Document v1waEkjR5yRN1LGymGDrm37Vm

COLUM BUS, O HIO OFFICE TW ELFTH FLOOR 21 E A S T S TATE S T R E E T CO LUM BUS. O H IO 43215-4221 614-221-2838 FAX: 614 -2 21 -2 0 07 Ro b e r t a . Bilott (513) 357-9638 bilott@taftlaw.com >)0 i>39 TAFT, STETTINIUS & HOLLISTER LLP 1800 FIRSTAR TOW ER 425 WALNUT STREET CINCINNATI, OHIO 45202-3957 513-381-2838 FAX: 5 1 3 -3 8 1 -0 2 0 5 w w w .taftlaw .com . A 6 . IJ U f March 6, 2001 Tt ~ 0 0 (o a NORTH ERN K EN TUCKY OFFICE THOMAS MORE CENTRE 2670 C H A N C E LLO R DRIVE C O V IN G T O N . K EN T U C K Y 4101 7-349 606-331-2638 513-381-2838 FAX: 513-381-6613 CLE VE LAN D . O HIO OFFICE SIXTH FLOOR BONO CO URT B U ILD IN G 1300 EAST NINTH STREET CLEVELAN D . O HIO 44114-1503 216-241-2838 FAX: 216-241-2637 CERTIFIED MAIL NO: 70000600002406963517 RETURN RECEIPT REQUESTED Christine T. Whitman Administrator United States Environmental Protection Agency 401 M. Street, S.W. Washington, DC 20460 FEDERAL EXPRESS The Honorable John D. Ashcroft Attorney General of the United States 5111 Main Street Building 10th Street and Constitution Avenue, N.W. Washington, DC 20530 FEDERAL EXPRESS Thomas Voltaggio Acting Regional Administrator United States Environmental Protection Agency Region III 1650 Arch Street Philadelphia, PA 19103-2029 FEDERAL EXPRESS Dr. Charles M. Auer Mary Dominiak United States Environmental Protection Agency Office Of Pollution, Prevention and Toxics Chemical Control Division 401 M Street, N.W., Room 403 Washington, DC 20460 FEDERAL EXPRESS John C. Cruden Assistant Attorney General United States Department of Justice Environment and Natural Resources Division -o 950 Pennsylvania Avenue, N.W. C5 t-o Washington, DC 20530-0001 FEDERAL EXPRESS CO wpn y--</crrIi Sarah Caspar United States Environmental Protection Agency Region III ac o oo rro- 841 Chestnut Building Philadelphia, PA 19107 f~ ' \ 1 L;U x - 1-- L'T c 'j -~ C O N T A IN N O C B I J .3 C) ;v R Oi 11 1 {u tU ^ '-O C'a -r 33Z 000:- USEPA 6461 March 6, 2001 Page 2 CERTIFIED MAIL NO: 70000600002406963524 RETURN RECEIPT REQUESTED Michael O. Callahan Director West Virginia Division of Environmental Protection 10 McJunkin Road Nitro, WV 25143 FEDERAL EXPRESS William Wentworth Project Manager United States Environmental Protection Agency Region III 1650 Arch Street Philadelphia, PA 19103-2029 FEDERAL EXPRESS West Virginia Health & Human Resources Department State Capital Complex Building 3, Room 206 Charleston, WV 25305 FEDERAL EXPRESS Allyn Turner Mike Zeto Water Resources/Waste Management Environmental Enforcement West Virginia Division of Environmental Protection 1356 Hansford Street Charleston, WV 25301-1401 FEDERAL EXPRESS Darrell V. McGraw, Esq. West Virginia Attorney General's Office State Capital Building Room 26E 1900 Kanawha Blvd., East Charleston, WV 25305 Re: Request For Immediate Governmental Action/Regulation Relating To DuPont's C-8 Releases In Wood County, West Virginia And Notice Of Intent To Sue Under The Federal Clean Water Act, Toxic Substances Control Act, And Resource Conservation And Recovery Act - NOTE: For Inclusion In USEPA Docket No. OPPTS-5Q639A_________________________________________________ Ladies and Gentlemen: Our law firm represents Wilbur Earl Tennant and Sandra K. Tennant (Route 3, Box 17, Washington, WV 26181, (304) 863-8787), James David Tennant and Della Marie Tennant (Route 3, Box 372, Parkersburg, WV 26101, (304) 863-5428), and Erwin Jackson Tennant (Route 3, Box 17A, Washington, WV 26181, (304) 863-6977) (collectively, the "Tennants") in connection with a lawsuit that is currently pending against E.I. duPont de Nemours & Co., Inc. ("DuPont") in Federal Court in Parkersburg, West Virginia, styled Tennant v. E.I. duPont de Nemours & Co., Inc., Civil Action No. 6:99-0488 (S.D. W.Va.). The Tennants have sued DuPont in connection with the release of various pollutants and contaminants from DuPont's Dry Run Landfill in Wood County, West Virginia. (See Exhibit 133.) The Tennants believe that OOOv-O.L March 6, 2001 Page 3 such releases have resulted in and continue to result in personal injury and property damage to the Tennants, including the death of several hundred head of the Tennants' cattle and serious health problems for the Tennants. During the course of the litigation, we have confirmed that the chemicals and pollutants released into the environment by DuPont at its Dry Run Landfill and other nearby DuPont-owned facilities may pose an imminent and substantial threat to health or the environment. More specifically, information currently available to the Tennants confirms that DuPont has been releasing and continues to release into the air, land, and water, including human drinking water supplies, an essentially unregulated, confirmed animal carcinogen known as ammonium perfluorooctanoate (a/k/a C-8/FC-143/APFO/PFOA) (CAS No. 3825-26-1) (hereinafter "C-8").1 Hundreds of head of cattle, along with numerous deer, fish, frogs, and other animals, have died in the area affected by the C-8 releases, and area residents exposed to the C-8 releases have been suffering ill health effects that are believed to be associated with C-8 exposure. For example, one of our clients, Wilbur Earl Tennant, has been in and out of the hospital repeatedly over the last few years suffering from respiratory problems, chemical bums, and other health problems after exposure to materials from the Dry Run Landfill. For the reasons discussed in more detail below, the Tennants hereby request that each of your agencies intervene in the Tennants' pending lawsuit and order the immediate investigation, assessment, containment, removal, and remediation of DuPont's C-8 releases into the environment from the Dry Run Landfill, including an order that DuPont immediately cease and desist all C-8 releases and that appropriate medical care/testing/evaluation be provided to the Tennants. The Tennants also request that DuPont's permit to operate the Dry Run Landfill be immediately revoked and that all operations at that landfill be suspended until adequate scientific demonstrations are made to prove that the C-8 releases have been abated and will not recur. In addition, the Tennants specifically request that USEPA exercise its authority under TSCA to order DuPont to immediately cease all manufacturing activities involving C-8 until DuPont can prove through appropriate scientific testing and research that its usage of C-8 does not pose an unreasonable risk of injury to health or the environment. In the meantime, the Tennants request that your agencies take those steps necessary to begin regulating C-8 releases into the environment. In that regard, the Tennants request that, at a minimum, USEPA include C-8 among the chemicals that it proposed in October of 2000 to regulate under TSCA on the grounds that the chemicals "may be hazardous to human health and the environment." (See Exhibit 123.) The Tennants believe that the information recently obtained from DuPont regarding C-8's potential threat to human health, (see e.g.. Exhibits 71, 125, and 126), warrants regulation of C-8 at least as aggressively as the related perflourinated chemicals manufactured by 3M. Currently available information also indicates unusual levels of iodide/iodine, along with Triton in Dry Run Creek. (See Exhibit 91.) OQOcO/; March 6, 2001 Page 4 This letter also constitutes notice on behalf of the Tennants and a class of other individuals similarly situated of their intent to bring citizen suit claims against DuPont in connection with DuPont's C-8 releases into air, land, and water from DuPont's Washington Works facility in Wood County, West Virginia under the Federal Clean Water Act ("CWA"), Toxic Substances Control Act ("TSCA"), and Resource Conservation and Recovery Act ("RCRA").2 The factual and legal basis of such citizen suit claims is explained in detail below. Additional documentation in support of the basic facts summarized below is available at our offices in Cincinnati, including a chronologically-organized database of the over 110,000 pages of documents produced to date by DuPont on this topic. I. DuPont Has Used C-8 Primarily At Its Washington Works Plant In Wood County, West Virginia.__________________________________________________________ C-8 is a perfluorinated detergent/surfactant manufactured in the United States by 3M Company that DuPont uses in connection with its manufacture of Teflon-related products. (See Exhibits 1 and 118.)3 DuPont has used C-8 as a reaction aid in its production of polytetrafluoroethylene (PTFE) and tetrafluoroethylene (TFE) co-polymers at its Washington Works facility outside Parkersburg, West Virginia since the early 1950s. (See Exhibit 118.) Wastes from the Washington Works' C-8 processes are either vented to the air following incineration, dumped into the Ohio River, sent to DuPont's Chambers Works facility in Deepwater, New Jersey for treatment and discharge, or disposed of at landfills. (See id.) The polymer product manufactured at the Washington Works is either sold directly to DuPont's customers (in the United States and abroad) or transferred to DuPont's Spruance Plant in Richmond, Virginia for use in the production of Teflon and PTFE-coated fibers or transferred to DuPont's Parlin Plant in Parlin, New Jersey for use in the production of Teflon finishes, some of which is then used in consumer cookware. (See id.) C-8 may remain in some of the products sold from DuPont's Washington Works, Spruance Plant, and Parlin Plant. (See id.) Some of DuPont's Teflon materials have been used in medical implants that are inserted directly into the human body. (See Exhibit 132.) Please note that, although the Tennants already have filed claims against DuPont under the CWA and RCRA, these pending claims relate only to releases from DuPont's Dry Run Landfill. This letter provides notice of the Tennants' intention to also bring separate claims against DuPont under the CWA, TSCA, and RCRA with respect to releases from DuPont's nearby Washington Works plant in Wood County, West Virginia, on behalf of themselves and a class of others similarly situated. DuPont's registered trademark. OGOUOt March 6, 2001 Page 5 II. DuPont Has Known That Excessive Exposure To C-8 Causes Adverse Effects. DuPont has worked closely with 3M since at least the 1970s to investigate the toxic and carcinogenic effects of C-8 on animal and human health. ("See id- and Exhibits 2, 24, and 49.) Through such company-sponsored studies, DuPont acquired knowledge by at least the early 1980s that C-8 was toxic and carcinogenic to animals, whether through inhalation, direct skin contact, or ingestion. (See Exhibits 12, 49, and 71.) Around the same time, DuPont also became aware that C-8 is biopersistent/bioaccumulative in animals and humans. (See Exhibits 30, 49 and 71.)4 In response to the mounting toxicity data on C-8, and because C-8 was essentially an unregulated chemical that, according to USEPA, had simply "sail[ed] under the agency regulatory radar screen" for decades, (see Exhibit 114), DuPont established in the 1980s its own internal standards for what it considered to be acceptable C-8 exposure levels for humans. For exposure to C-8 via air emissions/inhalation routes, DuPont determined that an "acceptable exposure limit" (AEL) for humans is 0.01 mg/m3(skin), with an acceptable "community exposure guideline" (CEG) for airborne emissions of 0.0003 mg/m3. (See Exhibits 2-4, and 9.) For human exposure to C-8 through contaminated water, DuPont established a CEG of 1 ppb. (See id.) DuPont also began routine monitoring of the levels of C-8 in the blood of its own employees, including employees at Washington Works, as early as 1981, (see Exhibit 118), and began looking for alternatives to C-8. By 1993, DuPont believed it may have found a viable, less toxic alternative to C-8, (see Exhibit 42), but decided to keep using C-8 anyway. Later in 1993, a study conducted by the University of Minnesota linked C-8 exposure with increased prostate cancer among human males. (See Exhibits 47 and 51.) By 1996, DuPont also had been informed that new tests were linking C-8 to DNA damage. (See Exhibit 60.) In response, DuPont, 3M, and others commissioned studies to further assess the potential effects of C-8 on humans through tests on monkeys. (See Exhibits 77, 84, 93, and 105.) By November of 1998, DuPont knew that one of the monkeys in the study receiving a 30 mg/kg dose of C-8 was suffering severe health effects. (See Exhibit 90.) By February of 1999, DuPont knew that one of the monkeys involved in the C-8 testing receiving the lowest dose of C-8 (3 mg/kg) had suffered such severe health effects that it had to be sacrificed. (See Exhibit 94.) By May of 1999, DuPont knew that a second monkey in the study had also suffered such severe health effects that it had to be sacrificed. (See Exhibits 103, 105, 107, 108 and 125.) The preliminary monkey study results also confirmed adverse liver effects among all of the monkeys in the study, regardless of exposure levels. (See id- and Exhibits 125 and 126.) Thus, because even exposure to the lowest DuPont also became aware of evidence as early as 1981 that at least two children bom to its Washington Works employees who worked with C-8 while pregnant appeared to have been bom with birth defects similar to those observed among rats exposed to high levels of C-8. (See Exhibit 13.) OOOvOi March 6, 2001 Page 6 dose of C-8 during the studies (3 mg/kg) produced adverse observable effects, a "no observable effects level" (NOEL) could not be found for C-8 in primates. (See Exhibits 105, 126.) 3M eventually notified USEPA of the preliminary results of the monkey study in a filing under TSCA, Section 8(e) during November of 1999. (See Exhibit 111.) Within only a few months, USEPA notified 3M that it intended to pursue more rigorous regulation of the perfluorinated chemicals manufactured by 3M. (See Exhibits 113 and 120.) Soon thereafter, 3M publicly announced that it would "voluntarily" withdraw from the market all of its perfluorinated chemical products, including the C-8 that it sells to DuPont for use in DuPont's Teflon products, and the chemicals 3M uses to make its Scotchguard products. (See Exhibits 113 and 114.)5 After learning that DuPont was one of the principal users of 3M's C-8 product, USEPA's TSCA Division requested in April of 2000 that DuPont supply information regarding DuPont's usage and release of C-8 within the United States. (See Exhibit 112.) DuPont produced some C-8 research data to USEPA on May 25, 2000, (see Exhibit 115), followed by preliminary usage and release information in a letter dated June 23, 2000. (See Exhibit 118.) In its C-8 disclosure letter to USEPA, DuPont confirmed that it has used C-8 primarily at its Washington Works site and that it had released C-8 into the air, water, and land at the Washington Works, into water at its Parlin Plant, Spruance Plant, and Chambers Works, into soils at the Chambers Works, and into soil and water at the "Local," Letart, and Dry Run Landfills owned and operated by DuPont near the Washington Works in West Virginia. (See id.) DuPont did not, however, reference any of the results of the C-8 monkey studies. (See id.) On October 18, 2000, USEPA proposed to begin regulating most of 3M's perfluorinated chemicals under TSCA on the grounds that the chemicals "may be hazardous to human health and the environment." (See Exhibit 123 (65 Fed. Reg. 62319-33 (Oct. 18, 2000)).) USEPA deferred, however, regulation of C-8, pending further review of the information being obtained from 3M and DuPont. After receiving a draft of this letter in November of 2000, DuPont sent revised C-8 usage and release information to USEPA in a letter dated January 25, 2001. (See Exhibit 136.) As of today's date, however, the Tennants are not aware of the results of the C-8 monkey studies having been "finalized" or published. III. DuPont Promised Not To Dispose Of Toxins Like C-8 In Its Dry Run Landfill. In the early 1980s, DuPont approached the Tennants seeking to buy several hundred acres of the Tennants' property for the purposes of constructing a landfill near the base of Dry Run Creek in Wood County, West Virginia. (See Exhibit 14.) In response to initial resistance from the Tennants to the idea of selling any portion of their land for a landfill, DuPont promised the Tennants that no hazardous materials would ever be disposed of in the landfill. (See Exhibit 14.) After receiving DuPont's verbal and written assurances that no harmful chemicals would ever be disposed of in the proposed landfill and that the Tennants would be permitted to graze their s 3M's registered trademark. 00 0(0 March 6, 2001 Page 7 cattle along the adjacent Dry Run Creek,6the Tennants eventually agreed to sell a portion of their property to DuPont for construction of the "non-hazardous" landfill. DuPont received a permit to operate the Dry Run Landfill as an unlined, non-hazardous, solid waste landfill in 1982, and began actual landfilling operations at the Landfill in 1984. (See Exhibit 5.) IV. DuPont Has Dumped Thousands Of Tons Of C-8 Wastes Into The Dry Run Landfill._________________________________________________________ Soon after DuPont began operating the Dry Run Landfill in 1984, DuPont received the results of internal sampling confirming that C-8 was leaching into groundwater beneath three old, unlined anaerobic digestion ponds at the Washington Works that DuPont previously had used for the disposal of thousands of tons of C-8-soaked sludges. (See Exhibits 9, 17, 20, and 31.) DuPont's internal sampling indicated that, not only was C-8 getting into the groundwater that DuPont used for the Washington Works' drinking water, but C-8 also was migrating through the groundwater under the Washington Works and into the Lubeck Public Service District's ("Lubeck PSD's") immediately-adjacent public drinking water wells. (See Exhibits 17, 18, 20, and 31.) Internal DuPont sampling confirmed C-8 in the Lubeck PSD community drinking water supply as high as 1.5 ppb in 1984, (see Exhibits 17, 18, and 20), increasing to as high as 1.9 ppb in 1987, (see Exhibits 19 and 20), and further increasing to as high as 2.2 ppb in 1988 (see Exhibits 27 and 28. See also Exhibit 33.) All of these levels exceed DuPont's own 1 ppb CEG for community drinking water. (See Exhibits 2-4, and 9.) Upon receipt of those results, DuPont decided to try to remove the source of the C-8 in the public and company drinking water supplies by digging up and removing the sludges from Washington Works' three anaerobic digestion ponds and dumping the tons of C-8-contaminated sludge7into the Dry Run Landfill. (See Exhibits 20, 21, 22, 23, and 26.) After DuPont submitted data to the West Virginia Division for Environmental Protection ("WVDEP") asserting that the sludges were "non-hazardous" under RCRA, WVDEP granted DuPont permission to dispose of approximately 7,100 tons of the sludge in the unlined Dry Run Landfill. (See Exhibits 21, 23, and 25.) DuPont completed the sludge disposal in 1988. (See Exhibit 6.) Rather than abate the presence of DuPont's C-8 in the public drinking water supply, DuPont simply purchased the Lubeck PSD well property and the wells were moved approximately two miles further down-gradient from the Washington Works. (See Exhibits 9, 30, 31, and 97.) DuPont then notified its employees to immediately cease all sampling of the DuPont even agreed to lease back to the Tennants for cattle pasture significant portions of the landfill property along the Dry Run Creek. Those leases remained in effect until the Tennants began complaining about the Dry Run Landfill to USEPA. (See Exhibit 5.) DuPont confirmed C-8 levels as high as 610 ppm in the sludge taken from the three ponds. (See Exhibit 9.) OOOt; if' March 6, 2001 Page 8 former Lubeck PSD wells and to destroy all previously-drawn, unanalyzed Lubeck PSD well samples. (See Exhibit 29.) Also in 1989, WVDEP informed DuPont that new landfill regulations had gone into effect in the State of West Virginia requiring existing, unlined landfills to be upgraded with more rigorous waste containment mechanisms, including liners and more extensive groundwater monitoring well systems. (See Exhibit 32.) In response, DuPont installed a series of new groundwater monitoring wells at its Dry Run Landfill and at its nearby, unlined Letart Landfill in Mason County, West Virginia where DuPont had been disposing of most of its Teflon and other C-8 wastes from the Washington Works as non-hazardous solid waste since the 1960s. (See Exhibit 121.) After DuPont's initial groundwater sampling at the Letart Landfill confirmed the presence of C-8 at 0.7 ppm, (see Exhibit 9), DuPont began investigating whether any C-8 also was leaching out of the waste at the Dry Run Landfill. (See Exhibit 6.) By April of 1990, DuPont had confirmed that C-8 was, in fact, leaching from the Dry Run Landfill and discharging directly into the Dry Run Creek at levels as high as 1.6 ppm - more than 100 times DuPont's own internal standard for drinking water of 1 ppb. (See Exhibits 9, 35, 37, 41, and 136.) Soon thereafter, DuPont abandoned its efforts to seek a new permit for the Letart Landfill, and notified WVDEP that it had decided, instead, to simply close that landfill "for economic reasons." (See Exhibits 74 and 121.) DuPont proceeded, however, with its efforts to get a revised permit for the Dry Run Landfill that would allow DuPont to continue to operate the landfill without having to install a liner. (See Exhibit 50.) After confirming elevated C-8 levels in the water at Dry Run, DuPont began investigating how to get rid of the approximately 7,100 tons of C-8-contaminated sludge that it dumped into the landfill in 1988, which DuPont assumed was a source of the C-8 being detected in Dry Run Creek. (See Exhibits 7, 8 and 38.) Although DuPont initially notified WVDEP that it would remove the C-8-contaminated sludges from the Dry Run Landfill and dispose of the material at its Letart Landfill, (see Exhibits 36 and 39), DuPont simply moved the sludges to another location within the Dry Run Landfill in 1991. (See Exhibits 5 and 6.) By the summer of 1993, WVDEP inspectors noticed increasingly excessive amounts of sediment and discoloration building up in the leachate collection ponds at the Dry Run Landfill. (See Exhibit 44.) In response, DuPont, despite knowledge that the leachate contained high levels of C-8 and despite knowledge that the Tennants' cattle were drinking the water in Dry Run Creek, ordered the drains on its leachate collection ponds opened for more than two weeks (after monthly sampling had been completed (see Exhibit 45)), so that the leachate could flow out of After DuPont finally shut down its unlined, "non-hazardous" Letart Landfill in 1996, it began paying to dispose of its C-8-contaminated wastes at a RCRA hazardous waste facility in Alabama. (See Exhibit 121.) 0 0 0 `. c ' March 6, 2001 Page 9 the ponds and directly into the Dry Run Creek. (See Exhibits 46 and 86.)9 Although WVDEP requested that DuPont submit acute toxicity sampling results for the leachate being discharged out of the sedimentation ponds, (see Exhibit 44), DuPont successfully avoided taking any such samples until four months after the original leachate had drained into the creek. (See Exhibit 48.) The acute toxicity results that DuPont did eventually submit to WVDEP confirmed a 15% mortality, even among neonates exposed to the water four months later. (See id.) In the meantime, dozens of the Tennants' cattle were dying along the Dry Run Creek bed and the Tennants and their family and friends were exposed to C-8. By the fall of 1994, DuPont had adopted a corporate plan to start routinely dumping C-8 wastes into the Dry Run Landfill, in anticipation of the upcoming closure of its Letart Landfill. (See Exhibit 130.) Thus, in furtherance of this corporate plan, but without any authorization or approval of any kind from WVDEP, DuPont began dumping its C-8-contaminated biocake wastes into the Dry Run Landfill that Fall. (See Exhibits 5 and 86.) According to DuPont's own analyses, the biocake contained 930 ppb of C-8. (See Exhibits 6, 58, 85, and 87.) By the spring of 1995, discolored, foul-smelling water was observed being discharged out of the Dry Run Landfill sedimentation ponds into Dry Run Creek, with almost knee-high suds and foam present along the Dry Run Creek bed, which DuPont assumed contained C-8. (See Exhibits 5, 53, 54, 56, 88 and 91.) At the same time, even more of the Tennants' cattle were dying. In response to repeated pleas from the Tennants that WVDEP force DuPont to take action to address the black odorous water and foam being discharged into the Dry Run Creek where their cattle were drinking and dying, WVDEP notified DuPont that it would need to start taking steps to address its improper discharges into Dry Run Creek and to upgrade the Dry Run Landfill. (See Exhibits 5 and 57.) After it became evident that little progress was being made by DuPont in response to WVDEP's requests,10the Tennants notified USEPA of the problem and provided copies of videotapes showing the discolored foaming water and dead animals along the Dry Run Creek bed. (See Exhibit 61.) Around the same time, the West Virginia Department of Natural Resources contacted DuPont in response to recent reports of numerous deer killed or dying in the area of the Dry Run Creek. (See Exhibit 59.) Despite such complaints, DuPont did nothing to disclose to the Tennants that C-8 was in the Dry Run Creek, nor did DuPont suggest in any way to the Tennants that their cattle should not be drinking the water in the Creek. (See Exhibit 74.) Instead, DuPont kept silent on the C-8 issue and took the position with the public and the regulatory agencies that all of the problems with the creek were simply the result of some high DuPont also ordered the landfill drain opened in 1989 and again in 1995 so that the contents of the sedimentation pond could flow directly into Dry Run Creek, without any apparent notice to or permission from WVDEP. (See Exhibits 34 and 55.) Discolored, foaming water continued in Dry Run Creek throughout the remainder of 1995, 1996, 1997, 1998, and into 1999.) (See Exhibits 62, 63, 89, and 92.) March 6, 2001 Page 10 iron sulfide levels that had been fully addressed and completely resolved. (See Exhibits 5, 74, and 78.)" In October of 1996, USEPA contacted DuPont and informed the company that it would be initiating an inspection of the Dry Run Landfill in response to the recent reports of hundreds of dead cattle and deer in the area of the Dry Run Creek. (See Exhibits 5, 64, and 68.) On the exact same day that DuPont learned of USEPA's pending inspection, Eli McCoy (with WVDEP's Water Division) forwarded to DuPont a draft complaint to aid DuPont in diffusing any potential enforcement action by USEPA relating to the discharge problems at the Dry Run Landfill. (See Exhibits 5 and 65.) Within a matter of weeks, DuPont completed its negotiations with the State and entered a consent decree to bar further governmental enforcement action in exchange for DuPont's payment to WVDEP of a $200,000 penalty. (See Exhibits 5, 67, and 69.) Soon thereafter Mr. McCoy left WVDEP and began working for the same DuPont consultant that would assist DuPont in complying with the consent decree - Potesta & Associates. (See Exhibit 73.) As part of the December 1996 settlement with WVDEP, DuPont finally agreed to begin implementing upgrades to the Dry Run Landfill, such as installation of the type of liner that was required under the State's landfill regulations since 1988, and construction of a leachate collection system. (See Exhibits 66 and 69.) DuPont also finally agreed to cease the disposal of its biocake wastes at the Dry Run Landfill. (See jd.) Thus, by the time USEPA actually commenced its ecological risk assessment activities in the Dry Run Landfill area in 1997, DuPont allegedly had stopped disposing of its C-8-contaminated biocake sludge at the Dry Run Landfill and had allegedly begun collecting C-8-contaminated leachate from the Landfill for transport to the Washington Works for treatment and discharge directly into the Ohio River. (See Exhibits 5, 70, and 72.) By the end of 1997, USEPA released to DuPont a draft of its Ecological Risk Assessment Report for the Dry Run Landfill. (See Exhibit 75.) USEPA's report indicated that, although adverse impacts were clearly evident among numerous animals, plants, and other wildlife in the area of the Dry Run Creek, USEPA had not been able to identify any particular known, regulated chemical as the clear cause of the observed problems. (See id. at 52) USEPA, therefore, recommended further assessment and identification of numerous "tentatively identified compounds" that had been detected in various environmental media in the area of Dry Run Creek that might be contributing to the problems. (See |d.) In response to the suggestion of further governmental investigation, DuPont immediately requested and USEPA agreed to discuss a "collaborative" effort to further investigate conditions in the area of Dry Run Creek. (See DuPont's practices with respect to making public the company's knowledge of the toxicity of its products was addressed in detail in In re E.I. duPont de Nemours & Co.. 918 F. Supp. 1524 (M.D. Ga. 1995) (court imposed over $100 million in sanctions against DuPont). 0 0 0 (: March 6, 2001 Page 11 Exhibits 79 and 83.) Part of that collaborative effort included DuPont's agreement that it would disclose more fully the precise identities of each of the various types of chemicals it had dumped into the Dry Run Landfill that DuPont had not previously identified for USEPA. (See Exhibit 83.) Although DuPont had been monitoring C-8 levels in Dry Run Creek for years and had confirmed C-8 in the water each time, DuPont eventually identified C-8 as being only "possibly" present in the Dry Run Landfill in a list of dozens of chemicals that it sent to USEPA in late 1998 - almost a year after the USEPA had completed its draft Risk Assessment Report. (See Exhibit 83.)12 Because of USEPA's persistent concerns that something in the Dry Run Creek was killing hundreds of head of the Tennants' cattle, (see Exhibit 78),13DuPont also agreed to jointly fund an investigation into the health of the Tennants' cattle. Specifically, DuPont agreed in the Spring of 1999 to create a "Cattle Team" to "independently" investigate such issues. By that time, however, less than a few dozen of the Tennants' cattle were even still alive. The Cattle Team was comprised of three veterinarians selected by DuPont, including Greg Sykes, a DuPont employee who had been involved in DuPont's internal investigations into the effects of C-8 on animals for many years, (see Exhibit 24), and three veterinarians selected by USEPA. (See Exhibit 95.) Despite DuPont's knowledge that C-8 was a toxic animal carcinogen (as reenforced to DuPont by the recent C-8 monkey study results (see, e.g.. Exhibits 87 and 166)), that the Tennants' cows were drinking out of Dry Run Creek, the information currently available to the Tennants does not indicate that anyone from DuPont ever disclosed such facts to the other members of the Cattle Team during the course of the Cattle Team's investigation. (See Exhibit 93.) Consequently, there is no evidence that the Cattle Team even considered the potential impact of C-8 on the Tennants' cattle, despite the release of the C-8 monkey study results to DuPont well before the final Cattle Team Report was released in December of 1999. (See Exhibit 109.) Again, DuPont kept completely silent on the C-8 issue and sat back and let the Cattle Team "independently" investigate the health of the Tennants' cattle, even though the USEPA-appointed Cattle Team members would never have any reason even to think to look at C-8. Over the last several years, while DuPont was working with USEPA on their "collaborative" effort to address environmental problems in the area of Dry Run Creek, several of the Tennants have been in and out of the hospital suffering from respiratory problems, chemical At around the same time, DuPont, again, ordered the Dry Run Landfill sedimentation pond drain opened, so that the foul-smelling contents could discharge directly into the Dry Run Creek where the few remaining head of the Tennants' "[cjattle were wallowing in the stream just beyond the fence." (See Exhibits 81 and 82.) At least two other local residents, including at least one current DuPont employee, also have complained that their cattle appear to have been harmed by something in Dry Run Creek. (See Exhibits 54 and 117.) March 6, 2001 Page 12 bums, and other health problems after having been exposed to fugitive air emissions and liquid discharge from DuPont's Dry Run Landfill. Moreover, despite installation several years ago of a leachate collection system that was supposed to prevent contaminants from the Dry Run Landfill from getting into the Dry Run Creek, DuPont's own monitoring reports confirm that C-8 is still getting into the Dry Run Creek with results as high as 87 ppb in the creek, as recently as the Summer of 1999, and as high as 27.6 ppb during the Fall of 2000 - readings more than twenty times DuPont's CEG for C-8 in water. fSee Exhibit 134.) Thus, DuPont's own monitoring reports confirm that, despite installation of a purported leachate collection system, there is a continuing, ongoing discharge of high levels of C-8 from the Dry Run Landfill into Dry Run Creek. V. DuPont Has Known That Its C-8 Wastes Have Leached Into Drinking Water. In addition to DuPont's failure to disclose to the Tennants or the USEPA-appointed Cattle Team members the full extent of its knowledge regarding the nature, extent, and likely effects upon wildlife of the C-8 it has been releasing and continues to release into Dry Run Creek, the information currently available to the Tennants indicates that DuPont also has not fully disclosed to USEPA, WVDEP, local governmental entities, its neighbors, or the public its knowledge of the full extent of the impact of its C-8 wastes on local drinking water. As part of its efforts to complete its RCRA Facility Investigation Report ("RFI Report") for the Washington Works, DuPont was required to investigate whether any of its former solid waste management units, including the three anaerobic digestion ponds that were closed in 1988, are contributing to any release of wastes onto neighboring properties and whether any wastes are exposing any persons to unreasonable health risks. (See Exhibits 98 and 99.) In connection with its RFI efforts, DuPont took more samples of the groundwater under the Washington Works site that it uses for drinking water at the Plant. (See Exhibits 10,11, 76, and 99.) DuPont also arranged for the sampling of groundwater under the neighboring GE Plastics Plant that GE uses for its own plant drinking water. (See Exhibits 10 and 11.) Sampling confirmed C-8 in the Washington Works' drinking water as high as 3.3 ppb14and as high as 0.71 ppb in the neighboring GE Plastics drinking water supply. iSee Exhibits 10, 11,43, 76, 96, 99, 102, 104, It is noted that, although DuPont had been sampling three drinking water wells at the Washington Works (wells 331, 332, and 336), when it came time to actually report the results to USEPA in its RFI Report, Dupont was careful to sample only the drinking water well that had previously yielded C-8 results less than 1 ppb (well 336), and conveniently did not even sample the wells that traditionally had yielded the higher C-8 results, nor did DuPont report these higher results in its RFI Report. (See Exhibits 76, 96, 99). Yet, when even the well with the C-8 readings traditionally below 1 ppb yielded a result of 1.9 ppb, DuPont fabricated a new 3.0 ppb "screening level" for C-8 to avoid having to reference any drinking water results exceeding DuPont's own l ppb CEG in its own plant drinking water. iSee Exhibit 99). March 6, 2001 Page 13 106, 110 and 129.) DuPont even found C-8 as high as 0.8 ppb in the new Lubeck PSD drinking water wells, which are now located approximately two miles farther away from the Washington Works site. (See Exhibits 10-11, 40, and 41.)15 Recent sampling of the private drinking water wells on the Tennants' property down-gradient from the Dry Run Landfill also has now confirmed C-8 in those drinking water wells. (See Exhibit 131.) DuPont has even investigated what C-8 levels might be present at various cities along the Ohio River, based upon DuPont's on going releases of C-8 into the River from the Washington Works facility. (See Exhibits 40, 100, and 118.)16 Approximately 24,000 pounds of C-8 also is discharged directly into the air every year from the Washington Works Site, although it is not clear that C-8 is actually permitted for such air discharge by DuPont. (See Exhibits 101 and 118.) Thus, it is evident that the residents living in at least the area near DuPont's Washington Works facility, Letart Landfill, and Dry Run Landfill (the "DuPont Sites") may have been and may continue to be exposed to DuPont's C-8 through DuPont's on-going and continuous releases of C-8 into the air, land, and water at and/or around those Sites, (see Exhibit 80), including direct ingestion of C-8 in the C-8-contaminated drinking water extracted from wells at the Washington Works Plant, the neighboring GE Plastics Plant, the Lubeck PSD well fields, and private residential and agricultural properties near DuPont's Sites.17 Local wildlife and the environment may be similarly exposed. Despite DuPont's knowledge for years of the nature, extent, and effect of these C-8 releases on human health and the environment, including the Sampling results from 1991 confirmed C-8 at 2.4 ppb in the new Lubeck wells with C-8 levels as high as 3.9 ppb in the tap water of several local, Lubeck-area homes. (See Exhibit 128.) Sampling in August of 2000 confirmed C-8 still present in the new Lubeck PSD wells at levels as high as 0.59 ppb. (See Exhibit 119.) DuPont has been evaluating the levels of C-8 in the Ohio River, which is a source of drinking water for numerous communities, since at least 1982. (See Exhibit 15.) In August of 2000, after the Tennants had made it known to DuPont that they had become aware of the C-8 in the Lubeck PSD wells, DuPont drafted a letter for the Lubeck PSD to send to its water customers to "disclose" the existence of the C-8. (See Exhibit 124.) In that letter, however, DuPont was very careful to refer only to the current C-8 levels in the current Lubeck PSD wells, and avoided any mention whatsoever of the earlier C-8 readings that were substantially above DuPont's 1 ppb CEG. (See id.) DuPont again was careful to avoid any public disclosure of its knowledge of earlier C-8 drinking water results that were well-above DuPont's 1 ppb CEG in recent statements provided to local Parkersburg newspapers, even though DuPont had received in November a draft of this letter referencing the higher C-8 levels. (See Exhibit 135.) 0 0 9 Gi March 6, 2001 Page 14 bioaccumulative/biopersistent nature of the material,18it appears that DuPont has allowed and continues to allow these releases to occur unabated for fear of not being able to continue to make its Teflon products, if it cannot use C-8. This situation is particularly disturbing, given that DuPont apparently has known of ways to remediate C-8-laden soils since the early 1990s but because of the expense, chose to do nothing "pending further actions that may be dictated by the EPA for remediation of the Washington Works site." (See Exhibit 122.) Even more disturbing is the fact that DuPont has known for years that C-8 levels in the Washington Works and old Lubeck PSD drinking water wells far exceeded its own 1 ppb CEG but has done absolutely nothing in response. DuPont has chosen, instead, to focus either on current, somewhat lower C-8 levels, or to simply fabricate a totally new drinking water "screening level" of 3 ppb for the Washington Works Plant when faced with having to disclose to USEPA in its RFI report for the Washington Works the existence of C-8 in the Plant's drinking water at levels well above 1 ppb. (See Exhibits 99 and 124.) VI. DuPont Should Be Ordered To Remediate Its C-8 Releases And To Immediately Shut Down Its Manufacturing Processes Involving C-8 Until Adequate Demonstrations Are Made That There Is No Unreasonable Risk To Health Or The Environment.____________________________________________________________ Over the years, DuPont has successfully avoided fully disclosing the nature and extent of the C-8 problem at its Dry Run Landfill by characterizing C-8 as an unregulated "non-hazardous" waste and/or substance under applicable law. Consequently, when the Federal and State agencies have asked questions about the nature and quantity of toxic wastes handled by DuPont at the Dry Run Landfill, DuPont has omitted any comprehensive discussion of C-8 on the grounds that it is not a "hazardous waste," "hazardous substance," or otherwise listed or regulated waste under current laws. DuPont shrewdly avoided any permit limits on its C-8 emissions and/or dumping at its Washington Works facility and Dry Run Landfill through similar corporate strategies. Thus, although DuPont has known for years that C-8 is an animal carcinogen and bioaccumulative/biopersistent substance, it has continued to knowingly dump thousands of tons of the waste into the environment at unlined, uncontrolled landfills and has allowed the waste to be disposed directly into the air, Ohio River, and local drinking water supplies, arguing that there has not been any improper disposal and/or release of any regulated material. In addition, DuPont has been careful to refer to the chemical in conflicting, inconsistent ways in its filings with regulatory agencies - sometimes calling it "C-8," sometimes calling it "FC-143," sometimes calling it "PFOA," sometimes calling it "APFO," and sometimes calling it by its full chemical name - "ammonium perfluorooctanoate" - thereby making it difficult for the agencies to understand how all the information interrelates. As confirmed by USEPA's recent DuPont's own employees even raised concerns about Teflon customer exposure to C-8 as early as 1983. (See Exhibits 16 and 52.) 0 0 0 .-f March 6, 2001 Page 15 proposal to begin regulating 3M's previously-unregulated perfluorinated chemicals, DuPont's past corporate strategy for diverting regulatory attention away from C-8 should stop now. Based upon the foregoing facts, the Tennants hereby respectfully request that your agencies intervene in the Tennants' pending Federal Court litigation and order the immediate investigation, assessment, containment, removal, and remediation of DuPont's on-going C-8 releases into the environment by virtue of the authority granted to your agencies under at least the following laws and their implementing regulations: The Toxic Substances Control Act, as amended, 15 U.S.C. 2601-2692; The Federal Clean Water Act, as amended, 33 U.S.C. 1251-1387; The Safe Drinking Water Act, as amended, 42 U.S.C. 300f-300j-26; The Federal Clean Air Act, as amended, 42 U.S.C. 7401-7671q; The Resource Conservation and Recovery Act, as amended, 42 U.S.C. 6901-6992k; The Comprehensive Environmental Response, Compensation and Liability Act, as amended, 42 U.S.C. 9601-9675; The West Virginia Air Pollution Control Act, W.Va. Code 22-5-1 through 22-5-18;. The West Virginia Water Pollution Control Act, W.Va. Code 22-11-1 through 22-11-28; The West Virginia Groundwater Protection Act, W.Va. Code 22-12-1 through 22-12-14; The West Virginia Natural Streams Preservation Act, W.Va. Code 22-13-1 through 22-13-15; The West Virginia Solid Waste Management Act, W.Va. Code 22-15-1 through 22-15-21; The West Virginia Hazardous Waste Management Act, W.Va. Code 22-18-1 through 22-18-25; and 0 0 0 0 ITS March 6, 2001 Page 16 The West Virginia Hazardous Waste Emergency Response Fund Laws, W.Va. Code 22-19-1 through 22-19-6. The Tennants also request that your agencies exercise their respective authority under the referenced laws to order DuPont to immediately cease and desist its C-8 releases into the environment, as addressed in this letter and to provide for immediate, appropriate medical care/testing/evaluation of the Tennants. The Tennants further request that DuPont's permit to operate the Dry Run Landfill be immediately revoked until adequate scientific demonstrations are made to prove that the C-8 releases have been abated, will not recur, and pose no unreasonable risk to human or animal health or the environment. With respect to minimizing harm to the public health and the environment from future C8 releases, the Tennants hereby specifically request that USEPA exercise its authority under the Toxic Substances Control Act to order DuPont to immediately cease all manufacturing activities using C-8, including DuPont's Teflon manufacturing operations, until DuPont either confirms that it has stopped its usage of C-8 entirely or has made adequate scientific demonstrations to prove that its continued usage of C-8 (whether from 3M or any other source) does not pose an unreasonable risk of injury to health or the environment. In the meantime, the Tennants request that your agencies take these steps necessary to regulate C-8 emissions/releases to the environment. As mentioned above, the Tennants believe that such steps should include, at a minimum, including C-8 among the list of perfluorinated chemicals that USEPA proposed in October of this year to begin regulating under TSCA on the basis that the chemicals "may be hazardous to human health and the environment." (See Exhibit 123.) VII. The Tennants Intend To Bring Citizen Suit Claims Against DuPont Under The CWA, TSCA, And RCRA If Appropriate Action Is Not Taken Immediately To Abate And Remediate DuPont's C-8 Releases From Its Washington Works Facility. As explained above, DuPont has been and continues to discharge C-8 from its Washington Works Facility in Wood County, West Virginia into the air, groundwater, and Ohio River. Moreover, the C-8 discharged by DuPont has been contaminating and continues to contaminate the land, air, and human and animal drinking water supplies. A. DuPont Is Violating The CWA. Section 505(a)(1) of the Clean Water Act ("CWA") permits citizens to commence a civil action against "any person ... who is alleged to be in violation of (A) an effluent standard or limitation under this chapter." 33 U.S.C. 1365(a)(l). "Effluent standard or limitation" is defined under the CWA to include, among other things, "a permit or condition thereof issued under Section 1342 of this title," such as state-issued but federally-enforceable NPDES discharge permits. Id. at 1365(F). Based upon information currently-available to the Tennants, DuPont's NPDES permit for its Washington Works facility specifies that DuPont shall not discharge any O iK /ui:, March 6, 2001 Page 17 effluent in violation of applicable Water Quality Standards. (See, e.g.. WV/NPDES Permit No. WV0001279, Conditions A. 1 - A.10, C.12, and H.2). The West Virginia Water Quality Standards prohibit DuPont from discharging into surface or groundwaters any "materials in concentrations which are harmful, hazardous, or toxic to man, animal, or aquatic life." W. Va. Code St. R. tit. 46, 46-1-3.2 (2000). Based upon currently-available information, as described above, DuPont has been discharging and continues to discharge C-8 into surface and groundwaters in concentrations exceeding DuPont's own CEG for human drinking water and at concentrations that are otherwise harmful, hazardous, or toxic to man, animal, or aquatic life, constituting a continuing violation of the West Virginia Water Quality Standards, and thereby constituting a continuing violation of DuPont's NPDES permit terms and the CWA. See, e.g.. 33 U.S.C. 1311(a), 1342. Notice is, therefore, hereby provided that the Tennants, on behalf of themselves and a class of others similarly situated, intend to file suit against DuPont, pursuant to Section 505(a)(1) of the CWA, within sixty (60) days of this notice to obtain appropriate relief for the violations of the CWA referenced herein. B. DuPont Is Violating TSCA. Section 20(a)(1) of the Toxic Substances Control Act ("TSCA") permits citizens to commence a civil action against "any person . .. who is alleged to be in violation of [TSCA] or any rule promulgated under Sections 2603, 2604, or 2605 of [TSCA], or Subchapters II or IV of [TSCA]." 15 U.S.C. 2619(a)(1). TSCA requires any "person who manufactures, processes, or distributes in commerce a chemical substance or mixture and who obtains information which reasonably supports the conclusion that such substance or mixture presents a substantial risk of injury to health or the environment" to "immediately" inform USEPA of "such information, unless such person has actual knowledge that" USEPA has been adequately informed of such information. Id. at 2607(e). TSCA also requires each person who manufactures or processes a chemical substance to comply with the regulations adopted by USEPA under TSCA governing the reporting to USEPA of certain research and adverse health effects information relating to such chemical substances. See id. at 2607(a), (c), (d); 40 C.F.R. Parts 716 and 717. Failure to comply with such TSCA requirements constitutes a violation of TSCA. See 15 U.S.C. 2614. As indicated above, the information currently available to the Tennants indicates that DuPont has not reported to USEPA all information within DuPont's possession regarding C-8 that is required to be reported to USEPA under Section 8(a), (c), (d), and (e) of TSCA, 15 U.S.C. 2607 (a), (c), (d), and (e), such as the results of the C-8 monkey studies and the Tennants' allegations of adverse health effects among themselves, their cattle, and area wildlife arising from exposure to DuPont's C-8. Notice is, therefore, hereby provided that the Tennants, on behalf of themselves and a class of others similarly situated, intend to file suit against DuPont, pursuant to Section 20(a)(1) of TSCA, within sixty (60) days of this notice to obtain appropriate relief for the violations of TSCA referenced herein. 00001/ March 6, 2001 Page 18 C. DuPont's C-8 Releases From Its Washington Works Facility May Present An Imminent And Substantial Endangerment To Health Or The Environment Under RCRA.___________________________________ Section 7002(a)(1)(B) of the Resource Conservation and Recovery Act ("RCRA") permits citizens to commence a civil action against: [a]ny person including any past or present generator, past or present transporter, or past or present owner or operator of a treatment, storage, or disposal facility, who has contributed or who is contributing to the past or present handling, storage, treatment, transportation, or disposal of any solid or hazardous waste which may present an imminent and substantial endangerment to health or the environment. 42 U.S.C. 6972(a)(1)(B). As discussed above, DuPont's past and on-going disposal of C-8 into soil, water, and air from DuPont's Washington Works Facility has resulted in C-8 in soil, water, and air at and/or around the Washington Works Facility in amounts, levels, and/or concentrations which, based upon the currently-available information, may present an imminent and substantial endangerment to health or the environment. Notice is, therefore, hereby provided that the Tennants , on behalf of themselves and a class of others similarly situated, intend to file suit against DuPont, pursuant to Section 7002(a)(1)(B) or RCRA, within ninety (90) days of this notice to obtain appropriate relief for the imminent and substantial endangerment referenced herein. Please confirm as soon as possible how your respective agencies plan to address our request for your involvement in this important public health and environmental matter. In that regard, please let us know if you will intervene in the Tennants' Federal Court proceedings or if 0 0 0 0 :1 8 March, 2001 Page 19 you would like to review any of the additional backup documentation maintained here at our Cincinnati offices. We would be happy to meet with you at your offices to discuss this matter in more detail. Thank you. On behalf of the Tennants, r. iliM-- Robert A. Bilott RAB/mdm Enclosures cc: Larry A. Winter, Esq. (West Virginia Counsel for the Tennants) (w/o ends.) Paula Durst Gillis, Esq. (Counsel for DuPont) (w/ ends.) (by CERTIFIED MAIL NO: 70000600002406963531, RETURN RECEIPT REQUESTED & REGISTERED MAIL NO: R410009299, RETURN RECEIPT REQUESTED) Registered Agent for E.I. duPont de Nemours & Co., Inc. (w/o ends.) (CT Corporation System, 707 Virginia Street, East, Charleston, WV 25301 by CERTIFIED MAIL NO: 70000600002406963500) H:\TENNANT\RequestLtr.wpd 0 0 0 0 .2 0 DuPont Material Safaty Data Sheet Page 1 05573515 C8 solution Revised 6-MAY-1999 Printed 6-MAY-1999 CHEMICAL PRODUCT/COMPANY IDENTIFICATION Tradename and Synonyma 20% Ammonium Perfluorooctanoate Solution Company Identification MANUFACTURER/DISTRIBUTOR DuPont 1007 Market Street Wilmington, DE 19898 PHONE NUMBERS Product Information s 1-800-441-7515 Transport Emergency s CHEMTREC 1-800-424-9300 Medical Emergency : 1-800-441-3637 COMPOSITION/INFORMATION ON INGREDIENTS Components Material Ammonium Perfluorooctanoate Water CAS Number 3825-26-1 7732-18-5 % 20 80 HAZARDS IDENTIFICATION Potential Health Effects Skin contact may cause skin irritation with discomfort or rash. Evidence suggests that skin permeation can occur in amounts capable of producing the effects of systemic toxicity. Eye contact may cause eye irritation with discomfort, tearing, or blurring of vision. Inhalation may cause irritation of the upper respiratory passages, with coughing and discomfort. Ingestion may cause gastrointestinal tract irritation; abnormal liver function as detected by laboratory tests; or abnormal blood forming system function with anemia. This compound is absorbed by the body and may be detected in the blood stream following ingestion, inhalation or skin contact. Animal and human experience indicate that this compound has a long half-life in the blood, and may be oooc EID087263 0SS73S1S DuPont Material Safety Data Sheet Page 2 (HAZARDS IDENTIFICATION - Continued) detected years after exposure. Individuals with preexisting diseases of the liver, or bone marrow may have increased susceptibility to the toxicity of excessive exposures. Carcinogenicity Information None of the components present in this material at concentrations equal to or greater than 0.1% are listed by IARC, NTP, OSHA or ACGIH as a carcinogen. FIRST AID MEASURES First Aid INHALATION If inhaled, remove to freBh air. If not breathing, give artificial respiration. If breathing is ..difficult, give oxygen. Call a physician. SKIN CONTACT In case of contact, immediately flush skin with plenty of water for at least 15 minutes while removing contaminated clothing and shoes. Call a physician. Wash contaminated clothing before reuse. EYE CONTACT In case of contact, immediately flush eyes with plenty of water for at least 15 minutes. Call a physician. INGESTION If swallowed, immediately give 2 glasses of water and induce vomiting. Never give anything by mouth to an unconscious person. Call a physician. FIRE FIGHTING MEASURES Flammable Properties Non- f1ammab le. Hazardous decomposition products including carbon dioxide, carbon monoxide, hydrogen fluoride, toxic gases or particles may be formed during combustion. These products may cause severe eye, nose, and throat irritation or toxic effects. EID087264 05573515 DuPont Material Safety Data Sheet Page 3 (FIRE FIGHTING MEASURES - Continued) Extinguishing Media Mater Spray, Foam, Dry Chemical, C02. Fire Fighting Instructions Wear self-contained breathing apparatus (SCBA) and full protective equipment. ACCIDENTAL RELEASE MEASURES Safeguards (Personnel) NOTE: Review FIRE FIGHTING MEASURES and HANDLING (PERSONNEL) sections before proceeding with clean-up. Use appropriate PERSONAL PROTECTIVE EQUIPMENT during clean-up. Evacuate personnel, thoroughly ventilate area, use self-contained breathing apparatus. Initial Containment Dike spill. Spill Clean Up Soak up with sawdust, sand, oil dry or other absorbent material. HANDLING AND STORAGE Handling (Personnel) Avoid inhalation. Avoid contact with eyes, skin or clothing. Hash thoroughly after handling. Hash clothing after use. Avoid circumstances that produce respirable particles unless suitable ventilation and respirator are used. Handling (Physical Aspects) Keep container tightly closed. Storage Store in a well ventilated place. 000023 EID087265 05573515 DuPont Material Safety Data Sheet Page 4 EXPOSURE CONTROLS/PERSONAL PROTECTION Engineering Control Use only with adequate ventilation. Vent heated extruder or dryer fumes outside work area. Do not aerosolize. In spray applications, use airless type pressure spray equipment at less than 60 psi, and exhaust ducts, drip pans, or other design features to minimize worker exposure to mists and overspray. Personal Protective Equipment EYE/FACE PROTECTION Wear safety glasses or coverall chemical splash goggles. RESPIRATORS Wear NIOSH approved respiratory protection, as appropriate. PROTECTIVE CLOTHING Where there is potential for skin contact have available and wear as appropriate Impervious gloves, apron, pants, and jacket. Exposure Guidelines Applicable Exposure Limits Ammonium Perfluorooctanoate PEL (OSHA) : None Established TLV (ACGIH) : 0.01 mg/m3, 8 Hr. AEL * (DuPont) : 0.01 mg/m3, 8 Hr. TWA, Skin, A3 TWA, Skin * AEL is DuPont's Acceptable Exposure Limit. Where governmentally imposed occupational exposure limits which are lower than the AEL are in effect, such limits shall take precedence. PHYSICAL AND CHEMICAL PROPERTIES Physical Data Boiling Point Freezing Point Form : 100 C (212 F) OTG000355 EID087266 0S573515 DuPont Material Safety Data Sheet Page 5 STABILITY AND REACTIVITY Chemical Stability Stable at normal temperatures and storage conditions. Incompatibility with Other Materials None reasonably foreseeable. Decompo sition Hazardous decomposition products including carbon dioxide, carbon monoxide, hydrogen fluoride, toxic gases or particles may be formed during combustion. These products may cause severe eye, nose, and throat irritation or toxic effects. Polymerization Polymerization will not occur. TOXICOLOGICAL INFORMATION Animal Data Ammonium Perfluorooctanoate: Inhalation 4 hour LC50: 980 mg/m3 in rats Skin absorption LD50: 4278 mg/kg in rabbits Oral LD50: 470 mg/kg in rats Ammonium Perf luorooctanoate is a skin and eye irritant, but is untested for animal sensitization. Effects of a single inhalation exposure include eye and nasal irritation, respiratory difficulty and liver enlargement. A single dermal exposure produced nonspecific effects such as weight loss and irritation, diarrhea, lethargy, labored breathing and cyanosis. A single ingestion exposure resulted in weight loss, gastrointestinal irritation and enlarged liver. Repeated exposures produced liver, kidney, pancreas and testes changes; anemia and cyanosis. Tests in male rats demonstrate tumorigenic activity based on an increased incidence of benign testicular, pancreatic, and liver tumors. Tests in animals demonstrate no developmental toxicity. Tests in animals for reproductive effects have not been performed. This compound does not produce genetic damage in bacterial cell cultures but has not been tested in animals. OTG000356 00QG5 EID087267 05573515 DuPont Material Safety Data Sheet Page 6 ECOLOGICAL INFORMATION Ecotoxicological Information Ammonium Perfluorooctanoate: 48 hour LCSO, fathead minnows: 1,500 mg/L. ' DISPOSAL CONSIDERATIONS Waste Disposal Treatment, storage, transportation, and disposal must be in accordance with applicable Federal, State/Provincial, and Local regulations. REGULATORY INFORMATION U .S . Federal Regulations TSCA Inventory Status : Listed. TITLE III HAZARD CLASSIFICATIONS SECTIONS 311, 312 Acute : Yes Chronic : Yes Fire : No Reactivity : No Pressure : No OTHER INFORMATION NFPA, NPCA-HMXS NPCA-HMIS Rating Health Flammability Reactivity :3 :0 :0 Personal Protection rating to be supplied by user depending on use conditions. The data in this Material Safety Data Sheet relates only to the specific material designated herein and does not relate to use in combination with any other material or in any process. Responsibility for MSDS Address Telephone J. S. Coates DuPont Specialty Chemicals Chambers Works 609-540-3251 EID087268 0S57351S DuPont Material Safety Data Sheet (Continued) End of MSDS Page 7 TG000358 0 0 OC: EID087269  T T f i C H f i l ~ AJ7~ 2 . /3 T S C * C 6 Z J>CAJ (30l 00006/V et l/crtf/V7 /i/o Sin U)& p f*o1/1tcet, cooc>;n CG0G23  Anthony J Playtls 08/04/2000 09:04 AM To: H David Ram sey/AE/DuPont@ DuPont cc: Subject: C -8 Exposure Limits Here's the information on C-8, aka ammonium perfluorooctanoate. Du Pont Acceptable Exposure Limit (AEL) 0.01 mg/m3, 8-hr TW A (skin); "Not likely to be a human carcinogen or developmental toxin" Du Pont Community Exposure Guidelines (CEG ) Airborne 0.0003 mg/m3 Drinking W ater 1 ug/L <? s ACGIH Threshold Limit Value (TLV) 0.01 mg/m3 TW A (skin, A3); The A3 notation means the following: "Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure." OSHA Permissible Exposure Limit (PEL) None established. -- EID089S13 00003 C-8 Control Levels TLV AEL CEGa CEGW 0.01 MG/M3, Liver Effects 0.01 MG/M3, Liver Effects Cancer Study Results Biopersistence 0.0003 MG/M3 1 PPB RJZ0073I2 3 o EID078904 RJZ007313 EID078905 A Com m unity Exposure Guideline ("C E G ") is an exposure guideline established by Haskell Laboratory. The CEG assumes a 24-h o u r lifetime exposure by ail, including the most sensitive individuals, in an exposed community population. Exposure above the CEG will not necessarily result in any adverse effects. W here data indicates that the CEG may be approached or exceeded, Haskell, the appropriate Business and Legal will evaluate, what action, if any should be taken. It is the Company's intent to maintain exposure below the CEG. c RJZ0073I C-8 OVERVIEW - MAN | Major Biological Concern: Long-Term Effects in Man Related to Persistence in Human Blood 1/2 Life > 1 Year (3-4 Best Estimate) C-8 OVERVIEW - MAN] No Liver Function Changes in Workers 3M DuPont Alleged Finding Relating Prostate Cancer in 3M Workplace with C-8 - Tenuous, 3M Working on Details EID078907 RJZ007315 U IT'0 Iv e> o a C-8 TOXICOLOGY REVIEW | ACUTE Moderate Acute Toxicology LD50, Rat 540 mg/kg Oral 7,000 mg/kg Dermal Rabbit 4,300 mg/kg Dermal ALC Rat 4 hr 800 mg/m3 Moderate Eye Irritant Non-Irritating to Skin RJZ007317 n EID078909 C-8 TOXICOLOGY OVERVIEW | REPEATED Rodent, Oral Striking Liver Enlargement 30 ppm - Little Effect 300 ppm - Pronounced Effect e> Monkey, Oral 10 mg/kg - No Effects 30 mg/kg - Not Tolerated C-8 TOXICOLOGY OVERVIEW | REPEATED Rat, Dermal 20 to 2,000 mg/kg Liver Damage Elevated Blood Levels Detected in Blood 47 Days Post-Exposure RJZ007319 EID078911 TOXICOLOGY OVERVIEW | t Inhalation -1 mg/m3 - NOAEL 7 + 84 mg/m3 - Liver Damage (Reversible) - Increased Blood Level - Male vs Female Rat Clearance Differs r-'j EID078912 RJZ007320 k TOXICOLOGY OVERVIEW] Lifetime Feeding - 30/300 ppm - Liver Effects Leydig Cell Tumors at 300 ppm Mechanism of Tumor Response Involves Chronic, Low-level Hormonal Change REASONING BEHIND AEL INHALATION NOAEL 1 WG/M3 EFFECTS AT 8 MG/M3 M I L D , REVERSIBLE LOW LEVEL ( ? ) A C T I V I T Y IN TESTES (TUMORS) 30 PPM IN DIET = 1 . 5 MG/KG/DAY - 1003 ABSORPTION OF INHALED DOSE, 70 KG WORKER s 1 0 .5 MG/M3 THIS IS 1) EFFECT LEVEL 2) HUMAN CLEARANCE FROM BODY SLOW SAFETY (UNCER TAINTY) FACTOR SHOULD BE LARGE ( 1 0 0 0 ) RECOMMEND 0 . 0 1 MG/M3 (1 0 .5 -f 1000) 000041 EID078913 73 N o o ro REASONING BEHIND CEG (COMMUNITY EXPOSURE GUIDELINE) AS FOR THE AEL ( 0 . 0 1 MG/ M?) ADDITIONAL FACTORS 1) 24 HR EXPOSURE I N COMMUNITY VS 8 HR AT WORK 2 ) DIVERSE POPULATION IN COMMUNITY 3) BIO-PE RS ISTE NC E IN MAN RECOMMEND 0 . 0 0 0 3 MG/M3 ( 3 3 FOLD REDUCTION) 0 0 EID078914 RJZ007322 HUMAN EXPOSURE Source Air Skin Adsorption Ingestion Preventative Method Reduce Air Levels Breathing Protection C-8 in Solution Chemical Gloves TYVEK Clothing Reduce Concentration in Drinking Water RJZ007323 0 \ ;0 a,*~i '' EID078915 u u r u n x n A a n i f i ' a i u w w u t (..> DRY RUN LANDFILL CHRONOLOGY -- 1995-1998 August 1994 Filter cake begins to be landfilled at Dry Run January 1995 TSS exceedence; start of high BOD/COD results; first notice of "black water" February/early March 1995 Pond Improvement Team organized Addition of antifoam March/April 1995 Water drainage improvements: diversion ditches and french drains installed Chemical treatment of fill area, pond, outfall begun (sulf control, hydrogen peroxide, antifoam) March 23, 1995 Cindy Musser inspection and recommendations May 1995 Beginning of enhanced monitoring and data collection on weekly basis Second sedimentation pond installed May 3 Cindy Musser inspection; progress noted June 1995 Lab testing confirmed filter cake contribution to high TOC problems 24-hour aeration begun in lower pond Algae control: copper sulfate treatment Lower pond visually improved October 1995 WTAP-TV news story November 1995 Musser/Britvec inspection (at our invitation); favorably impressed with progress February 1996 Zeto, Hill, Musser inspection to acquaint Zeto and Hill of Landfill operation October 15, 1996 DEP issued letter of intent to file civil action due to Washington Works' failure to meet new solid waste management standards November 1996 Final filtercake disposal at Landfill December 31, 1996 DEP issued Order and Washington Works agreed to settlement of all issues, including payment of $250,000 0 0 0 0 *15 EID089743 -2 - December 31, 1996, DuPont and the West Virginia Division of continued Environmental Protection (WVDEP) entered a settlement agreement pertaining to the operation and maintenance of the Dry Run Landfill, As part of the settlement agreement, DuPont agreed to perform additional maintenance on existing water diversion ditches, transport landfill leachate to Washington Works for treatment until design improvements planned for the landfill are completed, and stop disposal of plant filtercake in the landfill until design improvements planned for the landfill are completed. February 1997 Autopsy done in Belpre, OH (6-month-old bull calf) refers to "emaciation, poor nutritional state; intestinal parasites." March 1997 Autopsies (2 older cows) done for EPA: 1. "The only significant toxicologic finding in these two animals was low copper concentration. Since this may indicate a dietary problem, analysis of feed is recommended." 2. "No significant pathologic findings." 3. "No toxic compounds were detected by GC/MS* in the liver, kidney, urine or fat." June 1997 EPA ecosystem study July 1997 Public hearing; included testimony of local veterinarian interpreting autopsy data and concluding no Landfill effect on the autopsied animals, based on info in the autopsy reports December 1997 Draft report of EPA ecosystem study Doc 60531 DDJ001120 Q0 0 '1G EID089744 DRY RTIW LANDFILL EVENTS TIM ELINE * ACQUIRED DRY RUN PROPERTY.................................... * NUMEROUS LEASES.............................................. TENNANT COLLINS KAUFMAN * BEGAN LANDFILL OPERATION..................................... 1982-1983 1983-1984 1984 * DISPOSAL OF TFE POND SEDIMENT................................ 1989 * RELOCATION OF TFE POND MATERIAL (SUPERNATE) TOLINED CELL...... 10/25/91 * DISPOSAL OF FLUDGE OF DRY RUN STARTED................ (SUMMER) 93 OR 94 * STATE INSPECTION.............................................. 05/16/94 * FILTER PRESS INSTALLED AT WASTE WATER TREATMENT PLANT........ 08/94 * BEGAN DISPOSAL OF FILTER CAKE IN DRY RUN..................... 09/94 * BLACK WATER APPEARED......................................... * INSPECTION BY STATE DEPT ENV PROIN........................... * TENNANT MADE STREAM VIDEOS................................... * INSPECTION BY STATE.......................................... * ROUTINE INSPECTION OF DOWNSTREAM BEGAN....................... * BLACK WATER PROBLEM SOLVED................................... * INSPECTION BY STATE ENFORCEMENT & PERMIT WRITER.............. * TENNANT CONTACTED DNR (ELKINS OFFICE) ABOUT "STREAM POISONING DEER" & WV DEPT OF A G ........................... * TENNANT BEGAN TALKING IN COMMUNITY ABOUT CATTLE LOSSES....... 01/95 03/23/95 AP-MY95 05/03/95 05/95 05/95 10/95 12/95 95PM-96AM * DISCUSSION WITH WV DEPT OF AG VET, WV EXT SERV AGENT, & LOCAL LARGE ANIMAL VET.................................... SPRNG 96 * WASHINGTON WORKS COMMUNITY RESPONSIBLE CARETEAM STARTED....... 01/22/96 * EPA SOIL & WATER SAMPLING.................................... 10/96 * DRAFT COMPLAINT FROM WV DEP.................................. 10/96 * FREEDOM OF INFORMATION ACT REQUEST BY DuPONTTO EPA........... 11/06/96 * TERRADON/POTESTA.............................................. 11/96 * BEGAN DISPOSAL OF FILTER CAKE AT NORTHWEST LANDFILL.......... 12/96 * ADMIN SETTLEMENT REACHED WITH WV DEP CONCERNING ALLEGED VIOLATION.................................................. 12/96 * BEGAN TRUCKING LEACHATE BACK TO PLANT........................ * DISSECTION OF CATTLE VIDEO................................... * NOTIFICATION BY EPA OF CONCERNS QUESTION..................... * RESPONSE TO EPA............................................... * MEETING WITH COMMUNITY LEADERS............................... (LEGISLATORS - COMMUNITY AWARE? - ECC) * "OPEN HOUSE" FOR COMMUNITY AT DRY RUN........................ * EPA ENVIRONMENTAL RISK ASSESSMENT SAMPLING................... * FLUORIDE SAMPLES TAKEN BY DuPONT............................. * LETTER TO SITE EMPLOYEES BY PLANT MANAGEMENT................. * PERMIT APPLICATION PUBLIC HEARING............................ 01/97 02/97 02/97 03/20/97 05/97 06/97 06/97 06/23/97 07/27/97 07/97* * CEASED DISPOSAL OF ASBESTOS AT DRY RUN....................... * SPELTER BECAME ISSUE.......................................... * TENNANT LEASE CANCELLED...................................... * BEGAN SECURITY PATROLS ON WEEKENDS (CONTRACTAGENCY).......... * INSPECTION BY STATE........................................... * MEETING WITH WV DEP OFFICE OF WATER QUALITY TO ENGAGE" THEM IN EPA ACTIVITY....................................... 01/01/98 03/98 04/98 06/98 07/07/98 07/98 00004/ EID089745 0 0 0 0 '15 DRY RUN LANDFILL: C-8 HISTORY SUMMARY O SUPERNTE POND SOIL DISPOSAL: - 7100 TONS OF SOIL CONTAINING " 85 PPM C-8 DISPOSED OF NEAR THE BOTTOM OF THE LANDFILL 11/88. - THIS SOIL WAS MOVED TO THE TOP OF THE LANDFILL AND BURIED IN A CLAY-LINED SEPARATE CELL 10/91. 0 C-8 GROUNDWATER AND SURFACE WATER MONITORING: - BEGAN MONITORING ANNUALLY FOR C-8 IN 1991. - GROUNDWATER CONCENTRATIONS RANGE <1 - 15 PPB. - LEACHATE CONC. AT O.F. 001 RANGES 30 - 200 PPB. * PROPERTY BOUNDARY STREAM CONCENTRATION RANGES 2 - 2 5 PPB. - DATA REPORTED ANNUALLY TO WVDEP BEGINNING WITH 1991 ANNUAL REPORT. * 1998 RESULTS: LEACHATE = 56 PPB OUTLET 001 * 17 PPB STREAM #1 = 1 PPB STREAM *2 = A.6 PPB PROP. BND. = 0.88 PPB 0 _ 7 POUND/YR C-8 DISPOSED OF WITH BIOCAIE (930 PPB). 0 600M POUNDS/YR OF FLUQROPQLYMER WASTE DISPOSAL BEGAN 1/96; DOES NOT CONTAIN C-8. RJZ006998 00 *c* E ID 0 7 8 8 6 7 000G3G 0 8 HISTORICAL PROSPECTIVE Known Contaminant Sources - Supernate Ponds (Closed 1988) (Excavated Soil removed to Dry Run Landfill) Excavated Soil Levels - 234 ppm Max Residual Level in Remaining Riverbank Soil-173 ppm Max - Lubeck Public Service Division Test Well 27 - 1-2 ppb Employee Water Taps - 1-2 ppb - Letart Landfill Landfill Leachate - 3 ppm Groundwater Wells - 1.6 ppm (Poss. Construction Cont.) - Dry Run Landfill Landfill Leachate - 0.7 ppm Leachate Stream at Property Line - 0.1 ppm Regulatory Knowledge - EPA SWMU Survey - 6 /6 /8 6 C-8 in trace levels in Supernate waste C-8 found in ppb levels in aquifer - NPDES Permit Application - 9 /2 /8 6 Surfactants In 0 0 2 /0 0 6 Discharge (Not specific mention) - Supernate Sludge Disposal Request - 7 /3 0 /8 7 , 8 /2 3 /9 0 Supernate Sludge contained 85 ppm C-8 - Lubeck Public Service Division - 6 /1 3 /8 9 C-8 has been found in aquifer in ppb levels Stated no health hazard - Letart Landfill Permit Application - 9 /2 1 /8 9 C-8 in stream and wells reported in required analysis 000- X EED080125 V 8 r 0000 2 F AIM The aim of this meeting is to discuss what should be considered an acceptable level of C-8 in both surface water and ground water and to develop a plant strategy for dealing with the C-8 contamination at the Dry Run landfill. Review: o o o o Discuss: o o o AGENDA C-8 - What is it? C-8 - Overview of limits and guides Source of C-8 contamination at Dry Run Supernate pond sludge - 14,000,000 pounds C-8 concentration - 275 ppm Location and amount of current known contamination What is an acceptable level of C-8 in surface water? What is an acceptable level of C-8 in ground water? Based on these levels, what is the appropriate action to be taken at Dry Run at this time Some Options: o No Action, monitor for further contamination o Cap material in place, monitor for further contamination o Move material to Letart landfill o Incinerate o New technology o Calcining o RO o Ion Exchange 0000,53 v. EID080103 fir n * cf > e a r . is r s 0 0 0 ' * . bCtl b 3 0 ' j v t r s * Ho S o n -r` U oS 009G54 PFOA Concentrations Washington Works drinking water Outfall 005 1999 1999 1998 1990's 0.2 - 0.5 ppb (building samples) 0.082 ppb (drinking water wells) 1 .9,1.0, and 0.4 ppb (drinking water wells) 50-60 ppb GE Plastics drinking water 1999 0.5 ppb (drinking water well) Lbeck Public Service District Old LPSD wells + W W well 27 2000 1992 1984-88 1**Q: 0.8, 0.44, and 0.313 ppb 2"dQ: 0.315, 0.516, and 0.21 ppb 0.2, 0.4, and 0.09 ppb 9 samples ranging from 1 . 0 - 2.2 ppb Dry Run Landfill Leachate Outlet 001 Stream Sampling Station No. 1 Stream Sampling Station No. 2 Property Line 1999 34 ppb 66 ppb 0.54 ppb 87 ppb 39 ppb Letart Landfill 2000 t Monitoring wells are identified by Zones, with A nearest the surface and F the deepest. Zone A MW-1 17,400 ppb MW-7 219 ppb MW-8 2,100 ppb Zone D/E M W -4 172 ppb Zone F MW-2A 453 ppb MW-5B 1,030 ppb MW-6 9.4 ppb Blood Monitoring Data 1995 None higher than 5 ppm. Previously, levels had been detected up to 33 ppm. EID089310 00005S coo o PFOA Concentrations Washington Works drinking water Outfall 001 \ ' .* ` 1999 1999 1998 1999 0.2 --0.5 ppb (building samples) 0.082 ppb (drinking water wells) 1.9 ppb (drinking water wells) . ^ 66 ppb \ v> G E Plastics drinking water 1999 0.5 ppb (drinking water well) Lubeck Public Service District 1 2000 1992 Dry Run Landfill Leachate Outlet 001 Stream Sampling Station No. 1 Stream Sampling Station No. 2 Property Line 1999 0.8, 0.44, and 0.313 ppb t '* 0.2, 0.4, 0.09 ppb , l/ P 34 ppb 66 ppb 0 .5 4 ppb 87 ppb 39 ppb -y ( * . t * r. " ' O '* 4 -. . : \i u ii Letart Landfill 2000 Monitoring wells are identified by Zones, with A nearest the surface and F the deepest Zone A MW-1 17,400 ppb MW-7 219 ppb MW-8 2,100 ppb Zone D/E MW-4 172 ppb Zone F MW-2A 453 ppb MW-5B 1,030 ppb MW-6 9.4 ppb Blood Monitoring Data 1995 None higher than S ppm. Previously, levels had been detected up to 33 ppm. oooc <r 3 EID089516 OOOG-53 CC: R. J. Burger C. R. Campbell J. R. Broadway J. L. Granquist R. J. Zipfel P. Thistleton G. H. Stoltz C. A. Robinson K. G. Kronberg J . F . Doughty ; C-8 COMMUNICATIONS MEETING OUTLINE, TALK & CHARTS C. E. STEINER 7/31/80 PERSONAL & CONFIDENTIAL OOCiO' EID079399 C. E. S te in e r INTRODUCTION C -8 's d e sir a b le p ro cess q u a litie s S h o r t C -8 h i s t o r y i n TFE & FEP M a n u fa c tu r e TOXICITY O ral to x ic ity - s lig h t ly to x ic Com pare t o o th e r com pounds S k in c o n ta c t - s l i g h t l y to m o d e r a te ly t o x ic In h a la tio n t o x ic ity - h ig h ly to x ic Com pare to o th e r com pounds C o n cen tra tio n s found in a rea a r e lo w er IN IT IA L ' BLOOD' TE STS 3M Data Our R e su lts RECOGNIZING EXPECTED OPERATOR QUESTIONS - A transition Some disbelieve based on past experience Short history of chemicals in industry showing why we are careful MEDICAL RECORD STUDIES No evidence of health problem Studies thorough PROVISIONAL AEL AEL committee has set provisional AEL of 0.55 mpb Not yet firm AEL This very low number is to protect people who work with C-8 everj day The low provisional AEL and goal to reduce blood fluorine is the reason we are making changes in equipment and procedures. EQUIPMENT IMPROVEMENTS Goal, to reduce exposure to solid C-8, airborn C-8 and C-8 solutio Ingredients addition hood and stack Eliminate Weighing Citric Acid in C-8 hood Raising Dryer Air supply Inlets Seal Dryer Leaks Additional Dryer Windows Increase Ventillation During Outages Removing C-8 from Dryer Exhausts EID079400 2 PROTECTIVE EQUIPMENT Clothing and Gloves Needs to be disposable to prevent secondary contamination. An EOD is being prepared to evaluate clothing. Different protection levels for 3 exposure classes Breathing Equipment improvements will reduce airborne C-8 but high C-8 concentrations will still remain in some areas. Breathing air will be installed - ultimate- solution. Comfo II air respirator with GMAH cartridge acceptable. TESTING Personal Air Samples Will Resample. Blood Samples Blood sampling will be resumed. Frequent sampling is not necessary. rea Air Samples Will continue to define progress. Often exceed provisional AEL before improvements. SUMMARY C-8 is toxic but can be handled safely. People working with C-8 generally accumulate organic fluorine in the blood, and levels generally correlate with job exposure potential. Although this has caused no health effects continued exposure is hot tolerable. Our basic goals are to reduce exposures to below the provisional AEL, and to reduce organic fluorine levels in blood of exposed workers and prevent accumulation in new workers. This will require equipment changes that are being done. It will also require use of disposable protective clothing and us of breathing air or respirators for certain jobs. One other ingredientient is needed -- your cooperation in controlling this hazard. 0006' CES 6/3/80 EID07940I C - 8 COMMUNICATION MEETING The p u rp ose o f t h is m eetin g i s to b r in g ev ery o n e up to d a te on o u r fin d in g s r e g a r d in g C -8 , o u r im m ed iate program , and ou r lo n g term p la n s . Most of you know that C-8 is a fluorochemical surfactant that is used for producing fine powder, dispersion, granular and FEP. It has unique properties that allow it to wet Teflon's surface, shorten reaction cycle time, stabilize dispersions and provide sites for reactions. It has been used for Teflon manufactuz for over 25 years. Other chemicals have been tested but none match C-8's properties. Four years ago it was introduced in FEP manufacture where it was a manufacturing improvement. Let's look over the highlights of the Technical history of C-8. In 1965 tests showed that C-8 was slightly toxic when swallowed. This was not surprising. There is a dose level where almost every chemical becomes poisonous, even water. (Chart 1). This chart shows the oral toxicity of C-8 relative to some common chemicals. These tests were done on animals, and represent what dose would kill 50% of the animals tested. I've scaled up the dose from test data to animal weights comparable to an operator's weight. You can see that C-8 is not as toxic as acetone. It has a lower toxicity like table salt. C-8, like table salt, cam also be absorbed through the skin where it is about as toxic as it is orally. But, based on this low toxicity, no change in our safety program was necessary. 0 0 0 (; , 3 EID079402 2 In 1969 it was found that C-8 was more toxic by inhalation, Chart 2. This second chart shows the approximate concentration that will kill test animals in a 4 hour period. This approximate lethal concentration for rats exceeds anything we have measured in the plant. The highest level ever measured in the plant is about 1/4 of that level -- and that a l.lmpm leak at the feed end of No. 3 dryer which has been repaired. The other C-8 concentrations are generally about 1,000 to 10,000 times lower than this so people working in the area see no immediate effect.(.004Jnpai However, since 3M informed us in 1978 of organic fluorine being detected in the blood of their employees who worked with C-8, we have been reviewing and expanding our C-8 program. We have concluded that personnel routinely exposed to C-8 will absorb it in their body. Tests at Washington Works show that blood fluorine levels which indicate C-8 levels generally correlate with potential job exposure. Repeated exposures can result in accumulation of C-8 in the blood. One of the things that we are studying with the blood samples is the rate that C-8 is eliminated from the body. Some of the old timers remember when C-8 was treated with less respect and they wonder "Why is it suddenly harmful now?" 0 0 o*l EID079403 3 Throughout the chemical industries over the last 50 years this story has been repeated with the same disbelief but often with more drastic consequences. For example, carbon tetrachloride was used to clean auto parts and as a fire extinguisher for years, and now it is known to cause damage in some people and is used with care. The same story has been repeated several times for things like chloroform (which was used in cough suryp), methyl alcohol and other chemicals. The difference between the ending of the C-8 story and the others is that Du Pont is reacting while C-8 levels in the blood are low and before any damage is done in the body. The medical data show that no one has been injured by C-8 (Chart- 4). The Medical Division after a thorough study has concluded that ". . .there is no conclusive evidence of an occupationally related health problem among workers exposed to C-8.n All that was noted was a small increase in two liver enzyme levels. After 25 years of handling C-8 we see no damage among the workers. However, the potential is there -- C-8 has accumulated in the blood. Because of this accumulation we have decided to undertake programs to minimize accumulation.of C-8 in the blood of new workers. 0 G0 GG5 EID079404 4 The AEL Committee of Haskell Laboratories has set a provisional Allowable Exposure Limit or "AEL" at 0.55 mpb of C-8 in air. This very low proposal is based on a safety factor of 800 below the level where reversible liver effects were observed. An AEL is the same thing as a TLV or EGL -- it is a safe concentration in the air of a working environment. In order to meet the expected low AEL, equipment changes are necessary to protect from solid, liquid and airborn C-8. The next transparencies show the changes that have been made recently to protect against C-8 exposure. To date we have: Modified the Fine Powder/Dispersion ingredients addition hood to reduce C-8 emissions and bring the mixing operations into the hood. C-8 tools will also be stored in the hood where possible. .Improved the C-8 addition hood exhaust stack. The hood exhaust stack was close to an H & V inlet on the roof. Removed operations that don't have to be done in the C-8 hood -- like citric acid weighing. This has reduced exposure of concentration to the operators The dryers have been improved also: Air supply inlets have been raised to remove C-8 rich air from the ceiling. OOOC^-o EID079405  Seals of No. 3 dryer doors and seams have been improved. Inspection windows have been added to reduce need to open dryer doors. We have also put guards inside the dryer that will permit using the exhaust fans to remove C-8 when dryers are being cleaned. This has reduced some C-8 concentrations, but more work is to be done; for example, we plan to cover injection pump tanks, seal openings in floor and vent oscillating feeder compartments, sealing No. 3 dryer fans. The n e x t chart shows the three different protection levels required for three exposure classes: Low dry exposure, high dry exposure and wet exposure. A disposable garments of the appropriate design, gloves and air protection are recommended for each of these exposure classes. Sample garments, have been selected and an EOD will be run to evaluate this clothing. Tyvek was selected over cloth or paper garments because it is light fairly resistant to tearing, a good filter and disposable. Disposability is required to prevent secondary contamination when laundering. During this EOD, sample garments will be tried and evaluated by operators and mechanics. C-8 will permeate all glove materials over a period of time. New flock lined latex gloves will be used in jobs where C-8 exposure is likely. Even these gloves will be permeated by C-8 over a period of time, so these gloves will be disposed of after each shift. OGOtjsy EID079406 6 Breathing protection is very important to reducing C-8 exposures. Equipment improvements will reduce airborn C-8 in most areas but there will still be areas where exposure, is possible. A COMFO II air respirator with a special GMAH cartridge is required as a minimum. Breathing air is better and will be available soon. The yellow 3M masks are not acceptable. I've had some questions on future C-8 air samples and blood samples. We now have our baseline data and have mapped out the problem areas. The procedures are modified and equipment improved so C-8 exposures will be reduced. Blood sampling will probably be done on an annual basis in the future to define the real improvements in C-8 control. Let me summarize the items covered: C-8 is toxic but it can be used and controlled below the proposed toxic limit. In the past, people working with C-8 have accumulated organic fluorine in the blood and levels generally correlate with job exposure potential. Although this has caused no health effects, continued exposure should be minimized .with controls. Our objective is to reduce exposures to below the provisional AEL, and to reduce organic fluorine levels in blood of exposed workers and to limit accumulation in new workers. EID079407 0 -:s 7 This will require equipment changes that are partially comp It will also require use of disposable protective clothing and use of breathing air or respirators for certain jobs. One other ingredient is needed -- Total Division cooperation in controlling this material. 00 r . - yrof EID079408 V, 13 ^' 000670 ( Births and Pregnancies PPM C-8 in Bloody ^ p S T W ilJ 0.45 *0 ; Status Normal child - b o m June 1980. Transferred out of Fluorocarbons 4/79. 0.28 Normal child - born April 1981.. 0.078 Normal child - b o m April 1981. Umbilical cord blood 0.055 ppm. 1.5 Five months pregnane. O.Ol? ^fe<jpnthsv>pireg4rx. 2.5* Child - 2 plus years. Unconfirmed eye and tear duct defect. 0.048 >001 Child - 4 months. A fe c t' ' y< Jf /f Current blood level - in fluorocarbons area only one m onth before pregnancy. 1 1 E I D 0 7Q' O0 Q'/o V 14 r I I September 21, 1981 I TO: I CjUFROM: J. J. DI NICOLA D. H. SNYDER I WASHINGTON WORKS LANDFILL FACT SHEET I Ref: (1) Letter D. H. Snyder to C. W. Crowe 9/1/81, same title. I (2) Letter, C. W. Crowe to E. R. Kimrael, A. L. Skinner and J. L. Stowell# 9/11/81, same title. I Attached is a copy of the Landfill Fact Sheet which we reviewed by phone on 9/16/81. It will be used by J. R. Draper of the Real Estate Division of General Services Department in his I contacts with landowners. It is in response to requests by some owners. C. W. Crowe of the Departmental Engineers Office reviewed I this with both Legal and Public Affairs. They have approved its use. I* /jas(1669A) Attachment EXHIBIT 1 CF00I293 GGG EID022224 LANDFILL INFORMATION The landfill will contain nonhazardous wastes only, including ash from plant boilers, waste plastics, glass, scrap metal, paper, and trash, all transported by covered truck or closed containers. It will be designed and operated with full consideration for neighbors. The ash will be wetted, and the road will be paved to control dust and mud. The fill will be covered with dirt at the end of each day. Daytime only operation is planned. The site could receive 10 to 14 truckloads per day. The probable start-up date is late 1983. CTOOI294 0090/ EID022225 O0G75 The miracles o f science Study Title MODELING RELEASES OF AMMONIUM PERFLUOROOCTANOATE INTO THE OHIO RIVER Author William R. Berti D ra ft R e p o rt C o m p le te d o n May 22, 2000 Performing Laboratory E. I. du Pont de Nemours and Company Environmental and Microbiological Sciences & Engineering Corporate Center for Engineering Research Central Research & Development Glasgow, Building 300, P.O. Box 6101 Newark, DE 19714-6101 Report No. EMSE-054-00 Page 1 of 8 EID108608 CONTAINS CONFIDENTIAL BUSINESS INFORMATION DOOM 'S DuPont EMSE Report N o. 054-00 GENERAL INFORMATION Chemical Studied: Ammonium perfluorooctanoate Svnonvms/Codes: C-8, FC-143 DuPont Notebook No.: Not Applicable Sponsor; Robert Pinchot E. I. du Pont de Nemours and Company BARLML CRP-711/2210-B Study Initiated/Completed: September 1999 to May 2000 RP001968 Page 2 of 8 EID 108609 CONTAINS CONFIDENTIAL BUSINESS INFORM ATION 000C77 D uPont EMSE Report No. 054-00 MODELING RELEASES OF AMMONIUM PERFLUOROOCTANOATE INTO THE OHIO RIVER SUMMARY PDM indicated that C-8 concentrations of 1.0 g C-8/L would be exceeded about 50% of the time during the year. C-8 concentrations of in the river would exceed 0.1 g C-8/L 90% of the time during the year and 10 g C-8/L about 2.2% of the time during the year. Average annual C-8 concentrations in the Ohio River calculated by using a Microsoft Excel spreadsheet was 0.423 g C-8/L. Modeled C-8 concentrations in the river ranged from a low of 0.199 g C-8/L in March to a high of 0.965 g C-8/L in September, which correspond to high and low river flows, respectively. Average Ohio River flows and volume data calculated from the US Geological Survey was collected at the Belleville Dam and used in the spreadsheet model. The Belleville Dam is on the Ohio River 13 miles downstream of the Washington Works Plant. This river flow data is the closest location downstream from the plant where this type of information is available. Study Conducted and Report Prepared by: ____________________________________ William R. Berti (date) Senior Research Biologist RP001969 Page 3 of 8 EID108610 CONTAINS CONFIDENTIAL BUSINESS INFORM ATION 0 0 OC: / S D uPont EMSE Report N o. 054-00 INTRODUCTION/PURPOSE C-8 (ammonium perfluoroocatanoate) is a fluorinated surfactant used in the manufacturing of Teflon at Washington Works. A portion the C-8 (18,416 kg in 1996) was released to the Ohio River as part of an NPDES permitted release for the facility (WV0001279). The molecular weight of C-8 is 431.098 g/mole. Other properties of C-8 are listed below. Made by 3M Company Health rating of 2 Exposure limits 0.01 mg/m3skin 8 hr LD50acute oral rat = 680 mg/kg BOD20= nil Biodegradation = nil BCF = 18 Molecular formula CF3(CF2)6COO`NH4+ pH ~ 5 (0.5% aqueous) pKa = 2.8 (-COOH) Melting point = 56-58C (-COOH) C O D = 7 0 0 m g /k g Koc = 25 Water solubility > 1000 mg C-8/L Vapor pressure (at 22C) = 7.1* 10"05 mm Hg Our objective was to calculate the concentrations of C-8 that could reasonably be expected to occur in the Ohio River downstream of the NPDES permitted outfall at the DuPont Washington Works. MATERIALS/METHOD Releases of ammonium perfluorooctanoate (C-8) to the Ohio River from the DuPont Washington Works Plant were modeled using the Probabilistic Dilution Model (PDM Beta Version 4.0 Beta June 11, 1999, US EPA Office of Pollution Prevention and Toxics) and a constructed Microsoft Excel spreadsheet model. C-8 release data for 1996 were used in both modeling exercises. PDM inputs included the NPDES number of WV0001279. This corresponds to a reach number of 05030202039, a mean streamflow of 4.75E+04 million liters per day (MLD), a low streamflow of 9980.47 MLD and an effluent flow of 216.75 MLD. We assumed that C-8 was released 335 days/year, the loading was 55.138 kg/day, and the wastewater treatment efficiency was 0%. We then varied the C-8 concentration as the Concentration of Concern (COC) from 0.1 to 50 g C-8/L to determine the COC percent of year exceedence. Microsoft Excel spreadsheet used river flow data from the US Geological Survey (USGS: <http://waterdata.usgs.gov/nwis-w/WV/data.components/hist.cgi?statnum=03159530>). This is the mean daily river flow in cubic feet/sec measured at the Belleville Dam from 10/1/1974 to 9/30/1985. The Belleville Dam is on the Ohio River 13 miles downstream of the Washington Works Plant. This river flow data is the closest location downstream from the plant where this type of information is available. This river flow data compares well with Ohio River monthly average flows at Pittsburgh, PA, Huntington, WV, and Cincinnati, OH from the US Amy Corps of Engineers (ftp://www.lrd-wc.usace.army.mil/Monthly_htm/). The average daily river flow for the month was calculated from available data between those two dates. This was then converted to the average measured flow per month. We assumed the C-8 was discharged to the river at a constant rate except for the month of October when production at Washington Page 4 of 8 CONTAINS CONFIDENTIAL BUSINESS INFORMATION 00 On/9 E,D,086U DuPont EMSE Report No. 054-00 Works is usually suspended for annual maintenance. We assumed that the total discharge of was 18,416 kg C-8 (40,600 lbs C-8) divided by 11 months. Table shows the results of this spreadsheet model. RESULTS/DISCUSSION PDM indicated that C-8 concentrations of 1.0 g C-8/L would be exceeded about 50% of the time during the year. C-8 concentrations of in the river would exceed 0.1 g C-8/L 90% of the time during the year and 10 g C-8/L about 2.2% of the time during the year (Table 1). Figure 1 shows model input/output. Average annual C-8 concentrations in the Ohio River calculated by constructing and using a Microsoft Excel spreadsheet model was 0.423 g C-8/L (Table 2). Modeled C-8 concentrations in the river ranged from a low of 0.199 g C-8/L in March to a high of 0.965 g C8/L in September, which correspond to high and low river flows, respectively. Average Ohio River flows and volume data calculated from the US Geological Survey was collected at the Belleville Dam and used in the spreadsheet model. The Belleville Dam on the Ohio River 13 miles downstream of the Washington Works Plant. This river flow data is the closest location downstream from the plant where this type of information is available. RP001971 Page 5 of 8 EID 108612 CONTAINS CONFIDENTIAL BUSINESS INFORMATION 000050 D uPont EMSE Report No. 054-00 TABLE 1: Probabilistic Dilution Model (PDM) results of C-8 concentrations and percent of year that the concentration of C-8 will be exceeded in the Ohio River. Concentration Percent ot year of C-8 concentration exceeded o.i U.6 1 3 b 10 2b ------- 5 ... % 9(19 71.6 5TU ITB 6.1 2.2 0.2 0.0" RP001972 Page 6 of 8 EID108613 CONTAINS CONFIDENTIAL BUSINESS INFORMATION 0090 DuPont EMSE Report No. 054-00 Table 2. Month Microsoft Excel spreadsheet calculations of modeled C-8 concentrations in the Ohio River. Measured flow Measured tlow (J8 discharge to Ohio Estimated Cb River in 1996 concentration in Ohio River JtJ/sec January 64,001 February ------ W ------ March ------111,236----- Apnl 94,017 May 67,107 June 47,379 . July ------ 33S9 August ------ 3392------ September 25329 October ------ 3X59------ November ------ 42335------ December ------ 7O T5------ Average Total ------7T3324 Umo 4.69E+2 6.74E+12 8.43E+T2 6.90E+12 5.09E+T2 3.48H+12 2.35E+12 2.31E+12 1.73E+12 230E+T2 3.11E+T2 5.99E+T2 4.44E+12 5.33E+13 kg 1,674 1,674 1,674 1,674 1,674 1,674 TT574 H674 1,674 0 1,6/4 1,674 18,416 g/4 0757 0348 0239 0343 0329 0332 077T3 07724 o.yb 0300 0339 03S 1T423 0345 RP001973 Page 7 of 8 EID 108614 CONTAINS CONFIDENTIAL BUSINESS INFORMATION OOiKtS DuPont EMSE Report N o. 054-00 ADSORPTION-DESORPTION STUDIES OF AMMONIUM PERFLUOROOCTANOATE FIGURE 1: Probabilistic Dilution Model (PDM) Beta Version 4.0 input and output screen. PDM Site Specific Screen C -8 1 05030202039 1 1996 4.7S + 04 2 1 6 .' jI N P j J T DA'T jg fl 5 5 .1 3 8 EID 108615 coc (u g /L ) YEAR COC BXC8BDBD DAYS COC BXCEEDBD RBLKASE LOADING DAYS ( k g / s i t e / d a y ) WASTE WATER TREATMENT 0 .1 0 .5 1. s. 10. i L! 9 0 .9 7 1 .6 51. 8 .4 2 .2 3 3 1 .6 2 6 1 .5 186. 3 0 .6 8 .2 335. 335. 335. 335. 335. 5 5.1 SS. 1 5 5 .1 55 .1 5 5 .1 a : f e l K T. , : H iIf-u s .ivU.-i-- 1L 1-*tfA**ki4 k i * 0. 0. 0. 0. 0. WlOOdH Page 8 of 8 CONTAINS CONFIDENTIAL BUSINESS INFORMATION PERSONAL AND CONFIDENTIAL T. A. Foster R. N. Taylor P. Thistleton October 19, 1982 TO: R. J. ZIPFEL FROM: J. G. LOSCHIAVO ESTIMATE OF HUMAN C-8 EXPOSURE RESULTING FROM DRINKING OHIO RIVER HATER As you requested, I estimated human exposure to C-8 as a result of drinking Ohio River water. As a result, I've found human exposure to C-8 to be very low. Using 1982 manufacturing conditions (and no scrubbing of Fine Powder Dryer exhaust), persons would be exposed to a C^5 dose roughly equivalent to 0.08% of the acceptable exposure limit (AEL). Using pro jected manufacturing conditions for 1987 (with scrubbing of Fine Powder Dryer exhaust), persons would be exposed to a C-8 dose roughly equivalent to 0.35% of the AEL. It should also be mentioned that C-8 is more toxic via the inhalation route than the oral route. Therefore, these percentages would in actuality be even lower. Human C-8 exposure calculations were made using three separate sets of conditions: Case 1 - Reflects 1982 manufacturing conditions with no scrubbing of the Fine Powder Dryer exhaust. Case 2 - Reflects 1982 manufacturing conditions with scrubbing of the Fine Powder Dryer exhaust. Case 3 - Reflects projected 1987 manufacturing conditions with scrubbing of the Fine Powder Dryer exhaust. The results of my calculations are contained in the attached Table. My calculations are also attached. JGL:sdc 1799B-1 EID079287 TABLE 1. Estimated Ohio River C-8 Concentrations and Human C-8 Exposure Reflecting 1982 and 1987 Manufacturing Conditions C-8 Concentration in Average Daily Amount % of Equivalent Case No. River Water (ppm by wt.) of C-8 Ingested ^ g ) Act Dose 1 0.8 x 10-4 0.08 0.08 2 1.1 x 10-4 0.11 0.11 3 3.5 x 10-4 0.35 0.35 17998-2 0 0 0 s': V EID079288 CALCULATIONS General Assumptions: An average person drinks 1 liter of water per day. An average person inhales 10m3 of air over an 8-hour shift. Average Ohio River flow rate is 13,880,000,000 lb. water per hour. The scrubber on the Fine Powder Dryer stacks would be 90% efficient. When the Fine Powder Dryer exhaust is not scrubbed, 3% of the total C-8 added to Fine Powder/Oispersion goes to the River. When the Fine Powder Dryer exhaust is scrubbed, 31% of the total C-8 added to Fine Powder/Dispersion goes to the River. a Approximately 81% of the total C-8 added to FEP goes to the River. Specific Case Assumptions: Case 1 Fine Powder/Dispersion will manufacture 6.9 MMAP during 1982. An average of 0.0022 lb. of C-8 is added to make each pound of Fine Powder/Dispersion (35% solids). t FEP will manufacture 6.7 MMAP during 1982 An average 0.0016 lb. of C-8 is added to make each pound of FEP (low C-8 recipe). Case 2 Same as above except the Fine Powder Dryer exhaust is scrubbed throughout 1982. Case 3 Fine Powder/Dispersion will manufacture 16 MMAP during 1987. 9 An average 0.0033 1b. of C-8 will be added to make each pound of Fine Powder/Dispersion (45% solids). FEP will manufacture 11 MMAP during 1987. e An average 0.0030 lb. of C-8 will be added to mate each pound of FEP (high C-8 recipe). 1799B-3 GQCKi 8 EID079289 Case 1 Calculations Fine Powder/Dispersion: ,9 x 106 lb. TEFLON^ ^0.0022 lb. C-8 -) f-03)e - JLz lb. TEFLONSV \ J 365 days x 24 hr. yr. day 0.05 1b. C-8 hr. goes to River FEP: ^6.7 x 106 lb. TEFLON^ /0-0016 lb. C-8 I L t lb. TEFLON.; ) H 365 days 24 hr. y r . day 1.00 lb. C-8 hr. goes to River Total C-8 going to the River per hour * 1.00 + 0.05 = 1.05 lb. C-8 KF. C-8 Concentration in = f _____ 1.05 lb. C-8/hr.______106 * 8 x 10-5 ppm River (wt./wt.) \13,880,000,000 lb. water/hrj Amount of C-8 Ingested with Drinking Water Each Day ( l liter of water\[1000 gm water\/8 x 10- V liter water/\ 8 x 10-8 gm. op 0.O8 of C-8 Amount of C-8 Inhaled at the AEL Concentration over an 8-hr. Shift flO of C-8 A O m 3 of air\ \ m^ of air / \ > Ingesting 0.08 /rf) of C-8 is equivalent to: 0.08 ^g of C-8 x 100 0.08% of the AEL 100 q of C-8 . 100 ^g of C-8 1799B-4 00000; EID079290 Case 2 Calculations Fine Powder/Dispersion: 9 x 106 ib. f- TEFLON^ 365 days yr. ^0.0022 lb. C-8 lb. TEFLON/ 24 hr. 3ay 0.54 lb. C-8 hr. going to River FEP: Same as shown in Case 1. Total C-8 going to the River per hour 1.00 + 0.54 - 1.54 lb . C-8 FvFI C-8 Concentration in River (wt./wt.) _____ 1.54 lb. C-8/hr._____ \ x ig6 _ ^ x ^g-4 ppm 3,880,000,000 lb. water/hrj Amount of C-8 Ingested with f l liter of wateA A o O O gm w a t e A /l.l x 10~4 ppm} (10-e \ J\ /\Drinking Water Each Day liter water/\ * 1.1 x 10-7 gm. or o.ll ^g of C-8 Amount of C-8 Inhaled at the AEL Concentration * 100 yg of C-8 over an 8-hour Shift Ingesting 0 . 1 1 of C-8 is equivalent to: 0.11 of C-8 x 100 O . m of the AEL 100 /ug of C-8 17998-5 000C`Ab EID079291 5 chC4 0 Case 3 Calculations Fine Powder/Dispersion: C6 ) Mx 106 lb. TEFLON^ ^0.0033 lb. C-8 yr. lb. TEFLON>/ \ / 365 days 24 tir. yr. y 1.85 lb. C-8 hr. going to River FEP: 11 x 10 lb. TEFLON^ ^0.0030 1b. C-8 0 - i0*81)yr. lb. TEFLON/ \ J 365 days 24 hr. y r . day 3.06 lb. C-8 hr. going to River Total C-8 going to the River per hour * 1.85 + 3.06 = 4.91 lb. C-8 firT C-8 Concentration in i_____ 4.91 lb. C-8/hr.______q6 * 3 .5 x 10"4 ppm River (wt./wt.) U 3 , 880,000,000 lb. water/hr.< Amount of C-8 Ingested with = f l liter of water\A.000 gm w a t e A /3.5 x 1 0 - 4 ppni\no- Drinking Water Each Day \ /\ liter water/\. /\ 3.5 x 10"7 gm. or 0 .3 5 ^ of C-8 Amount of C-8 Inhaled at the AEL Concentration * 1 0 0 of C-8 over an 8-hour Shift Ingesting 0.11 ^ of C-8 is equivalent to: 0.35 jug of C-8 x 100 0.35% of the AEL 100 /*q of C-8 1799B-6 O# EID079292 000030 i f 7t7 t ~Ti Yi '$/lo>n ', J~ i F, <Ojv2 07o v a J ~ . 3 $ , i r l a - i /'ry U s^T n sy * P'A&u EID079735 sdifrvZs s ite ^ ^rTle/t oi\h3. s j7 C, ^ S & v-* -' ^'LP -'t/" s i* s- S S 7 r g / w * ' sh > Z t/* 1 > t$ ^ 4 V - ^ s(-< rn < U n sm J S & f ' rr<- P ^ e f r tfa d tL 4/p~ ' /'U j' -- ^ ^ C tr ^ tA . ^ 7 fP f- p P f^ -c , Q ^s P l S # ~ tC p f-T M< $fc &1SZJ$C J 0-& &1'-PJP J h * ' sU rSSi A. stf0~$ Scf. CA*y 7V f ^? ^d y s ) f t o o os aj. y n r^ s tf *^/y*+- jL \\* Z + tl' ^ T s tU P - /! - z f * r fl < L ^ ~ 7 /^ s iA s t Pt* & sC -yifctC < A s s& /\ - ^ L ^ic P T Y ^- s s ^ 'e` f ) C- f f J L ^ shh& tP Jt&Z J )v t P h f JlAvyo/fp^Ze,i, # 4 s tf jSj&ULt*&c4 t r v . < P tH rd ' ^ ,s(stn * u sb ^ o-- Y ^ Q ju g p lt-^ L ^ L ^ e f^ r f^ /xdL$nnJ!' -- - A > fa-1- 7 -7 ^SL^o, ), )7\ *$, ?S\j~2A-& fiJ2s F 'k J tn iZ s S 0y-d~ry- " <r7 ^ b t\ ^ JU A ^Q y^f^X < 2 6 / 7 J 7 7 , EID079736 1^ P m 1 o 4 ' <40 ^ M f-O /0 ~ fM y ^ tJ A J ^ L * ir "7* "* ~ td !o < Z sL f^ tA X ^ Z y s ^ -Q , S T Y L f ^ r y J ) AlL&Cs /r f > > d / X ^ 4 t i n ^ 2 v C A+7 000032. / ? 7 \A J?7& ryf- / I 000093 17 f PERSONAL h. CONFIDENTIAL 6/13/84 TO H. V. BRADLEY D. G. WIKA T. M. KEMP T. L. SCHRENK FROM: J. A. SCHMID C-8 IN WATER ************ BELOW IS A COMPARISON BETWEEN THE 3/13/84 SAMPLES, AND THDSE TAKEN ON 6/4/84. LOCATION ******** LITTLE HOCKING LUBECK WATER * POWELLS STORE C-8 IN PPB 3/13/84 ********* 6/4/84 ******** 0.8 NOT DETECTED 1.2 1 .0 * LUBECK HILL NOT SAMPLED 1.5 I WOULD HAVE TO CONCLUDE THAT IN THE CASE OF LITTLE HOCKING, THE C-8 DROPPED BELOW THE DETECTION LIMIT OF 0.6 PPB. ALSO, RECOGNIZING THAT WE ARE OPERATING AT THE EXTREME OF THE TEST'S SENSITIVITY, THE BEST WE CAN SAY ABOUT THE LUBECK WATER IS THAT IT IS PRESENT IN THE 1.0 PPB RANGE. REV.6/14/84 - 6/13/84 DATA WAS REPORTED AS FLUORINE NOT C-8. 00 0*; 0DO 19'M  000095 V 1 PERSONAL AND CONFIDENTIAL CC: T. A. Foster June 14*1984 TO: J. A. Schmid FROM: UPDATE on C-8 IN HATER SAMPLES The attached table shows the C-8 in water data including the -roost recent data. I conclude the new data confirm the original data. 1. The Du Pont data shows that the test does not see C-8 up river and the sampling system does not contaminate the sample. 2. The second Washington sample had essentially the same C-8 content as the first. 3. The new Lubeck sample shows essentially the same concentration as the Washington sample. Thus the Washington sample is from the Lubeck Water System as I suspect or at least the Lubeck system has the same concentration. 4. The original Little Hocking sample was very close to the detection limit for the test. The concentration now appears to be below the detection limit. I do not plan to do additional sampling unless further information is needed. The concentrations are very low and in my judgement are not cause for concern. 0 G0.i>3 r-i E1D079271 LOCATION DISTANCE (MILES) SIDE ppb C-8*** PARKERSBURG DU PONT (3/15/84) (6/4/84) DISTRIBUTION CENTER OF PARKERSBURG WASHINGTON (3/15/84) (6/4/84) LUBECK (6/4/84) LITTLE HOCKING (3/15/84) (6/4/84) BELLEVILLE REEDSVILLE RAVENSWOOD RACINE POINT PLEASANT ** GALLIPOLIS 7.5 u? stream 0.5 up stream WV WV 0.25 down stream* WV 0.25 down stream WV 0.25 down stream WV 3 down stream OHIO 12 down stream 14 down stream 29 down stream 50 down stream 74 down stream 79 down stream WV OHIO WV OHIO WV OHIO ND ND ND ND 1.2 1.0 1.5 0.8 ND ND ND ND ND ND ND *well is back from the river **first community to take water directly from the rive.r ***values obtained from Experimental Station multiplied by convert to C-8 vs F content originally reported ND = below the detection limit of 0.6 as C-8 (0.4 as F) 5 to Q O O u`3 ; ' EID079272 0 0 0 0 ss 19 r Du Po n t INTEROFFICE MEMORANDUM Date: From Dept : Tel No 12-May-1987 03:06pm EST TONY PLAYTIS PLAYTIS TEFTECH 2775 TO: ROGER ZIPFEL ( ZIPFEL ) CC: JOHN CRUM ( CRUM ) Subject: C8 In Water Attached is a copy of the analytical report for our five water sample-s, which are identified as follows. #1 - Washington Works drinking fountain, B3. #2 - Powell's General Store, Washington WJ * ' - Lubeck Pennzoil, Lubeck WV #4 - Mason's Village Market, Little Hocking OH #5 - 812 20th Street, Vienna WV C. L. Hill obtained samples 1-4 by driving to each location and asking to have a plastic bottle filled with drinking water. Sample 5 was taken by D. K. Moore at his home. All samples were taken on 3/13/87. Note that the results are expressed as ppb F. When converted to ppb C 8 , the result of 1.3 ppb becomes 1.9 ppb. This result is higher than those from 1984, but considering how close we are to the detection limit of the test, the difference is probably not significant. nA7/ A 'AVTM 000 0.3-3 E1D079091 Polymer Products Department Research & Development Division Experimental Station cc: M. A. Kaiser S. R. Laas M. Lombarski B. S. Shepard G. J. Sloan PRAL File I.C . - 256 - 256 - 269 - 323 - 323 - 256 - 323 ANALYTICAL REPORT May 7, 1987 To: A. J. Playtis - PPD, Washington Wrks From: M. J. Vilone and R. M. Vasta - PPD, ESL 269 - > n Qj*i (Job No. 870-441; PRAL Nos. 87-2933 - 2937, Notebook No. E44875) Five samples of water have been analyzed for perfluorooctanoate (C8) by electron capture gas chromatography. Method ES-567 was used with the following modifications: sample size was 10 g; lyophilization was -18-20 hours; concentration of perfluorodecanoate internal standard was decreased 10 fold. Spiked standards at concentrations of 0.4, 0.5, 0.8, 1.0 and 1.9 ppb were examined. A reproducible detectable peak was observed for 0.4 ppb and we have used this as our detection limit. No C8 peak was detected in the spiked standards <.4 ppb. For the quantitation we had linear calibration curves over the range of 0.4 to 1.9 ppb. The samples were freeze dried, derivitized, and analyzed in duplicate. The results are expressed as ppb fluoride where ppb F - 0.688 x ppb perfluorooctanoate. The results are given in the attached table. If you have any questions, don't hesitate to call. gmn Attachment Keywords: GC Perfluorooctanoate water 00900 EID079092 PRAL 87-2933 87-2934 87-2935 87-2936 87-2937 Perfluorooctanoate in Water Designation ngF/g. H,0 (ppb) * #1 n.d. - (O #2 #3 1.3 ^ #4 n.d. #5 n.d. * n.d. - none detected; detection limit 0.4 ppb 000j.0'L EID079093 ^uPont INTEROFFIC E MEMORANDUM Date: From: Dept: Tel No: 4 - M a v - 1937 02:09pm EST TONY FLAYTIS PLAYTIS TEFTECH 2775 TO: ROGER ZIPFEL ( ZIPFEL ) Subject: C3 in Water The -fallowing results have been received by phone; a letter will, -foil atby the end at the week. The detection limit o-f the test is 0.4 ppb. Samare esb_cs Washington Works drinking -fountain, E-f3 i..4 Powell's General Store, Washington WV 1.3 Lbeck Fennzoil, Lbeck WV 1.3 Ma so n's Vi 11 age Ma rke t, Little Hocking OH <0. 4 S12 20th Street, Vienna WV <0. 4 RJZ0092U 00002 EID079094 000103 C-8 REDUCTION & CONTROL PROGRAMS STATUS R. J. ZIPFEL 6-11-87 003546-19 - 06/09/87 - RJZrkst 0 0 0 J.Oi EID079685 WASHINGTON WORKS OFF PLANT EMISSIONS WATER POUNDS C-8 1983 1986 - 21,700 19,100 AIR 12,700 16,200 PRODUCT 8,000 8,300 OFF-PLANT DISPOSAL 7,700 8,300 50,100 51,900 003546-10&11 - 0 6 /0 3 /8 7 - HJZtkat 00*0105 EID079694 C-8 LEVELS IN DRINKING WATER DISTANCE FROM NO. 5 OUTFALL (miles) C-8 LEVEL - PPB 1984 1987 PARKERSBURG 7.50 UPSTREAM ND ND WASH. WORKS 0.50 UPSTREAM ND ND LUBECK WATER DISTRICT 0.25 DOWNSTREAM 0.25 DOWNSTREAM 1.1 1.5 1.9 1.9 LITTLE HOCKING 3.00 DOWNSTREAM 0.6 ND RAVENSWOOD 29.0 DOWNSTREAM ND ND = NOT DETECTABLE 0033*6-7 - 06/10/87 - RJZilut EID079695 SUPERNATE POND ELIMINATION BENEFIT - ELIMINATE C-8 CONTAMINATION OF LUBECK WATER SYSTEM AQUIFER FROM THESE PONDS STATUS - PROJECT APPROVED ($320M) 11/86 PERMIT APPROVAL 3Q87 START-UP 11/87 003546-33 - 06/10/87 RJZ:kst Q0010V EID079701 SOOO tAt M T * M l '`'ppcms*,a r - E. I. ou Po n t oc N cm ou * 3 & C o m p a n y P A * K * s u i a . W . V a. 2 102 OkYM CH AOOUCT* O C'A K TU CN T CC: R. V. Hlhillovlch, 3UH53 U.S. EPA Ragion III 841 Chastnut Bldg. Philadelphia, PA 19107 Grtg Hangar, Acting Suovr. WV 01y . of Watar Resources 6321 Emerson Avanua Parkersburg, WV 26101 CERTIFIED MAIL RETURN RECEIPT REQUESTED June IS, 1987 Mr. David W. Robinson. Chief WV Olvlslon of Watar Resources 1201 Greenbrier Straat Chariaston. Wast Virginia 25311 Attantlon: Industrial Wasta Section Dear Mr. Robinson: This la tte r 1s to comply with Section D .l, Page 21 of NPOES Pana1t WV0001279. and Section D .l. Page 17 of WV Permit IW623S~82. Informing you of planned physical changes at our Plant and a alnor change 1n discharge from o u tle ts 002 and 005. The changes planned were reviewed 1n a telephone conversation with Mr. Randy Sovlc of your s t a f f and are as follows: 1) Relocate the No. 006 ou tlet sample location . 2) Add Calgon H-900G mfcroblodde to our Process Watar w alls on Blennerhassett Island to control Iron bacteria, and 3) Close three anaerobic digestion ponds. The d e ta ils o f the planned changes are sham In Attachments 1, 2 I 3. Please c a ll as on 863-4271 I f you have any questions. Very truly yours ACH:hcw Attachments 1S73H Environmental Control Consultant Washington Worts mwrrmm r.iN a* row erre uvtwO 000109 EID076048  Appendix F - page 44 ATTACHENT 3 Page 1 of 3 CLOSE ANAER08IC DIGESTION PONDS Background Three anaerobic digestion ponds located on the Ohio River banks are used for contalmeent and treatment of some non-hazardous aqueous waste from our fluoropolymer production f a c i l i t i e s . The waste Includes water, Inert suspended so lid s and a non-1on1c detergent, and 1s held 1n the ponds to anaerobically digest the detergent. The three ponds have no ou tlet and are operated so they do not overflow. This requires shipment of digested waste o ff-s1 te to another Ou Pont location for further treatment and ultimate d isp osal. Since the cost of disposal of the waste stream has been Increasing rapidly and about SOI of the material shipped Is rainwater, a storage tank 1s being constructed for the waste to sig n ifica n tly reduce the volume. It Is anticipated that two ponds w ill be closed Immediately, with the third being closed by the end o f the year when tank construction Is complete. Description 1) The ponds are o f earthen construction, approximately 6 feet deep with sloped earthen banks about 22 fe e t wide at the base. All dike w alls were reconstructed 1n 1975 or 1976 with red clay. Bentonite was mixed 1n with the clay before replacing the w alls. Bentonite was also used to seal leaks 1n the bottom of the upriver pond.>i'y 2) Page 3 o f th is attachment (WSK-1367S) shows the location , size and elevation o f the three Impoundment u n its. 3) The combined volume o f the ponds 1s estimated to be about 3 million gallons. Closure PIam 1 ) The contents o f the digestion ponds w ill be pumped Into rail cars and shipped o f f - s i t e for d isp osal. 2) V isible TtMps o f polytetrafluoroethylene (Inert so lid s) are to be hand shoveled Into 55-gallon ste e l drums and la n d filled at Latart. 3) The bottom of the ponds w ill then be removed. Including sludge and discolored s o i l , to a depth o f 3 to 4 fe e t below the bottom of the ponds. 1573H-6 OOOJ.IG EID076049 Hppenaix r - nae 4s ATTACHMENT 3 Page 2 of 3 CLOSE ANAEROBIC DIGESTION PQNOS (Cont'd.) 4) The sludge and earth removed from the ponds will be disposed of 1n our Ory Run landfill (Permit IUL-6282-82). 5) It 1s then planned to push the earthen walls Inward, f i l l with clean s o il, le v e l, and plant grass on the leveled area. Sludge Test Results Analysis of a composite sample obtained from twelve locations within the eastern most (up river) pond showed the following resu lts: COMPOSITE SAMPLE COMPOSITION (ORY WEIGHT BASIS) FIuoropolymers Triton* Ammonita perfluorooctanoate (FC-143) Zinc* Inorganic fluoride Chloride 13. 61 9.,71 85 ppm 47 ppm 26 ppm 20 PP* In solu b le, at about background level The sludge tested non-haiardous by the RCRA EP to x ic ity te st as shown below: EP TOXICITY TEST Mitel Arsenic Berita Cadmium Chromium Lead Mercury Selenium Silver Concentration (ppm) 0.00 <1 <<0o..1s <0.5 <0.00S <0.05 <0.1 RCRA Limits (ppm) 5.0 100.0 1.0 5.0 5.0 0.2 1.0 5.0 1573H-7 OGQj.li EID076050 r~ TM rv ssMsAmwiNjiaTs. Ms xtA? iTx M- *M*o n mmrum to tmm tamp. J.~ o * E pj - j *ir>uaddw m oHk V c c : T. M. Kemp G. R. Alms/S. V J. G. Loschiavo J. E. Crum D. H-y Flensborg G"# if. Hs4df^J . C E V 'O.ine R. D. Lanyon W. A. Ott J. L. Post D. A. Schneider W. M. Stewart July 7, 1987 TO: C. A. DYKES J. A. SCHMID FROM: R. J. ZIPFEL C-8 CONTROL PROGRAM My review on this issue with Dr. Bruce Karrh on June 11, 1987, went very well with little change required to our present control program. Dr. Karrh was most interested in the presence of C-8 outside the plant boundaries. He stated that we need to place the highest priority on these environmental issues. Dr. Karrh also accepted the position that our employees will continue to have C-8 in their blood. My charts and the specific comments made' during the review are attached. The following is a restatement of the specific program items in our C-8 control plan with the necessary action steps indicated. I. ADMINISTRATIVE CONTROLS A. EQUIPMENT DESIGN 1. IMPLEMENT AN IMPROVED FINE POVDER DRYER GASKET DESIGN (RESP - KLINE) B. PROTECTIVE EQUIPMENT 1. AUDIT WASHINGTON WORKS C-8 IN BLOOD AND C-8 IN AIR DATA TO DETERMINE IF CURRENT PROTECTIVE EQUIPMENT (AND OPERATING PROCEDURES) ARE THE OPTIMUM AVAILABLE (RESP - LOSCHIAVO) RJZ026552 003855-1 - RJZ:kst 0 0 0 j.2 \ EID091375 c. A. DYKES / J. A. SCHMID C-8 CONTROL PROGRAM PAGE 2 JULY 7, 1987 C. C-8 MONITORING 1. REDUCE EMPLOYEE BLOOD TESTING TO ONLY THE FOLLOWING JOBS: RAW DISPERSION AUTOCLAVE OPERATOR DISPERSION OPERATOR FINE POWDER DRYER OPERATOR ENVIRONMENTAL OPERATOR (SUMP) DISPERSION PACKOUT OPERATOR GRANULAR POLYKETTLE OPERATOR FINE POWDER PACKOUT OPERATOR FEP POLYKETTLE OPERATOR FEP WET FINISHING OPERATOR FEP DISPERSION OPERATOR FIRST LINE SUPERVISION OF ABOVE PERSONNEL (RESP - LANYON) NOTE: BEFORE WE CHANGE OUR BLOOD SAMPLING PROGRAM, WE WILL WANT TO HAVE AN INTERNAL BTO COMMUNICATION (RESP - ZIPFEL) 2. PERSONAL C-8 IN AIR SAMPLING - MONTHLY SAMPLES SHOULD BE REQUIRED OF THE FOLLOWING JOBS: RAW DISPERSION AUTOCLAVE OPERATOR GRANULAR POLYKETTLE OPERATOR FINE POWDER DRYER OPERATOR DISPERSION OPERATOR FEP POLYKETTLE OPERATOR FEP WET FINISHING OPERATOR FEP DISPERSION OPERATOR (RESP - POLYMERS - OTT COPOLYMERS - POST) RJZ026553 003855-2 - RJZ:kst O O O J.i-5 EID091376 c. A. DYKES / J. A. SCHMID C-8 CONTROL PROGRAM PAGE 3 JULY 7, 1987 3. AREA C-8 IN AIR MONITORING - AS NEEDED BY AREA AROUND CRITICAL EQUIPMENT (e.g., FINE POWDER DRYERS) AND TO RESPOND TO HIGH LEVELS NOTED WITH PERSONAL SAMPLES (RESP - POLYMERS - OTT COPOLYMERS - POST) NOTE: IN GENERAL, WE ARE TAKING FAR TOO MANY AREA SAMPLES AND NOT ENOUGH PERSONAL SAMPLES 4. DOCUMENTATION - EXPLANATIONS OF REASONS AND ACTION RESPONSE FOR AIR LEVELS (PERSONAL SAMPLES ONLY) ABOVE 50* OF THE AEL (0.56 MPB) REQUIRE IMPROVEMENT IN THE DIVISION'S ENVIRONMENTAL SAMPLING BOOKS (RESP - POLYMERS - OTT COPOLYMERS - POST) D. C-8 CONTROL LEVELS 1. ESTABLISH MAXIMUM SAFE C-8 IN BLOOD AND C-8 IN DRINKING WATER LEVELS (RESP - G. L. KENNEDY - HASKELL) -- NOTE: ONCE A SAFE LEVEL IS ESTABLISHED, THOSE PERSONNEL EXCEEDING 50X OF THIS LEVEL WILL BE REQUIRED TO BE REMOVED FROM THE EXPOSURE AREA II. PROCESS CHANGES A. IMPLEMENT USE OF PURCHASED LIQUID C-8 AS IS BEING DONE AT DORDRECHT AND CHAMBERS WORKS (RESP - POLYMERS - CRUM COPOLYMERS - HERRIDGE) B. NEW SURFACTANTS 1. TBSA IN FEP - REDUCE PRIORITY ON THIS PROGRAM TO THE POINT WHERE BUSINESS NEEDS JUSTIFY FURTHER USE (QUALITY AND COST) (RESP HERRIDGE) 2. C-9, C-10, C-12 - NO ENVIRONMENTAL LIMITS ARE PLACED ON THE USE OF NEW SURFACTANTS C. C-8 RECOVERY 1. FINE POWDER DRYER VENT - DEVELOP BASIC DATA TO IDENTIFY RECOVERY PROCESS BY 4Q87 (RESP - SCHNEIDER) 2. FEP AQUEOUS STREAMS - APPLY ABOVE TECHNOLOGY IF ECONOMICAL (RESP SCHNEIDER) D. LBECK WATER DISTRICT CONTAMINATION 1. ELIMINATE SUPERNATE PONDS - GOAL IS NOVEMBER 1987 (RESP - FLENSBORG) 2. DETERMINE MODE OF CONTAMINATION (RESP - STEWART) Attachments 003855-3 - RJZ:kst 0 0 ..1 S EID091377 O O O liy v*. 23 E. I. ou Po n t oc N em o urs & C o m p a n y P.O . Box 1217 PAMKEXsauRO. W. Va. ZCI02 rokrM C R ^a o o u c t i oc*a* tm k n t CC: R. V. Minallovich, 3WM53 U.S. EPA Region III 841 Chestnut 81dg. Philadelphia, pa 19107 Greg Henger, Supervisor WV 01v. of Water Resources 6321 Emerson Avenue Parkersburg, WV 26101 CERTIFIED MAIL RETURN RECEIPT REQUESTED July 30, 1987 Mr. Oavld W. Robinson, Chief WV 01vision of Water Resources 1201 Greenbrier Street Charleston, West Virginia 25311 Attention: Industrial Waste Section Dear Mr. Robinson: Ref: Consolidated Permit WV/NPES Permit No. WV0001279 Permit Modification No. 5 dated 7/7/87 This le tte r 1s to comply with Item 3 of the reference Permit Modification and Section 0.1 o f WV Permit No. IWL-6282-82, Informing you of a planned physical change at our Plant which w ill resu lt 1n a minor change 1n the waste material disposed of 1n Dry Run L an dfill. The material to be disposed of w ill be approximately 7100 tons o f non-hazardous sludge and d irt from closin g three anaerobic digestion ponds. The sludge te s t resu lts are shown In Table 1 attached. Transportation of the sludge and d irt w ill be by road 1n open-top t r a ile r s . Please c a ll me on 863-4271 I f you have any questions. Very truly yours 'N JMM003564 /hew Attachment 1660H-1 Environmental Control Consultant Washington Works e rre * tminos ' o * scttc* uvino I EID007534 TABLE I SLUDGE TEST RESULTS Analysis of a composite sample obtained from twelve locations within the eastern most (up river) pond showed the following results: COMPOSITE SAMPLE COMPOSITION (DRY WEIGHT BASIS) Fluoropolymers Triton* Aimonlum perfluorooctanoate (FC-143) Zinc* Inorganic fluoride Chloride 13.6X 9. 7% 85 ppm 47 ppm Z6 ppm 20 ppm ` Insoluble, at about background level The sludge tested non-hazardous by the RCRA EP to x ic ity te s t as shown below: EP TOXICITY TEST Metal Concentration (ppm) RCRA Limits (oom) Arsenic Barlgm Cadmium Chromium Lead Mercury Selenium Silver 0.006 <1 <0 .1 <0.5 <0.5 <0.005 <0.05 <0 . 1 5.0 1 00.0 1.0 5.0 5.0 0 .2 1.0 5.0 1660H-3 000113 EID007535 000120 :: -30 Medicine H o Ith Phytic Indutriti Hygiene Toxicology Medical DeparlmenWM 3M Center St Ptul. Minnesota 551*4 612/7331110 FAX ( 6 1 2 ) 7 3 3 - 1 7 7 3 NC 2C2 FACSIMILE TRANSMISSION INFORMATION SHEET D a t _ M n o S O . 1*7V 7 N u m b o r ^ o l f ^ p a g r * ___________ A ttention OV f i . 1 0 . ^ c M a r d P h . b . L ocation t4 f r .5 k t .l l L ft S ' * * HO. _ . 3 D l > _? > - 5 2 ~ 7 Special Inatructiona or Inform ation: ORIGINATOR'S NAME Talaphona nuabar to varify coaplata tranaaiaaion* or to ralata problama: I s *7 3 3~ 3 -1- 0 EID071428 3M Medical Department Medicine Health Shyeice Industrial Hygl n c Tbilcology B- on; 220-2= C2 3V Ce-reSi Paul Minr.esoia S514--1000 6i2 "33 1no November 3C, 1937 3M Robert G. Geil, D.V.M. 3030 South 9th Street Kalamazoo, MI 1*9009 Dear Dr. Geil: A a follow-up to our recent telephone conversation regarding the "Two Year Oral (Diet) Toxicity/Carcinogenicity Study of riuorecheslcal FC-1U3 in Rata/ 1 ve are writing to you to grant permission to diacuaa the report with Greg Sykss, D.V.M. of Haskell Laboratory for Toxicology and Industrial Medicine. The enclosed materials Include Dr. Sykes' October 29, 1937 memo to Charles Reinhardt, K.D. regarding the study. A copy of the 3M report was provided to G. L. Kennedy, Jr* at Haskell. 8ykes' memo should serve as a guide to the matters he wishes to discuss with you. I should point out in passing that Dr. Sykes apparently did not realize that the primary interpretation of the data in the report was made by you, C. D. King, D.V.M., Ph.D. and J. L. Allen, Ph.D. I am not certain whether the people at Haskell are aware that you and Dr. King were external consultants retained by 3M Toxicology Serviees/Medleal Department and 3M Hiker Laboratories, respectively, to prepare the report. Additionally, enclosed are the first 31 pages of the report that waa issued in August 1937 The postmortem findings begin on page 1 U. The findings regarding Leydigcell adenomas are on page 18 . The discussion section begins on page 19 and the Leydig cell adenomas are dlseussed on page 22. If you would like a copy of the entire four volume report, please let me know and we will send it. To save you searching through your files, selected pages of the "final draft report," sailed to you with a May 12, 1988, cover letter from C. Chesney, D.V.M., Ph.D., are also enclosed. This enclosure Includes pages 1 ?, l6 , 22 and 23. Ve dlseussed the statistical analysis of the incidence of Leydig cell adenomas in comparison to the incidence in 95^ control rats at Haskell, 880 control rats in Charles River CD* Rat, 2U month published data and the incidence noted by you for 6l0 control male rats at IRDC. I think the data of these three control groups are similar and seem to support the fact that it is quite 0 0 "7 E1D071429 Robert 3. Cell, D.V.M. Page 2 November 30, 1987 unusual to find no Leydig cell adenoma* in sale rat* of 2L months age a* va* the cate in the FC-IU3 study. The Haskell data Is attached for your information. 1 believe you have the Charle* River report *ince you brought it to our attention. Enclosed also is an extract from a trip report prepared by 6. V. Elrod, Ph.D., 3M Riker Laboratories. The information presented at the seeting is certainly of Interest as regards the Leydlg cell adenomas noted in the FC--1L3 high dose animals. As discussed with you by telephone( ve feel that any further review of slide* froa this study and any additional sectioning of tissues should be done under your guidance. Ve thank you for assistance in this natter. Ve trust you will submit your statement for fees for services in connection with this additional consultation in the same Banner as before. In summary, please feel free to discuss this report with Dr. Sykes. If you need any further doeunents from our files, please let ne know. Thank you again for your assistance. Sincerely, Senior Toxicology Specialist Diplomats of the American Board of Toxicology RQP:bh (T8105 2.8) Zhelosures: 1) Memo Greg Bykes, D.V.M. to Charles Reinhardt, M.D. October 291 1987 2) Two Year Oral (Diet) Toxleity/Carclnogenieity ... first 31 pages of Volume 1 of k 3) Extracted pages from May 12, 1986 draft 1) Letter Gerry Kennedy to Roger Perkins October 16, 1987 3) Extract of Memo 8. V. Elrod to t. R. Erickson Voveaber IT, 1987 de: G. L. Kennedy, Jr. Haskell laboratory H k t o n Road, P.O. Box 30 Hevark, DE 19711* C. D. King, D.V.M., Ph.D. Xenos P.O. Box 5008 Korth Branch, EJ 08876 EID07I430 OOi ARCH A. MOORE, JR. Cow m of STATE OF WEST VIR G IN IA DEPARTMENT OF NATURAL RESOURCES OIVISION OF WATER RESOURCES 1201 Granbriar StrMt Chariwton, Wt Virginia 25311 Decenber 17, 1987 Mr. A. C. Huston E. I. du Font de Nemours & Company Incorporated P.0. Box 1217 Parkersburg, WV 26102 Plant file copy DO r;oT RONALD R. POTEST D irector ROBERT K. PARSONS Oaptrty Director RE: Water Pollution Control Penult No. IWL-6282-82 Dry Run Landfill (Wood Co.) WV Modification No. 1 Dear Mr. Huston: This serves as Modification No. 1 for the above referenced facility. This modification is granted pursuant to your letters of July 30, 1987 and September 15, 1987 requesting permission to dispose of approximately 7,100 tons of non-hazardous sludge and dirt, which will result from the closure of three (3) anaerobic digestion ponds at the Washington Works facility. Should you have any questions regarding the above information, please do not hesitate to contact John Britvec, Geologist at (304) 366-5880. Very truly yours DWR/jb/me cc: Greg Henger, Supv. Cindy Musser, Insp D. W. Robinson, Chief CF001520 000J.25 EIDOS 1114 9IT 000 1 4 1 ftWV. 1 /9 1 E. I. du Po n t dewrnNmtetmmtAoguu r s & C o m p a n y W il m in g t o n , D elaw are 19898 POLYMER PRODUCTS DEPARTMENT CC: D. G. WIKA, PPD W. H. MARTIN, FIBR R. W. MICHAUD, FIBR K. D. DASTUR, C&P R. Z. FORTNEY, INTL D. P. GLEASON, PPD April 27, 1988 TO: 0. L. DARBY, DU PONT TOKYO S. HAYASHI, SHIMIZU WORKS, JAPAN G. L. KENNEDY, HASKELL LAB R. D. LANYON, WASHINGTON WORKS R. J. ZIPFEL, WASHINGTON WORKS A. E. MORRIS, CHAMBERS WORKS K. J. HUISMAN, DORDRECHT J. P. BOLLMEIER, EXPERIMENTAL STA. T. W. OLCOTT. fAYETTEVILLE FROM: H. A. SMITH AMMONIUM PERFLUOROOCTANOATE (C-8 ) FOLLOW-UP MEETING Ref: H. A. Smith to R. D. Lanyon, e t a l, 2/29/88 A meeting to review our progress and path forward w ill be held: Date: Wednesday, June 29, 1988 Time: 8:00 a.n. - 4:30 p.o. Lunch w ill be provided Place: Kent Room Hotel du Pont We w ill be discussing: o Strategy for managing C- 8 in the workplace. o Strategy for managing C- 8 in the community. o Future program regarding C- 8 in blood - monitoring and g o a ls. Please come prepared to discu ss and share information on the following 1. Your personnel air monitoring r e su lts grouped by jobs. ' 2. Practices implemented to minimize skin contact. o o o i;i7 EID079641 BETTER T H IN O S FOR BETTER LIVIN O 0. L. DARBY, ET AL -2- April 27, 1988 3. A summary of your C-8 1n blood data if you have any. Summarize as follows: , o %+ Number of employees at a level of 0.5 ppm or less. o %+ Number of employees at a level of 1 ppm or less. o %+ Number of employees at a level of 5 ppm or less. o %+Number of employees at a level of 10 ppm or less. o %+Number of employees at a level of above 10 ppm. Ofl not overwork your blood data. If it is of questionable value or too sparce to be of real value, do nothing with it. We do not need to over focus on this subject at this time. 4. The CEG (Community Exposure Guideline) for C-8 is 0 .3 ug/n3. Does your s i t e meet th is guideline? 5. Any information available on C-8 in groundwater, public waters, etc. A copy of 3M's latest MSDS and Toxicity Summary Sheet dated February 1988 reflecting the results of their long-term (two-year) rat feeding study is attached. HAS/is Attachment lC 000i5 EID079642 27 00012S rr z INTEROFFICE MEMORANDUM Date: From: Dept: Tel No: 23-Aug-1933 03:43pm ANTHONY J. [TONY] F'LAYTIS PLAYTIS PPD-SPD 304-3S3-2775 TO: Roger J. 2ipfel ( ZIPFEL ) CC: JOHN E. CRUM CC: WALTER M. STEWART < CRUM ) C STEWART ) Subject: Test Results - C3 In Groundwater Mary Jane Vilone at ESL telephoned the results listed below for the samples we submitted in May as part of our monitoring program. She did t before writing the usual report because she was surprised by the very high levels seen in the Letart samples. Sample Description C8 Level 8212 Drinkinq Fountain 5/12/33, 14:00 none detected Lbeck Water - Playtis Home 5/12/3S, 17:00 2.2 ppb Little Hocking Water Ritenour Home, 5/12/88 none detected Test Well #27 5/11/33, 13:00 1.5 ppb Letart Upper Pond 5/10/88, 11:00 1.6 pom Letart Lower Pond 5/10/83, 11:00 2.3 ppm 0 0 0 1 .1 0 . EID079090 28 OCO t s l INTEROFFICE MEMORANDUM Date: From: Dep t: Tel No: 3Q-Jan-1989 01:18pm ANTHONY J. [TONY] PLAYTI3 PLAYTIS PPD-SPD 304-863-2775 TO: Roger J. Zipfel (ZIPFEL ) CC: JOHN E. CRUM CC: WALTER M. STEWART (CRUM ) (STEWART ) Subject: Test Results - C8 In Water The following results have been received from ESL for the November samples for monitoring C8 in local water sources. They had a terrible time getting their analysis to give the necessary level of sensitivity, but they are confident that they now know what caused their difficulties. Sample Description oob C8 6212 Drinking Fountain 11/2/88, 15:45 none detected Test Well #27 11/4/88, 08:30 1.3 Lubeck Water - Playtis Home 11/2/88, 17:00 1.4 Little Hocking Water - contaminated sample, analysis Ritenour Home, 11/7/88, 06:00 not possible E1D079089 000 V 29 rT 000133 INTEROFFICE MEMORANDUM Date: From: Dept s Tel No: 31-May-1389 10:54 WILLIAM E CRAWLEY CRAWLEWE PP0-*TEFLON'TECH 304-863-2742 ANTHONY J. [TONY] PLAYTIS < PLAYTIS ) Subject: C-8 Sampling We have decided that it is not necessary to continue sampling the Lubeck system for C-8 to see the impact of the Supernate Pond closure. Effective immediately, ue will not need to take any more sampling from the Lubeck system. Any Lubeck samples that are being held for analysis should be discarded to save the sampling cost. We do want to continue to sample Water Well No. 27 on a quarterly basis to monitor the impact of the Supernate Pond closure. We should also continue to take water samples around ? Dupont, Letart Landfill on a monthly basis. Please call me if you have any questions. Thanks, Bill. RJZ009200 OGOJ.ol . ' \ EID079087 V 30 0 0 0 J. H. V. BRADLEY WORKS MANAGER E . I. DU PONT DE NEMOURS & C O ., INC. WASHINGTON WORKS PLANT . 0. BOX 1217 PARKERSBURG, WV 26102 STANDBY PRESS RELEASE June 12, 1989 Du Pont's purchase of the Lubeck Public Service District (LPSD) facility on Rector Lane is progressing satisfactorily. The LPSD initiated the transaction in late 1986, offering sale to Du Pont to facilitate relocation of the LPSD's well field to a larger location to meet their forecast increased demands. After careful study, Du Pont agreed to purchase the wells to obtain additional process water and real estate to facilitate current and future Plant operations. The Plant has provided the LPSD with information to include in its response to a request from the West Virginia Public Service Commission for groundwater analytical data. Information has been provided from testing that has taken place in compliance with requirements of the permitting process of the Resource Conservation and Recovery Act (RCRA). This includes a test well that is the Plant's well closest to the LPSD wells. Additionally, since the mid-1970s, samples have been taken to ensure that Plant operations are not adversely affecting water quality. We believe that the data indicate that the water is safe and reliable. -m ore-- 0 0 Ox. E1D079154 DU PONT 6/6/89 STANDBY tGE 2 Both the LPSD and Washington Works agree that Du Pont's purchase of the LPSD wells will benefit both LPSD customers and Du Pont. The sale of the property will enable the LPSD to make a transition to its new facility more quickly and to reduce the cost increase to its customers. Benefits to the Plant include additional real estate adjoining the warehouse where products are stored, improving traffic flow and alleviating congestion around the warehouse. The water wells located on the property will also help fill the Plant's increasing needs for process water. Additionally, the purchase will allow the Plant to delay expansion of its well system on Blennerhassett Island. EDITORIAL CONTACT: H. D. RAMSEY PLANT SUPERINTENDENT WASHINGTON WORKS PLANT 304-863-2739 000:137 EID079155 Questions and Answers (Background Information for Plant Media Contacts) , Q; What is FC-143? A ; It's an ammonium salt of a fluorinated carboxylic acid. surfactant-- a detergent-like material. It is a 2. Q: What does Washington Works use FC-143 for? A : It is used in the manufacture of Teflon*. End uses of Teflon* include applications in the fields of medicine, space, the semiconductor industry, and non-stick cookware. 3. Q: Is FC-143 harmful? A ; The issue is concentration-- how much and when. Animal studies with rats have demonstrated that it is slightly to moderately toxic. In these animal studies, there was an indication of liver toxicity. The Material Safety Data Sheet (MSDS) notes human skin irritations, tearing, and respiratory discomfort with over-exposures. However, there has been no adverse effect on employee health associated with FC-143 exposure. 4, Q; How long has Washington Works been using FC-143? A : Since August of 1951, nearly 38 years. 5. Qi Where does FC-143 come from? A : We purchase it from 3M Corporation, and there is a Material Safety Data Sheet (MSDS) available to you that gives a good summary of its properties. 6. Q: Why were vou sampling for FC-143? A_L We began testing employees for FC-143 in 1979 when we were informed by 3M that it had been found to accumulate in human blood. We also initiated a program in 1983 to track FC-143 outside the areas where it was used. 7. Q; At the 1-2 ppb level, will it accumulate in the blood of those who drink it? Aj. We do not have the information to confirm it, but it is our technical judgment that it would not accumulate at these low levels. 0 0 0138. EID079156 8. Q: Why does it accumulate in the blood of humans? ft: We don't precisely know the mechanism. We do know that it >es not readily decompose, react, or break down in the biological processes of the human body. It is expelled from the body slowly. 3. Q; What is the allowable safe limit in drinking water? Ai. Du Pont has calculated a safe level of 5 ppb for drinking water. This was calculated by converting the daily dose based on Du Pont's AEL (acceptable exposure limit) for our plant workers, to an equivalent dose exposure were to occur via the drinking of 2 liters of water per day. Appropriate reductions were then incorporated as safety factors. if 10. Q: To what level has it been measured to accumulate in the blood of those who are exposed to it at the Plant? A s We have detected levels up to 33 ppm, with a significant percentage at 5 ppm or lower. There has been no adverse effect on employee health at these levels. 11. Q; How often is the blood of employees monitored for FC-143? Ai Every other year for Washington Works employees who work with FC-143. Consistent with our occupational health standards, we also ntinue to monitor to affirm the adequacy of our personal protection practices and procedures. 12. Q; How did FC-143 get into the LPSD water system? Ai We believe it could have come from three on-site collection ponds. Those ponds were closed in 1988 and replaced with metal collection tanks. The waste is shipped to another Du Pont site for disposal. This change was a result of Du Pont's Corporate Environmental Policy. 13. Q: What are you doing to reduce FC-143 emissions from vour plant? AlL We are currently in compliance with all regulatory requirements, but to comply with Corporate environmental direction, we have additional plans. We have a program to reduce air emissions going into operation during the last quarter of 1989 (at a cost of 3,800,000), and we are also studying means to remove FC-143 from wastewater. E1D079157 AiL--Qi I f t h e s t u f f i s n o t h a r m f u l , uhu a r e y o u s o e n d i n a anv money tn re d u c e the a ir and w ater e m i s s i o n s ? ----- - Aj. It continues to be Du Pont's policy to minimize aqueous and air emissions by reduction of waste. Even though the material has no known i n effects, it is our intent to minimize exposure which could cause concern associated with accumulation in the blood. 15. Q: Is the presence of FC-143 in the LPSD water system the reason for Du Pont's purchase of LPSD wells and orooertv adjacent to the Plant? A ; We would have made the purchase whether or not the FC-143 was present. We need an additional well water supply, and we will make good use of the additional real estate. Additionally, the purchase allows us to delay the expansion of our well system on Blennerhassett Island. 16. Q: What was detected in the water system? A 8 A full scale of normal water tests-- such as for hardness and chloride-- was conducted. Addi tionally, the water was analyzed for more than 240 compounds, using U.S. EPA monitoring requirements for groundwater as a reference, under the Resource Conservation and Recovery Act (RCRA). From the more than 240 materials that were analyzed, only trace quantities of 17 materials were detected. These results do not represent a concern. *7. Q: How long have vou known FC-143 was present in the Lubeck Water vstem? A: Since 1983. 18. Q: Why have vou not made this information public knowledge until now? A: At that time, we were not sure of the findings, since the level found was so low-- close to the detection limit. We did not regard the level to be a health problem. 19. Q: Isn't this a female reproductive concern? A: No. Initial tests by 3M with rats indicated a cause for concern, but more extensive testing demonstrated that the problem was not with FC-143, but with the original testing procedure. 20. Q: What is Du Pont paving for the wells? A: *1.8 million. RJZ009762 0 0 0 J. X'r'J. EID079158 0001 UtHOURS fjCO. ATTACHMENT 1 000113 GASTON CAPERTON Governor STATE OF WEST VIRGINIA DEPARTMENT OF NATURAL RESOURCES DIVISION OF WATER RESOURCES 1201 Greenbrier Street Charleston. West Virginia 25311 June 21, 1989 Mr. A. C. Huston E. I. DuPont de Nemours & Co., Ine P. 0. Box 1217 Parkersburg, WV 26102 J. EDWARO HAMRICK III Director LARRY W. GEORGE Deputy Director CERTIFIED RETURN RECEIPT REQUESTED RE: West Virginia Solid Waste Management Regulations Permit Numbers: IWL-6282-82 and 3494 Dear Mr. Huston: As you should be aware, the West Virginia Department of Natural Resources (DNR) filed Title 47, Series 38, "Solid Waste Management Regulations", which became effective on November 4, 1988 (on an emergency basis). This letter will serve as notification that your facility will now be governed by these regulations and to inform you of what you will be required to do to comply with these regulations. The regulations specify that all solid waste disposal facilities must have a liner under the site and that the liner system piust include a subbase, leachate detection zone, composite liner (compacted clay topped with a synthetic liner), and leachate collection with a protective cover zone. However, the regulations also acknowledge the fact that existing landfills may not have the specified liner system in place. To allow for the continued operation of existing facilities, a provision has been included in the regulations whereby a permittee may petition the director to allow use of an alternate system. The petition must include a demonstration that the currently employed system will provide protection of groundwater resources. The division wishes to begin reviewing these proposals as soon as possible. With this in mind, you are required to submit proposals for the groundwater protection demonstrations to the Division of Water Resources by July 31, 1989 using the Emergency Solid Waste Management Regulations. The results of your demonstration must be submitted with your application for permit renewal or Permit Application Addendum unless your permit expires within six (6) months of the date of this letter in which 0 0 0 j.4 EID007493 Mr. A. C. Huston Page Two instance this agency will entertain a request for a permit extension to allow a reasonable time period to complete the necessary demonstration. If your permit has already expired and all allowances exhausted for extension as provided by statute, you are advised to expeditiously submit your demonstrations. This agency will execute enforcement discretions in these instances. The purpose of soliciting proposals now is to assure both you and the division that the demonstration will be acceptable prior to its initiation. The proposal should contain a complianceschedule for completion of the demonstration. Should you require further information or assistance please l 00QJ.45 EID007494 O O O i-iS INTEROFFICE MEMORANDUM Date: From: Dept? Tel No 30-Jun-1989 03:51pm ANTHONY J. [TONY] PLAYTIS PLAYTIS PPD-SPD 304-863-2775 TO: WILLIAM E CRAWLEY CRAWLEWE ) CC: JOHN E. CRUM CC: WALTER M. STEWART CC: Bill Tice CC: Roger J. Zipfel ( CRUM ) ( STEWART ) ( TICE ) < ZIPFEL ) Subject: C8 In Water Test Results From SL SAMPLE test well 27, 5/4/89 P"*\2 drinking fountain, 5/8/89 Lubeck Water (Playtis), 5/7/89 Little Hocking Water (Ritenour) 5/4/89 SAMPLE Letart upper pond 11/23/88 lower " upper lower 12/30/88 upper lower 1/24/89 upper lower 2/28m/89 upper lower 3/17/89 upper lower 4/25/89 PPB C8 0.44 none detected 0.73 contaminated sample, analysis not possible PPM C8 4.2 2.3 0.96 1.5 3.2 3.1 1.2 1.9 1.1 1.1 0.49 1.5 0 0.U 7 . EID079124 OOOj.lS INTEROFFICE MEMORANDUM Date: From: Dept: Tel No: 3-Aug-1989 08:31am HAROLD BUMGARNER BUMGARHE Power & Services (304) 863-4796 '0: SEE BELOW Subject: LOWER POND LEAKAGE DRY RUN FOLLOWING OUR INSTRUCTIONS, BOSO DRAINED THE LOWER PONO, THEN DUG NTO THE BANK TO LOCATE AND REPAIR THE LEAK. THIS METHOO OF REPAIR, USING iENTONITE CLAY WAS RECOMMENDED BY THE W. VA. SOIL CONSERVATION SERVICE. 1ELVIN DID THE WORK ON 8/2. THE PATH OF WATER THROUGH THE GROUND WAS VERY IVIDENT AND HE WAS ABLE TO DIG THROUGH IT AND PACK THE HOLE AND ADJACENT AREAS 'ITH THE CLAY (HE USED A TON OF BENTONITE). WE ARE CONFIDENT THE LEAK IS EPAIRED BUT PROOF WILL REQUIRE PERMITTING THE POND TO REFILL WITH RAIN WATER. HE AMOUNT OF ALGAE PRESENT, BASED ON APPEARANCE, IS REDUCED OVER WHAT WE HAD IX WEEKS AGO. BUT WE DO SEE ALGAE SO BOSO WILL PUT A SMALL AMOUNT OF THE OPPER SULFATE ALGAECIDE IN THE POND AS IT FILLS. WE HAVE ASKED BOSO TO REMOVE THE SETTLED SOLIDS FROM THE UPPER POND 0 INCREASE ITS VOLUME. HE INTENDS TO DO THIS WORK OVER THE NEXT FEW DAYS. YOAK TELLS ME THAT HIS SAMPLE REPORT FOR JULY WILL SHOW NO FLOW ROM THIS POND. THE AUGUST SAMPLE WILL INDICATE THE SUCCESS OF THESE ODIFICATIONS. istribution: 0: FELIX DAVIS, JR. 0: R J YOAK 0: Billy D. Garner 0: ROBERT L. CARLSEN 0: ROGER C GAUL C: PENNY C MAHONEY C: WALTER M. STEWART C: Arthur C. (Art] Huston, Jr. DAVISF ) YOAKRJ ) GARNER ) CARLSERL ) GAULRC ) MAHONEPC ) STEWART ) HUSTON ) 3 s A 9 1 EID014083 0 00J.0 INTEROFFICE MEMORANDUM Dato: Fronti Dept I Tel Noi 12-Apr-1990 02:45pm ANTHONY J. [TONY] PLAYTIS PLAYTIS PPD-ER 304-863-2228 TOi Charles T. Alt TOs PENNY C MAHONEY TOs WALTER M. STEWART ( ALT ) ( MAHONEPC ) ( STEWART ) Subject: C8 At Dry Run Attached are results for various water samples taken at the Dry Run Landfill. The numbers refer to various stream sampling locations noted on my hand-drawn map. I asked Jim Yoak to take these samples because I was concerned about C8 leaching out of the material taken out of the Teflon* supernate pond sites. Since some of these results are nonzero, we may want tc do some additional testing. / A J I U V JO fI 00.*. EID080I67 INTEROFFICE MEMORANDUM Date: From: Dept: Tel No: 9-Apr-1990 03:50am Peter D.Spohn SPOHNPD PPD-SPD 363-4732 TO: ANTHONY J. [TONY] PLAYTIS ( PLAYTIS ) Subject: Dry Run C8 Analyses Here are the results: Samole D.R.#1 D.R.*2 D.R.*3 D.R.#4 D.R.#5 P.m C8 1 .6 0.0 0.0 0.6 0.4 alues were calculated from the area of the peaks EID080168 0 wt/o r* 3 H lW 3 OCO 51  j' ;t",: '. :-; -IT?': Jf'V `s*?\ SUPERNATE SLUDGE TO LETART LANDFILL (Letter, Stewart to Robertson, August 23, 1990) BCC: J. B. Allen, Legal C. F. Musica, Wilmington . c. c. Chien,'Louviers 'V Route to:." M. S. Eaton H. D. Ramsey C. R. Campbell F. Davis L. W. Goin L. K. Ireland A. C. Sobrero w. E. Crawley T. L. Byrd B. D. G a m e r R. C. Gaul. 'Route .to:? P. C. Mahoney EID051924 E. I. ou Pont de Nemours & Company P O. Box 1217 PAAKCftsau*a. W. Va. 26102 * A O O u C ',1 0 P A T w tN T CERTIFIED MAIL RETURN RECEIPT REQUESTED August 23, 1990 Mr. Max Robertson, Acting Chief Waste Management Section WV Division of Natural Resources 1260 Greenbrier Street Charleston, WV 25311 Re: Letter, Huston to Robinson, 7/30/87 Letter, Huston to Robinson, 9/15/87 Letter, Robinson to Huston, 12/17/87 NPDES Permit: WV0076244 NPDES Permit Application: WV0076066 Permit Number: 3495 Dear Mr. Robertson: This letter is to inform you of our intent to relocate fluoropolymer contaminated sludge from our Dry Run landfill to the Letart landfill. It is our site policy to segregate fluoropolymer waste from other plant wastes due to fire potential. In an effort to consolidate all of the fluoropolymer waste, we will be relocating approximately 7,000 tons of non-hazardous sludge and dirt from its current location at the Dry Run Landfill to the Letart Landfill in Mason County. This sludge is the only fluoropolymer waste known to have been disposed of in Dry Run. All other fluoropolymer waste has been disposed of in the Letart landfill. The sludge was generated during the closure of three fluoropolymer anaerobic digestion ponds during 1988. The movement of this soil to the Dry Run landfill was discussed with and approved by the DNR in the referenced letters (attached). We believe that the waste material to be relocated is covered under our existing Letart Landfill permit. We plan on beginning this movement early in September, 1990. If you have any questions or comments, please, feel free to contact me on 863-4271. Very truly yours, Attachments Environmental Control Consultant Washington Works erre* t h i n g s r o * erre* l i v i n g EID051925 OGJ. INTEROFFICE MEMORANDUM WASHINGTON WORKS POLYMERS March 27, 1991 TO: C. R. Campbell C. F. Muska L. W. Go in T. L. Byrd A. J. Platiss R. J. Yoak H. D. Ramsey W. M. Stewart L. K. Ireland M. G. McClusky L. Williams From: P. C. Mahoney QUARTERLY C-8 RESULTS AT DRY RUN LANDFILL Attached is an updated figure showing the C-8 results for the fourth quarter, 1990. Due to a miscommunication, samples were not taken during the third quarter, 1990. Samples were taken during the first quarter, 1991 but the results have not been received. The levels of C-8 appear to be decreasing, but with just two data points it would be premature to assume this will be a continuing trend. I will issue the first quarter results as soon as they are available. 0 0 0 j. EID080172 C -8 IN PPM - DRY RUN LANDFILL supnte. Dir. QUARTERLY ROUTINE SAMPLES Upper' Pond Pt.#1 7/26/90 0.4 10/31/90 0.1 |Pt.#2 o o o Lower .Pond, Outfall 001 Pt.#3 1000 ft Downstream Pt.#4 Property Line Pt.#5 0.4 0.2 0.7 0.5 0.3 0.15 0.1 0.045 EID080173 zs9i00cirv t V 38 O C O A .1,0 w 'r AIM TtTVIEyC-8 ISSUES AT WASHINGTON WORKS IN A WAY THAT ALL CONCERNS ARE AOORESSEO SO THAT 08 CAN BE EFFECTIVELY MANAGED AT THE SITE. AGENDA ITEM INTRODUCTION REVIEW OF AREAS AFFECTED 08 BALANCE FOR 1990 AIR DISPERSION MODEL RESULTS CEG STATUS, 08 IN WATER 08 TEST STATUS RECOMMENDATIONS FOR DETERMINING SIZE OF PLUME FROM SUPERNATE PONOS PLANS FOR TIEING IN LPSD WATER WELLS TO PLANT PROCESS WATER SYSTEM OTHER ISSUES RELOCATION OF SUPERNATE SLUOGE FROM DRY RUN t LETART PERMIT 727 RESPONSIBILITY STEWART MC CLUSKY STEWART MC CLUSKY CHIEN VANDELL IRELAND GARNER MAHONEY STEWART OOOi r.i EED080797 BACKGROUND C-8 WHAT IS C-8? AMMONIUM PERFLUOROOCTANOATE t FC-143 FC-118 (20% SOLUTION) CAS NO. - 3825-26-1 WHAT IS IT USED FOR? DISPERSING AGENT - POLYMERIZATION (USED SINCE LATE 1950's OR EARLY 1960's) WHERE IS IT USED? TEFLON) POLYMERS - ALL POLYMERIZATION BATCHES t TEFLON) COPOLYMERS - FEP POLYMERIZATION HOW IS IT RELEASED TO ENVIRONMENT? AIR - FINE POWDER AND FEP DRYERS WATER - DISPERSION & FEP SUPERNATE STREAMS - FLOAT TANKS - FEP COAGULATORS - POLYMERIZATION UNIT STREAMS LAND - SUPERNATE PONDS (NOW CLOSED) - SOLIDS (SOME WET) SENT TO LANDFILLS HOW TOXIC IS IT? ACUTE - MOOERATE CHRONIC - TREATED AS VERY TOXIC BECAUSE C-8 BIO-ACCUMULATES IN BLOOD AEL - 10^fG/M3 CEG - 0.3>VG/M3 /hew (4/15/91) 830 ~'- EID080798 WASHINGTON WORKS SITE SUPERNATE PONO AREA - CONTAMINATED SOIL - GROUNDWATER (-20 FT) WEST END OF SITE - GROUNDWATER (-75 FT) C-8 DETECTED LETART LANDFILL SURFACE WATER - LEACHATE PONO OVERFLOW t GROUNDWATER - OLD WELL SAMPLE DRY RUN LANDFILL SUPERNATE SLUDGE SURFACE WATER - UPPER PONO - SEDIMENTATION BASIN - DISCHARGE STREAMAT PROPERTY LINE t GROUNDWATER - MONITOR WELLS PPM 100 100 PPB 2-3 PPM 2-3 2-3 PPM 75-100 2-3 2-3 .04-.2 NO EID080799 C-8 IN DRY RUN MANAGEMENT PLAN PROPOSAL NO. 1 - LEAVE SUPERNATE SLUOGE IN PLACE, STABILIZE THE C-8 TC RETARD MIGRATION BY COVERING WITH 2 FT NATIVE CLAY PROS - EASY TO DO - LESS EXPENSIVE - NO TRUCKS ON HIGHWAYS - NOT A COMMUNITY ISSUE AT LETART - REDUCES SURFACE WATER CONTAMINATION LEVEL - PERMIT MODIFICATION NOT AN ISSUE CONS - MAY NOT PROTECT GROUNOWATER - SURFACE WATER CONTAMINATION MAY BE ABOVE CEG PROPOSAL NO. 2 - REMOVE SUPERNATE SLUDGE FROM DRY RUN AND RELOCATE THE MATERIAL TO LETART PROS - REMOVE SOURCE FROM THE LANDFILL - REDUCES SURFACE WATER CONTAMINATION LEVEL - GROUNOWATER CONTAMINATION POTENTIAL IS REDUCED CONS - TRUCKS ON HIGHWAY - COMMUNITY ISSUE AT LETART - NEED PERMIT FROM WY-DNR - SURFACE WATER MAY STILL BE ABOVE CEG - GROUNDWATER MAY STILL BE CONTAMINATED - COST EXPECTEO TO BE 75-100M $ - OTHER PERMIT ISSUES AT LETART 0 VV. EID080800 Supnta. Dlrt O O 0 1 w Outfall 001 Intar. Point 1000 ft Downatraam Proparty m Lina BOoO0Oo0 Prior Waak Rainfall C -8 IN PPM DRY RUN LANDFILL 2/13/90 4/25/90 5/22/90 0.6 ---------- 0.03 0.001---------------------------- < 1.6 0.05 0.15 1.68 0.76 1.71 6/19/90 2____ --2 _1 _1 0.2 0.72 GW006840 O G O SS V 39 r temporary operating instructions TOI NO. 91-6 TITLE: Relocation of supernate sludge within Dry Run Landfill AREA: Power and Services Dry Run Landfill Extent of work: 09/23/91 to 10/31/91 Objective: The objective of this work is to relocate the supernate sludge that was originally landfilled at Dry Run Landfill in 1988. The sludge will be moved from its current location to another location within the landfill. This new location will reduce the potential of leaching from the supernate sludge. All reasonable efforts will be made to completely remove the sludge from the existing location. SAFETY: All safety rules now in effect at the Dry Run Landfill will remain in effect during execution of this T.O.I. MSDS for FC-143 FLUORAD (C-8) is attached. (Attachment A-l) MSDS for Triton X-100 is attached. (Attachment A-2) PPE required during handling of the supernate material: Safety glasses with side shields Long sleeved shirts Rubber gloves No smoking materials will be permitted in the vicinity of the supernate material. Avoid breathing dust contaminated with the supernate material. If dust is generated during the excavation or movement of the sludge, the sludge should be sprayed with water to reduce the dust problem. If the dusting problem persists, the Site Occupational Health Coordinator (A. J. Playtis) will be consulted. RAK002923 000 EID024306 EID024307 RAK002924 WWM516 JOEGASTON SCALE* 1* 50' Ncck: l by gastonji at ws_26 on Thu May 02,1991 -Tl# Cl o 6 R I D i W E S T V E R G IN IA S T A T E P I_ A N E C O O R D I N A T E _ rar----- ; --^ - E.I. DUPONT DE NEMOURS & CO. NON HAZARDOUS--EANDFILL DRY RUN, .WOODviOUNTY, W.VA. T0P0 GR APH I(t 'MAP 1989 . ' * t INC. THIS DRAWING HAS BEEN FURNISHEO BY E.I.OUPONT OE NEMOURS A CO. THE INFORMATION ANO KNOW-HO* TtEREOH MAY NOT BE USED NOR THE DRAWING REPRO DUCED WITHOUT THE WRITTEN PERMISSION OF DUPONT. ALL REPRODUCTIONS IN WHOLE OR IN PART. INCLUDING VENDOR'S SHOP DRAWINGS. SHALL BEAR OR REFER TO THIS STAMP. J . G A S T O N LlSCALE_______L ____" 1 0 0 _______________ ! drawn by I. DATE -3 0 -9 1 G A S T O Nupdatedry J 1 i5 -l-9 1 i CHECKED B Y ___________________________________ 1_________ 1 APPROVED BY___________________________________ _____________ ELEC. COOE CLASS ' n j no. faa number PROJ. NO. WASHINGTON WORKS OF m .. ww M5 1 6 AR 0 1J - _ n i 1 1 rv i nn 000172 W A SHING TO N W ORKS P.O. B o x 1217 Pa r k e r s b u r g . W V 26102-1217 S S # *''" cc: T. L. Eichstdt L. W. Goin m ! M.' McClusky" P. C. Mahoney H. D. Ramsey W. M. Stewart October 3, 1991 CONFIDENTIAL TO: J. B. ALLEN - D7156 W. P. ANDERSON - 012026 T. R. BARRY - N9442-1 C. C. CHIEN - L3359 W. D. COBB - 011090 M. S. DEAK - 012016 M. S. EATON - WW J. C. LETTINGER - N7410 J. S. LINDELL - 011056 T. D. VANDELL - L33E63 D. M. VON SCHRILT 11090 FROM: R. J. ZIPFEL - WV > C-8 IN WATER SAMPLE RESULTS OHIO RIVER, SITE TEST WELLS, AND NEW LBECK WATER SYSTEM The site conducted an extensive sampling program of the Ohio River, plant site test wells and the new Lubeck Public Water System wells for the presence of C-8 1n September, 1991. This program was to further analyze the new Lubeck Public Water System wells, to gain further information on the C-8 levels in the Ohio River and 1n the aquifer beneath the site, and to begin to qualify an outside Du Pont analytical laboratory for C-8 in water data (CH2M HILL). The results of the sampling program showed the following: 1. Non-detect1b1e levels of C-8 in the Ohio River upstream of the site. 2. C-8 levels at expected values in the Ohio River downstream of the site and In the aquifer beneath the site (old Lubeck Water Systems wells). 3. Seven (7) of eight (8) results from the new Lubeck Water Systems wells showed non-detect1ble levels of C-8. The eighth sample gave a C-8 result near the lower analytical detection limit. The complete data package and path forward from this segment of work are attached. Any questions on these results or other items in this communication package should be directed to Penny Mahoney, Dave Ramsey or the writer. RJZ:sal Attachment BETTER THINGS FOR BETTER LIV IN Q EID079110 PRIVILEGED 1 CONFIDENTIAL SAMPLING PROGRAM SUMMARY OVERVIEW OF SAMPLING RESULTS SUMMARY PATH FORWARD 950-1 o o a -; EID079111 C-8 SAMPLING RESULTS Test Well #27 Well #331 Well MW-4 Ohio River -1 Ohio River -1 Duplicate Ohio River -2 Ohio River -2 Duplicate Ohio River -3 (Near Outfall) Ohio River -3 Duplicate Ohio River -4 Ohio River -4 Duplicate Ohio River -5 Ohio River -5 Duplicate Ohio River -6 Ohio River -6 Duplicate New Lubeck Well -F New Lubeck Well -F Dupl New Lubeck Well -B New Lubeck Well -B Dupl Old Lubeck Well -1 Old Lubeck Well -1 Dupl Old Lubeck Well -4 Old Lubeck Well -4 Dupl Experimental Station (PPB C-8) 7.1 <1 2.7 <1 <1 <1 3.9 19.6 16.8 5.2 3.1 4.2 2.8 <1 2.0 <1 <1 <1 <1 8.8 4.1 4.2 2.9 CH2M Hill* (PPB C-8) 1.2 0. 1 -v-4* 0.2 .if. Not Detected Not Detected Not Detected Not Detected 11.0 12.0 0.8 1.1 1.1 1.1 0.5 0.6 Not Detected Not Detected 0.3 Not Detected Destroyed 1.1 0.9 1.7 7^ * CH2H Hill experienced analytical difficulties. Absolute numbers may be low. 10/2/91 951 EID079112 -- Vc \' ' v- 7*__,_sa^1t.Nv --1- 'T ^ r / v-.' ^' r - VJ\skjV/> V.i 4*. .SiX , ORW- *~\ -- v~~S ' ^ i*"i. \ v ; kV / _ fvER ORW-2 C: ND/ND E: <1/ <1 / * ' C*>T _-- ORW-l C.-ND/NO E: * !/*] ) f~. /jr:ja ' / r^ ORW-5 C: 1.1/ 1.1 E: 4.2/2.8 7I r f // **T* /rl *4'*Tt*U--mu'u; Al]A4 V ' ^:S a . Vi . DRW-4 C: 0.8/1.1 E: 5.2/3.1 ORW-6 C: 0.5/0.6 E: -<-1/2.0 f* * % '( \'.V" F>li(;'js> r, ^ - z . . 7 T % xv '\ \ i- T 'V - v l-*j m UBKX RLLFIIU **.\'J P V Stndw X '^ i.-iJ ^ WK C-8 RESULTS (PPB) DETECTION LIMIT; ILL: 0.1 PP8 EXP. STAT: 1.0 PPB SAMPLE DATE: 9/11/91 )* / f i EID079113 t \ r - 7 i i\t\r7 C \ l MVEK LEVEL Ji ,TW M-2 TW WH TW R A M C Y KELL MT.m W E-4 TW E-5 n 99 l V TW M-4 C: 0.2 E: 2.7 A)% I 3 i C: 0.9/1.7 | E: 4 .2/2.9 |ECK\WAITER COj \ fc OLW-1 C: 1.1 E: 8.8/4.1 >.\ - '"N *ki* / / V P TMC: 27 1.2 m ` E: 7.1 Oo * VO i--* . H* 's ir * SLJU :l y> U w 57/. X i? 0 . ^ == .u C-8 RESULTS (PPB) 3600ZfH DETECTION LIMIT: CH2M HILL: 0.1 PPB EXP. STAT: 1.0 PPB SAMPLE DATE: 9/12/91 // \\ // U ll s / \i / S // // // // /S' 000 4N0V c r e e k ocmTHESIS C R O SS REFERENCED SITE MAP 41 r C00:1.7 3 TOXICOLOGY LIMITS - TLV - AEL - cega - CEGw ug/m3 100 10 0.3 - PPb 5.6 0.56 0.0015 1.0 CALCULATED DOSE - AEL - CEG 100 ug/day 6 ug/day 000 50 EID079258 C-8 DETECTED WASHINGTON WORKS SITE SUPERNATE POND AREA - CONTAMINATED SOIL - GROUNDWATER (-20 FT.) WEST END OF SITE - WELLS 27 & 4 - GROUNDWATER (-75 FT.) t NO. 5 OUTFALL - DISCHARGE TO OHIO RIVER WASHINGTON WORKS EMPLOYEES 1991 (VOLUNTARY TESTING) DRINKING WATER (LPSD) 1984 - 1989 1991 LETART LANDFILL SURFACE WATER - LEACHATE POND OVERFLOW GROUNDWATER - WELL SAMPLES DRY RUN LANDFILL SUPERNATE SLUDGE t SURFACE WATER - UPPER POND - SEDIMENTATION BASIN - DISCHARGE STREAM AT PROPERTY LINE GROUNDWATER - MONITOR WELLS Revised analytical method ooo.ui PPM 100 100 PPB 2-4 40 PPM UP TO 5 PPB 0.7 - 2.2 3.8* PPM 2-3 0.05 - 0.7 PPM 75-100 2-3 2-3 0.04 - .2 PPB 2-5 EID079259 GROUNDWATER ISSUES 1) P U N T SITE ROUTINE SAMPLE RESULTS v VERIFICATION INVESTIGATION 2) LETART UNDFILL LINER DEMONSTRATION SITE OVERVIEW PROPOSED STRATEGY 3) DRY RUN UNDFILL DETECTED IN DOWNGRADIENT WELLS 000J EID079269 INTEROFFICE MEMORANDUM TO: MAYNARD S EATON, JR TO: H. David Ramsey,, Jr. Date: From: Dept: Tel No 25-Jan-1993 08:13am TONY L EICHSTADT EICHSTTL POLY 304-863-2531 ( EATONMS ) ( RAMSEY ) Subject: C-8 ALTERNATE HDR00I553 000J.84 EID087668 INTEROFFICE MEMORANDUM Date Fro* Dept: Tel No 22-Jan-1993 12:23pm JAMES R LAWSON LAWSONJR PPD 304-863-4618 TO: Distribution List Subject: Great News on Surfactant Bruce, this is terrific news. The favorable reports on both acute toxicity and bioaccumulation combined with prior work showing this surfactant should be suitable for FEP means that, for the first time, we have a viable candidate to replace C8 in much of "Teflon". Even better, the candidate would be produced internally, improving our overall cost position. We have been waiting on this toxicity assessment before commencing additional polymerization testing. I think the focus of work should now switch to our organization. Obviously, we will need pure material for testing. Can you provide us with pound quantities? The focal point for our internal efforts should be Roger Zipfel. Please contact him to develop our path forward. Jim HDR001554 0 0 0 <5 s EID087669 INTEROFFICE MEMORANDUM Date: From: Dept: Tel Ho: 21-Jan-1993 09:55pm Bruce E. Baker BAKERBE AT A1 AT JLCL01 DuPont Chemicals 540-3490 TO: Hsu-Nan Huang TO: K. Spencer Prowse C HUANGH AT Al AT JLCL01 ) ( PEOWSEKS AT Al AT JLCL01 ) CC: A. Charles Sobrero CC: James R. Lawson ( SOBRERAC AT Al AT WWPS ) ( LAWSONJR AT Al AT WWPS ) Subject: C6-TBS: the rest of the story Folks: Gerry Kennedy has finished his bioaccumulation testing on C6-TBS, and I have some good news, and I have some even better news. If you'll recall, the good news (I've attached the previous memo, which explains it in detail) was that C6-TBS was between 32 and 53 times less bioaccumulative in the liver of male mice than was 3M's C8 product, in side by side comparison testing. As I said then, that was only half the picture; it said that C6-TBS was not as readily eliminated from the bloodstream into the liver, but could not say whether it was simply remaining in the bloodstream (and hence, still bioaccunulating). The better news is that the blood work on the mice is finished. A detailed report on the overall picture is forthcoming, but I wanted you all to be aware of the information Gerry shared with me today. Essentially, what was done was to feed 3 groups of mice meals spiked with varying levels of C6-TBS and C8 (the third group was a "control" group). We were then to allow up to 28 days of recovery, during which every 7 days blood samples were taken and ppm Fluorine in the blood was determined. As you will see, results were so good we halted the testing after the first 7 day sample was analyzed, to save unnecessary effort and expense. The results (in ppm Fluorine in the bloodstream, the average of five animals for each data point) are as follows: Day "Zero" of Recovery Day 7 of Recovery EID087670 HDR001555 Control 0.30 0.56 00 Ji. r 30 ppm diet C6-TBS 30 ppm diet 3M's C8 300 ppm diet C6-TBS 300 ppm diet 3M'S C8 5.30 33.23 8.19 71.52 0.35 19.26 0.45 22.20 Taken in combination, these results say that when equal doses are ingested by male mice, six to nine times more C8 is found in the bloodstream than C6-TBS. Furthermore, the half-life of C8 in the bloodstream appears to be around seven days, whereas the even at the highest concentration tested C6-TBS blood fluorine levels had returned to the control baseline in that same timeframe (Gerry's comment was that t-1/2 could have been as short as one day; it's tough to tell from the data because we had anticipated greater values and so did not take any samples between day zero and day seven). And finally, the liver data says that when the material does leave the bloodstream, somewhere between 30 and 50 times more of the C8 winds up in the liver than does C6-TBS. Taken as a whole. Gerrv's conclusion was that C6-TBS is indeecLmeasurably less bloaccumulative than CB. As I promised above, I'll be writing up a complete report very soon (with Gerry's assistance), and will have copies of this report sent to each of you when it is finished. Jim/Charlie-- Bruce I've left it to you to forward this note to other members of your organization, as you know much better than I who specifically is interested on your end. HDR001556 000 <5 EID087671 Hsu-Nan/Spencer: Some good news just in on the C6 homologue of Zonyl TBS, and since I'll be out of the office this week, I thought I'd share it with you "before I go." Gerry Kennedy just sent me a plot of percent increase in liver weight (vs. control) as a function of ppm fluorosurfactant in the diet. He tested Zonyl TBS, the C6-TBS, and perfluorooctanoic acid (3M's "C8"). The results are encouraging. At the higher end of the scale, both TBS and the C6 version look good relative to C8. Specifically, at 100% increase in liver weight gain, the values look like this: C8 -- 13.1ppm TBS -- 378ppm C6-TBS -- 705ppm The key data are at 50% increase in liver weight, which shows the C6-TBS to be clearly better than the other two: C8 -- 4.4ppm TBS -- 3ppm C6-TBS -- 142ppm Even at 25% increase in liver weight, the comparison between C8 and the C6-TBS is quite encouraging: C8 -- ca 2ppm C6-TBS -- ca 30ppm Gerry's cover note says: "C8 =* 30-50X more potent than C6-TBS." Please note that this is only half the storv? the percent flMoring.in-the bloodstream work is still being done. At this ; point , ye.can say it's clearly not accumulating in the the liver to the extent--that C8 floes,__What we don't know vet is whether that's because it's staying in the bloodstream to a greater extent than C$, or whether in fact it's being eliminated more efficiently. The blood testing should be finished soon? if it turns out to be as good as this result, we may in fact have found ourselves a less bioretentive fluorosurfactant. Keep those fingers crossed. 000135 EID087672 HDR001557 EID087673 HDR001558 > o 0) S to 000J.3 V 43 f' C-8 IN WASHINGTON WORKS DRINKING WATER Recent sampling of the four Washington Works drinking water wells have shown C-8 levels of 0.1, 0.5, 2.9 & 3.3 parts per billion. These values are surprisingly high but do not pose a health threat to our employees. The allowable exposure level of C-8 for our employees is set by our corporate AEL. This level is 0.01 mg/m3 or 0.56 ppb. This is an airborne control level. A control level for employee drinking water has not been set because such a control level was not deemed necessary. Exposure to C-8 is best understood by examining the AEL on a daily dose level basis. At the AEL an employee can be safety exposed to a 12 hour dose of 0.10 mg of C-8. If an employee were to drink water with a C-8 level of 3.3 ppb he would only be exposed to a daily dose of 0.006 mg., or l/20th of the AEL (note: C-8 is essentially fully absorbed by the human body if breathed or consumed). At this time all operating areas on site are in compliance to the AEL for airborne C-8 exposure. The slight additional exposure imposed by drinking water with C-8 levels of 3-4 ppb should not affect our compliance to the daily dose of C-8 allowed by the AEL. We should not get confused by the current CEG (Community Exposure Guideline) for C-8 in water of 1.0 ppb. This guide level is for exposure to the general public and not for the healthy workforce here on site. However, this situation should not be taken lightly. The site enviromental group and the C-8 team will endeavor to fully understand these recent sample results and provide you with future programs. Attached is the technical basis for the allowable dose exposure levels from Haskell. EID089421 V 44 Gaston Caporton Governor John M. Ranson Cabinet Secretary DEPARTMENT OF COMMERCE. LABOR 4 ENVIRONMENTAL RESOURCES D IV IS IO N O F E N V IR O N M E N T A L P R O T E C T IO N 1201 Greenbrier Street Charleston. WV 25311-1088 July 8, 1993 David C. Cailaghar Director Ann A. Spaner Deputy Director Mr. W.M. Stewart Sr. Environmental Control Consultant E.I. DuPont de Nemours and Company P.O. Box 1217 Parkersburg, WV 26102-1217 V Re: Solid Waste/NPDES Water Pollution Control Permit No. WV0076244, Dry Run Landfill V i K A D e a r Mr. Stewart: \ \ h is agency's June 28, 1993 field review of the above facility revealed non-compliance with Conditions D.l. and G.6. of the above permit as excessive sediment has accumulated in the lower sedimentation pond. Also, the upper sedimentation pond is not being operated in compliance with Condition D.l. due to excessive sediment accumulation. Furthermore, the discharge from the lower pond, Outlet No. 001, is causing a discoloration of the receiving stream, apparently due to an accumulation of algae within the pond. Therefore, the sedimentation ponds must be cleaned out and the cause of algal growth must be determined. To assist in determining the cause of algal growth, this agency requests that the Outlet 001 be analyzed for Nitrite, Nitrate, Ammonia Nitrogen, Total Phosphorus, and BOD. To facilitate the cleanout of the lower sedimentation pond, this agency suggests that the upper sedimentation pond be cleaned out and subsequently placed into service during the cleanout of the lower pond. This agency also requests that the discharge from Outlet No. 001 be analyzed for acute toxicity as determined by percentage mortality (fourty-eight hour screening bioassay) to fathead minnows and Daphnia. Dissolved Oxygen concentration shall be determined prior to running the bioassay. Within thirty days of the date of this letter, your company shall submit 1) acute toxicity Resting results, 2) the above referenced laboratory analyses, jand 3) a schedule for cleaning out the upper and lower sedimentation ponds. 9 GOO EIDO U563 Mr. Stewart Page two Should you have any questions concerning the above, please contact me at 367-2720. Sincerely, OFFICE OF WATER RESOURCES -' fd t&' b John G. Britvec, Geologist Industrial Branch JGB/jb cc: Cindy Musser, Insp., Environmental Enforcement, Dist. VI. Supervisor, Environmental Enforcement, Dist. VI. 00 01 EIDO12564 000193 45 PROCEDURE FOR CLEANING OUT LOWER SEDIMENT AT DRY RUN LANDFILL 1. In early August place bails of hay at the narrowest point of the hollow between the lower sediment pond and the active fill area to minimize sedimen going to the pond and out the outfall if it does rain. 2. After the August monthly samples have been taken remove the drain plug from the lower pond overflow line and drain the lower pond. 3. Allow the lower pond to dry out for approximately two weeks. 4. Remove the sediment from the lower pond using a backhoe and a bulldozer. Landfill the sediment in the active landfill area. 5. Measure the dimensions of the lower pond and note them on the a sketch of the pond. 6. Replace the drain plug in the overflow line to place the lower sediment pond back in service. 1 000 ij . *' EID017107 0001 INTEROFFICE MEMORANDUM Date: Fro: Dept: Tel No: 05-Aug-1993 01:31pm RICHARD A KIRSCHNER, JR KIRSCHRA POSTER & SERVICES (304) 863-2992 TO: Thomas R. Valdron ( VALDROTR ) Subject: Dry Run Pond Ton, I'm sure you've seen Valt's and Ed's memos. Then you talk to Boso please be sure he knows vhat's going on and vhat to expect. Also, if Melvin doesn't think it will do any harm, have him open the valve all the way. The faster this stuff leaves, the better. That silt fence is looking better and better all the time. Is he eventually going to use one? Thanks, The "worst" golfer around... EIDO17129 000J.93 47 f GWJ000077 950 Gilliland & Mandai M ortality in a PFOA Production Plant r i - c<? Mortality Among Employees of a Perfluorooctanoic Acid Production Plant Frank D. Gilliland, MD, PhD Jack S. Mandel, PhD, MPH Perfluorooctanoic acid (PFOA) has been found at low levels (10 to 100 parts per billion) in sera o f the general population a n d a t higher levels in occupationally exposed workers. Although PFOA has been reported to be a prom oter o f rodent hepatocarcinogenesis and to alter reproductive hormones in humans and rodents, there is little information on hum an health effects associated with PFOA exposure. The present study exam in ed the relationship between PFOA an d m ortality using a retrospective cohort m ortality design. The cohort consisted o f2788 m ale and 749fem ale workers em ployed between 1947 and 1983 at a plant that produced PFOA. The all-causes standardized m ortality ratio was .75 (95% confidence interval [C l], .56 to .99) fo r women an d .77 (95% C l, .69 to .86) fo r men. A m ong m en the cardiovascular standardized m ortality rate was .68 (95% C l, .58 to .80) an d the allgastrointestinal diseases was .57 (95% Cl, .29 to .99). There was no signifi cantly increased cause-specific standardized m ortality ratio fo r either men or women. Ten years o f em ploym ent in exposed jo b s w as associated with a 3.3-fold increase (95% C l, 1.02 to 10.6) in prostate cancer m ortality com pared to no em ploym ent in PFOA production. There were only six prostate cancer deaths overall an d fou r among the exposed workers; thus, the results must be interpreted cautiously. I f prostate cancer m ortality is related to PFOA, PFOA m ay increase prostate cancer m ortality b y altering reproductive hormones in m ale workers. From the Division of Environmental and Occupational Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota (Dr Gilliland, Dr Mandel); and Department of Internal Medicine, Occupational and Environmental Medicine Section, St Paul Ramsey Medical Center, St Paul, Minnesota (Dr Gilliland). Address correspondence to: Frank D. Gilliland, MD, University of New Mexico School of Medicine, New Mexico Tumor Registry, 900 Camino de Salud NE, Albuquerque, NM 87131. 0096-1736/93/3509-0950S03.00/0 Copyright C by American College of Occupational and Environmental Medicine erfluorooctanoic add (PFOA) and its salt, ammonium periluorooctanoate, are perfluorinated surfactants. Be cause o f their unique surface active properties they are used in a large number of industrial applications and consumer products including plasti cizers, lubricants, wetting agents, and emulsifiers.1*1 Despite their wide spread use, little is known about po tential adverse health effects. PFOA induced marked hepatomeg aly and peroxisome proliferation in rodent livers.1** The chemically di verse group of xenobiotics that induce peroxisomes is of concern because of its association with nongenotoxic hepatocarcinogenesis.1*10PFOA did not produce an increased number of hep atocellular carcinomas in a 2-year rat feeding study.* However, biphasic (initiation and promotion) and tri phasic (initiation, selection, and pro motion) hepatic carcinogenesis stud ies in rodents have shown significantly increased numbers of carcinomas in the PFOA-treated rats."11It has been suggested that the marked rodent hep atomegaly produced by PFOA is a marker for carcinogenic potential.11 The observations of increased Leydig cell tumors in a 2-year rat PFOA feed ing study and of disruption of the hypothalamic-pituitary-gonad axis in PFOA-treated rats* are consistent with the hypothesis that PFOA-associated tumors are mediated by a hormonal nongenotoxic mechanism. PFOA has a long half-life in hu mans. A study of occupationally ex posed workers showed that the halflife in men is greater than 1.5 years.14 Hence, accumulation of PFOA may occur from small, frequent PFOA doses. PFOA in the serum of the gen- OOOS'.OO EID088658 /wm oiume oo, numoer a,aepcemocr laao 31 eral populations of industrialized countries1*''* is Sikeiy re he the result of an accumuiauon ot small PFOA doses. No health problems related to PFOA exposure were observed in a cross-sectional study among workers employed at the PFOA production plant.1* Cross-sectional studies of PFOA-exposed workers at this plant have shown that PFOA was associated with decreased free testosterone and increased estradiol.20 To determine whether mortality from any cause was associated with occupational exposure to PFOA, a ret rospective cohort mortality study was conducted at a plant that has pro duced PFOA since 1947. Methods The plant consists of several divi sions, with PFOA production re stricted to the Chemical Division. A number of other specialty chemicals have been produced in this division. The study cohort consisted ofworkers who were employed at the plant for at least 6 months between Jan 1, 1947, and Dec 31, 1983. Data were ab stracted from plant personnel records, which were maintained on all workers ever employed at the plant. Vital status was ascertained from the Social Security Administration for the period 1947 to 1982 and from the National Death Index for the period 1979 to 1989. All workers with un known vital status were traced using a variety of tracing strategies such as directory assistance, Metronet and TRW searches, reverse directories, motor vehicle registration lists, con tacting neighbors and relatives, and the post offices. Death certificates were obtained from the appropriate state health departments for those identified as, or presumed to be, de ceased. Information concerning the data and cause of two deaths which occurred outside the United States was obtained from family members. A nosologist coded the death certifi cates for underlying cause of death according to the International Classi fication of Diseases, 8th revision. The reliability of the coding was evaluated by resubmitting a random sample of death certificates for coding by the same nesoiogist In the 2Z death cer tificates from 1970 to 1989 resubmit ted to the nosologist for ICD coding, there were no changes in the major categories of cause of death. Workers were categorized as ex posed or unexposed to PFOA based on their job histories. Exposed work ers were defined as all workers em ployed for 1 month or more in the Chemical Division. Unexposed work ers were employees who either never worked in the Chemical Division or worked in the Chemical Division for less than l month. Cumulative expo sure to PFOA was estimated using the surrogate measure of months of Chemical Division employment The observed numbers of causespecific deaths were compared to the expected numbers of deaths obtained by applying sex- and race-specific quinquennial age, calendar period, and cause-specific mortality rates for the United States and Minnesota pop ulations to the distribution of ob served person-time.21-22 Because less than 1% ofplant employees were non white, white male and white female rates were used for comparison. For women, only United States rates were used because cause- and calendar period-specific Minnesota rates for women were not available. The effects of latency, duration of employment, and work in the Chemical Division were examined using stratified stand ardized mortality ratio (SMR) anal yses. Cause-specific mortality rates were compared between exposed and unexposed workers using stratified SMRs.23 SMRs were calculated for men based on US and Minnesota white maie mortality retes for three latency intervals (10,15, and 20 years) and three categories of duration of employment (5, 10, and 20 years). The SMRs were calculated using the program developed by Moason.22 The relative risk (RR) and 9596 confidence interval (Cl) for deaths from all causes, cancer, cardiovascular diseases, and other selected causes were estimated using proportional hazard models.2*-23The time to event or censoring was defined as time from first employment to event or to De cember 31, 1989. In models for spe cific causes of death, deaths from other causes were censored at the time of death. Age at first employment, year of first employment, and dura tion of employment were included as covariates in the model. The analyses were stratified by gender. The appro priateness of the proportional hazard assumptions was tested using strati fied models with graphical analysis of log (-logfsurvival]) versus follow-up time relationships and models that tested the significance of a product term between exposure and log fol low-up time.23-24 Proportional hazard calculations were conducted using SAS.23 Results A total of 3537 workers employed at the plant between Jan 1, 1947 and Dec 31, 1983 were identified from company records. Six workers who had incomplete employment records were excluded from the study. The cohort consisted of 2788 (79%) men and 749 (2196) women (Table 1). Men TABLE1 Characteristics of Female and Male Employees, 1947-1989 C hem ical Non-Chemical Division Division Number of worter* Parson-years of ob- serration Mean foSow-up (y) Mean age at employmart (y) Mean year of death Mean year of death Mean age at death (y) Female 245 6029.0 24.6 28.8 1965.0 1981.3 58.7 Mala 1339 33385.3 24.8 25.6 1963.8 1978.3 54.2 Female 504 13280.4 26.4 26.9 1962.8 1979.2 54.4 Mala 1449 37732.4 26.0 28.9 1962.3 1978.1 58.1 Female 749 19309.4 25.8 27.6 1963.5 1979.6 55.4 Mala 2788 71117.7 25.5 27.3 1963.0 1978.2 56.4 EID088659 GWJ000078 contributed 71,117.7 person-years of observation, which were equally di vided between tic Chernies! Division ana non-Chemicai Division. Women contributed 19,309.4 person-years, two-thirds of which were in the nonChemical Division. Vital status was obiamcu foi 100% ofthe cohort (Table 2). There were 50 deaths among the women (11 in the Chemical Division cohort and 39 in the non-Chemical Division cohort) and 348 deaths among the men (148 deaths in the Chemical Division group and 200 in the non-Chemical Division group). Death certificates were obtained for 99.5% of deaths. For women, the SMR for all causes of death (SMR - .75; 95% Cl, .56 to .99) was significantly lower than ex pected (Table 3). There was no asso ciation with duration of employment or latency for deaths from all causes, cancer, and cardiovascular diseases (data not shown). Mortality among Chemical Division women was less than expected. In Chemical Division women, the all-causes SMR was .46 (95% Cl, .23 to .86) and the cancer SMR was .36 (95% Cl, .07 to 1.05). The all-causes SMR for the nonChemical Irivtacs women tvai .?! (yo% Cl, .cw to 1.24) and the cancer SMR was .91 (95% Cl, .49 to 1.52) (data not shown). Using Minnesota rates for compar ison, the SMR for men for all causes, for cardiovascular diseases, and for all gastrointestinal diseases was signifi cantly less than 1 (Table 4). None of the cause-specific SMRs was large nor was any significantly different from 1. The results were similar when the ex pected numbers of male deaths were based on US mortality rates. For the three latency intervals, the SMRs for deaths from all causes ranged from .75 to .77. For all cancers, the SMRs ranged from 1.06 to 1.12 and were nonsignificant Among men, theft was no associa tion between any cause of death and duration of plant employment The all-causes SMRs were .86 (95% Cl, .72 to 1.01) fer the Chemical Division group and .69 (95% Cl, .59 to .79) for the non-Chemical Division group (data not shown). The SMRs for pros TABLE 2 Vital Status and Cause of Death Ascertainment among Female and Male Employees. 1947-1989 Chemical Division Non-Chemicai Division Total Female Mala Female Mala Famela Mala Alive Dead Total No. % No. % No. % No. % No. % No. % 234 95.3 1191 88.9 465 91.6 1249 66.2 699 93.3 2440 87.5 11 4.7 148 11.1 39 8.4 200 13.8 50 6.7 348 12.5 245 100.0 1339 100.0 504 100.0 1449 100.0 749 10C.0 2788 100.0 TABLE 3 Observed (Obs) and Expected (Exp) Deaths, Standardized Mortality Ratios (SMR) and 95% Confidence Intervals (Cl) for 749 Female Employees Cause of Death Obs Exp SMR 95% a All causes 50 66.74 0.75 056-.99 Cancer 17 23.04 0.71 0.42-1.14 Gastrointestinal 2 4.54 0.44 0.05-1.59 Respiratory 4 4.72 0.95 0-26-2.43 Breast 3 5.87 0.51 0.10-1.49 Genital 2 3.37 0.59 0.07-2.14 Lymphopoietic 3 2.04 1.47 0.30- 2 9 CartSovascular 10 12.39 0.81 0.49-1.29 Cerebrovascular 3 3.51 0.86 0.01-4.80 Gastrointestinal 3 3.41 0.88 0.16-257 Injuries 4 6.23 0.84 0.17-1.64 Suicide 1 1.78 0-56 0.01-3.13 tate cancer were 2.03 (95% Cl, .55 to 1 4.59) in the Chemical Division group I and .; (95% CL .07 tc 209! in the I non-Chemicai mvision cohort In the i Chemical Division group, there were ' 4 observed and 2 expected deaths from prostate cancer. There was no significant association between any cause of death and latency in either i exposure group.JForthe Chemical Di- < vision cohort, the prostate cancer SMR was 1.61 (95% Cl, .32 to 4.70) i in the greater than 15-year latency group. Table 5 presents the final propor tional hazard mode! for all-causes, all cancer, and prostate-cancer mortality among the 2788 male workers em ployed for more than 6 months. The estimated relative risk for all-cause mortality for a 1-year increase in age at first employment was 1.08 (95% Cl, 1.07 to 1.09). Year of first em ployment and duration of employ ment were negatively associated with deaths from all causes. The risk asso ciated with months employed in the Chemical Division was small and nonsignificant. In the final prostate cancer mortal ity model, length of employment in the Chemical Division was positively and significantly associated with pros tate cancer risk. The relative ride for a 1-year increase in Chemical Divi sion employment time was 1.13 (95% Cl, 1.01 to 1.27) For 10 years' em ployment in the Chemical Division, the relative risk was estimated to be 3.3 (95% Cl, 1.02 to 10.6) compared with workers never employed in the Chemical Division. Age at first em ployment was positively associated with prostate cancer mortality. Length of time employed in the Chemical Division was not significantly related to mortality from lung cancer, gas trointestinal cancer, pancreatic can cer, or diabetes mellitus. Discussion This was the first retrospective co hort mortality study of workers em ployed in a PFOA production plant Mortality from all causes in both men and women was significantly less than expected. Because of the healthy worker effect, internal comparisons E1D088660 TABLE 4 Deaths and Standsrdi?t<i MonaFty Ratios (SMfij Based on Minnesota White Male Rates, Amcng &ivisie LiTipicryetr, ?S47~m9, anc 1339 Men Ever Employed In the Chemical Drvision, 1947-1989 Causes of Death AH Male Employees Ohs Exp 8MR 95% O Men Employed In Chemical Division Oba Exp SMR 9 5 % a Al causes 347 450.79 0.77 0.69-0.86 148 172.96 0.86 0.72-1.01 Cancer 103 97.29 1.05 0.86-1.27 40 36.31 1.10 0.79-1.50 Gastrointestinal 24 26.78 0.90 0.57-1.33 9 9.77 0.92 0.42-1.75 Colon 9 9.42 0.96 0.44-1.81 4 3.46 1.15 0.31-4.01 Pancreas 8 5.58 1.43 0.62-2.83 4 2.04 1.96 0.53-5.01 Respiratory 31 30.42 1.02 0.69-1.45 12 1126 1.07 0.55-1.86 Lung 29 28.94 1.00 0.67-1.44 11 10.70 1.03 0.51-1.84 Prostate 6 6.07 0.99 0.36-2.15 4 1.97 2.03 0.55-4.59 Testis 1 0.92 1.09 0.01-6.05 1 0.44 228 0.03-12.66 Bladder 3 2.18 1.37 0.28-4.01 1 0.75 123 0.02-7.40 Lymphopoietic 13 12.07 1.09 0.57-1.84 5 4.76 1.05 0.34-2.45 Cardiovascular 145 212.19 0.68 0.58-0.60 54 76.65 0.70 0.53-0.92 CHO* 110 159.09 0.69 0.57-0.83 43 57.74 0.74 0.54-1.00 Cerebrovascular 10 24.68 0.60 0.32-1.02 4 8.53 0.47 0.13-120 Al gastrointestinal 12 21.13 0.57 0.29-0.99 8 827 0.97 0.42-1.91 Al respiratory 13 21.75 0.60 0.32-1.06 7 7.77 0.91 0.36-1.87 Diabetes 8 6.52 1.23 0.53-2.42 3 2.55 1.18 024-2.44 Injuries 38 47.74 0.80 0.56-1.08 31 31.72 0.98 0.65-129 Suicide 12 15.09 0.79 0.41-1.39 10 6.99 1.43 0.68-2.63 'CHD, coronary and atneroscierotic heart disease. were made between Chemical Divi sion and non-Chemical Division em ployees. There were no significantly elevated SMRs in Chemical Division or non-Chemical Division employees. However, prostate cancer mortality was associated with length of employ ment in the Chemical Division in pro portional hazard analysis. Ten years of employment in the Chemical Di vision was associated with an esti mated 3.3-fold increase (95% Cl, 1.02 to 10.60) in prostate cancer mortality. The use ofprostate cancer mortality to assess the association between PFOA and prostate cancer occurrence is problematic. Age-adjusted prostate cancer mortality rates from 1983 to 1989 (949 per 100,000) were only 25% of the incidence rates (99.4).27 This low proportion of deaths among cases attributed to prostate cancer re flects the high risk of death for com peting causes for this disease ofelderly men. Given the small number of oh* served deaths from prostate cancer in the study, and the observed difference in incidence and mortality rates, the suggested association between PFOA exposure aod prostate csncer us; be viewed w hypothesis generating and should not be overinterpreted. The association may be real, may have been a chance finding, or may be the result of an unrecognized environ mental factor. However, the biologic plausibility for any association be tween PFOA employment and pros tate cancer is provided by anim) tox icologic and human epidemiologic data that show an association between PFOA and reproductive hormone changes." The all-causes, all-cancer, and allcardiovascular mortality among women was less than expected in the overall cohort The low SMRs are most likely to be a result ofthe healthy worker effect Latency and duration of plant employment did not have a strong relationship with the healthy worker effect The interpretation of this study re quires consideration of methodologi cal issues. SMRs for the subgroups of workers are not strictly comparable. We attempted to calculate standard ized rate ratios; however, the rates werebased on small numbersand pro duced unstable ratios. Estimates of PFOA exposure were based on job history, and categorization of workers into ever versus never employed in the Chemical Division may not reflect the biologic effective dose of PFOA. PFOA exposure was apparently wide spread among employees not directly exposed to PFOA,14and the exposure categorization may misclassify work ers as unexposed when they were ex- UWJ000080 TABLES Proportional Hazard Regression Model of Factors Predicting Mortality among All Male Employees* v aiM iim r AH Causes of Death 9 SCtf) P RRt Cancer Deatha 9 SCOT P RRt Prostate Cancer Deaths 9 SCOT P RRt Year of first employment -0.55 . 0.009 0.0001 0.946 -0.031 0.019 0.11 0.969 0.010 0.081 0.9 1.011 Age at first am- 0.079 0.006 0.0001 1.08 0.078 0.011 0.0001 1.081 0.082 0.045 0.06 1.085 pioymant(y) Duration of sm- -0 2 4 0.001 0.0001 0.967 -0.028 0.009 0.002 0.972 -0 .0 7 0.052 0.18 0.932 ptoyment(y) Months In 0.001 0.001 024 1.001 0.002 0.001 0 2 1.002 0.01 0.005 0.03 1.01 chemical divi sion * Abbreviations used are: 9, regression parameter; SCOT. standard error of the slope parameter, RR, relative rtsk. t Relative rtsk tar one unit change in Independent variable. EID088661 8 5 4 uuiuana a wianutu m u r u t m y in a r r v n r iu u u u u u u r u u u posed. Such misclassification would be expected tc bias the effect estimates toward the null if increased exposure increases death rates. Months em ployed in the Chemical Division may better reflect the biologic effective dcsc because cumulative exposure re flects the bioaccumulation of PFOA. Workers were exposed to many other xenobiotics, such as benzene and as bestos, during their employment at the plant. However, none ofthese ma terials has been associated with pros tate cancer. Although the mean age at first em ployment and mean year of first em ployment are similar in the Chemical Division and non-Chemical Division cohorts of men and women, the com parisons of the rates of disease are confounded by differences in the dis tribution of age at risk. The use of an internal comparison group may re duce, but not eliminate, confounding if the internal comparison groups have different distributions of these time factors. Because the disease oc currence relationship is defined in terms of cumulative exposure, the true effect of PFOA exposure may have been biased toward or away from the null by uncontrolled confounding by time factors.1,-J* Further research is needed to eval uate and confirm the association be tween PFOA and prostate cancer. The findings in this study are based on a small number of cases and could have resulted from chance or unrecognized confounding from exposure to other factors. Studies of prostate cancer in cidence in this and other PFOA-exposed work forces may clarify the sug gested increase in prostate cancer risk. Acknowledgments This work was supported in part by Na tional Institute for Occupational Safety and Health Grant TI50H07098-16. and the 3M Corporation. References 1. Guenthner R, Victor M. Surface active materials from perfluorocarboxylic and perfluorosulfonic acids. l&EC Product R e se a rc h a n d D e v r ic p m e n : rt2;l: I 6 i --69. 2. Griffith F, Lon* J. Animal toxicity stud ies with ammonium perfluorooctanoate. Am Ind Hyg Assoc J. 1980;41:576-583. 3. Olson C, Andersen M. The acute toxicity of periluorooctanoic and perfluorodecanoic adds in male rats and their effects on fatty tissue. Toxicol Appi Pharmacol. 1983;70:362-372. 4. Pastoor T, Lee K. Pern M. Gillies, P. Biochemical and morphological studies of ammonium perfluorooctanoate-in duced hepatomegaly and peroxisome proliferation. Exp M ol Pathol. 1987,47: 98-109. 5. Just W, Gorgas K, Haiti F, Heinemann P, Salazar M, Schimassek H. Biochemi cal effects and zonal heterogeneity of peroxisome proliferation induced by per* fluorocarboxylic adds in rat liver. Hepatology. 1989;9:570-581. 6. Kennedy G. Dermal toxidty of ammo nium perfluorooctanoate. Toxicol Appl Pharmacol. 1985,81:348-355. 7. Kennedy G, Hall G, Brittelli J, Chen H. Inhalation toxidty of ammonium per fluorooctanoate. Food Chem Toxicol. 1986;24:1323-1329. 8. Cook J, Murray S, Frame S, H unt M. Induction of Leydig cell adenomas by ammonium perfluorooctanate: A possi ble endocrine related mechanism. Taxicol Appl Pharmacol. 1991;113:209-213. 9. Reddy J, AzareofTD, Hignite C. Hypo lipidemic hepatic peroxisom prolifera ters form a novel class of chemical car cinogens. Nature. 1980^283:397--398. 10. Reddy J, Lalwani N. Cardnogenesis by hepatic peroxisome proliferators: evalu ation of the risk of hypolipidemic drugs and industrial plasticizers to humans. ` Crit Rev Toxicol. 1983;12:1-85. 11. Nilsson R, Bdje B, Preat V, Erixon K, Ramel C. On the mechanism of the hepatocarrinogenirity of peroxisome proliferators. Chem Biol Interact. 1991; 78:235-250. 12. AbdellatifA, Preat V, Vamecq J, Nilsson R, Roberfroid M. Peroxisome prolifera tion and modulation of rat liver carci nogenesis by 2,3-dichlorophenoxyacetic add, 2,4,5-trichlorophenoxyacetic add, periluorooctanoic ad d and nafeoopin. Carcinogenesis. 1990;11:1899-1902. 13. Takagi A, Sai K, Umemura T, Hasegawa R, Kurokawa Y. Short-term exposure to the peroxisome proliferators, periluorooctanoic ad d and periluotodecanoic acid, causes significant increases of 8hydroxydeoxyguanosine in liver DNA of rats. Cancer Lett. 1991;57:55-60. 14. Ubel F, Sorenson S, Roach D. Health status ci E*anf '-erlrrv exposed to fluorochemieaii: a preliminary report. Am In d H yg Assoc J. 1980-.41:584-589. ; 15. Guy W. Fluorocompounds of human plasma: analysis, prevalence, purifica tion, and characterization, PhD thesis. Rochester, NY: University of Rochester 1972. 16. Guy W, Taves D, Brey W. Organic fluo rocompounds in human plasma: preva lence and characterization. In: Filler R, ed. Biochemistry involving carbon-fluo rine bonds. AC S Symposium Series. New York: American Chemical Society; 1976:117-134. 17. Guy W. Ionic and organic fluorine in blood. In: Johansen E, Taves D, Olsen T, ed. Continuing evaluation o f the use o ffluoride. Boulder, CO: Westview Press; 1979. 18. Taves D. Evidence that there are two forms of fluoride in human serum. Na ture. 1968-217:1050-1051. 19. Taves D. Comparison of "organic" flu oride in human and nonhuman serums. J Dent Res. 197150:783. 20. Gilliland F. Fluorocarbons and human health: studies in an occupational cohort, PhD thesis. Minneapolis, MN: Univer sity o f Minnesota; 1992. 21. Berry G. The analysis of mortality by the subject-years method. Biometrics. 1983; 39:173-184. 22. Monson R. Analysis of relative survival and proportional mortality. Comput Biom edRes. 1974;7:325-332. 23. Miettinen O. Standardization of risk ratios. Am J Epidemiol. 1972:96: 383-388. 24. Cox D. Regression models and life tables. J R Stat Soc (B). 1972;34: 187-220. 25. SAS Institute. SAS User's Guide: Statis tics. 6th ed. Cary, NC: SAS Institute Inc, 1990. 26. Kalbfldsch J, Prentice R. The statistical analysis o ffailure tim e data. New York: John Wiley & Sons; 1980. 27. Miller R. Cancer statistics review 1973-- 1989. Bethesda, Maryland. US Depart ment of Health and Human Services, National Institutes of Health, National Cancer Institute. NIH Pub. No. 92-2789, 1992. 28. Checkoway H, Pierce N, CrawfordBrown D. Research methods in occupa tional epidemiology. New York: Oxford University Press; 1989. 29. Robins J. A new approach to causal in ference in mortality studies with a sus tained exposure period. Math Modeling. 1986;7:1393-1512. EID088662 000205 48 f Page I AH&M ENVIRONMENTAL, INC. 6404 MacCorkle Avenue, SW St. Albans, WV 25177 BIOASSAY REPORT FOR E. I. DUPONT WASHINGTON WORKS P. O . BOX 1217 PARKERSBURG, WV 26102 A1LV1 N O . 95-114 DAPHNIA PULEX DECEMBER 8 - 10, 1993, 48 HOUR STATIC ACUTE DEFINITIVE INTRODUCTION AH&.M Environmental, Inc. conducted a 48 hour static acute bioassay to determine the toxicity o f a landfill leachate collected by E. I. DuPont, Washington Works. A grab sample was collected on December 7, 1993. The sample was tested for toxicity using the freshwater organism, Daphnia pulex. F.. I. DuPont, Washington Works is located in Parkersburg, West Virginia 26102. The test was conducted on December 8 - 10, 1993. DILUTION WATER The dilution water used to perform the definitive toxicity test was moderately hard synthetic freshwater that is favorable to the aquatic organisms used in the test. The moderately hard synthetic fresh water is prepared according to EPA protocol w Methods for Measuring the Acute Toxicity _of Effluent a n d R eceivin g W a te r to Freshw ater and M arine O rganism s, E P A /600/4-90/027." The water is allowed to aerate for 24-48 hours prior to use in a test. Water quality analysis is conducted on the dilution water and if at any time water quality is not adequate, an additional batch w ill be prepared or an alternate source will be chosen. LEACHATE SAMPLE: The sample collected was a grab sample collected on December 7, 1993. The sample was collected by DuPont Washington Works personnel, refrigerated, and picked-up by AH&M Environmental, Inc. on December 8, 1993 at approximately 1100 hours. The effluent was translucent and had an orange color. An odor was observed and a small amount o f sediment was present. The receiving temperature o f the sample was 12.4C. Samples were stored at 4C and were used in the test prior to the 36 hour holding time. 000.-:- Oh WVDEP Q2i Fags 2 TEST METHODS: A definitive toxicity test was performed for E. I. DuPont, Washington Works according to EPA protocol "Methods for Measuring the Acute Toxicity of Effluent and Receiving Waters to Freshwater and Marine Organisms. EPA/600/4-90/027". Using a 0.5 dilution series, a concentration range of 100%, 50.0%, 25.0%, 12.5%, 6.25% and 0% (control) was used to test the toxicity of the sample. The test vessels were 30 ml plastic disposable test vessels. The test volume was 25 ml. Upon receipt, samples are logged in, assigned an AHM test number and initial parameters are recorded. The test concentrations are then mixed and decanted to the test vessels. Each test vessel is randomly distributed and at least 20 organisms o f a given species are exposed to each effluent concentration, five (5) per replicate. The test data measured in the tests are biological, chemical and physical data. Death/mortality is the effect measured in the acute test. Mortality o f the test chambers are monitored for early mortality during the first few hours, and only every 24 hours thereafter. Chemical and physical data (ie., pH, conductivity, dissolved oxygen and temperature) are measured at a minimum in all test concentrations every 24 hours. Total alkalinity and total hardness are measured in the controls and in the highest concentration at the beginning o f the test. The test temperature range is 2 5 + /-1 C . Dissolved oxygen is not allowed to exceed below 40% saturation. If however, the sample has a high oxygen demand and the test concentrations exhibit dissolved oxygen levels less than 40% saturation, aeration o f all test chambers will occur prior to introducing organisms to the test chambers. The test organisms used in the test were 1-24 hour Daphnia pulex which were cultured at AH&M Environmental, Inc. Daphnia pulex adults were isolated on 12/07/93 and received on 12/08/93. The Daphnia neonates produced are believed to be disease free and in the best o f health. AH&M Environmental, Inc. performs reference toxicant testing and maintains a coatrol chart for the Daphnia neonates cultured in house to assess the health o f our cultured organisms and the techniques applied by the technicians. RESULTS; The adverse effects measured in the 48 hour definitive test for E. I. DuPont, Washington Works was death/mortality. At 48 hours 15% mortality occurred in the 100%, 5% mortality occurred in the 50%, and 0% mortality occurred in the 25% , 12.5%, 6.25% and 0% (controls). The LC50 for Washington Works sample was >100% . The Acute Toxic Unit was not measurable. See Section V , o f the Test Summary for Daily Percent Mortality. All Chemical analysis o f effluent and dilution water are in appendix A. A copy o f the laboratory bench sheet is in appendix B. WVDEP 029 AH&M ENVIRONMENTAL, INC. 6404 MacCorkJe Avenue, SW St. Albans, West Virginia 25177 TEST SUMMARY SHEET Page 3 FACILITY: E. I. DuPont______________ Washington Works________ ADDRESS: Parkersburg_______________ CONTACT: Jim Yoak_________ OUTFALL N O : _______________ West Virginia 26102 NPDES NO: _WV______________ TELEPHO NE N O :.(304) 863-4633__________ SAM PLE ID: Landfill leachate TEST DATE: 12/08-10/93____________ REPORT DATE: 12/20/93 I. SAMPLE INFORMATION A . Method o f Sample Shipment: AH&M Environmental. Inc, courier_________ B. Condition Upon Arrival At Labortory: 1. Temperature 12.4 C_______ 2. pH 8.25 Std Units 3. Chlorine 0 m e/l_______ 4. Conductivity 500 umhos_____ 5. DO 10.1 mg/l _ 6. Appearance Translucent, orange colored liquid, odor present, and a small amount o f sediment________________________________________ C. Collection Dates: 12/07/93__________ D . Collection Location: Prior to discharge__________________________________ n . DILUENT INFORMATION A . Method o f Diluent Shipment: Not applicable prepared inhouse__ ___________ B. Treatment o f Diluent: Moderately hard synthetic freshwater preoared to EPA Protocol 6 0 0 /4 -9 0 /0 2 7 ._________________________________________ _________ ooo&os WVDEP 02S Page 4 AH&M ENVIRONMENTAL, INC. 6404 MacCorkle Avenue, SW St. Albans, West Virginia 25177 TEST SUMMARY SHEET C. Condition o f dilution water 1. Temperature 25.4 C__________ 2. pH 8.07 Std Units . 3. Chlorine 0 mg/1 4. Conductivity 300 umhoa 5. DO .L Q jl& fl_____ 6. Appearance Translucent, colorless liquid, with no sediment.and/or odor------------------------------------------------------------------------------------------- D . Collection/Preparation Dates: 12/01/93__________ E. Collection/Preparation Location: AH&M Environmental. Inc. IIL TEST START A. Test Organism: Daphnia oulex B. Age: < 2 4 hrs _ Isolated 12/07/93 C. Test Vessel Size: 30 ml____________ _ D . Test Volume: 25 ml______________ E. No. o f Replicates: 4 F. No. o f Organisms per Replicates: 20 G. Test Datcs/Times: Beginning Date: 12/08/93 Time: 1210 Ending Date: 12/10/93 Time: .1210 H. 100% Effluent at 0 Hours 1. Chlorine Initial 0 mgfl Adjusted Not Applicable 2. Salinity Initial ______0 oot Adjusted Not Applicable 3. pH Initial 8.19 std. units _ Adjusted Not Applicable oooob WVDEP 029 AH&M ENVIRONMENTAL, INC. 6404 MacCorkie Avenue, SW St. Albans, West Virginia 25177 TEST SUMMARY SHEET Page 5 4. Alkalinity 268 mg/1__________ 5. Hardness 200 mg/1__________ 6. Conductivity 600 umbos______ 7. DO Initial 8.1 mg/1________ _ Adjusted Not Applicable Aeration Period (if necessary) Not Applicable I. DILUENT at 0 Hours 1. pH Initial 8.05 std. units Adiusted Not Applicable 2. Salinitv Initial 0 oot Adiusted Not Applicable 3. DO Initial 8.0 mg/1 Adiusted Not Applicable Aeration Period (if necessary) -Hot Applicable 4. Alkalinitv 62 mg/l 5. Hardness 94 mg/1 6. Conductivity 310 umbos _ IV. TEST RESULTS A. Test Acceptability 1. Control Survival 100% .2 Average Weight per Control Organism B. Statistical Analysis 1. Method o f Statistical Analysis _Not Applicable 2. 48 Hour LC50 >100% 3. 95 % Lower and Upper Confidence Intervals Not Applicable. C. TU. 1. T U . - 100/LC50 = 1 0 0 /> 100% - AA (Below detectable) 000 k;i.0 WVDEP 029 Page 6 AH&M ENVIRONMENTAL, INC. 6404 MacCorkie Avenue, SW St. Albans, West Virginia 25177 TEST SLMMARY SHEET V. TABLE 1 DAILY PERCENT MORTALITY TEST CONCENTRATION 1 HOUR 0 24 48 CONTROL 0 0 0 6.25% 0 0 0 12.5% 0 0 0 25.0% 0 0 0 50.0% 0 5 5 100.0% 0 15 15 VI. COMMENTS OOO^.-i 1 WVDEP 02$ CG0212 HASKELL LABORATORY FOR DUPONT USE ONLY LIMITED DISTRIBUTION This review reflects the available toxicity literature, both published and unpublished. Studies have not been evaluated for scientific merit. Contact Haskell Laboratory if you have questions. Common N a m e : Ammonium P e r f l u o r o o c t a n o a t e (APFO) C h em ical Name: O c t a n o ic a c i d , p e n t a d e c a f l u o r o - , ammonium s a l t Synonyms: C-8 FC-143 CAS Registry N o . : 3825-26-1 Chemical Structure: Oit c f 3 - c f 2 - c f 2 - c f 2 - c f 2 - c f 2 - c f 2 - c - o- nh4 Physical Properties (5): Description: Molecular Weight: Boiling Point: Melting Point: Bulk Density: Vapor Pressure: Flash Point/Flammability: Explosive Limits: Solubility: Conversion Factors: Light-colored powder, slight odor 431 Sublimes @ 130C 0.6-0.7 g/mL 7 x 10-* mm Hg 20aC Soluble in water, ethanol and acetone 1 mg/L - 57 ppm 1 ppm - 17.6 mg/m3 This literature search contains 23 pages of text and 62 references. An * in the left margin indicates new data added at this update. This search was prepared by Richard C. Graham. See the last page of this document for its updating history. EID087793 Exposure Standards: DuPont AEL - 0.01 mg/m3 (8-hour TWA), skin * DuPo n t C o m m u n i t y Exposure G u i d e l i n e (air) (C E G , ) - 0.3 u g / m 3 * D u P o n t C o m m u n i t y Exposure Guid e l i n e (water) (C E G ,, ) - 1 ug/L * ACGIH TL V - 0.1 mg/m3 , skin DOT Classification: None E P A F.CRA Status: None FDA S t a t u s : None TSCA I n v e n t o r y : Yes TOXICITY Summary: C-8 has m oderate a c u t e o r a l t o x i c i t y w it h an LD50 in r a t s o f 470 m g /k g . An a q u e o u s p a s t e o f C-8 p r o d u c e d m i l d t o m o d e r a te i r r i t a t i o n on the sk in o f r a b b its . C l i n i c a l s ig n s o f t o x i c i t y w ere s e e n a t d o s e s as lo w a s 1500 m g /k g . I n s t i l l a t i o n o f th e s o lid m aterial in to the rabbit eye produced moderate corneal o p a c it y , i r i t i s and c o n j u n c t i v i t i s . The o c u la r e f f e c t s g r a d u a lly reced ed . Prompt washing o f the eye reduced th e e f f e c t s and th ese e y e s r e c o v e r e d more q u ic k ly . By th e a c u te i n h a l a t i o n r o u te , C-8 i s h i g h l y t o x i c w i t h a f o u r - h o u r ALC i n t h e r a t o f 0.8 m g / L . I n a t w o - w e e k s u b a c u t e i n h a l a t i o n s t u d y p e r f o r m e d a t 11 a n d 83 mg/m3 , l i v e r d e g e n e r a t i o n , e n la r g e d l i v e r s and i n c r e a s e s in l i v e r enzymes were ob served a t both c o n c e n t r a t io n s . A secon d stu dy was r u n a t 1, 7.6 a n d 83.9 m g / m 3 . No c o m p o u n d - r e l a t e d e f f e c t s w e r e s e e n in th e r a t s e x p o se d a t 1 mg/m3 . E x p o s u r e - r e l a t e d m o r t a l i t y was seen a t the h igh l e v e l o f ex p o su re. A d d it io n a lly , m acroscopic and m icroscop ic liv e r p ath ology was observed in the a n i m a l s e x p o s e d a t 7.6 and 83.9 mg/m3 . T h e s e l i v e r e f f e c t s appeared to be r e v e r s ib le . Subacute s t u d ie s by the o r a l and sk in a b s o r p t io n r o u t e s o f a d m in is t r a t i o n c o n fir m t h e e f f e c t s o f C-8 on the l i v e r . In two ch ro n ic fe e d in g s t u d ie s in r a t s , C-8 produced an in c r e a s e in th e in c id e n c e o f tumors in th e l i v e r , p an creas, and t e s t i s . C-8 was n o t t e r a t o g e n ic in t e s t s by in h a la tio n and gavage and was n o t m u ta g en ic in th e Ames t e s t . 2- - EID087794 000^:14 A. Acute 1. Oral ALD (rat) - 480 mg/kg (3.18). ALD (rat) - 670 mg/kg (3.1,3.5). * LD50 (rats) - 390 mg/kg (11.10). LD50 (male rats) - 470 mg/kg (3.15). LD50 (female rats) 482 mg/kg (3.15). LD50 (rats) - 540 mg/kg (5,12). LD50 (mice) - 457 mg/kg (3.16). LD50 (male guinea pigs) 178 mg/kg (3.14). LD50 (female guinea pigs) - 217 mg/kg (3.14). C-8 was slightly toxic when administered in single oral doses to the following groups of rats: we a n lings (21 days old): males, LD50 - 573 m g / k g and females, LD50 - 580 mg/kg; young adults (approx imately eight to ten weeks old): males, LD50 - 470 mg/kg and females, LD50 - 453 mg/kg; older rats: males, LD50 - 336 mg/kg and females, LD50 - 343 m g / k g ; n e w b o r n (< two d a y s old): m a l e s , L D 5 0 - 243 mg/kg and females, LD50 - 258 mg/kg. Toxicity in regards to the sex of the rats showed no significant difference. However, newborn (<two days old) and older rats had lower LD50 values than weanlings or young adult rats (3.32). C-8 is moderately toxic when a d m i n i s t e r e d orally to young adult male and female rats that'were untreated or surgically-modified (ovarectomized or castrated). Its LD50 is between 400 and 491 m g / k g of bo d y weight. No changes in liver weight to body weight ratios were seen in female rats given single doses of up to 200 mg/kg (ovarectomized or normal). A single oral dose of either 100 or 200 mg/kg produced an increase in liver weight of male rats. Castration reduced the magnitude of the liver weight increase but rats castrated and given 200 mg/kg had heavier livers than did the controls. Clinical signs seen in C-8 treated rats included stained face and perineal area and sporadic weight loss (3.21). HDR001723 -3- 0 0 0 i ,s EID087795  Two male beagles given a single dose of 450 mg/kg A P F O a i e d w i t h i n 48 hours. Pl a s m a e n z y m e s w e r e markedly elevated 24-48 hours after ingestion. Dogs given 200 mg/kg had elevated GPT and GOT in 24 hours which normalized after one week. This increase in plasma enzyme levels is indicative of c e l l u l a r damage (3.3). The oral LD50 of C-8 was determined in rats pretreated with phnobarbital sodium or proadifen hydrochloride. There were no significant differences in the LD50 value of C-8 (478 mg/kg) following pre-treatment with either phnobarbital sodium or proadifen hydrochloride (3.19). APFO w a s a d m i n i s t e r e d t o r a t s b y s t o m a c h t u b e i n s i n g l e d o se s ran gin g from 1.5-2250 m g/kg. C l i n i c a l sign s of t o x ic it y were in a c tiv it y , a red discharge around the n ose, p e r in e a l d is c o lo r a t io n and w eight l o s s . A n i m a l s r e c e i v i n g d o s e s >_ 200 m g / k g s h o w e d e n l a r g e d l i v e r s (3.1). R ats r e c e i v i n g i n t r a g a s t r i c d o s e s a s lo w a s 60-90 m g/kg had e n l a r g e d l i v e r s (3.5). G a s t r o i n t e s t i n a l i r r i t a t i o n w a s a l s o o b s e r v e d i n r a t s i n g e s t i n g APFO (3.5,3.6). APFO, given in single 12 mg/kg doses to three rats, produced no clinical signs of toxicity (3.2). Pre-dosing or post-dosing with Dowex* 1-X2-C1 Ion Exchange Resin at 1000 mg/kg changes the toxic effects of C-8 in rats. All rats dosed with the Dowex*, either before or after C-8 had reduced mortalities compared to the rats dosed wi t h C-8 alone (3.23). Groups of young adult rats were administered a single dose of ethanol at 6000 mg/kg or a 15% solution in their drinking water for 14 days and/or a single dose of C-8 at dose levels of 200, 480, or 670 mg/kg. In the rats administered a single dose of ethanol followed 24 hours later by C-8, all the rats administered 670 mg/kg of C-8 died within 8 days after dosing. In the rats administered ethanol for 14 days before C-8 dosing, all the rats administered 480 and 670 mg/kg of C-8 died within 6 days after dosing. Liver weight/body weight ratios showed a sharp increase in all the rats that received C-8 when compared to controls and to the rats that received only ethanol. There were no significant differences between the untreated controls and the rats that received only ethanol or between the ethanol pre-treated rats administered C-8 and the rats that received only C-8 (3.34). " 4" EID087796 r ooo;; HDR001724  See Related Reference 13 for information on the toxicity and kinetics of perfluorooctanoic acid. 2. S kin LD50 (rabbits) - 4278 mg/kg (3.10,6). Rabbits were dosed at 7500, 5000, 3000 and 1500 mg/kg. Skin irritation occurred at all levels. Clinical signs included weight loss and labored breathing at all levels, wetness underneath the body, cyanosis, diarrhea, and lethargy appearing most levels (3.10). at LD50 (male rats) - 6959 mg/kg (3.10,6). Male rats dosed at 3000, 5000 and 7500 mg/kg showed initial weight loss. Rats dosed at 5000 or 7500 mg/kg were lethargic on the day of treatment and the majority had wet and/or stained perineal areas. Chromodacryorrhea was seen in rats dosed at 7500 mg/kg (3.10,6). -- Female rats dosed at 5000 or 7500 mg/kg showed mild skin irritation and initial weight loss. At 7500 m 9/k9 a stained face and a wet and stained perineal area were also noted (3.12,6). Ammonium perfluorooctanoate did not produce i r r i t a t i o n w h e n a p p l i e d to the s k i n of rabbits (5). APFO (500 mg) was applied as an aqueous paste to the trunk and lateral areas of six male rabbits. After 24 hours semi-occluded contact, APF O caused mild to moderate skin irritation. O b s e r v a t i o n at 48 hours indicated slight to moderate irritation (3.9,6). Permeation of five types of gloves by C-8 was evaluated. Three of the gloves (Neoprene*, neosynthetic latex and natural latex) had a measurable breakthrough time and permeation rate after eight hours of continuous exposure to a 30% C-8 solution (3.22). See R e l ated R e f e r e n c e 14 for a d d i t i o n a l information. 3. Eyes APFO caused generalized moderate corneal opacity with a small area of severe opacity, intermittent moderate iritis and moderate conjunctivitis when 38.3 mg of solid test material was placed into the right conjunctival sac of a rabbit's eye. The ocular effects gradually receded, however, the small -5- EID087797 HDR001725 00 j area of corneal opacity persisted and at 21-28 days was mild with vascularization. An eye dosed with the test material and promptly washed had a small area of slight to moderate corneal opacity and moderate to slight conjunctivitis with no iritic effect. The eye was normal within seven days except for mild conjunctival redness, which was normal w i t h i n 14 d a y s (3.8). APFO' (100 mg) w a s m o d e r a t e l y i r r i t a t i n g 'to the eyes of rabbits (mean score - 14.0; highest possible score - 110.0). Iridial and conjunctival effects were evident in unwashed eyes, but only conjunctival effects appeared when eyes were washed after exposure (5). Rats exposed to APFO during a four-hour inhalation period exhibited corneal opacity and ulceration which were still m i c r o s c o p i c a l l y e v i d e n t after 42 days (3.6). 4. I n h a l a t i o n ~ Four-hour ALC (rats) - 0.8 mg/L (3.6,7). Groups of rats were exposed for four hours to concentrations of APFO ranging from 0.38 mg/L to 5.7 mg/L. At a concentration of 2.2 mg/L or higher, all rats died w i t h i n 48 hours after e xposure. Liver enlargement reached a maximum seven to 14 days after exposure returning to normal w i t h i n 42 days. APFO was highly toxic whe n inhaled but no changes in cell morphology were observed (3.6,7). 4-hour LC50 (rats) - 980 mg/m3 (11.12). No deaths resulted from a one hour exposure to a nominal concentration of APFO (18.6 mg/L). Clinical signs during exposure were red nasal discharge, yellow staining of the ano-genital fur, dry rales, red material around the eyes, excessive, salivation, and lacrimation. Similar signs appeared post exposure in a 14-day observation period. Bilateral mottling of the lungs was observed in eight of ten autopsies (5). 5. I n t r a p e r i t o n e a l i n j e c t i o n L D 5 0 (mice) 192 m g / k g (11.3). See Related References 15.and 16 for information on the toxicity of perfluorooctanoic acid. EID087798 HDR001726 OOOfciS B. Extended Studies 1. O r a l * Biochemical and morphological changes associated wi t h A P FO- induced hepatomegaly were studied in rats. G r oups of male rats were a d m i n i s t e r e d 50 m g / k g / d a y o f A P F O for 1, 3, or 7 days. S o m e rats r e c e i v e d C 1-labeled sodium acetate 24 hours after the last dose. T h e rats w e r e killed- a f t e r the l a s t daise or 3 hours after the administration of radiolabeled sodium acetate, and the livers were removed for examination. Liver weights were significantly increased in all APFO-treated rats. The relative amount of DNA/g of liver decreased; however, the total amount of hepatic DNA was not significantly affected. Cytochrome P-450 and benzphetamineN-demethylase activity were significantly increased by APFO administration. Carnitine-acetyltransferase and carnitine-palmitoyl-transferase activities were also significantly increased. Ethoxyresorufin-Odemethylase activity was decreased after one or three doses. Glutathione-S-transferase and uridinediphosphoglucuronyl-transferase were not significantly affected by APFO administration. Incorporation of radiolabeled sodium acetate into hepatic lipids except for diacylglycerols, squalene, and sterols containing 27 carbon atoms was significantly increased by APFO administration. Proliferation of the endoplasmic reticulum, mitochondria, and peroxisomes was observed in t r e a t e d rats. The h e p a t o m e g a l y i n d u c e d b y A P F O is due to hypertrophy rather than hyperplasia. Peroxisome proliferation does not necessarily result in hypolipidemia, as evidenced by the observed increase in lipogenesis in the treated rats (9). Administration of ten successive doses of 6.7 mg/kg to six rats caused moderate enlargement of the liver and slight enlargement of kidneys and testes. Simultaneously there was a slight depression of pancreatic weight and the lungs of rats showed slightly enhanced pneumonitis (3.2). e In a two-week feeding study, 25% Teflon* with APFO dispersing agent was administered in the diet of a group of six rats. After a two-week recovery period the treated animals had slightly heavier livers than the controls or animals receiving Teflon* without the APFO (3.2) . EID087799 -7- 00*. i s HDR001727  C-8 produced an increased incidence of Leydig cell adenomas in rats fed 200 p p m of C-S tor 1 years. A hormonal (non-genotoxic) mechanism was examined since C-8 was negative in short-terms tests for genotoxicity. Groups of adult male rats were administered C-8 by g a v a g e at d o s e s of 1, 10, 25, or 50 m g / k g / d a y for 14 days. Also included, in addition to an ad libitum control group, was a pair-fed control group to t h e : 50 mg/kg/day C-8 group. A dose-dependent decrease in body weight and relative accessory sex organ (ASO) weights was seen, wi t h the relative ASO weights of the 50 mg/kg/day group significantly less than those of the pair-fed controls. Serum e s t r a d i o l levels w e r e e l e v a t e d in the 10, 25, and 50 mg/kg/day groups. Estradiol levels in the 50 mg/kg/day group were 2.7-fold greater than those of the p a i r - f e d controls. The increase ^in s e rum estradiol levels occurred at the same dose levels as the increase in hepatic beta-oxidation activity. A significant d o w n w a r d trend w i t h dose was &een in serum testosterone levels when compared with the ad libitum controls. However, when the 50 mg/kg/day group was compared with their pair-fed controls, no significant differences were seen. Challenge experiments, which can identify the presence and location of a lesion in an endocrine axis, were undertaken to clarify the significance of this downward trend in serum testosterone following the administration of C-8. In this experiment, a group of rats was a d ministered 50 m g / kg/day of C-8 for 14 days. One hour before termination, rats received either a human chorionic gonadotropin (hCG), g o n a d o t r o p i n - r e l e a s i n g h o r m o n e (G n R H ), or n a l o x o n e challenge. Following hCG challenge, serum testosterone levels in the 50 mg/kg/day group were significantly decreased by 50% from those of the ad libitum controls. Similar decreases, although not significant, were seen in serum testosterone f o l l o w i n g G n R H and n a l o x o n e a d m i n i s t r a t i o n to the 50 mg/kg/day C-8 group. These studies suggest that the decrease in serum testosterone following C-8 administration was due to a lesion at the level of the testis. Androstenedione levels in the C-8 treated rats were decreased 60% from those in the ad libitum controls, suggesting the decrease in serum testosterone following hCG challenge may be due to a decrease in the conversion of 1 7-alpha-hydroxyprogesteron e to androstenedione. The conclusion was that the elevated estradiol levels in the C-8 treated rats may be responsible for the decreased relative 8- - EID087800 000 HDR001728 accessory sax crgan weight and serum testosterone Ic'-iii seen in tr.is, s t udy as w e l l as the ir.cieased incidence of Leydig cell adenomas observed in a chronic, 2-year feeding study in rats administered C-8 (2). * A group of male rats was a d m i n i s t e r e d by gavage 25 m g / k g / d a y of C-8 for 14 days. In a d d i t i o n to an ad libitum control group, a second control was pair-fed to the 25 mg/kg C-8 group. A decrease in body and accessory organ unit weights and an increase in liver weights was seen in the C-8 group when compared with the ad libitum control. When the C-8 group was compared to the pair-fed control group only the liver weight was increased. Although the serum testosterone concentration remained unchanged, the serum estradiol concentration was significantly higher in th C-8 group than in the pair-fed control group (1). An increased liver weight/body weight ratio was observed in mice fed 30 p p m of C-8 in t h eii diet for 14 days. W h e n C-8 was c o m b i n e d w i t h an e qual amount of nonadecafluorodecanoic acid, a similar effect was produced (3.31). Groups of ten mi c e we r e fed a d i e t c o n t a i n i n g 30, 300 or 3000 ppm of C-8 for 14 days. All the mice fed 3000 ppm of C-8 died. Deaths also occurred at 300 ppm. Body weight loss was indicated at 300 and 3000 ppm. Liver weight/body weight ratios showed a sharp increase over controls in the mice fed the 30 ppm C-8 d i e t (3.26,8). Gr o u p s of 32 mice w e r e fed a d i e t c o n t a i n i n g 10, 30, 100, 300, 1000, 3000 or 10,000 p p m of C-8 for 14 days. Deaths occurred in the 1000, 3000 and 10,000 ppm groups. Body weight loss was indicated at the end of each week at 300 ppm and more. Liver weight/ body w e ight ratios showed a s harp incr e a s e at 10 p p m and were dose-dependent. Clinical signs of toxicity included weakness, tremors, piloerection, pallor, stained perineal area and unkempt appearance (3.17). C-8 was administered three times a week for three weeks to rats and mice at three dose levels, 0.1, 1.0 or 10 mg/kg. Weakness followed by d eath occurred in two female mice dosed at 10 mg/kg. Sporadic weight loss was seen in the female rats and both sexes of mice. A significant liver weight increase was noted in both male and female mice administered 1 and 10 mg/kg. S i g n i f i c a n t l y increased liver weights were also noted in male rats administered 10 mg/kg (3.33). -9- ElD08780i 000/ Groups of mice were fed a diet containing 0.01, 0. G 3.. 0.1, CcO.- 1-0. Z, 10 or ZQ p p m cf C-8 for 21 days. Livers were s i g n i f i c a n t l y heavier at 30 ppm, slightly heavier at 3 ppm and appeared normal at 10 ppm. No changes in liver w e i g h t were seen in the groups fed 1 ppm or less of C-8 (3.29,8). Rats were fed 0-30,000 p p m A P F O d a i l y for 28 days. At 10,000 and 30,000 ppm all animals died within the first week. In general, animals showed decreased body weight and an increased liver weight (at >30 ppm, males and >300 ppm, females). Treatmentrelated histopathologic changes appeared in all test groups. In a similar test using mice all animals d o s e d at >^ 1000 p p m d i e d w i t h i n the f i r s t two we e k s . A t d o s e s o f >_ 3000 p p m a r o u g h h a i r c o a t a n d muscular weakness were evident in mice. Slight cyanosis, decreased body weight gain and increased average liver w e i g h t were also n o t e d (5). Groups of ten rats we r e fed d i e t s c o n t a i n i n g 10, 30, 100, 300 or 1000 p p m of C-8 for 90 days. -No c h a n g e s considered to be directly related to C-8 were seen in general behavior, appearance or survival. A slight decrease in body weight gain and food consumption was seen for male rats in the 300 and 1000 ppm groups. Hematologic, biochemical and urinalysis values for the female rats showed no changes considered to be related to C-8. A few values obtained for the males showed a slight deviation from the control values (i.e. slightly lower erythrocyte count, and elevated blood urea nitrogen and alkaline phosphatase values). Compound-related gross observations such as enlargement and varying degrees of discoloration on the surface of the liver were observed among male rats in the 1000 ppm group. There were no such observations among female rats from the 1000 ppm group or in males or females from lower dietary levels. Statistically significant v ariations in sex-group mean organ weights, which were considered compound related, occurred in liver of rats in the 300- and 1000 ppm groups. All other variations were unaccompanied by any morphologic alterations. Microscopically, compound-related lesions were confined to the liver. The lesions consisted of focal to multifocal, very slight to slight, cytoplasmic enlargement of hepatocytes located in centrilobular-midzonal regions of the affected liver lobules, accompanied in some instances by increased amount of yellowish-brown pigments resembling lipofuscin in cytoplasm of hepatocytes and occasionally in sinusoidal lining cells. The incidence and relative severity of the above lesions -10- EID087802 were p re d cm in a n tIv among males and more pronounced cunGn^ u *3 u Xm K wGO ppm. T h e s t r . e r c h a n g e s r e c o r d e d in the liver and o ther tissues were lesions of naturally occurring diseases and they were present in most instances among the control and test rats (5,11.1). * G r o u p s of rats w e r e fed d i e t s c o n t a i n i n g 1, 10, 30, or 100 p p m of C-8 for 13 weeks. B o d y w e i g h t and cumulative body weight gain for the 100 ppm rats were significantly lower than those of the control group. Hepatic palmitoyl CoA oxidase activity was s i g n i f i c a n t l y i n c r e a s e d in rats a d m i n i s t e r e d 30 and 100 ppm of C-8, and rats administered 10 ppm had transiently higher levels. Enzyme levels after 8 weeks of recovery foll o w i n g the 13 w e e k s of dietary administration were not significantly different from those of the controls. Administration of C-8 caused increased absolute and relative liver weights and hepatocellular hypertrophy in the livers of rats a d m i n i s t e r e d 10, 30, or 100 p p m of C-8 a f t e r 4, 7, and 13 weeks of treatment. The p r o g r e s s i o n of hepatocellular hypertrophy did not appear to be affected by the length of treatment. The changes observed are suggestive of a compound-related effect on intracellular metabolism and may be associated with peroxisome proliferation. At the end of recovery, these changes were not observed, indicating that the increase in liver weights was reversible. There was no consistent pattern for the hormone determinations which could be attributed to C-8 administration. None of the hormone levels were significantly different from controls although there appeared to be some indication of elevated estradiol for the 100 ppm group at the week 5 determination. The NOAEL was 1 ppm (11.13). e G r o u p s of four m o n k e y s w e r e a d m i n i s t e r e d 3, 10, 30 or 100 mg/kg of C-8 per day for 90 days. The monkeys treated with the higher dose, (100 mg/kg/day) all died during weeks two through five of the study. A t the 30 m g / k g / d a y d o sage level, three monkeys died during weeks seven through 12. They all showed signs of toxicity in the gastrointestinal tract (anorexia, emesis, sometimes brown in color, black stools), pale face and gums, swollen face and eyes, slight to severe decreased activity and prostration. The monkeys of the 30 and 100 mg/kg/day dosage levels showed body weight losses from the first week of the study. Because of the early deaths of the monkeys at the 100 mg/kg/day dosage level, the clinical laboratory tests were not conducted. The monkeys at the 30 mg/kg/day dosage level showed, in the first month of the study, - 11- EID087803 0 0 '):^ sli g h t ir rr?*r? ir> p r o t h r o m b i n t i m e a n d in a c t i v a t e d p a r t i a l m r o m r c p l a c t i r . time A ." 7 . 7 : ^iv.^5 . as well as decreased alkaline p h o s p h a t a s e a c t i v i t y in the serum (statistically significant). Only one monkey from this dosage level in this period showed a low albumin value. At the end of the study, the only remaining monkey from the 30 m g / k g / d a y dosage level showed apparent anemia, low blood glucose, alkaline phosphatase, total protein and albumin values. There was no m o r tality at:the 10 mg/kg/day ; dosage level. One monkey had black stool on several days in week 12 and occasionally anor e x i a and one monkey exhibited pale face and gums. At this dosage level there was a very slight increase in the A.P.T.T. values in the female monkeys during the first month of the study (not statistically significant). There were no changes in the other indices and no changes in the b o d y weight. In single monkeys from the 3 and 10 mg/kg/day dosage levels, there were trends toward decreased alkaline phosphatase in the serum. In the control and the 3 9/ k g / d a y d o s a g e l e vel t h e r e w a s n o m o r t a l i t y , no changes in the body weights and no signs of toxicity. Soft stool, diarrhea or emesis were observed occasionally. The mortality and the above mentioned signs of toxicity in the 30 and 100 mg/kg/day dosage levels were compound-related. There was a trend toward the same signs of toxicity in single m o n keys at the 10 m g / k g / d a y d o s a g e level. The 3 mg/kg/day dosage level seems to be free of signs of toxicity. There is an evident relationship between the administered doses and the degree of the toxicity. No gross or microscopic lesions which were considered compound-related were seen in tissues other than the adrenals, bone marrow, spleen and lymph nodes for male and female monkeys at the 30 and 100 m g / k g / d a y dosage levels. Microscopically, the a d renals fr o m male and f e m a l e m o n k e y s at the 30 and 100 mg/kg/day dosage levels have compoundrelated marked diffuse lipid depletion; the bone m a r r o w fr om male and female m o n k e y s at the 30 and 100 mg/kg/day dosage levels had compound-related slight to moderate h y p o c e l l u l a r i t y ; the spleen and l y m p h n o d e s f r o m m a l e and f e m a l e m o n k e y s a t the 30 and 100 mg/kg/day dosage levels had compound related moderate atrophy of lymphoid follicles. Statistically significant variations in sex group mean weights of a few organs o c c urred between the control and experimental groups. These variations were of unknown biological significance and were not accompanied by morphological alterations (5,11.2). -1 2 - EID087804 COOi Groups of 120 rale and 120 female rats were fed d i e t s contair.i.., ^iw*>c^ **- -- tw -t ** * for up to two years, while a control group received only untreated feed. The major in-life findings associated with C-8 administration consisted of a dose-dependent decrease in mean body weight gain and a treatment-related increase in food consumption in males; a slight treatment-related increase in the incidence of ataxia was observed in the females. There was no increase in mortality observed in either treatment group when compared to the control population. C-8 related hematologic changes seen in the treated rats consisted of decreased red blood cell counts, hemoglobin, and hematocrit values seen at various times throughout the two-year test period. While the decreases in erythrocyte counts were observed very early in the study, this condition did not progress into a generalized anemia by the end of the two-year study. Histopathologically, C-8 associated toxic changes were found in the liver. These changes were characterized by increased liver weights, increased size of the liver cells with vacuolation of the cytoplasm, and some evidence of hepatocellular degeneration with occasional signs of necrosis. As with the red blood cell findings, these liver changes were noted early in the study and showed very little evidence of progression over the remainder of the two-year study. The incidence of tumors found in this study was relatively low and the types of neoplasms found were not different from the tumor profiles commonly found in geriatric rats. Hepatocellular tumors were very slightly increased in the high-dose male rats; however, not to the extent that would be expected considering the morphological evidence of chronic hepatocellular stimulation first seen at the one-year necropsy (11.11). All of the liver tumors found in the above study w e r e c a r c i n o m a s a n d the i n c i d e n c e in the control, 30 ppm, and 300 ppm groups (males: 3/50, 1/50, 5/50; females: 0/50, 0/50, 1/50) did not appear to be dose related. The incidence of nodular h y p e r p l a s i a in the liver (males: 1/50, 0/50, 2/50; females: 0/50, 0/50, 3/50) was also slightly increased, though not statistically significantly (3.35). -13- 000//5 EID087805 All of the other remarkable tumor incidence values p r o d u c e d in this j t.vdy w e r e a s s o c i a t e d w i t h endocrine or endocrine-sensitive organs (3.35): The incidence of mammary gland fibroadenomas (10/50 (20%), 19/50 (38%), 21/50 (42%)) suggested a c o m p o u n d - r e l a t e d effect. However, w h e n compared to Haskell's historical control incidence for this strain of rat (37%), there does not appear to be any compound-related effect. The incidence of testicular Leydig cell adenomas (0/50 (0%), 3/50 (6%), 7/50 (14%)) was also suggestive of a compound-related effect. When compared to Haskell's control incidence for this strain of rat (6.1%, range 1-12%), the incidence in the 300 ppm group shows a statistically significant increase. C-8 was included in a mechanistic bioassay investigating extrahepatic. tumor induction by compounds which induce peroxisome proliferation. In this study, 300 ppm of C-8 was fed to rats for two years. Increased incidences of combined (single, multiple) hepatic adenomas (10/76 versus 2/80 in ad libitum controls and 3/79 in pair-fed controls), Leydig cell adenomas 8/76 versus 0/79 and 2/78 in control groups), and combined pancreatic acinar cell a d e n o m a s (7/76 v e r s u s 0/80 and 1/79 in control groups) were noted. The tumor incidences were outside the historical control incidence range for Haskell Laboratory, and in addition, ageadjustment statistics also supported the conclusion that the tumor incidences were elevated for the liver, pancreas, and testis (3.36,11.14). Skin Three groups of 15 male rats wer e exposed dermally for six hours/day, five d a y s/week for two weeks to 20 mg/kg, 200 m g / k g or 2000 m g / k g APFO.. A t 200 or 2000 mg/kg rats lost weight during the exposure period and showed slight reddening of the skin. Salivation was noted at 2000 mg/kg. Dose-related increases were noted in enzymes monitoring liver function. Liver damage was found in all groups following the tenth dose. During treatment there was an increase in liver weight. Coagulative necrosis of the epidermis at the dose site was noted in two rats dosed at 2000 mg/kg after ten days. Blood organofluoride levels were elevated on the tenth day of exposure. These decreased during a 14-42 day recovery period (3.11,6). -14- Ei D087806 3. I n h a l a t i o n G r o u p s c : 1 " r a t were- e x p o s e d , h e a d o n l y , to particular atmospheres of 11 or 83 m g / m 3 of C-8, six hours a day, five days a week for two weeks. The exposed rats showed a dose-related suppression of body weight. Liver injury or dysfunction was suggested by dose-related elevations of plasma enzymes for up to 28 days after the last exposure. Liver degeneration was detected histologically at the end of the exposure period. These liver effects were not observed after 14, 32 or 42 days of recovery. Eye examinations revealed no compoundrelated effects (3.7). Groups of rats were exposed six hours a day, five days a week for two weeks to 1.0, 7.6 or 83.9 mg/m3 of C-8. Observations of clinical signs during exposure showed only slight nasal and ocular discharge. However, after three to four days on test at 83.9 mg/m3 one rat died during exposure and a n o t h e r was s a c r i f i c e d in e x t r e m i s . B o t h xif th ese rats had lost a considerable amount of weight. Body weight of the 1.0 m g / m 3 groups were similar to those of the controls while the body weights of the 7.6 mg/m3 group were significantly higher. Organ to body weight ratios demonstrated a dose-related significant increase in lung, liver and testes weight immediately after exposure ended. The liver/body weight ratios were significantly higher in the 83.9 mg/m3 group through a 28-day recovery period. Clinical laboratory measurements demonstrated an increase in serum alkaline phosphatase in all exposure groups after ten exposures, which persisted in the 83.9 mg/m3 group through 14 days of recovery. P a t h o l o g i c a l evaluation revealed heavy livers and microscopic lesions in the 7.6 and 83.9 m g / m 3 groups. These changes were reversible following a 28-day recovery period. Blood fluoride analysis clearly d e m o n s t r a t e d a d o s e - r e l a t e d p r e s e n c e of. C-8 in all groups including the controls. The amount of C-8 in blood decreased with time, but was detectable after 84 days recovery in both controls and the 83.9 mg/m3 group (3.13,7). * Repeated exposure of rats to C-8 produced liver changes and elevated organofluoride levels (11.12), C. C a r c i n o g e n i c P o t e n t i a l * In chronic, 2-year feeding studies in rats, C-8 produced an increased incidence of tumors in the liver, pancreas, and testis (3.35,3.36,11.11,11.14). -15- EID087807 00` See "slated references 17-23 for indorsation on the neparoca i c m o g e n i c i t y of perfluoroccl&acic acid. Mutagenic Potential APFO was tested in microbial assays using Salmonella t y p h i m u r i u m s t r a i n s T A 98, T A 100, T A 1535") T A 1537 and TA 1538 and Saccharomyces cerevisiae strain D-4. All tests were negative with and without activation (5,12). C-8 had a low order of cytotoxicity in C3H 10T-1/2 cells and no evidence of transformation was observed (11.8). See R e l ated R eference 24 for i n f o r m a t i o n on the mutagenicity of perfluorooctanoic acid. E. D e v e l o p m e n t a l / R e p r o d u c t i v e T o x i c i t y The oral a d m i n i s t r a t i o n of A P F O at 25, 50, 75, 100 or 150 mg/kg/day to rats during the periocL.of organogenesis (days six through 15 of gestation) did not result in any deaths. A toxic effect of reduced body weight gain occurred between days six and nine of gestation in the 150 mg/kg/day dose group. The two nonpregnant 150 mg/kg/day rats had a more severe effect on body weight on day nine of the study than the pregnant high dose dams. They lost a considerable amount of weight and one was observed to have u r i n a r y incontinence on days 11, 12, and 13. The preg n a n t dams of the 25, 50, 75, a n d 100 g/kg/day dose groups did not have abnormal clinical signs and gained weight at comparable levels to the control group. Four fetuses were examined from each of four dams in the 25 and 150 m g / k g / d a y dose groups for eye changes. All of the readable fetuses sectioned had eye changes consisting of one or more of the following: large lens cleft, dark streak running one-half to three-quarters of the way through the lens or disorganized lens fibers. The lens abnormalities occurred in the same location as those observed in the two previous teratology studies on chemically related compounds. The abnormalities in this study appeared more pronounced than in the previous studies. In the previous studies, the teratogenic effect was a developmental eye abnormality which appeared to be an arrest in development of the primary lens fibers forming the embryonal lens nucleus, followed by secondary aberrations of the secondary lens fiber of the fetal nucleus. The same general morphological changes occurred in this study (11.6). - 16- EID087808 0 0 0 /:' S  Groups of pregnant rats were administered 0.05, 1.5, 50 or 2 ? C jRg/kg of C-S on o&ys t-'E c-f ge s t a t i o n . Three rats in the high dose group aiea. 1-c caused low mean body weights in this group. No teratogenic or embryotoxic effects were found (11.7). Pregnant rats were administered 100 mg/kg/day by . gavage on days 6-15 of gestation. Maternal deaths occurred and during the dosing period, the surviving dams gained a b o u t o n e - t h i r d less b o d y w e i g h t than; the control dams. External, visceral, and skeletal alterations were sought, and the eyes of several fetuses of each litter in both groups were examined stereoscopically and histologically for alterations. The only finding noted that could possibly be C-8 related was an increased incidence of fetuses with ossification sites on the first lumbar vertebrae versus the incidence in the control group. This difference in incidence was statistically significant only if analyzed by a one-tailed test. Its presence was probably a response to generalized stre s s e v o k e d b y the t o x i c s t a t e of the deyps. The postpartum viability, growth rate, and development of the offspring from additional dams given C-8 were not demonstrated to be adversely affected by the C-8 administered. Criteria of development included examination of the pups for external alterations and ophthalmoscopic examination of the eyes (3.25,10). Groups of pregnant rabbits were administered 1.5, 5 or 50 m g/k g of C-8 in d i s t i l l e d w a t e r on days 6-18 of gestation. At 50 m g/kg the dams lost more weight than the untreated controls. No teratogenic effects were observed (11.9). Groups of pregnant rats were exposed for six hours a day on days 6-15 of g e s tation to 0.14, 1.2, 9.9 or 21 m g / m 3 of C-8. M a t e r n a l d e a t h s o c c u r r e d at the 21 mg/m3 concentration and overt toxicity was evident among the surviving dams and among those of the 9.9 mg/m3 group. No teratogenic response was observed in any of the e x posed groups. Embryofetal toxicity was observed only in the 21 m g / m 3 group. Other than a temporary reduction in the body weight of the pups from the 21 m g / m 3 group, no adverse effects were seen in the offspring (3.24,10). Metabolism Animal Studies Sex and species differences in the excretion and disposition of radiolabeled C-8 were observed in a s t u d y irf rats, mice, h a m s t e r s , a n d ra b b i t s . The -17- E ID 087809 female rat and the male hams t e r e x c r e t e d over 99% of the minis t e red dose by 120 hours after dosing. Conversely, the as Is rat art the .he ms ter excreted 39 and 60% of the a d ministered dose by 120 hours post-dosing. Both sexes of rabbits excreted the C-8 as rapidly and completely as the female rat and male hamster. The male and female mice excreted only 21% of the administered dose in 120 hours .(3.28). Male and female rats were administered radiolabeled C-8 by i n t r a v e n o u s injection. F e m a l e s had exc r e t e d e s s e n t i a l l y 100% of the a d m i n i s t e r e d d o s e w i t h i n 24 hours while the males excreted only 20% of the administered dose. Radioactive tissue residues were not detectable after 17 days in the females, while at 36 days, male rats h a d 2.8% of the c a r b o n - 1 4 in the liver, 1.1% in plasma, and lower but still detectable amounts in other organs (11.5). The uptake and clearance of C-8 from the blood of female rats following a single oral dose was rapid with the peak reached one-two hours post-treatment and with virtual total clearance by 24 hours. A dose-response was demonstrated with no apparent changes in blood C-8 levels following multiple oral dosing. The slower clearance rate in male rats was demonstrated following a single oral dose. The same general statements apply following inhalation exposure. A single six-hour inhalation exposure resulted in peak blood levels within one hour after cessation of exposure, the material rapidly cleared from the blood, the number of exposures did not affect blood levels, and male rats cleared the compound much more slowly. Pregnant and non pregnant rats showed similar C-8 blood levels following either oral or inhalation exposures. Specific data follows (3.20): Oral administration, female rats, C-8 levels as a function of time post-dosing. C-8 levels of 14 ppm were seen 15 minutes following the dose (25 mg/kg). These levels rose to a peak of a p p r o x i m a t e l y 30 p p m at one to two hours, d r o pped to 26 p p m b y e i g h t h o u r s a n d to 0.7 a n d 0 . 0 4 5 p p m at 24 and 168 hours, respectively. Conclude: C-8 is absorbed and rapidly cleared from the blood of female rats given a single oral dose. -18- o o 0 r :: s o EID087810 O r a l a d m i n l s t r a t i o n , f e m a l e r a t s , C-8 l e v e l s as a f Uliw v t t V- V 'U*W^`G C-8 levels at 1/2 hour following treatment ranged from 3 to 162 ppm, doses administered 2.5 to 150 mg/kg. The same dose response was seen at 24 hours w i t h b l o o d values ranging f r o m 0.12 (2.5 mg/kg) to 18 (150 mg/kg) ppm. The response was linear. C onclude: C-8 in b lood i s d i r e c t l y r e la t e d to the amount o f C-8 a d m in ister e d o r a l l y . Oral administration, male and female rats following a single oral dose of 25 mg/kg. C-8 levels in female rats were 16 ppm (1/2 hour), 26 p pm (eight hours), 0.7 ppm (24 hours) and 0.045 ppm (168 hours). The corresponding values for male rats w e r e 23, 63, 50 and 23 ppm. Conclude: C-8 is retained in the blood of male rats to a greater extent than female rats following oral treatment. Oral administration, female rats, C-8 levels as a function of number of doses. Blood levels in female rats given one versus 11 doses of C-8 were not considerably different. Concentrations at 1/4 hours post-treatment were and 17 ppm, one and 11 doses, respectively. oral 14 At 1/2 hour C-8 concentrations were 16 and 25 ppm; at eight hours, 26 and 13 ppm; at 24 hours, 0.7 and 0.8 ppm; and at 168 hours, 0.045 and 0.10 ppm, one and 11 doses, respectively. Conclude: C-8 does not appear to accumulate in the blood of female rats following repeated oral treatment. The number of treatments does not seem to influence the C-8 blood level with dose remaining constant. Inhalation exposures, female rats, C-8 levels as a function of time post-exposure. C-8 levels of 96 ppm were seen 15 m i n u t e s following a single six-hour inhalation exposure to 10 m g / m 3 . This level stayed around 100-110 ppm through one hour, fell to approximately 70 ppm at eight hours, further decr e a s e d to 52 p p m at 24 h o u r s and dropped to 0.39 ppm 168 hours later. This same general pattern was seen in rats exposed to either 0.1 or 1 m g / m 3 . The lag phase seen in oral e x p o s u r e s is not -19- EID087811 seen here due to blood sam pling f o llo w in g a six -h o u r in h a la tio n exposure (rather than a s in g le oral dose at a given, f in it e tim e). Conclude: C-8 i s absorbed and r a p id ly c le a r e d from the blood of female rats given a sin g le six-hour inhalation exposure. In h a la tio n ex p o su res, fem ale r a ts , C-8 le v e l s as a function of dose. C-8 l e v e l s a t 1/2 hour f o l l o w i n g a s i n g l e s i x - h o u r i n h a l a t i o n e x p o s u r e ra n g e d from 2 t o 100 ppm, a i r b o r n e c o n c e n t r a t i o n s o f 0.1 t o 10 mg/m3 . The s a m e d o s e r e s p o n s e w a s s e e n a t t w o h o u r s (2, 17, 69 p p m ) , e i g h t h o u r s (0.85, 4, 71 ppm) a n d 24 h o u r s (0.14, 0.56, 52 ppm). - c o n c e n t r a t i o n s c o r r e s p o n d i n g t o 0.1, 1 and 10 mg/m3 . The r e s p o n s e i s l i n e a r a t 1/2 hour (correlation coefficient of 0.999). s. Conclude: C-8 in blood, i s d i r e c t l y r e la t e d to the amount o f C-8 in h a le d . At the h ig h e s t l e y g l u sed , the clea ra n ce r a te i s somewhat slow er than seen a t the lower l e v e l s . This su g g ests m assive overloads in the clearance system . Inhalation exposures, male and female rats following a single six-hour inhalation of 10 mg/mL. C-8 levels in female rats were 109 ppm (1/2 hour), 69 p p m (two hours), 71 p p m (eight hours), and 52 p p m (24 hours). The corres p o n d i n g va l u e s for male rats were 137, 157, 182 and 147 ppm. Conclude: C-8 i s r e ta in e d in th e b lo o d o f male r a ts to a greater ex ten t than female rats follow in g inhalation exposure. Oral administration to pregnant and non-pregnant female rats, C-8 levels following a single oral dose. C-8 levels in both pregnant and non-pregnant rats following a single 25 mg/kg oral dose were e s s e n t i a l l y the s a m e 16 a n d 10 p p m a t 1/2 hour, 33 a n d 39 p p m at two h o u r s , 26 a n d 31 p p m at e i g h t hours, non-pregnant and pregnant rats, respectively. C o n c l u d e : C-8 c l e a r a n c e f o l l o w i n g o r a l d o s i n g is not altered in pregnant vs. non-pregnant rats. - 20- EID087812 0 0 *l_?.o* Inha 1 s t : e n - r a l t r g a ts e n t, r regnant r a t s , C-8 1 e V e x & a & ct X- v**v*wAW** w *, . . . x O 6 C v *- Blood levels in pregnant rats given either one, six or ten doses of C-8 were essentially the same 1/2 and 24 hours following the last oral treatment. At 1/2 hour the levels were 18, 12 and 12 ppm, one, six and ten treatments, respectively. When comparing the levels seen at two and eight hours following a series of ten c o n s ecutive doses, there appears to be a lowering of C-8 blood concentrations in the rats given ten doses (15 compared to 25 pp m at two hours, 11 c o m p a r e d to 31 at e i g h t hours). Th i s m a y i n d i c a t e an e n h a n c e d .c l e a r a n c e of C - 8 w i t h m u l t i p l e dosing but w o u l d require c o n f i r m a t i o n p rior to acceptance as fact. Blood levels following one or ten consecutive six hours/day inhalation exposures were not different. Conclude: C-8 does not appear to accumulate in the blood of pregnant rats following repeated oral or inhalation exposures. Radiolabeled C-8 was transferred from maternal blood to the fetuses of pregnant rats. A single 10 mg/kg dose was administered orally on day 19 of gestation. Maternal blood and placental levels of C-8 increased between two and four hours after dosing then decreased between four and eight hours after dosing (3.27). In a previous study, Dowex* Ion Exchange Resin was able to reduce the acute lethal effects of C-8. in this study, rats a n d mi c e w e r e g i v e n D o w e x * resin 24 hours after dosing with C-8. No signs of enhanced elimination of C-8 via the feces, urine or exhaled air was seen (3.30). See Related References 26-39 for information on the metabolism of perfluorooctanoic acid. Also see Related References 61 and 62 for analytical methods for the determination of C-8 and perfluorooctanoic acid in biological samples. Human Studies Perfluorooctanoic acid has a long half-life in humans. A study of occupationally exposed workers at a plant which produces C-8 showed organic fluorine levels in the b l o o d r a n g i n g f r o m 1 to 71 ppm. One worker with a level of 70 ppm was removed from the fluorochemical production area and his blood analyzed for organic fluorine over several months. A f t e r 18 months, his o r g a n i c flu o r i n e level had d e c r e a s e d o n l y to 39 p p m (45% reduction) (12). -2 1 - e I>087813 G. Biochemical Studies * In ex vivo studies, Leydig cells were isolated from rats following 14 days of dosing. The hCG-stimulated Leydig cells from the C-8-treated rats had statistically greater increases in testosterone production than in controls. In contrast, c u l t u r e d L e y d i g c e l l s t r e a t e d iji v i t r o with C-8 produced a dose-dependent decrease in test o s t e r o n e and at 500 u M p r o d u c e d an i n c r e a s e in estradiol (1). * See Related References 40-60 for information on peroxisome proliferation and oxidative phosphorylation of perfluorooctanoic acid. H. Clinical Reports of Human Exposure * Health screening examinations were offered to the employees of a 3M plant that produced C-8 as well as other fluorochemicals. No health problems related to exposure to fluorochemicals were encountered among those examined. Additionally, no relationship was observed between deviations from normal between laboratory test results and blood levels of organic fluorine (the liver enzyme SGGT was the most frequently encountered test result exceeding the normal range). C-8 exposure levels ranged from 0.03 to 7.6 mg / m 3 (12). * A study was made of Washington Works employees potentially exposed to C-8. Results of blood chemistry testing (SGOT, LDH, AP, and bilirubin) indicated no conclusive evidence of an occupationally-related health problem among workers exposed to C-8 (3.38). I. Epidemiology A retrospective cohort mortality study was made of employees at a 3M plant where C-8, along with other f l u o r o c o m p o u n d s , is manufactured. R ecords on 4218 employees were reviewed. Only those who worked for six months or more (3688 workers) were included in the mortality follow-up. Of the 180 known deaths, 177 death certificates were obtained. Overall the number of deaths was significantly less than expected. The observed-to-expected ratio for cancer deaths was 1.0 (11.4,12). * In a retrospective cohort mortality study, the relationship between mortality and employment at a perfluorooctanoic acid (PFOA) production plant were investigated. The cohort consisted of 2788 male and IIUKUUl /</ -2 2 - E i&087814 749 female workers employed between 1947 and 1983. The all - c a u s e s s t a n d a r d i z e d m o r t a l i t y rate (SMR) was 0.75 for men and 0.77 for women. Among men, the cardiovascular SMR was 0.68 and the all-gastro intestinal diseases SMR was 0.57. There was no significantly increased cause-specific SMR for either men or women. The SMRs for prostate cancer were 2.03 in the Chemical Division group (exposed) and 0.58 in the non-Chemical Division group (not e x p o s e d to c h e m i c a l s ) . In :the C h e m i c a l D i v i s i o n group there were 4 observed and 2 expected deaths from prostate cancer. There was no significant association between any cause of death and latency in either group. In the Chemical Division group, the SMR for prostate cancer was 1.61 in the greater than 15-year latency group. For all men employed at this plant, 6 deaths were recorded for prostate cancer v e r s u s 6 expected. F u r t h e r r e s e a r c h is needed to evaluate and confirm the association be t w e e n P F O A and p r o s t a t e canc e r (4). J. Aquatic/En v i r o n m e n t a l Studies * 96-hour LC50 (bluegill sunfish) - 569 mg/L (11.12) 9 6 - h o u r LC50 (b l u e g i l l s u n f i s h } * 634 m g / L (3.37). 96-hour LC50 (fathead minnows) - 766 mg/L (11.12). 4 8 - h o u r LC50 (b l u e g i l l sunfish) - 1500 m g / L (3.4). 48-hour LC50 (snails) - 820 m g / L (3.4). 4 8 - h o u r E C50 (D a p h n i a m a g n a ) - 632 m g / L (11 .12). 50% growth reduction (diatoms) - 2400 m g / L ; safe level (seven days) - 720 mg/L (3.4). 14-day EC50 (green alga, Selenastrum capricornutum) - 73 mg/L (11.12) . COD - Nil? 20-day BOD - Nil (11.12). The Soil A b s o r p t i o n Coefficient (Kocj is 17? this i n d i c a t e s v e r y h i g h .m o b i l i t y in a s a n d y l o a m soil (11 .12). -23- 0 0 9>; 3.5 e ^087815 REFERENCES Biecfel, L. B. et al., The Toxicologist, 1 3 ( 1 ) : 3 9 9 (Abstract 1563) (1993) . Cook, J. C. et a l ., Toxicol. A p p l . Pharmacol., 113(2):209-217 (1992). DuPont Co., Haskell Laboratory Data: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 36. 37. 38. MR-604-7, HL-55-61 MR-604-7, HL-56-61 MR-639-1, HL-123-65 Acad. Nat. Sci. Philadelphia Data (1968) (C-17B2) MR-1070-1, HL-128-68 MR-1198-1, HL-160-69 MR-2753-1, HL-253-79 MR-3567-1, HL-635-79- MR-3567-1, HL-636-79 MR-3567-1, HL-659-79 MR-3567-1, HL-589-80 MR-5342-1, HL-682-80 _ MR-3692-1, HL-205-81 MR-5342-1, HL-291-81 MR-5342-1, HL-295-81 MR-5342-1, HL-329-81 MR-5418-1, HL-- 560-- 81 MR-5342-1, HL-565-81 MR-5342-1, HL-567-81 MR-4140-1, MR-4147-1, and MR-4152-1, HL-593-81 MR-5342-1, HL-600-81 MR-4198-1, HL-612-81 MR-5343-1, HL-828-81 MR-4129-1, HL-881-81 MR-4130-1, HL-1-82 MR-5418-1, HL-12-82 MR-4275-1, HL-61-82 MR-4153-1, HL-62-82 MR-5418-1, HL-323-82 MR-4370-1, HL-405-82 MR-5343-1, HL-537-82 MR-5454-1, HL-788-82 MR-5454-1, HL-138-83 MR-5343-1, HL-79-84 Letter, G. P. S y k e s to C. F. R e i n h a r d t , d a t e d 1 0 - 2 9 - 8 7 (AEL File) MR-5686-1 MR-9309-1 R e p o r t d a t e d 1 - 1 5 - 8 1 , W. E. F a y e r w e a t h e r , E p i d e m i o l o g y Division of Corporate Medical (C-4124) Gilliland, F. D. and J. S. Mandel, J. Occup. Med., 35(9):950-954 (1993). HDR001744 -24- EID087816 REFERENCES (CONT'D) 5. G r i f f i t h , F. D. and J. E. Long, Am. Ind. Hyq. A s s o c . J . , 41(8) :576-583 (1980). 6. K e n n e d y , G. L., Jr., T oxicol. A p p l . P h a r m a c o l . , 81(2):348-355 (1985). 7. K e n n e d y , . G . L., Jr. et a l ., F ood Chem. T o x i c o l . , 2 4 ( 1 2 ) :1325-1329 (1986). 8. K e n n e d y , G. L., Jr., T o x i c o l . L e t t . , 3 9 ( 2 - 3 ) : 2 9 5 - 3 0 0 (1987) . 9. P a s t o o r , T. P. et al., Exp. M o l . P a t h o l . , 4 7 ( 1 ) : 9 8 - 1 0 9 (1987). 10. S t a p l e s , R. E. et al., Fundam. A p pl. T o x i c o l . , 4(3,Part l):429-440 (1984). 11. 3M Co. Data. . 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. IRDC Report No. 137-089 (1978) (J-3546) IRDC Report No. 137-090 (1978) (J-3545) P e r s o n a l c o m m u n i c a t i o n , J. L o n g to P. J. G o r t (1/8/79) (C - 4 1 2 4 ) S c human, L. M. a n d J. S. M a n d e l , E p i d e m i o l o g y Associates Report (1980) (Submitted to EPA on 3-22-82, See L e t t e r W. H. P e a r l s o n to T. O ' B r y a n ) (C-4124) Riker Laboratories, Drug Metabolism Report 1-20 (1980) (Cited in Reference 11.11) Report M-601 (1981) Report No. 0681TR0110 (1981) (J-5918) Environmental Pathology Laboratory, Dept. Lab. Med. Path., Stone Research Laboratories (1981) (J-4124) G o r t n e r , E. G. et al., R i k e r L a b o r a t o r i e s D a t a (1982) (C-4124) Hazleton Laboratories America, Inc., Report Dated 2-6-87 (Submitted to EPA, TSCA8eCAP, Fiche 536984) Riker Laboratories, Inc., Report 0281CR0012 (1987) (J - 7 4 4 6 ) MSDS (1993) (Cited in DuPont MSDS No. 25617211) Hazleton Wisconsin, Inc., Report HWI-6329-100 (1993) (J -9878) EPA Submission (8e Notification Letter d ated 10-11-93 (AEL File) 12. U b el, F. A. et al., Am. Ind. Hyg. A s s o c . J., 4 1 ( 8 ) : 5 8 4 - 5 8 9 (1980). -25GOO EID087817 RELATED REFERENCES Oral 13. Kojo, A. et al., Arch. T o x i c o l . , S u p p l . 9:465-468 (1986). "Toxicity and kinetics of perfluorooctanoic acid in the wistar rat." Skin !< 14. DuPont Co., Haskell L a boratory Data, MR-4234-1, HL-735-81. "FC-143 occluded skin test on rabbits." Injection Studies 15. Olso n , C. T. a n d M. E. A n d e r s e n , T o x i c o l . A p pl. P h a r m a c o l . , 7 0 ( 3 ) :362-372 (1983). "The acute toxicity of perfluorooctanoic acid and perfluorodecanoic acid in male rats and effects oa tissue fatty acids." 16. Smith, F. A. et a l ., Toxicol. Appl. P h a r m a c o l . , 2 : 5 4 - 5 8 (1960) . "Screening of fluorine-containing compounds for acute toxicity." Carcinogenic Potential 17. A b d ellatif, A. G. et al., Arch. Int. Physiol. B i o c h i m . , 9 8 ( 5 ) :113 (1990) (B I O S I S / 9 1 / 1 4 2 7 8 ) . "The promoting activity of perfluorooctanoic acid. A novel promoter of rat liver carcinogenesis." 1 8 - A b d e l l a t i f , A. G. et al., C a r c i n o g e n e s i s , 1 1 ( 1 1 ) : 1 8 9 9 - 1 9 0 2 (1990). "Peroxisome proliferation and modulation of rat liver carcinogenesis by 2,4-dichlorophenoxyacetic acid, 2,4,5-trichlorophenoxyacetic acid, perfluorooctanoic acid, and nafenopin." 19. A b d e l l a t i f , A. G. et a l ., T o x i c o l . A p p l . P h a r m a c o l . , 111(3):530-537 (1991). "The modulation of rat liver carcinogenesis by p e r f l u o r o o c t a n o i c acid, a p e r o x i s o m e p r o l i f e r a t o r ." -26- EID087818 RELATED REFERENCES (CONT'D) Carcinogenic Potential (Cont'd) 20. N i l s s o n , R. et al., C h e m . - B i o l . I n t e r a c t . , 7 8 ( 2 ) : 2 3 5 - 2 5 0 (1991) . "On the mechanism of the h e p a t o c a rcinogenicity of peroxisome proliferators." 21. Revici, E., U.S. Patent No. 4 , 624,851 (1986) (CA 106:169039n). "Treatment of symptoms of neoplastic diseases." 22. Takagi, A. et al., C a n c e r L e t t . , 5 7 ( 1 ) : 5 5 - 6 0 (1991). "Short-term exposure to the peroxisome proliferators, perfluorooctanoic acid and perfluorodecanoic acid, causes significant increase of 8-hydroxydeoxyguanosine in liver DNA of rats." 23. Takagi, A. et al., J. E n v i r o n . P a t h o l . T o x i c o l . O ncol. , 11(3):145-149 (1992). "Hepatomegaly is an early b i o m a r k e r for hepatocarcinogenesis induced by peroxisome proliferators." Mutagenic Potential 24. K u b i n s k i , H. et a l ., M u t a t . R e s , 8 9 : 9 5 - 1 3 6 (1981). "DNA-cell binding (DCB) assay for suspected carcinogens and m u t a g e n s ." Developmental Toxicity 25. G o m b a r , V. K. et al., Quan t . S t r u c t . - A c t . R e l a t . , 1 0 ( 4 ) :306-332 (1991) (CA 1 1 7 : 2 4 9 8 8 ) . "A QSAR m o d e l of t e r a t o g e n e s i s ." Metabolism 26. Goe c k e , C. M. et a l ., Chem. Res. T o x i c o l . , 5 ( 4 ) : 5 1 2 - 5 1 9 (1992) . "A comparative toxicological investigation of perfluorocarboxylic acids in rats by fluorine-19 NMR spectroscopy." -27- EID087819 RELATED REFERENCES (CONT'D) Metabolism (Cont'd) 27. H a n h i j a r v i , H. et al., Proc. Soc. Exp. B i ol. Med., 171:50-55 (1982). "The sex-linked difference in perfluorooctanoate excretion in the r a t ." 28. H a n h i j a r v i , H. et al., P h a r m a c o l . T o x i c o l . , 6 1 ( 1 ) 6 6 - 6 8 (1987). "Elimination and toxicity of perfluorooctanoic acid during subfchronic administration in the Wistar rat." 29. H a n h i j a r v i , H. et al., N e w D e v e l o p m e n t s in B i o s c i e n c e s : Their Implications for Laboratory Animal Science; The Third Symposium of the Federation of European Laboratory Animal Science Associations, Amsterdam, pp. 409-412 (1988) (B I O S I S / 8 8 / 2 3 9 3 6 ). "A proposed species difference in the renal excretion of perfluorooctanoic acid in the beagle dog and rat." 30. P e r m a d i , H. et al., B i o c h e m . P h a r m a c o l . , 4 4 ( 6 ) : 1 1 8 3 - 1 1 9 1 (1992) . "Effects of perfluoro fatty acids on xenobioticmetabolizing enzymes, enzymes which detoxify reactive forms of oxygen and lipid peroxidation in mouse liver." 31. R o z n e r , M. A. a n d D. R. Taves, Fed. P r o c . , 40(3, Part 1 ) :675 (1981) . "A mechanism for lipid peroxidation by perfluorooctanoic acid." 32. S i n g e r , L. and R. Oph a u g , Crit. Rev. Cli n . Lab. Sci., 18(2)111-140 (1982). "Ionic and nonionic fluoride in plasma (or serum)." 33. V a n d e n Heuvel, J. P. et al., Lip i d s , 2 4 ( 6 ) : 5 2 6 - 5 3 1 (1989) (T O X B I B / 8 9 / 3 6 4 0 5 2 ). "Isolation and purification of perfluorodecanoic and perfluorooctanoic acids from rat tissues." 34. V a n d e n Heuvel, J. P. et al., J. B i o c h e m . T o x i c o l . , 6 ( 2 ) 8 3 - 9 2 (1991) (T O X B I B / 9 2 / 0 4 5 8 5 8 ). "Tissue distribution, metabolism, and elimination of perfluorooctanoic acid in male and female rats." -28- EID087820 00040 RELATED REFERENCES (C O N T 'D ) Metabolism (Cont'd) 35. V a n d e n Heuvel, J. P. et al., J. Biochem. T o x i c o l . , 7 ( 1 ) 3 1 - 3 6 (1992) (T O X B I B / 9 2 / 2 6 9 2 7 0 ). "Renal excretion of perfluorooctanoic acid in male rats: Inhibitory effect of testosterone." 36. V e n k a t e s w a r l u , P. et al., J. A s s o c . Off, A n a l . Chem. Int. 7 5 ( 4 ) : 6 7 2 - 6 7 7 (1992) (B I O S I S / 9 3 / 0 4 0 9 1 ). "Direct determination of individual organic fluorine compounds by aluminum monofluoride molecular absorption spectrometry." 37. Ylinen, M. et al., Arch. Environ. Contam. T o x i c o l . , 14(6) .-713-718 (1985). "Quantitative gas chromatographic determination of perfluorooctanoic acid as the benzyl ester in plasma and u r i n e ." 38. Ylinen, M. et al., Pharmacol. T o x i c o l , , 6 5 ( 4 ) :274-277 (1989) . "Stimulation by oestradiol of the urinary excretion of perfluorooctanoic acid in the male rat." 39. Ylinen, M. et al., Bull. Environ. Contam. T o x i c o l . , 44(1): 46-53 (1990). "Disposition of perfluorooctanoic acid in the rat after single and subchronic administration." Biochemical Studies 40. E l l e n b o g e n , E. a n d P. H. M a u r e r , Cong r . Int e r n . B i o c h e m . , Re s u m e s Commons., 3rd Congr., Brussels, p. 2 (1955) (CA 50 :1 6 8 9 5 e ). "Heat dnaturation of serum albumin in presence of perfluorooctanoic acid." 41. Hand l e r , J. A. et al., T oxicol. L e t t . , 6 0 ( l ) : 6 1 - 6 8 (1992) "Induction of peroxisomes by treatment with perfluorooctanoate does not increase rates of hydrogen peroxide production in intact liver." -2 9 - EID087821 RELATED REFERENCES (CONT'D) Biochemical Studies (Cont'd) 42. H a s e g a w a , R. et al., F ree R a d i c a l Biol. M e d . , 9 ( S u p p l . 1): 50 (1990) (B I O S I S / 9 1 / 0 7 8 2 0 ) . "Oxidative DNA damage in rat liver and kidney induced by p e r o x i s o m e p r o l i f e r a t o r s or f e r r i c n i t r i l o t r i a c e t a t e ." 43. I n t r a s u k s r i , U. a n d D. Fel l e r , Fed. Am. Soc. Exp. B i o l . , 5(6):A1571 (1991). "Characteristics of peroxisome proliferation by p e f l u o r i n a t e d o c t a n o i c a c i d in c u l t u r e d rat h e p a t o c y t e s ." 44. K a w a s h i m a , Y. et al., B i o c h e m . P h a r m a c o l . , 4 2 ( 1 0 ) :192 1-1926 (1991) . "Induction by perfluorooctanoic acid of microsomal 1-acylglycerophosphocholine acyltransferase in rat kidney: Sex-related difference." *_ 45. K a w a s h i m a , Y. a n d H. K o z u k a , T o x i c o l o g y , 7 1 ( 1 - 2 ) : 1 5 1 - 1 6 0 (1992) . "Cytosolic long-chain acyl-CoA hydrolase, a suitable parameter to measure hepatic response to peroxisome p r o l i f e r a t o r s ." 46. K e l l e r , B. J. et al., B i o c h i m . B i o p h y s . A c t a , 1 1 0 2 ( 2 ) :237-244 (1992) (B I O S I S / 9 3 / 0 0 3 3 3 ). "Several nongenotoxic carcinogens uncouple mitochondrial oxidative phosphorylation." 47. K e l l e r , B. J. et al., T o x i c o l o g y , 7 1 ( 1 / 2 ) : 4 9 - 6 1 (1992). "Inhibition of mitochondrial respiration and oxygendependent hepatotoxicity by six structurally dissimilar peroxisomal proliferating agents." 48. E l e v e n s , H. B. a n d E. E l l e n b o g e n , D i s c u s s i o n s F a r a d a y S o c . , 18:277-288 (1954) (CA 49:14430h). "Protein-fluoro acid interaction-bovine serum albumin-perfluorooctanoic acid." 49. L e v i t t , D. and A. Liss, J. T o x i c o l . E n v i r o n . Hea l t h , 2 0 ( 3 ) :303-316 (1987). "Perfluorinated fatty acids alter merocyanine 540 dye binding to plasma membranes." -30- EID087822 GOO RELATED REFERENCES (CONT'D) Biochemical Studies (Cont'd) 50. Levitt, D. and A. Liss, Toxicol. A p p l . P h a r m a c o l . . 86(1):1-11 (1986). "Toxicity of perfluorinated fatty acids for human and murine B cell lines." 51. S o h l e n i u s , A.-K. et a l ., B i o c h e m . J . , 2 8 5 ( 3 ) : 7 7 9 - 7 8 3 (1992) (B I O S I S / 9 2 / 3 0 0 8 7 ). "The effects of perfluorooctanoic acid on hepatic peroxisome proliferation and related parameters, show no sex-related difference in mice." 52. So h l e n i u s , A.-K. et al., J. Biochem. T o x i c o l . , 7 ( 4 ) : 2 0 5 - 2 1 2 (1992) (B I O S I S / 9 3 / 1 3 2 2 0 ). "Perfluorooctanoic acid has persistent effects on peroxisome proliferation and related parameters to mouse l i v e r ." 53. Sohlenius, A.-K. et al., Pharmacol. T o x i c o l . , 7 2 ( 2 ) : 9 0 - 9 3 (1993) . "Perfluorooctane sulfonic acid is a p o t e n t indu c e r of peroxisomal fatty acid beta-oxidation and other activities known to be affected by peroxisome proliferators in mouse l i v e r ." 54. Thottassery, J., Fed. Am. Soc. Exp. B i o l . , 4 { 3 ) : A 5 7 1 (1990). "Do hormones play a role in peroxisomal enzyme induction A study on the effects of perfluorooctanoic acid in adrenalectomized rats." 55. T h o t t a s s e r y , J. et al., H e p a t o l o g y , 1 5 ( 2 ) : 3 1 6 - 3 2 2 (1992) (T O X B I B / 9 2 / 1 3 7 9 1 1 ) . "Regulation of perfluorooctanoic acid-- induced peroxisomal enzyme activities and hepatocellular growth by adrenal h o r m o n e s ." 56. U y - Y u , N. et a l ., J. P h a r m a c o b i o . - D y n . , 1 3 ( 9 ) : 5 8 1 - 5 9 0 (1990) (B I O S I S / 9 1 / 0 3 7 3 5 ) . "Effects of chronic administration of perfluorooctanoic acid on fatty acid metabolism in.rat liver: Relationship among stearoyl-coenzyme A desaturase, 1-acylglycerophosphocholine acyltransferase, and acyl composition of microsomal phosphatidylcholine." -31- EID087823 000& -.13 RELATED REFERENCES (CONT'D) Biochemical Studies (Cont'd) 57. Uy-Yu, N. et al., Biochem. Pharmacol., 3 9 ( 9 ) : 1 4 9 2 - 1 4 9 5 (1990) (NIOSH/00197121). "Comparative studies on sex-linked difference in biochemical responses of livers to perfluorooctanoic acid between rats and mice." 58. V a n d e n Heuvel, J. P. et al., Chem. Biol, i n t e r a c t . , 82(3):317-328 (1992). "Covalent binding of perfluorinated fatty acids to proteins in the plasma, liver, and testes of rats." 59. W h i t e h o u s e , M. W. a n d I. F. S k i d m o r e , B i o c h e m . P h a r m a c o l . , 16:911-915 (1967). "Uncoupling of oxidative phosphorylation by some fluoro- compounds, nota b l y p e r f l u o r o p i n a c o l ." ^ 60. Wigler, P. W. and Y. B. Shah, Toxicol. A p p l . P h a r m a c o l . , 85(3) :456-463 (1986). "Perfluorodecanoic acid inactivation of a channel for 2-aminopurine in the L5178Y cell membrane and recovery of the channel." Analytical Methods 61. Belisle, J. W., 3M Co. Da t a (1978). "Analysis of serum for FC-143." 62. Belisle, J. and D. F. Hagen, Anal. B i o c h e m . , 1 0 1 ( 2 ) : 3 6 9 - 3 7 6 (L980) (H E E P / 8 0 / 0 8 6 2 1 ). "A method for the determination of perfluorooctanoic acid in blood and other biological samples." S. W. S n y d e r N o v e m b e r 24, 1975 U pdated by: Kimberly A Iverson:md April 16, 1981 R i c h a r d C. G r a h a m s m d : J uly 23, 1984 - INF19.4 J u n e 1, 1994 - D A T A 4 1 . 1 4 -32- EID087824 000*15 50 m im * W ASHING Tex'. WORKS P.O. Box 1217 Pa r k e r s b u r g , WV 26102-1217 DU FONT ROLYMERS Office of Env. Enforcement Div. of Env. Protection 2311 Ohio Avenue Parkersburg, WV 25101 John G. Britvec Office of Water Resources Industrial Waste Section 1304 Goose Run Road Fairmont, WV 26554 July 8, 1994 CERTIFIED MAIL RETURN RECEIPT REQUESTED Mr. Mark A. Scott, Chief Office of Water Resources Division of Environmental Protection 1201 Greenbrier Street Charleston, West Virginia 25311 Attention: Industrial Waste Section REF: WV/NPDES Permit Application WV0076244 Dear Mr. Scott: Enclosed is the original and four copies of our WV Solid Waste/NPDES permit application for the Dry Run Landfill. This application is being submitted for renewal of the referenced permit issued on January 12, 1990. The attached permit application does not include an approval letter from the Historical Preservation Office of the West Virginia Division of Culture and History. The results of an archaeological survey of the area were submitted to the Historical Preservation Office on June 10, 1994. The report indicates that there are no areas of a historical significance in the vicinity of the landfill. We will send you the approval letter from the Historical Preservation Office when it is received. Also, we have been working to obtain the storm event NPDES samples required for the permit application, but weather conditions have delayed completion of the sampling at the landfill. The results will be forwarded to you when they are available. A check for the $1,000.00 renewal application fee is attached. A signed affidavit for the Statement for Billing for the costs of publishing legal advertisement is also enclosed. If you have any questions or need additional information, please call me on 863-4271. A J Very truly yours, Attachments /vlw (6858-1) W. M. Stewart Sr. Environmental Control Consultant Washington Works BETTER THINQB FOR BETTER LIVING 0 0 0 .vs EID053308 51 r 0 0 0 * 1rj INTEROFFICE MEMORANDUM Oata: From: Dept : Tel No: 13-Sep-1994 09:51am EDT RITCHERL RITCHE RL91SCDCVM1GCDCIL1M TO: PLAYTIS9A1 Subject: Oucatnan VMSmail To information: HWPS::PLAYTIS Date: 09/13/94 09:30:49 To: ZIPFEL --WHPS PLAYTIS --WHPS MULHERFP--ULCL01 VALENTR --HSKVAX From: Bob Ritchey, FLPR SHEA, CRP711/130, 999-2870 Subject: Oucatman After our conference call yesterday, I called Judy Walrath back because I was curious for more information on the off-handed comment she had made that she had attended a conference and heard that 'PFOA was on a fast-track as a potential carcinogen*. Judy indicates that one of the co-authors of the JOM article associating PFOA production at the 3M plant to prostate cancer (the death certificate study) presented that paper at the National Cancer Institue's late April '94 conference on Occupational and Urogenital Cancers. Judy attended. The pape was presented without any disclaimers or qualifiers or limitations and Judy had to bite her tongue to avoid challenging it on the flaws we saw in it for fear of being branded the industry response. Aaron 81air, epidemiologis with NCI and known to be very interested in occupational cancers, then acknowledged the paper in front of the audience as an excellent paper. A person in attendance was Alan Oucatman, who is with WVU. He called Or. Karrh to and indicated to him his feeling that PFOA was on a fast-track to being identified as a potential carcinogen. Or. Karrh alerted Judy (see attached old email), who called Or. Zobel at 3M who indicated he would call Oucatman. We don't know what came of that call, but have not heard anything more from Oucatman or anyone else. I've asked Judy to contact Or. Zobel or Jeff Mendel with 3M and see what came of the followup with Oucatman. I pass this along to keep us all aware of the perceptions and linkages that are "out there* around C8. Regards, Bob Ritchey *** Forwarding note from HALAATJ --ISCOCVM1 09/13/94 08:54 ** To: RITCHERL--I8COCVM1 From: Judy Walrath Epidemiology/Haskell/CR&D, 38-68594 Subject: Oucatman Bob, For your information. I'll follow-up with 3M and let you know tdiat I learn. Judy *** Forwarding note from KARRHBH --ISCOCVM1 05/27/94 14:44 *** To: WALflATJ --ISCOCVM1 From: Bruce W. Karrh * 4-9513 N-10460-6 O O O k \s EID073255 Subject: Oucatman Alan Oucatman of University of WVa called me today. He was at the NCI conference where you gave the AN paper. His comment was that NCI has perfluorooctanoatic acid on a 'fast track" and, if we are planning any work on this compound, he would like to be involved. He was aware that we made or used it at a "West Virginia" plant, something Ididn't confirm nor deny but told him I would get in touch with the people who may be involved with that chemical and let them know of his interest. I tried to call Gerry Kennedy but he was not in. kill you please pass on to him Alan's interests?? Thanks cc: REINHACF--HSKVAX cc: KENNEDY --HSKVAX PEETDL --ISCDCVM1 David L. Peet SERINGCS--1SCDCVM5 HUQSONBL--kWPS flITCHERL--ISCOCVM1 Robert L. Ritch HOLMESOA--ISCOCVM1 Oave Holmes PORTERJB--CSOC 0 0 0 a .?.9 EID073256 52 0050 INTEROFFICE MEMORANDUM Date: From: Dept: Tel No: 09-NOV-1994 11:28am M i c h a e l E. G e l l GELLME AT A1 AT ENGG ENGR-SERO (704) 3 6 2 - 5 9 4 3 F a x 8-36 2 - 5 9 3 4 TO: See Below Subject: C-8 MSDS (suspect - small "c" carcinogen ?) Marshall, The attached MSDS for C-8 indicates that the compound causes tumors in mammals and is a suspect carcinogen. This compound is not listed as a known and federally controlled carcinogen, but Dupont Haskell lab considers it a suspect (small c c a r c i n o g e n ) . I asked Haskell lab about the exposure limits they have established for C-8 and they indicated that they considered it a potential carcinogen when they set the AEL and CEG(community exposure gui d e l i n e ) . I am not in a position to comment on the carcinogenicity of the C-8, but Haskell Lab is and I suggest we discuss this compound with Haskell. The CEG of 1 ug/1 in drinking water may be lower than the concentrations seen in our customers WWTP effluent, but I don't know enough about how they process the fiber and how much of the finish they would wash off and discharge to the environment. I am , however, concerned that we could potentially discharge this same material from any plant that makes or processes the finish. Will this compound find its way into the wastewater? Looking at the notes on the K-7762 finish I get the impression that we will not detect C-8 in the wastewater and that our customers will not see it in their air or water systems, but will it be there at some concentration? I am concerned that the C-8 will be there at some concentration and I am not sure what our obligation is to inform the site and the customer of that presence. I suggest that we discuss the potential exposure of the our WWT system and that of our customers to this compound in light of its potential carcinogenicity. I am concerned that we m a y have a product stewardship issue if we have a finish that contains a suspect carcinogen that is m a d e and processed on a DuPont site and then goes out to a potentially uninfo r m e d customer. If that customer does not handle the product with adequate precautions there could be a backlash to DuPont as the supplier. Please let m e know if I can be of any assistance w i t h the C-8 issue. 0 0 0 ,-,,' EID089977 V 53 N? '0025 QA LAB WORK REQUEST rnrvniv, M fcU U tS T REQUESTED BY:. \vr\l-Vniy^erK DATE: 4 UNIT, PROJECT OR DEPT THIS WORK SUPPORTS:. ______________________ REPORT RESULTS TO: (Name and phone number)__ DATE AND TIME RESULTS REQUIRED: i( j L t d V l f SCA ClA SAMPLE DESCRIPTION: (Sample Point, Container, Contents, Date, Time) ____ M B ------L*r \ Lt--1---- W U l i y V O ---------------- Li_L_y-----U U l V___________________________ SAFETY: (Circle One) Normal Hydrocarbon; Acidic; Caustic; Other ANALYSIS REQUIRED: ______C n O ^TS ^> d 1 5 u r& rA n r\-b ^ ) <=ly WHY IS WORK REQUIRED: fU C V Q h b o o r o c o m p io \n (~ \^ ANALYTICAL RESULTS: (Attach additional pages if necessary) C od m / o ,,J i ck,rf TSS t.y ! 1:7 DATE COMP ANALYST: FORM FOLIO NUMBER: C/f-gT' m'mrn 9002 1065 EPC5/94 SAMPLE DISPOSAL RETURN SAMPLE TO REQUESTER RETURN SAMPLE TO RETAIN DISPOSE OF SAMPLE OOO.v, CA 002 Water Sample from Dry Run, WV S a m p l e r e c e i v e d b y J i m H o l b e r t from E J T e n n a n t o n A p r i l 18, 1995. Sample was not preserved or cooled. p H of s a m p l e w a s 7.8. O h i o R i v e r p H o n A p r i l 12, 1995 w a s 8.0 thus consider pH of sample acceptable. Chemical Oxygen Demand was 1010 mg/L. Shell's treated water seldom goes above 25 mg/L so 1010 is extremely high. Surfactant level was 12.5ppm. This should be close to zero. Shows there are detergents present. Total suspended solids was 46.8 mg/L. The Ohio river when not flooded has solids of less than 10 mg/L. Given the smell and the detergents present. M y guess is the sample is c o n taminated with sewage and is harmful. CA 003 INTEROFFICE MEMORANDUM 06:08am PLOEGER a f e a i r s /l i t i g a t i o n s Date: From: Dept: Tel No: 26-Apr-1995 GERALD A PLOEGER EXT. 863-4248 TO: WALTER M. STEWART TO: GEORGE WOYTOWICH TO: LYNWOOD K. IRELAND TO: RICHARD A' KIRSCHNER, JR { STEWART ) ( WOYTOWIG ) ( IRELAND ) ( KIRSCHRA ) CC: DAWN D JACKSON ( JACKSOOD ) Subject: ATTACHED REGARDING CITIZEN COMMENTS INTEROFFICE MEMORANDUM 03:37pm Date: From: Dept : Tel No: 25-Apr-1995 D CHRIS KOELSCH KOELSCDC ZYTEL AUTOCLAVE 304-863-2291 TO: GERALD A PLOEGER TO: H. DAVID RAMSEY, JR. ( PLOEGER ) ( RAMSEY ) Subject: RE: DRY RUN LANDFILL Jerry, Rod Newell, a Eil mechanic in the Zytel* A/C area came to me yesterday morning asking me if I could help him in finding out some information about any trouble we might be having at the dry run landfill. Rod owns about 200 acres up by the landfill and raises about 80 to 90 head of cattle. There were basically three things that prompted him to seek further information; some of his cattle will start to graze in the fields next week, his neighbor's coanents to him, and the fact that he has noticed large amounts of foam coming from the run off as far down as Lee creek, as much as 18 inches in stagnate pools. During the conversation he did mention that within the last year he's had two calves that were still born and his neighbor had one. These were the first two he had ever had. He was not trying to link that to the landfill but did want to register it's presents. 000 V. EID007456 His neighbor, Earl Tennant, Rod is quick to point out, is a bit on the reactionary side. Earl has made comments to Rod that he has seen and collected dead fish and frogs out of the run off and has them frozen, has complained to the DNR and the EPA, and has had a sample tested himself and the results showed "bad stuff in the water". Earl owns about 700 acres out and around the landfill and also raises cattle. After Rod talked to me I contacted Ron Meloon and explained the situation. Ron was going to look into it and gat t back to me. He have missed each other several times in to last day and half. This morning I called George and relayed the same information to him. He assured me that surface water testing on about 29 different parameters are reported to the state each month and results from the 7 monitoring wells are reported quarterly. George stated to me there should not be a concern as far as the health and safety of his cattle. After my discussion with George I talked to Rod and relayed George's comments to him and offered to gather any other information for him if he still had concerns. Rod was satisfied and thankful for the information and now has a better understanding of the extent of monitoring we perform. He then mentioned that he was turkey hunting this morning and foam all the way down to the creek was very heavy in the run off. I then passed that information onto George and asked Rod to let me know if he did not see an improvement in a couple of days. That's about all I know. Let me know if there is anything else I should or can do. One other comment, Rod has approached this in a very calm and professional manner and is working with us. It gives us a great opportunity to improve our PR status with the abutting land owners to the landfill. Thanks, Chris 18 08:43am WOYTOWICH INTEROFFICE MEMORANDUM Date 04-May-1995 From GEORGE EID007457 V 55 000*5 3 Revised 3/93 STATE OF W EST VIRGINIA DIVISION OF ENVIRONMENTAL PROTECTION ENVIRONMENTAL ENFORCEMENT LANDFILL INSPECTION REPORT Applic/Permit/Order No. Expiration Date t - \ \ Municipal Industrial ^ ^ 0 o'? b2.u<j Name of Facility O u Pin W eath er. Tiv -v Current Monthly Tonnage Permit A creage_________ -0 Date of Last Inspection -3 3 Status of Operation: Active ( Inactive ( ), Not Started ( ), Closed ( ) _____Estimated disturbed acreage at time of inspection __ _______________________ Rating: S - Satisfactory, U - Unsatisfactory, N/A - Not Applicable. N/O - Not Observed, N/D - Not Determined M Marginal LEACHATE MANAGEMENT Liner System Construction AjA Monitoring Wells Ai c& Sewer Hook-up Liner System Maintenance *oft Monitoring Reports f* o Treatment Plan Leachate Collection System N A Leachate Treatment System Ni N Other Leachate Detection System KJk Sprayback Recirculation O th er Leachate Storage System U Pumpout and Transport JA Other Is there a leachate discharge into receiving stream: Yes ( X ) No ( ) Receiving Stream Q Outlet Status: Outlet Number P Ci \ Rating Comments U -S.J 1-2 An(Vvx v><a^ -CLl \^ Daily Cover Intermediate Cover Rnai Cover Erosion, Sediment Control, Diversion Ditches Revegetation Access Roads Access Control Operations Plan Placement and Compaction LSL JJL _LLSl IU U. Comments: <^VV'gLV-- Vfs -cL scvP^i11 ! . A Koo-vj' KVva . ev 3 * /o ^|srr^MANAGEMENT ^DXiPERATION QA/QC L_ H.W . Exclusion Plan/lnspections Certifications Contaminated Soils Disposal Control of Wind Blown Material Asbestos Disposal Odor Control Tire Disposal Dust Control Firs Control Vector Control Gas Management Records Equipment JA Drum Disposal Sludge Disposal Shredder Ruff Disposal Infectious Waste Disposal O th er O th er mOA C -- -I __ CSC vx___ ^ESl ^__k=L <W ^ * *ve* ^ a vT-r. =2/* Tb-- *<v W ARNING! You are hereby warned that the foito3wwiiir^ remerai measures must be taken on or before the Of. - 7 T nVg~va -s. _dau Number of N .O .V .'s issued on this date: *N>N-a ______ r S ^ S ^ N o n e 1 ) j Company Representative and Title: J. M . 'r'n h '-~*J~ *_-*______________ +-*-< __ ^*-- y 'rz^ A Signed: ^ \ - ^ st s> \3" (Inspector) . Oats: ^ Phone: ^ W hite Copy - District Yellow Copy Inspector Pink Copy - Charleston Goldenrod - Facility HIDOl'1 000X59 56 OOQS *7^7 4 'GO- jju-- INTEROFFICE MEMORANDUM Date: From: Dept: Tel Bo: 02-May-1995 03:00pa HALTER M. STEWART STEWART PPD-SHEA&EA . (304) 863-4271 TO: Distribution List Subject: MEETING - LANDFILL ISSUES THERE WILL BE A MEETING ON THURSDAY, 5/4 FROM 10:00 A.M. TO 12:00 NOON IN MY OFFICE TO DISCUSS ISSUES CONCERNING THE DRY RUN AND LOCAL LANDFILLS. THE TOPICS WILL INCUDE: DRY RUM 1) STATUS OF BLACKWATER IN THE POND AND STREAM 2} FOAM IN RUN BOTH ON AND OFF OUR PROPERTY 3) C-8 IN SLUDGE LOCAL 1) NEW PERMIT REQUIREMENTS 2) COMPLIANCE ORDER 3) STRATEGY - ACCEPT OR APPEAL LET ME KNOW IF OTHER ITEMS SHOULD BE ADDED TO THE AGENDA. THANKS. 0Q 026 EID080803 57 0 0 0 & &-La*tr*\^/ s^'*J_. D av/ 5- w / 'AftA S dati Kicirvto ------ 1 l i U r < T environmental O ffici GASTON CAPERTON GOVERNOR DIVISION OF ENVIRONMENTAL PROTECTION 1304 Goose Run Road Fairmont, W V 26554-1390 LAIDLEY ELI McCOY.Ph.D. DIRECTOR September 25, 1995 Mr. W. M. Stewart Senior Environmental Control Consultant Washington Works E.I. DuPont de Nemours and Company P.O. Box 1217 Parkersburg, WV 26102-1217 Re: Solid Waste/NPDES Water Pollution Control Permit Application No. WV0076244, Dry Run Landfill This agency's May 16, 1994 field investigation revealed numerous deficiencies regarding th operation of the Dry Run landfill. Although your company was advised of these deficiencies at that time, March 23, 1995 and May 3, 1995 field investigations conducted by an inspector from the Environmental Enforcement group revealed measures had not been taken to correct the deficiencies. These deficiencies, which are discussed in detail below, are of concern not only because of non-compliance with the operational requirements of Title 47, Series 38, Solid Waste Management Regulations (SWMR), but also because the structural integrity of the landfill could be effected. Said deficiencies included but were not`necessarily limited to the following: sparse vegetative cover, poorly defined benches which were not providing adequate routing of stormwater and leachate thus causing numerous erosional gulleys on the landfill surface, lack of interceptor channels to properly route stormwater and leachate to the surface impoundment, lack of a leachate collection system, lack of surface water diversion channels, and excessive solid waste lift thicknesses. Said deficiencies are primarily due to the design of the landfill which must be upgraded. For this purpose, tnis agency requests that your company contract the services of a consulting firm having expertise in landfill design. Your letter dated June 9, 1995 indicates that in response to the above referenced Environmental Enforcement inspections, diversion channels have been dug to prevent run-on to the active landfill area and furthermore, drain pipes have been installed in the fill area to aid in draining water from the area. Although these efforts are commendable, be advised that diversion channels must meet the requirements of Section 4.5.2.b. of the SWMR as further referenced in Section C.2.b.l. below. Also be advised that the installation of drain pipes does not preclude the placement of a leachate collection system (see Section C.2.e. below). Office of Water Resources Telephone: (304) 367-2724 Fax: (304) 367-2727 000*1'3 Ii E I D 0 12672 Mr. Stewart Page two Subsequent to the May 16, 1994 field review, a thorough review of Application No. WV0076244 was conducted. Based upon these reviews, and the March 23, 1995, and May 3, 1995 field investigations, said application has been found to be incomplete. Therefore, the following information is needed to continue the processing of Application No. WV0076244. Note that the sections referenced below correspond to these of the Class F application. A. 9 - Provide detailed information regarding the waste minimization program which shall include putrescible materials. Also provide details of the waste minimization programs which shall include a description of the technologies and methodologies of waste reduction, reuse, recycling, and energy recovery which are applicable to the wastes being disposed. B. l.b. - The application reaveals that the sludge filter cake will consist of approximately 22% sludge, 28% filter aid and 50% water. As the filter press has subsequently been placed into operation, provide actual sludge, filter aid, and water percentages. B. 2. - As indicated in revised Attachment 7 submitted with your letter dated September 14, 1994, % bio-solids of the sludge have increased dramatically pursuant to the recently started operation of a filter press to dewater sludge from the wastewater treatment plant from 4.8% (referenced in A.C. Hustons' 3/1/88 -2, letter to the writer) to 20%-30% as referenced in Attachment 7. The increase in biosludge concentration as well as increases in the amount of sludge disposed since the filter press became operational have apparently caused the presence of anaerobic bacteria and iron sulfide referenced in your April 13, 1995 and May 12, 1995 letters. Because of the dramatic increase in % bio-solids, your company should have requested that Permit No. WV0076244 be modified'to incorporate said sludge as Condition G.l. of Permit No. WV0076244 allows only for the disposal of sludge having a biomass of the concentration referenced in the above referenced 3/1/88 letter. Concurrently with the modification request, your company should have submitted a leachability analysis of the filter aid/sludge mixture. Therefore, this aqency requests that such be conducted by utilizing the Toxicity Characteristic Leaching Procedure (TCLP) for the parameters indicated in Mr. A.C. Huston's letter dated April 14, 1988. % weight dry solids of the filter aid/sludge mixture shall also be determined. C. l.c. - As this agency has no record of Well MW-12B, please provide boring logs and well construction information for said c well. C.2.a.l. - it is unclear which contours indicate 1991 conditions and those which reference 1994 conditions. Therefore, please differentiate. Also, please explain the volume calculations and how they were derived. f EIDO12673 Mr. Stewart Page three Regarding Section A - A of Drawing M677 (Attachment 11), the interval between the solid black line and the dashed line labeled "ravine bottom", appears to indicate an area which was filled prior to waste disposal, if this assumption is correct, please indicate materials utilized for filling as well as placement procedures. If the assumption is incorrect, please label the solid black line and indicate the significance of the interval between the solid black line and the dashed line. C.2.a.4. - Section 6.1.5. of the SWMR requires, unless otherwise approved by this agency in writing, that a cap consisting of a uniform and compacted one foot layer of clay that is no more permeable than 1 x 10-7 cm/sec shall be placed and graded over the entire surface of each final lift. As the landfill was not underlain by a leachate collection system prior to initial disposal operations, it is this agency's position that a one foot clay cap should be installed to minimize percolation of precipitation through the waste material. In accordance with Section 3.12. of the SWMR, provide a borrow area study identifying materials to be utilized for the above referenced one foot clay cap and a two foot topsoil cover (a lesser topsoil cover thickness will be considered providing sufficient rationale in support of such is provided) . Note that in accordance with Section 3.8.2. of the SWMR, test pits or test borings shall be utilized for this purpose. Refer to 3.8.2. to determine the required number of test pits or test borings and also to determine the information to be derived from test pits and borings. Said information shall be included in the borrow area study. Note that sufficient quantities of borrow materials must be available to provide the temporary cover referenced in this section but also the final cover requirements referenced in Section C.2.d.8. C.2.a.5, C.2.a.6, E.3.f., E.3.g. - The application indicated that "the surface will be crowned to provide a 1% to 2% slope to eliminate ponding on the surface and to direct surface water to diversion ditches on either side of the fill" to "mininize surface water flow through the fill and over the face of the lift." However, the May 16, 1994, the March 23, 1995, and the May 3, 1995 field investigations revealed that most of the benches of the landfill surface_ar*-Jiot well defined or are not sloped sufficiently to direetc^unoft) toward the sides of the landfill thus allowing runoff to TIow directly across the face of the landfill which is resulting in numerous erosional gulleys some of which have exposed waste materials. Those benches which are defined do not contain a sufficient slope to ro u te , leachate* toward either side of the landfill as pools of<fieachat wets observed on the benches. Therefore, the benches OOStToe redesigned to provide routing of stormwater and leachate to interceptor channels which must also be developed to continue routing of runoff to the surface impoundment for treatment. It must be determined if slope drains should be utilized to 000:;,fc5 EIDO12674 Mr. Stewart Page four route runoff from the benches to interceptor channels. If it is determined that slope drains are needed, provide detailed drawings of such and calculations verifying that the proposed design will fulfill their intended purpose. If it is determined that slope drains are not needed, provide appropriate rationale and calculations accordingly. During the May 16, 1994 field review, Mr. George Woytowich of , your staff informed the writer that individual lifts of waste / ^ materials are not placed in accordance with surveyed elevations/ As such is essential to provide proper drainage of the landfill) - surface, provide information detailing the implementation of ' surveying activities. ' Describe measures to be undertaken to revamp existing benches to assure each existing bench is well defined and properly constructed to provide proper drainage. Provide a detailed plan view map of scale 1M * 100' (or a more expanded scale) clearly indicating each reconstructed bench. Each reconstructed bench shall be designated by letter. Indicate proposed elevations for the front and back of each reconstructed bench (note that benches shall be sloped from front to back to facilitate drainage), and also directions of flow for each reconstructed bench toward intercepter channels. Note that each reconstructed bench shall be routed to an interceptor channel. (see Section C.2.b.l. regarding interceptor channel sizing). The reconstructed benches shall be designated Phase I of the disposal area (see paragraph below regarding Phase I). Each successive series of benches overlying Phase I shall be designated Phase II, Phase III, etc., until the proposed elevation of the completed fill referenced on Drawing M677 is reached. For each Phase, provide the above requested information for Phase I. Note that Attachment 12 is insufficient as it does not provide the information previously referenced in this section. The overall stability expressed, as a factor of safety of 1) the existing disposal area and 2) the final configuration of the disposal area must be determined using an approved method. Indicate on a plan view map the landfill section utilized for this purpose which shall extend from the toe of the fill to the top of the fill. Provide in table form soil properties utilized for the analysis. Calculations utilized to genrate the factor of safety shall also be included. The May 16, 1994 field review revealed that the upper surface impoundment was filled with sediment and therefore serving no useful purpose. At that time your company was advised that the impoundment should be drained to allow the sediment to thoroughly dry prior to disposing of waste materials thereupon. However, a representative of your company informed the Environmental Enforcement inspector present during the March 23, 1995 field investigation that no special measures were taken to drain the ooostf $ EIDO12675 Mr. Stewart Page five impoundment (other than its natural drainage) prior to placement of waste materials thereupon which was being effected that date. As the May 16, 1994 field review revealed that the natural drainage of the pond was poor, the pond could not have been properly drained. Insufficient drainage of the impoundment sediments is a concern to this agency as the structural integrity of the landfill could be affected. Placement of waste materials within the area of the upper surface impoundment has expanded the ravine being utilized for disposal to its ultimate footprint. Said placement, in addition to the area previously utilized for disposal, for purposes of this letter, constitute Phase I of the landfill. The application references that a "slope of 1:2 will be maintained during filling." Note that Section 4.6.2.a.A. of the SWMR requires that slopes of working faces shall not exceed 3:1. Also note that Section 6.1.5.a.D. of the SWMR requires that the grade of the final surface shall not exceed 3:1. Benches must be spaced to assure that the slopes of working faces and the final surface do not exceed 3:1; this requirement must be taken into consideration when preparing the map referenced in the above paragraph. Provide the following bench details the locations of which shall be clearly indicated on the plan view map referenced in the above paragraph: cross section to scale of a typical bench which shall include its upslope working face; plan view to scale of typical bench drainage to interceptor channels which shall include erosion control materials (provide documention that erosion control protection will not be required if such is not proposed to be utilized); plan view to scale of a typical bench corner; and cross-section to scale of typical bench erosion protection (provide documentation that erosion control protection will not be required if such is not proposed to be utilized). C .2.b .1.> i~7cs>vthe May 16, 1994 field investigation revealed that surface(run-on)has eroded a channel which in places is approximately three feet deep through the waste material on the southern side of the fill area, diversion channels are needed to route surface run-on around the site. Note that although Application No. WV0076244 dated August 19, 1987 indicated that a diversion channel would be constructed, the May 16, 1994 field investigation revealed that it had not. Note that diversion channels should also extend below the surface impoundment (see C.2 .b.3.) The application incorrectly states that diversion channels are shown on Attachment 10 with details and profiles of the channels being shown on Attachment 11. Note that in accordance with Section 4.5.2.b.A. of the SWMR that your company must design, construct, operate and maintain a run-on control system capable of preventing flow onto any part of the disposal area during peak discharge from at least a 25-year, 24-hour rainfall event. Note that it is unclear whether the drainage swales indicated our Drawing M641 (Attachment 10) meet this requirement. Furthermore, Section 4.5.2.b.B. of the SWMR requires that diversion channels shall have the capacity to pass safely the peak discharge from the contributing watershed from a 25-year, 24-hour rainfall event. Therefore, your company must provide the information required by Section 4.5.2.b.C. of the 000^7 E1D012676 Mr. Stewart page six SWMR for the diversion channels referenced in your June 9 letter. Should your company determine that the diversion channels referenced in said letter do not meet the requirements of Section 4.5.2.b .C ., submit the information required by 4.5.2.b.C. for alternative diversion channels. Attachment 13 incorrectly references that a cross-section of the diversion ditch is shown on Attachment 11 as such is not indicated on Attachment 11 or any other Drawing contained within the application. Furthermore, a determination cannot be made whether Attachment 13 contains the required information to verify that the diverson channel has sufficient capacity to pass safely the 25-year, 24-hour rainfall event. Therefore, this agency requests that a procedure approved by the United States Soil Conservation Service be utilized to determine the location and sizing not only of channels to divert surface run-on, but also to determine the location and sizing of interceptor channels referenced in C.2.a.5. above. At a minimum, the following factors must be included in the analysis: surface drainage area contributing to surface run-on; maximum, minimum, and average slope of the area contributing to surface run-on as well as the area where diversion channels are to be located; run off curve numbers; rainfall amount from a 25-yr/24-hr. storm event with its corresponding run-off depth, and peak rates of discharge in cubic feet per second. Based upon the analysis, the location and shapes (triangular or trapezoidal) of interceptor and diversion channels shall be determined. Said channels shall be indicated on a plan view map of scale 1' * 100' (or a more expanded scale) to accurately reference their locations. Provide cross sections of typical triangular and trapezoidal channels. For each interceptor and diversion channel, which shall be numbered in plan view, provide in table form the following information: the acreage of the contributing watershed, the design velocity in cubic feet per second based upon a 25-yr, 24-hr storm event, the type of section (trapezoidal or triangular), depth of channel, type of lining (grass, fabricform or rock - indicate rock size and type), thickness of lining, maximum velocity (feet per second), minimum slope (ft/ft), maximum slope (ft/ft), bottom width, and width of side slopes. For channels utilizing fabricform lining, provide minimum thickness and filter point spacing for centerline slopes less than or equal to 5%, 5%-10%, and greater than 10%. All calculations utilized to determine the design of the interceptor and diversion channels shall be provided. It must also be determined if geotextile should be utilized in the interceptor and diversion channels. If it is determined that geotextile should be utilized, provide the type(s) to be utilized and rationale for choosing said type(s). If it determined that geotextile should not be utilized, provide sufficient rationale accordingly. C.2.b.2. - Provide type and quantity (pounds per acre) of fertilizer to be utilized. Also note that Section 4.5.6.b.B. of the SWMR requires that for soils having a pH of less than 5.5, QOOVc 5 EID012677 Mr. Stewart Page seven lime shall be added to maintain a soil pH of 6.0. Therefore, based upon soil analyses, determine whether lime will be utilized and furthermore, indicate (if it is determined that lime is necessary) the amount to be utilized in pounds per acre. C . 2 . b . 3 . - As the discharge from Outlet No. 001 typically exceeds its maximum daily Total Suspended Solids limitation, and furthermore, as elevated BOD, TOC, and COD concentrations have been observed (see Section C.2.h.), the surface impoundment is not fulfilling its intended purpose. Be advised that the surface impoundment must meet the design requirements of Sections 4.5.2. C.A.(c), 4.5.2.C.A.fg)(B), and 4.5.2.C.A.(g)(C) of the SWMR. To determine if said requirements are being met, a procedure approved by the United States Soil Conservation Service shall be utilized. Therefore, provide documentation (calculations, drawings, verbage) regarding such. As the Environmental Enforcement inspector's May 3, 1995 field investigation revealed that the discharges from the diversion channels referenced in your June 9 letter are routed to the surface impoundment, said discharges must be included when determining if the requirements of Sections 4.5.2.C.A.(c), 4.5.2. c.A.(g)(B), and 4.5.2.c.A.(g)(C) are being met. Note that diversion channels should instead be routed around the surface impoundment to provide improved sedimentation control. If it is determined that the requirements are not being met, provide detailed drawings clearly indicating changes which will be made to upgrade the surface impoundment to conform with said requirements. Concurrently, with the revised drawings, provide documentation (calculations, verbage) to indicate that the revised design of the surface impoundment meets the requirements of the SWMR. It is the agency's understanding that the riser structure was changed concurrent with pond reconstruction in August 1993. Therefore, provide riser details. C.2.b.5. - Attachment No. 13 indicates that the discharge structure is a 15" diameter steel pipe. If this is correct, please confirm such. If not, indicate its type and diameter. C.2.C.I. - it is the writer's opinion that a haul road is required not only to provide access to the working face but also to provide protection for areas previously utilized for disposal. Therefore indicate haul road(s) m plan view on a map having a scale of 1" 100' for a more expanded scale). Station numbers (one per 100 feet minimum) shall also be indicated for each haul road on said plan view map. Provide haul road profile(s) referenced by station numbers. Also provide a typical cross-section of the haul road(s). Interceptor and diversion channels should be included in cross-sections of the haul road(s), if applicable. Note that access roads must be designed in accordance with Section 4.5.3.b. of the SWMR. As required by Sections 4.5.3.b.D. ooos.fa EIDO12678 Mr. Stewart Page eight and 4.5.3.b.F. of the SWMR, provide calculations documenting that drainage ditches and^culvert--openings--are-capable of passing the peak discharge of a: 1-year, 24-hour rainfall event. For each culvert, which shall'Tae numbered in plan v r e ^ provide in table form the following informations-- the-design-velocity_Jn cubic feet per second based upon a 25-yr, 24-hour storm eventD* the diameter expressed in inches, type T reinfm.e'gg concrete pipe, bituminous coated corrugated metal pipe, HOPE), length, % slope invert elevation of point of entry, site coordinates of point of entry, invert elevation of point of discharge, and site coordinates of point of discharge. C.2.d.l., E.3.A. - The application correctly references, as was observed during the May 16, 1994, March 23, 1995, and May 3, 1995 field investigations, that solid waste is being placed in eight foot lifts. This procedure in not in compliance with Section 4.6.2.a.C. of the SWMR which requires that solid waste shall be placed in layers not exceeding two feet in depth. The above field investigations revealed that waste materials were being landfilled which are difficult to compact such as large cardboard boxes and metal products. Although the application indicates that a waste minimization program is in effect, greater waste miminization efforts are in order to substantially reduce (preferably eliminate) materials which are difficult to compact as said materials pose a threat to the structural integrity of the landfill. Provide the size of the bulldozer which is utilized as Section 4.6.2.a.C. requires that an 815 Caterpillar compactor or other equipment of equivalent weight be utilized. c.2.d.2. - The application incorrectly states that layers up to two feet thick are disposed as field investigations referenced in c.2.d.l. revealed eight foot lifts were being utilized. Solid waste lift thickness must not exceed two feet. Describe measures which shall be implemented to comply with this requirement as the materials referenced in C.2.d.l. are difficult to compact to this thickness. C.2.d.4. - A detailed narrative is needed as Attachment 12 is insufficient for this purpose. The narrative must refer to the development of the Phases of designated benches previously referenced in Section C.2.a.5. C.2 .d.6., E.3.j. - As the application references that the landfill is not generally utilized during inclement weather, indicate where waste is stockpiled during inclement weather conditions. C.2.d.7. - Regarding the sludge fill area indicated on Attachment 9 (Drawing M688), although such was not observed during the May 16, 1994 field review, it is not marked inactive on said drawing. In addition to providing a time frame during which the sludge fill area was utilized, provide authorization by which such was effected, the quantity of sludge disposed and tne type and quantity of materials mixed with the sludge prior to disposal. OOOf-'.v fj EID O 12679 Mr. Stewart Page nine C . 2 . d . 8 . - Provide sedimentation control measures to be under taken at the sites on Drawing M688 designated "future cover material sites". During the May 16, 1994 field review, Mr. fj Woytowich of your staff indicated that archaeological investigations would be conducted upon said sites. Therefore, \ ^ either submit report(s) summarizing the findings of said tc investigations or provide a date by which they will be submitted'.'^ As the application indicates that soil will only be used as cover- on a temporarily closed area prior to seeding, provide an example of a temporarily closed area. Borrow area studies shall be conducted upon each "future cover material site" - see Section c.2.a.4. regarding borrow area study requirements. Note that sufficient quantities of borrow materials must be available to provide the final cover referenced in section C.2.a.4. but also the temporary cover requirements referenced in this section. C.2.e. The May 16, 1994, March 23, 1995, and May 3, 1995 field investigations revealed the presence of numerous seeps on the landfill surface which are likely due to the lack of a leachate collection system underlying the fill area. Therefore, to alleivate this problem, Mr. Woytowich was advised by the writer during the May 16, 1994 field Investigation that a leachate collection system must be placed upon the existing waste materials before an additional lift of waste materials is placed. Said system shall be designed in accordance with the requirements of Section 4.5.4.f. of the SWMR. To determine the amount of leachate flow from the site, which will be utilized in determining the proper design of the leachate collection system, the landfill modeling program entitled "Hydrologic Evaluation of Landfill Performance" created by the Waterways Experimental Station of the US Army Corps of Engineers shall be utilized. Leachate flow shall be determined from the existing site as it represents the ultimate footprint of the disposal area. The design properties-of the leachate collection system, based upon the requirements of Section 4.5.4.f., shall be incorporated into the HELP model analysis. Leachate flow shall also be determined utilizing the final configuration having a one foot clay cap, topsoil, and vegetative cover in place. Input data sheets and computer outputs derived from the program shall be submitted. Note that although Section 4.5.4.f.A.(b) requires that the leachate collection system be eighteen inches in thickness, a lesser thickness may be utilized if justified by the program. A maximum daily leachate discharge must be calculated not only to determine the thickness of the leachate collection system but also the sizing of pipes located within the leachate collection system; note that Section 4.5.4.f.A.(g) requires that perforated pipes be located within the leachate collection system. Provide calculations indicating that leachate collection system piping is of sufficient strength to support anticipated loadings without crushing. Also provide calculations indicating that the leachate collection system is of sufficient capacity to continue to function effectively should settlement of the underlying waste material occur. Routing of leachate away from the landfill area is critical to its structural integrity. A leachate collection system must overlie the entire areal extent of the series of Phase I benches /7 600 EIDO12680 Mr. Stewart page ten and associated working faces referenced in Section C.2.a.5. As disposal operations extend from the base of the disposal area to the top of the disposal area, the revampled Phase I benches referenced in Section C.2.a.5. shall be regraded immediately prior to the placement of the leachate collection system which shall placed immediately prior to the series of Phase II benches and their related working faces. Therefore on a plan view map of scale 1" * 100 * (or a more expanded scale) indicate piping within the leachate collection system, its routing to interceptor and diversion channels, and culverts. Interceptor channels, diversion channels, and culverts shall be numbered with each having a reference to a detailed drawing. Detailed drawings (cross-sections) shall be submitted for each type of interceptor channel, diversion channel, and culvert. For each culvert, provide in table form the design velocity in cubic feet per second based upon a 25-yr, 24-hr storm event, its diameter, the type of material from which it is composed, its length, its slope, inverted elevation of incoming flow, and inverted elevation of outgoing flow. Also provide detailed drawings indicating the interface between the leachate collection system and the interceptor ditches. Also indicate the type of material to be utilized for the leachate collection system. It must be determined if geotextile is needed 1) between the leachate collection system and the underlying subgrade, and 2) the leachate collection system and the leachate collection system and the overlying waste materials be evaluating particle movement and head loss in the filter material. If it is determined that geotextile is needed, specify the type(s) to be utilized and provide rationale for choosing said type(s). If it is determined that geotextile is not needed, provide sufficient rationale accordingly. It must be determined if oeotextile is needed for interceptor and diversion ditches. If it is determined that geotextile is needed, specify the type(s) to be utilized and provide rationale for'choosing said type(s). If it is determined that geotextile is not needed, provide sufficient rationale accordingly. C.2.h. - As the March 23, 1995, and May 3, 1995 field investigations indicated that the discharge from Outlet No. 001 was causing conditions not allowable in state waters referenced in Section 3.2. of Title 46, Series I, the surface impoundment is not providing sufficient leachate treatment. Insufficient treatment is further reflected by the elevated BOD, COD, and TOC concentrations observed at Outlet No. 001 during the first four months of 1995. Concentrations of this magnitude are not acceptable. As the surface impoundment does not contain a liner system, said concentrations will likely impact g r o u n d w a t e r .___ s Section 4.5.1. of Title 47, Series 58, Groundwater Protection OGO'/v? 1 EID0I2681 I Mr. Stewart Page eleven Regulations effective June 1, 1994 states "existing impoundments shall be evaluated for their potential to cause groundwater contamination. Where potential for contamination exists, action shall be taken to eliminate, to the degree practicable, the potential for groundwater contamination." Therefore, the surface impoundment must be retrofitted with a liner system which meets the design requirements or"section 4 .B.3 .C. of the SWMR. It must be determined if geotextile will be utilized in the liner system. It it is determined that geotextile will be utilized, provide the type(s) to be utilized and provide rationale for choosing said type is). If it is determined that geotextile is not necessary, ,provide sufficient rationale accordingly. Your May 1 2 1995 letter indicated that Sulf Control has been utilized to reduce the above referenced BOO, COO, and TOC concentrations. Therefore, provide a Material Data Safety sheet for the product. As use of such is merely a "stop gap" measure, provide detailed information regarding all steps being investigated - as was indicated in your May 12, 1995 letter - to eliminate the black water discharge from the fill area thereby resulting in the return of BOD, COD, and TOC to acceptable concentrations. C.3.a.3. - Available soil cover shall be determined by conducting^ the soil borrow area studies referenced in Section C.2.a.4. Ac C.3.c. - It is this agency's belief that utilization of the HELP modelling program previously referenced in Section C.2.e. would have been more appropriate for providing the information required by this Section. Therefore, it is requested that said program be utilized taking into consideration the deficiencies referenced in the paragraph below. Should your company believe that the data generated by the method referenced in Attachment 19 is as reliable as data generated by the HELP modelling program, this agency will accept the utilization of said method provided that you company provide de'tailed rationale in support of said method. Note that if the method referenced in Attachment 19 is utilized, the deficiencies referenced in the paragraph below must be taken into account. Attachment 19 indicates that "slope at the surface of each cell ,will be 1% - 2%". As the May 16, 1994, March 23, 1995, and May 3, 1995 field investigations revealed numerous areas of ponded 1 water, the writer does not concur with this assumption. Attachment 19 also states that "the remaining 16.9 acres of fill area is covered with an impermeable clay (1x10-7 cm/sec) which is placed in a 6" compacted layer." However, Attachment 6 of the application indicates that the cover material instead exhibits a permeability of 1x10-6. Although Attachment 19 indicates that said cover contains deep rooted grass, the May 16 field review revealed a sparse vegetative cover. It should also be noted that surface run-on must also be considered in your evaluation. E.2.e. - The application states that a 6" cover is applied as necessary "to maintain compaction and for dust and debris control during windy periods." Indicate factors which are considered when determining cover is to be applied. Also describe how cover material aids compaction. 0 0 Qy, f EIDO12682 Mr. Stewart Page twelve E .4.a . - Describe use of each type of equipment utilized. E.S.a.l. - Provide name, address, and qualifications of the landfill contractor. E.7. - Sections E.7.b. and E.7.c. indicate that a six-inch thick soil cover is applied as necessary to maintain compaction and for dust and debris control in windy periods while E.7.h. indicates that wastes are covered as soon as possible with a minimum ^ thickness of 6" of compacted cover material. Indicate if soil -5= cover referenced in E.7.b. and E.7.c. is the same soil cover referenced in E.7.h. E.10.a.2. - Section C.3. of Attachment 20 indicates PCBs having concentrations less than 50PPM are to be disposed. If PCBs have been disposed in the past, please provide the types and quantities of wastes containing PCBs which were disposed in addition to the dates they were disposed. If PCBs were not disposed in the past, please confirm such. Section C.4. of Attachment 29 indicates that maximum lift thicknesses of ten feet having a slope not exceeding 3:1 will be maintained. This is in conflict with Sections C.2.a.S. and C.2.d.6. of the application. Therefore, please reconcile. Section C.14. states that a minimum thickness of 6" of compacted cover material will be applied to the entire solid waste area once each working day. This conflicts with Section E.7. of the application which states that a 6" soil cover is applied as necessary to maintain compaction and for dust and debris control in windy periods. Therefore, please reconcile. Section F.3. of Attachment 20 indicates two feet of soil cover is to be placed over completed sections of the fill. Verify that "completed" sections refer to lifts which have reached final grade which will receive no additional waste materials. Quarterly Monitoring Well Reports (QMWRs) submitted as required by Permit No. WV0076244 reference that statistical comparisons of the data provided for downgradient wells 6A, 12A, and 13A with background well 14 are not meaningful as 14 monitors a different aquifer. Therefore, your company contends that background groundwater quality in the aquifer monitored by wells 6A, 12A, and 13A should be defined as the average of each parameter measured for the first four quarters in the data base, specifically the period covering the second quarter 1990 through the first quarter 1991. Be advised that the SWMR require that background groundwater quality be determined by sampling wells that are hydrogeologically upgradient of the disposal area. However, the SWMR allow background groundwater quality to be based on sampling of wells that are not hydrogeologically upgradient of the disposal area where other wells will provide background groundwater quality that is as representative or 000 .1 E1D012683 x Mr. Stewart page thirteen more representative than that provided by hydrogeololically upgradient wells. Therefore, as wells 6A, 12A, and 13A are located immediately downgradient of the disposal area, they must not be utilized to determine background groundwater quality. Therefore, other well(s) must be utilized. For this purpose, this agency will consider the utilization of wells MW-lA and/or MW-4A as they are not located immediately downgradient of the disposal area. Should your company elect to utilize MW-lA or MW-4A (in lieu of constructing new wells), it must be demonstrated that said well(s) will adequately provide groundwater data in the aquifer monitored by MW-6A, MW-12A, and MW-13A. Section 5.5.1. of the SWMR allows for the waiver or modification of various secions of the SWMR provided that sufficient documentation justifying the waiver or modification is provided. Based upon a review of Application Mo. WV0076244, waivers of Sections 4.4, 4*6.2.b.A, and 4.12.2 appear to be appropriate. Should your company desire to pursue waivers of these sections, provide sufficient justification. As was indicated in this agency's February 4, 1994 letter, Application No. WV0076244 must include a Quality Assurance/ Quality Control Plan consistent with the requirements of Section 3.7.7. of the SWMR. By letter dated November 30, 1990 to R.L. Weser, Chief, Compliance Division, Air Pollution Control Commission, you expressed a desire to incinerate solidified methacrylate sirup. Therefore, indiciate if methacrylate sirup ash has been disposed at the Dry Run landfill. If so, provide dates and quantities of disposal as well as all available leachability analyses. If methacrylate sirup ash has not been disposed, please indicate accordingly. An 1991 inspection by this agency revealed the lack of surface seals around wells MW-6 and MW-6A. Therefore, provide measure to be implemented to install surface seals around these wells. Attachment No. 14 references Stream Sampling Points 1 and 2. Indicate which location is utilized for collection of the sample obtained for semi-annual leachate analysis. A detailed narrative, where appropriate, shall accompany the above requested information. Please submit the original copy of the above requested information to Chief, Office of Water Resources ana four (4) copies of same to my attention at my Fairmont office in an expeditious manner but prior to January 11, 1996, so that the review of Application No. WV0076244 may continue. ooo; /h 1 EID012684 Mr- Stewart Page fourteen Should you have any questions concerning the above, please contact me at (304) 367-2724. Sincerely, OFFICE OF WATER RESOURCES John 6. Britvec, Geologist Industrial Branch JGB/jb cc: Cindy Musser, Insp., SW Dist. 000: EID012685 V 58 ^ r ZAK INTEROFFICE MEMORANDUM Date: From: Dept: Tel No: 05-Dec-1995 11:29am CRAIG K DILLON DILLONCK Fluoroproducts 304-863-4972 TO: Distribution List Subject: Meeting Notes - C-8 at Dry Run A meeting was held on November 30 to discuss the acceptable c-8 levels for Teflon* waste that is proposed to be landfilled at Dry Run. Those in attendance were Walt Stewart and Dan Weber (Environmental), Woody Ireland (Power & Services), John Doughty (Central Lab), and Roger Zipfel, Ed James, and Craig Dillon (tTeflon*). Zipfel presented data on various Teflon* waste samples that were extracted by Doughty for C-8 levels. Details of the samples extracted are recorded in book No. E56538 page 123 (Doughty Log?). Dan Weber also provided as reference extraction data furnished by Quality Analytical Lab on bio-cake. Summary of the data is as follows: DESCRIPTION POLYMER WATER EXTRACTION C-8 LEVEL EXTRACTED C-8 LEVEL PPM PPM** 150-1 Fine Powder Trench Scrap - undried 59 0.44 150-2 Granular Vacuum System Scrap - dry 2 0.08 150-3 PFA from Process K test dryer - dry 11 0.04 150-4 FEP-4100 from Line 3 - dry 7 0.04 150-5 1 ppm blank ^ - 1.04 NA Bio-cake sample (Quality Analytical) 0.004 0 H 1 in o Doughty extracted the sample that Quality Analytical analyzed. Weber noted that the analysis method used by Quality Analytical differed from the method used by Doughty on the polymer samples. Based on the bio-cake analysis, Weber indicated that approximately 7 pounds per year of C-8 is currently landfilled at Dry Run due to bio-cake. Using the test results as a guide, the group agreed that Granular scrap can be landfilled at Dry Run. In addition, any melted scrap PFA or FEP can be landfilled at Dry Run. For PFA, this would be scrap material generated at the exit side of the extruder and beyond (generally cubes). For FEP, this would be scrap material generated at the exit side of the humid heat treater and beyond (generally slabs, shred, cubes). It was the consensus of the group that the potential landfill amounts of these scrap materials would not significantly impact C-8 levels at Dry Run. For Fine Powder/Dispersion, no process scrap will be allowed at Dry Run. This was based on the test results and also on process configuration. There is concern that the process configuration would not allow for distinct EID016730 separation of C-8 and non-C-8 scrap. If .a Xaxjqa. amount of finished Fine Powder/Dispersion must be disposed, then this material should be tested for C-8 and handled on an individual basis. It was also the consensus of the group that Teflon* continue to drive the sale of all scrap to reduce the need for landfilling. \ E1D016731 -'3 V 59 OOOr-30 12/13/95 notes from Dawn Jackson jim Crum, Elkins DNR Office, called me today about a call that he had received from Earl Tennant about water flowing from DuPont's Dry Run Landfill poisoning the deer in the area. Tennant told Crum that he had also contacted Dr. Thomas, the State Veterinarian with the Dept, of Agriculture. Crum told Tennant that he (Tennant) should contact his local DNR office, which Tennant said he had done, but without satisfaction. Crum called the local office, and Jeff M c C r a d y told him to call me, knowing that I had some background info on Mr. Tennant. Tennant told Crum that numerous deer had been poisoned in the area recently. When Crum pinned him down on numbers, the total turned out to be five, between the months of April and October, with October being the last time that Tennant said that he had found one near Dry Run. Crum told Tennant that if he would contact the DNR office when he finds a fresh carcass, the DNR will do a tissue analysis. (Crum indicated to me that the DNR had done a number of such analyses when there was a virus killing whitetail deer in the Belleville area in 1988.) Tennant also provided several very specific kinds of details to Dr. Thomas and Jim Crum. He said that his water analysis indicated the presence of mercury in the Dry Run stream, that there was an arsenic level of .0097 ppm, and that the pH was "not right." He also said that DuPont was treating the landfill ponds on Tuesdays and Thursdays with 5 gallons of hydrogen peroxide. When Crum asked Tennant to share his water analysis info with the DNR, Tennant said that he wouldn't show the report to anyone until someone could give him some help with his cattle. Crum told him that the DNR couldn't address the cattle issue, but repeated that the DNR would do a tissue sample on a fresh deer carcass. Jim Crum (with whom our WHEC has worked on at least one project -- the osprey rintroduction) sounded very sympathetic and told me about the number of rumors that the DNR struggles with. He said that contacting us was a courtesy call, and he said that he would call us i he hears from Mr. Tennant again. He also asked me specifically if we are treating the ponds with something that Mr. Tennant may have seen and misinterpreted, and he asked me if we do an analysis of the materials that Mr. Tennant mentioned. I told him that I'd get back to him. I talked with Ron Meloon and Woody Ireland, and Woody pointed out that arsenic, mercury, and pH are among the parameters reported monthly to the DEP. Woody also recalled one hydrogen peroxide treatment on April 11 to change the pH of the pond, but he was not aware of any treatment that may have occurred as routinely as every Tuesday/Thursday. Ron and Woody are checking with Boso to see if anything like antifoam or algae treatment may have been used on a schedule during the summer that may have led Tennant to conclude that it was being done every Tue/Thur. In conclusion, Dawn loves her job, she hopes that these notes make sense, and she wishes Mr. Tennant a very Merry Christmas. 000;.,* EID010289 V 60 ooo;^ INTEROFFICE MEMORANDUM Date: From: Dept: Tel No: 27-Mar-1996 02:58pra EDT Roger J. Zipfel ZIPFEL Fluoroproducts 304-863-2567 TO: 7 addressees CC: GERALD L KENNEDY ( KENNEDY AT A1 AT HSKVAX ) Subject: Phone conversation with Gerry Kennedy Attached are the notes of a phone conversation I recently had with Gerry Kennedy. Since I an not good with sone of these words, I may have not got the story completely correnct. By this note, I an asking Gerry to correct any error in note taking on ny part. Per Gerry the botton line is that item 1 is not good news and itens 2&3 are good news. Roger. O G O <7 EID073253 C-8 Toxicity re: phone conversation with Gerry Kennedy on 3/20/96 1) 3M and Hoechst are running tests to fully expand our Geno Toxicity understanding. They ran an `Unscheduled DNA Synthesis' test. They found at high C-8 concentrations (1000 microg/ml) that C-8 gave equivocal results on geno toxicity. They are currently collaborating on why this happens. Where this will go in the future is not clear, but this is the first indication that C-8 could be affecting DNA. The worst case scenario is that C-8 could be classified as a large *C* carcinogen. 2) 3M and Hoechst have proposed to the APfC to look at the human relevance of the significance of the current rat pancreatic cancer concerns. 3) 3M has hired an epidemiologist to relook at 3M (1991) worker hormonal levels. Results of this effort are that the affects reported by the U.of Minn, can not be confirmed. The same worker population was also examined with data taken in 199341995 and again no relationships of C-8 exposure to hormonal affects were noted. A relook at the prostrate cancers noted in the 1991 UofMinn study showed that only 1 of the 6 cases was a C-8 worker. 3M plans to publish this work. ('li}-/' .<v EID073254 V 61 0005 INTEROFFICE MEMORANDUM Date: From: Dept: Tel No: 10-Sep-1996 04:59pm WALTER M. STEWART STEWART PPD-SHEA&EA (304) 863-4271 TO: See Below Subject: DRY RUN LANDFILL COMPLAINT I HAVE HAD TWO CONVERSATIONS SINCE YESTERDAY (9/9) WITH U.S. EPA, REGION III OFFICIALS REGARDING A COMPLAINT RECEIVED FROM MR. EARL TENANT. BOTH MARY BECK, REPRESENTING THE RCRA CORRECTIVE ACTION GROUP AND SARAH CASPAR, FROM THE SUPERFUND REMOVAL ENFORCEMENT AND OIL SECTION INDICATED THE COMPLAINT ALLEGED THAT 150 CATTLE DIED AS A RESULT OF WATER FLOW ACROSS HIS PROPERTY FROM OUR LANDFILL. HE OFFERED AS PROOF A STATEMENT FROM A VETERINARIAN (NO NAME) THAT TEETH EXAMINED FROM THE DEAD CATTLE SHOWED SIGNS OF FLUORIDE EXPOSURE. THEY BOTH REQUESTED NAMES OF THE STATE PEOPLE WE WERE WORKING WITH AND I GAVE THEM THE NAMES OF JOHN BRITVEC, OUR PERMIT WRITER AND CINDY MUSSER, THE ENFORCEMENT INSPECTOR. MS. CASPAR INDICATED SHE WOULD BE FOLLOWING UP WITH BOTH OF THEM. THE EPA IS TAKING THE COMPLAINT VERY SERIOUSLY AND IT WAS STATED BY MS. CASPAR THAT SHE EXPECTED TO VISIT THE SITE ABOUT TWO WEEKS FROM NOW. SHE INDICATED SHE WOULD LET ME KNOW WHEN, AND THAT THE STATE WOULD BE ASKED TO PARTICIPATE. I FILLED HER IN ON SOME OF THE BACKGROUND ABOUT THE SITUATION AND INDICATED THAT WE WOULD COOPERATE WITH THEM IN INVESTIGATING THE MATTER. I'LL KEEP YOU INFORMED WHEN I HEAR MORE ABOUT THIS. Distribution: TO: H. DAVID RAMSEY, JR. ( RAMSEY ) CC: MAYNARD S EATON, JR CC: RONALD W MELOON CC: LYNWOOD K. IRELAND CC: DAWN D JACKSON CC: GERALD A PLOEGER CC: Charles T. Alt CC: H RAY HODGES CC: GARY W. KLESEL CC: ROBERT L. RITCHEY CC: DANIEL A WEBER CC: GEORGE WOYTOWICH ( EATONMS ) ( MELOONRW ) ( IRELAND ) ( JACKSODD ) ( PLOEGER ) ( ALT ) ( HODGESHR ) ( KLESELGW ) ( RITCHERL ) ( WEBERDA ) ( WOYTOWIG ) G O n;- EID010291 62 OOOKS? INTEROFFICE MEMORANDUM TO: RONALD W MELOON TO: LYNWOOD K. IRELAND Date: From: Dept: Tel No: 16-Sep-1996 02:29pm Thomas R. Waldron WALDROTR PPD -POWER/SERVICE 304-863-2489 ( MELOONRW ) ( IRELAND ) CC: RICHARD A KIRSCHNER, JR CC: DANIEL A. WEBER ( KIRSCHRA ) ( WBBERDA ) Subject: Dry Run Landfill 09/16/96 I toured Dry Run Landfill today and made the following observations. 1) The newly sown grass seed is growing well and I saw no exposed areas. 2) The rip-rapped ditches were doing a good job of holding back most of the the run-off (it was raining at the time), the discharge from them was mostly clear. 3) The lower pond was still very green with some slight discoloration due to a small amount of solids in the runoff. 4) There was some foaming coming down into the lower pond from the upper pond and persisting downstream past the outfall. I instructed the operator to put a quart of anti-foam in the upper pond. 5) The waste was completely covered, except what had been deposited during the morning hours. Any questions, give me a call. \ Tom 0 0 0 -', 5 HID016848 V 63 o o o ^s INTEROFFICE MEMORANDUM Date: From: Dept: Tel No: 07-Oct-1996 01:55pm Thomas R. Waldron WALDROTR PPD-POWER/SERVICE 304-863-2489 TO: RONALD W MELOON TO: LYNWOOD K. IRELAND ( MELOONRW ) ( IRELAND ) CC: RICHARD A KIRSCHNER, JR CC: DANIEL A. WEBER ( KIRSCHRA ) ( WEBERDA ) Subject: Dry Run Landfill I toured the Dry Run landfill this afternoon and found a couple of things that I made corrections too. 1) The outfall had some considerable foam in and around the exit pipe. It also appeared to persist in the stream down to about the 500' foot level. I added about a quart of anti-foam to the pond via the air line and about a pint to the outfall exit itself. The foam began to immediately disipate. 2) I also found some small areas of exposed trash on the face of the active fill. Apparently the trash had lain uncovered all weekend. I instructed the landfill operator to cover the material before he left for the day and he told me he would get it done. Most of the recently seeded areas have a good crop of grass growing on them and those places that have been exposed by the recent rains will be reseeded this week. The meadows below the ponds have lots of 4 wheeler tracks in them as it would appear that someone is still running that area when we are not present. Any questions, give me a call. Tom ooo&so EID039281 w. 64 eoo <; m f i K * Ite. INTEROFFICE MEMORANDUM Date: Fro: Dept: Tel No: 15-0ct-1996 03:49pm WALTER M. STEWART STEWART PPD-SHEAAEA (304) 863-4271 TO: D istribution L ist Subject: EPA AUDIT I RECEIVED A PHONE CALL FROM MR. KEVIN SCOTT, PRC ENVIRONMENTAL MANAGEMENT THIS AFTERNOON (10/15) INFORMING ME THAT HE AND ANOTHER EPA PERSON WOULD BE CONDUCTING AN INSPECTION OF OUR DRY RUN LANDFILL FOR THE NEXT SEVERAL DAYS. HE INDICATED THAT THE INSPECTION WAS THE RESULT OF MR. TENNANT'S COMPLAINT AND THAT IT WOULD START THIS AFTERNOON. THE INSPECTION WILL INVOLVE VIEWING THE SITE, EXTENSIVE SAMPLING AT THE LANDFILL, AND SAMPLING DRINKING WATER WELLS IN THE VICINITY. I INDICATED THAT WE WANTED TO SPLIT SAMPLES OF ANY TAKEN AT OUR LANDFILL. MR. SCOn DID NOT WANT TO COME TO THE PLANT BUT WAS GOING DIRECTLY TO THE LANDFILL. I WILL KEEP YOU INFORMED ABOUT THE INSPECTION. IF THERE ARE ANY QUESTIONS, PLEASE CALL. 000.'-,!i?- EID024318 65 000&S3 GASTON CAPERTON GOVERNOR DIVISION OF ENVIRONMENTAL PROTECTION 10 McJunkin Road Nitro, WV 25143 LAIDLEY ELI McCoy. Ph.O. DIRECTOR October 15,1996 Mr. W. M. Stewart Senior Environmental Control Consultant E.I. DuPont de Nemours and Company Washington Works P.O.Box 1217 Parkersburg, West Virginia 26102 Re: Dry Run Landfill (WV/NPDES Permit No. WV0076244) and Washington Works facility (WV/NPDES Permit No. WV0001279) Dear Mr. Stewart: E.I. DuPont de Nemours and Company has always been a valued citizen o f West Virginia. However, over the past several months, inspectors with DEP have observed serious shortcomings in DuPont's operations of the Dry Run Landfill and the Washington Works facility. During numerous inspections, DEP employees noticed, among other violations, the following: 1. On several occasions, DuPont has allowed, and continues to allow, a large flow o f black and odorous leachate to be released from its Dry Run Landfill into Dry Run, in violation of its NPDES Permit and the West Virginia Code o f State Regulations; 2. On several occasions, DuPont discharged Teflon, Deiron, Nylon and wax beads from its Washington Works facility into the Ohio River, in violation o f its NPDES Permit and the West Virginia Code of State Regulations; 3. On several occasions, DuPont has failed, and apparently continues to fail, to prevent run-offfrom flowing across the Dry Run Landfill and has failed to collect and treat leachate generated by the Dry Run Landfill, in violation of the West Virginia Code of State Regulations; 4. On several occasions, DuPont has failed, and apparently continues to fail, to notify DEP that the quality of the leachate generated by the Dry Run Landfill has exceeded the design capacity of the treatment system, in violation of its NPDES Permit and the West Virginia Code of State Regulations; EID012733 000 C 1 r Mr. W.M. Stewart October 15, 1996 Page 2 5. On several occasions, DuPont has failed, and apparently continues to fail, to properly compact the wastes disposed at the Dry Run Landfill, in violation of the West Virginia Code of State Regulations; 6. On numerous occasions, DuPont has deposited, and continues to deposit, waste in the Dry Run Landfill in greater concentrations than the concentrations approved by DEP, in violation of its NPDES Permit and the West Virginia Code of State Regulations; 7. On several occasions, DuPont has failed to properly operate and maintain the Dry Run Landfill, in violation of its NPDES Permit 8. DuPont has failed, and continues to fail, to retrofit the Dry Run Landfill surface impoundment with a liner system and leak detection system, in violation of the West Virginia Code of State Regulations; 9. On numerous occasions, DuPont has allowed the effluent from the Dry Run Landfill to exceed the water quality standards, in violation of the West Virginia Code of State Regulations; 10. On numerous occasions, DuPont has allowed the effluent from the Dry Run Landfill to exceed the discharge limitations established in its NPDES Permit, in violation o f its NPDES Permit; and 11. On several occasions, DuPont has failed, and continues to fail, to comply with each and every condition of its NPDES Permit, in violation of its NPDES Permit Due to the foregoing violations at the Washington Works facility and Dry Run Landfill, DEP intends to file a civil action against DuPont in the Circuit Court of Wood County. The agency will seek injunctive relief to address current and prospective violations and will ask for the assessment of civil penalties for current and past violations. A copy of a draft complaint is attached. I have instructed DEP's Office of Legal Services to initiate formal proceedings against DuPont in circuit court by no later than January 15,1997. Should DuPont wish to enter into negotiations to explore potential resolution of the enforcement action before a complaint is filed, please contact DEP attorneys Matthew Crum or Scott Goldman at (304) 558-9160. OvK) o. s EIDO 12734 IN THE CIRCUIT COURT OF WOOD COUNTY, STATE OF WEST VIRGINIA LAIDLEY ELI McCOY, Director, West Virginia Division of Environmental Protection, Plaintiff, V. Civil Action E. I. DuPONT DE NEMOURS & COMPANY, INC.. Defendant C O M PL A IN T INTRODUCTION Plaintiff Laidley Eli McCoy, Director, West Virginia Division of Environmental Protection ("DEP"), by counsel, alleges the following: 1. This is a civil action brought under the Water Pollution Control A ct West Virginia Code 22-11-1 to -28 (1995) ("WPCA") and the Solid Waste Management Act, West Virginia Code 22-15-1 to -20 (1995) ("SWMA"), against Defendant E.I. DuPont De Nemours and Company, Incorporated, based on violations of the WPCA, SWMA, and the regulations promulgated thereunder for injunctive relief, the assessment of civil penalties, and attorneys fees. 000 EID012735 PARTIES 2. Plaintiff, Laidley Eli McCoy, for and on behalf of the State of West Virginia, is the duly appointed Director of DEP, and is thereby authorized by the WPCA, and the regulations promulgated thereunder, to enforce the water pollution control laws and regulations of this State. Specifically, W. Va. Code 22-11-22 states: Any person who violates any provision of any permit issued under or subject to the provisions of (the WPCA] is subject to a civil penalty not to exceed ten thousand dollars per day of such violation, and any person who violates any provision of this article or of any rule . . . is subject to a civil penalty not to exceed ten thousand dollars per day of such violation. Any such civil penalty may be imposed and collected only by a civil action instituted by the director (of DEP] in the circuit court of the county in which the violation occurred or is occurring or of the county in which the waters thereof are polluted as the result of such violation. Upon application by the director, the circuit courts of this state or the judges thereof in vacation may by injunction compel compliance with and enjoin violations o f the provisions of this article, the rules of the (environmental quality] board or director, effluent limitations, the terms and conditions of any permit granted under the provisions of this article, or any order of the director or board, and the venue of any such action shall be the county in which the violation or noncompliance exists or is taking place or in any county in which the waters thereof are polluted as the result of such violation or noncompliance. 3. Additionally, Director McCoy is authorized by the SWMA and the regulations promulgated thereunder, to enforce the solid waste management laws and regulations of this State. Specifically, W. Va. Code 22-15-15(d) and (e) state: (d) Any person who violates any provision of [the SWMA], [a]ny permit or any rule or order issued pursuant to [the SWMA] is subject to a civil penalty not to exceed twenty-five thousand dollars for each day of such violation, which penalty shall be recovered in a civil action either in the court wherein the violation occurs or in the circuit court of Kanawha County. (e) The director may seek an injunction, or may institute a civil action against any person in violation of any provisions of this article or any permit, rule or order issued pursuant to this article. 2 (U>0 EIDO12736 it 4. Defendant E. I. DuPont De Nemours & Company ("Defendant"), is a corporation duly authorized to conduct business in the State of West Virginia. Defendant owns and operates a facility ("Washington Works") in Wood County, West Virginia, which produces plastic and acrylic resins. Defendant also owns and operates a non-hazardous waste landfill ("Dry Run Landfill") in Wood County, West Virginia, that serves the Washington Works facility. At all pertinent times hereto, Defendant was and is doing business in Washington, Wood County, West Virginia. 5. Under the WPCA and SWMA, the definition of the term "person" includes "any industrial user, public or private corporation, institution, association, firm or company organized or existing under the laws of this or any other state or country." W. Va. Code 22-11-3(15) and -15-2(22). Defendant is a "person* as defined under the WPCA and SWMA. JURISDICTION AND VENUE 6. This Honorable Court has jurisdiction over this action pursuant to W. Va. Code 22-11-22 and 22-15-15(d). 7. Venue is proper in this court pursuant to W. Va. Code 22-11-22 and 22-1515(d) because Defendant's Washington Works facility and Dry Run Landfill are located in Wood County and because the violations referenced herein occurred or are occurring in Wood County. STATEMENT OF FACTS 8. Defendant was originally authorized to operate the Dry Rim Landfill in 1982 through issuance of permit No. IWL-6282-82 by the Department of Natural Resources ("DNR"), 3 GGO.-I EID012737 predecessor to DEP. Such permit authorized Defendant to discharge a specific amount and type of pollutants into Dry Run, a tributary of the North Fork of Lee Creek, which is a tributary of the Ohio River. Pursuant to W. Va. Code 22-11-3(23), Dry Run, the North Fork of Lee Creek, and the Ohio River are all "waters" of the State. 9. On January 12, 1990, DNR reissued IWL-6282-82 to Defendant as Solid Waste/National Pollutant Discharge Elimination System ("SW/NPDES") Permit No. WV0076244. As written, the SW/NPDES Permit was scheduled to expire on January 11, 1995. A copy of SW/NPDES Permit No. WV0076244 is attached hereto as Exhibit 1. 10. Solid Waste/National Pollutant Discharge Elimination System Permit No. WV0076244 incorporated by reference, as a term and condition thereof, information submitted by Defendant with SW/NPDES Application No. WV0076244, as well as information contained in correspondence from Defendant dated August 10,1987; September 15, 1987; March 1, 1988; April 14, 1988; March 16, 1989; and May 9, 1989. Sfifi Exhibit 1, page 1. 11. Under the federal Clean Water Act, 33 U.S.C. 1251, et seq. and the WPCA, the State of West Virginia, through DEP, is authorized to regulate discharges into the waters of the State of West Virginia through implementation of the National Pollutant Discharge Elimination System ("NPDES") Program. Specifically, the NPDES Program is "the [njational program for issuing, denying, modifying, revoking and reissuing, suspending, revoking, monitoring and enforcing permits, and imposing and enforcing pretreatment requirements under Sections 307, 318, 402, and 405 of [the federal Clean Water Act], including any approved [s]tate program." Sfifi National Pollutant Discharge Elimination System (NPDES) Program, ("NPDES Program"), West Virginia Code of State Regulations ("CSR"), Title 47, Series 10 2.27 (1993). 4 EID012738 12. On February 16, 1990, Defendant appealed the terms and conditions of SW/NPDES Permit No. WV0076244 to the Water Resources Board, predecessor to the Environmental Quality Board. The appeal was resolved by the Board's entry of an agreed order dated March 12, 1991, and resulted in a corresponding modification of SW/NPDES Permit No. WV0076244. The agreed order is attached hereto Exhibit 2. 13. By letter dated January 11,1995, DEP extended the expiration date of SW/NPDES Permit No. WV0076244 from January 11, 1995, to January 11, 1996. 14. By letter dated January 3, 1996, DEP conditionally extended the expiration date of SW/NPDES Permit No. WV0076244 to September 11,1996. Such extension was conditioned upon Defendant providing DEP with additional information regarding its Dry Run Landfill. 15. By letter dated August 22,1996, DEP extended the expiration date of SW/NPDES Permit No. WV0076244 to December 11,1996. 16. In addition to the Dry Run Landfill. Defendant also owns and operates the Washington Works facility which produces plastic and acrylic resins. On September 30, 1994, DEP reissued NPDES Permit No. WV0001279 to Defendant for its Washington Works facility, such permit authorizing Defendant to discharge a specific amount and type of pollutants directly into the Ohio River. NPDES Permit No. WV0001279 is attached hereto as Exhibit 3. COUNT I Violations o f Conditions Not Allowable in State W aters 17. Plaintiff hereby realleges and incorporates the allegations set forth in paragraphs 1 - 1 6 above as if fully restated herein. 5 OOOC.O'/ Ir EIDO12739 18. Pursuant to the Requirements Governing Water Quality Standards ("Water Quality Standards"), 46 CSR 1 V(1996)^entitled "Conditions Not Allowable in State Waters," No sewage, industrial waste, or other wastes present in any of the waters of the State shall cause therein or materially contribute to . . . distinctly visible floating or settleable solids, suspended solids, scum, foam, or oily slicks . . . [deposits or sludge banks on the bottom . . . [o]dors in the vicinity of the waters . . . [or] [d]istinctly visible color. 19. On March 23, 1995, Cynthia J. Musser, Inspector, Environmental Enforcement, DEP, inspected the Dry Run landfill. During the inspection, a flow of very black and odorous leachate was emanating from the subject landfill and entering Dry Run, thus discoloring Dry Run and imparting an odor thereto. 20. On May 3, 1995, Inspector Musser conducted an inspection of Defendant's Dry Run Landfill. The leachate from the landfill remained odorous and black, and the discharge from the subject landfill into Dry Run was odorous, turbid, and green with algae, thus discoloring Dry Run and imparting an odor thereto. 21. On August 13,1996, Inspector Musser conducted an inspection of Defendant's Dry Run Landfill. The leachate from the landfill remained odorous and black, and the discharge from the subject landfill into Dry Run was odorous, turbid, and green with algae, thus discoloring Dry Run and imparting an odor thereto. 22. On August 20, 1996, Inspector Supervisor Charles A. Moses, Inspector James C. Laine, Jr., and Inspector Musser conducted a river patrol of the Ohio River in the vicinity of Defendant's Washington Works facility. During the river patrol, the inspectors sampled deposits on the bottom of the Ohio River and along the river's banks immediately below Outfall 002 of the 6 OOOSOi EIDO12740 Washington Works facility. The sample contained beads made of Nylon, Deiron and Teflon - all materials manufactured at the Washington Works facility. 23. During the August 20, 1996, Ohio River patrol, the inspectors likewise sampled deposits along the banks of the Ohio River immediately below Outfall 003 of the Washington Works facility. The sample contained beads made of Nylon, Deiron and Teflon - all materials manufactured at the Washington Works facility. 24. During the August 20, 1996, Ohio River patrol, the inspectors sampled deposits on the bottom of the Ohio River below Outfall 005 of the Washington Works facility. The bottom deposit sample yielded beads which contained Teflon and Deiron - both materials manufactured at the Washington Works facility. 25. During the August 20, 1996, Ohio River patrol, the inspectors observed floating solids on the Ohio River and along the banks of the Ohio River which were determined to be a mixture of Teflon and wax and which had been discharged from Outfall 005 o f the Washington Works facility. The floating solids were located along the West Virginia river bank of the Ohio River for approximately one-half mile below Outfall 005. 26. On March 23, 1995, May 3, 1995, and August 13, 1996, Defendant was in violation of Water Quality Standards 46 CSR 1 3, (1996) "Conditions Not Allowable in State Waters," by discharging a turbid flow from Dry Run Landfill into Dry Run, such flow constituting the discharge of distinctly visible colon, turbid conditions, and odon in waters of the State. 27. On August 20, 1996, Defendant was in violation of Water Quality Standards, 46 CSR 1 3, (1996) "Conditions Not Allowable in State Waten," by discharging beads of material 7 000; i'.: EIDO12741 manufactured at Defendant's facility, from three separate discharge points, into the Ohio River, waters of the State. Such deposition of material constituted the illegal discharge of settleable solids into waters of the State as well as the impermissible deposition of materials on the bottom of the subject stream. 28. On August 20, 1996, Defendant was in violation of Water Quality Standards, 46 CSR 1 3, (1996) "Conditions Not Allowable in State Waters," by discharging a floating or suspended mixture of Teflon and wax, materials manufactured at Defendant's Washington Works facility, into the Ohio River. Such discharge constituted the illegal placement of distinctly visible floating or suspended solids into waters of the state. COUNTn Failure to Prevent R un-off and C ollect and Treat Leachate 29. Plaintiff hereby realleges and incorporates the allegations set forth in paragraphs 1 - 2 8 above as if fully restated herein. 30. Solid Waste Management Regulations ("SWMR") 47 CSR 38 4 .8 .l.b and d (1996), entitled "Leachate Management," state: 4.8.l.b Any liquid which comes in contact with waste or accumulates in a portion of the facility where active waste disposal operations are occurring must be handled as leachate and properly treated . . . unless otherwise approved by the director [of DEP] in writing. 4.8. l.d In the case of an industrial landfill, the leachate collection and treatment facility must be in place and operable prior to the commencement of landfill operations. 8 OGOo.fV; EIDO12742 31. Solid Waste Management Regulation, 47 CSR 38 4.5.2.b.A. (1996), entitled "Run-on Control System," states: (a) Permittees of all SWLFs [solid waste landfills] must design, construct, operate, and maintain: (b) A run-on control system capable of preventing flow onto any part of the disposal area including the active portion of the SWLF during peak discharge from at least a 25-year, 24-hour storm. 32. During a May 16,(^994, field review of the Dry Run Landfill conducted by John G. Britvec, Geologist, Office of Water Resources, DEP, and Inspector Musser, Mr. Britvec and Inspector Musser observed that Defendant had not installed a system which would collect and treat leachate, as required by SWMR, 47 CSR 38 4.8.1.d ^ 9 0 . 33. During the May 16^ 1994^ ^ review, Mr. Britvec and Inspector Musser observed that Defendant had not installed diversion ditches at the facility, as required by SWMR, 47 CSR 38 4.5.2.b.A. (1996). 34. During the May 16, 1994, field review and on other occasions, DEP personnel advised Defendant's managerial personnel that a leachate collection system and diversion ditches must be installed at the subject landfill. 35. During the March 23,1995, inspection of die Dry Run Landfill, Defendant did not have a collection system or treatment facility to collect or treat leachate generated by the Dry Run Landfill, as required by SWMR, 47 CSR 38 4 .8 .l.d (1996). 36. During the March 23,1995, inspection, Defendant did not have diversion ditches in place to re-direct surface flow or run-on away from the working surface of the landfill, as required by SWMR, 47 CSR 38 $ 4.5.2.b.A (1996). 9 OOOIm M EID012743 37. Upon information and belief, in April 1995, Defendant constructed two diversion ditches above the Dry Run Landfill to prevent run-on from flowing across the landfill. 38. During the August 13, 1996, inspection of the Dry Run Landfill, the diversion ditch on the upper side of the landfill was not properly maintained by Defendant, as required by SWMR, 47 CSR 38 4.5.2.b.A. (1996). 39. During the August 13, 1996, inspection of the Dry Run Landfill, the facility did not have a leachate collection system installed, as required by SWMR 47 CSR 38 4 .8 .l.d. (1996). 40. From May 16, 1994, until August 13, 1996, and upon information and belief, to the present date, Defendant has been in violation of SWMR 47 CSR 38 4 .8 .l.d . (1996), for failure to install a leachate collection system. 41. From May 16, 1994 until April 1995, Defendant was in violation of SWMR 47 CSR 38 4.5.2.b.A. (1996), for Mure to design, construct and operate a run-on control system. 42. On August 13, 1996, and, upon information and belief, to the present date. Defendant was and is in violation of SWMR 47 CSR 38 4.5.2.b.A. (1996), for failure to maintain a run-on control system. COUNT in Failure to N otify o f Violations 43. Plaintiff hereby realleges and incorporates the allegations set forth in paragraphs 1 - 4 2 above as if fully restated herein. 44. Solid Waste Management Regulation 47 CSR 38 4 .8 .l.j (1996), specifying notification requirements, states: 10 EIDO12744 The permittee must immediately notify the director [of DEP] and describe remedial steps to be taken i f . . . [ojperation of the leachate treatment facility under this rule cannot prevent the facility from . . . [violating the terms of its permit, [SWMR], the [federal] Clean Water Act and the rules and regulations promulgated thereunder, or W. Va. Code 22-11 and the rules and regulations promulgated thereunder; or . . . [clausing surface water pollution or groundwater degradation, contamination, or pollution. Further, Solid Waste Management Regulation 47 CSR 38 4.8.1-j (1996), states; The permittee must immediately notify the director [of DEP] and describe remedial steps to be taken i f . . . [t]he facility is generating a quality or quantity of leachate that exceeds the design capacity of the treatment system. 45. Defendant has failed to notify DEP that the operation of the Dry Run Landfill > exceeded the design capacity of the landfill's treatment system and that, as a result, such facility was in violation of the terms and conditions of the SW/NPDES permit, the WPCA, and regulations promulgated thereunder. 46. Upon information and belief, Defendant continues to fail to notify DEP when the quality of the leachate generated by the Dry Run Landfill exceeds the capacity of the treatment system, thus causing violations of established discharge limits into Dry Run. 47. On numerous occasions Defendant has been and, upon information and belief, still is in violation of SWMR 47 CSR 38 4.8.l.j (1996), for failure to notify DEP when operations of its facility exceeded the design capacity of its treatment system. COUNT IV Failure to Adequately Compact 48. Plaintiff hereby realleges and incorporates the allegations set forth in paragraphs 1 - 4 7 above as if fully restated herein. 11 000 r EID012745 49. Solid Waste Management Regulation 47 CSR 38 4.6.2.a.C, "Layering and Compaction," (1996) provides: Solid waste must be placed in layers not exceeding two (2) feet in depth and compacted with a minimum of three (3) passes with . . . equipment of [effective] compacting ability. 50. During the May 3, 1995, inspection, Defendant was compacting the wastes in the Dry Run Landfill in layers exceeding two feet in depth. 51. During the August 13, 1996, inspection, Defendant was continuing to compact the wastes in the Dry Run Landfill in layers exceeding two feet in depth. 52. On May 3, 1995, and August 13, 1996, and upon information and belief, to the present day, Defendant violated and continues to violate SWMR, 47 CSR 38 4.6.2.a.C. (1996), "Layering and Compaction," by failing to properly compact the wastes disposed in the Dry Run L an d fill. COUNTV Changing Composition o f W aste W ithout Proper Authorization 53. Plaintiff hereby realleges and incorporates the allegations set forth in paragraphs 1 - 5 2 above as if fully restated herein. 54. Section G. 1 of the SW/NPDES Permit No. WV0076244 states: Only the waste materials specified in [SW/NPDES] Permit Application No. WV0076244 and in the letter dated the 1st day of March 1988 may be disposed in the landfill. 55. Section C.4 of SW/NPDES Permit No. WV0076244 states: This Permit may be modified, revoked and reissued, suspended, or revoked for cause. The filing of a request by the permittee for a permit modification, 12 000. E1D012746 LKI000607 revocation, and reissuance or revocation or a notification of planned champ or anticipated noncompliance, does not stay anv permit condition. (Emphasis added.) 56. By letter dated September 14, 1994, Defendant informed DEP that it had changed the composition of wastes being disposed at its Dry Run Landfill. 57. During mid-1994, Defendant did dramatically alter the composition of wastes being disposed at the Dry Run Landfill. Jr 58. From mid-1994 through, upon information and belief, the present date, Defendant has disposed and continues to dispose of waste at the Dry Run Landfill, the composition of which differs substantially from that which was specified in Defendant's SW/NPDES Permit application and subsequently authorized in the SW/NPDES Permit No. WV0076244 without having obtained prior approval through a permit modification, in violation of SW/NPDES Permit No. WV0076244 G .l. COUNT VI Failure to Properly Operate and M aintain Facility 59. Plaintiff hereby realleges and incorporates the allegations set forth in paragraphs 1 - 5 8 above as if fully restated herein. 60. Section D.1 of SW/NPDES Permit No. WV0076244, entitled "Proper Operation and Maintenance," states: The permittee shall at all times properly operate and m a in ta in all facilities and systems of treatment and control. . . which are installed or used by the permittee to achieve compliance with the conditions of this permit. 13 EIDO12747 61. On May 1, 1995, upon information and belief, a drain valve for the sediment/leachate pond located at the Dry Run Landfill was opened to lower the level of the pond. \jkThe drain valve remained open until May 3, 1995. From May 1 until May 3, 1^ 6 a result o f Defendant opening the drain valve, an indeterminate amount of untreated leachate was discharged directly into Dry Run. 62. During the May 3, 1995, inspection, the discharge/sediment pond was approximately three (3) feet lower than the pond's normal elevation. This condition resulted from Defendant's failure to correcdy operate such pond. 63. From May 1 to May 3, 1995, Defendant was in violation of SW/NPDES Permit No. WV0076244, D .l, by failing to properly maintain and operate the drain valve on its sediment/leachate pond. COUNT vn Failure to Use a Leachate Liner and Leak Detection System 64. Plaintiff hereby realleges and incorporates the allegations set forth in paragraphs 1 - 6 3 above as if fully restated herein. 65. Solid Waste Management Regulation 47 CSR 38 4.8.3.C.B. (1996), setting forth requirements for surface impoundment, states that surface impoundments, such as the sediment/leachate pond at the Dry Run Landfill: must be constructed with a liner system of a minimum of two (2) liners and a leak detection system. Surface impoundments currently in use that do not have liners and a leak detection system as prescribed in [SWMR] must either be closed or retrofitted to conform to this section within six (6) months following the effective date of this rule. 14 EIDO12748 66. The Defendant has failed to construct a lining for its sediment/leachate pond at the Dry Run Landfill. 67. The surface impoundment used by Defendant to treat leachate has not been closed or retrofitted to properly treat and collect the leachate and does not use a leak detection system. 68. Defendant has violated SWMR, 47 CSR 38 4.8.3.c.B. (1996), by operating the Dry Run Landfill without retrofitting the surface impoundment with a liner system and leak detection system. 69. Upon information and belief, Defendant continues to violate SWMR, 47 CSR 38 4.8.3.C.B. (1996), by operating the Dry Run Landfill without retrofitting the surface impoundment with a liner system and leak detection system. COUNT v m Violations o f Numeric W ater Q uality Standards 70. Plaintiff hereby realleges and incorporates the allegations set forth in paragraphs 1 - 6 9 above as if fully restated herein. 71. Section C.12 of SW/NPDES Permit No. WV0076244, "Water Quality", states: The effluent covered by this permit may not cause a violation of applicable water quality standards adopted by the (Environmental Quality] Board. 72. Section G.8 of SW/NPDES Permit No. WV0076244 requires Defendant to sample Dry Rim approximately one thousand feet (1000 ft.) downstream of Outlet 001 for several water quality standard parameters and submit such results on the "Monthly Stream Sampling Report Form." 15 EID012749 73. The water quality standard for the concentration of total iron in Dry Run established in the Water Quality Standards, 46 CSR 1, App. E., 8.15 (1995), is 1.5 milligrams of iron per 1.0 liter of water (1.5 mg/1). 74. The water quality standard for the concentration of manganese in Dry Run established in the Water Quality Standards, 46 CSR 1, App. E., 8.17 (1995), is 1.0 mg/1. 75. Results submitted by Defendant on its Monthly Stream Sampling Report Forms for May, 1995, July 1995, September 1995, January 1996, and March 1996 showed the stream contained 4.8 mg/1, 1.7 mg/1, 1.9 mg/1, 6.0 mg/1, and 3.7 mg/1 of total iron, respectively - all exceeding the 1.5 mg/1 total iron water quality standard. 76. Results submitted by Defendant on its Monthly Stream Sampling Report Forms for February 1995, April 1995, and July 1995, showed the stream contained 2.5 mg/1, 1.1 mg/1, and 1.9 mg/1 of manganese, respectively - all exceeding the 1.0 mg/1 manganese water quality standard. 77. On at least eight separate occasions, Defendant has violated SW/NPDES Permit No. WV0076244, Section C.12, "Water Quality,'*by exceeding numeric water quality standards. 78. Upon information and belief. Defendant continues to occasionally violate SW/NPDES Permit No. WV0076244, Section C.12, "Water Quality,* by continuing to exceed the numeric water quality standards. COUNT EX Violations o f Discharge Limitations 16 000 EIDO12750 79. Plaintiff hereby realleges and incorporates the allegations set forth in paragraphs 1 - 7 8 above as if fully restated herein. 80. Section E.2.a of SW/NPDES Permit No. WV0Q76244, entitled "Reporting," states: Permittee shall submit each month according to the enclosed format, a Discharge Monitoring Report (DMR) indicating in terms of concentration, and/or quantities, the values of the constituents listed in Part A .l [of the Permit] analytically determined to be in the plant effluent(s). 81. Section A .l of SW/NPDES Permit No. WV0076244, entitled "Discharge Limitations and Monitoring Requirements," establishes a maximum daily discharge limit for total suspended solids ("TSS") as 60 mg/1 for Outlet 001. 82. Section A.1 of SW/NPDES Permit No. WV0076244, entitled "Discharge Limitations and Monitoring Requirements," establishes a maximum daily discharge limit for total iron as 7.0 mg/1 and an average monthly discharge limit for total iron as 3.5 mg/1. 83. Defendant's required Discharge Monitoring Reports ("DMRs") that were sent to DEP for January 1995, May 1995, and July 1995 show the effluent of the Dry Run Landfill contained TSS concentrations of 64 mg/1, 190 mg/1, and 75 mg/1, respectively - all exceeding the maximum daily discharge limit for TSS concentrations set forth in SW/NPDES Permit No. WV0076244 A .l. Copies of the DMRs for 1995 and 1996 are attached hereto as Exhibit 5. 84. The DMRs submitted by Defendant for May 1995 and May 1996 showed the effluent of the Dry Run Landfill contained total iron concentrations of 8.7 mg/1 and 3.6 mg/1, respectively - both exceeding the average monthly discharge limit for total iron concentrations set forth in SW/NPDES Permit No. WV0076244 A .l. See Exhibit 5. 17 009;- EIDO12751 85. Upon at least five separate occasions, Defendant has violated SW/NPDES Permit No. WV0076244, A .l, "Discharge Limitations and Monitoring Requirements," by exceeding the only two discharge limitations that were specifically established in SW/NPDES Permit No. WV0076244. 86. Upon information and belief, Defendant continues to violate SW/NPDES Permit No. WV0076244, A .l, "Discharge Limitations and Monitoring Requirements," by exceeding the only two discharge limitations that were specifically established in SW/NPDES Permit No. WV0076244. COUNT X Duty to Comply 87. Plaintiff hereby realleges and incorporates the allegations set forth in paragraphs 1 - 8 6 above as if fully restated herein. 88. Section C. 1.a of SW/NPDES Permit No. WV0076244, entitled "Duty to Comply" states: The permittee must comply with all conditions of this permit. Permit noncompliance constitutes a violation of the [federal Clean Water Act] and [State WPCA] and is grounds for enforcement action." 89. Issuance of SW/NPDES Permit No. WV0076244 was based, in part, upon information submitted by Defendant with SW/NPDES Application No. WV0076244, as well as information contained in correspondence from Defendant dated August 10, 1987, September 15, 1987, March 1, 1988, April 14,1988, March 16,1989, and May 9,1989. A copy of SW/NPDES Application No. WV0076244, dated August 10, 1987, is attached hereto as Exhibit 6. 18 ooo^i: EIDO12752 Ir 9 0 . In the information submitted by Defendant on August 1 0 , 1 9 8 7 , Defendant stated %that the surface of the Dry Run Landfill would be crowned to provide a 1 to 2 % slope to eliminate ponding on the surface of the landfill and to direct surface water to diversion ditches on either side of the landfill. Sfi Exhibit 6, page 7. 91. In the information submitted by Defendant on August 10, 1987, Defendant stated that compaction would be provided by a dozer operator who would spread the waste material in layers up to two feet thick. Ssfi Exhibit 6, page 7. % 2%92. During the March 21,1995, inspection, Defendant was not providing a 1 to crown to prevent ponding on the surface of the landfill as stated in Defendant's SW/NPDES Application No. WV0076244. 93. During the March 21,1995, inspection, Defendant was not adequately compacting the wastes at Dry Run Landfill, as stated in Defendant's SW/NPDES Application No. WV0076244. 1%94. During the May 3, 1995, inspection. Defendant was not providing a to 2% crown to prevent ponding on the surface of the landfill, as stated in Defendant's SW/NPDES Application No. WV0076244. 95. During the May 3,1995, inspection. Defendant was not adequately compacting the wastes at Dry Run landfill, as stated in Defendant's SW/NPDES Application No. WV0076244. % 2%96. During the August 13,1996, inspection, Defendant was not providing a 1 to crown to prevent ponding on the surface of the landfill, as stated in Defendant's SW/NPDES Application No. WV0076244. 19 000 EID012753 97. .During the August 13, 1996, inspection, Defendant was not adequately compacting the wastes at Dry Run Landfill, as stated in Defendant's SW/NPDES Application No. WV0076244. 98. Upon at least six separate occasions, Defendant has violated SW/NPDES Permit No. WV0076244 C.l, by failing to comply with every condition of the subject permit. 99. Upon information and belief, Defendant continues to violate SW/NPDES Permit No. WV0076244 C.l, by failing to comply with every condition of the subject permit. PRAYER FOR RELIEF WHEREFORE, pursuant to West Virginia Code 5 22-1-6, 22-11-4, 22-11-12, 22-11-15, 22-11-22, 22-15-5, 22-15-10, and 22-15-15, SW/NPDES Permit No. WV0076244 C .l and C.14, and otherwise, Plaintiff, Laidley Eli McCoy, Director, West Virginia Division of Environmental Protection, prays for an Order of Judgment against the Defendant, E. I. DuPont de Nemours & Company, that: 1. Preliminarily and permanently enjoins Defendant at its Dry Run Landfill from violating the Water Pollution Control Act, W. Va. Code 22-11-1 to -28, the regulations promulgated thereunder, the Solid Waste Management Act, W. Va. Code 22-15-1 to -20, the rules and regulations promulgated thereunder, SW/NPDES Permit No. WV0076244, and any and all other environmental laws, rules, or regulations which Defendant might be currently violating; 2. Preliminarily and permanently enjoins the Defendant from placing waste materials at the Dry Run Landfill until such time as the Defendant has installed a properly constructed 20 0 0 0 -a 1 5 E1D012754 landfill and leachate treatment facility, including a a lined impoundment, to prevent the current and future degradation of the waters and soils of the State of West Virginia; 3. Orders Defendant to construct a system of ditches and other permanent mechanical devices to prevent water from running onto the Dry Run Landfill and mixing with the waste deposited therein; 4. Levies a civil penalty not to exceed $10,000 (ten thousand dollars) per day against Defendant, as specifically authorized by the West Virginia Water Pollution Control Act, at W. Va. Code 22-11-22, for each of the Defendant's violations of SW/NPDES Permit No. WV0076244, the West Virginia Water Pollution Control Act, and the accompanying rules and regulations; 5. Levies a civil penalty not to exceed $25,000 (twenty-five thousand dollars) per day against Defendant, as specifically authorized by the West Virginia Solid Waste Management Act, at W. Va. Code 22-15-15(d), for each of the Defendant's violations of SW/NPDES Permit No. WV0076244, the West Virginia Solid Waste Management Act, and the accompanying rules and regulations; 6. Levies a civil penalty not to exceed $10,000 (ten thousand dollars) per day against Defendant, as specifically authorized by SW/NPDES Permit No. WV0076244 C. 14(a), for each of the Defendant's violations of SW/NPDES Permit No. WV0076244, the federal Water Pollution Control Act, the West Virginia Water Pollution Control Act, and the accompanying rules and regulations; LKJ0006I6 21 000 ! EID012755 7. Awards to Plaintiff its costs and disbursements, including reasonable attorneys fees, incurred in this action, as specifically provided by the West Virginia Solid Waste Management Act, at W. Va. Code 22-15-15(g); and 8. Awards such further relief that this Honorable Court deems appropriate. BY COUNSEL: Respectfully submitted, LAIDLEY ELI McCOY, Director, West Virginia Division of Environmental Protection MATTHEW B. CRUM, DEPUTY CHIEF SCOTT D. GOLDMAN, ASSISTANT CHIEF OFFICE OF LEGAL SERVICES WEST VIRGINIA DIVISION OF ENVIRONMENTAL PROTECTION 1356 Hansford Street Charleston, West Virginia 25301 Telephone: 304-558-9160 22 1 EID012756 0 0 0 o i.5 f DRY RUN LANDFILL LEACHATE COLLECTION AND TRANSPORT TO WASHINGTON WORKS (Letter, W. M. Stewart to Barbara S. Taylor, dated 11/8/96) BCC: P. McGee, Legal. D8065-1 In Turn: J. H. Little H. D. Ramsey W. M. Stewart R. W. Meloon / L. K. Ireland R. A. Kirschner In Turn: CTTT. Alt J. J. Mentink R. L. Ritchey G. Woytowich 0. A. Weber hew: 15633-3 OOOri-S E1D010842 DuPont '.YaSwton Works ?.0. Boi 1217 =kerstur7. WV 261C2- " 1? November 8, 1996 CERTIFIED MAIL RETURN RECEIPT REQUESTED Ms. Barbara S. Taylor, Chief Office of Waiter Resources WV Division of Environmental Protection 1201 Greenbrier Street Charleston, WV 25311-1088 RE: Letter, L. E. McCoy to W. M. Stewart, dated October 15, 1996 Dear Ms. Taylor: This letter is to inform you of our plans to collect leachate generated at Dry Run Landfill and transport it to Washington Works for treatment in our bio-oxidation wastewater treatment facility. The interim system described in this letter will be used until design modifications specified in our Dry Run Landfill permit renewal application have been completed and are in operation. Currently, approximately 15 - 20 thousand gallons per day of landfill leachate is collected in a leachate collection system servicing the bottom portion of the active fill area. This system drains through three separate pipe discharges to a surface impoundment (upper pond) for treatment, we propose to route the three existing discharge lines into a six-inch pipe that will gravity drain into an above-ground 50,000 gallon modular collection tank to be located above the upper pond (refer to Attachment 1 for location). Tank dimensions are 38` x 38' x 4'9" and the bolt-together design facilitates assembly at the site. Prior to erecting the tank, the area above of the upper pond will be cleared and prepared. The tank will be set on a one-foot compacted clay sub-base approximately 42' x 42' in size. If necessary, gravel will be used to stabilize the area prior to placement of the clay base. The tank wall panels comprised of 16 gauge galvanized steel will be supported by galvanized 2* x 2" x 1/8" and 2" x 2" x 3/16" steel angle and galvanized tension cables. A 10 mil geotextile material will be placed over the tension cables prior to installing the 20 mil HOPE tank liner. A photograph of a typical modular tank is included as Attachment 2. Stormwater will be routed around the tank into the upper pond. O 9 ;:-.,' EID010843 0 RAK007673 Hs. Barbara S. Taylor, Chief - 2- November 8 , 1996 A 3-HP submersible well pump will be mounted inside the tank to transfer XtLhe 1le_ a c_LhatXe- xthL roughL a__p__p__r__o__x_i_maxt-e1ly ^5A0A0 #f^e_ext _oif it.w_o-incih undaerground plastic pipe to a 5,000 gallon tanker truck located at the top of the hill, just east of the closed asbestos fill area. The well pump will deliver between 50-60 gpm of flow and will take approximately 90 minutes to fill a tank truck. We estimate three to five tankers per day will be transported to Washington Works for treatment primarily during daylight hours. The 50,000 gallon collection tank is sized to provide two feet of freeboard apd will be pumped to its minimum capacity each day to ensure that it will not overfill during the night. The collection tank will be inspected for leaks on a daily basis. An NPDES permit modification request to process the collected leachate through our site wastewater treatment facility will be submitted under separate cover letter. We request written approval to proceed with installation of our proposed interim leachate pumping system so that we may begin leachate collection and transport to Washington Works. If you have any questions or need additional information, please call me on 863-4271. Very truly yours Attachments hew: 15633-2 W. M. Stewart Sr. Environmental Control Consultant Washington Works cc: Ms. Cindy Musser Office of Env. Enforcement Div. of Env. Protection 2311 Ohio Avenue Parkersburg, WV 26101 Michael A. Zeto Water Resources/Waste Management Environmental Enforcement 1356 Hansford Street Charleston, WV 25301-1401 John G. Britvec Office of Water Resources Industrial Waste Section 1304 Goose Run Road Fairmont, WV 26554 OOO EID010844 is LOWER POND UPPER POND $0000 GAL MODULAR CONTAINMENT TANK ON PREPARED SUBBASE 6" COLLECTION PIPE CLOSED ASBESTOS FILL AREA RFi \ / ,------C" J LI _ 5000 GAL TANKER ATTACHMENT 1 Dry Run Landfill Leachate ectlon System 's . RAK007675 EXISTING LEACHATE COLLECTION SYSTEM . Il Attachment 2 : Modular Tank Photograph 000`;Vi GASTON CAPERTON GOVERNOR DIVISION OF ENVIRONMENTAL PROTECTION 10 McJunkin Road Nitro, WV 25143*2506 November 27, 1996 laidley eu m c c o y . Ph.o. d ir e c t o r Mr. H. Oavid Ramsey, Superintendent DuPont Washington Works Post Office Box 1217 Parkersburg, West Virginia 26102 I w mi copy 5 0 no t UMOVS J -'d q 7 .: 3 3 Dear Mr. Ramsey: I was very pleased that ve could reach a settlement in principal on the Dry Run Landfill issue. As soon as I have an opportunity, assuming 1 will, to discuss the small business loan program concept with Governor Underwood's staff, I will draft the body of the proposal. Once that occurs, I will call you and arrange a meeting. As it stands now, the $50,000 SEP (Supplemental Environmental Project) will be available to capitalize the loan program. If we are successful in establishing the program, that will constitute an end to DuPont's commitment. In the event that this loan program should not be adopted, I will contact you to decide how to redirect the Supplemental Environmental Project funding in the manner we have discussed. In this case, I will work with you directly to develop the new SEP, including other funding opportunities from DuPont as per our discussions. I do appreciate your assistance in this matter. Should you have questions, please feel free to call me at 304-759-0515. CT000328 cc: Matthew Crum, Deputy Chief, OLS O 0 0 .;-->5.5 E1D012824 V December 13. 1996 PRC Enwonm*<nal M*n*g*mnt. Inc. 1000 J a t n P Knn*oy BoulvrG Sxth Root PTwladeipfii*. pa 19103 215-972-0444 Fax 215-972-0484 Ms. Sarah Caspar On-Scene Coordinator U.S. Environmental Protection Agency Region 3 841 Chestnut Building Philadelphia, PA 19107 Subject: Field Trip Report Preliminary Assessment Dry Run/N. Fork Lee Creek Bovine Site Washington, Wood County, West Virginia TDD Number 03-9609-0013 Dear Ms. Caspar: PRC Environmental Management, Inc. (PRC), is submitting the enclosed trip report for the Dry Run/N. Fork Lee Creek Bovine site under the Site Assessment Technical Assistance (SATA) contract labor hour pool. Contract Number 68-S5-3002. If you have any questions about this report or need additional information, please contact me at (215) 656-8703. Kevin Scon Project Manager Enclosure cc: Bill Hagel, PRC Cate Brock. PRC SATA Dedicated Team (cover letter only) 000-.' IISFW C15 FIELD TRIP REPORT PRELIMINARY ASSESSMENT DRY RUN/N. FORK LEE CREEK BOVINE SITE WASHINGTON, WOOD COUNTY, WEST VIRGINIA Prepared for: U S. ENVIRONMENTAL PROTECTION AGENCY Region 3 841 Chestnut Building Philadelphia, PA 19107 EPA Region Date Prepared Contract Number TDD Number Prepared by On-Scene Coordinator Telephone Number 3 December 13, 1996 68-S5-3002 03-9609-0013 PRC Environmental Management, Inc. (Kevin Scott) (215) 656-8703 Sarah Caspar (215) 566-3283 0 0 0 : ;.,5,S USFW 015 TABLE OF CONTENTS Section Page 1.0 INTRODUCTION ................................................................................................. 1 2.0 BACKGROUND ................................................................................................................ 1 3.0 SITE ACTIVITIES .............................................................................................................. 1 4.0 DATA EVALUATION .................................................................................................... 11 5.0 CONCLUSIONS AND RECOMMENDATIONS ............................................................. 12 Afififiodix A SITE PHOTOGRAPHS B SAMPLE CHAIN-OF-CUSTODY RECORDS C LANCASTER LABORATORY SAMPLE ANALYSIS REPORT Figure 1 2 FIGURES Page Site Location Map .............................................. 3 Sample Location M a p .............................................................................................. 6 Table 1 2 3 4 TABLES Eagfi Sampling and Analysis Summary............................................................................. 7 Field Measurements ............................................................................................. 11 Summary of Laboratory Analytical Results (Aqueous Samples) ............................. 13 Summary of Laboratory Analytical Results (Sediment Samples)............................. 13 USFW 0151 GOOSES I lJ\N*W I3' Tnp RTT 1.0 INTRODUCTION PRC Environmental Management. Inc. (PRC), was tasked by the U.S. Environmental Protection Agency (EPA) to conduct a preliminary assessment at the Dry Run/N. Fork Lee Creek Bovine site, in Washington, Wood County, West Virginia. The work was conducted under Contract Number 68-S53002, Technical Direction Document Number 03-9609-0013. The purpose of the preliminary assessment was to investigate a citizen's complaint that hazardous materials are present in the surface water and sediments of Dry Run, a tributary of the North Fork of Lee Creek, a tributary to the Ohio River. 2.0 BACKGROUND Mr. Wilber Tennant, the citizen who placed the complaint, claims that contaminants are discharging into Dry Run from a landfill owned by the E. I. DuPont Company (DuPont). Dry Run flows across Mr. Tennant's land before it discharges to the North Fork of Lee Creek. Mr. Tennant raises cattle for beef on his land and his cattle drink from Dry Run. Mr. Tennant alleges that the numerous deaths, blindness, and other illnesses suffered by his herd are directly attributable to the contaminants in Dry Run. He also attributes some of the health-related problems experienced by members of his family to these contaminants. 3.0 SITE ACTIVITIES The following summary describes field activities conducted to investigate Mr. Tennant's allegations. October IS. 1P96 At about 1000 hours, PRC representatives Mr. Kevin Scon and Ms. Alicia Shultz arrived at the West Virginia Department of Natural Resources (WVDNR) in Parkersburg, West Virginia, where they met with Ms.Cynthia Musser, an enforcement officer for the West Virginia Department of Environmental Protection (WVDEP). The PRC personnel reviewed the state's files pertaining to the Dry Run landfill while awaiting the arrival of EPA Region 3 representative, Ms. Sarah Caspar. The Dry Run Landfill, as determined by the file review, is an active industrial solid waste landfill owned and operated by DuPont and the potential source of contamination entering Dry Run. The landfill is used by DuPont to i 000-00 USFW 015 l3Virt*l3\Tn* WH- dispose of waste that DuPont identifies as nonhazardous waste generated at its Washington Works facility located in Washington Bottom, West Virginia. The landfill is located in Washington, West Virginia, about 10 miles south of the Washington Works facility. The approximate location of the Dry Run landfill is shown in the site location map provided as Figure 1. The landfill permit application filed with the WVDEP lists wastes deposited at the landfill as fly ash and bottom ash from the facility's nonhazardous waste incinerator, "biosolids" (filter cake) from the facility's industrial wastewater treatment operation, polyamides, acrylics, polyacetyl, polyvinyl buryral, polyethylene terephthalate, cardboard, and construction debris. While at the WVDNR office, Mr. Scott placed a phone call to Mr. Tennant and arranged a meeting between EPA, PRC, and Mr. Tennant at the Tennant residence. Mr. Scott also contacted Mr. Walt Stewart, environmental manager for the DuPont Washington Works facility, to gain access to the Dry Run landfill. During the conversation between Mr. Scott and Mr. Stewart, Mr. Stewart indicated that DuPont would like to obtain split samples of all samples collected during the site assessment. He also requested a meeting at his office before EPA and PRC conducted the site assessment. EPA representative Ms. Caspar arrived at the WVDNR Parkersburg office at about 1500 hours. After further review of the state files, EPA and PRC personnel departed the WVDNR office and traveled to the Tennant residence in Washington, West Virginia. During the meeting between EPA, PRC, and Mr. Tennant, Mr. Tennant indicated that more than 200 cattle from his herd have died in the past 2 years from unknown health problems. He also said that he observed other dead wildlife in or near Dry Run, including, minnows, frogs, crows, raccoons, and deer. Mr. Tennant attributes the deaths of his cattle and the wildlife to exposure to the contaminants in Dry Run through ingestion and direct contact. While at the Tennant residence, Mr. Tennant showed the EPA and PRC personnel a cow skull that he had saved. Most of the teeth in the skull showed black staining and were easily removed from the jaw bone. According to Mr. Tennant, the discoloration of the cow's teeth was indicative of fluoride contamination. He also indicated that most of the cattle in his herd were or are affected similarly. EPA and PRC personnel traveled with Mr. Tennant and his daughter Amy to Dry Run, near its confluence with the North Fork of Lee Creek. Dead minnows were observed in Dry Run a short distance upstream from the confluence of the two water bodies. An oil-like sheen was also observed on the water when stream sediments were disturbed. A whitish-colored foam also was observed on the USFW 0160 2 IM \N 0*IJ'T np n r r 009;*<?.! USFW 0161 * / *> ' l / /o Y '/tJ n ' '/* > o o o c surface of the water at several locations along Dry Run. PRC took photographs of locations along the run that showed visible signs of contamination. The photographs taken by PRC during the site assessment are included in Attachment A. Mr. Tennant used a video camera to collect additional photographic documentation of stream contamination. PRC observed that the condition of the stream continued to degrade as they moved upstream, closer to the landfill. October 16. 1996 At about 0900 hours, EPA and PRC personnel met with Mr. Stewart at the DuPont Washington Works facility. Also present at the meeting were Mr. Daniel Weber, senior environmental engineer at the facility. Mr.Richard Kirschner, chemist and wastewater treatment plant engineer, and Tom Waldren, supervisor of operations at the Dry Run landfill. During the meeting, EPA and PRC informed the DuPont personnel of the site assessment sampling objectives and schedule. Mr. Steward suggested that EPA and PRC personnel be shown the landfill and leachate ponds in the morning and return after lunch to collect samples. Before traveling to the landfill, EPA and PRC personnel reviewed DuPont's files and analytical data pertaining to the landfill and Dry Run. At about 1100 hours, EPA, PRC. and DuPont personnel departed the Washington Works facility for the landfill. The Dry Run landfill is located off interstate Route 68, about 10 miles south of the DuPont facility. While at the landfill, a tractor trailer load of fly ash was dumped onto the upper lift of the landfill. A heavy equipment operator, operating a bulldozer, spread the fly ash across the lift. The bulldozer operator appeared to be the only worker present at the landfill during our visit. Failure to meet lift height and compaction specifications were noted as permit violations in several of the inspection reports prepared by Ms. Musser for the state. Based on PRC observations during the site visit, the current lift height appeared to be above the 2-foot permit limit. Additionally, the waste material did not appear adequately compacted. A sample of the wastewater treatment plant sludge was not obtained as planned because this material had been covered with fly ash and compacted before EPA and PRC personnel's arrival. Downgradient from the landfill were two leachate collection ponds. A steady stream of leachate was discharging into the upper pond from a single outfall at the foot of the landfill. According to DuPont, the flow rate of the leachate was approximately 20,000 gallons per day, and the outfall accounts for USFW 016 4 m\Nwo*tJ'Tr*nrr nearly all of the flow in Dry Run. An aeration system was in operation in the upper leachate collection pood. The system was powered by a diesel-powered air compressor, located west of the lower leachate collection pond. DuPont indicated that the aeration system is presently alternated between the upper and lower collection ponds. Mr. Weber indicated that DuPont was installing a permanent electrical system for continuous operation of the aeration system. Photographs of the leachate collection ponds and leachate discharge outfalls are included in Appendix A. At about 1245 hours, all personnel broke for lunch. DuPont agreed to meet EPA and PRC personnel back at the landfill at about 1400 hours. After returning to the landfill, PRC personnel prepared to collect a sample of the leachate from the outfall at the foot of the landfill. At about 1500 hours, leachate sample L-l was collected at this location. A sample location map is provided as Figure 2. A sufficient volume of the leachate was collected for multiple analytical parameters, including the target compound list (TCL) of volatile organic compounds (VOC) and semivolatile organic compounds (SVOC); and the target analyte list (TAL) of metals and cyanide; and fluoride, formaldehyde, and sulfate. The sample was collected in containers specific to each of the analytical parameters or laboratory conducting the analysis. Initially, the PRC sampling team had difficulty obtaining a viable sample for the VOC analysis due to a reaction between the leachate and the hydrochloric acid preservative in the sample vials. The reaction produced gas bubbles, which prevented the samplers from obtaining a sample with no headspace (as required by sampling and analytical protocols). The preservative was removed from the sample vials, and a viable sample was obtained. Three separate laboratories were contracted to analyze the samples for the various analytical parameters. Two EPA contract laboratory program (CLP) laboratories. American Analytical and Technical Services. Inc., and TMA/Skinner and Sherman Labs. Inc., were contracted to analyze for the TCL organic compounds and TAL inorganic compounds, respectively. Lancaster Laboratories, a PRC-subcontracted laboratory, was contracted to analyze samples for fluoride, formaldehyde, and sulfate. A summary of the sample collection information is presented in Table 1. In addition to the laboratory-contracted analytical parameters, the leachate samples were screened in the field by PRC for pH, temperature, and dissolved oxygen concentration. Due to an instrument 5 0C \W \ USFW 016 ]W\N**l3'TnpRPT (DRIKAQI) \ nji)r i k s i -:d i ) (IIKGAQI) (MKiiSliDI) o o o LRGENI) DRY RUN Sample Location n> Outfall -------- Stream (n o t t o s c a l e ) USFW 0164 DRY RUN LANDFILL 0 2) Lower Leachate Collection Pond <1*D'-*)(L-I) O D -2)^ "t >( Upper Leachate Collection Pond Dry Ruii/N f o i l I t c Cicck Burine Sue Wuhinalun, Wuuii ( uumy. Wert Vngnm f ig u r e 2 SAMPl.b I OCA IION MAP / U C ENVIRONM ENTAL M A N A G EM EN T INC. TABLE I SAMPLING AND ANALYSIS SUMMARY DRY RUN/N. FORK LEE CREEK BOVINE SITE (Page I of )) 1 li Discharge pipe at foal of landfill LD 1 Nonhern bank of upper leachate collection pond L 2 Lower leachate collection pond discharge pipe I ,x) i m * Leachate 1507; TCL VOCs (Aqueous) 10/16/96 TCL SVOCs. Pesticides, and PCBs TAL Metals TAL Cyanide Fluoride Formaldehyde Sulfate Sediment 1537; TCL VOCs 10/16/96 -Km ) ii .j CLP Protocol (3/90) 3 t 40 ml. VOA vial. HCI to pll < 2. cool to 4 "C CLP Protocol (3/90) 2 x 80 ox., amber glass, cool to 4*C CLP Protocol (3/90) CLP Protocol (3/90) EPA 340 2 Draft EPA 8315 EPA 375 4 CLP Protocol (3/90) 1 x 1 liter, poly bottle, UNO* to pH > 2 1 x 1 liter, poly bottle, NaOH to pH > 12 100 ml, glass, cool to 4 C 40 ml, glass, cool to 4 *C 100 ml. glass, cool to 4 *C 2 x 4 ox, wide-mouth clear glass jar, cool to 4 "C Sediment TCL SVOCs. Pesticides, and PCBs TAL Metals and Cyanide Fluoride Formaldehyde Sulfate 1647, TCL VOCs 10/16/96 CLP Protocol (3/90) 2 x 1 ox. wide-mouth clear glass jar. oool to 4 "C CLP Protocol (3/90) CLP Protocol (3/90) Draft EPA 315 Ion Chromatography CLP Protocol (3/90) 1 x ox, wide-mouth clear glass jar 1 i ox. wide-mouth clear glass jar 1 x 1 ox, wide-mouth clear glass jar 1 x 8 ox, wide-mouth clear gtua jar 3 x 40 ml. VOA vial. H O to pH < 2. cool to 4 *C TCL SVOCs, Pesticides, and PCBs TAL Metals TAL Cyanide Fluoride Formaldehyde Sulfate CLP Protocol (3/90) 2 x 80 ox., amber glass, coot to 4 "C CLP Protocol (3/90) CLP Protocol (3/90) EPA 340.2 Draft EPA 8315 EPA 375.4 1 x 1 liter, poly bottle, HNO, to pH > 2 1 x 1 liter, poly bottle. NaOH to pH >12 100 ml, glass, cool to 4 "C 40 ml. glass, cool to 4 *C 100 ml. glass, cool to 4 *C '" 1 AATSLA AATSLA TMA/Skitmer TMA/Skinner 1anraurr Lancaster Lancaster AATSLA AATSLA TMA Skinner Lancaster Lancaster Lancaster AATSLA AATSLA TMA/Skittncr TMA/Sk inner Lancaster Lancaster Lancaster 7 i9)vN9609i i\Tiip art TABLE I SAMPLING AND ANALYSIS SUMMARY DRY RUN/N. FORK LEE CREEK BOVINE SITE (Page 2 of )) IID , >f'- LD2 D'lKhargc drainage swale downstream of lower leachate collection pond BKGAQI Unnamed tributary of Dry Run. west of leachate collection ponds BKGSEDI Unnamed tributary of Dry Run. west of leachate collection ponds filnutj Sediment SPBBSS'* P m n rw w n 164?. TCL VOCs 10/16/% CLP Protocol (3/90) Surface Water (Aqueous! TCL SVOCs. Pesticides, and PCBs TAL Metals and Cyanide Fluoride Formaldehyde Sulfate 1710; TCL VOCs 10/16/% CLP Protocol (3/90) CLP Protocol (3/90) CLP Protocol (3/90) Draft EPA 8313 Ion Chromatography CLP Protocol (3/90) Sediment TCL SVOCs. Pesticides, and PCBs TAL Metals TAL Cyanide Fluoride Formaldehyde Sulfate 1727; TCL VOCs 10/16/% TCL SVOCs. Pesticides, and PCBs TAL Metals and Cyanide Fluoride Formaldehyde Sulfate CLP Protocol (3/90) CLP Protocol (3/90) CLP Protocol (3/90) EPA 340.2 Draft EPA 8313 EPA 375 4 CLP Protocol (3/90) CLP Protocol (3/90) CLP Protocol (3/90) CLP Protocol (3/90) Draft EPA 8315 Ion chromatography 2 a 4 oi. widc-mouth clear glass jar. cool to 4 C 2 a 8 oi. widemouih clear glass jar, cool to 4* C 1 a 8 o i, widc-mouth clear glass jar 1 a 8 oz, widc-mouth clear glass jar 1 a 8 oz, widc-mouth clear glass jar 1 a 8 oz, widc-mouth clear glass jar 3 a 40 ml, VOA vial. MCI to pH < 2. cool to 4* C 2 a 80 oz, amber glass, cool to 4 *C 1 a 1 liter, poly bottle, UNO, to pit >2 1 a 1 liter, poly battle, NaOH to pH >12 100 ml, glass, cool to 4 *C 40 ml, glass, cool to 4 *C 100 ml, glass, cool to 4 *C 2 a 4 oz, widc-mouth clear glass jar, cool to 4 "C 2 a 8 oz, widc-mouth dear glass jar, cool to 4 C 1 a 8 oz, widc-mouth clear glass jar 1 a 8 oz, wide mouih clear glass jar 1 a 8 oz, wide mouih clear glass jar 1 a 8 oz, widc-mouth clear glass jar AATSLA AATSLA TMA/Sk rner Lancaster Lancaster Lancaster AATSLA AATSLA TMA/Skinner TMA/Sk inner Lancaster Lancaster Lancaster AATSLA AATSLA TMA/Skinocr Lancaster Lancaster lancasicr 8 i*]\NMo*i>vrrtp an TABLE 1 SAMPLING AND ANALYSIS SUMMARY DRY RUN/N. FORK LEE CREEK BOVINE SITE (Page ) of 3) i*'*> < DRIKAQI Dry Run. 1.000 feel downstream of Outlall No 001 d r k sd T Dry Run. 1.000 red dtiwnsiream of Outrai! No 001 'm Surface water (Aqueous) np ml 1807; 10/16/96 TCL VOCs TCL SVOCs, Pesticides, and PCBs TAL Metals TAL Cyanide Fluoride Formaldehyde Sul(ate Sediment 1827; TCL VOCs 10/16/96 CLP Protocol (3/90) 3 a 40 ml, VOA vial, HCI to pH < 2. cool to 4 C CLP Protocol (3/90) CLP Protocol (3/90) CLP Protocol (3/90) EPA 340 2 Draft EPA 8315 EPA 375.4 CLP Protocol (3/90) 2 a 80 or. amber glass, cool to 4* C """ 1 a 1 liter, poly bottle, UNO, to pH >2 1 a 1 liter, poly bottle, NaOH to pH >12 100 ml, glass, cool to 4 "C 40 ml, glass, cool to 4 "C 100 ml, glass, cool to 4 *C 2 x 4 oz, widc-mouth clear glass jar, cool to 4 *C TCL SVOCs. Pesticides, and PCBs CLP Protocol (3/90) 2 a 8 oz, widemouth dear glass jar. cool to 4 "C TAL Metals and Cyanide CLP Protocol (3/90) 1 a 8 oz. widemouth clear glass jar Fluoride CLP Protocol (3/90) 1 a 8 oz, widc-mouth clear glass jar Formaldehyde Draft EPA 8315 1 a 8 oz, widc-mouth dear glass jar m M ti U lM tkm | i Rnr wiriFcmnRh r ln r la iar B AATSLA AATSLA TMA/Skinner TMA/Skinner Lancaster Lancaster Lancastd AATSLA AATSLA TMA/Skinner Lancaster Lancaster m JS ^ Notes: TCL VOC CLP TAL ml rMA/Skinner Target compound list Volatile organic compounds Contract laboratory program Target analyte list Milliliter TMA/Skinner and Sherman Labs, Inc. SVOC VOA Hd C AATSLA Semivolatile organic compounds HNOj Volatile organic analysis NaOII Hydrochloric acid PCB Centigrade oz American Analytical and Technical Services, Inc. Nitric acid Sodium hydroxide Polychlorinated biphenyl Ounce USFW 016 9 !t)\N * 0 9 i)\T fip APT malfunction, however. pH measurements were not obtained. Dissolved oxygen and temperature measurements for the samples were recorded in the logbook and are summarized in Table 2. At about 1540 hours, sediment sample SD-1 was collected from the upper leachate collection bank. A sufficient volume of sample was collected for the same set of analytical parameters as described above. At 1600 hours, PRC personnel collected leachate sample L-2 from the discharge pipe of the lower leachate collection pond. The outfall is a routine sample collection station for DuPont and is identified as No. 001 by a sign staked in the ground near the outfall. From this location, the leachate flows a short distance through an underground culvert and empties into Dry Run. Sediment sample LD-2 was collected in the same vicinity as L-2. Background surface water and sediment samples were collected from a small unnamed tributary of Dry Run, which converged with Dry Run several hundred feet downstream from Outfall No. 001. Aqueous sample BKGAQ1 and sediment sample BKGSED1 were collected at about 1730. Between 1800 and 1830 hours, PRC personnel collected aqueous sample DR1KAQ1 and sediment sample DR1KSED1 from a location along Dry Run about 1,000 feet downstream of Outfall No. 001. This location is a routine sampling station for DuPont. A thick film was observed on the surface of the creek at this location. A violent reaction occurred again in the sample bottle when PRC personnel attempted to collect a water sample for VOC analysis. PRC emptied the preservative from the sample vial and recollected the sample. Aqueous and sediment split samples were again provided to DuPont. TABLE 2 FIELD MEASUREMENTS DRY RUN/N. FORK LEE CREEK BOVINE SITE L-l 17.7 80 L-2 16.2 73 BKGAQ1 18.7 62 DR1KAQ1 15.7 80 10 USFW 0168 m \N 0IJ\Tnp W T DuPont personnel were provided with split samples for each of the locations sampled by PRC. At about 1830 hours, all personnel departed the site. PRC personnel returned to the hotel to complete the sample paperwork. All samples were logged onto laboratory-appropriate chain-of-custody (COC) records, identified with sample-specific sample tags, and placed into coolers in preparation for shipment to the appropriate laboratory. Copies of the EPA organic and the inorganic traffic report and COC records are provided in Appendix B. October 17.1996 . -i . - At about 0900 hours, EPA and P ^uoonnel returned Works facility to meet with Mr-Stewart. ' l^ spar updfttedMn !te w it .ro^e_**iij^5ig activities conducted the previous day. Ms. Shuto rignflg jftgjymplajgdflOC rcconH&e split samples, officially relinquishing the samples to DuPont. andmifclflOO hours7EPA aad PRC.personnel departed the ^ _ft w. ... Washington Works facility and traveled to the WVDNR office in Petersburg, West Virginia, to gather additional information about the site. Ms. Musser was unavailable, and the EPA and PRC personnel departed shortly after their arrival. PRC personnel completed sample shipment preparations and traveled to the local Federal Express office to ship the samples. At about 1230 hours, PRC personnel departed Parkersburg, West Virginia to return to Philadelphia, Pennsylvania. 4.0 DATA EVALUATION Table 3 summarizes fluoride, formaldehyde, and sulfate analytical data from samples collected during the site assessment. The results of analyses of the samples were compared with EPA numeric removal action levels (RAL) for contaminated drinking-water sites, EPA Region 3 risk-based concentrations (RBC) for up water (developed by Roy Smith, EPA toxicologist), and background sample concentrations. No concentrations of fluoride, formaldehyde, or sulfate exceeded either of the EPA action limits or guidelines. Fluoride was observed at concentrations above background in both of the leachate samples and in the downsteam sample. Fluoride was detected at concentrations of 220 and 160 micrograms per liter (ug/L) in leachate samples L-l and L-2, respectively, and at a concentration of 130 ug/L in sample DR1AQ1. Fluoride was not detected in the background sample (BKGAQ1). The highest concentration of sulfate (34,500 ug/L) was detected in the background sample. 11 0 0 0 > .-10 USFW 0169 TABLE 3 SUMMARY OF LABORATORY ANALYTICAL RESULTS (AQUEOUS SAMPLES) DRY RUN/N. FORK LEE CREEK BOVINE SITE T Notes: ID Identification NA Not Applicable ug/L Micrograms per liter Table 4 presents a summary of fluoride, formaldehyde, and sulfate analytical data from samples of the sediment collected during the site assessment. The results of analyses of the samples were compared with EPA Region 3 RBCs for fish and to background sample concentrations. Fluoride was detected at concentrations of 396 and 411 milligrams per kilogram (mg/kg) in sediment samples LD-1 and LD-2, respectively; 335 mg/kg in the downstream sediment sample (DR1KSED1); and 198 mg/kg in the background sample (BKGSED1). The fluoride concentrations in these samples are significantly above the EPA guidance level of 81 mg/kg. Fluoride concentrations that exceeded EPA limits are shaded in Table 4. Appendix C provides die Lancaster Laboratories Sample Analysis Report for the aqueous and sediment samples. The analytical results for the samples submined to the CLP laboratories are not included in this evaluation. Upon receipt and evaluation of the remaining sample analytical data, PRC will prepare and submit to EPA an addendum to this trip report. USFW 0170 12 ooo;-.-.i a I93VW*0I J'T np HPT TABLE 4 SUMMARY OF LABORATORY ANALYTICAL RESULTS (SEDIMENT SAMPLES) DRY RUN/N. FORK LEE CREEK BOVINE SITE Notes: Sediment simple analytical raadfts are presented as dry weight results. Fluoride coocengarions that exceed EPA criteria are~shaded. ID Idendficadoo 7 -* --N Noocarcinogemceffects ' NA Not applicable mg/kg Milligrams perkilogram % by wt Percent by weight % 5.0 RECOMMENDATIONS ^ - J -<SL *" Based on the limited sample analytical data available to PRC at the present time, PRC recommends that an in-depth evaluation of the CLP analytical data be conducted before conducting further sampling at the site. If the evaluation of the CLP data shows that additional sampling is warranted, PRC will make this recommendation to the EPA. USFW 0171 13 IM\NWO*IJ'Tr**rr 000-:--'.u V 69 GASTON CAPERTON GOVERNOR DIVISION OF ENVIRONMENTAL PROTECTION 1356 Hansford Street l a id l e v e l i m c c o y . PhD Charleston, W V 25301-1401 d ir e c t o r ORDER ISSUED UNDER THE WATER POLLUTION CONTROL ACT WEST VIRGINIA CODE, CHAPTER 22, ARTICLE 11 and THE SOLID WASTE MANAGEMENT ACT WEST VIRGINIA CODE, CHAPTER 22, ARTICLE 15 ORDER NO. 3850 DATE: December 31, 1996 RECEIVED JAN 2 9 1997 SreaRESCjaCES TO: Mr. H. David Ramsey, Jr. E. I. Du Pont de Nemours and Company Washington Works Post Office Box 1217 Parkersburg, West Virginia 26102-1217 Attention: Mr. Ramsey, Jr. This order is issued by the Director of the West Virginia Division of Environmental Protection (or "WVDEP"), through his authorized representatives, under the authority of the West Virginia Code, as amended (hereinafter, the "Code"), Chapter 22, Article 11 and Chapter 22, Article 15 to E. I. Dupont de Nemours and Company (hereinafter "Dupont"). FINDINGS OF FACT As a result a result of inspections conducted at Dupont's Dry Run Landfill and the Washington Works facility by authorized representatives of the Director and in support of this Order, the Director of the West Virginia Division of Environmental Protection hereby finds the following: Office of Legal Services Telephone: (304) 558-9160 Fax: (304) 558-4255 OC*0 Page 2 H. David Ramsey, Jr. E. I. Dupont de Nemours and Company December 31, 1996 A. Dupont is a person as defined in Chapter 22, Article 11, Section 3 of the Code and Chapter 22, Article 15, Section 2. Dupont is a corporation duly authorized to conduct business in the State of West Virginia; and owns and operates a facility ("Washington Works") in Wood County, West Virginia. Dupont also owns and operates a non-hazardous waste landfill ("Dry Run Landfill"), also in Wood County, West Virginia, which serves the Washington Works facility. B. Dupont is authorized to operate the Dry Run Landfill under Solid Waste/West Virginia National Pollutant Discharge Elimination System ("SW/WVNPDES") Permit No. WV 0076244. The permit authorizes Dupont to discharge a specified amount and type of pollutant into Dry Run, a tributary of the North Fork of Lee Creek, which is a tributary of the Ohio River. Dupont also holds a WVNPDES Permit No. WV001279 for the Washington Works facility, which allows the facility to discharge a specified amount and type of pollutant into the Ohio River. C. Authorized representatives of the Director conducted an inspection of the Dry Run Landfill on March 23, 1995, May 3, 1995 and August 13, 1996 and noted a discolored leachate flowing from the landfill into Dry Run. D. Authorized representatives of the Director conducted an inspection of the Ohio River in the vicinity of the Washington Works facility on August 20, 1996. The inspectors noted solids of wax and polymeric materials of the type manufactured at the Washington Works facility in the Ohio River and its banks. E. Authorized representatives of the Director inspected the Dry Run Landfill on May 16, 1994, March 23, 1995 and August 13, 1996 and noted the absence of a leachate collection system. Inspectors also noted an absence of diversion ditches during the May 16 and March 23 inspections. F. Subsequent to the inspection, Dupont constructed two diversion ditches above the landfill to prevent run-on from flowing across the landfill. Dupont incorporated designs for a leachate collection system into the permit application for renewal of the permit for the landfill. G. Authorized representatives of the Director inspected the compaction procedures used at the landfill on May 3 and August 13, 1996 and noted that the wastes were being compacted in layers exceeding two feet in depth. H. Dupont notified the WVDEP in September 1994 of a change in the ratio of wastes being disposed at the landfill. Such wastes were disposed of at the landfill through September 1996. Office of Legal Services Telephone: (304) 558-9160 Fax: (304) 558-4255 0K Page 3 H. David Ramsey, Jr. E. I. Dupont de Nemours and Company December 31, 1996 I. Representatives of the Director have noted that the surface impoundment at the landfill does not use a leak detection system or a liner. Dupont incorporated designs for leak detection and liner systems into the permit application for renewal of the permit for the landfill. J. Authorized representatives of the Director inspected the leachate pond located near the landfill on May 3, 1995 and noted that the water level was approximately three (3) feet below normal elevation. Dupont had opened a drain value in preparation for treatment of the pond. K. Water quality standards were exceeded at Dry Run Landfill and permit discharge limits were exceeded for Total Suspended Solids, manganese, and iron as reported on Dupont's Monthly Discharge Monitoring Reports. L. Authorized representatives of the Director inspected the landfill on March 21, 1995, May 3, 1995 and August 13, 1996 and noted that a 1-2% crown was not; provided to prevent ponding on the surface of the landfill. REQUIREMENTS OF ORDER Now, in accordance with Chapter 22, Article 15, Section 15 and Chapter 22, Article 11, Section 15 of the Code, it is hereby agreed between the parties and ordered by the Director as follows: In settlement of all issues in the Findings of Fact, Dupont agrees to the following: 1. Immediately upon the effective date of this Order, Dupont shall cease disposal of filter cake from the Washington Works wastewater treatment system at the Dry Run Landfill. Dupont will refrain from future disposal of such filter cake at the Dry Run Landfill until such time as the installation and operation of all improvements to the landfill as required under the SW/WVNPDES Permit to be issued by the WVDEP for the subject landfill are completed. 2. Immediately upon the effective date of this Order, Dupont shall collect the leachate generated at the Dry Run Landfill and transport it for treatment to the Washington Works wastewater treatment facility upon approval of WVDEP of the necessary permit modifications of the Washington Works WVNPDES permit to allow such treatment. Dupont will continue to collect such leachate and transport it to the Washington Works water treatment facility until the installation and operation of all improvements to the landfill as Office of Legal Services Telephone: (304) 558-9160 Fax: (304) 558-4255 OOO-.-v Page 4 H. David Ramsey, Jr. E. I. Dupont de Nemours and Company December 31, 1996 required under the SW/WVNPDES Permits to be issued by the WVDEP for the subject landfill are completed. 3. Immediately upon the effective date of this Order, Dupont shall perform such maintenance on the diversion ditches currently in place at the Dry Run Landfill as necessary for controlled flow of surface water through such ditches and away from the active face of the landfill. 4. Within thirty (30) days of the effective date of this order, Dupont will send via certified mail or shall hand deliver to the office of Environmental Enforcement for deposit in the Water Quality Management Fund a check of two-hundred thousand dollars ($200,000) payable to "West Virginia Division of Environmental Protection. " 5. Dupont will perform a supplemental environmental project ("SEP") to accrue to the benefit of the environment but which shall not be directed towards facilitating Dupont's compliance with statutory or regulatory requirements. Dupont will make a contribution of fifty thousand dollars ($50,000) to an escrow account to be held for the agency responsible for developing and/or implementing a loan program designed to facilitate environmental compliance by small business. If by May 1, 1997 such a loan program has not been developed, the fifty thousand dollars ($50,000) held in escrow will be returned to Dupont and an alternative SEP shall be developed between the parties, which shall be valued at not less than fifty-thousand dollars ($50,000). In the event that the parties fail to negotiate a mutually acceptable SEP by July 1, 1997, Dupont will send via certified mail or will hand deliver to the office of Environmental Enforcement for deposit in the Water Quality Management Fund a check for fifty-thousand dollars ($50,000) payable to "West Virginia Division of Environmental Protection." GENERAL PROVISIONS 1. WVDEP reserves all rights and defenses which they may have pursuant to any legal authority, as well as the right to raise as a basis for supporting such legal authority or defenses, facts other than those enumerated in the Findings of Fact. 2. Dupont hereby waives its right to appeal this order under the provisions of Chapter 22, Article 15, Section 15 and Chapter 22, Article 11, Section 21 of the Code. Under this Order, Dupont agrees to undertake all actions required by the terms and conditions of this Order and consent to and will not contest the jurisdiction of the Director regarding this Order. However, Dupont does not admit any factual or legal determinations made in this Order and reserves all rights and defenses available regarding liability and Office of Legal Services Telephone: (304) 558-9160 Fax: (304) 558-4255 0 0 0 ^ / Page 5 H. David Ramsey, Jr. E. I. Dupont de Nemours and Company December 31, 1996 responsibility in any proceedings regarding these facilities other than proceedings, either administrative or civil, to enforce this Order. 3. This Order becomes effective on the date indicated and shall terminate upon notification from the Agency that Dupont has satisfactorily completed all tasks set forth in the requirements of the Order. n J . Z i IQ l ___________ Effective Date Name / /I West Virginia Division of Environmental Protection E. II Dupont de Nemours and Company Title P lant S u perintend ent Title Office of Legal Services Telephone: (304) 558-9160 Fax: (304) 558-4255 0 0 Or, \ s  p Q z t t 3 $ S O E. I . DU PONT DE NEMOURS AND COMPANY FINANCE - VENOOR PAYMENT J q& ~ Q u J b tf, A fr n J t MHILMINGTON OELAXARE 1 9 6 9 8 <>2-20 SU CHECK NUMBER amount ^ 12/1 52892530 $****200,000.00 STATE OF WEST VIRGINIA DEPT OF ENVIRONMENTAL PROT 10 MC GUNK IN RO NITRO WV 251A3 HOT V A U D AFTER 90 DAYS TO; citibank oelamaac Swocldlary Clttear Qna Pfn*% w*v n w Ciitl. QC 1*720 II* 5 2 a *9 a S 3QII* :o 3 i too ao a?aa5?7f B A t f r Thing for 8 t H > r Living from Ou Pont PAY TO THE ORDER OF E . I . DU PONT DE NEMOURS AND COMPANY FINANCE - VENDOR PAYMENT MXLMXNCTON, DELAHORE 1 9 8 9 8 62-20 SU DATE 12/16/96 CHECK HUMBER 52892531 AMOUNT $***50 ,000.00 STATE OF WEST VIRGINIA DEPT OF ENVIRONMENTAL PROT 10 MC GUNKIN R0 NITRO WV 25143 MOT VAiXO AFTER 90 DAYS TO; eiTIBAMl OtLAHARC A Swacld*.rv %* Ctictr On* A*n*i n 8 C'la H 19129 g g ^ " 5 g a i 2 s a i* >: a i i o o 2 0 su a a 7 3 3 5 7 7' Thiwgt for 6#ttr livtwg . . . f r o m D u Pour 5 * 000-A * ') 70 QGQr. 0 INTEROFFICE MEMORANDUM rO: Distribution List Date: From: Dept: Tel No: 03-Jan-1997 0 4 :20pm RONALD W MELOON MELOONRW EP P&S 304-863-4753 Subject: Leachate to the BioPond Early this afternoon we successfully brought our first full load sf leachate from Dry Run back to the new dewatering facility. All pumps, equipment and logistics worked well. At this point we intend to continue handling leachate over the weekend. EID029946 ooocs 71 / DuPont Haskell Laboratory January 9, 1997 HAZARD CHARACTERIZATION FOR HUMAN HEALTH C8 EXPOSURE CAS REGISTRY NO. 3825-26-1 Prepared by: L. B. Biegel, Ph.D. Senior Research Toxicologist MAB000010 1 O0< EED080808 h a z a r d c h a r a c t e r iz a t io n f o r HUM AN HEALTH C8 e x p o s u r e CAS REGISTRY NO. 3825-26-1 Table of Contents INTRODUCTION.............................................................................................................. 3 I. MAMMALIAN TOXICOLOGY................................................................................... 3 1.1. Acute Toxicity Studies............................................................................................. 3 1.1.a. Acute Oral Toxicity............................................................................................ 3 1.1. b. Acute Dermal Toxicity................................................................................... 5 1.1. c. Acute Ocular Toxicity..................................................................................... 5 1.1.d. Acute Inhalation Toxicity.................................................................................. 6 1.1. e. Acute Injection Toxicity................................................................................. 7 1.2. Subchronic Toxicity Studies.................................................................................... 7 1.2. a. Subchronic Oral Toxicity...............................................-............................... 7 1.2. b. Subchronic Inhalation Toxicity..................................................................... 10 1.2. c. Subchronic Dermal Toxicity......................................................................... 10 1.3. Developmental Toxicity......................................................................................... 11 1.4. Reproductive Toxicity............................................................................................ 13 1.5. Mutagenicity........................................................................................................... 13 1.6. Chronic Toxicity and Oncogenicity....................................................................... 13 II. METABOLISM.......................................................................................................... 15 11.1. Animal Studies...................................................................................................... 15 11.2. Human Exposure................................................................................................... 19 III. MECHANISMS OF ACTION................................................................................ 20 III. 1. Investigation of C8s' Effect on the Liver......................................................... 20 111.2. Investigation of C8s' Effect on Testicular Leydig Cells.................................... 21 111.3. Investigation of C8s' Effect on the Pancreas....................................................... 22 IV. CLINICAL REPORTS OF HUMAN EXPOSURE............................................... 22 V. EPIDEMIOLOGY......................................................................................................23 VI. DISCUSSION OF ENDPOINTS............................................................................... 23 VI. I. Discussion of Target Organs............................................................................... 23 VI.2. Discussion of Differences in Species-Specific Sensitivities............................... 24 VT.3. Tumors Associated with C8 in the Rat................................................................ 24 VI.3.a. Significance of C8-Induced Rodent Tumor to Human Risk......................... 24 VII. SUMMARY.............................................................................................................25 REFERENCES.................................................................................................................27 2 EID080809 GOOLc HAZARD CHARACTERIZATION FOR HUM AN HEALTH C8 EXPOSURE CAS REGISTRY NO. 3825-26-1 INTRODUCTION This document is a Hazard Characterization of C8 for human health. C8 is also known as ammonium perfluorooctanoate (AFPO; CAS # 3825-26-1) and is the primary ingredient in FC-143 FLUORAD Brand Fluorochemical Surfactant. Within this document the chemical will be referred to as C8. However, it is acknowledged that many of the studies discussed actually tested the product FC143, which is a mixture of several straight-chain perfluorocarboxylic acids containing approximately 93.0-97.0% C8. I. MAMMALIAN TOXICOLOGY 1.1. Acute Toxicity Studies I.l.a. Acute Oral Toxicity Numerous acute oral toxicity studies, in several species (rats, mice, guinea pigs, dogs), have been conducted with C8 (see Table 1-1). The results of the various studies have been consistent in their results. Administration of a single dose of 12 mg/kg to 3 rats produced no clinical signs of toxicity. Studies demonstrate that newborn and older adult rats appear to be more sensitive than weanlings and young adults. Additionally, while mice and rats appear to be equally sensitive to the acute toxicity of C8, guinea pigs are more sensitive than mice or rats. In the rat, acute oral exposure generally results in enlarged livers, elevations of liver enzyme levels, gastrointestinal irritation, and weight loss. C8 is considered to have moderate acute oral toxicity. In addition to the numerous studies listed below, several other studies were conducted which investigated the effects of C8 alone or on animals pre-exposed to other chemicals or drugs. Pre-treatment of rats with phnobarbital sodium or proadifen hydrochloride does not result in an alteration of the LDso of C8 (478 mg/kg). Pre or post dosing with Dowex 1-X2-C1 Ion Exchange Resin at 1000 mg/kg reduced the mortality compared to rats dosed with C8 alone. A study was conducted to determine if pretreatment with ethanol (a single dose of 60% or a 15% aqueous solution (v/v) in drinking water for 14 days) modifies the effects of C8 on liver weight. This study determined that pre-treatment with ethanol did not alter C8's effect on liver to body weight ratios. 3 . 000 r3 EID080810 HAZARD CHARACTERIZATION FOR HUMAN HEALTH C8 EXPOSURE CAS REGISTRY NO. 3825-26-1 Table I-1 SUMMARY OF ACUTE ORAL TOXICITY STUDIES WITH C8 Study Type ALD ALD Species Rat (tii M/sex/d ose 10 Male 1 Male Dose (mg/kg) 200,480,670 .5, IMd,lib.Yob,30o,4d,7d. iddd. 1500.2250 Vehicle Comoil Water Results mg/kg 480 616 Reference HL-565-81 HL-55-61 AL'6 Rat 1 Mate 1, f.5.2.3,34,5.1.26,40.#5, 11,90.12, 130.170,200,300,450,670,2250 Water 670 Hl-i28-68 LD Lt)w flat 5 Rat .................... 6 dd,'2'5,464, iddd,2f5d 20b,4bd, 43d, d, 670, rood Acctonc(49%) Com oil (60%) Com oil Males: 680 Females: 430 Males: 470 Females: 482 (Griffith and Long, 1980) llL-295-81 LD as a function Rat of age 10 Weanling males 10 Weanling females 10 Young adult females 10 Mature adult males 10 Mature adult females 10 Newborn males 10 Newborn females 350,400,450,525,670,710 350,400,450,670 350,425,500,670 200,240,300,350,400,500,720 225,350,400,450,670 130,200,240,280,330,370 130,180,200,220,240,280,320 Com oil HL-788-82 573 580 453 336 343 243 258 LOmcastrated vs. intact adults Rat 10 intact males 10 intact females 10orehidectomized males 10ovariectomized females 200,480,670 200,480,670 200,480,670 200,480,670 Com oil HL-600-81 439 491 459 400 LB Rat 10 males 4, 5C0,650 Comoil 478 HL-567-81 ...... lb ......... Rat ' Li* Mice id '250,500,166, Iddd, 2. 4000 Com oil 3*5 Hazleton Laboratoiy America, Inc. 2-6-87 457 IIL-329-81 ...... d m ...... ' Dog function 3Males 450,200 Not stated Lethal at 450 mg/kg by 48 hours Elevated GPT and GOT which normalized within 1week at 200 mg/kg Ht;i3-65 LD Guinea Pig Id i5d, 2,250,300.4(5(5,67d Gomoil Males: 178 Females: 217 a). Weanling = 21-days old b). Young adult = 8-10 weeks old c). Mature adult = >10 weeks old d). Newborn = < 2 days old HL-29I-8I EID080811 eiooooavw 4 HUMANH A Z A R D C H A R A C TE R IZA TIO N FOR HEALTH C8 EXPOSURE CAS REGISTRY NO. 3825-26-1 I.l.b. Acute Dermal Toxicity Acute dermal toxicity and irritation studies in rats and rabbits have been conducted with C8. C8 is considered to be mild - moderately irritating to the skin and moderately toxic by the dermal route of exposure. Rat skin showed less irritation than rabbit and in general the effects were more pronounced in males than in females. In addition to dermal irritation several clinical signs of toxicity were observed in both rats and rabbits in response to C8 exposure. These observations included body weight loss, wet and/or stained perineal area, cyanosis (rabbits only), diarrhea (rabbits only), lethargy (rabbits only), labored breathing (rabbits only), and chromodacryorrhea (rats at 7500 mg/kg) Table 1-2 SUMMARY OF ACUTE DERMAL TOXICITY/IRRITATION STUDIES WITH C8 Study Type LD30 Species Rat Skin Absorption Rat LD #/sex/dose 5 5 Females Dose (mg/kg) 3000,5000, 7500 5000 and 7500 Results Male LDjos 6959 mg/kg Female LD = >7500 mg/kg LDjo>7500 mg/kg Mild skin irritation Reference HL-659-79 (Kennedy, 1985) HL-682-80 Skin Absorption LD Rat 5 Females 5000 and 7500 LD5o>7500 mg/kg Mild skin irritation HL-682-80 LD Rabbit 5 Males 1500,3000, (2 at 7500) 5000, 7500 LDjo* 4278 mg/kg HL-659-79 (Kennedy, 1985) Rabbit 4 100, 1000,2000 Lethal 4/4 at 2000 3/4 at 1000 0/4 at 100 Riker Laboratories Report No. 09790AB0485 Skin Irritation Rabbit 6 500 mg on intact and abraded sites Non-irritating (Griffith and Long, 1980) Skin Irritation Rabbit 6 Males 500 mg Mild-moderate irritation at 24 hours Slight-moderate irritation at 48 hours HL-636-79 MAB000014 I.l.c. Acute Ocular Toxicity Eye irritation studies in rabbits have been conducted with C8. C8 is considered to be moderately irritating to the eye. Instillation of solid C8 into rabbit eyes produced moderate comeal opacity, iritis, and conjunctivitis. These ocular effects gradually receded over time. Prompt washing of the eye reduced the effects and provided a more rapid recovery. In addition to the eye irritation studies that have been conducted, rats 5 0 0 0 ,- k-' - EID080812 HAZARD CHARACTERIZATION FOR H UM AN HEALTH C8 EXPOSURE CAS REGISTRY NO. 3825-26-1 exposed to C8.during a 4-hour inhalation period exhibited comeal opacity and ulceration, which were microscopically evident 42 days post-exposure. Species Rabbit Rabbit Table 1-3 SUMMARY OF EYE IRRITATION STUDIES WITH C8 #/sex/dose 2 (1 unwashed, 1 washed) 6 unwashed 6 washed Dose Results (mg) 38.3 Unwashed eye Moderate-severe comeal opacity Moderate iritis Moderate conjunctivitis At 21-28 days Comeal opacity Mild vascularization Washed eye Slight-moderate corneal opacity Slight-moderate conjunctivitis At 7 days Mild conjunctival redness At 14 days Normal *100 Unwashed eye Moderate irritation Conjunctivitis Iritis Washed eye Conjunctivitis At 7 days 4/6 eyes were free of irritation Reference HL-635-79 Biosearch, Inc. Report No. T1395 (Griffith and Long, 1980) 1.1 .d. Acute Inhalation Toxicity Acute inhalation toxicity studies in rats have been conducted with C8. Acute exposure to C8 by inhalation is considered to be highly toxic, with a 4-hour approximate lethal concentration (ALC) in rats of 0.8 mg/L. At concentrations of 2.2 mg/L C8 and higher, all rats died within 48 hours of exposure. At concentrations between 0.38 and 0.83 mg/L C8, rats experienced an initial weight loss following exposure and an increased liver-to-body weight ratio which returned to the high end of the normal range 42 days post-exposure. Additionally, all rats exposed to 0.81 mg/L C8 and higher showed comeal opacity and corrosion. 6 pp U L* EID080813 Species Rat Rat HAZARD CHARACTERIZATION FOR H UM AN HEALTH C8 EXPOSURE CAS REGISTRY NO. 3825-26-1 Table M SUMMARY OF ACUTE INHALATION STUDIES WITH C8 #/sex/dose 6 Males Concentration (mg/L) 4-hour exposure to: 0.38,0.81,0.83,2.2,4.8,5.7 Results Reference 4-hour ALC = 0.8 mg/L H L -160-69 LC = 0.98 mg/L (Kennedy, et al., 1986) 5 1-hour exposure to:18.6 mg/L No deaths (Griffith and Long, Eye and respiratory 1980) irritation 1.1 .e. Acute Injection Toxicity Acute toxicity o f C8 when administered by intraperitoneal injection was assessed in mice (3M, 1979). The LD50 by intraperitoneal injection in mice is 192 mg/kg. 1.2. Subchronic Toxicity Studies 1.2.a. Subchronic Oral Toxicity Numerous subchronic oral toxicity studies in several species (rats, mice, and monkeys), have been conducted with C8 (see Table 1-5). The results o f the various studies have been quite consistent in their results. Administration of C8 in the diet or by daily gastric intubation produced death at concentrations of 1000 ppm and higher for rats and mice and at 30 mg/kg/day for monkeys. The primary target organ for toxic responses in all species studied is the liver. C8 produces increased liver weights, increased liver enzyme activity, hepatocellular hypertrophy, and hepatic peroxisome proliferation. In addition to the numerous studies listed below, other studies were conducted which investigated the mechanism o f action o f C8. These studies are summarized in Section III. Mechanisms of Action. 7 00 */ i EID080814 HAZARD CHARACTERIZATION FOR HUMAN HEALTH C8 EXPOSURE CAS REGISTRY NO. 3825-26-1 Study Type 14-day feeding Species Mice 14-day feeding Mice 21-day feeding Mice 14-day feeding Mice 9-dose gavage Mice Rat 14-day feeding with a 2-week recovery period 14-day feeding With a 56 day recovery period Rat Rat Tabic 1-5 SUMMARY OF SUBCHRONIC ORAL TOXICITY STUDIES WITH C8 #/sex/dose 5 Concentration (ppm unless specified) 10,30, 100,300, 1000,3000,10000 Results 100% mortality at >3000; deaths at 1000; increased liver weight/body weight ratio at >10 Reference HL 560-81 5 30, 300,3000 100% mortality at 3000; deaths at 300; weight loss at HL12-82 > 300 increased liver weight/body weight ratios at > 30 (Kennedy, 1987) 5 6,0.01,0.03,6.1,0.3, 1,3,10,30 Significantly increased liver weight at 30 HL 323-82 (Kennedy, 1987) 5 30 Increased liver weight; HL 537-82 when C8 was combined with an equal amount of nonadecafluorodecanoic acid, a similar effect was produced 5 0.1, 1.0,10 mg/kg Weight loss, death in 10mg/kg females, increased liver HL 138-83 weight at 1and 10mg/kg 5 0.1, 1.0,10 mg/kg Weight loss, increased liver weight in 10mg/kg males 6 Males 5 Males 25% Teflon with C8 as the dispersing agent 30,300 Slightly increased liver weights following the recovery period Decreased body weights at 300; increased liver weights at theend of thefeeding period at 30 and 300 and on recovery days 7 and 28 (300 ppm only; elevated blood fluoride levels out to recovery day 7 (final day tested) HL 56-61 HL 326-95 EID080815 looooevw 8 HAZARD CHARACTERIZATION FOR HUM AN HEALTH C8 EXPOSURE CAS REGISTRY NO. 3825-26-1 Study Type Species 28-day feeding Rat Mice 90-day feeding Rat 90-day gavage Monkey 90-day feeding with an 8-week recoveiy period Rat Table 1-5(Con't) SUMMARY OF SUBCHRONIC ORAL TOXICITY STUDIES WITH C8 Sex (#/sex/dose) 5 Concentration (ppm unless specified) 30,100,300, 1000,3000, 10000, 30000 Results 100% mortality at >3000; decreased body weights at> 1000 and 3000 for females; increased liver weight/body weight ratios at > 30 for males and > 300 for females Reference (Griffith and Long, 1980) 5 30, 100,300, 1000,3000, 10000, 100% mortality at > 1000; deaths at > 30; decreased body 30000 weights at > 30; cyanosis and muscle weakness at > 3000; increased liver weight/body weight ratios at > 30; panlobular diffuse hypertrophy of hepatocytcs 5 10, 30, 100,300,1000 Decreased body weights at > 300; increased liver weights at > 300; panlobular diffuse hypertrophy o f hepatocytcs at > 1000 with males more affected than females; serum fluoride concentration increased 75 to 226 fold with higher concentrations observed in males 2 3, 10,30, 100mg/kg/day 100% mortality at > 100; deaths at > 30 (females only); decreased body weights at > 30; no signs of toxicity at 3 mg/kg/day; dose dependent increases in serum and liver fluorine levels (no apparent sex difference) 55 Males 1,10,30, 100 Reduced body weigh at 100; increased palmitoyl CoA oxidase activity at > 30 and transient increases at 10; palmitoyl CoA oxidase activity returned to normal after the 8 weeks of recovery; increased liver weights and hepatocellular hypertrophy at > 10which was reversible following therecovery period. Serum estradiol, testosteroneand lutienizing hormone levels werenot affected by dietary exposure to C8, while estradiol levels were slightly elevated at 100ppm at week 5. The NOAEL = 100ppm; theNOEL = 1ppm (Perkins, 1992) EID080816 8I0000HVW 9 H A Z A R D C H A R A C TE R IZa T iI'. FO R H U M A N H E A L T H C8 E X P O SU R E CAS REGISTRY NO. 3825-26-1 I.2.b. Subchronic Inhalation Toxicity Similar to the oral toxicity studies, inhalation exposure to C8 produces reduced body weight, increased liver weights, increases in plasma enzymes indicative of liver injury, and pathological lesions in the liver. Measurement of the blood fluoride levels (indicative of the presence of C8) determined that the blood half-life of C8 in the rat is 57 days following inhalation exposure. Table 1-6 SUMMARY OF SUBCHRONIC INHALATION TOXICITY STUDIES WITH C8 IN THE RAT Study Type 10 exposure with a 42-day recovery Sex (#/sex/dose) 20 Concentration 11, 83 mg/m1 for 6 hours/day Results (mg/kg) Dose related decrease in body weight, suppression of body weight m ain tain ed during the 42-day recovery period at 83; increased plasma enzymes indicative of liver injury present up to 28 days following the last exposure; granular degeneration of hepatocytes; increased liver weights, no ocular effects were observed. The liver effects were not observed after 14,32, or 42 days of recovery. Reference HL 253-79 10 exposure 24 I, 8, 84 mg/m3 Deaths at 84; increased lung, liver and testes HL 205-81 with an 84- for 6 hours/day weights, no ocular effects observed; increased (Kennedy, Hall et al., day recovery plasma enzymes indicative of liver injury; 1986) increased liver weights at > 8 mg/m3;panlobular and centrilobular hepatocellular hypertrophy and necrosis. The liver effects were reversible following a 28- dav recovery period. Dose related presence of C8 in theblood, which decreased with time during the recovery period but was still detectable after 84 days of recovery. NOAEL " 1mg/m5,, although 13ppm organofluoride was detected immediately following exposure to 1mg/m3 MAB000019 I.2.C. Subchronic Dermal Toxicity The subchronic dermal toxicity of C8 has been studied in the rat and rabbit (see Table 1-7). Similar to the oral toxicity studies, dermal exposure to C8 produces reduced body weight, increased liver weights, increases in plasma enzymes indicative of liver injury and lesions in the liver. Measurement of blood fluoride levels (indicative of the presence of C8) determined that the blood half-life o f C8 in the rat is 5-7 days following dermal exposure. A comparison o f the dermal exposure studies to the feeding studies leads to the conclusion that the rates of absorption of C8 by these two routes are not significantly different. io EED080817 HAZARD CHARACTERIZATION FOR H UM AN HEALTH C8 EXPOSURE CAS REGISTRY NO. 3825-26-1 Table 1-6 SUMMARY OF SUBCHRONIC INHALATION TOXICITY STUDIES WITH C8 IN THE RAT Study Type 10 dose with an 84 day recovery Species (#/sex/dose) 15 Male Rats Concentration (mg/kg) 20,200,2000 for 6 hours/day, 5 days/week Results (mg/kg) Skin irritation at > 200; reversible reduction in body weight at > 200; increased plasma enzymes indicative of liver injury; increased liver weights at > 20; hepatocellular hypertrophy and necrosis at 20 ; no ocular effects observed The liver effects were generally reversible following a 42-day recovery period at < 200. Dose related presence of C8 in the blood, which decreased with time during the recovery period but was still detectable after 42 days of recovery. Reference HL 589-80 (Kennedy, 1985) Range-finder 10 exposure with a 14 day recovery 4 Rabbits (sex not specified) 10 Rabbits 100, 1000, 2000 Lethal to 4 of4 at 2000,3 of 4 at 1000, 0 of 4 at 100 100 for 6 hours/day, 5 days/week Reversible reduction in body weight; Blood fluorine levels were 5.4,6.8,4.6 ppm for males and 10.1,12.1, and 3.5 for females at 7, 14, and 28 days of the study, respectively. Riker Laboratories, Report 09790AB0485, March 15,1981 1.3. Developmental Toxicity Developmental toxicity studies have been conducted in rats and rabbits (See Table 1-7). The original developmental toxicity study in rats indicated that C8 might be a teratogen in rats. However, because the results were questionable, additional studies were conducted to clarify the result. The additional studies did not confirm the original result. Overall, C8 is not considered to be uniquely hazardous to the conceptus. The two areas o f question were apparent lens abnormalities and skeletal alterations. In the original study, the lens alterations consisted of the following: large lA V*lens cleft, dark streak running to of the way through the lens; or disorganized lens fibers. In the subsequent studies, the lens alterations were determined to be an artifact created in the lens during freehand sectioning. Processing Bouin's-fixed fetal heads that were trimmed on either side of the orbit, instead of through the center o f the eye, essentially eliminated this artifact Examination of the eyes o f offspring using focal illumination, indirect ophthalmoscopy, and slitlamp microscopy were also used and did not detect any C8-related eye alterations. The skeletal alterations included ossification sites on the first lumbar vertebrae in rats and 13 ribs in rabbits. Both o f these alterations are considered to represent stress-related changes indirectly related to C8-administration. MAB000020 ll EID080818 HAZARD CHARACTERIZETION FOR HUM AN HEALTH C8 EXPOSURE CAS REGISTRY NO. 3825-26-1 Table 1-7 SUMMARY OF DEVELOPMENTAI7REPRODUCTTVE TOXICITY STUDIES WITH C8* Species (#/dose) Rats (# not specified) Concentration 25,50, 75, 100, 150 mg/kg by gavage Results mg/kg Reduced maternal body weight gain and clinical signs of toxicity at 150; eye abnormalities at 25 and 150 Reference 3M Report M-601 (1981) 25 Rats* 100 mg/kg by gavage Maternal deaths, decreased maternal body weight gain; no developmental toxicity or abnormalities observed. HL 1-82 (Staples, et al., 1984) 12 Rats' 100 mg/kg by gavage Maternal deaths, decreased maternal body weight gain; no alterations in postpartum viability, growth rate, or development. No ocular effects observed. Rats 0.05, 1.5,50, 150 mg/kg (# not specified) by gavage Maternal deaths at 150; C8 was not embryotoxic, no abnormal gross findings, no malformations'1. Fetal lens findings were observed in all groups. Determined to be a processing artifact No effect on ovaries, reproductive tract, male/female ratio, implantation sites, corpora lutea, or fetal weights. 3M Report 0681TR0110, 1981 Rats O'.14,1.2,9.9, 2'i mg/m1 Maternal deaths at 21; overt maternal HL 881-81 by inhalation toxicity at 9.9; No teratogenic effects were (Staples, et al., observed in any of die exposed groups; 1984) embryo-fetal toxicity was observed at 21; processing artifacts were observed on lens'. 18 Rabbits 1.5, 5,50 mg/kg by gavage Reduced maternal body weight gain at 50, C8 was not embryotoxic or teratogenic' 3M Product Toxicity Sheet, May 24,1996 a. Pregnant rats were dosed by gavage on days 6-15 of pregnancy. Pregnant rabbits were dosed by gavage on days 6-18 of pregnancy. b. Sacrificed on Day 21 of gestation. c. Pups sacrificed on day 35 postpartum. d. A significantly higher incidence of the skeletal finding "one stemabrae missing", occurred in the high- dose group. This was a minor skeletal aberration and was not considered a malformation in this study. Furthermore, the incidence of this finding did not differ from the control group or the 3 lower-level treatment groups. The incidences of skeletal findings associated with delayed ossification and rib aberrations were not different among the treatment groups and controls. e. There was a statistically significant increase in the incidence of 13 ribs in the high dose group and 13 ribs spurred in the mid-dose group. While the findings are significantly greater in the treated animals than in the controls, they are not considered to be teratogenic changes or malformations, rather they are considered to represent stress-related changes to compound administration. MAB000021 12 G0 0 ;a' EID080819 HAZARD CHARACTERIZATION FOR H UM AN HEALTH C8 EXPOSURE CAS REGISTRY NO. 3825-26-1 1.4. Reproductive Toxicity No information is available on the reproductive toxicity of C8 1.5. Mutagenicity It has been demonstrated that C8 is not mutagenic in a variety of mutagenicity tests (See Table 1-9). Study Type Table 1-9 SUMMARY OF MUTAGENICITY STUDIES WITH C8 IN THE RAT Study Description Results Reference Mutagenicity assay Assayed in S. Typhimurium (TA1535, TA1537, TA1538, and TA100) and S. cerevisiae D4 yeast, with and without metabolic activation. Negative Litton Bionetics; LBI Project 20838, Feb. 1,1978 (Griffith and Long, 1980) In vivo mouse micronucleus 3 mice/sex were dosed with 200,400, 600,800, and 1000 mg/kg and bone marrow was evaluated at 24,48 and 72 hours after dosing. Negative Corning Hazleton, 17388-0-455, May 16, 1996 Chromosomal aberration Assayed for ability to induce chromosomal aberrations in CHO cells with and without metabolic activation. Negative Coming Hazleton, 17388-0-437, April 25,1996 M a m m a lia n cell transformation assay Assayed for cell transformation potential LD = 50 g/mL; low cytotoxicity and cytotoxicity in C3H 10T1/2 colony No evidence of cell transformation cells. University of Minnesota Environ. Path Lab, T2942, April 9, 1981 1.6. Chronic Toxicity and Oncogenicity The chronic toxicity and oncogenicity o f C8 has been investigated in two 2-year feeding studies in rats (see Table I-10). MAB000022 13 s EID080820 HAZARD CHARACTERIZATION FOR H UM AN HEALTH C8 EXPOSURE CAS REGISTk i N u . ^825-26-1 Table I-10 SUMMARY OF CHRONIC TOXICITY AND ONCOGENICITY STUDIES WITH C8 IN RATS #/sex/dose Concentration (mean daily intake, mg/kg/day) Results Reference 50 0, 30, 300 ppm (0, 1.5, and 15 rnglcg/day) Decreased body weight gain and food consumption, increased ataxia. Decreased REC counts, hemoglobin, and hematocrit values. Increased liver weights, liver cell hypertrophy, degeneration and necrosis. Not considered to be carcinogenic. Riker Laboratory 0281CR001 (April 1981-May 1983) 156 Males 0, 0-pair-fed, 300 ppm Decreased body weight gain and food consumption. Increased estradiol levels. Increased incidence of liver, Leydig cell and pancreatic acinar cell adenomas. (Cook, et al., 1994) DuPont MR-5686 In the original study, in-life findings consisted o f a dose dependent decrease in mean body weight gain and increase in food consumption in males, and a slight treatment-related increase in the incidence of ataxia in females. No increase in mortality was observed. C8-related hematologic alteration included decreased red blood cell counts, hemoglobin and hematocrit values observed at various times throughout the 2year test period. However, the decreases in erythrocyte counts were observed early in the study and did not progress into generalized anemia. Histopathologically, C8-associated alterations were observed in the liver. These changes were characterized by increased liver weights, hypertrophy, hepatocellular degeneration, and necrosis. As with the erythrocyte counts, the hepatic alterations were observed early in the study and showed little progression over the remainder o f the 2-year study. The incidence o f tumors was relatively low, and the types o f neoplasms found were not different from the tumor profiles commonly observed in geriatric rats. Hepatocellular tumors were slightly increased in the 300 ppm males, however, not to the extent that would be expected considering the morphological evidence of hepatocellular stimulation observed at the 1year necropsy. The incidence of testicular Leydig cell adenomas (0/50,3/50, and 7/50 at 0, 30, and 300 ppm, respectively) was suggestive of a compound-related effect. However, because the incidence was within the historical control range, it was not considered to be a compound-related effect. Based on the tumor incidence, types of tumors, time o f tumor appearance, and the survival rate at the 2 year time point, the overall conclusion was that C8 was not carcinogenic in the rat (Riker Laboratory, 0281CR0012). However, in this original study, some of the pathological findings were equivocal (liver and Leydig cell tumors), even when evaluated by an outside laboratory, and therefore a second 2-year study was conducted to clarify some of these findings. The second study included many mechanistic endpoints to help determine the mechanism o f tumor formation (DuPont MR-5686, Cook, et al., 1994). In addition to the adlibitumcontrol, a second control was pair-fed to the C8 group. Peroxisome proliferation (B-oxidation activity) and cell proliferation (BrdU, 6-day osmotic pumps) MAB000023 14 EID080821 O0O;-h' g HAZARD CHARACTERIZATION FOR HUMAN HEALTH C8 EXPOSURE CAS REGISTRY NO 382*-'6-1 were measured in the liver and testis. Serum hormone levels (testosterone, estradiol, lutienizing hormone (LH), follicle stimulating hormone (FSH) and prolactin) were also measured. Interim sacrifices were performed at 3-month intervals as well as at 1 month. Increased relative liver weights were observed in the C8-treated rats. Hepatic B-oxidation activity was also increased in the C8-treated rats at all time points. In contrast, hepatic cell proliferation was not significantly increased in the C8-treated group. C8 did not significantly alter the rate of Lcydig cell B-oxidation or Leydig cell proliferation. Moreover, the rate of B-oxidation in Leydig cells was approximately 20-times less than the rate of hepatic B-oxidation, irrespective of treatment. Serum testosterone, FSH, prolactin, and LH levels were unchanged in the C8-treated rats when compared to the controls. There were, however, significant increases in serum estradiol levels in the e s treated rats at 1,3,6, 9,12,15,18 and 21 months. Histopathological evaluation revealed compound-related increases in liver, Leydig cell, and pancreatic acinar cell tumors in C8treated rats. Based on the data, the Leydig cell tumors appear to be due to the combination of elevated estradiol levels and reduced prolactin levels. The pancreatic acinar cell tumors are related to an increase in serum cholecystokinin (CCK) levels. II. METABOLISM Numerous studies have been conducted investigating the excretion and disposition o f C8 in various species. Additionally, studies have been conducted with exposed workers at a manufacturing plant which produces C8. Sex and species differences have been noted, whereas reproductive status in females did not have an effect on excretion or disposition in rats. Rabbits (both sexes), female rats, and male hamsters rapidly excrete C8, while male rats and female hamsters excrete C8 more slowly. Mice (both sexes) excrete C8 even more slowly. C8 also has a long '/2-life in humans. Measurement of C8 blood levels in an exposed worker showed that the '/-life in men is greater than 1.5 years. II.l. Animal Studies The excretion and disposition of C8 has been investigated in rats, mice, hamsters and rabbits. Studies have also investigated the influence of route of exposure. These studies are summarized below. II. 1.a. Male and female rats were administered radiolabeled C8 by intravenous injection. Females excreted essentially 100% of the administered dose by 24 hours, while males had excreted only 20% of the administered dose. Radioactive tissue residues were not detectable after 17 days in the females, while at 36 days males had 2.8% o f the UC in the liver, 1.1%in the plasma and lower but detectable levels in other organs (Riker Laboratory drug Metabolism Report 1-20 (1980)). II. 1.b. Sex differences in the excretion and disposition of radiolabeled C8 were observed in a study of rats, mice, ham sters, and rabbits. Male and female animals o f each species were dosed by gavage with 10 mg/kg C8, and urine and feces were collected at 24,48, 72, 96, and 120 hours post-dosing. Animals were then sacrificed, and blood and 15 . 0v'} EID080822 HAZARD CHARACTERIZATION FOR H UM AN HEALTH C8 EXPOSURE tissues were analyzed. The urine and feces of rabbits was also collected at 144 and 168 hours post-dosing, and rabbits were sacrificed at 168 hours. The female rat and male hamster had excreted over 99% of the administered dose at the time of sacrifice. The male rat and the female hamster had excreted 39 and 60% of the administered dose, respectively, at the time o f sacrifice. Both sexes of rabbits excreted the C8 as rapidly and completely as the female rat and male hamster. The male and female mice retained substantial amounts of the total administered radioactivity in their tissues at the time of sacrifice, only excreting 21% o f the administered dose at 120 hours post-dosing (HL 62-82) 11.1. c. Cholestyramine, a non-absorbable anion-exchange resin, was demonstrated to protect rats from the acute lethal effect of C8 when administered within 2 hours of C8 dosing (HL 828-81). A second study was conducted to investigate the effect of cholestyramine on the elimination of l4C-C8 (10 mg/kg by gavage) from rats and mice (HL 405-82). Adult male rats and mice were given cholestyramine (1000 mg/kg by gavage) 24 hours after dosing with 14C-C8. The cholestyramine did not enhance the elimination of C8 via the feces, urine, or exhaled air. Similarly, Dowex Ion Exchange Resin was also able to reduce the acute lethal effect of C8. When rats and mice were given Dowex resin 24 hours after dosing with C8 no signs of enhanced elimination of C8, via the feces, urine or exhaled air, were observed (HL 405-82). To further investigate the use of cholestyramine to enhance C8 elimination, a third study was conducted in rats. In this study, rats were dosed with l4C-C8 (13.3 mg/kg, by iv.) and then were fed diets containing 4% cholestyramine for 14 days. The cholestyramine increased the elimination of C8 via the feces by 9.8 fold and decreased the concentration of C8 found in the liver, plasma, and red blood cells (Johnson, et al., 1984). 11.1. d. A series of experiments was conducted to evaluate the uptake and clearance of C8 from the blood of male and female (pregnant and non-pregnant) rats following oral exposure, and inhalation exposure. The uptake and clearance of C8 from the blood o f female rats following a single oral dose was rapid, with peak reached 1-2 hours post-treatment and virtual total clearance by 24 hours. A dose-response was demonstrated with no apparent changes in blood C8 levels following multiple oral dosing. The slower clearance rate in male rats was demonstrated following a single oral dose. The same general statements apply following inhalation exposure. A single 6-hour inhalation exposure resulted in: peak blood levels within 1 hour after cessation o f exposure; the material rapidly cleared from the blood; the number o f exposures did not affect blood levels; and male rats cleared the compound much more slowly. Pregnant and non-pregnant rats showed similar C8 blood 16 C-*. c.i EID080823 H il.**!? T'.P.IZA- I O * r ? R H U M A N H E A L T H C 8 E X P O SU R E CAS REGISTRY NO. 3825-26-1 levels following either oral or inhalation exposure (HL 593-91). Specifics of the experiments are summarized below. II.l.e.1. Oral administration-Blood levels of C8 as a function of time post-dosing (female rats) C8 levels of 14 ppm were seen 15 minutes following administration of C8. These levels peaked at 30 ppm at 1-2 hours, dropped to 26 ppm by 8 hours, and to 0.7 and 0.045 ppm at 24 and 168 hours, respectively. C8 is absorbed and rapidly cleared from the blood of female rats given a single oral dose. II. 1.e.2. Oral administration-Blood levels of C8 as a function of dose (female rats) C8 levels 30 minutes following administration of 2.5 - 150 mg/kg ranged from 3 -162 ppm. The same dose response was observed at 24 hours with blood levels ranging from 0.12 -18 ppm. The response was linear. The level of C8 in the blood is directly related to the amount of C8 administered. II. 1.e.3. Oral administration-Blood levels of C8 as a function of number of doses (female rats) Blood levels in female rats given 1 versus 11 doses of C8 were not considerably different. Concentrations at 15 minutes following administration were 14 and 17 ppm for 1 and 11 doses, respectively. At 30 minutes C8 concentrations were 16 and 25 ppm; at 8 hours 26 and 13 ppm; at 24 hours, 0.7 and 0.8 ppm; and at 168 hours, 0.045 and 0.10 ppm for 1 and 11 doses, respectively. C8 does not appear to accumulate in the blood of female rats following repeated oral administration. The number o f treatments does not appear to influence the C8 blood level. II.l.e.4. Oral administration-Blood levels of C8 following a single 25 mg/kg dose (male and female rats) Time following single oral dose (hours) A 8 24 168 Blood Levels of C8 (ppm) Male Rats Female Rats 23 16 63 26 50 0.7 23 0.045 C8 is retained in the blood of male rats to a greater extent than female rats. II.l.e.5. Inhalation exposure-Blood levels o f C8 as a function o f time post-exposure (female rats) C8 levels o f 96 ppm were observed 15 minutes following a single 6-hour exposure to 10 mg C8/m . The level was m a in ta in e d through 1 hour, fell to approximately 70 ppm at 8 hours, 52 ppm at 24 hours, and dropped to 0.39 ppm at 168 17 EID080824 O O O .-.c 9 L. CHARACTERIZATION FOR H U M A N HEALTH C8 EXPOSURE CAS REGISTRY NO. 3825-26-1 hours post-exposure. This same general pattern was observed in rats exposed to either 0.1 or 1mg/m3. The lag phase seen following oral exposure was not observed here due to blood sampling following a 6-hour inhalation exposure (rather than a single dose at a given time). C8 is absorbed and rapidly cleared from the blood of female rats following a single inhalation exposure. II. 1.e.6. Inhalation exposure -Blood levels of C8 as a function of dose (female rats) Time following single inhalation exposure dose (hours) A 2 8 24 Blood Levels of C8 (ppm) Following exposure to C8 at 0.1 mg/m1 1 m g/m 1 27 2 17 0.85 4 0.14 0.56 10 mg/mJ 109 69 71 52 The response is linear at 30 minutes. C8 blood levels are directly related to the amount of C8 inhaled. At the high concentration used, the clearance rate is somewhat slower than observed at the lower levels. This suggests massive overloads in the clearance system. II. 1.e.7. Inhalation exposure -Blood levels o f C8 following a single 6 hour exposure to 10 mg/m3(male and female rats) Time following single oral dose (hours) '/i 2 8 24 Blood Levels of C8 (ppm) Male Rats Female Rats 137 109 157 69 182 71 147 52 C8 is retained in the blood of male rats to a greater extent than female rats following inhalation exposure. II.l.e.8. Oral administration-Blood levels of C8 following a single 25 mg/kg (pregnant and non-pregnant female rats) Time following single oral dose (hours) Vi 2 8 Blood Levels of C8 (ppm) Pregnant Rats Non-pregnant Rats 16 10 33 39 26 31 C8 clearance following oral dosing is similar in pregnant and non-pregnant female rats. MAB000027 18 OOOiv.-'O EID080825 H A Z A R D C H A P A C 1"?RIZATION FO R H U M A N H E A L T H C8 E X P O S U R E CAS REGISTRY NO. 3825-26-1 II.ie.9. Oral and Inhalation exposure -Blood levels of C8 as a function of number of exposure concentration (pregnant female rats) Time following single oral dose of 25 mg/kg (hours) A 2 8 24 Blood Levels of C8 (ppm) Following 1exposure 6 exposures 10 exposures 18 12 12 39 37 15 31 nd* 11 2 nd 1 Time following single inhalation exposure to 10 mg/m3 (hours) A 2 a. nd = not done Blood Levels of C8 (ppm) Following 1 exposure 10 exposures 77 53 90 nd When comparing the C8 levels seen at 2 and 8 hours, following 10 consecutive oral doses, there appears to be a lowering of the C8 blood levels. Blood levels following 1 or 10 consecutive inhalation exposures (6 hours/day) were not different. C8 does not appear to accumulate in the blood of pregnant rats following repeated oral or inhalation exposures. Ill.f. The ability o f UC-C8 to transfer through the placenta was investigated in rats (HL 61-82). A single dose of 10 mg/kg UC-C8 was administered to pregnant rats on the 19thday of pregnancy. Maternal blood and placental levels o f UC-C8 increased between 2 and 4 hours post-dosing, and decreased between 4 and 8 hours post-dosing. Time following single oral dose of 10 mg/kg (hours) 2 4 8 Levels of C8 Maternal (fig equivalents/mL blood) 12 20 12 Fetal (fig equivalents/mL tissue) 0.7 3 3 n.2. Human Exposure Determinations of organic fluorine blood levels in workers exposed to C8 in an industrial environment were performed. Approximately 90% o f the organic fluorine was composed o f the C8 anion. The highest levels were found in workers with the longest work history in fluorochemical production. The majority o f the values remained at lAapproximately the same level throughout the 2 year monitoring period. Monitoring of C8 blood levels o f a worker who was removed from the fluorochemical production site due to high C8 blood levels (70 ppm) suggests that fluorochemicals are very slowly 19 EID080826 HAZARD CHARACTERIZATION FOR H UM AN HEALTH C8 EXPOSURE 1S JL .V J LkJ a I V NO. 3825-26-1 eliminated. From this limited data it is hypothesized that the `/2-life of C8 is 1.5 years in men (Ubel, et al., 1980). Group Normal human sera Industrial controls Laboratory personnel (>20 years exposure) Plant workers Number analyzed from published literature 4 8 49 Blood Organic Fluorine Levels (ppm) 0.01-0.13 0.01-0.08 0.04-2.00 1.00-71.00 III. MECHANISMS OF ACTION C8 is not metabolized in rats. C8 produces hepatomegaly, induces hepatic peroxisomes in mice and rats, and has been shown to produce hepatic, Leydig cell, and pancreatic acinar tumors in a 2-year feeding study in rats. The male rat is more susceptible to the toxic effects of C8 than the female rat, presumably due to the longer Vilife in males. Short-term studies have been conducted investigating the mechanisms of action responsible for the various effects. III. 1. Investigation of C8s' Effect on the Liver. III. 1.a. Because C8 had been shown to induce a striking hepatomegaly in rats, a study was conducted to investigate the hepatic biochemical and morphological changes associated with C8-induced hepatomegaly in rats (Pastoor, et al., 1987). In this study male rats were dosed daily for 1,3, or 7 days with 50 mg C8/kg body weight by intragastric intubation. The total cytochrome P450 content and activity o f benzphetamine Ar-demethylase was increased in the livers of C8-treated rats, indicating the proliferation of smooth endoplasmic reticulum. In contrast, the soluble, cytoplasmic enzymes, glutathione 5-transferase and UDP-glucuronyltransferase, were unaffected. Carnitine acetyltransferase activity was disproportionately increased relative to carnitine palmitoyl transferase activity, confirming the predominant proliferation o f peroxisomes versus mitochondria. Electron microscopy confirmed the proliferative response o f the endoplasmic reticulum, peroxisomes, and microsomes in the livers of the C8-treated rats. This study also demonstrated that C8 does not possess hypolipidemic activity. m.l.b. C8 increased serum estradiol concentrations in 2-week gavage studies, and feeding studies at various time points up to 2 years. This was accompanied by increases in liver weights, and hepatic P-oxidation activity (Cook, et al., 1992; Cook, et al., 1994). Since peroxisome proliferators induce both p-oxidation activity and cytochrome P450 enzymes, an investigation was conducted to determine if C8 increases serum estradiol levels by stimulating aromatase activity (Liu, et al., 1996a). Fourteen days o f treatment with up to 40 mg C8/kg/day produced dose-dependent increases in liver weights, serum estradiol, and hepatic aromatase activity. A significant linear correlation Invitrowas established between estradiol and hepatic aromatase activity. experiments using cultured hepatocytes suggest that the increase in serum estradiol is at least partly 20 ooo; EID080827 HAZARD CHARACTERIZATION FOR H UM AN HEALTH C8 EXPOSURE r -,c R F ^ rsT F .y N C . 3825-26-1 due to a direct effect on the liver to increase synthesis of estradiol through induction of aromatase cytochrome P450 in the endoplasmic reticulum. III.2. Investigation of C8s' Effect on Testicular Leydig Cells Because C8 produced an increased incidence of testicular Leydig cell tumors in a 2-year feeding study in rats, and because C8 was negative in short-term tests for genotoxicity, a non-genotoxic (hormonal-mediated) mechanism for tumor formation was investigated. The studies summarized below support a hormonally-mediated mechanism of Leydig cell tumorigenesis: C8 produces an increase in hepatic aromatase activity, which elevates serum estradiol concentrations, which in turn modulates growth factors in the testis, which results in tumor formation. 111.2. a. Fourteen days of treatment with up to 50 mg C8/kg/day produced dose- dependent increases in hepatic p-oxidation activity, and serum concentrations of estradiol, and decreases in serum testosterone concentrations, body weights, and relative accessory sex organ weights in male rats (Cook, et al., 1992). Challenge experiments, using human chorionic gonadotropin (hCG), gondaotropin-releasing hormone (GnrH), or naloxone challenges, suggest that the decrease in testosterone may be due to a lesion at the level of the testes, due to a decrease in the conversion of 17a-hydroxyprogesterone to androstenedione. m.2.b. Using invitro, invivoand ex vivo studies, C8 was examined for its ability invitroto directly affect Leydig cells using isolated Leydig cells from untreated rats, and ex vivo using Leydig cells isolated from C8-treated rats. Additionally, the ability o f C8 to affect testicular interstitial fluid hormone levels and induce aromatase activity was invitroinvestigated (Biegel, et al., 1995). The studies demonstrated that C8 directly inhibits testosterone production, while the ex vivo studies demonstrated that this invivoinhibition is reversible. In the study, serum and testicular interstitial fluid estradiol were increased and testicular interstitial fluid transforming growth factor a were increased. Additionally, hepatic aromatase activity was increased while aromatase activity levels were not affected in the testis, muscle, or fat These data suggest that the increases in estradiol levels are primarily due to increases in aromatase activity. 111.2. C. Previous studies with C8 showed a direct effect on Leydig cells to alter steriodogenesis. It was therefore proposed that peroxisome proliferators, in general, may directly affect Leydig cell function to produce Leydig cell tumors. A study investigating whether several peroxisome proliferators (including C8), directly affect Leydig cell invitrofunction was conducted. This study showed that peroxisome proliferators, as a class of compounds, directly modify the steroidogenic function of Leydig cells invitro. invitroThis also suggests that compounds which directly affect Leydig cell function may also induce Leydig cell tumors invivo(Liu, et al., 1996b). 21 EID080828 GO o:v H A Z A R D CH.A.o*rTERIZATTOW r OR JIviAN H E A L T i l CS E X P O S U R E CAS REGISTRY NO. 3825-26-1 III. 3. Investigation of C8s' Effect on the Pancreas Several peroxisome proliferators have been shown to produce pancreatic acinar incell hyperplasia/adenocarcinomas in 2-year feeding studies, including C8. Therefore, vitroand invivoinvestigations of C8's (invitroonly) and Wyeth-14, 643's (a model peroxisome proliferator) mechanism of tumorigenesis in the pancreas were conducted. These mechanisms include cholecystokinin receptor agonism (CCKa ) trypsin inhibition, alterations in gut fat content, cholestasis and altered bile flow/composition. All of these mechanisms enhance pancreatic growth either by binding to the CCKa receptor or by increasing plasma CCK levels. C8 did not bind directly to the CCKa receptor and it Invivofailed to inhibit trypsin, a common mechanism for increasing plasma CCK levels. studies with Wyeth-14,643 suggest that these peroxisome proliferators produce pancreatic tumors by cholestasis, which may be responsible for the decrease in bile acid output which contributes to the increase in plasma CCK levels. Therefore, for Wyeth-14, 643 (and perhaps C8), the pancreatic tumors may be secondary to hepatic cholestasis (Oboum, et al., 1997). IV. CLINICAL REPORTS OF HUMAN EXPOSURE IV. 1.a. Health screening examinations were offered to employees o f a 3M plant that produced C8, as well as other fluorochemicals. No health problems related to exposure were encountered among those examined. Additionally, no relationship was observed between deviations from normal laboratory test results and blood levels of organic fluorine (the liver enzyme SGGT was the most frequently encountered test result exceeding the normal range. C8 exposure levels ranged from 0.03 to 7.6 mg/m3 (Ubel, et al., 1980). IV.l.b. A study was made of Washington Works employees potentially exposed to C8. Results o f blood chemistry testing (SGOT, LDH, AP, and bilirubin) indicated no conclusive evidence of an occupationally related health problem among workers exposed to C8 (Fayerweather, 1981). IV. 1.c. Although C8 is the major organofluorine compound found in humans, little information is available concerning human responses to C8 exposure. Therefore, a study was conducted among 115 workers exposed to C8 occupationally (serum fluorine levels varied between 0 and 26 ppm, with a mean of 3.3). In an examination o f the crosssectional associations between C8 and hepatic enzymes, lipoproteins, and cholesterol, there was no significant clinical hepatic toxicity o f the C8 levels observed in this study (Gilliland and Mandel, 1996). Serum C8 levels were positively associated with estradiol and negatively associated with free testosterone and not associated with luteinizing hormone. The negative association between testosterone and C8 was stronger in older men. Thyroid stimulating hormone and C8 were positively associated. Prolactin and C8 were positively associated in moderate drinkers. The effect of adiposity on serum glutamyl oxaloacetic acid and glutamyl pyruvic transaminase decreased as C8 increased. The induction o f gamma glutamyl transferase by alcohol was decreased as C8 increased. The effect of alcohol on HDL was reduced as C8 increased. A positive association 22 EID080829 2?. ClK A 1A S T - C tL A P J .C T E K Z A T IC r,: HUJ.LAN H E A L T H E X PO SU R E CAS REGISTRY NO. 3825-26-1 between hemoglobin, mean cellular volume, and leukocyte counts with C8 was observed. These results suggest that C8 affects male reproductive hormones and that the liver is not a significant site of toxicity in humans at the C8 levels observed in this study. However, C8 appears to modify hepatic and immune responses to xenobiotics (Gilliland and Mandel, 1993). V. EPIDEMIOLOGY V. 1.a. A retrospective cohort mortality study was made o f employees at a 3M plant where C8 and other fluorocompounds are manufactured. Records on 4218 employees were reviewed. Only those who worked for 6 months or more (3688 workers) were included in the mortality follow-up. Of the 180 known deaths, 177 death certificates were obtained. Overall the number of deaths was significantly less than expected. The observed-to-expected ratio for cancer deaths was 1.0 (Ubel, et al., 1980). V. Lb. In a retrospective cohort mortality study, a relationship between mortality and employment at a plant where C8 and other fluorocompounds are manufactured were investigated (Gilliland and Mandel, 1993). The cohort consisted of 2788 male and 749 female workers employed between 1947 and 1983. The all-causes standardized mortality rate (SMR) was 0.75 for males and 0.77 for females. There was no significantly increased cause-specific SMR for men or women. The SMRs for prostate cancer were 2.03 in the exposed group and 0.58 in the not-exposed group. In the exposed group there were 4 observed and 2 expected deaths from prostate cancer. Among men, 10 years of employment in C8 production was associated with a significant 3-fold increase in prostate cancer mortality when compared to no employment in production. Given the small number of prostate cancer deaths and the natural history of the disease, the association between production work and prostate cancer must be viewed as hypothesis generating and not over interpreted. If the prostate cancer mortality excess is related to C8, the results o f this study and other clinical studies suggest that C8 may increase prostate cancer mortality through endocrine alterations. VI. DISCUSSION OF ENDPOINTS VI. 1. Discussion of Target Organs The primary target organ for C8-induced toxicity is the liver in mice, rats, and dogs, regardless o f route of exposure. The hepatotoxicity manifests as increased liver weights, hepatocellular hypertrophy, liver degeneration, increases in liver enzymes, necrosis of the liver, and induction o f peroxisomes (rats and mice only). Many o f these effects were demonstrated to be reversible when animals were provided with a recovery period. Evidence of hepatotoxicity was not evident in studies in monkeys or humans. In contrast with the rodent, the target organs in the monkey were the M AB000032 23 0 0 0 . EID080830 U C T E R IZ a T IC iS i OK H U M A N H E A L T H C 8 E X P O SU R E CAS REGISTRY NO. 3825-26-1 gastrointestinal tract and the reticuloendothelial system (Griffith and Long, 1980). While the liver does not appear to be a primary target organ in humans, exposure to C8 appears to modify the hepatic and immune response to xenobiotics (Gilliland and Mandel, 1996). VI.2. Discussion of Differences in Species-Specific Sensitivities The induction of peroxisome proliferation by xenobiotics is generally determined as an increase in the activities of certain peroxisome-specific enzymes, or as an increase in the numerical or volume density of peroxisomes in the affected organ. Peroxisome proliferation is associated with: increases in number and volume o f peroxisomes; an increase in DNA synthesis and liver growth; and liver, Leydig cell, and pancreatic acinar cell tumors. The phenomenon of peroxisome proliferation is not uniform across all species. While rats and mice are particularly sensitive to this phenomenon, guinea pigs, cats, dogs and primates (including man), are predominantly non-responsive. VI.3. Tumors Associated with C8 in the Rat C8 has been demonstrated to be a peroxisome proliferator in the rat. C8 exposure in the rat was found to be associated with tumors in the liver, Leydig cell, and pancreatic acinar cell. Peroxisome proliferators, in general, were initially recognized to be associated with hepatocarcinogenesis in rats. However, more recently peroxisome proliferators have been associated with the induction of a triad o f tumors in rats: liver, Leydig cell, and pancreatic acinar cell. Hyperplasia o f these cell types is typically observed prior to, and along with, the occurrence o f neoplasia. Several known peroxisome proliferators (clofibrate, HCFC-123, methylclofenapate, and Wyeth-14,643) are reported to induce this triad of tumors in rats. Hence, this tumor profile appears to be common phenomenon for at least a subset of compounds that are peroxisome proliferators. VI.3.a. Significance of C8-Induced Rodent Tumor to Human Risk VI.3.a.l. Liver Tumors The abundance of data indicates that there is a hepatocarcinogenic hazard of peroxisome proliferators to responsive species (rats and mice) in chronic studies, whereas the carcinogenic hazard to non-responding species, such as humans, is clearly questionable. The epidemiology data, albeit limited, strongly support that the relevance o f the hepatocarcinogenic effects of C8 and other peroxisome proliferators for human hazard assessment should be considered negligible. VI.3.a.2. Leydig Cell Tumors Leydig cell hyperplasia and adenomas are commonly observed in laboratory rats. The incidence o f spontaneous Leydig cell adenomas in Crl:CDBR rats ranges from approximately 0-12% by 2 years of age, and ranges from approximately 64-100 %in F344 rats. In contrast, the rate in humans has been reported to be approximately 0.4 per 24 000 EID080831 .-iA ilA R B C rlA ivA v,ic RIZa i i O N rOR. H U M A N H E A L iri CS EXPOSURE CAS REGISTRY NO. 3825-26-1 million (0.00004%). Although a direct comparison is somewhat tenuous, the data suggest a substantial difference in the susceptibility of rodents and humans to Leydig cell tumorigenesis. This is supported by epidemiology data from compounds that clearly produce Leydig cell tumors in rodent studies but are commonly ingested by humans and are not associated with Leydig cell tumorigenesis in humans. C8 and other peroxisome proliferators do not produce increases in peroxisomes in Leydig cells and are hypothesized to produce these tumors via a different mechanism than the liver tumors. The mechanism of tumorigenesis is not completely understood, and therefore relevance to humans can not be completely ruled out. However, it is known that non-genotoxic compounds (such as C8) produce Leydig cell tumors by altering the endocrine system. Therefore, a threshold for tumorigenesis is expected. If this is the case, use of a margin of safety approach is appropriate for the quantitative dose-response assessment. It is important to consider the slope o f the dose-response at the low end of the observed range in determining an acceptable margin o f safety. VI.3.a.3. Pancreatic Acinar Cell Tumors C8 and other peroxisome proliferators do not produce increases in peroxisomes in the pancreas and are hypothesized to produce these tumors via a different mechanism than the liver tumors. The mechanism of tumorigenesis is not understood, and therefore relevance to humans can not be completely ruled out However there is a growing weight o f evidence that the pancreatic acinar cell tumors are hormonally mediated, therefore they should be treated similarly to peroxisome-proliferator-induced Leydig cell tumors. Vn. SUMMARY C8 has moderate acute oral toxicity with LDjo*s ranging from 178 mg/kg in male guinea pigs to 680mg/kg in adult male rats. An aqueous paste of C8 produced mild to moderate dermal irritation in rabbits and clinical signs of toxicity were observed at doses as low as 1000 mg/kg. Instillation of solid C8 into the rabbit eye produced moderate comeal opacity, iritis, and conjunctivitis. These ocular effects gradually receded. C8 has high acute inhalation toxicity with a 4-hour ALC of 0.8 mg/L in the rat Subchronic inhalation exposure to C8 produced reversible liver effects at concentrations as low as 8 mg/m3(measured as 7.6 mg/m3). Oral and skin absorption subchronic studies confirmed the hepatotoxicity of C8 in the rat. In chronic feeding studies in rats, C8 produced an increased incidence of tumors in the liver, pancreas, and testis. C8 was found not to be a developmental toxic or mutagenic in several tests for mutagenicity. The relevance to human health o f tumors induced by peroxisome proliferators in rodents has been the focus o f several investigators. Regarding the liver, there is a strong association and probable link between peroxisome-proliferator-induced liver growth and the subsequent development of rodent liver tumors. A combination of invivoand invitro studies as well as epidemiology data, has led several investigators to conclude that humans appear to be insensitive or unresponsive to peroxisome-proliferator-induced hepatic effects, and therefore these nongenotoxic agentspose little or no 25 ooo; EID080832 HAZARD CHARACTERIZATION FOR H UM AN HEALTH C8 EXPOSURE CAS REGISTRY NO. 3825-26-1 hepatocarcinogenic hazard to humans. Evidence is also accumulating that the initiating events, which lead to the development of Leydig cell and pancreatic acinar cell tumors are from changes in the liver. These hepatic changes appear to alter the hormonal control of the testis and pancreas. Although these relationships need to be confirmed, it is likely that these extrahepatie tumors pose little or no carcinogenic hazard to humans. Additionally, programs monitoring the health of C8-exposed workers and retrospective cohort studies of workers exposed to C8 provide no evidence of an association between C8 exposure and adverse human health effects. Of primary concern in humans is the slow clearance of C8 from human blood, the opportunity for exposure in the work place, and the moderate-high acute toxicity, regardless of route of exposure. 26 E1D080833 c o o ;. ; r.,} HAZARD CR*. ~ ACTERIZATION TOR H U M A N HEALTH C8 EXPOSURE _______________________________ C A S R EG ISTR Y N O . 382 5 -2 6 -1________________________________ REFERENCES DuPont Co.. Haskell Laboratory Report NumbersCHLT 55- 61, Acute Oral Test. 1961, H. Sherman. 56- 61, Subacute Feeding Study. 1961, H. Sherman. 123- 65, Effects of Fluorocarbon Disbursing Agents on the Livers o f Rats and Dogs.1965, J. R. Bames and H. Sherman. 124- 65, Two-Week Feeding Study. 1965, H. Sherman. 128-68, Acute Oral Test. 1963, S. B. Fretz. 160-69, Acute Inhalation Dust Toxicity. 1969, F. O. Tayfun and R. S. Waritz. 253-79, Inhalation Subacute. 1979, G. T. Hall. 635- 79, Eye Irritation Test in Rabbits. 1979, D. F. Edwards. 636- 79, Skin Irritation Test on Rabbits. 1979, D. F. Edwards. 659-79, Skin Absorption LDso - Rabbit and Rat.1979, D. F. Edwards. 589-80, Rat Skin Absorption Subacute Study with FC-143.1980, L. S. Silber. 682-80, Skin Absorption LDso-Female Rats.1980, J. E. Henry. 205-81, Subacute Inhalation Toxicity of Pentadecafluorooctanoic Acid, Ammonium Salt. 1981, S. D. Nash and M. A. Britelli. 291-81, Oral LD50 Test in Guinea Pigs. 1981, J. A. Hall. 295-81, Oral LDso Test in Rats. 1981, J. A. Hall. 329-81, Oral LD50 Test in Mice.1981, J. A. Hall. 560-81, Mouse Feeding Study - 14 Day. 1981, L. S. Ford. 565-81, Acute Oral Toxicity Comparison Test in Rats.1981, L. Hinckle. 567-81, Oral LD50 Test in Rats. 1981, J. E. Henry. 593-81, Ammonium Perfluorooctanoate Blood Levels in the Female Rat 1981, Kennedy, G. L. 27 000 EED080834 HAZARD CHARACTERIZATION FOR HUM AN HEALTH C8 EXPOSURE _________________________ C A S R EG ISTR Y N O . 3 8 2 5 -2 6 -1 _________________________ 600-81, Liver Weight Comparison in Castrated and Ovariectomized Rats vs. Normal Rats. 1981, L. Hinckle. 537-82, Fourteen-Day Feeding Study in Male and Female Mice. 1982, J. E. Henry. 788-82, Acute Oral Toxicity of FC-143 as a Function of Age. 1983, L. Hinckle. 138-83, C-8 Liver Weights in Rats and Mice: Oral Administration to Males and Females. 1983, C. N. Wyle. DuPont MR 5686, Investigation of Hormonally-Mediated Mechanisms for XenobioticInduced Leydig Cell Tumors in Male Rats. (1989). 3M Co. Reports: Personal communication, J. Long to P.J. Gort, January 8, 1979. 3M Report M-601 (1981). 3M Report 0681TR0110, 1981. 3M Product Toxicity Sheet, May 24,1996. Biosearch, Inc. Report No. T1395, March 4,1976. Coming Hazleton, 17388-0-455, May 16,1996. Coming Hazleton, 17388-0-437, April 25,1996. Hazleton Laboratory America, Inc. 2-6-87 (Submitted to EPA, TSCA 8eCAP Submission, Fiche 536984). Litton Bionetics; LBI Project 20838, February 1, 1978. Riker Laboratory Drug Metabolism Report 1-20 (1980). Riker Laboratories, Report 09790AB0485, March 15,1981. Riker Laboratory 0281CR0012, April 1981-May 1983. University o f Minnesota Environ. Path Lab, T2942, April 9,1981. Published References: Biegel, L. B., R. C. M. Liu, M. E. Hurtt, and J. C. Cook (1995). Effects o f ammonium perfluorooctanoate on Leydig cell function: Invitro, invivo, and ex vivostudies. Toxicol. A ppL Pharmacol. 134: 18-25. ; ooo;-.,28 EID080835 HAZARD CHARACTERIZATION FOR HUM AN HEALTH C8 EXPOSURE CAS REGISTRY NO. 3825-26-1 Cook, J. C., M. E. Hurtt, S. R. Frame, and L. B. Biegel (1994). Mechanisms of extrahepatic tumor induction by peroxisome proliferators in Crl:CDBR (CD) rats. Toxicologist (abstracts 14. Cook, J. C., S. M. Murray, S. R. Frame, and M. E. Hurtt (1992). Induction of Leydig cell adenomas by ammonium perfluorooctanoate: A possible endocrine-related mechanism. Toxicol. AppI. Pharmacol. 113: 209-217. Fayerweather, W. E., Liver study of Washington Works employees exposed to C8: Results of blood biochemistry testing. DuPont, Epidemiology Division of Corporate Medical, January 15,1981. Gilliland, F. D. and J. S. Mandel (1993). Mortality among employees of a perfluorooctanoic acid production plant. J. Occup. Med. 35: 950-954. Gilliland, F. D. and J. S. Mandel (1996). Serum perfluorooctanoic acid and hepatic enzymes, lipoproteins, and cholesterol: A study of occupationally exposed men. American Journal of Industrial Medicine 29: 560-568. Griffith, F. D. and J. E. Long (1980). Animal toxicity studies with ammonium perfluorooctanoate. Am. Ind. Hvg. Assoc. J. 41: 576-583. Johnson, J. D., S. J. Gibson, and R. E. Ober (1984). Cholestyramine-enhanced fecal elimination of carbon-14 in rats after administration of ammonium [14C]perfluorooctanoate or potassium [ 14C]perfluorooctanesulfonate. Fundam. AdpI. Toxicol. 4: 972-976. Kennedy, Jr., G.L. (1985). Dermal toxicity of ammonium perfluorooctanoate. Toxicol. AppI. Pharmacol. 81: 348-355. Kennedy. Jr., G.L., G. T. Hall, M. R. Brittelli, J. R. Barnes, and H. C. Chen (1986). Inhalation Toxicity of Ammonium Perfluorooctanoate. Fd. Chcm. Toxic. 24(12): 13251329. Kennedy Jr., G. L. (1987). Increase in mouse liver weight following feeding of ammonium perfluorooctanoate and related fluorochemicals. Toxicol. Letters 39: 295300. Liu, R. C. M., C. Hahn, and M. E. Hurtt (1996a). The direct effect of hepatic peroxisome proliferators on rat Leydig cell function invitro. Fundam AppI.Toxicol. 30: 102-108. Liu, R. C. M., M. E. Hurtt, J. C. Cook, and L. B. Biegel (1996b). Effect o f the peroxisome proliferator, ammonium perfluorooctanoate (C8), on hepatic aromatase activity in adult male Crl:CDBR (CD) rats. Fundam. AppI. Toxicol. 30: 220-228. 29 0 0 0 = EID080836 HAZARD CHARACTERIZATION FOR H UM AN HEALTH C8 EXPOSURE CAS REGISTRY NO. 3825-26-1 Oboum, J. D., S. R. Frame, R. H. Bell Jr., D. S. Longnecker, G. S. Elliott, and J. C. Cook (1997). Mechanisms for the pancreatic oncogenic effects of the peroxisome proliferator Wyeth-14, 643. Toxicology and Applied Pharmacology 145: 425-436. Pastoor, T. P., K. P. Lee, M. A. Perri, and P. J. Gillies (1987). Biochemical and morphological studies of ammonium perfluorooctanoate-induced hepatomegaly and peroxisome proliferation. Experimental and Molecular Pathology 47: 98-109. Perkins, R. G. (1992). Investigation of ammonium perfluorooctanoate effect on hormone levels and peroxisomal proliferation in the rat. The Toxicologist 12(1): 52. Staples, R. E., B. A. Burgess, and W. D. Kems (1984). The embryo-fetal toxicity and teratogenic potential of ammonium perfluorooctanoate (APFO) in the rat. Fundamental and Applied Toxicology 4: 429-440. Ubel, F. A., S. D. Sorenson, and D. E. Roach (1980). Health status of plant workers exposed to fluorochemicals-a preliminary report. Am. Ind. Hvg. Assoc. J. 41(8): 584589. 30 EID080837 COO,-- \\server\name PSCRIPT Page Separator MAUUUU4U o o o ; :-.?ri EID080838 DRAFT Proposal to Conduct a General Human Health and Environm ental Effects Risk Analysis on C-8 Purpose: The purpose of this project is to evaluate the risks to human health and the environment from exposure to C-8 during manufacture, transport, product use, and disposal of C-8. The analysis will be conducted in a fashion that will provide semi-quantitative estimates of risks so that exposures yielding the highest risks can be identified and recommendations on reducing these risks can be developed. Risks from manufacture, transport and product use will developed in a way that will facilitate future comparisons of risks estimated for potential C-8 alternatives. The project will be conducted in three parts. The first two will be conducted in parallel, in which human health and ecological risks will be characterized. The final part will develop conclusions on exposures that contribute the highest risks so that recommendations for risk management strategies and alternatives can be developed. The projectis estimated to take 12 months to complete from the time of initiation. The Exposure analyses listed below will require collaboration with appropriate plant personnel. (The dates presented assume a Feb. 1, 1997 SBU approval date.) Scope: I. Human Health Risk A. Hazard Identification Time Line 4 /1 8 /9 7 Est. Cost($) 8000 Hazards to human health will be reviewed and summarized in this section. The critical toxicity endpoints of relevance to human health risk will be identified and potential dosimeters to be used for interspecies extrapolation of risk will be discussed. The Haskell toxicity summary will be updated as part of this task. B. Dose-Response Analysis 9 /3 0 /9 7 43,200 The dose-response characteristics of C-8 will be evaluated. This may include conducting benchmark dose analyses to identify no-observed adverse effect levels where necessary. Appropriate dosimeters for interspecies extrapolation will also be developed based on the likely mode of action. The pharmacokinetics of C-8 will also be reviewed. If possible, rudimentary physiologically-based pharmacokinetics approaches will be developed to facilitate interspecies extrapolation of risk. Risks vs. dose relationships will be developed in this phase C. Exposure Analysis 9/30/97 16,000 Reasonable exposure scenarios for C-8 will be developed. This are likely to include airborne, drinking water, dermal, and other oral ingestion pathways. Intake rates and durations of exposure will be developed. Haskell will work with an assigned person(s) from the plant site to help characterize these exposure pathways for manufacturing, transport, product use, and waste disposal operations. The business will provide Haskell with data on concentrations of C-8 in the affected media (air, water, soil). These data will be tabulated. Monte Carlo techniques may be used to calculate expected upper confidence limits for these exposures, depending the availability of data. The cost associated with this task include only Haskell personnel time. D. Risk Characterization 1 2 /1 5 /9 7 16,000 Risks will be summarized according to the major routes of exposure (air, water, dermal, other oral) for each C-8 application (manufacture, transport product use, disposal). The risks will be characterized by comparing the likely exposure concentrations to the dose-response relationship, This method is generally referred MAB000041 EID080839 DRAFT to as a Margin of Exposure. The characterization will provide the risk manager with information that will help identify the operations and exposure pathways that present the highest risk. The characterizations will also enable future comparisons to be made of potential risks posed by C-8 alternatives. II Ecological Effects A. Hazard Identification B. Dose-Response Analysis C. Exposure Analysis D. Risk Characterization III. Recommendations on Risk Management Strategies and Alternatives 12/15/97 4800 This section will evaluate collectively the risks identified to human health and ecological receptors. Based on these analyses, recommendations will be made as to which operations could be targeted to reduce the largest risks for the least cost. This will be a very subjective exercise (narrative) and will require some input from the plant people. MAB000042 00 EID080840 i O 0 0 s;- ,Jc. 72 INTEROFFICE MEMORANDUM Date: From: Dept: Tel No: 09-Jun-1997 09:32am EDT DANIEL A. WEBER WEBERDA ENGINEERING POLYMERS 8-863-4415 TO: 7 addressees CC: 3 addressees Subject: EPA REGION III ECOSYSTEM ASSESSMENT OF DRY RUN CREEK EIDO17890 0 THIS MORNING, WOODY IRELAND AND I MET WITH SARA CASPAR (REGION III EPA, PHILADELPHIA) FOR ABOUT A HALF HOUR TO REVIEW HER PLANS TO OBTAIN SAMPLES NEEDED TO CONDUCT AN ECOLOGICAL RISK ASSESSMENT OF THE ORY RUN CREEK. THE PURPOSE OF THIS ASSESSMENT IS TO LOOK FOR POTENTIAL CONTAMINATION IN THE DRY RUN CREEK DRAINAGE AND IDENTIFY POTENTIAL TOXINS WHICH MAY BE RESPONSIBLE FOR THE OBSERVED DECLINE AND PHYSIOLOGICAL ABNORMALITIES IN CATTLE WHICH USE THE DRY RUN CREEK AREA AS A SOURCE OF WATER AND FOOD. SARA AND A TEAM OF 4 TO 5 PEOPLE WILL BE IN THE DRY RUN CREEK AREA FROM TODAY THROUGH FRIDAY TO COLLECT SAMPLES FOR THE RISK ASSESSMENT. SOME SAMPLES WILL BE TAKEN ON OUPONT PROPERTY ANO SARA MENTIONED THAT WE WOULD RECEIVE A COPY OF THE DATA RESULTS. {AS AN ASIDE, SHE ALSO PLANS TO SEND US SOME INFORMATION ON RESULTS OF COW TISSUE ANALYSES PERFORMED AT MICHIGAN STATE.) SARA PROVIDED ME A COPY OF A DRAFT WORK PLAN FOR COLLECTING SOIL, SEDIMENT, WATER AND BIOTA (ANIMAL SPECIMENS) FROM THE DRY RUN CREEK. A COPY OF THIS WORK PLAN HAS BEEN SENT TO THE ADDRESSEES AND CONTAINS ADDITIONAL INFORMATION NOT SUMMARIZED IN THIS NOTE. BASED ON OUR DISCUSSIONS THIS MORNING WITH SARA AND A REVIEW OF THE DRAFT WORK PLAN, LISTED BELOW ARE THE TYPES OF SAMPLING WHICH WILL BE PERFORMED. VARIOUS TOXICITY ASSESSMENTS AND ANALYSES WILL BE MADE ON THESE SAMPLES. NOT ALL SAMPLES WILL BE TAKEN FROM DUPONT PROPERTY AND EXACT SAMPLING LOCATIONS HAVE NOT YET BEEN DETERMINED. - OBTAIN FIVE SEDIMENT AND SURFACE WATER SAMPLES FOR TOXICITY TESTING. - FATHEAD MINNOWS, EARTHWORMS AND "HYALELLA" TO BE USED FOR TOXICITY TESTING. - PERFORM BENTHIC SURVEYS WHERE SAMPLES ARE TAKEN. - PERFORM ELECTROSHOCK FISH SAMPLING FOR TISSUE ANALYSIS AT SURFACE WATER SAMPLING LOCATIONS. - OBTAIN FROG EGGS FOR ANALYSIS OR LIVE ADULT FROGS FOR BREEDING. - COLLECT GRASS SAMPLES FOR ANALYSIS. - COLLECT SMALL ANIMALS (DEER MOUSE AND MEADOW VOLE IMPLIED BASED ON WORK PLAN) FOR TISSUE ANALYSIS. EXAMINE JAW BONES AND TEETH FOR DISCOLORATION. - USE OATA OBTAINED ABOVE ANO APPLY TO A FOOO CHAIN MODEL TO ASSESS POTENTIAL HEALTH EFFECTS ON A ROBIN, RED-TAILED HAWK, AND RED FOX. SARA INDICATED THERE WOULD BE AN ATTEMPT TO CATCH THESE ANIMALS BUT I DIDN'T SEE THIS MENTIONED IN THE WORK PLAN. THE WORK PLAN CONCLUDES WITH A LIST OF 17 TESTABLE HYPOTHESES, OR QUESTIONS, WHICH THE STUDY IS DESIGNED TO HELP ANSWER. DAN 000, *3 EIDO17891 000^89 73 Potesta & Associates, Inc. Telephone: (304) 357-4990 Engineers and Environmental Consultants_____________ ___________ Fax: (304) 357-4983 U niverfity of Charleiton, Cox H all, 2300 M icC orU e Avenue S .E ., Cberleiton, W V 25304 July 28, 1997 Mr. Daniel Weber Senior Engineer E.I. DuPont DeNemours and Company Washington Works, Building 1 P.O. Box 1217 Parkersburg, West Virginia 26102 v * m u ear. >0 NOTHHMOVi 3 ^ 3:foc Dear Mr. Weber: RE: Response to Affiliated Construction Trades Foundation comments on the Dupont, Dry Run Landfill Permit Application, For U se at Public Hearing. I was asked to offer my thoughts on the four comments made by the Affiliated Construction Trades Foundation regarding the Dry Run Landfill draft permit. These comments are offered without researching the specific federal and/or state statute or regulation, and are intended to be general in nature. My first thought is that DuPont should not attempt to respond to these questions at the hearing, but let the agency answer them. These are accusations that challenge the agency's integrity, which will be addressed in the agency's formal response to comments. COMMENT 1 The draft allows for new landfill on top o f existing. The existing landfill must be closed in accordance with state regulations, and state should not allow a landfill on the area, which is already impacted as is indicated by the elevated fluoride levels. The facility has not been closed out, a new cell is being added. The state has allowed "piggy backing'' o f a new cell on or against an existing cell in other cases. There is no prohibition against it. The director is given a great deal o f flexibility to control industrial wastes. The code and the regulations allow best engineering judgements to be made on facilities such as this. The existing area has been covered and graded and has an excellent stand o f vegetation. It is not an open hole that encourages the infiltration o f rainwater, which results in leachate formation. A s die new cell expands the leachate collection system w ill serve the same purpose as a liner system. The Division o f Environmental Protection (DEP) has approved the use o f this system for future groundwater protection, so it should serve as an adequate cap o f the old facility. The only negative issue here is the 10 years it will take to cover the old facility with the new cell and associated impervious layer. OGOl-SO EID052803 Mr. Daniel Weber Page 2 July 28, 1997 If I understand the facts correctly, the fluoride value in the groundwater was a one time occurrence. The regulations specify what a facility is to do when monitoring w ells show elevated levels. I would assume that the agency and the company are following the procedures as required. If elevated fluoride levels are shown to be a problem, the appropriate action w ill be taken. A ct is encouraging DuPont to move to a "green fields" site for the new cell. The agency should encourage the use o f those existing industrial sites to the degree possible. The waste should logically be in the same place to affect the best control possible. COMMENT 2 Additional treatment o f leachate to meet water quality limits. The available information on quality o f the discharge into Dry Run is based upon the quantity and quality o f the leachate, as well as the efficiency o f the existing treatment system. Those performance levels cannot be used to estimate the effectiveness o f the new system. The new system, with its larger area and baffled aeration area, is expected to have higher removal efficiencies. In the event that the limits cannot be met, DuPont can either truck the leachate to their plant on the Ohio River (I assume they have a permit modification in place to allow this) or add additional treatment to the existing site. There is no proof that the new system will not meet the limits. The bottom line is DuPont will have to meet them or apply to Environmental Quality Board (EQB) for a variance for Dry Run. It is a compliance issue if they fail to meet the limits. COMMENT 3 Limits for fecal coliform, boron and formaldehyde. The director must first determine that these materials are, or may be, discharged at a level to contribute to an excursion o f the water quality standards. The director or his representatives have reviewed the information and determined that they do not need to be limited at this time. The agency should evaluate the effectiveness o f the new system and, if additional limits are needed, modify the permit accordingly. There are no water quality standards promulgated by the EQB for boron or formaldehyde. EPA suggested ambient goals are not regulations until adopted by the EQB. The inclusion o f these as limits are discretionary on the part o f the agency. They can be added if they are felt to be a problem. COMMENT 4 WET testing on a continuing basis. Potest & Associates, Inc, OOOSSi EID052804 Mr. aniel Weber Page 3 July 28, 1997 The agency is requiring the initial whole effluent toxicity (WET) testing on the facility. It is standard practice to discontinue that requirement, should toxicity be shown not to be a problem. It is a waste o f resources to require such testing when it does not appear to be a problem. The agency can at any time take WET tests on the effluent. The agency can require DuPont to do WET tests on the effluent. Should the agency decide that toxicity is an issue o f concern, the permit can be modified to require it, but to require it where there is no history o f toxicity problems is useless. I am available to discuss these issues further, if you feel that would be helpful. LEM/srs cc: Mr. Ronald R. Potest Mr. Mark Kiser Potest & Associates, Inc. 000 co EID052805 eoo$: 74 y i` CONFIDENTIAL Dry Run Landfill Task Team Anticipated Questions -- FINAL (7/29/97) General Information / Physical Features / Operation 1. Why wasn't a liner installed when the landfill was constructed, and why is the WVDEP making you install one now? (Quoted material is from the draft permit.) The landfill permit predated the Solid Waste Management Regulations of 1990 and "the design requirements of the SWMR are now being incorporated into the design.of the Dry Run landfill" to improve groundwater protection. 2. How long will you be operating the landfill? For the foreseeable future. 3. When the current cell is full, will you expand the landfill to another area, open another cell? Decisions about expansion in the future will depend upon economical considerations and the regulations/requirements in effect at the time. 4. Why were those new tanks installed at the landfill? To collect leachate for transport to the Site for disposal. This practice is required by the State in the interim until modifications required by the new permit are completed. 5. What about all the windblown trash that comes off Boso's trucks as he's hauling the waste down to the landfill? All trucks are covered, with the exception of truck loads of dirt from excavations during current construction activity. Blowing material is unusual -- we'd like to be contacted so that we can follow-up. Please call 863-2000. 6. What about illegal dumpings at night? Why isn't the landfill more secure? Protected by locked gate. No scheduled activity after dark. Operated only during daylight hours. If you witness any activity after hours, please contact us at 863-2000. 7. If you do such a good job, how come you had to close down your other landfills? Local landfill -- reached capacity. Letart -- The amount of plastic waste being landfilled has decreased over the years, and landfill operations are being consolidated for economic reasons. EID08I089 General Information, continued -2- 8. Are you going to start dumping into Dry Run some of the bad actors that used to go elsewhere? Only nonhazardous solid waste materials are landfilled at Dry Run. 9. Why were materials taken to Letart in the first place? Teflon* wastes were segregated from other waste materials because of the potential at the time for a landfill fire resulting from the disposal of hot polymer waste. The involvement of Teflon* waste in a landfill fire had the potential to release dangerous fumes. Since hot polymer waste is no longer landfilled, there is no longer a need to segregate the Teflon* wastes.. 10. What determines what is landfilled and what is incinerated? Two factors primarily influence the determination: permitting and handling. First, with our waste minimization effort, we try to reuse or recycle whatever we can. Next, we try to process as much nonhazardous waste material as possible that is acceptable and permitted for burning in our alternate fuel boiler (AFB) so that we can recover heat value for plant steam needs. Finally, nonhazardous waste materials which can't be processed through the AFB are landfilled. 11. Leachate a. What is leachate? Any liquid that might have contacted disposed waste. b. Why is the State requiring that you transport leachate to Washington Works for disposal? What is their concern? This practice is required by the State in the interim until modifications required by the new permit are completed. The concern is about such conditions as iron content, total suspended solids, and biochemical oxygen demand in unlined landfill operations. The State is interested in protecting the groundwater to the greatest extent possible, and we are complying. coo; ^ EID081090 -3- Leachate, continued c. How long will you be hauling leachate out? We don't know -- at least until the new permit construction is complete. d. Do you have DOH or DOT approval to haul leachate? The operation for hauling the leachate meets all State requirements for hauling nonhazardous materials. Such requirements include licensed drivers, weight limit compliance, etc. e. I saw it leak out on the road; did you report the leak? No record of any leak; vehicles inspected for integrity. Material hauled is nonhazardous. However, if concerned, let us know. Call 863-2000. f. Is your contractor licensed to transport the leachate? Meets all requirements within his existing PSC license. Also, contract, not commercial hauler. B. Black Water Issues 1. Why did the water turn black and smelly? This was a temporary situation (about five-months) that has been resolved for approximately two years. The color and odor were caused by the presence of iron sulfide and hydrogen sulfide. Aerating the ponds -- that is, bubbling air through the water -- eliminated the color and odor, and they have not reappeared since aeration began in June 1995. 2. What effect did it have on the ecology of the stream? Frequent stream surveillance has provided no evidence of a negative impact on the wildlife or vegetation of the area. 3. If you've messed up in the past with that black water, how can we be sure you won't mess up again in some other way? We are cpnfident that our work with the WVDEP to upgrade the landfill to, comply with new regulations, in combination with increased routine surveillance (monitoring) required by the State, will enhance the overall operation of the facility. DDJ00029U 0 0 0 1 c* EID081091 -4- C. Contents / Materials Landfilled 1. What carcinogens, hazardous wastes, toxic wastes, etc., are being placed in the "dump?" The landfill is a nonhazardous solid waste landfill. The only material requiring special handling is, as,we described earlier, asbestos, which is considered a possible carcinogen to those directly exposed to it. However, asbestos is a hazard only when it is in the air and can be inhaled. When handled properly and buried or wet, it presents no hazard. 2. What else is in that landfill that is not on the list of 19 parameters? What aren't you reporting? We dispose of only those materials specified in the permit; we must report their amounts annually; we are subject to unannounced inspections by the.WVDEP to monitor landfill operations. 3. Is there fertilizer or other chemicals in the landfill water going into Dry Run? Consistent with State regulations and recommendations, we do add fertilizer from time to time to establish vegetation growth. We use no pesticides or herbicides. D. Toxicity / Other Harmful Effects 1. Is the antifoam additive toxic? No. EC-210 (Antifoam) is used in accordance with manufacturer specifications. (MSDS sheet is on file; mineral oil.) 2. Is the algae poisonous to cattle if they drink water with algae in it? The algae are not harmful. (Report faxed from Haskell Lab is on file regarding fresh water blue-green algae bloom that can cause lethal poisoning; most problems reported have occurred in northern plains states. Furthermore, it is likely that this question would be asked from this perspective: "If leachate from your landfill contacts algae in the stream, would the polluted algae in the stream be toxic to cattle?" Suggested answer: To-date, neither the DEP nor the EPA has established a connection between the landfill and poor animal health.) .000.- EED081092 -5 - D. Toxicity / Other Harmful Effects, continued 3. Is the groundwater near the landfill contaminated? If so, will contaminated groundwater get into my drinking water? (Quoted material is from the draft permit.) Analysis of quarterly groundwater data "has revealed that the Dry Run site has not caused a statistically significant impact upon groundwater relative to background groundwater concentrations." 4. Is it possible that some chemical that you don't know about is coming out of your landfill and causing harm? It is unlikely, since the permit requires quarterly screening for a large number of possibilities in the. landfill leachate. In addition, we do several nonspecific chemical and biological tests, monitoring such indicator parameters as BOD (biochemical oxygen demand), COD (chemical oxygen demand), and TOC (total organic carbons). With regard to causing harm, we have no evidence that the landfill operation is causing harm. We have observed no impact on vegetation or wildlife. We conducted the State's standard acute toxicity testing in 1993. The results were within established limits. 5. Can the nonhazardous materials that you put in your landfill degrade to other things that could be more hazardous? Materials placed in the anaerobic environment of a landfill (that is, buried so that oxygen cannot penetrate) have been observed to degrade extremely slowly. Excavations at municipal landfills have uncovered such items as newspapers and various foodstuffs that have survived intact for decades. The materials that we put into the Dry Run Landfill are at least as durable. If any degradation products formed that were harmful, they would appear so slowly that their concentrations would remain too low to be detrimental. 6. Are there harmful bacteria in the water discharge from the landfill? If so, where does it come from -- the filtercake? We have no reason to believe that there is a problem. The new permit requires monthly monitoring for fecal coliform, so we'll be checking for that as well as other parameters. ooo;;i s EID081093 -6fV . D. Toxicity / Other Harmful Effects, continued 7. Why don't you tell everyone about the C-8 coming out of your landfill and why you're so worried about it? C-8, or ammonium perfluorooctanoate, is a surfactant used in our Teflon*'area. Although C-8 is not regulated by any government agency, DuPont controls it voluntarily because of our high internal standards. Based on our 40 years of experience with handling it at th Plant, we are confidnt that the levels detected at the landfill are not harmful. No ill effect in our employees has been observed to-date. Additional information for our use that may be too detailed or too alarming for the general public: If C-8 were to have a negative.health impact, the target organ would be the liver. We have collected epidemiologic data on our employees over the life of the plant, and the incidence of liver cancer is no higher than expected'. C-8 is a weak animal carcinogen. We have reported the presence of C-8 in the leachate to the WVDEP. E. Filtercake Issues 1. What exactly is filtercake? Filtercake is a concentrated form of sludge that is removed from the site waste water treatment plant. It is composed of waste biosolids, microorganisms from the waste water treatment plant, fly ash, and water. It is different from sludge in that excess water is removed and fly ash is added. The components of filtercake are similar to those produced by municipal waste water treatment plants and commonly either disposed of- in municipal landfills or applied as fertilizer. 2. Why did you stop disposing of filtercake in the landfill and start taking it to the Northwestern Landfill? This practice is required by the State in the interim until modifications required by the new permit are completed. 3. How much filtercake have you put in the landfill? tons: 1994 -- 568.57 1995 -- 3,888.27 1996-- 3,952.81 4. How long did you dispose of filtercake in he landfill? From late August 1994 to mid-November 1996 000, 0 EID081094 009400 75 DRAFT REPORT DRY RUN CREEK WASHINGTON, WOOD COUNTY, WEST VIRGINIA NOVEMBER 1997 PREPARED BY: Mark D. Sprenger, Ph.D. Environmental Response Team AND Michael T. Horne, Ph.D. U.S. Fish & Wildlife Service/Environmental Response Team IN CONJUNCTION WITH: Mark Huston REAC/ERT Environmental Response Team Center Office of Emergency & Remedial Response 000- USFW 0579 TABLE OF CONTENTS LIST OF TA B LES ..............................................................................................................................................vi LIST OF FIGURES ......................................... ................................................................................................viii SECTION I. 1.0 2.0 3.0 TECHNICAL APPROACH. SUMMARY OF FIELD EFFORT RESULTS, AND PRELIMINARY RISK SCREEN........................................................................................................................ 1 INTRO DUC TIO N................................................................................................................... I 1.1 Objective .................................................................................................................... I 1.2 Site Background......................................................................................................... 1 METHODOLOGY ....................................................................................................... I 2.1 Soil Sampling ............................................................................................................ 1 2.2 Sediment Sampling..................................................................................................... 2 2.3 Surface Water Sampling .................................................................................... } . 2 2.4 Drinking Water Well Sampling................................................................................. 2 2.5 Biological Sampling .................................................................................................. 3 2.5.1 Small Mammal Study.................................................................................... 3 2.5.2 Vegetation Sampling .................................................................................... 3 2.5.3 Aquatic Macroinvertebrate Sampling........................................................... 4' 2.5.4 Fish Collection.............................................................................................. 4 2.6 Toxicity Testing.......................................................................................................... 4 2.6.1 Eiseniafoetida (Earthworm) Toxicity Tests.................................................. 4 2.6.2 Hyalella azteca (Amphipod) Toxicity Tests.................................................. 5 2.6.3 Pimephales promelas (Minnow) Toxicity Tests ........................................... 5 2.7 Sampling Equipment Decontamination........................................................................ 5 2.8 Standard Operating Procedures .................................................................................. 5 2.8.1 Documentation.............................................................................. 5 2.8.2 Sample Packaging, Shipment, Storage, Preservation, and Handling .......... 5 2.8.3 Field Sampling and Analytical Techniques.................................................. 5 2.8.4 Health and S afety.......................................................................................... 6 RESULTS....................................................................................................................... '. . . 6 3.1 Water, Soil, and Sediment Analysis ............................................................................ 6 3.1.1 BNAs ............................................................................................." . . . . 6 l COO .u:s USFW 0580 3.1.2 TAL Metals.................................................................................................. 7 3.1.3 Pesticides/PCBs........................................................................................... 8 3.1.4 VOCs ............. 8 3.1.5 Total Fluoride ............................................................................................. 9 3.1.6 Organofluorides ........................................................................................... 9 3.1.7 Total Organic Carbon and Grain Size of Soil and Sediment...........................10 3.1.8 Water Quality Parameters.............................................................................. 10 3.1.9 Bovine Fecal Samples ................................................................................... 10 3.2 Biotic Sampling and Tissue Analysis..........................................................................10 3.2.1 Benthic Macroinvertebrates............................................................................11 3.2.2 Mammal......................................................................................................... 12 3.2.3 Fish................................................................................................................ 13 3.2.4 Earthworm .................................................................................................... 13 3.2.5 Vegetation.......................................................................................................14 3.3 Histological assay of small mammal liver and kidney............................................... 14. 3.4 Toxicity Testing............................................................................................................ 14 4.0 SUMMARY OF PRELIMINARY ECOLOGICAL RISK ASSESSMENT SCREEN ...............15 5.0 DISCUSSION ...........................................................................................................................15 SECTION II 1.0 2.0 ECOLOGICAL RISK ASSESSMENT .........................................................................16 INTRO DUCTIO N............................................................................ : ..................................... 16 1.1 Objective......................................................................................................................16 1.2 Site Background............................................................................................................ 16 PROBLEM FORMULATION .................................................................................................. 16 2.1 Ecological Risk Assessment .........................................................................................16 2.2 Identification of the Contaminants of Concern........................................................... .17 2.3 Exposure Characterization ........................................................................................... 17 2.4 Hazard Characterization/Toxicity Assessment..............................................................17 2.4.1 Fluoride..........................................................................................................17 2.4.2 Organofluorides..............................................................................................18 2.4.3 Aluminum....................................................................................................... 18 2.4.4 Arsenic ..........................................................................................................18 2.4.5 Beryllium ....................................................................................................... 19 it ib~t rs, OV USFW 0581 2.4.6 Chromium.......................................................................................................19 2.4.7 Copper........................................................................................................... 20 2.4.8 Iro n ................................................................................................................ 21 2.4.9 Lead .............................................................................................................. 21 2.4.10 Manganese .................................................................................................... 21 2.4.11 Nickel ........................................................................................................... 22 2.4.12 Vanadium.......................................................................................................22 2.4.13 Zinc .............................................................................................................. 23 2.5 Selection of Assessment Endpoints.............................................................................. 23 2.6 Production of Testable Hypotheses.............................................................................. 24 2.7 Conceptual Model .......................................................................................................25 2.8 Selection of Measurement Endpoints............................................................................26 2.9 Life History/Exposure Profile Information ...................................................................29 2.9.1 The amphipod (Hyallela caeca) as Representative of Benthic Invertebrates ...................................................................................................................... 29 2.9.2 Earthworm (Eiseniafoerida) as Representative of Terrestrial Invertebrates ...................................................................................................................... 30 2.9.3 Fathead Minnow (Pimephalespromelas) as Representative of Fish Community 31 2.9.4 American Robin (Tardus migratorius)as Representative ofWorm-eating Birds .......................................................................................................................... 32 . 2.9.5 Red-tailed Hawk (Buteojamaciensis) as Representative of Carnivorous Birds. .................................................................................................................... 33 2.9.6 Red Fox ( Vulpes wipes) as Representativeof Carnivorous Mammals . . . . 34 2.9.7 Mink (Musiela vison) as Representative of Carnivorous Mammals ...............35 2.9.8 Raccoon (Procyon lotor) as Representativeof Omnivorous Mammals . . . . 37 2.9.9 Short-tailed Shrew {Blarina brevicauda) as Representative of Insectivorous Mam m als......................................................................................................38 2.9.10 Meadow Vole (Microtus pennsylvanicus) as Representative of Herbivorous Mammals 40 A S S U M P T IO N S ............ 42 EFFECTS PROFILE . . . 43 4.1 Fluoride............. 43 4.2 Organofluorides............................................................. 4.3 Aluminum .................................................................... 4.4 Arsenic ......................................................................... 4.5 Beryllium ....................................................................... 4.6 Chromium .................................................................... 4.7 Copper ......................................................................... 4.8 Iron .............................................................................. 4.9 Lead .............................................................................. 4.10 Manganese.................................................................... 4.11 N ic ke l............................................................................ 4.12 Vanadium....................................................................... 4.13 Zinc .............................................................................. 5.0 RISK CHARACTERIZATION................................................... 5.1 Benthic Invertebrate Community Structure and Function 5.2 Soil Invertebrate Community Structure and Function . . 5.3 Fish Communities ...................................................... 5.4 Worm-eating Birds....................................................... 5.5 Carnivorous Birds ........................................................ 5.6 Carnivorous Mammals (Terrestrially feeding)............... 5.7 Piscivorous Mammals.................................................. 5.8 Omnivorous Mammals ................................................. 5.9 Insectivorous Mammals................................................. 5.10 Herbivorous Mammals ................................................. 6.0 UNCERTAINTY ANALYSIS ................................................... 7.0 CONCLUSIONS......................................................................... 7.1 Benthic Invertebrate Community Structure and Function 7.2 Soil Invertebrate Community Structure and Function . 7.3 Fish Communities ...................................................... 7.4 Worm-eating Birds...................................................... 7.5 Carnivorous Birds ...................................................... 7.6 Carnivorous Mammals ............................................... 7.7 Piscivorous Mammals................................................. 7.8 Omnivorous Mammals ............................................... IV 11-J - 5 43 43 44 44 44 45 45 45 46 46 46 47 47 47 4? 48 48 48 48 48 49 49 49 49 50 50 50 51 51 . 51 . 51 . 51 . 51 7.9 InsectivorousMammals.................................................................................................52 7.10 Herbivorous Mammals ............................................................................................... 52 8.0 SUM M A RY............ .................................................................................................................J2 LITERATURE C IT E D ......................................................................................................................................... 53 APPENDIX A Small Mammal Data Sheets.................................................................................................................. 60 APPENDIX B Analytical Reports ................................................................................................................................ 61 APPENDIX C Toxicity Testing Reports........................................................................................................................... 62 APPENDIX D Field N otes............................................................................................................................................... 63 APPENDIX E Statistical Analysis ...................................................................................................................................64 000 '0 V LIST OF TABLES TITLE 1 Concentration of BNA's in Water 2 Concentration of BNA's in Soil 3 Concentration of BNA's in Sediment 4 Concentrations of Metals in Water 5 Results of Concentrations of Metals in Soil '6 Results of Concentrations of Metals in Sediment 7 Results of the Analysis for Pesticide/PCB in Water 8 Results of the Analysis for Pesticide/PCB in Soil 9 Results of the Analysis for Pesticide/PCB in Sediment 10 VOA Concentrations in Water 11 VOA Concentrations in Soil 12 VOA Concentrations in Sediment 13 Concentrations of Fluoride in Water 14 Concentrations of Fluoride in Soil 15 Concentrations of Fluoride in Sediment 16 Results of the Organo-fluoride Analysis in Sediment 17 Concentrations of TOC in Soil 18 Results of the Analysis for Grain Size in Soil 19 Concentrations of TOC in Sediment 20 Results of the Analysis for Grain Size in Sediment 21 In Siru Water Quality Parameters 22 Concentrations of Bromide, Chloride, Nitrate, Phosphorus, and Sulfate in Water vi OOOr.OV USFW 0585 23 C oncentrations o f B N A 's in Fecal Sam ples 24 Concentrations of Metals in Fecal Samples 25 Concentrations of Fluoride in Fecal Samples 26 Frequency and Abundance of Benthic Macroinvertebrates 27 Concentrations of Metals in Small Mammals 28 Concentrations of Fluoride in Small Mammals 29 Lipid Concentrations in Mammal Tissue 30 Concentrations of Metals in Fish Tissue 31 Concentrations of Fuoride in Fish Tissue 32 Lipid Concentrations in Fish Tissue 33 Results of the Analysis for TAL Metals in Earthworm Tissue 34 Results of the Analysis for Fluoride in Earthworm Tissue 35 Lipid Concentrations in Earthworm Tissue 16 Concentrations of Metals in Vegetation Concentrations of Fluoride in Vegetation Lipid Concentrations in Plant Tissue Results of Histopathology for the (Meadow Vole, Short-tail shrew. Meadow jumping mouse, and White-footed mouse) Summary of Toxicity Test Results Summary of Initial Risk Screen Risk Calculations Based on Wet Weight i yi - vii NUMBER 1 LIST OF FIGURES ITELE Sampling Site Map Vili 0 0 0 - `- s USFW 0587 SECTION I. TECHNICAL APPROACH, SUMMARY OF FIELD EFFORT RESULTS, AND PRELIMINARY RISK SCREEN 1.0 INTRODUCTION 1.1 Objective The objective of this project was to provide technical support to the U.S. Environmental Protection Agency Region III Removal Program in conducting an evaluation of ecological risks from alleged contamination of soil, sediment, and water at a working beef production farm located down gradient of a landfill. The effort resulted in the collection of soil, sediment, surface water, and biota samples for contaminant analyses and soil, sediment, and surface water for laboratory toxicity testing. The p rimary goals of the project were to: 1) identify contaminants present, 2) determine the extent of contamination, and 3) produce an ecological risk assessment based on the collected data. 1.2 Site Background The site is a working beef production farm located in Washington, Wood County, WV. The owner of the farm has filed numerous complaints with the West Virginia Department of Natural Resources and the U. S. EPA alleging that contaminants are being discharged from an industrial landfill owned by the DuPont corporation, into Dry Run. Dry Run flows through the farmer's property and is a primary source of water for his cattle. The fanner maintains that numerous deaths, blindness, and other unusual illnesses observed in his herd are directly attributable to the contaminants that are discharged into Dry Run from the DuPont landfill. It has also been reponed that fish and wildlife kills have also occurred in the area, which may be associated with the abnormalities observed in the cattle. 2.0 METHODOLOGY The approach used in this document followed current U.S. EPA guidance for designing and conducting ecological risk assessments (U.S. EPA 1997). Based on the problem formulation phase of the risk assessment design, the following field study was conducted to provide data needed to complete the assessment. A screening-level ERA was conducted after the field investigation, as little data on site contamination was available prior to the effort. Numerous fish and wildlife kills, in addition to problems in the cattle, had been reported prior to this activation. 2.1 Soil Sampling Surface soil samples were collected at 4 sample areas along Dry Run and in one reference sample area (Figure l). Sample areas were selected based on distance from the landfill outfall in an anempt to identify a contaminant concentration gradient. Sampling was concentrated in the meadows along the stream bed. Three replicate samples were taken in each sampling area. Replicate sampling locations were determined by gridding the sampling area and randomly choosing three grid nodes for sampling through the use of a random numbers table. Sampling grid nodes were determined by using a random numbers table. Surface soil samples were collected using a decontaminated stainless steel trowel or spoon from the top 6 inches of the soil according to ERTC/REAC Standard Operating Procedure (SOP) #2012, Soil Sampling. All soil samples were analyzed for total organic carbon (TOC); grain size; target analyte l 0 0 0 - .10 USFW 0588 list (TAL) metals; TCL pesticides/PCBs; TCL Base, Neutral, and Acid Extractable (BNAs) compounds; TCL volatile organic compounds (VOCs), total fluoride, and organofluoride compounds. Additional soil was collected from the sample node closest to the stream bed for use in an earthworm toxicity test. A vegetation sample was also taken at each of the soil sampling nodes. 2.2 Sediment Sampling Sediment samples were collected at 5 sample areas on site in Dry Run, one reference sample area, and one area in Lee Creek. Sample areas were selected based on distance from the landfill outfall in an attempt to identify a contaminant concentration gradient. Sampling was concentrated in the depositional areas along the stream bed. All sediment sampling was conducted according to ERTC/REAC SOP #2016, Sediment Sampling. At each sample station, sediment was collected from the top 6 inches using a decontaminated trowel. The sample was composited into a decontaminated S-gallon stainless steel bucket, homogenized, and divided into the appropriate sample containers for chemical analyses. Additional sediment was collected in the reference area. Tributary A, Tributary B, Area II, and Area IV , for use in a Hyaiella azteca whole sediment bioassay. 2.3 Surface Water Sampling Surface water samples were collected at locations which corresponded to each of the seven sediment sample stations. Surface water samples were collected directly into two 1-liter polypropylene bottles for metals analyses and into 1-liter glass bottles for organic (i.e.,' BNAs, Pesticide/PCBs, VOCs) analyses as per ERTC/REAC SOP #2013, Surface Water Sampling. Water samples were collected prior to collecting sediment samples and upstream of any stream disturbances caused by the sampler. One sample at each location was filtered through a 0.45 micron Cum) filter in the field prior to TAL metals analysis; all the remaining TAL metals samples and all the organic samples were analyzed unfiltered. All samples analyzed for metals were preserved by adding 40 percent nitric acid until a pH of less than 2 in the sample was obtained. The filtered sample submined for TAL metal analysis was preserved after the sample was filtered. All surface water samples were submitted for TAL metals, TCL BNAs, TCL Pesticide/PCBs, TCL VOCs, chloride, fluoride, bromide, nitrate, sulfate, and phosphate analyses. Additional sample was taken in the reference area. Tributary A, Tributary B, Area II, and Area IV , for use in a Pimephales promelas aquaeous phase toxicity test. Water quality parameters were measured using a HoribaTM water quality meter. The meter was used to measure temperature in degrees Celsius (*C ), pH, dissolved oxygen [milligrams per liter (mg/L)]. conductivity [millimhos per centimeter (mmhos/cm)], oxidation reduction potential [volts (V )]. The meter was calibrated prior to and after data collection. In-siru water quality data was transcribed from the digital display of the HoribaTM into a field logbook at the time of collection. The HoribaTM was used in accordance the manufacturer's operating manual. 2.4 Drinking Water Well Sampling Water was sampled from a drinking water well on the Tennant farm. Parameters were analyzed as outlined above. Samples to be analyzed were taken from a tap that was located directly on the pump head after the well had been purged for a period of approximately five minutes. 2 000- .i". USFW 058$ 2.5 Biological Sampling 2.5.1 Small Mammal Study Small mammals were collected from the site to determine body burden levels of TAL metals and total fluoride and to evaluate histopathological effects of exposure to site contaminants. Tissue burdens of small mammals trapped on site were compared to animal* collected from the reference area. All field trapping activities were conducted in accordance with ERTC/RJEAC Draft Standard Operating Procedure SOP #2029, Small Mammal Sampling and Processing. Four trapping areas were established on site in areas corresponding to the soil sampling locations. A fifth grid was established on a reference area located just to the north of Dry Run in similar meadow habitat as that observed along the stream corridor (Figure 1). The reference area was chosen because the habitat present was sim ilar to that in the meadows near Dry Run, and because it was outside the area that could be directly influenced by surface water from Dry Run. The length of the trapping period and the trapping effort varied among each of the trap areas and was based on the length of time and effort required to capture a sufficient number of mammals for statistical evaluation. Sampling was performed using Museum Special snap traps set in grids. All traps were spaced 10 feet apart and baited with a rolled oats and peanut butter mixture. The traps were checked1 twice daily, once in the morning and once in the evening. During trap checks, traps were rebaited and reset as necessary. Recovered animals were labeled with the trap area, trap number, species, and date of capture while in the field and then were transferred in coolers to the staging area for processing. For each animal, prior to performing the necropsy, data from the specimen label was transferred to a small mammal data sheet (Appendix A). Body metrics including total body weight, body length, tail length, ear length, liver weight, and kidney weight were measured and recorded on the data sheet. During the necropsy any abnormalities were noted and the contents of the gastrointestinal tract were removed from each specimen. Sections of the liver and kidney (approximately 0.5 g each) were removed for histopathological analyses. The sections were placed in a labeled 40-mL glass vial and preserved with 10 percent neutral buffered formalin. Preserved liver and kidney sections were submitted to Animal Reference Pathology (ARP) for histopathological evaluation. The remaining tissue was submitted for homogenization and TAL metal, total fluoride, percent moisture, and percent lipid analysis. 2.5.2 Vegetation Sampling Vegetation was collected by hand for residue analysis per ERTC/REAC SOP #2038 Vegetation Assessment Field Protocol. The most abundant grass taxa observed at all sampling locations was targeted for residue analysis. Grass samples were taken in each area at the same grid nodes as the soil samples were taken. The above ground portion of plants from the immediate vicinity of the soil sampling node were collected by cutting the stems at the soil surface with a decontaminated knife. All samples were analyzed for TAL metals, total fluoride, percent moisture, and percent lipids. 2.5.3 Aquatic Macroinvertebrate Sampling 3 @Q9 USFW 0590 The infaunal macroinvenebrate community was sampled per Draft ERTC/REAC SOP #2032 Benihic Macroinvenebraie Sampling and U.S. EPA (1983, 1989, and 1990). Macroinvenebrate samples were collected for evaluation of community structure. In this investigation, macroinvenebrates were defined as organisms that impinged on a 0.5 millimeter (mm) sieve. A total of three replicates were collected from each of five sediment sampling locations (Figure 1). A long-handled, D-frame kick net, measuring approximately 45 centimeters wide and 20 centimeters tall, with 0.5 mm mesh was used. The net was used to disturb submerged vegetation and debris and collect dislodged invenebrates. Each replicate collection was performed over a uniform area at each sampling location. Benthic invertebrate samples were transferred to 500 ml polyethylene jars and preserved with a 70 percent 2-propanol solution. In the laboratory, the sample was rinsed in clean water and placed in a white 12 x 18-inch polyethylene pan with just enough water added to allow complete dispersion of the material within the pan. Large debris, stones, and other extraneous materials were removed from the tray and inspected for attached or clinging organisms. All organisms picked from the pan were identified to the lowest positively identified taxonomic level, enumerated, and recorded on a laboratory bench sheet. The size and life history stage of the organisms and state of taxonomic knowledge of the group determined the level of identification. The organisms were identified using appropriate taxonomic references and a representative' subsaraple were identified by a second individual to meet the Quality Assurance/Quality Control (QA/QC) requirements of the taxonomic analysis. 2:5.4 Fish Collection Fish were collected from Dry Run to determine body burden levels of TAL metals and total fluoride. A CoffeltTVbattery powered backpack electroshocker was used and operated as per the manufacturer's instructions. The sampling team-consisted of one individual operating the electroshocker and one individual collecting stunned fish with a dip net. Stunned fish were placed in a 5-gallon bucket filled with site water. Following collection, fish were identified to the lowest taxonomic level possible in the field and live specimens were released. Voucher and dead specimens were preserved with a dilute formaldehyde solution and returned to the ERT/REAC biological laboratory for confirmation of field taxonomic analyses. Fish tissue was homogenized and submitted to the laboratory for TAL metal, total fluoride, % lipid and % moisture analysis. Toxicity Testing 2.6.1 Eiseniafaetida (Earthworm) Toxicity Tests Five soil samples were taken for evaluation in an earthworm toxicity test. Four of the samples were taken in the meadow sampling areas along Dry Run and one in the reference meadow area as outlined above. The test was run for a period of 28 days, at which time mortality and growth in each of the test soils was enumerated. Earthworm tissue resulting from each of the treatments was submined for TAL metals, total fluoride, % lipid, and So moisture analysis. Figure 1.details the earthworm toxicity test soil sampling locations. 2.6.2 Hyalella azteca (Amphipod) Toxicity Tests 000- -3 4 USFW 0591 Five sediment samples were taken for evaluation in an ampbipod toxicity test. Four of the samples were taken in Dry Run and one in a reference area stream. The test was run for a period of 10 days, at which time mortality and growth in each of the test sediments was enumerated. Figure 1 details the amphipod toxicity test sediment sampling locations. 2.6.3 Pimephales promelas (Minnow) Toxicity Tests Five surface water samples were taken for evaluation in a fathead minnow toxicity test. Four of the samples were taken in Dry Run and one in a reference area stream. The test was run for a period of 7 days, at which time mortality and growth in each of the test waters was enumerated. Figure 1 details the fathead minnow toxicity test water sampling locations. 2.7 Sampling Equipment Decontamination The following sampling equipment decontamination procedure was employed prior to and subsequent to sampling in the following numerical sequence: 1. physical removal 2. nonphosphate detergent wash 3. potable water rinse 4. 10 percent nitric acid rinse 3. distilled water rinse 6. solvent rinse [acetone] 7. air dry 2.8 Standard Operating Procedures 2.8.1 Documentation Documentation was conducted in accordance with the following SOPs: -ERTC/REAC SOP #2002, Sample Documentation -ERTC/REAC SOP #4001, Logbook Documentation -ERTC/REAC SOP #4005, Chain of Custody Procedures 2.8.2 Sample Packaging. Shipment, Storage, Preservation, and Handling Sample packaging, shipment, storage, preservation and handling were conducted in accordance with the following SOPs: -ERTC/REAC SOP #2003, Sample Storage, Preservation and Handling -ERTC/REAC SOP #2004, Sample Packaging and Shipment 2.8.3 Field Sampling and Analytical Techniques Field sampling activities and field analytics were conducted in accordance with the following SOPs: -ERTC/REAC SOP #2001, General Field Sampling Guidelines 5 OOO-.Vi- USFW 0592 -ERTC/REAC SOP #2005, Quality Assurance/Qualiry Control Samples -ERTC/REAC SOP #2006, Sampling Equipment Decontamination -ERTC/REAC SOP #2012, SoilSampling -ERTC/REAC SOP #2013, Surface Water Sampling -ERTC/REAC SOP #2016, Sediment Sampling -REAC SOP #2029, Small Mammal Trapping and Processing -REAC SOP #2032, Benthic Sampling 2.8.4 Health and Safety Health and Safety was conducted in accordance with the following SOPs: -ERTC/REAC SOP #3001, R E A C Health and Safety Program Policy and Implementation -ERTC/REAC SOP #3012, R E A C Heath and Safety Guidelines at Hazardous Waste Sites -ERTC/REAC SOP #3020, Inclement Weather, Heat Stress and Cold Stress RESULTS 3.1 Water, Soil, and Sediment Analysis 3.1.1 BNAs Surface Water Analysis of the surface water samples from Dry Run, the reference stream, and Lee Creek produced only one detection on the standard BNA scan. A sample taken in the Upper Tributary B location contained an estimated concentration of 2 ug/L of Bis(2Ethylhexyl)phthalate. In addition, numerous Tentatively Identified Compounds (TICs) including unknown alkane and alkene compounds were found in the surface water samples. Results for the BNA analysis of surface water samples taken in in Dry Run are presented in Table 1 and in Appendix B. Well Water The sample taken at the Tennant Farm well produced no detections from the standard BNA list. Several TICs were identified, however only one of the detected compounds could be tentatively characterized and identified as an alkene. Results for the BNA analysis of the well water sample taken at the Tennant farm is presented in Table 1 and in Appendix B. Soil Analysis of the surface soil samples from the meadows adjacent to the streambed and the reference meadow area produced a few isolated hits from the standard BNA list. Fluoranthene was detected at an estimated concentration of 23 ug/Kg in one of the three reference samples. Carbazole was detected at an estimated concentration of 41 ug/Kg in one of the three Area I soils. Di-n-butylphthalate was detected at concentrations of 22, 27, 26. and 30 ug/kg in one sample from area II, one sample from area three, and two of the three samples from area IV, respectively. Bis(2-Ethylhexyl)phtha!ate was detected at estimated concentrations of 27 and 62 ug/Kg in one sample from Area III and one sample 6 000-/; 5 USFW 059: from Area IV. Di-n-octylphthalate was detected at as estimated concentration of 180 ug/kg in one of the samples from area IV. In addition, numerous TICs including unknown alkane, cycloalkane, aikene, aldehyde, sterols, alcohols, PAH, acid, and other organic compounds were found in the surface soil samples. Results for the BNA analysis of soil samples is presented in Table 2 and in Appendix B. Sediment Analysis of the sediment samples from the five site and two off-site stream locations produced only a few isolated detections of BNA compounds. Di-n-butylphthalate was detected in the Area IV sediment sample at an estimated concentration of 30 ug/Kg. Bis(2Ethylhexyl)phthalate was detected in the Area III sediment sample at an estimated concentration of 52 ug/Kg. No other standard list compounds were found in any of the Lee Creek, reference stream, or Dry Run sediment samples. Numerous TICs including unknown alkane, cycloalkane, aikene, aldehyde, sterols, alcohols, PAH, acid, and other organic compounds were found in the Dry Run, Lee Creek, and reference sediment samples. Results for the BNA analysis of sediment samples is presented in Table 3 and in Appendix B. 3.1.2 TAL Metals Surface Water Analysis of the surface water samples from Dry Run, the reference stream, and Lee Creek included both filtered and unfiltered samples for TAL metals analysis. Antimony, arsenic, beryllium, cadmium, cobalt, mercury, nickel, selenium, silver, thallium, and vanadium were not detected in any of the filtered or unfiltered water samples. Aluminum, barium, calcium, copper, iron, magnesium, manganese, potassium, sodium, and zinc were detected in the filtered water samples. Of the list of detected metals in the filtered samples, it appears that aluminum, copper, and zinc are found in higher concentrations in the Dry Run Creek drainage, including the reference stream, than in Lee Creek. Aluminum, barium, calcium, copper, iron, magnesium, manganese, potassium, sodium, and zinc were detected in the unfiltered samples. Of the list of detected metals in the unfdtered samples, concentrations of aluminum, iron, and zinc appear to be higher in Dry Run thaB those measured in Lee Creek. Detailed results of the TAL metals analysis in filtered and unfiltered water samples are presented in Table 4 and in Appendix B. w.dl water Well water sampled from the well on the Tennant farm was analyzed as an unfiltered sample. Antimony, arsenic, beryllium, cadmium, chromium, cobalt, mercury, nickel, selenium, silver, thallium, and vanadium were not detected in the well sample. Concentrations measured for the remaining list of TAL metals are presented in Table 4 and in Appendix B. 7 000. USFW 0594 Soil Three replicate surface soil samples from the four Dry Run meadow areas and the reference meadow area were analyzed for TAL metals. Antimony, cadmium mercury, selenium, silver, and thallium were not detected in any of the soil samples. One-way analysis of variance determined that soil manganese concentrations were significantly higher in Area II compared to the reference area, but the same as those noted in areas I, HI. and IV (p=0.094). Area II had the highest mean manganese concentration with mean concentrations from the other areas ranging from 680 to 1310 mg/kg. Further results of the TAL metals analysis of site and reference soil samples are presented in Table 5 and Appendix B. Scdinicm Seven sediment samples were submitted for TAL metals analysis. Five of the samples were taken in the streambed of Dry Run, one was taken in Lee Creek, and one was taken in the reference stream. Antimony, cadmium, mercury, selenium, silver, and thallium were not detected in any of the sediment samples. In comparison to the levels measured in the Lee Creek sample, it appears the Dry Run Creek reach may be enriched in aluminum, arsenic, barium, calcium, chromium, cobalt, copper, iron, lead, magnesium, manganese, nickel, potassium, sodium, vanadium, and zinc. Based on the results of the aluminum, barium, chromium, cobalt, copper, iron, lead, manganese, nickel, vanadium, and zinc analysis, there also appears to be a general trend that metal concentrations decrease with increasing distance from the landfill. Further results of the TAL metals analysis of site and reference sediment samples are presented in Table 6 and Appendix B. 3.1.3 Pesticides/PCBs Water No pesticides or PCBs were detected in the Dry Run samples, the Lee Creek sample, or in the reference stream sample (Table 7; Appendix B). Soil No pesticides or PCBs were detected in the Dry Run meadow samples, or in the reference meadow samples (Table 8; Appendix B). Sediment No pesticides or PCBs were detected in the Dry Run samples, the Lee Creek sample, or in the reference stream sample (Table 9, Appendix B). 3.1.4 VOCs Water No volatile organic carbon compounds were detected in the Dry Run samples, the Lee Creek sample, or in the reference stream sample (Table 10; Appendix B). 8 000 USFW 059E Soil Trichlorofluoromcthanc was detected in every soil sample taken in the meadows adjacent to Dry Run at concentrations ranging from 0.9 to 3.6 ug/Kg. In addition, tetrachloroethene was detected in one replicate Area III soil sample a: a concentration of 4.4 ug/Kg. No other volatile organic carbon compounds were detected in the Dry Run samples, the Lee Creek sample, or in the reference stream sample. Results of the VOC an alysis of site and reference soil samples are presented in Table 11 and Appendix B. Sediment Acetone was detected in the Area IV sample at a concentration of 7.2 ug/Kg. Chloroform was detected at a concentration of 0.5 ug/kg in the Area III sample. No other volatile organic carbon compounds were detected in the Dry Run samples, the Lee Creek sample, or in the reference stream sample. Results of the VOC analysis of site and reference sediment samples are presented in Table 12 and Appendix B. 3.1.5 Total Fluoride Water / Well Water Fluoride was not detected in the Dry Run samples, the Lee Creek sample, the reference stream sample, or in the well sample taken on the Tennant farm (Table 13; Appendix B). Soil Fluoride was detected in the Dry Run meadow and in the reference meadow samples. Soil fluoride concentrations ranged from a low of 180 mg/kg in Area IV to a high of 370 mg/kg in Area III. There appear to be no statistically significant differences in total soil fluoride concentration. Results of the soil fluoride analysis are presented in Table 14 and Appendix B. Sediment Fluoride was detected in the Dry Run creekbed and in the reference creekbed samples, but not in Lee Creek. Fluoride concentrations ranged from a low of 290 mg/kg in the Area IV sampling area to a high of 450 mg/kg in the Upper Tributary A sampling area. Fluoride was not detected in Lee Creek. Overall, fluoride concentrations tend to decrease with increasing distance from the landfill. Sediments sampled in the Dry Run Creek reach appear to be enriched with fluoride, which is not found in Lee Creek. Results of the sediment fluoride analysis are presented in Table 15 and in Appendix B. 3.1.6 Organofluorides Sediment Because of methodology problems, specifically in obtaining appropriate standards, and the high volatility of some standards, only a limited suite of organofluoride compounds could be scanned for in the sediment samples. These compounds are presented in Table 16. Of the list that was analyzed for (Tetrafluoroethylene, hexafluoropropylene. 9 000-115 USFW 0596 chlorodifluoromethane, perfluorocyclobutane, l-Chloro-l, 1,2,2, tetrafluoroethane, 2Chloro-l,1.1.2,3,3,-hexafluoropropanc, and Perfluoroisobutylene), none of the organofluoride compounds were detected in site sediments. Results of the organofluoride analysis is reported in Table 16 and in Appendix B. 3.1.7 Total Organic Carbon and Grain Size of Soil and Sediment Summaries of total organic carbon and grain size analysis are presented in Tables 17-20 and in Appendix B. TOC in the soil ranged from an average low of 5.6% in Area III soils to an average high of 9.2 in Area IV soils. Soil grain size determinations are summarized in Table 18. TOC in the sediment ranged from a low of 1.9% in Lee Creek to a high of 4.5 % in Area IV. Sediment grain size determination is presented in Table 20. 3.1.8 Water Quality Parameters Water quality parameters including pH, conductivity, turbidity, dissolved oxygen, temperature, bromide, chloride, nitrate, phosphate, and sulfate was measured in the Dry Run Creek reach, the reference stream, and in Lee Creek. The most notable observations were that conductivity and sulfate concentration decreased with increasing distance from the landfill. Other parameters appeared to be in the expected range. Results of these measurements and analyses are presented in Tables 21 and 22. 3.1.9 Bovine Fecal Samples Six fecal samples were taken to determine if environmental contaminants were showing up in the digestive products of the affected cattle. BNAs Phenol was detected in all six fecal samples at concentrations ranging from 2.6 to 8.0 mg/kg. Additionally, 4-methylphenol was detected in all six samples in concentrations ranging from 45 to 110 mg/kg. Benzoic acid was detected in two of the samples at a concentration of 30 mg/kg. Additional information is presented in Table 23 and in Appendix B. TAL Metals Aluminum, barium, calcium, copper, iron, lead, magnesium, manganese, potassium, sodium, vanadium, and zinc were detected in the fecal samples. Additional information presented in Table 24 and in Appendix B. Fluoride Fluoride was not detected in any of the fecal samples (Table 25; Appendix B). Biotic Sampling and Tissue Analysis 3.2.1 Benthic Macroinvenebrates 10 0 0 0 - A '.7 USFW 0597 A total of 27 taxonomic groups were collected from the 5 locations sampled (Table 26). Of these, there was 1 Oligochaetc, 1 Mollusc, 1 Turbellarian, 3 Crustaceans, anH 21 Insect taxa. Of the latter, the dominant group, in terms of taxonomic diversity, were the Coleopteria which were represented by 7 taxa. The Dipteria were represented by 4 taxa and the Ephemeropteria were represented by 3 taxa. The Plecopteria, Hemipteria Tricopteria, and Megaloptera were the least diverse groups and were represented by one or two taxa. The greatest taxonomic diversity was observed at the reference location, where 19 taxa were collected. Fewer taxa were observed at locations I through IV, and the lowest diversity was observed a: location IV where 11 taxa were collected. The difference in taxonomic diversity between the reference location and locations I, II, HI, and IV was primarily due to the presence of a greater number of rare taxa at the former location. Tne number of individuals collected per replicate ranged from 203 at the reference location (replicate A) to 24 at location IV (replicate C). The observed density of individuals throughout the study area is primarily the result of the numerical abundance of only several taxa (Table 26). The numerically dominant taxa collected from the study area includes Leucrocuta and Asellidae. When present, these taxa were typically the most numerically abundant organisms and were represented by 221 and 391 individuals, respectively. Other taxa, including Perlista, Chironomidae, Hyalella, the Turbellaria, and to a lesser extent, Leptophlebia, Baetis, and Pseudolimnophilia, were present at most locations in consistendy significant proportions. In general, most taxa collected were relatively rare and were represented by five or fewer individuals at most locations. For example, of the 129 total taxonomic observances, 54 were represented by one individual. 36 were represented by two to five individuals, 11 by six to 10 individuals, 15 by 11 to 20 individuals, and 13 by greater than 21 individuals. Several taxa were collected from all locations sampled including Leucotricia, Perlesta, Chironomidae, and Asellidae (Table 26). Several taxa were not collected from all locations but were broadly represented throughout the drainage including Leptophlebia, Agabus, Hyalella, and Turbellaria. Of the nine taxa observed at only one location, four, including Elmidae, Scirtidae, Pseudolimnophila, and Stratiomyidae were collected only from the reference location. The most common distribution observed was one where a taxa was collected in relatively low numbers, and at few locations. For example, Elmidae, Hydropsyche, Limnophilidae, Nigronia, and Ceratoponidae were collected infrequently and in low numbers. Similarly. Lipogomphus, Dytiscidae, Curculidae, Elmidae, Scirtidae, Histeridae, Pseudolimnophila, Stratiomyidae, and Physa were collected in low numbers at only one location. Five functional feeding groups were collected from the Dry Run drainage (Table 26). Resulting from the presence of Asellidae and Hyalella, omnivores were the dominant functional group at most locations. Although less dominant, collector-gatherers and scrapers were consistently collected from all locations in the study area and included the mayflies Leucrocuta and Leptophlebia. The dominant scraper was the mayfly Leucrocuta. Predators were dominant at locations II and III and were represented primarily by the stonefly Perlesta. The overall assessment of ecological condition first focuses on the evaluation of habitat quality, and secondly on the analysis of biological components in light of habitat. Habitat, 11 0 0 0 - .,- 0 USFW 0598 as the principal determinant of biological potential, sets the stage for interpreting biosurvey data and can be used as a general predictor of biological condition. High quality habitat will support high quality biological communities and responses to minor alterations will be subtle and of little consequence. However, as a habitat declines in quality, disceraable biological, impairment results. When habitat and biological data are systematically collected together, empirical relationships can be quantified and subsequently used for screening impact and discriminating water quality effects from habitat degradation. The watershed that drains the Dry Run study area has been modified as a result of past and present land use, particularly with respect to cattle grazing and other agricultural practices, as well as the siting of commercial and industrial facilities. The loss of riparian vegetation, through replacement by species resistant or adapted to grazing, or elimination by grazing has several consequences that should be considered when evaluating the distribution of benthic macroinvertebrates and macroinvertebrates in the current study. The attainable biological potential of a stream or river is primarily determined by the quality of the habitat at a particular location. The Dry Run study area is situated in a rural area utilized primarily for grazing cattle and, although historic indications of grazing are evident, significant portions of the riparian area remain vegetated, and there are few areas with a completely open canopy and exposed soil. Portions of the Dry Run drainage, though somewhat degraded, support a surprisingly diverse and apparently robust aquatic community. The taxonomic diversity and numerical abundance of the macroinvenebrate was relatively high at the reference area. In contrast, the diversity and abundance at locations I, II. Ill, and IV was reduced substantially. Since habitat considerations at all locations in Dry Run are similar, the presence of contamination at the latter locations may be significant. 3.2.2 Mammal Four species of small mammals (meadow voles, short-tailed shrews, white-footed mice, and meadow jumping mice) were caught during the trapping effort. Whole bodies were submitted for lipid, TAL metal and total fluoride analysis. The trapping effort revealed at least one important field observation, which was there was extremely low trapping success in Area I, the area nearest the landfill outfall, as compared to the other areas. This is highly irregular given the similar habitats present site-wide, and may indicate an ecological threat. Field necropsies identified several significant problems with the small mammals collected in the meadow areas adjacent to Dry Run. Short-tail shrews sampled from all areas showed blackened and degenerating teeth. Shrews commonly have what is known as chestnut tipped teeth, where the extreme points of the dentitia are a light brown color. The black, mottled, and degenerating teeth observed in this study are not normally observed in shrews. One meadow vole sampled from the area was missing the left kidney, and another appeared to have and extra kidney or an extra lobe on the right kidney, independent of the adrenals. Sufficient numbers of meadow voles were caught from the Reference Area, Area II, Area III, and Area IV for statistical comparisons of tissue concentrations. Lipid concentration of meadow voles was significantly depressed in the Reference Area, Area II, and Area III, compared to that observed in Area IV (p<0.001). Barium concentration was significantly lower in the Reference Area, Area II. and Area III. compared to that observed in Area IV 12 00*5- USFW 0599 (p=0.067). Sufficient numbers of short-tail shrews were caught from the Reference Area and Area III for statistical comparisons. There were no differences in body concentration of lipid. TAL metals, and fluoride in shrews taken from these two areas. Results of the trapping success, TAL metals, and fluoride analysis are presented in Tables 27-29, and in Appendix B. Results are presented by species and trapping location. 3.2.3 Fish Four species of fish were collected from Dry Run in Areas II, III, and IV. No fish were observed in Area I or the Reference Area. Creek chubs and fantail darters were collected in Area IV. Creek chubs and river chubs were collected in area III. Creek chubs, river chubs, fantail darters, central stone rollers, and black-nose dace were collected in Area II. Fish sampled during the electrofishing effort in Dry Run were submitted for whole body lipid, TAL metal and fluoride analysis. A composite sample that was taken during a historical fish kill in Dry Run was also analyzed. Since creek chubs were the only species common to all three sampling locations, statistical analysis concentrated on differentiating between tissue concentrations in this species. Aluminum, arsenic, barium, beryllium, cobalt, iron, lead, manganese, thallium, and vanadium were significantly higher in creek chubs from area II than those sample in Areas m and IV. Likewise, concentrations of these metals in Area III creek chubs were higher than those in Area IV. Conversely, cadmium and silver concentrations showed the reverse trend, with tissue concentrations in Area IV significantly higher than those measure in Areas II or III. In spite of this result, it is clear that fish inhabiting upper reaches of Dry Run. nearer to the landfill are being dosed with a significantly higher amount of metals than those in the lower reaches. There were no difference in lipid or fluoride concentration. Results of the chemical analyses are presented in Tables 30-32 and in Appendix B. 3.2.4 Earthworm Three replicate eanhworm samples were produced from each of the earthworm toxicity test soil samples. One-way analysis of variance was used to look for significant differences in tissue concentrations between earthworms exposed to each of the five soil treatments. Cadmium and thallium concentrations in the eanhworm tissue was significantly higher in the Area I exposures than those in Areas II, III, IV, or the Reference soils. Cobalt levels were lower in worms taken from the reference area, but tended to increase with increasing distance from the landfill. Copper and nickel concentrations were higher in worms taken from the reference soils than those observed in worm taken from the other soil area exposures. Further results of the earthworm tissue analyses for lipid, TAL metals and fluoride concentration are presented in Tables 33-35 and in Appendix B. 3.2.5 Veaetation 13 000.,,?."; USFW 060C Three replicate samples of meadow grass were taken in each of the five soil sampling locations. One way analysis of variance was used to look for differences in plant tissue concentrations across the five sampling areas. Barium concentration was significantly higher in the Area I vegetation than in the Area III and IV vegetation, but similar to that observed in plants take in the Reference and in Area II. Manganese concentration was significantly higher in the Area I and reference vegetation than in the Area II. Ill and IV vegetation. Cobalt was significantly higher in Area IV vegetation than that taken in any of the other areas. There was no difference in the fluoride or lipid concentration. Results of the TAL metals and fluoride analysis are presented in Tables 36-38 and in Appendix B. 3.3 Histological assay of small mammal liver and kidney Histological analysis of liver and kidney sections of meadow voles, short-tail shrews, meadow jumping mice, and white-footed mice trapped in each of the five trapping areas concluded that there were no substantive changes in liver or kidney morphology. The absence of a kidney in one animal, and the presence of an extra lobe on the right kidney of another provide anecdotal evidence of an effect, however we are unable to ascertain the importance of these observations. Full summaries of the histopathological work are presented in Table 39 and in Appendix B. 3.4 Toxicity Testing Earthworm Based on the toxicity evaluation of soils, there is no evidence for growth or survival effects on earthworms tested in any of the soil samples collected at the Dry Run Creek site. Survival was 100% in all treatment replicates and growth ranged from 32.4 to 54.3%. Further results of the earthworm toxicity test are presented in Table 40 and in Appendix C. Fathead minnpw Based on the toxicity evaluation of surface water samples to the fathead minnow, it appears that surface water taken in the Upper Tributary A location induced significant mortality. Survival in the Upper Tributary A sample was 58% while survival in all other samples, including the reference location, ranged from 87 to 100%. There appear to be no growth related effects water, on the minnows in any of the water samples taken from Dry Run Creek. Survival was negatively correlated potassium concentrations, however these correlations are not statistically significant at the 0.10 level. There was a significant positive correlation between fathead survival and iron concentrations in the filtered water samples. Further results of the fathead minnow toxicity test are presented in Table 40 and in Appendix C. Amohinod Based on the results of the 10 day solid phase whole sediment toxicity test with the amphipod, Hyalelln azteca, growth of the organisms was inhibited in the sediment samples taken at the Upper Tributary A. and Area II locations. There were no effects observed on survival in any of the samples taken. The observed negative growth effect was significantly negatively correlated with 14 0 0 0 f>ejl * USFW 0601 fluoride, alu m i n u m , calcium, magnesium, nickel, potassium, and sodium. Further, there were strong negative associations between the growth endpoint and chromium, copper, lead, and zinc concentrations, although the relauonships were not significant at the 0.10 level. Further results of the amphipod toxicity test are presented in Table 40 and in Appendix C. 4.0 SUMMARY OF PRELIMINARY ECOLOGICAL RISK ASSESSMENT SCREEN Sediment, soil and water concentrations were compared against Region III BTAG screening values (U.S. EPA 1995). Hazard quotients were generated by dividing the maiimnm site concentration measured in each matrix by the corresponding Region III benchmark values. All contaminants for which maiimnm concentrations exceeded benchmarks for sediment, soil, and water in the initial screening-level risk assessment are listed in the following sections. Contaminants that failed the initial screening process will be further evaluated in a final risk assessment for the site. Sediment Table 1 lists m a i i m u m concentrations, screening criteria, and quality criteria factors for sediment contaminants. The maximum concentration recorded at the site exceeded the benchmark values for the following compounds: arsenic, chromium, copper, manganese, and nickel. Because of the lack of a screening benchmark, the following compounds are still considered as risk factors as well: fluoride, alu m inum , barium, beryllium, cobalt, iron, and vanadium. Water Table 1 lists m ax im u m concentrations, benchmarks, and quality criteria factors for water con t a m i n a n t The maximum concentration recorded at the site exceeded the benchmark values for the following compounds: aluminum, copper, and iron. Because of the lack of a screening benchmark, fluoride is considered to be a potential risk factor. Soil Table l lists maximum concentrations, screening criteria, and quality criteria factors for soil c o n ta m in a n ts. The maximum concentration recorded at the site exceeded the benchmark values for the following compounds: aluminum, beryllium, chromium, copper, iron, lead, manganese, vanadium, and zinc. Because of the lack of a screening benchmark, the following compounds are still considered as risk factors as well: fluoride and trichlorofluoromethane. 5.0 DISCUSSION The data generated during the field effort suggests that there are potential problems associated with conditions at the Dry Run Creek site. Minimally, the results of the sediment and water toxicity tests suggest potential problems in the stream. Some metals appear in higher tissue concentrations in biota sampled nearest the outfall of the landfill, with those levels progressively dropping with increasing distance from the landfill area. Likewise, sediments sampled in Dry Run near the landfill outfall appear to have higher fluoride and metals concentrations than those sampled further downstream. A preliminary screen of potential risk factors suggests that other problems, specifically elevated levels of fluorides, organofluorides, and some metals, may be present as well. Data gathered during the field effort will be further analyzed through a base-line ecological risk assessment for the Dry Run Creek site 15 0 0 0 - .;'; 5 USFW 0602 SECTION II ECOLOGICAL RISK ASSESSMENT 1.0 INTRODUCTION 1.1 Objective The objective of this risk assessment was to provide technical support to the U.S. Environmental Protection Agency Region III in conducting an evaluation of potential ecological threat due to existing contaminant levels in soil, sediment, and water at a working beef production farm located down gradient of a landfill. Soil, sediment, surface water, and biota samples were collected for contaminant analyses and soil, sediment, and surface water were collected for laboratory toxicity testing. The information gathered during this field effort was incorporated into in an ecological risk assessment for the Dry Run Creek site. 1.2 Site Background The site is a working beef production farm located in Washington, Wood County, WV. The owner of the farm has filed numerous complaints with the West Virginia Department of Natural Resources and the U. S. EPA alleging that contaminants are being discharged from an industrial landfill owned by the Dupont corporation, into Dry Run. Dry Run flows through the farmer's property and is a primary source of water for his cattle. The fanner maintains that numerous deaths, blindness, and other unusual illnesses observed in his herd are directly attributable to the contaminants that are discharged into Dry Run from the Dupont landfill. In addition to these abnormalities, numerous fish and wildlife kills have also been reported in Dry Run since the construction of the landfill. : 2.0 PROBLEM FORMULATION This risk assessment was designed to evaluate the potential threats to ecological receptors from exposure to site contaminants. During the preliminary risk assessment, the problem formulation process included the identification of COCs and a comparison of the maximum concentration of COCs with accepted benchmarks. This information was then used to identify complete exposure pathways of compounds exceeding benchmarks to ecological receptors and their appropriate measurement endpoints. The first step of the preliminary risk assessment process compared all chemicals analyzed in soil, sediment, and water during the field with established toxicological benchmarks. Benchmarks for sediment and soil were used to identify potential contaminants of concern for the protection of aquatic biota (U.S. EPA 1995, Long and Morgan 1990, Long et al. 1995, Persuad et al. 1992, U.S. EPA 1992, Suter and Mabrey 1994). Compounds exceeding benchmarks were retained for further evaluation using ingestion-based exposure models for higher vertebrates, and direct exposure assays for fish, benthic and terrestrial invertebrates. 2.1 Ecological Risk Assessment This ecological risk assessment was written to determine the risk associated with the exposure of biota to site-related contaminants. The following steps were completed for this preliminary risk assessment: (1) A literature search was conducted to locate life history information for selected indicator species, to determine ecotoxicological effects of site contaminants, and to locate bioconcentration factors for site contaminants. (2) An evaluation of ecological receptors was prepared. This consisted of the following: Exposure scenarios were determined based on site contaminant levels, the extent and magnitude of contamination, and the toxicological mechanisms of the 16 USFW 06( contaminants. Indicator species were selected based on species present and/or potentially present on site, the availability of toxicity information from the literature, and the potential far exposure to site contaminants based on habitat use or behavior. Exposure pathway(s) were determined for each indicator species. Exposure and effect profiles were written for each indicator species and each site contaminant A risk characterization was conducted which involved the calculation of hazard quotients (HQs) for each species for a range of exposure scenarios. Based on the results of this evaluation, the COCs identified in the initial screen were further evaluated through the use of conservative risk models. Identification of the Contaminants of Concern The contaminants of potential concern were identified using the initial contaminant screen. The COCs for this site that were retained through the preliminary screen include metals, fluoride, and organofluoride compounds. Exposure Characterization The objective of the exposure assessment is to determine the pathways and media through which receptors may be exposed to sitecontaminants. Potential exposure pathways are dependant on habitats and receptors present on site, extent and magnitude of contamination, and environmental fate and transport of COCs. In this base-line ecological risk assessment, it will be concluded that "a potential risk" exists if the HQ calculated from the maximum site concentration and the No Observed Apparent Effect Level (NOAEL) equals or exceeds 1. Exposure to COCs present in forage and prey species via ingestion could cause toxicity in higher trophic level organisms. In addition to exposure via consumption of contaminated forage, ecological receptors may also be exposed through ingestion of water and incidental ingestion of soil/sediment. The exposure of benthic invertebrates, terrestrial invertebrates, and fish was determined by examining results of the toxicity tests. Hazard Characterization/Toxicity Assessment To determine the effects of contaminants on biota, it is necessary to understand the mechanisms of toxicity of the chemicals and the systems that they affect. Knowledge of the fate, effects, and mode of action of the COCs allows for the selection of appropriate assessment endpoints. Next is a review of the general toxicological information for the COCs identified in Section 2.4. 2.4.1 Fluoride Inorganic fluoride compounds are ubiquitous in nature. However, industrial processes such as manufacturing and mining have contributed to the environmental load of fluoride, primarily through atmospheric deposition._Jn low doses, it is accepted that fluoride is 17 eeo /`.j *> USFW 0604 protective of teeth in humans as well as other animals. How.ver In higher levels it is generally accepted that fluoride can be toxic to both plant and animal life. Dental and skeletal lesions, lameness, stiffness of gait, appetite impairment, decreased weight gain, decreased milk production, posture abnormalities, tremors, stillbirths, overgrowth of hooves, severe diarrhea, and death have been associated with mammalian fluoride toxicity (Suttie, 1977; Shupe et al, 1992). In addition to the effects known in mammals, birds are also susceptible to fluoride toxicity. Mortality, decreased growth rates, depressed appetite, and decreasedeggshell quality have been reportedastoxicological endpoints of fluoride exposure in birds (Fleming and Schuler 1988; Fleming et al. 1987; Guenter and Hahn 1986). 2.4.2 Organofluorides Organofluorides are used in a variety of industrial processes including the production of Teflon"4, propellants, and refrigerants. Available toxicological data generally concentrates on inhalation exposure and dermal absorption. Acute (10 day) exposure of rats to chlorodifluormethane produced decreased maternal and fetal weights, aswell as an increased frequency of anopthalmia and subsequent blindness in newborn fetuses (IARC 1986). Hexafluoropropene exposure induced an increased incidence of hamster ovary cell aberrations and increased frequency grossly abnormal cells (HSDB 1997). 2.4.3 Aluminum Because of its strong reactivity, aluminum (Al) is not found as a free metal in natures Aluminum has only one oxidation state (+3), thus its behavior in the environment depends on its ordination chemistry and the surrounding conditions. In soils, a low pH generally results in an increase in aluminum mobility. In water, an equilibrium with a solid phase is established that controls the extent of aluminum dissolution (ATSDR 1990). Plants vary in their ability to remove aluminum from soils, although bioconcentration factors for plants are generally less than one. Biomagnification of aluminum in terrestrial food chains does not appear to occur. There is no data on the biomagnification of aluminum in aquatic food chains (ATSDR 1990). The nervous system may be a target area for aluminum. Aluminum accumulates in neurofibrillary tangles in humans with Alzheimer's disease. Aluminum may also interact with neuronal DNA to alter gene expression and protein formation. Mammalian studies do not indicate that aluminum affects reproduction although some developmental effects have been reported in mammals (ATSDR 1990). Aluminum is known to interfere with gill transport of oxygen and carbon dioxide in fish, and has also been identified in ionoregulatory disruption. 2.4.4 Arsenic Several review articles are available which discuss the toxic effects of As (Eisler 1988a, Nxiagu 1994). Arsenic tends to be widespread in the environment (Woolson 1975) and is constantly being oxidized, reduced, or mobilized (Eisler 1988a). Physical processes are important in determining As bioavailability in aquatic environments. For example, arsenates are readily adsorbed onto sediments with high organic matter, and arsenates are more strongly adsorbed onto sediments than other As forms. However, absorption depends on the As concentration, sediment characteristics, pH, and ionic concentration of other compounds 18 G O O 27 USFW 060i (Eisler 1988a; U.2. SP*. 19811. The U.S. EPA (1981) noted that arsenate (pentavalent) is the predominant As form in oxygeuo--- 'car *nd that arsenite (trivalenx) isthe predominant As form in anaerobic conditions. Arsenic is not significantly concentrated in aquatic invertebrates; whole body concentration factors for invertebrates range from 3 to 17 for exposure to arsenic trioxide (trivalent) and from 0 to 7 for arsenic pentoxide (pentavalent). Arsenic may be bioconcentrated by orzanisms at the bottom of the food chain; however, data do not indicate that significant biomagnification occurs (U.S. EPA 1985). 2.4.5 Beryllium The majority of the beryllium (Be) in the environment is the result of coal and oil combustion. Beryllium naturally enters waterways through the weathering of rock and soil, and through deposition of annospheric beryllium. Upon reaching water and soil, beryllium is most likely retained as an insoluble form that is generally immobile. However, beryllium chloride, fluoride, nitrate, phosphate, and sulfate (tetrahydrate) are all water-soluble forms (ATSDR 1993a). Due to its geochemical similarity to aluminum, beryllium may be expected to adsorb onto clay surfaces at low pHs, and it may remain precipitated as insoluble complexes at higher pHs. Therefore, beryllium is expected to have limited mobility in soil (ATSDR 1993a). ; Beryllium is not expected to bioconcentrate in aquatic animals and no evidence for significant biomagnification within food chains has been found. Beryllium is extremely toxic to warmwater fish in soft water. The degree of toxicity decreases with increasing hardness (ATSDR 1993a). Major exposure routes for aquatic ecological receptors include ingestion of contaminated soil and sediment. Although several studies point out the negative effects of beryllium in mammalian systems, no studies that evaluated the relationship between sediment beryllium concentration and observed toxicity to benthic organisms could be found (ATSDR 1993a). 2.4.6 Chromium Chromium (Cr) can exist in oxidation states ranging from -2 to +6, but is most frequently converted to the relatively stable trivalent (--3) and hexavalent (+6) oxidation states (Eisler 1986a). In both freshwater and marine systems, hydrolysis and precipitation are the most important processes that determine the fate and effects of Cr, whereas adsorption and bioaccumulation are relatively minor. Precipitated Cr'1 hydroxides remain in sediments under aerobic conditions. However, under anoxic and low pH conditions, Cr*1hydroxides may solubilize and remain as ionic Cr*1unless oxidized to Cr** through mixing and aeration (Eisler 1986a). In soils, the solubility and bioavailability of Cr are governed by soil pH and organic complexing substances, although organic complexes play a more significant role (James and Bartlett 1983a; James and Bartlett 1983b). TH* trivalent state <sthe form usually found in biological materials. This form functions as an essential element in mammals by maintaining efficient glucose, lipid, and protein metabolism (Stevens et al. 1976). Chromium is beneficial but not essential to higher plants (Eisler 1986a). The biomagnification and toxicity of Cr*1is low relative to Cr** because of 19 GO USFW 0606 its low membrane permeability and its noncorrosivity. However, a large degree of accumulation by aquatic and terrestrial plants and animals in the lower trophic levels has been documented (Eisler 1986a), although, the mechanism of accumulation remains largely unknown. Chromium is mutagenic, carcinogenic, and teratogenic, with Cr** exhibiting the greatest toxicity; relatively less is known about the toxicity of Cr*1. At high concentrations, Cr*4 is associated with abnormal enzyme activity, altered blood chemistry, lowered resistance to pathogenic organisms, behavioral modifications, disrupted feeding, histopathology, osmoregulatory upset, alterations in population structure, and inhibition of photosynthesis. Rabbits fed dietary Cr accumulated hyaluronates, chondroitin sulfates, and neutral mucopolysaccharides in the soft tissues, causing pericapillary sclerosis (Kucher and Shabanov 1967). This accumulation blocked blood tissue barriers, which are permeable under normal conditions, preventing the normal transport of metabolites. One manifestation of this condition was the inhibition of insulin production in the pancreatic islets due to damage to the beta-cells contained therein. Chromium also leads to nephron damage via swelling and loss of microvilli, the formation of intracellular vacuoles, mitochondrial swelling, and cytoplasmic liquefication and loss of ceils lining the nephron surface (Evan and Dail 1974). The preliminary step in Cr-induced respiratory cancer is speculated to be the scarring of alveolar tissue, followed by the elicitation of inflammatory reactions in lung tissue leading to bronchopneumonia, alveolar epithelial changes, atrophy, and benign tumor formation. Dire skin contact with highly corrosive chromic acid and its anhydride produces skin ulcers and necrosis by a mechanism independent of any allergic response (Steven et al. 1976). 2.4.7 Copper Copper (Cu) does not appear to have mutagenic properties (IRIS 1990), but it is a teratogen (RTECS 1991) and a possible carcinogen (Venugopal and Luckey 1978). Copper is caustic, and acute toxicity is primarily related to this property (Hatch 1978). Copper is an essential element for animals and is a component of many metalloenzymes and respiratory pigments (Demayo et al. 1982). It is also essential to iron (Fe) utilization and functions in enzymes for energy production, connective tissue formation, and pigmentation (Venugopal and Luckey 1978). Excess Cu ingestion leads to accumulation in tissues, especially in the liver. High levels of Cu modify hepatic metabolism (Brooks 1988), which may leadto inability of the liver to store and excrete additional Cu. When liver concentration exceeds a certain level, the metal is released into the blood, causing hemolysis and jaundice. High Cu levels also inhibit essential metabolic enzymes (Demayo et al. 1982). Toxic symptoms appear when the liver accumulates 3 to 15 times the normal level of Cu (Demayo et al. 1982). Although the exact mechanism oftoxicity isnot known, the following mechanisms have been proposed: formation of stable inhibitory complexes with cytochrome P-450 (Wiebel et al. 1971); impairment of function of NADPH-cytochrome c reductase and alteration of mixed function oxidations (Reiners et al. 1986); and inhibition ofheme biosynthesis (Martell 1981). Intranuclear inclusions may act as a detoxifying mechanism where Cu is complexed by 20 000 :'L,7(j1 USFW 060 protein ligands, protecting cytoplasmic organelles (Demayo et al. 1982). Ruminants are the most sensitive mammal species to Cu toxicosis. Young animals retain more dietary Cu than older animals and are more sensitive to Cu toxicity (Venugopal and Luckey 1978). 2.4.8 Iron Iron (Fe) is commonly detected in concentrations of 5 percent or more in soil. It is used primarily in the production of steel and other alloys as well as a major source of hydrogen. Iron is a constituent of hemoglobin and is essential to plant and animal life as well as being an important component in cellular oxidative processes. The disposition of ingested iron is regulated by a complex mechanism to maintain homeostasis. Therefore, bioconcentration in biota is not expected to be a significant process for iron. Generally, about 2 to 15 percent of ingested iron is absorbed from the gastrointestinal tract, and elimination is approximately 0.01 percent of the body burden per day. Adverse effects of iron toxicity may include renal failure and hepatic cirrhosis. The mechanism of toxicity begins with acute mucosal cell damage and absorption of ferrous ions directly into circulation, resulting in capillary endothelial cell damage to the liver (Shacklette and Boemgen 1984). 2.4.9 Lead Lead does not biomagnify to a great extent in food chains, although accumulation by plants and animals has been extensively documented (Wixson and Davis 1993, Eisler 1988b). Older organisms typically contain the highest tissue Pb concentrations, with the majority of the accumulation in the bony tissue of vertebrates (Eisler 1988b). Predicting the accumulation and toxicity of Pb is difficult since its effects are influenced to a very large degree, relative to other metals, by interactions among physical, chemical, and biological variables. In general, organolead compounds are more toxic than inorganic Pb compounds, and young, immature organisms are most susceptible to its effects (Eisler 1988b). In plants, Pb inhibits growth by reducing photosynthetic activity, mitosis, and water absorption. The mechanism by which photosynthetic activity is reduced is attributed to the blocking of sulfhvdryl groups, inhibiting the conversion of coproporphyrinogen to prcporphyrinojen (Holl and Hampp 1975). The toxic effects of Pb on aquatic and terrestrial organisms are extremely varied and include mortality, reduced growth and reproductive output, blood chemistry alterations, lesions, and behavioral changes. However, many effects exhibit general trends in their toxic mechanism. Generally, Pb inhibits the formation of heme, adversely affects blood chemistry, and accumulates at hematopoietic organs (Eisler 1988b). At high concentrations near levels causing mortality, marked changes to the central nervous system occur prior to death (Eisler 1988b). Plants can uptake Pb through surface deposition in rain, dust, and soil, or by uptake through the roots. The ability of a plant to uptake Pb from soils is inversely related to soil pH and organic matter content. Lead can inhibit photosynthesis, plant growth, water absorption. 2.4.10 Manganese 21 0 0 0 - ..; r * USFW 060' Manganese (Mn) does not occur as a free metal in the environment but is a component of numerous minerals. Elemental manganese and inorganic manganese compounds have negligible vapor pressures, but may exist in air as suspended particulate matter derived from industrial emissions or the erosion of soil. Removal from the atmosphere is mostly through gravitational sealing. The transport and partitioning of manganese in water is controlled by the solubility of the specific chemical form present. The metal may exist in water in any of four oxidation states (2+. 3+, 4+, or 7+). Divalent manganese (Mn-K2) predominates in most waters (pH 4 to 7), but may become oxidized at a pH greater than 8 or 9. Manganese isoften transported in moving water as suspended sediments. The tendency of soluble manganese compounds to adsorb to soils and sediments depends mainly on the cation exchange capacity and the organic composition of the soil. Manganese in water may be significantly bioconcentrated at lower trophic levels. However, biomagnification in the food chain may not be significant (ATSDR 1990). The amount of manganese absorbed across the gastrointestinal tract is variable. There does not appear to be a marked difference between manganese ingested in food or in water. One of the key determinants of absorption appears to be dietary iron intake, with low iron levels leading to increased manganese absorption. This is probably because both iron and manganese are absorbed by the same transport system in the gut (ATSDR 1990). 2.4.11 Nickel Pure nickel (Ni) is a hard, white metal that is usually used in the formation of alloys (such as stainless steel) and Ni combined with other elements is found in all soils. Nickel is the 24* most abundant element and is found in the environment as oxides or sulfides. Nickel may be released into the environment through mining, oil-burning power plants, coal-burning power plants, and incinerators. Nickel will attach to soil or sediment particles, especially those containing Fe or manganese (Mn). Under acidic conditions, Ni may become more mobile and seep into the groundwater. The typical Ni concentration reported in soils is from 4- 80 milligrams per kilograms (mg/kg). The speciation and physicochemical state of Ni is important in considering its behavior in the environment and its availability to biota. The most probable exposure routes of Ni are through dermal contact, inhalation of dust, and ingestion of Ni-contaminated soil. The respiratory system is the primary target of Ni exposure following inhalation. Manifestations such as inflammation of the lungs, fibrosis, macrophage hyperplasia, and increased lung weight have been noted in animals exposed to Ni. Animals exposed to Ni through oral exposure were noted to have lethargy, ataxia, irregular breathing, salivation, and squinting (ATSDR 1996). 2.4.12 Vanadium Elemental vanadium does not occur naturally but it can exist in 50 different ores and fossil fuels. Other anthropogenic sources include acid-mine leachate, sewage sludge, and fertilizers. The principal use of vanadium is as an alloy constiment, especially in steel. The addition of vanadium to steel removes oxygen and nitrogen, which improves the strength. The average concentration of vanadium in the earths crust is 150 mg/kg and in the U.S. soils are 200 mg/kg (Byemum et al. 1974). The release of vanadium to water and soil occurs as a result of the weathering of rocks and from soil erosion. This process usually converts the less-soluble trivalent form to the more- 22 000 USFW 06C soluble pentavalent form. The mobility of vanadium in soil is affected by pH, redox potential, and the presence of particulates. Relative to other minerals, vanadium is mobile in neutral or alkaline soils and its mobility decreases in acidic soils (ATSDR 1991; Van Zinderen Bakker and Jaworski 1980). In the terrestrial systems, bioconcentration is more common in lower plant species. In addition, vanadium concentrations in plants are dependent on the amount of water-soluble vanadium, pH, and growing conditions. Vanadium appears to be present in all terrestrial mammals but the concentrations are usually below the detection limits. The highest concentration of vanadium is usually found in the liver and skeletal tissues (ATSDR 1991). Vanadium is very poorly absorbed into the gastrointestinal tract and the toxic mechanism of vanadium on the respiratory system is similar to other metals (Castronova et al. 1984). Vanadium damages the alveolar macrophages by decreasing the macrophage membrane integrity. Damaged macrophages inhibit the ability of the respiratory system to clear itself of other particles. In vitro experiments indicate that the mechanism of toxicity of vandium is by inhibiting sodium-potassium ATPase activity, which inhibits the sodium-potassium pump. This pump is necessary for the transport of material across cell membranes (Nechay and Saunders 1978). 2.4.13 Zinc Zinc (Zn) is essential for normal growth and reproduction in plants and animals and is regulated by metallothioneins. Metallothioneins act as temporary Zn storage sites and aid in reducing the toxicity ofZn to both vertebrates and invertebrates (Olsson et al. 1989). Zinc is not known to bioaccumulate in food chains, because it is regulated by the body and excess Zn is eliminated. Zinc has its primary metabolic effect onZn-dependant enzymes that regulate the biosynthesis and catabolic rate of ribonucleic (RNA) acid and deoxyribonucleic acid (DNA). High levels of Zn induce Cu deficiency and interfere with metabolism of calcium (Ca) and Fe (Goyer 1986). The pancreas and bone seem to be the primary targets of Zn toxicity in birds and mammals. Pancreatic effects include cytoplasmic vacuolation, cellular atrophy, and cell death (Lu and Combs 1988, Kazacos and Van Vleet 1989). Zinc preferentially accumulates in bone, and induces osteomalacia (a softening of bone caused by a deficiency of Ca, phosphorus and other minerals) (Kaji et al. 1988). Gill epithelium is the primary target site in fish. Zinc toxicosis results in destruction of gill epithelium and tissue hypoxia (Spear 1981). Selection of Assessment Endpoints The information gathered during a site reconnaissance and during the field work, and subsequent discussions with the U.S. EPA on-scene coordinator and the Region III Biological Technical Assistance Group, allowed for the selection of assessment endpoints that corresponded to the habitat types present at the Dry Run Creek site. The site is composed of a variety of habitats including forested and old-field uplands, grassy meadows, the creek, and associated riparian areas. A variety of birds, mammals, and fish may use the site for feeding and nesting. Likewise, terrestrial and benthic invertebrates are key elements in the functions of these systems. Therefore, the assessment endpoints focused toward these faunal groups. Viability of terrestrial, avian, and aquatic populations and organism survivability were selected as assessment endpoints for this risk assessment. Listed next are 23 0& Q -J5 USFW 0610 the specific assessment endpoints selected for this ecological risk assessment. Ten assessment endpoints were chosen to evaluate the risk of contaminants at the Dry Run Creek site: 1) protection of benthic invertebrate community structure and function 2) protection of soil invertebrate community structure and function 3) protection of fish communities to ensure that direct exposure to contaminants does not have a potential negative impact on growth, survival, or reproductive success. 4) protection of worm-eating birds to ensure that ingestion of contaminants in forage does not have a potential negative impact on growth, survival, or reproductive success. 5) protection of carnivorous birds to ensure that ingestion of contaminants in forage does not have a potential negative impact on growth, survival, or reproductive success. 6) protection of carnivorous mammals to ensure that ingestion of contaminants in forage does not have a potential negative impact on growth, survival, or reproductive success. 7) protection of piscivorous mammals to ensure that ingestion of contaminants in forage does not have a potential negative impact on growth, survival, and reproductive success. 8) protection of omnivorous mammals to ensure that ingestion of contaminants in forage does not have a potential negative impact on growth, survival, and reproductive success. 9) protection of insectivorous mammals to ensure that ingestion of contaminants in forage does not have a negative impact on growth, survival, and reproductive success. 10) protection of herbivorous mammals to ensure that ingestion of contaminants in forage does not have a negative impact on growth, survival, and reproductive success. Production of Testable Hypotheses The testable hypotheses are specific risk questions that are based on the assessment endpoints. Based on the mechanism of contaminant toxicity, the number of exposure pathways that may exist for an assessment endpoint, or other factors, there may be more than one question for each assessment endpoint. Are levels of site contaminants sufficient to have negative effects on benthic invertebrate community structure and function? Are levels of site contaminants sufficient to have negative effects on soil invertebrate community structure and function? Are levels of site contaminants sufficient to cause direct toxicity to fish growth, survival, and reproductive success? Are levels of site contaminants sufficient to cause negative impacts on growth, survival, or reproductive success of worm-eating birds due to the ingestion of contaminated forage, soil, and water 24 000 USFW 061 on the site? Are levels of site contaminants sufficient to cause negative impacts on growth, survival, and reproductive success of carnivorous birds due to the ingestion of contaminated forage, soil, and water on the site? Are levels of site contaminants sufficient to cause negative impacts on growth, survival, and reproductive success of carnivorous mammals due to the ingestion of contaminated forage, soil, and water on the site? Are levels of site contaminants sufficient to cause negative impacts on growth, survival, and reproductive success of piscivorous mammals due to the ingestion of contaminated forage, soil, and water on the site? Are levels of site contaminants sufficient to cause negative impacts on growth, survival, and reproductive success of omnivorous mammals due to the ingestion of contaminated forage, soil, and water on the site? Are levels of site contaminants sufficient to cause negative impacts on growth, survival, and reproductive success of insectivorous mammals due to the ingestion of contaminated forage, soil, and water on the site? Are levels of site contaminants sufficient to cause negative impacts on growth, survival, and reproductive success of herbivorous mammals due to the ingestion of contaminated forage, soil, and water on the site? 2.7 Conceptual Model The conceptual model relies on contaminant and habitat characteristics to identify critical exposure pathways to the selected measurement endpoints. At the Dry Run Creek site, contaminants in the soil may come in contact with subsurface (earthworms) and above-ground terrestrial receptors (small mammals) inhabiting the wooded, wetland, and open field areas of the site. Subsurface terrestrial receptors in these areas may be exposed to site contaminants through direct contact with the soil, and in some cases, the intentional ingestion of soil. Above-ground terrestrial receptors may be exposed to contaminants through direct contact with the soil, the ingestion of subsurface terrestrial organisms, the ingestion of other above-ground terrestrial receptors, the incidental ingestion of soil adhered to food items, and the intentional ingestion of surface water from any of the on-site surface drainages. The wooded areas, riparian area, and meadow areas provide distinct habitat types that may support a variety of terrestrial and avian receptors. For example, a small omnivorous mammal may occupy one or all the habitat types, whereas, an individual carnivorous mammal may regularly traverse all three habitats daily in search of food items. Avian piscivores and carnivores may be exposed to site contaminants in much the same way as an above-ground terrestrial receptor. The consumption of contaminated prey, the incidental ingestion ofsoil/sediment, and the consumption ofsurface water may transfer contaminants to these receptors. The conceptual model relies on contaminant and habitat characteristics to identify critical exposure pathways to the selected measurement endpoints. The preliminary risk screen identified metals, fluoride, and crichlorofluoromethane as the primary contaminants exceeding benchmarks in site sediment, soil, and water. Benthic macroinvertebrates, fish, and terrestrial invertebrates may be 25 000 USFW 0612 exposed to contaminated sediment, water, or soil through direct toxicity. For the purposes of this risk assessment, the concentration of thecontaminants of concern found in the sediment, water, or soil were correlated with toxicity levels identified in the corresponding toxicity tests to determine if benthic invertebrates fish, or terrestrial invertebrates may be at risk. Terrestrial receptors may be exposed to contaminants by feeding on organisms which have accumulated COCs in their tissues. Higher trophic level receptors may also be exposed to contaminants from food ingestion and via incidental ingestion of soil/sediment and water. The pathway to the reference area meadow is unknown, however the pathway to the reference area stream may involve groundwater transport. The following pathways were evaluated in this risk assessment: I. Benthic invertebrates a) Direct exposure to sediment II. Soil invertebrates a) Direct exposure to soil III. Fish a) Direct exposure to water IV. Worm-eating bird a) Ingestion of earthworms b) Incidental ingestion of soil c) Incidental ingestion of water V. Carnivorous bird a) Ingestion of small mammals b) Incidental ingestion of soil c) Incidental ingestion of water VI. Carnivorous mammal a) Ingestion of small mammals b) Incidental ingestion of soil c) Incidental ingestion of water VII. Piscivorous mammal a) Ingestion of forage fish b) Incidental ingestion of sediment c) Incidental ingestion of water VIII. Omnivorous mammal a) Ingestion of forage fish b) Incidental ingestion of sediment c) Incidental ingestion of water IX. Insectivorous mammal a) Ingestion of earthworms b) Incidental ingestion of sediment 0 Incidental ingestion of water X. Herbivorous mammal 26 0 004 3 USFW 0613 a) Ingestion of vegetation b) Incidental ingestion of sediment c) Incidental ingestion of water Selection of Measurement Endpoints Measurement endpoints are measurable ecological characteristics that are related to the valued characteristics selected as assessment endpoints. Measurement endpoints should be linked to the assessment endpoints by the mechanism oftoxicity and the route of exposure. Measurement endpoints are used to derive a quantitative estimate of potential effects, and form a basis for extrapolation to the assessment endpoints. Measurement endpoints were selected on the basis of potential presence of receptors on site, and the potential for exposure to contaminants of concern. The availability of the appropriate toxicity information on which risk calculations could be based was also an important consideration. Endpoints selected were determined to be representative of exposure pathways and assessment endpoints identified for the site. Next is a list of specific measurement endpoints that correspond to the assessment endpoints identified in Section 2.5. Measurement endpoints for assessment endpoint: protection of benthic invertebrate communities structure and function To evaluate the structure and function of the benthic community, benthic macroinvertebrates were collected from five locations in Dry Run. Existing community structure was evaluated at each of the five locations by determining taxonomic diversity and through an evaluation of functional feeding groups. Sediment was also collected in each of the five areas for toxicity testing using the amphipod, Hyallela azieca. The endpoints of these testswere survival and growth. Collocated sediment samples were also collected and analyzed for target analyte list (TAL) metals. BNA's, PestTCBs, VOCs, fluoride, grain size, and total organic carbon (TOC). The chemistry results were then correlated with observed adverse biotic responses in the toxicity tests in order to determine risk potential. Measurement endpoints for assessment endpoint: protection of soil invertebrate community structure and function To evaluate the structure and function of the benthic community, soil was collected from each of the meadow locations and tested using the earthworm, Eistniafoetida in toxicity tests. The endpoints of these tests were survival and growth. Collocated soil samples were also collected and analyzed for target analyte list (TAL) metals, BNA's, Pest/PCBs, VOCs, fluoride, grain size, and total organic carbon (TOC). Measurement endpoints for assessment endpoint: protection of fish communities to ensure that direct exposure to contaminants does not have a negative impact on growth, survival, and reproductive success. 27 0G0-'. i USFW 0R14 Fathead minnow, Pimephalespromelas, toxicity tests were used to determine the toxicity of the water in Dry Run. The endpoints of these tests were survival and growth. Collocated water samples were also collected and analyzed for target analyte list (TAL) metals, BNA's, Pest/PCBs, VOCs, fluoride, grain size, and total organic carbon (TOC). The chemistry results were then correlated with observed adverse biotic responses in the toxicity tests in order to determine risk potential. Measurement endpoints for assessment endpoint: Protection of worm-eating birds to ensure that ingestion of contaminants in forage does not have a negative impact on growth, survival, and reproductive success. Food chain accumulation studies were selected to evaluate risk to avian species which utilize the site as a feeding area. The selected measurement endpoint receptor species is the American robin, Turdus migratorius. Appropriate forage species (earthworms) were identified for the above receptor, and the dietary exposure of receptors to contaminants was quantified and compared to existing toxicity data for these, or other closely related species. Measurement endpoints for assessment endpoint: Protection of carnivorous birds to ensure that ingestion of contaminants in forage does not have a negative impact on growth, survival, and reproductive success. Food chain accumulation studies were selected to evaluate risk to avian species which utilize the site as a feeding area. The selected measurement endpoint receptor species is the red-tailed hawk, Buteo jamaciensis. Appropriate forage species (small mammals) were identified for the above receptor, and the dietary exposure of receptors to contaminants was quantified and compared to existing toxicity data for these, or other closely related species. Measurement endpoints for assessment endpoint: Protection of carnivorous mammals to ensure that ingestion of contaminants in forage does not have a negative impact on growth, survival, and reproductive success. Food chain accumulation studies were selected to evaluate risk to mammalian species which utilize the site and adjacent areas. The selected measurement endpoint receptor species is the red fox, Vulpes vulpes. Appropriate forage species (small mammals) were identified for the above receptors and the dietary exposure of receptors to contaminants was quantified. Measurement endpoints for assessment endpoint: Protection of piscivorous mammals to ensure that ingestion of contaminants in forage does not have a negative impact on growth, survival, and reproductive success. Food chain accumulation studies were selected to evaluate risk to mammalian species which utilize the site and adjacent areas. The selected measurement endpoint receptor species are the mink, Mustela vison. Appropriate forage species (fish) were identified for the above receptors and the dietary exposure of receptors to contaminants was quantified. Measurement endpoints for assessment endpoint: 28 000 USFW 061 Protection of omnivorous mammals to ensure that ingestion of contaminants in forage does not have a negative impact on growth, survival, and reproductive success. Food chain accumulation studies were selected to evaluate risk to mammalian species which utilize the site and adjacent areas. The selected measurement endpoint receptor species is the raccoon, Procyon lotor, as a model for omnivorous mammalian species. Appropriate forage species (fish) were identified for the above receptors and the dietary exposure of receptors to contaminants was quantified. Measurement endpoints for assessment endpoint: Protection of insectivorous mammals to ensure that ingestion of contaminants in forage does not have a negative impact on growth, survival, and reproductive success Food chain accumulation studies were selected to evaluate risk to mammalian species which utilize the site and adjacent areas. The selected measurement endpoint receptor species is the short-tail shrew, Blarina brevicauda, as a model for insectivorous mammalian species. Appropriate forage species (earthworms) were identified for the above receptors and the dietary exposure of receptors to contaminants was quantified. Measurement endpoints for assessment endpoint: Protection of herbivorous mammals to ensure that ingestion of contaminants in forage does not have a negative impact on growth, survival, and reproductive success Food chain accumulation studies were selected to evaluate risk to mammalian species which utilize the site and adjacent areas. The selected measurement endpoint receptor species is the meadow vole, Microtuspennsylvanicus, as a model for herbivorous mammalian species. Appropriate foraae species (vegetation) was identified for the above receptors and the dietary exposure of receptors to contaminants was quantified. Life History/Exposure Profile Information Receptor species were selected from several trophic levels. Organisms which were likely to be exposed to contaminants because of specific behaviors, patterns of habitat use, or feeding habits were selected for evaluation in this risk assessment. The availability of appropriate toxicity information on which risk calculations could be based was also an important consideration. The terrestrial invertebrate receptor selected for this assessment is the earthworm. The terrestrial vertebrate receptor species selected for this risk assessment are: meadow vole, short-tail shrew, raccoon, mink, and red fox. The avian receptor species selected for this risk assessment are: American robin and red-tailed hawk. The aquatic vertebrate receptor species for this risk assessment is the fathead minnow. The aquatic invertebrate receptor is H. azteca. 2.9.1 The amphipod (Hyallela azteca) as Representative of Benthic Invertebrates Justification Hyallela azteca was selected as representative of benthic invertebrates due to their direct contact with sediment for a significant portion of their life cycle, ubiquitous distribution in aquatic systems, importance as a food item for aquatic-invertebrate consumers, and ease of 29 OOOo.oS U S F W DR1 fi use in laboratory toxicity evaluations. These species are also likely to occur in the surface sediment at the Dry Run Creek site. Life History,(Hvallela azteca1 The amphipod, Hyallela azteca, is commonly found in freshwater lakes, streams, ponds, and rivers throughout North and South America. In preferred habitats, they are known to reach densities in excess of 10,000 per square meter. They may also be found in sloughs, marshes, and ditches, but generally in lower numbers (U.S. EPA 1994). Hyallela azteca are epibenthic detritivores that feed on coarse paniculate organic material. They typically burrow into surface sediment, and avoid bright light. Because of their feeding and behavioral characteristics, they are ideal test organisms for toxicological evaluation of freshwater sediments. Avoidance of light by movement into the sediment keeps these organisms almost constantly in contact with sediment contaminants (U.S. EPA 1994). Reproduction in this crustacean is sexual. Males are larger than females and have larger front gnathopods that are presumably used for holding the female during amplexus and copulation. During amplexus, the male and female feed together for a period of up to one week. The pair separates temporarily while the female goes through a molting period. Immediately after the molt, the two rejoin and copulation begins. During copulation, the male releases sperm near the female's marsupium. The female sweeps the sperm into her marsupium. and simultaneously releases eggs from her oviducts, into the marsupium, where fertilization takes place. The average brood size for female Hyallela azteca is 18 eggs per brood, but this number can vary with environmental conditions and physiological stress (U.S. EPA 1994). Developing embryos and hatched young are kept inside the female's marsupium until she undergoes a second molt. At that time, the juvenile Hyallela azteca are released into the surrounding environment. Under favorable conditions, each female produces approximately one brood during every ten day time period (U.S. EPA 1994). Hyallela azteca have a minimum of 9 instars, with 5 to 8 pre-reproductive stages. The first five stages arejuvenile stages; instars 6 and 7 form the adolescent stages; and stages 8 and higher are considered adult (fully reproductive) stages (U.S. EPA 1994). Exposure Profile for Hvallela azteca Since direct contact with contaminated sediment in the toxicity evaluation is the primary route of exposure for Hyallela azteca in this risk assessment, the results of the test will be used to indicate exposure. 2.9.2 Earthworm (Eisertiafoetida) as Representative of Terrestrial Invertebrates Justification Earthworms were selected as representative of terrestrial invertebrates due to their feeding habits, ubiquitous distribution throughout many habitats and soil conditions, and importance in providing a food base for many small- to medium-sized predators. A diet of detritus, microflora, and microfauna, combined with direct contact with the surrounding soil, presents a potential link between soil contaminants and soil-invertebrate consumers. In addition, 30 OOO-1.,? USFW 061 earthworms were observed in both the wooded and open field areas of the Dry Run Creek site. l ife History Earthworms feed on dead and decaying plant and animal remains and on free-living soil microflora and microfauna. Their primary source of food is dead plant material, especially plant litter. Next to food, their most important requirement is adequate moisture. Water conservation mechanisms are poorly developed: respiration depends on diffusion of gases through the body wall which must be kept moist. Earthworms are generally absent or rare in soils with very coarse texture, in soils with high clay content in regions of high rainfall, and in soils with a pH of less than 4 (Lee 1985). Earthworms are hermaphroditic and most species reproduce by cross-fertilization, although many species can also produce cocoons parthenogenetically. Sexual reproduction cannot occur without a clitellum, ovaries, oviducts, and possibly the ovisacs, but male organs are not essential. The population of an earthworm species at any one time consists of young immature, well-grown immature (adolescent), mature, and senescent individuals (Edwards and Lofty 1977). Earthworms have several ways of surviving adverse environmental conditions such as soil desiccation and ambient cold and heat. In terms of population survival, the cocoons can resist desiccation and temperature extremes much more easily than mature individuals. Worms may also migrate to deeper soil or undergo states of inactivity until environmental conditions become favorable once again (Edwards and Lofty 1977). Some species of worms grow throughout their lives by continually adding segments proliferated from a growing zone locatedjust in front of the anus. Other species, such as . foetida, possess the adult number of segments upon hatching and increase in size without increasing the number of segments. The life span of Eisentafoetida was reported to be approximately 4.5 years under laboratory conditions (Edwards and Lofty 1977). Exposure Profile Direct contact with contaminated soil is the primary route of exposure for earthworms in this risk assessment. Survival and growth endpoints following exposure to site soils will be used to evaluate risk to these organisms. Tissue residue analysis will also be conducted on the worms to determine exposure to higher trophic level organisms. 2.9.3 Fathead Minnow (Pimephales promeias) as Representative of Fish Community Jvsiif'C4Uon The fathead minnow was selected as representative of omnivorous fish due to its dietary composition, direct contact with water throughout the life cycle, ubiquitous distribution in aquatic systems, importance as a food item for fish-eating consumers, and ease of use in laboratory toxicity evaluations. Life History 31 009 0 U S F W nio The fathead minnow, P. promelas, is widely distributed in North America and is found in a variety of habitats such as small streams, ponds, and small lakes. It is uncommon or absent in streams of moderate and high gradients. It is tolerant of high temperature, high turbidity, and low oxygen concentrations (U.S. EPA 1985). The fathead minnow is primarily omnivorous. Young typically feed on detritus, algae, and zooplankton. Adults feed on aquatic insects, worms, small crustaceans, and other animals. This species is considered an important food source for other fish and birds (U.S. EPA 1985). Adult fathead minnows spawn in the spring and continue to spawn throughout most of the summer. The minimum spawning temperature appears to be approximately I6C. The ovaries of the females contain eggs in all stages of development, and they spawn repeatedly as the eggs mature. The average number of eggs per spawn per female is 100 to 150. Larger females may lay 400 to 500 eggs per spawn. Hatching times depend on temperature and average about six days. In warm water with an ample food supply, spawning may occur as early as the fust year. In cooler water with a moderate food supply, spawning usually occurs during the second year. Survival to the third year is relatively uncommon (U.S. EPA 1985). Exposure Profile Since direct contact with contaminated water in the toxicity evaluation is the primary route of exposure for fathead minnows in this risk assessment, the results of the test will be used to indicate exposure. 2.9.4 American Robin (Turdus migratorius) as Representative of Worm-eating Birds Justification The American robin was selected as representative of omnivorous and carnivorous birds because of its ubiquitous distribution and dietary composition. The preference for soil invertebrates in its omnivorous diet allows this species to be used as both an omnivorous and carnivorous receptor in this risk assessment. This species is also likely to occur at the Dry Run Creek site. Lift Higgs' The American robin (Turdus migratorius) occurs throughout most of the continental U.S. and Canada, wintering in the southern half of the U.S., Mexico, and Central America. Given the increase in open habitat and lawns, the robin's breeding range has expanded in the recent times. Habitat requirements for breeding robins include access to fresh water, protected nesting sites, and productive foraging areas. These requirements are commonly met in moist forests, swamps, open woodlands, and other open areas. Non-breeding robins occupy similar habitats although proximity to fruit bearing trees is of more importance. The primary foraging technique for robins is to hop along the ground in search of ground dwelling invertebrates, although they commonly search for insects and fruit in tree branches as well. The robin's diet during the breeding season consists mainly of invertebrates and some fruit, but fruit is the primary food consumed outside of the breeding season. As robins exhibit a low digestive efficiency for fruit, they often consume more than their own body weight in fruit to meet their metabolic needs (U.S. EPA 1993). 32 COO-. USFW 0619 Breeding territories are established by male robins. Most foraging occurs close to these territories during the breeding season; however, if densities of robins are high in a given area or if food resources are limited, adult robins will leave to temporarily forage elsewhere. Outside of the breeding period, robins typically return to the same foraging sites and roost within 1 to 3 kilometers (km) of these areas (U.S. EPA 1993). Exposure Profile Adult American robins are reported to weigh from 77.3 to 133.8 g (U.S. EPA 1993). Territory sizes vary from 0.3 to 1 acre, with foraging home ranges reported up to 2 acres (U.S. EPA 1993). The lowest reported body weight (77.3 g) and the smallest reported home range of (0.3 acres) were assumed for this risk assessment. A food ingestion rate of 0.89 to 1.52 g/g BW/day and a water ingestion rate of 0.14 g/g BW/day are reported for this species (U.S. EPA 1993). Assuming a 77.3 g body weight, an American robin can be expected to consume 117.5 g/day of food and 10.8 g/day of water. The diet of the American robin consists of seasonally variable proportions of invertebrates (e.g., earthworms, snails, beetles, caterpillars, spiders) and fruit (e.g., dogwood, cherry, sumac, hackberries, raspberries) (U.S. EPA 1993, Ehrlich et al. 1988). During spring, summer, and fall, the dietary composition is reported to change from 93 percent invertebrates and 7 percent fruit in the spring (nesting season) to 92 percent fruit and 8 percent invertebrates in fall (migratory season). The summer dietary proportion is reported as 68 percent fruit and 32 percent invertebrates (U.S. EPA 1993). For the purposes of this risk assessment, a diet of 100% earthworms will be assumed. An incidental soil ingestion rate for the American robin could not be found in the literature. However, a soil ingestion rate of 10.4 percent of the diet reported for the American woodcock will be used as a substitute ingestion rate for the American robin (Beyer et al. 1994). Assuming a food ingestion rate of 117.5 g/day, the soil ingestion rate for the American robin is 12.2 g/day. 2.9.5 Red-tailed Hawk (Buteojamaciensis) as Representative of Carnivorous Birds. Justification The red-tailed hawk was selected as representative of a carnivorous bird due to its dietary composition, relative abundant distribution, and likelihood of occurrence at the Dry Run Creek site. Its diet allows for the evaluation of contamination in site soils. In addition, the concentration of contaminants found in small mammal tissue will also provide an accurate dose to the red-tailed hawk which allows for the evaluation of contaminants in the food source. Life History Red-tailed hawks are the most common and widespread American Buteo (Bull and Farrand 1977). Their habitat is highly variable, but they are commonly found in wooded areas near open land. They also inhabit plains, prairie groves, and deserts in the western United States (NGS 1987). This species is absent, however, from tundra, and rare in extensive unbroken forest. An opportunistic feeder, the red-tailed hawk hunts from a perch or on the wing for i ispw food items such as small mammals (e.g., mice, chipmunks, rabbits), birds (usually grounddwelling species), reptiles, insects, and occasionally, prey species that are too heavy to lift off the ground (Burton 1989). The breeding season starts with aerial courtship displays, commonly followed by mating on a perch and nest-building by both sexes. Nests are placed in tall trees, high rock ledges, or tall cacti and are often refurbished annually for use in consecutive years. Incubation of two to three eggs iscarried out by both sexes and lasts for approximately 30 days. The young are able to feed themselves at 4 to 5 weeks and fledge in about 45 days (Bull and Farrand 1977; Burton 1989). Exposure Profile Adult male and female red-tailed hawks are reported to weigh 960 g and 1,235 g, respectively (DeGraaf and Rudis 1983; U.S. EPA 1993). Home ranges vary from 148.26 to 395.36 acres (Kirkwood 1980). The lowest reported body weight of 0.960 kg and the smallest reported home range of 148J26 acres were assumed for this risk assessment. The diet of a red-tailed hawk consists of mammals, birds, reptiles, and insects which vary in importance with season and availability (U.S. EPA 1993). For the purposes of this risk assessment, the hawk will be assumed to consume 100% small mammals. Food ingestion rates are reported to range from 136 to 400 g/day (Kirkwood 1980). The highest reported food ingestion rate of400 g/day was assumed for this risk assessment. A water ingestion rate of approximately 0.059 g/g BW/day has been estimated for this species (U.S. EPA 1993). To express this value in units of g/day, the water ingestion rate was multiplied by the lowest reported body weight of 960 g to yield a water ingestion rate of 56.64 g/day (56.64 mLVday). A soil ingestion rate for the red-tailed hawk could not be found in the literature; therefore, the amount of soil predicted to be entrained in the digestive tract of a white-footed mouse was used to calculate this value. A soil ingestion rate of less than 2 percent of the total diet has been reported (Beyer et al. 1994) for the white-footed' mouse. From this value, a conservative soil ingestion rate of 1.9 percent of the total diet was assumed for the white footed mouse. To express this value in units of g/day, the soil ingestion rate of 1.9 percent was multiplied by the food ingestion rate of the white-footed mouse (4.50 g/day) (U.S. EPA 1993) to yield a soil ingestion rate of 0.09 g/day. This value was assumed to represent the amount of soil entrained in the digestive tract of the white-footed mouse that remains constant over time. To express 0.09 g in units of grams of soil per gram of mouse body weight, this value was divided by the lowest reported body weight ( 13 g) of the white-footed mouse (Merritt 1987) to yield a value of 0.007 g/g BW. This value was then multiplied by the food ingestion rate of the red-tailed hawk (400 g/day) to yield a soil ingestion rate of 2.8 g/day. 2.9.6 Red Fox ( Vulpes vuipes) as Representative of Carnivorous Mammals Justification The red fox was selected as representative of a carnivorous mammal due to its dietary composition, relative abundant distribution, and likelihood of occurrence at the Dry Run Creek site. Its diet allows for the evaluation of contamination in site soils. In addition, the concentration of contaminants found in small mammal tissue will also provide an accurate 34 000 USFW 062 dose to the red fox which allows for the evaluation o f contaminants in the food source. L ifg .H istg n Red fox inhabit open meadows, ditch banks, field and wood edges, fencerows, stream and lake borders, and farmlands (Hoffineister 1989; Jones and Bimey 1988; Merritt 1987). With the exception of the breeding season, red fox have no permanent home but sleep on the ground (Schwartz and Schwartz 1981). A den, usually modified from an existing woodchuck or fox den, is dug during the breeding season and exceptionally cold winters (Barbour and Davis 1974). These scent-marked dens have multiple rooms, entrances, and trails leading to and from hunting areas (Schwartz and Schwartz 1981). In addition to their dens, both males and females will defend their scent-marked hunting territory from intruders (Jones and Bimey 1988). The red fox is primarily an opportunistic carnivore, consuming food items such as rabbits, opossums, muskrats, skunks, rodents, birds, eggs, carrion, invertebrates, snakes, and frogs (Barbour and Davis 1974; Merritt 1987). Some vegetable matter such as fruits and nuts are also consumed when in season (Jones and Bimey 1988). During times of abundant food supply, the red fox will bury surplus food to return to for consumption at a later time (Schwartz and Schwartz 1981). Male and female foxes pair for life, remaining together from midwinter to summer. Females bear one liner per year usually between March and April (Merritt 1987). Gestation periods last from about 49 to 56 days, with most averaging 53 days (Schwartz and Schwartz 1981). The pups are weaned at about 60 days, leave the den in the autumn, and are sexually mature by their first winter (Merritt 1987). Natural predators of the red fox are few but include large hawks and owls, and possibly coyotes (Merritt 1987; Schwartz and Schwartz 1981). Red fox may live from six to ten years in the wild (Schwartz and Schwartz 1981). Exposure Profile Adult red fox weigh from 2.7 to 7 kg (Barbour and Davis 1974; Jones and Bimey 1988). Home ranges vary from 245 to 1,235 acres (Merritt 1987). The food ingestion rates of the red fox range from 0.069 g/g BW/dav for a nonbreeding adult, to 0.16 g/g BW/day for ajuvenile (U.S. EPA 1993). The water ingestion rate for an adult red fox is estimated to be approximately 0.086 g/g BW/day (U.S. EPA 1993). To express these values in units of g/day, the highest reported food ingestion rate of 0.16 g/g BW/day and the water ingestion rate of 0.086 g/g BW/day were multiplied by the lowest reported body weight of 2.7 kg (2,700 g) to yield a food ingestion rate of 432 g/day and a water ingestion rate o f232.2 g/day (232.2 mL/day). For the purposes of this risk assessment, a diet of 100% small mammals will be assumed. A soil ingestion rate of 2.8 percent of the total diet has been reported (Beyer et al. 1994) for the red fox. To express this value in units of g/day, the soil ingestion rate of 2.8 percent was multiplied by the food ingestion rate of432 g/day to yield a soil ingestion rate of 12.1g/day. 2.9.7 Mink (Mustela vison) as Representative of Carnivorous Mammals Justification 35 0 0 v- USFW 0622 The mink was selected as representative of a carnivorous mammal due to its dietary composition, relative abundant distribution, and likelihood of occurrence at the Dry Run Creek site. Its diet allows for the evaluation of contamination in site soils. In addition, the concentration of contaminants found in clams and fish tissue will also provide an accurate dose to the mink which allows for the evaluation of contaminants in the food source. Lift H is a c Mink are distributed over much of boreal North America, southward throughout the eastern United States and in the west to California, New Mexico, and Texas (Jones and Bimev 1988). They can be found in virtually any habitat containing permanent water thus, they are not commonly found in upland areas (Jones and Bimey 1988). Although primarily nocturnal, their activity often extends into midday (Hoffrneister 1989). Dens are always near water, and they are usually an old muskrat burrow or constructed by the mink itself (Jones and Bimey 1988). Males tend to live in their own burrows which are less elaborate than ones occupied by females (Barbour and Davis 1974). Home ranges tend to be linear since mink often follow a shoreline (Jones and Bimey 1988). Mink are solitary and mark their territories by spraying (Merritt 1987). Seasonal food availability governs the dietary composition (Barbour and Davis 1974). Their diets may consist of crayfish, frogs, fish, snakes, rodents, rabbits, and plants among other items (Jones and Bimey 1988; Schwartz and Schwartz 1981). Crayfish are a major portion of the summer diet in many regions of North America (Barbour and Davis 1981; Jones and Bimey 1988; Merritt 1987). Breeding occurs from January to early April with highly variable gestation periods ranging from 40 to 75 days (Merritt 1987; Schwartz and Schwartz 1981). A highly variable single litter of 1to 17 young may be produced (Schwartz and Schwartz 1981). Average liner sizes vary among regions (Barbour and Davis 1974; Hoffrneister 1989; Jones and Bimey 1988; Merritt 1987; Schwartz and Schwartz 1981). Young are weaned at about five to six weeks of age and are sexually mature by ten months (Merritt 1987; Schwartz and Schwartz 1981). Occasionally great homed owls, foxes, coyotes, bobcats, and dogs will prey on mink (Merritt 1987; Schwartz and Schwartz 1981). Although some individuals have lived up to six years, mink seldom exceed two years of age in the wild (Schwartz and Schwartz 1981). Effects Profile Adult mink weigh from 520 to 1,730 g (Merritt 1987; U.S. EPA 1993). Home ranges vary from 19 to 1,900 acres (U.S. EPA 1993). A year-round food ingestion rate of 0.22 g/g BW/day has been estimated for both male and female mink (U.S. EPA 1993). To express this value in units of g/day, the food ingestion rate was multiplied by the lowest reported body weight (520 g) to yield a food ingestion rate of 114 g/day. An estimated water ingestion rate of 0.11 g/g BW/day was reported for farmraised females (U.S. EPA 1993). To express this value in units of g/day, this water ingestion rate was multiplied by the lowest reported body weight of 520 g to yield a water ingestion rate of 57.2 g'day (57.2 mL/day). For the purposes of this risk assessment, a diet of 100% fish will be assumed. 36 0 0 0 - '5 USFW 062 An incidental sediment ingestion rate was not available from the literature; therefore, a predicted incidental ingestion rate for sediment that may be entrained in the digestive system of the prey item (fish) was used for this risk assessment. Consumption of this prey item was assumed to be the primary mechanism by which mink may incidentally ingest sediment. The derivation of the predicted level of incidental sediment ingestion via consumption of fish is described next. Life history information for the bluegill (Lepomis machrochirus) was used to predict the amount of sediment that may be ingested by mink via consumption of fish. Adult bluegills range in size from 100 to 230 mm (Pflieger 1975; Smith 1985). In keeping with the conservative approach of this risk assessment, the amount of sediment entrained in the lowest body size of 100 mm in length was predicted. The weight of a 100 mm bluegill was calculated to be 18.11 g based on the following algorithm relating length to weight (Hillman 1982); log Weight (g) * -5.374 + 3.316 log Length (mm) A daily food ingestion rate of 1.75 percent BW/day has been reported for the bluegill (Kolehmainen 1974). This provides a predicted intake rate of 0.32 g of food per day for a 18.11 g fish. A study evaluating the stomach contents of 153 bluegills reported an average content of detritus and sediment to be 9.6 percent of the total diet (Kolehmainen 1974). If a conservative assumption is made that 9.6 percent of the food ingested is entirely sediment, ` it can be predicted that a fish of this size may contain 0.03 g of sediment in its digestive system. For the purpose of this model, it was assumed that the level of sediment contained in the digestive system of a fish remains constant over time. This value (0.03 g) was divided by the predicted fish body weight (18.11 g) to express sediment entrained in fish digestive systems in units of grams of sediment per gram of fish body weight. This provided a value of 0.0017 g sediment/g body weight. When this value is multiplied by the food ingestion rate of the mink (114 g/day), the predicted sediment ingestion rate for the mink through consumption of fish is 0.2 g/day. 2.9.8 Raccoon (Procyon lotor) as Representative of Omnivorous Mammals Justification The raccoon was selected as representative of a omnivorous mammal due to its dietary composition, relative abundant distribution, and likelihood of occurrence at the Dry Run Creek site. Its diet allows for the evaluation of contamination in site sediment. In addition, the concentration of contaminants found in forage fish tissue and clams will also provide an accurate dose to the raccoon which allows for the evaluation of contaminants in the food source. LifcH,istaty Raccoons are medium-sized omnivores and are abundant throughout North America. Raccoons prefer aquatic habitats, particularly hardwood swamps, flood plains, freshwater wetlands, and salt marshes (Kaufmann 1982). Raccoons have also adapted well to residential areas and farmlands. Raccoons rely heavily on surface waters for foraging and as a source 37 000-, i i g !=\a/ n aoA. of drinking water (Stuewer 1943). Raccoons are active primarily from dusk to dawn (Stuewer 1943) but will alter their activities to opportunistically feed on whatever is available (Sanderson 1987). For example, raccoons living near a salt marsh may become active during the day to take advantage of feeding opportunities during low tide (Ivey 1948). Raccoons feed primarily on fruits, nuts, acorns, grains, insects, frogs, crayfish, and eggs (Palmer and Fowler 1975). Raccoons in the southern regions of the United States are active year round (Goldman 1950). Adult raccoons are normally solitary but will come together for short periods of time during mating (Kaufman 1982). Mating occurs from March to June in southern areas and each male may mate with several females during each season (Sanderson 1987; Kaufman 1982). Young males are normally not sexually mature in the first breeding season but mature later in the summer, while females mature in the first year (Sanderson 1951). The home range of a raccoon depends on the animal's age, habitat, food resources, and season (Sanderson 1987). Home ranges are typically a few hundred hectares (ha) but ranges as large as a few thousand ha have been reported (Sanderson 1987). Population densities also depend strongly on the amount of resources in the area. Numbers of 0.1 to 0.2 animals per ha are common (Hoffman and Gottschang 1977). Raccoons are found near every aquatic habitat. During the last 50 years raccoon populations have increased greatly (Sanderson 1987). In Alabama, adult mate raccoons weighed up to 8.8 kilograms (kg) (mean 43 1kg) while adult females can weigh up to 5.9 kg (mean 3.67 kg) (Johnson 1970). Adult raccoons weigh between 2 and 12 kg (Nowak 1991), and consume 0.5 kg of food per day (Newell et al. 1987). Raccoons feed primarily on fruits, nuts, acorns, grains, insects, frogs, crayfish, eggs (Palmer and Fowler 1975). In a Maryland forested bottom land, the dietary composition of raccoons during the summer was principly made up of insects (39 percent), wild cherry (17 percent), blackberries (16 percent), crayfish (8 percent), snails (5 percent), herptiles (5 percent), fish (2 percent), rodents (2 percent), com (l percent), and trace amounts of Smilax, acoms and pokeberry (Llewellyn and Uhler 1952). At Washington state tidewater area raccoons displayed the following dietary composition: molluscs, mussels and oyster (44 percent), Crustacea, shrimp and crabs (25 percent), fish (9 percent), marine worms (20 percent), and Echiurida worms (1 percent) (Tyson 1950). The home range of a raccoon depends on the animal's age, habitat, food resources, and season (Sanderson 1987). Home ranges are typically a few hundred hectares but ranges as large as a few thousand hectares have been reported (Sanderson 1987). The home range for adult male raccoon found in coastal Georgia raccoons is approximately 65 ha ( 18 SE) while the home range for adult females in the same area is approximately 39 ha ( 16 SE) (Lotze 1979). Population densities also depend strongly on the amount of resources in the area. Numbers of 0.1 to 02 animals per hectare is common (Hoffman and Gottschang 1977). Exposure Profile For the purposes of this risk assessment, a body weight of 2 kg, an ingestion rate of 0.5 kg'day, and a diet of 80 percent forage fish and 20 percent clams were assumed. A soil ingestion rate of 9.4 percent of the diet has been reported for raccoons (Beyer et al. 1991). Multiplying the ingestion rate by 9.4 percent yields a sediment ingestion rate of 0.047 kg/day. 38 000 USFW 062! A daily water ingestion rate of 0.18 Liters per day (Uday) was calculated using an allometric equation derived by Calder and Braun (1983). A diet of 100% fish will be assumed. r ^'>rr.railed Shrew (Blarina brevicauda) as Representative of Insectivorous Mammals Juaiifitaiian The short-tailed shrew was selected as representative of insectivorous mammals because of its dietary composition, relative abundant distribution in both moist and dry habitats, and likelihood of occurrence at the Dry Run Creek site. Although their diets may consist of plants as well as insects, they tend to favor soil invertebrates when they are in abundance. Hence, by assuming that their dietary composition comprises solely invertebrates in this risk assessment, this species may represent an insectivorous mammal. Life Histotv The short-tailed shrew is an extremely active, large, and heavy-bodied shrew common within its range (Jones and Bimey 1988). It occupies a variety of moist and dry habitats such as marshes, bogs, moist forest floors with ample decaying matter, brushland, fencerows, weedftelds, and pastures (Barbour and Davis 1974; Jones and Bimey 1988). Short-tailed shrews are active both day and night throughout the year, although most of this activity is subnivean (Merritt 1987). During harsh winters, this species may undergo a period of torpor' (Hoffmeister 1989). The home range of this species varies with their dramatic population cycles. In peak years, animal density may be greater than 25 individuals per acre (Schwartz and Schwartz 1981). In other years, this species may have an animal density of one individual per acre (Merritt 1987). Although short-tailed shrews strongly prefer animal matter, they'are opportunistic omnivores and will voraciously consume whatever food items are in ample supply (Barbour and Davis 1974). These food items include earthworms, slugs, snails, insects, arthropods, fungi, vegetable matter, seeds, snakes, salamanders, small mammals, and young birds (Barbour and Davis 1974; Jones and Bimey 1988; Schwartz and Schwartz 1981). Plant matter is generally consumed to a greater extent in winter (Schwartz and Schwartz 1981). In some regions, plant matter may constitute up to 20 percent of the shrew's diet (Barbour and Davis 1974). Submaxiliary glands pioduce a venom that quickly immobilizes their prey (Merritt 1987). Prey items that are not consumed immediately are stored in a cache (Merritt 1987). Using echolocation and scent-marking, short-tailed shrew rely heavily on their hearing and sense of smell to locate food and to move about (Hoffmeister 1989). An elaborate system of runways and tunnels are constructed usually just a few inches below the ground surface (Schwartz and Schwartz 1981). Two types of nests are built by this species, a breeding nest and a resting nest. Both nests are built underground beneath a log, rock, or other cover, and have multiple entrances. The breeding nest is typically larger than the resting nest (Merritt 1987). Breeding appears to commence in early spring and extend into the fall, although in some regions, breeding may subside in early and midsummer but peak again in early fall (Hoffmeister 1989; Jones and Bimey 1988). Gestation periods are approximately 21 to 22 39 00 *t?' USRA/ neon days with litter sizes of approximately four to ten young (Jones and Bimey 1988; Schwartz and Schwartz 1981). The young are fully mature from one to three months of age (Barbour and Davis 1974; Schwartz and Schwartz 1981). Both sexes may breed their fast spring (Schwartz and Schwartz 1981). Natural predators of the short-tailed shrew include fish, snakes, owls, hawks, shrikes, opossums, raccoons, foxes, weasels, bobcats, skunks, and feral cats, although most of these predators do not consume the shrew (or at least all of the shrew) because of their distasteful musk glands (Barbour and Davis 1974; Jones and Bimey 1988; Merritt 1987; Schwartz and Schwartz 1981). The life expectancy of a short-tailed shrew in the wild is approximately one year (Schwartz and Schwartz 1981). Exposure Profile Adult short-tailed shrews weigh from 12 to 30 grams (g) (Jones and Bimey 1988; Merritt 1987). Home ranges vary from 0.5 to 1 acre (Memtt 1987). Therefore, it was assumed that a short-tailed shrew could obtain 100 percent of its diet from the contaminated area (area use factor of 1), since the area comprising the on-site sampling locations was approximately 20 acres. Food ingestion rates ranging from 0.49 to 0.62 gram per gram of body weight per day (g/g BW/day ) have been reported (U.S. EPA 1993). An average food ingestion rate of 7.95 g'day has also been reported (U.S. EPA 1993). To express the former food ingestion rates in units of g/day for comparison to the latter ingestion rate, the former ingestion rates were multiplied by the lowest reported body weight of 12 grams to yield food ingestion rates of 5.38 to 7.44 g/day. Of these values, the highest food ingestion rate of 7.95 g'day will be used for the purposes of this risk assessment. A water ingestion rate of 0.223 g/g BW/day has been reported (U.S. EPA 1993). To express this value in units of g/day, the water ingestion rate was multiplied by the lowest reported body weight of 12 g to yield a water ingestion rate of 2.7 g'day (2.7 milliliters per day [mL/day]). A soil ingestion rate for the short-tailed shrew was not available from the literature, therefore, the soil ingestion rate of the opossum was used. The opossum's diet is similar to that of the short-tailed shrew since they are both opportunistic omnivores with a strong preference for animal matter (Schwartz and Schwartz 1981). A soil ingestion rate of 9.4 percent of the diet was reported for the opossum (Beyer et al. 1994). This value was multiplied by the highest food ingestion rate of the short-tailed shrew (7.95 g'day) to yield a soil ingestion rate of 0.74 g day. For the purposes of the food chain model in this risk assessment, it was assumed that 100 percent of the diet of the short-tailed shrew was comprised of earthworms. .9.10 Meadow Vole (Microtus pennsylvanicus) as Representative of Herbivorous Mammals Justification The meadow vole was selected as representative of herbivorous mammals because of its dietary composition, abundance in North America, preference for moist areas, and likelihood of occurrence at the Dry Run Creek site. 40 USFW 0627 Lift Hiaag The meadow vole is one of the largest and most abundant voles in North America (Jones and Bimey 1988; Merritt 1987). Although they are more commonly found in habitats such as moist meadows, bogs, swamps, stream banks, and lakeshores, they have also been known to inhabit cultivated fields, roadside ditches, and fencerows (Barbour and Davis 1974; Jones and Bimey 1988; Merritt 1987; Schwartz and Schwartz 1981). Dense vegetative cover appears to be cne of the major prerequisites for habitation (Hofftneister 1989; Jones and Bimey 1988). The home range of the meadow vole varies in size with season, habitat, and population size (Jones and Bimey 1988). Populations tend to fluctuate drastically every two to five years, with peak population density levels exceeding 100 voles per acre (Barbour and Davis 1974; Jones and Bimey 1988). Activity occurs during both day and night, and throughout the year, although it is greatest at dawn and dusk (Barbour and Davis 1974). Well-worn intersecting runways under vegetative cover are distinctive of meadow vole inhabitation (Jones and Bimey 1988). Elaborate spherical nests are commonly built aboveground in the center of a tussock of grass, although underground nests are also built in drier areas (Barbour and Davis 1974; Jones and Bimey 1988). The meadow vole is herbivorous, feeding primarily on grasses, sedges, legumes, tubers, and roots (Merritt 1987); however, insectivory and cannibalism have been reported in some individuals (Barbour and Davis 1974; Hoffmeister 1989). Bluegrass (Poa sp.) is a major component of the diet in some regions (Jones and Bimey 1988; Hofftneister 1989). This species hoards food for the winter in above- and below-ground caches (Merrirt 1987). The meadow vole is one of the most prolific mammals, producing litter after liner in rapid succession (Barbour and Davis 1974). Breeding occurs during the warmer months of the year (Jones and Bimey 1988). The gestation period is about 21 days with liner sizes ranging from 1 to 11 young (averaging four to seven) (Barbour and Davis 1974; Jones and Bimey 1988). The helpless young mature rapidly and may breed by 25 days of age (Barbour and Davis 1974). Meadow voles are preyed upon by nearly all species of predatory birds and mammals (Barbour and Davis 1974). These predators include owls, hawks, shrikes, bluejays, crows, foxes, weasels, mink, cats, raccoons, skunks, opossums, shrews, and snakes (Barbour and Davis 1974; Merrin 1987). Due to heavy predation, only a small proportion of the population exceeds sixty days of age (Schwartz and Schwartz 1981). Exposure Profile Adult meadow voles weigh from 20 to 65 grams (Merrin 1987; U.S. EPA 1993). The home range of this species varies from less than one acre to 3.2 acres (Merrin 1987). Therefore, it was assumed that a meadow vole could obtain 100 percent of its diet from the contaminated area (area use factor of 1), since the area comprising the on-site sampling locations was approximately 20 acres. A food ingestion rate ranging from 0.30 to 0.35 g/g BW/day, and a mean water ingestion rate of0.21 g;g BW/dav is reported for this species (U.S. EPA 1993). To express these values in units of g;day, the highest reported food ingestion rate of 0.35 g/g BW/dav and the water . 41 GOQ-'.^O U S F W 0628 ingestion rate of 0.21g/g BW/day were multiplied by the lowest reported body weight of 20 g to yield a food ingestion rate of 7.0 g/day and a water ingestion rate of 42 g/day (4 ? ml/day). " 7v A soil ingestion rate of 2.4 percent of the total di*r*--*--n rer--- u k^eyer et al. 1994) for the meadow voie. to express this me in units of g/day, the soil ingestion rate of 2.4 percent was multiplied by the food ingestion rate of 7.0 g'dav to vi*1-*- Ui-cauon rate of 0.17 g/day. For the purposes of the food chain model in this risk assessment, it was assumed that 100 percent of the diet was comprised of plants. 3.0 ASSUMPTIONS This risk assessment evaluates exposure to contaminants through food and incidental sediment/soil ingestion. The following conservative assumptions were made to conduct this risk assessment in the absence of sitespecific data: The maximum of the contaminant levels measured in sediment, soil, or water collected on site was used in risk calculations. The maximum concentrations of COCs reported in sediment, soil, water, and biota were assumed to be present site-wide. An area use factor (AUF) of 1 was assumed for all species using the site for feeding. Contaminants were assumed to be 100 percent bioavailable. Dietary composition information was obtained from the literature for the receptor species. However, simplifications of complex diets were performed for the receptors. A literature search was conducted to determine the chronic toxicity of the contaminants of concern when ingested by the indicator species. If no toxicity values could be located for the receptor species, values reported for a closely related species were used. All studies were critically reviewed to determine whether study design and methods were appropriate. When values for chronic toxicity were not available, LDja (median lethal dose) values were used. For purposes of this risk assessment, a factor of 100 was used to convert the reported LDS0 to a No Observed Apparent Effect Level - (NOAEL). A factor of 10 was used to convert a reported Lowest Observed Adverse Effect Level (LOAEL) to a NOAEL. and a factor of 10 was used to convert a reported LDS0to a LOAEL. If several toxicity values were reported for a receptor species, the most conservative value was used in the risk calculations regardless of toxic mechanism. Toxicity values obtained from long-term feeding studies were used in preference to those obtained from single dose oral studies. No other safety factors were incorporated into this risk assessment. In some cases, contaminant doses were reported as part per million contaminant in diet. These were converted to daily intake (in milligrams per kilogram body weight per day; mg'kg-day) by using the formula: Intake (mg'kg/day)*Contaminant Dose (mg/kg diet) x Ingestion Rate (kg'day) x 1/Bodyweight (kg) 42 000 USFW 062! This conversion allows dietary toxicity levels cited for one species to be converted to a daily dose for a different species based on body weight. For the purposes of this risk assessment, incidental cnii/sediment ingestion was also included in the calculation to determine the total daily intake for the recepto. - r t v :- j , ; iv dose may then be used to evaluate the risk to other species if no specific toxicity data a n available for a ,cccpiu.. Some contamin*--of c^r-.cer' (e.g. aluminum) are not food chain accumulators, but instead are direct toxins when ingested at the prescn--I levels. 4.0 EFFECTS PROFILE Many contaminants detected at the Dry Run Creek site do not have benchmarks. This excluded them from further consideration in this risk assessment, but does not exclude them as potential contaminants of concern. Based on the results of the preliminary risk assessment, the following compounds were considered COCs and their toxic effects are presented next: fluoride, trichlorofluoromethane, aluminum, arsenic, beryllium, chromium, copper, iron, lead, manganese, nickel, vanadium, and zinc. Based on the chemistry results, these compounds will be further evaluated using food chain accumulation models. Contaminants exceeding their respective benchmarks are assumed to be affecting receptor species and negatively impacting species, populations, and communities in the aquatic and terrestrial ecosystems at the Dry Run Creek site. 4.1 Fluoride Maurer et al (1990) identified skeletal and dental abnormalities in rats that were exposed to sodium fluoride for a period of 99 weeks. The LOAEL identified in this study was 4 mg Fl/kg BW/day. A NOAEL was calculated from the LOAEL using an accepted conversion factor of 10. Based on these results, a LOAEL of 4mg/kg BW/day and an estimated NOAEL of 0.4/kg BW/day will be used to evaluate the risk posed by fluoride mammalian receptors Fleming etal. (1987) found significant growth rate reduction in European starling fed a diet containing as low as 13 mg Fl/kg BW/day. No effects were observed at 10 mg Fl/kg BW/day. As such, this risk assessment will estimate fluoride related risk using a LOAEL of 13 mg-kg BW/day and a NOAEL of 10 mg'kg BW/day. 4.2 Organofluorides No studies pertaining to the dietary toxicity of trichlorofluoromethane or any other fluorinated organic compound was found in the literature. 4.3 Aluminum Dixon et al. (1979) conducted a study that evaluated the reproductive success of rats exposed to aluminum in drinking water for 90 days prior to breeding. The highest dose administered was 77.5 milligrams per kilogram body weight per day (mg/kg BW/day) and did not result in reproductive abnormalities. Lai et al. (1993) conducted a 180-day drinking water study in which rats were exposed to 55 mg'kg BW/day of aluminum. At this dose, behavioral effects were observed, including a significant reduction in spontaneous locomotor activity and significant deficits in acquisition and retention of learned responses. Based on these results, a LOAEL of 55 mg/kg BW/day and an estimated NOAEL of 5.5 mgkg BW/day will be used to evaluate the risk posed by aluminum to mammalian receptors (Table 1). 43 IIOC7\A/ nmo No effects were observed when Japanese quail were fed a diet containing 0.05 percent (84 mg/kg BW/day) aluminum for four weeks (Hussein et al. 1988). When quail were fed a diet containing 0.1 percent (165 mg/kg BW/day) aluminum, a decrease in egg shell breaking strength was observed. Finally, when quail were fed a diet containing 0.15 percent (257 mg/kg BW/day) aluminum, a decrease in body weight, egg shell strength, and egg shell production was observed. A 48-dav feeding study using chickens concluded that dietary levels of 28.4 mg/kg BW/day aluminum resulted in a decrease in weight gain, feed intake, and plasma inorganic phosphorus, as well as an increase in plasma calcium (Hussein 1990). However, only the altered metabolism of calcium and phosphorus could be attributed to the direct effects of aluminum. The associated NOAEL for this effect is 22.8 mg/kg BW/day. Because a range of concentrations were used and the endpoints were ecologically significant and related to the dose, the study by Hussein et al. (1988) was used to the develop the NOAEL and LOAL values. A NOAEL of 84 mg/kg BW/day and a LOAEL of 165 mg/kg BW/day will be used to evaluate the risk posed by aluminum to avian receptors (Table 1). 4.4 Arsenic Several studies were located which determined the effects of As to mammals. A study conducted on cats indicated that a chronic oral toxicity dose was 1J mg/kg BW/day (Pershagen and Vahter 1979). In addition. National Resources Council of Canada (1978) states that mammals in general have oral LD^s that range from 10 to 50 mg/kg of lead arsenate. A study conducted on mice indicated an oral dose LDjo of 39.4 mg/kg BW/day and an oral dose LD0of 10.4 mg/kg BW/day after 96 hours (NAS 1977). For the purposes of this risk assessment, the chronic value for the cat was used to calculate HQs for mammals (1.5 mg/kg BW/day). This value was converted to a NOAEL by dividing by a factor of 10. Eisler (1988a) reviewed several studies in which the toxicity of inorganic arsenicals were measured. Inorganic As is more mobile than organic As and may pose greater risk by leaching into surface water. Studies were also described in which organoarsenical compounds were measured. Studies indicate that sensitive species include the California quail (single oral dose LDJfl of 47.6 mg/kg BW/day) (Hudson etal. 1984) and chicken (single oral dose LDWof 33 mg/kg BW/day) (NAS 1977). For the purposes of this risk assessment, a value of 3.3 mg/kg BW/day was used to determine the HQ to birds. This value was converted to a NOAEL by dividing by a factor of 10. 4.5 Beryllium Two separate chronic dietary exposure studies using rats reported similar musculoskeletal effects. Guyart et al. (1933) fed large amounts of beryllium carbonate to rats at concentrations of 10,20,40, 80, 160, and 240 mg/kg BW/day. Rats from all exposure levels developed rickets, with the fragility of the bones varying directly with the exposure concentration. Similar results were reported by Jacobson (1933) who reported severely weakened bones in rats fed beryllium carbonate at dietary levels of 121 and 242 mg/kg BW/day. For this risk assessment, a dietary exposure level of 10 mg/kg BW/day was used to estimate risk of beryllium to the short-tailed shrew. A NOAEL of 0.10 mg/kg BW/day was derived from this LOAEL using an accepted conversion factor of 10. No studies pertaining to the dietary toxicity of beryllium to avian receptors were found in the literature. 4.6 Chromium 44 GOO- USFW 0631 Heinz and Haseltine (1981) exposed 2- to 3-year old breeding pairs of black ducks (Anas rubripes) to a diet containing 0, 20, or 200 mg/kg, wet weight, (0. 2.77, or 27.77 mg/kg BW/day) of Cr*3as chromium potassium sulfate [CrK (S O ^' ^HjOj for a period of approximately five months, until the onset of egg-laying by the females. Hatched ducklings were then fed a mash diet containing the same Cr concentrations that the parents were fed. Seven-day old chicks were tested for avoidance behavior in response to a fright stimulus. None of the Cr concentrations resulted in alteration of avoidance behavior. However, Haseltine et al. (1985), in an unpublished study reported by Eisler (1986a) notes that black duck ducklings suffered reduced survival and altered growth patterns when exposed to 10 mg/kg and 50 mg/kg of an unspecified Cr*3compound in their diets. The percent reduction in survival and a detailed explanation of the altered growth patterns were not available in this unpublished study. For the purposes of this risk assessment, dietary levels of 10 mg/kg (1 mg/kg BW/day) of Cr in prey was used as a LOAEL for the avian species. However, due to the conflicting results, a NOAEL was derived from the same study in which the LOAEL was selected to maintain a degree of consistency regarding the Cr species evaluated. A NOAEL of 0.1 mg/kg BW/day was derived from the LOAEL using a conversion factor of 10. A study conducted with dogs indicated that 2.5 mg/kg/day of Cr** ingested in the diet caused death (Steven et al. 1976). For the purposes of this risk assessment, a LOAEL of 0.25 and a NOAEL of 0.025 were used for the red fox, raccoon, and mink. 4.7 Copper One study was located which determined the effects of ingestion of Cu to mammalia species. An oral dose of 100 mg'kg/day to a dog caused death (OHMD 1987). For the purposes of this risk assessment, a LOAEL of 10 mg/kg/day was used and a NOAEL of 1 mg/kg/day were used for the exposure of mammals. Several studies were located which determined the effects of Cu on chickens. A dose of 350 mg/kg (61.3 mg'kg/day) caused a significant decrease in growth and food consumption (Smith 1969). Another study found that a dose of 325 mg/kg (23.5 mg/kg/day) caused respiratory problems (Hatch 1978). Assuming that respiratory problems are an acute effect, a LOAEL of 2.35 mgkg/day and a NOAEL of 0.235 mg/kg/day were used to determine risk to avian species. 4.8 Iron No studies pertaining to the dietary toxicity of iron to mammalian or avian receptors were found in the literature. 4.9 Lead The gastric motility of adult male and female red-tailed hawks fed 0.82 and 1.64 mg Pb/kg BW/day in a single oral dose was evaluated through the use of surgically implanted transducers for a period of three weeks following the dose. Neither concentration had any effect on gastric contractions or egestion of undigested material pellets (Lawler et al. 1991). A study conducted on red-tailed hawk found that 3 mgkg/day of Pb caused the clinical symptoms of Pb poisoning (Reiser and Temple 1981). A similar study found that 3 m gkg'day fed to starlings caused a reduction in muscle condition and altered their feeding activity (Osborne et al. 1983). For I ictrw n co the purposes of this risk assessment, a LOAEL of 3 mg/kg/day was used to determine risk to avian species and a NOAEL of 0.3 was used. Several studies were located which determined the effects of Pb ingesrion to mammals. A study conducted on mice indicated that 1.5 mg/kg/day of Pb caused a reduction in success of implanted ova (Clark 1979). Another study found that 2 2 mg/kg/day caused a reduction in the frequency of pregnancy when the dose was administered 3 to 5 days following mating (Clark 1979). For the purposes of this risk assessment, a NOAEL of 0.15 mg/kg/day and a LOAEL of 1.5 mg/kg/day were used to determine risk to mammals. 4.10 Manganese The effects levels for manganese toxicity vary widely, most likely attributable to the form of manganese tested. Rats exposed to 13 mg/kg BW/day of manganese as Mn304 in their diet for 224 days exhibited reduced testosterone levels (Laskey et al. 1982). In mice, a dietary' level of 140 mg/kg BW/day, also of Mn304 for 90 days resulted in decreased activity (Gray and Laskey 1980). A much higher exposure concentration of 2,300 mg/kg BW/day of manganese as MnC12 resulted in reduced dopamine levels (Gianutsos and Murray 1982). In contrast, levels as high as 930 mg/kg BW/day of manganese as MnS04 for 103 weeks had no effect on the respiratory, cardiovascular, gastrointestinal, hematological, musculoskeletal, hepatic, renal, dermal, and ocular systems of mice (Hejtmancik et al. 1987). For this risk assessment, a dietary exposure level of 13 mg/kg BW/day will be used as a LOAEL to estimate risk of manganese to the selected mammalian receptor. A NOAEL of 1.3 mgkg BW/day was derived from this LOAEL using an accepted conversion factor of 10. No studies pertaining to the dietary toxicity of manganese to an avian receptor were found in the literature. 4.11 Nickel Several studies were available which determined the effects of Ni ingestion to mammals. Wistar rats fed Ni sulfate indicated a NOAEL of 187.5 mg/kg/day to most systems except for body weight. This level of Ni sulfate caused a 27 to 29 percent decreased body weight (Ambrose et al. 1976). In a similar study with a beagle, a NOAEL of 62.5 mg/kg/day was noted (Ambrose et al. 1976). For the purposes of this risk assessment a NOAEL of 62.5 mg/kg/day was used to determine risk to mammals. This value was converted to a LOAEL of 625.0 mg/kg'day by multiplying the NOAEL by a factor of 10- No studies were available that determined the dose of Ni to avian species. Tnerefore, the risk to avian species from ingested Ni will not be determined. 4.12 Vanadium Gavage studies in mice have found an LC50 of 31 mg Vn/Kg diet (Schroeder and Balassa 1967). This dose was convened to a LOAEL of 3.1 mg/kg and a NOAEL of 0.31 using an accepted factor of 10 conversion. This food dose was convened to a daily dose by multiplying the LOAEL or NOAEL concentration by an ingestion rate commonly observed in mice (0.003 kg of food/day) and then by the inverse of the body weight (0.025 kg)(RTECS 1985). This calculation resulted in a LOAEL of 0.372 46 0 0 0 5 USFW 063: mg V/kg BW/day and a NOAEL of 0.0372 mg V/kg BW/day. These values will be used to estimate risk to mammalian receptors in this risk assessment. Rosomer (1960) exposed chickens to varying concentrations of vanadium. The study involved feeding 4 replicates of 13 chickens varying concentrations of vanadium for a period of 21 days. The study found that a dietary level of 40 mg/kg in the diet resulted in a marked depression in weight gain and efficiency of food utilization. At levels of 200 mg/kg, mortality was noted in all test chickens. The authors reported that a dietary level of 20 mg/kg could be tolerated with no resultant toxic effects. This dietary level was convened to a daily dose as above by multiplying the dietary concentration by a representative chicken ingestion rate (0.140 kg/day) and then by the inverse of the body weight (0.800 kg)(RTECS 1985). This calculation resulted in LOAEL of 7 mg V/kg BW/day and a NOAEL of 3.5 mg V/kg BW/ day. These values will be used to estimate risk to avian receptors. 4.13 Zinc Several studies were available which determined the effects of ingested Zn to birds. A concentration of 144.5 mg/kg/day caused a decrease in growth and anemia in chickens (Stahl et al. 1989). In a similar study conducted on chickens, a concentration of 361 mg/kg/day caused a reduction in body weight (Dean et al. 1991). In a study conducted on Japanese quail, a concentration of 139 mg/kg/day caused 7 percent morality in chicks and reduced food inake (Hill and Camardese 1986). For the purposes of this risk assessment, a LOAEL of 139 mg/kg/day was used to determine the effects to avian species. This value was converted to a NOAEL of 13.9 mg/kg/day by dividing the LOAEL by a factor of 10. A study conducted on dogs, indicated that 1,000 mg/kg (25 mg/kg/day) caused no effects after one year (NAS 1979). For the purposes of this risk assessment, a LOAEL of 250 and a NOAEL of 25 were used to determine risk to the fox and the mouse. In a study conducted on ferrets, a dose of 370 mg/kg day caused a decrease in food intake and weight loss. Because the ferret is similar to the mink, a LOAEL of 370 mg/kg/day was used and a NOAEL of 37 was used to determine risk to the mink. 5.0 RISK CHARACTERIZATION The following method was used to calculate risk. To estimate the risk to wildlife in the model systems utilizing the Dry Run Creek site, implications of the exposure concentrations need to be determined. The HQ method (U.S. EPA 1989, Bamthouse et al. 1986) compares exposure concentrations to ecological endpoints such as reproductive failure or reduced growth. The comparisons are expressed as ratios of potential intake values to population effect levels, or: Hazard Quotient (HQ) _______Mean Exposure Concentration No Observed Adverse Effect Level (NOAEL) A HQ greater than one indicates that exposure to the conaminant has the potential to cause adverse effects in the organism. A HQ less than one does not indicate a lack of risk. The HQ should be interpreted based on the severity of the effect reported. The results of the risk characterization are presented next. 5.1 Benthic Invertebrate Community Structure and Function The benthic invertebrate community in Dry Run appears to be at risk for nvo reasons. The benthic community survey showed a decrease in community taxonomic diversity and abundance in Dry Run as compared to the Reference stream. Since land use and available habitat are the same along both 47 eoo- streams, the decrease in diversity and abundance in Dry Run may be attributed to contamination present in sediments in Dry Run. In addition, the amphipod toxicity test dearly demonstrates that acute exposure sub-Iethai effects can be produced in the benthic community, especially under conditions present in Tributary A and in Area II. The observed negative growth effect was siznificantly negatively correlated with fluoride, aluminum, calcium, magnesium, nickel, potassium, and sodium. Further, there were strong negative associations between the growth endpoint and chromium, copper, lead, and zinc concentrations, although the relationships were not significant at the 0.10 level. Since the sediments closer the landfill along the whole Dry Run reach appear to be enriched with metals, the observed toxicity may represent a significant threat. 5.2 Soil Invertebrate Community Structure and Function The soil invertebrate community does not appear to be at risk based on current soil conditions at Dry Run. The earthworm toxicity test identified no problems with survival or growth. 5.3 Fish Communities The fish community at Dry Run may be at risk. Results of the fathead minnow toxicity bioassav show that water conditions in Upper Tributary A induce mortality to larval fish. This mortality could not directly be associated with a suite of contaminants as in the amphipod test, but survival was negatively correlated with potassium concentrations, however this correlation was not statistically sig n ifican t at the 0.10 level. There was a significant positive correlation between fathead survival and iron concentrations in the filtered water samples. Low species diversity and abundance observed during the electroshocking effort may be reflected by the results of the toxicity test. 5.4 Worm-eating Birds A conservative risk assessment model based on wet-weight concentrations of contaminants for the Dry Run Creek site has determined that worm-eating birds may be at risk due to ingestion of contaminated forage, soil, and water. The model predicts that aluminum, chromium, copper, lead, vanadium, zinc, and fluoride are risk factors based on conservative inputs. By default, beryllium, iron, manganese, nickel, and trichlorofluoromethane are risk factors due to lack of toxicological benchmarks for these compounds. Food chain risk calculations and resultant hazard quotients are presented in Table 42. 5.5 Carnivorous Birds A conservative risk assessment model based on wet-weight concentrations of contaminants for the Dry Run Creek site has determined that carnivorous birds may be at risk due to ingestion of contaminated forage, soil, and water. The model predicts that aluminum, chromium, copper, lead, zinc, and fluoride are risk factors based on conservative inputs. By default, beryllium, iron, manganese, nickel, vanadium, and trichlorofluoromethane are risk factors due to lack of toxicological benchmarks for these compounds. Food chain risk calculations and resultant hazard quotients are presented in Table 42. 5.6 Carnivorous Mammals (Terrestrially feeding) A conservative risk assessment model based on wet-weight concentrations of contaminants for the Dry Run Creek site has determined that carnivorous mammals may be at risk due to ingestion of contaminated forage, soil, and water. The model predicts that aluminum, chromium, copper, lead. 48 0 0 0 -., USFW 0635 manganese, vanadium, and fluoride are risk factors based on conservative inputs. By default, iron and trichlorofluoromethane are risk factors due to lack of toxicological benchmarks for these compounds. Food chain risk calculations and resultant hazard quotients are presented in Table 42. 5.7 Piscivorous Mammals A conservative risk assessment model based on wet-weight concentrations of contaminants for the Dry Run Creek site has determined that piscivorous mammals may be at risk due to ingestion of contaminated forage, soil, and water. The model predicts that chromium, manganese, and fluoride are risk factors based on conservative inputs. Trichlorofluoromethane is not considered a risk factor because it was not detected in site sediments. Food chain risk calculations and resultant hazard quotients are presented in Table 42. 5.8 Omnivorous Mammals A conservative risk assessment mode! based on wet-weight concentrations of contaminants for the Dry Run Creek site has determined that omnivorous mammals may be at risk due to ingestion of contaminated forage, soil, and water. The model predicts that arsenic, chromium, copper, manganese, vanadium, and fluoride are risk factors based on conservative inputs. Trichlorofluoromethane is not considered a risk factor because it was not detected in site sediments. Food chain risk calculations and resultant hazard quotients are presented in Table 42. 5.9 Insectivorous Mammals A conservative risk assessment model based on wet-weight concentrations of contaminants for the Dry Run Creek site has determined that insectivorous mammals may be at risk due to ingestion of contaminated forage, soil, and water. The model predicts that aluminum, chromium, copper, lead, manganese, vanadium and fluoride are risk factors based on conservative inputs. By default, iron, and trichlorofluoromethane are considered risk factors due to lack of toxicological benchmarks for these compounds. Food chain risk calculations and resultant hazard quotients are presented in Table 42. 5.10 Herbivorous Mammals A conservative risk assessment model based on wet-weight concentrations of contaminants for the Dry Run Creek site has determined that herbivorous mammals may be at risk due to ingestion of contaminated forage, soil, and water. The model predicts that aluminum, chromium, lead, manganese, and fluoride are risk factors based on conservative inputs. By default, iron, vanadium, and trichlorofluoromethane are considered risk factors due to lack of toxicological benchmarks for this compound. Food chain risk calculations and resultant hazard quotients are presented in Table 42. 6.0 UNCERTAINTY ANALYSIS There are factors inherent in the risk assessment process which contribute to uncertainty and need to be considered when interpreting results. Major sources of uncertainty include natural variability, error, and insufficient knowledge. Error can be introduced by use of invalid assumptions in the conceptual model. Conservative assumptions were made in light of the uncertainty associated with the risk assessment process. This was done to minimize the possibility of concluding that no risk is present when a threat actually does exist (e.g., elimination of false negatives). Whenever possible, risk calculations were based on conservative values. For example, NOAELs 49 OOO-AcS i l o t r t a / ncnc used to calculate HQs were the lowest values found in the literature, regardless of toxic mechanism. An important contributor to uncertainty is the incompleteness of the data or information upon which the risk assessment is based. Risk calculations are based on maximum COC levels in sediment, water, and soil samples. Literature values for the toxicity of COCs were not available for all receptor species. An attempt was made to identify studies using closely related species to make risk estimates for the selected receptors. Species respond differently to exposure to toxins; responses to COCs by the indicator species may be different from species for which the toxicity data are reported. Methodological problems were also apparent in several of the studies from which NOAELs were obtained. Unfortunately, studies which were more suitable for this assessment were not found for some of the selected receptors. A literature search was conducted to identify appropriate NOAELs and LOAELs for this risk assessment. The values used to calculate HQs were the lowest values found in the literature. In many of the studies reviewed, adverse effects were observed at the lowest exposure concentration. This made it impossible to identify appropriate NOAELs for some receptors. In these cases, a factor of 10 was used to convert the LOAEL to a NOAEL, which adds uncertainty to the NOAEL-based calculations. Doses in toxicological studies can be reported in units of mg contaminant/kg diet, or in units of mg contaminant/kg body weight/day. All doses reported as mg/kg in diet were convened to units of mg/kg BW/day. If body weights were reported for the test animals in a given study, these values were used for making this conversion. Otherwise, the body weight and ingestion rate for the species reported in other literature sources were used. Another source of uncertainty arises from the use of toxicity values reported in the literature which are derived from single-species, single-contaminant laboratory studies. Prediction of ecosystem effects from laboratory studies is difficult. Laboratory studies cannot take into account the effects of environmental factors which may add to the effects of contaminant stress. NOAELs were generally selected from studies using single contaminant exposure scenarios. Species utilizing the Dry Run Creek site are exposed to a variety of contaminants. There is very linle information available in the literature regarding the rates of incidental soil/sediment ingestion for wildlife species. In this risk assessment, most of these values were based on estimates reported for species similar to the indicator species. Exposure concentrations were calculated for each target receptor species based on levels of contaminants detected in site media, daily food ingestion rates, incidental soil/sediment ingestion rates, and body weight reported in the literature. Tnis ecological risk assessment was conducted with the intent of completing a baseline risk assessment. In this risk evaluation it is concluded that a "potential ecological risk" exists if the HQ calculated from the maximum area concentration and the NOAEL equals or exceeds one. Within the calculation spreadsheets, alternate calculations were made using LOAEL toxicity benchmarks. CONCLUSIONS 7.1 Benthic Invertebrate Community Structure and Function Data from both the benthic survey and the toxicity tests indicate that fluoride and metal contamination may be a significant problem in Dry Run. Numerous fish kills historically reported in Dry Run also 50 0 0 9 7 rJ USFW 0637 provide evidence for potential effects on the benthic community. 7.2 Soil Invertebrate Community Structure and Function The structure and function of the soil invertebrate community does not appear to be at risk under current conditions found at the Dry Run Creek site. However, since earthworms comprise a significant amount of the forage base of some organisms (e.g. American robins, short-tail shrews, etc.), food chain problems may result from contaminants being tied up in the earthworm tissue. Based on our food chain models, it appears that this may be the case. 7.3 Fish Communities It was shown through the results of the fathead minnow bioassay, that larval fish were susceptible to contamination currently present near the landfill outfall at Dry Run. This finding is further supported by the results of the benthic invertebrate toxicity tests, where toxicity was observed at the same location. Negative effects of contaminants on the benthic community may directly affect fish communities, in that a portion of the fish food base in Dry Run (i.e. benthic invertebrates) may also be removed from the system. Reports of historical fish kills are also an important piece of evidence that suggests an ecological risk. In addition, high levels of metals were noted in the fish, which may present problems to upper level consumers due to dietary toxicity. 7.4 Worm-eating Birds Results of the food chain model for worm-eating birds such as the American robin indicate a potential risk due to metals, fluoride, and trichlorofluoromethane. This risk is associated with these contaminants in the soil and/or in earthworm tissue. Reports of historical wildlife kills also suggest ecological risk to avian receptors. 7.5 Carnivorous Birds Results of the food chain model for carnivorous birds such as the red-tail hawk indicate a potential risk due to metals, fluoride, and trichlorofluoromethane. This risk is associated with these conraminants in the soil and'or in small mammal tissue. Reports of historical wildlife kills also suggest ecological risk to avian receptors. 7.6 Carnivorous Mammals Results of the food chain model for terrestrially feeding carnivorous mammals such as the red fox indicate a potential risk due to metals, fluoride, and trichlorofluoromethane. "his risk is associated with these contaminants in the soil and/or in small mammal tissue. Reports of historical wildlife kills also suggest ecological risk to mammalian receptors. 7.7 Piscivorous Mammals Results of the food chain mode! for piscivorous mammals such as the mink indicate a potential risk due to metals, fluoride, and trichlorofluoromethane. This risk is associated with these contaminants in the soil and'or in fish tissue. Reports of historical wildlife kills also suggest ecological risk to mammalian receptors. 7.8 Omnivorous Mammals 51 0 0 0 * :G i iocxa/ nfi38 Results of the food chain mode! for omnivorous mammals such as the raccoon indicate a potential risk due to metals, fluoride, and trichlorofluoromethane. This risk is associated with these contaminants in the soil and/or in fish tissue. Reports of historical wildlife kills also suggest ecological risk to mammalian receptors. 7.9 Insectivorous Mammals Results of the food chain model for insectivorous mammals such as the short-tail shrew indicate a potential risk due to metals, fluoride, and trichlorofluoromethane. This risk is associated with these contaminants in the soil and/or in earthworm tissue. Physiological abnormalities, specifically the tooth structure of the shrews taken on site, further suggest ecological risk. In addition to the direct potential risk for the shrews, some of these animals had high concentrations of metals and fluoride in their tissues. This could present problems to organisms that feed on shrews and other small mammals on the site due to dietary toxicity. Reports of historical wildlife kills also suggest ecological risk to mammalian receptors. 7.10 Herbivorous Mammals Results of the food chain model for herbivorous mammals such as the meadow vole indicate a potential risk due to metals, fluoride, and trichlorofluoromethane. This risk is associated with these contaminants in the soil and/or in plant tissue. In addition to the direct potential risk for the voles; some of these animals had high concentrations of metals and fluoride in their tissues. This could present problems to organisms that feed on voles and other small mammals on the site due to dietary toxicity. Reports of historical wildlife kills also suggest ecological risk to mammalian receptors. SUMMARY During the past several years, a farmer who grazes his cattle along the reach of Dry Run Creek, has reported severe abnormalities in his herd. These abnormalities have included an increased incidence of stillborn calves, blindness in newborn and adult cattle, erratic behavior, stiffness of gait in adult cattle, abnormal posture, mottled teeth, and a high mortality rate across all age classes of his herd. In addition to problems with his herd, the farmer and others have also reported numerous fish kills in Dry Run, and wildlife kills (e.g. deer) for animals drinking from Dry Run. The results of this risk assessment support his assertion that effluent from the Dry Run Creek landfill may be having adverse effects on the ecological communities that inhabit the old field, deciduous forest, meadow, stream, and riparian habitats that are present on the site. These effects may be related to enriched levels of metals, fluoride, and trichlorofluoromethane that appear to be resultant of the landfill drainage. At a minimum, the symptoms manifest by the herd are characteristic of fluoride toxicity, and consistent with the conclusions of the risk assessment. In addition to the compounds that were studied in this risk assessment, numerous other compounds were present in Dry Run (specifically those identified as TICs or Tentatively Identified Compounds in the BNA scan) that could not be accurately identified. These compounds may also present a threat to the system, an certainly merit further investigation. The DuPont landfill that drains into Dry Run is the only apparent source of trichlorofluoromethane in soils adjacent to the stream. 52 c-oo 1ISFW 063S LITERATURE CITED Agency for Toxic Substances and Disease Registry (ATSDR). 1990. Toxicological Profilefo r Aluminum. Prepared by Sciences International Inc. Under U.S. Department of Health and Human Services Contract No. 205-93-0606. Research Triangle Park, NC. Agency for Toxic Substances and Disease Registry (ATSDR). 1990. Toxicological Profilefo r Manganese. Prepared by Sciences International Inc. Under U.S. Department of Health and Human Services Contract No. 205-93-0606. Research Triangle Park, NC. Agency for Toxic Substances and Disease Registry (ATSDR). 1991. Toxicological Profilefo r Vanadium. Prepared by Sciences International Inc. Under U.S. Department of Health and Human Services Contract No. 205-93-0606. Research Triangle Park, NC. Agency for Toxic Substances and Disease Registry (ATSDR). 1993. Toxicological Profilefo r Beryllium. Prepared by Sciences International Inc. Under U.S. Department of Health and Human Services Contract No. 205-93-0606. Research Triangle Park, NC. Agency for Toxic Substances and Disease Registry (ATSDR). 1996. Toxicological Profile fo r Nickel. Prepared by Sciences International Inc. Under U.S. Department of Health and Human Services Contract No. 205-93-0606. Research Triangle Park, NC. Ambrose, A.M., P.S. Larson, and J.F. Borzelleca. 1976. "Long-term toxicological assessment of nickel in rats and dogs." J. Food. Sci. Technol.. 13:181-187. Barbour, R.W. and W.H. Davis. 1974. Mammals o f Kentucky. Lexington, KY: University of Kentucky Press. 322p. Bamthouse, L.W., G.W. Suter, S.M. Bartell, J.J. Beauchamp, R.H. Gardner, E. Linder, R.V. O'Neill and A.E. Rosen. 1986. Users Manualfar Ecological Risk Assessment. Publication Number 2679. ORNL-6251. Environmental Services Division, Oak Ridge National Laboratory, Oak Ridge, TN. Beyer, W.N., E.E. Conner, and S. Gerould. 1994. "Estimates of Soil Ingestin bv Wildlife." J. Wildl. Manage., 5S(2):375-382. Brooks, L. 1988. "Inhibition of NADPH-cytochrome c reductase and attenuation of acute diethylnitrosamine hepatotoxicity by copper." Ph.D. Dissertation, Rutgers University, New Brunswick, N.J Bull, J. And J. Farrand, Jr. 1977. The Audubon Society Field Guide to North American Birds. Eastern Region. New York, NY: Alfred A. Knopf, Inc. Burton, P. 1989. Birds o f Prey o f the World. New York, NY: W.H. Smith Publishers. Byerrum, R.U., R.E. Eckardt, L.L. Hopkins. 1974. Vanadium. Washington, D.C. National Academy of Sciences. 53 ooo.;-. Calder, W.A., and E.J. Braun. 1983. "Scaling of osmotic regulation in mammals and birds." American Journal o f Physiology, 244: R601-R606. Castranova, V., L. Bowman, and J.R. Wright. 1984. "Toxicity of Metallic Ions in the Lung: Effects on Alveolar Macrophages and Alveolar Type II Cells." J. Toxicol. Environ. Health 13:845-856. Clark, D.R. Jr. 1979. "Lead Concentrations: Bats vs. Terrestrial Mammals Collected near a Major Highway." Environ. Sci. Tech.. 13:338-341. Dean, C.E., B.M. Hargis and P.S. Hargis. 1991. "Effects of Zinc Toxicity on Thyroid Function and Histology in Broiler Chicks." Toxicol. Letters. 57:309-318. DeGraaf, R.M. and D.D. Rudis. 1983. New England Wildlife: Habitat. Natural History, and Distribution. Amherst, MA. The University of Massachusetts Press. DeMayo, A., M.C. Taylor and K.W. Taylor. 1982. 'Effects of Copper on Humans, Laboratory and Farm Animals, Terrestrial Plants and Aquatic Life." CRC Critical Reviews in Environmental Control. 12(3): 183-255. Dixon, R.L., R.J. Sherins, and I.P. Lee. 1979. "Assessment of Environmental Factors Affecting Male Fertility." Environmental Health Perspectives. 30:53-68. Edwards, C.A. and J.R. Lofty. 1977. The Biology o f Earthworms. John Wiley and Sons, New York, NY. Ehrlich, P.R., D.S. Dobkin, and D. Wheye. 1988. The Birders Handbook. Simon and Schuster, Fireside. New York. 785 PPEisler, R. 1986. "Chromium Hazards to Fish, Wildlife, and Invertebrates: a Synoptic Review." U.S. Fish and Wildlife Service Biological Report, 85(1.86). 60p. Eisler, R. 1988a. "Arsenic Hazards to Fish, Wildlife, and Invertebrates: A Synoptic Review." U.S. Fish and Wildlife Service Biological Report 85(1.12). Eisler, R. 1988b. "Lead Hazards to Fish, Wildlife, and Invertebrates: A Synoptic Review." United States Fish and Wildlife Biological Report. 85(1.14). Evan, A.P. and W.G. Dail. 1974. "The Effects of Sodium Chromate on the Proximal Tubules of the Rat Kidney." Lab. Invest., 30:704-715 In: Steven, J.D., L.J. Davies, E.K. Stanley, R.A. Abbott, M. Inhat, L. Bidstrup, and J.F. Jaworski. 1976. "Effects of Chromium in the Canadian Environment." Nat. Res. Counc. Can., NRCC No. 15017. 168p. Fleming. W.J. and C.A. Schuler. 1988. "Influence of the Method of Fluoride Administration on Toxicity and Fluoride Concentrations in Japanese Quail." Environmental Toxicology and Chemistr 7(10):841-846. Fleming, W.J., C.E. Grue, C.A. Schuler, and C.M. Bunck. 1987. "Effects of Oral Doses of Fluoride on Nestling European Starlings." Arch. Env. Cont. Toxicol. 16(4): 483-490. Gianutsos, G. and M.T. Murray. 1982. "Alterations in Brain Dopamine and GABA Following Inorganic or Organic Manganese Administration." Neurotoxicol. 3:75-81. Goldman, E.A. 1950. Raccoons o f North and Middle America. Washington, DC: U.S. Fish and Wildl. Service. 54 o o o . *r USFW 0641 Effects on Aquatic Biota: 1994 Revision. ES/EF/TM-96/R1, Martin Marietta Energy Systems, Inc. Suttie, J.W. 1977. "Effects of Fluoride on Livestock." Journal o f Occupational Medicine. 19(l):40-48. Tyson, E.L. 1950. "Summer Food Habits of the Raccoon in Southwest Washington." J. Mammal., 31:448-449. U.S. Environmental Protection Agency (U.S. EPA). 1981. An exposure and risk assessmentfor arsenic. Office of Water Regulations and Standards, Criteria and Standards Division, Washington, D.C. EPA-440/4-85-005. U.S. Environmental Protection Agency (U.S. EPA). 1985. Ambient water quality criteriafo r arsenic. Office of Water Regulations and Standards, Criteria and Standards Division, Washington, D.C. U.S. Environmental Protection Agency (U.S. EPA). 1985. Methodsfo r Measuring the Acute Toxicity o f Effluents to Freshwater and Marine Organisms. United States Environmental Protection Agency. EPA/600/4-85/013. ' U.S. Environmental Protection Agency (U.S. EPA). 1989. Risk Assessment Guidance fo r Superfund. Volume I. Washington, D.C. EPA/540/1-89/002. U.S. Environmental Protection Agency (U.S. EPA). 1992. Ambient Water Quality Criteriafo r the Protection o fAquatic Life. Federal Register. Volume 57. No. 246. December 22. U.S. Environmental Protection Agency (U.S. EPA). 1993. Wildlife Exposure Factors Handbook, Volume l o fII. United States Environmental Protection Agency, Office of Research and Development, Washington, D.C. EPA/600/R-93/187a. U.S. Environmental Protection Agency (U.S. EPA). 1994. Methodsfo r Measuring the Toxicity and Bioaccumulation o fSediment-Associated Contaminants with Freshwater Invertebrates. United States Environmental Protection Agency. EPA/600/R-94/024. U.S. Environmental Protection Agency (U.S. EPA). 1995. Revised Region III BTAG Benchmark Values. U.S. EPA Region III BTAG. Technical Support Section. Philadelphia, PA. Van Zinderen Bakker and J.F. Jaworski. 1980. Effects o f Vanadium in the Canadian Environment. Ottawa, Canada: National Research Council of Canada, Associate Committee Scientific Criteria for Environmental Quality. Venugopal, B. and T.D. Luckey. 1978. Metal Toxicity in Mammals: 2. Chemical Toxicity o f Metals andMetalloids. Plenum Press, New York, NY. Wiebel. F.J., J.C. Leutz. L.Diamond and H.V. Gelboin. 1971. "Aryl Hydrocarbon (Benzo(a)pyrene) Hydroxylase in Microsomes from Rat Tissues: Differential Inhibition and Stimulation by Benzoflavones and Organic Solvents." Arch. Biochem. Biophys., 144:78-86. Wixson, B.G. and B.E. Davis. 1993. "Lead in Soil." Lead in Soil Task Force, Science Reviews, Northwood. 132 pp. Woolson, E.A. 1975. Arsenical pesticides. ACS Ser 7:1 - 176 (as cited in Eisler, 1994). 59 000*:^ U S F W Dfi4P USFW 0643 \ 76 O0Olt?6 I N T E R O F F I C E ri 3 M r- R A N D O M Date* From Dept Tel No 14-Nov-1997 02:11pm EDT DANIEL A. WEBER WEBERDA ENGINEERING POLYMERS 0-863-4415 TO LYNWOOD K. IRELAND TO RONALD W MELOON TO* ROBERT L . RITCHEY TO* H. DAVID RAMSEY, JR TO* David C. Harrison ( IRELAND ) ( MELOONRW ) ( RITCHERL ) ( RAMSEY ) ( HARRISDC ) Subject C-8 DATA FOR DOMESTIC WATER WELLS FYI, C-8 LEVELS IN THE EAST FILED DOMESTIC WATER SERVICE WELLS AND WEST FIELD (OLD LUBECK WELLFIELD) WELL #1 ARE SUMMARIZED BELOW: WEST WELLFIELD (OLD LUBECK WELLFIELD) WELL #1 5/93 8/94 5/97 0.6 PPB 2.1 PPB (RETEST) 1.5 PPB 7.9 PPB 8 - 11 % 60 - 75 % 30 - 38 % 120 - 126 % SURROGATE RECOVERY SURROGATE RECOVERY SURROGATE RECOVERY SURROGATE RECOVERY BAST WELLFIELD WELL # 336 6/93 4/96 5/97 0.5 PPB 0.48 PPB 0.79 PPB 52 - 76 % SURROGATE RECOVERY 29 - 85 % SURROGATE RECOVERY 36 - 41 % SURROGATE RECOVERY WELL JL 331 6/93 4/96 5/97 2.9 PPB 0.52 PPB 0.55 PPB 55 - 78 % SURROGATE RECOVERY 40 - 101 % SURROGATE RECOVERY 43 - 45 % SURROGATE RECOVERY DAW000638 WELL JL 332 6/93 3.3 PPB 69 - 87 % SURROGATE RECOVERY SURROGATE RECOVERY PERTAINS TO THE PRACTICE OF ADDING COMPOUNDS WITH SIMILAR C8 ORGANIC STRUCTURE TO THE SAMPLE TO GAGE THE PER CENT RECOVERY OF THE ANALYTICAL METHOD USED TO DETERMINE THE C8 RESULT (IE, -AN INDICATION OF HOW MUCH OF THE C-8 PRESENT IN THE SAMPLE WAS IDENTIFIED). EID091600 0 0 0 .c I 77 OO..16 S kennedgl ! / 12/08/97 09:41 AM To: ZIPFEL, KOENINMC, CHAPMAGA cc: COOKJC Subject: C-8 MONKEY STUOY MET WITH APME APFO GROUP LAST WEEK-MINUTES WILL COME WITH OFFICIAL ITEMS BUT HERE IS A QUICK PREVIEW: 1) 0.FARRAR WILL WORK TO GET CONTRACTS ON PLACE BY YEARS END 2) 6 1/2 SHARES (650,000) COMMITTED TO MONKEY AND RAT WORK 3) FINAL COST TO BE IN THAT REGION, 2 DETAILS INCLUDE ANALYTICAL WORK BY 3-M (BST 50,000) AND BIOCHEMICAL DETERMINATIONS BY HASKELL (AROUND 20,000). THIS WILL BE DETAILED THROUGH BY PAUL LEIDER-- PERHAPS THE DOLLAR AMOUNTS CAN BE ADJUSTS. IT IS THE DESIRE OF THE TOX WORKING GROUP TO NOT GO ASK FOR MORE MONEY. 4 ) TIMING--MONKEY PILOT TO START IN TEB, 1998, RESULTS AVAILABLE MAY,1998. MONKEY MAIN-TO START JUNE 1998, RESULTS AVAILABLE MAY 1999. WE DECIDED THAT THERE WAS LITTLE CHANCE THAT THE STUDY WOULD GENERATE ENOUGH SOLID INFORMATION TO ALLOW CONCLUSION AFTER 3 MONTHS-- SO IT IS A 6 MONTH STUDY. 5) COMMUNICATION INTERFACE WILL NEED BE MAINTAINED AND EXPEDITED-ALL TOX MEMBERS MADE TIMING COMMITMENTS TO MEET THE ABOVE SCHEDULE-- THIS WILL INCLUDE 2 US AND 2 EUROPEAN MEETINGS DURING AND AFTER COMPLETION OF THE IN LIFE PHASES. FURTHER DEAILS TO COME-- WORKING GROUP WAS THE MOST COOPERATIVE TO DATE- LOOKS LIKE EVERYONE IS IN LINE TO GET AFTER THE ISSUE. CO NOTE THAT THE RISK ASSESSMENT WILL RELY HEAVILY ON THIS MONKEY, AND TO A LESSER EXTENT THE RAT, STUDIES AND HENCE WILL NOT.BE COMPLETED IN 1998. 0 0 0 EID081907 78 OOO-.V/O i INTEROFFICE MEMORANDUM Date: 17-Feb-1998 11:29am EDT From: ROBERT L. RITCHEY RITCHERL Dept: EP - Env TelNo: 863-4271 TO: See Below Subject EPA Visit to Dry Run Landfill We hosted today a pre-scheduled visit by Mike Taurino, EPA Region HI, to Dry Run Landfill. Mike was assigned to EPA's Dry Run efforts several weeks ago. He is a Fund On-Scene Coordinator. As such, he gets involved under Superfund/CERCLA when there is a potential "removal" project He explained that his role is dealing with situations that require immediate attention (thus removal) as opposed to their group that handles remedial responses which are longer term in nature. He would define what response is required to a given immediate need. Mike is a Civil Engineer with an Environmental Masters and has been with EPA five years. What drew Mike into this Dry Run effort is the perception by EPA that our landfill may be having an impact on Dry Run Creek. The basis for this is obviously influenced by claims of historical cattle, fish, and other wildlife impacts which are reflected in the EPA risk assessment report on Dry Run. Mike indicated that he had read the conclusions (only) of this report and also has available to him the 104e information we submitted on Dry Run. With that background, he was predisposed to believe that there are problems at Dry Run Creek. Presentations and Q&A sessions with Woody Ireland and Dan Weber were successful in casting serious doubt on the science and credibility of the EPA risk assessment. Mike at one point stated something like "so if I am deciding what actions are needed, it sounds like I really can't rely on this report." We did acknowledge that in 1995 we had an episode of "black water", but explained the cause, disassociated it from fluorides, explained our corrective actions and that it has not reoccurred since. We also discussed the numerous design improvements and additional monitoring and permit requirements which will be incorporated in our new permit when it is finally issued. We indicated our desire to begin working on those ASAP. I believe Mike is of the opinion that what we have already done and what we plan to do under the new permit will resolve the issue. He reserved the right to decide otherwise, including a decision to do more study. However, he was clearly having trouble thinking of what else we could do and what else would be justified. We took Mike to the Landfill and he got a good tour. He does not have a background in dealing with landfills, so we did most of the talking and he had few questions. Everything looked good. Diy Run Creek did not have the appearance of being adversely effected at all. As Dan summarized afterwards, Mike came to see ugly and he didn't Mike will be at our meeting with EPA next Monday in Philadelphia. I believe he can help stabilize EPA's unattached emotional reaction to KLKUUI /J 000 . EID067733 some of the assertions and conclusions of the study. I believe based on this Interaction today that it will be important to hit hard on the aquatic and mammalian tox issues and when we visit EPA. Distribution: TO: WILLIAM H. HOPKINS TO: BARRY L. HUDSON TO: JOHN H. LITTLE TO: H. DAVID RAMSEY, JR. ( HOPKINWH ) fH U D S O N B L } ( LITTLEJH ) ( RAMSEY ) CC: LYNWOOD K. IRELAND ( IRELAND ) CO: JOHN R. MATHEWS (MATHEW S) CC: RICHARD A KIRSCHNER, JR ( KIRSCHRA ) CC: DAWN D JACKSON ( JACKSODD) CC: RALPH G. STAHL. JR. CSTAHLRG AT A1 AT CSOC ) CC: KEITH B. PERSOCI ( PIERSOKB AT A1 AT ESVAX ) CC: ANDREW S. HARTTEN ( HARTTEAS AT A1 AT CSOC ) CC: Chartes T. Alt (A LT) CC: JOHN J MENTINK ( MENTINJJ ) CC: JOHN M MIGLIORE ( MIGLIOJM ) CC: DANIEL A. WEBER (W EBERDAj CC: GEORGE WOYTOWICH ( WOYTOWIG ) 00vA- EID067734 79 ooo-i > May 14, 1998 CERTIFIED MAIL RETURN RECEIPT REQUESTED Ms. Sarah L. Caspar (3HW32) U.S. Environmental P ro tectio n Agency 841 Chestnut Building P h ila d e lp h ia , PA 19107 RE: EPA D r a f t Report, Dry Run Creek, November 1997 Dear Ms. Caspar: Thank you f o r providing DuPont Washington Works a copy o f the subject r e p o rt and f o r meeting w ith DuPont on February 23, 1998, to hear our concerns regarding the v a lid ity of the report's conclusions. The purpose o f t h i s l e t t e r is to document those concerns and others which time p r o h ib ite d review ing in our meeting. A summary o f key comments is provided, follow ed by a more d e t a i le d discussio n. We recognize t h a t the r e p o rt we reviewed i s a " D r a ft" copy. While our discussion on February 23 raised the prospect o f making changes to t h i s d r a f t re p o rt to remove some of the im p lic a tio n s t h a t the co-authors in d ic a te d they did not in te n d , upon review we b e lie v e t h a t a major r e w r i t e would be necessary to accomplish t h i s . We do not b e lie v e t h a t prospect was o f f e r e d . Therefore, we have e le c te d instead to l i m i t our comments to t h is l e t t e r . We share an i n t e r e s t in determ ining whether Dry Run Creek has been or is being adversely a f f e c t e d , and i f so, determ ining the cause. However, i t is our opinion th at the conclusions of the d ra ft report with respect to these questions are not supported by a v a il a b l e d a ta . As in d ic a te d a t our February 23 m eeting, i t is our i n t e n t to work w ith you to design and consider a c o lla b o r a tiv e n ext-step to advance a s c i e n t i f i c understanding o f the issues behind the ris k assessment. Sincerely yours, Robert L. Ritchey Sr. Environmental Control Consultant Washington Works Attachment hew: 19675-1 USEPA 062 V 80 Rogar J. ZipfeT <ZIPFELW WPS-A1.EMAIL.DUPONT.COM > on 0 9 /1 4 /9 9 04:38:51 PM To: Roger J Zipfel/AE/DuPont cc: Subject: (C-8 ENVIROMENTAL SAMPLING/24-Jun-1998)FC-143 Results Availab Date: Wed, 24 Jun 1998 13:38:00 EDT From: VERA L WIGAL <WIGALVL0wwps-al.email.dupont.com> Subject: FC-143 Results Available To-Date (Woytowich) To: "ANDREW S. HARTTEN" <HARTTEAS0CSOC-A1.EMAIL.DOPONT.COM>, "ROBERT L. RITCHEY" <RITCHERL0wwps-al.email.dupont.com>, "DANIEL A. WEBER" <WEBERDA0wwps-al.email.dupont.com>, "LYNWOOD K. IRELAND" <IRLAND0wwps-al.email.dupont.com>, "Roger J. Zipfel" <ZIPFEL0wwpa-al.email.dupont.com>, "RICHARD A KIRSCHNER, JR" <KIRSCHRA0wwps-al.email.dupont.com>, GEORGE WOYTOWICH <WOYTOWIG0wwps-al.email.dupont.com> MIME-version: 1.0 Content-type: MULTIPART/MIXED; BOUNDARY-"Boundary_(ID_2NbORBOXIUKUMFSQRO/NFA)" Delivery-date: Wed, 24 Jun 1998 13:44:00 EDT " Posting-date: Wed, 24 Jun 1998 13:42:00 EDT Importance: normal Al-type: MAIL Date: Wed, 24 Jun 1998 11:07:00 EDT Subject: FC-143 Data from Landfills MIME-version: 1.0 Content-type: text/plain Importance: normal Al-type: DOCUMENT June 24, 1998 Details of FC-143 Sample Data From CH2M Hill Available To-Date: Location Date Site Sampled Site Location Result ug/L EID082057 Dry Run Landfill 5/19/98 Stream I Stream II 001 Outlet Leachate FBLK21 1.0 4.6 17 56 0 .1 Letart Landfill 5/28/98 Lower Rond Upper Pond WWXLTLMW6 WWKLTLKW2A WWKLTLKW7 WWKLTLMW1 WWKLTLMW8 Trip Blank FBLK02 1100 480 30 990 260 24000 2700 0.1 0.1 Local Landfill 6/2/98 Outlet 101 Stream 2 15 Outfall 004 12 Outfall 005 39 PBLK05 54 0.1 Plant Site Weet WellFld 16 16058 (vlw) 000 EID082058 81 000-.V/5 INTEROFFICE MEMORANDUM Date: From: Dept: Tel No: 08-Aug-1998 11:33am Thomas R. Waldron WALDROTR PPD-POWER/SERVICE 304-863-2489 TO: LYNWOOD K. IRELAND TO: JOHN R. MATHEWS ( IRELAND ) ( MATHEWS ) CC: Gary W. Klesel CC: RICHARD A KIRSCHNER, JR ( KLESELGW ) ( KIRSCHRA ) Subject: Dry Run Landfill I came in this morning at about 0830 to look at Dry Run Landfill. The pond is being drained to the stream, at a very slow rate. The level of the pond had dropped about a foot or so. On my way out, I ran into one of Richard's hands and he said he had opened the valve a little, earlier this moring, and was just checking on the progress. He also said he was told to turn it off before dark.(?) I took some water samples (just for visual comparison) at #001, one at the 2,000 ft level and one at the property line. Richard Construction has installed a couple of check dams at 001 and also installed silt fences and hay bales in the outfall itself. The water was running through them both but not all the solids were staying behind. The stream was turbid down to about a thousand foot or so but beyond.that, was fairly clear. There is still a lot of activity down near the property line, and Wilbur Earl has installed a metal gate at the line fence, my guess would be to give him easier access on to our property when he so desires. Someone is running the fill from his end quite a lot. If I get a chance, I may check on things down there tomorrow. Tom 000 EID030998 82 000^10 INTEROFFICE MEMORANDUM Date: From: Dept: Tel No: 09-Aug-1998 03:57pm Thomas R . Waldron WAIiDROTR PPD-POWER/SERVICE 304-863-2489 TO: LYNWOOD K. IRELAND TO: JOHN R. MATHEWS ( IRELAND ) ( MATHEWS ) CC: Ga*y W. Kiesel CC: RICHARD A KIRSCHNER, JR ( KLESELGW ) ( KIRSCHRA ) Subject: DRY RUN LANDFILL I came in today at 1400 to check on Dry Run. The pond has now drained down about 3 to 4 feet. I again took samples (for visual inspection only), just below the #001 Outfall, as I did yesterday, at about the 2,000' level and again at the property line. The outfall is still pretty turbid and the sample at the 2,000' level is also slightly turbid. The sample at the property line is still clear. Wilbur's cattle were wallowing in the stream just beyond the fence at the property line. I got several pictures both yesterday and today. You can notice an odor from the sample at the outfall but it does not smell like leachate. I will bring them down in them in the morning and let you all have a look. I talked to the Security Guard at the fill and he said the same couples as last week came down on 4-wheelers and went back up the old road just beyond the old 1,000' sample point. I am going to check that out soon and see if I can find some wackyweed perhaps being grown up there. Problem is, I don't know what the stuff looks like. I may have to take Roger with me!! I hear they grow a lot of that stuff over in Meigs County. As I write this message, looking out my office window, it sure looks a lot like rain on the way! Just what we need at the landfill... More solids in the stream... Tom C0 EIDO17500 I AG2NDA 8/11/98 DRY RUN LANDFILL o Commitment to work together o Purpose of Collaborative Effort o Materials Potentially Landfilled o DuPont Inputs on what to look for * Mammalian effects * Organofluorides * TICs o 7/22/98 Split Sample Results o Collaborative Program Proposal OOO'-ii USEPA 0821 gSJBEQSB s t a t e ;iCW*? FOR COLLABORATIVE PROGRAM: A collaborative effort between EPA and DuPont, including scope development, data collection, and interpretation, will be undertaken to characterize environmental conditions in order to: 1) investigate potential causes of environmental effects 2) determine if causes are connected to landfill constituents and exposure pathways 8/11/98 * GOO-.'.tf EIDO17942 Group i: Materials known or suspected to have been sent to Dry Run Landfill in significant quantities at some time in history include the following. This listing represents a good faith effort to evaluate disposal history for materials meeting this criteria. flyash (coal-fired boilers) boiler bottom ash (coal-fired and alternate fuels boilers) dirt/rubble from plant excavations absorbed biosludge biocake bio-waste treatment settlings (equalization tank) superaste pond dirt polyacetal resins nylon resins polyester resins elastomeric polymers acrylic polymers polyvinyl butyral fluoropolymers polyethylene wood cardboard scrap metal glass asbestos 8/11/98 OOO-.iS EID000244 Group l Appendix: Major monomers and constituents of Group l resins. RESIN polyacetal resins nylon resins polyester resins elastomeric polymers acrylic polymers polyvinyl butyral fluoropolymers polyethylene Kfi.TOB MONOMERS /CONSTITUENTS formal dehyde adipic acid hexamethylene diamine caprolactam dodecanedioic acid teraphthalic acid* ethylene glycol* butylene glycol* ethylene-propylene-hexadiene elastomer* ethylene/methacrylic acid copolymers* butylene/poly(alkylene ether)phthalate* methyl methacrylate ethyl acrylate ethyl methacrylate n-butyl methacrylate isobutyl methacrylate methacrylic acid butyraldhyde polyvinyl alcohol tetra ethylene glycol diheptanoate tetrafluoroethylene hexafluoropropylene ethylene ethylene * not handled at manufacturing site as monomers (already polymers) 9/1/98 0 0 0 . -'i JL f EID000245 Group 2: Low and trace volume chemicals of In te re st which could - posslblv he present it the Drv Run ' an d flll Include the following chemicals usee- as solvents, p la stic iz e rs, refrig e ra n ts, surfactants, e t c ., which could be present in de minimis amounts on f i l t e r s , gaskets, insulation, rags, absorbents, e tc ., or as laboratory or maintenance chemicals. The l i s t is not complete as to create such a l i s t would be an exhaustive exercise a t a f a c ility as diverse as ours; however, a good fa ith effo rt has been made to include those chemicals o f g reatest in te re st given the in ten t of the EPA request. acetic acid formic acid methanol acetone chloroform carbon te tra chloride heptanes mixed isomers heptanol mixed isomers s te a ric acid and sa lts N-butyl benzene sulfonamide biphenyl and biphenyl oxide difluorochloromethane (F-22) trichlo ro triflu o ro eth an e (F-113) methylene chloride te tra c h 1oroethy1ene trichloroethylene methyl chloroform phenol m-cresol benzyl alcohol hydroxyethyl cellulose methyl ethyl ketone toluene hydrocarbon o ils silicon oils polyethylene glycol ethers succinic acid ammonium perfluorooctanoate ethylene glycol gasoline di-2 ethylhexoate of polyethylene glycol numerous hindered phenol compounds d-limonene phthalic anhydride alkaline batteries A lternate Fuels Boiler flyash (one time event) diesel fuel 8/12/98 000./. v EID000246 V 84 G 00.$ V) \ n i-: ; ICL-L_ LWt- IU , , K lL'L' Vj DRAFT c\> 'V Purpose: . Proposal to Conduct a General Human Health and Environmental Effects Risk Analysis on C-8 The purpose of this project is to evaluate the risks to human health and the environment from exposure to C-fl during manufacture, transport, product use and disposal of -8. The analysis will be conducted in a fashion that will provi semi-quantitative estimates of risks so that exposures yielding the highest risks can be identified and recommendations on reducing these risks can be developed. Risks from manufacture, transport and product use will developed In a way that will facilitate Future comparisons of risks estimated for potential C-8 alternatives. The project will be conducted in three parts. The first two will be conductod in parallel, in which H u m a n health and ecological risks will be characterized. The final part will develop conclusionc on oxposures that contribute the highest risks so that recommendations for risk management strategies and alternatives can be developed. The project is estimated to take 12 months to complete from the time of initiation. The Exposure analyses listed below wilt require collaboration misappropriate plant personnel. /The datas presented assume a Feb. 1. t o 9 S p U approval date.) Scope: I. H u m a n Ile&tth Risk A. Hazard Identification 0 / tTi:--m--e-I Li--ine 4/18/9) ESI. C a s t($ } 8000 T P fY ; 5Z Hazards to human health will he reviewed and summarized in this section. The critical toxicity endpoints of relevance to human health risk will he identified and potential dosimeters to be used for interspaces extrapolation of risk will be discussed. The Haskell toxicity summary will be updated as part of this task. Oose-Hesponse Analysis 9/30/9^) 43,200 The dose-response characteristics of C-8 wilt be evaluated. This may include conducting benchmark dose analyses to identify no-observod adverse effect levels whoro necessary. Appropriate dosimeters for interspecies extrapolation will also be developed based on the likely mode of action. The pharmacokinetics of C-8 will also be reviewed. If possible, rudimentary physiologically-based pharmacokinetics approaches will be developed to facilitate interspaoias extrapolation of risk. Risks vs. dose relationships will be developed in this phase 43 c. Exposure Analysis 9/30/97 16,000 Reasonable exposure scenarios for C-8 will be developed. Thi6 are likely to include QSl- airborne, drinking water, dermal, and other oral Ingestion pathways. Intake rates and durations of exposure will be developed. Haskell will work with an assigned person(s) from the plant site to help characterize these exposure pathways for manufacturing, transport, product use, and waste disposal operations. Tho business will piovide Haskell with data on concentrations of C -8 in tho afloctod media (air, water, soil). These data will be tabulated. Mnnts Carlo techniques may be used to calculate expected upper confidence limits for these exposures, depending the availability of data. The cost associated with this task includes only Haskell personnel time. D. Risk Characterization 12/15/97 16.000 Risks will be summarized according to the major routes of exposure (air, water, dermal, other oral) for each C-8 application (manufacture, transport, product use, disposal). The risks will be characterized by comparing the likely exposure concentrations to the dose-response relationship. This method is generally referred to as a Margin of Exposure. The characterization will provide the risk manager with 0 ^^ oP I^ * \A^ EID087228 0 0 9 . 'ii in DRAFT ,1. f information that will help identify the operations and exposure pathways that present the highest risk. The characterizations will also enable future comparisons to be made of potential risks posed by C-8 alternatives. Ecological Effects Time Lina Est. Cnst($) Hazard Identification Hazards to key environmental health indicator species will be reviewed and summarized in this section. The critical toxicity endpoints will be identified. Based on the current literature search, chronic studies In aquatic species will need to be undertaken. Avian reproduction and avian food-chain accumulation will need assessment; however this may be extrapolated using mammalian toxicology and PB- PK data and E Fate Information. The Haskell toxicity summary will be updated as part of this task. 1.) Hazard Assessment 9/15/9) '$ib.<och 2. ) Testing (Fish ELS and Daphmd Chronic) 8/15/9? $80X100 y ' fThjsis-wLh-siatk: renewal and analytical) ) Avian (if needed?^. 8/15/0? Exposure Analysis * Reasonable exposure scenarios for C-8 will be developed for the higher environmental oxposure areas at the three manufacturing sites, including their respective disposal sites and a customer site. Intake rates and durations of exposure will be developed. Haskell will work with an assigned person(s) from the plant site to help characterize these exposure pathways for manufacturing, transport, product use, and waste disposal operations. The business wilt provide Haskell with data on concentrations of C-8 in the affected media (air. water, soil). These data will be tabulated. Monte Carlo techniques may be used to calculate expected upper confidence limits tor these exposures, depending on the availability of data. The cost associated with this task includes only Haskell personnel time. 1. ) Exposure Assessment - Washington Works 6 /1 5 /9 / 8 ^ 0 2. ) Exposure Assessment - Dordrecht 8/15/97 S.fity) 3. ) Exposure Assessment - Shimi2U9/1 & / 9 \ 2jOOO 4. ) Exposure Assessment D. Risk Characterization Customor 410/15/9721000 / Risks wilt bo summarized according to the major media of environmental exposure (water, soil, air) for oach C 8 application (manufacture, transport, product use, disposal). The risks wifi be characterized by comparing the likely Predicted Environmental Concentrations (PEC) to the Predicted No Effect Concentrations (PNEC). This method is generally referred to as Hazard Quotient. The characterization will provide the risk manager with Information that will help identify the operations and exposure pathways that present the highest risk. The characterizations will also enable future comparisons to be made of potential risks posed by C-8 alternatives. 12/15/9^r 16.000 27 III. Recommendations on Risk Management Strategies and Alternatives 12/15/9/4800 This section will ovaluato collectively the risks identified to human health and ecological receptors. Based on these analyses, recommendations will be made as to which operations could be targeted to ensure risks are appropriately managed in the most cost effective manner. This will be a very subjective exercise (narrative) and will require some Interaction with the appropriate people from the business. ! EID087230 i 85 OOri 9 * "Roger J. Zlpfai* <ZIPFEL@WWPS-A1 .EMAIL.OUPONT.COM > on 0 9 /1 4 /9 9 08:51 :1 2 PM To: Roger J Zipfel/AE/DuPont cc: Subject: (C-8 REVIEWS/10-Sep-1998)C-8 Review Date Data: Thu, 10 Sap 1998 11:28:00 EDT Prom: "ROBERT L. RITCHEY" <RITCHERL@wwps-al.email.dupont.com> Subjact: C-8 Raviaw Data To: Bernard J Reilly <REILL2BJ8NANOTESl.EMAIL.DUPONT.COM>, "ISIDOROS J. ZANXKOS, P.E." <ZANIKOIJ0CSOC-A1.EMAIL.DUPONT.COM>, TRINI GARZA <GARZAOT@wwpa-al.aaall.dupont.coa, "Roger J. Zipfel" <ZIPPEL@wwps-al.email.dupont.eom>, "ROBERT R. MATTSON" <MATTSORR@wwps-al.email.dupont.com>, "DANIEL A. WEBER" <WEBERDA0wwps-al.email.dupont.com>, DAWN D JACKSON <JACKSODD@wwps-al.email.dupont.com> Ce: "H. DAVID RAMSEY, JR." <RAMSEY@wwps-al.email.dupont.cqm>, JOHN M M1GLIORE <MIGLIOJM@wwps-al.email.dupont.com>, Andrea V Malinowski <MALIN2A0NANOTES1.EMAIL.DUPONT.COM>, L Craig Skaggs <SKAGG2LC@NANOTESl.EMAIL.DUPONT.COM>, Maurice Astorga <ASTORGM@ISCDCVM5>, Robert P Pinchot <PINCH2RP0NANOTES1.EMAIL.DUPONT.COM> MIME-version: 1.0 Content-type: text/plain Delivery-date: Thu, 10 Sep 1998 11:56:00 EDT Posting-date: Thu, 10 Sep 1998 11:49:00 EDT Importance: normal Al-type: MAIL The C-8 review has been set for 12:30-4:30 October 5 in the B21 upstairs small conference room. Tentative Agenda appears below. Visitors: I will be arranging your passes and you should plan to have receptionist call me. We can go to cafeteria for lunch if you arrive early enough. Craig and Andrea: Please feel free to attend. Let me know. AGENDA: 10/5/98 C-8 Review C-8: What is it ? - Punetion and use - Vendor and competitor information - Molecular structure and biopersistence - Toxicology 000-: EID082020 FLPR Management System Global team structure Goals, Program Summary Reduction and replacement effort progress Product Stewardship view; mass balance Dry Run Landfill Fluoropolymers disposal history Sampling data Government Communications 104 RFI Permits Drinking Water Risk Assessment Program Criala Management Plana ooo-:. EID082021 V-_ 86 009.* g rI DuPont Wchingtor Worts ?.0.BcsV2V Pirtersburj, WV 25102-1217 September 11, 1998 CERTIFIED HAIL RETURN RECEIPT REQUESTED M r. John G. B r itv e c , G eologist In d u s t r ia l Waste Section O f f ic e o f Water Resources, WV-DEP Goose Run Road F airm o n t, WV 26554 Dear John, During our September 10, 1998 conference c a ll w ith EPA regarding Dry Run L a n d f i l l , you asked me to send you th e seven items I summarized as our answer to EPA's question about changes we had made in th e 1993-1994 tim efram e. As in d ic a te d when I covered t h is m a t e r ia l, we are sim ply re p o rtin g changes in the nature o f the waste o r the physicals o f the l a n d f i l l , w ith o u t a tte m p tin g to c o r r e la te these changes to any e f f e c t s . I t would be our judgment th a t most o f these changes would have low p r o b a b ilit y o f an e c o - e f f e c t . This would be f u r th e r supported by EPA's r e v e la tio n during th e conference c a ll th a t the alle g atio n s o f e ffe c t date to a t le a s t the m id -1 9 8 0 's . EPA also commented th a t the question about the 1993-1994 tim efram e predated t h e i r understanding o f th a t h is to r y o f a lle g a t io n , and th a t any question about changes during th a t o r o th e r tim efram es is probably not a p p ro p r ia te . However, since you had asked f o r the summary, I am in c lu d in g i t b e lo w . 1) Some grades o f p o lyac eta l re s in s were tra n s itio n e d beginning around 1992 to a d iffe r e n t s t a b i l i z e r . . . a polyacrylam ide s t a b i l i z e r . . . to improve product performance a t processing tem peratures. Only fin is h e d resins have the s t a b i l i z e r , and maximum co n c e n tra tio n o f polyacrylam ide present in them is .5wt%, which would be in c o rp o rated in the r e s in . This would probably not present an issue since re s in is stable. 2 ) At the same time as the s t a b i l i z e r change and f o r those same products, we changed to a b e t t e r a n t i-o x id a n t, irg anox 2 4 5 . T h is m a te ria l is also incorporated in th e s ta b le polym er. The amount in the finished product is less than .lw t% . 3 ) As the r e s u lt o f a global program to reduce polymer to l a n d f i l l by fin d in g new o u tle ts f o r s a le o f o ff-s p e c m a te ria l and through in cin eratio n fo r recovery o f heat valu e, s ig n ific a n t reductions in the q u a n tity o f p o ly a c e ta l, n ylo n , p o ly e s te r, and elastom ers being la n d f ille d a t Dry Run occurred each y e a r from 1993 through 1995. EID000228 '. *4: > S*T ' m-.. r t 0 a 4c.r:rt o * John G. Britvec -2- September 11, 1998 4) As in d ic a te d p re v io u s ly to OWR and EPA, in 1994, in p re p a ra tio n f o r in s t a llin g the new b io s o lid s f i l t e r press a t th e p la n t s i t e , th e amount o f sorbed s o lid s being sent to Dry Run l a n d f i l l was s ig n ific a n tly increased in the Spring o f 1994. 5) Also as in d ic a te d p re v io u s ly , in August 1994, we began disposing o f b io s o lid s in f i l t e r cake form , which increased b io m a tte r co n cen tratio n and put more t o t a l biomass to the l a n d f i l l because th e new f i l t e r press was more e f f i c i e n t in removing s o lid s . 6) Because o f s o lid s accum ulation, the low er pond was d rain ed and sediments were removed in August, 1993 to m ain tain pond c a p a c ity requirem ents. As you know, t h is was done in communication w ith WV-OWR. Steps were taken to preven t th e re le a s e o f sediment to th e receiving stream. 7) We began l a n d f il li n g a t the low er s e c tio n o f th e l a n d f i l l in September, 1994, having completed the f i r s t pass on th e upper section. I a ls o in d ic a te d during the September 10, 1998 conference c a l l t h a t we do n o t have in fo rm atio n on what changes the neighboring farm er may have in tro d u ced in th is same tim e period and t h a t we would hope t h a t EPA is investigating this area. S in c e re ly Robert L. Ritchey S r. Environmental Control Consultant Washington Works 20770-2 OOO.AS-S EID000229 JL 87 OOO- : INTEROFFICE MEMORANDUM Date From Dept * Tel Noi 3O-Sep-1990 09:26am EDT DANIEL A. WEBER WEBERDA ENGINEERING POLYMERS 8-863-4415 TO DANIEL A. WEBER ( WEBERDA ) Subjects C-8 INFO SLIDES FOR RLR MEETING: 10/5/98 DAW000631 EID091595 000-: 3 5 DRY RUN LANDFILL: FC-143 HISTORY SUMMARY SUPERNATE POND SOIL DISPOSAL: - 7100 TONS OF SOIL CONTAINING - 85 PPM FC-143 DISPOSED OF NEAR THE BOTTOM OF THE LANDFILL IN 11/88. - THIS SOIL WAS LATER MOVED TO THE TOP OF THE LANDFILL AND BURIED IN A CLAY-LINED SEPARATE CELL IN 10/91. FC-143 GROUNDWATER AND SURFACE WATER MONITORING: - BEGAN MONITORING ANNUALLY FOR FC-143 IN 1991. - GROUNDWATER CONCENTRATIONS RANGE <1 - 15 P P B . - LEACHATE CONC. AT O.F. 001 RANGES 30 - 200 PPB * PROPERTY BOUNDARY STREAM CONCENTRATION RANGES 2 - 2 5 PPB. - DATA REPORTED ANNUALLY TO THE WVDEP BEGINNING WITH THE 1991 ANNUAL REPORT. STILL MONITORING AND REPORTING ANNUALLY.* * 1998 RESULTS: LEACHATE = 56 PPB OUTLET 001 = 17 PPB STREAM #1 = 1 PPB STREAM #2 = 4.6 PPB PROP. BND. = 0.88 PPB - 7 POUND/YR FC-143 DISPOSED OF WITH BIOCAKE (930 P P B ) . 600M POUNDS/YR OF FLUOROPOLYMER WASTE DISPOSAL BEGAN 1/96; DOES NOT CONTAIN FC-143. EID091596 V i 88 r '""C 000cG0 INTEROFFICE MEMORANDUM Date: From: Dept: Tel No: 13-0ct-1998 05:11pm DANIEL A. WEBER WEBERDA ENGINEERING POLYMERS 8-863-4415 Subject: POTENTIAL COAMING MATERIALS AT DRY RUN LANDFILL FYI, BASED ON A REVIEW OF GROUP 1 & 2 LISTED MATERIALS, BELOW IS A LIST OF MATERIALS WHICH MAY HAVE GONE TO DRY RUN LANDFILL THAT ARE KNOWN TO CAUSE FOAM. N-butyl benzene sulfonamide - this compound was identified in a sample of foam taken from a Dry Run Landfill leachate discharge. stearic acid and salts polyethylene glycol ethers ammonium perfluorooctanoate Triton X-lOO (tm) - not specifically listed but contained in supernate dirt and possibly empty containers ucon oil - not on group 1 & 2 list biological foams - from biocake and bacteria growth in ponds \ 0000.:l EID016841 V 89 r 000502 INTEROFFICE MEMORANDUM Date: From: Dept: Tel No: 29-Oct-1998 10:29am DANIEL A. WEBER WEBERDA ENGINEERING POLYMERS 8-863-4415 TO: See Below Subject: FOAM AT DRY RUN LANDFILL JOHN, I WENT DOWN TO DRY RUN LANDFILL TODAY WITH TOM WALDRON. I NOTICED FOAM FORMING DOWN IN THE LOWER POND BELOW THE LEACHATE DISCHARGE PIPE. THERE IS CURRENTLY NO POND DISCHARGE TO DRY RUN CREEK. BARBARA DEEM WILL BE TAKING A SAMPLE TODAY OF THE FOAM AND THE LEACHATE DISCHARGE. PLEASE TAKE A LOOK AT THESE SAMPLES AND LET ME KNOW WHAT YOU CAN DETERMINE IS CAUSING THE FOAM - SAME MATERIALS AS LAST TIME ? CAN THE LEVELS BE QUANTIFIED ? PLEASE REFRIGERATE THE UNUSED PORTION OF THE SAMPLES IN CASE WE WANT TO DO ADDITIONAL ANALYSES LATER. THANKS FOR YOUR HELP, DAN Distribution: TO: JOHN F. DOUGHTY CC: ROBERT L. RITCHEY CC: LYNWOOD K. IRELAND CC: RICHARD A KIRSCHNER, JR CC: Thomas R. Waldron CC: Gary W. Klesel { DOUGHTJF ) { RITCHERL ) ( IRELAND ) ( KIRSCHRA ) ( WALDROTR ) ( KLESELGW ) RAK008791 e o o ; ;C3 i EID030763 I I 90 r INTEROFFICE MEMORANDUM Date: From: Dept: Tel No: 02-NOV-1998 02:36pm GERRY KENNEDY KENNEDGL AG 366-5259 TO: Oscar T Garza TO: Matthew C Koenings TO: Roger J. Zipfel TO: WILLIAM J BROCK ( GARZA20T AT CDCLNM3 ( KOENI2MC AT CDCLNM1 ( ZIPFEL AT Al AT WWPS ( BROCKWJ ) ) ) ) Subject: C-8 MONKEY STUDY PROGRESS REPORT THROUGH FIRST 30 DAYS OF MONKEY STUDY: 1) TOP DOSE 30MG/KG NOT TOLERATED BY 2 OF 6 MONKEYS, DOSING WAS DISCONTINUED AFTER 11 DOSES OF 30 FOR 11 DAYS THEN WAS RESTARTED AT 20 MG/KG. AFTER THIS LOWERING, 1 OF THE 6 (AFFECTED AT 30) WAS SACRIFICED IN DISTRESS AFTER 7 DOSES. A NUMBER OF CLINICAL PARAMETERS WERE ALTERED IN THIS ANIMAL ALONG WITH MARKED HYPOCHOLESTEROLEMIA, MILD HYPERBILIRUBINEMIA, AND MARKED INCRESE IN HEPATIC ENZYMES. THE MOST APPARENT EXPLANATION FOR THE RESPONSE IN THIS ANIMAL IS LIVER DEGENERATION/NECROSIS WITH IMPAIRED LIVER FUNCTION, POSSIBLE BLOOD LOSS, AND INFLAMMATION IN EITHER THE LIVER OR GI TRACT. PATHOLOGY WILL ADD DETAIL TO THIS. 2) 3 AND 10 MG/KG MONKEYS TO DATE LOOK FINE. 4)REMAINING 5 MONKEYS AT 20 MG/KG DOING FINE; CLINICALS DO NOT SEEM TO INDICATE ANY PROBLEMS INCLUDING THE LIVER. NOTE)NO EFFECTS SEEN IN 4 WEEK PILOT AT 20 MG/KG. IT IS OBVIOUS THAT AT LEAST SOME OF THE POPULATION CAN NOT TOLERATE 30/20 MG/KG, 3 AND 10 MG/KG COULD PRODUCE EFFECTS AS THE TIME OF DOSING EXTENDS FROM 1 TO 6 MONTHS. REMEMBER THE CUMULATIVE POTENTIAL HERE IS WHAT WE ARE LOOKING AT/FOR. NEXT REPORT WILL BE A 2 MONTHS UNLESS STRIKING FINDING INTERVENE. GWJ000189 000-WS EID088762 91 ( < INTEROFFICE MEMORANDUM ; Date: 04-Nov-1998 08:10am From: JOHN F. DOUGHTY DOUGHTJF Dept: PPD Tel No: (304) 863-2801 TO: See Below Subject: SAMPLES FROM DRY RUN LANDFILL Paul Rowan and I have spent several man days on the two samples using the FT-IR, the Mass Spec and the x-ray on the electron microscope. The foam sample collected from the Lower Pond on 10-29-98 at 11:39AM was analyzed to identify the cause of the foam. Because the foam was very concentrated and stable, we were able to isolate material by drying at room temperature and a simple methanol wash. The major material in the foam is the sodium salt of an acrylic polymer with a high acid content. As you know these resins have become a major product in recent years. We have never identified this material before so to confirm the identity. I made some in the laboratory using Elvacite 2627 and sodium hydroxide. The scans were a match. Later we did our normal extraction procedure and isolated enough total material to be very roughly 3500 mg/L in concentration. I speculate the high acid acrylic resins which are insoluble as they are made are being converted to the sodium salt in the landfill and become soluble. We know there is sodium in the fly ash and the fly ash is basic. I am not aware of any other major sources of sodium. The resin itself could originate either from the filter cake in Acrylics or from acrylic polymers that accumulate in the biosludge and the bottom of the equalization tank. Mass Spec work done on the extracts also identified smaller amounts of ortho and para toluene sulfonamide and butyl benzene sulfonamide, nylon oligomers, a fluorocarbon that we believe is C8 and a complex mixture that we believe is biological in origin. Lots of microbiological organisms were evident under the microscope. X-ray work also detected sodium, chlorine, magnesium, calcium, potassium, aluminum, silicon, sulfur, iodine and iron. Most of these could be from dirt or the fly ash but the iodine in particular is not expected. The source must be the potassium iodide and cuprous iodide used as stabilizers in Zytel products. One of our Mass Spec scans also seems to indicate an iodine containing compound. The other sample was taken from the discharge of the 4 inch pipe at the Lower Pond at the same time. We did our normal extraction procedure to isolate the organics in the sample. We weighed the recovered material to determine the concentration which was roughly 35 mg/L. We found the major component was nylon oligomers. Also present was some material that we believe is biological in origin as well as ortho and para toluene OOOokw EID030773 sulfonamide and butyl benzene sulfonamide. Di s t r i b u ti on: TO: DANIEL A. WEBER TO: ROBERT L. RITCHEY TO: GEORGE WOYTOWICH WEBERDA ) RITCHERL ) WOYTOWIG ) OOO,'0 *3 EID030774 CC: `PAUL E ROWAN CC: CHARLES J REFSHAUGE CC: PAULA G CRAWLEY 'CC: CYNTHIA H KIRSCHNER CC: RICHARD A KIRSCHNER. JR ( ROWANPE ) ( REFSHACJ ) ( CRAWLEPG ) ( KIRSCHCH ) ( KIRSCHRA ) 0 0 0 , C:: EID030775 000: 92 f INTEROFFICE MEMORANDUM Date: From: 13-Jan-1999 10:26am Thomas R. Waldron Dept: Tel No: PPD-POWER/SERVICE 304- TO: JON F. MOORE CC: LYNWOOD K. IRELAND CC: RICHARD A KIRSCHNER, JR ( MOOREJF ) ( IRELAND ) ( KIRSCHRA ) Subject: Dry Run Landfill While touring the facility yesterday, I witnessed quite a bit of solids in the stream. I talked to Melvin Boso and we took steps to contain as much as we could. This would be to add fresh bales of hay/straw in the stream and the ditch line itself. The pond was running out the outfall and appeared to be in very good shape. Tom JI;M000400 0 0 0 iA E1D030784 I V 93 000 KOENI2MC@CDCLN05.LVS.DUPONT.COM on 0 1 /2 6 /9 9 0 9 :5 2 :0 0 AM To: PINCH2RF@CDCLN05.LVS.DUPONT.COM@SMTP \ cc: ASTOR2M@CDCLN05.LVS.DUPONT.COM@SMTP, BROCKWJ, ZIPFEL. G A R Z A 20T @ C D C L N 05.L V S .DUPONT.COM@ SMTP Subject: Re: C-8 Human Risk Assessment and Analysis Rob, I like your outline for risk assessment. It may not prove to be perfect, but it is an excellent start. I don't see any flaws at this point in time, but I have experienced evolution in these type of processes once they are put in use for the first time. I would suggest that we use at least one other alternative case. We exit the use of C-8 in all product lines that do not "heat treat" the resin in such a way that the C8 levels are dramatically reduced in our product and the C8 used in the process can be aggressively contained/destroyed. Dispersions are my first concern, but there may be a few other types/grades that do not receive adequate heat treatment in this respect. The attempt here is to eliminate situations where we distribute a product with "high" levels of C8 that go outside of our control, but manage the use of C8 where the levels are low and the applications are known to either adequately destroy and or control the ultimate fate. It is an attempt to mitigate the risk where practical and eliminate the risk where we loose control. There may be a few of these intermediate positions to discuss/explore. Thanks. Matt Robert F Pinchot 01/22/99 02:50 PM (Embedded image moved to file: PIC23720.PCX) To: Oscar T Garza/AE/DuPont@DuPont, "Roger J. Zipfel" <ZIPFEL@wwps-al.email.dupont.com>, Matthew C Koenings/DuPontSDuPont, "WILLIAM J BROCK" <BROCKWJ@esvax-al.email.dupont.com> cc: Maurice Astorga/AE/DuPont@DuPont Subject: C-8 Human Risk Assessement and Analysis I've been putting a lot of thought into and talking to a lot of people about how we might use the output of the C-8 monkey study and the subsequent risk assessment. In this thought process I've come to some conclusions as to what I think will be the outcome based on intuition. Hopefully, the data will uphold my intuitive thoughts but we'll have to wait until the data is available. But that isn't the purpose of this note. What I want to do with this note is to get you thinking about the approach that I'm proposing and giving me feedback on how to upgrade the process. Comments are welcome and needed...Here goes. EID087029 Assumptions: Output of the Risk assessment will be a series of results that will be in the form of "for toxic endpoint X, the risk is Y cases/lOOOyr at z exposure." We will have exposure data that will allow calculation the risk of the exposed population in the form of Y' cases/1000 yr. Any C-8 replacements will have at least 10X less risk for toxic endpoints as C-8. Proposed Approach: Select a base case and 4 alternative cases as options for our C-8 strategy. Compare the financials of the five cases ( using NPV as the best indicator) with the risk calculation for these cases. Utilize the following data measures as the comparison points: Absolute change in the risk for human health effects i.e. strategy A reduces risk by X cases/lOOOyr vs. strategy B Relative change in the risk for human health effects i.e. strategy A reduces risk by X% vs. strategy B Relative change in the risk for human health effects on a financially weighted basis i.e. utilize the metric of X cases reduced/1000yr/$MM NPV change vs. the base case Consider the DuPont image vs. the competitor's image based on the various strategies. Would the strategies hold up to public scrutiny? Consider the relative risk of the various C-8 strategies with other risks of industrial occupation and every day life, (just for your information, some risk numbers are listed at the end of this note. I thought that these are enlightening) Consider the premise that the goal for exposures and emissions is ZERO. Consider the relative risk reduction of the C-8 strategies vs. other risk reduction activities in our business.. Options to Consider Base Case: Replace C-8 where technically feasible and market conditions allow. Aggressively minimize exposure/emissions at our manufacturing plants and customer locations Alternate Case 1: Do not replace C-8 in any application. Aggressively minimize exposure/emissions at our manufacturing plants and customer locations Alternate Case 2: Replace all C-8 use Aggressively minimize replacement emissions/exposure 000,'viA EID087030 E xit fin e powder market Alternate Case 2a: Replace all C-8 use Aggressively minimize replacement emissions/exposure Develop Fine powder replacement surfactant Alternate Case 3: Do nothing beyond emission reduction/exposure minimization beyond that in place year end 1999. RFP Thoughts One may think that a decision could be made based solely on the relative risk reduction ( i.e. the metrics above) of the various options. I contend that the most likely outcome of the risk study will be that the metrics won't matter much and the decision on the best strategy will have to be made based on the last four considerations above. The human risk hierarchy (from highest to lowest) is AC3, BC, AC2a, AC2. When you also consider environmental risk the picture gets even fuzzier and can be very site specific. In that case the risk numbers will only tell us if we have a definite problem with our past or current practices. Comments/Upgrades Requested Please comment on the following aspects of this plan. Note that this is very preliminary and will probably go through many iterations prior to getting the data. Metrics to be used Assumptions made Considerations to take into account Cases to be studied Risk Numbers Number of endpoints/1000 Endpoint considered people Event/Criteria 0.001 Cancer California Prop 65 Labeling Law 0.02 Death IMeasured value for motor EID087031 |vehicle accident deaths >---------------- --------------------------------------------------- +- 1 ----------------------------------------------------------------------------------- + - . >------------------------ Criteria used by OSHA to set occupational exposure limits for carcinogens >------------------------------------ ----------------------------------------------------------------------------------- + -- 2.7 ----------------------------------------------------------------------------------- + . >---------------------------------- Measured value for Average occupational risk >------------------------------------------------------------------- + 20 ----------------------------------------------------------------------------------- + . >----------------------------------- Measured value for mine worker death due to occupational accident >----------------------------------- ----------------------------------------------------------------------------------- + . 27 ----------------------------------------------------------------------------------- + . >----------------------------------- Measured value for fire fighter death in the line of duty >----------------------------------- Cancer > > ----------------------- > Death | ------------------------------------------ > -----------------------> Death | -----------------------> ----------------------- > Death f ----------------------- > EID087032 630060013 / T^G o3 ^rTTr^>ir^ rv3'* ~ rry^-or^ nr^f A-yr^ "p ^ v o 'O rj^ ^ ^ r o &j, . . . . . . . ............................................................................................................ ^ .......... ............................................................................ 'Cyfe rv--V/T") ^` c* ^ (r f7 * 'S ^ ^or-7 **ycy>*~r'p nrmf^ i I f v ^ x v y t rc r v W p K? >nO V\znr^eu?C/ ^ 2T>^>rr^ *^ r 7 - rro^o- if'/vyM ^***9 ' " ' 7 I" ^ ^ o ro y ^ r jr o -- ^ / - y r~TrT ^ ^r~r~~~x<i^f v - Kfr^rn - v ^ _ yypnry efpQ^) -vo & ^ T ^ f y ir>y>^-rty ^ t?vva/^ p ^ -fT^^f r-jjTMVTV^ 2 ^ . *? v / 3 s^>pryT^~ry^~&-^*a&^> ^ m -oQ D ^ ^ -* 0 G~O rj r y y ^ ^yjp^zryn <=>ry pyrer m / / -- T* ^ ;>-* / ^ V V e r s ( '1 , - ^,-: 1- ' 'T RJZO16397 009M 3 V 94 ifi>I., KENNEDGL 0 2 /2 4 /9 9 12:43 PM To: BR0CK2WJ, K0ENI2MC, ZIPFEL, GARZAOT cc: Subject: C8 MONKEY STUDY CURRENTLY IN 21ST WEEK OF 26 WEEK STUDY. LAST WEEK A MONEY (1 OF 4) IN THE LOW DOSE (3MG/KG) SHOWED RAPID DETERIORATION AND WAS SACRIFICED. NO OUTSIDE CAUSE FOR THE DEATH WAS DETECTED; TREATMENT RELATIONSHIP IS A STRONG POSSIBILITY. THIS IS BEING FOLLOWED CLOSELY WITH THE CONTRACTOR (COVANCE-MADISON). THE OTHER 3 ANIMALS IN THIS GROUP ARE FINE AS ARE ALL 6 MONKEYS RECEIVING 10 MG/KG. THERE SEEMS TO BE AN AFFECTS 1 ANIMAL, NOT ANOTHER PHENOMENON GOING ON. ANALYSIS OF EFFECTS VS BLOOD C-8 LEVELS WILL BE INSTRUCTIVE-PRELIMINARY FINDINGS SHOW LITTLE DIFFERENCES IN BLOOD LEVELS BETWEEN MONKEYS RECEIVING 3, 10, OR 20 MG/KG. RECALL THAT MORTALITIES HAVE OCCURRED AT THE 30/20 MG/KG GROUP-- THE TOX FOLKS WILL BE GATHERING IN MADISON AT DOSING EBD TO REVIEW DATALOOK AT RECOVERY PARAMETERS. PLEASE CALL WITH ANY QUESTIONS (366-5259), I 'M CONCERNED ABOUT THE LACK OF DOSE RESPONSE AND SERIOUS FINDINGS IN 1 OF 4 LOW DOSE ANIMALS. KJZU12241 QG0.;`- & EID087006 i 000<S0 95 C attle Team K ickoff M eeting March 9, 1999 Sum m ary T h e "C a ttle Team " m et lor the first tim e on M arch 9 at the Univ of Pennsylvania's N e w Bolton C enter. M any thanks to N ew Bolton C enter for hosting the m eeting and providing the conference room. A tte n d e e s Sarah Caspar (EPA Region III), Mike Horne (U S FW S ), M ark Sprenger (EPA O E R R ), Perry Habecker (U of Pa). Bob Poppenga (U of Pa), Peter Moisan (Rolling Laboratory), Lisa Heller (private practice), Greg Sykes (DuPont Pharm a), Paul Ross (DuPont Haskell Lab), Rudy Valentins (DuPont Haskell Lab), and Ralph Stahl (DuPont Corp. Remediation Group). E x p e c ta tio n s T h e C attle T e a m is expected to be an objective, independent body that will advise EPA and DuPont as to the existing condition of Mr. T en n an t's herd and any associated exposures or param eters that might im pact the overall health of the herd. T h e T e a m is expected to be technically sound in its approach and reach a consensus on the herd's condition and recom m endations to mitigate possible future impacts to the herd's health. Team Structure and Logistics > T h e C attle T e a m is a subset of the Dry R un Technical T e a m and is com posed of v e tem aria n s and scientists with expertise in large anim als, especially cattle. T h e T e a m will conduct detailed evaluations of M r. T en n a n t's herd and report back to the Technical T e a m in approxim ately 2 -3 months. A written report that details the findings of the T eam and recom m endations for action will be prepared. Th e T eam m em bers are: H abecker, Heller, Moisan Poppenga, and Sykes. W here needed, Caspar, Horn, Sprenger, Stahl and Valentine will support the Team . ^ Dr. G reg S ykes w as elected to be the coordinator of the C attle T e a m , with Dr. Perry H a b e c k e r acting as the Scientific L eader. G reg will be responsible for handling logistics and other coordinator duties, while Perry will be responsible for leading the herd evaluation, interpretation of the results, and the drafting of the findings and recom m endations. > Dr. Lisa H e lle r will act as the local vetem iaria n and will be involved with all the T e a m 's activities. In addition, because of h e r proximity to Mr. T e n n a n t's farm , she will b e responsible, w here n eed ed , for exam ining any of the herd that . m ight exhibit untoward signs or that is found dead or m oribund. Mr. T en n an t 003 EID042172 9 15:eg !D ::lPC,NT E!W!RCM"E\~-L .-ex: 302-3S2-7641 -GE will be responsible for notifying Dr. H eller when such anim als are noted or found. > S arah C asp ar will act as the interface with Mr. T e n n a n t on the initial site visit and all com m unications. No m em ber of the Cattle T e a m is expected to respond to any questions from Mr. Ten n an t or others regarding findings, conclusions or recom m endations on the herd. S arah will be responsible for fielding any questions from the media and responding on behalf of EPA. Ralph Stahl will be responsible for referring the sam e questions to Ms. Dawn Jackson at DuPont W ashington Works who will respond on behalf of DuPont. > EPA will be responsible for supporting the work of Drs. H ab e c k e r and PofJpenga; D uP ont will be responsible for supporting Drs. H e lle r and Moisan. Analytical work conducted on the herd including blood analysis, etc., adm inistrative support (copying, mailing, etc.) will be billed 5 0 % to EPA , 50 % to DuPont. The T e a m agreed that Mr. Tennant would not be com pensated for cattle subjected to sacrifice since he w as gaining substantial benefit from this effort at little or no cost. > While contacted on March 9 by Sarah Caspar and Mike H om e, Mr. Tennant noted that he currently has 40 head of cattle, 36 of which are expected to calve this spring. T w o cows are currently exhibiting signs of distress and m ay require exam ination by Dr. H eller in the n ear term . H e has a cinder-block barn foundation that can be used as a corral, and a steel head-gate that can be used to hold cattle during examination. > EPA determ ined that they would fund and undertake a study to exam ine w hite-tailed d e e r in W o o d C ounty and other areas this spring. E P A m ay use the Cattle T e a m for consultation on this study, including its design and the interpretation of the results. Action Item s 1. T h e visit to M r. T en n an t's farm is April 8, 1999. Mr. T e n n a n t will be informed of this d ate by S a rah and M ike. T h e T e a m will conduct an evaluation on all 40 head of cattle, obtain a detailed herd history from Mr. Tennant, and may visit the grazing areas including those on or near Dry Run Landfill. 2. Dr. H eller will visit Mr. Ten n an t's farm to ensure that the corral and head gate are safe and appropriate for use in exam ining the herd. S h e will report back to G reg S ykes and Perry H ab e c k e r on this point in the next few w eeks. 3. T h e T e a m will hold a conference call to review the 13 potential problem s and differential diagnostic indicators produced during the M arch 9 meeting. Greg and Perry are responsible for setting this up. EID042173 000 GPS000987 4. Mike. Horne will provide the T e a m with a copy of the W o o d w ard Clyde small m am m al sampling effort. 5. Ralph Stahl will provide the T e a m with the lists of substances and materials deposited in Dry Run Landfill. 6. T h e majority of the t e a m 's correspondence will occur by em ail. Dr. H eller will get an email account so that she can com m unicate electronically with the Team. 7. Hom e phone numbers of the T eam and supporting individuals were distributed so everyone could be notified in the event of an anim al exhibiting morbidity or mortality prior to or after the April 8 site visit. 8. Th e next meeting of the T eam and supporting individuals will be sometime after the April 8 visit to Mr. Tennant's farm. Th e exact date will depend on when analytical results are obtained from blood sam ples, etc. and whether or not the T e a m has drafted its findings and recom m endations. Ralph and S arah will check with G reg and Perry after the April 8 visit and determ ine when this m eeting m ay take place. Phone, fax, em ail information Sarah Caspar Wo: Fax: Home: Email: 215 814-3283 610 873M 237 P **" casoar.sarah@eDamail.epa.aov ^ > 5 -3 1 0 - -JO IT-M -iS l? Perry Habecker Wo: Fax:' Home: Email: 610 444-5800, ext. 2385 610 444-0892 610 384-0452 habecker@ vet.uoenn.edu Mike Horne Wo: Fax: Home: Email: 732 321-6717 732 321-6724 610 923-9701 horne.m ichael@ eoam ail.eoa.gov Peter Moisan Wo: Fax: Home: Email: 919 733-3986 919 363-3523 GPS000988 EID042174 Greg Sykes Wo: Fax: Home: Email: Bob Poppenga Wo: Fax: Home: Email: Mark Sprenger Wo: Fax: Home: Email: Lisa Heller Wo: Fax: Home: Email: Ralph Stahl Wo: Fax: Home: Email: Rudy Valentine Wo: Fax: Home: Email: 302 366-6070 302 366-6065 610 869-8469 area.D .svkes@ d u D o n tD h arm a.com 610 444-580 0. ext. 2217 610 444-4617 610 268-4112 D O D D enaa@ vet.uD enn.edu 732 906-6826 732 321-6724 SDrenaer.mark@ eoamail.eDa.aov 304 684-9495 itldtJL <3JSyJO. Com 302 892-1369 302 892-7641 302 478-9253 ralDh.a.stahl-ir@ usa.duDont.com 302 366-5315 302 rudolDh.valentine@ usa.duoont.com GPS000989 0 0 0 ^ ;-M EID042175 0 0 0 o .,' 5 96 INTEROFFICE MEMORANDUM Date From Dept Tel No lO-May-1999 08:08am EDT DANIEL A. WEBER WEBERDA ENGINEERING POLYMERS 8-863-4415 TO ROBERT L. RITCHEY TO JOHN M MIGLIORE (RITCHERL ) (MIGLIOJM ) CC ALISON A CRANE (CRANEAA ) Subject C8 IN EAST FIELD WELLS BOB/JOHN, FYI, PER P&S, OUR DRINKING WATER SUPPLY WELLS ARE 331 AND 336. 332 IS ALSO OCCASIONALLY USED FOR DRINKING WATER. C8 CONCENTRATIONS MEASURED IN THESE WELLS BY CH2MHILL ARE AS FOLLOWS: WELL JUNE 1993 APRIL 1996 MAY 1997 331 2.9 ug/L 0.52 ug/L 0.55 ug/L 336 0.5 ug/L 0.48 ug/L 0.79 ug/L 332 3.3 ug/L DAN DAW000627 000, EID091591 V 97 / 00 INTERO FFIC E MEMORANDUM Date: From: Dept: Tel No : 21-May-1999 10:11am ANTHONY J. [TONY] PLAYTIS PLAYTIS POLYMERS SHE&EA 34-863-2228 TO: ROBERT L. RITCHEY ( RITCHERL ) CC: DAWN D JACKSON CC: Roger J. Zipfel ( JACKSODD ) ( ZIPFEL ) Subject: C-8 In Drinking Water Communications Bob, I checked my files for any communications that we might have issued on C-8 in drinking water. The only pertinent documents I could find are attached. I don't believe we ever actually released any communication on the subject. I'll stop by your office on Tuesday morning at 8:00 to discuss the Thursday meeting in Wilmington. Roger may or may not be able to make it. Tony 009, EID089418 OOO^'S V. 98 / From: Dawn D Jackson on 0 6 /2 3 /9 9 0 7 :5 5 AM To: Robert L Ritchey/CL/DuPont<s>DuPont, Anthony J Playtis/CL/DuPont@DuPont, Roger J Zipfel/AE/DuPont@DuPont cc: Subject: Outline of communications with GE Plastics regarding C-8 Gentlemen, I have attached a draft of an outline of points to be made in communications with GE Plastics. If there are omissions or errors, please let me know. I will attempt to send you a revision before I leave today at 4 :3 0 . I will be out of town until Monday. Dawn GE Com munication 000;-.. EID082078 iI 6/22/99 Bob Ritchey, Tony Playtis, Roger Zipfel, Dawn Jackson Planning for Communications with GE Plastics regarding C-8 Scenario 1: Results of early June testing of GE drinking well show <3 ppb Recommended communication: John Little calls Dallas Silverthome to report test results and speak from talking points such as those below; John also offers to send MSDS on C-8 and Community Exposure Guideline (CEG) information. Outline of talking points (in brief form; to be developed further): Why ? - Why we did the sampling (RFI; C-8 in groundwater; need to know if it crosses site boundary; model says no; WW wanted to sample to be sure.) What ? -- What is C-8? (Explain what it is: detergent-like material; surfactant; used in manufacture of Teflon fluoropolymer resins) Where? - Where is it coming from? (old supernate ponds - anaerobic digestion ponds constructed in mid-1950's (one) and mid-1970's (two); decommissioned in 1988.) % Re: concentration -- represents dose lower than TLV would allow; it's ___ of the TLV; below the CEG. Toxicity piece: Refer to MSDS; offer to provide copy of MSDS; at these levels, no acute health effects ever observed; however, it does persist in the bloodstream; in animal testing at high doses, liver is the target organ. Path forward: Emphasize that concentration in GE well is comparable to concentration in WAVdrinking water; WW will continue to monitor; if there is an increase at WAV, we will contact GE; Site EA will prepare standby statement and Qs/As, in the event of media inquiries. Scenario 2: Test results - 3-25 ppb Recommended communication: John Little calls Dallas Silverthome to request a meeting (1/2-day?) with Silverthome and his Playtis, Ritchey counterparts; to attend from WAVLittle, Ritchey, Playtis, Zipfel. Outline of talking points (to be more detailed than for first scenario): Why? - Same info as above, + some detail about its being the only chemical in the RFI above EPA screening levels; assurance that WW will work with EPA to define levels acceptable to EPA and methods/controls to reach those levels. What? - Same info as above + a review of the C-8 molecule itself; possible other applications outside DuPont Where? - Same info as above + hydrogeology, including river recharge, plume in groundwater EID082079  Re: concentration: Provide MSDS; discuss toxicologic information in detail, such as major exposure routes (inhalation, skin absorption) vs. ingestion; discuss CEG and intent to reduce or eliminate human health exposure route. Toxicity piece: Talk through elements of MSDS, vs. just providing a copy; provide occupational health background - animal studies details, human health-related information, U. of Minnesota paper (flawed study); review what we've done with our own employees since 1981, including employee communications; share Pace Team strategies? Path forward: DuPont will take necessary action to protect human health and meet regulatory requirements; Site EA will prepare standby statement and Qs/As, in the event o f media inquiries. Anticipated Qs from GE: 1. What kind of engineering controls are effective to handle elevated levels of C-8? 2. What exposure routes are there besides drinking water? 3. Do the levels in GE drinking water indicate a probability of measurable levels in employees' blood? 4. ... txV rAj '-Jvt' E1D082080 99 (gJPDN) Gu?Ont ?0 Go*121/ ?jrkcrsburg. WV 26192 12l 1 CERTIFIED MAIL RETURN RECEIPT REQUESTED June 24, 1999 Mr. Martin Kotsch Project Manager U.S. EPA, Region III 1650 Arch Street Philadelphia, PA 19103-2029 RE: Permit WVD045875291 * Dear Mr. Kotsch: Please find enclosed the RCRA Facility Investigation (RFI) Report of Findings for your review and comment. If you have any questions or comments, please contact me at (304) 863-4271. Very truly yours, Attachment CC: Mr. Mark Priddy Office of Waste Management WV-DEP 1356 Hansford Street Charleston, WV 25301 Mr. B. F. Smith, Chief* Office of Waste Management Charleston, WV 25301 1356 Hansford Street * cover letter only R. L. Ritchey Sr. Environmental Control Consultant Washington Works Ms. Barbara Taylor, Chief* Office of Water Resources WV-DEP 1201 Greenbrier Street Charleston, WV 25311 &D073527 AL-UUJJ'tO TABLE 6.8 HEALTH-BASED SCREENING FOR PRODUCTION WELL WATER Constituent Arsenic -- JJnits mg/L Potable Water Well (1) 0.01 Process Water Wells (2) Screening Level Typ* 0.0068 0.05 MCL Max > SL? No Barium mg/L 0.07 0.16 2 MCL No Cadmium mg/L ND (<0.01 ) NO (<0.01 ) 0.005 MCL No Lead Nickel FC-143 mg/L mg/L ug/L ND (<0.003) ND (<0.05) 1.9 0.0022 NO (<0.05) 16.2 0.015 0.14 3 MCL No MCL No PSL Potable - No Process - Yes (3) T etrachloroethy lene ug/L ND (<5) 5 5 MCL No Trichloroethylene ug/L ND (<5) 22 5 MCL Potable - No Process - Yes (4) Methyene Chloride ug/L ND (<5) - 5 MCL No Freon 113 ug/L ND (<10) 270 LfiSfimL MCL = Maximum Contaminant Level for drinking water. PSL = Preliminary Screening Level; see Table 6.6 and Section 6.4.2. RBC - Risk-based concentration for tap water (USEPA Region III, 1999) - - Not analyzed. 59000 RBC No Notes: (1) Well 336 (AM07-PW01) (2) Process Water Wells: K16-PW01 K16-PW01 L17-PW01 L17-PW01 V05-PW01 V05-PW01 L04-PW01 L04-PW01 (3) Trichloroethylene exceeded the MCL in production well V05-PW 01. (4) FC-143 exceeded the preliminary SL in production wells K16-PW01, V05-PW01. and L04-PW01. GLK002756 5 < ra b ic i \ i - '*> io :< \ m 000 E ID 109784 Pauc I <-M 0 0 Or ^3foZ 100 William R Berti 0 8 /1 1 /9 9 02:11 PM To: Roger J Zipfel/AE/DuPont@DuPont cc: Guat-Lian C Kreamer/AE/DuPont@DuPont Subject: Estimated C-8 in river Hi Roger, Attached is the Excel file that I put together on Ohio River flows and estimated C-8 concentrations that we talked about earlier. Estimated C -8 concentrations in Ohi Best regards, Bill DuPont Central Research & Development Voice: (302) 366-6762 Fax: (302) 366-6602 Pager: (888) 548-9264 Internet e-mail: William.R.Berti@usa.dupont.com 0 0 EID082037 Ohio River monthly average flows at Pittsburgh, PA River flow data from <ftp://www.lrd-wc.usace.army.mil/Monthly_htm/> Assume: 1 ft3/sec = 0.0283m3/sec; 1 m3 = 1*10A6 cm3; 1 cm3 = 1 mL Long Estimated Measured term of normal flow, normal, flow, r-Yr ft3/sec % ft3/sec Jun-98 28,480 120 23733 Jul-98 17,192 124 13865 Aug-98 9,111 76 11988 Sep-98 7,312 72 10156 Oct-98 7,966 66 12070 Nov-98 6,144 28 21943 Dec-98 9,440 25 37760 Jan-99 53,865 124 43440 Feb-99 46,314 94 49270 Mar-99 52,898 77 68699 Apr-99 60,741 105 57849 May-99 23,053 61 37792 Estimated normal flow, m3/sec Estimated normal Estimated flow, normal m3/mo flow, L/mo 6.72E+02 1.74E+09 1.74E+12 3.92E+02 1.05E+09 1.05E+12 3.39E+02 9.09E+08 9.09E+11 2.87E+02 7.45E+08 7.45E+11 3.42E+02 9.15E+08 9.15E+11 6.21 E+02 1.61E+09 1.61E+12 1.07E+03 2.86E+09 2.86E+12 1.23E+03 3.29E+09 3.29E+12 1.39E+03 3.37E+09 3.37E+12 1.94E+03 5.21 E+09 5.21 E+12 1.64E+03 4.24E+09 4.24E+12 1.07E+03 2.86E+09 2.86E+12 Total flow Jun-98 to May-99, L 2.88E+13 C8 discharge to Ohio River in 1996, lbs 40600 r-i E1D082038 11-Aug-99 C8 discharge to Ohio River in 1996, kg Estimated C8 concentration in Ohio River, kg/L Estimated C8 concentration in Ohio River, mg/L Estimated C8 concentration in Ohio River, ug/L 18416 6.39E-10 6.39E-04 0.639 0 0 1* EID082039 Ohio River monthly average flows at Belleville Dam, WV River flow data from < http://waterdata.usgs.gov/nwis-w/WV/data.components/hist.cgi?statnum=03159530> Based on USGS mean daily flows from 10/1/1974 to 9/30/1985 Estimated C8 Estimated Estimated Estimated Measured normal normal normal Estimated C8 C8 concentrt discharge discharge ion in to Ohio to Ohio Ohio flow, flow, flow, flow, normal River in River in River, Mo ft3/sec ft3/sec m3/sec m3/mo flow, L/mo 1996, lbs 1 9 9 6 ,kg kg/L Jan 64000.79 64001 1.81E+03 4.69E+09 4.69E+12 Feb 88908.68 88909 2.52E+03 6.74E+09 6.74E+12 Mar 111235.8 111236 3.15E+03 8.43E+09 8.43E+12 Apr 94016.67 94017 2.66E+03 6.90E+09 6.90E+12 May 67107.33 67107 1.90E+03 5.09E+09 5.09E+12 Jun 47378.91 47379 1.34E+03 3.48E+09 3.48E+12 Jul 30989.47 30989 8.77E+02 2.35E+09 2.35E+12 Aug 30501.91 30502 8.63E+02 2.31 E+09 2.31 E+12 Sep 25339.3 25339 7.17E+02 1.73E+09 1.73E+12 Oct 33029.62 33030 9.35E+02 2.50E+09 2.50E+12 Nov 42329.7 42330 1.20E+03 3.11 E+09 3.11E+12 Dec 78985.92 78986 2.24E+03 5.99E+09 5.99E+12 Total 7.14E+05 7.14E+05 2.02E+04 5.33E+10 5.33E+13 40600 18416 3.45E-10 0 0 0 >i EID082040 Estimated C8 concentrat Estimated C8 ion in Ohio concentration River, in Ohio River, mg/L ug/L 3.45E-04 0 .3 4 5 000541- EID082041 Ohio River monthly average flows at Huntington, W V River flow data from < ftp://www.lrd-wc.usace.army.mil/Monthly_htm/> Assume: 1 ft3/sec = 0.0283m3/sec; 1 m3 = 1*10*6 cm3; 1 cm3 = 1 mL Mo-Yr Measured flow, ft3/sec Long term of normal, % Estimated normal flow, ft3/sec Estimated normal flow, m3/sec Estimated normal Estimated flow, normal m3/mo flow, L/mo Jun-98 97,300 172 56570 1.60E+03 4.15E+09 4.15E+12 Jul-98 68,742 190 36180 1.02E+03 2.74E+09 2.74E+12 Aug-98 28,484 94 30302 8.58E+02 2.30E+09 2.30E+12 Sep-98 17,733 78 22735 6.43E+02 1.67E+09 1.67E+12 Oct-98 19,710 80 24638 6.97E+02 1.87E+09 1.87E+12 Nov-98 18,233 41 44471 1.26E+03 3.26E+09 3.26E+12 Dec-98 28,710 36 79750 2.26E+03 6.04E+09 6.04E+12 Jan-99 141,810 126 112548 3.19E+03 8.53E+09 8.53E+12 Feb-99 108,500 84 129167 3.66E+03 8.84E+09 8.84E+12 Mar-99 142,350 86 165523 4.68E+03 1.25E+10 1.25E+13 Apr-99 112200 82 136829 3.87E+03 1.00E+10 1.00E+13 May-99 57484 62 92716 2.62E+03 7.03E+09 7.03E+12 Total flow Jun-98 to May-99, L 6.90E+13 C8 discharge to Ohio River in 1996, lbs 40600 OOOo EID082042 C8 discharge Estimated C8 Estimated C8 to Ohio River concentration in concentration in in 1996, kg Ohio River, kg/L Ohio River, mg/L Estimated C8 concentration in Ohio River, ug/L 18416 2.67E-10 2.67E-04 0.267 OO^.-Iis Ei E>082043 Ohio River monthly average flows at Cincinnati, OH River flow data from <ftp://www.lrd-wc.usace.army.mil/Monthly_htm/> Assume: 1 ft3/sec = 0.0283m3/sec; 1 m3 = 1*10*6 cm3; 1 cm3 = 1 mL Mo-Yr Estimated Estimated Estimated Measured Long-term normal normal normal Estimated flow, of normal, flow, flow, flow, normal ft3/sec % ft3/sec m3/sec m3/mo flow, l/m o Jun-98 131,400 175 75086 2.12E+03 5.51 E+09 5.51E+12 Jul-98 94,452 211 44764 1.27E+03 3.39E+09 3.39E+12 Aug-98 28,387 80 35484 1.00E+03 2.69E+09 2.69E+12 Sep-98 21,200 74 28649 8.11E+02 2.10E+09 2.10E+12 Oct-98 21,065 77 27357 7.74E+02 2.07E+09 2.07E+12 Nov-98 21,400 40 53500 1.51 E+03 3.92E+09 3.92E+12 Dec-98 34,548 35 98709 2.79E+03 7.48E+09 7.48E+12 Jan-99 178,190 131 136023 3.85E+03 1.03E+10 1.03E+13 Feb-99 134,860 81 166494 4.71 E+03 1.14E+10 1.14E+13 Mar-99 180,260 85 212071 6.00E+03 1.61E+10 1.61E+13 Apr-99 118000 66 178788 5.06E+03 1.31E+10 1.31E+13 May-99 60226 49 122910 3.48E+03 9.32E+09 9.32E+12 Total 1.02E+06 1.18E+06 3.34E+04 8.74E+10 8.74E+13 C8 discharge to Ohio River in 1996, lbs 40600 000, EID082044 Estimated C8 C8 discharge concentration to Ohio River in Ohio River, in 1996, kg kg/L Estimated C8 concentration in Ohio River, mg/L Estimated C8 concentration in Ohio River, ug/L 18416 2.11E-10 2.11E-04 0.211 OCo; ' \ EID082045 Ohio River monthly average flows at Pittsburgh, PA, Huntington, W V , and Cincinnati, OH River flow data from <ftp://www.lrd-wc.usace.army.mil/Monthly_htm/> Mo 1 Jan 2 Feb 3 Mar 4 Apr 5 May 6 Jun 7 Jul 8 Aug 9 Sep 10 Oct 11 Nov 12 Dec Pittsburgh, PA 3.29E+12 3.37E+12 5.21 E+12 4.24E+12 2.86E+12 1.74E+12 1.05E+12 9.09E+11 7.45E+11 9.15E+11 1.61 E+12 2.86E+12 Belleville Huntington, Cincinnati, Dam, W V WV OH 4.69E+12 8.53E+12 1.03E+13 6.74E+12 8.84E+12 1.14E+13 8.43E+12 1.25E+13 1.61E+13 6.90E+12 1.00E+13 1.31E+13 5.09E+12 7.03E+12 9.32E+12 3.48E+12 4.15E+12 5.51E+12 2.35E+12 2.74E+12 3.39E+12 2.31 E+12 2.30E+12 2.69E+12 1.73E+12 1.67E+12 2.10E+12 2.50E+12 1.87E+12 2.07E+12 3.11E+12 3.26E+12 3.92E+12 5.99E+12 6.04E+12 7.48E+12 O E o 75 E>_ oc T3 O CS E 3 (A Ili Jan Feb Mar Apr May Jun Jul Aug 000. EID082046 burgh, PA eville Dam, W V tington, W V innati, OH Sep Oct Nov Dec EID082047  T T ftC H triEAjT / Oi i s T S C P i Cfii. b c U ,3 0 / 0 0 0 0 0 /* / AJo S a n i i i t c d l I/ r s i o n U J a S p r o w : <fa>J . 102 00 Q M 9 OuPont Washington Wortes P. 0. Box 1217 Parieerstw. WV2B102-1217 August 31, 1999 Mr. D allas Silverthom e, Plant M anager GE Plastics P. O. B ox 68 W ashington, W V 26181 D ear Dallas: A s w e discussed by telephone on A ugust 30, I have enclosed the lab report on the water sample taken at your facility on June 3, 1999, for analysis o f levels o f ammonium perfluorooctanoate. I have also enclosed the DuPont M aterial Safety Data Sheet. Both docum ents refer to the material as FC -143, but it is com m only known as C-8. I'd like to reiterate that the 0.552 ug/1 concentration detected in your site's sam ple represents a dose lower than the TLV w ould allow . In fact, it's approximately 1% o f the TLV and is in the same range as what w e see in our site's drinking water w ells. N o human health effects have been observed at concentrations many tim es this level. I hope that this information is useful to you. I f you have any (further) questions, you can reach me at 863-4305. Sincerely, E n clo su res Plant Manager E. I. eu d* Mefticyf and Csmoany COPY EID089407 fibfam d an fectort Paar '# ' Analysis Rep Lancaster Laboratories W h e r e q u a lit y is a science. LLI Sample No. WW 3167122 Collected: 6/3/99 by GW Submitted: 6/ 5/99 Reported: 6/16/99 Discard; 7/17/99 Account No: 07032 CRG-E.I.OuPont da Nemours 4 Co P.0. Box 47 Old HlcKory TN 37138-0047 P.0. LBIO-62248-1 Rei. LE458 WWK-G-R-2 Water Sample ANNUAL Cfl SAMPLING 1999 CAT NO. ANALYSIS NAME AS RECEIVEO RESULTS moo DETECTION LIMIT UNITS 2324 FC-143 1n Water 0.552 0.029 ug/1 The stated QC limits are advisory only until sufficient data points can be obtained to calculate statistical limits. SAMPLE SAMPLE MOL UNITS 2324 FC-143 in Water 0.029 ug/1 BLANK 0.032 J ug/1 QUALITY CONTROL REPORT DUP RPD MS MSD 96 -38 MS LCS LCS LCS LIMITS RPO LCS OUP RPO -LOW HIGH 36 21 50 150 2324 FC-143 1n Water SURROGATE SUMMARY TRIAL ID SURROGATE PFNA 11H-PFUA PFDOA RECOVERY X 35 0 5 SURROGATE LIMITS LOW HIGH 9 81 13 88 SO 150 CAT NO 2324 2325 ANALYSIS NAME FC-143 1n Water Pesticide Alternate Water Extr LABORATORY CHRONICLE METHOO FC-143 by GC/ECO 10/91 FC-143 10/91 TRIAL 1 1 ANALYSIS IO 0ATE ANO TIME 06/10/99 0328 06/08/990730 ANALYST Carolyn J. Koch Deborah M. Zlmmarman EID089408 RECEIVED 1 COPY TO Woodward Clyde Diamonds ATTN: Ms. Sara Seastroa JUN 18 1999 Questions? Contact your Client Services Representative Nancy Bornholm at (717) 656-2300 07:17:34 0 0001 1 135803 668971 0.00 00022500 ASR00Q CEDLoad Date t J f y f t t Accuracy Check bv ^ Holding Tima Chtck Tim* I 3 Pat A h l Date iJ M LM UtiR Respectfully Submitted .HV.rVK-t H /'i N.-V INkr Jenifer E. Hess. B.S. Group Leader Pesticides/PCSs IXJ Bo* 14/S LilKiiMi-l.I`Al/MSHi\ Inutter laborattxn-t h a tubiidiary ol Thenno terraTeth h u . * Tlinnm Uettran Company. / ! / i-*n. Mia- L i. M/SM1 iSSl Ve itw iw \ide (or --xpUnation ol jymolt atbrevUuunv DuPont Material Safety Data Sheet Page i FC-143 FLUORAD BRAND FLUOROCHEMICAL SURFACTANT (3M) V0003045 Revised 15-JAN-1997 Printed 5-AUG-1999 CHEMICAL PRODUCT/COMPANY IDENTIFICATION Tradenames and Synonyms FLUORAD FC-143 Company Identification MANUFACTURER/DISTRIBUTOR Revised 23-AUG-1996 3M General Offices 3M Center * St. Paul MN USA 55144-1000 PHONE NUMBERS Product Information : 612-733-1110 Transport Emergency : 800-424-9300 * V COMPOSITION/INFORMATION ON INGREDIENTS Components Material Ammonium Perfluorooctanoate Ammonium perfluoroheptanoate Ammonium perfluoropentanoate Ammonium perfluorohexanoate CAS Number 3825-26-1 6130-43-4 68259-11-0 21615-47-4 % 93-97 1-3 1-3 0.1-1 EXPOSURE CONTROLS/PERSONAL PROTECTION Exposure Guidelines Applicable Exposure Limits Ammonium Perfluorooctanoate PEL (OSHA) : None Established TLV (ACGIH) : 0.01 mg/m3, 8 Hr. TWA, Skin, A3 AEL * (DuPont) : 0.01 mg/m3, 8 Hr. TWA, Skin * AEL is DuPont's Acceptable Exposure Limit. Where governmentally imposed occupational exposure limits which are lower than the AEL are in effect, such limits shall take precedence. EID089409 V0003045 DuPont Material Safety Data Sheet Page 2 OTHER INFORMATION Additional Information ************************************************************ * Information in the above Sections are provided by DuPont* * and should be used as the primary source for these * * categories. * *********************************************************** Vendor MSDS Text 3M MATERIAL SAFETY DATA SHEET 3M General Offices 3M Center St. Paul, MN 55144-1000 612-733-1110 Copyright, 1996, Minnesota Mining and Manufacturing Company All rights reserved. Copying and/or downloading of this information for the purpose of properly utilizing 3M products is allowed provided that: 1) the information is copied in full with no changes unless prior agreement is obtained from 3M, and 2) Neither the copy nor the original is resold or otherwise distributed with the intention of earning profit thereon. Abbreviations: N/D - Not Determined N/A - Not Applicable DIVISION: SPECIALTY CHEMICALS DIVISION TRADE NAME: FC-143 FLUORAD Brand Fluorochemical Surfactant 3M ID NUMBER/U.P .C .: ZF-0002-0378-4 98-0211-0008-0 00-51135-09138-8 98-0211-0891-9 00-51135-09365-8 98-0211-5489-7 00-51135 -02941-1 98-0211-6581-0 00-51135-10405-7 98-0211-7394-7 00-51135 -10762-1 1. INGREDIENT C.A.S. NO. PERCENT AMMONIUM PERFLUOROOCTANOATE AMMONIUM PERFLUOROHEPTANOATE AMMONIUM PERFLUOROPENTANOATE AMMONIUM PERFLUOROHEXANOATE 3825-26-1 6130-43-4 68259-11-0 21615-47-4 93 - 97 1-3 1-3 0.1 - 1 PHYSICAL DATA Boiling Point: 7apor Pressure: 7apor Density: N/A N/A N/A 000 > EID089410 V0003045 DuPont Material Safety Data Sheet Page 3 (Continued) Evaporation Rate: Solubility in Water: Sp. Gravity: Percent Volatile: pH: Viscosity: Melting Point: Appearance and Odor: N/A Apprec. 0.4 - 0.5 Water=l (Bulk) N/A ca. 5 (0.5% Aqueous) N/D N/A Light colored powder; slight odor 3. FIRE AND EXPLOSION HAZARD DATA Flash Point: Non-flammable Flammable Limits -LEL: N/A Flammable Limits -UEL: N/A Autoignition Temperature: N/A Extinguishing Media: Water, carbon dioxide, dry chemical, foam Special Fire Fighting Procedures: Wear full protective clothing, including helmet, self-contained, positive pressure or pressure demand breathing apparatus, bunker coat and pants, bands around arms, waist and legs, face mask, and protective covering for exposed areas of the head. Unusual Fire and Explosion Hazards: 3ee Hazardous Decomposition section for products of combustion. 4. REACTIVITY DATA Stability: Stable Incompatibility - Materials to Avoid: Not applicable Hazardous Polymerization: Will not occur Hazardous Decomposition Products: larbon monoxide and carbon dioxide, oxides of nitrogen, hydrogen fluoride, ammonia. 5. ENVIRONMENTAL INFORMATION Spill Response: EID089411 Observe precautions from other sections. Collect spilled material. Use wet sweeping compound or water to avoid dusting. Clean up residue. Place in a closed container. Recommended Disposal: Incinerate in an industrial or commerical facility in the presence of a combustible material. Combustion products will include HF. Disposal V0003045 DuPont Material Safety Data Sheet (Continued) page alternative: Dispose of waste product in a facility permitted to accept chemical waste. Environmental Data: Chemical Oxygen Demand (COD) = Nil(.00070 g/g); 20-day Biochemical Oxygen Demand (BOD20) = Nil; Theoretical Oxygen Demand (ThOD) = 0 . 3 2 g/g; Fathead Minnow (Pimephales promelas) 96-hr LC50 = 740 mg/L; Water flea (Daphnia magna) 48-hr EC50 = 460 mg/L; Green Algae (Selenastrum capricornatum) 14-day EC50 (cell dry weight) = 73 mg/L; Green Algae (Selenastrum capricornutum) 14-day EC50 (cell count) = 43 mg/L Bioconcentration factor (BCF) for ammonium perfluorooctanoate (PFO = 1 . 8 ) Regulatory Information: Volatile Organic Compounds: N/A VOC Less H20 & Exempt Solvents: N/A Since regulations vary, consult applicable regulations or authorities before disposal. U.S. EPA Hazardous Waste Number = None (Not U.S. EPA Hazardous). The components of this product are in compliance with the chemical registration requirements of TSCA, EINECS, CDSL, AICS, MITI and KTCCL. EPCRA Hazard Class: Fire Hazard: No Chronic: Yes Pressure: No Reactivity: No Acute: Yes 6. SUGGESTED FIRST AID Eye Contact: t Immediately flush eyes with large amounts of water for at least 15 minutes. immediate medical attention. Ge Skin Contact: Flush skin with large amounts of water. attention. Inhalation: If irritation persists, get medical EID089412 If signs/symptoms occur, remove person to fresh air. If signs/symptoms continue, call a physician. If Swallowed: Do not induce vomiting. Drink two glasses of water. Call a physician. 7. PRECAUTIONARY INFORMATION ooo;>c5 V0003045 DuPont Material Safety Data Sheet Page 5 (Continued) Eye Protection: Avoid eye contact. Wear vented goggles. Skin Protection: Avoid skin contact. Wear appropriate gloves when handling this material. A pair of gloves made from the following material(s) are recommended: Butyl rubber. Use one or more of the followig personal protection items as necessari to prevent skin contact: head covering, coveralls. Protective garments (other than gloves) should be made of either of the following materials: Polyethylene/polyvinylidene chloride (Saranex). Ventilation Protection: Use with appropriate local exhaust ventilation. Provide sufficient ventilation to maintain emissions below recommended exposure limits. If exhaust ventilatio is not adequate, use appropriate respiratory protection. Respiratory Protection: Avoid breathing of airborne material. Select one of the following NIOSH approved respirators based on airborne concentration of contaminants and in accordance with OSHA regulations: full-face high-efficiency filter respirator, full-face supplied air respirator. Prevention of Accidental Ingestion: Do not eat, drink or smoke when using this product. Wash exposed areas thoroughly with soap and water. Wash hands after handling and before eating. Recommended Storage: Do not store containers on their sides. Store at room temperature. Keep container dry. Keep container closed when not in use. PREVENT MOISTURE CONTAMINATION TO KEEP POWDER FREE FLOWING.** EID089413 Fire and Explosion Avoidance: Keep container tightly closed. No smoking while handling this material. Other Precautionary Information: HMIS HAZARD RATINGS: HEALTH: 3 FLAMMABILITY: 0 REACTIVITY: 0 PERSONAL PROTECTION: X (See precautions, section 7.) EXPOSURE LIMITS Ingredients Ammonium Perfluorooctanoate Ammonium Perfluoroheptanoate Ammonium Perfluoropentanoate Value 0.01 0.1 0.1 Unit mg/m3 mg/m3 mg/m3 Type TWA TWA TWA Auth ACGIH 3M 3M Skin* Y Y Y V0003045 DuPont Material Safety Data Sheet Page 6 (Continued) Ammonium Perfluorohexanoate 0.1 mg/m3 TWA 3M Y * Skin Notation: Listed substances indicated with "Y" under SKIN refer to the potential contribution to the overall exposure by the cutaneous route includinc mucous membrane and eye, either by airborne or, more particularly, by direct contact with the substance. Vehicles can alter skin absorption. Source of Exposure Limit Data: - ACGIH: American Conference of Governmental Industrial Hygienists - AIHA: American Industrial Hygiene Assoc. Workplace Environmental Exposure Level - 3M: 3M Medical Department Guideline 3. HEALTH HAZARD DATA EYE CONTACT: Moderate eye irritation: signs/symptoms can include redness, swelling, pain, rearing, and hazy vision. Airborne product may cause eye injury consisting of corneal opacity. SKIN CONTACT: Product is not expected to be irritating to the skin. Mild skin irritation (after prolonged or repeated contact): signs/symptoms can include redness, swelling, and itching. fay be absorbed through the skin and persist in the body for an extended time. INHALATION: Illness requiring medical attention may result from a single exposure by inhalation to moderate quantities of this material. May be absorbed by inhalation and persist in the body for an extended time. Repeated inhalation of airborne product above the exposure guideline can result in elevated organofluoride levels in the blood. Single overexposure, above recommended guidelines, may cause: Irritation (upper respiratory): signs/symptoms can include soreness of the nose and throat, coughing and sneezing. Prolonged or repeated overexposure, above recommended guidelines, may cause: Liver Effects: signs/symptoms can include yellow skin (jaundice) and tenderness of upper abdomen. IF SWALLOWED: EID089414 Ingestion is not a likely route of exposure to this product. VO003045 DuPont Material Safety Data Sheet page y (Continued) Illness may result from a single swallowing of a moderate quantity of this material. CANCER: A mixture of ammonium perfluorooctahoate, ammonium perfluoroheptanoate ammonium perfluoropentanoate and ammonium perfluorohexanoate, that was 93 to 9 AMMONIUM PERFLUOROOCTANOATE (3825-26-1) was fed to albino rats for 2 years, no compound induced carcinogenicity was found in the study. There were statistically significant compound realted benign testicular tumors. In a second two-year study there were statisticallly significant compound related benign tumors in the liver, pancreas, and testis when compared to ad libitum ai pair-fed controls. Based on the current knowledge, these findings have no hum health implications. (1983 and 1993 studies conducted jointly by 3M and DuPont). s MUTAGENICITY: Not mutagenic in invitro mutagenicity assays. Did not cause cel] transformation in a mammalian cell transformation assay. REPRODUCTIVE/DEVELOPMENTAL TOXINS: Not teratogenic in rabbits by oral administration. Not teratogenic to rats by gavage or inhalation exposures. OTHER HEALTH HAZARD INFORMATION: A 3M Product Toxicity Summary Sheet is available. SECTION CHANGE DATES HEADING Section changed since May 20, 1996 issue MSDS: FC-143 FLUORAD Brand Fluorchemical Surfactant August 23, 1996 The information in this Material Safety Data Sheet (MSDS) is believed to be correct as of the date issued. 3M MAKES NO WARRANTIES, EXPRESSED OR IMPLIED, INCLUDING, BUT NOT LIMITED TO, ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE OR COURSE OF PERFORMANCE OR USAGE OF TRADE. 'Jser is responsible for determining whether the 3M product is fit for a particular purpose and suitable for user's method of use or application. Given che variety of factors that can affect the use and application of a 3M product, some of which are uniquely within the user's knowledge and control, it is essential that the user evaluate the 3M product to determine whether it is fit for a particular purpose and suitable for user's method of use or application. 3M provides information in electronic form as a service to its customers. Due co the remote possibility that electronic transfer may have resulted in errors, omissions or alterations in this information, 3M makes no representations as to its completeness or accuracy. In addition, information obtained from a databasi nay not be as current as the information in the MSDS available directly from 3M The data in this Material Safety Data Sheet relates only to the specific material designated herein and does not relate to use in combination with any other material or in any process. End of MSDS EID089415 01 3M Environmental Lab A / A* n - c? Kris Hanaen 3M Environment! Lab Fluorine Analytical Chemistry Team 2-3E-09 September 2,1999 Paul Lieder 3M Toxicology Services 220-2E-02 Dear Paul Lieder Here are preliminary restilts for POAA levels in sera and liver for TOX026 (POAA Monkey Study). As I said in my original email message, please do not make these results public. We provide them only to help you make better decisions about the status of current and future projects. I understand you need to use the data to ascertain trends, but please do not publish or release specific values. As stated in an earlier communication, this data has all been QCd, but not QA'd. These are interim results that L. /e been through peer review by the scientific staff in the Environmental Lab. By definition, interim results may change before they are entered in final reports if errors are discovered as the data move through the review process, including pending review by the Environmental Lab QAU. I trust you understand the potential risks involved with interim data Sincerely, /V- /4i-- Kris Hansen 3M Environmental Lab cc Dale bacon 2-3E-09 John Butenhoff 220-2E-02 GWJ000050 Fluorine A n alytical Chem istry Team VyWVVW.WM-.-AW.VW EID088631 009<> K Covnncctf 6329-231 Study: Product Number(Tcst Substance): Matrix: Mclhod/Revision: Analytical Equipment System Number: Instrument Soilware/Version: Dale of Exlraclion/Analyst: Date of Analysis/Analyst: Dale of Data Reduction/Analyst: Sample Data 6 Month Capsule T T-6889.2 (POAA) Monkey Liver FACT-M-l.O A FA Soup020l99 MassLynx 3.2 7/13/99 SF.E 07/21/99 DRB 07/22/99 l)RB MONKEY LIVER Week 20 and 40 Croii| Sample W Dose Method Blk U20Blk-l 1120 Blk-2 Matrix Blk Rabbit liver Btk-1 Rabbit Liver Blk-2 QC - 230 ppb I03718M-MS-U I037I8M-MSD-I2 C roup 1, WHO I037I8M 0.0 mg/kg/day I05720M C roup 2, IVHO 10572IM C roup 3, WHO tf '7 ;2 M 10 mg/kg/day I057I6M POAA Perfliiorooctanoate Limit ofQuant ilalion (LOQ) - 30 ppb lim it of Detection (LOD) 13 ppb POAA Cute. Cone, " i'e 0.0 0.0 2.8 0.0 297 278 12.3 11.8 17874 286 84.4 Amount of POAA ug/ <LOD <LOD CLOD CLOD 99% 92% 0.0123 0.0113 179 0.286 0.0844 Date Enlercd/Dy: Dale Verified/ ny: 07/26/99 LAC 08/03/99 GML EID088632 ISOOOOfAYO EID088633 O O <D `J4 ZSOOOOfAYO FACT-M-2.0 Covaticci/ 6329-231 Study Product Numbcr(Tcsl Substance): Matrix: Mcthod/Rcvision: Analytical Equipment System Number: Instrument Soflwarc/Version: Dale of Extraction/Analyst: Dale of Analysis/Analyst: Date of Data Reduction/Analyst: Sample Data 6 Month Capsule T T-6889.2 (POAA) Monkey Uver FACT-M-I.O & FA Soup020l99 Missl.ynx 3.2 06/21/99 SAII 06/23/99.07/28/99 06/25/99.07/29/99 MONKEY LIVER Week 27 Croup Sample ff Dose Method nik 1120 nik-l 1120 Blk-2 Matrix Blk Rabbit Liver Illk-I Rabbit IJvcr Ulk-2 Q C- 250 ppb I05709M-MS-3 I05709M-MSD-3 Croup t I05709M Wk27 Control I057I4M Wk27 0.0 mg/kg/day 1057ISM Wk27 10S72SM Wk27 Croup 2 105702M Wk27 Mid Dose I05706M Wk27 3.0 mg/kg/day I05717M Wk27 5721M replacement I05723M Group 3 I05707M Wk27 Mid-lligh Dose I05708M Wk27 10 mg/kg/day I057I0M Wk27 I057I9M Wk27 Group 4 105703M Wk27 lligh Dose I05704M Wk27 30 mg/kg/day 10571 IM Wk27 105713M Wk27 I05722M Wk27 I05724M Moribund POAA * Pcrfluorooctanoale Limit of Quantitation (LOQ) " 30 ppb Limit of Detection (IjOD) - 15 ppb POAA Calc. Cne. "R'R 10.7 00 11.8 14.0 219 184 93.5 543 235 41.8 15723 19209 11629 16873 22764 6488 9069 19444 1350 16582 224 86933 : - 0 E. 160808 Amount ofTOAA " R' <LOD <LOD <I.OD <LOD 74*/. 62*/. 0.0935 0.0543 0.235 0.0418 15.7 19.2 11.6 169 22.8 6.49 9.07 19.4 1.35 16.6 0.224 86.9 0.00 161 Date F-nteted/Dy: Dale Verified/ Dy: 06/24/99,06/25/99,07/29/99 LAC 08/03/99 OML 9/7/99 EID088634 O o o esoooofAvo FACT M-4 I C.'ovHiicW/ (J2V -2JI Slinty 6 Month Capsule Toxicity Study with APFO in Cynomolgus Monkeys Product NuvnbcrfTcst Sulntince) T-6889 2(POAA) Malfix: Monkey Sera Mcthod/Rcvision: Analytical Equipment System Number; FACT-M-3 I A FACT-M-4 I Amelia 062498 Irutnment Software/Verston MassLynx 3 I Filename See Attachments R-Squared Value; See Attachments Slope; See Attachments Y-Infercept: See Attachments Dite of Extraction/Analyst Dale of Analysis/Analyst 11/13/91 IAS 11/16/91,11/24/98,12/03/98 >IOJ Date of Data Reduction/Analyst: 11/17/98. H /30/98.12/07/98 HOI Sample Dala Day 9 MONKEY SERA Croup Sample R POAA Average BSD Dose Reported Ug/mly POAA ug/mL Sid Dev. Method Blk 1120 Blk-1 <MDL Matrix Pik ll2 0 B lk -2 Rahbil Sere Btk-I <MDL <MT)L <MDL chfDL Q C -W O ppb Rabbit Sera Blk*2 RBSI 1134-MS <MDL 109% <MDf. <MDL RBSII11S-MSD 100% 104% 8% Croup 1 Control 10S709M 10S7I4M 00372 01158 0 0 mgAg/day I057I5M <MDL I0S7IIM I05720M 00638 <MDL 695 105725M 00214 0 0595 00414 G roup} I05702M 86 1 Low Dose I0S706M 173 105717M 110 10572IM NR 295 I05723M 124 123 364 G roups I05707M 224 M tdlligh Dose I05708M 91 5 10 mg/kg/dy I057I0M 162 I05712M 172 I057I6M 222 212 I05719M 213 III 509 Croup 4 I05701M 6656 High Dote I05704M 291 30m^kg/day 10571 IM 1741 I057I3M 20S I05722M I05724M 164 111 1 1657 152 2522 Limit of Quantitation (LOQ) 10 ng/mL Method Detection Limit (MDL); 5 Ang/mL POAA.* Pcffluorooctanoate Tentative value, sample evaporated to dryness D ue Enleied/By: Dale Verified/ By: 11/11/91,12/07/98 LAC 06/21/99 EAD 088635 I frSOOOOfMO FACT-LM I Covjiiicc//6329*231 Slwly Piduct Number(Test Substance): Matrix: Mcthod/Rcvision: Anatylka) Equipment SystemNumber: Instrument Software/Venion Filename. R-SquarcdValue Slope Y-lnlcrccpt: Date of Extraction/Analyst DaleofAnalysis/Analyst Date of Data Reduction/Analyst 6 MonthCapsule Toxicity Studywith APFOin CynocnolgmMonkeys T-6W9 2(POAA) MonkeySera FACT-M-3 I A FACTM-4 I Amelia062491 Masst.ynx 3 1 Sec Attachment See Attachments See Attachments See Attachments 11/13/9* IAS 11/16/91.11/24/91.12/03/91.01/04/99 IIOI 11/17/9. 11/30/98, 12/07/91.01/07/99 IIOI Sample Data Week 4 MONKEY SERA Croup Dom Sample# Methodnik 1120DIM 112001k-2 MatrixBtk Rabbit SeraBlk-1 Rabbit SetaBlk-2 QC 500ppb RnSlll3S-MS RBSI1I3SMSD Group 1 I05709M Control 10S7I4M 0 0 mg/kg/day IOS715M 10571IM I0S720M I05725M Group 2 I05702M LowDose I05706M 1057I7M I0572IM IOS723M Group 3 I05707M Mid-High One 105708M 10mg/fcg/diy 105710M IOS7I2M I057I6M I057I9M Group 4 I05703M HighDose I05704M 30mg/kg/dsy 10571IM I057IJM I05722M I05724M LimitofQuantitation(LOQ). 10ng/mL MethodDetectionLimit (MIX.): 50 ng/mL POAA8 PeriluovDoctanoate POAA Average RSD Reported POAA std. Dev. ug/ml. ug/mL <MDL <MDL <MDL <MDL <MDL <MDL <MDL <MDI. 109% 100% 10454 1% Oil] 0 240 00119 0162 0174 51 1 0119 0215 0110 97 2120 * 43 4* 115 91.1* 404* 54 5 112 NR 1025 1864 206 71 279 E 124 41 1 201 t0 751 297 264 4962 694 511 178 IK 1011 1922 * Outlier, wasnot includedinthesevalues NR Samplenot receivednorreported ESampleevaporated, not analyzed. Dite EiMcrcd/B)r: Dale Verified/ Dy 11/21/98.12/07/91,01/12/99 LAC 06/21/99 EAD EID088636 O o '; J w SSOOOOfAVO ETS-8 I i.'iiviiiicc// <>J2!>-2JI Study' lynJuct Nwnbci< l est Substance): 6 Month Capsule Toxicity Study with ATFO in Cynomolgus Monkeys T-6889 2 (POAA) Matrix. Monkey Seta Mclhod/Rcvision: E T S-M .l and ETS I 5 I Analytical Equipment System Number: Amelia 062498, Soup020199 Inslnanent SoAware/Version MassLynx 3 2 Filename: See AtlachmcnU RSquarcd Value: See Attachments Slope: See Attachments Y-Intercept: See Attachments Date of Extraction/Analyst: Date of Analysis/Analyst: Dale of Data Reduclion/Analyst 03/12/99 SAI I 06/03/99,06/07/99.06/10/99,06/16/99 IIOJ/SAII/MEE/LAC 06/04/99.06/08/99,06/11/99,06/17/99 IIOJ/LAC Sample Data Week 6 MONKEY SERA Group Sample a POAA Average RSD Dose Reported ug/mL POAA ug/mL Std. Dev. Method Rlk H 20 Elk-1 <MDL ll200lk-2 <MDL <MDL <MDL Matrix Blk Ribhil Sera Blk-I <MDL QC 250 ppb Rabbit Sera Blk-2 RBS0S129-MS-3 <MDL 78H <MDL <MDL RDS05I29MSD-3 78*4 71% 0% RRS05129 MS-4 17% RDS05129MSD-4 1255 14% 5% Group 1 I03709M 0166 Control I057I4M 0160 OOmg/kg/day 10571SM 0093 I0S7IIM 0133 I0S720M I05725M 0092 0096 0123 279 00343 G ro u p ! I0S702M 70S Low D o I05706M 120 105717M >73 I0572IM 149 328 IOS723M NR 107 351 G roup3 I05707M 88 Mid-High Dose I0570JM 122 lOmg/kgMiy I057I0M 1074 I057I2M 92 I057I6M 90 215 I057I9M 140 1000 215 Group 4 I05703M 169 High Doie JOmg/kgMiy I0S7O4M 10571IM III 1679 I057I3M 161 149 I05727M 143 ISI 23 Limit of Quantitation (LOQ): lOngfanL Method Detection Limit (MDL) 5 0 ng/mL NR * Sample not received nor reported. POAA * Perfluorooctanoate Date Entered/By: Dale Verified/ By: 06/08/99,06/14/99,06/17/99 LAC 06/21/99 EAD EID088637 9S 0000fM .D ETS I 5 I CovHiicctf (J29-2JI Study: Product Number(Tcst Subitmcc) Matrix Mclhod/Rcvision: Analytical Equipment System Number Instrument SoAware/Veriton' Filename: RSquwcd Value: Slope: Y-Interccpt: Date of Extraction/Analyst: Date o f Analysis/Analyst Date of Data Reduction1Analyst: 6 Month Capsule Toxicity Study with APFO in Cynomolgus Monkeys T-6889 2 (POAA) Monkey Sera ETS-l-4 I and ETS-8-5 I Amelia 062498 MassLynx 3 2 See AlUchiKnu Sec Attachments See Attachments See Attachments 03/12/99 SAJI 06/03/99,06/07/99,06/10/99 110J 06/T>4/99.06/08/99.06'| 1/99 HO) Sample Data Week 8 MONKEY SERA Croup Dote Method Blk Matrix Dlk QC - 250 ppb Croup 1 Control 0 0 mg/Vg/day Sample # IUOBIk-1 II20BH-2 Rebhil Sera Blk-1 Rabbit Sera T)tk<2 RBS05129 MS-3 RBS05I29 MSD-3 RBS05I29MSA RBSOSI29MSCM I03709M 10S7I4M 105715M 1037I8M POAA Reported ug/mL <MDL <MDL <MDL <MDL 71% n% tl% 1755 0 242 0162 00726 00166 Avenge POAA tig/mL <MDL <MDL 78% 84% RSD Sid Dev. <MDL <MDL 0% 5% I03720M I05725M 0129 0 0923 0119 655 00780 Croup 2 I03702M 791 Low Dose I05706M 106 I057I7M 735 I0572IM 105723M 136 211 NR 99 215 Croup J M idllighDoie lOmg/Vg/dey - I05707M I0S70SM I0S7I0M 101 707 924 I057I2M 16 I0S7I6M 107 24 1 I057I9M 131 1019 24 6 C r* u p 4 llilh Dose lOmg/Vg/dey Limit of Quantitation (LOQ) |0 ng/mL I05703M I0S704M 10571IM 103713M I05722M 113 127 1061 103 396 349 173 103 Method Detection Limit (MDL) 3 0 ng/ml. NR * Sample not received not reported POAA * Perilitoroocianoaie D ue Entcred/By: Dele Verified/ By: os/o1/99. 06/14/99 lac 06/21/99 EAD EID088638 SOOOOfM.0 C'ovHiitc// 6J29-2JI stuly 6 Month Capsule Toxicity Study with APFO in Cynomnlgus Monkeys Product NumbctfTcst Subtlance) T-6889 2 (POAA) Matrix Monkey Sera Methml/Rcvisian* ETS-8-4 I andETS-l-5 I Analytical Equipment System Number Madeline 041091 Instrument Software/Version MassLynx 3 2 Filename: See Attachments R-Squared Value: See Attachments Slope: Sec Attachments V-Intercept: See Attachments Date of Extraction/Analyst; 05/13/99 SRP/JCP Date o f Analysis/Analyst 03/17/99.03/19/99.06/10/99 MEE/KJH/IIOJ Date of Data Reduction/Analyst: 05/18/99,05/20/99. 06/1 |/99 KJH/MEE/HOl Sample Data W eek 10 M ONKEY SKRA Group Sample 0 rOAA Average RSD Dose Reported POAA Sid. Dev. gimU ug/mL Method Dlk IDO Dlk-1 <LOQ 1120 Dlk-2 <MDL <MDL <MDL Matrix Blk Matrix Blk Rabhil Seta Dlk-1 Rahbit Sera Dlk-2 Monkey Sera Blk-1 0 03174 003434 008671 0 03314 0 q c .jso n * Monkey Sera Dlk-2 RBS05I29-MS-7 RBS03I29-MSD-7 0 04897 103% 105% 006784 104% 0 2% RBS05129-MS-S 103% KBS05I29-MSD-* !27% 115% 20% Creup 1 IfllW M 0 202 Control I0S7MM OHI 0 0 mg'kg/day IOS7I5M 00976 I0S7IIM 0137 I0S720M I05725M 0136 O lii 0134 27 5 00367 Group 2 IOS7D2M 792 Low Dose I05706M 119 I0S7I7M 710 I0S72IM 161 360 I05723M NR 109 394 G roup3 I05707M 102 Mid-lligh Dose I0570IM 760 lOmg/kgiday I057I0M 917 I05712M 107 I05716M I057I9M 107 14 6 112 977 > 14 3 Group 4 I05703M 327 High Dose I05704M 134 30 mg/kg/day 10S7IIM 703 I057I3M 217 661 I05722M 488 247 165 Limit of Quantitation (LOQ)- lOng/mL Method Detection Limit (MDL) 50ng/mL NR * Sample not received nor reported E Sample evaporated not analyzed POAA * Periluorooctancate Date Entered/Dv: 05/20/99.05/25/99.06/14/99 LAC EID088639 O o 8SOOOOfMO FACT-M-4 I t.o v jim c // <iJ2V-2JI Study Numhcit leM Substance) Maliix Mclhod/Rcvision: Analytical Hquipircnl System Number: 6 Month Capsule Toxicity Study with APFO in Cynomolgus Monkeys T 6889 2 (POAA) Monkey Sera FACT M 3 I A FACT-M-4 I Madeline 041098 Instrument Soflware/Version Masslynx 3 I Filename R-Squved Value: Slope Y-Intercept; Date of Extraction/Analyst Date of Analysis/Analyst Date of Data Reduction^Analyst See Attachments See Attachments See Attachments See Attachments 01/08/99 SA11/JCP 01/21/99, 01/27/99 IIOI/MEE 01/25/99.01/28/99 KJII/MHE Sample Data W eek 12 MONKEY SERA Group Dost Sample tf POAA Reportai Average POAA RSD Sld.Drv. ug/mL ug/mL Method nik 1120 RIM <MUL Matrix Blit QC - 250 ppb II20BHC-2 Rabbit Seta DIM Rabbit Sera Blk-2 RDS0I019MS <MDL <MDL <MDL 101% <MDL <MDL <MDL <MDL Croup 1 Control OOrngAgMay RBS0I089MSD I05709M I057I4M 105715M I057IIM 99% 0214 0101 oor.19 0139 100% 2% Group 2 Low Dose I0S720M I05725M I05702M I05706M 0143 0 0852 67 9 901 0124 435 00540 1057I7M 519 IOS72IM 121 321 IOS723M NR 84 7 271 Group 3 I0S707M too Mid-lligh Dose lOmg/kg/day I0570IM I0S7I0M 105712M <02 838 142 I057I6M 19 9 279 I0S7I9M 105 967 270 Croup 4 High Dose 30 mg/Vf/diy I05703M I05704M 10571IM 240 no 34 3 I057I3M I05722M 193 141 54 3 I05724M NR 145 719 Limit of Quantitation (LOQ) lOng/mL Method Detection Limit (MDL): 5 0ng/mL POAA * Perilnorooctanoate Dale F.nleicd/Bjf Dite Ventici/ By. 01/27/99,01/21/99 LAC 06/21/99 F.AD EID088640 6S0000MD Covuiicc// GJ29-2J1 Study 6 Month Capsule Toxicity Study with APFO in Cynomolgm Monkeys Priduct NumbcifTest Substance) T-68B92(POAA) Mibix: Monkey Sera Mdhod/Rcvision FACT-M-3.1 A FACT-M-4 I Analytical Equipment System Number Madeline 041098 Instrument Softwire/Vcrsion M m lynx 3 I Filename See Attachments R-Squarcd Value: See Attachments Slope; See Attachments Y-Interccpl: See Attachments Date o f Extraction/Analyst: 01/08/99 SAH/JCP Date of Analysis/Analyst: 01/21/99 HOI Dale ofDala Reduction/Analyst 01/23/99 K ill Sample Dala W eek 14 MONKEY SERA Group Sanqtte tt POAA Arrragc RSI) Dote Reported POAA Std Der. Method nik Il20nik.| 1120 nik-2 ug/mL <MDL <MDL ug/mL <MDL -MDL Matrix Dlk Rabbit Sera Blk-I <MDL QC-2S0ppb Rabbit Sen Dlk-2 RBS0I0S9-MS <MDL 101% <MDL <MDL R13SOIOK-MSD 99% 100% 2% Croup 1 I0S709M 0211 Control I057I4M 0159 OOmgAg/day I0S7ISM 00973 10S718M 0 157 105720M 0112 419 I05725M 0 103 0 165 00689 Group 2 I03702M 774 Low Dose I05706M 116 105717M 62 0 I0572IM 124 316 I03723M NR 949 300 G roupJ 105707M 700 Mid-High Dose I0570IM 105 tOmgAg/day I057IOM 65 2 I0S7I2M 145 105716M 139 29 5 I057I9M 115 964 214 Group 4 I05703M S9.6 High Dose 105704M 116 30tngAtg/diy 10571IM 721 10571 )M 315 I05722M 105 361 I0S724M NR 14 2 304 Limit of Quantitation (LOQ): lOng/mL Method Detection Limit (MDL) $ 0 ng/mt POAA * Perilucxooclanoate Date EnteraVBy; Date Verified/By; 01/27/99 LAC 06/21/99 EAD (.'iivaiiu-tf 6J2V -2JI Stialy ricxtucl NumbcrfTcit Substance) 6 Month Capeula Toxicity Study with ATFO in Cynomolgua Monkey T4889 2 (POAA) M ilin: Mclliod/Revnion: Analytical Equipment System Number Instrument Softwwe/Venion; Filename; R-Sqnared Value; Slope: Y-Interccpt. Dele of Extraction/Analytt. Pate of Analysis/Analyst Monkey Sera ETS-I-4 I andETS-8-5 I Madeline 041098 MmLym 3.1 See Attachment Sea Attachments See Aitachmcnti Sea Aitachmcnti 05/13/99 SRP/JCP 05/17/99.0V I9/99, OfA 0/99 MEE Pala of Data Reducimr>/Anilyst: 0VI8/99,05/20/99. Ofi/I I /99 KJIUKfEIVlIOI Sample Data Week 16 MONKEY SERA Group Dm * Sample I rOAA Reported Average POAA uso Sid. Dev. ug/mL ag/mt. Method Pik 1120 Olk-I <I.OQ Matrix Pik 1120 Dlk-2 Rabbit Sera Blk-I <MDL 003174 RDfV/01 *DIVAN Rabbit Sera Dlk-2 003454 003314 0 Matrix Rlk Monkey Sera Plk-I 008671 Monkey Sera Blk-2 0 04897 006784 0 QC 500 ppb RDS05I29-MS-7 104% RI1S05I29-MSD-7 106% 105% 2% KRS05129-MS-8 104% O Croup 1 RDS05129-MSD-8 I05709M 128% 0298 116% 20% O Control 0 0 mf/Vg/day 105714M 5 7 15M 0.152 00840 57 IBM 0161 Group 2 Low Dote W5720M I0572SM K15702M 5706M 016 0 0870 577 737 0159 488 00778 K137I7M 572IM 5723M 453 in 379 NR 71 6 27 1 Group J Mid-High Doit lOmg/kg/day I05707M IOS70IM I0S7I0M S7I2M 104 62 8 764 in EID088641 IOS7I6M 57I9M 95 2 430 903 103 44 1 Croup 4 5703M Itigli Dote I0S704M 30 mg%g/day I0S7I1M 57I3M 105722M I05724M Limit of Quantitation (LOQ) 10 ng/mL 71.2 ut 13 174 603 69 7 NR 17 6 61 1 Method Detection Limit (MDL). 5 0 pg/mL NR " Sample not received nor reported. POAA Pcrfluorooctanoata E " Sample evaporated, not analyzed 090000fMO P>u Enlercd/By: DaU VcnHcd/ Hy. 05/20/99.06/1 4/99 LAC 06/21 /99.06/22/99 EAD/LAC nre a a l EID088642 O O O l9 0 0 0 0 f/^ O ETS-l-5 I Covancc# 6J29-23I Study 6 Month Capsule Toxicity Study with APFO in Cynomolgus Monkeys Product NumberfTest Substance) T-6889 2(POAA) Matrix: Monkey Sera Mcthod/Revision: ETS-8-4 I andHTS-l-5.1 Analytical Equipment System Number Instnancnt Soflwsre/Veninn Madeline 041098, Amelia 062498 Massl.ynx 3 2 Filename: See Attachments R-Squared Value: See Attachments Slope: See Attachments Y-Intercept See Attachments Date of Extraction/Analyst: 05/14/99 SEE Date of Analysis/Analyst: 05/11/99.05/24/99.05/25/99.06/07/99 MEE/llOi/SAII Date of Data Reduction/Analyst : 05/19/99,05/25/99,05/27/99.06/08/99 MEE/HOI Sample Data W eek 18 M ONKEY SERA Croup Dose Method nik Sampled 1120 B lkl POAA Reported ug/mL <MDL Average POAA uft/mL KSD Sid. Dev. Matrix Dtk 1120 Blk-2 Rsbbil Sets Btk-I <MDL <LOQ <MDL <MDL QC - 250 ppb Rabbit S en Blk-2 RBS05I49-MS-M <MDL 105% <MDL <MDL RBS0SI49MSD-II 84% 94% 22% RDS05I49-MS-I2 88% RDS05I49-MSD-I2 7IH 80% 22% Croup 1 I05709M 0 275 Control I057I4M 0 254 00m*/k*/d*y 10571SM 00991 1057IIM 0172 I05720M I05725M 0 202 0144 0191 341 00665 G roup! 105702M 116 Low Dose I05706M 167 1057I7M 697 165 IOS72IM 249 307 266 Group 3 I05707M 140 M td-lli|h Dose lOmf/kg/dey I0570IM I05710M 101 414 IOS7I2M 14 3 1057I6M I05719M 10 3 12 1 I I I 112 149 Group 4 High Dose 30 rn*/k(/dy I05703M I05704M 10571IM 711 209 191 I05713M I05722M 215 515 479 371 221 Limit of Quantitation (LOQ) lOng/mL Method Detection Limit (MDL) 5 0ng/mL POAA .Pcrfluorooctanoate Dite Entcrcd/By: Dite Verified/ By: 05/19/99.05/25/99,05/27/99.06/01/99 LAC 06/21/99 EAD EID088643 O O O Z90000fMD ETSI5I C'ovMncc# 6J29-231 Study 6 Month Capsule Toxicity Study with APFO in Cynomolgus Monkeys Product Numba(Tcit Substance): T-68892(POAA) Matrix* Monkey Sera Melhnd/Revision ETS-l-4 I a n d E T S 1 5 | Analytical Equipment System Humber: Madeline M l09, Amelia 062498, Soup 020199 Instrument SoAware/Venion MassLynx 3 2 Filename: See Attachments R-Squarcd Value: See Attachments Slope: See Attachments Y-Intercept: See Attachments Date of ExtractVAnalyst: OVI4/99 SEE Date o f Analysis/Analyst Dale o f Data Reductinn/Analyst 05/18/99,05/24/99,05/25/99.06/10/99.06/16/99 MEMIOI/SAII/LAC 05/19/99.05/25/99,05/27/99,06/11/99,06/17/99 MEE/110J/1.AC Sample Data Week 20 MONKEY SERA Croup Date Sample 4 I'OAA Repotted Average POAA RSI) Sid. Dev. itn/ml. ug/mL Method Blk 1120 Blk-1 <MDL Method Dlk ll2 0 B lk -2 <MDL <MDL <MDL Matrix Blk Rabbit Sera Dlk-I <MDL Matrix Blk QC - 250 pph Rabbit Sera B!k-2 RBS05149-MS-II <MDL 104% <MDL <MDL RBS05I49MSD-II 3% 94% 22% QC *250 pr* KBS05I49 MS-12 17% RQSOS149-MSD-12 70% 79% 22% Group 1 I05709M 0357 Control 105714M 0 221 OOmg/kg/day 105715M 0120 105718M 0234 I05720M 0 253 326 I0572SM 0216 0 234 00762 Croup 2 I05702M 116 Low Dose I05706M 119 I0S7I7M 341 78 1 10572IM 726 345 272 C roupS 105707M 112 Mid-High Doie I0570IM 643 I0mg/kg/day I057I0M 715 * I057I2M 141 I057I6M 953 276 I057I9M 112 lot 278 Group 4 I0S703M 406 High Doie I05704M 966 10 mg/kg/day 10571 IM 249 I05713M 336 132 I05722M 344 102 135 Limit of Quantitation (LOQ): lOng/mL Method Detection Limit (MDL): SOng/mL POAA PerfUaorooctmaatc Dale Enteredy: Dtle Verified/ By: 05/20/99,05/25/99.05/27/99. 06/14/99.06/17/99 LAC 06/21/99.06/22/99 EAD/LAC ^880ai3 O O O 900001 ETS-I-S.I (.'ovante// 6J29-2J1 SluJy 6 Month Capsule Toxicity Study w ith AFFO in Cynomolgus Monkeys Product N on b cr(l est Substance) T-68I9 2 (POAA) M atrix Monkey Sera Method/Revision ETS I-4 I and ETS 8-5 I Analytical Equipment System Number: Am elia 062491, Madeline 041098 Instrument Software/Version* MassLynx 3 2 Filename: See Attachments R-Squared Value: Sec Attachments Slope: See Attachments Y -In te iccp t: See Attachments Dale o f Extraction/Analyst 05/14/99 M O I Date o f Analysis/Anatyst Date o f Data Reduction/Analyst: 05/20/99,05/26/99.05/28/99. 06/10/99 IIO I/M E E 05/24/99.05/27/99,06.'0|/99.06/11/99 IIO I/M E E Sample Data Week 22 MONKEY SFRA G roup Sample 0 POAA Average RSD Dose Reported POAA Sid. Dev. ug/m L ug/m L Method Blk M atrix B lk 1120 Blk-9 1120 Hlk-IO Rabbit Sera (Ilk-9 <MDL <MDL <MDL <M D L <M D L QC - 250ppb Rabbit SeraBlk-10 R B S 05I49-M S -9 <MDL 103% <M D L <MDL RBS05I49M SD-9 108% 106% 4% G roup 1 C on tro l I05709M I052I4M 0410 0164 0 0 mg/kg/day I0S7ISM OUI 10571IM 0 210 I0572OM 03 495 I05725M 0169 0 254 0126 G roup 2 I05702M 729 Low Dose I05706M no 321 I0S7I7M 600 110 260 G roup 3 I05707M 127 M id-H igh Dose I0570SM 665 10 mg/kg/day I057I0M 916 I057I2M 175 I057I6M 111 34 I0S7I9M 9 1099 379 G roup 4 t05703M 172 High Dose 105704M 961 30 mg/kg/day 10571 IM 1 91 I057I3M 100 771 I05727M 897 61 7 476 L im it o f Quantitation (I.O Q ) lO ng/m l. Method Detection L im it (M O L): SOng/mL POAA r Pcrfluorooctanoate Date F.ntered/By: Dale V erified/B y: 0505/99,05/27/99. 06/02/99. 06/14/99 LAC 06/21/99,06/22/99 EAD/LAC EID088645 t/90000f/&O ETS-l-2 I Covuncctf 6J29-2 J I Study: 6 Month Capsule T oxicity Study w ith APFO in Cynom olpu Monkeys Product Numbcr(Tc** Substance): T-6889 2 (POAA) M atrix Monkey Sera M cthod/R evision: E T S -M I and ETS-B- 5 I Analytical Equipment System Number: Amelia 062491 Instrument Soflware/Version MaasLynx 3 2 Filename See Attachments RSquared Value See Attachments Slope: See Attachments Y-Intcrcept: See Attachments Date o f Extraction/Analyst 05/14/99 M O ! Date o f Analysis/Analyst: Dale o f Data Reduciion/Analyst: 05/20/99,05/26/99,05/28/99 HO J/5AII/M EE 05/24/99,05/27/99.064)1/991IOJ/MEE Sample Data Week 24 MONKEY SERA G roup Sample 4 POAA Average R sn Hose Reported POAA Std O rr. ug/m L ug/m L Method Oik 1120 fllk -9 <MDL M atrix B lk 1120 Btk-10 Rabbit Sera B lk-9 <MDL <MDL <MDL <MDL QC - 250 pph Rabbit Sera Blk>10 RBS05M 9M S-9 <MDL 103% <M D L <MDL R B S05M 9M SD 9 108% 106% 4% G roup 1 I05709M Ext C ontrol 105714M Ext OOmgAg/day 105715M 0171 1057ISM 0190 I0S720M 0 362 464 105725M 0139 0216 00999 G roup 2 I05702M 106 Low Dose I05706M 153 95 3 105717M 621 75 4 71 1 G roup3 I05707M 30 M id-H igh Dose I05708M 641 lO m g/kg/day I057I0M 154 105712M 121 I057I6M 151 233 1057I9M 120 949 22 1 G roup 4 I0570JM 21 25 High Dose I05704M 94 3 JOmg/kg/day 10571IM 441 1057U M 119 119 I0S722M 171 65 4 776 L im it o f Quantitation (LO Q ) lO ng/m L Ext: Samples lost during sample extraction. Method Detection L im it (M D L): 50ng/m L POAA * Pevfluorooctanoatc Dale Entercd/By: Dale V erified/B y: 05/25/99,05/27/99,06/02/99 LAC 06/21/99 EAD EID 0 8 8 6 4 6 O O O S90000MO ET5-I-5I Covarne# 6J29-2JI Study: 6 M onth Capsule Toxicity Study w ith APFO in Cynomolgus Monkeys Product Numbcr{Tcst Substance): T-6889 2 (POAA) M atrix: Monkey Sera M ethod/R evision: ETS 8-4 I A ETS-8-5 I Analytical Equipment System Number: Am elia 062491 Instrument Softwwe/Versinn MassLynx 3 2 Filename Sec Attachments R S q u vtd Value: See Attachments Slope: See Attachments Y 'lnlcrcept See Attachments Dale o f Extraction/Analyst 04/29/99.03/14/99 SAM D r it o f Analysts/Analyst: Date o f Data Reduction/Analyst 05/17/99,05/20/99,05/26/99,06/10/99 HOJ/SAH/MEE 05/19/99.05/24/99.05/27/99.06/| 1/99 IIO J/M EE Sample Data Week 26 MONKEY SERA G raup Sample M POAA Average RSD D a ti Reported POAA Sid. Der. ujg/mL. itg /m L Method B lk ll2 0 B lk -l <MDL Method B lk M atrix B lk 1120 B lk 2 Rabbit Sera B lk-I <M D L <M D L <M D L <M D L M atrix B lk Rabbit Sera Blk-2 <M D L <M D L <M D L Q C -250ppb M KS05I49M S 80% M KS05I49M SD 16% IW 7% C roup I 105709M 0451 Centred IOS7I4M 0102 0 0 m g/kg'diy 10S715M 0 095 10571IM 0 215 I05720M 0 322 75 1 IOS72SM 0 057 0201 0156 G ro u p ! I05702M 130 M id D oie I0S706M 147 233 105717M 914 123 28 7 G roup 5 M id i fifth Dose I05707M I0S708M II 3 571 10 m ^ k |/d ty I057IO M 101 211 I057I9M 13 1 80S 17 6 G roup 4 I05703M 11.6 High Dose 30 m ft'kg/diy I05704M 10571 IM 644 147 105713M 312 162 I0S722M 165 ti 1 131 L im it o f Quantitation (LOQ): lOng/m L Method Detection L im it (M D L) 50ng/m L POAA Perfluorooctanoate Dale Entered/By: Date V erified/ By: 05/19/91.05/27/99.06/14/99 LAC 06/21/99,0642/99 EATVLAC EID088647 990000f/WO Covante// 6J 29-231 Study: 6 M onth Capsule T oxicity Study w ith A P fO in Cynomolgui Monkeys Product NumberfTest Substance): T-6W 9 2(P O A A ) M iiru . Monkey Sera M ethod/R cvision: Analytical Equipment System Number E T S -M I A ETS -l-5 I Am elia 06249S Instnanent SoAware/Venion: MassLynx 3 2 Filename See Attachments R>Squed Value: See Attachments Slope: Y-Intercept: Date o f Extraction/Analyst: Dale o f Analysis/Analyst Dale o f Data Reduction/Analyst; See Attachments See Attachments 04/29/99 S A II 04/3099.05A)3W . 0 5 W P 9 .05/05/99 KJI1/MEE/JIOJ 05/03/99.05AW 99.05X15/99.05/25/99 IIO J/K IH Sample Data Week 26,27 MONKEY SERA_____________________ C roup Sanale 0 rO A A Average KSD Dote Reported POAA SUL Dev. mr/ir L ug/m L Method B lk Method D lk 1120 B lk-1 1120 Blk-2 <M D L <MDL <MDL <M D L M atrix B lk Rabbit Seta Olk-1 <MDL M atrix B lk Rabbit Sera Blk-2 <M D L <M D L <M D L QC - 250ppb I0S709M M S I057I4M M S 79% 101% 94% 17% C roup 1 Control I05709M Wk27 105714M Wk27 0 393 0229 0 0 mg/kgMay I0S7ISM Wk27 l05 7 IIM W k2 6 0099 0215 I05720M Wk26 I05725M Wk27 0 322 0142 0 233 471 0110 C roup 2 I05702M Wk27 49 7 M id Dose I05706M Wk27 669 I0S7I7M Wk27 45 7 I0572IM Moribund 477 174 IOS723M 622 545 941 G ro u p s I05707M Wk27 126 M id-H igh D ost lO m ^kgM ay 1057D1M Wk27 !057IOM W k27 33 3 494 I057I2M Wk26 104 I0S7I6M Wk26 110 447 I037I9M Wk77 676 769 344 C roup 4 I05703M Wk27 776 II^ i Dok I03704M Wk27 60S 30 mgfleg/day 105711M W 327 0909 IOS713M Wk27 192 I05722M Wk27 690 151 I03724M Moribund 501 537 110 L im it o f Quantitation (LOQ): 10 ng/mL Method Detection L im it (M D L): S.Ong/mL FOAA Perfiuorooctanoate Date Entercd/By: Date Verified/ By: 05/04/99,05/05/99.05/25/99 LAC 06/71/99 EAD CuvMticc# 6329-231 Study. 6 M onth Capsule Toxicity Study w ith APFO in Cynomolgus Monkey* Product N um bofTest Substance): T-6889 2(PO AA) M atrix' Monkey Sen M ethod/R vision E T S I-4 1 A ETS I-) I Analytical Equipment System Number: Soup 020199. Am elia 062491 Instrument SoAwve/Vcrsion: MassLyruc 3 2 Filcrum e: See Attachments R-Squared Value: See Attachments Slope: See Attachments Y -In tcrccp t: Sec Attachments Date o f Extraction/Analyst 06/11/99 RWW Date o f Anatysis/Analyst 06/22/99.06/23/99 DRJVMEE Date o f Data Reduction/Analyst: 06/23/99,06/24/99 DRJVMEE Sample Data Week 28 MONKEY SERA G roup Sample 0 POAA Average RSD Dose Reported POAA Sid. Dev. ug/m L uft/m L Method BIk 1120 D lk l <MDL ll2 0 B lk -2 <M D L <MDL <M D L M atrix B lk Rabbit Sera B lk *l <MDL Rabbit Sera Dlk-2 <M D L <MDL <MOL M atrix BIk Monkey Sera D lk-I <M D L Monkey Sera Dlk-2 <M D L <MDL <M D L Q C -230ppb M K S 06II9-M S -I 106% M K S 0 6 II9 M S D -I I0 4 H 105% IH G roup 1 I0 5 7 IS M 0160 216 C ontrol, 0 0 m ftfa/dey I0S720M 0211 0119 00408 G rottpS I057I2M 724 27.26 IO m g/kg/day 1057I6M 219 271 740 L im it o f Quantitation (LO Q ) lOng/m L Method Detection L im it (M D L): SOng/mL POAA Pcrfluorooctanoate Date EnlcredLDy: Date V erified/ By: 06/2V 99.06/25/99 LAC 0S/04/99 GM L HID 0 8 8 6 4 8 90000IAVO ETS-l-51  'V' w"> Covante// I Study Ptnducl Num bofTest Substance): M atrix 6 Month Capsule Toxicity Study w ith APFO in Cynomolgua Monkeys T-6889 2(PO AA) Monkey Sera M elhod/R cvision E T S I-4 I A ETS I 5 I Analytical Equipment System Number Instrument Soflware/Venion Sowf) 020199. Am elia 062491 MassLynx ) 2 Filename: See Attachments ((Squared Value: See Attachments Slope: Sec Attachments Y*Intercept: Date o f Extraction/Analyst: Dale o f Analysis/Analyst; Dale o f Data ReArctinn/Analyst See Attachments 06/11/99 RWW 06/22/99,06/23/99 DRH/M I-E 06/23/99,06/24/99 DRB/MEE Sample Data Week 30 MONKEY SERA C roup Dost Sample 91 POAA Reported ug/mL Am ap POAA ug/mL. RSD std . D er. Method B lk M atrix B lk IC O B lk-I ll2 O 0 tk -2 Rabbit Sera B lk-I <M D L <MDL <M D L <MDL <MDL M atrix B lk Rabbit Sera Blk-2 Monkey Sera B lk-I <M D L <MDL <M D L <MDL QC - 250 ppb Monkey Sera Blk-2 M K S 06II9-M S -I <MDL 106% <M D L <M D L M K S 06II9-M S D -I 104% 105% Itt C roup 1 C ontrol, 0 0 fne/kgMay 1057IIM I0S720M 013) 0168 0150 166 00248 C roup J lO m n/kg/day I0 5 7 I2 M 156 452 I0S7I6M 101 I I I 535 L im it o f Quantitation (LQ): 10 n^m L Method Detection L im it (M D L): 30ng/m L POAA * Pcrfluorooctanoate Date EntemVBy: Date V erified/ By: 06/23/99,06/25/99 LAC 08/04/99 GM L EID088649 890000fMO ETSI-51 Covillicc// iiSV)-XS\ Study: 6 Month Capsule Toxicity Study w ith APFO in Cynomolgus Monkeys Pimluct NumbcifTest Substance) T-6889 2(PO AA) M tliix ; Monkey Sera M cthod/R eviston: E T S -M I * ETS I 5 I Analytical Equipment System Number: Soup 020199. Am elia 062498 Inslnxnent Sortware/Venion Massl.ynx 3 2 Filename' See Attachments R-Squarcd Value: See Attachments Slope: See Attachments Y lntercept See Attachments Date o f Extractinn/Analyst 06/11/99 RWW Date o f Analysis/Analyst 06/22/99.06/23/99 DRB/MEE Dale o f Data Reduction/Analyst: 06/23/99.06/24/99 DRP/MF.E Sample Data Week 32 MONKEY SERA C roup S in p lc ti POAA Average RSD Dow Reported POAA Std Dev. ug/m L ug/m L Method B lk 1120 B lk -1 <M D L 1)20 Blk-2 <M D L <M D L <MDL M atrix B lk Rabbit Sera B Ik-l <M D L Rabbit Sera Blk-2 <MDL <MDL <MDL M atrix Blk Monkey Sera U lk*l Monkey Sera Blk-2 <M D L <MDL <M D L <MDL Q C -250ppb MKS06119-M S-l 106% M KS06I19-M SD -I 103% 106% IH G roup 1 I057U M 00984 198 Control. 0 0 mgAs/day I0S720M 0 133 0114 00226 C roups 105712M 108 SI 3 > lO ntaAii/day I057K M 307 795 408 L im il ofQ uantitation (LO Q ) lOng/m L Method D eled ion L im it (M D (.) J O i n iL POAA * P eriluorooctanoate Date EnleroVBy Dale V erified/ B r 06/23/99,06/25/99 LAC 01/04/99 GM L e ID088650 690000fAVD ETS-l-5 I TOX-026-sen 231Aemnh O o o g OOOoo ps O^OOOOfAVO Lovmiicc// <>J2!7-2JI Study: Product N isnbcrfTest SubUnce): 6 M onth Cipsule Toxicity Study w ith APFO in Cynomolgus Monkeys T-68B9 2 (POAA) M atrix; Monkey Sera M ethods evision: E T S -M .I A E T S I S I Analytical Equipment System Number Instrument Softwarc/Vcrsion: Filename; Soup 020199. Amelia 062491 MassLynx 3 2 Sec Attachments R-Squared Value: See Attachments Slope: See Attachments Y-lm lcfccpt: See Attachments Date o f Extraction/Analyst: Date o f Analysii/Analyst. 06/11/99 RWW 06/22/99.06/23/99 D R fi/M EE Dale o f Data Reduction/Analyst: 06/23/99,06/24/99 DRB'M EE Sample Data Week 34 MONKEY SERA C reup Dose S a tiric 0 POAA Reported ug/m L Average POAA ug/m L RSD Std.D cv. Method B lk 1120 B tk-t <MDL M atrix B lk M atrix B lk II2 0 B H -2 Rabbit Seta B lk-I Rabbit Sera Blk-2 Monkey Sera B lk -I <MDL <MDL <MDL <MDL <MDL <MDL <MDL JJ VV QC >250 ppb Monkey Sera BIk-2 M K S 06II9-M S -I 106% <MDL cM DL C roup 1 Control. 0 0 mftAft/day M K S 06II9-M S D -I I0 S 7 IIM I05720M 105% 00710 0109 I0 6 H 00199 i% 29 7 0 0267 C reup 3 I057I2M I0m ft/kft/day I0S716M L im it o f Quantitation (LO Q ) lOng/m L 569 260 4 M 529 219 Method Detection L im it (M D L): SOng/mL POAA Perfluam ctanoatc Date Entered/By: Date V erified/ By: 06/23/99.06/25/99 LAC 0I/W /99O M L CovmiccIt(J29-2JI SluJy Product NumbcrfTest Substance). M affix 6 Month Capsule Toxicity Study w ith APFO in Cynomolgus Monkeys T -6 II9 2 (POAA) Monkey Sera M cthod/R cvition: Analytical Equipment Syiicm Number Instrument SoAwarc/Vcnion Filename RSquared Value Slope Y -ln tcrccp l. Dale o f E xtractionAnalyst Date o f Analysis/Analyst Date o f D m* RcAiclion/Analyst: E T S -M I A B T 3 I-5 .I Soup 020199 M auLynx 3 2 See Attachments See Attachments See Attachments Sea Attachments 07/13/99 MCH 07/14/99.07/21/99 OM UDRD 07/15/99.07/22/99 G M U D R fl Sample Data Week 38 MONKEY SERA (raup Sample M POAA Average RSD Dose Method lllk 1120 nik-I Reported gfad. <MDL FOAA fjmL S td .D rv . 1120 n ik -2 <MDL <MDL <MDL M atrix flk Rabbit Sera D I M <MDL Rabbit Sera B lk -2 <MDL <MDL <MDL Matoix B lk M onkey Sera G lk-I <MDL Monkey Sett D lk-I <MDL <MDL <MDL rs Q C - 250ppb M K S 07119-M S . 1 92% o M K S 07I 39-M S I3-I MW 11% 9W o C raup 1 I057I IM 00717 34 1 Control, 0 0 mg/kg/day I05720M 0124 00991 00341 C raupJ I057I 2M 299 772 i 10 m |/kg /d *y I0S7I 6M O il 19) 1 49 L im it o f Quantitation (LO Q ) 25 ng/mL Method Detection L im it (M D L): 12 ng/mL POAA Pcrfhwrooclnotte Date E rta cd /B y Date V erified/ By 07/20/99.07/23/99 LAC 01/04/99 G M L E ID 088652 UOOOOfMD KTS-I-J I CovanccW (J29-2JI Study Product N ixnbcrfTcsl Substance) 6 M onth Capsule Toxicity Study w ith APFO to Cynomolgua Monkeys T -6 il9 2 (P O A A ) M atrix: Monkey S a t M cihod/Rcvision Analytical Equipment System Number: E T S -M l A B T 3 I 5 I Soup 020199 Instrument SoAware/Vrrsion MassLynx 3 2 Filename See Attachments R-Squared Value See Attachments Slope Y -lntctccpl. See Attachments See Attachments Dale o f ExtractiocVAnalysl: Dale o f Analysis/Analyst 07/11/99 MCH 07/14/99.07/21/99 GM L/DRB D ae o f Data Reduction/Analyst: 07/15/99.07/22/99 GML/DRB Sample Data Week 38 MONKKY SEKA G roup D a it Sample N POAA Reported IG/ml, Average POAA ug/m L HSD S td.D rv. Method lllk ID O B tk -l <M I7L M atrix Blk M atrix B lk 1120 Blk-2 R ib b ii S n i Olk-1 Rbbit S o t Blk-2 Monkey Sera B lk-1 Monkey Sera Blk-2 <M I7L <M PL <MDL <M PL <MDL <MDL <MDL <MDL <M D L <MDL <MDL Q C -250ppb M KS07139M S-I 97% M K S 07I39M S D -I 14% 11% 9% G roup I Control. 0 0 mg/kgM iy 1057ISM I05720M 00757 0124 0099 341 00341 G raup 2 lOm f/Vg/day I057I2M 299 772 I057I6M O il 193 149 l.im it o f C^iantitatran (LO Q ) 25 ng/mL Method Detection L im it (M D L). 12 ng/mL POAA * Perfluorooctanoale Dale Entaed/By; Dale V erified/ By 07/20/99,07/23/99 LAC 01/04/99 GM L EID088653 ^OOOOfMO Cova litre# 6J29-2JI Study 6 M onth C ym ric Toxicity Study w ith APFO in Cynomolpts Monkeys Ptoduct Num bo(Tcst S ubiU nu); T -6 tt9.2(P O A A ) M atrix M elhod/Rcvision Monkey Sera ETS M I A ETS-I-S I Analytical Equipment System Number: In iInanent Softwarc/Vcnion: Soup 030199 MassLynx 3 2 Filename* See Attachments RSquared Value: See Attachment* Slope: Y 'ln la ccp t See Attachment* See Attachments D ite o f E xbection/Aiulyst 07/11/99 M Q I Date o f Analysis/Analyst Dale o f Data Reduciion/Analyst: 07/14/99,07/21/99 GML/DRB 07/15/99.07/22/99 GM UDRB Sample Dala Week 40 MONKEY SERA Crawp Dmc Sairple# MethodBlk Maui* Bile M ail Blit Q C.2Mppb Criup 1 Control.00mx/kg/day Group3 lOmc/kg/day 1120Dlkl m onft.J Rabbit SetaDlk-1 Rabbit SeraBlk-2 Monkey Sera Blk-I MonkeySeraBlk-2 MKS07I39MS-I MKS07IJ9MSD-I I057IIM I0S77OM IOS7I2M IQ17I6M FOAA Reported ftfaiL <MDL <MI3I. <MOL <MDL <MDL <MDL 92% in 00751 0011 ltd 063 Average POAA ug/ml. <ua. <MDL <MDL 11% 00779 127 RSD SldDrv. <MDI. <MDL <MDL 9% SI oooto 97 016 L im it o f Q ia n tiu iio n (I.O Q ) 23n$/m L Method D dection L im it (M D L ) l2 n t/m L POAA Pcrfluorooctanoate Dale EmertxVBy: Dale V erified/D y 07/20/99.07/23/99 LAC 01/04/99 G M L EID088654 OOOOfAVO TOX-026-Sera231 6 Month POAA study in Monkeys GWJ000074 ----Control 0.0 mg/kg/day -- Low Dose 3 mg/kg/day --A--Mid Dose 10 mg/kg/day --H--High Dose 30 mg/kg/day EID088655 TOX-026-Sera231 6 Month POAA study in Monkeys Magnified View ---- ConUol 0.0mg/kg/day - O-- Low Dose 3mg/kg/day - A -- Mid Dose 10mg/kg/day --H-- High Dose 30mg/kg/day 'K O o o 104 f 000, 5 <9 Andrew S Hartten 09/03/99 02:48 PM To: cc: Subject: Robert L Ritchey/CL/DuPont@OuPont Robert F Pinchot/DEV/AE/DuPont@DuPont, Isidores J Zanikos/AE/DuPont@DuPont, Andrea Malinowski/DPL/DUP@DUP, 8emard J. Reilly/DPL/DUP@DUP, Michael J Lukas/AE/DuPonl@DuPont. Alison A Crane/AE/DuPont@DuPont, Michael A Turco/AE/DuPont@DuPont, H David Ramsey/AE/DuPont@DuPont, John M Migliore/AE/DuPont@DuPont, Roger J Zipfel/AE/DuPont@DuPont, Dawn D Jackson/CL/OuPont@DuPont, Anthony J Playtis/CL/DuPont@DuPont, George Woytowich/CL/DuPont@DuPont, "LYNWOOD K. IRELAND" <IRELAND@wwps-a1.email.dupont.com>, John E Auger/AE/DuPont@DuPont, Jon F Moore/CL/DuPont@DuPont, David C Harrison/CL/DuPont@DuPont, Timothy S Bingman/AE/DuPont@DuPont Re: Plant Manager communication to GE J?) Bob, Great to hear that additional communication has occurred with GE. Related to this subject, we need to be prepared to address EPA questions concerning this issue during their Sept. 23 site visit, especially if Martin Kotsch (EPA PM) visits the GE site first and arrives "enlightened". As you know, he will also be visiting GE during his trip to Parkersburg as they are also currently immersed in the RFI process. Hopefully, we can defer most questions to the formal "Wash Works RFI Results Summary" presentation he wants me (and Tim) to give to his project team (i.e., toxicologist, hydro) in mid-October. Andrew e e o ; v'i E1D072367 105J oc o :- o * TO: / FAX: DATE ,V FA C SIM ILE COVER SH E E T DU PONT FLUOROPRODUCTS y y PHONE: 1 'R O M : ?-/ / ' / '- LO CA TIO N : CRP-711/ PHONE: FAX: (302) 999-5123 N o . o f Pages in c lu d in g co ver sheet: M essage: Deliver Immediately Confidential EID087238 C-8 Monkey Study Goal: A) to determine toxicologic effects of C-8 in the primate following an extended exposure period B) to determine potency for producing change (NOEL-LOEL-EL) Surprises: - Potency at lower dose (3 mg/kg) - Failure of all animals in group to respond similarly - Quick plateau of C-8 in blood A) Quick clearance from blood B) Lack of proportional response (exposure of x, 3x, 6x did not lead to blood concentrations of x, 3x, 6x) Subtle vs major toxicity end points Hormones unchanged Pathology unrem arkable, especially in severely affected monkeys EID087239 OTG000257 F 11 .F' [!. c,<d I I inrfiUFflNT i.'.F 711 Oy w y ?,\y` PvatF C-8 Monkey Study Sponsor: APME Ad-Hoc APR) Toxicology Working Group Testing Facility: Covancc Laboratories Madison, WT Study ID: 6329-231 Study Director: Peter Thomford Study Monitor: Paul Lieder - 3M Study Representatives: David Farrar - LCI Reinhart Jung - Clariant Gerry Kennedy - DuPont [Giovanni Costa' - MitaniJ [George Lin - Daikin | In Lite 9/23/98 - 7/2/99 EID087240 O0Q:>3O OTG000258 FILE I - F x - i 10 7 '00 I[ i:[il.lFijMT t;p 711 :00 000 51 PVH.tE C-8 Monkey Study Kxnerimental Details Oral closing - gelatin capsules Diet - primate diet, 1 or 2 x/day - supplemented t'ruit/vegetables Young aduit/adult - 3 -*5 kg O T G 0 0 0259 0 0 0 Y 3 .1 EID087241 FII> N--,. 5>;d 1i l'-.}*, Ir<:niiFl'ItIT r.F 711 0? yyy 517': Fhi_- C-8 Monkey Study U e s lu n G ro u p I s* Control - 6 cynomolgus males 4 6 months 2 6 months &. 3 months recovery r Group 2 Group 3 3 mg/kg - 4 males - 6 months (1 monkey - died day 137) 10 mg/lcg - 6 males 4 6 months 2 6 months &. 2 months recovery Group 4 20/30 mg/kg - 6 males 30 - day 1-11 0 - day 12-21 20 - day 22 ->6 months 3 monkeys - dosing discontinued Days 43 *-81 1 monkey - diedxlay 20) ^ All sacrificed at 6 months /^ e IE>087242 hr F IL F l'k'. CA4 10 7 '-'I 1y - ID : MJPOMT fR 711 >;> OO'.-t P-Mf C-8 Monkey Study Parameters I. In Vivo Observed 2x/day Body weight - weekly Food consumption - estimate daily Ocular exams - pre-test/weeks 27 8c 40 II. Clinical Pathology Timing - Pre-test, days 30, 60, 90, 180 Recovery days 30, 60, 90 Hematology - RBC, Hb, PcV, platelets WBC 8c diet, reticulocytes, cell-indices Coagulation - APTT, pro time, fibrinogen Clin Chem - glucose, UN, creatinine, prot, bilirubin, cholesterol, triglycerides, ALT, AP, AST, GGT, SDH, ions (Ca, etc), amylase, lipase Urine - standard & urobilinogen, bilirubin OOO.S33 EID087243 'FILE'I- Z9Z000Drn C-8 Monkey Study ITT. Blood Hormones - Timing - 3x pre-dosing, day 30, 60, 90, 180 Recovery day 30, 60, 90 - Estradiol Estrone Fstriol Thyroid stimulate hormone Total & tree iodothyronine (T3) Total & Tree thyroxin (T4) Testosterone Cholecystokinin IV. Exposure Indices - Serum APFO - 7 days & every 2 weeks thereafter - Urine APFO - as serum - Feces APFO - as serum - Liver APFO - at sacrifice 000, EID087244 r l l t I K- `. V - 4 1'. 17 I l.i: i.iiJM II Ii i F, 711 C-8 Monkey Study V. Pathology Complete nescropsy Organ weights adrenal, brain, epididymis, kidney, liver, pancreas, testes, thyroid (parathyroid) Histopathology (36 tissues) Additional parameters - Palmitoyl CoA oxidase - Cell proliferation - Rile acid determination (receptor level determinations) (bone marrow smear) OTG000263 EID087245 e c o ; 'S ' F [I.F 'M'>. c A d 1 1`< -f i r:riJPfll IT i'R 71 1 C-8 Monkey Study - Results l. Clinical Observations Control - none 3 mg/kg - I monkey - week 18 - ataxic, hypoactive no food consumption, limited use of hind limbs ^^^ week 20 - sacrificed, lost 9.5% bwt 3 monkeys - none 10 mg/kg - 6 monkeys - none 30 mg/kg - week 1 - low food consumption lost 3-1.5% bwt 20 mg/kg - week 3 - 3 monkeys - same as above withou marked vvt loss, treatment discontinued week 7, 10, 12 1 monkey died week 4 2 monkeys - no clinical signs after week 2 OTG000264 00OS2S EID087246 FILE-N. 10 7 'li ID:[il.TO.IT lF 711 C-8 Monkey Study - Results II. Ophthalmology - no findings 111. Body Weight 0/3/10 mg/kg - no differences * 20 mg/kg - lower wk 7, 9, 24 (14.390 wt gain of controls) [30 mg/kg - lower wk l] IV. Food Consumption 0/3/10 mg/kg - no differences 20/30 mg/kg - lower (some no food consumption) V . B1ood Honm>ne No significant effects (0 30 mg/kg) Unexplained total thyroxin lower 20 mg/kg free triiodothyronine lower 20 mg/kg VI. Clinical Pathology 0/3/10 mg/kg - no differences 30/20 mg/kg - mild * triglycerides mild * neutrophil, protein, albumin EIDOS7247 OTG000265 FILE No. 10 7 'OO 1 [[i:DUPONT i!F 711 Tjlljl 7 1 FvhItI C-8 Monkey Study - Results VII. Palmitoyl CoA oxidase - expect <4 wks Cell proliferation - expect <2 wks Bile acid - no differences VITT. Pathology Gross pathology - unremarkable Organ weight - liver weights elevated 7 - 0/3/10/2IT30--------------------------- ' ^ 60/82/83/90^ ^ ^ Mean (all test*) 1.5/1.8/1.9/2.4 Organ/bwt (all ;t*) Histopathology - unremarkable Cause of death - unclear in both moribund animals ooo^es EID087248 o H Ooooto On ON IMDd'l']:O ] OI r>: `':'M T I M 2 r 3 94 li* oj irj I 4 /4 3 0 13 3 /1 0 4 IS 2/2S 4 , 12 7/12 9 IsU /l.v.J | I 14 /204 ,/ 3 / 3 , H..vO.iM n . l H i l . f t HID087249 OTG000267 Ir OJ o o o A 1 77 1 ID: Hi Pl'iMT i.'.R 711 C-8 Monkey Study Liver C-8 Levels (ppm) Group (mg/kg) 0 3 10 20/30 Recovery fLiverl 0.04 (0-0.04) 5.9 (4.1-6.8) L 5.9(3.6-8.7) / 17.2 (8-28) 0.8 (0.03-1.2) EID087250 ' I- ! I .F* N.-,. U> ;-Y 1X : f f.i : f.if if i'll JT i'.R - ~ \ \ PR#! C-8 Monkey Study - Conclusions Monkeys do not tolerate 20 mg/kg or higher - Non-specific response involves liver - Recovery complete in oft-dosing monkeys - Effects include body weight, liver weight - No specific histopathological changes hormonal changes Effects at 10 mg/kg only liver weights Effects at 3 mg/kg - 1 death (relationship to treatment?) liver weights C-8 cleared quickly from urine (proportional to exposure C-8 clears quickly from blood (not proportional) _ - Reaches plateau quickly - Leaves system quickly C-8 in liver proportional to exposure, '+k~ A ck recovery quick and complete C-8 in feces - will get "matrix information" 000G0. 0087251 o H OoooCtoV VO r u_c i io. iv i':1 i i l UUUPMT f..R 711 02 .1 C-8 Monkey Study - Conclusion -------/o ' 1 flvu Potential serious effect in I/4 monkeys at low dose (liver effect unexplained currently; best explanation i could be enzyme induction) At AEL/TLV of 0.01 mg/m3, daily exposure to man is 0.001 mg/kg X^fk 0 0 0 6 O f; EID087252 o H ~oOootoJ FfiFN.-.. 10 ;>7 'O'-' V? IH :M.CliNT OR 711 ft- ' '.j'.-.i'-i R,1y FvtGF C-8 Monkey Study - Issues Liver effect (will answer) ^ * . y i c ^ d ! ' Death of low dose monkey Lack of slow elimination as seen in man (does human data reflect mulli-phase clearance) Evaluation of monkey-by-monkey data (in progress) OTG000271 OOOftO'i EID087253 .r 11 r .r-j.-.. 111: 1ii iH ir 11 i h . 1 1 Cry R] F v n .'iF Thanks for Hanging in there OTG000272 QOOSO EID087254 I 106 0 0 K-. 5 C x /- C w - V ,. /X . A- JMM008028 roon O O e> i ,,O 0 0 LOI I f T Roger J Zipfel D ' , 1/17 /9 3 -j i ;27 AM To: Robert F Pinchot/DEV/AE/DuPont@DuPont cc: Oscar T Garza/AE7DuPont@DuPont Subject: Re: C-8 Monkey Study and Allowable Exposure Limit Rob, I don't fully support the first burger dot as it is stated. I don't think that we can rule out death due to C-8 exposure. Thus I believe it should read similar to the second burger dot. Roger. Robert F Pinchot 1 1 /1 5 /9 9 0 3 :0 6 PM Robert F Pinchot 11 /1 5 /99 0 3:06 PM .v /iw .M -A w .w :v To: Robbin Ranerjee/AE/DuPont^OuPont. Oscar T Garza/AE/DuPont@DuPont, Anthony J Ptaytis/CL/DuPont@DuPont, Stephen J Gissy/AE/DuPont@DuPont, Roger J Zipfel/AE/DuPont@DuPont, Matthew C Koenings/EUR/DuPont@DuPont, Arie J Vermeulen/EUR/DuPont@DuPont, Seiichi Tanaka/PO/DuPont@DuPont, Norifumi Ohtsuka/PO/DuPont@DuPont, Barbara J Gayda/AE/OuPont@DuPont, Barbara J Gayda/AE/DuPont@DuPont, Thomas J Cavanaugh/AE/DuPont@DuPont, Romain Van_Aken/EUR/DuPont@DuPont, Barbara J Dawson/AE/DuPont@DuPont, Susan S Mileti/DuPont@DuPont, Richard J Angiullo/AE/DuPont@DuPont, Maurice Astorga/AE/DuPont@DuPont, Marianne Marsi/DuPont@DuPont, David M Rurak/AE/DuPont@DuPont, Michael E McCord/AE/DuPont@>DuPont, Robert J Cavanaugh/DuPont@DuPont, Clarence P Mihal/AE/DuPont@DuPont, Earl W . MacFariane/DPL/DUP@DUP, Andrea V Malinowski/AE/DuPont@DuPont @ DUP, Sharron Laas/AE/DuPont@DuPont cc: Diane R Shomper/AE/DuPont@DuPont, Gary W Jepson/AE/DuPont@DuPont, Gerald L Kennedy/AE/DuPont@DuPont Subject: C-8 Monkey Study and Allowable Exposure Limit Most of the results of the 6 month monkey study are available. Due to some of the findings of the study, the study is reportable to the US EPA under TSCA Section 8(e) by the 3 M company. This notification will be made by Friday, November 19th and the letter will become a public document shortly thereafter. Since employees potentially exposed to C -8 have a right to know about the findings of the study, Diane Shomper and I are developing an employee communication framework for you to use for your communications. This communication package should be available for you to use by Monday November 2 2 . To give you a preview of w hat w e will be in the communication, here are the key points: One monkey in the low dose group died for reasons that are unclear. One monkey in the highest dose group died for reasons that are unclear but may be related to C-8 exposure. All monkeys showed some liver effects (liver weight increases in all dosage groups, liver enzyme increases in the high dose group monkeys that were in distress. The recovery animals did n o t show these effects suggesting th at the liver effects w ere reversible. No other clinical or pathological changes were observed other than the deaths and the liver effects. The study results are not complete. W e w o n 't have a full analysis of the data until January. The AEL (0.01m g /m 3 8 and 12 hr TW A with a skin notation) and Community Exposure Guideline (3micrograms/day) will, for now , stay the same. The Committee will revisit this QOQVtOS EID081959 a fter the full results are in and analyzed. Please w ait for the formal communication package to com m unicate this broadly. The purpose of this note is to give you a heads up th a t this com m unication is com ing. Regards, Rob . r, EID081960 108 r .-KSfC OOOh.'.O C-8 Monkey Study Communication Plan Communication to Employees DuPont Legal opinion is that communication is required to US employees. No specific time frame is given in the OSHA Hazard Communication Standard. To be conducted on Thursday, December 9 to all DuPont and employees potentially exposed to C-8 (Sites include WW, Parlin, Spruance, CW, DW, Mechelen, Shenzhen, Madurai, and Shimizu). Summary of study made public on November 22 through TSCA 8(e) filing by 3M. Messages to be conveyed at all sites ' 1. Current AEL is protective of human health 2. Liver effects seen at all doses, effects were reversible after ceasing exposure 3. Two deaths occurred in the test groups. One at low dose and one at high dose. The cause of the deaths is unknown. 4. More data will be communicated when analysis is complete (early 2000) Some sites adding site specific information on exposure levels at their site (all of which are less than the AEL). WW communicating that C-8 is in drinking water at the site, at levels less than the Community Exposure Guideline. WW is communicating the results to GE Plastics management. Communication to Customers No MSDS changes have been made at this time. No need to communicate to all dispersion customers. May have to change the MSDS once the final results are analyzed and will need to communicate to customers Chem Fab and Gore have been told about the monkey study. We will share the results with these two customers in the near future. (Gore meeting set up in January). RP000141 EID083021 109 r Tennant Farm Herd Health Investigation Caule Team Repo Tennant Farm Herd Health Investigation Cattle Team Report Kji E P A /D u P o n t C attle T e a m D r. Perry L. H abecker D r. L isa A . D a v is -H e lle r D r. Peter G . M o is an D r. R o b e rt J. M u n s o n D r. Robert H . Poppenga D r. G reg P. Sykes Decem ber 2 0 Oi/b. DUP 242 Tennant Farm Herd Health Investigation TABLE OF CONTENTS Section 1. 0. 1. 1. ' SUM M ARY S ig n a tu re s 2.0. IN T R O D U C T IO N 3.0. 3.1. 3.1.1. 3.1.2. 3.2. . 3.2.1. 3 ) ) 3.2.3. 3.2.4. 3.2.5. M ETHO DS C attle T eam mem bers m eetings A nim al Data videotapes diagnostic pathology reports A p ril 1999 site visit data m iscellaneous data w ildlife 4.0. 4.1. 4.1.1. 4.1.2. 4.1.3. RESULTS C a ttle videotapes diagnostic pathology repons A p ril 1999 site visit data a. herd history (4 /8 /9 9 in te rvie w ) b. physical exam in atio n o f cattle (4 /7 /9 9 ) - age. pregnancy status - bod> condition scores, ginh - clinical sians c. clinical pathology - hem atology - clinical chem istrv - special chem istrv - serolocy i - parasitology 1 d. hav and grain analvsis 4.2 4.3. 4.3.1. 4.3.2. 4.3.3. M iscellaneous Data W ild life videotapes sm all m am m al data deer studies 5.0. D IS C U S S IO N - endophyte toxicity - pinkeye - m alnutrition Cattle Team Report Page 4 5 ~ ------6 6 6 6 7 7 7 8 8 11 12 1 12 12 12 14 15 15 16 16 16 16 16 16 16 17 17 18 18 19 19 19 19 19 20 20 22 23 00 OC DUP 243 1 Tennant Farm Herd Health Investigation Cattle Team Report TABLE OF CONTENTS (continued) S e c tio n 5.0. D IS C U S S IO N (continued) - copper deficiency - to xico lo g y issues Pase 23 24 6.0. R E C O M M E N D A T IO N S 24 7.0 C O N C L U S IO N 26 8.0 R E F E R E N C E S 26 9.0 G R A P H S G r a p h 1: I n d i v i d u a l P r o l a c t i n V a l u e s 29 30 10.0 F IG U R E S Figures 1 and 2: Faceflies Figure 3: C orneal opacity 1 Figure 4: D elayed shedding 31 32 33 | 33 | Figures 5 and 6: C oronitis j F ig u res 7 and S: C a ttle s ta n d in g in w a te r 1 1 11.0 | T A B L E S 34 35 ( 36 | T a b le !: R eview of Tennant Farm Videotapes | 37 | T a b le 2: In d iv id u a l A n im a l D a ta: C lin ic a l S igns | 44 1 T a b le o : di vid ual A n im a l D ata: H e m a to lo g y (eryth ro n . platelets') T a b le d : Individual A n im a l Data: H em ato log y (leukon). and Special C hem istry | T ab le : Individual A n im a l Data: C linical C hem istry 46 48 | 50 ! T ab le : Individual A n im al Data: Serology and Fecal E xam j 52 j T a b le 7: T e n n a n t F a rm G ra in an d H a y : N u tritio n a l A n alys is 54 !1 12.0 A P P E N D IC E S 55 A ppendix A: A bbreviated C u rriculu m V ita e o f Cattle T eam M em b e rs | 56 A ppendix B: D iagnostic Pathology Reports (O h io Dept. A gric.: # 4 9 7 7 97: M ich ig an A n im a l H ealth D iagnostic Lab.: #1792571; U n iv . Penn. Lab. o f L arg e A n im a l Pathol, and T oxicol.: # U P 9 9 0 2 7 0 2 , #9901437) A p p en dix C: D ry R un Safety Plan A p p en d ix D : Figures 1-42 : Photographs o f the 4 2 adult cattle Figures 4 3 -6 6 : M iscellaneou s photographs o f the T e n n a n t F a rm and cattle. A ppendix E: H erd H ealth H istory (A p ril 8, 1999 interview ) A p p en dix F: D iet Analysis: C o m p u ter S oftw are Sim ulation 58 70 71 106 | 109 000 3 DUP 244 Tennant Farm Herd Health Investigation Cattle Team Report 1.0 SUMMARY In tro d u c tio n : T h e o b je c tiv e o f this in v e s tig a tio n w as to e v a lu a te the h ealth status o f M r. E arl T e n n a n t's cattle herd and d e te rm in e possible causes o f an y p ro b lem s. T h e inv es tig atio n in c lu d e d an e x a m in a tio n o f re le v a n t h is to ric a l d a ta as w e ll as th e c o lle c tio n and ev alu atio n o f n e w data. T h e in v e s tig a tio n te rm in a te d in the p ro d u c tio n o f this report, w h ich outlines study find ing s and m akes re co m m en d a tio n s to im p ro v e herd health. M e th o d s : T h e T e n n a n t fa rm h erd h ealth in v es tig atio n w as c o n d u cte d b y a te a m o f six veterin arian s w ith c o lle c tiv e e x p e rie n c e in b o v in e diseases, h erd h ealth m a n a g e m e n t, to x ic o lo g y , p a th o lo g y , and w ild life diseases. In a d d itio n to n u m e ro u s m e e tin g s and discussions, the cattle te a m visite d the T e n n a n t F a rm o n A p ril 7 -8 , 1 9 9 9 in o rd e r to collect relevant data. T h e cattle tea m re v ie w e d historical d ata (e.g., vid eo tap es, diagnostic lab o rato ry re p o n s) and c o n te m p o ra ry data (e.g., clin ic a l e x a m in a tio n s , b lo o d tests). D iag n o s es an d re c o m m e n d a tio n s w e re based u p o n the d ata co lle cte d . R esu lts: T h e m u ltifa c e te d disease in v es tig atio n o f the ad u lt cattle in the T e n n a n t b e e f herd revealed h ealth p ro b lem s that w e re related to en d o p h yte to x ic ity , in fe ctio u s keratoconjunctivitis (p in keye), m aln u tritio n , and co p per d eficien cy. C lin ic a l and historical data, w ith p ro lactin valu es o f so m e an im als, w e re consistent w ith en d o p h yte m ycotoxicosis. A n e x am in atio n o f vid eo tap es m ade d u rin g the s u m m e r m o n th s and clinical exam in atio n s o f p rev io u sly affected ad u lt an im als d u rin g the h erd visit indicated p r o l o n g e d s e v e r e e n z o o t i c s o f f a c e f i y (M u s c a a u t u m n a lis ) i n f e s t a t i o n a n d c o n c o m i t a n t p in keye. H a y an alysis, cattle b o d y c o n d itio n scorin g , an d an e v a lu a tio n o f the m in era l and grain rations fed w ere consistent w ith p ro te in -e n e rg y m a ln u tritio n an d m a cro m in eru l/tru ce nutrient d eficien cies. E a rlie r lab o rato ry data, c lin ica l signs, and se ru m testin g at the tim e o f th e h erd v is it w e re in d ic a tiv e o f se ve re c o p p e r d e fic ie n c y in the cattle. C o n c lu s io n : T h e re w as c o n c lu s iv e e v id e n c e th at the T e n n a n t ca ttle her'd w a s . an d co n tin u es to be. s u ffe rin g fro m fo u r m a jo r disease en tities, s o m e o f w h ic h w e re p otentially interrelated: en d o p h yte to x ic ity (fescue m y co to x ic o sis). p in ke ye , m aln u tritio n , and co p p er d eficien cy. A s substantiated b y the clin ical and lab o rato ry findings, and h istorical data, these fo u r con dition s re ad ily acco un t fo r the ch ro n ic herd health p ro blem s on the T e n n a n t farm . T h e herd h ealth in v e s tig a tio n re v e a le d d e fic ie n c ie s in h erd m a n a g e m e n t, in c lu d in g p o o r n utrition, inadequate ve terin ary care, and lack o f fly co n tro l. T h e lack o f va cc in atio n and in tern al parasite c o n tro l p ro g ra m s d id n o t ap p ear to h a v e a su b stan tial im p a c t o n this re la tiv ely isolated herd. D esp ite an exh au stive re v ie w o f h istorical and c o n te m p o ra ry h erd data, there w as no evid ence o f to x ic ity associated w ith c h e m ic a l c o n ta m in a tio n o f the e n v iro n m e n t. OOOv-j.^ DUP 245 4 Tennant Farm Herd Health Investigation 1.1 Signatures Cattle Team Report Perry D abecker, VMD, Dipl. ACVP Date Tisa. Davis-Heller, DVM /JzM /Cy Dat' / Peter G. Moisan, DVM, Dipl. ACVP, ABVP a u=m Date Robert J. Murson, VMD >J joe Date Robert H. Poppenga, DVM. PhD, Dipl. ABVT Date ^/ 7 Greg P. Sykes, VMD, Dipl. ACVP, ABT Date eoe DUP 246 5 Tennant Farm Herd Health Investigation Cattle Team Report 2.0 INTRODUCTION T h e o b jec tiv e o f this in v es tig atio n w as to ev a lu a te the h e a lth status o f M r . E a rl T e n n a n t's cattle nerd and d e te rm in e possible causes o f an y p ro b le m s . T h e in v es tig atio n in clu d ed an e x a m in a tio n o f re le va n t historical data as w e ll as the c o lle c tio n and e v a lu a tio n o f n e w data. T h e in vestig atio n term in a ted in the p ro d u ctio n o f this report, w h ic h outlines study find ing s and m akes re c o m m e n d a tio n s to im p ro v e herd h ealth 3.0 METHODS 3.1. Cattle Team 3.1.1. Members T h e T en n a n t F a rm H e rd H e a lth In vestig atio n w as assigned to a tea m o f six veterinarians ( "cattle te a m "). T h e team w as co n stitu ted to in c lu d e e x p e rtis e in b o v in e diseases, herd health m a n a g e m e n t, to x ic o lo g y , p a th o lo g y , and w ild life diseases. R e p res en tatives o f the D u P o n t C o m p a n y (D u P o n t) selected three m e m b ers (D rs . S yk es , D a v is -H e lle r. M o is a n ); represen tatives o f the U n ite d States E n v iro n m e n ta l P ro te c tio n A g e n c y (E P A ) selected th ree m e m b e rs (D r s . H a b e c k e r. P o p p e n g a , M u n s o n ). A b b r e v ia te d Curriculum Viwe o f the cattle tea m m e m b e rs are in c lu d e d in this repo rt (A p p e n d ix A ). Cattle Team Members Associations Perry Habecker. VMD. Dipi. ACVP Lisa Davis-Heller. DVM Chief. Large Animal Pathology. Laboratory of Pathology and Toxicology. Univ. of Penn. School of Veterinary Meo ine. New Bolton Center. Kennett Square. PA. Private Practitioner. St. Mary's Veterinarv Clinic. St. Marv's. \VV Peter Moisan. DVM. Dipl. ACVP. Dipl. ABVP Robert Munson. VMD Veterinary Pathologist. Rollins Animal Disease Diagnostic Laboratory (state laboratory). Raleieh. N'C. Field Investigator. Center for Animal Health and Productivity. Unit , of Penn. School of Veterinary Medicine. Kennett Square. PA. Robert Poppenga. DVM. PhD. Dipl. ABVT Greg Svkes. VMD. Dipl. ACVP. Dipl. "a b t Chief. Toxicology. Laboratory of Pathology and Toxicology, Univ. of Penn. School of Veterinary Medicine. New Bolton Center. Kennett Square. PA. Pathologist. Safety Assessment, DuPont Pharmaceuticals ComDany. Stine Research Center. Newark. DE. DVM. VMD = Docior ot'Veterinary Medicine Dipl. ACVP = Diplomate. American College of Veterinary Pathologists Dipl ABVP = Diplomate. American Board of Veterinary Practice (Food Animal and Beef Cattle Specialist) Dipl. ACVT = Diplomate. American College of Veterinary Toxicologists Dipl. ABT = Diplomate. American Board of Toxicology A t the first m e e tin g o f the cattle tea m (M a rc h 9. 19 99 ), P e rry H a b e c k e r w as elected S cien tific L e a d e r (i.e.. ch airm an ) and G re g S ykes w as elected C o o rd in ato r. T h e 009` .5 DUP 247 6 Tennant Farm Herd Health Investigation Cattle Team Report c h airm an and c o o rd in ato r w ere in stru cted to c o m m u n ic a te w ith the " steerin g c o m m itte e '' leaders, D rs. S arah C a sp ar (E P A , R e g io n III) an d R a lp h S tah l (D u P o n t C o rp o ra te R e m e d ia tio n G ro u p ), as n eed ed . T h is " steerin g c o m m itte e " in c lu d e d D rs . C a s p a r, S tah l, M ik e H orne (U S F W S ), M a rk Sprenger (E P A -O E R R ), and R u d y V alen tin e (D u P o n t S p ecialities C h em ic als to xico lo g ist). 3.1.2. C a ttle T e a m M e e tin g s T h e cattle te a m m e t fo rm a lly on fo u r o ccasio n s, in c lu d in g the T e n n a n t F a rm site visit. C a ttle T e a m M e e tin g s Date I Location March 9. 1999 New Bolton Center. Kennett Square. PA March 23. 1999 New Bolton Center, Kennett Square. PA April 7-8. 1999 Tennant Farm. Wood County. WV* JulV 2S-29. 1999 New Bolton Center. Kennett Square. PA * including pre-meeting planning session ai Holiday Inn. Parkersburg. WV In ad d itio n , several in-person discussions to o k place at N e w B o lto n C e n te r b e tw e e n and am o n g D rs. H a b e c k e r. M u n s o n . P o p p en g a, and S yk es b e tw e e n M a rc h 1 9 9 9 and the issuance o f this report. A ll cattle te a m m e m b e rs u tilize d the telep h o n e, in te rn et e m a il, and I 'S postal system s fo r p a ir and g ro u p discussions an d in fo rm a tio n sh arin g . 3.2. A n im a l D a ta 3.2.1. V id e o ta p e s T w o vid eo tap es w e re su p plied to the cattle team b y tne steerin g c o m m itte e . E a c h o f the tapes w as a c o lle c tio n o f vid eo tap es m a d e , and n arrate d , b y M r . E arl T e n n a n t o n his fa rm and the adjacent lan d fill area. A lth o u g h the tapes w e re ed ited and in c lu d e m a te ria l fro m d iffe re n t se aso n s, it a p p e a re d th a t th e s e tap es w e r e a ll p ro d u c e d b e tw e e n 1 9 9 5 a n d 1 9 9 7 . T e n n a n t F a rm V id eo tap es Tape Title 1 "Tennant Farm: New Enciand. Wood Countv. WVa - Januarv and Februarv. 1997" #2 "Dry Run: Harris PC. Wood Co.: Off North Fork of Lee Creek. New England. WVa" Animal Case Numbers 1 - IS 19 - 60 B o th o f these tapes w ere v ie w e d , in th e ir en tirety , b y the cattle tea m m e m b e rs i n d i v i d u a l l y . T h e y w e r e a l s o r e v i e w e d a t a c a t t l e t e a m m e e t i n g o n J u l y 2 8 th ( D r . D a v i s H e lle r not present). A total o f 6 0 a n im a l cases, ran g in g fro m a dead cray fis h to groups o f sick co w s, w ere evalu ated . Item s on the tapes that w e re n o t a n im a l related (e.g ., w a te r tre a tm e n t) w e re n o te d b u t n o t e v a lu a te d . T a b le 1 is a c o m p ila tio n o f th e re le v a n t a n im a l health data d e riv e d fro m these tapes. T h is table does n ot in clu d e m a n y assertions and eoo-i-' DUP 248 7 Tennant Farm Herd Health Investigation Cattle Team Report in te rp reta tio n s, m a d e b y the n a rra to r in the tapes, w h ic h the te a m m e m b e rs c o n s id e re d to be incom plete o r erroneous. 3.2.2. D ia g n o s tic P a th o lo g y R e p o rts T w o p ath o lo g y re p o n s (A p p e n d ix B ) w e re su p plied to the cattle te a m b y the steering co m m itte e . B o th w e re issued b y state a n im a l d iag n o stic lab o rato ries in response to the su b m issio n o f d ead a n im als or tissues fro m the T e n n a n t F a rm . T h e s e repo rts w e re re v ie w e d b y the cattle team . A th ird p a th o lo g y rep o rt (A p p e n d ix B ) w as p ro d u ce d su b seq u en t to the e le c tiv e sacrifice o f one an im al (# 3 7 ) on June 10, 19 99 . T h e cattle c o m m itte e d e c id e d , at a m e e tin g on M a y 2S. 1 9 9 9 , th at it w o u ld b e in fo rm a tiv e to h ave a to x ic o lo g y screen o n tissues fro m one or tw o o ld e r co w s. M r. T e n n a n t w as asked to select o n e o r tw o o f the cattle that he co n sidered to be in the w o rst co n d itio n . H e chose to sa crifice c o w # 3 7 . a 7 -y e a r o ld red c o w that had fresh en ed a fe w m o n th s earlier. T h is a n im a l w a s e u th a n ize d b y g un sh o t b y M r . T e n n a n t o n the fa rm on Ju n e 10, 19 9 9 . M r . T e n n a n t p e rfo rm e d the d is s e c tio n in the presence o f D r. D a v is -H e lle r. Tissu es w e re co llected (D r. D a v is -H e lle r) fo r h istop ath o lo g y and an alytical to xico lo g y. In d iv id u a l A n im a l P ath o lo g y R e p o rts Pathology Report j Date ! Name of Diagnostic Laboratory March 0. 199' | Animal Disease Diagnostic Laboratory. Ohio 1 Department of Agriculture. Re\noldsburg. OH March 2. 1997 Animal Health Diagnostic Laboratory, College of Veterinary Medicine. Michigan State University. Lansing MI July 5. 1999 1 Laboratory of Large Animal Pathology and Toxicology. New Bolton Center. University of ! Pennsylvania. Kennett Sauare. PA Case Material (case number' dead 6-month-o!d bull calf (#4977-97) tissues 4-year-old Holstein coyv (#1792571) tissues 9-year-old Holstein coyy (#1792571) tissues 7-vear-old coyy (#UP9902702: UP9901437) 3.2.3. A p ril 19 99 S ite V is it D a ta T h e cattle te a m v is ite d the T e n n a n t F a rm and ad jacen t D r y R u n la n d fill site o n A p ril 7 and 8. 1 9 9 9 in o rd e r to c o lle c t d ata an d b io lo g ic a l sam p le s re le v a n t to th e h e rd h ealth in vestig atio n . B e fo re p ro c e e d in g to the site on A p ril 7 th , a b rie f s a fety m e e tin g w as held at the P arkersb u rg H o lid a y In n d u rin g w h ic h the D ry R u n S a fe ty P lan (A p p e n d ix C ) w as re view ed . T h e 6 cattle team m em b ers, 2 o f the steering c o m m itte e m e m b e rs (C asp ar. H o rn e i and 2 U S F W S em p lo yees w ere present. A p ril 7, 1999 T h e cattle te a m had p lan n ed to inspect the fa rm and a d jac en t la n d fill, v ie w the herd g ra z in g , a n d in te r v ie w M r . T e n n a n t o n th e a fte rn o o n o f W e d n e s d a y A p r il 7 th. H o w e v e r , 000^,Vf> DUP 249 8 Tennant Farm Herd Health Investigation Cattle Team Report d u e to a m is u n d e rs ta n d in g , M r . T e n n a n t h ad c o rra lle d his e n tire h erd o n W e d n e s d a y m o rn in g . W h e n the cattle team and E P A /U S F W S p erso n n el arrived at a p p ro x im a te ly 3 :1 5 P M , the h erd had been co n tain e d in a s m a ll en clo su re , w ith o u t fo od o r w a te r, fo r several hours. T h e tea m th erefore elected to co n d u ct the in d iv id u a l a n im a l e x a m in a tio n s and sp ecim en co llection s im m e d ia te ly . A n e w h e a d -h o ld restraint device h ad b een in s talle d n ext to the en clo su re to fa c ilita te a n im a l h a n d lin g . M r . E a rl T e n n a n t an d his b ro th e r w e re v e ry h e lp fu l in h a n d lin g the c a ttle an d m o v in g th e m in to the re stra in t d e v ic e . T h e 41 adult cattle w ere in d iv id u a lly run into the ch u te, secured w ith the h ead h o ld and a h a lte r, a n d e x a m in e d . E a c h a d u lt (3 8 c o w s , 2 b u lls , a n d 1 ste e r) w'as g iv e n a g e n e ra l physical ex am in atio n inclu d in g observation o f gross ab n orm alities, g rad ing o f b o d y co n d itio n , and es tim atio n o f age based on the incisors. B lo o d w as co llected b y ju g u la r venip un ctu re (2 red top, 1 green top, and 1 lave n d e r top tubes) fro m each c o w and fecal sam p les w ere re cta lly co llected fro m each ad u lt. C o w s w e re re cta lly p alp a ted to d e te rm in e th eir p reg n an cy status. A ll e x a m in e d ad u lt a n im a ls received tw o e a r tags, one w ith an id e n tificatio n n u m b e r and o ne w ith an im p re g n a te d insecticide. O n e H e re fo rd c o w ( i . e . , t h e 3 9 Ih c o w , 4 2 nd a d u l t ) e s c a p e d t h e c h u t e p r i o r t o e x a m i n a t i o n , a g i n g , u t e r i n e p alp atio n , b lo o d co llection , and ear tagging. E ach adult b o vin e w as in d iv id u a lly p h o to g rap h ed and id en tified (A p p e n d ix D . photographs 1-42). O n ly 1 cow- (a n im a l # 2 2 ) received treatm ent - a m ass, m o st consistent w ith a d e rm o id cyst, w as incised and d rain ed (A p p e n d ix D , p h o to g rap h s 4 9 -5 1 ). A d d itio n a l p h o to g rap h s o f the fa rm (A p p e n d ix D . p h o to g rap h s 4 3 . 5 4 -5 8 ), in d iv id u a l a n im a l "le s io n s " o b s e rv e d on A p ril 7, 1 9 9 9 (A p p e n d ix D , p h o to g - ,phs 4 4 -4 8 . 5 2 , 5 3 ). p ho to grap hs su p p lied to the team b y M r. T e n n a n t (A p p e n d ix D , p hotographs 6 0 -6 5 ). and a p h o to g rap h o f cattle team and steerin g c o m m itte e m e m b e rs (A p p e n d ix D , p h o to g rap h 6 6 ) are also in c lu d e d in this report. Adult Cattle Procedures physical examination bodv condition scored ace estimation rectal precnancv examination cirth measurement fecal sample collection blood collection ear tapped: animal identification ear tapped: insecticide photographed T w e lv e ca lv es w e re e x a m in e d as a g ro u p . T h e s m a lle r seven re ce iv ed in s e c tic id a l ea r tags: the larg er fiv e re c e iv e d no ea r tags as M r . T e n n a n t in d ic a te d that th ey w e re to be sold in the v e ry n ear future. A lth o u g h the cattle tea m w as p rep ared to d o a p o s t-m o rte m e x a m in a tio n on o n e o r m o re cattle, the tea m d ecid ed that there w as no a n im a l s u ffic ie n tly ill to ju s tify eu th an asia and n ecrop sy at the tim e o f the visit. DUP 250 9 Tennant Farm Herd Health Inv estigation Cattle Team Repon A ll an im al b io lo g ical sam p les (b lo o d an d feces) w e re taken b a c k to N e w B o lto n C e n te r b y D r. H a b e c k e r. B lo o d sam p les w e re su b jected to h e m a to lo g y , se ru m c h e m is try , and se ro lo g y. R a n d o m ly selected fe c a l s a m p le s w'ere s u b je cte d to fecal flo ta tio n . T h e fo llo w in g clinical p ath o lo g y param eters w ere evaluated: H e m ato lo g y leukocvte itotal and differentia!) count "hematocrit ervthrocvte count "mean corpuscular hemoglobin hemoglobin concentration "mean corpuscular hemoglobin concentration mean corpuscular volume "red cell distribution width platelet count "platelet distribution width mean platelet volume "These parameters were calculated using the measured data. S e ru m C h e m is trv aspartate aminotransferase potassium gamma clutamvl transferase calcium creatine kinase chloride blood urea nitrogen magnesium creatinine phosphorus total protein copper albumin selenium "globulin pepsinogen sodium ""prolactin globulin '.'.a? calculated rrom the measured albumin and total protein data, prolactin wa> measured from blood plasma derived from EDTA tubes (lavender top). S erolo gy bovine leukemia virus >ei epizootic hemorrhagic disease of deer tagidi bov ine viru> diarrhea viru> !sn i M y c o b a c t e r i u m p a r a t u b e r c u l o s i s iJohne'si (e) bovine virus diarrhea virus mo i leptospirosis (sn) blue tongue virus iacidi brucellosis (sn) (e ) = elisa test, ism = serum neutralization test: imp) = microplate assay; (agid) = agarose gel immunodiffusion test A p ril 8. 1999 T h re e m em b ers o f the cattle tea m (D rs . M o is a n , M u n s o n , an d D a v is -H e lle r) m e t w ith M r. E a rl T e n n a n t and reco rd ed his re c o lle c tio n o f the 1 9 9 8 -1 9 9 9 h erd h ealth h is to ry (A p p e n d ix Ei. D rs. C asp ar and H o m e g ave all o f the cattle te a m m e m b ers a d riv in g to u r o f the p ro p erty b etw een the T e n n a n t barn and the D r y R u n la n d fill, in c lu d in g a d rive w ith in the lan d fill. D u rin g those tw o trips, the te a m m e m b e rs w e re able to see the c o n n e c tin g pastures. 0 0 Ov DUP 251 io Tennant Farm Herd Health Investigation Cattle Team Report adjacent creeks, n eig h b o rin g cattle g razin g , and w ild life . T h e lan d fill w as open and b e in g u tiliz e d at .the tim e o f the site visit. W h ile on site, the cattle tea m m a d e g en eral o b servatio n s re g a rd in g the e n v iro n m e n t, in clu d in g the flora, fauna, and m a n -m a d e structures. C o re sam p les o f three larg e round h ay bales w e re co lle cte d (3 s a m p le s /b a le ) fro m bales in the b a m yard . M r . T e n n a n t g ave the team so m e receipts (dates ran g ed fro m 2 /9 8 to 1 2 /9 8 ) fro m c o m p le te , m ix e d feed, and m ineral supplem ent he had purchased. A ll plant b io lo g ical sam ples (b aile d h ay co re sam ples an d g rain sa m p le ) w e re subjected to n u tritio n al analysis b y the F o ra g e T e s tin g L a b o ra to ry o f the N o rth C a ro lin a D e p a rtm e n t o f A g ric u ltu re (T a b le 7). T h ese data w e re used in an E x c e l spreadsheet p ro g ram (C N C P S v 3 .1 ) fro m C o rn e ll U n iv e rs ity to e v a lu a te the diets in tw o c o w m o d els u nder tw o feed in g situations (A p p e n d ix F, m o d els 1-4). T h e f o llo w in g n u tritio n a l p a ra m e te rs '.'ere e v a lu a te d : H a v an d G ra in A n alysis 1 drv matter i crude protein i unavailable protein 1 adjusted crude protein i acid detergent fiber , total digestible nitrogen NE (lactation) i calcium ! phosphorus i sodium ! magnesium 1 sulphur I potassium 1 copper I iron I manganese i zinc ! nitrate ion I selenium 1 3.2.4. M iscellan eo u s D ata D u rin g the site visit in A p ril. M r . T e n n a n t w as a s ke d to n o tify D r. L is a D a v is -H e lle r or D r. S arah C a s p a r if there w e re a n y fu ture signs o f d isease p ro b le m s in his h erd . T h e tea m w is h e d to c o lle c t w h a te v e r d ata m ig h t be re le v a n t to th e ir assessm en t o f th e h ealth status o f the T e n n a n t herd. B e tw e en A p ril S and D e c e m b e r 23, 1999. M r. T en n a n t co n su lted tw ice w ith D r. D avisH e ller. S ubseq uent to n o tify in g D r. C asp ar o f a n e w b o rn c a lf w h ic h w as b orn w ith a "c lo u d y e y e ". M r. T e n n a n t b ro u g h t the c a lf to D r. D a v is -H e lle r's clin ic (A p ril 21 . 1999). D r. D a v is -H e lle r e x a m in e d the c a lf and m a d e a d iag n o sis. M r . T e n n a n t left w ith the calf. O n M a y 26. 1999. D r. D a v is -H e lle r e x am in ed c o w # 3 0 fo r a lu m p u nd er the right m andible. 000 OUP 252 11 Tennant Farm Herd Health In\estimation Cattle Team Report 3.2.5. W ild life E P A and D u P o n t each sponsored e n v iro n m e n ta l studies that in clu d ed the tra p p in g o f sm all m a m m a ls in the g razin g fields o f M r. T e n n a n t's cattle. T h ese re p o n s w e re su p plied to the ca ttle te a m b y th e s te e rin g c o m m itte e . T h e d a ta in c lu d e d in these re p o n s , as it relates to sm a ll m a m m a l p a th o lo g y , w e re e v a lu a te d b y the ca ttle team . S m a ll M a m m a l S tu dies Reoort Date 1 Report Title November. 1997 (draft) Dry Run Creek: Washington, Wood County, West Virginia. USEPA Environmental Response Team December 3. 1998 (letter) Small Mammal Trapping Effort: Dry Run Landfill, Washington. WV (URS Greiner Woodward CKde studv) Animal Data Section Table 39: Results of Histopathology for the Meadow Vole Table 1: Data Summary. Small Mammal Investigation T h e cattle tea m w as also m ad e a w a re o f p erio d ic d eer re p ro d u c tio n su rveys c o n d u c te d b y D r. C ru m and associates o f the W e s t V irg in ia D e p a rtm e n t o f N a tu ra l R eso u rces ( W V D N R ) in the D ry R u n area, h o w e v e r n o re p o n s w e re a v a ila b le . 4.0 RESULTS 4.1. C a ttle 4.1.1. V id e o ta p e s (T ab le i) T w o vid eo tap es o f several hours d u ratio n w e re re v ie w e d . F o rty cattle scenes and 2 0 w ild life scenes w ere presented, d ep ic tin g n u m ero u s lesions. T h e in d iv id u a l scenes (i.e.. cases), alo ng w ith the cattle te a m 's d ia g n o s is /c o m m e n t, are presen ted in T a b le 1 in the o rd e r in w h ic h th e y w e re p resen ted in the v id e o ta p e s . T h e h e rd h ea lth p ro b le m s i d e n t i f i e d in. t h e s e v i d e o s w e r e s u m m a r i z e d a s f o l l o w s : 1. K e r a titis : C o rn e a ! u lc e rs , sc a rs a n d o p a c itie s , as w e ll as b le p h a r o s p a s m , w e r e o bserved in m a n y cattle. T h e s e w e re all c o n sid e re d to be m a n ife s ta tio n s o f " p in k e y e " , an in fe c tio u s k e r a to c o n ju n c tiv itis c a u s e d b y b a c te ria s u c h as More.xella bovis. T h e f a c e f ly i M itsca autumnalis) p r o b le m o b s e r v e d in th e s e v id e o s a n d th e lack o f effe ctive fly control w ere consistent w ith the diagnosis o f severe "p in k e y e " in these cattle. A ffe c te d y o u n g an d a d u lt cattle w e re o b s erv ed to h a v e 2 -3 to 2 5 -5 0 or m o re faceflies feeding at the m e d ia l canthus o f each eye and on the la c rim a l secretions. Fig u res 1 and 2 are p rints fro m vid eo tap e # 2 , illu stratin g the fa c e fly p ro b le m on a c a lf and her d am , resp ectively. B o th o f these an im als w e re b lin d fro m ch ro n ic kerato co n ju n ctivitis. F ig u re 3 (vid eo tap e # 2 ) dem onstrates an e a rly central co rn eal u lc er on the left eye o f a ca lf; fac eflie s are seen b y the lo w e r e y e lid . 00 0 DUP 253 Tennant Farm Herd Health Investigation Cattle Team Report 2. H a ir loss, n eck and ta il: T h e c e rv ic a l a lo p e c ia w a s m o s t co n sistent w ith a lice p ro b lem . T h e alo p e cia o b s erv ed o n the tails o f so m e cattle (e.g., loss o f "s w itc h ") m a y also h ave been due to lice, o r m a y h ave b een related to fescue m y c o to x ic ity . 3. P o o r sh ed d in g o f h air c o a ts : T h is c lin ic a l sign, m o s t p ro m in e n t in the late spring a n d s u m m e r s e g m e n ts o f th e v id e o ta p e s , is c o n s is te n t w it h m u ltip le n u tritio n a l d eficien cies as w e ll as fescue m y c o to x ic o s is . F ig u re 4 d em o n stra tes a c o w fro m vid eo tap e # 2 that w as d escrib ed b y M r . T e n n a n t as h a v in g d e la y e d sh ed d in g o f the w in te r coat. 4. H a ir d e p ig m e n ta tio n : T h e d is c o lo ra tio n o f the c a ttle h a ir co ats is a c h a n g e m o st o ften asso ciated w ith a n u tritio n a l d e fic ie n c y , an d is e s p e c ia lly c o m m o n in cases o f copper deficiency. 5. C o ro n itis : A lo p e c ia and e ry th e m a abo ve the c o ro n a ry b an d m a y be seen w ith fescue m y c o to x ic o s is . m e c h a n ic a l tra u m a , o r as a n o n -s p e c ific d e rm a titis . F ig u res 5 and 6 (vid eo tap e # 2 ) are represen tative o f the eryth em ato u s fo o t lesions observed by M r . T e n n a n t in m a n y o f his cattle. F ig u re s 7 an d 8 (v id e o ta p e # 2 ) ) d e m o n s tra te the c a ttle 's p refe re n c e fo r sta n d in g in the w a te r w h e n these lesions w e re present. Fescue m y co to x ic o sis (" fescue fo o t") w as considered the m ost lik e ly diagnosis o f this c o n d itio n . 6. " H u n c h e d u p " o r p a in fu l s ta n c e : T h is is a c lin ic a l sig n o fte n a s s o c ia te d w ith a b d o m in a l o r fo o t p ain , b u t has b een s p e c ific a lly d e s c rib e d as a m a n ife s ta tio n o f the fescue en d op h yte to xicity c o m p lex . T h in b o d v c o n d itio n : P o o r b o d y c o n d itio n is a n o n -s p e c ific fin d in g a n d the cases presented m ost lik e ly represented d ifferen t etio lo g ies. T h e em aciated dead c a lf w ith serous atro p h y appears to h ave starved w h ile others ap p e a r to h ave had d ia rrh ea o r m a stica tio n p ro b le m s . C o n s id e rin g the o th e r fin d in g s in this herd (e.g.. feed an alysis), n u tritio n al in s u ffic ie n c y (p ro te in -e n e rg y m a ln u tritio n ) w as also a likely c o n trib u tin g fac to r to p o o r b o d y co n d itio n . S o m e fin d in g s d esc rib ed in these tapes w e re d iffic u lt to e v a lu a te b y v id e o alth o u g h they p ro b ab ly w ere real. F o r e x a m p le , the d escrib ed "lu m p s " in a c o w u d d e r (case # 5 4 ) w as d iffic u lt to see b u t w o u ld be c o n s id e re d an in c id e n ta l fin d in g in a n y case. A fe w cattle w e re d esc rib ed as " h u n c h e d -u p " o r " h u m p e d -u p " (cases ff 1 ,5 , 17) - these m a y h ave b een related to lam eness, h a rd w a re disease (trau m atic re tic u lo p e rica rd itis), fescue m yco toxico sis, o r o ther co n dition . A n in d ivid u al c o w that w as slo bb erin g , losing cud. and u rinatin g (case # 1 3 ) m a y also h ave h ad h a rd w a re disease, alth o u g h the d iagn o sis w as not clear. A n o th e r in d ivid u al c o w (case # 4 5 ) w h ic h w as p an tin g w as consistent w ith fescue m y c o to x ic o s is (i.e.. " s u m m e r fes cu e" h y p e rth e rm ia ), a lth o u g h this p resen tatio n w as certain ly n on -sp ecific. OOOt DUP 254 3 Tennant Farm Herd Health Investisation Cattle Team Report 4.1.2. D iag n o s tic P ath o lo g y R e p o rts (A p p e n d ix B ) O n ly fo u r o f M r . T e n n a n t's cattle w ere su b m itte d fo r p o s t-m o rte m d iag n o stic ev a lu a tio n o f so m e type. T h e m o st s ig n ifican t fin d in g w as m o d e ra te to m a rk e d c o p p e r d e fic ie n c y in the three co w s a n a ly ze d fo r h e a v y m e tals. K e ra titis w a s o b s e rv e d in the o n ly a n im a l that w as fo rm a lly necropsied. T h is 6 -m o n th o ld b u ll c a lf a p p are n tly died fro m w in te r starvation (i.e., neg ative en erg y b alan ce o r p ro te in -e n e rg y m a ln u tritio n ) c o m p lic a te d b y u ntreated intestinal coccidiosis. T h e s e re p o n s are in c lu d e d in A p p e n d ix B ; s u m m a rie s are presented b elow : a. D e a d 6 -m o n th old b ull c a lf s u b m itted to the A n im a l D isease D iag n o s tic Laboratory. O h io D epartm ent o f A g ricu ltu re, R eyn old sb urg, O H on 2 /27 /97; L ab orato ry report dated 3 -1 0 -9 7 (A p p en d ix B ) H istory: G ross diagnosis: H is to p a th o lo g ic diagnosis: 6 -m o n th o ld b ull calf; u n d erw e ig h t; d iarrh ea fo r one m o n th ; received no m ed icatio n ; co rn eal opacities; d ie d . E m a c ia tio n w ith serous atro p h y o f fat Intestinal parasitism (trichuriasis) E nteric coccidiosis K eratitis, m oderate, ch ro n ic, fo callv extensive b. T issu es fro m a 4 -y e a r o ld H o ls te in c o w su b m itte d to th A n im a l H e a lth D iag n ostic L ab o rato ry. C o llege o f V e te rin a ry M e d ic in e . M ic h ig a n State U n iversity. L an sing M I on 3/4/9 7: L ab orato ry report dated 3 -1 2 -9 7 (A p p e n d ix B ) H istory: 4 -y e a r o ld H o ls te in c o w ; d ied 2 -1 S -9 7 ; dissected by o w n e r; tissues s u b m itte d b y E P A H e a v y m etal screen: C o p p e r d e fic ie n c y in liv e r ( 1.9 p p m vs. 2 5 -1 5 0 reference range) and kid ney (2.37 p p m vs. 4 - 6 p p m reference range). M a n g a n e s e w a s m a rg in a lly lo w in liv e r; c a d m iu m w as slig h tly increased in the kid n e y. N o h e a v y m e tals fo u n d in u rin e (u rin e flu o rid e w as 6.6 u g /m l)[re fere n c e range: toxic if 14 p g /m L ] c. T issu es fro m a 9 -y e a r o ld H o ls te in c o w s u b m itte d to the A n im a l H e a lth D iag n ostic L ab o rato ry. C o llege o f V e te rin a ry M e d ic in e . M ic h ig a n State U n iv e rs ity . L an sing M I on 3/4/9 7; L ab orato ry report dated 3 -1 2 -9 7 (A p p e n d ix B ) H istory: 9 -v e a r o ld H o ls te in c o w ; d ied 3 -2 -9 7 ; dissected b y o w n e r; tissues s u b m itte d b y E P A ta DUP 255 Tennant Farm Herd Health Investigation Cattle Team Report H isto p ath o lo g ic diagnosis: (o n ly heart, liver, and k id n e y s su b m itted : autolvsis and freeze/th aw artifact) M y o c a rd ia l sarcocysts Heavy m e ta l s c re e n : C o p p e r d e ficien cy in liv e r (2 .0 3 p p m vs. 2 5 -1 5 0 reference range) and kid n e y (2.33 p p m vs. 4 - 6 p p m reference range). M a n g a n e s e w as m a rg in a lly lo w in liv er; iro n w as elevated in the liver; c a d m iu m w as slig h tly increased in the k id n e y . U rin e h eavy m etals w ere n o rm al (u rin e flu o rid e w as 5.55 u g /m l)[referen ce range: toxic if > 14 u g /m L ] C linical pathology: N o significant findings d. Tissues fro m a 7 -y e a r o ld red c o w (eu th an ize d on 6 /1 0 /9 9 an d dissected b y M r. T e n n a n t i su b m itted to the L a b o ra to ry o f L a rg e A n im a l P a th o lo g y an d T o x ic o lo g y . S chool o f V e te rin a ry M e d ic in e . U n iv e rs ity o f P en n sylvan ia. K e n n ett S q uare, P A on 6/27 /99: Laboratory report dated 7 -5 -9 9 (A p p en d ix B ) H istory: 7 -y e a r old red c o w ; e u th a n ize d 6 -1 0 -9 9 ; dissected by o w n e r: tissues s u b m itte d b v D r. D a v is -H e lle r. H isto p ath o lo g ic diagnosis: E n teric lesions o f m in im a l sig n ifican ce (fo res to m ach abscesses', in te s tin a l c o c c id io s is ; m y o c a rd ia l sarcocysts). H e a v \ m etal screen: C o p p e r d e fic ie n c y in liv e r (7 .7 1 p p m vs. 2 5 -1 5 0 reference range). 4 .1 .3 . A p r il 1 9 9 9 S ite "Visit D a ta a. H e rd H is to ry (A p p e n d ix E ) T h e herd history (A p p e n d ix E ) w as based on M r. T e n n a n t's re co lle ctio n s d u rin g the in te rvie w on A p ril 8, 1999. A w ritte n record o f herd health w as co n sp ic u o u sly absent. M u c h o f this c a n be a ttrib u te d to th e la c k o f o u ts id e in te rv e n tio n . T h e re is n o re c o rd o f veterin ary care o r co n su ltatio n w ith an a n im a l n utritionist. M in im a l m e d ic a tio n s have been used on these anim als, and there has been no use o f vaccin es o r m o d e rn d ew o rm ers. E x c e p t fo r the fe w a n im a ls n o te d in this d o c u m e n t (see D ia g n o s tic P a th o lo g y R e p o n s , ab o ve), no d ia g n o stic la b o ra to ry tests w e re d o n e on d ead a n im a ls . T h e le v e l o f cattle herd m a n a g e m e n t has not ch an g ed since the installation o f the lan d fill. 000 DUP 256 15 Tennant Farm Herd Health Investigation Cattle Team Report b. P h ysical E x a m in a tio n (T a b le 2) A g e. Pregnancy Status O n A p ril 7, 19 9 9 , the cattle tea m e x a m in e d 41 an im als, in c lu d in g 3 8 ad u lt co w s, 2 adult bulls, and 1 ad u lt steer (T a b le 2). E s tim a te d ages fo r th e a d u lt c o w s ra n g e d fro m 4 to g rea ter th an 9 y e a rs . T h is is a h e rd o f a g e d c a ttle ; 3 2 o f th e 3 8 c o w s w e re e s tim a te d to be o ld er that 9 years. T w e n ty -s e v e n (2 7 /3 8 ) co w s w e re p reg n an t. B o d v C o n dition Scores B o d y co n d itio n scores (B C S ) w e re based on a 1-9 scale. S cores ran g ed fro m 2 to 7; the a v e ra g e sco re w a s 3 .5 (3 = th in , 4 = b o r d e r lin e , 5 -7 is c o n s id e re d o p tim u m ). C lin ica l Signs H a irc o a t a b n o rm a litie s w e re e v id e n t in 9 o f the 41 cattle. O n e a n im a l h ad an e p id e rm a l inclusion cyst that w as lanced and em p tied . M a m m a ry g la n d lu m p s , consistent w ith ch ro n ic m astitis, w e re in te rp rete d as abscesses o r a c c u m u la tio n s o f fib ro u s c o n n e c tiv e (s c a n tissue. R e ctal e x a m in a tio n o f o ne c o w suggested the p res en ce o f in tra -a b d o m in a l fat necrosis. c. C lin ic a l P a th o lo g y (T a b le s 3 - 6; G ra p h 1) H em atology E r y t h r o n ( T a b l e 3 >: R e d b l o o d c e l l i n d i c e s w e r e g e n e r a l l y i n t h e l o w - n o r m a l r a n g e . N o anim ais w ere co n sidered an em ic. L e u k o n ( T a b l e 4 : T h e t o t a l w h i t e b l o o d c e l l c o u n t s w e r e w i t h i n t h e n o r m a l r a n g e . D iffe re n tia l cell co u nts w e re co n sid ered in v a lid due to the 3 6 h o u r d e la y b e tw e e n co llectio n and testing. C linical chem istry (T a b le 5 1 M o s t elec tro lyte valu es w e re in the h ig h -n o rm a l to s lig h tly e le v a te d ran g e, co n sistent w ith m iid d e h yd ratio n . S in ce the cattle w e re p en ned d u rin g the d a y lig h t h ours o f A p ril 7. w h ic h w as u n s eas o n a b ly w a rm , and had no access to w a te r, c lin ic a l d e h y d ra tio n w as not u n e x p e c te d . D e h y d r a tio n is also the m o s t lik e ly e x p la n a tio n fo r th e e le v a te d c re a tin in e in 4 0 /4 1 cattle. M o s t (2 7 /4 1 ) o f the cattle had e lev ate d total p ro tein, w h ic h also co rrelates h ig h ly w ith a d iagnosis o f d e h y d ra tio n (to tal p ro te in = g lo b u lin fra ctio n + a lb u m in fra c tio n ). In all cattle (4 1 /4 1 ) the g lo b u lin fractio n w as elevated w h ile the a lb u m in fra c tio n w as w ith in the referen ce range. 0G0 .r'; DUP 257 16 Tennant Farm Herd Healrh Investigation Cattle Team Report G a m m a g lu tam yltran s fe ra se (G G T ), a sensitive in d ic a to r o f active liv er disease, w as consistently w ith in the n orm al referen ce range. C reatin e kin ase (C K ), an in d icato r o f m u scle necrosis, w as also n o rm a l in all o f the cattle. H o w e v e r, aspartate a m in o tra n s fe ra s e (A S T ) , a less s e n s itiv e in d ic a to r o f liv e r a n d m u s c le d e g e n e ra tio n , w a s m in im a lly e lev ate d in 3 3 /4 1 cattle. T h is m ig h t be fro m le u k o c y te d isso lu tion , the result o f the 3 6 h o u r in terval b e tw e e n b lo o d c o lle c tio n an d testing. S pecial chem istry P rolactin: P las m a p rolactin levels (T a b le 4 and G ra p h 1) w e re s ig n ifican tly depressed. A c c o rd in g to the testing lab o rato ry (D r. N e a l S c h ric k , U n iv e rs ity o f T en n e s s e e ), an averag e p ro la ctin level fo r cattle on fes cu e-fre e p asture (fo r A p ril) w as 1 7 1 .6 m ic ro g ra m s /lite r (n g /m L ) (i.e.. referen ce m e a n = 1 7 1 .6 n g /m L ). T h e av erag e o f the 41 T e n n a n t sam p les w as 110.1 n g /m L an d 3 6 /4 1 o f the T e n n a n t cattle w ere b e lo w the reference m ean (1 7 1 .6 n g /m L ). In contrast, an averag e p ro la ctin level fo r cattle on en d o p h yte-in fected fescue (sim u lated b y erg o tam in e tartrate ad m in istratio n ) w as 105.8 n g /m L (data fro m D r. S ch rick). T h is av erag e w as s im ila r to the T e n n a n t h erd av erag e (1 1 0 .1 n g /m L ) and 2 4 /4 1 o f the cattle w e re b e lo w this re fe re n c e level (1 0 5 .8 n g /m L ). A c c o rd in g to D r. S c h ric k . these fin d in g s w e re h ig h ly s u p p o rtiv e o f e n d o p h y te to x ic ity in the T e n n a n t herd. C o p p e r: B lo o d c o p p e r lev els w e re in the d e fic ie n t ra n g e fo r 2 6 o f 41 a n im a ls : o n e co p p e r assay w as b e lo w the lim it o f detectio n . S e le n iu m : B lo o d s e le n iu m levels w e re n o rm a l fo r 41 o f 41 cattle. P ep sin og en : P ep sin o g en , a b lo o d e n z y m e in d icato r o f p arasite d am a g e to the a b o m a s u m , w as m e as u red in 10 c o w s , o ne steer an d o n e b u ll. A ll valu es w e re w ith in the n o rm al referen ce range. T h ese data su p po rted the co n clu s io n that ab o m asal ostertagiasis w as not a p ro b le m in ad u lt cattle in this herd. S erolo gy (T ab le 6) B L V (B o vin e L eu kem ia V iru s) J o h n e 's (Mycobacterium pararuberculosis a n tig e n ) B ru cella B V D (B o v in e V iru s D iarrh ea antigen) B V D M ic ro p la te A ssay (v ire m ia detectio n ) B luetongue L ep to sp ira interrogans (5 subvarieties) E H D type 2 (E p izo o tic H e m o rrh a g ic D isease o f deer) 1/41 p o s itiv e 1/14 p ositive 0 /4 1 2/41 positive 0 /4 1 0 /4 1 3/41 positive 2 /12 positive N o n e o f the se ro lo g y values suggested a h e rd -w id e p ro b le m . P o sitive titers fo r B V D and L e p to s p ira m ig h t reflect residual va cc in atio n titers in p u rch ased an im als o r n atu ral ex p o su re to these diseases. T h e discovery' o f tw o p o s itiv e E H D titers w as e v id e n c e that this disease has b een in the lo c al d e e r p o p u la tio n . Qw DUP 258 17 Tennant Farm Herd Health Investigation Cattle Team Report P arasito lo g y R o u tin e fecal flo ta tio n (T a b le 4 ) re ve aled parasite o v a in 11 o f 14 ra n d o m ly selected fecal sam p les. T h e m a g n itu d e o f o v a sh ed d in g c o u ld be c a te g o rize d as rare to m o d e ra te . Parasite g roups in c lu d e d co cc id ia, ta p e w o rm s , and s tro n g y le -ty p e n e m a to d e s . In te stin a l p arasitism w as not co n sid ered to be a m a jo r herd p ro b le m in the ad u lt cattle. T h e s h e d d in g o f s m a ll n u m b e rs o f o o c y s ts a n d h e lm in th o v a is e x p e c te d o f m a tu r e ca ttle . d. Hay and Grain Analysis (Table 7) D u rin g the cattle te a m 's v isit to the T e n n a n t fa rm (4 /8 /9 9 ), M r . T e n n a n t w a s in te rv ie w e d re g a rd in g h erd fe e d in g practices. T h re e larg e ro u n d bales o f h a y in th e b a rn y a rd , id e n tifie d as re p re s e n ta tiv e o f the h e rd 's fo ra g e , w e re v is u a lly in s p e c te d a n d c o re s a m p le s (3 /b a le ) w ere co lle cte d fo r analysis. T h is fo rag e (i.e., h ay, g rass/fescu e) w a s fed ad lib itu m . D u rin g the site v isit, fo ra g e q u a lity w a s s u b je c tiv e ly e v a lu a te d as p o o r. T h e fib e r le v e l o f the h ay ap p eared to be h ig h and fo ra g e an alysis (T a b le 7 ) later su b stan tiated th at o bservation. F ib e r levels o f fo rag e p la y an im p o rtan t ro le in d e te rm in in g h o w m u c h o f a fe e d can be c o n s u m e d . D r y m a tte r in ta k e ( D M I ) is in v e rs e ly re la te d to fib e r le v e ls . A c c o rd in g to M r . T e n n a n t, m a tu re a n im a ls , o n the T e n n a n t fa rm , w e re also fe d fiv e pounds per head p er d ay o f a grain m ix co m p o sed o f d ry ear corn, so yb ean m e al, and m in erals (rate co u ld n ot be v a lid a te d , d esp ite the existen ce o f g rain receip ts). A sam p le o f this feed w a s ta k e n an d a n a ly z e d . A n E x c e l spreadsheet p ro g ra m (C N C P S v 3 .1 ) fro m C o rn e ll U n iv e rs ity w a s used to ev alu ate the diets. U s in g th e fo ra g e an d g ra in n u tritio n a l an alysis c o n d u c te d b y th e F orag e T estin g L ab o rato ry o f the N o rth C a ro lin a D e p a rtm e n t o f A g ric u ltu re (T a b le 7), tw o m o d els fo r m a tu re co w s (e a rly lacta tio n and d ry p reg n an t) w e re selected to e x a m in e the cu rren t fee d in g p ro g ra m (A p p e n d ix F ). A c c o rd in g to the c o m p u te r m o d e ls , a c o w in e a rly la c ta tio n (m o d e l # 1 ) in th e sp rin g o f 1 9 9 9 fed fiv e p o u n d s o f this g ra in an d fre e ch o ic e h a y w a s in seve re n e g a tiv e e n e rg y b alan ce (7 2 .5 % o f re q u ire m e n t) a n d less severe p ro te in d e fic ie n c y (9 0 .9 % o f re q u irem en t). T h e lim ite d n utrients a v a ila b le w o u ld h a v e a n e g a tiv e im p a c t o n m ilk p ro d u ctio n , p ersisten cy o f p ro d u c tio n , an d c a lf g ro w th . A c o w u n d e r this fe e d in g system w o u ld req u ire 2 .4 tim es the co rn c u rre n tly b ein g fed to b e is o c a lo ric (m o d e l # 2 ). S im ila rly , a d ry p re g n a n t c o w (m o d e l # 3 ) in the sam e fe e d in g s y s te m w o u ld also b e in n egative en erg y b alan ce (7 5 .2 % o f re q u ire m e n t) but not d e fic ie n t in p ro tein (1 2 5 % ). T h e sam e d ry p reg n an t c o w m a x im iz in g d ry m a tte r in take (m o d e l # 4 ) w o u ld still b e in neg ative en erg y b alan ce (8 7 .7 % ). 0 0 0 '-'c. ? DUP 259 18 Tennant Farm Herd Health Investisation Cattle Team Report T h e b od y co n d itio n scores (B C S s ) o f the herd w e re consistent w ith the en erg y d eficit o f the diets. T h e im p a c t o f the p o o r q u a lity fo ra g e o n this fa rm and su b seq u en t e n e rg y deficits w e re co n sid ered to h ave ch ro n ic effects w e ll afte r the co w s return to adequate pasture. 4.2. M is c e lla n e o u s D a ta F o llo w in g the site visit. M r . T e n n a n t c o n su lte d w ith D r. D a v is -H e lle r re g a rd in g a suspected sick a n im a l. M r . T e n n a n t b ro u g h t a c a lf w ith a "c lo u d y e y e " to D r. D a v is H e lle r's clin ic (A p ril 21, 1999). D r. D a v is -H e lle r e x a m in e d the c a lf and d e te rm in e d that there w as n o th in g w ro n g w ith the eye, ex ce p t fo r a slig h t m u c o id exu d ate on the co rn ea w h ich w as easily w ip e d aw ay. O n M a \ 26. 1999. D r. D a v is -H e lle r e x a m in e d c o w # 3 0 fo r a lu m p u nder the right m an d ib le. T h e lesion w as aspirated (p us) and su b seq u en tly lanced. 4.3. W ild life 4 .3 .1 . V id e o ta p e s (T a b le 1) T h e 2 0 w ild life cases presen ted in the vid eo tap es w e re all d ead and. ex ce p t fo r o n e case (case = 4 9 ). o f no d iag n o stic value. T h e s e w e re all co n sid e re d to be in c id en tal deaths since there d id not a p p e a r to be an y c o n s is te n c y in the sp ecies. lo c atio n , o r tim in g o f the deaths. In fact, these deaths ap p eared to be m ost con sistent w ith the ra n d o m w ild life carcasses w h ic h w o u ld be fo u n d in a h e a lth y eco system . T h e in d iv id u a l d ead d e e r (case # 49.) w h ic h p re s e n te d w ith h e m o rrh a g e fro m the n o s trils m a y h a v e d ie d fro m e p iz o o tic h e m o rrh a g ic disease (E H D ). T h is d iagn o sis w o u ld co rres p o n d w ith the k n o w n existen ce o f this disease in lo c a l d e e r (p e rs o n a l c o m m u n ic a tio n : D r. C r u m to D r. S y k e s ) an d the fin d in g o f so m e E H D se ro p o sitive cattle in the T e n n a n t herd. 4.3.2. S m a ll M a m m a l D a ta T w o p ath olo gists re v ie w e d the liv e r and k id n e y h is to lo g y fro m 45 sm all ro dents (vo les, sh rew s, and m ic e ) cap tu red on the T e n n a n t p ro p e rty in 1 9 9 7 (U S E P A E n v iro n m e n ta l R esponse T e a m d raft report: D ry R u n C reek . W a s h in g to n , W o o d C o u n ty, W e s t V irg in ia ; T a b le 39). N o lesions characteristic o f h ep ato to x ic ity o r n ep h ro to xicity w ere evid ent. A lth o u g h several an o m alies w ere id entified , none w ere considered suggestive o f toxic te ra to g e n e s is . T h e 1998 sm all m a m m a l trapping (U R S G re in e r W o o d w a rd C ly d e study, D e c e m b e r 3, 1 9 9 8 ) o b s erv ed no gross a b n o rm a litie s in the c a p tu re d a n im a ls (vo les, sh rew s, and m ic e ). 4.3.3. Deer Studies T h e cattle te a m w as m ad e aw are o f the p erio d ic d e e r re p ro d u ctio n surveys co n d u cted b y the W e s t V irg in ia D e p a rtm e n t o f N a tu ra l R e so u rce s ( W V D N R ) in the D ry R u n area. A lth o u g h the te a m re v ie w e d so m e o f the d ata sheets fro m these studies, n o reports w e re a v ailab le . O n e te a m m e m b e r (S y k e s ) had a telep h o n e co n versa tio n w ith D r. C ru m o f the DUP 260 19 Tennant Farm Herd Health Investigation Cattle Team Report W V D N R re g a rd in g d eer h erd h ealth in the D r y R u n area in o rd e r to ac q u ire so m e a d d itio n a l in fo rm a tio n . F ro m this c o n v e rs a tio n , it w as the c a ttle te a m 's u n d e rs ta n d in g that: - ev id e n c e o f lo w fe rtility rates in y o u n g does w as p ro b a b ly attrib u ta b le to d eer o v e rp o p u la tio n ; - ep izo o tic h e m o rrh a g ic disease (E H D ) has been d ia g n o sed c lin ic a lly and s e ro lo g ic a lly in d ead an d ca p tu re d d eer, re sp ec tiv ely; - b ovin e virus d iarrh ea ( B V D ) has been d iag n o sed se ro lo g ic ally in d eer not far from D ry Run; In ad d itio n , the team has learn e d that o u tb re aks o f E H D in W e s t V irg in ia d e e r w e re reported betw een 1980 and 19S9 [S outheastern C o o p erative W ild life D isease S tu d y p u b lic a tio n . F ie ld M a n u a l o f W ild life D iseases in the S o u th eastern U .S ., 2 n d ed .]. S ince there w as no evid en ce o f an E H D o r B V D o u tb re ak in the T e n n a n t h erd , the deer p o p u latio n w as not co n sidered to be a c o n trib u tin g facto r in the cattle h erd h ealth p ro b lem s. A lso , there w as no ev id e n c e that the d eer herd w as a useful sentinel species fo r a n v o f the disease entities id e n tifie d in the T e n n a n t herd. 5.0 DISCUSSION T h e six veterin arians c o m p ris in g the cattle te a m ag reed that there w as c o n c lu s iv e e v id e n c e that the T e n n a n t h erd w as s u ffe rin g fro m fo u r m a jo r disease en tities: en d o p h y te to xicity, p in keye, m aln u tritio n , and co p p e r d eficien cy. T h e clinical, lab o rato ry, and h istorical data substantiate that these fo u r co n d itio n s can re ad ily account fo r the ch ro n ic herd health p ro b lem s on the T e n n a n t farm . E n d o p h vte toxicitv A c c o rd in g to the h is to ry a c q u ire d o n A p ril 8. 1 9 9 9 . the h erd has been fed a d ie t o f K Y fescu e h a y in the w in te r an d p astu re th at a p p ro a c h e s 1009c K Y 3 1 fes cu e d u rin g the su m m er. T h e re has been no s u p p lem en tal pasture o r o th er forage fed to these anim als. T h e c lin ic a l signs in the T e n n a n t h erd that h ig h ly suggest en d o p h y te to x ic ity (fes cu e m y co to x ic o sis) include: s w e llin g and p ain at the c o ro n a ry b a n d (c o ro n itis ) and ab o v e , w ith ca ttle that stand in the creek d u rin g hot w e a th e r (F ig u re s 5 -8 ); p o o r shedding o f w in te r coats (F ig u re 4); p atch y tail alo p e cia w ith loss o f tail sw itch ; birth o f u nd ersized calves; p o o r co n cep tion and c a lv in g rates: n u m ero u s va g u e diseases su g g e stive o f im m u n e d y s fu n c tio n ; <> DUP 261 2 Tennant Farm Herd Health Investigation Cattle Team Report O th e r clin ical signs that are consistent w ith e n d o p h y te to x ic ity include: fat necrosis, p re s u m p tiv e , as d ia g n o s e d b y rectal p a lp a tio n in c o w # 1 5 ; con co m itan t presence o f co p per deficiency; . p an tin g in c o w # 4 5 , suggestive o f h yp erth erm ia; general failu re o f the cattle to th rive. V a s o c o n s tric tio n is seen as a re s u lt o f in g e s tio n o f a n u m b e r o f e r g o t-lik e a lk a lo id s . T h e e n d o p h y te fu n g u s a s s o c ia te d w it h fe s c u e m y c o to x ic o s is is Acrem onium coenophialum w h ich produces p erlo lin e, p erlo lid in e, N -a cety l lo lin e, an d N -fo rm y l lo lin e (S tu ed em an n . et al.. 1985). T h e s e alka lo id s a c c u m u la te in the fescu e grass seed d u rin g g ro w th , acqu iring the h ighest co n cen tratio n s at the greatest m a tu rity o f the grass. A d d itio n a lly , the alk a lo id s m a y b e fo u n d in sto red hay. T h e co ro n itis p ro b le m o b served in the vid eo tap es (F ig u re s 5 an d 6 ) w as ty p ic a l o f that p ro d u ced b y e n d o p h y te to x ic ity in the " fescue fo o t" s y n d ro m e . S ig n s o f fescue foot g e n e ra lly start w ith re d u c e d w e ig h t g ain , o r loss o f w e ig h t, ro u g h h a ir co at, a rch ed b a c k , and soreness in o n e o r b o th re a r lim b s . H y p e re m ia o f th e c o ro n a ry b a n d o c c u rs b e tw e e n the d e w c la w s a n d h o o v e s an d is g e n e ra lly a c c o m p a n ie d b y s o m e s w e llin g ( H e m k e n . et al.. 19S 4). A rc h in g o f the b ack w as re p o rte d b y the o w n e r in the vid e o ta p e s as "h u n c h e d " and " h u m p e d " p osture in so m e cattle. P erip h eral va s o c o n s tric tio n fro m these vaso ac tiv e a lk a lo id s results in d ecrea sed a b ility to d is sip a te h eat d u rin g h o t w e a th e r. T h is p h e n o m e n o n is k n o w m as " s u m m e r s lu m p " (O sb o rn e , et al.. 1 9 9 2 T h e p an tin g and d ro o lin g b y a red c o w (# 4 5 ) in v id e o ta p e # 2 w as suggestive o f the s u m m e r slu m p synd ro m e. T h e b irth o f u n d ersized calves to darns ing estin g a d iet h ig h in e n d o p h y te -in fe s te d fescue has also b een d o c u m e n te d (B o lt, et al.. 1 9 8 6 ). T h is m a y b e b y a m e c h a n is m s im ila r to the va so co n strictio n caused b y the e rg o t-lik e alkalo id s. V a s o c o n s tric tio n o f the uterine b lo o d vessels m a y result in decreased circ u la tio n to the g ro w in g fetus. T h e e ffe c t has been d o c u m e n te d in m ic e that w e re exp o sed to the e n d o p h y te d u rin g g estatio n . M o u s e pups fro m fem ales fed the m a teria l d u rin g gestation w e re a lig h te r b irth w e ig h t, w ere d elay ed in p o s t-p a rtu m d e v e lo p m e n t, and g re w s lo w e r th an co n tro l m ic e (V a rn e v , et al., 1 9 9 1 i. E v id e n c e th at e n d o p h y te to x ic ity in fescu e g ra z in g c a ttle m a y b e re s p o n s ib le fo r the loss o f the tail s w itc h is la rg e ly a n e c d o ta l, fro m v e te rin a ry p ra c titio n e rs th at h a v e e x p e rie n c e w ith s im ila rly a ffe cted cattle. T h e m o st severe fo rm s o f e n d o p h y te -in d u c e d vaso co n strictio n result in d ry g an g ren e o f the tail an d d ig its (R a d o stits, et al., 1994: H e m k e n . et al., 19S 4). R e p ro d u ctive effects fro m the ing estio n o f e n d o p h y te -in fe s te d fescue in c lu d e in c re m e n ta lly d ep res se d c o n c e p tio n rates in cattle g ra z in g in fe c te d p astu re (P ate rs o n , et al.. 1 9 9 5 ). In the T e n n a n t h erd , th e g razin g o f pastures w ith 1 0 0 % K Y 3 1 fescu e co u ld p o te n tia lly p la y a m a jo r role in the u n a cce p ta b le c o n c e p tio n rate. A p o o r c o n c e p tio n rate DUP 262 21 Tennant Farm Herd Health In\esusation Cattle Team Report c o u ld also be s e c o n d a ry to a la c k o f in te n s iv e b re e d in g m a n a g e m e n t at the T e n n a n t fa rm , w h e re b re e d in g occurs year ro u nd . T h e a d v a n c e d age o f m o s t an im als in the b re e d in g h erd c o u ld also b e e x p e cte d to be a cause fo r d ep ressed fe rtility an d an e x te n d e d c a lv in g in te rva l. I.ik e lv . a c o m b in a tio n o f all th ree facto rs h a v e c o n trib u te d to s u b o p tim a l fe r tility . T h e p oo r g ro w th o f the nursing calves c o u ld be m u ltifa c to ria l as w ell. T h e ad van ced age o f the co w s or a lim ite d genetic p o te n tial in the h erd c o u ld lead to p o o r m ilk p ro d u c tio n and p o o r c a lf g ro w th . S im ila rly , lack o f p ro p e r n u tritio n o r a lack o f a b alan ce d diet am o n g the b ro od cow s could depress c a lf g ro w th . T h e in g estio n o f en d o p h yte-in fested fescue c o u ld lead to depressed m ilk p ro d u c tio n d u e to p ro la c tin in h ib itio n (H u rle y , et al.. 1 9 8 0 ; P ate rs o n , et al.. 1 9 9 5 ). T h e m e c h a n is m is c o n s id e re d to be d u e to the d o p a m in e rg ic effects o f the en d o p h yte e rg o p ep tid es on p ro la c tin p ro d u ctio n in the b o v in e p itu itary gland (S ch u ltze . et al.. 19 99 ). E n d o p h y te in to x ic a tio n is ,also c o n s id e re d to h a v e an im m u n o s u p p r e s iv e e ffe c t b y an ap p aren tly ind irect route. A lth o u g h an ecd o tal e v id e n c e exists to suggest that fescue in to x ic a tio n is re s p o n s ib le fo r d e p re s s e d im m u n e f u n c tio n , th e re a p p e a rs to b e n o ap p arent lack o f im m u n e response to v a c c in a tio n s o f ca ttle fed diets h ig h in fescu e (R ic e , et al.. 1 9 9 7 ). In d ire c tly , h o w e v e r , th e re is a r e la tio n s h ip b e tw e e n im m u n e fu n c tio n , en d o p h yte in to xica tio n and co p p er status o f cattle on a h ig h fescue diet (D e n n is , et al.. 1 9 9 S ; S a k e r . e t a l . . 1 9 9 8 1. S t e e r s g r a z i n g e n d o p h y t e - i n f e s t e d t a l l f e s c u e h a v e l o w e r seru m co p p e r co n cen tratio n s than those not on a h ig h -e n d o p h v te tall fescue diet, resu ltin g in d e p re s s e d m o n o c y te -m a c ro p h a g e fu n c tio n s . T h is is a p p a re n tly an e ffe c t o f th e decreased u ptake o f co p p er b y the in fected tall fescue p lants. A n o th e r source has re co rd ed d ep ressed g lo b u lin levels in a n im a ls g ra zin g in fe c te d pastures (S c h u ltz e . et a!.. 1999). F a t n e c ro s is is a h e rd p ro b le m o f c a ttle g r a z in g ta ll fe s c u e w ith h ig h e n d o p h y te le v e ls . T h e necrotic fat accu m u latio n s are m o s tly w ith in the o m e n ta l an d re tro p e rito n ea l fat depots, and consist o f hard m asses o f p artly m in e ra liz e d fat. C o w = 15 had p alp a b le m asses w ithin the ab d o m in al ca vity that w e re id e n tifie d d u rin g the herd e x a m on A p ril 7. 1999. T h e se m asses w ere m ost su g gestive o f m asses o f n ecro tic fat. T h e b io c h e m ic a l re a c tio n c a u s in g th e fat n ecro s is is u n c le a r, h o w e v e r , in a ffe c te d a n im a ls th a t are o n a d ie t h ig h in N -fo r m y l an d N -a c e ty l lo lin e . th e re is a c o n s is te n t re d u c tio n o f c irc u la tin g le v e ls o f ch o lestero l (S tu e d e m a n n . et al.. 19 8 5 ). A n im a ls w ith in creased d ie tary levels o f e n d o p h y te -in fe c te d fescue had d ecreased b o d y c o n d itio n and increased fat necrosis. P inkeve F a c e flie s w e re a serious p ro b le m in the cattle in the v id e o ta p e d re co rd in g s ta k e n o n the T e n n a n t fa rm (F ig u res 1 and 2). A d d itio n a lly , th ey h a v e also b een a p ro b le m in o th er years, a c co rd in g to the h istory p ro v id e d b y M r . T e n n a n t d u rin g the A p ril 8, 19 9 9 in te rv ie w . F ace flie s w ere seen in sm all n u m b e rs at the eyes o f the cattle d u rin g the A p ril 7. 19 99 herd visit, representing an e a rly sp rin g in festatio n . T h e fac efly, Musca ciuuunnalis. is a v e c t o r fo r M oraxella bovis. th e e t io lo g y o f m o s t b o v in e p in k e y e . C o n t r o l 0 0 0 c .- DUP 263 Tennant Farm Herd Health Investigation Cattle Team Report o f th ese in s e c ts is b a s e d o n p r e v e n tin g th e flie s f r o m fe e d in g o n th e la c r im a l s e c re tio n s o f the cattle. Insecticid es and in s ec tic id al ea r tags, as a p p lie d d u rin g the visit, are effe c tiv e c o n tro ls . S e c o n d a r ily , th e in s e c tic id e s te n d to lim it th e s p re a d o f M. bovis b e tw e e n susceptible cattle d u rin g o u tb re aks o f p in k e y e . S evere fac efly infestations can result in p o o r feed c o n s u m p tio n and co n versio n a m o n g affected cattle. S o m e o f the p o o r w e ig h t g ain d escrib ed in the h is to ry o f the h erd and the vid eo s m a y be d u e to " fly w o rry " T h e m a n ic s ta m p e d in g o f the cattle, that w a s d esc rib ed in o ne o f the v id eo tap es , w a s lik e ly d u e to the larg e n u m b e r o f flies. M aln u tritio n M a ln u tritio n w as co n sid ered to be a s ig n ific a n t p ro b le m in the T e n n a n t h erd . T h e o w n e r had id e n tifie d p o o r g ro w th rates an d in fe rtility as sp ecific p ro b le m s a m o n g his cattle. T h is w as co n sid e re d a m a n ife s ta tio n o f p ro te in -e n e rg y in s u ffic ie n c y an d w a s re fle c te d in the lo w b od y co n d itio n scores. D ie ta ry req u irem en ts o f b e e f cattle ch an g e d ra m a tic a lly d urin g the life cycle o f the an im als and d u rin g the year, p a rtic u la rly w ith respect to such e n v iro n m e n ta l and p h y s io lo g ic a l stressors as flu c tu a tin g a m b ie n t te m p e ra tu re s an d m oisture co n dition s, lactation, g ro w th , and b reed in g (R ic e . 1 9 9 1 ). T h e c lin ic a l im p ressio n o f m a ln u tritio n that fo llo w e d the visits o f A p ril 7 and 8 w e re c o n firm e d b y the results o f the feed an alysis o f the h a y an d g ra in m ix ratio n s taken d u rin g the visits. C o p p e r deficiency' A s ind icated b y the h eav y m e tal analysis p e rfo rm e d b y tw o lab orato ries, o n tissues fro m th ree a n im a ls , c o p p e r d e fic ie n c y is a p ro b le m in the T e n n a n t h e rd (A p p e n d ix B ). In 1 9 9 7 c o p p e r d e fic ie n c y w as d ia g n o s e d in a 4 -y e a r o ld H o ls te in c o w an d a 9 -y e a r o ld H o lstein co w b y the A n im a l H e a lth D iag n o s tic L ab o rato ry o f M ic h ig a n State U n iv e rs ity in E ast L a n s in g . M ic h ig a n . In 1 9 9 9 . c o p p e r d e fic ie n c y w as re v e a le d in tissues fro m a sacrificed 7 -y e a r o ld red c o w b y the L a b o ra to ry o f L arg e A n im a l P a th o lo g y and T o x ic o lo g y o f the U n iv e rs ity o f P e n n sy lv an ia . K en n ett S q uare. P en n sy lv an ia . F u rth e rm o re , serum sam ples taken fro m 41 adult an im als at the fa rm on A p ril 7. 19 99 revealed that 26 o f the 41 (6 3 9 c ) h ad se ru m co p p e r levels b e lo w that c o n sid e re d d eficien t at the reference lab orato ry (T a b le 4). C lin ic a l signs o f co p p e r d e fic ie n c y seen on the T e n n a n t fa rm w e re lig h te n in g o f the hair coats, p oo r q u ality hair on the co w s, and o v e rg ro w n hooves. T h is w as rep o rted b y M r. T e n n a n t and sh o w n in vid eo tap es m a d e o f the herd. T h e clinical effects o f co p per d e fic ie n c y are m u ltip le , and the clin ica l and p h y sio lo g ica l effects o f such d eficien cy are w e ll d o cu m en ted (N R C , 1996). T h e effects inclu d e im m u n e deficiencies, p oo r q u a lity h air coats, increased fra g ility o f b o n e an d sudden death in e x tre m e cases. D u rin g d isease, c o p p e r d e fic ie n c y can resu lt in d ep ressed le v e ls o f tu m o r necrosis fa c to r (a c y to k in e ) w ith re s u ltin g a b n o rm a l te m p e ra tu re resp on ses to infection s and depressed feed in take (G e n g e lb a c h , et al.. 19 9 7 ). 000 DUP 264 Tennant Farm Herd Health Investigation Cattle Team Report Im m u n e d e fic ie n c ie s related to co p p er d e fic ie n c y are m u ltip le and in c lu d e depressed acute phase p ro tein response and ly m p h o c y te re sp o n siven ess to m ito g e n stim u latio n (A rth in g to n , et ai., 1996: G en g e lb ac h . et al., 1997). A s there has been no d o c u m en tatio n o f an y co p p e r s u p p le m e n ta tio n o f the h erd, the d e fic ie n c y is e x p e c te d to be p re s e n t at th is tim e a n d to c o n tin u e . T h e re la tio n s h ip b etw een h ig h e n d o p h yte fescue g razin g and co p p e r status in the feed has b een described (D e n n is , et al., 1 9 9 8 ). C o p p e r d e fic ie n c y is w id e s p re a d th ro u g h o u t th e U n ite d S tates (D a rg a tz, et al.. 1999). T o x ic o lo g y issues B ased upon the d raft report entitled D ry R u n C re e k . 1 9 9 7 fro m the E n v iro n m e n ta l R esponse T e a m o f the U S E P A , carn ivo ro u s, p is civo ro u s , o m n iv o ro u s , insectivorou s and h e rb iv o ro u s m a m m a ls in the D r y R u n C re e k s tu d y a re a are at in c re a s e d h e a lth risk d u e to expo su re to m etals, flu o rid e and tric h lo ro flu o ro m e th a n e . A t least w ith reg ard to m etals o f co n cern, d ia g n o stic ev a lu a tio n o f tissue an d flu id s c o lle c te d fro m th ree an im als fro m the T e n n a n t fa rm (tw o su b m itted to M ic h ig a n S tate U n iv e rs ity an d o ne s u b m itted to N e w B o lto n C e n te r) do not suggest elevated co n cen tratio n s o f an y m etal. In ad d itio n , urine (tw o sa m p le s s u b m itte d to M ic h ig a n S tate U n iv e rs ity ) a n d b o n e (o n e s a m p le s u b m itte d to M ic h ig a n State U n iv e rs ity fro m the c o w e v alu ated at N e w B o lto n C e n te r) sam p les fo r fluo rid e analysis d id not m easure co n cen tratio n s ab o ve ex p e c te d or "b a c k g ro u n d " values. T h e u rin a ry flu o rid e values w ere 6 .6 0 p p m and 5 .5 5 p p m an d one b on e flu o rid e valu e w as 1090 p p m (exp ressed on a fat free, d ry w e ig h t basis). U rin e and b o n e flu o rid e co n cen tratio n s in ad u lt cattle consistent w ith flu o ro sis are 15 to 2 0 p p m o r g reater and 3 0 0 0 p p m or g reater (expressed on a fat free, dry w e ig h t b asis), re sp ec tiv ely (O s w e ile r et al.. 19 85 ). In ad d itio n , there w as no c lin ica l e v id e n c e o f c h ro n ic flu o ro sis in the T e n n a n t herd. E xp o su re to tric h lo ro flu o ro m e th a n e w as co n sid ered to b e a d e fa u lt risk fa c to r based upon a lack o f to x ic o lo g ic b e n c h m a rk s fo r this c o m p o u n d . H o w e v e r , a v a ila b le to x ic ity d ata d erive d fro m in h a la tio n studies using c o m m o n la b o ra to ry a n im a ls in d icate that c h lo ro flu o ro c a rb o n s such as tric h lo ro flu o ro m e th a n e h a v e low ' acu te an d c h ro n ic to x ic ity (M a g d a . 19 99 ). S igns associated w ith acute to x ic ity are re ve rsib le effects on the central n ervo u s sy ste m such as le th a rg y an d in c o o rd in a tio n . C h lo ro flu o ro c a rb o n s are not d evelo p m en tal toxicants, do not affect reprod u ctive p e rfo rm an ce and are not genotoxic. 6.0 R E C O M M E N D A T IO N S T h e m ost im p o rtan t general re co m m en d a tio n fro m th e cattle te a m , after co m p le tio n o f the herd visit and re v ie w o f the in v es tig ato ry data, w o u ld be fo r the o w n e r o f the T e n n a n t herd to en g ag e v e te rin a ry and n u tritio n al co n su ltants in the d esig n o f a herd h ealth program . 000- DUP 265 24 Tennant Farm Herd Health Investigation Cattle Team Report E n d o p h vte to x ic itv : W ith d ietary fo rag e that contains n early 1 0 0 % K Y 3 1 fescue, fed d u rin g all seasons, the im m e d ia te g o al w o u ld be fo r the d ilu tio n o f the e n d o p h y te in the diet b y m ix in g the h ay and pasture w ith e ith e r n o n -e n d o p h y te infested fescu e o r an o th er d iffe ren t fo rag e source. A sh o rt-te rm g oal w o u ld be to redu ce the co n ten t o f e n d o p h y te infested h ay and pasture to 5 0 % o r less o f the diet, p rim a rily b y s u p p le m e n tin g the diet w ith h ig h er q u a lity forage. A n acceptable lo n g -term p lan w o u ld be to rep lace the fescue pasture and h ay fields w ith a n o n -en d o p h y te-in fe ste d forage crop or crops o v e r tim e, again w ith the goal o f d ilu tin g the d ie tary en d o p h yte co n su m p tio n . C ro p m a n a g e m e n t sh o uld be attem p ted u n d er the su p e rv is io n o f specialists in fo rag e an d g ra zin g m anagem ent. P in k e v e : P re v e n tio n o f p in k e y e (k e ra to c o n ju n c tiv itis ) in the im m e d ia te fu tu re sh o u ld be a tte m p te d b y an a p p ro a c h that lim its th e sp read o f the in fe c tio u s o rg a n is m . M oraxella bovis, fro m c a rrie r ca ttle to s u s c e p tib le c a ttle . E ffe c tiv e fly c o n tro l, th ro u g h th e use o f in s e c tic id e -im p re g n a te d e.artags o r s o m e o th e r p ro v e n m e th o d , is p e rh a p s th e m o s t effe ctive co n tro l m e th o d that sh o uld be p racticed d u rin g the w a rm m o n ths. T h e in s ec tic id e-lad en eartags sh o u ld be ro tated e v e ry y e a r in o rd e r to c irc u m v e n t the d ev e lo p m e n t o f insecticide resistance b y the local face fly p o p u latio n . A n ad d itio n a l lo n g -te r m a p p ro a c h th at m a y b e e m p lo y e d is th e b re e d in g fo r c a ttle th a t h a v e d a rk faces. B y s e le c tin g fo r d a rk -fa c e d c a ttle , th e c o rn e a l d a m a g e th at is c a u s e d b y th e u ltra v io le t lig h t o f th e s u n is m in im iz e d . H o w e v e r , w h ile m in im iz in g th e d a m a g e to th e c o rn e a s o f the cattle m a y p rev en t o vert lesions o f k e ra to c o n ju n c tiv itis , the loss o f c o n d itio n fro m severe fly infestatio ns w ill not be a v o id e d b y selectin g fo r face c o lo r in ca ttle . T h u s regardless o f the type o f cattle in the h erd , in secticid e fly rep ellan ts sh o u ld b e used e v e ry year. M a ln u tritio n : R atio n s and pasture n u tritio n should be p lan n ed w ith the assistance o f a specialist in b e e f cattle n u tritio n . In the T e n n a n t herd , th ere w as e v id e n c e o f gross p ro te in -e n e rg y m a ln u tritio n , as w e ll as co n cern s ab o u t m a c ro m in e ra l (c a lc iu m , phosphorus, and m ag n esiu m ) nutrition. T rac e m in eral and vita m in d eficien cies are c o m m o n to m a n y b e e f herds and sh o u ld also be addressed. In the d e v e lo p m e n t o f a ratio n fo r this h erd , p articu lar atte n tio n sh o u ld be p aid b y the n u tritio n ist to th e lo cal trace m ineral and m acrom in eral deficiencies. C o p p e r d e fic ie n c y : C o p p e r is a tra c e m in e r a l th a t is c ru c ia l to th e h e a lth o f c a ttle y e t is m issin g fro m the diet o f cattle in m a n y areas o f the N o rth A m e ric a . A s c o p p e r d e fic ie n c y w as suspected c lin ic a lly and c o n firm e d b io c h e m ic a lly in the T e n n a n t h erd , the p ro visio n o f a high co p p er trace m in e ra l s u p p lem en t, ag ain u n d er the su p ervision o f a b e e f cattle n u tritio n is t, s h o u ld be a p rio rity y e a r ro u n d . T h is is e s p e c ia lly c ritic a l c o n s id e rin g th e p revalen ce o f en d o p h yte-in fested fescue on the T e n n a n t farm . 000^ V DUP 266 Tennant Farm Herd Health Investigation Cattle Team Report 7.0 CONCLUSION T h e re w as co n c lu s iv e ev id e n c e that the T e n n a n t cattle h erd w as. and co n tin u es to be. su fferin g fro m fo u r m a jo r disease en tities, so m e o f w h ic h w e re p o te n tia lly interrelated : endophyte to xicity (fescue m yco to x ic o sis), p in keye, m a ln u tritio n , and co p p er deficiency. A s substantiated b y the clin ica l and lab o rato ry fin d in g s, an d h istorical data, these fo ur conditions re ad ily acco un t fo r the ch ro n ic herd h ealth p ro b le m s on the T e n n a n t farm . T h e herd h ealth in vestig atio n re ve aled d eficien cies in h erd m a n a g e m e n t, in c lu d in g p oo r nutrition, inadequate veterin ary care, and lack o f fly co n tro l. T h e lack o f vaccin atio n and in tern al p arasite c o n tro l p ro g ra m s d id not a p p e a r to h a v e a su b stan tial im p a c t o n this re la tiv ely isolated herd. D espite an exh au stive re v ie w o f historical and c o n te m p o ra ry herd data, there w as no evid ence o f to x ic itv associated w ith ch e m ic a l co n ta m in a tio n o f the e n v iro n m e n t. 8.0 REFERENCES E n d o p h y te T o x ic itv R eferences 1. B o l t D J . B o n d J: E f f e c t s in p r e g n a n t b e e f h e i f e r s g r a z i n g f u n g u s - i n f e c t e d t a l l f e s c u e on c a lf birth w e ig h t, m ilk yield , and c a lf g ro w th . J A n im Sci 6 3 (s u p p l):2 9 7 . 19S6. 2. D e n n is S B . A lle n Y G . S a k e r K E . F o n te n o t JP. A y a d J Y M . B ro w n C P : In flu e n c e o f Seoryphodium coenophialwn_o\\ c o p p e r c o n c e n tr a tio n in ta ll fe s c u e . J A n i m S c i 76:2687-2693. 199S. 3. H e m k e n R \Y . J a ck so n J.A. B o lin g J A : T o x ic fac to rs in ta ll fescu e. J A n im Sci 58:101 1-1016. 1984. 4 . Hurley \ Y L . C o n v e y E M . L e u n g K . H e m k e n R W : B o v i n e p r o la c t i n . T S H . T 4 a n d T 3 con cen tratio n s as affected b y tall fescue s u m m e r to xico sis and tem p e ra tu re . J A n im Sci 51 :37 4-37 9. 1980. 5. O sborne T G . S ch m id t SP. M a rp le D N . R ahe C H . Steenstra JR: E ffec t o f consum ing fu n g u s-in fected and fu n g u s-fre e fescue and e rg o ta m in e tartrate on selected p h ysio lo g ical variab les o f cattle in e n v iro n m e n ta lly c o n tro lle d co n d itio n s. J A n im Set 70:2501-2509. 1992. 6. Paterson J. F o rc h e rio C , L a rs o n B , S a m fo rd M , K e rle y M : T h e e ffe c ts o f fescue toxicosis on b e e f cattle p ro d u c tiv ity . J A n im Sci 7 3 :8 8 9 -8 9 8 , 1995. 7. R adostits O M . B lo o d D C . G a y C C : D iseases cau sed b y to xin s in plants, fungi, c y a n o b a c te ria , cla v ib a c te ria . insects, and a n im als . In: V e te rin a ry M e d ic in e : A OGOo.J DUP 267 26 Tennant Farm Herd Health Investigation Cattle Team Repon t e x t b o o k o f t h e d is e a s e s o f c a t t l e , s h e e p , p i g s , g o a t s , a n d h o r s e s , 8 Ih e d . , R a d o s t i t s O M . B lo o d D C , G a y C C , editors. B a illi re T in d a ll, P h ilad elp h ia 1 5 3 2 -1 6 1 1 , 1994. 8. R ice R L , B lo d g ett D J, S churig G G , S w e c k e r W S , Fontenot JP, A lle n V G , A kers R M : E v a lu a tio n o f h u m o ral im m u n e responses in cattle g razin g e n d o p h y te -in fe c te d o r en d o p h yte-free fescue. V e t Im m u n L m m u n o p ath o l 5 9 :2 8 5 -2 9 1 , 1997. 9. S a k e r K E . A lle n V G , K a ln its k y J, T h a tc h e r C D , S w e c k e r, Jr. W S , F o n te n o t, JP: M o n o c y te im m u n e cell resp o n se an d c o p p e r status in b e e f steers th at g raze d e n d o p h y te -in fe c te d tall fescue. J A n im S ci 7 6 :2 6 9 4 -2 7 0 0 , 1998. 10. S c h u ltz e A E . R o h rb a c h B W , F rib o u rg H A , W a lle r J C , O liv e r J W : A lte ra tio n s in b o vin e seru m b io ch em istry p ro files associated w ith p ro lo n g ed c o n su m p tio n o f e n d o p h y te -in fe c te d tall fescue. V e t H u m a n T o x ic o l 4 1 :1 3 3 -1 3 9 , 19 99 . 11. S tu e d e m a n n J A . R u m s e y T S , B o n d J, W ilk in s o n S R , B u s h L P , W illia m s D J , C a u d le A B : A s so ciatio n o f b lo o d ch o le ste ro l w ith o ccu rren ce o f fat necrosis in c o w s an d tall fescue s u m m e r to xico sis in steers. A m J V e t R es 4 6 :1 9 9 0 -1 9 9 5 , 19 85 . 12. V a rn e y D R . V a rn e y L A . Z a v o s P M . W ig le s w o rth M D . Siegel M R : T a ll fescue en d o p h yte: e ffe c t on c o n g e n ita l d e v e lo p m e n t and p u p g ro w th in m ic e . J D a iry Sci 74:460-466. 1991. M a ln u tritio n R eferences 13. R ic e L E : T h e effect? o f n u tritio n o n re p ro d u c tiv e p e rfo rm a n c e in b e e f ca ttle . V e t C lin N o rth A m e r - Food A n im Pract 7:1-26. 1991. C o p p e r D e fic ie n c y R eferences 14. A rthin gto n JD . C orah L R . B le c h a F: T h e effect o f m o lyb d e n u m -in d u ce d copper d eficien cy on acute-phase p ro tein concentrations, superoxide d ism utase activity, leu ko cyte n u m b ers, and ly m p h o c y te p ro liferatio n in b e e f heifers in o cu lated w ith b o v in e h e r p e s v ir u s - 1. J A n i m S c i 7 4 : 2 1 1 - 2 1 7 , 1 9 9 6 . 15. D a rg a tz D A . G a rry F B . C la rk G B : S e ru m c o p p e r co n cen tra tio n s in b e e f c o w s and heifers. J A V M A 2 1 5 :1 8 2 8 -1 8 3 2 , 1999. 16. D enn is S B , A lle n V G . S aker K E , F on ten o t JP, A y a d J Y M . B ro w n C P : In flu en ce o f Neothyphodiw n coenophialum _ o n c o p p e r c o n c e n tr a tio n in ta ll fe s c u e . J A n i m S c i 76:2687-2693. 1998. DUP 268 eV -*7 Tennant Farm Herd Health Investigation Cattle Team Report 17. G en gelb ach G P . W a rd JD , Spears J W , B ro w n T T : E ffec ts o f co p per d e ficien cy and co p per d e fic ie n c y co u p led w ith h ig h d ie tary iron o r m o ly b d e n u m on p h a g o c y tic cell fu nctio n and response o f calves to a resp irato ry disease ch allen g e . J A n im Sci 75 :11 12-1 1 IS . 1997. IS . N a tio n a l R e se arc h C o u n c il: M in e ra ls , in: N u trie n t R e q u ire m e n ts o f B e e f. 7th ed. N atio n al A c a d e m y Press. W a s h in g to n , D . C . 5 4 -7 4 , 1996. T o x ic o lo g y Issues R e fe re n c e s 19. M a g d a S: F lu o ro carb o n s. In: T o x ic o lo g y , 1st ed., M a r q u a r d t H , S c h a fe r S G , M c C le lla n R and W e ls c h F, editors.. A c a d e m ic Press, S an D ie g o , 6 5 9 -6 6 2 . 1999. 20. O sw eile r G D . C arson T L . B u c k W B , V a n G e ld e r G A , editors: F lu o rid e . C lin ic a l and D iagnostic T o x ic o lo g y . K e n d a ll/H u n t P u blish in g , D u b u q u e , IA , 1 8 3 -1 8 8 , 1985. 21. L '.S .E .P .A . E n viro n m en tal R esponse T e a m : Dry' R u n C re e k . 1997 (d raft). 0 0 0 !') DUP 269 28 Tennant Farm Herd Health Investigation Cattle Team Report 9.0 GRAPHS G r a p h 1: I n d i v i d u a l C a t t le P la s m a P r o la c t in ( A p r i l 7 , 1 9 9 9 ) . H e p a rin iz e d b lo o d sam p les tak en fro m 4 1 ad u lt cattle d u rin g the cattle tea m 's visit to the T e n n a n t fa rm w e re a n a ly ze d fo r the e n d o p h y te responsive h o rm o n e , p ro la ctin . G ra p h illustrates the lab o rato ry's reference m eans for endop h yte-free (1 7 1 .6 n g /m L ) and en dophyteinfested (1 0 5 .8 n g /m L ) A p ril pasture. T h e averag e p la sm a p ro lactin v a lu e fo r the T e n n a n t h e rd ( l 10.1 n g /m L ) w a s s im ila r to the en d o p h yte-in fested referen ce. T h e s e results w ere h ig h ly su p p o rtive o f the diagnosis o f en d o p h yte m y c o to x ic o s is in the T e n n a n t herd. (T estin g laboratory: D r. N e il S ch ric k, U n iv e rs ity o f T en nessee) coo* ' DUP 270 Cirnpli 1: Individual ('aillo Plasm a Prolaolin (April /, 1090) D C 13 ro -nI O W. 'j- c> Animal Number a Prolactin 1716 110 1 105.8 Tennant Farm Herd Health Invesuaation Cattle Team Report 10.0 FIGURES F ig u re 1: F a c e flie s on th e h e a d o f a c a lf. F a c e f l y (M u s c a a u t u m n a l i s ) i n f e s t a t i o n w a s c o n s i d e r e d t o b e a m a j o r d i s e a s e p ro b le m on the T e n n a n t farm . In ad d itio n to the constant h arassm ent by flies, this c a lf h ad severe b ilate ra l k e ra to c o n ju n c tiv itis an d a p p eared to be c lin ic a lly b lin d on the vid eo tap e (p h o to w as tak en fro m T e n n a n t videotape # 2 ). F ig u re 2: F aceflies on the head o f a co w . T h is c o w w a s the d a m o f the c a lf in F igure 1. L ik e h e r c a lf, she h ad se ve re b ilateral keratocon jun ctivitis, (p ho to w as taken fro m T e n n a n t vid eo tap e #2). F ig u re 3: L e ft eye o f a c a lf w ith faceflies and ce n tral co rn eal opacity. F ace flie s are a vecto r fo r the bacterial agents o f p in k e y e (k e r a to c o n ju n c tiv itis ) su ch as M oraxella bovis. C e n tr a l c o rn e a l o p a c itie s m a y p rogress to d iffu s e co rn ea l u lc e ra tio n a n d c lin ic a l b lin d n ess, (p h o to w as taken fro m T en n an t videotape #2). F ig u re 4: D e la y e d sh edding o f the w in te r coat on a b e e f co w . T h e v ideotapes presented m u ltip le cattle w ith d e la y e d sh ed d in g o f w in te r c o a ts . T h is is a c lin ic a l sig n o fte n a s s o c ia te d w ith e n d o p h y te to x ic ity as w e ll as n u tritio n a l d eficien cies , (p h o to w as ta k e n fro m T e n n a n t v id e o ta p e = 2). F ig u re 5: A lo p e c ia and e ry th e m a ab ove the c o ro n a ry b an d (co ro n itis). T h is le s io n w a s p re s e n t in se v e ra l c a ttle in th e v id e o ta p e s . It is a c o m m o n s ig n o f e n d o p h y te to x ic ity a n d is g e n e r a lly r e fe r r e d to as " fe s c u e fo o t" , (p h o to '"as taken fro m T e n n a n t vid eo tap e # 2 ). F ig u re 6: A lo p e c ia and ery th e m a ab o ve the c o ro n a ry band (co ro n itis). T h is e x a m p le o f " fe s c u e fo o t" is s im ila r to th a t p re s e n te d in fig u r e 5. (p h o to w as taken fro m T en nant videotape #2). F ig u re 7: T h re e cattle stand ing in the creek. A u nu su al p red ilectio n for standing in w a te r w as d escrib ed fo r the T e n n a n t c a ttle in th e s u m m e r . T h is b e h a v io r is k n o w n to b e a s s o c ia te d w it h e n d o p h y te to x ic ity as it p ro v id e s s o m e r e lie f fo r b o th c o ro n itis ("fe s c u e fo o t") and h yp erth erm ia (" su m m er fescue"), (p h o to w as taken fro m T en nant videotape #2). F ig u re S: T w o cattle stand ing in a p ud d le. A s d e s c rib e d fo r fig u re 7, s ta n d in g in w a te r p ro v id e s s o m e c lin ic a l re lie f to cattle w ith co ro n itis. A lth o u g h n o n -s p e c ific , a p re d ile c tio n fo r this b e h a v io r is a s s o c ia te d w ith " fe s c u e fo o t" , (p h o to w a s ta k e n f r o m T e n n a n t v id e o ta p e DUP 272 31 Figure 1 Figure 2 OOOv,.' \ DUP 273 n Figure 3 DUP 274 35 Figure 6 P G O-:-. DUP 275 3+ Figure 7 Figure 8 0 G9 - : DUP 276 & Tennant Farm Herd Health Investigation Cattle Team Report 11.0 TABLES T ab le I: R e v ie w o f T e n n a n t F a rm V id eo tap es T a b le 2: In d iv id u a l A n im a l D ata: C lin ic a l S igns T a b le o : In d iv id u a l A n im a l D ata: H e m a to lo g y (eryth ro n , p latelets) T ab le 4: In d ivid u al A n im a l D ata: H e m a to lo g y (leu ko n ), and S p ecial C h em istry T ab le 5: In d ivid u al A n im a l D ata: C lin ica l C h em is try T a b le : In d ividu al A n im a l D ata: S erology and Fecal E x a m T a b le 7: T e n n a n t F a rm G ra in and H a y : N u tritio n a l A n a ly s is o o o -..; DUP 277 ib Tennant Farm Herd Health Investigation Cattle Team Repon Table 1: Review of Tennant Farm Videotapes Tape #1 (cases 1- 18): Tennant Farm: New England, Wood Co., WVa - __________________ January & February, 1997__________________ nil S u b j e c t P re se n ta tio n D ia g n o s is /C o m m e n t A n im al(s) l C o w , H e re fo rd neck: alo p e cia, scaling , p ro b a b le lice, d escrib ed as " h u m p e d - " h u m p e d -u p " d iffic u lt to ap p reciate u p '\ (sn o w in g) on tape. 2 C o w , H e refo rd corneal opacity, co rn eal scar, p ro b a b ly seco n d ary to (sn o w in g) p in keye. 3 2 b lack bulls possible d isco lo ratio n not clear fro m tape. o f hair (not clear), . (sn o w in g) 4 C o w , H e re fo rd thin, v e ry th in , p ro b a b ly due to d esc rib ed as p o o r teeth, decreased food co n su m p tio n and (sn o w in g) m asticatio n p ro b lem , although teeth not seen on video, age u n k n o w n ; cause o f possible teeth p ro b lem u n kn o w n . 5 C o w . H e re fo rd possible hun ch ed back n ot clear fro m tape. (not clear). (sn o w in g) 6 Cow uani alopecia, tail sw itch , tail h a ir loss d iffe re n tia l d iag n o sis (sn o w in g) w o u ld in clu d e m e c h a n ic a l, lice, fescue toxicosis, and selen iu m to x ic o s is . 7 Cow alo pecia, tail sw itch , tail h air loss d iffe re n tia l d iagn o sis (sn o w in g) w o u ld in clu d e m e c h a n ic a l, lice, fescue toxicosis, and selen iu m to x ic o s is . 8 C a lf, b lack d ead (d ated 2 /9 /9 7 ) in h o o ves a little lo n g er than n o rm a l, snow, b ut not unusual, . overgrow n hooves, "co ld cataracts" (post m o rte m ), b ilateral lens o pacities, teeth n o rm al, b la c k /b ro w n teeth, fecal m ucous n orm al for stagnant m ucous on feces, feces in rectu m , necropsy: no other n ecropsy: lack o f fat; serous le s io n s , a tro p h y o f fat: em ac ia tio n , stated: had d iarrh ea p ro b a b ly due to starvation . Table 1: Review of Tennant Farm Videotapes 000> DUP 278 Tennant Farm Herd Health Investigation Cattle Team Report Table 1 (continued):Review of Tennant Farm Videotapes Tape #1 (cases 1- 18): Tennant Farm: New England, Wood Co., WVa - __________________ January & February, 1997 _____________ # S u b ject A n im al(s) 9 C alf, b lack/w h ite face P re se n ta tio n neck: alopecia, diarrhea, lens o r co rn eal o pacities D ia g n o s is /C o m m e n t p ro b a b le lice, cause o f d iarrh ea u n k n o w n , p ro b a b le co rn eal scar (h ard to tell). 10 C o w , H ereford thin, corneal o pacity, ab o ve hooves: alopecia and h yp erem ia, d iarrh ea corneal o pacity p ro b ab ly secondary to p in keye, d ifferen tial d iagn o sis o f h o o f lesions in clu d e m e ch an ical d erm atitis, fescue to xico sis, and m o ist d erm atitis d u e to u n k n o w n cause o f d ia rrh ea and th in n in g unknown. 11 C o w . black neck: alopecia p ro b a b le lice. 12 C o w , red neck: alopecia p ro b ab le lice. 13 C o w . red 14 C o w . red 15 C o w . red 16 C o w . red slo bb erin g , losing cud (on g ro un d ), urinatin g , tail s w itc h alo p ecia neck: alopecia, tail sw itch : short h air neck: alopecia slo b b erin g /u rin atin g d ifferen tial diagnosis in clu d es h a rd w a re and ch o lin esterase in h ib itio n (less lik e ly d ue to in d iv id u a l c o w a ffe c te d ), alo pecia d iffe re n tia l diagnosis includes m e c h a n ic a l, lice, and fescue o r s e le n iu m toxicosis. neck: p ro b ab le lice, tail h air d iffe re n tia l d iagn o sis inclu d es m e c h a n ic a l, lice, and fescue o r se le n iu m toxicosis. . p ro b a b le lice. odd c h e w in g b eh avio r not clear fro m tape. 17 C o w , H e refo rd possible h un ch ed b ack not clear fro m tape; d iffe ren tial diagnosis in clu d es h ard w a re disease (tra u m a tic reticulo pericard itis). 009 Table 1: Review of Tennant Farm Videotapes DUP 279 3S Tennant Farm Herd Health Investigation Cattle Team Report Table 1 (continued):Review of Tennant Farm Videotapes Tape # 1 ( c a s e s 1 - 1 8 ) : Tennant Farm: New England, Wood Co., WVa - __________________ January & February, 1997__________________ rur Subject Animal(s) Presentation Diagnosis/Comment 18 C o w , red d ead in b a m , (is this the 9 -y e a r-o ld c o w (sam e as # 1 3 ) corneal o pacity, su b m itted to M ic h ig a n ? ), necropsy: no other co m e al opacity m a y be postm o rtem le s io n s a rtifa c t, necropsy: serous atrophy o f fat, noted: n orm al p o stm o rtem changes in c lu d e m o d erate to severe autolysis, p seu d om elan osis o f intestines, in te rlo b u la r e m p h y s e m a (ag o nal), also noted: n o rm a l front teeth large g allb lad d er suggests p eriod o f a n o re x ia , cause o f death u nkno w n. Table 1: Review of Tennant Farm Videotapes 0 0 V V. 'f DUP 280 3? Tennant Farm Herd Health Investigation Cattle Team Report Table 1(continued):Review of Tennant Farm Videotapes Tape #2 (cases 19 - 60): Dry Run Harris PC. Wood Co. - Off North Fork of _________________Lee Creek, New England, WYA__________ # Subject Animal(s) Presentation Diagnosis/Comments 19 C alves, m u ltip le corneal opacities o f varyin g severity; som e fly p ro blem w ith secondary p in keye, w ith ex u d ate an d /o r . hair coat sh ed d in g and co lo rin g b lep h aro sp asm , p ro bably due to a n utritio nal fly p ro b lem (sum m er), problem . som e w ith p oo rly shedded a n d /o r lig h t- co lored coats 20 F ish (su cker? ) dead incidental death: no diagnosis p o s s ib le . 21 S m all m a m m a l . skeleton (ra c c o o n ? ) incid en tal death: no diagnosis p o s s ib le . 22 1 Cow corneal opacity co m e al scar se co n d a ry to p in keye. ! 23 C a lf co rn eal o pacities, p ossible h ead tilt (n ot c le a r) c o m e a l scar s e c o n d a ry to p in k e y e , head tilt not c le a r o n tape. 24 C a lf . co rn eal o pacities. corneal scar s e co n d a ry to p in keye. flies 25 C a lf dead (-1 m o n th-o ld). corneal opacity, cause o f death u n k n o w n . corneal scar s e c o n d a ry to p in ke ye . 26 Snake (b urnin g carcass) j dead incidental death: no d iagn o sis 27 C a lf i corneal o pacities, p o s s ib le . fly p ro blem w ith secondary- fly p ro b lem p in keye. 28 Fish dead incidental death: no d iagnosis p o s s ib le . 29 C a lf corneal o pacity c o m e a l scar s e c o n d a ry to p in keye.. 30 C a lf corneal o pacity corneal scar se co n d a ry to p in keye. Table l: Review ot' Tennant Farm Videotapes DUP 281 00 OC.if; Tennaru Farm Herd Health Investigation Cattle Team Report Table 1 (continued): Review of Tennant Farm Videotapes Tape #2 (c a s e s 19 - 60): Dry Run Harris PC. Wood Co. - Off North Fork of ______________ Lee Creek, New England, WYA_____ nu S u b j e c t P re se n ta tio n D ia g n o s is /C o m m e n ts A n im a l(s ) 31 C ow . dead, cause o f d iarrh ea, em aciatio n and w o rn incisors, death u n kn o w n , . diarrhea, w o rn incisors m a y be age o r feed em aciated , sunken eyes re la te d , (d eh yd rated ? ), serous lun g em p h ysem a w as agonal and atrop h y o f fat (heart), in s ig n ific a n t. agonal lung em physem a 32 C row . dead in c id e n ta l death: n o diagnosis p o s s ib le . 33 C row . dead in c id en tal death: no diagnosis p o s s ib le . 34 C alves. corneal o pacity co rn ea l scar se c o n d a ry to p in ke ye . m u ltip le 35 C o w corneal opacity, thin co rn e a l scar se c o n d a ry to p in k e y e , d ia g n o sis o f the cause o f thin c o n d itio n not possible. 36 Fish dying in c id en tal death: no diagnosis p o s s ib le . 37 C rayfish dead in c id e n ta l death: no diagnosis p o s s i t ' . 38 S alam an d er dead in c id e n ta l death : no diagn o sis p o s s ib le . 39 Toad dead in c id en tal death: no diagnosis p o s s ib le . 40 N e w b o rn c a lf contracted tendons, d iffic u lt to e v a lu a te fro m tape; m a y b ig hocks be co n genital contracted tendons. 41 Deer dead in c id e n ta l d eath : no diagn o sis p o s s ib le . 42 Cow dead (rotten) no diagnosis possible. 43 Deer 44 Deer rotten carcass bones in c id e n ta l death: n o diagn o sis p o s s ib le . in c id e n ta l death: no diagnosis p o s s ib le . Table 1: Review of Tennant Farm Videotapes 0 0 ') DUP 282 ii Tennant Farm Herd Health Investigation Cattle Team Report Table 1 (continued):Review of Tennant Farm Videotapes Tape #2 ( c a s e s 19 - 60): Dry Run Harris PG. Wood Co. - Off North Fork of _________________Lee Creek, New England, WVA_________________ nu Subject Animal(s) Presentation Diagnosis/Comments 45 C o w panting; increased d ifferen tal d iagnosis includes re s p ira tio n h yp erth erm ia due to s u m m e r fescue to x ic o s is , diagnosis u ncertain . 46 C o w diarrh ea cause o f d iarrh ea u n k n o w n . n <oS'-- i 47 R a c c o o n 48 D e e r 49 D e e r 50 R a b b i t 51 T u r k e y 52 H a w k 53 F i s h 54 skull skeleton dead (fresh). b lo o d y nose dead dead . dead dead lum pv udder incidental death: no d iagnosis p o s s ib le . incidental death: no d iagnosis p o s s ib le . death p ossibly d u e to ep izo o tic h em o rrh a g ic disease o f d eer (E H D ). incidental death: no d iagn o sis p o s s ib le . incidental death: no d iagnosis p o s s ib le . incidental death: no d iagn o sis p o s s ib le . incidental death: no diagnosis p o s s ib le . unclear fro m vid eo tap e. 55 C o w s , m u l t i p l e a b o v e h o o v e s : a l o p e c i a , d i f f e r e n t i a l d i a g n o s i s i n c l u d e s possibly eryth em a, m echanical d erm atitis, fescue overgrow n hooves toxicosis, and m o ist d erm atitis due to u n k n o w n , h o o f length not sig n ifican t. 56 B u l l , c o w s , corneal o pacities, c o m e a l scar seco n d ary to p in ke ye . m u ltip le alo p e cia and e ry th e m a h o o f d iffe ren tial d iag n o sis includes above hooves m echanical d erm atitis, fescue toxicosis, and m o ist d erm atitis due to u n kn o w n . 57 C o w lu m p y udder u nclear fro m vid eo tap e. Table I: Review of Tennant Farm Videotapes 000 DUP 283 Hi Tennant Farm Herd Health In v e s titio n Cattle Team Report Table 1 (continued): Review of Tennant Farm Videotapes Tape #2 (cases 19 - 60): Dry Run Harris PC. Wood Co. - Off North Fork of _________________Lee Creek, New England, WVA_________________ # j S u b ject ! A n im aK s) Presentation Diagnosis/Comments 5 8 C o w s , m u ltip le ab o ve hooves: alopecia, h o o f d iffe re n tia l d iagn o sis includes possibly eryth em a. m ech an ical d erm atitis, fescue p oo r sh ed d in g o f coat toxicosis, and m o ist derm atitis due in so m e an im als to u n k n o w n , p o o r h air co at sh ed d in g suggests n utritio nal p ro b le m o r fescue m yco toxico sis. 59 C o w (tan) unusual gait lam e due to u n k n o w n cause. 6 0 C o w s , h eifers, thin. d e fin itiv e d iagn o sis not possible m u ltip le d elayed shedding fro m tape - p ro b a b ly a n utritio nal d e fic ie n c y . I Note: This table excludes man> of the clinical signs and pathological conditions that were proposed by the videotapes' narrator but were considered by the cattle team to be inaccurate. For example, the team did not agree with the narrator's assertion that blackened teeth or patchy melanosis were abnormal. Also numerous speculative comments regarding normal organs, during the dissections shown in the videotapes, were not included in this tabie. Table 11 Review of Tennant Farm Videotapes 000 t;. DUP 284 Tennant Farm Herd Health Investigation Cattle Team Report Individual Animal Dala: Calile from Tennant Karin (Washington, West Virginia) Table 2: Clinical Signs Animal Age Preg. Number Status Description Body Condition Score il -10) Clinical Signs | years Girth DCS .(in.). (MO) __ ____c >9 2 >9 4 in yellow open red, white lace 3 possible lice 3 lice, corneal scar (i) 3 >9 open yellow, while face 3 (large uterus) 4 >9 7 ni red, while face 70 4 lice 5 >9 6 nt red, while face 75 4 corneal scar (1) 6 >9 3 m red, while face - 4- 7 >9 6 m red, while face 71 4 hair loss (switch) 8 >9 open red, white face -4 9 >9 open red, white face 70 4 (muzzle: melanin considered normal) 10 >9 term red, white face 70 3 - 11 >9 8,5 in red, white face - 3- 12 >9 1 term red, white face .... 72...... 3 light coat color; small corneal scar (r) 13 > 9 open red, white face 66 2 slight corneal scar (1), 14 > 9 calf red, white face 78 4 alopecia (brisket) D C uo ro Uj % 9*9 CJ1 7*) 15 >9 __ open yellow 16 _6 __ open__ hlack_ 17 >9 4 nt red, while face 18 >9 4 m red, white face 19 >9 Calf red, brockleface 20 >9 6 m red, white face 21 >9 ! 5 m red, while face 22 >9 5 in red, brockleface 71 68 78 78 ' ! 68 74 69 76..... 2 3 7 ~7 ' 3 3 3 4 palpation difficult (fat necrosis?) - mammary gland lumps (right front)(abscesses?) slight corneal scars (1 and r) - small corneal scar (l)(5 mm) mass (12 cm) prescap. neck (r) - lanced: brown scrum + hair 23 - bull black -4 24 >9 6 tn red, white face 4 hair loss (neck) Photo' # 1 ....2 3 4 5 6 7 8 9 10 II 12 13 14 15 16 7 18,53 19 20 21 22.49-51 23 24 Data Tables Tennant Farm Herd Health Investigation Cattle Team Report Individual Animal Dala: Calde from Tennanl Farm (Washington, West Virginia) Tabic 2: C linical Siffnx (continued) Anlitiitl Age Prcg. Description Number Status Hotly Condition Score (1-10) Clinical Signs Photo # years Girth BCS (in.) 0-1) 25 4 5 m black 72 4 corneal scar (1) 25, 44 26 6 bull black 5 corneal opacity (1) 26, 45 27 >9 8 m red, brockleface (4 3- 27 28 7 8 m black, while face 74 4- 28 29 >9 term red, brockleface 77 2 mammary gland lumps (left rear) (abscesses?) _____ 29_ 30 >9 8 m red, while face 72 3 lice, hair loss (abd.), extra teat, corneal opacity (l=3mm; r=5mm) 30, 46 31 8 6 m red, while face 77 5 corneal scar (r) (2 mm); (longue: melanin considered normal) 31,52 32 >9 6 m black, white face 70 lice 32 33 >9 8 m red, white face 72 3 - 33 34 >9 8 m__ red, brockleface '73 2- 34 35 >9 36 >9 5 m red, white face 8 m red, white face 72..... 3 - 75 i - 3 - corneal scar (1), severe 35 36 a 37 7 calf red, brockleface 77 ___ 4___ cortical scar (r) (1 cm) c 38 >9 7 m red. white face 73 4 - TJ 39 >9 calf red, while face 68 .... 2 __ - ro 40 4 6 m black ' 75 4 ~ ' light hair color, corneal opacity (1) (2mm) ocno 41 1 cow 4 - steer black, while face - red, whiteface 71 -1 lame (Ir), corneal opacity (r) severe; phthysical eye (1) cow escaped run before being lagged or examined 37,47 38 39 1---4-0-,4-8- 41 42 calves < 6 m - 12 mise, calves -! 5 bigger calves not tagged; 7 smaller calves tagged - Cattle examinations conducted on April 7, 1999. Age determined by teeth examination (Dr. Moisan); Pregnancy Status determined by rectal palpation ^ (Dr. Munson); Girth measured by tape (Dr. Habeeker); PCS assigned by Drs. Moisan and Munson; Clinical Signs identified by cattle team (Drs. O Davis-Heller, Habeeker, Moisan, Munson, Poppenga, Sykes); Photos taken by Dr. Sykes. f*' Cow #22: Gross diagnosis (no histology) of skin lesion: epidermal inclusion cyst (incidental lesion of no significance). ______________________ C Data Tables Tennant Farm Herd lleallli Investigation Cattle Team Report cO "a ro 00 -c o Individual Animal Data: Caille from Tennant Farm (Washington, West Virginia) T a b le 3 : H e m a to lo g y (E ryth ro n , P la te le ts) Animal Ago Prog. Number Status IIHC Hgb Hct --dy.-e-a-r-s-- ---------- -- xIOVul fi/dl Reference 5-10 8-15 % 24- Range: 46 1 4 4 m 5.85 9.91 28.8 2 3 open 4.68 8.82 26.0 3 >9 open 6.22 12.0 34.8 4 >9 7m 5.81 10.4 29.7 5 >9 6m 5.86 9.87 29.2 6 >9 3m 5.21 10.1 28.8 7 >9 6 m 5.06 10.6 29.3 8 >9 open 4.44 9.58 26.6 9 >9 open 4.48 8.66 25.2 10 >9 term 5.23 10.5 29.7 11 >9 8.5 m 4.81 9.84 28.2 12 >9 term 4.99 9.41 27.9 13 >9 open 4.29 8.62 23.7 14 >9 calf 6.04 12.0 33.7 15 >9 pres-n. 4.65 8.41 24.9 16 6 open 5.47 9.58 28.2 17 >9 4m 6.16 13.1 37.7 18 >9 4 m 6.30 12.5 35.2 19 >9 calf 4.92 9.98 29.1 20 >9 6 m 4.85 9.51 28.0 21 >9 5 m 5.80 10.7 30.9 22 >9 5m 23 _ ! bull 5.55 10.5 .30.3 6.13 12.4 34.8 24 >9 6 m 6.02 11.8 33.5 MCV MCH MCHC RDW PLT MPV PCT PDW n 40-60 J> _ g/tii % xIO'/ul 11 . % 19.3 10.9 34.4 18.3 55.6 18.8 33.8 19.5 55.9 19.3 34.6 17.8 51.1 17.9 35.1 19.3 49.8 16.9 33.8 18.6 55.2 19.4 35.1 19.3 58.0 21.0 36.1 17.8 59.9 21.6 36.0 19.2 56.3 19.3 34.3 20.2 56.9 20.1 35.3 17.1 58.6 20.4 34.9 17.8 55.9 18.9 33.7 19.0 55.2 20.1 36.4 20.4 55.8 19.9 35.7 18.8 53.6 18.1 __ 33.7__ 20.6 51.5 17.5 34.0 ~20.0_ 61.1 21.2 ' 3 4 .7 ... ... 19.2 " 55.9 19.9 35.6 194 59.2 20.3 34.3 17.3 57.7 19.6 34.0 18.0 53.2 18.5 34.8 l o o 54.7 18.9 34.6 19 1 56.7 2 o . r .... 35.7 ' 19.0 55.7 __19.6_ 1 1 21.8 378 186 233 259 142 201 378 448 184 369 142 113 595 361 238 284 _ 8T4 368 317 275 320 391 283 270 7.04 .266 _ 15.9 9.10 .170 19.0 8.50 .198 18.9 8.08 .209 18.4 8.82 .126 19.7 8.98 .180 18.7 6.49 .246 16.9 6.42 .287 17.2 13.1 .240 23.4 8.02 .296 18.1 - -- 10.9 .123 21.8 6.73 .400 17.7 8.91 .321 19.2 7.73 .184 19.2 __8^27__ .235 18.3 --- 7.71 .283 17.2 5.75 .182 16.1 7.55 .207 18.6 _8.30_ __.266 _ 19.4 7.24 .283 ' 18.2 8.74 .248 20.9 8.23 .222 17.9 " Data laities Tennant Farm Herd Heallli Investigation Calile Team Report Individual Animal Dala: Cattle from Tennant Farm (Washington, West Virginia) co "Q 0o0o 00 o o o Table 3: Hematology (Erylhron, Platelets) (continued) Animal Age Prog. l i n e Hgb Hot MCV MCH MC'HC RDW PLT MPV Number Status years xl06/ul g/di % n _.PS _ Mit % xloVnl n Reference 5-10 8-15 24- 40-60 Range: 46 25 4 5 m 6.93 12.5 35.9 51.8 18.0 3-1.8 18.8 231 8.33 26 6 bull 6.13 11.4 33.1 5-1.0 18.5 3 1.3 18.4 278 7.71 27 >9 8m 4.90 9.8 28.3 57. 20.1 34.9 18.3 406 7.05 28 7 8 m 6.12 11.7 34.1 55.7 19.2 .34.4 17.8 180 7.18 29 >9 term 5.37 9.93 28.7 53.4 18.5__ J 4 .6 _ 19.2 220 9.57 30 >9 8m 5.08 10.2 28.6 56.3 20.0 j 3.V6 20.1 407 7.09 31 8 6 m 6.03 12.6 36.0 59.7 20.9 1__ 35. 19.5 ..T n '"' 8.07 32 >9 6 m 6.17 I t .3 32.4 52.5 18.2 34/7 ' 19.2 138 7.33 33 >9 8m 5.42 10.1 30.1 55.5 __ [8.7__ 33.6 17.8 186 7.77 34 >9 8 m 5.41 11.6 33.0 60.9 35.1__ 18.2 361 7.20 35 >9 5m 5.86 I I I 32.2 55.0 19.0 34~6 21.2 246 _ 6.33 36 >9 8 m 4.34 9.44 26.3 60.6 JM.7__ 35.9 _ 18.1 " .315 8.00 37 7 calf 5.48 10.9 30.9 56.4 19.8 .35.1 18.8 363 8.56 38 >9 7m 5.88 11.5 32.2 54.8 19.6 35.7 18.3 397 5.82 39 >9 calf 4.68 8.34 24.5 52.4 17.8 34.1__ 18.5 345 6.28 40 4 41 4 6m steer 6.94 6.78 12.4 34.4 12.2 34.7 49.6 51.1 17.9 36~1 18.0 ' 35.2 19.1 20.0 449 298 6.65 6.94 hours before hematology was run on an Abbott Cell-Dyne 3500. Reference values are for cattle (New Rollon Center), but not from the Cell-Dyne 3500. per PDW % .19.7 ...J .[-_.215 .286 17.8 .129 17.6 .21 1 24.4 .288 __ [6.9__ .175 " 18.2 .101 19.5 .145 20.2 .260 17.8 .156 16.8 .252 18.0 .310 19.5 .231 16.7 .217 16.4 .298 17.4 .207 17.6 -<F1 Dala Tables Tennant Farm Herd Health Investigation Cattle Team Report Individuili Animal Dala: Calile from Tennant Farm (Washington, West Virginia) Table 4: Hematology (lenkon), Special Chemistry, and Fecal Exam Animal Age Prep. WI1C Netti Lymph Mono Eos Number Sfnlus years Reference Range: l4 4m 23 open 3 >9 open 4 >9 7m 5 >9 6m 6 >9 3m 7 >9 6 m 8 >9 open 9 >9 open 10 >9 term 11 >9 8.5 m 12 >9 term 13 >9 open 14 >9 calf 15 >9 pregn. 16 6 open 17 >9 4 m 18 >9 4 m 19 >9 calf 20 >9 6m 21 >9 5m 22 >9 5m 23 . bull 24 >9 6m xio'/nl 4-12 8.74 8.46 7.10 6.32 6.69 8.48 6.80 7.38 4.81 6.54 6.25 6.13 5.37 5.21 4.29 7.38 6.83 8.44 5.28 3.59 7.90 5.58 6.02 5.84 % 15-45 % 45-75 % 2-7 35.9 28.7 7.48 32.0 44.2 9.36 63.6 5.39 10.0 42.5 28.9 7.39 31.6 29.4 7.41 35.6 25.1 7.07 58.9 6.15 7.42 53.7 16.3 .207 43.9 33.6 9.93 62.2 15.3 10.5 34.8 35.8 9.72 45.7 33.0 7.75 61.4 18.0 1(H) 31.2 41.9 8.25 56.5 25.0 12.1 49.7 33.7 J O . 7 44.8 " - - - - - HT2 45.1 23.7 5.2.3 57.2 19.4 11.3 53.4 __ 19.2__ _ 8.19 32.0 22.6 4.68 44.6 M 3 __121 59.1 - 2T 2 _7AI 42.5 25.5 10.6 % 2-20 27.9 14.4 21.0 21.1 31.6 32.3 27.5 29.8 12.6 11.8 19.6 13.5 10.4 18.5 5.89 5 76 17.5 26.0 ~ 11.9 19.2 40 *7 28.9 12.4 21 A ~ Huso % 0-2 .016 .037 .021 .109 0.00 0.00 .029 O.(H) .054 .113 .061 .037 .151 .137 .428 .240 _ 0.00 0.00 .058 0.00__ o'on .167 0.(8) .028 Prolactin Cu Sc-A A plasma ng/inl 171.6 (mean) 58.71) 137.60 124.68 197.19 48.34 37.01 51.61 40.21 113.08 562.10 106.50 124.43 38.18 54.40 141.36 .32.04 92.87 142.25 42.28 .3.3.35 ." '17.37 62.95 89.60 87.94 scrum blood ppm __ PPTM 0.6- > 0.080 1.20 .282 .121 .305 .091 .518 .120 .593 .121 .693 .091 .667 .110 .473 .138 .633 .105 .518 .105 .525 .105 .344 .102 .462 .104 1 .586 .100 .549 .128 .244 .115 .487 .101 .838 .156 .773 .174 .414 .091 .205 .134 .623 .1.35 .415 ~ . r i r .437 . 1 2 1 .649 .135 Peps scrum odu 0.0-0.3 Fecal E\nm - t; s (f) .276 - - -- - _c(r)M___ -- -- -- -- -- -- -- .304 s(f) -- .302 S(0 - S(0 .334 s (0 .390 - -- - c(r);s(f) - 1- - c(r);s(m) -- -cC*> Data Tables DUP 289 Tennant Farm Herd Health Investigation Cattle Team Report Individual Animal Data: Cattle from Tennant Farm (Washington, West Virginia) Tabic 4: Hematology (leukon), Special Chemistry, and Fecal Exam (continued) Animal Age l'rcg. W1IC Number Status years 1 Reference Range: xIOVuI 4-12 Ncut % 15-45 Lymph Mono % 45-75 % 2-7 Eos % 2-20 Buso % 0-2 Proluditi elusile ng/ml 171.6 (105.8) Cu Sc*AA Peps mint ppm 0.61.20 hliinil __ PP1" > 0.080 scrum odu 0.0-0.3 Fedii cxnm 25 4 5 m 8.98 54.8 6.61 7.76 30.8 .026 47.76 .643 .161 -- 26 6 bull 6.09 64.6 17.4 6.87 10.9 .168 27 >9 8 m 5.69 56.4 16.2 8.79 18.4 .160 68.95 .778 .142 .184 S(m) 122.27 .443 .116 -- 28 7 8 m 5.92 69.9 19.1 .525 10.5 0.00 86.90 .396 .114 -- 29 >9 term 5.49 53.5 13.7 7.72 25.1_ 0.00 106.37 <0.20 .146 .224 neg. 30 >9 8 m 3.58_ 64.8 14.5 5.79 15.0 _ 0.00 44.53 .289 .114 -- 31 8 6 m 5*4r 59.2 18.2 ...3.61 _ J9 3 )_ 0.00 ' 157.00 .683 .139 s m - 32 >9 6 m 6.86 59.0 19.8 3.36 17.8 0.00 361.97 .488 .132 _ neg. 33 >9 8 m 6.76 70.4 4.69 6.72 18.2 .026 34 >9 8 m 5.19 57.6 19.5 9.81 13.0 __3)56_ 35 >9 5 m 5.40 383) 24.0 12.8. 25.1 .055 36 >9 8 m 4.39 57.1 ....17.5 ' 13.5 __ 113)__ 0.00 64.19 109.60 47.45 3064 0 .533 .434 ,679 .596" .105 .161 .140 .101 - .324 - - --------------- 1 - - s(D 37 7 calf 5.89 54.0 14.4 10.2 21.3 3)90 43.89 .732 .142 -- 38 >9 7 m 6.49 53.8 10.7 9.62 25.9 .022 143.13 .681 .124 -- co 39 >9 calf 4.72 35.5 35.5 7.47 21.5 03X) 48.70 .762 .109 qns - 40 4 6m 9.05 26.7 29.7 12.6 ! 30.9 .055____ ______ 207.43 .607 .146 . s (0 41 4 steer 9.57 52.3 31.3.......... 2.73 13.7 ' 0.00 80.12 .582 1 .143 .304 - N > Blood collected by jugular venipuncture during examination while cattle restrained in a head-hold device. Blood refrigerated for approximately 36 CD hours before hematology was run on an Abbott Cell-Dyne 3500. WBC (WIC values) considered valid; WBC differential (neutrophils, Oo lymphocytes, monocytes, eosinophils, basophils) considered invalid due to 36-hour storage of blood. c> V? Hematology reference values are for cattle (New Bolton Center), but not from the Cell-Dyne 3500. Selenium values of 0.050 ppm are considered marginal; below 0.050 ppm arc selenium deficient. Prolactin (heparin tubes)(Dr. N. Schrick, Univ. of Tcnn., Dept. An. Sci ). Ref. means: April non-fescue (171.6) anil ergotamine tartrate (105.8 ng/rnl). Cu = copper; Se-AA = selenium. (New Bolton Center) Peps = serum pepsinogen; odu = optical density units (Texas Veterinary Diagnostic Laboratory, College Station, TX) Fecal exam: c = coccidia oocysts; s = strongyle eggs; t = Monezia tapeworm eggs; (r) = rare; (f) - few; (m) = moderate. (New Bolton Center).______ * Data Tables Tennniil Poni) Herd I(colili Investigatimi C olile Teom Report Individual Animal Dala: Cattle from Tennant Farm (Washington, West Virginia) Table 5: Clinical Chemistry Animal Ago Frog. HUN Croat Nil+ K+ Cl- Cu Mg Pitos Number Status years mg/dl Reference 6 -2 2 Range: l4 4 m 14.7 23 open 10.5 3 >9 open 11.5 4 >9 7 m 10.8 5 >9 6 m 7.9 6 >9 3m n n 7 >9 6 m 13.5 8 >9 open 10.0 9 >9 open 8.5 10 >9 term 17.0 11 >9 8.5 m 11.6 12 >9 term 21.0 13 >9 open 15.9 14 >9 calf 19.6 15 >9 pregn. 21.2 16 6 open 17.8 17 >9 4 m 12.0 18 >9 4 m 8.2 19 >9 calf 14.3 20 >9 6 m 11.3 21 >9 5 m 17.4 22 >9 5 m 15.6 23 bull 8.5 24 >9 6 m 9.6 ine/ill 0.5 1.1 1.68 1.23 2.00 1.59 1.82 1.73 2.30 1.47 1.49 2.15 1.86 1.62 1.06 1.72 1.83 1.78 1.87 1.73 1.69 2.09 1.47 2.09 2.55 1.98 miwil/l 134 144 145 143 144 144 146 145 143 145 145 150 149 146 145 146 144 140 151 144 147 146 146 145 143 148 tnmol/I niiiMil/l 4.0- 965.7 K)4 5.14 102 4.95 106 6.00 105 4.78 106 5.06 107 4.55 107 6.27 102 6.13 106 5.60 104 4.91 109 4.81 III 4.64 109 5.52 105 5.55 103 5.02 104 5.44 J 0 1 6.46 _ 109 4.85 102 4.72 105 5.36 __107_ 4.77 1OS 5.42 _108 4.55 102 4.67 1 110 id^AII mp/dl iiift/d 8.2- 2.0- 4.7 - 10 2.8 9.0 9.8 2.3 5.73 8.75 1.9 7.02 9.42 2.2 5.80 9.21 2.1 7.24 7.71 2.0 9.31 9.87 2.2 5.09 9.00 1.7 6.66 9.58 1.9 5.30 9.39 2.1 5.35 9.93 2.2 6.11 10.24 2.3 5.02 9.56 1.7 4.76 9.10 1.8 5.20 9.83 1.8 7.35 8.42 2.0 6.37 9.44 2. j 7 5549_ 10.29 '2.1 ' 9.52 2.0 676 9.34 2.0 5.07 10.32 2.1 5.95 10.25 " 2 .3 ~ ' 63)7 10.40 . ,,22.22~~ 4.93 9.42 5.55 jKiL'L- 2.1 ' 7.03 Tot Alb Prot gA K/dl 5.8- 2.4 7.5 3.5 7.2 2.79 7.6 2.70 7.8 3.20 7.3 2.92 7.8 2.96 7.6 3.17 7.6 3.15 8.0 3.03 7.6 2.85 7.0 3.04 7.1 2..86 7.6 2.86 7.8 2.74 7.9 3.30 7.0 2.46 6.8 2.82 8 3 _ 3.35 7.9 ~ 3.42 7.1 3.01 8.1 3.07 7.9 3.06 '7.8 ' 3*25 7.6 3.08 7.5 3.03 (lob gA 3.03.5 4.41 4.90 4.60 4.38 4.84 4.43 4.45 4.97 4.75 3.96 4.24 4.74 5.06 4.60 4.54 3.98 4.95 4.48 4.09 5.03 4.84 4.55 4.52 4.47 AST CK CJGT U/L U/L U/L 58 - 22 - 100 64 126 _89_ 40 98 77 36 138 110 32 84 57 29 98 71 45 126 181 37 109 155 30 141 187 49 111 83 34 99 49 35 101 l j 97 76 27 37 141 97 42 127 86 35 106 52 34 96 85 30 109 87 31 141 298 39 126 79 28 113 92 35 103 96 __30_ 101 90 34" 109 97 33 109 116 37 $ Data Tables 000 DUP 291 Tennant Farm Herd Health Investigation Cattle Team Report Individual Animal Data: Cattle from Tennant Farm (Washington, West Virginia) Table 5: Clinical Chemistry (continued) Animal Ago P r e HIJN Creut Nt+ K+ Cl- Cu M Plios Tot Alb d o b AST CK COT Number sta i us Prot ------------- 1 years mg/dl mg/dl ininol/l nnnol/l nimnl/l mji/ril mg/dl g/dl g/dl g/dl U/L U/L U/L Reference 6 -22 0.5 - 134 - 4.0- 96- 8.2 - 2.0- 4.7 - 5.8- 2.4 - 3.0- 58- 22- Range: 1.1 144 5.7 104 10 2.8 9.0 7.5 3.5 3.5 100 _64_ 25 4 26 6 5 m 10.0 1.99 149 4.9.3 108 9.90 2.4 7.12 7.7 3.34 4.36 122 __138_ 29 _ bull 7.6 2.08 147 4.69 107 9.72 2.2 5.31 7.7 3.13 4.57 139 150 "54" 27 >9 8 m 14.3 1.72 149 4.97 113 10.18 1.8 3.67 7.4 2.94 4.46 138 133 39 28 7 8 m 14.7 2.07 147 5.44 110 9.83 2.4 5.04 7.6 3.20 4.40 102 123 33 29 >9 term 12.9 2.16 146 5.26 _109 _ 10.19 2.2 5.35 7.3 2.83 4.47 98 50 37 30 >9 8 m 14.1 1.64 143 5.42 ' 103 8.80 1 2.3 6.77 7.5 2.99 4.51 132 90 35 31 8 6 m 11.3 ~ 1.66 148 4.55 109 _ 10.33 ! ' 2.2 ~ 5.24 7.3 3.25 " 4.05 111 99 29 32 >9 6 m 18.8 1.72 143 4.36 106 9.80 2.2 4.72 7.3 2.98 4.32 89 126 43 33 >9 8 m 13.0 1.95 152 4.50 112 9.61 1.4 7.14 7.9 3.14 4.76 150 137 38 34 >9 8 m 19.6 2.56 149 6.27 n o 10.79 2.5 6.75 7.9 3.52 4.38 139 99 35 35 >9 5 m 7.9 1.81 148 5.77 _ 107 9.82 _ "2.3 5.30 _8.0_ 3.27 4.73 120 106 30 36 >9 8 m 15.1 2.09 147 5.56'" " n o ' 9.50 "~23 ' 5~43 "' 7.7 1 3.05 4.65 112 92 29 37 7 calf 9.8 1.92 146 5.55 106 9.43 2.0 4.12 8.2 3.43 i ?? ; 119 94 36 38 >9 7 m 13.0 1.97 149 4.35 112 9.65 2.1 5.34 8.2 3.47 4.73 206 173 39 39 >9 calf 6.4 2.03 145 4.90 102 9.44 1.9 5.31 8.1 3.01 5.09 135 79 33 40 4 41 4 6 m 15.0 1.94 147 5.05 108 J0.20 2.2 6.28 7.6 3.12 4.48 147 79 37 steer ! 8.3 1.72 "1 143 6.37 106 ' 9.95 ' "2.3 6.99 7.4 3.10 4.30 n o 192 26 ^ Blood collected by jugular venipuncture during examination while cattle restrained in a head-hold device. Blood refrigerated for approximately 36 hours C i before serum chemistry was run on a Kodak Ektachem. O Cattle were coralled for several hours on a warm day, without water, before blood samples were collected. Reference values are for cattle (New Bolton Center, Kodak Ektachem), except for globulin (Duncan and Prassc). **-1,1 --i i--i - - --" ' _ DUP 292 ' j Data Tables Tennant Farm Herd Health Investigation Cattle Team Report Indi vidimi Animal Data: Calile from Tennant Farm (Washington, West Virginia) co T> FO CD 03 o o > Table 6: Serology Animal Age Prig. Il LV .!oh tit's Um edia UVD UVD tlluc I.tpto Number Status Tnnpue ivrsl scrum test: elisa clisa sn sn micrnplatc AGID sn serum Reference samples Range: 14 4m neg neg . i,LT . . . "eg neg neg neg 23 open neg neg non neg neg neg neg 3 >9 open neg neg nep ncg neg neg ncg T 1 >9 7m neg ....neg....... neg neg neg neg. ncg 5 >9 6m neg neg neg neg neg neg neg 6 >9 3m neg neg neg__ neg ncg ncg neg 7 >9 6m neg neg nen neg neg "eg___ neg 8 >9 open neg neg neg neg neg neg neg 9 >9 open neg neg neg neg ncg ncg ncg 10 >9 term neg neg neg neg neg ncg neg 11 >9 8.5 m neg neg neg . "eg___ ncg " eS neg 12 >9 13 >9 14 >9 term open calf neg neg neg neg neg m ___ j i g s ___ "CE___ JS___ neg neg . neg___ ___ neg___ neg neg neg ___neg___ neg ___ ncg__ ___ neg__ ___ 1B___ i 15 >9 16 6 17 >9 18 >9 19 >9 20 >9 pregn. open 4m 4m calf 6m neg neg neg neg neg neg_ neg neg___ W E m I "eg___ n?g___ neS___ neg neg neg "eg. neg ......"eg___ neg neg "eg neg ncg neg neg neg ___neg___ neg "eg neg neg ...... ncg..... ncg ___ncg___ neg neg ___ neg___ neg neg ___neg___ 1:101) 21 >9 22 >9 23 . 5m 5m bull neg neg neg non ___neg___ neg ___neg___ neg__ "eg__ neg ___neg___ neg neg__ __ neg ___ neg___ neg neg neg neg ___neg___ ncg 24 >9_ 6 m __ ___neg___ ..... "eg . "eg..... neg neg . "eg...... ___ ncg___ EHD (type 2) AGID ncg ncg neg >1:8(1 - neg neg - - - - - 1 ______ Data Tables Tennant l'arm Herd Health Investigation Cattle Team Report Individual Animal Data: Caille from Tennant Farm (Washington, West Virginia) Table 6: Serology (continued) Animal Age Prt. Number Status BLV .lohne'* Brucella BVI) UVD Blue Tongue U'ptu Kill) (type 2) fyrs) scrum test: elisa clisa sn sn mieroplatc ACilD sn AGID serum Reference samples Range: " ~25~ 4 26 6 27 >9 5m bull 8m neg (neg)1 ... neg..... neg neg neg neg neg POS neg neg 1:256 neg ...."eg...... neg neg _ "eg___ neg neg neg neg - neg - 28 7 29 >9 8m term ne___ neg neg _ ne neg neg neg .. 1c- .._ "eg....... neg neg neg neg NIKI >1:80 30 >9 8m neg neg neg neg ncj* neg neg - 31 8 6m neg neg neg ne___ cg "eg___ neg neg 32 >9 6m neg neg neg neg neg "eg neg - 33 >9 8m neg neg neg neg neg neg___ 1:100 - 34 >9 8m neg neg __ neg___ ___ neg___ ___ neg___ ___ neg___ ___ neg___ neg. o 35 >9 36 >9 5m 8m neg neg neg- neg neg neg neg ___neg___ neg neg neg "eg neg ___ "eg . . 1 c uft 37 7 calf neg neg neg neg neg neg neg 38 >9 7m neg neg neg neg neg neg ___ "eg - IV) ro 39 >9 calf neg neg ___neg___ neg ___ n eg __ ___ neg___ neg & 40 4 6m neg POS neg ___ rlL___ .,,.n eg .__ ___ ."eg___ neg 1 41 4 steer neg neg | neg neg neg "eg neg neg O BLV = bovine leukemia virus antibody Cs Johne's =,M y c o b a c te r iu m p a r a tu b e r c u lo s is antibody (technique has a \ % false positive error rale) sCP Brucella = B r u c e lla a b o r tu s antibody :'V, Leplo = antibody to L e p to s p i r a s p p . ( L p o m o n a , L ic te r a h e n w r r h a g ia e , L h a r d j o, L g r ip p o ty p h o s a , L c a n ic o la ) . ! BLV, Johne's, Brucella, and Lepto assays conducted by the Animal Diagnostic Laboratory, Penn. State Univ., University Park, PA. EHD = 2 of 12 tested cattle were "positive" for HUD-type 2 (Alberta strain); ('rexas Vc[crinary Diagnostic Laboratory, College Station, TX). U* Data Tables Tennant Farm Herd Health Investigation Cattle Team Report Tennant Farm (Washington, West Virginia): Crain and Hay Analysis Table 7: Nutritional Analysis Huy Gruln Analyte Dry Malter units % as sampled basis 86.34 dry matter basis - as sampled basis 89.66 dry matter basis - Crude Protein Unavailable Protein Adj. Crude Protein % % % 6.77 1.90 5.55 7.84 2.20 6.42 10.21 - 11.39 '- - Acid Detergent Fiber % 40.44 46.84 7.59 8.46 TDN % 47.67 55.21 69.35 77.35 NE (Lactation) Mcal./lb 0.33 0.38 0.72 0.81 Calcium Phosphorus ppm ppm 0.40 0.10 0.46 0.12 0.95 0.30 1.07 0.33 Sodium % 0.02 0.02 0.37 0.48 Magnesium %. 0.13 0.15 0.30 0.34 Sulfur % 0.18 ~~ 0.21 0.13 0.14 cO Potassium Copper " Iron ro CD Manganese CJl o Zinc Nitrate Ion Selenium 1% ppm ppm ppm ppm % ppm 0.87 5 206 331 43 0.00 LOI 6 239 384 50 0.00 0.12 0.60 6 305 ! 22 39 0.67 7 340 24 43 1 0.19 Hay and grain feed analysis performed by NC Dept. Agric., Food and Drug Protection Division. Forage Testing Laboratory, 4000 Reedy Creek Rd, Raleigh, NC 27607. Hay and grain samples collected by cattle team during April 1999 site visit to Tennant Farm. Hay sample consisted of 3 core samples each from 3Jarge round bales of 1998 cut bay. Data Tables Tennant Farm Herd Health Investigation Cattle Team Repon 12.0 A PPE N D IC E S Appendix A: Abbreviated Curriculum Vitae of Cattle Team Members Appendix B: Diagnostic Pathology Reports Ohio Department of Agriculture: #4977-97 Michigan Animal Health Diagnostic Laboratory: #1792571 University of Pennsylvania Laboratory of Large Animal Pathology and Toxicology: #UP9902702, #9901437 Appendix C: Dry Run Safety Plan Appendix D: Figures 1-42 : Photographs of the 42 adult cattle; Figures 43-66 : Miscellaneous photographs of the Tennant Farm and cattle Appendix E: Herd Health History (April 8, 1999 interview) Appendix F: Diet Analysis: Computer Software Modelling 00 DUP 296 J"-T Tennant Farm Herd Health Investigation Cattle Team Report Appendix A: Abbreviated C u rricu lu m V itae oftheCattleTeam Members Name: Degrees. Certifications: Employment: Education: Dr. Perry L. Habecker V M D . Diplomate ACVP Chief. Large Animal Pathology. Laboratory o f Pathology and Toxicology. Univ. o f Penn. School o f Veterinary Medicine, New Bolton Center. Kennett Square, PA. Juniata College (BS. 1972-1976) University o f Pennsylvania. School o f Veterinary Medicine (V M D 1969-1973) University o f Pennsylvania. School o f Veterinary Medicine (resident. 1989-1992) Affiliations: American College o f Veterinary Pathologists Pennsyl vania Veterinary Medical Association American Association o f Veterinarv Laboratory Diagnosticians Name: Degrees. Certifications: Employment: Education: Affiliations: Dr. Lisa Davis-Heller DVM Private Practitioner. St. Mary's Veterinary C linic. St. M ary's. W V. Ohio State University Ohio State University. College o f Veterinary Medicine (D V M . 1979-198?> American Veterinary Medical Association Ohio Veterinary Medical Association Wes; Virginia Veterinary Medical Association International Veterinary Acupuncture Society Holistic Veterinary Societv Name: Degrees. Certifications: Employment: Education: A ffilia tio n s : Dr. Peter G. Moisan D V M . Diplomate ACVP.. Diplomate A B V P (food animal specialist: beef cattle specialist) Veterinary Pathologist and Field Investigator. Rollins Animal Disease Diagnostic Laboratory. North Carolina Department o f Agriculture. Raleigh. N C Cleveland State Community College (AS. 1974) East Tennessee State University (BS. M icrobiology. 1975) East Tennessee State University (MS. M icrobiology. 1978) University o f Tennessee. College o f Veterinary Medicine (D V M . 1981) Michigan State University (Resident, Veterinary Pathology, 1995) Kansas State University (Research. Veterinary Pathology, 1995-1998 American Board o f Veterinary Practitioners American College o f Veterinary Pathologists American Association o f Bovine Practitioners American Association o f Swine Practitioners Academy o f Veterinary Consultants American Veterinary Medical Association American Association o f Veterinary Laboratory Diagnosticians Appendix A; Abbreviated C u r r i c u l u m V it a e o f Cattle Team Members DUP 297 I noj r~ bcc: Andrew Hatien Rob Pinchot Sharron Laas J.HLLittIe HLD.Ramsey D.D.Jackson J.M.Migliore R-Baneijee KJ.Zipfel AJ.PIaytis PO^-70 EID089382 A N D R E A V. M A L I N O W S K I , ESQ. Senior Counsel DuPont Legal, Room D-7078 1007 Market Street Wilmington, DE 19898 Phone: (302)774-6443 Fax; (302)774-4812 January 12, 2000 VIA FAX (cover letter only) [413-448-6553] VIA OVERNIGHT MAIL (with attachments) Douglas Johns, Esquire Legal General Electric Plastics One Plastics Avenue Pittsfield, MA 01201 Dear Mr. Johns: This letter is further to our conversation of last week and more specifically in reply to items 1-3 of Mr. Dale Van De Velde's January 5,2000 e-mail to Bob Ritchey of DuPont concerning FC-143 (also referred to as C-8 or ammonium perfluorooctanoate). Item 1: TSCA 8(e) Decision Regarding item 1, DuPont did not submit a TSCA 8(e) notification to EPA concerning the presence of FC-143 in environmental media. The 8(e)-reportability of the presence of FC-143 in environmental media was reviewed within DuPont and determined to not be reportable. The reasons for that decision are as follows: The toxicology of FC-143 has been reported to EPA by both DuPont and 3M in numerous TSCA 8(e) submissions. I faxed to you last week a copy of the latest TSCA 8(e) submission, dated November 19, 1999 and made by 3M. Other submissions were made both before and during the TSCA 8(e) Compliance Audit Program. * The discharge of FC-143 into the Ohio River has been reported to EPA Region HI and the West Virginia Division of Water Resources (WVDWR). For example, in a June 9, 1981 letter (attached Document 11to the WVDWR (copy to EPA Region HI), it is stated that FC-143 is present in outfall 005 (permit WV0001279) in a concentration of about 0.1 mg/L. Outfall 005 discharges into the Ohio River. Note it EID089383 E. I. du Pont de Nemours and Comoany C. '';M 0 Printed on Recycled Paper LG-4178 Rev. 2/9a General Electric Plastics -2- January 12, 2000 was later determined that the defects observed in the study referenced in this letter were not caused by FC-143. i The presence of FC-143 in the aquifer underlying the Washington Works site has been reported to EPA Region III and the WVDWR. For example, attached Document 2 is an excerpt from Washington Works' Solid Waste Management Unit Survey submission made in 1985 to EPA Region III (copy to the WVDWR). In section B-4, paragraph entitled "Releases, Spills, etc.", it is stated that FC-143 has been detected in the aquifer at ppb levels. The presence of FC-143 in the Lubeck public supply wells in ppb levels has been reported to EPA Region in and the West Virginia Department of Natural Resources (WVDNR). For example, attached Document 3 is an excerpt from Washington Works' Verification Investigation Work Plan (VI) report submitte'd in 1990 to EPA Region HI (copy to WVDNR and the West Virginia Pollution Control Division). On page numbered 18 of the VI, it is stated that the Lubeck public supply wells have detectable levels (ppb) of ammonium perfluorooctanoate (also called C-8). Based upon the above correspondences, it was determined that the EPA Administrator had knowledge of the presence of FC-143 in various environmental media, both at the plant site and outside the boundary of the plant site. In addition, as you know, EPA guidance on the criteria for environmental TSCA 8(e) reporting is vague, uncertain, and currently (for the past several years) being rewritten. In its last Notice o f Clarification on TSCA 8(e) reporting criteria (58 FedReg 37735; July 13, 1993), EPA stated that "With regard to non-emergency environmental contamination information, EPA interprets section 8(e) to require reporting of information that provides evidence of widespread environmental distribution of a chemical substance or mixture, and which because of the extent, pattern, and amount of the contamination seriously threatens or may seriously threaten: (1) Humans with cancer, birth defects, mutation, death or serious or prolonged incapacitation ... or (2) non-human organisms with large-scale or ecologically significant population destruction. Thus, the mere presence of a chemical substance in an environmental media, absent some other relevant information as noted above, would not trigger reporting under section 8(e)." At the levels FC-143 is present in environmental media, DuPont concludes that FC-143 does not pose the threat or potential threat described above. In making the decision on 8(e) reportability, DuPont recognized that the guidance on 8(e) environmental reporting was in flux and it was decided that this decision would be reviewed again once EPA issues the new environmental guidance. EID089384 General Electric Plastics -3- Januaiy 12, 2000 Items 2 and 3: Correspondences to the Town and Test Data on Town Wells We have located the following correspondences about FC-143 to the town (Lubeck) and test data on the town wells: June 13, 1989 letter (attached Document 4) to the Lubeck Public Service Division (LPSD) in which it is stated on page 2 of the cover letter that FC-143 was detected in LPSD water taps in concentrations ranging from 1.0 to 2.2 ppb. We are not aware of any written response to this letter from the LPSD. Note that DuPont subsequently purchased these wells and that the LPSD now draws its drinking water from different wells, samples of which have also been tested by DuPont (see next bullet). March 23,1992 letter (attached Document 51 to the LPSD providing results of analyses performed on samples taken from three of the new LPSD wells. Results ranged from 0.09JX ppb to 0.4 ppb. Note that JX means estimate. We are not aware of any written response to this letter from the LPSI>. Follow-up If you need any additional information or further clarification, please do not hesitate to contact me. If GE should decide to submit an 8(e) notification, we would appreciate receiving a copy of it. Very truly yours, Andrea V. Malinowski Attachments cc: Steve Austin [Fax:413-448-6590] GE Plastics One Plastics Avenue Pittsfield, Mass 01201 Dale Van De Velde [Fax: 304-863-7128] Manager, Environmental Programs General Electric Company, Plastics Mfg. Div. P.O. Box 68 Washington, WV 26181 Robert Ritchey, DuPont Washington Works Bernard Reilly, DuPont Legal, Wilmington, DE EID089385 VV^OO in \ * Katherine E. Reed. Ph.O. Executive Director 3M Environmental Technology and Safety Services 900 Bush Avenue Building 42-2E-26 PO Box 33331 St Paul. MN 55133-3331 651 778 4331 3M November 19, 1999 CERTIFIED MAIL Document Processing Center (7407) (Attn: Section 8(e) Coordinator) Office of Toxic Substances T ic F P A 401 M Street, SW Washington, DC 20460 j .J J h i Qp-Mj- ( -c rsj CO zir~\ Re: TSCA 8(e) SUBSTANTIAL RISK NOTICE ON: Ammonium Perfluorooctanoate CAS# 3825-26-1 Dear Sir: 3M has recently completed a review of the draft report on a 6-month primate feeding study performed with ammonium perfluorooctanoate (PFOA) by Covance Laboratories, Madison, Wisconsin. Male cynomologus monkeys were given daily doses by intragastrie capsule deposition of 0 (n=6), 3 (n=4), 10 (n=6) and 30 (n=6) mg/kg ammonium perfluorooctanoate. Significant illness occurred in the 30 mg/kg dose group within several weeks. Dosing was stopped while the animals recovered. Dosing was resumed at 20 mg/kg. At the end of the six month dosing period, two animals in the control, mid and high dose groups were allowed to recover for 90 days. One high dose animal was sacrificed in moribund condition on day 29. This animal suffered hepatic lesions which are felt to be compound-related. Other high dose animals also exhibited liver toxicity. The following findings are being reported by 3M under TSCA 8(e): - Significant increased liver-to-body weight ratios were observed in all dose groups. There was no corresponding adverse pathology in the two lowest dose groups (3 mg/kg/day, 10 mg/kg/day) at terminal sacrifice. Liver weight increases were reversed after a 90 day recovery period. US ri <^=> - Preliminary analytical results indicate the serum levels of PFOA for these two lower 3= dose groups are similar to those found among the highest PFOA serum levels y? observed in a small number of 3M Cottage Grove chemical production employees. -- Workplace medical surveillance activities have been conducted at 3M since die 1970's. Employees' fluorochemical levels, whether measured as total organic fluorine or as PFOA, have not been associated with clinical hepatic toxicity. EID 102775 >< 3I0M 1 clcIO m A1*1'ITIM 8EHQ-99-1459G 88000000036 009 Document Processing Center (7407) (Attn: Section 8(e) Coordinator) Office of Toxic Substances US EPA Page No. 2 November 19, 1999 - In addition, one low dose (3 mg/kg/day) test animal was sacrificed in moribund condition on study day 139. An independent pathology review of this case did not reveal a specific cause of morbidity. The effects observed in this animal were not consistent with the significant hepatoxicity observed at the high dose and may not be compound-related. There were no effects, other than increased liver weight, in the remaining three animals tested at the low dose. This chemical is produced by 3M and is used by industrial customers as a process aid. 3M has and will continue to conduct medical monitoring of its chemical production workers and to reduce potential for worker exposure. A copy of the final study report will be sent to the EPA when received. Please contact Dr. William Weppner, 651-733-6374, for further information. Sincerely, EID102776 AVM000210 112 eoo Dear Gerry, As discussed on April 13 by phone, EPA needs to review complete copies of final reports and any other relevant information in your possession or control on carboxylated and sulfonated perfluorochemicals, with initial focus on PFOA (perfluoro octanoic acid). The requested information includes health effects studies (including pharmacokinetics), environmental effects studies, environmental fate studies and information, and human and environmental exposure studies and information, including monitoring. If final reports are not available, we request that you clarify the status of any ongoing studies with regard to projected completion date and provide us with the latest and most complete version of any preliminary reports in your possession or control. We request that you provide us with the above information on PFOA by May 26, 2000. Regarding the sulfonated perfluorochemicals, our initial interest is focused on perfluorooctyl sulfonic acid (PFOS) and we request that you provide the above information on PFOS by April 28, 2000. If you have any of the above information on other carboxylated or sulfonated perfluorochemicals, we request that, by April 28, 2000, you initially identify the chemicals to allow us to confirm our interest, and then provide the requested information in your possession or control on other sulfonated perfluorochemicals by May 19, 2000 and on other carboxylated perfluorochemicals by a week later, May 26, 2000. The information on these additional chemicals can most usefully be provided in chemical specific increments as they are completed, with completion of the full submissions by the dates requested. A few points of clarification regarding this request: >duPont need not resubmit copies of studies already provided to EPA (e.g., under TSCA 8(e), as FYIs, under FIFRA) although we do request that you provide a comprehensive bibliography of the studies already submitted so we can check this against our holdings. >copies of acute systemic toxicity studies can be limited to the key or critical studies as described in the Data Adequacy and robust summary guidance developed for the HPV Challenge Program. Under this approach all studies will be cited in a bibliographic listing although full copies can be limited to studies which (1) serve to identify lowest (i.e., most toxic) lethal dose values by different routes or (2) report observed effects which differ from those seen in studies (using the same route) submitted under (1). >skin and eye irritation studies can be handled in a manner consistent with that outlined for acute systemic toxicity (i.e., submit copies of the key or critical studies which serve to set out the irritation potential of the chemical and other irritation studies which show effects which differ from those reported in submitted studies). >the initial request is generally limited to studies conducted during or after 1976. For studies conducted prior to 1976, we ask for a bibliography listing all studies and for full copies of studies in the following endpoint areas: genetic toxicity; subchronic toxicity; reproductive tjoxicity; developmental toxicity; immunotoxicity; uptake/metabolism; chronic toxicity/carcinogenicity; neurotoxicity. regarding exposure information, we are most interested in receiving information and data of the types found in the Use and Exposure Information Profile {UEIP; the UEIP has been used to support SIDS assessments in the US) and information on results of exposure or monitoring studies (human and environmental), including full copies of studies where available and including details on procedures and methods used for sampling and analysis. We are also interested in studies relating to the ultimate environmental fate and distribution of these chemicals. v C00- EID080127 In order to maintain the integrity of your submissions, please submit all information on a given chemical as a separate "For Your Information" (FYI) submission. You may also submit the information as supplements to any prior submissions by your company under TSCA 8{e) relating to these chemicals. As always, any CBI must be submitted in accordance with applicable procedures. If you have any questions with regard to the submission procedures, or you wish to work out the arrangements in advance, please contact Terry 0?Bryan (202-260-3483). If you have any general questions regarding this request, please contact me by email or phone (202-260-3749). I thank you in advance for your cooperation. Charles M. Auer, Director Chemical Control Division Office of Pollution Prevention and Toxics/OPPTS/EPA AJP001522 * 000 E 1D 0S0^2S 113 OOOfcO H David Ramsey 05/19/2000 12:42 PM To: cc: Subject: John L Granquist/AE/DuPont@DuPont, Robert L Ritchey/CL/DuPont@DuPont, Lynwood K lreland/CL/DuPont@DuPont, John E Auger/AE/DuPont@DuPont, John M Migliore/AE/DuPont@DuPont, Robbin Banerjee/AE/DuPont@DuPont, Dawn D Jackson/CL/DuPont@DuPont, Anthony J Playtis/CL/DuPont@DuPont, Roger J Zipfel/AE/DuPont@DuPont, Oscar T Garza/A/DuPont@DuPont EPA Side of PFOS Story - NY Times -------------- Forwarded by H David Ramsey/AE/DuPont on 06/19/2000 12:41 PM .... ...... ..... -- From: Bernard J Reilly on 05/19/2000 06:32 AM To: cc: Subject: Robert F Pinchot/DEV/AE/DuPont@DuPont, Michael E McCord/AE/DuPont@DuPont, Richard J Angiullo/AE/DuPont@DuPont, John S Sieg/EUR/DuPont@DuPont, H David Ramsey/AE/DuPont@DuPont, Paul J Bossert/AE/DuPont@DuPont EPA Side of PFOS Story - NY Times May 19, 2000 E.P.A. Says It Pressed 3M for Action on Scotchgard Chemical By DAVID BARBOZA CHICAGO, May 1 8 - The Environmental Protection Agency said today that it had pressed Minnesota Mining and Manufacturing to come up with a solution after the company's own tests had shown that a chemical compound used in Scotchgard and an array of household products could pose a risk to human health and the environment. The E.P.A. account differs from that of 3M, which said on Monday that it had voluntarily decided to stop making the chemical used in Scotchgard and many other products by the end of the year because the tests showed that the chemical compounds failed to decompose in the environment. Officials of 3M say they have no evidence that the chemicals pose a long-term threat to human health. While the E.P.A. said it did not see an immediate safety risk for consumers using products now on the market, agency officials said that if 3M had not acted they would have taken steps to remove the product from the market. The officials said they grew concerned about potential long-term health risks to humans after a 3M study showed that the chemical, perfluorooctanyl sulfonate, lingered for years in human blood and animal tissue and that high doses were known to kill laboratory rats. T h e results raised a number of concerns," said Stephen Johnson, who works in the office of prevention, pesticides and toxic substances at the E.P A "What it suggests to us is that there are potentially long-term consequences. But we don't have evidence it is unsafe now." Officials of 3M, however, say they are absolutely confident that their products are safe, and that there are no long-term consequences to human health. T h is isn't a health issue now, and it wont be a health issue," said Lany Zobel, the medical director at 3M., which is based in St. Paul. T o the question of whether this builds up in humans, it would have to be a long time, like hundreds of thousands of years, to be a threat," he said. Many scientists have praised 3M's decision to stop production of perfluorooctanyl and related chemicals. \ ooo E1D080088 "The real issue is this stuff accumulates, and if it accumulates in the ecosystem, you have to be worried about that because it could be trouble," said John Doull, a retired professor of clinical toxicology at the University of Kansas Medical Center in Kansas City. "No chemical is totally innocuous, and it seems inconceivable that anything that accumulates would not eventually become toxic." In addition to Scotchgard products, the chemical is used as stain repellant and protective coating on textiles, carpets and leather, and in paper packing, snack-food bags, pet- food bags, firefighting foam and pesticides. The E.P.A. said its decision to press 3M rested on four concerns: the compound is persistent in the environment; it appears in wildlife and human tissue around the world; it appears in human blood samples taken from around the world; and, based on the study of laboratory rats, it has the potential to harm humans. The E.P.A. said it was first alerted to the study of laboratory rats shortly after it was conducted in 1998. In that study, male and female rats were given doses of the chemical and then mated. When a pregnant rat continued to get regular doses of about 3.2 milligrams per kilogram of body weight, most of the offspring died within four days. "With all that information, we finally talked to 3M and said that raises a number of concerns. What are you going to do?" said Mr. Johnson at the E.P.A. There is still a difference of interpretation, however. Officials of 3M said the doses given to the rats were extremely high, but E.P.A. officials said that few other chemicals would have as severe an effect. "This is fairly toxic stuff in rats," one E.P.A. official said. "There's clear evidence it presents a problem in rats." But 3M said it had not yet determined the cause of death in the rats nor how humans or animals ingested the chemicals so that it appeared in tissue or blood samples. "That's a very interesting question," Mr. Zobel said. "We cant say how it gets into anybody's blood." As a result of that uncertainty, and the persistence of the compound in the environment, 3M said it would do away with the chemistry by the end of the year. The company said it negotiated with the E.P.A. but its decision was voluntary and there was never a discussion of a recall of the products. 3M, which is the only company known to make perfluorooctanyl, has been searching for alternatives. But in recent weeks, after the E.P A asked 3M to come up with a solution, the company decided to discontinue using the chemistry behind most of its Scotchgard products, which account for about $300 million in sales, or less than 2 percent of the company's $16 billion in annual revenue. Since the announcement on Monday, the company's shares have gained $1.125, closing at $87.0625 today. 3M, which also produces Post-it notes and Scotch tape, will stop supplying the chemical to other companies that use it for their products. v. 00 0c EID080089 V 114 f OOO c / H David Ramsey 05/19/2000 12:46 PM To. cc: Subject: Dawn DJackson/CL7DuPont@DuPont, Robert L Ritchey/CLiDuPont@OuPont, John M Migiiore/AE/DuPont@DuPont, Anthony J Playtis/Cl/DuPont@DuPont, Roger J Zipfel/AE/DuPont@DuPont, Oscar T Garza/AE/DuPont@DuPont, Lynwood K lreland/CL/DuPont@DuPont, John E Auger/AE/DuPont@DuPont EPA and Canada on PFOS and Related Perfluoroalkyls - SNA News Clip Forwarded by H David Ramsey/AE/DuPont on 05/19/2000 12:45 PM From: Bernard J Reilly on 05/19/2000 06:48 AM To: Robert F Pinchot/DEV/AE/DuPont@DuPont, John S Sieg/EUR/DuPont@DuPont, Paul J Bossert/AE/DuPont@DuPont, H David Ramsey/AE/DuPont@DuPont, Andrea V Malinowski/AE/DuPont@DuPont, Jim E Pesek/AE/DuPont@DuPont, Susan S Mileti/DuPont@DuPont, Robert C Buck/DuPont@DuPont, Richard J Angiullo/AE/DuPont@DuPont. Martha L Rees/AE/DuPont@DuPont@DuPont, John R Bowman/AE/DuPont@DuPont@DuPont, Earl W MacFar1ane/AE/DuPont@DuPont, James K Higgins/AE/DuPont@DuPont, Erin Mariani/AE/DuPont@DuPont, Gerald L Kennedy/AE/DuPont@DuPont, Marjorie W Doyle/AE/DuPont@DuPont, Isidoros J Zanikos/AE/DuPont@DuPont, Hugh J Campbell_Jr/AE/DuPont@OuPont, Michael S Parr/AE/DuPont@DuPont, Darwin G Wika/AE/DuPont@DuPont cc: Subject: EPA and Canada on PFOS and Related Perfluoroalkyls - BNA News Clip No. 98 Friday, May 19, 2000 Page A-14 ISSN 1521-9402 News Chemical Safety EPA Has No Regulatory Plans on PFOS; 3M Has Major Research, Testing Under Way It is too early to know whether regulatory action is needed on a group of chemicals being pulled from the market by 3M, an Environmental Protection Agency official told BNA May 17. At the same time, the company has vowed to conduct further health and environmental tests to better understand how perfluorooctanyl sulfonate (PFOS) chemicals, which are used in certain stain-resistant Scotchgard products, persist and move through the environment, even though the company said the chemicals posed no health threat. The St. Paul, Minn.-based company announced plans May 16 to phase out a profitable product line that uses PFOS-based chemicals after sending EPA a substantial risk report and boxes of follow-up information. The Toxic Substances Control Act requires submittal to EPA of information about the adverse effects of industrial chemicals (96 DEN A-1, 5/17/00). EPA Searches for 'Cousins.' JMM008I63 C0 0 >'J- EID072413 EPA is trying to determine how many discrete PFOS chemicals are being made and how may related "cousin chemicals" are being made, Charles Auer, director of EPA's Chemical Control Division in the Office of Pollution Prevention and Toxics, told BNA May 17. The agency is particularly interested in identifying the polymers that are being made with a similar chemistry, he said, although most polymers are not measured in the TSCA reporting and tracking mechanisms. Because PFOS is an old product--its production began more than 50 years ago-EPA has not required manufacturers to conduct environmental or health tests on it. However, as one top 3M official said, the company has conducted virtually every toxicity test known on PFOS, and some studies have been done more than once. EPA expects to identify "tens of substances" in commerce that may need to be reviewed for possible regulatory controls, Auer said. Auer said that while 3M was the predominant manufacturer of PFOS materials, it was not the only company making or handling the substance in the United States. He said data collected periodically by EPA on chemicals made or imported into the United States indicate that there are other companies that at least have the capability of making the materials. The technology used to make the substance-electrochemical fluorination or EC F-is used in other countries, he said. Because the technology for making PFOS-related chemicals exists in other countries, U.S. officials will lead a discussion about whether worldwide controls are needed at an upcoming working group meeting of chemical regulators from the Organization for Economic Cooperation and Development, Auer said. PFOS are not reported to the annual Toxic Release Inventory, he said. However, chemical companies that handle more than 10,000 pounds of the material are required to report production volume and other information to EPA every four years in the "TSCA Inventory Update" of chemicals in commerce, Auer said. He also said PFOS chemicals are not among the chemicals currently being looked for in any of the federally funded exposure studies that seek to measure and identify levels chemicals and pesticides in human blood and tissue. Some agency staff have described PFOS as "sailing under the agency regulatory radar screen," Auer said. "It's too early to know whether a regulation is needed'' under TSCA that would require companies to report or control their production, or whether letters to companies encouraging action on their part, such as 3M's voluntary withdrawal from the market, would address this issue, Auer said. Company's Responsibility Top 3M officials interviewed by BNA said the company was undertaking research and testing for the chemical because the company has a responsibility to understand how its products interact with the environment, even after a product's commercial life has ended. Bill Coyne, senior vice president for research and development at 3M, told BNA "the reason we are phasing out this product is that it is not sustainable," even though it has been shown to be safe in dozens of toxicity tests. The fact that minute quantities of this material have been identified in the environment and persist in the environment is reason enough to act. he said. 0 0 9 ( EID072414 3M has turned in several boxes of data on this chemical, and more boxes are expected to arrive shortly, an EPA official said. The information is housed in the TSCA public docket in Washington. The 3M materials are identified as HQ-04-00373 in the TSCA Section 8(e) substantial risk and "for your information" reports, the official said. The primary PFOS chemical that has been the subject of most of 3M's testing and analysis is potassium perfluorooctane sulfonate (CAS No. 2795-39-3), an EPA official said. No Substitutes Yet Researchers at 3M have said they are three to five years away from finding a substitute for PFOS in most of its Scotchgard products, Coyne said. He noted that a few Scotchgard products will remain in commerce because they are formulated differently. Coyne said that by the end of 2000, production will be halted at both 3M manufacturing sites-one in Alabama, the other in the Netherlands. The decision to abandon a $300 million product line without a substitute ready was "not all that hard" once the data showed the presence of PFOS in places where it was not expected, he said. The company began efforts to reduce releases of the substance when it was discovered in minute quantities in blood from a blood bank two years ago, Katherine Reed, a top 3M scientist, explained. 3M scientists have developed and refined the laboratory methods that were used to detect the chemical, she said. The methodology, which has good laboratory practices associated with it, will be submitted for publication in a scientific journal soon, she said. Canada Welcomes 3M Oecision O TTAW A-The Canadian government welcomes the decision by 3M to phase out by the end of 2000 the use of perfluorooctanyl chemistry in some of the company's specialty materials, Environment Minister David Anderson said May 16. Perfluorooctanyl chemicals were among the commercial chemicals in the perfluoroalkyl (PFA) class of substances identified in 1999 under the Canadian Environmental Protection Act (CEPA) as requiring further review as potential threats to the environment or human health, Anderson said in joint statement with Health Minister Allan Rock. The Canadian government learned in March 2000 that the U.S. Environmental Protection Agency was also studying that class of chemicals, the statement said. "In the coming weeks, Health Canada and Environment Canada officials will use the authorities in CEPA to identify all manufacturers and importers of the chemicals and gather information on Canadian usage and toxicological information," it said. By Peter Menyasz Copyright 2000 by The Bureau of National Affaire, Inc., Washington D.C. EID072415 3M Phasing Out Some of its Specialty Materials ST PAUL. Minnesota - May 16, 2000 - 3M today announced it is phasing out of the perfluorooctanyl chemistry used to produce certain repellents and surfactant products. The affected product lines represent about two percent of 3M's nearly S16 billion in annual sales. These include many Scotchgard products, such as soil, oil and water repellent products; coatings used for oil and grease resistance on paper packaging; fire-fighting foams; and specialty components for other products. 3M said it plans to substantially phase out production by the end of the year and will work with customers to accomplish a smooth transition "Our decision anticipates increasing attention to the appropriate use and management of persistent materials," said Or. Charles Reich, executive vice president, Specialty Matenal Markets. "While this chemistry has been used effectively for more than 40 years and our products are safe, our decision to phase out production is based on our principles of responsible environmental management." "We're reallocating resources to accelerate Innovation in more sustainable opportunities and technologies. This decision is not only in the public interest, it's in the best interests of all our constituencies ... our employees, customers, communities and investors," Reich said. Sophisticated testing capabilities - some developed in only the last few years - show that this persistent compound, like other materials in the environment, can be detected broadly at extremely low levels in the environment and in people. All existing scientific knowledge indicates that the presence of these materials at these very low levels does not pose a human health or environmental risk. 3M expects to meet consensus earnings estimates for the rest of. 2000. This excludes a one-time charge on the order of $200 million, that will be taken sometime this year. "Our growth engines are more powerful than ever and we're confident in our ability to continue delivering on expectations," said L.O. OeSimone, chairman and CEO. "Many of our new technology platforms directly address the fastest-growing segments of the new economy such as electronics, telecommunications and flat-panel displays." "We expect the positive momentum in our financial performance to continue into 2001 with earnings somewhat above current analyst estimates," OeSimone said. 3M is a leading manufacturer of innovative products for industrial, consumer, trans-portation, safety, health care and other markets, with operations in more than 60 countries worldwide. The company is well known for its "Pollution Prevention Pays' environmental initiative, and its emission reduction programs including water-based replacement of solvents in manufacturing and replacements for ozone-depleting chlorofluoroearbons (CFCs). Forward-Looking Statements Certain portions of this news release that do not relate to historical financial information constitute forward-looking statements. These forward-looking statements are subject to certain risks and uncertainties. Actual future results and trends may differ materially from historical results or those expected depending on a variety of factors, including: (1) worldwide economic conditions; (2) foreign exchange rates and fluctuations in those rates; (3) the timing and acceptance of new product offerings: (4) raw materials, including shortages and increases in the costs of key raw materials; and (5) legal proceedings. Scotchgard is a trademark of 3M company. From: 3M Public Relations 3M Center, Building 225-1S-15 St. Paul, MN 55144-1000 Phone: (651) 733-6805 E-mail: www.3m.oom [3M Home] [News and Profile] [Press Box] Copyright O 1997 3M. All rights reserved. Legal Guidelines eoo;- EID0724I6 fr r COOf 5 aaUBDs DuPont H askell Laboratory DuPont Haskall Laboratory for Toxicology and Industrial Medicine Ekton Road, P.0. Bax SO Newark, DE 13714-0050 RECEIVED JU L 0 6 7pfi0 LEGAI May 25, 2000 Mr. Charles M. Auer, Director U. S. Environmental Protection AgencyOffice of Pollution Prevention & Toxics Chemical Control Division 401 M Street, N.W. - Room 403 Washington, D.C. 20460 Dear Mr. A uer As requested, enclosed are the summaries of studies conducted at DuPont Haskell Laboratory with Ammonium Perfluorooctanoate and Perfluorononanoate. If you have questions, please contact me at (302) 366-5259. GLKijhh Enclosures E. L du P o n t do Nem ours end Com pany Director - Applied Toxicology and Health 000 EID091521 @ Printed on R ecyd ed P tp tr SUMMARY OF A STUDY CONDUCTED WITH POTASSIUM PERFLUOROALKYL SULFONATE (PFOS) AT DUPONT Type: Species/Strain: Sex/Number: Exposure Period: Frequency of Treatment: Exposure Levels: Method: Biopersistence Screening Study Rats/Crl:CDSD(IGS)BR Male/5/group 5 or 10 days; 94 days of recovery Ad libitum for 5 or 10 days Ammonium perfluorooctanoate: 20 mg/kg Potassium perfluoroalkyl sulfonate (PFOS): 10 mg/kg Six groups of rats were administered ammonium perfluorooctanoate, 1 group received the test substance for 5 consecutive days and the other 5 groups received the test substance for 10 days. Approximately 2 hours after the first dose, blood was collected from each rat from the group designated for 5 doses. These same rats were sacrificed on test day 5 approximately 2 hours post-dosing, and blood and livers were collected. The remaining groups received the test substance for 10 days. Five rats were sacrificed and had blood and livers collected on test days 10 (2 hours post-dose), 13, 24, 52, or 93/94. The total fluorine content of the blood was determined by using a Wickbold torch combustion method, followed by analysis with a fluoride ion selective electrode. Body weights and clinical signs were recorded throughout the test. Liver weights were recorded, but not reported. Six groups of rats were administered potassium perfluoroalkyl sulfonate as described above. Food and water were available ad libitum throughout the test. Com oil was used as the vehicle for the ammonium perfluorooctanoate test groups. GLP: Test Substance: Potassium perfluoroalkyl sulfonate was dissolved in acetone before suspending it in com oil. The ratio of acetone to com oil was 20:80. Negative controls of com oil and com oil/acetone were also tested as described above. No Ammonium perfluorooctanoate, purity 93-97% Results: Potassium perfluoroalkyl sulfonate, purity 82-86% CAS #2795-39-3, 3-8% CAS #3871-99-6,3-7% CAS #29420-49-3, 1-3% CAS #60272-25-1 Rats dosed with am m onium perfluorooctanoate exhibited wet perineum and diarrhea during the dosing period. Alopecia was observed during the recovery period. The normalized jjM equivalents (blood organofluoride levels) in rat blood.peaked after EID091522 Reference: 5 days of dosing and then decreased throughout the testing period. The Cmax was 518.12 44.89 ppm with a terminal half-life of 8.3 days. The AI (Accumulation Index) was 12.5 and the BI (Bioaccumulation) was 6497.5. An area under the curve (estimated to infinity) (AUCINF/D) was calculated and normalized for fluorine content. The AUCINF/D was calculated as 70,789.6. Rats dosed with potassium perfluoroalkyl sulfonate exhibited diarrhea, salivation, alopecia, black ocular discharge, and staining of various parts of the body during the dosing period. Alopecia was observed during the recovery period. The normalized lM equivalents (blood organofluoride levels) in rat blood continued to rise throughout the dosing period and may not have reached steady-state. The Cmax was 989.85 116.90 ppm with a terminal half-life of 40.5 days. The AI was 59.0 and the BI was 58382.2. The AUCINF/D was calculated as 566,479.1. DuPont Co. (2000). Unpublished Data, Haskell Laboratory Report No. 2922. SUMMARY OF STUDIES CONDUCTED WITH AMMONIUM PERFLUOROOCTANOATE AT DUPONT Ecotoxicity Type: Value: Breakdown products: Method: GLP: Test Substance: Results: Biodegradation 13% at Day 28 C02 Modified Strum Test (OECD 301 B). In this test, biodegradability was measured as C 0 2evolution. Activated sludge was used as the inoculum. No Ammonium perfluorooctanoate, purity assumed 100% Ammonium perfluorooctanoate (30% solution) did not demonstrate "Ready Biodegradability." Note that failure to pass a "Ready Biodegradability Test" does not imply that the test substance will persist in the environment for an extended period of time. The toxicity test, which included both the test substance and the reference chemical (sodium benzoate) in the same flask, yielded < 25% biodegradation within 14 days; therefore, ammonium perfluorooctanoate was considered inhibitory to microorganisms in the inoculum. EID091523 Reference: Type: Method: DuPont Co. (1997). Unpublished Data, AEM Laboratory Report No. 24-97. Adsorption-Desorption Screening Studies * Ammonium perfluorooctanoate adsorption/desorption screening studies were performed on several test materials, including two clays, a washed sand, peat moss, and an agricultural soil from Delaware, USA. The adsorption/desorption screening studies were also performed using two surface soils and two sediments from the Ohio River collected in the vicinity of the DuPont Washington Works plant near Parkersburg, West Virginia. s The adsorption/desorption procedure used in this study was adapted from a metho<?developed by the Office of Prevention, Pesticides and Toxic Substances (OPPTS), United States Environmental Protection Agency for use in the testing of pesticides and toxic substances, and the development of test data iUS EPA (1998). Fate, transport and transformation test guidelines: OPPTS 835.1220 sediment and soil adsorption/desorption isotherm. United State Environmental Protection Aeencv. Office of Prevention, Pesticides, and Toxic Substances, EPA712-C-98-048). Except for the clays, all samples were screened through a 2-mm (10 mesh) stainless steel sieve in preparation for the absorption/desorption screening test. Furthermore, the sand was washed using DI (deionized) water through 2-mm and 50-|im stainless steel sieves. Material retained on the 50 pm sieve was used in the study. The sand, soils, and sediments used in the studies were air-dried prior to use. Data calculations, however, were based on oven-dry weights of the samples. Oven-dry weights were determined after drying a subsample of material in an oven at 105C for a minimum of 24 hours. The pH of the samples was determined in a ratio of 1:1 (test substance to water). Percent organic matter was determined using the loss on ignition method. Screening Test: Adsorption Studies The adsorption test was performed in duplicate on each material. A blank containing 0.01M CaG^ solution with test materials and no ammonium perfluorooctanoate and a single control at each ammonium perfluorooctanoate concentration but no material were also included. Each material was equilibrated with the aqueous phase of a solution of the test substance at 50, 500, and 5000 pg/L EID091524 3 0 0 9k. ST: prepared in 0.01M CaCl2 Sterile 50 mL polypropylene centrifuge tubes were used as the test vessels. One part air-dried material (4.0 g) was weighed and 5 parts test solution (20 mL) were decanted into centrifuge tubes, except the control tube. The centrifuge tubes were secured on an end-over-end mixer and agitated at approximately 30 rpm for 24 hours. Samples were centrifuged for 20 minutes at 4000 x g, and then filtered through a 0.2 pm nylon syringe filter into a new centrifuge tube. The volume of aqueous supernatant was measured and refrigerated at approximately 5C until analyzed for the parent compound using an LC-MS. The blank and the control tubes were subjected to the same steps as the test systems, including filtering. Screening Test: Desorption Studies GLP: Test Substance: Results: A fresh volume of 20 mL of 0.01M CaCl2 solution without the test substance was added to each solid phase (pellet). The sample was mixed, centrifuged, filtered, stored, and analyzed as was done in the adsorption studies. This desorption step was repeated a second time, resulting in two washings that were analyzed separately. No Ammonium perfluorooctanoate, purity not applicable Five of 9 materials tested for the adsorption/desorption characteristics of ammonium perfluorooctanoate (peat moss, Upstream sediment, East Wood soil. Garden Area soil, and Kaolin clay) exhibited significant adsorption (> 25% of ammonium perfluorooctanoate added) at one or more of the added concentrations of ammonium perfluorooctanoate. Sand, Montmorillonite clay, Downstream sediment, and Sassafras soil did not adsorb a significant amount of ammonium perfluorooctanoate at any concentration. Only peat moss, however, adsorbed a significant amount at all three concentrations of added ammonium perfluorooctanoate. Kaolin clay adsorbed a significant amount of ammonium perfluorooctanoate at 500 and 5000 pg/L. The Garden Area soil collected at Washington Works also adsorbed significant amounts of ammonium perfluorooctanoate at 500 pg/L. Upstream sediments from the Ohio River and East Wood soil adsorbed a significant amount of ammonium perfluorooctanoate at 50 pg/L only. Once adsorbed on peat moss, most of the ammonium perfluorooctanoate (> 76%) did not desorb after two washings with a solution of 0.01M CaCl2 . For the Kaolin clay, most of the A HID091525 eook-i.'-* h Reference: ammonium perfluorooctanoate adsorbed when added at 5000 pg/L desorbed with washing (> 60%). At ammonium perfluorooctanoate added at 500 pg/L, however, an average of 98% did not desorb from the Kaolin clay after two washings. The East Wood soil, which adsorbed 46% of the ammonium perfluorooctanoate added at 50 pg/L desorbed only about 2%. For the Garden Area soil 57% of the ammonium perfluorooctanoate desorbed when adsorbed from the 500 pg/L solution. No measurable desorption of ammonium perfluorooctanoate from the Upstream sediment after two washings was observed when the ammonium perfluorooctanoate was added at 50 pg/L. DuPont Co. (2000). Unpublished Data, Report No. EMSE-053-00. Acute Toxicity to Fish Type: Species: Value: Method: L96ep-hoomuirsmLCac5r0ochirus(bluegill sunfish) 634 mg/L (95% fiducial interval, 567-725 mg/L) A rangefinding study was conducted using nominal test concentrations of 0,0.1, 1, 10, 100, and 1000 mg/L. For the definitive study, nominal test concentrations were 0, 262, 328,410, 512, 640, 800, and 1000 mg/L. Glass aquaria (20 L) containing 10 L of test solution were employed. Positions of test chambers in the water bath used to maintain constant temperature were assigned using random numbers. Ten fish were added to each replicate using random numbers ( 2 replicates per concentration; total 20 fish per concentration). Control fish ranged from 1.2-2.8 cm standard length (mean 2.1 cm) and 0.0451-0.524 g wet weight (mean 0.228 g). Control loading was 0.23 g/L at test conclusion. Fish were not fed approximately 24 hours prior to and during the test. A photoperiod of 16 hours light (312-344 Lux) versus 8 hours darkness was employed with 25 minutes of transitional light (<2.15 Lux) preceding and following the 16-hour light interval. Observations for mortality and behavioral effects were made daily. Dissolved oxygen, pH, and temperature were measured in each replicate before addition of fish at test start, daily, at total fish mortality, and/or at test end. Total alkalinity, EDTA hardness, and conductivity of the control water were measured before fish were added at test start. A continuously recording thermometer in a water-control replicate was used to check temperature variations during the 96-hour test. Chemical analyses of the test substance concentrations in water were not performed. EID091526 GLP: Test Substance: Results: The LC50 value and its 95% fiducial interval were calculated. Yes Ammonium perfluorooctanoate, purity 99% Mortality in the rangefinding study after 96 hours was 0, 0, 0, 0, 0, and 80% at 0, 0.1, 1, 10, 100, and 1000 mg/L, respectively. Total mortality was 0, 5, 10, 15, 30, 40, 65, and 95% in the 0, 262, 328, 410, 512, 640, 800, and 1000 mg/L concentrations, respectively. All deaths occurred within 24 hours, with the exception of 1 death at 48 hours at 1000 mg/L. No behavioral effects were noted at < 640 mg/L. Surviving fish at 800 and 1000 mg/L were lethargic. Reference: Type: Species: Value: Method: All chemical and physical parameters were within expected ranges. Total alkalinity, EDTA hardness, and conductivity of the dilution water control were 79 mg/L CaCC^, 76 mg/L CaC0 3 , and 165 pmhos/cm, respectively. During the test, dissolved oxygen concentrations ranged from 6.7-8.5 mg/L, pH ranged from 6.9-7.4, and temperature ranged from 21.4-22.1C. DuPont Co. (1994). Unpublished Data, Haskell Laboratory Report No. 61-94. LC96-hour 50 Oncorhynchusmykiss(rainbow trout) 4001 mg/L (95% confidence interval, 3327-4932 mg/L) A static rangefinding study with 5 fish per concentration was conducted using a dilution water control and nominal concentrations of 50, 100, 500, 1000, and 5000 mg/L. Nominal concentrations of 625, 1250, 2500, 5000, and 10,000 mg/L (20% solution of ammonium perfluorooctanoate in water) were chosen for the definitive test based on the results of the preliminary rangefinding study. Test chambers were stainless steel aquaria that held approximately 9 L of test solution. Two replicate test chambers were used per.test concentration with 1 0 fish in each chamber (total of 2 0 fish per concentration). Each chamber was covered with a glass plate to prevent fish from escaping. Random numbers were used to assign test concentrations to the test chambers and position of test concentrations in the water bath. Rainbow trout used in this study were not fed approximately 29 hours prior to and during the test, and were assigned to the test chambers using random numbers. Addition of fish to the test solutions was initiated approximately 41 minutes after mixing of EID091527 OOCK-cU,- the test solutions was completed. Mortality and behavioral observations were made at test start, every 24 hours thereafter, and at test end. At test conclusion, all surviving fish were sacrificed. A recirculating water bath was used to maintain mean temperature in the test chambers during the 96-hour test. In addition, a continuously recording thermometer was used to check for temperature variation in l replicate of the dilution water control. A photoperiod of 16 hours light (approximately 199-450 Lux) and 8 hours darkness was employed, which included 30 minutes of transitional light (11-157 Lux) preceding and following the 16-hour light interval. Dissolved oxygen, pH, and temperature were measured in all replicate chambers of the control and test substance concentrations. These measurements were taken before fish were added at test start, every 24 hours thereafter, and at test end or at total mortality in a concentration. Total alkalinity, EDTA hardness, and conductivity of the water were measured before fish were added at the beginning of the test. Test solutions were not aerated during the test. Concentrations of ammonium perfluorooctanoate were measured directly by high performance liquid chromatography/tandem mass spectrometry (LC/MS/MS). At test conclusion, fish from the water control ranged from 2.5-3.2 cm in standard length (mean 2.8 cm) and 0.15-0.30 g in wet weight, blotted dry (mean 0.21 g). Standard length of the longest fish was not more than twice the length of the shortest fish in the control. Loading in the water control was 0.23 g/L at test conclusion. GLP: Test Substance: Results: The LC50 value was calculated using the moving average-angle method. Yes ' Ammonium perfluorooctanoate, purity 99.4% At the end of 96 hours in the rangefinding study, the mortality was 0, 0, 0 ,0 ,0 , and 60% at 0, 50, 100,500, 1000, and 5000 mg/L, respectively. Test substance solutions were clear and colorless with no insoluble test substance present during the study. In the definitive study, mean measured concentrations of ammonium perfluorooctanoate were 554, 1090, 2280, 4560, and 9360 for the 625, 1250, 2500,5000, and 10,000 mg/L dose levels, respectively. Control solutions showed no detectable EID091528 000c concentrations of ammonium perfluorooctanoate. All test substance solutions were clear and colorless with no insoluble test substance present during the test. All chemical and physical parameters for the definitive test were within expected ranges. Total alkalinity, EDTA hardness, and conductivity of the dilution water control were 49 mg/L CaC0 3 , 122 mg/L CaC0 3 , and 240 pmhos/cm, respectively. During the test, dissolved oxygen concentrations ranged from 7.5-11.2 mg/L, pH ranged from 7.1-7.2, and mean temperature was 11.8C (range 11.6-12.1C). No mortality or sublethal effects were seen in the dilution water control fish. No mortality or sublethal effects were observed at <concentrations 2500 mg/L. At 5000 mg/L, mortality was 8/20, 11/20, 14/20, and 15/20 at 24, 48, 72, and 96 hours, respectively. At 10,000 mg/L all fish were dead by 24 hours. Reference: Surviving fish exposed to 5000 mg/L exhibited sublethal effects such as swimming at the surface, labored respiration, dark coloration, lethargy, partial loss of equilibrium, rapid respiration, and erratic swimming. DuPont Co. (1999). Unpublished Data, Haskell Laboratory Report No. Dupont-3381. Mammalian Toxicity Acute Toxicity Type: Species/strain: Value: Oral LDso Male rats/Crl:CD Male rats receiving ammonium perfluorooctanoate alone: 478 mg/kg (95% confidence limits, lower 361 mg/kg, upper 571 mg/kg, slope 7.9) Male rats receiving ammonium perfluorooctanoate and pre-treatment of phnobarbital sodium: 547 mg/kg (95% confidence limits, lower 517 mg/kg, upper 582 mg/kg, slope 22.1) Method: Male rats receiving ammonium perfluorooctanoate and pre-treatment of proadifen hydrochloride: 520 mg/kg (95% confidence limits, lower 450 mg/kg, upper 618 mg/kg, slope 9.8) Ammonium perfluorooctanoate was administered by intragastric intubation as a suspension in com oil in single doses to 10 rats/group at concentrations of 400,500, or 650 mg/kg. Another 30 rats, 10/group, were treated by single intraperitoneal injections EID091529 8 009^ with aqueous solutions of phnobarbital sodium at 80 mg/kg/day for 3 days. One day after the final treatment, the rats were administered ammonium perfluorooctanoate by intragastric intubation using the same treatment as described above. An additional group of 30 rats, 10/group, were treated with an intraperitoneal injection of aqueous solutions of proadifen hydrochloride at 50 mg/kg. One hour after this treatment, ammonium perfluorooctanoate was administered by intragastric intubation, using the same treatment as described above. The surviving rats from all treatments were weighed and observed during a 14-day recovery period and then sacrificed. The T.nso values were calculated from the mortality data. GLP: Test Substance: Results: The phnobarbital sodium phase of the study was repeated. The rats from both phases #ere combined and the LD50 value was based on all 60 rats. No Ammonium perfluorooctanoate, purity approximately 100% There were no significant differences in the LD50 values of ammonium perfluorooctanoate, either when tested alone or following pre-treatment with either phnobarbital sodium or proadifen hydrochloride. Mortality ratios of 2/10, 7/10, and 8/10 were observed for the rats treated with 400, 500, and 650 mg/kg ammonium perfluorooctanoate, respectively. Wet and/or stained perineal area and weight loss were observed at all levels tested. Other clinical signs observed included stained face (500 and 650 mg/kg), weakness (500 and 650 mg/kg), and chromodacryorrhea (500 mg/kg). All deaths occurred within 6 days after dosing. Mortality of 0/20,4/20, and 19/20 was observed for the rats pretreated with phnobarbital sodium and then treated with 400, 500, and 650 mg/kg ammonium perfluorooctanoate, respectively. Wet and/or stained perineal area, stained face, diarrhea, and weight loss were observed at all levels tested. Other clinical signs observed included weakness (500 and 650 mg/kg) and lethargy (650 mg/kg). All deaths occurred within 4 days after dosing. Mortality of 1/10, 5/10, and 8/10 was observed for the rats pretreated with proadifen hydrochloride and then treated with 400, 500, and 650 mg/kg ammonium perfluorooctanoate, respectively. Stained face, wet and/or stained perineal area, weight loss, and weakness were observed at all levels tested. Other clinical signs observed included tremors (400 mg/kg), chromodacryorrhea (400 mg/kg), diarrhea (500 and 650 mg/kg), and lacrimation EID091530 9 000r i Reference: (650 mg/kg). All deaths occurred within 5 days after dosing. DuPont Co. (1981). Unpublished Data, Haskell Laboratory Report No. 567-81. Type: Species/strain: Value: Oral LD50 Male and female rats/Crl:CD Male rats: 470 mg/kg (95% confidence limits, lower 403 mg/kg, upper 536 mg/kg, slope 8.6) Method: GLP: Test Substance: Results: Female rats: 482 mg/kg (95% confidence limits, lower 438 mg/kg, upper 541 mg/kg, slope 12.3) The test substance, as a suspension in com oil, was administered by intragastric intubation in single doses to 6 groups of male and 6 groups of female young adult rats. Ten male and female rats/group were administered 200,400, 450, 500, 670, or 1000 mg/kg of the test substance. The surviving rats were weighed and observed during a 14-day recovery period and then sacrificed. The LD50 values were calculated from the mortality data. No Ammonium periluorooctanoate, purity approximately 100% Mortality ratios of 2/10, 3/10, 4/10, 6/10, 9/10, and 10/10 were found in the 200, 400,450, 500, 670, and 1000 mg/kg male groups, respectively. Mortality ratios of 0/10, 0/10, 5/10, 7/10, 9/10, and 10/10 were found in the 200,400, 450, 500, 670, and 1000 mg/kg female groups, respectively. Clinical signs observed in male rats included stained and/or wet perineal area, weakness, and weight loss at all levels tested. Other clinical signs observed in the male rats included stained face (450 mg/kg and above), chromodacryorrhea (500 and 1000 mg/kg), hunched posture (500 mg/kg), morbundity (670 mg/kg), eyes half closed (670 mg/kg), and gasping (670 mg/kg). All deaths occurred within 4 days of dosing. Reference: Clinical signs observed in female rats included stained and/or wet perineal-area and weight loss at all levels tested. Stained face was observed at all levels except 200 mg/kg. Other clinical signs noted in female rats included alopecia (400 mg/kg), weakness (400,450, 670, and 1000 mg/kg), hunched posture (450 and 670 mg/kg), chromodacryorrhea (670 mg/kg), eyes half closed (670 mg/kg), and ataxia (670 mg/kg). All deaths occurred within 3 days after dosing. DuPont Co. (1981). Unpublished Data, Haskell Laboratory Report No. 295-81. EID091531 10 0 0 0 ^ Type: Species/strain: Value: Oral LD50 Male and female rats/Crl:CD Male newborn rats: 243 mg/kg (95% confidence limits, undefined, slope 55.7) Female newborn rats: 258 mg/kg (95% confidence limits, lower 244 mg/kg, upper 276 mg/kg, slope 19.9) Male weanling rats: 573 mg/kg (95% confidence limits, lower 514 mg/kg, upper 664 mg/kg, slope 8.0) Female weanling rats: 580 mg/kg (95% confidence limits, lower 470 mg/kg, upper 2258 mg/kg, slope 4.7) Male young adult rats: 470 mg/kg (95% confidence limits, lower 403 mg/kg, upper 536 mg/kg, slope 8.6) Female young adult rats: 453 mg/k'g (95% confidence limits, lower 413 mg/kg, upper 503 mg/kg, slope 15.0) Male older rats: 336 mg/kg (95% confidence limits, undefined) Method: GLP: Test Substance: Results: Female older rats: 343 mg/kg (95% confidence limits, lower 285 mg/kg, upper 390 mg/kg, slope 8.0) The test substance, as a suspension in com oil, was administered by intragastric intubation in single doses to groups of rats. The groups (10 rats/group) were male and female newborn rats (< 2 days old), male and female weanling rats (21 days old), male and female young adults (-8-10 weeks old), and male and female older rats (age undefined). Male newborn rats were administered 130,200, 240, 280, 330, or 370 mg/kg. Female newborn rats were administered 130, 160, 200, 220, 240, 280, or 320 mg/kg. Male weanling rats were administered 350, 400, 450, 525, 670, or 710 mg/kg. Female weanling rats were administered 350,400, 450, or 670 mg/kg. Young adult rats were administered 350, 425, 500, or 670 mg/kg. Young adult male rat data are reported in DuPont Report No. 295-81. Older male rats were administered 200, 240, 300, 350,400, 500, or 720 mg/kg. Older female rats were administered 225, 350,400,450, or 670 mg/kg. The surviving rats were weighed and observed during a 14-day recovery period and then sacrificed. The LD50 values were calculated from the mortality data. No Ammonium perfluorooctanoate, purity approximately 100% Mortality ratios for male newborn rats were 0/10, 0/10, 0/10,10/10, EID091532 11 0 0 0 V00 References: 10/10, and 10/10 for the 130, 200, 240, 280, 330, and 370 mg/kg groups, respectively. No clinical signs were reported. Deaths occurred up to 6 days after dosing. Mortality ratios for female newborn rats were 0/10, 0/10, 0/10, 0/10, 5/10, 6/10, and 10/10 for the 130, 160, 200,220, 240, 280, and 320 mg/kg groups, respectively. No clinical signs were reported. Deaths occurred up to 4 days after dosing. Mortality ratios for male weanling rats were 0/10,2/10, 2/10, 3/10, 7/10, and 8/10 for the 350,400, 450, 525, 670, and 710 mg/kg groups, respectively. Stained and wet perineal area, weakness, and weight loss were observed. Deaths occurred up to 3 days after dosing. Mortality ratios for female weanling rats were 1/10, 3/10, 3/10, and 6/10 for the 350, 400, 450, and 670 mg/kg groups, respectively. Stained and wet perineal area, stained face, weakness, and weight loss were observed. Deaths occurred up to 3 days after dosing. Mortality ratio data for the young adult males are covered in DuPont Report No. 295-81. Mortality ratios for female young adult rats were 1/10, 2/10, 8/10, and 10/10 for the 350, 425, 500, and 670 mg/kg groups, respectively. Stained and wet perineal area, stained face, nasal discharge, diarrhea, and weight loss were observed. Deaths occurred up to 4 days after dosing. Mortality ratios for the older male rats were 0/10,0/10, 0/10,9/10, 10/10, 10/10, and 10/10 for the 200, 240, 300, 350,400, 500, and 720 mg/kg groups, respectively. Stained face, stained and wet perineal area, weakness, tremors, lethargy, chromodacryorrhea, diarrhea, and weight loss were observed. Deaths occurred up to 9 days after dosing.- < Mortality ratios for the older female rats were 1/10, 5/10, 6/10, 9/10, and 10/10 for the 225,350,400,450, and 670 mg/kg groups, respectively. Stained face, stained and wet perineal area, weakness, tremors, lethargy, and weight loss were observed. Deaths occurred up to 5 days after dosing. DuPont Co. (1982). Unpublished Data, Haskell Laboratory Report No. 788-82. DuPont Co. (1981). Unpublished Data, Haskell Laboratory Report No. 295-81. EID091533 12 ooovo.?. Type: Species/strain: Value: Oral L D 5o Rangefinder and Liver Weight Comparison Test Male and female rats/Crl:CD Male rats: 439 mg/kg (confidence limits, lower 294 mg/kg, upper 554 mg/kg, slope 6.1) Castrated male rats: 491 mg/kg (confidence limits, lower 276 mg/kg, upper 619 mg/kg, slope 6.7) Female rats: 459 mg/kg (confidence limits, lower 315 mg/kg, upper 607 mg/kg, slope 5.2) Method: Overiectomized female rats: 400 mg/kg (confidence limits, lower 259 mg/kg, upper 494 mg/kg, slope 7.2) In an LD50 rangefinder test, the test substance, as a suspension in com oil, was administered by intragastric intubation in single doses to normal male rats, castrated male rats, normal female rats, and ovariectomized female rats. Dose levels of 200, 480, and 670 mg/kg were tested in each of the test systems mentioned above (10 rats/group). GLP: Test Substance: Results: In the liver weight comparison test, 5 rats/group were administered the test substance, as a suspension in com oil, as a single dose. Male groups were defined as male control, male 100 mg/kg, male 200 mg/kg, male castrated control, and male castrated 200 mg/kg. Female groups were defined as female control, female 100 mg/kg, female 200 mg/kg, female ovariectomized control, and female ovariectomized 200 mg/kg. All rats were weighed and observed during a 14-day recovery period. The rats were then sacrificed and the livers were weighed. No Ammonium perfluorooctanoate, purity approximately 100% In the LD50 study, mortality in the male rats occurred in 0/10, 7/10, and 8/10 rats in the 200,480, and 670 mg/kg groups, respectively. Mortality in the castrated male rats occurred in 0/10,5/10, and 8/10 rats in the 200,480, and 670 mg/kg groups, respectively. Mortality of the female rats occurred in 0/10,7/10, and 7/10 rats in the 200,480, and 670 mg/kg groups, respectively. Mortality in the ovariectomized female rats occurred in 0/10, 8/10, and 9/10 mg/kg at 200,480, and 670 mg/kg, respectively. In the liver weight comparison study tested at dose levels of 0,100, and 200 mg/kg, no changes in liver weight or in liver to body weight ratios were seen in the female rats given single doses of up to 200 mg/kg (ovariectomized or normal). A single oral dose of either 100 or 200 mg/kg produced an increase in liver weight of EID091534 13 OOQ'AL'i Reference: Type: Species/strain: Method: GLP: Test Substance: male rats. Castration reduced the magnitude of the liver weight increase, but rats castrated and given 200 mg/kg had heavier livers than did the controls. Clinical signs seen in the am m onium perfluorooctanoate-treated rats included stained face and perineal area, and sporadic weight loss. No deaths occurred in this phase of the experiment. DuPont Co. (1981). Unpublished Data, Haskell Laboratory Report No. 600-81. Acute Oral Toxicity Male rats/Crl:CD The test substance, ammonium perfluorooctanoate (3M) and ammonium perfluorooctanoate (Rimar Co.), as suspensions in com oil, were administered by intragastric intubation in single doses to young adult male rats. Rats (10/group) were administered 200, 480, or 670 mg/kg of the test substance. The surviving rats were weighed and observed during a 14-day recovery period and then sacrificed. No Ammonium perfluorooctanoate (3M), purity approximately 100% Results: Ammonium perfluorooctanoate (Rimar Co.), purity 95% minimum Mortality ratios of 0/10, 6/10, and 10/10 were found in the 200, 480, and 670 mg/kg ammonium perfluorooctanoate (3M) groups, respectively. Mortality ratios of 0/10,10/10, and 10/10 were found in the 200, 480, and 670 mg/kg ammonium perfluorooctanoate (Rimar Co.) groups, respectively. Clinical signs observed in ammonium perfluorooctanoate (3M) rats included stained and/or wet perineal area, stained face, and weight loss at all levels tested. Other clinical signs observed included weakness (480 and 670 mg/kg), diarrhea (480 mg/kg), and alopecia (200 mg/kg). All deaths occurred within 4 days after dosing. Reference: Clinical signs observed in ammonium perfluorooctanoate (Rimar Co.) rat's included stained and/or wet perineal area, stained face, and weight loss at all levels tested. Other clinical signs noted included weakness (480 and 670 mg/kg) and lethargy (670 mg/kg). All deaths occurred within 4 days after dosing. DuPont Co. (1981). Unpublished Data, Haskell Laboratory Report No. 565-81. Type: Species/strain: Value: Method: Oral ALD (Approximate Lethal Dose) Male rats/ChR-CD 670 mg/kg The test substance, as an aqueous solution (pH -6), was EID091535 14 000V\l .'5 GLP: Test Substance: Results: administered by intragastric intubation to young adult male rats (1 rat/group) in single doses. Concentrations tested were 1, 1.5, 2.3, 3.4, 5.1, 26, 40, 60, 77, 90, 120, 130, 170, 200, 300, 450, 670, and 2250 mg/kg. Survivors were sacrificed 14 days later, and body weights and liver weights were recorded. No Ammonium perfluorooctanoate, purity not specified Deaths did not occur at dose levels of 1-450 mg/kg. The rat dosed with 670 mg/kg died 2 days after dosing, and the rat dosed with 2250 mg/kg died 1 day after dosing. Reference: Slight initial weight losses occurred at 26 mg/kg and above for 1-2 days. At 90 mg/kg and above, the fece$ were small and irregularly-shaped for 1-6 days after dosing, and the rats were uncomfortable for 1-5flays after dosing. The compound caused liver enlargement in rats with single doses as low as 60-90 mg/kg. Based on clinical signs, it also acted as a gastrointestinal irritant. Additional toxic signs at the lethal doses (670 and 2250 mg/kg) included chewing motions, polyuria, increased respiration rate, and face-pawing on the day of dosing. Shovel-nosing was observed at 2250 mg/kg and slight salivation after dosing occurred at 670 mg/kg. DuPont Co. (1968). Unpublished Data, Haskell Laboratory Report No. 128-68. Type: Species/strain: Vale: Method: GLP: Test Substance: Results: Oral ALD Male rats/ChR-CD 670 mg/kg The test substance was administered by intragastric intubation to male rats (1 rat/group) in single doses. Concentrations tested were 1.5, 12, 40, 120, 200, 300, 450, 670, 1000, 1500, and 2250 mg/kg. Survivors were sacrificed 14-15 days later, and body weights and liver weights were recorded. No Ammonium perfluorooctanoate, purity 99% Mortality occurred at 670 mg/kg and above. Clinical signs of toxicity included inactivity (120, 1000, 1500, and 2250 mg/kg), red discharge around the nose (670, 1500, and 2250 mg/kg), perineal discoloration (300 and 450 mg/kg), ruffled fur (300 and 450 mg/kg), irritability (670 mg/kg), and weight loss (40, 200,300, 450, 670, and 1000 mg/kg). Animals sacrificed 14-15 days after having received doses down to and including 200 mg/kg had enlarged livers when compared to control rats weighing between 500-550 g with liver weights of 22.6, 20.7,19.1, and 21.7 g and liver weight/body weight percentages of 4.2, 3.8,3.6, and 3.8, respectively. Liver weights at 200, 300, and 450 mg/kg were 30.6, EID091536 15 OOO'/O Reference: 25.2, and 28.2 g, with liver weight/body weight percentages of 5.6, 5.3, and 6.2, respectively. Liver enlargement was also possible in rats dosed below 200 mg/kg, but additional test and control rats would have to be compared in order to establish this. DuPont Co. (1961). Unpublished Data, Haskell Laboratory Report No. 55-61. Type: Species/strain: Method: GLP: Test Substance: Results: Reference: Type: Species/strain: Value: Method: Acute Oral Effects, Does pretreatment with ethanol modify the toxicity of ammonium perfluorooctanoate? Male rats/Crl:CD Young adult male rats (6/group) were administered ammonium perfluorooctanoate as a 60% aqueous solution at dose levels of 200, 480, and 670 mg/kg. Additional groups of rats were pre-treated with ethanol (15% v/v) in drinking water for 14 days and then dosed with ammonium perfluorooctanoate at the same concentrations as listed above on day 15. Three other groups of rats were pretreated with a single 6000 mg/kg dose of ethanol via intragastric intubation followed 24 hours later with the ammonium perfluorooctanoate treatment at the levels listed above. An additional group of untreated rats served as controls. Groups of rats were also treated with ethanol alone at either 6000 mg/kg or 15% v/v in drinking water for 14 days. Clinical signs and body weights were recorded. Liver weights were recorded at the 14-day sacrifice. No Ammonium perfluorooctanoate, purity approximately 100% All rats died within 8 days after dosing with ammonium perfluorooctanoate at 670 mg/kg. Liver weight/body weight ratios showed an increase in all rats that received ammonium perfluorooctanoate when compared to the untreated controls and the animals that received only ethanol. There were no significant differences between the untreated controls and the animals that received only ethanol. There were no significant differences between rats that received ethanol and ammonium perfluorooctanoate and the rats that received only ammonium perfluorooctanoate. DuPont Co. (1984). Unpublished Data, Haskell Laboratory Report No. 79-84. Oral LD50 EID091537 Male and female mice/CD-1 Male and female mice: 457 mg/kg (95% confidence limits, lower 344 mg/kg, upper 560 mg/kg, slope 6.6) The test substance, as a suspension in com oil, was administered by intragastric intubation in single doses to 6 groups of male and 6 groups of female young adult mice. Ten male and female 16 0 0 0 / .1 r.: GLP: Test Substance: Results: mice/group were administered 250, 500, 750, 1000, 2000, or 4000 mg/kg of the test substance. The surviving rats were weighed and observed during a 14-day recovery period and then sacrificed. The LD50 values were calculated from the mortality data. The male and female 4000 and 2000 mg/kg dose levels were not calculated in the LD50 data due to limitations of the computer. No Ammonium perfluorooctanoate, purity approximately 100% Mortality ratios of 1/10, 4/10, 10/10, 10/10, 10/10, and 10/10 were found in the 250, 500, 750, 1000, 2000, and 4000 mg/kg male and female groups, respectively. Clinical signs observed in male mice included stained and/or wet perineal area, weakness, and weight loss in all surviving mice. Other signs included eyes half closed (250 and 1000 mg/kg), ruffled fur (250 and 500 mg/kg), ataxia (250, 500, and 1000 mg/kg), and tremors (500 and 750 mg/kg). All deaths in male mice occurred within 6 days after dosing. Reference: Clinical signs observed in female mice included stained and/or wet perineal area, weakness, and weight loss in all surviving mice. Other signs included eyes half closed (750 mg/kg), stained face (750 mg/kg), tremors (750 mg/kg), ataxia (500 mg/kg), and ruffled fur (250 and 750 mg/kg). All deaths in female mice occurred within 7 days after dosing. DuPont Co. (1981). Unpublished Data, Haskell Laboratory Report No. 329-81. Type: Species/strain: Value: Oral L D 50 Male and female guinea pigs/Duncan Hartley Male guinea pigs: 178 mg/kg (95% confidence limits, lower 144 mg/kg, upper 202 mg/kg, slope 8.9) Method: GLP: Test Substance: Results: Female guinea pigs: 217 mg/kg (95% confidence limits, lower 187 mg/kg, upper 246 mg/kg, slope 8.6) The test substance, as a suspension in com oil, was administered by intragastric intubation in single doses to 6 groups of male and 6 groups of female young adult guinea pigs. Ten male and female guinea pigs/group were administered 150, 200, 250, 300, 400, or 670 mg/kg of the test substance. The surviving guinea pigs were weighed and observed during a 14-day recovery period and then sacrificed. The LD50 values were calculated from the mortality data No Ammonium perfluorooctanoate, purity approximately 100% Mortality ratios of 3/10, 6/10,9/10, 10/10,10/10, and 10/10 were EID091538 17 eoovos found in the 150, 200, 250, 300, 400, and 670 mg/kg male groups, respectively. Mortality ranos of 2/10, 1/10, 8/10, 9/10, 10/10, and 10/10 were found in the 150, 200, 250, 300, 400, and 670 mg/kg female groups, respectively. Clinical signs observed in male guinea pigs included stained and/or wet perineal area and weakness at all levels tested. Other clinical signs observed in the male guinea pigs included stained face (150, 200, and 670 mg/kg), eyes half closed (200 and 300 mg/kg), lacrimation (150 and 200 mg/kg), ataxia (670 mg/kg), tremors (150 mg/kg), and hunched posture (200 mg/kg). Weight loss occurred at all levels tested except 400 and 670 mg/kg. All deaths occurred within 4 days after dosing. Reference: Clinical signs observed in female guinea pigs included stained and/or wet perineal area and weakness at all levels tested except 400 and 670 mg/kg. Other clinical signs noted in female guinea pigs included convulsions (670 mg/kg), ataxia (670 mg/kg), gasping (670 mg/kg), eyes half closed (150 and 250 mg/kg), tremors (400 mg/kg), lacrimation (250 mg/kg), stained face (200 mg/kg), and lethargy (150 mg/kg). Weight loss occurred at all levels tested except for 670 mg/kg. All deaths occurred within 6 days after dosing. DuPont Co. (1981). Unpublished Data, Haskell Laboratory Report No. 291-81. Type: Species/strain: Method: GUP: Test Substance: Results: Acute Toxicity Male dogs/beagie Dogs (2/group) received either 200 or 450 mg/kg of the test substance. The following biochemical measurements were made on the blood: sugar, urea nitrogen, total cholesterol, and alkaline phosphatase. When the 450 mg/kg dose was administered, the level of activity of lactic dehydrogenase (LDH), isocitric dehydrogenase (ICDH), aldolase, glutamic oxalacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) were also measured. A routine hematological examination and an analysis of a 24-hour urine specimen was made at intervals on these animals. The level of various components of the blood following dosing was compared with an average value observed prior to exposure and with a similar measurement made at the same time on specimens from stock colony dogs. For the enzyme activities, a normal range was established from measurements made on stock dogs. The activity was also measured at least once prior to treatment. No Ammonium perfluorooctanoate, purity 99% The GPT and GOT levels were elevated within 48 hours in both EID091539 18 Reference: dogs that received 200 mg/kg. One week later, they were in the normal range. When 450 mg/kg was administered, all of the enzymes measured were markedly elevated 24 to 48 hours later. The greatest change occurred in the GPT and ICDH. Both animals that received 450 mg/kg died within 48 hours after dosing. DuPont Co. (1965). Unpublished Data, Haskell Laboratory Report No. 123-65. Type: Species/strain: Exposure Time: Value: Method: Inhalation ALC (Acute Lethal Concentration) Rats/ChR-CD 4 hours 0.8 mg/L Male rats (6/exposure level), weighing 250-270 grams were exposed to dusts of ammonium perfluorooctanoate at exposure levels of 0.38, 0.81, 0.83, 2.2, 4.8, or 5.7 mg/L. Exposures were head-only, except for the 2.2 mg/L exposure level where rats had whole-body exposure. Two different methods of dust generation were used to generate ammonium perfluorooctanoate aerosols. In the first method, a heavy cloud was generated by blowing approximately 30 L/minute of air through a high velocity Cu-tubing jet submerged in a mechanically stirred reservoir of the test substance. The air carried the dust particles into an 8 L exposure chamber. Suitable diluting air was introduced between the generator and the chamber to achieve lower concentrations. The generator did not fractionate the dust, and all particle sizes, large and small, were delivered into the exposure chamber. In the second method, a generator was used for low atmospheric dust concentrations. A falling stream of dust particles from a stirred reservoir impinged on a pneumatic jet. The air stream from this jet carried the particles to a cyclone head where the larger ones were returned to the reservoir. This generator achieved some particle size fractionation. The generator was run under constant conditions and dust concentrations were lowered by diluting the stream with air between the generator and the exposure chamber. The airborne concentrations were determined 5 times during each 4-hour exposure. At the mid-point of each exposure, a particle size distribution measurement was made. GLP: Test Substance: Results: Clinical signs were recorded. The eyes of the rats were stained with fluorescein immediately after exposure. Rats were sacrificed for histopathologic examination at 1,7,14,27, or 42 days post-exposure. Tissues from two rats dying during exposure were also examined microscopically. No Ammonium perfluorooctanoate, purity approximately 100% The mortality ratios for the 0.38,0.81,0.83, 2.2,4.8, and 5.7 mg/L EID091540 19 000 VO exposure groups were 1/6 (not test substance-related), 2/6, 1/6, 6/6, 6/6, and 6/6, respectively. All deaths occurred either during exposure or within 48 hours after exposure. Clinical signs observed during exposure included gasping (all exposure levels), irregular breathing (all exposure levels), red discharge around the eyes and nose (all exposure levels), and salivation (2.2,4.8, and 5..7 mg/L). Clinical signs observed post-exposure included some rupture of eyes, all other eyes opaque (2.2 and 4.8 mg/L), and > 80% rats having opaque and corroded-appearing eyes (0.81 and 0.83 mg/L). External damage of the eyes was confirmed with fluorescein stain (0.81,0.83, and 2.2 mg/L), with the eyes appearing normal after 20 days (0.81 mg/L). References: Inhalation of the test substance caused liver enlargement which reached a maximum (2 times normal) 7-14 days after exposure. Liver weights returned to the normal range 42 days after exposure. No changes in liver cell morphology were observed. Microscopic examination indicated that acute pulmonary edema developed promptly, but disappeared in approximately 1 week, leaving no residual injury. No dust particles were seen in the lungs microscopically. There was irritation of the stomach that cleared in 2 weeks. Ammonium perfluorooctanoate also caused comeal opacity and ulceration that were still microscopically evident 42 days after exposure. DuPont Co. (1969). Unpublished Data, Haskell Laboratory Report No. 160-69. Kennedy, G. L., Jr. et al. (1983). The Toxicologist. 3:22. Kennedy, G. L., Jr. et al. (1986). Food Chem. Toxicol.. 24:1325-1329. Type: Species/strain: Exposure Time: Value: Method: Dermal LD50 Male rats/ChR-CD 24 hours 6959 mg/kg (95% confidence limits undefined) Rats were clipped free of hair over the back and trunk area. Five male rats/dose level were dosed with 3000,5000, and 7500 mg/kg ammonium perfluorooctanoate. The test substance, as a 50/50 aqueous suspension, was applied to the back of each rat under a square of aluminum foil and held in place with elastic bandages. After 24 hours of exposure, the rats were unwrapped, sponged off with a mild detergent, rinsed, dried, and returned to their cages for 13 days observation or until death. During the EID091541 20 OOO'/O^ GLP: Test Substance: Results: References: observation period, the rats were weighed and observed for clinical signs. Gross pathology was done on all survivors and 1 animal that was found dead at 7500 mg/kg. Liver weights were recorded in all rats except 1 . The LD50 value was calculated from the mortality data. No Ammonium perfluorooctanoate, purity approximately 100% Mortality ratios were 0/5; 0/5, and 4/5 at 3000, 5000, and 7500 mg/kg, respectively. Death occurred within 2 days of dosing. All rats dosed at 3000, 5000, and 7500 mg/kg had initial weight loss. Clinical signs observed included lethargy (5000 and 7500 mg/kg), wet perineal area (5000 and 7000 mg/kg), stained perineal area (7500 mg/kg), stained nose (a500 mg/kg), and chromodacryorrhea (7500 mg/kg). Gross pathology showed an increase in liver weights in all surviving rats examined at 14 days post-treatment. DuPont Co. (1979). Unpublished Data, Haskell Laboratory Report No. 659-79. Type: Species/strain: Exposure Time: Value: Method: GLP: Test Substance: Results: References: Kennedy, G. L., Jr. (1985). Toxicol. Appl. Pharmacol.. 81:348-355. Dermal LD50 Female rats/ChR-CD 24 hours > 7500 mg/kg (the maximum feasible dose) Rats were clipped free of hair over the back and trunk area. Five female rats/dose level were dosed with 5000 or 7500 mg/kg ammonium perfluorooctanoate. The test substance, as a 50/50 aqueous suspension, was applied to the back of each rat under a square of aluminum foil and held in place with elastic bandages. After 24 hours of exposure, the rats were unwrapped, sponged off with a mild detergent, rinsed, dried, and returned to their cages for 13 days observation or until death. During the observation period, the rats were weighed and observed for clinical signs. Surviving rats were sacrificed. No ' Ammonium perfluorooctanoate, purity approximately 100% The mortality was 0/5 and 1/5 at 5000 and 7500 mg/kg, respectively. Death occurred 3 days after treatment. Ammonium perfluorooctanoate caused mild skin irritation and weight loss at both dose levels. In addition, stained face and wet and stained perineal area were observed at 7500 mg/kg. DuPont Co. (1980). Unpublished Data, Haskell Laboratory Report No. 682-80. EID091542 0 0 > . j..;> Kennedy, G. L., Jr. (1985). Toxicol. A p p I. Pharmacol.. 81:348-355. Type: Species/strain: Exposure Time: Value: Method: GLP: Test Substance: Results: References: Dermal LD50 Male rabbits/New Zealand White 24 hours 4278 mg/kg (95% confidence limits, lower 2369 mg/kg, upper 9814 mg/kg, slope 6.2504) Rabbits were clipped free of hair over the back and trunk area, and were fitted with plastic collars. Five, 5,- 5, and 2 male rabbits were dosed with 1500, 3000, 5000, and 7500 mg/kg ammonium perfluorooctanoate, respectively. The test substance was made into a slurry with water, was applied to the back of each rabbit, and the test site was occluded (wrapped with plastic wrap, gauze, and elastic bandages). After 24 hours of exposure, the animals were unwrapped, washed with water, dried, and returned to their cages for 14 or 15 days observation or until death. During the observation period, the animals were weighed and observed for clinical signs. Gross pathology was done on all survivors and 1 animal that was found dead at 3000 mg/kg. The LD50 value was calculated from the mortality data. No Ammonium perfluorooctanoate, purity approximately 100% Mortality ratios of rabbits were 0/5, 1/5, 3/5, and 2/2 at 1500, 3000, 5000, and 7500 mg/kg, respectively. Death occurred within 4 days of dosing. Gross pathological examination showed no compound-related changes; however, there was skin irritation at all dose levels. Clinical signs included weight loss and labored breathing at all dose levels. In addition, lethargy (3000 mg/kg), nasal discharge (5000 mg/kg), shallow breathing (5000 mg/kg), pallor (5000 mg/kg), diarrhea (5000 mg/kg), weakness (5000 mg/kg), wet underneath the body (5000 and 7500 mg/kg), and cyanosis (7500 mg/kg) were observed. DuPont Co. (1979). Unpublished Data, Haskell Laboratory Report No. 659-79. Kennedy, G. L., Jr. (1985). Toxicol. AppI. Pharmacol.. 81:348-355. Type: Species/strain: Method: Dermal Irritation Male rabbits/New Zealand White Six male rabbits were clipped free of hair on the trunk and lateral areas, and placed in FDA-type stocks. Doses of 0.5 g solid ' ammonium perfluorooctanoate were applied as an aqueous paste to the intact skin under gauze squares, and the test site was semi-occluded (rubber sheeting was loosely wrapped around the EID091543 GLP: Test Substance: Results: Reference: trunk and secured with adhesive tape). After 24 hours, the rabbits were removed from the stocks, the patches removed, and the reactions observed. Observations were also made at 48 hours. No Ammonium perfluorooctanoate, purity approximately 100% Ammonium perfluorooctanoate caused mild to moderate skin irritation in 24 hours, and slight to moderate irritation in 48 hours when tested on the shaved intact skin of rabbits under semi-occluded conditions. DuPont Co. (1979). Unpublished Data, Haskell Laboratory Report No. 636-79. Type: Species/strain: Method: GLP: Test Substance: Dermal Irritation Male rabbits/New Zealand White Twenty-one male rabbits were clipped free of hair over the back and trunk areas, and fitted with plastic collars. Ammonium perfluorooctanoate impregnated Teflon strips or ammonium perfluorooctanoate impregnated Kevlar strips were applied to the back of each rabbit. Three rabbits served as controls and were wrapped in non-ammonium perfluorooctanoate-treated material. The trunk of each rabbit was then occluded (wrapped with a layer of plastic wrap, gauze stretch bandage, and adhesive stretch tape). After 4-, 8-, or 24-hour exposure periods, the wrappings were removed and the exposed areas were wiped with gauze pads that were soaked in a 50:50 ethanokwater solution. The animals were observed after unwrapping for skin irritation. No Ammonium perfluorooctanoate impregnated Teflon (48% Teflon fibers, 38% Teflon resin that included 2.9% Triton X-100 and 0.061% ammonium perfluorooctanoate, and 14% dimethylsilicone oil) Results: Reference: Ammonium perfluorooctanoate impregnated Kevlar (40.5% Kevlar fibers, 42% Kevlar resin that included 3.2% Triton X-100 and 0.067% ammonium perfluorooctanoate, and 17.5% dimethylsilicone oil) No skin irritation was observed during the study. DuPont Co. (1981). Unpublished Data, Haskell Laboratory Report No. 736-81. Type: Species/strain: Method: Eye Irritation Rabbits/New Zealand White One-tenth mL (38.3 mg) of solid test substance was placed into the right conjunctival sac of each of 2 rabbits (sex not specified). After 20 seconds, 1 treated eye was washed with tap wate.r for 1 minute. The treated eye of the other rabbit was not washed. Observations EID091544 0*1 GLP: Test Substance: Results: Reference: of the cornea, iris, and conjunctiva were made with a hand-slit lamp at 1 and 4 hours, and at 1,2, 3,7, 14, 21, and 28 days. Fluor-I-strip stain and a biomicroscope were used at examinations after the day of treatment. No Ammonium perfluorooctanoate, purity 100% Ammonium perfluorooctanoate caused generalized moderate comeal opacity with a small area of severe opacity, intermittent moderate iritis, and moderate conjunctivitis when tested in a rabbit eye that was unwashed after treatment. The ocular effects gradually receded; however, the small area of comeal opacity persisted, and at 21-28 days was mild with vascularization (sign of healing). An eye dosed with the test substance and promptly washed had a small area of slight to moderate comeal opacity and moderate to slight conjunctivitis with no iritic effect. The eye was normal within 7 days, except for mild conjunctival redness, which was normal within 14 days. DuPont Co. (1979). Unpublished Data, Haskell Laboratory Report No. 635-79. Repeat Dose Toxicity Type: Species/Strain: Sex/Number: Exposure Period: Frequency of Treatment: Exposure Levels: Method: GLP: Test Substance: Results: Repeated Dose Oral Toxicity Study Mice/CD-1 Rats/Crl:CD Male and female/5/group 9 doses (3/week) 3 weeks 0 , 0.1 , 1 .0, 10 mg/kg The test substance, as aqueous solutions, wo.s administered by intragastric intubation to rats and mice. Control rats and mice received water only. Body weights and clinical signs were recorded. Animals were sacrificed 3 days after the final dose and the livers were removed and weighed. No Ammonium perfluorooctanoate, purity approximately 100% A significant liver weight increase was noted in both male and female mice at the 1 and 10 mg/kg levels. Significantly increased liver weights were noted in male rats, but only at 10 mg/kg. There were no significant changes in the liver weights of female rats at any dose. EID091545 Reference: Mortality occurred in 2/5 female mice at 10 mg/kg. No mortality occurred in male mice, male rats, or female rats at any dose level tested. Sporadic weight loss occurred in the 0.1, 1.0, and 10 mg/kg female rats and in the 0 .1 , 1 .0, and 10 mg/kg male and female mice. Weakness was observed in the 10 mg/kg female mice. DuPont Co. (1983). Unpublished Data, Haskell Laboratory Report No. 138-83. Type: Species/S train: Sex/Number: Exposure Period: Frequency of Treatment: Exposure Levels: Method: GLP: Test Substance: Results: Repeated Dose Oral Toxicity Study Rats/Crl:CD Male/12 12 days; 14 days of recovery 10 daily doses (5 doses, 2 non-dose days, 5 doses) 0, 6.7 mg/kg Each of 6 rats received 10 daily doses of ammonium perfluorooctanoate by intragastric intubation as an aqueous solution. Body weights were recorded. Three rats were killed 4 hours after receiving the 10th dose, and the remainder were killed 14 days later. Organ weights were recorded. Six undosed rats served as controls. No Ammonium perfluorooctanoate, purity 99% The most prominent effect of the test substance was enlargement of the liver, which, at the end of the dosage regimen, was about 45% heavier than that of the control rats. This change persisted after cessation of dosage, but the weight discrepancy was somewhat less since 14 days later the livers were only 20% heavier than those of control rats. The renal weights were 20% heavier than those of corresponding control rats, and this increase persisted after cessation of dosage, being 22% above that of the control rats 14 days later. These weight changes were not accompanied by morphological changes. Reference: The pancreatic weights were slightly depressed, being 8% and 12% lower than those of controls at the end of the test and recovery phases, respectively. The adrenals and testes were slightly increased in weight after the last dose, +14% and +11%, respectively, but returned to normal 14 days later. DuPont Co. (n.d.). Unpublished Data. EID091546 Q Q 9 V -J..--- Type: Species/S train: Sex/Numben Exposure Period: Frequency of Treatment: Exposure Levels: Method: 14-Day Feeding Study Rat/Crl:CDBR Male/20/group 14 days; 56 days of recovery ad libitum for 14 days 0, 30, 300 ppm Rats were approximately 6 weeks old at arrival. At study start, the body weights ranged from 196 to 240 g. Rats were housed singly and were fed food and water ad libitum. During the test period each group were fed diet that contained 0, 30, or 300 ppm of the test substance. Diets were prepared once for the 2-week feeding period and were stored refrigerated until used. All rats were weighed and observed for clinical signs of toxicity. Rats not sacrificed at the end of the feeding period were weighed and observed during the recovery period. Cageside examinations to detect moribund or dead rats were conducted twice daily. Five rats/group were sacrificed at the end of the 14-day feeding period, and on recovery days 7, 28, and 56. Livers were removed and weighed at each sacrifice period. Blood samples were taken for organofluoride concentration analysis from rats sacrificed at the end of the feeding period and on recovery day 7. GLP: Test Substance: Results: Appropriate statistical methods were used to analyze body weights, body weight gains, and organ weight data. No Ammonium perfluorooctanoate, purity approximately 100% Diets were not analyzed. No mortalities were observed during the study. Clinical signs of toxicity noted in the 30 and 300 ppm groups during the feeding period included irregular respiration, rapid breathing, red nasal discharge, and hunched posture. Statistically significant decreases in mean body weights were observed in rats from the 300 ppm dose group on days 7 and 14 of the feeding period and on recovery day 7. Mean body weight gains from this same group were significantly depressed during the first week of feeding. Significant increases in mean absolute liver weights were observed in rats from the 30 and 300 ppm dose groups sacrificed at the end of the feeding period and on recovery days 7 and 28. Significantly increased mean relative liver weights were observed in rats from the 30 and 300 ppm dose groups sacrificed at the end of the feeding EID091547 period and on recovery day 7, and in the 300 ppm dose group rats sacrificed on recovery day 28. Reference: Mean blood organofluoride concentrations of rats sacrificed on recovery day 0 were 0.3 ppm in control rats, 33.2 ppm*m the 30 ppm rats, and 71.5 ppm in the 300 ppm rats. On recovery day 7, mean blood organofluoride concentrations were 0.9 ppm for controls, 19.3 ppm for the 30 ppm group, and 22.2 ppm for the 300 ppm group. DuPont Co. (1995). Unpublished Data, Haskell Laboratory Report No. 326-95. Type: Species/S train: Sex/Number. Exposure Period: Frequency of Treatment: Exposure Levels: Method: GLP: Test Substance: Results: References: 14-Day Feeding Study Mice/Crl:CD-l # Male and female/5/group ^ 14 days ad libitum for 14 days 0, 30, 300, 3000 ppm Male and female mice (age 43 and 44 days, weighing 21 to 38 g) were fed diets containing ammonium perfluorooctanoate for 14 consecutive days. Male and female controls were observed concurrently and fed only ground chow. Individual body weights, food consumption, and clinical signs were recorded. Liver weights were recorded at the 14-day sacrifice. No Ammonium perfluorooctanoate, purity approximately 100% All male and female mice died after dosing with 3000 ppm. One female mouse died at 300 ppm. Body weight loss occurred at 300 and 3000 ppm. Liver weight/body weight ratios showed a dose- response increase at > 30 ppm in male and female mice. Clinical signs observed included unkempt head area (300 and 3000 mg/kg) and weakness (300 mg/kg). DuPont Co. (1982). Unpublished Data, Haskell Laboratory Report No. 12-82. Kennedy, G. L., Jr. (1987). Toxicol. Lett.. 39:295-300. Type: Species/S train: Sex/Number. Exposure Period: 14-Day Feeding Study Mice/Crl:CD-l Male and female/5/group/gender 14 days EID091548 Frequency of Treatment: Exposure Levels: Method: GLP: Test Substance: Results: ad libitum for 14 days 0, 10, 30, 100, 300, 1000, 3000, 10,000 ppm Male and female mice (age 41 and 42 days, weighing 19 to 30 g) were fed diets containing ammonium perfluorooctanoate for 14 consecutive days. Male and female controls were observed concurrently and fed only ground chow. Individual body weights, food consumption, and clinical signs were recorded. Liver weights were recorded at the 14-day sacrifice. No Ammonium perfluorooctanoate, purity approximately 100% Death occurred at 1000, 3000, and 10,000 ppm. All female mice at 3000 ppm and all male mice at 10,000 ppm were dead at the 2-week time point. All 10,000 ppm female mice and 3000 ppm male mice were dead at the 1-week time point. Although death occurred in the 1000 ppm mice, details on the number of deaths was not reported. Reference: Body weight loss occurred at the end of each week at 300, 1000, 3000, and 10,000 ppm male and female mice. Liver weight/body weight ratios showed a dose-response increase at > 10 ppm in male and female mice. Clinical signs observed included weakness (100 - 3000 ppm), tremors (300 and 1000 ppm), piloerection (100, 1000, and 3000 ppm), pallor (10,000 ppm), stained perineal area (100 - 1000 ppm), weight loss (100,1000, 3000, and 10,000 ppm), and unkempt appearances (300 - 10,000 ppm). DuPont Co. (1981). Unpublished Data, Haskell Laboratory Report No. 560-81. Type: Species/Strain: Sex/Number: Exposure Period: Frequency of Treatment: Exposure Levels: Method: 14-Day Feeding Study Mice/Crl:CD-1 Male and female/5/group 14 days ad libitum for 14 days Ammonium perfluorooctanoate: 0, 30 ppm Nonadecafluorodecanoic acid: 3,10, 30, 300, 3000 ppm Mixtures of nonadecafluorodecanoic acid/ammonium perfluorooctanoate: 15/15, 5/25,25/5 ppm Male and female mice (age 44 days, weighing 24 to 35 g) were fed diets containing either am m onium perfluorooctanoate, nonadecafluorodecanoic acid, or mixtures of the two test substances for 14 consecutive days. Male and female controls were observed concurrently and fed only ground chow. Individual body EID091549 GLP: Test Substance: Results: Reference: weights and clinical signs were recorded. Liver weights were recorded at the 14-day sacrifice. No Ammonium perfluorooctanoate, purity approximately 100% Liver weight/body weight ratio showed an increase at all levels tested. Mixing the 2 test substances did not alter the effects. Liver enlargement appeared to be dose-related with nonadecafluorodecanoic acid appearing the more potent of the two substances. DuPont Co. (1982). Unpublished Data, Haskell Laboratory Report No. 537-82. Type: Species/S train: Sex/Number: Exposure Period: Frequency of Treatment: Exposure Levels: Method: GLP: Test Substance: Results: References: 21-Day Feeding Study Mice/Crl:CD-l Male and female/5/group 21 days ad libitum for 21 days (Mice were mistakenly fed ground chow, without compound, for 2 days) 0, 0.01, 0.03, 0.1, 0.3, 1, 3, 10, 30 ppm Male and female mice (age 41 and 42 days, weighing 21 to 33 g) were fed diets containing ammonium perfluorooctanoate (suspended in 1% com oil before being mixed in ground chow) for 21 consecutive days. Male and female controls were observed concurrently and fed only ground chow. Individual body weights and clinical signs were recorded. Liver weights were recorded at the 21-day sacrifice. No Ammonium perfluorooctanoate, purity approximately 100% Livers were significantly heavier at 30 ppm, slightly heavier at 3 ppm, and appeared normal at 10 ppm in male and female mice. No changes in liver weight were seen at feeding levels of 1 ppm or lower, and the significance of the change observed at 3 ppm, in light of no differences at 10 ppm, is questionable. The only clinical sign observed was sporadic weight loss. DuPont Co. (1982). Unpublished Data, Haskell Laboratory Report No. 323-82. Kennedy. G. L.. Jr. (T987L Toxicol. Lett.. 39:295-300. Type: Species/S train: Sex/Number Exposure Period: 2-Year Feeding Study Rat/Crl:CDBR Male/156/group 2 years EID091550 29 CG0V-* Frequency of Treatment: Exposure Levels: Method: adlibitumfor 2 years 0, 0 (pair-fed), 300 ppm Male rats were administered either 0 (adlibitumcontrol group (control)), 0 (control pair-fed to the ammonium perfluorooctanoate group (CP-C8)), or 300 ppm ammonium perfluorooctanoate in the diet for approximately 2 years. After assignment to treatment groups each rat was designated for either hormonal evaluation (10/group/time point), cell proliferation evaluation (6/group/time point), or evaluation of peroxisome proliferation (6/group/time point). All rats were provided food and tap water adlibitum. Stability of ammonium perfluorooctanoate was confirmed by analyses at the beginning, middle, and end of the study. Throughout the study, concentration of the test compound in the diet and the homogeneity of the test diets were determined. All rats were approximately 49 days of age on the day of study start. Body weights, food consumption, and clinical signs were monitored throughout the study. Blood was collected for hormonal analyses at approximately 1,3, 6,9,12, 15,18, and 21 months after initiation of the study. Serum was analyzed for testosterone, estradiol, luteinizing hormone (LH), follicle stimulating hormone (FSH), and prolactin concentrations. Rats were sacrificed at the following interim time points: 1, 3, 6, 9, 12, 15, 18, and 21 months for cell proliferation and peroxisome proliferation evaluations. The following organs were weighed: testes, epididymides, accessory sex gland (ASG) unit with fluid, coagulating gland/seminal vesicle with fluid removed, prostate, and liver. Immediately after weighing, the liver and testes from animals selected for peroxisome proliferation evaluation were placed in ice-cold homogenization buffer for peroxisomal preparation. The following tissues were collected from the rats selected for cell proliferation evaluation: right and left testes, epididymides, ASG, liver, duodenum, pituitary, and ail organs with gross lesions. All rats surviving the 24-month test period were sacrificed and necropsied. Brain, heart, liver, spleen, kidneys, ASG unit, coagulating gland/seminal vesicles with fluid removed, prostate, epididymides, and testes were weighed at necropsy. The liver, testes, epididymides, pancreas, and organs with gross lesions were examined microscopically. GLP: Data were analyzed by appropriate statistical methods. No EID091551 3A e o o ' Test Substance: Results: Reference: Ammonium perfluorooctanoate, purity 98-100% Increased relative liver weights were observed in the ammonium perfluorooctanoate-treated rats. Hepatic 8-oxidation activity was also increased in the ammonium perfluorooctanoate-treated rats at all time points. Ammonium perfluorooctanoate did not significantly alter the rate of Leydig cell 8-oxidation or Leydig cell proliferation. Moreover, the rate of B-oxidation in Leydig cells was approximately 20-times less than the rate of hepatic 8-oxidation. Serum testosterone, FSH, prolactin, and LH levels were unchanged. There were, however, significant increases in serum estradiol levels in the ammonium perfluorooctanoate-treated rats at 1, 3, 6, 9, 15, 18, and 21 months. At 12 months, the am m onium perfluorooctanoate-treated rats had elevated serum estradiol levels when compared to the pair-fed control. Histopathological evaluation revealed compound-related increases in liver, Leydig cell, and pancreatic acinar cell tumors. Based on these data, .the Leydig cell tumors appear to be due to the combination of elevated estradiol levels and reduced prolactin levels. DuPont Co. (2000). Unpublished Data (Draft Manuscript). Type: Species/S train: Sex/Numben Exposure Period: Frequency of Treatment: Exposure Levels: Method: Repeated Exposure Inhalation Study Rats/ChR-CD Male/20/group 2 weeks; 42 days of recovery 6 hours/day, 5 days/week 0, 8, 80 mg/m3 Houseline air (approximately 20 L/min) was passed through a cyclone-head dust generator connected to a particle agitator-reservoir that contained ammonium perfluorooctanoate. The resulting airborne particulate was passed into a 30 L battery jar exposure chamber. The atmospheric concentration of ammonium perfluorooctanoate in the exposure chamber was monitored at 30-mihuite intervals. Rats were exposed, head only, for 5 consecutive days, 6 hours per day. After 5 days, the rats were given a 2-day recovery (weekend), which was followed by 5 daily, consecutive 6-hour exposures. All rats were weighed and observed daily (except weekends) during the adexposure and recovery periods. Food and water were available libitumat all times other than during the actual exposure. Clinical laboratory examinations were performed on 10 rats from each group at 0,14, and 28 days post-exposure. After a total of EID091552 10 exposures, 5 rats from each group were pathologically evaluated at 0, 14, 32, and 42 days post-exposure. Organs were weighed, and absolute and relative organ weights were calculated. GLP: Test Substance: Results: On the 5thand 9thdays of exposure, 10 rats were selected from each group for eye examinations. No Ammonium perfluorooctanoate, purity approximately 100% Overall mean concentrations were 0, 11 5, 83 17 for the 0, 8, and 80 mg/m3 exposure levels, respectively. Rats exposed to ammonium perfluorooctanoate showed a suppression of body weight throughout the test. The 83 mg/m3 group was more severely affected during exposure and for 14 days of recovery. During each exposure, sporadic cases of blinking, pawing, chewing, and red eye and nasal discharge were seen in all groups. Some rats exposed to ammonium perfluorooctanoate dust displayed elevated alkaline phosphatase activity. Effects were seen in glutamic-pyruvic transaminase and glutamic-oxalacetic transaminase after 0, 14, and 28 recovery days. The incidence was related to dose; higher activities were found at the higher exposure level. However, only the latter activity at 83 mg/m3 was statistically different from controls. Pathologic evaluations showed cloudy swelling or granular degeneration of hepatocytes in the livers of rats exposed to ammonium perfluorooctanoate for 10 days with no recovery. This effect was not seen after a 14-day or longer recovery period. No other compound-related histologic changes were noted. Exposurerelated increase in liver weights was observed. References: No comeal, iritic, or conjunctival effects were seen in any of the rats examined after 5 or 9 exposure days. DuPont Co. (1979). Unpublished Data, Haskell Laboratory Report No. 253-79. Type: Species/Strain: Sex/Number: Exposure Period: Kennedy, G. L., Jr. et al. (1983). The Toxicologist. 3:22. Repeated Exposure Inhalation Study Rats/Cri:CD Male/24/group 2 weeks; 84 days of recovery EID091553 Frequency of Treatment: Exposure Levels: Method: 6 hours/day, 5 days/week 0, 1, 8, 80 mg/m3 Dust atmospheres of ammonium perfluorooctanoate wfere generated by passing air through a glass generator. For the high concentration (80 mg/m3), chamber atmosphere concentrations were primarily determined by gravimetric analysis. For the intermediate and low concentrations (8 and 1 mg/m3, respectively), chamber atmospheres were determined by a chemical analyses. Male rats (age 7-8 weeks, weighing 240-279 g) were exposed head-only to dust atmospheres for 6 hours/day, 5 days/week for 2 weeks (weekends excluded). During exposure, rats were observed and clinical signs were noted. Post-exposure rats were weighed and observed daily for 14 recovery days, then weighed and observed 2 times/week through 84 days of recovery. Five, rats/group were sacrificed at 0, 14, 28, 42, and 84 days of recovery, for a total of 96 test days. Clinical laboratory examinations were performed on 5 rats from each group at 0, 14, 28,42, and 84 days post-exposure. After a total of 10 exposures, 5 rats from each group were pathologically evaluated at 0, 14, 28, 42, and 84 days post-exposure. The rats were examined grossly and tissues and organs were saved for microscopic evaluation. In addition, lungs, heart, thymus, spleen, liver, testes, and kidneys were weighed. GLP: Test Substance: Results: At necropsy, blood was collected for analysis of organofluoride levels in rat blood. Blood samples from the 0 and 80 mg/m3groups were analyzed at each recovery period. Blood samples from the 1 and 8 mg/m3 groups were analyzed only at 0 and 28 recovery days. No Ammonium perfluorooctanoate, purity approximately 100% Overall mean concentrations were 1.0 0.5,7.6 2.5, and 83.9 12.8 mg/m3 for the 1,8, and 80 mg/m3groups, respectively. Body weight analysis demonstrated no significant differences between controls and 1 mg/m3. Body weights from animals exposed to 8 mg/m3 were significantly higher than controls from test days 17-33. Body weights from animals exposed to 80 mg/m3were significantly lower than controls from test days 2-16. Observations of clinical signs during exposures showed only slight signs of nasal and ocular discharge. However, at the high concentration, after 3-4 days on test 1 rat died during exposure and 1 rat was sacrificed e ID091554 000';':", inextremis. Both of these rats had severe weight loss. Mortality was probably exposure-related, although pathologic evaluation could not determine the cause of death. Three of 24 rats in the 80 mg/m3exposure group exhibited lung noise during the 12-day exposure period. Organ to body weight ratios demonstrated a significant, dose-related increase in lung, liver, and testes weights after 0 recovery days. The liver/body weight ratios were significantly higher in animals exposed to 80 mg/m3 through 28 days of recovery. Mean absolute liver weights were significantly higher in the 8 mg/m3 animals through 28 days of recovery, but this may be an artifact caused by an unexplainable increase in body weight accompanied by a normal increase in liver weights at 8 mg/m3. Clinical laboratory measurements demonstrated an increase in alkaline phosphatase in all groups exposed to ammonium periluorooctanoate after 10 exposures, but this finding was significant only at 8 and 80 mg/m3. This increase persisted in the 80 mg/m3 animals through 14 days of recovery. After 28, 42, and 84 days of recovery no differences were found. Compound-related pathologic findings included heavy livers, panlobular hepatocellular hypertrophy, centrolobular hepatocellular hypertrophy, and hepatocellular necrosis in animals exposed to 8 and 80 mg/m3. These findings showed an exposure-response relationship, but were reversible by 28 days of recovery (8 mg/m3) or 42 days of recovery (80 mg/m3). References: Blood organofluoride analysis clearly demonstrated an exposure-related presence in all groups (including the controls, this finding remains unexplained). Blood organofluoride levels decreased with time, but was detectable after 84 days of recovery in both the control and 80 mg/m3 exposure levels. DuPont Co. (1981). Unpublished Data, Haskell Laboratory Report No. 205-81. Kennedy, G. L., Jr. et a1. (1983). The Toxicologist. 3:22. Type: Species/Strain: Sex/Numben Kennedy, G. L., Jr. et al. (1986). Food Chem. Toxicol.. 24:1325-1329. RepeatedDose Dermal Study Rats/ChR-CD Male/15/group EID091555 000V;-/. Exposure Period: Frequency of Treatment: Exposure Levels: Method: 2 weeks; 42 days of recovery 6 hours/day, 5 days/week 0, 20, 200, 2000 mg/kg Male rats (age 8 weeks, weighing 210-245 g) were collared to prevent ingestion of the compound when preening and grooming during the 2-week exposure period. A m m onium perfluorooctanoate, as an aqueous paste, was applied to the backs of each rat that had been shaved free of hair. Daily 6-hour exposures ended when the compound was wiped from the rats' backs with a gauze pad. Collars were removed after exposure day 10. Throughout the test period, food and water were available adlibitum. Body weights and clinical signs were recorded. After exposure day 10 and on recovery days 14 and 42, blood was taken from 5 rats from each group for hematology measurements. Gross necropsy and histopathological examinations were performed on 5 rats/group after exposure 10, and on recovery days 14 and 42. Mean absolute and relative organ to body weight analyses were performed. After exposure 10 and on recovery days 14 and 42, blood was collected from 5 rats/group for organofluorine determinations. Eye examinations were performed on each rat after exposure 9, and on recovery days 13 and 41. The procedure included gross observation of the eyes using a bright light, and semimicroscopic observation using a hang magnifying lamp and a slit-lamp biomicroscope. GLP: Test Substance: Results: Data were analyzed by appropriate statistical methods. No Ammonium perfluorooctanoate, purity approximately 100% Rats treated with 20 mg/kg ammonium perfluorooctanoate showed normal body weights and no unusual clinical signs during the experiment. During the 10-day exposure period, rats treated with either 200 or 2000 mg/kg lost weight, followed by a normal growth after the exposure period. Slight redness of the skin was observed in these 2 groups, along with salivation in the 2000 mg/kg group only. Clinical enzyme determinations monitoring liver function (alkaline phosphatase, GPT, and GOT) showed dose-related increases in all treated groups after exposure 10. These values returned to normal at recovery days 14 and 42. Liver damage characterized by coagulative necrosis,was observed in all treated groups following the 10thdose. The incidence and EID091556 009V:' severity of liver damage was dose-related. Recovery was complete in the 20 mg/kg group 14 days following the 10* dose, and was essentially complete in the 200 mg/kg group at the same time. On recovery day 42, reversal of liver damage was essentially complete in the 2000 mg/kg group. Two rats exposed to 2000 mg/kg had coagulative necrosis of the epidermis at the dose site following 10 exposures. Liver weights, both on an absolute and relative to body weight basis, showed a dose-related increase on exposure day 10, with a return to normal weight seen in the 20 mg/kg group at 14 days and in the 200 mg/kg group at 42 days of recovery. The increased liver weight persisted for 42 days in the 2000 mg/kg group, although a trend toward normal was observed. On exposure day 10, the mean kidney weights of the 20 mg/kg group were significantly greater than controls, and the mean absolute spleen and kidney weights from the 2000 mg/kg group were significantly less than controls. The mean relative testicular weights from the 2000 mg/kg group showed a statistically significant increase on exposure day 10. On recovery day 14, there was a statistically significant increase in the mean relative kidney and testes weights of the 200 and 2000 mg/kg groups. References: Blood organofluoride levels showed dose-related elevation on exposure day 10, followed by a decrease in the levels at recovery days 14 and 42. These values after the 10* exposure ranged from 52, 81, and 118 ppm (20, 200, and 2000 mg/kg, respectively) to 1,4, and 8 ppm (20, 200, and 2000 mg/kg, respectively) at recovery day 42. At a blood organofluoride concentration of approximately 10 ppm, there were normal liver weight to body weight ratios and serum enzyme activity, and no clinical signs or body weight differences from controls. One rat showed liver changes at this level. At a blood organofluoride level of approximately 50 ppm, there were marked liver changes and significant increases in the mean absolute and relative liver weights. No other toxic effects were evident at this blood organofluoride concentration. DuPont Co. (1980)1 Unpublished Data, Haskell Laboratory Report No. 589-80. Kennedy, G. L., Jr. (1985). Toxicol. Annl. Pharmacol.. 81:348-355. Developmental Toxicity Type: Species/Strain: Sex/Numben Route of Administration: Developmental Toxicity in Rats Rats/Crl:CD(SD)BR Females/6-15/group Inhalation EID091557 nc. 000' Exposure Period: Frequency of Treatment: Exposure Levels: Method: Days 6-15 of Gestation 6 hours/day 0, 0.1, 1.0, 10.0,25.0 mg/m3 Female rats were mated to males, and mating was verified by detection of spermatozoain the vaginal lavage each morning following overnight cohabitation. The day that spermatozoa were detected was designated as Day 1 of gestation (Day 1G). For Experiment I (females sacrificed before parturition), a total of 24 mated females were to have been assigned to each group (12 females/group/Run). However, due to the degree of maternal toxicity in evidence in the 25.0 mg/m3group in Run I, this concentration was reduced to 10.0 mg/m3 for Run II, and 15 mated females were assigned to this new group. Furthermore, two more control groups (6 mated females/group) were added to Run II; one was pair-fed to the 25.0 mg/m3group, and the other was pair fed to the 10 mg/m3group. For Experiment II (females allowed to give birth), in Run I 12 mated female rats were distributed to each group. With the addition of the 10.0 mg/m3 group in Run II, 6 mated females were added to both the control and the 10.0 mg/m3groups. Rats were exposed whole-body to atmospheres of ammonium perfluorooctanoate in 150 L glass and stainless steel Rochestertype chambers within which the rats were housed individually in wire-mesh modules. Chamber concentrations were determined by Vigravimetric analysis either each hour (1.0 mg/m3, and 10 or 25 mg/m3) or each hour (0.1 mg/m3), and by a spectrophotometric technique (on each 0.1 mg/m3sample, and on 5-6 samples per exposure day for the other levels tested). Dams .were weighed and observed for clinical signs. Feed consumption was measured during gestation (2 females/cage). The dams were coded from before sacrifice until all maternal and fetal data were collected, and until all structural alterations noted among the fetuses were classified. After sacrifice, the dams were examined for gross pathologic changes, liver weight was recorded, and reproductive status was determined. The number of corpora lutea and implantation sites were counted, and the number and position of all live, dead, and resorbed fetuses were recorded. All live and dead fetuses were weighed and sexed externally and EID09I558 37 009V internally, and the live fetuses were examined for external' Vialterations. Approximately of the fetuses of each litter that were alive when removed from the dam were examined for visceral alterations, and all stunted or malformed fetuses were examined similarly. The fetuses that were examined for visceral alterations were also examined for head alterations. Sections, containing the eyes of 3 fetuses from each litter of the 25.0 mg/m3group and of 2 fetuses from each litter of the control group, were processed histologically for examination. In Run II, one fetal head from each of 4 litters from the 10.0 mg/m3 group and the control group were examined. In addition^ the heads from all fetuses in the group pair fed to the 25 mg/m3group were processed for examination. All fetuses were examined for skeletal alterations. For Experiment II, the procedures used until Day 21G were the same as for Experiment I, except that the dams were weighed less frequently during gestation, feed consumption was not measured, and the identity of each offspring within litters was not retained. Before expected parturition, each dam was housed in a polycarbonate cage that contained bedding. The date of parturition was noted and was termed Day 1 PP. The dams were weighed and examined for clinical signs. For each test group fertility index and gestation index were calculated, and for each litter viability index and lactation index were calculated. All dams were sacrificed on Day 22 PP. The pups from each dam were counted, sexed, weighed, and examined for external alterations toward the end of Day 1 PP. Thereafter, each pup was weighed and inspected for adverse clinical signs on Day 4, 7, 14, and 22 PP. The eyes of the pups in all groups of Run I (Experiment II) were examined by an ophthalmologist on Days 15,16, or 17 PP, shortly after the eyes opened. This examination was conducted with the exposure levels coded. On Day 35 PP, each pup was sacrificed and the eyes were fixed for possible future evaluation. GLP: Test Substance: Results: Data were analyzed by appropriate statistical methods. Yes Ammonium perfluorooctanoate, purity >95% The actual mean concentrations achieved were 0 and approximately 0.14, 1.2, 9.9, and 21.0 mg/m3 for the 0, 0.1, 1.0, 10.0, and 25.0 mg/m3exposure groups. No effects were observed at 0.1 or 1.0 mg/m3. None of the 21 dams exposed to ammonium perfluorooctanoate at 10.0 mg/m3 died, but they showed similar clinical signs to a lesser degree than EID091559 'JJOO 0 0 0 f. ' that seen at the 25.0 mg/m3level. At 25 mg/m3, ammonium perfluorooctanoate was overtly toxic to rats in that 5/24 did not survive to term, most of the survivors had wet abdomens; reddishbrown discoloration around the eyes, nose, and mouth; lethargy; decreased feed consumption and body weight gain during the exposure period; and an unkempt appearance. Maternal liver weight changes among groups on a relative weight basis indicated that exposure to ammonium perfluorooctanoate at 10.0 mg/m3 or greater resulted in significantly larger livers. This increase in liver weight occurred despite the significant decrease in body weight gain in these groups, which significantly reduced the relative liver weights of the pair-fed contrcA groups. No differences from control were observed in the mean number of implants, mean number of corpora lutea, or fetal death in any dose level tested. Developmental toxicity was not demonstrated upon sacrifice of the dams on Day 21 of gestation at any concentration of ammonium perfluorooctanoate tested. Concentration-related embryo-fetal toxicity, expressed as decreased fetal weight, occurred only at 25.0 mg/m , which was overtly toxic to the dams. This decreased body weight persisted to Day 1 PP, but not to Day 4 PP. inOn Days 15, 16, or 17 PP, coded examination of the pups' eyes vivo from Run I did not reveal concentration-related malformations. In view of these negative results, similar invivo examination of the eyes of the pups from Run II was not conducted. Reference: Ammonium perfluorooctanoate did not demonstrate a unique hazard to the conceptus. DuPont Co. (1981). Unpublished Data, Haskell Laboratory Report No. 881-81. Staples, R. E. et al. (1984). Fundam. Appl. Toxicol.. 4:429-440. Type: Species/Strain: Sex/Number: Route of Administration: Exposure Period: Developmental Toxicity in Rats Rats/Crl:CD(SD)BR Female/25/group (Experiment I), 12/group (Experiment II) Gavage Days 6-15 of Gestation EID091560 J7 OQQV.'S Exposure Levels: Method: 0, 100 mg/kg In a pretest, 2 non-pregnant female rats were administered ammonium perfluorooctanoate by gavage at 150 mg/kg/day or 100 mg/kg/day to determine the maximum dose that the Hami could tolerate for the planned exposure period of 10 days. For the definitive study, female rats were mated to males, and the day that spermatozoa were detected in vaginal lavage was designated as Day 1 of gestation (Day 1G). For Experiment I, body weights, clinical signs, and feed consumption during gestation were recorded. The dams were coded fromjust before sacrifice until all maternal and fetal data were collected, and until all structural alterations noted among the fetuses were classified. After sacrifice of the dams on Day 21G, gross pathologic changes were examined, liver weight was recorded, and reproductive status was determined. The number of corpora lutea and implantation sites were counted, and the number and position of all live, dead, and resorbed fetuses were recorded. All live and dead fetuses were weighed and sexed externally and internally, and the live fetuses Viwere examined for external alterations. Approximately of the fetuses of each litter that were alive when removed from the dam were examined for visceral alterations. In addition, all stunted or malformed fetuses were similarly examined. The heads of all fetuses examined for visceral alterations and a sufficient number of the remainder to total 2/3 of each litter were fixed and examined for head alterations. All fetuses, except the heads of those that were fixed, were examined for skeletal alterations. For Experiment II, the procedures used until Day 21G were the same as for Experiment I, except that body weights were collected on different gestation days, feed consumption was not measured, and the. identity of each offspring within litters was not retained. At least two days before expected parturition, each dam was housed in a polycarbonate cage with bedding. The date of parturition was noted, and was termed Day 1 PP. The dams were weighed and examined for clinical signs. For each test group fertility index and gestation index were calculated, and for each litter viability index and lactation index were calculated. All dams were sacrificed on Day 23 PP, without pathological examination. The pups from each dam were counted, sexed, weighed, and examined for external alterations toward the end of Day 1 PP. EID09I561 40 0 0 0 ' Thereafter, each pup was weighed and inspected for adverse clinical signs on Day 4, 7, 14, and 22 PP. The eyes of the pups in both groups were examined by an ophthalmologist between Days 27 and 31 PP. This examination was conducted with the exposure levels coded. On Day 35 PP, each pup was sacrificed and the eyes were fixed for histologic evaluation. GLP: Test Substance: Results: Data were analyzed by appropriate statistical methods. Yes Ammonium perfluorooctanoate, purity > 95% In the pretest, one rat (weighing 278 g) dosed at 150 mg/kg showed severe clinical signs of toxicity by the 4thday and was found dead on the morning of the 5thday, by which time it had lost approximately 40 g body weight. Another rat (weighing 260 g) dosed at 150 mg/kg lost approximately 11 g by the 3rdday. After 5 days of dosing at 100 mg/kg, adverse clinical signs were not noted in 1 rat that lost approximately 6 g, and were minimal in the other rat that lost approximately 14 g. On this basis, the 100 mg/kg/day dosage level was judged to be the maximum that the dams could tolerate for the planned exposure period of 10 days. In Experiments I and n, 5 of the 37 dams given ammonium perfluorooctanoate were found dead and 1 was sacrificed in a moribund state, as compared to 0 of the 37 control animals. During the dosing period, all but 1 of the dams that subsequently died had wet perineal areas and were lethargic. Two also had chromodacryorrhea and chromorhinorrhea. Among the remaining dams, 4 developed alopecia, 1 had lung noise, and 1 had diarrhea. In the control group, the only clinical sign noted was focal alopecia that developed in 1 dam. From Days 6-15G, the treated group in Experiment I gained approximately 1/3 less than the control group, and during the post-treatment period (Days 16-21G), the body weight gain of the ammonium perfluorooctanoate-treated group significantly exceeded that of the control group. In Experiment II, the Day 16G body weight was not taken, therefore, Days 6-15 body weight gains were not calculated. Feed consumption was measured only for Experiment I. During the dosing period, the treated group consumed significantly less feed than the control group. Feed consumption was similar to the control value in the post-exposure period. Mean maternal liver weight for the treated group was increased, but the difference was not statistically significant. At sacrifice, 1 of the EID091562 4i ooovjo dams given ammonium perfluorooctanoate was observed to have several red areas on the visceral surface of the median lobe of the liver. In Experiment I, the maintenance of pregnancy, the incidence of resorptions, and fetal body weight were not adversely affected by ammonium perfluorooctanoate administradon. Similarly, in Experiment II, no adverse effect on reproductive performance or on pup viability or growth was demonstrated. The only embryo-fetal toxicity finding noted that could be compound-related was an increased incidence of fetuses with ossification sites on the first lumbar vertebrae versus the incidence in the control group. This difference in incidence was statistically significant only if analyzed by a one-tailed test Its presence was probably a response to generalized stress evoked by the toxic state of the dams. The postpartum viability, growth rate, and development of the offspring from additional dams given ammonium perfluorooctanoate were not affected. In vivo examination of pups' eyes between Days 27 and 31 PP revealed no compound-related alterations in the pups. Reference: Ammonium perfluorooctanoate did not demonstrate a unique hazard to the conceptus. DuPont Co. (1982). Unpublished Data, Haskell Laboratory Report No. 1-82. Miscellaneous Type: Species/stxain: Method: Metabolism Female and male rats/Crl:CD Female albino rats (7-8 weeks old and weighing approximately 200 g); pregnant primigrvida females (weighing approximately 200 g); and male rats (approximately 8 weeks old and weighing approximately 250 g) were used. The rats were housed 2/cage and allowed food and water ad libitum. Groups A-E rats were tested to measure blood organofluoride levels in female rats as a function of post-exposure time following oral administration and to investigate multiple versus single doses. Group A (21 female rats) was dosed with 25 mg/kg orally and 3 rats were sacrificed at !4, Vz, 1, 2,4, 8, and 24 hours after dosing. Groups B and C (12 female rats/group) were orally dosed with 2.5 or 150 mg/kg, respectively, and 3 rats were sacrificed at Vz, 2, 8, and 24 hours after dosing. Group D (21 female rats) was dosed ErD091563 0 0 0 VoV 11 days with 25 mg/kg orally each day and 3 rats were sacrificed at lA, Vi, 2, 4, 8, 24, and 168 hours after the 11th dose. Group E (12 male rats) was dosed at 25 mg/kg orally and 3 rats were sacrificed at Vi, 8, 24, and 168 hours after dosing. Groups F-I rats were tested to measure blood organofluoride levels in female rats following inhalation exposure. Group F (24 female rats) was exposed to a single 6-hour exposure of 10 mg/m3and 3 rats were sacrificed at lA, Vz, 1, 2,4, 8,24, and 168 hours after exposure. Groups G and H (12 female rats/group) were exposed to a single 6-hour exposure of 1 mg/m3 or 0.1 mg/m3, respectively, and 3 rats were sacrificed at Vi, 2, 8, and 24 hours after exposure. Group 1(12 male rats) was exposed to a single ,6-hour exposure of 10 mg/m3 and 3 rats were sacrificed at Vi, 2, 8, and 24 hours after exposure. Groups J-N were tested to compare blood organofluoride levels in pregnant versus non-pregnant rats and to compare oral exposure versus inhalation exposure. Group J (12 pregnant female rats) was administered 25 mg/kg orally on gestation day 15 and 3 rats were sacrificed at Vz, 2, 8, and 24 hours after dosing. Group K (6 pregnant female rats) was administered 25 mg/kg orally on gestation days 6-11 and 3 rats were sacrificed at Vz and 2 hours after the 6th dose. Group L (12 pregnant female rats) was administered 25 mg/kg orally on gestation days 6-15 and 3 rats were sacrificed at Vz, 2, 8, and 24 hours after the 10thdose. Group M (6 pregnant female rats) was exposed via a single 6-hour inhalation exposure to 10 mg/m3 on gestation day 15 and 3 rats were sacrificed at Vz and 2 hours after exposure. Group N (3 pregnant female rats) was exposed via inhalation, 6 hours/day, to 10 mg/m3 on gestation days 6-15 and 3 rats were sacrificed at Vz hour after the 10thexposure. GLP: Test Substance: Results: Blood samples were obtained from each rat. No Ammonium perfluorooctanoate, purity approximately 100% The uptake and clearance of ammonium perfluorooctanoate from the blood of female rats following a single oral dose was rapid with the peak reached 1-2 hours post-treatment and with virtual total clearance by 24 hours. A dose-response was demonstrated with no apparent changes in blood organofluoride levels following multiple oral dosing. A slower clearance rate in male rats was demonstrated following a single oral dose. A single 6-hour inhalation exposure resulted in peak blood levels within 1 hour after cessation of exposure. The test substance EID091564 rapidly cleared from the blood, and the number of exposures did not affect blood levels. Male rats cleared the compound much more slowly. Pregnant and non-pregnant rats showed similar organofluoride blood levels following either oral or inhalation exposures. Reference: The amount of ammonium perfluorooctanoate present as the straight chain isomer increases relative to the non-straight chain isomers as the time following ammonium perfluorooctanoate administration increases. This suggested that the non-straight chain isomers are cleared from the blood more rapidly than the straight chain isomer, or that a metabolite is present. DuPont Co. (1981). Unpublished Data, Haskell Laboratory Report No. 593-81. Type: Species/strain: Method: GLP: Test Substance: Results: Metabolism Male rats/Crl:CD Male mice 14C-Ammonium perfluorooctanoate (0.5 uCi/mg) as an aqueous solution was administered by intragastric intubation to 8 young adult male rats and 6 adult male mice at a dose of 10 mg/kg. One control group (2 rats and 2 mice) was sacrificed at 24 hours and 1 control group (3 rats and 2 mice) was sacrificed at 96 hours. The treated group (3 rats and 2 mice) was dosed with cholestyramine (1000 mg/kg) 24 hours after dosing with the test substance and then sacrificed at 96 hours. After dosing, rats and mice were placed in individual glass metabolism chambers. Exhaled 14C was sampled at 24,48, 72, and 96 hours. Feces and urine were collected. At sacrifice time, 1-2 mL of blood was removed from the mice and approximately 8 mL of blood was removed from the rats. Livers were removed, homogenized, weighed, and 0.5 g samples were oxidized and counted. No Ammonium perfluorooctanoate, purity approximately 100% Although a previous study (DuPont Report No. 828-81 - described below) indicated that cholestyramine resin could reduce the acute lethal effects of ammonium perfluorooctanoate in this study, there was no sign of enhanced elimination of t4C-ammonium perfluorooctanoate via feces, urine, or exhaled air. The differences between the 2 studies are most likely because of differences in absorption of the test substance. In the previous study, much of the dose was probably still in the gastrointestinal tract when cholestyramine was administered. The non-absorbed ammonium perfluorooctanoate then associated with cholestyramine, was removed before absorption could occur, and thus prevented the EID091565 Reference: acute lethal effects of ammonium perfluorooctanoate. For both rats and mice, the primary route of excretion was urinary, followed by fecal and expired air. After 96 hours, fecal elimination was nearly the same for both species; however, the mouse expired significantly more 14C in the air than the rat. Most notably, the mouse excreted less in the urine than the rat. This difference in urinary excretion was reflected as a greater concentration in mouse liver. DuPont Co. (1982). Unpublished Data, Haskell Laboratory Report No. 405-82. \ Pastoor, T. P. et al. (1983). The Toxicologist. 3:82. Type: Species/strain: Method: Metabolism Male and female rats Male and female mice Male and female hamsters Male and female rabbits A male and female of each species received a single 10 mg/kg dose of I4C-ammonium perfluorooctanoate via intragastric intubation. The rats, mice, and hamsters were housed individually in glass metabolism units immediately after dosing. Expired CO2, urine, and feces were collected at 12, 24, 48, 72, 96, and 120 hours after dosing. The male and female rabbits were individually housed in stainless steel metabolism cages immediately after dosing. Urine and feces were collected 24,48, 72, 96, 120, 144, and 168 hours after dosing. Expired CO2 was not collected. Blood was drawn from the rabbits 168 hours after dosing. The rats, mice, and hamsters were all sacrificed 120 hours after dosing and blood was drawn. All animals were dissected with following tissues excised, weighed, and frozen: heart, lungs, liver, kidneys, spleen, testes or ovaries, brain, G. I. tract, and muscle, skin, and fat samples. The carcasses were then weighed and frozen. Metabolism units were washed and the cage washes were collected and refrigerated. GLP: Urine, CO2 samples, and cage washes were analyzed directly for radioactivity using a liquid scintillation counter. Blood, feces, tissues, organs, and homogenized carcass samples were analyzed for 14C content by tissue oxidation using a tissue oxidizer and liquid scintillation counter. Rabbit carcasses were not analyzed for 14C content. No E ID 09I566 45 Test Substance: Results: Reference: Ammonium perfluorooctanoate, purity 70% Substantial sex differences in rats and hamsters were observed in the excretion of 14C activity following a single oral dose. The female rat and the male hamster excreted over 99% of the original 14C activity by 120 hours after dosing, conversely the male rat and the female hamster excreted 39 and 60% of the original l4C activity, respectively, by 120 hours post-dosing. Both sexes of rabbits excreted the l4C activity as rapidly and completely as the female rat and the male hamster. The male and female mice excreted only 21% of the original 14C activity by 120 hours post-dosing. The rapid excretors (female rat, male hamster, and male and female rabbits) contained negligible amounts of 14C in organs and tissues at sacrifice. The slow excretors exhibited the highest 14C concentrations in the blood and liver with substantial levels in the kidneys, lungs, and skin. DuPont Co. (1982). Unpublished Data, Haskell Laboratory Report No. 62-82. Type: Species/strain: Sex/Number: Method: Placental Transfer Pregnant rats/strain not specified Females/6 14C-labeled ammonium perfluorooctanoate was labeled on the carbonyl position and had a specific activity of 0.5 pCi/mg. Water was used as the dosing vehicle. The pregnant female rats received a single 10 mg/kg dose of 14C-labeIed ammonium perfluorooctanoate by gavage on the 19th day of gestation. The rats were individually placed in glass metabolism units immediately after dosing. Two rats were sacrificed at each time interval of 2,4, and 8 hours after dosing. Blood was drawn at sacrifice and refrigerated. The placentas, umbilical cords, and fetuses were then removed, dissected from each other, and weighed. The umbilical cords and placentas were individually placed into paper combustion cones and fetuses were frozen. Organs and tissues were also excised, weighed, and frozen. The carcasses were also weighed and frozen. Urine and fecal samples excreted between dosing and sacrifice were collected and frozen. The metabolism units were washed successively with dilute detergent, water, and acetone. The washes were collected and stored. The placentas, umbilical cords, and fetuses were oxidized in their entirety. Samples of the maternal tissues, carcass, and feces were also oxidized and analyzed for l4C activity by liquid scintillation counting. The urine and cage washes were analyzed directly by liquid scintillation counting. EID091567 ** GLP: Test Substance: Results: Reference: No Ammonium perfluorooctanoate, purity approximately 70% Placental transfer of 14C-labeled ammonium perfluorooctanoate was shown to occur after administration of a single oral dose of 14C-Iabeled ammonium perfluorooctanoate. The comparison of fetal levels of ammonium perfluorooctanoate at 2 and 4 hours relative to the concentrations observed in the maternal blood, placenta, and other organs revealed evidence of resistance to placental transfer of the test compound. However, by 4 hours, the fetal concentrations of ammonium perfluorooctanoate increased substantially more than all other organs and tissues examined. In contrast to other tissues examined, ammonium perfluorooctanoate in the fetuses did not decrease between 4-8 hours. The peak fetal ammonium perfluorooctanoate concentrations were similar in magnitude to the levels observed in the spleen, heart, lungs, and fat. Significant quantities of ammonium perfluorooctanoate can, therefore, be transferred from the placenta to the fetus with the placental barrier offering minimal resistance to transfer. DuPont Co. (1982). Unpublished Data, Haskell Laboratory Report No. 61-82. Type: Species/strain: Method: Effects of Dowex Ion Exchange on the Toxicity of Ammonium Perfluorooctanoate in Rats Male rats/Crl:CD A range-finding study was conducted prior to the test to find the tolerated dose of Dowex 1-X2-C1 (cholestyramine). In that study, rats were dosed from 200-1000 mg/kg, 1 rat/dose level, and 6 rats dosed at 1000 mg/kg. No clinical signs of toxicity were noted in this study. GLP: Test Substance: Results: Ammonium perfluorooctanoate, as a suspension in com oil, was administered by intragastric intubation to young adult male rats. Four groups, 6 rats/group, were used in the study. Group I was dosed with 500 mg/kg of ammonium perfluorooctanoate, Group II was dosed with 500 mg/kg of ammonium perfluorooctanoate and immediately dosed with 1000 mg/kg of Dowex 1-X2-C1, Group in was dosed with 1000 mg/kg Dowex 1-X2-C1 and 2 hours later dosed with 500 mg/kg of ammonium perfluorooctanoate, and Group IV was dosed with 500 mg/kg of ammonium perfluorooctanoate and 2 hours later dosed with 1000 mg/kg of Dowex 1-X2-C1. All rats were weighed and observed over a 14 day recovery period and then sacrificed. No Ammonium perfluorooctanoate, purity approximately 100% Pre-dosing or post-dosing with Dowex 1-X2-C1 Ion Exchange Resin at 1000 mg/kg changes the toxic effects of ammonium An-rt EID091568 perfluorooctanoate in rats. All rats dosed with the Dowex 1-X2-C1, either before or after the ammomiuni perfluooctanoate had reduced mortalities compared to the rats dosed with ammomium perfluooctanoate alone. Mortality ratios were 5/6, 0/6, 1/6, and 0/6 for Groups I, n, m , and IV, respectively. Reference: A follow-up study (DuPont Report No. 405-82 - described above) was performed to determine whether cholestyramine would enhance the elimination of absorbed ammonium perfluorooctanoate from the body. DuPont Co. (1981). Unpublished Data, Haskell Laboratory Report No. 828-81. Type: Method: GLP: Test Substance: Results: Reference: Respirator Evaluation The purpose was to evaluate M.S.A. Combination Type GMA-H respirator cartridges against ammonium perfluorooctanoate dust for breakthrough. The cartridge pairs were tested against an average concentration of 0.56 mg/m3 ammonium perfluorooctanoate generated in a dust generator, and introduced into an air blow of 60 L/min maintained at 50% relative humidity and ambient room temperature. Both upstream and downstream airborne concentrations were monitored for ammonium perfluorooctanoate dust by filter paper cassettes backed up with an impinger sampling train to absorb possible ammonium perfluorooctanoate vapors. Aliquots of the aqueous extracts of the filter paper and aliquots of the aqueous impinger samples were analyzed colorimetrically for ammonium perfluorooctanoate. No Ammonium perfluorooctanoate, purity not specified After 40 hours of continuous exposure, no detectable amount of ammonium perfluorooctanoate dust or vapor was found downstream on the breathing side of the cartridge pairs tested. The minimum detectable limit was 1.5 pg of ammonium perfluorooctanoate.' Based on a 420 L air sample, this would calculate to be 0.004 mg/m3. The mean upstream airborne concentrations were 0.67 0.33 and 0.48 0.15 mg/m3 at 40 and 54 hours, respectively. The results demonstrated that the M.S.S. combination type GMA-H cartridges effectively filter ammonium perfluorooctanoate dust and vapor concentrations at the test conditions for a minimum of 40 hours. DuPont Co. (1980). Unpublished Data, Haskell Laboratory Report No. 664-80. EID091569 AQ OOO'i Type: Method: GLP: Test Substance: Results: Glove Permeation Testing Five types of gloves (neoprene; neo-synthetic latex rubber, floe lined; latex; natural latex; neoprene rubber) were evaluated for their permeation resistance to a 30% aqueous solution of ammonium perfluorooctanoate and ammonium perfluorooctanoate dry powder. Samples of the gloves were tested in duplicate in 10 mL glass permeation cells with water used as a collection medium on the inside surface of the gloves. A 10 mL aliquot of the collecting medium was analyzed for ammonium perfluorooctanoate by spectrophotometry after an 8-hour exposure. Breakthrough was determined when a detectable amount of ammonium perfluorooctanoate was found in the collection medium. The minimum detection limit for ammonium perfluorooctanoate was 1 pg/mL in the collection medium. No Ammonium perfluorooctanoate, purity not specified Results of the evaluation show that 3 of the glove samples (neoprene; neo-synthetic later rubber, floe lined; and-natural latex) do have a measurable breakthrough time and permeation rate after 8 hours of continuous exposure to a 30% solution of ammonium perfluorooctanoate. However, the permeation rates are very low indicating that the materials do offer some resistance to the test substance. Reference: Type: Results of the tests performed with ammonium perfluorooctanoate powder show that in 4 of the samples (neoprene; neo-synthetic latex rubber, floe lined; latex; and neoprene rubber) no breakthrough was observed after 8 hours of continuous exposure, and only a very small amount permeated the latex sample. DuPont Co. (1981). Unpublished Data, Haskell Laboratory Report No. 612-81. Biopersistence Screening Study Summarized in the PFOS section, see DuPont (2000). Haskell Laboratory Report No. 2922. EID091570 0 0 0 '/ J 5 SUMMARY OF STUDIES CONDUCTED WITH AMMONIUM PERFLUORONONANOATE AT DUPONT Mammalian Toxicity Acute Toxicity Type: Species/strain: Value: Method: GLP: Test Substance: Results: Reference: Oral ALD Male rats/ChR-CD 187 mg/kg The test substance, as a solution in water, was administered by intragastric intubation to young adult male rats (1/group) in single doses. Concentrations tested were 1.0, 1.5, 2.3, 3.4, 5.1, 7.7, 12, 17, 26, 40, 60, 90, 130, 187, 300, 450, 670, 1000, 1500, and 2250 mg/kg. Survivors were sacrificed 14 days later, and body weights and liver weights were recorded. No Ammonium perfluorononanoate, purity not specified Mortality was observed at concentrations of 187 mg/kg and above. Deaths occurred within 6 days after dosing. Slight initial weight losses occurred at 26 and 40 mg/kg. Weight loss occurred for 9, 12, and 15 days at 60, 90, and 130 mg/kg, respectively. No clinical signs were observed below 26 mg/kg. Clinical signs observed at 26 mg/kg and above included pallor, salivation, polyuria, and chewing-motions. Additional clinical signs observed at 187 mg/kg and above included belly-crawling, half-closed eyes, incoordination, ruffled fur, diarrhea, and emanciation. Increased liver weights and increased liver/body weight ratios occurred at 3.4 mg/kg and above. DuPont Co. (1968). Unpublished Data, Haskell Laboratory Report No. 129-68. Type: Species/strain: Value: Method: Inhalation ALC Male rats/Crl:CD(SD)BR 590 mg/m3 Male rats (6/group), 8 weeks old and weighing between 234 and 298 g, were exposed via nose-only inhalation for a single, 4-hour period to a dust atmosphere of ammonium perfluorononanoate in air. Concentrations tested were 620, 910,1600, and 4600 mg/m3. Dust atmospheres were generated with a bin feeder regulated with a volumetric feed controller. The bin feeder metered test substance into a glass transfer tube. Air introduced at the tube swept the test substance through a size-reducing cyclone and into the exposure chamber. For the lowest exposure concentration, the atmosphere was generated by passing pressurized air through a glass generator. A flask at the bottom of the generator served as a dust reservoir. A EID09157I TA OOYc'if GLP: Test Substance: Results: cyclone elutriator was inserted above the reservoir. A motorized stirring rod agitated dust in the generator. Air introduced at the bottom of the reservoir and at the cyclone elutriator swept dust particles into the exposure chamber. The atmospheric concentrations was determined at approximately 30 minute intervals by drawing calibrated volumes of chamber atmosphere through filters. The atmospheric concentration of particulate was determined from the filter weight differential before and after sampling. Chamber temperature, relative humidity, and chamber oxygen content were measured. Except during exposure, food and water were available ad libitum. Body weights and clinical signs were recorded. Survivors were sacrificed 14 days later. N To monitor the effectspf ammonium perfluorononanoate on the liver, 2 groups of 10 rats, 8 weeks old and weighing between 237 and 277 g, were exposed to 67 and 590 mg/m3, respectively. Two groups of 10 rats, 8 weeks old and weighing 231 and 267 g, were exposed to air only. Each control group was exposed concurrently with one of the test groups. Five rats/group were sacrificed 5 or 12 days after exposure for pathologic examination of the liver. Yes Ammonium perfluorononanoate, purity >99% Chamber temperatures ranged between 23-27C, relative humidities ranged from 19-45%, and chamber oxygen contents were 21%. One of the rats in the 590 mg/m3died on the 12th day of exposure. Mortality ratios of 0/6, 4/6, 6/6, and 6/6 were observed in the 620, 910, 1600, and 4600 mg/m3. Clinical signs observed during or immediately post-exposure included red or brown facial discharge (67-1600 mg/m3), test substance on the head (620, 1600, and 4600 mg/m ), labored breathing (4600 mg/m ), profuse clear nasal and oral discharges (4600 mg/m3), and diminished startle response (4600 mg/m3). No adverse clinical signs were observed in rats exposed to 67 mg/m3 throughout the recovery period. Common clinical signs at higher concentrations included hunched posture, ruffled or discolored fur, red or brown facial discharges, wet or stained perineum, pallor, lung noise or labored breathing, lethargy, limpness, and hair loss. Rats exposed to 67 mg/m3 lost 1-9% of initial body weight 1 day post-exposure, followed by normal weight gain. At concentrations greater than 67 mg/m3, rats lost approximately 6-15% of initial body weight 1 day post-exposure, and continued to lose weight either throughout the recovery period or until they died. Most EID091572 51 0 0 0 ', surviving rats exposed to 590, 620, or 910 mg/m3 weighed only 54-71% of initial body weight when they were sacrificed 12 days post-exposure or at the end of the recovery period. References: Rats exposed to 67 mg/m3had significantly elevated mean liver weights and liver-to-body weight ratios on the 5th and 12thdays after exposure. Rats exposed to 590 mg/m3 had significantly elevated liver-to-body weight ratios on the 12thday after exposure. Liver weights for these rats were not significantly different from the controls on the 5thday of recovery, and mean liver weights were significantly depressed on the 12th day of recovery. However, these seemingly inconsistent changes were due to severe body weight loss in rats exposed to 590 mg/m3. Gross pathologic examination of rats exposed to 590 mg/m3 revealed discolored livers with prominent lobular patterns in 4/5 rats sacrificed on the 5thday of recovery, and similar gross liver lesions in 2/5 rats sacrificed on the 12th day of recovery. DuPont Co. (1985). Unpublished Data, Haskell Laboratory Report No. 293-85. Kinney, L. A. et al. (1989). Food Chem. Toxicol.. 27:465-468. Repeat Dose Toxicity Type: Species/S train: Sex/Numben Exposure Period: Frequency of Treatment: Exposure Levels: Method: GLP: Test Substance: Repeated Dose Oral Toxicity Study Mice/Crl:CD-1(ICR)BR Male and female/5/group 14 days Ad libitum for 14 days 0, 1, 3, 10, 30, 100,300, 1000, 3000, 10,000 mg/kg Male and female mice (5-6 weeks old) were fed diets containing ammonium perfluorononanoate for 14 consecutive days. Verification of the concentration of the test substance in the prepared diets were performed. Body weights and clinical signs were recorded throughout the test. After sacrifice, liver weights were recorded. Body weights and liver weights were analyzed with appropriate statistical methods. Sacrifices occurred on test day 6 at concentrations of 1000 ppm and greater, on test day 8 at concentrations of 100 and 300 ppm, and on test day 14 for the remaining test groups. No Ammonium perfluorononanoate, purity 99% EID091573 52 0 0 9 V - . 1 Results: Reference: Mortality ratios of 0/5, 0/5, 0/5, 3/5, and 1/5 were observed for the male mice fed 100, 300, 1000, 3000, and 10,000 ppm, respectively. Mortality ratios o f 0/5, 3/5, 4/5, 5/5, and 3/5 were observed for the female mice fed 100, 300, 1000, 3000, and 10,000 ppm, respectively. Mice fed concentrations o f 100 ppm or less exhibited slight to severe sporadic weight loss. Mice fed concentrations of 300 ppm and higher exhibited severe weight loss, ruffled fur, lethargy, low posture, and limpness. Male and female mice fed diets o f 3 ppm or higher had significantly increased mean absolute and mean relative liver weights. The mean relative liver weights o f male mice fed the 1 ppm diet were also significantly heavier than the controls. Comparisons o f mean body and liver weights o f mice fed diets above 30 ppm were not possible because there were no concurrent control groups. DuPont Co. (1985). Unpublished Data, Haskell Laboratory Report No. 401-85. EID091574 009 1<, r > 116 O O O V'.J.o  Anthony J Playtis 06/09/2000 02:59 PM To: cc: Subjsct Paul J Bossrt/AE/DuPontDuPont, Robert L Ritchey/CL/DuPontQDuPont, Dawn D Jackson/CL/DuPontDuPont Oscar T Garza/AE/DuPontQDuPont C-6 TLV I checked the ACGIH TLV listing for ammonium perfluorooctanoate, and they do indeed give it an A3 notation, which means: "Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in animals at a relatively high dose, by route(s) o f administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure." EID076894 I 117 000V ix r ^ /P ' ... H David Ramsey 06/13/2000 02:48 PM To: cc Subject: Dawn D Jackson/CL/DuPont@DuPont, Lynwood K lreland/CL/DuPont@OuPont, Paul J Bossert/AE/DuPont@DuPont. Robert L Ritchey/CL/DuPont@DuPont, John S Sieg/EUR/DuPont@DuPont Mr. Graham of Dry Run -------------------------- Forwarded by H David Ramsay/AE/DuPont on 06/13/200002:48PM --------------------- ;----------- From: Bernard J Reilly on 06/13/2000 01:51 PM To: cc: Subject: H David Ramsey/AE/DuPont@DuPont, Ralph G Stahl_Jr/AE/DuPont@DuPont, Isidores J Zanikos/AE/DuPont@DuPont. John R Bowman/AE/DuPont@DuPont@DuPont, Andrea V Malinowski/AE/DuPont@DuPont, Paula Durst-Glllis/STB/DUPQDUP, M. Ann Bradley/STB/DUP@DUP Mr. Graham of Dry Run -------------------------- Forwarded by Bernard J ReiDy/AE/DuPont on 06/13/2000 01:48 P M ---------------------------------"Dr. Perry Habecker" <habecker@ vetupenn.edu> on 06/13/2000 12:58:06 PM To: 'Bob Poppenga" <poppenga, 'Bob Munson' <munson, 'GREG P. SYKES 6-6070* <SYKESGP cc: REILL2BJ Subject Mr. Graham of Dry Run I just talked to Cyril Graham, the Jersey cow dairyman from the Dry Run area, about his concerns for potential toxicities. In short, he has already contracted a lab to analyze his cowDs milk. He said he was testing for cadmium, arsenic and several other items. When I said Dheavy metal screenD , he affirmed this. He prefers to wait to see what results this lab generates before contacting us. I offered him Bob PoppengaOs (sorry Bob) and my NBC phone numbers if he needs clarification or thinks he needs more testing. During a previous phone conversation, I had suggested that testing milk was probably not the most expeditious route to finding trouble. So, for the moment, we donQt need to talk with him. Perry DDJ001516 att1.htm -------------------------- Forwarded by H David Ramsey/AE/DuPont on 06/13/2000 02:48 PM ---- -- ---- -- -- ---- From: Bernard J Reilly on 06/13/2000 02:04 PM To: cc: Subject: H David Ramaey/AE/DuPontQDuPont, Ralph G Stahl_Jr/AE/DuPorrtDuPont Isidores J Zanikos/AE/DuPontDuPont John R Bowman/AE/DuPcnt@DuPont@DuPont M. Ann Bradley/STB/DUPQDUP. Paula Ourst-Gillis/STB/DUP@DUP. Greg P Sykes/RND/Pharma@DPC RE: Mr. Graham of Dry Run Forwarded by Bernard J Reilly/AE/DuPont on 06/13/2000 02:00 P M -----------------------"Dr. Perry Habecker" <habecker@ veLupenn.edtP- on 06/13/2000 02:02:11 PM 'lo o o v 1 f E'O 0S6 l4 6 To: RE1LL2BJ Subject RE: Mr. Graham of Dry Run I should tell you that I cc'd that e-mail message to Sarah Caspar of the EPA regional office. I don't think that this will make for complications, but the cattle team had agreed a long time ago that we would notify her of relevant consultations with the WV locals. ---- Original Message---From: Bernard J Reilly [mailto:Bernard.J.Reilly0USA.dupont.com] Sent: Tuesday, June 13, 2000 1:52 PM To: Dr. Perry Habecker Cc: GREG P. SYKES; Ralph G Stahl_Jr Subject: Re: Mr. Graham of Dry Run Perry, Thank you for following up. -- Bernie DDJ001517 0 00 * t EID086147 VV 'S 18 I c 0 0 0 7 *' 5 June 23, 2000 Dr. Charles M. Auer, Director U.S. Environmental Protection Agency Office of Pollution Prevention and Toxics Chemical Control Division 401 M Street NW, Room 403 Washington, D.C. 20460 Dear Dr. Auer: As you requested in your April 19, 2000 letter and during our subsequent meeting on May 1, 2000, attached is a summary o f DuPont's U.S. uses o f Ammonium Perfluorooctanoate (APFO, CAS# 3825-26-1) as a fluoropolymer reaction aid including releases from DuPont site and the fate o f APFO in fluoropolymer dispersion products, a summary of industrial hygiene data collected at our U.S. fluoropolymer manufacturing site, and a summary o f the employee blood data from a site in the U.S. A summary o f the toxicology available to DuPont was sent under separate cover on May 26, 2000. It is important to emphasize the following points: > DuPont does not manufacture APFO. All APFO used in our processes as a reaction aid is purchased from an outside supplier. > Most of the APFO used is removed from the fluoropolymer products before they are sold to outside customers. A relatively small amount o f APFO (worldwide, in the U.S.) leaves DuPont facilities in fluoropolymer dispersion products. > O f the APFO in the products sold, most (>97%) is destroyed during customer processing to a non-carboxylated hydrofluorocarbon. > All o f the U.S. DuPont operations that use APFO with significant exposure potential are concentrated at one location; Washington Works in Washington, WV. Therefore, most of the industrial hygiene data and blood serum data presented in this document are from that location. > 0 0 f. EID070482 Dr. Charles M. Auer, Director U.S. Environmental Protection Agency Page 2 > Extensive industrial hygiene data collected on workers potentially exposed to APFO show airborne exposures to be significantly below the ACGIH TLV of 0.01mg/m38 hr. TWA. Exposure levels of plant workers have dropped significantly since the conversion to an APFO solution from a dry powder. > As part of the ongoing surveillance of workers potentially exposed to APFO, in March and April of this year a series of blood samples were taken from workers in the U.S., The Netherlands and Japan to be analyzed for serum APFO concentration. DuPont has not received the results from our contract laboratory at this time. DuPont will submit a summary of the results when they become available. The format of the information in the attached is a modified UEIP format. If you wish to discuss the information contained in the attachment, please contact Robert F. Pinchot at (302) 999-4074 or e-mail at Robert.F.Pinchot@usa.dupont.com or me at (302) 366-5259. Very truly yours. Gerald L. Kennedy Director, Applied Toxicology and Health 009V.G EID070483 Voluntary UE!P, Ammonium Perfluorooctanoate V o lu n ta ry Use and E xp o su re In fo rm a tio n P ro file A m m o n iu m P erflu o ro o ctan o ate (A P F O ) I. CHEMICAL IDENTIFICATION Chemical Name: CAS Number: Ammonium Perfluorooctanoate 3825-26-1 II. COMPANY IDENTIFICATION Company Name: E. I. du Pont de Nemours and Company Site Locations: Site where APFO is used as a reaction aid: Washington Works Route 892 Washington, WV 26181 Sites where APFO containing products made at Washington Works are processed: Parlin Plant Cheesequake Road Parlin, NJ 08859 Spruance Plant 5401 Jefferson Davis Hwy. Richmond, VA 23234 Site which disposes of waste containing APFO: Chambers Works Rte. 130 Deepwater, NJ 08023 Technical Contact: Robert F. Pinchot (302) 999-4074 DuPont Fluoroproducts Chestnut Run Plaza Bldg. 711/2210 Centre Boulevard Wilmington, DE 19805-0711 EID070484 Voluntary UEIP, Ammonium Perfluorooctanoate III. DUPONT AND CUSTOMER ACTIVITIES Narrative Description of APFO Use The block diagram on the back page titled "DuPont US APFO Balance" describes the processes discussed below. DuPont uses APFO as a reaction aid in the production of polytetrafluoroethylene (PTFE) and tetrafluoroethylene (TFE) co-polymers. The process utilized at DuPont's Washington Works for making PTFE and co-polymers consists of polymerizing TFE (and other co-monomers if desired) in an aqueous media with a small amount of APFO to aid in the reaction. Following the polymerization step, the polymer dispersion is either dried to remove water and APFO or concentrated (removing some of the APFO), stabilized and sold as an aqueous dispersion. The dried polymer contains very little, if any, APFO. The APFO removed from the polymer is recovered for recycle, captured and destroyed off site in an incinerator, captured and sent to an offsite industrial landfill, and/or emitted to air or water at the Washington Works. The stabilized polymer dispersions are sold by DuPont to industrial customers (both in the US and outside the US) for a variety of uses, internally transferred to the DuPont Spruance Plant for the production of Teflon fibers and PTFE coated synthetic fibers, or internally transferred to the DuPont Parlin Plant for the production of Teflon Finishes. A small amount of non-hazardous waste polymer, water, APFO and other additives generated at Washington Works is treated in a wastewater treatment facility at DuPont's Chambers Works. This material is either emitted in the Chambers Works water discharge or captured on carbon and landfilled in a secure landfill. The internal process at the DuPont Spurance Plant to produce Teflon fibers involves, for most of the product, a "sintering" step in which the APFO contained in the product is destroyed by the following reaction:1 CF3(CF2)6COO-NH4+ - CF3(CF2)5CF2H + C 02 +NHj This reaction goes to completion at 350C and 0.2s residence time. A small amount of product processed at DuPont's Spruance plant does not get sintered and thus contains a small amount of residual APFO. These products are used for industrial pump, valve and compressor packing materials. 1P.J. Krusic, D.C. Roe. `Thermal decomposition of C8 fluorinated surfactants and related materials studied by high temperature gas-phase l9F NMR. A new Alternative to thermal gravimetric analysis, DuPont Internal Report. 0 0 9 7 . ' r. EID070485 Voluntary UEIP, Ammonium Perfluorooctanoate The process for making Teflon finishes at the DuPont Parlin Plant involves a blending operation of fluoropolymer dispersions with other additives including solvents, binders, and pigments. The small amount of APFO emissions to water from this facility is due to waste generated during product changeovers. Some of the fluoropolymer dispersion is processed at contract facilities where the material is dried at temperatures >350C thus destroying the APFO according to the reaction above. This dried material is then incorporated into finishes products. The final product produced is then sold to applicators that apply the product to a substrate (such as cookware) via automated spraying or rollercoating. Emissions of APFO from these operations consist of overspray that is either captured on filters and landfilled or absorbed into water resulting in a water emission. Product that is applied to the substrate is then typically "sintered" at temperatures approaching 800F resulting in the removal of the APFO from the substrate and subsequent destruction according to the reaction above. Customers of dispersion products use the material for a variety of applications. However, most applications involve a "sintering" step where the APFO is destroyed. There are a small number of applications where the customer heats the dispersion products to temperatures that allow the APFO to sublime resulting in air emissions. There are also a small number of applications where the customer's product is not heated resulting in the APFO staying with the product. These applications include industrial packings, and industrial filter fabrics. IV. SITE RELEASE AND TRANSFER INFORMATION FOR TRI CHEMICALS Not applicable- APFO is not listed on the TRI V. SITE RELEASE AND TRANSFER INFORMATION FOR NON-TRI CHEMICALS A. On-site Air Releases Fugitive Stack (Point Source) Estimated Total Annual Releases ( lbs. 1999) Washineton Works Parlin Snruance Chambers Works Negligible 0 0 0 24000 00 0 Comments Air emissions are estimated using engineering calculations and judgements and limited measurements of specific point sources conducted in the past. ooo'; EID070486 Voluntary UEIP, Ammonium Perfluorooctanoate B. On-site Water Releases Point Source Estimated Total Annual Releases ( lbs. 1999) Washineton Works Pari in Soruance Chambers Works ~j 55000 300 150 9500 Comments Water emissions are estimated using engineering calculations and judgements and limited measurements of specific sources conducted in the past. Washington Works emissions occur for approximately 350 days/yr while the other sites' emissions occur for 10-100 days/yr. Releases of APFO to the Ohio River from the DuPont Washington Works Plant were modeled using the Probabilistic Dilution Model (PDM Beta Version 4.0 Beta June 11, 1999, US EPA Office of Pollution Prevention and Toxics) and a constructed Microsoft Excel spreadsheet model. APFO release data for 1996 were used in both modeling exercises.2 The PDM indicated that APFO concentrations of 1.0 ug C8/L would be exceeded about 50% of the time during the year. APFO concentrations of in the river would exceed 0.1 pg APFO/L 90% of the time during the year and 10 pg APFO/L about 2.2% of the time during the year. Average annual APFO concentrations in the Ohio River calculated by using a Microsoft Excel spreadsheet was 0.423 pg APFO/L. Modeled AFPO concentrations in the river ranged from a low of 0.199 pg APFO/L in March to a high of 0.965 pg APFOC-8/L in September, which correspond to high and low river flows, respectively. Average Ohio River flows and volume data calculated from the US Geological Survey was collected at the Belleville Dam and used in the spreadsheet model. The Belleville Dam is on the Ohio River 13 miles downstream of the Washington Works Plant. This river flow data is the closest location downstream from the plant where this type of information is available. In 1999 a drinking water sample obtained from GE plastics, Washington WV, immediately downstream on the Ohio River from DuPont Washington Works showed 0.552pg/l APFO. In addition samples obtained in January 2000 from three different wells at the Lubeck Public Service District, downstream of Washington Works on the Ohio River, showed 0.8pg/l, 0.44pg/l and 0.313 pg/1. APFO. 2 W.R.Berti, Modeling releases of ammonium perfluorooctanoate into the Ohio River, DuPont Internal Report EMSE-054-00. 000 t* A EID070487 Voluntary UEIP, Ammonium Perfluorooctanoate C. On-Site Land Releases Chambers Works treats APFO containing waste in a wastewater treatment system. Engineering calculations and measurements indicate that approximately 30% of the APFO in'the wastewater treated is absorbed on to a carbon media that is landfilled on site. These land releases are estimated to be 39001b in 1999. Prior operations have resulted in measurable APFO concentrations in three landfills operated by the Washington Works in West Virginia. At Letart3 landfill surface water measurements in 1999 and 2000ytd range from 2.23pxg/1 to 3240pg/l with an average of 1392ug/l. Groundwater measurements taken during the same time period at Letart landfill range from 60.3(ig/l to 17400pg/l with an average of 2537|ag/l. At the "local landfill" the groundwater concentrations range from 0.046pg/l to 39|ig/l with an average of 8.83|ig/l. Surface water samples at the "local landfill" range from 0.54pg/l to 87|ig/l with an average of 18.5pg/l. At Dry Run landfill there are limited measurements of groundwater and surface water with maximum concentrations in groundwater of 15pg/l and the maximum concentration in the permitted outfall has been 33(jg/l. In 1999 a RCRA Facility Investigation was completed for Washington Works and was submitted to EPA Region III in June 19994. The report contains data on groundwater concentrations of APFO at Washington Works. D. Transfers to Off-site Locations Washington Works: Incineration Wastewater treatment Underground Injection Hazardous Waste Landfill Other landfill Recycle or recovery Estimated Total Annual Releases or Transfers db. 1999 16000 T343 0 2600 0 IV. ON-SITE W ORKPLACE EXPOSURE A. Information on the Number of Employees Potentially Exposed 5Maps of the landfill locations and specific monitoring locations and results are available upon request. 4Report was submitted to Martin. T. Kotsch. Remedial Program Manager, EPA Region III, Philadelphia. 5This is the same material that was described above in paragraph 1 of section V.D. 09 EID070488 Voluntary UEIP, Ammonium Perfluorooctanoate The tables below describe the number of workers that may be exposed to APPO during their normal work activities for each of the three sites where APFO is used or APFO containing product is processed. Hours/Day <0.25 0.25-1 1-8 >8 <10 Washington Works Days/yr 10-100 100-250 242 >250 Routine worker activities that have potential for exposure: > Handling raw material APFO > Handling raw dispersions containing APFO > Maintenance of polymerization reaction systems > Polymer dryer operation and maintenance > Packout of PTFE and co-polymer dispersion products > Operation and maintenance of APFO recovery systems EID070489 Voluntary UEIP, Ammonium Perfluorooctanoate Hours/Day <0.25 0.25-1 1-8 >8 <10 Parlin Plant Days/yr 10-100 100-250 18 >250 Routine worker activities that have potential for exposure: > Handling of PTFE and Co-polymer dispersion products > Operation and maintenance of blending facilities > Packout of finished product Note that at no time is the material handled at the Parlin Plant at an elevated temperature where the APFO could sublime. Therefore there is little potential for exposure to airborne APFO at this facility. All exposure potential is through skin contact during handling of the polymer dispersion materials all of which contain <1% APFO with most containing <0.25% APFO. Hours/Day <0.25 0.25-1 1-8 >8 <10 Spruance Plant Days/yr 10-100 100-250 <10 >250 Routine worker activities that have potential for exposure: > Handling of PTFE and Co-polymer dispersion products > Operation and maintenance of fiber coating facilities > Operation and maintenance of sintering rolls > Packaging of non-sintered product. Note that the PTFE and co-polymer dispersion products used at the Spruance site contain <0.9% APFO with most containing approximately 0.3% APFO. B. Information on the Exposure Levels of Washington Works Employees Since most of the processing done in the US with APFO and APFO containing intermediates and products is done at Washington Works, DuPont's airborne industrial hygiene data is concentrated at that site. The limited measurements of airborne APFO concentrations at the other sites where APFO containing products are used have shown much lower levels (mostly non-detectable) levels of APFO. The data in the table below COOV-i"1' EID070490 Voluntary UEIP, Ammonium Perfluorooctanoate reflect monitoring done over the last 5 years at Washington Works. The sample results are a combination of chemical operator and maintenance worker personal samples. Year Sample Type 1999 Partial 1998 Shift 1997 (mostly 1996 6-8 1995 hours) # of Samples 100 83 100 73 32 Minimum Concentration (mpb6) <0.01 .001 <0.01 N/D N/D Maximum Concentration (mpb) 0.58 0.78 2.4 0.29 0.16 Mean Standard (mpb) Deviation 0.061 0.103 0.146 0.055 0.067 0.151 0.145 0.378 0.069 0.063 Partial shift air samples are taken at the rate of 200 mL/min using a Tenax collection tube that has been pretreated with sodium hydroxide/ethylene glycol/methanol. The APFO is desorbed from the tubes using methanolic hydrogen chloride, which also serves as a derivatizing reagent, converting the APFO to its methyl ester. After workup, the methyl ester is quantified using a gas chromatograph equipped with an electron capture detector. The methyl ester of perfluorodecanoic acid is used as an internal standard, and at least three calibration samples are prepared to cover the concentration range of interest. Precision is estimated to be +/- 10% relative. The data above show averages consistently below the AGCHITLV of 0.01mg/m3 with only a very few samples above the TLV. Where results are above or near to the TLV, the event is investigated and corrective action (additional personal protective equipment or engineering controls) to reduce the exposure levels is undertaken. Older data from the 1980's show higher levels of exposure. In the early 1990's Washington Works switched from receiving the APFO as a powder to receiving it as an aqueous solution. This change was done to reduce the potential for exposure during handling of the dry powder. It should be noted that in the 1997 time period, the site was starting up new APFO recovery facilities. Operating and maintenance difficulties associated with the start-up of these facilities may have contributed to the higher levels of APFO in the personal samples during that year. Task specific monitoring data and wipe monitoring data exist. However these data are not indicative of employee exposure and are not presented here. These samples are taken to identify areas where additional exposure controls may be necessary. Engineering controls to reduce exposure consist of the following: > Reaction systems are closed systems with continuous ambient monitoring for monomer concentrations > Ventilation systems are installed where airborne concentrations are significant > The polymer dryers operate under negative pressure to contain APFO and other materials. > Recovery systems are in place to reduce airborne emissions. 6 mpb* moles per billion. 0.56mpb is equivalent to the ACGIH TLV of 0.0lmg/m, EID070491 Voluntary UEIP, Ammonium Perfluorooctanoate Personal protective equipment that workers regularly wear consist of the following: > Safety shoes and side-shield safety glasses in all areas. > Impervious gloves when handling APFO solutions or aqueous dispersion products! > Chemical protective coveralls and goggles or face shields when the possibility of splashes of APFO containing solutions is present. > Airline respirators or cartridge respirators where monitoring has shown to have high exposure potential. At Washington Works, blood serum levels of APFO have been measured since 1981. Prior measurements of blood fluoride levels have been taken prior to 1981 but are of limited value in assessing exposure to APFO. A summary of results of employees with identified APFO exposure potential the 1995, 1989-90, 1985,and 1984 volunteer sampling events is in the table below. Due to significant job assignment movement during this period of time, analysis of trends of data are difficult. The data in the table below prior to 1995 are for employees included in the 1995 sampling data so that comparisons of relative levels of APFO in blood serum can be compared. The entire data set of blood concentrations is available upon request. Year 1995 1989-90 1985 1984 #of Samples 73 23 21 19 Minimum Concentration (ppm) 0.12 0.4 61 Odjf Maximum Concentration (ppm) 4.5 8.5 18* 24* Mean Concentration (ppm) 1.57 3.13 2.44 3.82 7 This individual was working in a job that has APFO exposure potential at the time of the sample. *This individual consistently has had the highest blood concentration of APFO since APFO specific samples were taken. This employee left an APFO exposure potential assignment in 1991. In 1995 this employee's blood serum level was 4.4ppm. OOOV'ot? EID070492 V. 8/15/00 LPSD Water Sample Analytical Results (Letter, R. L. Ritchey to Mr. James C. Cox, LPSD dated 10/4/00) BCC: A. V. Malinowski, Legal, D7078 M. A. Bradley, Spilman, Thomas, & Battle P. J. Bossert /H. D. Ramsey/D. D. Jackson I. J. Zanikos/A. S. Hartten R. F. Pinchot R. Banerjee/R. J. Zipfel dsw/ 2:817.2 4 0 0 0 '. EID090036 October 4, 2000 Mr. James C. Cox Lubeck Public Service District P.O. Box 700 Washington, W V 26181 RE: LPSD Water Sample Analytical Results Dear Mr. Cox: Attached are copies of the analytical results for water samples taken on August 15, 2000 from three LPSD wells and the LPSD Building 1 main water line. If you have any questions or need additional information, please contact me at 304-863-4271. Sincerely, R. L. Ritchey Sr. Environmental Control Consultant Washington Works RLR/gw.dsw Attachments cc: William J. Gibbs Lubeck Public Service District P.O. Box 700 Washington, W V 26181 EID090037 # Lancaster Laboratories Where quality isa science. L a n c a s t e r L a b o r a t o r i e s S a m p l e N o . WW 3 4 3 9 7 3 9 C o l le c te d :0 8 /1 5 /2 0 0 0 1 3 :4 0 b y BJD S u b m itte d : 0 8 /1 5 /2 0 0 0 0 9 :1 0 R e p o r t e d : 0 9 / 1 2 / 0 0 a t 0 9 : 2 8 PM D is c a rd : 1 0 /1 3 /0 0 WWK-G-LPWD-WELL_A U n s p i k e d W a te r LUBECK WELLS 3Q00 S am ple Page 1 of 1 A cco u n t N um ber: 07032 C R G -E .I.D u P o n t d e N em ours & Co B a r le y M ill. P la z a , B ld g . 27 R o u tes 141. & 48 W ilm in g to n DE 1 9 8 0 5 WELLA S D G #: X X X 01-01BK G CAT H o. 02324 A n a l y s i s Hama CAS H u m b e r As R aceiv ed R e su lt F C -1 4 3 3 8 2 5 -2 6 -1 0.S 3 S T he- F C -1 4 3 r e c o v e r y i s o u t s i d e t h e QC l i m i t s f o r t h e L CS, MS, T he sam p le w as r e - e x tr a c te d p a s t h o ld in g tim e w ith a c c e p ta b le O rig in a l r e s u lts w ere re p o rte d . As R e ceiv ed M ethod D e te c tio n L im it 0 .0 2 9 a n d MSD. LCS r e c o v e r y . T h e 11 H -P F U A a n d PFDDA s u r r o g a t e r e c o v e r i e s a t r e o u t s i d e t h e QC l i m i t s . U n its u g /1 D ilu tio n F acto r 1 CAT H o. 02324 0232S A n a l y s i s Hame F C -1 4 3 P e s tic id e A lte r n a te W ater E x tr Laboratory Chronicle A n a ly sis M ethod T r i a l # D a te a n d T im e F C -143 b y GC/ECD 1 0 /9 1 1 0 8 / 3 1 / 2 0 0 0 2 1 : OS FC-143 1 0 /9 1 1 0 8 /2 4 /2 0 0 0 0 8:00 A n aly s t R ick S h o b er D ilu t Fact 1 D e b o r a h M. Z im m e rm a n 1 -ncasTsr-flcrsrcn -lit 3 .Vi 3 H .3 New -icilar.o eoovi'ri EID090038 L a n c a s t e r L a b o r a t o r i e s S a m p l e N o . WW 3 4 3 9 7 4 0 C o l le c te d :0 8 /1 5 /2 0 0 0 1 3 :2 5 b y BJD S u b m itte d : 0 8 /1 S /2 0 0 0 0 9 :1 0 R e p o r t e d : 0 9 / 1 2 / 0 0 a t 0 9 : 2 8 PM D is c a rd : 1 0 /1 3 /0 0 WWK-G-LPWD-WELL_B W a te r S a m p le LOBECK WELLS 3Q 00 Page 1 of A cco u n t N um ber: 07032 C R G -E .I.D u P o n t d e N em ours & Co B a rle y M ill P la z a , B ld g . 27 R o u te s 141 & 48 W ilm in g to n . DE 1 9 8 0 5 WELLB CAT N o. 02324 AS R e c e iv e d A n a ly s is Name CAS N u m b e r As R eceiv ed R e su lt M ethod D e te c tio n F C -143 3 8 2 5 -2 6 -1 0 .1 5 9 L im it 0 .0 2 9 T h e F C -1 4 3 r e c o v e r y i s o u t s i d e C h e QC l i m i t s f o r t h e L C S, MS, a n d MSD. The sam p le w as r e - e x tr a c te d p a s t h o ld in g tim e t o c o n firm o r i g i n a l r e s u l t s . T he LCS r e c o v e r y f o r t h e s e c o n d e x t r a c t i o n w as w i t h i n a c c e p t a n c e l i m i t s . S im ila r r e s u lts w ere o b ta in e d in b o th e x tr a c ts . O rig in a l r e s u l t s w ere re p o rte d . T h e 11H -P F U A a n d PFDDA s u r r o g a t e r e c o v e r i e s a r e o u t s i d e t h e QC l i m i t s . u n its u g /1 D ilu tio n F acto r 1 CAT N o. 02324 02325 A n a l y s i s Name F C -143 P e s tic id e A lte r n a te W ater E x tr Laboratory Chronicle M ethod F C -1 4 3 b y GC/ECD 1 0/91 FC-143 1 0 /9 1 T ria l# 1 A n aly sis D a te a n d T im a 0 8 /3 1 /2 0 0 0 2 2 :3 7 1 0 8 /2 4 /2 0 0 0 0 8 :0 0 A n aly st R ick S hober D ilu Fact 1 D e b o ra h M. Z im m erm an 1 / AA I ] 3. 3 ---- irn csstsr '.accrsisnes 1425 M iw -loilana r'ke 3 0 X "2*15 -sn cstsr. ?A 'I z d 'A ll EID090039 A ;-.ar .ac.'..'3'c-.'ie; : .sicisr/ ::r~nerrr.c TerraTeen `r,c,, a T'.crrnr. l-rr.cnv L a n c a s t e r L a b o r a t o r i e s S a m p l e N o - WW 3 4 3 9 7 4 1 C o lle c te d :0 8 /1 5 /2 0 0 0 1 3 :1 5 b y BJD S u b m itte d : 0 8 /1 6 /2 0 0 0 0 9 :1 0 R e p o r t e d : 0 9 / 1 2 / 0 0 a t 0 9 : 2 8 PM D is c a rd : 1 0 /1 3 /0 0 WWK-G- LPWD- W ELL_F W a t e r S a m p l e LUBECX WELLS 3Q 00 Page 1 of A cco u n t N um ber: 07032 C R G -E. I .D u P o n t d e N em o u rs & Co B a rle y M ill P la z a , B ld g . 27 R o u te s 1 4 1 .& 48 W ilm ington-D E 1980S WELLF M N o. 02324 As R eceiv ed As R e ceiv ed M ethod A n a ly s is Name CAS N u m b e r R e su lt D e te c tio n F C -1 4 3 3 3 2 5 -2 6 -1 0 .0 7 3 J L im it 0 .0 2 9 T h e F C - 1 4 3 r e c o v e r y i s o u t s i d e t h e QC l i m i t s f o r t h e L C S , MS, a n d MSD. T he sam p le was r e - e x tr a c te d p a s t h o ld in g tim e to c o n firm o r ig in a l r e s u l t s . T h e LCS r e c o v e r y f o r t h e s e c o n d e x t r a c t i o n w a s w i t h i n a c c e p ta n c e l i m i t s . S im ila r r e s u lts w ere o b ta in e d fo r b o th e x tr a c ts . O rig in a l r e s u lts w ere re p o rte d . U n its u g /1 D ilu tio n F acto r 1 T h e 11H -P F U A a n d PFDDA s u r r o g a t e r e c o v e r i e s a r e o u c s i d e t h e QC l i m i t s . CAT No. 02324 02325 A n a ly s is Name F C -143 P e s tic id e A lte r n a te W ater E x tr Laboratory Chronicle M ethod F C -143 1 0 /9 1 F C -143 b y GC/ECD 1 0/91 T ria l# 1 A n aly sis D a ta a n d T im e 0 8 /3 1 /2 0 0 0 2 3 :0 8 1 0 8 /2 4 /2 0 0 0 0 8 :0 0 A n aly st R ick S hober D ilu Fac 1 D e b o r a h M. Z im m e rm a n 1 0 7 fA0 A .n M 2 \ji S ..2!v:astar Lacararoriaa 2*25 ."fc ila n d ??C Ar 3ox cas t1i '242a5 E ID 090040 5 L jt ic :a v :r ii i * :ucs;<r*r' ,t ..13- ^ 2 r.z . : J -;-::m Lancaster Laboratories Where quality is a science. L a n c a s t e r L a b o r a t o r i e s S a m p l e H o . WW 3 4 3 9 7 3 8 C o lle c te d :0 8 /1 5 /2 0 0 0 1 2 :4 5 th ro u g h 0 8 /1 5 /2 0 0 0 1 2 :4 5 S u b m itte d : 0 8 /1 6 /2 0 0 0 0 9 :1 0 R e p o rte d : 0 9 /1 4 /0 0 a t 0 8 :5 4 D isc a rd : 1 0 /1 5 /0 0 W W K-D-BUILDING- 1_MAIN W a te r LUBECK WELLS 3Q 00 b y BJD AM S am ple Page 1 of A c c o u n t H um ber.- 0 7 0 3 2 C R G -E. I .D u P o n t d e H em o u rs & Co B a rle y M ill P la z a , B ld g . 27 R o u tes 141 & 4a W ilm in g t o n DE 1 9 8 0 5 BBAAA CAT Mo. 02324 A3 R e c e iv e d As R e c a iv a d M ethod A n a ly s is Hama F C -1 4 3 CAS N u m b e r 3 8 2 5 -2 S -1 R e su lt 0 .5 8 9 D etectio n L im it 0 .0 2 9 T h e F C -1 4 3 r e c o v e r y i s o u t s i d e t h e QC l i m i t s f o r t h e L C S , MS, a n d MSD. S in c e th e r e w as i n s u f f i c i e n t sam ple am ount f o r a r e e x t r a c t io n , Che r e s u l t s w ere re p o rte d . T h e 1 1 H -P F U A a n d PFDDA s u r r o g a t e r e c o v e r i e s a r e o u t s i d e t h e QC l i m i t s . U n its u g /1 D ilu tio n F acto r 1 CAT N o. 02324 02325 A n a ly s is Name F C -143 P e s tic id e A lte r n a te W ater E x tr Laboratory Chronicle A n aly sis M ethod T r i a l # D a te a n d T im e F C -1 4 3 b y GC/ECD 1 0 8 /3 1 /2 0 0 0 2 0:34 1 0 /9 1 FC-143 1 0 /9 1 1 0 8 /2 4 /2 0 0 0 08:00 A n aly st R ick S hober D ili; Fac D e b o r a h M. Z im m e rm a n 1 MEMBER Lancaster Laboratories 1425 N ew Holland Pike PO Sox 12425 'ncauer Pft i7 fir .ii?a r -nr-.':..' EID090041 ooove >nihudiars atTirana .SerraTetfi Inc. I Thermo clectrcn Z in c a r IP Environment CHEMICALS and the rest of that stuff. What we are accustomed to seeing is decades-long o'c' arguments about whether a chemical is really toxic." 3MS BIG ** NOTICE: The long and tortuous trail that led 354 to its decision highlights the grow I th::;maTcRial may ing concern within the chemical industry iil BEPROTECTEDBY over persistent chemicals, a relatively recent environmental worry. There are CLEANUP COPYRIGHTLAW scores of these chemicals, woven into (TITLE17U.S.CODE) the very fabric of modern life, that re sist natural processes of decay and can linger in the environment for decades. Some have already been banned-- most prominently DDT, PCBs, and CFCs--but no one is quite Why it decided to foremost among them its ubiquitous certain what damage, if Scotchgard fabric protector. Since there any, the rest might pull the plug on is no replacement chemical as yet, that be causing. The means a potential loss of $500 million in annual sales, out of total corporate rev its best-selling enues of $16 billion, and one-time re structuring charges of up to $200 mil stain repellant lion. The news caused a rush to stockpile Scotchgard by the clean and the care A t first, Dr. Larry R. Zobel and other researchers at 354 Co. fig ured the findings had to be a mis take. Investigators from Cornell less. Heloise, author of the syndicated "Hints from Heloise" housekeeping column, says everyone from dothesconsrious t v hosts to flight atten University, using a powerful new tecdhants have fretted to her about nique to scan the blood of 354*3 factory the loss of Scotchgard. Even workers, were testing some serum they she, an expert a t stain-re bought from commercial blood banks to moval, admits: "When my hus establish base lines for the machines. band gets a new tie I spray it The highly sensitive devices kept turn on right away." ing up the same odd result: Tiny "CUTS.* Scotchgard's popularity amounts of a chemical 3M had made for makes its removal particularly nearly 40 years were showing up in noteworthy, given that 354 was un blood drawn from people living all der no mandate to act. "354 de across the country, even in places far serves great credit for identifying from 3M factories. "I t took months be this problem and coming forward fore all the chemists were convinced voluntarily," says Environmental Pro that it was there," recalls Zobel, 354*3 tection Agency Administrator Carol medical director. T here was disbelief." 54. Browner. Even environmental ac For 3M. the late 1997 test results tivists like Linda E. Greer, senior sci were troubling. If they held up, it meant entist at the Washington-based Natural that virtually all Americans--and folks Resources Defense Council, gives plau Car beyond the U.S.--may be carrying dits to the company. "I t took guts," she some minuscule amount of a 354 chemi says, even if they did it out of fear of cal, called perfiuorooctane sulfonate government action. "The fact is that (PFOS), in their systems. How PFOS got most companies, when faced with gov there, whether it could pose a health ernment nudging, go into anger, denial, risk and, more important, what should be done about it, were questions that 354 executives felt driven to ask. Although they have yet to come up with definitive answers--and they insist that there's no evidence of danger to humans--the Min nesota company's research led it to a drastic derision. On May 16, 354 decided to phase out PFOS and products containing related chemicals, first and THE PROBLEM WITH SCOTCHGARD fIgorccleutaerepglctnolseosar.tlinniusnntirwtcaeonfi,anlmPuitsneFoaPrtOromOaiSnaSnm,Fedsw,aetohh<cliimoeLaanntnIditt DANCES The chemi cals persist in the envi ronment for decades, and' PFOS shows up in trace amounts in human blood.. EFFECT At very high daily doses, PFOS has killed monkeys and new bom rats in lab tests. \rt . is :ed w- -iy ire ito re an <I4 j ..*1 EPA 3 pressing the chemical industry al ailments in the living workers and, when certain precursor chemicals get to reduce the manufacture of these sub after scanning death records, nothing into the cells. These precursors are part stances, however, and is currently ne unusual in the deaths of former workers. of the chemical makeup of Scotchgard gotiating international conventions with "Physicians who were seeing the fabric protector and are valued precise Canada aimed at reducing their pres employees generally found no significant ly. for their hardiness. They repel water ence in the Great Lakes. health problems, no health problems tHaf. and ofl like nothing else, making them pfos is not on environmentalists' list would be unexpected in a typical potent stain-resisters. Indeed, 3M has of the most worrisome persis long revered the in-house sci tent chemicals. But 3M, which is responsible for most of the THE PATH TO A PAINFUL CHOICE entists who developed the man made 'chemicals, after a lab world's supply of the substance, 1968 A researcher at the University of Rochester staffer in the early 1950s decided not to wait until all the finds organic fluorine in human blood samples from chanced on them. The staffer scientific cards fell into place. the general population. Publishes finding in Nature. It took its costly step based on scientific detective work that 1976 Academic researchers refine the earlier find, had spilled one of the chemi cals bn her sneaker, found it impossible to wash out with ei has built up incrementally over and the Rochester investigator, D.R. Taves, discovers ther w ater or solvents, and the past 30 years--and far the chemical in his own blood. started investigating its re more damningly in the past two years. Its choice threatens the jobs of some 1,500 3M workers in Alabama, Minnesota, even 1978 3M reviews 30 years of death records among factory workers exposed to organic fluorine on the job but finds nothing unusual. pelling powers. While routine employee mon itoring continued throughout the 1980s, the company had lit Belgium. It also discomfits EARLY 1990s 3M uses enhanced mass spectrometry tle reason to worry. Even when scores of industrial customers, chiefly papermakers and textile mills, who apply the 3M chemi cals to goods as far-ranging as pet-food bags, candy wrappers, to scan workers' blood. Reliably detects contamina tion down to the level of 0 .5 parts per million. 1993 Researchers at University of Minnesota report finding no increased mortality in workers exposed to blood tests grew more sophis ticated in the early 1990s--and 3M could screen for specific flu orines such as pfos or related chemicals--the lack of any and carpeting. an organic fluorine. Elsewhere, it is linked to cancer damning health effects kept BLOOD TESTS. The first big in rodents and changes in reproductive hormones in concerns to a minimum. Re twist in the tale took place in humans. peated medical reviews seemed 1968, with a physician at the University of Rochester. Dr. Donald R. Taves was studying the effects of water fluorida 1996 University of Minnesota researchers publish study finding no toxicity to the fiver in 115 3M work ers from PFOS exposures. to clear the chemicals of any problems. Then, in 1997, powerful new detection techniques changed tion when he found tiny quan tities of an unusual form of flu orine--a kind that didn't come from fluoridated water--in hu 1997 Researchers at Michigan State University and 3M report that organic fluorine chemicals are appear ing in water, air, and soil. everything. The new tests turned up evidence of the chemicals in levels as low as 0.5 parts per million in human man blood. Just how it got (WAY, 1998 3M advises EPA that it found organic blood. `That is not much," says there and what its presence fluorine in blood-bank samples in tiny amounts. Zobel drily! "It's like 50 sec meant were unclear. But scien Company decides to move away from this chemistry. onds in 32 years." It was by tists familiar with the organic fluorines, known as POST, took note. The finding drew still more attention when Taves, SEPTEMBER, 1998 Company tells EPA of disturbing animal-test findings. The offspring of rats heavily dosed with organic fluorine die within days. using the new techniques that the Gornell University lab, working for 3M, found the PFOS in blood from the scattered working with colleagues at the SEPTEMBER, 1999 3M researchers find no adverse University of Florida, con health effects from on-the-job exposure to PFOS. firmed the results in a 1976 blood banks. 3M promptly launched an international test ing program, screening blood study. Chillingly, Taves even FEBRUARY, 2 0 0 0 Researchers alert 3M that PFOS from 18 U.S. blood banks found the fluorine in his own is found in tissue of birds from the Pacific Ocean to along with samples from Eu blood, though he lived fa r from the Baltic. rope and Asia. It even scanned any potential factory source. Researchers at 3M, which says it is vigilant about chem ical MARCH, 2 0 0 0 3M and EPA discuss latest findings, including the deaths of heavily dosed monkeys. old, stored blood samples from Korean War veterans. The re sult: tiny amounts of contami exposure of its workers, were MAY 16, 2 0 0 0 3M and EPA announce that the com nation in the U.S. and Europe, rn.paying particular attention. pany will voluntarily phase out the organic fluorines. They quickly launched programs OMA. EM.HOMESWEK except in the veterans' blood, which predated the Scotchgard to test employees at plants in chemical. Cottage Grove (Minn.), Decatur (Ala.), population like this," says Zobel. 3M regularly updated the EPA on all and later Antwerp (Belgium), to see if For 3M veterans, the cheerfiil medical of its research. For their part, EPA offi fluorine exposures were high. While they results were not surprising. Although cials were particularly concerned by the found that fluorines were registering at unusually hardy, organic fluorines for persistence of Pfos. It is so hardy that higher levels in workers' blood than in decades were thought to be inert. PFOS, no one knows when, if ever, it will the general population, the medical evi a 3M product used in fire-fighting foams break down. Worse, it accumulates in dence suggested that they posed no and industrial add-suppression products, human and animal tissues. "With things problem. Researchers found no unusu is also produced in animals and humans that are persistent, the only way for 000' BUSINESS WEEK / .U N E 5 . 2000 37 E1D089503 Environment "3M deserves great credit for identifying this problem and coming forward voluntarily," says the EPA's Browner the concentrations to go is up--in our ples of animal tissue from all across the times what humans would ever likely be bodies and in wildlife," says the Nat globe, which he keeps on hand in lab exposed to. The investigators found that ural Resources Defense Council's Greer. freezers, Giesy found the chemical in the rats' offspring were dying within "And pretty much every chemical in "various animals from various places." days of birth. Then, this past March, the world is toxic at some close." While he won't list the animals or loca they reported that two monkeys that Because pfos is both enduring and tions--for fear of preempting scientific were also dosed heavily died, after suf widespread, 3M made some crucial publication-- >M executives say pfos fering severe gastrointestinal problems choices in mid-1998. Company execu turned up in flesh-eating birds in the and convulsions. The company promptly tives decided they would--eventually-- Pacific Ocean and the Baltic regions. notified the EPA of the results. abandon such formulations and find re Giesy is now halfway through tests on Those animal tests got the agency's placements for the troublesome 2,000 tissue samples drawn from as far attention. Although 3M had kept the fluorines. "We began to realize then, away as the Arctic and Antarctic. EPA informed of all its pfos studies, the and came to realize more animal mortality data--and later, that this would be a especially the rat fatalities-- chemical that would con sparked a steady series of stantly be Involved in envi "no lunch, no refresh ronmental debate," says ments... roll-up-your-sleeves" Charles Reich, a chemist in meetings in March at epa charge of Scotchgard as the headquarters in Washington, company's executive vice- one top epa official recalls. president for specialty-ma Says the official: "The seri terial markets. ousness of the issues grew NO SURE THING. Still, 3M's over time." top executives argued over When the 3M executives ju st how long they could finally decided to pull the continue. Could they wait plug on PFOS and related until replacements for the products, they didn't need chemicals were found? That the heavy hammer of an epa might take seven years or ruling--but that possibility more, and was not a sure hung heavily in the back thing. And what about the ground. "They could see the effect on corporate cus writing on the wall," argues tomers, who valued the 3M the senior EPA official. "They products for their ability to could see we were going to repel water or oil? Shouldn't REICH AND COYNE: SM data showed no adverse health effects continue our assessment of 3M keep the supplies com- ------------- this and it would get more ing, since there was no hint of human When Giesy started presenting his detailed and at the end of the day we danger. "All the data we had on initial results to 3M officials in February, would make some kind of decision... 3M health...pointed toward no health the concern level at the company rose decided that the better course of action effect," says William E. Coyne, senior sharply. He was summoned back to re was to get out of it early." For their vice-president for research and peat his presentation for Chief Execu part, 3M officials say they would have development. tive Officer Livio D. DeSimone and his made the same decision whether the But then 3M took a couple of crucial most senior executives. "This was very epa pushed them or not. steps that sped up its decision to chuck important to 3M," recalls the researcher. Just how quickly 3M can adapt to its the product: It ordered up studies on Since neither Giesy nor in-house sci far-reaching decision isn't clear. It in rats, monkeys, and other animals to see entists could say ju st how pfos got tends to be out of production on most, if what heavy doses of pfos might do. into the far-flung animal tissues, the not all, PFOS-related products by yearend. And it commissioned more research, 3M scientists now plan a global re With a few products, such as fire-fight forking over 3800,000 for an investigator search effort aimed at tracking the ing foams, it may take longer to adjust. at Michigan State University to test chemical's sources and destinations. With over $1 billion pouring in each year wildlife samples to see just how perva Says Katherine E. Reed, a chemist who from all sorts of new products that don't sive the chemicals were. The results of is 3M's executive director of environ use the chemicals, the company feels both sets of tests, though preliminary, mental technology: "We believe that sure it can come up with substitutes-- proved fatal for the chemicals. our responsibility for materials contin ideally, nonpersistent ones. And it ex The wildlife tests confirmed the initial ues... into disposal. It's a concept we pects it will find jobs elsewhere or will fears of the 3M executives. Michigan call life-cycle management." pay separation benefits to affected work State University researcher John P. The most damning evidence against ers. Meanwhile, the worries about PFOS Giesy, a zoologist and a faculty mem PFOS began emerging in September, 199$. are not yet oven For years to come, 3M ber of the school's National Food Safety That's when 3M got the results of animal will be keeping track of the stuff it has & Toxicology Center, found pfos in tests in which heavy doses of PFOS were already put out there. some very odd places. Scanning sam administered to rats--10.000 to 100.000 B y Joseph Weber in S t Paul, Minn. MC C 0 0 0 / '{) LA1NC ft{HN(OV 121 /i - W% --' m w A J PAGE 3 OF 13 F-rEVISI0NNa: 2 r v r ^ ^ 11/5 DATE: 8/1/56 EXPIRATION PATE: 02/01/97 T E F L O N N O N -S A L A B L E PR O C E S S W A S T E D IS P O S A L . ABOUND '.iste disposafai the DuPont Letart Lan d fill w ill cease effective January 1, 1996. This landfill had been the disposal > : for T S P L O N `s process waste (excluding R C R A hazardous waste). The process waste that T E F L O N is to L e ta rt can generally be classified as C -8 contaminated waste and non-C-8 waste. Since the Letart Landfill is dosing, alternate disposal sites w ill have to be used fo r T E F L O N 's process waste. A portion o f T E F L O N 's process waste is currently sold as scrag, however, not a ll o f the process waste is salable. F or the T E F L O N Division at Washington W orks, the C -8 contaminated process waste w ill be sent to a hazardous waste landfill in Emelle, Alabama. It is anticipated that the m ajority o f T E F L O N '* C -8 contaminated waste that is sent to to Em elle w ill be shipped in 55-gallon steel drums. The estimated cost to send process waste to Emelle is S145 per drum. Process waste that does not contain C -8 w ill be sent to DuPont's D ry Run L an d fill fo r disposal. The D ry Run L an d fill is not permitted fo r disposal o f waste in steel o r plastic drums; therefore, process waste sent to D ry Run w ill have to be shipped in fiber containers. It is estimated that the disposal cost at D ry Run w ill be S15-S25 per drum. T H IS P R O C E D U R E D O ES N O T C H A N G E T H E D IS P O S A L PR O C ESS F O R R C R A H A Z A R D O U S W A S T E . Consult the T E F L O N W aste Disposal M anual (#30) for disposal o f R C R A hazardous waste. 3Q C E D U R E The process waste has been tabulated in the attached tables. Some o f the m aterial in the tables might currently be sold as scrap. Areas should continue to sell scrap where possible. However, i f the scrap cannot be sold, it should be properly disposed. I f there are questions as to how a particular waste should be disposed, contact the area shift supervisor on duty. I f additional assistance is still needed, contact our environmental coordinator. (Today, this is K eith Cof&nan, X 4 3 7 0 ). I T IS E X T R E M E L Y IM P O R T A N T T H A T N O C -8 C O N T A M IN A T E D W A S T E B E S E N T T O D R Y R U N L A N D F IL L . Packaging o f C -8 Contam inated Process W aste - Em elle L a n d fill 1. W aste w ill be packaged in a red 55-gallon steel drum . Drum s w ill be available at the T E F L O N Pad northwest o f B -164 (see attached B -164 W est Pad diagram ). Contact Polly Shackelford i f additional drums are needed. E X C E P T IN T H E CASE O F N O A V A IL A B L E S U P P L Y , T E F L O N W IL L N O L O N G E R USE B L A C K S T E E L D R U M S FO R W A S T E D IS P O S A L . T41U2.4M * Dm Paai't r*tiiitrr4 ln < ta n k EID031901 1 ILW CONTROLLED DOCUMENT IF RED V f t iT R c h i m e v T / * a. Js T S C A CX. t)C U 6 3 o / o o o O O I f _ . ifijo S a n + ` 1/ e r S i o - n ujas p r o v i d e d - 000773 V Federal R egister/ Vol. 65. No. 202 ' W ednesday, October 18. 2000 / Proposed Rules 6231 P A R T 8 0 1 -- LABELING 1 . The authority citation for 21 CFR part 801 continues to read as follows: Authority: 21 U.S.C. 321. 331. 351 352. 360i. 360j. 371. 374. 2. S ection 801.430 is am en d e d by revising the table in paragraph (e)(1) to read as follows: 8 0 1 .4 3 0 User labeling for menstrual tampons. *** (e)* * (1) * * * Ranges of absorbency m grams' Corresponding term of absorbency 6 and under 6 10 9 9 to 12 12 to 15 15 to 18 Above 18 Light absorbency Regular absorbency Super absorbency Super plus absorbency \ Ultra absorbency. No term. 1These ranges are defined, respectively, as follows: Less than or equal to 6 grams (g): greater than 6 g up to and including 9 g; greater than g up to and including 12 g; greater than 12 g up to and including 15 g; greater than 15 g up to and including 18 g; and greater than 18 g. Dated: October 2. 2000. Margaret M. Dotzel. Associate Commissioner for Policy. (FR Doc. 00-26249 Filed 10-17-00: 8:45 am) BILLING COOE 418O-01-T ENVIRONMENTAL PROTECTION AGENCY 40 CFR Parts 52 and 81 [MO 114-1114; FR L-6885-7] Approval and Promulgation of Implementation Plans; State of Missouri; Designation of Areas for Air Quality Planning Purposes; Dent Township AGENCY: E n v iro n m en tal P rotection Agency (EPA). ACTION: P ro p o sed rule. SUMMARY: EPA p roposes to approve a State Im p lem en tatio n P lan (SIP) revision subm itted by the state of M issouri and M issouri's request to redesignate the lead nonattainm ent area in w estern Iron County. M issouri, to attainm ent of the National Am bient Air Q uality Standards (NAAQS). EPA proposes to ap p ro v e th e m aintenance plan for this area including a consent order w hich was subm itted w ith the redesignation request, and also proposes to ap p ro v e the revision to M issouri's Restriction of Emissions of Lead From Specific Lead Smelter-Refinery Installations rule w hich ensures the perm anent and enforceable em ission reductions by clarifying the em issions lim its for the Doe Run Resource Recycling Facility, and removes the text w hich could have allow ed this facility to resum e op eratio n as a prim ary sm elter. In the final rules section of to d a y 's F ed era l Regi5ter. EPA is approving the state's SIP revision and redesignation request as a direct final rule w ithout prior proposal because the Agency views this as a noncontroversial action and anticipates no relevant adverse com m ents to th is action. A d etailed rationale for the approval is set forth in the direct final rule. If no relevant adverse com m ents are received in response to this action, no further activity is co n tem p lated in relation to this action. If EPA receives relevant adverse com m ents, the direct final rule w ill be w ithdraw n and all public com m ents received w ill be addressed in a subsequent final rule based on this proposed action. EPA w ill not institute a second com m ent period on this action. Any parties interested in com m enting on this action should do so at this time. DATES: C om m ents on th is p ro p o sed action m ust be received in w riting by N ovem ber 17, 2000. ADORESSES: C om m ents m ay be m a ile d to Kim Johnson, Environm ental Protection Agency, Air Planning and Developm ent Branch, 901 North 5th Street. Kansas City, Kansas 66101. FOR FURTHER INFORMATION CONTACT: Kim Johnson at (913) 551-7975. SUPPLEMENTARY INFORMATION: See th e inform ation provided in the direct final rule w hich is located in the rules sectio n of to d a y 's F ed era l R egister. Dated: September 27. 2000. Dennis Grams, Regional Adm inistrator. Region 7 [FR Doc. 00-26502 Filed 10-17-00: 8:45 ami BILLING COOC 5560-50-P ENVIRONMENTAL PROTECTION AGENCY 40 CFR Part 721 OPPTS-50639; FRL-6745-5 RIN 2070--AD43 Parfluorooctyl Sulfonate; Proposed Significant New Use Rule AGENCY: E n v ironm ental Protection Agency (EPA). ACTION: P ro p o sed rule. SUMMARY: EPA is proposing a significai new use rule (SNUR) under section 5(a)(2) of the Toxic Substances Control Act (TSCA) for the following chem ical substances: Perfluorooctanesulfonic acid (PFOSA) and certain of its salts (PFOSS), perfluorooctanesulfonyl fluoride (PFOSF). certain higher and lower hom ologues of PFOSA and PFOSF, and certain other chemical substances, including polymers, that co n tain PFOSA a n d its hom ologues as substructures. All of these chem ical substances are referred to collectively i this proposed rule as perfluorooctyl sulfonates, or PFOS. This proposed ruli would require manufacturers and im porters to notify EPA at least 90 days before com m encing the m anufacture or im p o rt o f th ese ch em ical su b stan ces foi the significant new uses described in this docum ent. EPA believes that this action is necessary because the chemic; substances included in this proposed rule may be hazardous to hum an health and the environm ent. The required notice w ould provide EPA w ith the opportunity to evaluate an intended new use and associated activities and. i necessary, to prohibit or lim it that activity before it occurs. DATES: C om m ents, id e n tifie d by the docket num ber OPPTS-50639. are due N ovem ber 17, 2000. 62320 Federal Register / Voi. 65, Na. 202 / W ednesday. October 18, 2000 ' Proposed Rules ADDRESSES: C om m ents may be subm itted by mail, electronically, or in person. Please follow the detailed instructions for each m ethod as provided in U nit I. of the SUPPLEMENTARY INFORMATION. To en su re proper receipt by EPA. it is im perative that you identify docket control num ber OPPTS--50639 in the subject line on the first page of your response. FOR FURTHER INFORMATION CONTACT: For general inform ation contact: Barbara Cu n n ingham Director, Office of Program M anagement and Evaluation, Office of Pollution Prevention and Toxics (7401), Environm ental Protection Agency. 1200 Pennsylvania Ave., NW,, W ashington, DC 20460; telephone num ber: (202) 554--1404; e-m ail address: T SC A -H otline@ epa.gov. For technical inform ation contact. Mary Dominiak. Chemical Control Division (7405), Office of Pollution Prevention and Toxics, Environm ental Protection Agency, 1200 Pennsylvania Ave., NW,, W ashington. DC 20460; telephone num ber: (202) 260-7768: fax num ber: (202) 260-1096; e-mail address: dominiak.mary@ epa.gov. SUPPLEMENTARY INFORMATION: I. G en eral In fo rm a tio n A. Does this N otice A p p ly to Me? You may be affected by this action if you m anufacture (defined by statute to include import) any of the chem ical substances that are listed in Table 2 or Table 3 of this unit. Persons who intend to im po rt any ch em ical su b stan ce governed by a final SNUR are subject to the TSCA section 13 (15 U.S.C. 2612) import certification requirem ents, and to the reg u latio n s codified at 19 CFR 12.118 through 12.127 and 12.728. Those persons m ust certify that they are in co m p lian ce w ith the SNTJR requirem ents. T he EPA policy in support of im port certification appears at 40 CFR p art 707, su b p art B. In addition, any persons who export or intend to export any of the chem ical substances listed in Table 2 or Table 3 of this u nit are subject to the export notification provisions of TSCA section 12(h) (15 U.S.C. 2611(b)), and m ust com ply w ith the export notification requirem ents in 40 CFR 721.20 and 40 CFR p art 707, su b p art D. E ntities potentially affected by the SNUR requirem ents in this proposed rule may in clu d e, b u t are n ot lim ited to: Table 1.-- E ntities Potentially Affec ted by the S N U R R e q u ir em en ts Categories NAICS codes Examples of potentially affected entities Chemical manufacturers or importers Chemical exporters j 325 | I 325 i Persons who manufacture (defined by statute to include import) one or more of the sub|ect chemical substances , Persons who export, or intend to export, one or more of the subject chemical substances T his listing is not in te n d ed to be exhaustive. Instead, it provides a guide for readers regarding entities likely to be affected by this action. Other types of entities not listed in Table 1 of this unit could also be affected. The North American Industrial Classification System (NAICS) codes have been provided to assist in determ inations of w h eth e r th is actio n m ig h t ap p ly to certain entities. To determ ine if you or your business is affected by this action, you should carefully exam ine the applicability provisions at 40 CFR 721.5 for SNUR-related obligations. Also, co n su lt U nit ED. N ote th a t because th is proposed rule w ould designate certain m anufacturing and im porting activities as significant new uses, persons that solely process the chem ical substances that w ould be covered by this action w o u ld n o t be subject to th e rule. If you have any questions regarding the applicability of this action to a particular entity, consult the technical p erso n liste d u n d e r FOR FURTHER INFORMATION CONTACT. T able 2.--C hemicals Requiring a Significant N ew U se Notice O n or After January 1,2001 CAS No./PMN Ninth Collective Index chemical name 383-07-3 ........... 2-Propenoic acid, 2-[butyl((heptadecaf1uoroocty1)sulfonyl]amino]ethyl ester. 423-82-5 ........... 2-Propenoic acid. 2-[ethyl[(heptadecafluorooctyl)sulfonyl]amino]ethyl ester. 2250-98-8 ......... 1-Octanesulfonamide. N,N',N"-[phosphinylidynetns(oxy-2,1 -ethanediyl)]tris(N-ethyl-l,1.2,2.3.3.4.4.5,5.6,6.7,7,8.S,8- heptadecafluoro-. 14650-24-9 ...... 2-Propenoic acid. 2-methy!-, 2-([(heptadecafluorooctyl)sulfonyl]methylamino]ethyl ester. 30381-98-7 ...... 1-Octanesulfonamide. N,N'-[phosphinicobis(oxy-2,1-ethanediyl)]bis(N-ethyl-l.1.2,2,3,3,4,4,5.5.6,6,7.7,8,8,8-heptadecaf1uoro- , ammonium salt. 55120-77-9 ...... | 1-Hexanesulfonic acid, 1,1.2.2.3.3.4,4,5.5.6.6,6-tridecafluoro-. lithium salt. 57589-85-2 ......... Benzoic acid. 2.3.4,5-tetrachloro-6-(I[3-[[(heptadecaf1uorooctyl)sulfonyl]oxy]phenyl]amino]caft>onyl]-. monopotassium salt. 61660-12-6 ...... i 1-Octanesulfonamide, N-ethyl-l,1.2.2.3,3.4.4,5,5,6.6.7,7,8.8.8-heptadecafluoro-N-{3-(trimethoxysilyl)propyl]-. 67969-69-1 ...... 1-Octanesulfonamide. N-ethyM.1,2.2.3.3.4.4.5.5.6.6.7.7.8.8.8-heptadecafluoro-N-(2-(phosphonooxy)ethyll-. diammonium salt. 68156-01-4 ...... Cyciohexanesulfonic acid, nonafluorobis(trifluoromethyl)-. potassium salt. 68329-56-6 ...... 2-Propenoic acid, eicosyl ester, polymer with 2-([(heptadecafluorooctyl)sulfonyl]methylamino]ethyl 2-propenoate. hexadecyl 2-propenoate, 2-[methyl[(nonafluorobutyl)sulfonyl]amino|ethyl 2-propenoate, 2- [methyl((pentadecafluoroheptyl)sulfonyl]amino]ethyl 2-propenoate. 2-[methyl[(tridecafluorohexyl)sulfony!]amino]ethy! 2- propenoate, 2-(methyl((undecatluoropentyl)sulfonyl]amino)ethyl 2-propenoate and octadecy! 2-propenoate. 68555-91-9 ...... 2-Propenoic acid. 2-methyl-, 2-(ethyl[(heptadecafluorooctyl)sulfonyl]ammo]ethyl ester. polymer with 2- [ethyl[(nonafluorobutyl)sulfonyl]amino|ethyl 2-methyl-2-propenoate. 2-(ethyl[(pentadecafluoroheptyl)sulfonyl]amino)ethyl 2- methyl-2-propenoate, 2-(ethyl((tndecafluorohexyl)sulfonyl]amino)ethyl 2-methyl-2-propenoate, 2- [ethyl[(undecafluoropentyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate and octadecyl 2-methyl-2-propenoate. 68555-92-0 ...... 2-Propenoic acid. 2-methyl-, 2-([(heptadecafluorooctyl)sulfonyl]methylammo]ethyl ester, polymer with 2- [methyl((nonafluorobutyl)sulfonyl]amino)ethyl 2-methyl-2-propenoate. 2- [methyl((pentadecaf1uoroheptyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate. 2- [methyl[(tridecafluorohexyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate. 2-(methyl[(undecafluoropentyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate and octadecyl 2-methyl-2-propenoate. Federal Register Vol. 65. No. 202 ' W ednesday. O ctober 18. 2000 ; Proposed Rules 62321 Table 2.--C hemicals Requiring a S ignificant New Use Notice O n or After J anuary 1, 2001-- Continued CAS No.PMN Ninth Collective Index chemical name 63608-1*1-0 68909-15-9 70776-36-2 73772-32-4 .... 311#0--38--7 ..... 94133-90-1 ...... 117806-54-9 .... 127133-66-8 129813-71-4 .... 143240-73-2 .... 148240-79-3 .... 148240-80-6 148240-81-7 .. . 148240-82-8 . 148684-79-1 .... 178535-22-3 . .. P-83-1102 ........ P-84-1163 ........ P-84-1171 ...... P-86-0301 ....... P-89-0799 ....... P-94-0545 . . P-94-0927 ...... P-94-2205 ....... P-94-2206 ........ P-96-1645 ...... P-97-0790 ....... P-98-0251 P-98-1272 ....... P-99-0188 ....... P-99-0319 Sulfonamides. C4-8-alkane, perfluoro. N-ethyl-N-(hydroxyethyt). reaction products with 1.T-methyleneois(4- isocyanatobenzene]. 2-Propenoic acid, eicosyl ester, polymers with branched octyl acrylate. 2-{[(heptadecafluorooctyi)sulfonyl]methylammo]ethyl acrylate. 2->methyl[(nonafluorobutyl) sulfonyl]aminojethyi acrylate. 2-(methyt[(pentadecafluoroheptyl)sulfonyl]aminolethyl acrylate. 2-(methyl((tndecafluorohexyl)sulfonyi]amino]ethyl acrylate. 2-[methyl[(undecafluoropentyl) sulfonyllaminojethyi acrylate, polyethylene glycol acrylate Me ether and stearyt acrylate. 2-Propenoic acid. 2-methyl-. octadecyl ester. polymer with 1.1-dichloroethene. 2- ;:(heptadecafluorooctyl)sulfonyl]methylamino!ethyl 2-propenoate. N-(hydroxymethyl)-2-propenamide 2- ;methyl[(nonafluoroPutyl)suitonyl]aminolethyl 2-propenoate. 2-[methyl[(pentadecafluoroheptyl)sulfonyl]ammo]ethyi 2- propenoate, 2-(methyt((1ndecafluorohexyHsulfonyljamino|elhyl 2-propenoate and 2- [methyl((undecafluoropentyl)sulfonyljamino]ethyl 2-propenoate. 1-Propanesulfonic acid. 3-([3-(dimethylamino)propyl][(tndecafluorohexyl)sulfonyl]aminol-2-hydroxy-. monosodium salt. 1-Propanammium. N-(2-hydroxyethyi)-3-[(2-hydroxy-3-sulfopropyi) ((tndecafluorohexyl)sulfonyl]ammo|-N.N-dimethyi-. hy droxide. monosodium salt. 1- Propanesulfonic acid. 3-[[3-(dimethyiaminolpropyi][(heptadecafluorooctyl)sulfonylJamino]-2-hydroxy-. monosodium salt. 1-Heptanesulfonic acid. 1.12.2.3.3,4.4.5.5,6.6.7,7.7-pentadecafluoro-. lithium salt. 2- Propenoic acid. 2-methyl-, polymers with Bu methacrylate, lauryl methacrylate and 2-[methyl((perfluoro-C4-8- alkyl)sulfonyl]aminoiethyl methacrylate. Sulfonamides. C4-8-alkane, perfluoro. N-methyl-N-loxiranylmethyl). Fatty acids. Cl8-unsatd.. trimers. 2-([(heptadecafluorooctyl)sulfonyllmethyiamino]ethyl esters. Fatty acids. Cl8-unsatd., tnmers. 2-[methyl[(nonafluorobutyl)sulfonyl]amino|ethyl esters. Fatty acids. Cl8-unsatd.. tnmers. 2-[methyl[(tridecafluorohexyl)sulfonyi]amino]ethyl esters. Fatty acids. 018-unsatd.. tnmers. 2-[methyl[(undecafluoropentyl)sulfonyl]amino]ethyl esters. Fatty acids. 018-unsatd.. trimers. 2-[methyl((pentadecafluoroheptyl)suifonyl]aminolethyl esters. Sulfonamides. C4-8-alkane. perfluoro. N-(hydroxyethyl|-N-methyf. reaction products with 1.6-diisocyanatohexane homopolymer and ethylene glycol. Sulfonamides. C4-8-alkane. perfluoro. N-ethyl-N-(hydroxyethyt)-. polymers with 1,l'-methylenebis(4-isocyanatobenzene] and polymethylenepolyphenylene isocyanate. 2-ethylhexyl esters. Me Et ketone oxime-blocked. Fatty acids, linseed-oit. dimers. 2-([(heptadecaftuorooctyl)sulfonyt]methylaminolethyt esters. Propanoic acid. 3-hydroxy-2-(hydroxymethyl)-2-methyl-, polymer with 2-ethyl-2-(hydroxymethyl)-1,3-propanediol and N.N',2- tns(6-isocyanatohexyl)imidodicarbomc diamide, reaction products with N-ethyl-1,1,2.2.3.3.4,4.5.5.6.6.7.7,8.8.8- heptadecafluoro-N-(2-hydroxyethyl)-l -octanesulfonamide and N-ethyl-1,1.2,2.3.3.4,4,5.5,6.6.77,7-pentadecafluoro-N-(2- hydroxyethyl)-1-heptanesullonamide. compds. with tnethylamine. Propanoic acid, 3-hydroxy-2-(hydroxymethyl)-2-methyl-, polymer with 1.1'-methylenebis{4-isocyanatobenzene] and 1.2.3- propanetnol, reaction products with N-elhyl-l,l.2.2.3.3.4.4.5.5,6.6,7,7.8.8.8-heptadecafluoro-N-(2-hydroxyethyl)-l- octanesultonamide and N-ethyl-1.l.2.2.3.3,4,4.5.5.6.6,7,7,7-pentadecafluoro-N-(2-hydroxyethyl)-l-heptanesulfonamide. compds. with morpholine. Sulfonamides. C4-8-alkane. perfluoro. N-(hydroxyethyl)-N-methyl. reaction products with 12-hydroxystearic acid and 2.4- TDI. ammonium salts. Sulfonamides. C4-8-alkane. perfluoro. N-ethyl-N-(hydroxyethyl). reaction products with 2-ethyM-hexanol and polymethylenepolyphenylene isocyanate. 1-Hexadecanamimum. N.N-dimethyl-N-[2-[(2-methyl-l-oxo-2-propenyl)oxy]ethyl]-. bromide, polymers with Bu acrylate. Bu methacrylate and 2-[methyl((perfluoro-C4-8-alkyl)sulfonyl]amino]ethyl acrylate. 2-Propenoic acid. 2-methyl-, 2-methyipropyl ester, polymer with 2.4-diisocyanato-l-methylbenzene. 2-ethyl-2- (hydroxymethyl)-i ,3-propanediol and 2-propenoic acid. N-ethyl-N-(hydroxyethyl)perfluoro-C4-8-alkanesulfon amides- biocked. Polymethylenepolyphenylene isocyanate and bis|4-NCO-phenyl)methane reaction products with 2-ethyl-1-hexanol. 2-buta- none. oxime. N-ethyl-N-(2- hydroxyethyl)-t-C4-C8 perfluoroalkanesulfonamide. Siloxanes and Silicones. di-Me. mono(3-[(2-methyl-i-oxo-2-propenyl)oxy]propylgroup]-terminated. polymers with 2- [methyii(perfluoro-C4-8-alkyl)sulfonyl]amino]ethyl acrylate and stearyl methacrylate. Fatty acids. Cl8-unsatd.. dimers. 2-[meihyl((perfluoro-C4-8-alkyi)sulfonyl]aminoJethyl esters. i-Decanaminium. N-decyl-N.N-dimethyl-, salt with 1.1 2.2.3.3.4,4.5.5.6.6.7.7,8.8.8-heptadecatluoro-l-octanesultonic acid (IT ). 2-Propenoic acid, butyl ester, polymers with acrylamide. 2-[methyl[(perfluoro-C4-8-alky!)sulfonyl]amino]ethyt acrylate and vinylidene chloride. 2-Propenoic acid. 2-methyl-. 3-(tnmethaxysilyl)propyi ester, polymers with acrylic acid. 2-[methyi((perfluoro-C4-8- alkyl)sulfonyilammo]ethyl acrylate and propylene glycol monoacrylate, hydrolyzed, compds. with 2.2- (methylimino)bis(ethanoi]. Hexane, 1.6-diisocyanato-. homopolymer. N-(hydroxyethyl)-N-methyi perfluoro C4-8-alkane sulfonamide- and stearyl ale - blocked. Poiy(oxy-l.2-ethanediyl), alpha.-[2-(methylammo)ethyi]-.omega.-[(1 T .3.3-tetramethylbutyl)phenoxy]-, N-((perfiuoro-C4-8- aikyilsulfonyl] derivs.. T a b l e 3.-- C h e m ic a l s S u b j e c t t o V o l u m e C a p R e s t r ic t io n s O n o r . A f t e r J a n u a r y 1, 2001 a n d R e q u ir in g a S ig n if ic a n t N e w U s e N o t ic e O n o r A f t e r J a n u a r y 1, 2003 CAS No PMN 307-35-7 .......... 307-51-7 376-14-7 ........ Ninth Collective Index chemical name 1-Octanesulfonyi fluoride. 1.1.2.2.3.3.4.4.5.5.6.6.7,7.8.8.8-heptadecaftuoro1- Decanesulfonyl fluoride. 1.1.2.2.3.3.4,4.5.5.6.6.7.7.8.8.9.970.10.10-heneicosafluoro2- Propenoic acid. 2-methyl-. 2-!ethyi[(heptadecafluorooctyl)suifonyi]amino)ethyl ester 62322 F ederal Register 1VoL 65. \'o. 202 / W ednesday. October 18. 2000 >Proposed Rules Table 3.-- C hemicals S ubject to Volume C ap i-il STRctons On or After J anuary 1, 2001 and Requiring a S ignificant New Use Notice O n or After J anuary 1 ,2 0 0 3 -- Continued CAS No /PMN Ninth Collective Index chemical name 423-50-7 ........ 1-Hexanesulfonyl fluonde. 1.1.2.2.3,3.4.4,5,5.6.6.6-tridecafluoro- 754-91-6 ........... 1-Octanesulfonamide. 1.1,2.2.3.3.4,45.5,6.6.7.7.8.8.8-heptadecafluoro1652-63-7 ......... 1-Prooanamimum. 3-[[(heptadecafluorooctyl)sulfonytlammo|-N.N.N-tnmethyl-. iodide 1691-99-2 ...... 1-Octanesulfonamide. N-ethyl-1.1.2.2.3.3.4.4.S.5.6.6.7.7.8,8.8-heptadecafluoro-N-(2-hydroxyethyl)- 1763-23-1 1-Octanesulfonic acid. H 2.2.3.3.4.4.5.5.6,6.77.8.8.8-heptadecafluoro- 2795-39-3 ...... 1-Octanesulfonic acid. 1.1.2.2.3.3.4.4.5,5,6.6.7.7.8.8.8-heptadecafluoro-, potassium salt 2991-51-7 ........ Glycine. N-ethyl-N-[(heptadecafluorooctyl)sulfonyl]-. potassium salt 4151-50--2 ......... 1-Octanesulfonamide. N-ethyl-1,1.2.2.3.3.4.4.5.5.6.6.7.7.8,8.8-heptadecafluoro- 17202--41--4 ....... 1-Nonanesulfomc acid. 1.1,2,2,3.3.4,4.5.5.6,6.7.7,8.8.9.9.9-nonadecafluoro-. ammonium salt 24448-09-7 ...... 1-Octanesulfonamide. 1.1.2.2.3.3.4.4.5.5.6.6.7.7.8.8.8-heptadecafluoro-N-(2-hydroxyethyl)-N-methyl- 25268-77-3 ........ 2-Propenoic acid. 2-([(heptadecafluorooctyl)sulfonyt]methylamino]ethyl ester 29081-56-9 ........ 1-Octanesulfonic acid. 1,1.2,2.3,3.4,4.5.5,6,6,7.7.8.8.8-heptadecafluoro-, ammonium salt 29117-08-6 ... Poly(oxy-l.2-ethanediyl). alpha.-[2-(ethyl((heptadecafluorooctyl)sulfonyl]amino]ethyl]-.omega.-hydroxy- 29457-72-5 ........ 1-Octanesulfonic acid, 1.1,2.2.3,3.4.4.5.5.6.6.7.7,8.8.8-heptadecafluoro-, lithium salt 31506-32-8 ....... 1-Octanesulfonamide. 1.1,2.2.3.3.4.4,5.5.6.6.7.7,8.8,8-heptadecafluoro-N-methyl- 38006-74-5 ....... 1-Propanammium. 3-[[(heptadecafluorooctyl)sulfonyl]amino)-N.N.N-tnmethyl-. chlonde 38850-58-7 ....... 1-Propanamimum. N-(2-hydroxyethyl)-N.N-dimethyl-3-((3-sulfopropyi)((tndecafluorohexyl)sulfonyi]aminol-, inner salt 67584--42-3 ........ Cyclohexanesultomc acid, decafluoro(pentafluoroethyl)-, potassium salt 67906--42-7 ...... 1-Decanesulfomc acid. 1,1.2,2,3.3.4,4.5.5.6.6.7.7.8.8.9.9.10.10,10-heneicosafluoro-, ammonium salt 68298-62--4 ....... 2-Propenoic acid. 2-(butyl((heptadecafluorooctyl)sulfonyl]amino)ethyl ester. telomer with 2- [butyi((pentadecafluoroheptyl)sulfonyl]ammo]ethyl 2-propenoate. methyloxirane polymer with oxirane di-2-propenoate. methyloxirane polymer with oxirane mono-2-propenoate and 1-octanethiol 68541-80-0 ...... 2-Propenoic acid, polymer with 2-(ethyl[(heptadecafluorooctyl)sulfonyl]ammo]ethyl 2-methy1-2-propenoate and octadecyl 2- propenoate 68555-90-8 ....... 2-Propenoic acid, butyl ester, polymer with 2-[[(heptadecafluorooctyl)sulfonyl] methylammolethyl 2-propenoate. 2- [methyl[(nonafluorobuty1)sulfonyl]amino]ethyi 2-propenoate. 2-[methyi[(pentadecaf1uoroheptyl)sulfonyl]amino]ethyl 2- propenoate. 2-[methyl((tridecafluorohexyl)sulfonyl]ammo]ethyl 2-propenoate and 2- [methyl[(undecafluoropentyl)sulfonyljamino|ethyl 2-propenoate 68586-14-1 ....... 2-Propenoic acid, 2-[[(heptadecafluorooctyl)sulfonyilmethylamino]ethyl ester, telomer with 2- [methyl((nonafluorobutyl)suHonyl]amino]ethyl 2-propenoate, alpha.-(2-methyl-l-oxo-2-propenyl)-.omega.-hydroxypoly(oxy- 1 2-ethanediyl), alpha.-(2-methyl-1-oxo-2-propenyl)- omega.-[(2-methyl-1-oxo-2-propenyl)oxy]poly(oxy-1.2-ethanediyl). 2- [methyl((pentadecafluoroheptyl)sulfonyl)aminolethyl 2-propenoate, 2-[methyl((tridecafluorohexyl)sulfonyl]amino]ethyl 2- propenoate. 2-[methyl((undecafluoropentyl)sulfonyl]ammo]ethyl 2-propenoate and 1-octanethiol 68649-26-3 ......... 1-Octanesulfonamide. N-ethyl-l,1.2.2.3.3.4.4,5.5.6,6.7.7,8.8,8-heptadecafluoro-N-(2-hydroxyethyl)-, reaction products with N-ethyl-1.1.2,2.3.3.4.4,4-nonafluoro-N-(2-hydroxyethyl)-l-butanesulfonamide. N-ethyl-1,1,2,2.3,3.4,4,5.5.6.6.7.7.7- pentadecafluoro-N-(2-hydroxyethyl)-l-heptanesulfonamide, N-ethyl-1.1.2.2.3,3.4.4,5.5.6.6.6-tridecafluoro-N-(2-hydroxy- ethyl)-i-hexanesulfonamide. N-ethyl-1.1,2.2.3,3.4,4,5,5,5-undecafluoro-N-(2-hydroxyethyl)-1-pentanesutfonamide. polymethylenepolyphenylene isocyanate and stearyl ale. 68867-60-7 ......... 2-Propenoic acid. 2-[[(heptadecafluorooctyl)sulfonyl]methylamino]ethyl ester, polymer with 2- [methyi[(nonafluorobutyl)sulfonyl]amino]ethyl 2-propenoate. 2-(methyl((pentadecafluoroheptyl)sulfonyl]amino)ethyl 2- propenoate. 2-[methyl((tridecafluorohexyl)sulfonyl]amino]ethyl 2-propenoate. 2- (methyi((undecafluoropentyl)sulfonyllamino!ethyl 2-propenoate and alpha.-(1-oxo-2-propenyl)- omega.-methoxypoly(oxy- 1 2-ethanediyl) 68867-62-9 ....... 2-Propenoic acid. 2-methyl-, 2-(ethyl[(heptadecafluorooctyl)sulfonyl]aminolethyl ester. telomer with 2- (ethyl[(nonafluorobutyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate. 2-[ethyl((pentadecafluoroheptyl)sulfonyllamino]ethyl 2- methyi-2'-propenoate. 2-{ethyl((tridecafluorohexyl)sulfonyl]aminolethyl 2-methyl-2-propenoate. 2- [ethyl((undecafluoropentyl)sulfonyl]amino)ethyl 2-methyl-2-propenoate. 1-octanethiol and alpha.-(1 -oxo-2-propenyl)- omega. -methoxypoly(oxy-1.2-ethanediyl) 68891-96-3 ....... Chromium. diaquatetrachloro[.mu.-[N-ethyl-N-[(heptadecaffuorooctyl)sulfonyl]glycmato- kappa.Oi.kappa.O']]- mu - hydroxybis(2-methylpropanol)di- 68958-61-2 ........ Polyioxy-1.2-ethanediyl), .alpha.-[2-[ethyl[(heptadecafluorooctyl)sulfonyl]ammolethyl)-.omega.-methoxy- 70225-14-8 ........ 1-Octanesulfonic acid. 1.1.2.2.3.3,4,4.5.5.6.6.7.7.8.8.8-heptadecafluoro-. compd. with 2.2'-iminobis(ethanol) (1:1) 71487-20-2 ......... 2-Propenoic acid. 2-methyl-. methyl ester. polymer with ethenylbenzene. 2- [[(heptadecafluorooctyl)sulforryllmethylammolethyl 2-propenoate, 2-[methyl((nonaftuorobutyl)sulfonyl]aminolettiyl 2- propenoate, 2-[methyl[(pentadecafluoroheptyl)sulfonyl]amino]ethyl 2-propenoate. 2- [methyl[(tridecafluorohexyl)sulfonyl]amino)ethyl 2-propenoate. 2-[methyl[(undecafluoropentyl)sulfonyl)amino]ethyl 2- propenoate and 2-propenoic acid 91081-99-1 ....... 1-Octanesulfonamide, l.1,2,2,3,3.4.4.5.5.6.6.7.7,8.8.8-heptadecafluoro-N-(2-hydroxyethyl)-N-methyl-. polymer with(chloromethyl)oxirane, 1.1.2.2.3.3.4.4,4-nonafluoro-N-(2-hydroxyethyl)-N-methyl-t -butanesulfonamide. 1.1.2.2.3.3.4,4.5.5.6.6.7.7.7-pentadecaffuoro-N-(2-hydroxyethyl)-N-methyl-1-heptanesulfonamide. 1.1.2.2.3.3.4.4.5.5.6.6.6- tridecafluoro-N-(2-hydroxyethyl)-N-methy!-i-hexanesulfonamide and i,l,2.2.3,3,4.4,5.5.5-undecafluoro-N-(2-hydroxyethyl)- N-methyl-1-pentanesulfonarnide. hexanedioate (ester) 98999-57-6 ........ Sulfonamides. C7-8-alkane, perfluoro. N-methyl-N-{2-((1-oxo-2-propenyl) oxylethyl], polymers with 2-ethoxyethyl acrylate. glycidyl methacrylate and N.N,N-trimethyl-2-[(2-methyl-1-oxo-2-propenyl)oxy]ethanaminiumchloride 182700-90-9 1-Octanesulfonamide. 1.1.2.2.3.3,4.4,5.5,6.6,7,7.8.8,8-heptadecafluoro-N-methyl-, reaction products with benzene-chlonne- sulfur chlonde (S2CI2) reaction products chlondes L-92--0151 2-Propenoic acid. 2-methyl-, butyl ester, polymer with 2-methyl-. 2-(ethyl [(heptadecafluorooctyljsulfonyljaminolethyl 2-meth- yl-2-propenoate. 2-[ethyl[(nonafluorobutyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate, 2- [ethyl((pentadecafluoroheptyl)suffonyl]amino]ethyl 2-methyl-2-propenoate. 2-[ethyl[(trideca<luorohexyl)sulfonyl!amino]ethyl 2-methyl-2-propenoate. and 2-propenoic acid P-80-0183 Sulfonamides. C4-8-alkane, perfluoro. N-(3-(dimethylamino)propyl], reaction products with acrylic acid Federal Register VoL 65. N'o. 202 W ednesday. October 18. 2000 Proposed Rules 62323 T a b le 3.--C hemicals S ubject to Volume Cap Restrictions On or After J anuary i . 2001 and Requiring a S ignificant New Use Notice On or After J anuary 1, 2003-- Continued CAS No PMN Ninth Collective Index cnemical name p gg_0958 p' p qo-0111 p"qi_1419 p g3_ i 444 ...... p 95-0120 ....... 9*96-1262 ......... p 96-1424 ......... p . 9 6 - 1 4 3 3 ......... 2-Propenoic acid. 2-methyl-, dodecyl ester, polymers with 2-(methyl[(perfluoro-C4-8-aikyi)sulfonyi]amino]ethyi acryiate and vmylidene chloride Sulfonamides. C4-8-alkane. pertluoro. N-methyl-N-((3-octadecyl-2-oxo-5-oxazolidmyi)methyl] Poly(oxy-1,2-ethanediyO. alpha-hydro-omega.-hydroxy-, polymer with 1,6-dnsocyanatonexane. N-(2-hydroxyethyl)-N-methyi pertluoro C4-8-alkane sulfonamide-blocked 2-Propenoic acid. 2-methyl-, dodecyl ester, polymers with N-(hydroxymethyl)-2-propenamide. 2-[methyi[(perfluoro-C4-8aikyltsuifonyl|ammo)ethyl methacrylate, stearyl methacrylate and vinylidene chloride Sulfonamides C4-8-alkane. pertluoro. N.N'-[1,6-hexanediylbis([2-oxo-3 5-oxazolidinediyl)methylene]]bis[N-methylSulfonic acids. C6-8-alkane. pertluoro. compds. with polyethylene-polypropylene glycol bis(2-ammopropyi) ether 2-Propenoic acid. 2-methyl-. 2-(dimethylamino|ethy! ester, telomers with 2-[ethyl[(perfluoro-C4-8-alkylsulfonyl]ammojethyl methacrylate and 1-octanethioi. N-oxides Sulfonamides. C4-8-alkane. pertluoro. N-(3-(drmethyloxidoammo)propyl). potassium salts B How Can I get A dditional Information. Including Copies o f this Document or O ther Related D ocum ents? 1 . Electronically. You may obtain electronic copies of this docum ent and certain other related docum ents that might be available electronically, from the EPA Internet Home Page at http:// www.epa.gov/. To access this document, on the Home Page select Law and R egulations," "R egulations and Proposed Rules." then look up the entrv for this docum ent under "Federal Register--Environm ental D ocum ents.'' You can also go directly to the Federal Register listings at http://w w w .epa.gov/ fedrgstr/. To access the OPPTS Harmonized G uidelines referenced in this docum ent, go directly to the guidelines at http://w w w.epa.gov/ opptsfrs/h o m e/g u id elin .h tm . Ln addition, you may access other inform ation about the Office of Prevention. Pesticides and Toxic Substances (OPPTS) and related programs at http://w w w.epa.gov/ intem et/oppts/. - 2. In p erso n . T he Agency has established an official record for this action under docket control num ber OPPTS-50639. The official record consists of the docum ents referenced in this action, any public com m ents received during the com m ent period, and other inform ation related to this rulemaking, including inform ation claim ed as C onfidential Business Inform ation (CB1). T his official record includes the docum ents that are physically located in the docket, as well as all d o cu m en ts that are referenced in those docum ents. The public version of the official record does not include any inform ation claim ed as CBI. T he public version of the official record, w hich includes printed paper versions of any electronic com m ents that may be submitted during an applicable com m ent period, is available for inspection in the TSCA N onconfidential Inform ation Center. Room NE B -607. 401 M St.. SW.. W ashington. DC. T he C enter is o p en from noon to 4 p.m .. M onday through Friday, excluding legal holidavs. The telephone number of the C enter is (202) 260-7099. C. H o w a n d to W h o m Do S u b m it C om m ents7 You may subm it com ments through the mail, in person, or electronically. To ensure proper receipt by EPA. your com m ents m ust identify docket control num ber OPPTS-50639 in the subject line on the first page of your response. 1. B y m a il. S ubm it y o u r com m en ts to: Docum ent Control Office (7407). Office of Pollution Prevention and Toxics (OPPT), Environm ental Protection Agency. 1200 Pennsylvania Ave., NW.. W ashington. DC 20460. 2. In p e r so n o r b y courier. D eliver your com m ents to: O PPT 's D ocum ent Control Office (DCO). East Tow er Room G -099. W aterside Mall. 401 M St.. SW.. W ashington. DC. T he DCO is o p en from 8 a.m. to 4 p.m.. M onday through Friday, excluding legal holidays. The te lep h o n e n u m b er for the DCO is*(202) 260-7093. 3. E le ctro n ica lly. You m ay subm it your com m ents electronically by e-mail to: oppt.ncic@ epa.gov. or mail or deliver your com puter disk to the addresses iden tified in U nit I.C .l. or I.C.2. Do not subm it any inform ation electronically that you co n sid er to be CBI. E-m ailed com m ents m ust be subm itted as an ASCII file, avoiding the use of special characters or any form of encryption. Comments will also be accepted on standard com puter disks in W ordPerfect 6.1/8.0 or ASCII file format. All com m ents in electronic form m ust be identified by docket control num ber OPPTS-50639. Electronic comments may also be filed online at many Federal Depository Libraries. D. H o w S h o u ld l H a n d le CBI in fo rm a tio n th a t I W ant to S u b m it to the Agency? Do not subm it any inform ation electro n ically th a t you co n sid er to be CBI. You may claim in fo rm atio n that you subm it in response to this docum ent as CBI by m arking any part or all of th a t in fo rm atio n as CBI. Inform ation so m arked w ill not be disclosed except in accordance with p ro ced u res set forth in 40 CFR part 2. In ad d itio n to one com plete version of the com m ents that include any in fo rm atio n claim ed as CBI. a sanitized copy of the com ments which does not c o n tain th e inform ation claim ed as CBI m ust be subm itted for inclusion in the public version of the official record. Inform ation not marked confidential will be included in the public version of the official record by EPA w ithout prior notice. If you have any questions about CBI or the procedures for claim ing CBI. co n su lt th e tech n ical person listed u n d e r FOR FURTHER INFORMATIN CONTACT. E. W h a t S h o u ld I C o n s id e r as l P repare M y C om m ents for EPA? We invite you to provide your views on the various options we propose, new approaches we have not considered, the potential im pacts of the various options (including possible unintended consequences), and any data or inform ation that you w ould like the Agency to consider during the developm ent of the final SNUR. You may find the following suggestions helpful for preparing vour comments: 1. E x p lain y o u r view s as clearly as possible. 2. D escribe an y assu m p tio n s that you used. 3. P ro v id e copies of an y tech n ical inform ation and/or data you used that support your views. C09V 62324 Federal Register ' Vol. 65. No. 202 ' W ednesday, October 18. 2000 ' Proposed Rules 4 If you estim ate potential b urden or costs, explain how vou arrived at the estimate. 5. Provide specific exam ples to illustrate your concerns. 6. Offer alternative w ays to im prove the proposed rule or data collection activity. 7. Make sure to subm it your com m ents by the d ea d lin e specified in this docum ent. 8. At the beginning of your com m ents, be sure to properly identify the docum ent you are com m enting on. To ensure proper receipt by EPA. vour comments must identify the docket control num ber assigned to this action in the subject line on the first page of your response. You may also provide the title, date, and Federal Register citation. II. B ackground A. W h a t A c tio n is th e A g e n c y T aking? This proposal w ould require persons to notify' EPA at least 90 days before com mencing the m anufacture or import of the chem ical substances identified in Table 2 or Table 3 of U nit I.A., for the significant new uses described in this docum ent. The chem ical substances identified in Table 2 and Table 3 of Unit l.A. include PFOSA, PFOSS. PFOSF, certain higher and lower homologues of PFOSA and PFOSF, and certain other chemical substances, including polymers, that contain PFOSA and its homologues as substructures. These chemical substances are collectively referred to throughout this proposed rule as PFOS. The significant new uses described by this notice are: 1. T he m an u factu re or im port for any use of amy*of the chem icals listed in Table 2 of U nit l.A. on or after January 1. 2001. 2. T he m anufacture or im port for any use of any one or more of the chemicals listed in Table 3 of U nit l.A. in excess of an aggregate volum e of 1.100.000 pounds per person per calendar year on or after January 1. 2001 a n d before January 1. 2003. 3. T he m anufacture or im p o rt for any use of any of the chem icals listed in Table 3 of U nit l.A. on or after January 1. 2003. B. W h a t is th e A g e n c y 's A u th o r ity fo r Taking this Action? Section 5(a)(2) of TSCA (15 U.S.C. 2604(a)(2)) authorizes EPA to determ ine that a use of a chem ical substance is a `significant new use." T he A gency makes this determ ination by rule after considering all relevant factors, in cluding those listed in TSCLA section 5(a)(2). These factors include the volume of a chem ical substance's p roductio n ; the extent to w hich a use changes the type, form, m agnitude, or duration of exposure to the substance; and the reasonably anticipated manner of producing or otherw ise managing the substance. Once EPA m akes this d eterm in atio n an d prom ulgates a SN'UR, TSCA section 5(a)(1)(B) requires persons to subm it a significant new use notice (SNUN) to EPA at least 90 days before they manufacture, import, or process the chem ical substance for that significant new use (15 U.S.C. 2604 (a)(1)(B)). C. W h ich G en era l P ro visio n s A p p ly ? General provisions for SNURs are published under 40 CFR part 721, sub p art A. T hese p rovisions describ e persons subject to the rule, recordkeeping requirem ents, exem ptions to reporting requirem ents, and applicability of the rule to uses occurring before the effective date of the final rule. Note that because this proposed rule w ould designate certain manufacturing and im porting activities as significant new uses, persons that solely process the chem ical substances that w ould be covered by this action w ould not be subject to the rule. Provisions relating to user fees appear at 40 CFR part 700. Persons subject to this proposed SNUR w ould be required to com ply w ith the same notice requirem ents and EPA regulatory procedures as subm itters of Prem anufacture Notices (PMNs) under TSCA section 5(a)(1)(A). In particular, these requirem ents include: the inform ation subm ission requirem ents of TSCA section 5(b) and 5(d)(1); the exem ptions authorized by TSCA section 5 (h)(1). (2), (3), an d (5): the export notification provisions of TSCA section 12(b); and the export notification requirem ents in 40 CFR part 707, subpart-D. Once EPA receives a SNUN. EPA may take regulatory action under TSCA sectio n s 5(e), 5(f). 6, or 7, if appropriate, to control the activities on w hich it has received the SNUN. If EPA does not take action, EPA is required u n d e r TSCA sectio n 5(g) to ex p lain in the Federal Register its reasons for not taking action. III. Summary of this Proposed Rule T he ch em ical sub stan ces su b ject to this proposed SNUR are listed in Table 2 and Table 3 of U nit l.A. These chem ical substances include PFOSA. PFOSS. PFOSF. certain higher and lower homologues of PFOSA and PFOSF. and certain other chem ical substances, including polymers, that contain PFOSA and its hom ologues as substructures. All of these chem ical substances are referred iu cullectivelv in this proposed rule as perfluorooctyl sulfonates, or PFOS. All of these chem ical substances have the potential to degrade back to PFOSA in the environm ent, and PFOSA does not degrade further. PFOSA is highly persistent in the environm ent and has a strong ten d en cy to bioaccum uiate. Studies have found PFOS in verv small quantities in the blood of the general hum an population as well as in wildlife, indicating that exposure to the ch em icals is w id esp read , an d recent tests have raised concerns about their potential developm ental, reproductive, an d sy stem ic toxicity (Refs. 1, 2. an d 3). These factors, taken together, raise concerns for long term potential adverse effects in people and w ildlife over time if PFOS sh o u ld co n tin u e to be produced, released, and built up in the environm ent. EPA believes that the chem ical substances listed in Tables 2 and 3 of Unit l.A. are m anufactured and im ported in the United States only by the M innesota Mining and M anufacturing Com pany (3M) (Refs. 4 an d 5). 3M has co m m itted to p h ase o ut these chem icals voluntarily by discontinuing the m anufacture of certain of these chemical substances on a global basis for their m ost w idespread uses by the end of December 2000. by steadily reducing their production volume on the rem aining chemicals through 2001 and 2002. and by entirely discontinuing the m anufacture of all of these PFOS chem icals by December 31. 2002 (Ref. 6). T h e chem icals listed in T able 2 of U nit l.A. are those w h ich 3M has com m itted to cease m anufacturing by December 31. 2000. The chem icals listed in Table 3 of U nit l.A. are those w hich 3M has com m itted first to reduce, and then to cease m anufacturing by December 31. 2002. EPA believes that any m anufacture or im port of these PFOS chem icals occurring after 3M's global phase-out dates w ould increase the m agnitude and duration of exposure to th ese ch em icals. T herefore. EPA is proposing to designate the following as significant new uses: 1. A ny m an u factu re or im port for any use of the chem icals listed in Table 2 of U nit l.A. on or after January 1, 2001. 2. .Any m an u factu re or im p o rt for any use of the chem icals listed in Table 3 of U nit l.A. in excess of an aggregate annual m anufacture and im port volum e cap for all of these chem icals of 1.100.000 pounds per person per ca le n d ar year on or after January 1. 2001 an d before January 1. 2003. 3. .Any m an u factu re or im p o rt for any use of any of the chem icals listed in Federal Register Voi. 65, N'o. 202 ' W ednesday. October 18. 2000 Proposed Rules 62325 Table 3 of Unit l.A. on or after January 1. 2003. Given that no companies other than 3M are currently producing the chemicals listed on Table 3 of Unit l.A., and given the negative commercial and regulatory- environment associated with these chemicals. EPA believes it is unlikely that companies would incur the costs associated with establishing new manufacturing capacity for these chemicals in order to enter this market. This proposed rule, when finalized, would require persons who intend to manufacture or import the PFOS chemicals listed in this proposed rule to notify EPA, through the submission of a SNUN, at least 90 days before commencing the manufacture or importation of any of these chemicals for any use designated by this proposed SNLR as a significant new use. The required notice would provide EPA with the opportunity to evaluate the intended use. and. if necessarv. to prohibit or limit that use before it occurs. These proposed requirements are summarized in the following Table 4: Table 4.-- S ummary of P roposed SNUR Requirements Manufacture or import: You must file a significant new use notice (SNUN) if you: 1 When7 How much? Chemical suostances listed m Table 2 of Unit l.A After December 31, 2000 Any amount Chemical substances listed in Table 3 of Unit l.A January 1. 2001 through December 31, Aggregate amount exceeding 1.100.000 lbs per 2002 person per calendar year Chemical substances listed in Table 3 of Unit l.A After December 31. 2002 Any amount IV. C hem ical C om pound H istory .3. D e fin in g PFO S This proposed rule applies to a large group of fully fiuorinated alkyl sulfonate-containing substances, none of which occur naturally. The Ninth Collective Index chem ical names and CAS Registry N um bers (CAS No.) (w hen available) provided in Table 2 and Table 3 of U nit I.A. are for the specific chem ical substances that are subject to the provisions contained in this proposed SNUR (for exam ple, entry #8 on T able 3 of U nit I.A. lists CAS No.1763-23-1 for the com pound nam ed 1-octanesulfonic acid. 1.1.2.2.3.3.4.4.5.5.6.6,7.7,8,8,8heptadecafluoro-. com m only referred to as PFOSA). All of the chem ical substances listed in Table 2 and Table 3 of U nit I.A. have a com m on chem ical structure consisting of a PFOS moiety, as illu strate d here, som ew here in the m olecule. F FO I iI F - C - C* -- S -- Y ! Ii F FO SILLING CODE 5560-50-C The num ber of carbon atoms present in the m oiety varies from 4 to 10 (x = 3-9) am ong the listed chem icals. In addition, there are many examples of different chem ical functionality (free acids (Y = OH), m etal salts (Y = O- M*), sulfonvl h alid es (Y = X). sulfonam ides (Y= N H 2), and o ther derivatives). T he listed chem ical substances also include polym ers. The class of chemical substances including the perfluoroalkyl sulfonvl moiety described by the structure show n in this unit contains more chem ical substances than are specified in the lists in Table 2 and Table 3 of U nit [.A. O nly the listed chem ical substances, w hich are m anufactured or im ported exclusively by 3M and w hich 3M has voluntarily com m itted to cease producing, are subject to this SNUR. EPA is ev alu atin g further this overall structural class of chemical substances and may take additional regulatory action as appropriate. B. E nvironm ental Fate The basic building block of all of the PFOS ch em icals is PFOSF, w h ich is used as an interm ediate in the production of the PFOS chemicals. PFOSA results from the chem ical or enzym atic hydrolysis of PFOSF. Current inform ation strongly supports that PFOSA is an extrem ely stable substance w hich resists breakdown by chem ical or biological processes. Therefore PFOSA is the ultim ate degradation pro d u ct from PFOS chem icals and will persist tn that form (Refs. 1 an d 2). EPA cannot currently conduct a definitive assessm ent of the environm ental transport and partitioning of PFOS. The available data are lim ited and their accuracy uncertain. Also, the accuracy of the estim atio n m odels is lim ited by the quality of data input into them. Depending on what data are consulted and utilized, the environm ental fate and transport of PFOS vary. Biological sam pling recently discovered the presence of certain perfluoroalkyl com pounds in fish and in fish-eating birds across the United States and in locations in Canada. Sweden, and the S outh Pacific (Ref. 1). T he w ide distribution of the chemicals in high trophic levels is strongly suggestive of the potential for bioaccum ulation/ bioconcentration. The widespread presence of PFOS suggests the p o ssib ility of tran sp o rt in air as w ell as water, but the m ultim edia equilibrium criterio n m o d el (EQC) suggests o th erw ise (Ref. 7). U sing data p ro v id ed by 3M as inputs, the model indicates that PFOS w ould fall out of air and partition alm ost equally in water and soil. T he H en ry 's Law values calcu lated u tiliz in g th e v ap o r pressu re of 3.31 E-4 Pa@20 C and w ater solubility values of 370, 570, 5. an d 25 m illigram /Liter (mg/ L) in fresh w ater, p ure water, u n filtered seawater, and filtered seawater, resp ectiv ely y ie ld ed H enry's Law values of 4.7 E-9 , 7.2 E-9. 6.4 E -ll, an d 3.2 E10 atm .m 3 /m o le (atm ospheres per m eter cubed per mole), respectively. The vapor pressure and water solubility values w ere obtained from Table 4. p.16 of the M arch 1, 2000. w h ite p ap e r by 3M. S u lfo n a te d P erflu o ro ch em ica ls in the E nvironm ent: Sources. D ispersion, F ate a n d E ffe c ts (Ref. 1). T hese Henry' s Law values suggest that volatilization from w ater to air is not very likely. A ccording to 3M. testing is planned and/or underw ay for the environm ental properties, fate, and transport of PFOS (Ref. 1). W ith m ore com p lete data. EPA w ould be able to make more definitive assessm ents. W ith the present data, the Agency can only speculate on environm ental transport and partitioning of PFOS. although current in fo rm atio n suggests strongly th a t it is persistent and may bioaccum ulate. C. H e a lth E ffe cts The A gency's hazard analysis for PFOS is a review of health hazard and b io m o n ito rin g d ata (Ref. 8). Toxicologystu d ies show th a t PFOS is w ell absorbed 62326 Federal Register / Vol. 65. No. 202 / W ednesday. October 18. 2 0 0 0 /Pronosed Rule? orally and distributes primarily m the serum and liver PFOS can also be formed as a m etabolite of other p erfluorinated sulfonates. It does not appear to be further m etabolized. Elim ination from the body is slow and occurs via both urine and feces. Serum PFOS levels in three retired m ale 3M chemical workers have been followed for 51 years and suggest a m ean elim in atio n half-life (t 11 of 1.428 days (approxim ately 4 years). Based on the pharm acokinetic data obtained from a 28-dav oral study in male and female m onkeys, a volum e of d istrib u tio n (Vd) of 0.19 L/kilogram (kg) was reported: no sex differences in the pharm acokinetic parameters were noted. PFOS has show n m oderate acute toxicity by the oral route w ith a rat LD;o of 251 mg/kg. A 1-hour LCso of 5.2 mg/ L in rats has been reported. PFOS was found to be m ildly irritating to the eyes and non-irritating to the skin of rabbits. PFOS was negative in m utagenicity studies in five strains of salm onella and did not induce m icronuclei in an in vivo mouse bone marrow m icronucleus assay. Numerous repeat-dose oral toxicity studies on PFOS have been conducted in rats and prim ates. A dverse signs of toxicity observed in rat studies included increases in liver enzymes, hepatic vacuolization and hepatocellular hypertrophy, gastrointestinal effects, hematological abnorm alities, weight loss, convulsions, and death. These effects were reported at doses of 2 mg/ kg/dav and above. Adverse signs of toxicity observed in Rhesus monkey studies included anorexia, emesis, diarrhea, hypoactivitv. prostration, convulsions, atrophy of the salivary glands and the pancreas, marked decreases in serum cholesterol, and lipid depletion in the adrenals. The dose range for these effects was reported between 1.5-300 m g/kg/dav. No monkeys survived beyond 3 weeks into treatm ent at 10 m g/kg/dav, or beyond 7 weeks into treatm ent at doses as low as 4.5 m g/kg/day. At doses as low as 0.75 mg/kg/day. Cvnomolgus monkeys exhibited low food consum ption, excessive salivation, labored breathing, hypoactivitv. ataxia, hepatic vacuolization and hepatocellular hypertrophy, significant reductions in serum cholesterol levels, and death. Postnatal deaths and other developm ental effects w ere reported at low doses in offspring in a 2-generation reproductive toxicity study in rats. At the two highest doses of 1.6 and 3.2 mg/ kg/day. pup survival in the first generation was significantly decreased. All first generation offspring (F l pups) at the highest dose died w ithin a day after birth w h iie d o s e to 30'o of the F l pup s in the 1.6 m g/kg/day dose group died w ithin 4 days after birth. As a result of the pup m ortality in the two top dose groups, only the two lowest dose groups. 0.1 and 0.4 m g/kg/day. were continued into the second generation. The no observed adverse effect level (NOAEL) and low est observed adverse effect level (LOAJEL) for the second g eneration offspring (F2 pups) were 0.1 m g/kg/day and 0.4 mg/ kg/day, respectively, based on reductions in pup body weight. Reversible delays in reflex and physical developm ent were also observed in this study, raising concerns about the potential for developm ental neurotoxicity following exposure to PFOS. D evelopm ental effects were also reported in prenatal developm ental toxicity studies in the rat and rabbit, although at slightly higher dose levels. Signs of developm ental toxicity were evident at doses of 5 m g/kg/day and above in rats adm inistered PFOS during gestation. Significant decreases in fetal body w eight and significant increases in external and visceral anom alies, delayed ossification, and skeletal variations were observed. Abnorm alities of the lens of the eye were also reported at doses as low as 1 m g/kg/day in one rat prenatal developm ental study, but could not be repeated in a second study of sim ilar design. At doses of 2.5 m g/kg/day an d above, significant reductions in fetalbody weight and significant increases in delayed ossification were observed in rabbits adm inistered PFOS during gestation. In hum an blood sam ples. PFOS has been detected in the serum of occupational and general populations in the parts per m illion (ppm) to parts per billion (ppb) range. In the U nited States, recent blood serum levels of PFOS in m anufacturing em ployees have been as high as 12.83 ppm . w hile in the general population, serum collected from blood banks and commercial sources have indicated mean PFOS levels of 30-44 ppb. Levels in a very sm all sam ple of children yielded even higher results, w ith a mean level of 54 ppb. Sam pling of several wildlife species from a variety of sites across the U nited States has show n w idespread distribution of PFOS. In recent analyses, PFOS was detected in the ppb range in the plasm a of several species of eagles, w ild birds, and fish. Endogenous levels of PFOS have also been detected in the ppb range in the livers of unexposed rats used in toxicity studies, presum ably through a dietary source (fishmeal). A lthough the PFOS levels detected in the blood of the general population are low. this w idespread presence, com bined w ith the persistence, the bioaccum ulative potential, and the reproductive and subchronic toxicitv of the chem ical, raises concerns for potential adverse effects on people and w ildlife over time should the chemical sub stan ces co n tin u e to be produced, released, and accum ulated in the environm ent. D. E x p o su r e D ata As in d ic ated in U nit IV.C., PFOS has been detected at low levels in the blood of hum ans and wildlife throughout the U nited States, providing clear evidence of w id esp re ad exposure to the chem ical. PFOS has been in commercial use since the 1950's, predom inantly in soil and stain-resistant coating products on fabrics, carpets, and leather, and in grease and oil resistant coatings on paper products, including food contact papers. O ther uses leading to environm ental releases include fire fighting foams. The various surface treatm ent uses constitute the largest volum e of PFOS production and are believed to present the greatest potential for w idespread hum an and environm ental exposure to PFOS. Studies are underw ay to determ ine the routes of exposure w hich have led to the detection of PFOS in hum an and animal blood. There are several potential pathw ays that may account for the w id e sp re a d ex p o su re to PFOS including: Dietary intake from the consum ption of food w rapped in paper containing PFOS derivatives; inhalation from aerosol applications of PFOScontaining consum er products; and inhalation, dietary, or dermal exposures resulting from m anufacturing, as w ell as industrial, com m ercial, and consum er use and disposal of PFOS-derived chem icals and products. E. U se D ata PFOS and related sulfonvl-based fluorochem icals are used in a variety of products, w hich can be divided into three m ain categories of use: Surface treatm ents, paper protectors, and p erfo rm an ce ch em icals (Ref. 4). T he various surface treatm ent and paper protection uses constitute the largest volum e of PFOS production and are believed to present the greatest potential for w idespread hum an and environm ental exposure to PFOS. PFOS chem icals produced for surface treatm ent applications provide soil. oil. and w ater resistance to personal apparel and hom e furnishings. Specific applications in this use category include protection of apparel and leather, fabric/ upholstery, and carpet. These applications are undertaken in Federal R egister/Vol. 65, No. 202 / W ednesday. October 18. 2000 / Proposed Rules 62327 industrial settings by custom ers such as textile mills, leather tanneries, finishers, fiber producers, and carpet m anufacturers. PFOS chem icals are also used in afterm arket treatm ent of apparel and leather, upholstery, carpet, and automobile interiors by the general public or professional applicators (Ref. 4 ). Ln 2000. the d om estic p ro d u ctio n volume of PFOS chem icals for this use category is estim ated to be approxim ately 2.4 m illion pounds (Ref. 6) . PFOS chem icals produced for paper protection applications provide grease, oil. and w ater resistance to paper and paperboard as part of a sizing agent form ulation. S pecific applications in this use category include food contact applications (plates, food containers, bags, and w raps) regulated by the Food and Drug A dm in istratio n (FDA) u n d er 21 CFR 176.170. as w ell as non-food contact applications (folding cartons, containers, carbonless forms, and masking papers). The application of sizing agents is u n d ertak en m ainly bypaper m ills and. to som e extent, converters who m anufacture bags, wraps, and other products from paper and p ap erb o ard (Ref. 4). In 2000. the dom estic production volume of PFOS chem icals for th is use category is estim ated to be ap p ro x im ately 2.7 m illion p o u n d s (Ref. 6). PFOS chem icals in the perform ance chem icals category are used in a wide variety of specialized industrial, commercial, and consum er applications. Specific applications include fire fighting foams, m ining and oil well surfactants, acid m ist suppressants for metal plating and electronic etching baths, alkaline cleaners, floor polishes, photographic film, denture cleaners, shampoos, chem ical interm ediates, coating additives, carpet spot cleaners, and as an insecticide in bait stations for ants (Ref. 4). Ln 2000. the dom estic production volume of PFOS chem icals for th is use category is estim ated to be approxim ateiv i.5 m illion p o u n d s (Ref. 6). On May 16. 2000. follow ing d iscu ssio n s w ith the Agency. 3M issued a press release an n ouncing that it w ould discontinue the production of perflu o ro o ctan v l chem icals used to produce some of its repellent and su rfactan t p ro d u cts. In its statem ent. 3M com m itted to "substantially phase out production" by the end of calendar vear 2000 (Ref. 9). In subseq u en t co rresp o n d en ce w ith the Agency. 3M provided a schedule docum enting its com plete plan for discontinuing all m anufacture of specific PFOS and related chem icals for most surface treatm ent and paper protection uses (including food contact uses regulated by the FDA) by the end of 2000. and discontinuing all m anufacture for any uses by the e n d of 2002 (Ref. 6). This schedule, and 3M's anticipated p ro d u ctio n volum es, are sum m arized in T able 5. T able 5.-- An ticipated Annual U.S. P r o d u c tio n Vo lum e (P o u n d s ) for PFOS U se C ateg o ries Use category 2000 2001 I 2002 2003 Surface treatment Paper protection Performance chemicals Total 2.356.700 2.670,700 1,462,500 6.469,900 '0 :0 1.011.900 1,011.900 So ;o ; 443.700 ; 443,700 0 0 io ;o A ccording to the inform ation currently available to EPA. 3M is the sole m anufacturer of PFOS chem icals affected by this pro p o sed SNUR (Ref. 5). 3M p lans to d isc o n tin u e the manufacture of the chem icals identified in Table 2 of U nit I.A. (in general, those associated w ith surface treatm ent and paper protection uses) by the end of 2000 an d to d isc o n tin u e the chem icals id entified in T able 3 of U nit I.A. (in general, those associated with performance chemical applications) by the end of 2002. V. Objectives and Rationale for this Proposed Rule In determ ining w hat w ould constitute a significant new use for the chem ical substances that are the subjects of this proposed SNUR. EPA considered relevant inform ation on the toxicity of the substances, likely exposures associated with potential uses, inform ation provided by industry sources, and the four factors listed in TSCA section 5(a)(2) an d U nit II.B. Based on these considerations. EPA w ants to achieve the follow ing objectives w ith regard to the significant new uses that are designated in this proposed rule. EPA w ants to ensure that: 1. EPA w o u ld receive n o tice of any person's intent to m anufacture or im port PFOS chem icals for a designated significant new use before that activity begins. 2. EPA w o u ld have an o p p o rtu n ity to review and evaluate data subm itted in a SNUN before the notice subm itter begins m anufacturing or im porting the subject chem ical substances for a significant new use. 3. EPA w o u ld be able to regulate prospective manufacturers and im porters of the subject chem ical substances before a significant new use occurs, provided such regulation is w arranted pursuant to TSCA section 5(e) or (f). EPA has concerns regarding the toxicity, persistence, and bioaccum ulative potential of the chem ical substances that are included in this proposed SNUR. 3M, the sole m anufacturer of these chem icals in the U nited States, has chosen voluntarily to discontinue their m anufacture and sale for all uses by December 31. 2002. and to substantially reduce their m anufacture for their most w idespread uses bv D ecem ber 31. 2000. W ith 3M 's exit from the m arket. EPA believes that all m anufacture of these chemicals likely w ill cease. H ow ever. EPA is concerned that m anufacture could be reinitiated in the future, and wants the opportunity to evaluate and control, if appropriate, exposures associated with that activity. T he notice that w ould be required by the SNUR would provide EPA w ith the o pportunity to evaluate activities associated w ith a significant new use as proposed herein and an opportunity to protect against unreasonable risks, if any. from exposure to the substances w hich could result. Given that no com panies other than 3M are currently producing the ch em icals listed on T able 3 of U nit I.A., and given the negative commercial and regulatory environm ent associated with these ch em icals, EPA believes it is unlikely that com panies would incur the costs associated w ith establishing new m anufacturing capacity for these chem icals in order to enter this market. EPA will use inform ation subm itted pursuant to the Inventory U pdate Rule (40 CFR part 710) to track the production volum es of these chemicals. In the event th at the phase-out of these chem icals does not progress as 000 62328 F ederal Register / Vol. 65, No 202 / W ednesday, October 18. 2000 / Proposed Rules described in this proposed ruie. EPA may pursue additional regulatory action as ap p ro p riate u n d er TSCA sections 4. 6, and 8. VI. A ltern ativ es Before proposing this SNUR. EPA considered the following alternative regulatory actions for the chem ical substances listed in Tables 2 and 3 of U nit I.A. In addition, EPA determ ined that these chem ical substances are currently not subject to Federal notification requirements. 1. Prom ulgate a chem ical-specific TSCA section 8(a) reporting n ile for the chemical substances listed in Tables 2 and 3 of U nit I.A. U nder a TSCA section 8(a) rule, EPA could require any person to report inform ation to the Agency w hen they intend to m anufacture or import the substances listed in Tables 2 and 3 of U nit I.A. for the significant new uses Listed in this p roposed rule (15 U.S.C. 2607). H ow ever, th e use of TSCA section 8(a) rather than SNUR authority w ould not provide the opportunity for EPA to review hum an and environm ental hazards and exposures associated w ith the new uses of these substances and, if necessary, to take imm ediate regulatory action under TSCA section 5(e) or section 5(f) to prohibit or lim it the activity before it begins. In addition, EPA may not receive im portant inform ation from sm all businesses, because those firms generally are exem pt from TSCA section 8(a) reporting requirem ents. In view of EPA's concerns about these chem ical substances and its interest in having the opportunity to regulate these substances further as needed, pending the developm ent of exposure and/or hazard inform ation should a significant new use be initiated, the Agency believes that a TSCA section 8(a) rule for those chem ical substances w ould not meet all of EPA 's regulatory objectives. 2. Regulate the chem ical substances listed in T ables 2 an d 3 of U nit I.A. under TSCA section 6. EPA m ust regulate under TSCA section 6 if there is a reasonable basis to conclude that the manufacture, im port, processing, distribution in commerce, use, or disposal of a chemical substance or m ixture "presents or w ill p rese n t" an unreasonable risk of injury to hum an health or the environm ent. Given the decision by the sole m anufacturer 3M to discontinue manufacturing these chem icals, and th us to rem ove the bulk of the existing potential risk w hich they present. EPA concluded that risk management action under TSCA section 6 is probably not necessary at this tim e. This proposed SNUR will allow the Agency to address the potential risks associated w ith any intended significant new use of these substances. If the phase-out of these chemicals does not occur as anticipated, EPA may reconsider this decision and pursue additional regulatory action as appropriate. VII. A pplicability o f Proposed Rule to Uses O ccurring Before the Effective Date of the Final Rule EPA believes that the intent of TSCA section 5(a)(1)(B) is best served by designating a use as a significant new use as of the proposal date of the SNUR. rather than as of the effective date of the final rule. If uses begun after publication of the proposed SNUR were considered to be ongoing, rather th an new, it w ould be difficult for EPA to establish SNUR notice requirem ents, because any person could defeat the SNUR by initiating the proposed significant new use before the rule becam e final, and then argue that the use was ongoing. Persons who begin commercial m anufacture or im port of PFOS for the significan t new u ses Listed in th is proposed SNUR after the proposal has been published m ust stop that activity before the effective date of the final rule. Persons w ho ceased those activities w ill have to m eet all SNUR notice requirem ents and w ait until the end of the notice review period, including all extensions, before engaging in any activities designated as significant new uses. If. how ever, p erso n s w h o begin com m ercial m anufacture or im port of these chem ical substances between the proposal and the effective date of the SNUR meet the conditions of advance com pliance as codified at 40 CFR 721.45(h), those persons w ill be considered to have m et the final SNUR requirem ents for those activities. v m . Test D ata and O ther Inform ation EPA recognizes that under TSCA section 5. persons are not required to develop any particular test data before subm itting a SNUN. Rather, persons are required only to subm it test data in their possession or control and to describe any other data know n to. or reasonably ascertain ab le by th em (15 U.S.C. 2604(d); 40 CFR 721.25). However, in view of the potential health and environm ental risks posed by the significant new uses of the chem ical substances listed in Table 2 and Table 3 of U nit I.A.. EPA requests that potential SNUN subm itters include data that would permit a reasoned evaluation of risks posed by these chem ical substances w hen used for an intended significant new use. EPA currently believes that the known or reasonable ascertainable results of the following tests could help adequately characterize possible health effects of these chem ical substances: Reproductive and developm ental toxicity studies, mutagenicity, gene m utation, im m unotoxicity, neurotoxicity, carcinogenicity, and acute, subchronic, and chronic toxicity studies, as w ell as pharm acokinetics and m echanistic studies. Because of the specific concerns that EPA has for the persistence and bioaccum ulation potential of these chem icals. EPA also encourages SNUN subm itters to provide inform ation on environm ental fate and transport, specifically including m easured values for the octanoL/water p artitio n coefficient (log P), log of the so il/sed im en t adsorption coefficient (log Koc), bioconcentration factor (BCF), melting and/or boiling point, vapor p ressu re, H en ry 's Law constant, biodegradation, atm ospheric oxidation and the fugacity-based m ultim edia eq u ilib riu m criterio n level LU (EQC 111) m odel (Ref. 10). H ow ever, com pletion of those studies may not be the only means of identifying potential risks. For exam ple, analyses of potential exposure may dem onstrate that associated risks w ould be of low concern. A SNUN " subm itted w ithout accom panying test data may increase the likelihood that EPA w ill take action under TSCA section 5(e). EPA encourages persons to consult w ith the Agency before subm itting a SNUN for any of the PFOS substances listed in T ab le 2 or T able 3 of U nit I.A. As part of this optional pre-notice consultation. EPA w ill discuss specific test data it believes are necessary to evaluate a significant new use of the chem ical substances and advise the subm itter on the selection of test protocols. The Agency requests that all test data be developed according to the TSCA Good Laboratory Practice Standards in 40 CFR part 792. Failure to do so m ay re su lt in EPA 's finding th a t subm itted data are insufficient to reasonably evaluate the health effects and public health im plications of these chem ical substances. EPA urges SNUN subm itters to provide detailed inform ation on hum an and environm ental exposures that would result or could reasonably be anticipated to result from the significant new uses of the chem ical substances listed in T able 2 an d T able 3 of U nit I.A. and at 721.9582 of the proposed regulation. In addition. EPA encourages persons to subm it inform ation on potential benefits of these chem ical substances and inform ation on risks posed by these chem ical substances com pared to risks posed by possible substitutes. c o o 1; Federal Register/ Vol. 65. No. 202 1W ednesdav. October 18. 2000 / Proposed Rules 52329 DC. Econom ic C onsiderations EPA has evaluated the potential costs of establishing a SNUR for PFOS listed in Table 2 a n d T able 3 of U nit I.A. These potential costs are related to the submission of SNUNs. the export notification requirem ents ofTSCA section 12(b), and the developm ent of test data. EPA notes that, w ith the possible exception of the export notification requirem ents, these costs will not be incurred by any com pany unless that com pany decides to pursue a significant new use as defined in this SNUR. A. S N U N s Because of uncertainties related to predicting the num ber of SNUNs that will be subm itted as a result of this SNUR. EPA is unable to calculate the total annual cost of com pliance w ith the final rule. However. EPA estim ates that the cost for preparation and subm ission of a SNUN ranges from approxim ately 58.500 to 59.800. w hich includes a $2.500 user fee (Ref. 11). EPA notes that small businesses w ith annual sales of less than 540 m illio n are subject to a reduced user fee of 5100. Based on past experience w ith SNURs and the low num ber of SNUNs w hich are subm itted on an annual basis, EPA believes that there w ould be few. if any, SNUNs subm itted as a result of this SNUR. F urtherm ore, no com pany is required to subm it a SNUN for the chemicals listed in this SNUR unless that com pany decides to begin manufacture or im portation those chemicals. As a result. EPA expects that com panies w ould be able to determ ine if the burden of subm itting a SNUN would be likely to create significant adverse econom ics im pacts for the com pany prior to incurring SNUNrelated costs. B. E xp o rt N o tific a tio n As noted in U nit II.A., persons w ho intend to export a chem ical substance identified in a proposed or final SNUR are subject to the export notification provisions ofT S C A section 12(b) (15 U.S.C. 2611 (b)). T hese provisions require that a com pany notify EPA of the first shipm ent to a particular country of an affected chem ical. EPA believes that m ost com panies com ply with these provisions by com piling a list of products that are subject to TSCA section 12(b) reporting. O utgoing orders are checked to see if the chem ical or product is on the list, an d w h eth e r it is the first sh ip m en t to the im porting country or the first shipm ent of the calendar year to that country. If so, a form letter is sen t to EPA. In m ost cases. the entire process is com p u terized . The estim ated cost of the TSCA section 12(b)(1) export notification, w hich w ould be req u ired for the first export to a particular country of a chemical subject to the rule, is estim ated to be 583.38 for the first time that an exporter m ust com ply with TSCA section 12(b)(1) export notification requirem ents, and 519.08 for each subsequent export notification subm itted by th at ex p o rter (Ref. 12). EPA is un ab le to estim ate the total num ber ofTSC A section 12(b) notifications that will be received as a result of this SNUR, or the total num ber of com panies that w ill file these notices. However, EPA expects that the total cost of com plying w ith the export notification provisions of TSCA section 12(b) w ill be lim ited based on historical experience w ith TSCA section 12(b) notifications, the relatively few com panies w ith fluorocarbon production capabilities, and the lim ited num ber of chem icals listed in this SNUR. If co m p an ies w ere to m anufacture any of the chemicals covered by this SNUR for export only, these com panies w ould incur costs associated w ith export notification even if these co m p an ies d ecid ed to forgo any dom estic significant new use. EPA is not aware of any com panies in this situation, and expects that any potential im pact w ould be lim ited to the sm all burden of export notification. C. T e stin g In U nit VIII.. EPA has id en tified certain tests that SNUN subm itters may choose to conduct to assist EPA in evaluating the risks posed by these chem ical substances w hen used for an intended significant new use. The estim ated cost of these tests ranges from 51.450 for the acute oral toxicity test using the up-o r-d o w n m eth o d to S2.24 m illion for the 2-species carcinogenicity test by the in h a latio n route (Ref. 13). As n o te d in U nit VIII., d ev elo p m en t of any particular test data w ould be at the discretion of the subm itter of the SNUN. EPA is not able to predict w hich specific tests will be conducted for chem icals that are the subject of SNUNs. However. EPA notes that com panies w o u ld be able to d eterm in e if the burden of developing test data w ould be likely to create significant adverse econom ic impacts for the com pany prior to incurrin g these testing costs. X. References These references have been placed in the official record that was established under docket control number OPPTS50639 for this rulem aking as indicated in U nit I.B.2. Reference d o cu m en ts identified w ith an adm inistrative record n u m b er (AR) are cross-indexed to nonregulatorv. publicly accessible inform ation files m aintained in the TSCA N onconfidential Information Center. Copies of these docum ents can be o b tain ed as d escrib ed in Unit I.B.2. 1. (A R 226-0620) Sulfonated Perfluorochem icals in the Environment: Sources. D ispersion. Fate, and Effects. 3M. St. Paul. MN. M arch 1. 2000. 2. (A R 226-0547) T he S cience of O rganic F luorochem istry. 3M. St. Paul, MN. February 5. 1999. 3. (AR226--0548) P erfluorooctane Sulfonate: Current Summary of Human Sera. H ealth and Toxicology Data. 3M. St. Paul. MN. January 21. 1999. 4. (A R 226-0550) F luorochem ical Use. D istrib u tio n , an d Release O verview . 3M. St. Paul. MN. May 26. 1999. 5. Rice, Cody. D om estic M anufacturers or Importers of PFOS Chem icals O ther Than 3M. USEPA/ OPPT/EETD. W ashington. DC. A ugust 31. 2000. 6. (AR226--0600) W eppner. W illiam A. P h ase-o u t P lan for POSF-Based P ro d u cts. 3M. St. P au l. MN. July 7, 2000. 7. M acKay, D., D iG uardo. A.. P aterso n , S., a n d Cow an. C.E. Evaluating the Environm ental Fate of a Variety of T vpes of C hem icals Using the EQC Model. Environm ental Toxicology and Chem istry. SETAC Press. H ouston. TX. 1996. Vol. 15. No. 9. p p .1627-1637. 8. Seed. Jennifer. H azard A ssessm ent and Biom onitoring Data on Perfluorooctane Sulfonate--PFOS. U SEPA /EPA /RA D . W ashington. DC. August 31. 2000. 9. 3M P hasin g O u t Som e of its S p ecialty M aterials. 3M News. 3M. St. Paul. MN. May 16, 2000. 10. G uidelines for the requested fate and transport data can be found in OPPTS H arm onized Test Guidelines, Series 835. Fate. Transport And Transform ation Test Guidelines. These guidelines, both Public Drafts and Finals, are available electronically in PDF (portable docum ent format) on the EPA W orld W ide Web site, see Unit I.B.I.. or in paper by contacting the OPP Public Docket at (763) 305-5805 or by e-m ail at: opp-docket@ epa.gov. Final guidelines, only, are available from the U S. G o v ern m en t P rin tin g Office Bookstore. 810 N orth Capitol St.. NW.. W ashington. DC or by calling (202) 5121800 and ordering ASCII disks or paper copies. T he EQC m odel is available for dow nload from the Trent University web site at http://w w w .trentu.ca/ envm odel. 11. (AR 2 0 4 -0 0 1 ) TSCA S ection 5(a)(2) Significant New Use Rules for ooov 62330 F ederal R e ^ ste r/V o l. 65. No. 202 / W ednesday. October 18, 2 0 0 0 / ProDosed R n 1a c Existing C hem icals. ICR <1 188.06, OMB No. 2070-0038 (Undated). 12. (AR 205-001) TSCA S ection 12(b) N otification of C hem ical Exports. ICR #0795.10. OMB No. 2070-0030 (Undated). 13. Rice. Cody. E stim ated C osta of Testing Recom m ended for PFOS SNUR. USEPA/OPPT/EETD. W ashington. DC. July 25, 2000. XI. R egulatory A ssessm ent Requirem ents Under Executive Order 12866. entitled Regulatory Planning and R eview (58 FR 51735, O ctober 4. 1993), the Office of M anagem ent and Budget (OMB) has determ ined that SNURs are not a ``significant regulatory ac tio n " subject to review by OMB. because SNURs do not meet the criteria in section 3(f) of the E xecutive Order. Based on EPA's experience w ith past SNURs. State, local, and tribal governm ents have not been im pacted by these rulem akings, and EPA does not have any reasons to believe that any State, local, or tribal governm ent w ill be im pacted by this rulem aking. As such, EPA has determ ined that this regulatory action does not impose any enforceable duty, contain any unfunded m andate, or otherw ise have any affect on small governm ents subject to the requirem ents of sections 202. 203. 204. or 205 of the U nfunded M andates Reform Act of 1995 (UMRA) (Public Law 104--4). Sim ilarly, this action is not subject to the requirem ent for prior consultation w ith Indian tribal governm ents as specified in Executive O rder 13084, entitled C onsultation and Coordination w ith In d ia n T ribal G o v e rn m e n ts (63 FR 27655. May 19.1998). Nor will this action have a substantial direct effect on States, on the relationship between the national governm ent and the States, or on the distribution of pow er and responsibilities among the various levels of governm ent, as specified in Executive Order 13132. entitled F ederalism (64 FR 43255, A ugust 10. 1999). In issuing this proposed rule, EPA has taken the necessary steps to elim inate drafting errors and am biguity, m inim ize potential litigation, and provide a clear legal standard for affected conduct, as required by section 3 of Executive Order 12988, en title d C ivil Ju stic e R e fo rm (61 FR 4729. F ebruary 7, 1996). EPA has com plied w ith Executive Order 12630. entitled G overnm ental A ctions an d Interference with C onstitutionally Protected Property R ights (53 FR 8859, M arch 15.1988). by examining the takings im plications of this proposed rule in accordance with the "A ttorney General's Supplem ental G uidelines for the Evaluation of Risk and Avoidance of U nanticipated Takings" issued under the Executive Order. This action does not involve special considerations of environm ental justice related issues as required by Executive O rder 12898. entitled Federal A c tio n s to A d d ress E nvironm ental Justice in M inority P opulations and Low-Income P o p u la tio n s (59 FR 7629. February 16. 1994). This action is not subject to Executive Order 13045. entitled Protection o f Children from E nvironm ental Health R isks a n d S a fe ty R isks (62 FR 19885, A pril 23. 1997). because this is not an econom ically significant regulatory action as defined by Executive Order 12866, and this action does not address environm ental health or safety risks disproportionately affecting children. In addition, since this action does not involve any technical standards, section 12(d) of the N ational Technology Transfer and A dvancem ent Act of 1995 (NTTAA), Public Law 104-113. section 12(d) (15 U.S.C. 272 note), does not apply to this action. Pursuant to section 605(b) of the R egulatory F lexibility A ct (RFA) (5 U.S.C. 601 e t seq.), the Agency hereby certifies that prom ulgation of this SNUR will not have a significant adverse economic im pact on a substantial num ber of small entities. A SNUR applies to any person (including sm all or large entities) w ho intends to engage in any activity described in the rule as a "significant new use." By definition of the word "new ," and based on all inform ation currently available to EPA. it appears that no sm all or large entities currently engage in such activity. Since a SNUR requires merely that any person w ho intends to engage in such activity in the future m ust first notify EPA (by subm itting a SNUN), no econom ic im pact w ill even occur until someone decides to engage in those activities. As a voluntary action, it is reasonable to presum e that this decision w ould be based on a determ ination by the person subm itting the SNUN that the potential benefits w ould outw eigh the costs. A lthough some sm all entities may decide to co nduct such activities in the future, EPA cannot presently determ ine how m any, if any. there may be. EPA's experience to date is that, in response to the prom ulgation of over 530 SNURs, th e A gency has receiv ed few er th a n 15 SNUNs. Of those SNUNs subm itted, none appear to be from sm all entities. In fact. EPA expects to receive few. if any, SNUNs from either large or sm all entities in response to any SNUR. Therefore, EPA believes that, the economic im pact of com plying w ith a SNUR is not ex p ected to be significant or adversely im pact a substantial num ber of small entities. This rationale has been provided to the Chief Counsel for Advocacy of the Small Business A dm inistration. A ccording to the Paperw ork R eduction Act (PRA), 44 USC 3501 et seq.. an agency may not conduct or sponsor, an d a p erso n is not req u ired to respond to a collection of inform ation that requires OMB approval under the PRA. unless it has been approved by OMB and displays a currently valid OMB control number. The OMB control n u m b ers for EPA 's regulations, after initial display in the Federal Register and in addition to its display on any related co llectio n in stru m en t, are Listed in 40 CFR p art 9. The inform ation collection requirem ents related to this action have already been approved by OMB pursuant to the PRA under OMB control n u m b er 20 7 0 -0 0 3 8 (EPA ICR No. 1188.06). This action does not im pose any burden requiring additional OMB approval. If an entity w ere to subm it a SNUN to the Agency, the annual burden is estim ated to average betw een 98.98 and 118.92 hours per response at an estim ated reporting cost of between $5,957 and $7,192 per SNUN. This burden estim ate includes the tim e needed to review instructions, search existing data sources, gather and m aintain the data needed, and com plete, review and subm it the required significant new use notice, and m aintain the required records. This burden estim ate does not include 1 hour of technical tim e at $64.30 per hour estim ated to be required for custom er notification of SNUR requirem ents, or the $2,500 user fee for subm ission of a SNUN ($100 for businesses w ith less than $40 m illion in an n ual sales). Send any com m ents about the accuracy of the burden estim ate, and any suggested m ethods for m inim izing respondent burden, including through the use of autom ated collection te ch n iq u e s, as in stru c te d in U n it I.C. or to the D irector. C ollection Strategies Division, Office of Environm ental Inform ation.. Environm ental Protection Agency (2822), 1200 Pennsylvania Ave., NW., W ashington. DC 20460. Please rem em ber to include the OMB control number in any correspondence, but do not subm it any com pleted forms to this address. List of Subjects in 40 CFR Part 721 Environm ental Protection. Chemicals. H azardous m aterials. Recordkeeping and reporting requirem ents. COOVi/i Federal Register >Vol. 65. N'n. 202 / W ednesday. October 18, 2000 / Proposed Rules 62331 Dated. October 12. 2000 William H. Sanders. 01 Director. Office o f Pollution Prevention and Toxics. Therefore, it is proposed that 40 CFR chapter I be am ended as follows: PART 721--[AMENDED] 1. T he au th o rity citatio n for part 721 w ould continue to read as follows: Authority: 15 U.S.C. 2604. 2607 and 2625(e). 2. By ad d in g new 721.9582 to subpart E to read as follows: 72* .S5S2 Certain perriuorooctyi sulfonates. (a) C h e m ic a l s u b sta n c e s a n d sig n ific a n t n e w uses sub/ect to reporting. (1) T h e ch e m ic al substances listed in Tables 1 and 2 of this paragraph are subject to reporting under this section for th e sig n ifican t new uses described in paragraph (a)(2) of this section. T a b l e 1.-- C h e m ic a l s R e q u ir in g a S i g n if ic a n t N e w U se N o t i c e O n o r A f t e r J a n u a r y 1, 2001 CAS No./PMN Ninth Collective Index chemical name 3 8 8 -0 7 -3 ... 4 2 3 -8 2 -5 ... 2250-98-8 14650-24-9 30381-98-7 55120-77-9 57589-85-2 61660- 12-6 67969-69-1 6 8 1 5 6 - 0 1 --4 68329-56-6 68555-91-9 68555-92-0 68608-14-0 86909-15-9 70776-36-2 73772-32--4 . 81190-38-7 . 94133-90-1 . 117806-54-9 127133-66-8 129813-71-4 148240-78-2 148240-79-3 148240-80-6 148240-81-7 148240-02-8 148684-79-1 178535-22-3 P-83-1102 ... P -84-1163 .... . 2-Propenoic acid, 2-(butyl((heptadecafhjorooctyi)sut1onyl]amino)ethyl ester. 2-Propenoic acid, 2-(ethyl((heptadecaf1uorooctyt)sulfony!]aminojethyl ester. 1-Octanesultpnamide. N,N',N"-[phosphinylidynetris(oxy-2,l-ethanediyl)]tris(N-othyl-i,l.2.2,3.3,4,4,5.5.6.6.7.7.8.8.8- heptadecatluoro-. 2- Propenoic acid, 2-methyl-. 2-[[(heptadecafluorooctyt)sulonyt]methylaminojethyl ester. 1- Octanesulfonamide, N,N'-[phosphinicobis(oxy-2,l-ethanediy1)]bis(N-ethyt-1,1,2,2.3,3,4,4,5.5,6.6.7,7,8,8.8-heptadecafluoroammonium salt. - 1-Hexanesulfonic acid. 1,1.2.2.3.3.4.4,5.5.6.6.6-tndecafluoro-, lithium salt. Benzoic acid. 2.3.4.5-tetrachloro-6-([[3-{[(heptadecafluoroocty1)sutfonyl]oxylphenyl]amino]cait>onyi]-, monopotassium salt. [ 1-Octanesulfonamide. N-ethyl-1,1,2.2.3.3,4,4,5.5.6,6,7,7.8.8,8-heptadecafHjoro-N-{3-(trimethoxysifyl)propyi]-. : 1-Octanesulfonamide. N-ethyl-1,1.2,2.3.3,4,4,5.5,6,6,7,7.8,8,8-heptadecafluoro-N-(2-(phosphonooxy)ethyl]-, diammonium [ salt. 1 Cyclohexanesulfonic acid, nonafluorobis(trifluoromethyl)-, potassium salt. i 2-Propenoic acid, eicosyl ester, polymer with 2-{[(heptadecaftuorooctyl)sut1onyl]methytamino]ethyt 2-propenoete. hexadecyl | 2-propenoate. 2-[methyl((nonat1uorobutyl)sulfony1]amino]ethy1 2-propenoate, 2- | [methyl((pentadecaftuoroheptyl)su!fonyl]amino]ethyt 2-propenoate. 2-(methyl{(trrdecafluorohexy1)sulfony1]amino]ethyl 2- j propenoate, 2-[methyl[(undecafluoropemy1)sulfonyl]amino)ethyt 2-propenoate and octadecyl 2-propenoate. 2-Propenoic acid. 2-methyl-, 2-iethyl((heptadecaf1uoroocty1)sultony1]arrano)ethyl ester, polymer with 2- [ethyl((nonafluorotouty1)sulfonyt]amino)ethyl 2-methyl-2-propenoate, 2-{ethy1[(pentadecafluoroheptyt)sulfonyt]arninojelhy1 2- methyl-2-propenoate. 2-{ethyl((tridecafluorohexyl)sulfonytlaminolethyl 2-methyt-2-propenoate, 2- [ethyt[(undecafluoropentyl)sulfonyl]amino]ethyt 2-methy!-2-propenoate and octadecyl 2-methyl-2-propenoate. 2-Propenoic acid, 2-methyl-, 2-[[(heptadecaftuorooctyl)sulfonyl]mettiylamiro]ethyl ester, polymer with 2- [methyt[(nonafluorobutyt)sulfonyl]amino]ethy( 2-methyt-2-propenoa*e, 2- [methyt[(pentadecafluoroheptyt)sulfonyljamino]ethyl 2-methy1-2*ptopenoate, 2- (methy1((tndecafluorohexyl)sultonyl)amino)ethyl 2-methy1-2-propenoate, 2-{methy!((undecafluoropentyQsulfonyl]arnino]etfiyl 2-methyt-2-propenoate and octadecyl 2-methyl-2-propenoate. I Sulfonamides, C4-8-alkane. perfluoro, N-ethyi-N-(hydroxyethyi), reaction products with 1.1'-methylenebts(4- j isocyanatobenzene], j 2-Propenoic add, eicosyl ester, polymers with branched octyl acrylate, 2-Q(heptadecaftuorooctyt)su<fonyl}methytamino]ethyt acrylate. 2-{methyl((nonaftuorobutyl) sultony1)amino)ethyl acrylate. 2-[mettyt[(pentadecafluoroh6ptyf>suttonyt)airiino]ethyl acrylate, 2-(methyl((tridecafluorohexy1)sulfonyt]amino]ethyl acrylate, 2-[rnethyi{(undecafluoropentyl) suitonyljammoethyl acrylate, polyethylene glycol acrylate Me ether and stearyl acrylate. 2-Propenoic add. 2-methyt-, octadecyl [[(heptadecaduoroocty1)sultony1]methylamino)ethyi ester, polymer with 1 ,1 -dich loroethane, 2-propenoate. N-(hydroxymethyl)-2-propenamide. 22- [methyl[(nonaftuorobutyl)sultony1]amino)ethy1 2-propenoate, 2-{methyl((pentadecafluoroheptyt)sutfony!]amino)ethyl propenoate, 2-{methyl{(tndecafluorohexy1)suttonyl)amino)ethyl 2-propenoate and (methyl((undecafluoropentyl)suIfonyljamlno(ethyl 2-propenoate. 22- 1-Propanesulfonic add, 3-([3-(dlmethytamino)propylX(tncleca8uorohexyl)sulfonyl)amino]-2-hydroxy-, monosodium salt. 1-Propanaminium, N-{2-hydroxyethy1)-3-{(2-hydroxy-3-suttopropyl) [{tridecaf1uorohexyl)sulfonyt]amirio]-N,N-dimethyf-, hy droxide. monosodium salt. 1-Propanesulfonic add. 3-fl3-{dimethytamino)propytK(heptadecafluoroocty1)sulfonyl]aminol-2-hyckoxy-, monosodium salt. 1- Heptanesulfonic add. 1.1,2,2.3,3,4,4,5,5,6,6,7,7,7-pentadeeafluoro-. lithium salt. 2- Propenoic add. 2-methyl-, polymers with Bu methacrylate, lauryl methacrylate and 2-[methy1((perfluoro-C4-8alkyi)sultonyt]amino]ethyt methacrylate. Sulfonamides, C4-8-alkane, perfluoro, N-methyl-N-(oxiranylmethyl). Fatty acids. C18-unsatd.. trimers, 2-([(heptodecafluorooctyt)sulfony1]methylamino]ethyl esters. Fatty acids, C18-unsatd., trimers, 2-{methyl((nonatluorobutyl)sulfonyt]amino]ethyl esters. Fatty adds. C18-unsatd.. trimers. 2-{methyl[(tridecafluorohexyt)sulfonyl]amino]ethy1 esters, i Patty acids, C18-unsatd,, trimers. 2-(methyl{(undecaftuoropentyl)sultony1]amino]ethy1 esters, j Fatty acids, C18-unsatd.. trimers. 2-imethyl[(pentadecafluoroheptyl)sultonyl)aminolethyl esters. | Sulfonamides, C4-8-alkane, perfluoro, N-(hydroxyethyl)-N-methyl, reaction products with 1,6-diisocyanatohexane j homopolymer and ethylene glycol. I Sulfonamides, C4-8-a!kane. perfluoro. N-ethyl-N-ihydroxyethyl)-, polym'ers with 1 .1'-methylenetofS[4-isocyanatobenzene] and polymethylenepolyphenylene isocyanate. 2-ethylheicyl esters. M e Et ketone oxime-blocked. | Fatty acids, linseed-oil, dimers. 2-([(heptadecafluorooctyl)sulfonyl]methytamino)ethyl esters. i Propanoic add, 3-hydroxy-2-(hydroxymethyl)-2-methyl-, polymer with 2-ethyl-2-(hydroxymethyl)-1.3-propanediol and N.N',2- ! tns(6-isocyanatohexyl)imidodicarbonic dlamide, reaction products with N-ethyl-1,1.2.2.3.3,4,4,5.5.6.6.7.7.8.8.8l ' heptadecafluoro-N-(2-hydroxyethyt)-1-octanesulfonamide and N-ethyl-1,1,2,2,3,3,4,4,5,5,6,6,7,7,7-pentadecafluoro-N-(2- hydroxyethyl)-i-heptanesulfonamide. compds. with Methylamine. 0 0 OV 62332 Federa! Register ' Vol. 65. No. 202 / W ednesday. October 18. 200Q / Proposed Rules ! T a b l e 1.-- C h e m ic a l s R eq u ir in g a S ig n if ic a n t n e w u s e No t ic e O n o r A f t e r Ja n u a r y 1, 20 01-- Continued CAS No./PMN Ninin Collective Index cnemical name P-84-1171 ....... Propanoic acid. 3-hydroxy-2-(hydroxymethyl)-2-methyl-. polymer with 1 1'-methylenebis(4-isocyanatobenzene] and 1.2.3- propanetriol, reaction products with N-ethyl-1,1,2.2.3.3.4.4.5.5.6.6.7.7,8.8.8-heptadecafluoro-N-(2-hydroxyethyl)-l- octanesulfonamide and N-ethyl-1,1.2.2,3,3.4,4,5.5.6.6.7.7.7-pentadecaf!uoro-N-(2-hydroxyethyl)-1 -heptanesultonamide. P-8&-0301 ....... P-89-0799 ....... P-94-0545 ....... compds. with morpholine. Sulfonamides. C4-8-alkane, perfluoro. N-(hydroxyethyl)-N-methyl. reaction products with 12-hydroxysteanc acid and 2.4- TDI. ammonium salts. Sulfonamides. C4-8-alkane. perfluoro. N-ethyl-N-(hydroxyethyl), reaction products with 2-ethyi-i-hexanol and polymethytenepolyphenytene isocyanate. 1-Hexadecanamimum. N.N-dimethyl-N-[2-((2-methyl-l-oxo-2-propenyl)oxy)ethyl]-. bromide, polymers with Bu acrylate. Bu methacrylate and 2-{methyi((perfluoro-C4-8-alkyl)sulfonyl]amino]ethyl acrylate. P-94-0927 ........ 2-Propenoic acid. 2-methyl-. 2-methylpropyl ester, polymer with 2.4-diisocyanato-l-methylbenzene. 2-ethyl-2(hydroxymethyl)-l,3-propanediol and 2-propenoic acid. N-ethyl-N-(hydroxyethyl)perfluoro-C4-8-alkanesulfon amides- ! blocked. P-94-2205 ........ Polymethylenepolyphenylene isocyanate and bis(4-NCO-phenyl)methane reaction products with 2-ethyl-l-hexanol. 2-buta- none. oxime, N-ethyl-N-(2- hydroxyethyl)-1-C4-C8 perfluoroalkanesulfonamide. P-94-2206 ....... ; Siloxanes and Silicones. di-Me, mono{3-[(2-methyl-1-oxo-2-propenyl)oxy]propylgroup]-terminated, polymers with 2[methyl[(perfluoro-C4-8-alkyl)sulfonyl]amino)ethyl acrylate and stearyl methacrylate. P-96-1645 ........ Fatty acids. C18-unsatd.. dimers, 2-(methyl((perlluoro-C4-8-alky1)sulfonyl]amino)ethyl esters. P-97-0790 ....... 1-Decanammium. N-decyl-N,N-dimethyl-, salt with 1,1.2.2,3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-l-octanesulfonic acid : (1:1). P-98-0251 ......... 2-Propenoic acid, butyl ester, polymers with acrylamide, 2-[methyl[(perfluoro-C4-8-alkyl)sullonyl]amino]ethyl acrylate and vinylidene chloride. P-98-1272 ........ 2-Propenoic acid, 2-methyl-. 3-(trimethoxysilyl)propyl ester, polymers with acrylic acid. 2-[methyt[(perfluoro-C4-8- alkyl)sulfonyl]amino]ethyl acrylate and propylene glycol monoacrylate, hydrolyzed, compds. with 2.2'- (methylimino)bis(ethanol]. P-99-0188 ......... Hexane. 1.6-dlisocyanato-. homopolymer. N-(hydroxyethyl)-N-methyl perfluoro C4-8-alkane sulfonamide- and stearyl alc.- blocked. P-99-0319 ......... i Poly(oxy-l .2-ethanediyl), i alkyl)sulfonyl] denvs.. alpha.-[2-<methylamino)ethyl]-.omega.-{(1,1,3,3-tetramethylbutyi)phenoxy]-, N-{(perfluoro-C4-8- ; i T able 2 .-- C hemicals Subject to V o lum e C ap Re str ic tio n s O n or After Janu ary 1, 2001 and R eq u ir in g a S ig nific ant N ew U se No t ic e O n or After Ja n u a r y 1, 2003 CAS No./PMN Ninth Collective Index chemical name 3 0 7 -3 5 -7 .............. 3 0 7 -5 1 -7 .............. 3 7 6 -1 4 -7 .............. 4 2 3 -5 0 -7 .............. 7 5 4 -9 1 -6 .............. 1 6 5 2 -6 3 -7 .......... 1 6 9 1 -9 9 -2 ............ 1763-23-1 ........... 2 7 9 5 -3 9 -3 ............ 2 9 9 1 -5 1 -7 ............ 4 1 5 1 -5 0 -2 ............ 1 7 2 0 2 -4 1 -4 ........ 2 4 4 4 8 -0 9 -7 ......... 2 5 2 6 8 -7 7 -3 ......... 2 9 0 8 1 -5 6 -9 ......... 2 9 1 1 7 -0 8 -6 ......... 2 9 4 5 7 -7 2 -5 ......... 3 1 5 0 6 -3 2 -8 ......... 3 8 0 0 6 -7 4 -5 ......... 3 8 8 5 0 -5 6 -7 ......... 67584--4 2 -3 ......... 67906--4 2 -7 ......... 682 98 -6 2 --4 ......... 6 8 5 4 1 -8 0 -0 ......... 6 8 5 5 5 -9 0 -8 ......... 6 8 5 8 6 -1 4 -1 ........ 1-Octanesulfonyl fluoride, 1.1.2.2.3.3,4.4.5,5.6,6,7,7,8,8.8-heptadecafluoro- 1- Decanesulfonyl fluoride. 1,1,2,2.3,3,4,4,5.5,6,6,7,7,8,8,9,9,10.10,10-heneicosafluoro- 2 - Propenoic acid. 2-methyl-, 2-[ethyl((heptadecafluorooctyf)sulfonyl]aminolethyl ester 1-Hexanesulfonyl fluoride. 1.1.2.2.3,3.4,4,5.5.6,6,6-tridecafluoro- 1-Octanesulfonamide, 1,1,2.2.3,3.4,4,5,5.6.6.7,7,8,8.8-heptadecafluoro- 1-Propanaminium. 3-([(heptadecafluorooctyl)sulfpnyl]amino]-N.N,N-trimethyl-, iodide 1-Octanesulfonamide, N-ethyl-1,1.2.2,3,3.4,4.5.5,6,6,7.7.8.8,8-heptadecafluoro-N-(2-hydroxyethyl)- 1-Odanesulfonic acid. 1,1,2,2.3.3,4,4,5,5,6,6,7,7,8,8,8-heptadecaftuoro- 1-Octanesulfomc acid. 1,1.2,2.3,3,4.4,5,5,6,6,7,7,8,8,8-heptadecafluoro-, potassium salt Glycine. N-ethyl-N-{(heptadecafluorooctyl)sulfonyl]-, potassium salt 1- Octanesulfonamide. N-ethyl-1,1,2.2,3,3.4,4,5.5.6,6,7.7,8,8.8-heptadecafluoro 1-Nonanesulfonic acid. 1,1,2.2.3.3.4.4,5,5,6.6.7,7,8,8,9.9.9-nonadecafluoro-. ammonium salt 1-Octanesulfonamide, 1,1,2.2,3,3.4.4,5.5.6.6,7,7.8.8,8-heptadecafluoro-N-(2-hydroxyethyl)-N-methyl- 2 - Propenoic acid. 2-{[(heptadecafluorooctyl)sulfonyl]methylamino]ethyl ester 1-Octanesulfomc acid, 1,1,2,2.3,3,4.4,5,5,6,6,7,7,8,8.8-heptadecafluoro-, ammonium salt Poiy(oxy-l.2-ethanediyl), .alpha.-(2-[ethyl[(heptadecaftuorooctyl)sulfonyl]amino]ethyl]-.omega.-hydroxy- 1-Octanesulfomc acid, 1,1,2,2.3,3,4,4,5,5,6,6,7,7,8,8,8-heptadecafluoro-, lithium salt 1-Octanesulfonamide. 1,1,2,2,3,3,4,4,5,5.6.6.7.7,8,8.8-heptadecafluoro-N-methyl- 1-Propanaminium. 3-([(heptadecafluorooctyl)sulfonyl]amino)-N,N.N-tnmethyl-, chloride 1-Propanaminium. N-(2-hydroxyethyl)-N.N-dimethyl-3-[(3-sulfopropyl){(tridecafluorohexyl)sulfonyl]amino)-, inner salt Cyclohexanesulfonic acid, decafluoro(pentafluoroethyl)-, potassium salt 1- Decanesulfomc acid, 1.1,2.2.3,3.4,4.5.5.6.6.7.7.8.8.9.9.10.10.10-heneicosafluoro-. ammonium salt 2- Propenoic acid. 2-[butylftheptadecafluorooctyl)sulfonyl]amino]ethyl ester, telomer _ with [butyl[(pentadecafluoroheptyl)sulfonyl]amino]ethyl 2-propenoate, methyloxirane polymer with oxirane d'i-2-propenoate. methyloxirane polymer with oxirane mono-2-propenoate and 1-octanethiol 2-Propenoic acid, polymer with 2-[ethyl[(heptadecafluorooctyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate and octadecyl 2- propenoate 2-Propenoic acid, butyl ester, polymer with 2-[[(heptadecafluorooctyl)sulfonyt] methylamino)ethyl 2-propenoate. 2- [methyl[(nonafluorobutyt)sulfonyl]amino)ethyl 2-propenoate. 2-(methyl[(pentadecafluoroheptyf)sulfonyl]amino)ethyl 2- propenoate. 2-[methyl((tridecafluorohexyl)sulfonyl]amino|ethyl 2-propenoate and 2- (methyl((undecaftuoropentyl)sulfonyl]amino]ethyl 2-propenoate 2-Propenoic acid. 2-([(heptadecafluorooctyl)sulfonyl]methylamino]ethyl ester, telomer with 2- (methyl[(nonafluorobutyl)sulfonyl]ammo)ethyl 2-propenoate. ,alpha.-(2-methyl-1-oxo-2-propenyl)-.omega.-hydroxypoly(oxy- 1 2-ethanediyl). alpha.-(2-methyl-1 -oxo-2-propenyl)- omega.-{(2-methyl-l -oxo-2-propenyl)oxy]poly(oxy-l .2-ethanediyl). 2- (methyl[(pentadecafluoroheptyt)sulfony!]amino]ethyl 2-propenoate, 2-{methyl[(tridecafluorohexyl)sulfonyl]amino]ethyl 2- propenoate. 2-[methyi((undecafluoropentyl)sulfonyt]aminolethyt 2-propenoate and 1-octanethiot 2 I Federad R egister/ Vol. 65. No. 202 / W ednesday, October 18. 2000 / Proposed Rules 62333 Ta b l e 2.-- C h e m ic a l s S u b je c t t o 'V o l u m e C a p R e s t r ic t io n s O n o r A p i ER J a n u a r y i , 2001 a n u RtQuiRiNG a S ig n ific a n t n e w U s e No t ic e O n o r A f t e r J a n u a r y 1, 2003-- Continued CAS NO./PMN Ninth Collective Index chemical name 50649-26-3 50867-60-7 50867-62-9 66891-96-3 68956-61-2 70225-1 A--8 71407-20-2 91081-99-1 98999-57-6 182700-90-9 L-92-0151 .... P-80-0183 P-86-0958 P-90-0111 P-91-1419 P-93-1444 P-95-0120 P-96-1262 P-96-1424 P-96-1433 1-Octanesulfonamide. N-ethyl-1.1.2.2.3.3.4.4.5.5.6.6.7,7.8.8,8-heptadecat1uoro-N-(2-hydroxyethyl)-, reaction products with N-ethyl-1, 1,2,2.3.3,4.4.4-nonafluoro-N-(2-hydroxyethyl)-i-butanesultonamide. N-ethyl-1,1.2.2,3.3.4.4.5.5.6.6.7 7 7- pentadecafluoro-N-(2-hydroxyethyl)-1-heptanesulfonamide. N -e th y l-1 ,1 ,2 ,2 ,3 .3 .4 ,4 ,5 .5 .6 .6 .6-tridecafluoro-N-(2-hydroxy- ethyl)-1-hexanesulfonamide. N-ethyl-1.1.2.2.3.3.4.4.5.5.5-undecafluoro-N-(2-hydroxyethyl)-1-pentanesulfonamide. polymethylenepolyphenylene isocyanate and stearyl ale. 2-Propenoic acid. 2-[[(heptadecafluorooctyl)sul<onyl]methylaminolethyl ester, polymer with 2- [methyl[(nonafluorobutyl)sulfonyl]amino]ethyl 2-propenoate. 2-{methyl[(pentadecafluorohep1yl)sulfonyl]aminolethyl 2- propenoate. 2-[methyl((tndecaf1uorohexyl)sulfonyl]amino]ethyt 2-propenoate. 2- (methyl[(undecafluoropentyl)sulfonyl]ammo|ethyl 2-propenoate and alpha.-(1-oxo-2-propenyl)-.omega.-methoxypoly(oxy- 1,2-ethanedlyl) 2-Propenoic acid. 2-methyt-, 2-[ethyl((heptadecafluorooctyl)sulfonyl]amino)ethyl ester, telomer with 2- [ethyl((nonafluorobutyl)sulfonyl]aminolethyt 2-methyl-2-propenoate. 2-{ethyl[(pentadecafluorohepty1)sultonyl]aminolethyl 2- methyl-2-propenoate. 2-[ethyl[(tridecafluorohexyl)sulfonyl]amino)ethyl 2-methy1-2-propenoate. 2- [ethyl((undecafluoropentyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate, 1-octanethiol and alpha.-(1-oxo-2-propenyl)- .omega.-methoxypoly(oxy-1,2-ethanediyl) Chromium. diaquatetrachloro(.mu.-(N-ethyl-N-[(heptadecafluorooctyl)sulfonyl]glYcinato- kappa.O:.kappa.O'fl- mu - hydroxybisf 2-methylpropanol)dl- Poly(oxy-i,2-ethanediyl), alpha.-(2-[ethyl((heptadecafluorooctyl)sulfonyl]amino]ethy1]- omega.-methoxy- 1- Octanesultonic acid, 1,1,2,2.3,3,4.4,5.5,6,6,7.7.8.8.8-heptadecafluoro-, compd. with 2.2'-iminobis(ethanol] (1:1) 2 - Propenoic acid. 2-methyl-. methyl ester, polymer with ethenylbenzene. 2- [[(heptadecafluorooctyl)sulfonyl]methylamino]ethyl 2-propenoate. 2-(methyl[{nonafluorobutyl)sulfonyl]amino]ethyt 2- propenoate. 2-(methyl((pentadecaftuoroheptyl)sulfonyl]amino]ethyt 2-propenoate. 2- [methyl((tndecafluorohexyl)sulfonyl]amino]ethyl 2-propenoate. 2-[methyl((undecaf1uoropentyl)sulfonyl]aminolethyl 2- propenoate and 2-propenoic acid 1-Octanesultonamide. 1,1.2.2,3.3,4.4.5.5.6.6.7,7.8.8.8-heptadecaf1uoro-N-(2-hydroxyethy1)-N-methyt-. polymer with(chloromethyl)oxirane, 1.1.2.2.3.3.4,4.4-nonaftuoro-N-(2-hydroxyethy1)-N-methy1-1-butanesulfonamide, 1.1.2.2.3.3.4.4,5.5,6.6,7,7,7-pentadecalluoro-N-(2-hydroxyethyl)-N-methyt-l-heptanesulfonaiTiide, 1,1,2,2.3,3,4.4,5,5,6,6.6- tndecafluoro-N-(2-hydroxyethyl)-N-methyl-1-hexanesulfonamide and 1,1,2,2.3,3,4,4,5,5,5-undecafluoro-N-(2-hydroxyethyl)- N-methyl-1-pentanesutfonamide, hexanedioate (ester) Sulfonamides. C7-8-alkane,-perftuoro, N-methyl-N-{2-((l-oxo-2-propenyl) oxy)ethyl], polymers with 2-ethoxyethyl acrylate, glycidyl methacrylate and N,N,N-tnmethyl-2-{(2-methyl-l-oxo-2-propenyl)oxyjethanaminiumchk>hde 1-Octanesulfonamide, 1.1.2.2,3,3,4,4,5.5.6.6,7.7.8.8,8-heptadecafluoro-N-methyl-, reaction products with benzene-chlorine- sulfur chloride (S2CI2) reaction products chlorides 2- Propenoic acid, 2-methyl-, butyl ester, polymer with 2-methyl-. 2-{ethyl [(heptadecafluorooctyl)sulfonyl]amino}ethyl 2-meth- yl-2-propenoate, 2-[ethyl[(nonafluorobutyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate. 2- [ethyl((pentadecafluoroheptyl)sulfonyl]amino]ethyl 2-methyl-2-propenoate, 2-{ethyl((tridecafluorohexyl)sulfonyllaminolethyl 2-methyl-2-propenoate, and 2-propenoic acid Sulfonamides, C4-8-alkane. perfluoro, N-{3-(dimethylamino)propyl], reaction products with acrylic acid 2-Propenoic acid, 2-methyl-, dodecyl ester, polymers with 2-(methy1((pertluoro-C4-8-alkyl)sutfonyl|amino]ethyl acrylate and vinylidene chloride Sulfonamides. C4-8-alkane. perfluoro. N-methyl-N-[(3-octadecyl-2-oxo-5-oxazolidinyl)methyl] Poly(oxy-l ,2-ethanediyl), alpha.-hydro-.omega.-hydroxy-, polymer with 1,6-diisocyanatohexane, N-(2-hydroxyethy1)-N-methyt perfluoro C4-8-alkane sulfonamide-blocked 2-Propenoic acid. 2-methyl-, dodecyl ester, polymers with N-(hydroxymethyl)-2-propenamide, 2-[methyl{(perfluoro-C4-8- alkyl)sulfonyl]amino]ethyl methacrylate, stearyl methacrylate and vinylidene chionde Sulfonamides, C4-8-alkane, perfluoro, N,N'-(1,6-hexanediylbis([2-oxo-3,5-oxazolidinediyl)methylenel!bis(N-methyl- Sulfonic acids. C6-8-alkane. perfluoro, compds. with polyethylene-polypropylene glycol bis(2-aminopropyl) ether 2-Propenoic acid, 2-methyl-, 2-(dimethylamino)ethyl ester, telomers with 2-[ethyl[(perfluoro-C4-8-alkylsulfonyl]ammo]ethy! methacrylate and 1-octanethiol. N-oxides Sulfonamides. C4-8-alkane, perfluoro, N-(3-(dimethyloxidoamino)propyl), potassium salts (2) T he significant n ew uses are: (i) A ny m an u factu re or im port for any use of any chem ical listed in Table 1 of paragraph (a)(1) of this section on or after January 1, 2001. (ii) Any m an u factu re or im port for any use of any one or more of the chemicals listed in Table 2 of paragraph (a)(1) of this section in excess of an aggregate volum e for all of these chem icals of 1,100.000 pounds per person per calendar year on or after January 1. 2001 an d before January 1. 2003. (iii) .Any m a n u factu re or im p o rt for any use of any of the chem icals listed in T able 2 of p arag rap h (a)(1) of this sectio n on or after January 1. 2003. (b) (Reserved). (FR Doc. 00--26751 Filed 1 0 -1 7 -0 0 : 8:45 dm) BILLING C O O C 8 4 *0 -5 0 -3 0O3V<? r> 000T3 ^/24 L (OS' S 0 \ XH/XXI 1HX 0 0 / 6 0 / 1 1 LUBECK P u b lic S e rv ic e D istrict p.o.Box 700, Washington, West Virginia 26181-0700 James M. Cox, Manager Telephone Facsimile (304) 863-3341 (304) 863-3791 D ear L ubeck P S D Custom ers: O ctober 3 1 ,2 0 0 0 C O M M IS S IO N E R S : James E. Smith, Chairman David D. Steele, Secretary Lee "Ox" Johnson, Treasurer In com pliance w ith the Safe D rin kin g W a te r A c t A m endm ents and the W est V irg in ia B ureau for P ublic H e a lth , Lubeck P u b lic Service D istrict (L P S D ) m ust p ro vid e o ur custom ers w ith an annual w ater q u ality rep o rt, w h ich w as done in an advertisem ent in T h e Parkersburg N ew s and T h e Parkersburg Sentinel on July 1, 2000. In order to insure th at tap w ater is safe to d rin k , the U . S. E n v iro n m e n ta l P ro tectio n A g en cy (E P A ) prescribes regulations w h ich lim it the am ount o f certain contam inants in w a te r p ro vid ed by p u b lic w ater systems T h e presence o f those contam inants does not necessarily in d icate th a t w a te r poses a h ealth risk. L P S D ro u tin e ly m onitors yo u r d rin k in g w ater acco rd in g to F ed eral and State law s. T h e July 1, 2 0 0 0 advertisem ent p rovided the results o f m o n ito rin g fo r reg u lated contam inants. A n unregulated ch em ical fo r w hich L P S D has m o n ito rin g data is am m o n iu m p erfluorooctanoate (also know n as P F O A , A P F O , F C -1 4 3 , and C -8 ), w h ic h is used a t D u P o n t W ash in g to n W orks. A tten tio n has recen tly been focused on P F O A because it is one o f several products b ein g phased out by its m anufacturer, the 3 M Com pany. P F O A is a persistent ch em ical that is slo w to be e lim in a te d fro m the b lo o d stream o f p eo p le who have been exposed to it. D u P o n t reports that it has to xico lo g ical and e p id e m io lo g ic a l data to support confidence th at exposure guidelines established by D u P o n t are p ro tective o f hum an health. A lth o u g h P F O A is u nregulated fo r d rin kin g w a te r purposes (th at is, it has no lim it established by a regulatory agency), th e D u P o n t C om pany has established its o w n d rin k in g w a te r g u id elin e o f 1 p a ri per b illio n . T h e D u P o n t C om pany has advised the D is tric t that lo w co ncentrations have been fo u n d in d rin kin g w ater ax W ash in g to n W o rks (0 .2 parts p er b illio n , or ppb, as o f A u g u st 2 0 0 0 ) and in th e L P S D w ells (0 .2 , 0 .5 , and 0.1 ppb, also as o f August 2 0 0 0 ). These levels are b e lo w th e D u P o n t g u id e lin e and D uP ont has advised the D is tric t th at it is co n fid en t these levels are safe. L P S D is co m m itted to p ro vid in g safe w ater to o ur custom ers. I f you h ave any questions, you can reach the D is tric t at 8 6 3 -3 3 4 1 o r D a w n Jackson at D u P o n t at 8 6 3 -2 5 1 3 . 30 39Vd SNIlNIdd AQ33dS dIS 8frI3S8t>fr0 EZ'PT 0003/60 T 009 r;'Q i V' O-1 12 5 la.ma. m u tuam MCU1UL U a UL u. 3311 r. 1/ J Z3 **> 3 J f;.iBNt^i' Group name: Group type: Description: Members; 3'v*,*'Z::: W - 1: APFO TOX WORKING GROUP MuM-purpose_____________ CONFERENCE CALL LIST peter.thomford@oovance.com T T o * Paul Lieder David Fanar-iCHFaoc 011-44-1928-515-146 CE(combe-Dundee-(011-44-1382-669 -993) R Jun0-Hoechst(O11-49-6190-807-354 M Mistrorigo -Miteni(Ol 1-39-0445-963-847) G Costa - Verona (011-39-0445-963-647) S Shirvya - Asahi (011-81332-11-7671) G Kennedy - Dupont (302-366-5207) G Un - Daikin (614-365-9515) Y2. < 73*> Administration Owners: Administrators: Foreign directory sync allowed: Rosamaria Maldonado/US-Corporata/SM/US Rosamaria Maldonado/US-CorponateftMAJS Yas 1ST CLASS M AIL gn~9. -rhomt-cA 8T0OE s c i !m rn s s & ADDL. DIST. L .Bi'iyL T O X FILE CLI 0304 Covance Laboratories Madison, Wl MAY 1 9 1 999 Received # 1 5 h a !, m. isss &:44am > t MtUlUL U C. U a v . 33 11 r. u 3 May 19,1999 To: APFO Sub-committcc: APME From: Paul H. Lieder Attached is the preliminary analytical results for the animals at the end of the dosing phase o f the study. One animal in the low dose group died during the dosing phase o f the study as did one high dose animal. In sum mary, the low dose and mid dose animals had similar serum and liver values. Three high dose animals became very sick during dosing and consequently dosing was terminated mid-study. The serum and liver PFOA levels from these animals appear to be much lower than the high dose animals still receiving compound, indicating a relatively (vs, humans) short half-life(?) The results o f the histopathology and hormone analysis w ill be sent by Peter Thomford shortly. Regards, PHL 00073 CLI 0305 mai. ia. taaa o: 4 4 am MCUUAL u UL nu. 33 11 r. j / j 6 Month Capsule Toxicity Study wit APFO in Cynomolgus Monkeys Sera and Liver Analysis at Study Termination Preliminary Results: 18/5/99 Part 1: Serum Analysis Control Group 0 mg/kg/da I.D. Cone (ue/mL) 5709 0.393 5714 0.229 5715 0.099 5718 0.215 5719 0.322 5725 0.142 Average=0.233 Low Dose 3 mg/kg/da Cone (ug/mL) 5702 49.7 5706 66.9 5716 45.7 5721 47.7 5723 62.2 Average=54.5 Mid-high Dose 10 mg/kg/da I.D. Cone (ug/mD 5707 87.0 5708 33.3 5709 49.4 5712 104 5717 81.0 5718 67.6 Averages 70.5 OOOV-3'5 CLI 0306 may. ia. i yyy b : 44am MtULlAL u a \u hu. s a il r. v o High Dose 20 to 30 mg/kg/da On dosing (receiving compound at end of 6 months) I.D. Cone (ue/mL) 5703 60.8 5713 192 Averages 125 High Dose-- Moribund-sacrificed mid-study I.D. Cone (ug/mD 5724 403 High Dose-Recovery-removed from dosing mid-study due to toxicity I.D. Cone Oig/mU 5703 7.76 5711 0.909 5722 6.90 Average=5.19 Part 2: Liver Analysis Control Group 0 mg/kg/da I.D. Cone (ug/g) 5709 <MDL 5714 <MDL 5715 0.0474 5725 <MDL Average=0.0474 Low Dose 0 mg/kg/da I.D. Cone (ug/g) 5702 5.77 0GQ CLI 0307 MM. 13. 1333 O:<HM1 MCUIUAL L L U LC UL u. 33 11 I . J/ J 5706 6.81 5716 4.12 5723 6.80 Averages5.88 Mid-high Dose 0 mg/ks/da I.D. Cone (ug/mL) 5707 8.7 5708 3.61 5709 5.64 5719 5.50 Average=5.86 High Dose 30-- 20mg/kg/da On Compound--receiving compound at end of study I.D. Cone fue/mU) 5704 8.03 5713 28.3 Average^ 17.2 High Dose-Recovery-removed from dosing mid-study due to toxicity I.D. Cone (ug/mD 5703 1.05 5711 0.0278 5722 1.218 Average=0.766 5724 30.3 Moribund-sacrificed mid-study ooo'; 3 CLI 0308 John L. Butenhoff, et al. DRAFT 11/20/00 mTitle: Toxicity of Ammmonium Perfluorooctanoate (APFO) in Cynomolgus Monkeys after Twenty-Six Weeks of O ral Dosing Authors in sequence to be determined EID101453 D RAFT July 28, 2000 coor2 r* Page John L. ButenhofF, et al. DRAFT 11/20/00 Abstract: The purpose o f this study was to identify the earliest clinically measurable biological response from repeated daily exposure to ammonium perfluorooctanoate (APFO) and to correlate this response to serum concentrations for purposes o f risk assessment and medical monitoring of exposed populations. Groups o f male Cypomolgus monkeys received daily doses o f 0 (six per sex), 3 (four per sex), 10 (six per sex), or 30/20 (six per sex) mg/kg/day ammonium perfluorooctanoate for 26 weeks by gelatin capsule via gastric intubation. The high-dose group received 30 mg/kg for 11 days, after which dosing was discontinued for ten days (through study dosing day 21) due to signs o f few feces, low food consumption and weight loss. Beginning on study dosing day 22, the high-dose group was given 20 mg/kg and remained on this dose through termination of the dosing phase with the exception of three animals for which dosing was discontinued between days 43 and 81 due to emaciated appearance, weight loss, few or no feces and low or no food consumption. Two males in the control and mid-dose (10 mg/kg) group were followed for ninety days after cessation o f dosing and observed for reversibility, persistence, or delayed occurrence o f toxic effects. One high-dose male was sacrificed in moribund condition on day 29 after exhibiting hypoactivity, body cold to the touch, few feces, low or no food consumption and weight loss. One low-dose male was sacrificed in moribund condition on day 137 after exhibiting limited use and paralysis o f the hind limbs, ataxic and hypoactive behavior, few feces and no food consumption. There were no effects on estrone, estradiol, estriol, testosterone, cholecystokinin, thyroid stimulating hormone, or thyroxin. Triiodothyronine tremded down in three high-dose monkeys who were taken off compound for the remainder o f the study. T3 values for these monkeys trended up after cessation of dosing.. At all dose groups, significant increases in mean absolute liver weight and mean liver-to-body weight percentages were observed. The liver weight increase in the low dose animals occurred at a mean serum concentration o f approximately 50 ppm. Mean liver-to-brain weight ratios were increased in the mid-dose group. Organ weight and body weight effects were not evident at the end o f the recovery period. No test material related macroscopic or microscopic changes were observed in any organs, including liver, adrenal, spleen, pancreas and testis. The liver weight increase at the low dose occurred at serum concentrations which overlap those which have been observed in some workers with high exposure; therfore, the liver enlargement was considered a significant effect and the low dose o f 3 mg/kg/day is characterized as the lowest observed effect level (LOEL). D R AFT July 28, 2 0 0 0 EID101454 O O O C iO Page 2 John L. B u ten h o ff, et al. DRAFT INTRODUCTION 11/20/00 Ammonium perfluorooctanoate (C7F,3COO'NH4+; C.A.S. Registry number 3825-26-1; ammonium perfluorocaprylate, ammonium pentadecafluorooctanoate; FLUORAD TM Brand FC-143 Fluorochemical Surfactant; C-8; APFO1; PFOA1; Mol. Wgt. 431.1 g) is used as a surfactant in the aqueous polymerization o f fluorinated monomers such as tetrafluoroethylene. The assumed presence of PFOA in general population blood and in exposed worker blood, coupled with the observed persistence in workers, has led to extensive research into the potential health risk o f exposure to APFO (Guy, 1972; Venkateswarlu, 1975; Guy and Taves, 1976; Guy et al, 1976; Belisle and Hagen, 1978; Belisle and Hagen, 1980; Singer, 1979; Paez, 1980; Ubel, 1980; Belisle, 1981; Yamamoto, 1989). APFO has been produced since the early 1950's. Medical monitoring o f employees involved in PFOA production began in 1976, by measuring serum levels o f organic fluorine (OF) and performing medical assessments. Serum PFOA levels in production workers have been measured as high as 114 ppm. Eighty percent o f the workers had serum PFOA levels less than 10 ppm. Average serum concentrations have been approximately 2 ppm and individual values have range from 0 to 114 ppm. Past studies have demonstrated that the primary target organ for APFO-induced toxicity is the liver (refs). The hepatotoxicity manifests as increased liver weights, hepatocellular hypertrophy, liver degeneration, increases in liver enzymes, necrosis o f the liver, and proliferation of endoplasmic reticulum, microsomes, and peroxisomes (rats and mice only) yet does not result in hypolipidemia (Pastoor et al, 1987). Many o f these effects were demonstrated to be reversible when animals were provided with a recovery period. APFO has been demonstrated to be a peroxisome proliferator in the rat. APFO exposure in the rat was found to be associated with tumors in the liver, Leydig cell, and pancreatic acinar cell. Peroxisome proliferation is associated with: increases in number and volume o f peroxisomes; an increase in DNA synthesis and liver growth; and liver, Leydig cell, and pancreatic acinar cell tumors. Several known peroxisome proliferators (clofibrate, HCFC-123, methylclofenapate, and W yeth-14,643) are reported to induce this triad o f tumors in rats. The phenomenon o f peroxisome proliferation is not uniform across all species. While rats and mice are particularly sensitive to this phenomenon, guinea pigs, cats, dogs and primates (including man), are predominantly non-responsive. As noted above, chronic dietary studies in rats have produced hepatocellular adenoma, pancreatic acinar cell adenoma and Leydig cell adenomas (refs). The mechanisms of tum or formation have been studied. Hepatocellular tumors in the rat may arise from the proliferation o f peroxisomes (refs). In investigating the role of increased cholecystokinin (CCK) or CCKa receptor binding as possible mechanism for pancreatic tumors, APFO D R A FT July 28, 2000 EID101455 Page 3 John L. B utenhoff, et al. DRAFT 11/20/00 failed to bind directly to the CCKAreceptor and it failed to inhibit trypsin, a common mechanism for increasing plasma CCK levels (ref). In vivo studies with Wyeth-14, 643, a model peroxisome proliferator, suggest that these peroxisome proliferators produce pancreatic tumors by cholestasis, which may be responsible for the decrease in bile acid output which contributes to the increase in plasma CCK levels (Oboum et al, 1997). Therefore, the pancreatic tumors produced by APFO may be secondary to hepatic cholestasis. The Leydig-cell tumors appear to arise from an induction o f aromatase with a consequent increased conversion o f testoterone to estradiol an ?tijcohprt;jnortahly.^study;pf workers engagesdinAPTO/pioduotion found -no .. _j i Hepatic toxicity and hypolipidemia have not been associated with the PFOA levels measured in APFO production workers (Gilliland and Mandel, 1993; Gilliland, 1992; Gilliland and Mandel, Am J Ind Med 129:560-568; Olsen et al, 2000). Based on toxicological findings that suggested PFOA may increase estradiol due to an induction o f hepatic aromatase activity, Gilliland examined and found a positive association between serum total organic fluorine levels, used as an approximate measurement for PFOA, and estradiol (Gilliland, 1992). Gilliland and Mandel also observed that serum total organic fluorine negatively modulated the effect alcohol has on high-density lipoprotein (HDL) levels and exacerbated the effect that obesity has on hepatic enzyme tests among these workers (Gilliland and Mandel, AmsfrlndMfedri-29:560*568). However, an analysis o f two subsequent medical surveillance examinations on this APFO production workforce, which specifically assayed for PFOA, did not confirm these associations (Olsen et al, 1998 and Olsen et al, 2000). Neither did Olsen et al find an association between plasma cholecystokinin and measured serum PFOA levels (Olsen et al, 2000). The occupational exposure limit in current use is the American Conference o f Governmental Industrial Hygienists (ACGIH) Threshold Limit Value (TLV) o f 0.01 m g/m \ as an 8-hour, time-weighted average with a notation for skin exposure and an A3 designation for animal carcinogen with questionable relevance to humans [13,45] The purpose o f this study was to assess the effect o f APFO on critical enzyme levels, hormones, and other selected biochemical parameters when administered daily by oral capsule to cynomolgus monkeys for at least 26 weeks and to assess reversibility, persistence, or delayed occurrence o f toxic effects for 13 weeks after the 26-week treatment period. MATERIALS AND METHODS EID101456 A nim als and husbandry. Young adult to adult male Cynomolgus monkeys were obtained from Covance Research Products Inc. (Denver, PA) on August 25, 1998, and *,f7 A n 'in D R A FT July 2 8 ,2 0 0 0 eoo& tf: Page 4 John L. Butenhoff, et al. DRAFT 11/20/00 weighed 3.2 to 4.5 Kg at initiation o f treatment. Animals were acclimated for 35 days before initiation o f treatment. Each animal was assigned a permanent number upon arrival and identified with a collar tag. The animals were housed individually in suspended stainless-steel cages. The animal room was environmentally controlled to maintain 18 to 29C, a relative humidity o f 30 to 70%, and a 12-hr light/dark cycle. Certified primate diet, (#8726C,Harlan Teklad) was provided once or twice daily along with fruits or additional supplements. Water was provided a d libitum. Samples o f the water were analyzed for specific microorganisms and contaminants. Duringthe-study, rovend/animals experiencing low food consumption in the high^ose group'were offered supplements to rehydrate and stimulate food consumption. Animals were assigned to treatment groups using a computerized blocking procedure designed to achieve body weight balance within each treatment group. M aterials, dose preparation and treatm ent Ammonium perfluoroocatnoate (APFO, lot 332) was obtained from 3M (Saint Paul MN; purity xxx). Gelatin capsules (Torpac, Inc., Fairfield, NJ, Size No. 2, Lot No. 122932) containing the appropriate dose o f APFO were used for dose administration. Control animals received empty gelatin capsules. Capsules were prepared at least weekly. Individual daily doses were calculated based on the most recently recorded body weights. The dose preparations were stored at room temperature. Since the APFO was added directly to capsules as supplied without the use o f a vehicle, no dose analysis was performed. Dose levels were 0 (control group, n = 6), 3 mg/kg (low-dose group, n = 4), 10 mg/kg (mid-dose group, n = 6) or 30 reduced to 20 (30/20) mg/kg (high-dose group, n = 6). The capsules were administered orally once a day, seven days per week, for at least 26 weeks (183 days) except as noted below. One female in the low-dose group needed to be replaced for non-treatment-related issues. The replacement animal (105721) received his initial dose on day 17. High-dose animals were initiated on 30 mg/kg; however, due to toxicity, dosing was discontinued from day 12 through 21 and recommenced on day 22 at 20 mg/kg. Also due to toxicity, dose administration was also discontinued for three highdose animals on either day 43 (105711), day 66 (105722) or day 81 (105703). Two animals in both the control and mid-dose groups were designated as recovery group animals and were observed for reversibility, persistence, or delayed occurrence o f toxic effects for 13 weeks after the 26-week treatment period. D R AFT July 28, 2000 EID101457 ooo^ors Page 5 John L. Butenhoff, et al. DRAFT 11/20/00 Observations. The animals were observed twice daily for general health, behavior and qualitative food consumption. Ophthalmic examinations were conducted on each animal before treatment and on weeks 27 and 40 (recovery animals). Body weights were recorded weekly before initiation o f treatment, on the day before initiation o f treatment for dose calculation, on the first day o f treatment, and weekly thereafter. Determination o f blood hormones. Blood was collected from the femoral vein o f nonfasted animals 18, 8, and 4 days prior to initiation o f treatment and on days 35, 66, 94 and 183 o f treatment. Blood collection from recovery animals occurred on days 220, 248 and 276 after initiation o f treatment prior to collection. Blood samples were split into serum and plasma samples for further analysis for various hormones. Plasma samples were analyzed for cholecystokinin and testosterone (with the exception o f recovery animals in which case serum samples were used for testosterone). Serum was analyzed for estradiol, estrone, estriol, thyroid stimulating hormone, total and free triiodothyronine, total and free thyroxin. Clinical pathology observations. A clinical laboratory evaluation was conducted before initiation o f treatment, on days 31, 63, 91 and 182 o f treatment and during recovery on days 217, 245, and 275 after initiation o f dosing. At each sampling time, blood and urine samples were collected from animals that had been fasted overnight. Urine was collected overnight on wet ice before blood sampling; water was provided ad libitum. Blood was collected from the femoral vein. Sodium citrate was used as the anticoagulant for coagulation tests, and potassium EDTA was the anticoagulant used for hematology tests. Anticoagulants were not used for the clinical chemistry test sample collection. Blood was collected from animals with unscheduled sacrifices. Otherwise, animals with scheduled collections were bled in random order. The following hematological parameters were measured or calculated: erythrocyte (RBC) count, leukocytes (WBC) and platelets (PLAT); hemoglobin concentration (Hb) and hematocrit (Hct); mean corpuscular volume (MCV);mean corpuscular hemoglobin (MCHh); mean corpuscular hemoglobin concentration (MCHC); differential blood cell count o f segmented neutrophils (N-SEG), lymphocytes (), eosinophils () basophils (); and blood cell morphology and reticulocyte count. Blood cell counts, hemoglobin concentration hematocrit MCV, MCH, MCHV, were determined on a Abbott Cell-Dyn 35000 hematology analyzer. Differential cell counts were determined on an Abbott Cell-Dyn 3500 and reticulocyte counts were obtained using a Miller Disk microscopy technique. Bone marrow smears were prepared at euthanization EID101458 D R AFT July 28, 2000 C yr> :c*.vt- Page 6 John L. B u ten hoff, et al. DRAFT 11/20/00 Coagulation parameters measured were prothrombin time, activated partial thromboplastin time, and fibrinogen. Clinical chemistry measurements were made for glucose, urea nitrogen, creatinine, total protein, albumin, globulin, total bilirubin, cholesterol, triglycerides, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, gamma glutamyl transferase, sorbitol dehydrogenase, creatine kinase, calcium, inorganic phosphorus, sodium, potassium, chloride, bile acids, amylase, lipase, and pancreatic-specific amylase. Clinical chemical analytes were measured on a Hitachi Model 704 Chemistry Analyzer. Serum globulin concentration was calculated from the total protein and albumin concentrations. Urine was analyzed for volume (approximately 16 hours overnight), specific gravity, pH, protein, glucose, ketones, bilirubin, blood, urobilinogen, microscopic examination o f sediment, and general appearance. Determination o f serum and liver PFOA content Approximately 2 ml o f whole blood (for serum) were collected from the femoral vein o f non-fasted animals during week 2 and every two weeks thereafter. A section o f liver was collected at sacrifice from each animal, weighed, flash frozen in liquid nitrogen, and stored at -6 0 to -8 0 degrees C until shipped on dry ice to 3M for analysis. Sera and liver samples were anlalyzed for PFOA content by 3M methodology (refs). Concurrent with blood collections for PFOA determination, at least 2 ml o f urine was collected on wet ice and at least 5 g o f feces (overnight) were collected from each animal. Results o f urine and fecal analysis will be discussed in a future paper. A natom ic pathology. After 26 weeks o f treatment, four animals in the control, low and mid-dose groups, and the five surviving animals in the high-dose group were fasted overnight, anesthetized with ketamine and xylazine, weighed, exsanguinated, necropsied. Similarity the two animals in the control and mid-dose recovery groups were sacrified 13 weeks following the last dose. Necropsies were also performed on the low-dose and high-dose animals that had unscheduled sacrifices on treatment days 137 and 29, respectively. The adrenals, brain, epididymides, kidneys, liver, pancreas, testes and thyroids with parathyroid were collected and weighed. Organ to body weight and organ to brain weight ratios were calculated. The following tissues were collected for microscopic evaluation: adrenal; aorta; brain; cecum; colon; duodenum; epididymus; esophagus; eyes; femur; gall bladder; heart; ileum; jejunum; kidney; lesions; lung; mammary gland; mesenteric lymph node; pancreas; pituitary; prostate; rectum; salivary gland (mandibular); sciatic nerve; seminal D R A FT July 28, 2000 EID101459 000 i}- Page 7 John L. ButenhofF, et al. DRAFT 11/20/00 vesicles; skeletal muscle (thigh); skin; spinal cord; spleen; sternum with bone marrow; stomach; testes; and thyroid; trachea; and, urinary bladder. Tissues were embedded in paraffin, stained with hematoxylin and eosin and examined by light microscopy. Palmitoyl CoA oxidase determinations. Samples o f the right lateral lobe o f the livers from each animal at scheduled and unscheduled sacrifices were flash-frozen in liquid nitrogen at necropsy and analyzed for palmitoyl CoA oxidase activity (need C liffs method here). Cell proliferation determinations. Representative samples o f the left lateral lobe o f the liver, left and right testes and pancreas were collected from each animal. After fixation^formalin or zinc formalin), samples were embedded in paraffin,and sections stained with hemotoxylin and eosin were prepared. Previously described methods were used to stain tissues for PCNA (Eldridge et a l, 1993). B ile acid determination. Bile (up to 5 ml) was collected at sacrifice o f each animal, flash frozen in liquid nitrogen and analyzed for specific bile acids (insert C liff s methods) Statistics. Levene's test (Levene, 1960) was used for variance homogeneity. In the case o f heterogeneity o f variance at p < 0.05, transformations were used to stabilize the variance. One-way analysis o f variance (ANOVA, Winer 1971a) was used to analyze initial body weights, body weight changes, continuous clinical pathology values, and organ weight data. ANOVA was done on the homogeneous or transformed data. If the ANOVA was significant, Dunnett's t-test (Dunnett, 1964) was used for control versus treated group comparisons. One-way analysis o f variance (ANCOVA, Winer, 1971b) was used to analyze body weights, with initial body weights as the covariate. Although Levene's test for variance homogeneity was done, no transformations were used because covariance adjustment removed extraneous heterogeneity. If the ANCOVA was significant, covariate-adjusted means were used for control versus treated group comparisons. Dosed groups were compared to the controls at the 5% two-tailed probability level. Blood hormone levels were compared by ANCOVA with significance at the p=0.05 level. For CCK, all data were analyzed using Jonckheere's test for trend {p < 0.05). RESULTS Clinical observations. During the first week o f dosing, all animals in the 30 mg/kg dose group had qualitatively low food consumption and and lost from 3.1 to 7.5 percent o f D R AFT July 28, 2000 EID101460 OOO&tff- Page 8 John L. B utenhoff, et al. DRAFT 11/20/00 body weight. Four o f the six animals also had few or no feces. Dosing was suspended on Day 12 and recommenced at 20 mg/kg/day on day 22. Only two animals were continuously treated at the 20 mg/kg/day dose for the remainder o f the dosing period. Dosing o f the other three high-dose animals was discontinued on Days 43, 66 and 81. These animals exhibited low or no food consumption, few or no feces, and dramatic body-weight losses prior to being suspended from dosing. Bodyweight losses were 17.5, 23.1 and 18.7 percent prior to suspension o f dosing on days 43, 66 and 81, respectively. The remaining high-dose animal was sacrified in moribund condition on day 29. This animal had lost 12.5 percent o f body weight, was hypoactive, cold to the touch, exhibited low or no food consumption, and few or no feces. There was a lack o f opthalmic effects in all animals. Overall, body-weight losses in the 30/20 mg/kg dose group were significantly lower than controls (14.3 percent over the 27 week period). Dosing at 30 mg/kg during the first two weeks caused considerable weight loss. After commencing the 20 mg/kg/day dosing on day 22, weight loss was significant compared to controls during weeks 7, 9 and 24 (Table 1). Clinical signs and body-weights were normal in monkeys receiving 10 mg/kg and all but one monkey receiving 3 mg/kgc. However, one low-dose animal was sacrificed in mroibund condition on day 137. In this one animal, paralysis o f the hind limbs and ataxia occurred as well as few feces and low or no food consumption and loss o f 9.5 percent of body weight in the week prior to sacrifice. B lood homone determinations. No effects on estrone, estradiol, estriol or testosterone were noted. Mean group estradiol values in all groups including the controls tended to be considerably lower dutring the treatment period than the corresponding pretreament values. In the high-dose animals these values appeared to be lower than the other groups. The estradiol values in the recovery animals tended to be similar to the predose values. No significant changes in testosterone values were seen during the treatment period. In the last recovery sampling, mean values (9 and 15 ng/ml) tended to be higher than means during the rest o f the study (1-8 ng/ml). Taken collectively, values for the thyroid hormones in APFO-treated monkeys appeared to be unaffected. With total and free T3, mean values from test day - 4 through to the end o f the study remained relatively constant; although, monkeys in the high-dose group exhibited generally lower group mean values. It should be pointed out that values on pretest days - 8 and -18 were considerably higher than those during the rest o f the study. Group mean total T3 values are shown in Figure 1, page 56). During the treatment period, the three high-dose animals that were eventually taken o ff compound for toxicity tended to have decreasing T3 values prior to removal from treatment. These values tended to increase toward pre-study values after cessation o f treatment. Figures 2 (page DRAFT July 28, 2000 EID101461 000, Page 9 John L. B utenhoff, et al. DRAFT 11/20/00 57) and 3 (page 60) represent the individual trends in Total T3 for the control and highdose groups, respectively. No statistically significant or biologically significant alterations in plasma CCK concentrations were observed. Clinical pathology. Administration o f APFO at 3 or 10 mg/kg produced no apparent effects on measured clinical parameters including hematology, coagulation, clinical chemistry, and urinanalysis. The 3 mg/kg dose group animal that was sacrifced in moribund condition on day 137 showed marked hyperfibrogenemia, moderate lymphopenia, moderate hypoalbuminemia and mild hypocholesterolemia. Findings in the 30/20 mg/kg dose group were complicated by the unscheduled sacrifice o f one animal on day 29 and the cessation o f treatment for three others by day 80. Only two animals remained on treatment during clinical pathology tesing intervals on days 91 and 182. In this group, mild increases in triglycerides and mild to marked decreases in absolute neutrophile count, total protein concentration, and albumin concentration occurred. The differences in triglycerides were statistically significant on days 31 and 91, The other differences were not statistically significant but were consistent over time. Absolute neutrophile count and albumin concentration were mildly decreased prior to cessation o f treatment for the three animals for which treatment was stopped early. One monkey at this dose had moderate increases in serum activities o f aspartate aminotransferase, alanine aminotransferase and creatine kinase when dosing was stopped on day 66 and moderate increases in serum bile acids on day 63. The high-dose dose group animal which was sacrificed in moribund condition on day 29 had numerous non specific clinical pathology findings commonly observed in animals that are very ill along with marked serum activities o f aspartate aminotransferase , alanine aminotransferase, sorbitol dehydrogenase and creatine kinase as well as unusually low cholesterol (14 mg/dL). Eleven days prior to initiation o f treatment (day -1 1 ), the animal in the low-dose group which was sacrificed in moribund condition had a high hematocrit (49.7%) and albumin concentration (5.6 g/dL), possibly indicative o f mild dehydration, and it had the lowest neutrophil count (1,600/pL) o f all animals. PFOA levels in Serum and Liver. Steady-state values for PFOA in the serum were attained within 4 to 6 weeks o f dosing. In the 3 mg/kg group, this value was approximately 1lOppm and in the 10 mg/kg group it was 1OOppm. Although difficult to determine because o f discontinuous treatment, peak values were highly variable and averages o f around 150 to lOOOppm were seen in animals receiving 30/20 mg/kg. It is apparent that the relationship between APFO administered and APFO in the serum is not linear (Table X) EID101462 D R AFT July 28, 2000 0 4.n - <V>'fJc v- vT- P age 10 John L. ButenhofF, ct al. DRAFT 11/20/00 Amounts o f APFO in monkey liver averaged 14 to 16 ppm in the 2 lower dose groups (Table Y).In the higher group the values for the 2 monkeys which continued through the entire treatment period were 17 and 87 ppm. In animals from this group that were removed from dosing, liver concentration o f from 0.2 to 1.5ppm were obtained. In the 2 mid-dose recovery monkeys, APFO concentrations in the liver went from a mean o f 14 ppm to 0.1 and 0.3 ppm respectively. Preliminary data from urine analysis for PFOA suggests that most PFOA is excreted in the urine. This will be presented in a future manuscript. Palm itoyl CoA determinations. There ^reincrehsfcs'nver control inpidinitoyliGoA oxadase^adtreity. Cell proliferation results. There were no significant differences in cell proliferation observed in liver, pancreas or testes as measured by PCNA. Anatom ic Pathology. Increases occurred in mean absolute liver weights and mean liverto-body weight percentages in all dose groups at terminal sacrifice after 26 weeks o f dosing (Table Z). Liver weight increases showed a positive dose-response trend. The low-dose and mid-dose animals group mean absolute and relative liver weights were similar and significantly elevated over control values. The two high-dose animals that were treated until the end o f the dosing period had absolute and relative liver weights which were significantly elevated over the other treatment groups and control. No APFO-related macroscopic or microscopic changes were observed in any organs at the terminal sacrifice. This includes key organs such as the liver, adrenal, spleen, pancreas and testis. At the recovery sacrifice o f the 10 mg/kg animals, there were no effects on terminal body weight, there were no macroscopic or microscopic findings, and liver weights were normal. Table Z: Absolute and relative liver and body weights at scheduled dosing termination. Dose group, Body weight Liver weight % Control L wgt/B wgt % Control mg/kg (n) (g) 0 Control (4) 3947 591 (g) 60.16 6.93 100 (%) 1.53 0 .0 7 100 3(3) 4486 30 81.79 2.81 135 1.82 0 .0 5 119 10(4) 4447 498 83.17 9 .6 6 138 1.87 0 .0 6 122 30/20 (2) 3925 583 90.39 4 .2 2 150 2.40 0.51 157 Two animals were found in moribund condition and sacrificed at unscheduled times during the dosing period. A 30/20 mg/kg animal was sacrificed on day 29 and found to have edema and inflammation o f the esophagus and stomach indicative o f dosing injury. This animal also had liver lesions, including mid-zonal and centrilobular hepatocellular EID101463 D R A FT July 28, 2000 000 00 P age 11 John L. B utenhoff, et al. DRAFT 11/20/00 degeneration and necrosis, diffuse hepatocellular vacuolation, and hepatocyte basophilia in centrilobular areas indicative o f liver regeneration. Involution o f the thymus, a common stress response, and degeneration and necrosis o f the heart, probably agonal changes, were also observed in this animal. Although the esophageal and gastric lesions are complicating factors, the contribution o f APFO to this animals moribund condition cannot be dismissed due to findings in the liver, which were likely due to APFO exposure. A 3 mg/kg animal was found in moribund condition with hind-limb paralysis and ataxia and sacrificed on day 137. The blood supply to this animals hind limbs was severely compromised, as indicated by the cool temperature o f the hind limbs on final medical examination and the fact that ketamine injected into the thigh muscle failed to reach the systemic circulation. The microscopic and macroscopic findings did not reveal evidence o f spinal cord injury or impaired blood circulation. DISCUSSION Quality o f the study (GK) Dose-level selection (PL) High-dose unscheduled sacrifice (JB) High-dose cessation o f dosing (JB) Liver findings (JB) Sex hormones (GK) Thyroid hormones (JB) Recovery story (PL) Mechanistic endpoints (PcoAO, PCNA, CCK, bile acids) (GK) Pharmacokinetics (PL) LOEL / NOEL (GK) Low-dose death (GK) Relate to rhesus study (JB) Relate to rodent story (PL) Relate to human story (JB) CONCLUSIONS D R AFT July 28, 2000 EID101464 ooo-;. Page 12 John L. ButenhofT, et al. DRAFT 11/20/00 Resource material for discussion follows: These findings were non-specific and, with the exception o f low albumin concentration, were not consistent with the findings observed for animals in the high-dose group that were withdrawn from treatment. Therefore, the clinical pathology results for this lowdose animal were not assumed to be due to APFO exposure. There are no known metabolic processes that degrade PFOA. The urinary elimination of PFOA in rats appears to be hormonally regulated (refs). Female rats and castrated male rats rapidly clear PFOA in the urine; whereas, male rats have a significantly longer urinary clearance half-life (refs). Sex differences in urinary clearance have not been found in [species] (ref). PFOA is excreted in the bile and enters enterohepatic circulation (Johnson, J.D. et al. 1980; Johnson, J.D., et al., 1984). Follow-up on blood levels in retired workers indicated that, although the concentrations detected were in the few ppm range, the chemical was present in some individuals well after the possibility o f exposure had ceased, suggesting an elimination half-life on the order o f 18 months (Ubel, 1980). A recent study o f 3M retired chemical plant workers suggests that the mean serum elimination half life is approximately 300 days (Burris et al, 2000). Liver tumors The finding o f liver enlargement in male cynomolgous monkeys at all doses in this study is significant in ligt o f prior information available from a 90-day oral gavage study in male and female rhesus monkeys. The rhesus study was conducted with APFO (FC-143, Lot 340) in male and female rhesus monkeys at doses o f 0 (control), 3, 10, 30 and 100 mg/kg/day in 0.5% Methocel.. Unfortunately, all animals in the 100 mg/kg/d group and 3 o f 4 animals in the 30 mg/kg/d group died. No treatment related gross pathological lesions or alterations in urinalysis values were seen. Significant effects (and LOELs in mg/kg/day) included: weight loss (30); anorexia (10); emesis (30); black stools (10); pale, swollen face (10), swollen eyes(30); decreased activity (30); prostration and trembling (100); anemia (30), slightly increased prothrombin and activated partial thromboplastin times (30), decreased serum alkaline phosphatase activity (30); increased serum aspartate aminotransferase (SGOT) activity (30); increased serum creatinine phosphokinase (CPK) activity (30); diffuse lipid depletion o f the adrenals (30), bone marrow hypocellularity (30), splenic and lymph node follicular atrophy (30). The NOAEL for this study was 3 mg/kg/d (ref). Subsequent analysis o f serum and liver samples showed dose-related FC143 concentrations. There was no apparent difference in serum or liver FC-143 levels between males and females (ref). Testosterone inhibits urinary elimination o f PFOA in male rats. It has been suggested that the gender difference in elimination may be due to a testosterone inducible serum or tissue protein which binds PFOA [48], D R A FT July 28, 2000 E ID 1 0 1 4 6 5 P age 13 John L. B utenhoff, et al. DRAFT 11/20/00 No changes in liver weight to body weight ratios were seen in female rats given single oral doses o f up to 200 mg PFOA/kg. In male rats, single oral doses o f either 100 or 200 mg PFOA/kg produced an increase in relative liver weight. Castration reduced the magnitude o f the liver weight increase [13]. Estradiol treatment o f castrated or intact male rats produced PFOA excretion rates similar to those in females. Castration without estradiol treatment also enhanced PFOA excretion but not as effectively as estradiol treatment [51]. PFOA induced hepatomegaly, peroxisomal P-oxidation, microsomal 1acylglycerophosphocoline acyltransferase and cytosolic long-chain acyl CoA hydrolase in male rats to a much greater extent than in female rats. Testosterone was shown to be necessary for these effects and estradiol blocked these effects in male rats [53]. Activities o f liver microsomal 1-acylglycerophosphocholine acyltransferase (AGA), microsomal stearoyl-CoA desaturase (SD) and peroxisomal P-oxidation and the acyl composition o f liver microsomal phosphatidylcholine (PC) were measured in rats fed a diet containing 0.01 % PFOA for 2 ,2 2 or 26 weeks. Females showed only slight changes in these parameters. In males, activities for all three enzymes were elevated by two weeks. Activities o f AGA and p-oxidation remained unchanged throughout 26 weeks. The activity o f SD declined but was still higher than controls at 26 weeks. The acyl composition o f microsomal PC was significantly altered in males. All o f these parameters returned to control levels within 4 weeks after PFOA was withdrawn from the diet [72], PFOA in the diet o f mice at a concentration o f 0.02-0.05% for 5-10 days caused increased hepatic peroxisomal fatty acid p-oxidation, decreased hepatic mitochondrial size and increases in the following hepatic enzyme activities: to-hydroxylation o f lauric acid and cytosolic epoxide hydrolase, glutathione transferase and DT-diaphorase. There were no significant differences between males and females [85]. PFOA has been shown to induce hepatic peroxisomal proliferation in rats and mice There was a marked sex difference in rats [38, 53, 54, 58, 83]. PFOA-induced hepatic peroxisomal proliferation in male rats is most prevalent in the centrilobular region and is associated with increased peroxisomal palmitoyl-CoA oxidation, marked hypolipidemia, an almost 10-fold increase in hepatic free acid soluble CoA, and altered peroxisomal polypeptides [83]. Perfluorooctane, CgFu, did not induce peroxisomal proliferation in rats, indicating the importance o f the carboxylic acid group in causing this effect [54], PFOA caused peroxisomal proliferation in primary cultures o f rat hepatocytes. PFOAmediated increases in the peroxisomal enzyme fatty acyl-CoA P-oxidase (FACO) were inhibited by cycloheximide and correlated with elevations in FACO mRNA levels. Thus, EID101466 D R AFT July 28, 2000 P age 14 John L. Butenhoff, et al. DRAFT 11/20/00 PFOA appears to induce peroxisomal proliferation through the regulation o f gene transcriptional and translational processes [69]. PFOA-induced hepatomegaly is due predominantly to cell hypertrophy resulting from proliferation o f smooth endoplasmic reticulum, mitochondria and peroxisomes [38]. PFOA-induced DNA synthesis (hyperplasia) has also been shown to occur in rat liver, primarily in the periportal region. Increased DNA synthesis occurred in the absence o f necrosis, suggesting that the cell proliferative activity is not a regenerative response to hepatocellular injury. Peroxisome proliferation occurred primarily in the centrilobular region suggesting that PFOA-induced hyperplasia and peroxisomal proliferation are independent processes[73]. PFOA in the diet o f male mice at concentrations o f 0.02 to 0.1 % for 2-10 days caused decreased body weight and the following hepatic effects: hepatomegaly, decreased mitochondrial size, increased microsomal P450, P450 reductase and epoxide hydrolase, increased cytosolic epoxide hydrolase and DT-diaphorase, and decreased mitochondrial lipid peroxidation. Hepatic microsomal,b5and cytosolic glutathione transferase, glutathione peroxidase and superoxide dismutase were not significantly affected [84]. Hepatomegaly, but not peroxisome proliferation, caused by PFOA in rats was shown to be dependent on corticosterone, the primary adrenal glucocorticoid in rodents [73]. Unlike many hepatocarcinogenic peroxisome proliferators, PFOA did not cause hypolipidemia. Rather, PFOA caused a marked increase in hepatic lipid synthesis [38]. Dietary treatment o f male rats with PFOA (0.02% for 7-14 days) caused decreased serum cholesterol and triacylglycerols and increased liver free cholesterol. Hepatocytes isolated from treated rats showed reduced synthesis o f cholesterol from acetate, pyruvate and hydroxymethylglutarate but not from mevalonate, increased oxidation o f palmitate and reduced fatty acid synthesis. Activities o f liver hydroxymethyl glutaric acid-CoA reductase and acyl-CoA:cholesterol acyltransferase were reduced [82]. PFOA in the diet o f mice for up to 10 days caused greater increases in liver weight, hepatic mitochondrial protein, hepatic peroxisomal palmitoyl-CoA oxidation, lauroyl CoA oxidase activity and catalase activity than did perfluoroacetic, -butyric or decanoic acids. PFOA increased peroxisomal fatty acid (3-oxidation (which produces H202) to a much greater extent than catalase (which reduces H202to water and molecular oxygen). Dietary levels o f PFOA as low as 0.001 % caused significant changes[61], PFOA caused enhanced affinity and reduced maximal binding capacity o f hepatic inositol triphosphate (ITP) receptors in male rats. ITP is a second messenger involved in the mobilization o f calcium from intracellular stores and may be involved in the process o f peroxisomal proliferation [74]. EID101467 D R AFT July 28, 2000 P age 15 John L. Butenhoff, et al. DRAFT 11/20/00 Valproate (2-propylpentanoic acid), a non-fluorinated analog o f PFOA, is a hepatotoxin which impairs mitochondrial function and fatty acid metabolism [97], Induction o f peroxisomes by treatment with PFOA did not increase rates o f hydrogen peroxide production in rat or mouse liver [12]. Oxidative stress resulting from the increased production o f hydrogen peroxide has been postulated as a mechanism by which peroxisome proliferators cause liver damage and cancer. PFOA induced hepatic microsomal carboxylesterase isozymes in male rats [106]. PFOA (5-dimethylaminonapthalenesulfphonyl)-undecanoic acid (DAUDA) from L-FABP was m easili^'nn'//?0`asMij'5ercent'QoSs-ofifutial;fltlOTesceiice. 10 pfr^F@&<igttsed%4% reductiSfrof initial fluorescence When added to solutions containing 1 4iMiT>FMJF4and 1pM DAUDA. The LOEL for PFOA in this assay was 0.5 -1 .0 pM . By comparison, 10 ' p.M o f th e known or suspected peroxisome proliferators: perfluorooctane sulfonic acid (PFOS), iWyeth, N-Ethyl perfluorooctanesulfonamide (F X -12) and N E thylp^uoro(^tane;nnlfonam ide ethanol (N-`EtFO SE)oaused:6i% v48% >j4S^>and:39% reducfron^fdnitialflU orescenW jM respectively.-T lesultsforB E A -w erevery^iiinlarlo^hose seen w ith L-FABP [1 0 9 ,122]. The serum concentration at which this liver enlargement occurred (approx. 50 ppm) is within the range experienced by workers with higher exposures. Studies in exposed workers have not indicated liver toxicity. However, the enlargement at the low dose in the cynomolgus monkey was not associated with any clinical manisfestations o f liver toxicity; therefore, it is not possible to know if workers with similar body burdens, as represented by serum concentration, experience similar liver enlargement. Pancreatic tumors The absence o f an increase in cholecystokinin is also also significant in light o f Cook et al.'s findings in rats (ref). This may indicate a decreased risk o f pancreatic tumors in primates. It is also important to point out that CCKA receptors are distributed differently in the rodent as oppsed to humans and primates (ref), [comment on CCKAreceptor agonism] PFOA has been asssociated with elevated CCK levels and pancreatic tumors. PFOA did not bind directly to the CCKAreceptor in a competition binding assay, and did not inhibit trypsin in vitro, thus two possible contributing mechanisms for pancreatic carcinogeneis were ruled out [111]. Leydig cell tum ors EID101468 D R AFT July 28, 2000 C O O c.j. ; Page 16 John L. Butenhoff, et al. DRAFT 11/20/00 In the male rat, estradiol is elevated and testoterone decreased on repeated exposure. The absence o f this effect in the present study and in studies o f workers suggests that the primate is not responsive to the hormonal changes seen in the rat. Since these changes are thought to occur in the rat via induction o f aromatase and are related to the formation o f Leydig cell tumors in the rat, the risk o f testicular tumors in primates from exposure to APFO is assumed to be much lower than that in the rat. In fact, the spontaneous incidence o f Leydig cell tumors in rats is orders o f magnitude higher than in the humans (insert detail and refs). The historical incidence o f Leydig cell tumors in Sprague-Dawley rats ranges from 1.4 to 10% with a mean o f 4.7% [60]. The incidence o f Leydig cell tumors in man is estimated to be less than 0.0003%. A number o f chemical agents, nutritional and hormonal factors have been shown to cause Leydig cell tumors in rodents. However, where there have been studies on the same chemicals in man, there appears to be no evidence o f Leydig cell tumor formation in man [50]. Elevated estrogen levels have been associated with Leydig cell tumors in mice, rats and humans [91,95,96]. Serum estradiol levels were significantly elevated in rats treated with PFOA at doses o f more than 10 mg/kg/d and accessory sex organ relative weights were significantly reduced in rats fed 50 mg/kg/d PFOA for 14 days. In addition, serum testosterone levels showed a dose-dependent decrease which was, however, not statistically significant. This decrease in testosterone levels was shown, by human chorionic gonadotropin (cHG) challenge, to be associated with inhibition o f steroidogenesis in Leydig cells [10] The increase in serum estrogen caused by PFOA appears to be due to induction o f the enzyme aromatase (Cytochrome P450 XIX) which metabolizes testosterone to estradiol. A two-fold increase in serum estradiol showed a linear correlation with a 16-fold increase in total hepatic aromatase activity [57, 118]. PFOA caused a dose-dependent decrease in hCG stimulated testosterone secretion and also reduced the basal release o f estradiol by rat Leydig cells exposed in vitro, suggesting that PFOA may have a direct effect on the ability o f Leydig cells to produce testosterone and estradiol [55,119]. In contrast, ex-vivo studies demonstrate an increase in testosterone production in hCG-stimulated Leydig cells from rats treated with 25 mg/kg/day APFO for 14 days, indicating that the direct inhibition o f testosterone synthesis seen in-vitro is reversible in-vivo. Furthermore, in the in vivo studies serum estradiol and testicular interstitial fluid estradiol and transforming growth factor alpha (TGF alpha) levels were also increased, consistent with the hypothesis that estradiol may modulate growth factor expression within the testis. APFO produced a 4.5 fold increase in hepatic aromatase invivo, suggested as the primary cause o f increased serum estradiol [120]. PFOA at 300 ppm in the diet for 1 year in male rats caused increased serum estradiol levels, increased hepatic p-oxidation (peroxisome proliferation) and increased relative D R AFT July 28, 2000 EID101469 Page 17 John L. B u ten h o ff, et al. DRAFT 11/20/00 liver weights. PFOA had no effect on hepatic or Leydig cell proliferation, Leydig cell poxidation, or serum testosterone, FSH, prolactin or luteinizing hormone concentrations. Thus, PFOA did not induce peroxisome proliferation in Leydig cells at dietary levels which did induce hepatic peroxisome proliferation [56]. The lack o f peroxisome proliferation seen in this study in not unexpected. Primates are less responsive to peroxisome proliferation from xenobiotic compounds than rodents, partially due to the fact that primates have much fewer PPARa receptors than rodents. Since the hepatocelluar tumors observed in rats with APFO are thought to derive from peroxisome proliferation and the pleiomorphic response from activation o f PPARa, the risk o f these tumors occuring in primates is considered low. Waxman et al (1999) have studied the effects o f PFOA on transactivation o f PPARa and PPARy in COS-1 cells transfected with mouse and human PPARa and PPARy receptors. Human PPARa was less sensitive to PFOA than mouse PPARa. Human and mouse PPARy were non-responsive to PFOA. Thyroid hormones All T4 values were within the range published for Rhesus monkeys o f 0.8 - 6.6 ug/mL for males, and 1.3 .-7.6 ug/mL for females (DePaolo and Masaro. 1989). Taken together, the data suggest that the changes in T4 values observed appear to be systemic trends that are not compound related and not biologically significant. All T3 values were within the reference range for male and female Macaques (54 -115 ng/lOOml and 65- 295 ng/100 ml for males and females, respectively (DePaolo and Masaro 1989). Cell proliferation discussion M embrane Effects: At sub-lethal concentrations, PFOA did not alter the expression or secretion o f IgM from cultured human or mouse B cells. At lethal concentrations (> 0.8 mM), PFOA caused a detergent-like solubilization o f membrane proteins. The authors have suggested that some o f the biochemical changes and target organ effects observed in vivo with PFOA may be secondary to cell lysis [92], PFOA caused lipid peroxidation in vitro [80]. PFOA and other perfluorinated surfactants cause alterations in the fatty acid composition, organization and fluidity o f cell membranes [62,92,93,94]. EID101470 D RAFT July 28, 2000 00 9 P age 18 John L. Butenhoff, et al. DRAFT 11/20/00 At sub-lethal concentrations, PFOA did not affect migration or capping o f cell surface immunoglobulins after antigen recognition in lymphoblastoid cells in vitro. However, PFOA (0.9 mM for 15 min) did cause changes in membrane lipid architecture. It was suggested that direct, physical disruption o f cell surface membranes is the likely mechanism o f acute PFOA toxicity [93]. Sodium perfluorooctanoate had a much higher affinity for dipalmatoylphosphatidylcholine vesicle membranes than did the corresponding nonfluorinated compound, sodium octanoate. This difference was attributed to the greater hydrophobicity o f the fluorinated acid [compound [94]. PFOA did not inhibit cell-to-cell communication in cultures o f freshly isolated or established (ARL) rat liver cells as did PFDA [76]. PFOA uncoupled (ED50= 0.18 mM) and at higher concentrations inhibited rat mitochondrial oxidative phosphorylation in vitro. The authors hypothesized that uncoupling o f mitochondrial oxidative phosphorylation by PFOA in vivo would lead to . reduced cellular ATP levels and elevated intracellular unsaturated fatty acids which would activate protein kinase c leading to increased cell turnover which is believed to be involved in the carcinogenic process for nongenotoxic carcinogens [67]. PFOA (100 pM) exhibited a general detergent-like effect on mitochondrial membranes as reelected by a decrease in respiratory control without uncoupling oxidative phosphorylation in-vitro. FC-143 slightly increased the activity o f enzymes o f oxidative phosphorylation and respiratory chain, the most probable mechanism being the fluidisation o f the inner mitochondrial membrane [121]. PFOA at concentrations up to 500 pg/ml did not impair clone-forming ability in L5178Y mouse lymphoma cells in vitro [77]. DRAFT July 28, 2000 EID101471 GOO^Y P age 19 John L. B utenhoff, et al. 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Synthesis and Characterization o f FC-95-uC. Project No. 8900310200, Riker Laboratories, Inc., St. Paul, MN. Johnson, J.D., Gibson, S.J. and Ober, R.E. 1979. Extent and route o f excretion and tissue, distribution o f total carbon-14 in rats after a single i.v. dose o f FC-95-uC. Project No. 8900310200, Riker Laboratories, Inc., St. Paul, MN. Johnson, J.D., Gibson, S.J. and Ober, R.E. 1980. Enhanced elimination o f FC.-95-14C and FC-143-14C in rats with cholestyramine treatment. Project No. 8900310200, Riker Laboratories, Inc., St. Paul, MN. Johnson, J.D., Gibson, S.J. and Ober, R.E. 1984. Cholestramine-enhanced fecal elimination o f carbon-14 in rats after administration o f ammonium [14C]perfluorooctanoate or potassium [14C]perfluorooctanesulfonate. Fund. Appl. Toxicol. 4, 972-976. Just W. W., Gorgas K., Hartl F-U., Heinemann P., Salzer M. and Schimassek H. 1989. 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July 13 1999. 26-week Capsule Toxicity Study with Perfluorooctane Sulfonic Acid Potassium Salt (TFOA-.T-62951 in Cvnomologus Monkeys - Draft Pathological Report (Ancilliarv Study) Electron Microscopic Evaluation o f Liver in Cvnomoloeus Monkeys. Client Number 6329-223 PAI Study Number EM 99.76. Pathology Associates International, Durham NC. Nold, J.B. May 30,2000. 26-week Capsule Toxicity Study with Perfluorooctane Sulfonic Acid Potassium Salt (PFOA:T-6295i in Cvnomoloeus Monkeys - Draft Pathological Report (Ancilliarv Study') Electron Microscopic Evaluation o f Liver in Cvnomoloeus Monkeys (Recover Animals). Client Number 6329-223 PAI Study Number EM 99.76. Pathology Associates International, Durham NC. O'Conner J.C., Frame, S.C., Biegel L.B. Cook J.C. and Davis L.G. Sensitivity o f a Tier 1 screening battery compared to an in-utero exposure for detecting the estrogen receptor agonist 17 p-estradiol. Tox. Sci. 44, 1 6 9 - 184,1998. Olsen G.W., Burris J.M., Mandel J.H., Zobel L.R. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. JOEM 41:799-805. Reimers J.R. 1999. Hormones. In: The C lin ical C h em istry o f L a b o ra to ry Anim als. S eco n d edition . Eds.: Loeb W.F and Quimby F. W. pp 455-499, Philadelphia PA. Taylor and Frances. Smith, D.R. 1998. Animal models: Nutrition and lipoprotein metabolism. C urrent O pin ion in L ipidology. 9:3-6. Turley, S.D., Spady D.K., and Dietschy J.M. 1995. Role o f liver in the synthesis o f cholesterol and the clearance o f low density lipoproteins in the Cynomolgus monkey Journal o f Lipid Research. 36:67-79. Wagner, J.D., Zhang, L., and Adams, M.R. 1997. Effect o f estrogens on arterial LDL metabolism. In H orm onal, m etabolic, a n d cellu lar influences on ca rd io va scu la r d isea se in w om en. Ed. T.L. Forte, pp 153-174. New York: Futura Publishing Co. Wallace K. B. and Starkov A. 1998. The effect o f perfluorinated arylalkylsulfonamides on bioenergetics o f rat liver mitochondria. Dept o f Biochemistry and Molecular Biology, University o f MN School o f Medicine. Duluth, MN 55812, USA. Supported by a grant from 3M Company. EID101496 DRAFT July 28, 2000 00 9 L Page 44 27 Pathology Associates International A C om pany o f Science Applications International Corporation CorscSfiy Pathology Associates Int'l 15 Worman's Mill Court Suite 1 Frederick, MD 21701 September 29, 2000 Dr. Peter J. Thomford, Ph.D. Covance Laboratories Inc. 3301 Kinsman Blvd. Madison WI 53704 Dear Dr.Thomford, Enclosed please find a copy of the Draft Cell Proliferation Report for the Study identified below: 26-Week Capsule Toxicity Study with Ammonium Perfluorooctanoate (APFO) in Cynomolgus Monkeys Covance Study Number 6329-231 Sincerely, Kim Claggett Research Assistant Cell Kinetics Division 301-624-2917 Enclosure Covance Laboratories Madison, W! COT 0 2 2000 Received # 1 5 S D _______________ S T J y f n / i :u A y sc addl. oist. TOX FILE 15 W orm an's Mill Court. Suite I Frederick, M aryland 21701 (301) 663-1644 * (301) 663-8994 FAX Pathology Associates International A Company of Science Applications International Corporation An Employee-Owned Company DRAFT CELL PROLIFERATION REPORT 26-WEEK CAPSULE TOXICITY STUDY WITH AMMONIUM PERFLUOROOCTANOATE (APFO) IN CYNOMOLGUS MONKEYS COVANCE STUDY NUMBER 6329-231 PREPARED FOR: 3M TOXICOLOGY SERVICES BUILDING 220-2E-02, 3M CENTER ST. PAUL, MN 55144-1000 PREPARED BY: PATHOLOGY ASSOCIATES INTERNATIONAL 15 W ORM AN'S MILL COURT, SUITE I FREDERICK, MD 21701 SEPTEMBER 26, 2000 IS Worman's Mill Court, Suite I * Frederick, Maryland 21701 * (301) 663-1644 * (301) 663-8994 FAX 0 0 0 -.V ' % TABLE OF CONTENTS Report Narrative Tables Figures Individuai Animal Histopathology Findings Signature Page Quality Assurance Statement Section I II III IV V VI 0 0 0 * . . , 'ri 3M Covance Study No. 6329-231 Draft Cell Proliferation Report Page 1-1 CELL PROLIFERATION REPORT FOR: 26-WEEK CAPSULE TOXICITY STUDY WITH AMMONIUM PERFLUOROOCTANOATE (APFO) IN CYNOMOLGUS MONKEYS COVANCE STUDY NUMBER 6329-231 INTRODUCTION The purpose o f the study was to assess the effect o f the test material on critical enzyme levels, hormones, and other selected biochemical parameters when administered daily by capsule to cynomolgus monkeys for at least 26 weeks. This report, submitted by Pathology Associates International (PAI) to the study Sponsor, 3M Toxicology Services, represents the cell proliferation findings and interpretation for Covance Study Number 6329-231 entitled " 26-Week Capsule Toxicity Study with Ammonium Perfluorooctanoate In Cynomolgus Monkeys" . REGULATORY COMPLIANCE All aspects o f the tasks associated with PAI's portion o f this study were conducted in compliance with the Environmental Protection Agency Good Laboratory Practice (GLP) Regulations as set forth in Title 40 o f the US Code o f Federal Regulations, Part 792, issued November 29, 1983(effective December 29, 1983), and with any applicable amendments. MATERIALS AND METHODS Experimental Design Treatment Group 1 (Control) 2 (Low-dose) 3 (Mid-dose) 4 (High-dose) Dose Level (mg/kg/day) 0 3 10 30 Number o f Animals Main Study Recovery 42 40 42 42 All animals (main study and recovery) were treated for up to 26 weeks. Two animals in groups l, 3 and 4 were designated as recovery animals. Treatment in these animals was discontinued and the Sponsor determined the recovery period. 3M Covance Study No. 6329-231 Draft Cell Proliferation Report Page 1-2 Tissue Collection for Ceil Proliferation Representative samples o f the left lateral lobe of the liver, left and right testes, and pancreas from each o f the 22 animals was fixed and processed to paraffin block by Covance per protocol specifications. Tissue blocks were shipped to PAI for sectioning and staining. From each block, slides were prepared for H&E evaluation and immunohistochemical detection o f proliferating cell nuclear antigen (PCNA), a marker o f cell proliferation. Immunohistochemistry for Cell Proliferation Sections o f paraffin-embedded tissues were cut = 5 pm and placed on positively charged slides (Superfrost Plus, Fisher Scientific, Pittsburgh, PA) to ensure adhesion during processing for PCNA. Standard immunohistochemical methods for PCNA (Eldridge, et al., 1993) were used to stain tissues. Briefly, tissue sections were incubated with a monoclonal antibody to PCNA ( Lot # 107 Exp. 11/00 DAKO, Carpinteria, CA) and reagents required for the avidin-biotin peroxidase (MslgG Kit Lot# PK6102 Exp. 4/22/00, Vector, Burlingame, CA) method for the detection o f the antigen-antibody complex. PCNA expression in cells in all phases o f the cell cycle (G l, S, G2 and M) was localized by the chromagen 3,3'-diaminobenzidine (DAB Lot# 108H8210 Exp. 8/20/01; Sigma Chemical Co., St. Louis, MO). Tissue sections were counterstained with hematoxylin. Cell Proliferation Measurements Positive staining for PCNA was categorized based on cellular distribution and intensity o f the brown to black reaction product that correlated with the different phases o f the cell cycle (Eldridge et al., 1993). Uniform, dark brown to black nuclear staining was judged to be positive for S phase cells. A cell in the G, phase o f the cell cycle had diffuse, stippled nuclear staining that was lighter than a cell in S phase. Cells in the G2 phase exhibited distinct, diffuse cytoplasmic stippling with or without nuclear staining. Mitotic figures were conspicuous with diffuse cytoplasmic stippling. A negative control slide was included in the staining run and consisted o f study tissue (animal no. 105709) that was not incubated with the primary antibody. For cell proliferation evaluations, slides were first perused at low magnification (100X) to judge quality o f staining, processing and sectioning, pattern o f cell labeling (e.g., centrilobular or panlobular, extrahepatocellular proliferation, such as Kupffer cells, bile duct epithelium, endothelium), and histomorphologic changes. The later was further assessed by evaluating the serial H&E slide for each animal evaluated for cell proliferation. Cell proliferation was then quantified at higher magnification (200X) as described above. For cell proliferation measurements in the liver, the percentage o f dark, nuclear-stained hepatocytes that represent cells in S-phase was determined by scoring at least 3000 hepatocytes in 10 randomly selected fields per animal. Cell proliferation within islet and exocrine cells o f the pancreas was scored subjectively with 3 = exocrine stained greater than islets, and 4 = islets and exocrine stained heavily as determined by positive PCNA staining. The entire tissue section 000>.-/ 3M Covancc Study No. 6329-231 Draft Cell Proliferation Report Page 1-3 represented on the slide was perused at 100X and 400X. For measuring cell proliferation in the testes, the section farthest from the slide label was scored. The percentage o f PCNA-labeled Leydig cells was determined by scoring at least 100 Leydig cells in the entire section that was examined. Statistical Analysis Due to the small samples sizes within main study and recovery groups, and because not all animals within a treatment group were sacrificed on the same day, statistical analysis was not performed on cell proliferation data. RESULTS Cell Proliferation Individual animal cell proliferation data are presented in Section II (Table II-1) and graphically in Figures III-l - 3. Clearly, cell proliferation was not increased by treatment in the pancreas or testes o f monkeys as determined by examining the scatter plots in Section II, Figures III-2 and III-3. In the liver, however, there did appear to be an enhancement o f cell proliferation in the highest dose tested (30 mg/kg/day) as revealed in Section II, Figure (III -1). Data points 6, 8, 9 and 10 (30 mg/kg/day; animals 105704,105713,105711,105722, and 105703, respectively) were greater than or equal to the highest control value (data point 1; animal 105714). The lowest dose tested (data point 3; 3 mg/kg/day), however, had one animal (animal 105706) with a labeling index that exceeded all animals examined. Thus, an apparent increase in cell proliferation was not necessarily dose-related. Histopathology Sections from the same tissue blocks used for preparation o f PCNA-stained slides were stained with hematoxylin and eosin (H&E) for histopathologic evaluation to facilitate the interpretation o f the immunostained slides. Individual animal findings are presented in Section IV. Representative sections o f liver, pancreas and testes from 22 monkeys were evaluated histologically. Each tissue section was stained with hematoxylin and eosin. The purpose o f this evaluation was to determine whether or not morphologic changes were occurring in these tissues that may alter or confound the specificity o f the PCNA staining observed in these animals. The results showed that no significant changes that would alter the interpretation o f the PCNA staining in this study were observed in the liver, pancreas or testes from male monkeys. Although chronic inflammation was reported for several animals, it was minimal in severity and occurred across all groups. Furthermore, the PCNA labeling index did not correlate with the observation o f inflammation in the liver. For example, inflammation was not observed in the animal with the highest liver labeling index (animal 105706). Numerous findings were reported for animal 105724 that included hypertrophy, inflammation, fat infiltration and possibly bacterial 3M Covance Study No. 6329-231 Draft Cell Proliferation Report Page 1-4 colonization. Based on the substantial non-specific PCNA staining observed in the liver o f this animal, clearly these lesions confounded the ability to measure hepatocellular proliferation; therefore, no attempt was made to evaluate the PCNA labeling index in animal 105724. DISCUSSION In the present study, cell proliferation was measured within the liver, pancreas and testes o f male monkeys from control and treated groups after up to 26 weeks on study, as well as a recovery period. An increase in cell proliferation, as determined by the PCNA labeling index, was not observed in the pancreas or testes o f male monkeys. Cell proliferation in the liver, however, was equivocal. SUMMARY After up to 26 weeks on study, enhanced cell proliferation was not evident in the pancreas or testes o f male monkeys, whereas in the liver the findings were equivocal. LITERATURE CITED Eldridge, S.R., Butterworth, B.E., Goldsworthy, T.L. (1993). Proliferating cell nuclear antigen: a marker for hepatocellular proliferation in rodents. Environ. H ealth P erspec. 101:211-218. II. TABLES eoo TABLE 11-1. CELL PROLIFERATION IN MONKEYS 3M Covance Study No. 6329-231 Page 11-1 Dose Group 0 mg/kg/day (Control) 0 mg/kg/day (Control) 0 mg/kg/day (Control) 0 mg/kg/day (Control) 0 mg/kg/day (Control) 0 mg/kg/day (Control) 3 mg/kg/day (Low dose) 3 mg/kg/day (Low dose) 3 mg/kg/day (Low dose) 3 mg/kg/day (Low dose) 10 mg/kg/day (Mid dose) 10 mg/kg/day (Mid dose) 10 mg/kg/day (Mid dose) 10 mg/kg/day (Mid dose) 10 mg/kg/day (Mid dose) 10 mg/kg/day (Mid dose) 30 mg/kg/day (High dose) 30 mg/kg/day (High dose) 30 mg/kg/day (High dose) 30 mg/kg/day (High dose) 30 mg/kg/day (High dose) 30 mg/kg/day (High dose) Day of Death 26 Weeks 26 Weeks 26 Weeks 26 Weeks Recovery animal Recovery animal 26 Weeks 26 Weeks 26 Weeks Sacrificed week 20 26 Weeks 26 Weeks 26 Weeks 26 Weeks Recovery animal Recovery animal 26 Weeks 26 Weeks Sacrificed day 29 Stopped dosing week 7; Sacrificed week 27 Stopped dosing week 10; Sacrificed week 27 Stopped dosing week 12; Sacrificed week 27 Animal Number IO5709 105714 105715 105725 105718 IO5720 IO5702 IO5706 105717 105721 IO5707 IO5708 105710 105719 105712 105716 IO5704 105713 105724 105711 I05722 IO5703 Labeling Index Liver 0.025% 0.075% 0.000% 0.074% 0.025% 0.000% 0.000% 0.170% 0.099% 0.000% 0.075% 0.050% 0.024% 0.025% 0.073% 0.000% 0.100% 0.075% ND 0.126% Labeling Index Pancreas 3 3 3 4 3 3 4 3 3 NP 3 3 3 3 3 4 3 4 3 4 Labeling Index Testes 22.86% 11.00% 14.91% 27.00% 41.51% 23.42% 10.58% 21.78% 22.77% 13.00% 15.53% 17.14% 17.92% 35.17% 18.81% 10.89% 10.78% 15.84% 16.35% 21.70% 0.149% 3 14.29% 0.075% 3 20.19% Skip slide=negative control; animal no. IO5709 ND, not determined due to too much non-specific staining NP. tissue not present on slide O Liver; Only dark nuclear stained hepatocytes scored as S-phase; 200X 3 Pancreas: Scored subjectively with 4=islets and exocrine stained heavily (>50% labeled); 3=exocrine stained greater than islets; perused at 100X and 400X .P Testes; Section farthest from slide label scored; Leydig cells scored at 400X III. FIGURES Legend for data points on Figures III-l - 3 Group 1 2 3 4 5 6 7 8 9 10 Treatment 0 mg/kg/day 0 mg/kg/day 3 mg/kg/day 10 mg/kg/day 10 mg/kg/day 30 mg/kg/day 30 mg/kg/day 30 mg/kg/day 30 mg/kg/day 30 mg/kg/day Day of Death 26 weeks Recovery animal 26 weeks 26 weeks Recovery animal 26 weeks Sacrificed day 29 Stopped dosing day 43 Stopped dosing day 66 Stopped dosing day 81 3M Covance Study No. 6329-231 Page 111-1 OO 3M IV. INDIVIDUAL ANIMAL HISTOPATHOLOGY FINDINGS Individual Animal Findings 3M Covance Study No. 6329-23 1 Page IV-1 26-WEEK CAPSULE TOXICITY STUDY WITH AMMONIUM PERFLUOROOCTANOATE (APFO) IN CYNOMOLGUS M ONKEYS A N IM A L NUM BER SEX D O SE GROUP H ISTO LO G IC FIN D IN G S 105709 105714 105715 105725 105718 105720 105702 105706 105717 105721 M M M M M M M M M M 1 Liver - chronic inflammation, minimal Pancreas - autolysis, focal Testes - crush artifact Spleen - NSF 1 Liver - chronic inflammation, minimal Pancreas - NSF Testes - NSF Spleen - NSF 1 Liver - NSF Pancreas - NSF Testes - NSF Spleen - NSF 1 Liver - NSF Pancreas - NSF Testes - NSF Spleen - NSF 1 Liver - NSF Pancreas - NSF Testes - crush artifacts Spleen - NSF 1 Liver - NSF Pancreas - NSF Testes - NSF Spleen - NSF 2 Liver - NSF Pancreas - NSF Testes - NSF Spleen - hemosiderin deposition, mild 2 Liver - NSF Pancreas - NSF Testes - NSF Spleen - NSF 2 Liver - NSF Pancreas - NSF Testes - crush artifact Spleen - NSF 2 Liver - chronic inflammation, minimal Pancreas - NSF Testes - NSF Spleen - NSF Legend: NSF = no significant findings 000 Individual Animal Findings 3M Covance Study No. 6329-231 Page IV-1 26-WEEK CAPSULE TOXICITY STUDY WITH AMMONIUM PERFLUOROOCTANOATE (APFO) IN CYNOMOLGUS MONKEYS ANIMAL NUMBER SEX DOSE GROUP HISTOLOGIC FINDINGS 105707 105708 105710 105712 105716 105719 M M M M M M 3 Liver - NSF Pancreas - NSF Testes - NSF Spleen - hemosiderin deposition, minimal 3 Liver - NSF Pancreas - NSF Testes - NSF Spleen - NSF 3 Liver - NSF Pancreas - NSF Testes - NSF Spleen - NSF 3 Liver - chronic inflammation, minimal Pancreas - NSF Testes - NSF Spleen - NSF 3 Liver - NSF Pancreas - NSF Testes - NSF Spleen - NSF 3 Liver - NSF Pancreas - NSF Testes - NSF 105703 105704 105711 M M M 105713 M 4 Liver - NSF Pancreas - NSF Testes - NSF Spleen - NSF 4 Liver - chronic inflammation, minimal Pancreas - NSF Testes - NSF Spleen - hemosiderin, minimal 4 Liver - chronic inflammation, minimal - hemosiderin, minimal Pancreas - NSF Testes - NSF Spleen - NSF 4 Liver - chronic inflammation, minimal Pancreas - NSF Testes - NSF Spleen - NSF L egend: N SF = no significant findings Individual Animal Findings 3M Covance Study No. 6329-231 Page IV -1 26-WEEK CAPSULE TOXICITY STUDY WITH AMMONIUM PERFLUOROOCTANOATE (APFO) IN CYNOMOLGUS MONKEYS ANIMAL NUMBER SEX DOSE GROUP HISTOLOGIC FINDINGS 105722 105724 M M 4 Liver - hemosiderin, minimal Pancreas - NSF Testes - NSF Spleen - NSF 4 Liver - periportal, fat infiltration, severe periportal, cellular hypertrophy, severe periportal, chronic inflammation,moderate midzonal, necrosis, moderate to severe centrilobular, fat infiltration, severe centrilobular, cellular hypertrophy, severe random distribution, bacterial colonies??? Pancreas - islets, fat infiltration, mild to moderate Testes - NSF Spleen - NSF L egend: N SF = no significant findings V. SIGNATURE PAGE Submitted by: Project Manager: Sandra R. Eldridge, Ph.D. Project Pathologist: Date Carolyn Moyer, D.V.M., Diplomate, A.C.V.P. Date VI. QUALITY ASSURANCE STATEMENT Pat h o l o g y Associates International A Compary o f Science Applications International Corporation AnSmeieiH+OmyuCcrrony C ell Proliferation R eport 26-W eek C apsule T oxicity Study W ith A m m onium Perfluorooctanoate (A P F O ) in C ynom olgus M o n k ey s Covance Study Number: 6329-228 Q UALITY ASSURANCE STA TEM EN T This cell proliferation project has been inspected and audited by the PAI Quality Assurance Unit (QAU) as required by the Good Laboratory Practice (GLP) regulations promulgated by the U.S. Environmental Protection Agency. The cell proliferation report is an accurate reflection of the recorded data. The following table is a record of the inspections/audits performed and reported by the QAU. Date of Inspection 10/25/99 09/06,07/00 09/06,07,25/00 Phase Inspected Date Findings Reported to PAI Management/Proiect Manager PCNA Dilutions/Staining Study Data and Supporting Documentation Draft Cell Proliferation Report 10/25/99 09/07/00 09/07/00 a Dorarne Dundee Quality Assurance Auditor .<*5. 0iOQ^> 7 Date *7 000-- 15 W orm an's Mill Court, Suite I Frederick, Maryland 21701 (301) 6 6 3 -1 6 4 4 (301) 663-8994 FAX APPENDIX I 000 PROTOCOL DEVIATION REPORT Date: September 28, 2000 Study Number: Covance Study No. 6329-231 Title: 26-Week Capsule Toxicity Study with Ammonium Perfluorooctanoate In Cynomolgus Monkeys Protocol Deviation #1: Representative samples of liver, testes and pancreas were to be collected for cell proliferation evaluation, which included preparation of an H&E slide for correlative morphologic interpretation of the cell proliferation findings. Samples of spleen were inadvertently submitted to PAI and the H&E slide examined for this tissue. Reason: Spleen was inadvertently submitted. The H&E slide was inadvertently evaluated microscopically and the histologic findings reported. This deviation had no impact on the study. Submitted by: Sandra R. Eldridge, Ph.D. PAI Project Manager Sandra R. Eldridge PAI Project Manager Date 128 L*Ca| LP Mg- o4 /ng - o c /VvJ- oq l?rv 31 IW > Il .H aj i a/A oev e<o lp 0OI oTLT L-EACWAT $T*E+* X ffctfECTV a*4HiV mo- i3 MM- 0 J*G ^X q.q ir 0TW*. ORBITE Mito U>iK wu A jii 2.H S i t e o e w t x i k Trfc LOG 3 U>G- ZIZ ..Q L.f 33 /> Cz n II I. o Z. o , * V o . l.X / o filA ASI IOI()|56 EID103018 C00.5*r V InJASH-WG-T/O WokS iqnjirn C-% SamPujug- Results " / l L e t a t Lc l T ? L A ^ n r' ui_ l 0<6 E r - --i / t ICO i/ P P F il Pc -'j D '--30 A no-G 30 qqc / .: - i 'ilv - 1 ZGO a 1-: e c o 5 ^ re f e.-v- : r ' .'' .uL/ i l ___ >r- ` f..'-: , T L C 'P -r ! 1-0 0 / ; r* tJ A Poe P- e L ZG M i- 0(d - o9 ( : - 0 9 A^C z z J5 S JiG oo ] C,r. P&o S3 5 'O C 2ooo a. o M8-0 "?tn l Ll II Aj ) -P U < vT C ;p r' , .S i [M il EE ! ,`J L : ^^ U/TS1 Lof(_( p-f(.P .0 M AJA JZ.ss~ q , ) M f E . W l P*T4 f o f'L .'1/-J-T G l T C 4_(_< ^ /' .'il-.' i ' i M ie - l i G 5fi?F-M X C-TR--, r r '-- e .* i r e IF;-C M ^7 Ml'J- ' i M Li ' 3- Ve - 2 4 M- - G \ M v j ' !2 -*- : . C - C 'Lf' PlLL IW ri A) ! 0 4G 11- CG <u ajO 'V e , r- *-* A v .' o- vi. Il 33 6G l.o aJ v 15 I. e ---i ^ f c o f w r v Bcok^ y to c e p z 0 .5 . 2. 0 Z - s -" > v: X EID103019 0 0 0 .-.- r-; C - 9 QF F S I T E SAM PLIN G 3 /1 3 /8 7 3 /1 2 /8 8 1 1 / 2 /8 8 3 / 7 /8 9 LUBECK BUSINESS TAP LPSO HOME TAP - P LPSO HOME TAP - P LPSD HOME TAP - P <2 > 3 /2 3 /9 1 3 /2 9 /9 1 8 / 8 /9 1 LPSO HOME TAP -M LPSD HOME TAP - C LPSD HOME TAP -M W W W pf pfrfllfI__ I__ 1 I- i- I I <- j < * I > ` ` ` 1 -- 1- t_ I-- -- 1- -L- - 1 - 1 * I 3 /1 3 /8 7 3 /1 3 /8 7 3 /1 2 /8 8 U IEM sW HOME TA P -M L IT T L E HOCKING B U S IN E S S TAP L IT T L E HOCKING HOME T A P -R L 1 1 1 1- 1- I I -i- t L I I t l t 1 I1 i 1 1 /2 8 /9 0 8 / 3 /9 1 LUBECK PRIVIATE WELLS ( 2 ) LUBECK PR IVA TE WELLS < 2 ) Q z jm 1 .9 , 2.2 1 .4 0 .7 1 .9 3 .8 3 .8 3 .9 < 0.6 <0.6 < 0.6 <0.6,<0.6 <1.0 , <1.0 6 /2 3 /9 1 ( ) NEW LUBECK WELL C H 2M H ILL CONFIRMED "PRESENCE* OF C -8 2 .4 ( * ) ASI 1010161 EID103Q20 C-8 HUMAN EXPOSURE; L IM IT S TLU (3M ) AEL (DUPONT) CEG ( A I R , W ATER) u G /M 3 100 10 HASKELL ESTABLISHED: uG C -8 PER 2 4 HOURS 90% BY A I R ................. 6 . 4 u G / 2 0 M 3 0 . 3 2 OR O ^ u G /M 3 20% BY WATER ........... 1 . 6 u G / 2 L 0 . 8 0 OR 1 PPB O U TS ID E CONTRACT LAB! CH 2M H ILL 2 3 M AUTH TO PROVIDE 0 ^ 1 PPB C - 8 IN WATER 4 *W L Y S IS ASI K) 10 162 EID103021 000^/0 C-9 SAMPLING (MARCH - JUNE 19fl<n L O C A T IO N PKSBG-HOME TAP WW-DRINK f t n D I S T . CTR-WELL WASHINGTON-STORE TAP LUBECK-STORE TAP L . HOCKING-STORE TAP B E L L E V IL L E -P R IV A T E WELL REED SVILLE-STO R E TAP RAVENSWOOD-STORE TAP RA CINE-STORE TAP PO INT PLEASANT-STORE TAP G A LLIPO LIS-STO R E TAPC*) 0 1STANCE ( M I L E S ^ 7 . 3 UPSTREAM -- 0 . 2 3 DOt+4 0 . 2 5 DOLN 0 . 2 5 DOWN 3 DOMM 1 2 DOWN 1 4 DOUfsi 29 D O m 50 D O m 7 4 DOWN 7 9 DOWN C-B PPfiiO.4 L I N T T < < < 1 . 2 , 1 .0 1 .3 0 9 1 0 a 6 < < < < < < ( * ) NEAREST C O hfiU N ITY TO TAKE WATER D IR E C T L Y FROM O H I O R I V E R . ASI IO10163 EID103022 C - 8 ON S I TE S A P L I N G TEST W ILL 2 7 6 / 4/Q 7 3 /1 1 /8 8 1 1 / 4 /8 8 3 / 4 /8 9 8 / 1 /8 9 1 0 /2 4 /8 9 2 /2 7 /9 0 4 /2 0 /9 0 7 /1 3 /9 0 8 / 9 /9 0 1 0 /1 9 /9 0 R EVISED TEST 1 /1 3 /9 1 4 /1 8 /9 1 7 /2 4 /9 1 8 / 2 /9 1 ADJACENT M ELL:M 4-4 3 /1 3 /9 1 8 / 1 /9 1 H 4 D R IN K IN G MATER 3 /1 3 /8 7 1 1 / 2 /8 8 1 3 /1 2 /8 * 3 / 8 /8 8L0Q 3 8L08 212 8L03 212 BLD<3 2 1 2 c-a ppa 2.0 1.5 1 .3 <0.6 1 .3 1 .3 1 .3 1 .3 1.6 <10 <10 2.9 3.0 3.9 3.0 1.3 1.4 < 0.6 < 0.6 < 0.6 < 0.6 (3.0) (3.0) ASM0I0I64 EID 103023 000  Robert L Ritchey 09/14/2000 03:52 PM To: cc: Subject H Oavid Ramsey/A/OuPont@DuPont George Woytowich/CL/DuPontDuPorrt, Andrew S Hartten/AE/DuPont@DuPont (bcc: Robert L Ritchey/CL/DuPont) GE sampling results Spoke with Dale Van de Velde at GE this afternoon. He got his FC-143 results back a few days ago from their August 15,2000 sampling of drinking water wells. Weil #3 analyzed at .707 ug/l. Well #4 analyzed at .275 ug/l. Well #3 is closest to us. He estimated #4 to be 600-700 feet further downriver. He believes they pump about 50% from each well, which would be consistent with the earlier composite result at a site tap. He asked if we had seen numbers as high as the .707 ug/l and I pointed out to him that in the TSCA material we sent to EPA, which he has a copy of, we discuss a .8 ug/l result on a Lubeck well and a .965 ug/l modeled result in the river. We briefly discussed influences such as river flow, distance downriver, and test accuracy. He indicated that they plan to continue to sample periodically. RLR003302 EID103379 tiuyv*.? v- flT T A C H m e AJT 13 0 )s TSC C L c AJ Ct>3 Dt o OO 0 0 / 4 A io s - n + Z .ec/ V e r s i t vy ou a.s p ro vi aieoi. 131 m -o q< I I <"= A.: _ - J _ C = 0 A N I C 5 A N A L / S I S D A T A S H E E T C L I E N T 5 A N P L N _ao Name =ACIFIC ANALYTICAL, Tj t " l X LATER larrj i e j : / v j 1 1 0 0 0 0 0 0 ml O::cin:ra:50 Extract Volume: Im jectvon volume: 1 ul INC. 1000 ul '1om p o .n : Samp 1e Cone u g /L Lab Samp 1e ID. Lab File ID: Date Sampieb: Date Extracted: Date Analyzed: Time Analyzed: ITDL ug /L sur r j rt3: : sr , 3 j - r I u o -o octan o ic Acid c =t? 0. 1 7 2 7 0. 1187 s t 'i V - Undetected J D = Dilution Resulte na = C om o ou n j na s no ~0L = R~acti:al Quan Estimated Concentration B = Found in E = Result Exceeds Calibration Curve correspond ing labeled reference tacion Limit Sian* 1 0 0 0 T 2568 3 ; - = a C _a S_ C=Oa n ICS ANAL / S I S DATA SHEET C L I E N T AH.= _ ,v ~ _a: Nji 'a "r ; x :3"C i ; =aCI,-IC ANALYTICAL/ INC. 1 1000 COO .Hi Extract Volume. vslum: 1 u I 1000 ul Samp 1e Cone :po ug/L Ferricprpjccanoic Acid Esce 0 1205 Lab Sample ID Lap File ID Dace Sampled Date Extracted Date Analyzed Time Analyzed. MDL ug/L 0. 1137 01 ft TR0 4 26/0 0 1- AQ - = Underacted J = Estimated Concentration B * Found m D = Oilucion Results E = Result Exceeds Calibration Curve *U 4J mp our d has no corresponding labeled reference race: cal Quanitation Limit 3 Ia r,< *u T 2578 132 The Arizona Republic, April 29, 1990 Page 23 FOCUS for faster computers. * Carborundum Co., Niagara Falls, N.Y., opened a plant in Phoenix last year to develop ceramic materials and products for microelectronic compenents. The company makes silicon carbide, aluminum nitride and boron nitride, which are all used as insulators and heat dissipaters for semiconductor chips. * W.L. Gore & Associates Inc., based in Delaware, has teams in Flagstaff and Phoenix still finding uses for a substance patented in 1937: Teflon. Gore researchers in Flagstaff work on new medical products, such as liners for casts, synthetic blood vessels and artificial ligaments. Researchers there and in Phoenix work on electronic products such as cables to detect leaks in buried fuel tanks. * Hexcel Corp., San Francisco, has been making lightweight structural materials since 1986 in Casa Grande. Its composite, honeycomb-textured materials lighten many aircraft and cushioned the first manned landing on the moon. GRAPHIC: Photo LANGUAGE: ENGLISH UMI-ACC-NO: 9021645 LOAD-DATE: June 10, 1994 LEXIS'- NEXIS' LEXIS'-NEXIS' LEXIS'-NEXIS' Page 3 321ST STORY of Level 1 printed in FULL format. Copyright 1986 UMI Inc.; Copyright Manning Publications Inc 1986; Business Dateline; Vermont Business January, 1986 SECTION: Sec 1; pg 24 LENGTH: 1749 words HEADLINE: Grand Isle's One Manufacturer a One-of-a-Kind BYLINE : Michele Patenaude DATELINE: South Hero; VT; US BODY: There is only one manufacturer in the entire county of Grand Isle -- Phoenix Wire Inc. Not only is the firm unique in its county, but it is also one-of-a-kind in the world, according to company officials. "We do only one thing," says Horace Corbin, the firm's president, "we insulate wire with Teflon." The company's claim to fame is not in insulating wire with Teflon. Many companies do that. Phoenix insulates the tiniest wires in the world. Called micro miniature wires, some of them are several times finer than a human hair. Single strands can be virtually invisible. They were to Tom Parizo, Phoenix's vice president and product engineer, until he started wearing glasses six months ago. "Product quality has improved tremendously since I got them," he jokes. These tiny wires may end up in such extraordinary places as the inside of a human brain or an instrument panel on the space shuttle. The combination of small size and Teflon coating makes them ideal in applications involving medicine and electronics. In most cases the wire makes a long and complicated journey from its origins at Phoenix to its final home in a piece of equipment, so Corbin is not sure where it all ends up. But NASA is a regular customer and so are medical establishments famous around the world. He does know for sure that it is used in cardiac catheters (tubes), pacemakers, probes and sutures. Teflon, a DuPont trade name for polytetrafluoethelene or PTFE, has some unique properties that make it especially appropriate for use inside the body. Chemically, it is inert; it doesn't react to other substances such as body tissues and fluids, which makes it one of the safest materials available for implantation in the body. Also, because Teflon can be applied to wire in extremely thin layers, it is LEXIS-NEXIS Vermont Business, January, 1986 Page 4 ideal for use in miniaturized electronics. And it's one of the best of all materials for electrical insulation. The most obvious property of Teflon -- one known to anyone familiar with a modern kitchen -- is that nothing sticks to it. For that reason some of Phoenix's product is used in such "low tech" operations as cookie cutting, chocolate cutting and the cutting of plastic bags. Phoenix Wire is a small company. Only five full-time and two part-time employees work on the South Hero side street in a building as small and unassuming as its products. Except for listings in Thomas' Register and the Yellow Pages, advertising is a word-of-mouth affair. Ohmer Corbin, Horace's cousin and the firm's sales manager, says a recent phone call he received is indicative of how that works. An Irish doctor called to place an order for some wire he had been shown by a Spanish doctor at a conference in Isreal. The wire had been coated at Phoenix. Customers call from as far away as France, India and Japan, and as nearby as the University of Vermont 20 miles south. All the work is done on a custom basis. The customer ships the wire to Phoenix, where it is coated to the specified thickness and color, and then shipped back to the customer. Horace and Ohmer Corbin, as well as Tom Parizo, live within five miles of the business. That, probably more than any other factor, is the reason for the plant's location on Station Road in South Hero. Because they all love living near the water- and the boating and fishing it affords, Grand Isle's Lake Champlain environs offer them a perfect place to live and work. And much to their delight they have discovered that being off the beaten path helps keep salespeople from beating a path to the company door. The firm maintains a profile so low they'd have to camouflage the building to make it any harder to find. Conspicuously absent is any kind of an identifying sign. The location, while convenient for the principals, is not a critical concern for the business. Production requires little space, few resources and shipping is done through United Parcel Service. "Our product is a lightweight, high-value product," says Horace Corbin, "We could be anywhere we wanted." That fact has led Parizo to suggest they put the whole operation into a large trailer truck and drive south to Florida as the winter approaches and the lake begins to freeze over. Eight miles wide and more than 30 gently rolling miles long, Grand Isle County is the state's smallest. Located in the northwestern corner of Vermont and comprised mostly of islands, it is known for its beauty, its shoreline, its farms and apple orchards. Tourists and cows form the bedrock of its economy and undoubtedly will for a long time to come. Parizo, a native of the county, would like to see more light industry there to broaden the tax base. Present development in the county is primarily residential. Parizo explains that houses, and the families they bring to the community, consume more in services than the taxes they put into the coffers. "To have a good economic system you have to have a balance between residential, commercial and industrial. LE X IS -N E X IS LEXIS'-NEX1S' Vermont Business, January, 1986 Page 5 Rebecca Kaiser agrees with him. As the executive director of the Grand Isle County Development Corporation (GICDC), she would also like to see more light industry in the county. GICDC is a two-year-old, nonprofit organization, one of 12 Vermont development corporations, and is supported by public and private funds. Its board of directors are resident volunteers and its mission is to provide more jobs for the community. Presently the GICDC is developing a couple of sites as potential locations for manufacturing concerns. A recently completed countywide survey indicates residents are opposed to heavy industry being located there, but are more favorable to light industry. Kaiser says the survey results show "residents generally support an expansion of the tax base and the generation of more local jobs." Ironically, for a county surrounded by water, water is the major obstacle to industrial development -- both getting it and getting rid of it. The area's clay soil is a poor one for septic leaching. And although water can be pumped in from the lake to shoreside sites, away from shore water must be drilled for, and even then it is often found to be contaminated with sulfur. Water is not a probelm for Phoenix Wire because so little is used in the production process. In that process, called "dispersion coating," wire is drawn through a milky looking liquid which is actually a Teflon and water suspension. The wire then travels through an oven which bakes the coating on. The process is repeated over and over until the required thickness of insulation is reached. Most other types of wire are insulated with polyvinyl chloride or polyethylene using an extrusion process. Unlike Teflon dispersion coating, this process does not ensure uniform thickness of insulation around the wire. It is also more prone to pinholes because the coating is a single layer rather than the multi-layers of the Teflon process. The only major disadvantage of Teflon as a wire insulator is that it is soft and subject to abrasion. Sometimes a layer of a harder material is applied over the Teflon to solve this problem. Over the years, Phoenix has developed its methods and equipment to perform the operation efficiently. The company owns six complex machines, each of which very slowly feeds the wire from the spools through the Teflon suspension into an over and then back on the spools again. Production continues around the clock from Monday morning until Thursday afternoon. Three-day weekends and long summer vacations are the rule at Phoenix Wire. (Nobody here is overworked," says Horace Corbin.) It's for benefits such as these that the company policy is to stay small. Corbin says the demand for small wires is growing and he intends for the company to keep pace and grow to meet the demand. But expanding into other areas is definitely not in the picture. The headaches and problems that go with a large business are something he has every intention of avoiding, after experiencing them himself. At one time the business employed 350. That was before a fire destroyed it in January of 1969. At that time the company was known as Thermal Wire, and besides coating wire of all types, the company was also a sub-contractor for electronic sub-assemblies. IBM was a major customer. LEXIS-NEXIS' Vermont Business, January, 1986 Page 6 It all began in 1956 when Horace Corbin got out of the service and decided to start his own business. His initial inclination was toward hardware or boating supplies, but a friend convinced him of the profits to be found in wire. Parizo and cousin Ohmer came in on it almost from the beginning. The business was indeed profitable and it grew. It was housed in a large modern plant only a short distance away from the present Phoenix Wire location. Then came the fire. At about the same time IBM phased out the product for which Thermal was making the subassemblies. In December after the fire the company resumed operation in an unscathed Thermal warehouse which is the present site. The business was renamed Phoenix after the mythological bird that burned itself on a furneral pyre and rose up anew from the ashes. It was at this time a deliberate decision was made to keep the business small. Teflon dispersion wire coating, only a small fraction of what had been Thermal's business, was chosen to be the sole business of Phoenix because it was both profitable and required few employees. "With 350 people you've got 350 problems," Corbin says of the decision. "We're much happier doing it this way." It was a good choice for many reasons, not just the personal preferences of the principals. The large wire companies that had been coating miniature wires began to drop out to concentrate on other aspects of the wire business that, for them, were more profitable and did not require extensive employee training. (Corbin says it takes a minimum of two years to properly train an operator.) Eventually Phoenix was the only one left. And so customers from all over the world who need the tiny Teflon insulated wires must do business with Grand Isle's one and only manufacturer. "We'll do anything we can to help a customer develop a product," says Horace Corbin, "however we don't have the philosophy that the customer is always right. We've been in this business long enough to know our wire is good wire, we know what can and can not be done. We're independent Vermonters. If they push us too far we'll tell them to go someplace else." The question is -- where? LANGUAGE: ENGLISH UMI-ACC-NO: 8602610 LOAD-DATE: October 9, 1995 LEXIS-NEXIS LEXIS-NEXIS 000s\ LEXIS-NEXIS )33 G00&35 / V -J FOR IN THE UNITED STATES DISTRICT CO)U lf THE SOUTHERN DISTRICT OF WEST VE lGJf f i y y'The or'9in31washiedm PARKERSBURG DIVISION fBeXTerk's Office at Charleston on WILBUR EARL TENNANT, ERWIN JACKSON TENNANT, JAMES DAVID TENNANT, DELLA MARIE TENNANT, and SANDRA K. TENNANT, Plaintiffs, V. OCT2 I 099 i :' ami i"' K y, CLE3K U S D: irLi. ' Souf' nrn Disrr'ct n` CIVIL ACTION NO. 6:99-0488 E.I. DUPONT DE NEMOURS & CO., INC., Defendant. SECOND AMENDED COMPLAINT Now come plaintiffs Wilbur Earl Tennant, Erwin Jackson Tennant, James David Tennant, Della Marie Tennant and Sandra K. Tennant ("Plaintiffs") and state as follows for their Second Amended Complaint against defendant E.I. DuPontde Nemours&Co., Inc. ("DuPont") herein; NATURE OF ACTION 1. This is a civil action for declaratory, injunctive, and equitable relief, monetary damages, and response costs incurred and to be incurred by Plaintiffs for bodily injury and property damage to Plaintiffs and their property arising from the acts and/or omissions of DuPont during the ownership and/or operation of DuPont's Dry Run Landfill in Wood County, West Virginia, defined herein as the "Site" under the authority of; (i) the Comprehensive Environmental Response, etseq:,Compensation and Liability Act of 1980, as amended ("CERCLA"), 42 U.S.C. 9601 (ii) etseq:,the Federal Declaratory Judgment Act, 28 U.S.C. 2201 (iii) the Resource Conservation etseq:,and Recovery Act of 1976, as amended ("RCRA"), 42 U.S.C. 6901 the Clean Water Act, as amended ("CWA"), 33 U.S.C. 1251 et seq:, (v) the West Virginia Hazardous Waste 009 Management Act fthe "Waste Act"), W Va. Code 22-18-1 et seq.\ and (vi) principles of common law. JURISDICTION AND VENUF. 2. This Court has jurisdiction over this action pursuant to: 28 U.S.C. 133 1, 1332. 1367, 2201. and 2202, Sections 107 and 113 of CERCLA 42 U.S.C. 9607 and 9613, Section 7002(a) of RCRA, 42 U.S.C. 6972(a); and Section 505(a) of CWA, 33 U.S.C. 1365(a). 3. This Court has pendant and ancillary/supplemental jurisdiction over Plaintiffs' claims arising under state statutory and federal and state common law. 4. Venue is proper in this District pursuant to 28 U.S.C. 1391(b); Sections 107 and 113 o f CERCLA, 42 U.S.C. 9607 and 9613; Section 7002(a) o f RCRA, 42 U.S.C. 6972(a); and Section 505(c) of CWA 33 U.S.C. 1365(c), because the discharge, disposal and/or release of solid, toxic and/or hazardous wastes, substances, pollutants, and/or contaminants that gives rise to these claims occurred and/or is occurring in this District, because the real property that is the subject of this action is located within this District, and because a substantial part of the events or omissions giving rise to these claims occurred and continues to occur within this District. PARTIES 5 Plaintiff Wilbur Earl Tennant is an individual residing at Route 3, Box 17, Washington. Wood County, West Virginia 26181. 6. Plaintiff Erwin Jackson Tennant is an individual residing at Route 3, Box 17A. Washington, Wood County, West Virginia 26181. 7, Plaintiff James David Tennant is an individual residing at Route 3, Box 372. Parkersburg, W'ood County, West Virginia 26101 9 000 3. Plaintiff Della Marie Tennant is an individual residing at Route 3. Box 3" 2. Parkersburg, Wood County, West Virginia 26101. 9. Plaintiff Sandra K.. Tennant is an individual residing at Route 3. Box 17. Washington. Wood County. West Virginia 26181, 10. Defendant E.I. DuPont de Nemours ("DuPont") is a Delaware corporation authorized to conduct business in the State of West Virginia and has a principal place of business at 1007 Market Street, Wilmington. Delaware 19898. GENERAL ALLEGATIONS 11. Since approximately 1982, DuPont has owned and/or operated a facility known as the E.I. DuPont Dry Run Landfill located adjacent to Route No. 68 in the Harris District o f Wood County, West Virginia, near the town of Lubeck, which facility is referred to herein as the "Site" and identified generally for illustrative purposes only as the "Site" on Exhibit A to Plaintiffs' First Amended Complaint. 12. During DuPont's ownership and/or operation of the Site, DuPont has disposed of one or more solid, toxic, and/or hazardous wastes, substances, pollutants, and/or contaminants at the Site, including but limited to, asbestos, fly ash, bottom ash, boiler ash, coal ash, filter cake sludges, polyamides, acrylics, polyacetai, polyvinyl butyrai, polyethylene terephthalate, fluropolymers, paraffin wax, sludges from DuPont's Washington Works plant, filter aids, construction dirt, paper, cardboard, glass, scrap piping and metals, and railroad ties. 13. During DuPont's ownership and/or operation o f the Site, DuPont has failed to compact wastes appropriately at the Site. J 000 a N. 'vj, 14 During its ownership and/or operation of the Site, DuPont has failed to adequate!-, control fugitive dust at the Site. 15. During its ownership and/or operation of the Site. DuPont has failed to maintain adequate slopes of its landfill surface areas at the Site. 16. During its ownership and/or operation of the Site. DuPont has failed to properly control stormwater runoff at the Site. 17. During its ownership and/or operation at the Site, DuPont has failed to adequate!;, control landfill leachate and runoff at the Site. 18. During its ownership and/or operation of the Site, DuPont has failed to install and. or maintain an appropriate leachate collection and/or treatment system at the Site. 19. During its ownership and/or operation of the Site, DuPont has failed to install and or maintain appropriate catch basins at the Site. 20. During its ownership and/or operation of the Site, DuPont has failed to install and. or maintain appropriately lined sedimentation/settling ponds at the Site. 21. During its ownership and/or operation of the Site, DuPont has failed to install and. or maintain appropriate runoff'leachate diversion ditches at the Site. 22. During its ownership and/or operation of the Site, DuPont has failed to appropriates close and/or retrofit surface impoundments at the Site. 23. During its ownership and/or operation of the Site, DuPont has failed to submit timely notice o f its violation of applicable surface and/or groundwater protection standards at the Site 24. Durina its ownership and/or operation of the Site. DuPont has tailed to notify appropriate government officials that it changed the nature of the waste DuPont disposed at the Site 4 e o o ,-.,3C:/ 25. During its ownership and/or operation of the Site, DuPont has disposed of wastes, including certain sludges, without first obtaining appropriate government approvals. 26. During its ownership and/or operation at the Site, DuPont failed to close a drain valve for one o f its leachate/sedimentation ponds resulting in the discharge of pollutants into the environment, including the nearby Dry Run stream. 27. As a result of DuPont's ownership and/or operation of the Site, one or more solid, toxic and/or hazardous wastes, substances, pollutants, and/or contaminants have been and continue to be disposed, discharged, and/or otherwise released into environmental media at the Site (the "Contaminants"), including surface and groundwaters at the Site, including the nearby Dry Run stream. 28. At all times relevant hereto, Plaintiffs collectively have owned, leased, and/or otherwise possessed several hundred acres of real property adjacent and/or contiguous to the Site which properties are collectively referred to herein as "Plaintiffs' Properties" and are depicted generally for illustrative purposes only as "Plaintiffs' Properties" on Exhibit A to Plaintiffs' First .Amended Complaint. 29. At all times relevant hereto, one or more of the Contaminants originating from the Site have entered and continue to enter one or more portions of Plaintiffs' Properties through various pathways, including but not limited to the Dry Run stream, resulting in the contamination of environmental media, including but not limited to soils and surface and groundwaters, at Plaintiffs' Properties (the "Contamination"). 30. Several hundred o f Plaintiffs' cattle have been and continue to be killed, injured, or otherwise adversely affected by the Contamination. 5 000 3 I The Contamination has adversely impacted and continues to adverselv impact flora and fauna at Plaintiffs' Properties, and has impacted and continues to otherwise adversely impact the value of Plaintiffs' Properties. 32 The Contamination .has made and continues to make Plaintiffs physically ill or otherwise physically damaged, and has caused and continues to cause associated emotional and/or mental stress, anxiety, and/or fear of current and/or future illnesses. FIRST COUNT (CERCLA) 33. Plaintiffs incorporate herein the allegations contained in Paragraphs 1 through 32 of this Complaint as if fully restated herein. 34. Plaintiffs and DuPont are each "persons" within the meaning o f Section 101(21) of CERCLA, 42 U.S.C. 9601(21). 35. The Site is and was at all times relevant hereto, a "facility" within the meaning of Section 101(9) of CERCLA, 42 U.S.C. 9601(9). 36. At all times relevant hereto, and at the time o f disposal and/or release and/or threatened release at the Site o f one or more "hazardous substances," as that term is defined in Section 101(14) o f CERCLA, 42 U.S.C. 9601(14), DuPont owned and/or possessed hazardous substances and/or materials containing hazardous substances and by contract, agreement, or otherwise arranged for the treatment and/or disposal of such hazardous substances and/or materials containing hazardous substances at the Site, and is, therefore, a liable party within the meaning ot Section 107(a)(3) o f CERCLA, 42 U.S.C. 9607(a)(3). 6 C00T.'3.i 37 At all times relevant hereto, and at the time of disposal and/or release and. or threatened release at the Site of one or more "hazardous substances," as that term is defined in Section 101(14) of CERCLA, 42 U. S C 9601(14), DuPont is and/or was at the time of disposal of such hazardous substances, an owner and/or operator o f the Site and is, therefore, a liable partv within the meaning of Section 107(a)(1) and/or (2) of CERCLA, 42 U.S.C. 9607(a)(1) and/or (2) 38. At all times relevant hereto, and at the time of disposal and/or release and or threatened release of one or more "hazardous substances," as that term is defined in Section 101(14) of CERCLA. 42 U.S.C. 9601(14), DuPont is and/or was a person who accepts or accepted one or more such hazardous substances for transport to the Site and is, therefore, a liable party within the meaning of Section 107(a)(4) of CERCLA, 42 U.S.C. 9607(a)(4). 39. As a result of the actions of DuPont as referenced in Paragraphs 1 through 38 above, a "release" and/or "threatened release," as those terms are defined in Section 101(22) o f CERCLA, 42 U.S.C. 9601(22), of one or more hazardous substances has occurred, is continuing to occur, and all relevant times hereto was occurring at, under, and/or from the Site. 40. Plaintiffs have incurred and will continue to incur costs to investigate and/or otherwise respond to the release and/or threatened release, of hazardous substances at, under, and/or from the Site, within the meaning of Section 101(25) of CERCLA, 42 U.S.C. 9601(25). 41. Plaintiffs' actions taken in response to the release and/or threatened release of one or more hazardous substances at, under, and/or from the Site and the costs incurred incident thereto were necessary and undertaken in a manner consistent with the National Contingency Plan set torth at 40 C.F.R. Pan 300. 7 42 Plaintiffs have satisfied any and ail conditions precedent to the undertaking of response actions, the incurrence of response costs, and to the recovery of such costs from DuPont under CERCLA. 43. L'nder Section 107(a).of CERCLA. 42 U.S.C. 9607(a). DuPont is strictly liable to Plaintiffs, jointly and severally, for all response costs, including prejudgment interest, incurred and to be incurred by Plaintiffs in response to hazardous substances at, under, and/or from the Site 44. Under Section 113(f) of CERCLA. 42 U.S.C. 9613(f), Plaintiffs are entitled to contribution from DuPont for DuPont's equitable share of all liability, response costs, and damages incurred and to be incurred by Plaintiffs in response to hazardous substances at, under, and/or from the Site. SECOND COUNT (RCRA) 45. Plaintiffs incorporate herein the allegations set forth in Paragraphs 1 through 44 of this Complaint as if fully restated herein. 46. Plaintiffs and DuPont are each "persons" within the meaning of Section 1004( 15) of RCRA, 42 U.S.C. 6903(15). 47. DuPont is a past or present generator, past or present transporter, and/or past or present owner and/or operator of a treatment, storage, and/or disposal facility, who has contributed and/or is contributing to the past and/or present handling, storage, treatment, transportation, and/or disposal o f "solid waste" within the meaning of Section 1004(27) of RCRA, 42 U.S.C. 6903(27). and/or "hazardous waste" within the meaning of Section 1004(5) of RCRA, 42 U.S.C. 6903(c). at. under, and/or from the Site, which may present an imminent and substantial endangerment to health 8 eoo^ u or the environment, within the meaning of Section 7002(a)( 1)(B) of RCRA, 42 L' S C 6972(a)(1)(B). 4S. As a direct and proximate result of DuPont's acts and/or omissions contributing to the past and/or present handling, storage, treatment, transportation, and/or disposal of solid and or hazardous waste at, under, and/or from the Sice, which may present an imminent and substantial endangerment to health or the environment, DuPont is liable for such endangerment under Section 7002(a)(1)(B) of RCRA, 42 U.S.C. 6972(a)(1)(B). 49. DuPont does not dispute that Plaintiffs have complied with the notice requirements set forth in Section 7002(b)(2) of RCRA, 42 U.S.C. 6972(b)(2), and at least ninety (90) days have past between the date of such notice and the date of filing this Second Amended Complaint. 50. Plaintiffs have complied with all conditions precedent to bringing their claim against DuPont under Section 7002(a)(1)(B) of RCRA, 42 U.S.C. 6972(a)(1)(B), and no action has been taken which could prevent the filing of this RCRA claim under Section 7002(b)(2) o f RCRA. 42 U.S.C. 6972(b)(2). 51. Plaintiffs are entitled to an injunction against DuPont ordering DuPont to undertake and/or pay tor any and all investigations, studies, monitoring, response, removal, and remedial actions and/or any other activities and/or actions necessary and/or required to respond to, abate, remediate and/or otherwise address any environmental contamination at, under, and/or from the Site and, or Plaintiffs' Properties that may present an imminent and substantial endangerment to health or tne environment, and ordering DuPont to take all such other actions as this Court may deem necessary, pursuant to Section 7002(a)(1)(B) of RCRA, 42 U.S.C. 6972(a)(1)(B). 9 {?G0 U THiRD COUNT (DECLARATORY JUDGMENT! 52. Plaintiffs incorporate herein the allegations set forth in Paragraphs 1 through 51 of this Complaint as if fully restated herein. 53. .An actual, substantial and justiciable controversy exists between Plaintiffs and DuPont regarding their respective rights and obligations for the response costs and/or damages that have been and will be incurred in connection with the release and/or threatened release o f one or more hazardous substances at, under, and/or from the Site. 54. Plaintiffs seek a declaratory judgment against DuPont under Section 113(g)(2) of CERCLA, 42 U.S.C. 9613(g)(2), and the Federal Declaratory Judgment Act, 28 U.S.C. 2201, 2202, holding DuPont strictly liable, jointly and severally, for all and/or DuPont's equitable share of the response costs incurred and to be incurred by Plaintiffs that will be binding in any subsequent action to recover further response costs or damages. 55. Pursuant to Section 113(g)(2) of CERCLA, 42 U.S.C. 9613(g)(2), and 28 U.S.C. 2201, 2202, Plaintiffs are entitled to a declaration from this Court that DuPont is strictly liable, jointly and severally, to Plaintiffs for all and/or DuPont's equitable share of the response costs and damages incurred or to be incurred by Plaintiffs. FOURTH COUNT (CLEAN WATER ACT) 56. Plaintiffs incorporate herein the allegations contained in Paragraphs 1 through 55 of this Complaint as o f fully restated herein. 57. Plaintiffs are each "citizens" within the meaning of Section 505(g) ofCWA. 33, U.S.C 1365(g). 10 OOOa '?S 5S. DuPont is a "person" within the meaning of Section 502(5) of CWA, 33 L' S C i 1362(5). 59. On April 14, 1998, the West Virginia Division of Environmental Protection f'WVDEP") renewed and reissued a National Pollutant Discharge Elimination System permit (Permit No. WV0076244) (the "Permit"), to DuPont for water discharges from the Site through authority of Section 1342 o f CWA, 33 U.S.C. 1342. 60. Monthly monitoring reports submitted to WVDEP by DuPont for at least the months of May, July, and August, 1998 confirm that DuPont has discharged and continues to discharge waste from Outlet 001 at the Site in amounts and concentrations that exceed applicable limits established under the Permit for at least iron, manganese, aluminum, and total suspended solids, thereby violating at least conditions A. I, B. 1, C. 1, C.3, C. 12, D. 1, F.2, F.3, F.4, G.7, and G. 17 of the Permit. 61. Monthly monitoring reports submitted to WVDEP by DuPont for at least the months o f May, July, and November of 1998 confirm that DuPont has discharged and continues to discharge waste from the Site into the nearby Dry Run stream in amounts and concentrations that exceed applicable limits established under the Permit for at least aluminum and iron, thereby violating at least conditions C .l, C.3, C.12, D. I, F.2, F.3, F.4, G.7, G.8, and G.17 o f the Permit. 62. Monthly monitoring reports submitted to WVDEP by DuPont for at least the months of May, July, August, and November o f 1998 confirm that DuPont is currently in violation of at least Paragraphs 1 and 3 of the Compliance Order set forth on Page 4 of the April 14, 1998, Findings and Order issued by WVDEP to DuPont as a result of violations of the CWA and Permit standards and limitations referenced above (Findings and Order No. 4015). 11 63 DuPont's continuing and on-going violations referenced above constitute continuing and on-going violations of at least Sections 301(a) and 405(a) of the CWA, 33 L' S C 13 11(a). 1345(a), and Sections 22-1 1-6, 22-11-S, 22-11-16, and 22-11-18 of the West Virginia Water Pollution Control Act, W.Va. Code 22-11-1 et seq. (collectively the "Law"). 64. The Permit limits. Law, and compliance order provisions referenced above constitute "effluent standards or limitations" within the meaning of Section 505(f) of the CWA, 33 U.S.C. 1365(f). 65. By virtue o f DuPont's violations o f the effluent standards or limitations referenced above, DuPont is in violation of "(A) an effluent standard or limitation under this chapter or (B) an order issued by the Administrator or a State with respect to such a standard or limitation" within the meaning of Section 505(a)(1) of the CWA, 33 U.S.C. 1365(a)(1). 66. DuPont does not dispute that Plaintiffs have complied with the notice requirements set forth in Section 505(b)(1)(A) o f the CWA, 33, U.S.C. 1365(b)(1)(A), and at least sixty (60) days have passed between the date of such notice and the date o f filing this Second .Amended Complaint. 67. Plaintiffs have complied with all conditions precedent to bringing their claim against DuPont under Section 1365(a)(1) of the CWA, 33 U.S.C. 1365(a)(1), and no action has been taken which could prevent the filing of this CWA claim under Section 505(b)(1)(B) of the CWA, 33 L.S.C. 1365(b)(1)(B). 68. Plaintiffs are entitled to an injunction against DuPont ordering DuPont to comply with the effluent standards or limitations and compliance order referenced above, to pay appropriate civil penalties under Section 309(d) of the CWA, 33 U.S.C. 1319(d), to pay all costs of litigation 12 (including reasonable attorney and expert witness fees) and to take all such other action as the Court may deem necessary, pursuant to Section 505fa)(1) of the CWA, 33 C S C . 1365(a)(1). FIFTH COUNT (WEST VIRGINIA HAZARDOUS WASTE MANAGEMENT ACT) 69 Plaintiffs incorporate herein the allegations contained in Paragraphs 1 through 6 7 of this Complaint as if fully restated herein. 70. Plaintiffs and DuPont are each "persons" within the meaning o f Section 22-18-3( 1!) o f the Waste Act, W.Va. Code 22-18-3(11). 71. As a result of the acts and/or omissions of DuPont as referenced in Paragraphs 1 through 70 above, DuPont has and continues to operate the Site in violation of applicable permit requirements set forth in Section 22-18-8 of the Waste Act, W.Va. Code 22-18-8. 72. As a result of the acts and/or omissions o f DuPont as described in Paragraphs 1 through 71 above, Plaintiffs are entitled to bring a citizens suit against DuPont to obtain DuPont's compliance with applicable law, pursuant to Section 22-18-19(a) of the Waste Act, W.Va. Code 2218-19(a). 73. Dupont does not dispute that Plaintiffs have complied with the notice requirements set forth in Section 22-18-19(a) of the Waste Act, W.Va. Code 22-18-19(a), and at least sixty (60) days have passed between the date of such notice and the date of filing this Second Amended Complaint. 74. Plaintiff; have complied with all conditions precedent to bringing their claim against DuPont under Section 22-18-19(a) of the Waste Act, W. Va. Code 22-18-19(a), and no action has 13 V a i**.' *." . been caken which could prevent the filing of this Waste Act claim under Section 22-18- 19(d) o f the Waste Act, W.Va. Code 22-18-19(a). 75 Plaintiffs are entitled to an injunction against DuPont, ordering DuPont to comply with the requirements set forth in Section 22-18-8 of the Waste Act, W.Va. Code 22-18-8. and ordering DuPont to take all such other action as this Court may deemed necessary', pursuant to Section 22- i S19(a) o f the Waste Act, W.Va. Code 22-18-19(a). SIXTH COUNT (CONTRIBUTIONS 76. Plaintiffs incorporate herein the allegations contained in Paragraphs 1 through 75 of this Complaint as if fully restated herein. 77. To the extent Plaintiffs have incurred damages and response costs and will continue to incur damages and response costs in the future in response to the release and/or threatened release of one or more solid, toxic, and/or hazardous wastes, substances, pollutants, and/or contaminants at. under, and/or from Site, DuPont is liable, jointly and severally, to Plaintiffs for contribution pursuant to Plaintiffs1right of contnbution arising under Federal and State common law and applicable statutes SEVENTH COUNT (NEGLIGENCE) 78. Plaintiffs incorporate the allegations contained in Paragraphs 1 through 77 o f this Complaint as if fully restated herein. 79. In connection with its ownership and/or operation of the Site, DuPont has had and continues to have a duty of ordinary and reasonable care to operate and manage the Site in such a way as to not create a nuisance or situation causing any injury or damage to human health or the environment. 14 ooo;v*r? 80 DuPont breached its duty of ordinary and reasonable care by negligently operating and/or managing the Site and/or conducting other operations and/or activities at the Site in such a manner as to cause, permit, and/or allow the release and/or threatened release of solid, toxic, and. or hazardous wastes, substances, pollutants, and/or contaminants at, under, and/or from the Site 81. DuPont's negligent acts and/or omissions proximately caused and continue to proximatelv cause damage to Plaintiffs in the form of property damage and bodily injury, in addition to creating a situation harmful to human health and the environment, for which DuPont is liable. EIGHTH COUNT (NEGLIGENCE PER SE) 82. Plaintiffs incorporate herein the allegations contained in Paragraphs 1 through 81 of this Complaint as if fully restated herein. 83. By its acts and/or omissions resulting in the release and/or threatened release of one or more solid, toxic, and/or hazardous wastes, substances, pollutants, and/or contaminants at. under, and/or from the Site, DuPont violated and continues to violate one or more applicable State and. or Federal statutes, including but not limited to Sections 22-11-6, 22-11-8, 22-11-16, 22-11-18, 22-1 c10, and 22-18-8 of the West Virginia Code, constituting negligence per se. 84. DuPont's violation of law proximately caused and continues to proximately cause damage to Plaintiffs in the form o f property damage and bodily injury for which DuPont is liable. NINTH COUNT (NUISANCE) 85. Plaintiffs incorporate herein the allegations contained in Paragraphs 1 through 84 of this Complaint as if fully restated herein. 15 ooosor* 86 DuPont's acts and/or omissions in operating and/or otherwise managing the Site caused and continue to cause a substantial and unreasonable interference with Plaintiffs' use and enjoyment of Plaintiffs' Properties and has materially diminished and continues to diminish the value of Plaintiffs'Properties. 87. DuPont's substantial and unreasonable interference with the use and enjoyment of Plaintiffs' Properties and continuing substantial and unreasonable interference with such use and enjoyment of Plaintiffs' Properties constitutes a continuing private nuisance. 88. DuPont's creation and continuing creation of a continuing private nuisance proximately caused and continues to proximately cause damage to Plaintiffs in the form of property damage and bodily injury, including diminution in the value of Plaintiffs' Properties, for which DuPont is liable. TENTH COUNT (TRESPASS! 89. Plaintiffs incorporate herein the allegations contained in Paragraphs 1 through 88 of this Complaint as if fully restated herein. 90. DuPont's acts and/or omissions resulting in the release and/or threatened release of one or more solid, toxic, and/or hazardous wastes, substances, pollutants, and/or contaminants at. under, and/or from the Site have resulted and continue to result in the release and/or threatened release o f one or more such solid, toxic, and/or hazardous wastes, substances, pollutants, and/or contaminants at, under, onto, and/or into Plaintiffs' Properties. 9 1. The solid, toxic, and/or hazardous wastes, substances, pollutants, and/or contaminants present on Plaintiffs' Properties originating from the Site were at all relevant times hereto, and continue to be, the property of DuPont. 16 COOSO.;. 92. The invasion and presence of DuPont's solid, toxic, and/or hazardous wastes, substances, pollutants, and/or contaminants at. under, onto, and/or into Plaintiffs' Properties vsas and continues to be without permission or authority from Plaintiffs or anyone who could grant such permission or authority. 93. The presence and continuing presence of DuPont's solid, toxic, and/or hazardous wastes, substances, pollutants, and/or contaminants at Plaintiffs' Properties constitutes a continuing trespass. 94. DuPont's past and continuing trespass upon Plaintiffs' Properties proximately caused and continues to proximately cause damage to Plaintiffs in the form o f property damage and bodily injury, including diminution in the value of Plaintiffs' Properties, for which DuPont is liable. ELEVENTH COUNT /PUNITIVE DAMAGES) 95. Plaintiffs incorporate herein the allegations contained in paragraphs 1 through 94 of this Complaint as if fully restated herein. 96. DuPont's acts and/or omissions as described above were conducted with such malicious, wanton, willful, and/or reckless indifference to Plaintiffs' rights and/or flagrant disregard for the safety and/or property of Plaintiffs that DuPont is liable for punitive damages. W H E R E FO R E , Plaintiffs hereby demand that this Court: A. Enter a judgment against DuPont, pursuant to Section 107 ofCERCLA, 42 U.S C 9607, that DuPont is strictly liable, jointly and severally, to Plaintiffs for all response costs and damages that Plaintiffs have incurred and will incur in connection with the release and/or threatened 17 coos release of hazardous substances at, under, and/or from the Site in an amount according to the proof at trial, plus attorneys' fees (to the extent recoverable), costs, and prejudgment interest; B In the alternative, enter a judgment against DuPont, pursuant to Section 113(f) of CERCLA 42 U.S.C. 9613(f), that DuPont is strictly liable to Plaintiffs for DuPont's fair, equitable, and proportionate contribution for all response costs and damages that Plaintiffs have incurred and will incur in connection with the release and/or threatened release of hazardous substances at. under, and/or from the Site in an amount according to the proof at trial, plus attorneys' fees (to the extent recoverable) costs, and prejudgment interest; C. Enter a declaratory judgment against DuPont, pursuant to Sections 107 and 113( g) o f CERCLA 42 U.S.C. 9607, 9613(g), and/or 28 U.S.C. 2201, 2202 that DuPont is strictly liable, jointly and severally, to Plaintiffs for all response costs and damages that Plaintiffs have incurred and will incur in connection with the release and/or threatened release o f hazardous substances at, under, and/or from the Site in an amount according to the proof at trial, plus attorneys' fees (to the extent recoverable) costs, and prejudgment interest; D. In the alternative, enter a declaratory judgment against DuPont, pursuant to Section 113(f) and (g) of CERCLA, 42 U.S.C. 9613(f), (g), and/or 28 U.S.C. 2201, 2202 that DuPont is strictly liable to Plaintiffs for DuPont's fair, equitable, and proportionate contribution tor all response costs and damages that Plaintiffs have incurred and will incur in connection with the release and/or threatened release of hazardous substances at, under, or from the Site in an amount according to the proof at trial, plus attorneys' fees (to the extent recoverable), costs, and prejudgment interest, E. Enter an injunction against DuPont, pursuant to Section 7002(a)(1)(B) o f RCRA. 42 U.S.C. 6972(a)(1)(B), ordering DuPont to undertake and/or pay for any and all investigations. IS studies, monitoring, response, removal, remedial, and/or any other actions necessary and/or other.'. required to respond to. abate, remediate, and/or otherwise address any environmental contamination at. under, and/or from the Site and/or Plaintiffs' Properties that may present an imminent and substantial endangerment to health or the environment, and ordering DuPont to pay all costs o f litigation (including reasonable attorney and expert witness fees) and prejudgment interest. F. Enter an injunction against DuPont, pursuant to Section 505(a)(1) o f the CWA. 33 U.S.C. 1365(a)(1), ordering DuPont to comply with the effluent standards or limitations and compliance orders that DuPont is violating, to pay appropriate civil penalties under Section 309(d) of the CWA, 33 U.S.C. 1319(d), and ordering DuPont to pay all costs of litigation (including reasonable attorney and expert witness fees) and prejudgment interest; G. Enter an injunction against DuPont, pursuant to Section 22-18 -19(a) of the Waste Act. W.Va. Code 22-18-19(a), ordering DuPont to comply with applicable provisions of Section 22-188 o f the Waste Act, W.Va. Code 22-18-8, and ordering DuPont to pay all costs of litigation (including reasonable attorney and expert witness fees) and prejudgment interest; H. Enter a judgment against DuPont under Federal and/or State common law that DuPont is liable to Plaintiffs in contribution for DuPont's fair, equitable, and proportionate share of all liability, response costs, and damages incurred and to be incurred in connection with any environmental contamination at the Site; I Enter a judgment against DuPont that DuPont is liable to Plaintiffs for negligence m an amount to be determined at trial; J. Enter ajudament against DuPont that DuPont is liable to Plaintiffs for negligence per ie in an amount to be determined at trial; 19 K. Enter ajudgment against DuPont that DuPont is liable to Plaintiffs for nuisance in an amount to be determined at trial; L. Enter a judgment against DuPont that DuPont is liable to Plaintiffs for trespass in an amount to be determined at trial; M. Enter a judgment against DuPont that DuPont is liable to Plaintiffs for punitive damages in an amount to be determined at trial, and N. Enter a judgment against DuPont for Plaintiffs' costs, attorneys' fees, and interest and all such other and further relief as this Court may deem just and appropriate. JURY DEMAND Plaintiffs hereby demand trial by jury on all issues so triable. WILBUR EARL TENNANT, ERWIN JACKSON TENNANT, JAMES DAVID TENNANT, DELLA MARIE TENNANT, and SANDRA K. TENNANT ___________ Larry A. Winter Carey, Hill, Scott, Winter & Johnson PLLC P.O. Box 3384 Charleston, WV 25338 (304)345-1234 Robert A. Bilott J. Steven Justice Taft, Stettinius & Hollister LLP 1800 Firstar Tower 425 Walnut Street Cincinnati, OH 45202-3957 (513)381-2838 20 CERTIFICATE OF SERVICE I hereby certify that a filed, date-stamped copy of the foregoing Second Amended C om p lain t, which was filed with the Court on October 21, 1999, was served upon the following parties by regular L' S mail, postage prepaid, this 2T` day o f October, 1999: The Honorable Janet Reno Attorney General o f the United States 5111 Main Street Building 10th Street and Constitution Ave., N.W. Washington, D.C. 20530 Carol Browner, Administrator United States Environmental Protection Agency 401 M Street, SAV. Washington, D.C. 20460 W. Michael McCabe, Regional Administrator United States Environmental Protection Agency, Region III 1650 .Arch Street Philadelphia, PA 19103-2029 Michael Miano, Director WV Division o f Environmental Protection 10 McJunkin Road Nitro, WV 25143 Eric M. James, Esq. Paula Durst Gillis, Esq. Spilman, Thomas & Battle P.O. Box 273 Charleston, WV 25321 Larry A. Winter OOOSO' M ichael W C arey N * n c y C- H ill P hillip B S c o t t i i^v?. L arry A. W inter D a v i d D Jo h n s o n . [[I P w i e l a C D eem MG e o r g e Scott of C ounsel C a r e y , .i l l , S c o t t , W in t e r & Jo h n s o . I7 0 1 B ank O ne C enter 707 V irginia S treet. E ast P O Box 3884 C h a rlesto n . W est V irginia 25338 October 21, 1999 R eceived - IS d H D ate OCT 2 5 V *'-' Phone' 304, 345,1234 F \x , 3114 I 343.1 [( 15 Email. chvAjctsh.s 1 c m Web s i t e AM'LiL y.rT.LLiiii hvir.ter cos'.'. ; . ;:r. Samuel L. Kay. Clerk United States District Court P 0 . Box 1526 Parkersburg, WV 26101 Re: Wilbur E. Tennant, et al. v. ./. DuPont de Nemours & Co., Inc. Civil Action No. 6:99-0488 Dear Mr. Kay: I enclose herewith a Second Amended Complaint for filing in the above-referenced civil action. Thank you very much for your assistance in this matter. If you have any questions, please do not hesitate to contact me. Very truly yours, LAW: sms Enclosure cc: The Honorable Janet Reno Carol Browner W Michael McCabe Michael Miano Eric M. James, Esq. Paula Durst Gillis, Esq. Larry A. Winter TAFT, oTETTI N I US & HOLLISTE,. LLP COLUMBUS. O h io OFFICE TWELFTH f l o o r 21 E A S T STAT E S T R E E T 614.221.2S38C O L U M B U S . O H I O 4 3 2 1 5 - 4 2 2 1 FAX: 614-221 -2007 1800 FIRSTAR TO W ER 425 W ALN UT STREET CINCINNATI. OHIO 45202-3957 5 13-38 1-2838 FAX: 5 13-381 -0205 w w w .taftlaw .com ROBERT A. 8IL0TT b{il5o1c3t@}t3af5t7-w9.6c3c^8 August 18, 1999 REGISTERED MAIL NO. R410009615 RETURN RECEIPT REQUESTED N O R T H E R N K E N T U C K Y O P F C E Th o m a s m o r e c e n io e 2670 C H A N C E LLO R OR'VE C O V I N G T O N K E N T U C K Y 4 10 ' 7 3 4 3 i 6 0 S - 3 3 I 26 38 513-361 2638 FAX 5 13-361-6613 C LEVELAN D . O h io OFFICE SIXTH FLOOR BONO C O U R T BUiLOiNG 1300 EAST N IN TH STREET CLEVELANO. O h io 44ii.iS 03 216-241-2638 FAX 216.241-2837 Statutory Agent E .I DuPont de Nemours & C o . , Inc. 1007 Market Street Wilmington, DE 19898 Re: Notice Of Intent To Amend Complaint To Bring Citizens Suit Under Federal Clean Water Act In Connection With DuPont's Dry Run Landfill In Wood County, West Virginia: Tennant, et al-. v. B.I. D u P o n t d e N e m o u r s & Co., Inc. (S.D. W.Va. Civil Action No. 6:99-0488_____ Dear Statutory Agent: On behalf of our law firm's clients, Wilbur Earl Tennant (Route 3, Box 17, Washington, West Virginia 26181), Erwin Jackson Tennant (Route 3, Box 17A, Washington, West Virginia 26181), James David Tennant (Route 3, Box 372, Parkersburg, West Virginia 26101), Della Marie Tennant (Route 3, Box 372, Parkersburg, West Virginia 26101), and Sandra K. Tennant (Route 3, Box 17, Washington, West Virginia 26181) (collectively the "Tennants"), E.I. DuPont de Nemours & Co., Inc. ("DuPont") is hereby notified that the Tennants intend to amend their Complaint currently pending against DuPont in the referenced action in Federal Court in the Southern District of West Virginia to bring a claim against Dupont, pursuant to Section 505 of the Federal Clean Water Act, as amended ("CWA"), 33 U.S.C. 1365. Section 505(a)(1) of the CWA permits the Tennants to commence a civil action against "any person . . . who is alleged to be in violation of (A) an effluent standard or limitation under this chapter or (B) an order issued by the Administrator or State with respect to such a standard or limitation." 33 U.S.C. 1365(a)(l). "Effluent standard or limitation" is defined under the CWA to include, among other things, "a permit or condition thereof issued under Section 1342 of this title, which is in effect under this chapter (including requirement applicable by reason of section 1323 of this t i t l e ) Id. at 1365(f). 0 0 0 V 01 Statutory Agent August 18, 1999 Page 2 Based upon a review of the information provided to date by the State of West Virginia's Division of Environmental Protection ("WVDEP") in response to a Freedom of Information Act request, the Tennants have determined that DuPont is currently in violation of at least the following provisions of the NPDES permit reissued to DuPont by WVDEP on April 14, 1998, under authority of Section 1342 of the CWA (Permit No. WV0076244) with respect to discharges from Dupont's Dry Run Landfill in Wood County, West Virginia: 1. Monthly monitoring reports submitted to WVDEP by DuPont for at least the months of May, July, and August, 1998, confirm that DuPont has discharged and continues to discharge waste from Outlet 001 at the DuPont Dry Run Landfill in amounts and concentrations that exceed applicable permit limits for at least iron, manganese, aluminum, and total suspended solids, thereby violating at least conditions A.l, B.l, C.l, C.3, C.12, D.l, F.2, F . 3, F .4, G.7, and G.17 of Permit No. WV0076244. >' 2. Monthly monitoring reports submitted to WVDEP by DuPont for at least the months of May, July, and November of 1998, confirm that DuPont has discharged and continues to discharge waste from the DuPont Dry Run Landfill into the nearby Dry Run stream in amounts and concentrations that exceed applicable permit limits for at least aluminum and iron, thereby violating at least conditions C.l, C.3, C.12, D.l, F.2, F.3, F .4, G.7, G. 8, and G.17 of Permit No. WV0076244. In addition, the Tennants have determined from the information produced to date by WVDEP that DuPont is currently in violation of at least Paragraphs 1 and 3 of the Compliance Order set forth on Page 4 of the April 14, 1998, Findings and Order issued by WVDEP to DuPont as a result of violation of the CWA standards or limitations referenced above (Findings and Order No. 4015) . The continuing and on-going violations referenced herein also constitute continuing violations of at least Sections 301(a) and 405(a) of the CWA, 33 U.S.C. 1311(a), 1345(a), and Sections 22-11-6, 22-11-8, 22-11-16, and 22-11-18 of the West Virginia Water Pollution Control Act, W.Va. Code 22-11-1 et sea. As indicated above, the continuing and on-going violations referenced in this notice are based upon the information that has actually been produced to date by WVDEP. We did not find within WVDEP's publicly-available files many of the monthly, quarterly, and annual monitoring reports that DuPont is required to submit to WVDEP under the terms of Permit No. WV0076244. Thus, the OOO&O?? Statutory Agent August 18, 1999 Page 3 Tennants reserve their right to allege and assert additional violations of the CWA, if additional information is obtained from WVDEP, U.S. EPA, or any other source indicating additional CWA violations. Nevertheless, DuPont is hereby notified that the Tennants intend to amend their Complaint currently pending against DuPont in the above-referenced litigation to include a citizens suit claim against DuPont, pursuant to Section 505(a)(l) of the CWA, within sixty (60) days after issuance of this notice to obtain relief at least for DuPont's violations of the CWA referenced above. The following are receiving copies of this notice. 1. Carol Browner RBGISTBRBD MAIL NO. R410009616 Administrator RBTPRN RBCBIPT RBOPBSTBD United States Environmental Protection Agency 401 M Street, S.W. Washington, DC 20460 2. W. Michael McCabe RBGXSTBRBD MAXL NO. R410009617 Regional Administrator RBTPRN RBCBIPT RBOBSTBD United States Environmental Protection Agency, Region III 1650 Arch Street Philadelphia, PA 19103-202: 3 . Michael Miano Director West Virginia Division of Environmental Protection 10 McJunkin Road Nitro, WV 251434 RBGXSTBRBD MAIL NO. R410009620 RBTPRN RBCBIPT RBOPBSTBD 4. Registered Agent for E .I . Dupont de Nemours & Co., Inc. CT Corporation System 707 Virginia Street, East Charleston, WV 25301 RBGXSTBRBD MAIL NO. R410009621 RBTPRN RBCBIPT RBOPBSTBD Statutory Agent August 18, 1999 Page 4 5. Paula Durst Gillis, Esq. REGISTERED MAIL MO. R410009622 Spilman Thomas & Battle, PLLC RETURN RECEIPT REQUESTED Spilman Center 300 Kanawha Boulevard, East P.O. Box 273 Charleston, WV 25321-0273 / R A B :mdm cc: Wilbur Earl Tennant Erwin Jackson Tennant James David Tennant Della Marie Tennant Sandra K. Tennant Larry A. winter, Esq. J. Stephen Justice, Esq. |3 4 /A y c- 'i/ CERTIFIED MAIL RSTURM,RECEIPT R5QUBSTSP Mr. William D. Brannon, Acting Chief Office of Water Resources Division of Environmental Protection 1201 Greenbrier Street Charleston, WV 25311 Attention: Industrial Branch f Re: WV/NPDES Permit Number WVO076244 Dear Mr. Brannon: DuPont Washington Works P. 0. Box 1217 Parkersburg, WV 26102-1217 January 31, 2000 pom *ncops OO HOT UMOV Enclosed is the 19 99 annual report summarizing the operations of our Dry Run industrial landfill. If you have any questions or need additional information, please call me on 863-4271. Very truly yours, R. I t . Ritchey Sr. Environmental Control Consultant Washington Works Attachments RLR/GW :vlw U'* cc: John G. Britvec * Office of Water Resources Division of Environmental Protection 1304 Goose Run Road Fairmont, WV 26354 Attention: Industrial Branch 3u P irn tiM w w u n and C a^canv EID076133 0 0 O f .'i CF008243 t e c j ?tsv -2- I certify under penalty of law that this document and all attachments were prepared under my direction or supervision in accordance with a system designed to assure that qualified personnel properly gather and evaluate the information submitted. Based on my inquiry of the person or persons who manage the system, or those persons directly responsible for gathering the information, the information submitted is, to the best of my knowledge and belief, true, accurate, and complete. I am aware that there are significant penalties for submitting false information, including the possibility of fine and imprisonment for knowing violations. 1/31/00 R. L. Ritchey Sr. Environmental Control Consultant Washington Works EID076134 000 CF008244 -3 - 1999 DRY RUN LANDFILL OPERATIONAL REPORT Facility Users All the waste disposed o f in the Dry Run Landfill originates from E. I. du Pont and Company, Washington Works site and its auxiliaries. Landfill Shipments A summary o f the 1999 landfill shipments is attached. Surface and Groundwater Monitoring A summary o f the 1999 surface and groundwater monitoring activities is attached. Landfill Operation. Construction and Maintenance Activity Summary Approximately 6.1 acres o f leachate collection system were constructed during 1999 at the landfill. Project work included construction of: 267,000 square feet (6.1 acres) o f leachate collection system. This included subgrade preparation, 1,670 linear feet of anchor trench, 16 ounce/square yard nonwoven geotextile, 60-mil textured HDPE geomembrane, HDPE drainage net, 10 ounce/square yard nonwoven geotextile, and 12-inch soil layer. 390 linear feet o f 4-inch diameter leachate seep collection drain. 360 feet o f 8-inch dimeter perforated HDPE pipe leachate collection drain. 1,430 linear feet o f 4-inch diameter perforated HDPE pipe leachate collection drain. 1,090 linear feet o f riprap ditch. 60 linear feet o f 24-inch diameter corrugated metal pipe culvert One gas ven t Revegetation o f 12 acres o f disturbed area. An existing landslide was also repaired just south o f the landfill area. The area was regraded and approximately 350 feet o f riprap ditch reconstructed. A collection system to enable truck transport o f leachate generated by the landfill remained in service throughout the entire year. 2.9 million gallons o f leachate were transported to Washington Works for treatment in 1999. An updated topographic map o f the landfill and cross section map showing the landfill space filled is attached. eCKH:-.' EID076135 -4- Drv Run Landfill Remaining Capacity Calculations Calculation o f 1999 fill: Net Waste Fill Volume Method: Waste volume hauled in 1999: = 3,857 truck loads x 39.7 yd3/truck load (avg) = 153,123 ~ 153,000 yd3 Average net waste compaction (daily cover allowance included) estimated at 80% for 1999: Total 1999 fill volume = 153,000 x 80% = 122,400 yd3 122,400 - 122,000 Ravine #1 (existing cell) Capacity remaining at the beginning o f 1999 = 810,000 yd3 Capacity used in 1999 = 122,000 yd3 Capacity remaining at the beginning o f 2000 = 688,000 yd3 Based on 122,000 yd3 per year net fill volume consumption: 688,000 y d 3 / 122.000 = 5.6 years remaining life on existing cell CF008246 c o o k 's EID076136 Material Coal Ash Paper, Cardboard, Wood Glass, Miscellaneous Solids, Metal, Nonasbestos Insulation Plastic Wastes (Polyamides, Acrylics, Polyacetal, PolyethyleneTerephthalate, Fluoropolymers) Dirt fill 1999 DRY RUN LANDFILL SHIPMENTS Number o f Shipments 1294 1137 Total Weight Tons 18,604 40,765 Total Weight Pounds 37,207,060 81,529,340 1326 7,615 15,230,320 M l 1242 2.498.620 Total 3,857 68,233 136,465,340 ooo^.j- EID076137 -6- 1999 DRY RUN LANDFILL QUARTERLY LEACHATE ANALYSIS REPORT SUMMARY Date Submitted Report 07/01/99 10/01/99 1/14/00 Second Quarter Leachate Monitoring Report Third Quarter Leachate Monitoring Report Fourth Quarter Leachate Monitoring Report 1999 DRY RUN LANDFILL QUARTERLY POND UNDERDRAIN ANALYSIS REPORT SUMMARY DalS-Subcutled Report 07/16/99 10/01/99 1/14/00 Second Quarter Pond Underdrain Monitoring Report Third Quarter Pond Underdrain Monitoring Report Fourth Quarter Pond Underdrain Monitoring Report 1999 DRY RUN LANDFILL QUARTERLY WELL MONITORING REPORT SUMMARY Date-Submitted Report 04/13/99 07/02/99 10/06/99 01/07/00 First Quarter Monitoring Well Report Second Quarter Monitoring Well Report Third Quarter Monitoring Well Report Fourth Quarter Monitoring Well Report 1999 DRY RUN LANDFILL SEMI-ANNUAL STORMWATER MONITORING REPORT SUMMARY Date Submitted * 1/21/00 Report Second Half Stormwater Monitoring Report * No samples obtained for first half stormwater monitoring report because o f lack o f adequate rainfall. CF008248 000? r. t EID076138 -7 - 1999 DRY RUN LANDFILL MONTHLY DISCHARGE MONITORING REPORT SUMMARY Date Submitted Renort 02/12/99 January Discharge Monitoring Report 03/08/99 February Discharge Monitoring Report 04/15/99 March Discharge Monitoring Report 05/11/99 April Discharge Monitoring Report 06/16/99 May Discharge Monitoring Report 07/15/99 June Discharge Monitoring Report 08/13/99 July Discharge Monitoring Report 09/16/99 August Discharge Monitoring Report 10/20/99 September Discharge Monitoring Report 11/08/99 October Discharge Monitoring Report 12/20/99 November Discharge Monitoring Report 01/20/00 December Discharge Monitoring Report 1999 DRY RUN LANDFILL ACUTE TOXICITY AND BENTHIC SURVEY REPORTS (Not otherwise included with the reports listed above) No benthic surveys performed during the year because o f extremely dry weather. CF008249 EID076139 -8- DRY RUN LANDFILL 1222 GRQLTNDWATER/SURFA.CE WATER MQMTQBJNG SUMMARY OF FC-143* ANALYTICAL RESULTS Sample Date: 07/22/99 Sample Location Well #6A Well #12 Well #12A Well #12B Well #13 WeU #13 A Well #14 WeU #15 Sample Date: 12/29/99 Sample Location Leachate Outlet 001 Stream Sampling Station No. 1 Stream Sampling Station No. 2 Property Line FC-143 Result (ug/L) 0.096 0.134 0.081 5.4 3.6 0.070 2.5 0.263 FC-143 Result (ue/Ul 34 66 0.54 87 39 * FC-143 is ammonium perfluorooctanoate ionic surfactant AU analyses performed by : Lancaster Laboratories 2425 New HoUand Pike PO Box 12425 Lancaster, PA 17605-2425 coot EID076140 qF008250 ION LINE 0 0 0 S;', ' E .I. DUPONT DE NEMOURS & CO. INC. NON HAZARDOUS LA N D FILL DRY RUN, WOOD C O U N TY , W.VA. THIS ORAIING HAS BEEN FURNISHED BY E.I.OUPONT DE ICMXRS t CO. THE INFORMATION AND KNOI-HO TTCREON MAY NOT BE USEO NOR TtC DRAHNS REPROOUCEO I1TH0UT THE IRITTEN PERMISSION OF DUPONT. ALL REPRODUCTIONS IN (HOLE OR IN PART, INCLUDING VENDOR'S SHOP DRAV1N6S. SHALL BEAR OR REFER TO THIS STAIN*. SCALE.. _ i : -_ _ 6 0 i_________ d r a in ar J. I . GASTON u *oatfo V JOE GASTON DATE 2-8-94 1-28-00 F IL L VOLUME AV AILAB LE ELEC. CODE CLASS IJ NO. FAA M M E R CHECKED B Y _________ ______ ^ -- APPROVED Bt__ _____ _ _____ ---- --- PftOJ. NO. WASHINGTON WORKS OF ww M 6 7 7 AR CF008251 EID076141 o oo ID076142 N 255.000 - + * MONITOR WELLS STREAM SAMPLE POINT U\N0OO>OT0>f K> GRID WEST VIRGINIA STATE PLANE COORDINATE PHOTO DATE*4 -2 4 -R 8 E .I. D U PO N T DE N EM O U R S & C O . IN C . amnmmaammwuunraciam.MM|anmaKcnSsoHrmiammawnasncmoiiusaWnnnido m tu -no r n . AU.M Q U C T I M 1H M U 1 INNA. U C U O M m <t M P DMCPM. uu flus 9 D O T not IM#. S O L ID W A S TE IN D U S T R IA L L A N D F IL L v u - _ J I _3J38.`_ ______ | m V . A L _QASTP____ 'jBrU-JQ # E J?ASJQ.N______ j 1- & - 3 ;D R Y R U N , W OOD C O U N T Y , W V IWIU 1 _ r . -- WM. M MDI rm x m. 9 WASHINGTON WORKS WW M 7 6 0 AR 199 9 ANNUAL LANDFILL REPORT WV/NPDES PERMIT NUMBER: WV007_244 (Letter, R.L. Ritchey to W.D. Brannon, dated 01/31/00) BCC: A. V. Malinowski, Legal, D7078 M. A. Bradley, Spilman, Thomas & Battle A. S. Hartten, BMP-27 M. L. Press, CH Works in m m : J. H. Little H. D. Ramsey, Jr. J. E. Auger W. H. Hopkins R. Banerjee D. C. Koelsch R. L. Ritchey L. K. Ireland/J. F. Moore/33.05.02.05 G. W. Klesel/J. S. DeBee In Turn: D. F. Altman A. A. Crane W. E. Lively J. J. Mentink M. M Pagels G. Woytowich RLR/DFA:vlw 0 0 0 ? .; EID076143 2000 AN N U A L LANDFILL R EPO R T W V/N PD ES PERM IT NUMBER: W V0076244 (Letter, R. L. Ritchey to A. G. Turner, W V -D E P , O W R dated 1 /2 6 /0 1 ) BCC: A. V. Malinowski, Legal, D 7078 A. S. Hartten, BM P-27, 2160 M. L. Press, C H W orks M. A. Bradley, Spilman, Thom as, & Battle In T u rn : P. J. Bossert, Jr. H. D. R am sey, Jr. J. E. Auger R. Banerjee D. C. Koelsch R. L. Ritchey J. F. M oore/33.05.02.0 5 In T u rn : G. W . Klesel J. S. DeBee In T u rn : D. F. Altman A. A. Crane W . E. Lively J. J. Mentink M. M Pagels G. Woytowich dsw/2:1Q7 E1DU4142 POCtt-TU tidirnieon QONOrQEMOVE DuPont Washmgtor Works P.0. 8cxUT Parkersburg, WV 26102-1217 January 26, 2001 C E R TIFIE D M AIL RETURN R EC EIPT REQUESTED Ms. Allyn G . Turner, Chief z. V o o Office of W ater Resources Division of Environmental Protection 1201 Greenbrier Street Charleston, W V 25311 Attention: Industrial Branch 7 P '7 /?<? Re: W V /N P D E S Permit Num ber W V 0076244 Dear Ms. Tum en Enclosed is th e 2 0 0 0 annual report sum m arizing the operations of our Dry Run industrial landfill. If you h ave any questions or need additional information, please contact m e at (3 0 4 ) 863-4271. - Sincerely, R. L. Ritchey Sr. Environmental Control Consultant W ashington W orks R L R /g w :d s w A ttach m en ts . cc: John G . Britvec -- J^7 Office of W ater Resources Division of Environmental Protection 1304 Goose Run Road Fairmont, W V 26554 Attention: Industrial Branch ........ ryn :s awnaunncCor-nny 0 0 9 `. EID114143 fir 3rmi?C.or, 2 I certify u n d er penalty o f law th at this d o cu m en t an d all attach m en ts w e r e p re p a re d u n d e r m y d irectio n o r su p ervisio n in a c c o rd a n c e w ith a system d esig n ed to assu re that qualified personnel properly g ath er an d e v a lu a te the inform ation subm itted. B ased on my inquiry of the person or persons w ho m a n a g e the system , or those persons directly responsible for g a th e rin g th e inform ation, th e in fo rm atio n su b m itted is, to th e b e s t o f m y know ledge and belief, true, accurate, and com plete. I am a w a re that there a re significant p enalties for subm itting false Inform ation, including the possibility o f fine an d im prisonm ent for know ing violations. R. L Ritchey 1/26/01 Sr. Environmental Control Consultant Washington Works E I D l14144 3 2000 DRY RUN LANDFILL OPERATIONAL REPORT Facility Users All the w aste disposed of in the Dry Run Landfill originates from E. I. DuPont, W ashington W o rk s and its auxiliaries. Landfill Shipments A sum m ary of the 2 0 0 0 landfill shipments is attached. Surface and Groundwater Monitoring A sum m ary of the 2 0 0 0 surface and groundw ater monitoring activities is attached. Landfill Operation. Construction and M aintenance Activity Sum m ary T h e leachate collection system constructed during 19 9 9 rem ained in service throughout th e entire ye a r of 2 0 00. Alm ost 3 .3 million gallons of leachate w ere transported to W ashington W o rk s fo r treatm ent in 2 0 0 0 . A cross section m ap showing the approxim ate landfill elevation at the end of the y e a r 2 000 and a topographic map o f the landfill indicating the proposed final grading plan are attached. D rv Run Landfill Remaining Capacity Calculations C alculation of 2 0 0 0 fill: N e t W a s te Fill V olum e M eth o d : W a s te volum e hauled in 20 00: = 4 ,1 4 7 truck loads x 3 8 .6 yd3/truck load (avg.) = 160,074 - 160,000 yd3 A verage net waste compaction (daily cover allowance included) estimated at 8 0 % for 2000: T o ta l 2 0 0 0 fill volum e = 1 6 0 ,0 0 0 x 8 0 % = 1 2 8 ,0 0 0 yd3 Ravine #1 Capacity remaining at the (existing cell) beginning of 2000 = 688,000 yd3 C apacity used in 2 0 0 0 != 128,000 yd3 Capacity remaining at the beginning of 2001 = 560,000yd3 B ased on 1 2 8 ,0 0 0 yd3 per y e a r net fill volum e consumption: 5 6 0 ,0 0 0 yd3 /1 2 8 ,0 0 0 = 4 .4 years rem aining life on existing cell eoo EID114145 4 2000 DRY RUN LANDFILL SHIPMENTS M aterial Coal Ash Number of ShiDments 1347 Total W eight Tons 19767:5 Total W eight Pounds 3 9 ,5 3 5 ,0 0 0 Paper, Cardboard, Wood Glass, Miscellaneous Solids, M etal, N on-Asbestos Insulation 1362 6 1 7 8 .7 8 12,357,560 Plastic W astes (Polyam ides, Acrylics, Polyacetal, PolyethyleneTerephthalate, F lu o ro p o lym ers) 1073 6339.32 12,678,640 Dirt, Construction Total 365 4147 6502.38 38,787.98 13,004,760 7 7 ,5 7 5 ,9 6 0 c o o s* V.J EID114146 5 2000 DRY RUN LANDFILL QUARTERLY LEACHATE ANALYSIS REPORT SUMMARY D ate Submitted Report 0 3 /2 9 /0 0 07/20/00 10/09/00 1/16/01 First Q uarter Leachate Monitoring Report Second Q uarter Leachate Monitoring Report Third Quarter Leachate Monitoring Report Fourth Q uarter Leachate Monitoring Report 2000 D R Y RUN LANDFILL Q UA R TER LY PO N D U N D ER D R A IN A N A LYSIS R EPO R T SUM M ARY D ate Submitted Report 0 4 /0 5 /0 0 0 7 /2 0 /0 0 10/09/00 1/16/01 First Q uarter Pond Underdrain Monitoring Report Second Quarter Pond Underdrain Monitoring Report Third Q uarter Pond Underdrain Monitoring Report Fourth Q uarter Pond Underdrain Monitoring Report 2 0 0 0 D R Y R UN LANDFILL Q U A R TE R LY W E LL M O N ITO R IN G R E P O R T SUM M A R Y D ate Submitted Report 0 4 /1 2 /0 0 0 7 /2 0 /0 0 10/20/00 1/17/01 First Q uarter Monitoring W ell Report Second Q uarter Monitoring W ell Report Third Q uarter Monitoring W ell Report Fourth Q uarter Monitoring W ell Report 2000 D R Y R U N LANDFILL SEM I-ANNUAL S TO R M W A TE R M O N IT O R IN G R E P O R T SUM M ARY D ate Submitted Report 7 /2 4 /0 0 1/23/01 First H alf Storm water Monitoring Report Second Half Storm water Monitoring Report 000' EID114147 6 2000 DRY RUN LANDFILL MONTHLY DISCHARGE MONITORING REPORT SUMMARY D ate Submitted ReDort 02/03/00 January Discharge Monitoring Report 03/13/00 February Discharge Monitoring Report 04/14/00 March Discharge Monitoring Report 05/16/00 Aprii Discharge Monitoring Report 06/15/00 M ay Discharge Monitoring Report 07/17/00 June Discharge Monitoring Report 08/15/00 July Discharge Monitoring Report 09/18/00 August Discharge Monitoring Report 10/09/00 Septem ber Discharge Monitoring Report 11/02/00 October Discharge Monitoring Report 12/15/00 N ovem ber Discharge Monitoring Report 01/16/01 D ecem ber Discharge Monitoring Report 2000 DRY RUN LANDFILL B EN TH IC S U R V E Y R E P O R TS 06/27/00 Benthic Macroinvertebrate Survey: M ay 11/28/00 Benthic M acroinvertebrate Survey: August C00V30 EID114148 7 DRY RUN LANDFILL 2000 G R O U N D W A TER /SU R FA C E W ATER M O NITO RING SUM M ARY O F FC -143* ANALYTICAL RESU LTS Sam ple Date: 07/19/00 Sam le Location F C -143 Resultfua/LI W ell #12 0.160 W ell #12A 0.128 Sam ple Date: 07/20/00 Well #6A 0.212 Well #12B <0.029 W ell #13 . 9.8 W ell #13A 9.9 W ell #14 0.115 W ell #15 0.763 Sam ple Date: 10/3/00 Leachate 27.4 Outlet 001 31.5 Stream Sampling Station No. 1 0.758 Stream Sampling Station No. 2 2 7 .6 Property Line 10.3 * F C -1 4 3 is am m o n iu m perfluorooctanoate ionic surfactant All analyses perform ed by: Lancastr Laboratories 2425 N ew Holland Pike PO Box 12425 Lancaster, PA 17605-2425 EID114149 990 980 970 960 730 720 E ID l14150 PONT DE .NEMOURS & CO. INC AZARDOUS LANDFILL UN, WOOD COUNTY, W.VA. VOLUME AVAILABLE oe CLASS fJ MO. F A A NUhflCR PROJ. NO. THIS WAVING HAS BEEN FURNISHED BY E.I.OUPONT K tcHOURS t CO. THE INFORMATION ANO KNOW-1-01 nCREON HAY NOT BE USED NOR TFC BRAVING REPRO- OUCEO VITHOUT THE VRITTEN PERMISSION OF OUPQNT. ALL REPROOUCTIONS IN IHOLE W IN PART. INCLUOI VENOOR'S SHOP CRAVINGS. SHALL BEAR OR REFER TO i l 601__THIS STAW. SCALE_____ BATE DRAIN BY___. GASTON 2_-8-_94 UPOATED BY- JOE_ G A S T O N 1- 2-01 APPROVEO BY- W A SH IN G TO N WORKS OF ww M 6 7 7 AR POO; KJ\ 1 Title O PROPOSED FINAL WASTE ^. GRADINO PLAN 2 O PRELIMINARY Owner E.l. DuPont de Nemours 6 Company DUPONT WASHINGTON WORKS PARKERSBURC, W EST VJRCINIA P, EN( 000S34 FE3-02-Q I 10:18AM FROM-NOE OFFICE EQUIPMENT Lubeck PSD: Chemical in 1groundwater not a health threat yHOOSIAOHM ______________ 3taff W riter A lale ammonium pcrfluorooctanoata with yaw w ew ? Alao called C-, PPOA, a PFO and FC-143, the surfhctont chemical {bund in groundwater consumed by Lubeck Public Service District customers does not pose a health throat, offi cials said. Pcprecennrivac of DuPont Washington Works rod (he Lubeck PSD said ifae presence a t C -l is not dangerous at cur rant levels. The levels of die chemical bars been monitored fbr a long time. Jim Cos. district manager for the Luback PSD. said Tuesday. The chemical has been detected in the drinking water sc Washington Weeks el a leva! o f 0.2 p m par U nan and in Luback Public Service District wells at levels tanging bom 0.1-0.5 p m per billion. These levels are lower ten D u P o at'a own guideline of no poetar than 1 p m p v b U lk .. Low levels of this chemical have been dseKm d'iirjpoundw atir walls in the Lubeck atea ft mote (han 10,yarns. Dawn Jackson, external affairs assistant at Washington Wades, said its presence at current levis posas oo danger people or the environmo*. "W e've got many years of m aniiorlnf date bom (ha 3M TabsCompany, bom IXPonr and b a n other that have d m soidiea," Jackson said. "There isn't anything in the scientific d a a to indicate a need far concern. That* is nothing to indicate that (here is any human health effect.'' However, ana mason the community la --"--n -* is bacause C- is a persistent chemical, meante it remate in the longhuman body and theacosynm far a time; Jaefcron said. " h is a p a rs lin t chemieaL moanlns dtac it dooe sick around in the^anvirentnant. and m the human body," Jw kiflii said. "A iao M in aied lalely n ietm S sd m d aU m in aB d .T lu t j~ t - - p r u r if Thun the n a r ntTT mp<k<inlhTlitiWsa "1 ....... a it does cake longer far it to be elim ihaidd'frointhc body.** Washington Works uses C-S in some o f its manufacturing processes, Jackson said. 3-M, the company that manufacturas C-8, said in a press release Out this persistent compound. Uka otlax matenala in the environment, can be detected broadly at extremaly low levels in the environment and in people. A ll existing scientif ic knowledge indicates that tne presence o f (tea* materials at such low levels does not pose a human health or environ mental risk. 3044287895 T -1 3 3 P Q i / 3 2 s--333 of C-8 m drinking water. Lhe>t^uj. wiucq serves j . juu. uj- tomets is giynat/ederaJ snd-statnagnklel1iys an what (a mon itor. It monitors C-8 levels even though it's not required to. " If we And something e litrin the w a , ^och as the C-8, we will monitor far th at," Coatadded. `'jSdtthr all of our lev els a n fine. Certainly we will continue to monitor th an to make sura they remain that w ay." Jackson said that although th e n la no federal standard regulating the acceptable level of C-8. Washington Works sets strict guidelines to protect people end the environment. "There Is not a regulatory lim it on it," Jackson said. "A lot of times, for what materials we use, we sot our own tu n - dotd." Jackson said that DuPont's guidelines ore so stria that the company will have no trouble adbving to federal or other regulatory standards, if established. "O ne of the dungs we-have mid our own employees Is (hat if a regulatory agancy ever does set g level, we will be able to com ply," Jackson said. . Recent atteodqn has been draw n 'to C # because 3M decided to phaseo u t on entire branch of chemistry, called perfluoroctanyl chemistry, and PPOa is one of the minor products of that line. "T hey're phasing out a lot of different product!," Jackson said. "T his ia Just one of them ." When 3M decided u phase out perfluoroctanyl chemistry, local concerns were raised. W ashington Works and the PSD, which continually work together to monitor chemical levela, decided lo inform the community o f the sltuatioo. "Jim (Cox) got a couple of questions from people in the community last spring." Jackson said. "W e started to look at it and find out what people's questions were: We made the decision together that the thing to do was send a let to the customers of this district.". .. Although health issues were raised when 3M decided to phase out perfluoroctanyl cheaustty, .W ashington Works officials remain confident in thssbm paay's products. "Thoy're confident that their products am safe," Jackson said. "W e've been confident as w ell, but w e've continued to monitor, just as a precaution. We'vw been using it st the plant for yean and w e've been monitoring it far 20 yean or m ere.'' M oreover, 3M, which has manufactured C-8 and other chemicals like it Tor approximately 40 yean, continually studies its products, according to e statement on the compa ny's Web tite. Jackson said that in die past. DuPont employees who worked wuh C-8 on a dpily.basis were exposed to it through skin absorption beoa^qg icj^ipjjjjk to be available in powder form. ' 1">, i . >-r *' "O ur employees were exposed to it at higher levels, at that tim e." she said. 'The company then started to prepare it for us in a solution form add that reduced it (the exposure level) considerably. / ' 'Through better control measures, better forms dial we can purchase it in and better ways to handle it, over the yean w e've been able to reduce it at the p la n t" Jackson said. "O f course reducing levela at the plant also would contribute to reducing emissions into the environm ent." Jackson said the curr ent acceptable employee exposure limit for C-8 is 0 .0 1 m Ulipam s per cubic m ew at an eight hour time-weighted average far skin absorption. "Somebody could be exposed to that level constantly over an eight-hour work sh ift." Jackson said. "T hat's not the same thing as somebody lit the community who is not exposed to it for eight hours at a tu n e." Standards in the workplace are different than they are ui the community. Therefore, DuPont came up with an accept able level for C -8's presence in drinking water. "Through calculations done about exposure guidelines we've come up with keeping it below one part per billion.'' Jackson said Jackson added that these are the guidelines that DuPont has set for (he safety o f its employees and the general public. However, they ate prepared to comply with any regulatory standards chat may bo set in the future. "A t some point the EPA may come to us or Jim tod tell us, something different and we will comply with that." Jackson said. 00 O fficiais: Chem ical in grounaw ater no threat By ROGEH AM1NS Staff Wrtbr Repreaetodver of DuPest WasUnfea Warta sad fe L rtrd r PrMir Seaie t Dbafce nM fe fraseoce af satUctto ebendcil m (N M fe fe r cennoaed by Lteeck PSD r a im e n don M fOM i heafdi ttnett. Lo* Heasb af fe cbeadeai, a f 1 u o a lta yaflaorfoctuNMte (abie cvOed C l, PFOA, WPO ad FC-1 4)x heve beentnootwed brf tbe toeck PuWk Snior Distrito h >loa* tie, ln On. stifct maniger fot fe Luteck PSD. i*id Tbcuby. TT* cbanjcil tin beca detecte! ia fe <triaHn ime u W tshiafn a W o tis tt i levW af 0.1 pero pa tiiHtaa Md tn luhcdt F ilie Setvic Dbtnrt welb >t lewds rsngiDg beTM 0. t J ptfrt prr binko Ttieje W-.el) lewer Dun DvPMft * foMetlc* of o eceqmen fe M | M% fe fe n a li. m terfea l peto per b ilie * " li b a(nteadM dieal, w a a la t ai 1 Lo* Uvei af fe i chetateli lave te a dna teck arom i b fe a ilw a tu . a d la drtrctisf U y iw b d weils U f e Lteeck fe b a u body," faeboa a id *** b col am fe n o * t a 10 pean. Dana faeton, UEMdUiely aneeeOardal fe fe n d . TM a n n i l i h k t u b a ta li t W rrbkyto J------1-- - " *~~ --j - t r i n u n irli V eto , a id Ri fm eote c b m levali behaae,bacate* k dora e te Unger U rti tabe peaa m datar la pH fle or f e eavinanet. efeUated ben f e body." "We've p a n a ? yens efneaiM itaf dita W irbU fea Verta ne r C-d h rode <f Ita beta fe )M C nfany, te n (M tia a d iMiiUnaUg prooenq. U t a * a ld bea afea Ubato t lave fe a aridit.*' faci- JM. fe ccopany it o nnw fa ia n C -l, Ma a fA "Tbev to '! aytM tlf U fe lefcrtiif- oM ir a pveurefeasr fe i tbia ycoiaMat ceti k datalo todkrfc erad fe concerta T to tfa prend. U ti o ta r enterite In f e e n tra noto) la M irate thol fere u a y bnaa t o c a be dbecied tin n fly al emeiaely beai* e fftc t" la * Irvteii In fe env fc a a a rad ia prcfde Htwrver. eoerea* ite coatanty lacea- AB eahdaf icittU flc knnwltdge inriiolea cemedis becaitaeC -l la aparisin! tie n ili. fea fe p r ima, of fe w rsterU lj M sacl itteauag Sranoira In tbe tiram i tiody od fe -------------=j^-- lo * kveb does boi pan i tirane tiealth et Chemical enUato to d eUL O r tfd fe n b w tegOikay f e t o ! io fe ti fe U n ii afC 4 h dtltehn a n o. Tte PSD. Mib a m a U to . iman an b tre* fcdefalid<iatiefaSdttUesan a te i bram a le*. kaeabaes C-* letali cacafeagk i ' i a ri teqakedto " l i w fiad srm kU g tb t U fe nato, t o t m fe C -l. *e di m o t t a fcr OtrC' C a added. "Sa ha a l r f sur laveU ara bue. CeatoUy *e rii cantata am ailer te a aa to te it o feyieaaU ita way " la t t o tabi fea f fe iajb diere b ao (ad erii naadifdR |fedata tncptaMs Uvei af C-d, WfnMagtina V a iti tea tiric i galdetkxs taprotactpecyk ndfeeavkeaaKM. Saa CHORCAI, Faga SA --v J '/ ' c- CosnvtiE n o ti Pa IA ta do aa scad a b ite r fe cas- "OT enne redada teieb ta Brarrr of fe r dbtifct" yijMrt aho areuld t e d tito tir "Ititte h m i a iryabrery Unti A lfengb tiento batel ate todac* tteaafaai tati] fe eavtim- m k ." faeton it o " A M of tto n . fcr arto n r tn ift 4 tn , *e sei oar o*a ra d ia i" Jacto aid fe t DePoaTi feWelinea ac n k t fe l fe n to d bea 1M dedded aa fteM 0 *1 perflootocbayl chefestay. fn lfe fe a Verta oOfcbb lem bi coafldeat in die coafeay'i pod- oeta. aeu" facto u H fe cnaeal recep. fee *(te|e t*pw e lUt * * C- 8 a d d i RdHrrauperafHe torte a ti b tira itUne-adjUed aeer- (fodacli ne tale.'' IrrtSMadpaay a d hace ao cable adberinf "Tbay'ie ceafideot fe l fe b lo Metal or a tto itgatatoy feda, if Ibey aie ever ejafebbed "V e ' * baca ceofideat m eB. hd "Om of fe A U p *e bave M . *e've cmfinvrd to taaadba. jto n tur OM enployeer ta tu r If a itg t- (m m ito W e'vt beta asini B * tfttrik iM k ta p tk m 'Veartedy eoald be eifored ta ut Uvei eooilKady ver la eiktfeoer otti dad." faeton atte T t o i ncatoc ta to tU if U anae- lamy ayetvy enee doer sei a tevet, *< wUtie itile lo cnaply." b e to n fe pinot for yent red rn've beca aaotoUt Ur ao )ar ortacat-" tedy U fe o n m a itr * N b etpoMd ao ba el|U bont M a sabL Rem.t Mteetea bai beta dttwn M C -l bearne 1M dedded to (tele m* ia totSie beanti of ctjeniitry, cabed yei flarrocm yl ebeniatey. and ffO A b ore of f e ana (red Mneaier. JM. U d bai n a to Iticued C -l rad ta ctinaicab R b N fet ^tfrotabandy 40 yem, oanOnally atudiei H ftodueb. acconiiaf M a s td e m l m fe m uoiaj"~ Web site. tose." Sbadato U f e ortpUct ara direnai tkaa fe y e U fe cotaantoty. TVrekae. DuPonte n * i f o titi ae n re itrtfe to r i fe e l i pinne ttiiU cf wUef. acta o f f e I to "Tbey'ie pbaan| eid aUt of f- fercM prodotta," Jackroa aaid. "T b ii b ju it eoe of b e a ." bea JM dedded M fhaae a perflnoroctaayt ctieoirtry. locai oonrtras ere la b e l W nhtaiti W a ti a d fe rSD. bich n ta ta Uy wtek lopoter aomoaHoi fe n - teai teicb, decided In Ubata fe cfinm nby r f fe litvadra. *rn(C orifei empie ofqaar- tiots bori (afl< ia fe moneady b s t p h o t - " laeksoa ia to - ' " U t Uarttifio look m ul G iti uot * to ---UMkm* n -a f* Wfti CTIfef^ Urtasa raid tto U fe pad, DuFotd eiapfor ubo orted r i C -l * i M y basii *en etposed ta it tb tu fk it o ObaatpOoa beconse h ned to be rn rtte iapewder Amo. "Our enplayees wett etposed to it si M|ber In-ela. ito itine," itM ir il 'TbeoonyaayfeostKted to p e p u ri farai In aartidim tiw it aod ito ledaceli it (toe expaiae le tti) ooasidenly. "Itra u fb beser anbol neraoro, better binai thoi *e caa yurttine it in and he<rrr>yito loadle li over tKe veaia *e *e ben aMe to "TUmyfc cakuhOtn i dooe boa espouia oideUaas to v e COK f w i* b*e(!* il bete* om pan perbiltioa. " faetonsaid Ijckaoa teded fe t dure to fe ganMnei lU t OuFto Ito et fe dir idfery of <ts emptoem and tot geoenl jtobtir. Hovievtr, fe y an (ttp to d to cctfey witli aay tefula M r/ lUBdotb ito ras te Jet i lite Ukr. "A t uri poi* fe EPA it coras to ai fan m i te i a nonrthjng tofTernit ad e il comp'. ftti dna." JKkaon aaid. CeoUit t n y r A tin i io evneff 1 tt c t 02/02/01 FRI 10:18 [TX/RX NO 52331 O i 1 coo nV1 r _H i> D uPont Haskell Luboratorv January 25, 200! Dr. Charles M. Auer, Director U.S. Environment;!! Pr.'iecti.-r. 'e -urn. Of: tee <>f P Orami Prevention and Toxics Chemical Control Division -MO M Street NW Room, -a . : dmgion. D.C. 204&0 Dear Dr. Auer In my June 23, 2000 letter that transmitted DnPontN Voluntary Use ana Exposure Information Profile fUEIP' for Ammonium Perrluorooctanoace fAPFO, CAS43825-261), I noted that, as part of the ongoing surveillance of workers potentially exposed to APFO, a series of blood samples were taken in year 2000 from workers and that DuPont would voluntarily submit a summary of the results when they became available. The results of the blood serum tests are raw. ,, ..mm.a. a nummary of this year's results for workers with mmmiiee At'1*0 exposure potential is beiow. Year 4 of ; ' Samples ; L_____ l _________ ~1 ' j 2000 1 72 i Minimum Concentration (PPm> 0.02 Maximum j Mean Concentration j Concentration yppnaj___ ;___ _ ( ppm) WO ; 1.53 Note the following concerning the above data. ^ Five samples, ail from workers in one particular job, tested greater than 5.0 ppm. Among the jobs with potential APFO exposure, this jon should have the least exposure obtcntial. We are investigating the cause or these elevated results in this group of workers. Eliminating the five data points from these workers gives a maximum concentration of 4.9 ppm and a mean concentration of 1.16 ppm. > Some employees not routinely working with APFO provided blood samples. APFO levels in this group of people are consistently iess than 0.2 ppm. EID114198 OOO^S 1 January 25, 2001 Dr. Charles M. Auer > Blood serum APFO concentration seems to he a function of length of time in assignments with potential APFO exposure. Due to variances in length of service among workers in assignments with potential APFO exposure, average values may be influenced not only by exposure potential but also by average length of service of the volunteer group. Additional groundwater and surface water measurements have been reported and some older cjata has been located. These additional data are reported on pages 5 and 6 of a revised Voluntarv ( HETP Please replace *ho prc. ions submisocr. a ith the attacned crsion. Wte that there is public copy ana a copy containing Confidential Business Information. 1; }i<a Alsu to discuss he nfonuauon contained in this document, please contact Robert F. Pinchot at (302)999-4074 or e-mail at Robert.F.Pinchot(gu.sa.dunnnt.com o r me at r?02 3AA- ' <o Attachments Very tally yours. IT Gerald L. Kennedy Director, Applied Toxicology and Health PUBLIC COPY \ nluntaiy l i'.ll*. Aiiiiiiimmm I'crfliiorooctanoutc Revised January 2001 Voluntary Use and Exposure Information Profile Ammonium Perfluorooctanoate (APFO) (revised January 2001) V o te : T h e in fo r m a t io n c o n ta i n e d in th is d o c u m e n t is s u b m it t e d v o lu n ta rily a n d m a y be su b je c t to f u t u r e revision and/or m odification. C O N F ID E N TIA L B U SIN E SS IN F O R M A T IO N RED AC TED I. CHEMICAL IDENTIFICATION Chemical Name: CAS Number: Ammonium Peril uorooctanoate :s2'-2- ! II. COMPANY IDENTIFICATION Company Name: E. I. du Pone de Nemours and Company Nile Locations: . Site where APFO is used as a reaction aid: Washington Works Route 892 Washington. WV 26181 Sites where APFO containing products made at Washington Work' arc processed. Purlin Plant Cheesequake Road Parlin, NJ 08859 Spruunce Plant 5-10! Jetterson Davis Hwv. Richmond, VA 2 ;2 3-1 Site which disposes of waste containing APFO: Chambers Works Rte. 130 Deepwater, NJ 08023 Confidential Utisincss Information Redacted COOL-' < EID114201 \ 'limitary ( PIP, Amiimimmi l'erflmii onctanoatc K c v t s c d ( a m i a i v 2t)t) l Technical Contact: Robert F. Pinehot (302) 999-4074 DuPont Fluoroproducts Chestnut Run Plaza Bldg. 71 1/2210 Centre Boulevard Wilmington, DE 19805-0711 III. DUPONT AND CUSTOMER ACTIVITIES Narrative Description of APFO Use The block diagram on the back page titled "DuPont US APFO Balance" describes the i'i'Vo v - discussed 'eiov. aim. Itie esi:mate: i etnW'to:t< u>snc:a:cd >.*. tch these acti\ ties DuPont uses APFO as a reaction aid in the rroducuon or'nob. tetrar'luoroctlv lene . !r tet:..:uuu\.e:n;.:ene ilid ii cc-peUir.ets. The ptvccss utilized at DuPont's Washington Works for making PTFE and co-polymers consists of polymerizing TFE (and other co-monomers if desired'' in an aoueous media with a ^mnl! amount of APFO n aid m the reaction. Following the polymerization step, the polymer dispersion is either dried to remove water and APFO or concentrated (removing some of the APFO), stabilized and sold as an aqueous dispersion. The dried polymer contains very little, if any, APFO. The APFO removed from the polymer is recovered for recycle, captured and destroyed off sice in an incinerator, captured and sent to an offsite industrial landfill, and/or emitted to air or water at the Washington Works. The stabilized polymer dispersions are sold by DuPont to industrial customers (both in the US and outside the US) for a variety of uses, internally transferred to the DuPont Spruance Plant for the production of Teflon fibers and PTFE coated synthetic fibers, or internally transferred to the DuPont Parlin Plant for the production of Teflon Finishes.' . A small amount of non-hazardous waste polymer, water, APFO and other additives generated at Washington Works is treated in a wastewater treatment facility at DuPont's Chambers Works. This material is either emitted in the Chambers Works water discharge or captured on carbon and landfilled in a secure landfill. The internal process at the DuPont Spruance Plant to produce Teflon fibers involves, for most of the product, a "sintering" step in which the APFO contained in the product is destroyed by the following reaction:' 1 P i. Krusic, D.C. Roe, "Thermal Decomposition o f C.S Ruonnated Surfactants and Related Materials Studied by High Temperature Gas-phase WF N M R . A New Alternative to Thermal Gravim etric Analysts" , DuPont Internal Report. Cun/ldcntiai Business Information Redacted E1D114202 Page : \ iiltiiK.uy I RII*. Ammonium I'eriluorooctannate Revised J.mnaiv 2001 CFjtCFiACOO'NHC ~ y CFjiCFOiCFdd + CO: +NH, This reaction goes to completion at 350CC and 0.2s residence time. A small amount of product processed at DuPont's Spruance plant docs not get sintered and thus contains a small amount of residual APFO. These products are used for industrial pump, valve and compressor packing materials. The process for making Teflon finishes at the DuPont Parlin Plant involves a blending operation of fluoropolymer dispersions with other additives including solvents, binders, and pigments. The small amount of APFO emissions to water from this facility is due to waste generated during product changeovers. Some of the fluoropolymer dispersion is processed at contract facilities where the material is dried at temperatures >350C thus destroying the APFO according to the reaction abo\c This dried materia! is then U 1 ; U ' f , f C U U '. t O i ; i U s f . C b p 1 O c l U e l s . Tlie final product produced is then v id to -1 ;..toC' that apply 'die product to a vuh>;:a: tsuch as cookware; via automated spraying or roiiercoating. Emissions of APFO from these operations consist of overspray that is either captured on Filters and landfilled or absorbed :nro '.vatcr resulting ::i a v.ucr emission. Product trail is applied to lire substrate ts then typically "sintered" at temperatures approaching 800F resulting in the removal of the .APFO from the substrate and subsequent destruction according to the reaction above. Customers of dispersion products use the material for a variety of applications. However, most applications involve a "sintering" step where the APFO is destroyed. There are a small number of applications [ ] where the customer heats the dispersion products to temperatures that allow the .APFO to sublime resulting in air emissions. There are also a small number of applications [ ] where the customer'' product is not ho,.ted rooking in the APFO staying with lire product. These applications include industrial packings, and industrial filter fabrics. IV. SITE RELEASE AND TRANSFER INFORMATION FOR TRI CHEMICALS Not applicable- APFO is not listed on ihe TR1 V. SITE RELEASE AND TRANSFER INFORMATION FOR NON-TRI CHEMICALS A. On-site Air Releases ! Washington Works Parlin Spruance Fugitive Negligible ' 0 0 Stack (Point Source) 24000 .o 0 (.'nnfidential Business Information Redacted E lD l14203 Chambers Work 0 Rage i V o l u n t a r y l i C I P . A m m o n i u m I'o r f h i n r n n c t a n o a t c Revised .Januarv 2001 Comments Air emissions are estimated using engineering calculations and judgements and limited measurements of specific point sources conducted in the past. B. On-site Water Releases Point Source C nmme nts Estimated Total Annual Releases ( lbs. 1999) Washington Works Parlin Spruance Chambers Works ! 55000 300 150 18,500 Water emissions are estimated using engineering calculations and judgements and limited measurements of specific sources conducted in die past. Washington Works emissions occur for approximately 350 davs/vr while the 'tiler sites emissions occur tor iO-lOO Jajs/sr. Releases or APFO to the Ohio River from the DuPont Washington Works Plant were modeled using the Probabilistic Dilution Model (PDM Beta Version 4.0 Beta June 11, 1999. US EPA Office of Pollution Prevention and Toxics) and a constructed Microsoft T Excel spreadsheet model. APFO release data for 1996 were used in both modeling exercises.' The PDM indicated that APFO concentrations of 1.0 ptAPFO/1 would be exceeded about 50% of the time during the year. APFO concentrations of in the river would exceed 0.1 ug APFO/1 90% of the time during the year and 10 ug APFO/1 about 2.2% of the time during the year. Average annual APFO concentrations in the Ohio River calculated by using a Microsoft Excel spreadsheet was 0.423 pig APFO/L. Modeled AFPO concentrations in the river ranged from a low of 0.199 pig APFO/L in March to a high of 0.965 pig APFO/1 in September, which correspond to high and low river flows, respectively. Average Ohio River flows and volume data calculated from the US Geological Survey was collected at the Belleville Dam and used in the spreadsheet model. The Belleville Dam is on the Ohio River 13 miles downstream of the Washington Works Plant. This river flow data is the closest location downstream from the plant where this type of information is available. In 1999, a drinking water sample obtained from GE plastics, Washington WV, immediately downstream on the Ohio River from DuPont Washington Works showed 0.562ptg/l APFO. 3 W .R .Berti, " M odeling Releases o f Am m onium Perfluoroocianoute imo the Ohio R iver", DuPont Interna! Report EMSE-0S4-00. EID114204 Confidential Business Information Redacted 000F..U Pativ 1 V o l u n t a r y I . l-J11*. \ i n n i o i i i u n i P c r l l n o r o o c t u n o n t e R e v i s e d . / a n u a r y 21)0 1 In addition, samples obtained in January 2000 from three different wells at the Lubeck Public Service District, downstream of Washington Works on the Ohio River, showed 0.8ug/l, 0.44jag/l and 0.3 13 u.g/1 APFO. Subsequent samples in April, May, and August 2000, showed a maximum of 0.59 ug/1 and a minimum of 0.07u.g/l. C. On-Site Land Releases Chambers Works treats APFO containing waste in a wastewater treatment system. Engineering calculations and judgements and limited measurements of specific sources in the past estimate that approximately 30% of the APFO in the wastewater treated is adsorbed on to a carbon media that is landfilled on site. These land releases are estimated to be 8,000 !h in 1999. Prior operations have resulted in measurable APFO concentrations in three landfills operated by the Washington Works in Wom Virginia. At Letart' Lmdfiil. surface water measurements in 199y and 2000 ytd range from 2.23ug/l to 3240(J.g/l, with an average of 1392ug/l. Groundwater measurements taken during die same lime period at Leieii nuiuiiil range mom OO.iug/1 to I7400u.g/1, with an average of 2537fJ.g/1. At the "local landfill", the groundwater concentrations range from 0.046ug/l to 39|ig/l with an average of 8.S3p.g/1. Surface water samples at the "local landfill" range from 0.54ug/l to 87jig/l, with an average of 18.5u.g/l. At Dry Run landfill, there are limited measurements of groundwater and surface water, with the maximum concentration in groundwater of 15pg/l and the maximum concentration in the permitted outfall of 200ug/l. In 1990, samples of surface water were taken and showed concentrations as high as 1.6mg/iJ. In 1992. samples in the "upper" and 'lower" ponds near Dry Run landfill menu:red 220u.g/l and 230u.g/l, respectively. Samples taken in these locations at Dry Run landfill have since shown lower concentrations. In 1999, a RCRA Facility Investigation was completed for Washington Works and was submitted to EPA Region III in June. 1999\ The report contains data on groundwater concentrations of APFO at Washington Works. 3 Maps o f (he lan dfill locations and specific m onitoring locations and results are available upon request. 4 The validity o f tnese 1990 analyses cannot bo verified since the method used for analysis, the sample technique, the chain o f custody, the sample quality control/quality assurance procedures, and therefore the accuracy o f the results are not known. 5 Report was submitted to M artin. T. Kotsch, Remedial Program Manager, EPA Region III, Philadelphia. Confidential Business Information Redacted E I D 1 14205 00 OS.5 Page ; Voluntary I.'KIP. Ammonium PcrfluoroucMnoate Revised January 2001 D. Transfers to Off-site Locations Washington Works: 11! Incineration Wastewater treatment Underground Injection Hazardous Waste Landfill Other landfill Recycle or recovery Estimated Total Annual Releases or Transfers (lb. 19991 16000 134006 0 2600 25000 VI. ON-SITE WORKPLACE EXPOSURE A. Information on the Number of Employees Potentially Exposed The tables below describe the number of workers that may be exposed to APFO in year 2000 during their normal work activities for each of the three sites where APFO is used or APFO cenLtmii'.g product is processed. Hours/Day <0.25 0.25-1 1-8 j i <10 i i ! Washineton Works Davs/vr : lo-ioo i 100-250 ;1 i i 242 ! >250 ! j ! ^ Routine worker activities that have potential for exposure: > Handling raw material APFO > Handling raw dispersions containing APFO > Maintenance of polymerization reaction systems > Polymer dryer operation and maintenance Packout of PTFE and co-pol\mer dispersion products r- Operation and maintenance of APFO recovers systems 6Transferred lo Chambers Works facility (see section B and C ahuvej Confidential Business Information Redacted EIDI14206 OOOT.'T, -i Page Voluntary l,'HIP, Ammonium PerfiuoroocUmoale Revised .January 2001 oo A1 i Hours/Day i <0.25 : 0.25-1 1 1-8 <10 Parit Plant 10-100 Days/vr 100-250 !1 18 >250 "i -------- ] -- 1 ------- ---- ----- -} i 1 Routine worker activities that have potential for exposure: > Handling of PTFE and Co-polymer dispersion products > Operation and maintenance of blending facilities > Packout of finished product Note that at no time is the material handled at the Parlin Plant at an elevated temperature where the APFO could sublime. Therefore, there is little potential for exposure to airborne APFO at this facility. All exposure potential is through skin contact during handling of the polymer dispersion materials, all of which contain <1 % APFO with most contammo <0 25C APFO. Hours/Day <10 <0.25 0.25-1 ____________ >8 Spruance Plant Days/vr i 10-100 100-250 II T <10 I 1 i! >250 ! i ! : 1 Routine worker activities that have potential tor exposure: > Handling of PTFE and Co-polymer dispersion products > Operation and maintenance of fiber coating facilities > Operation and maintenance of sintering rolls > Packaging of non-sintered product. Note chat the PTFE and co-polymer dispersion products used at the Spruance site contain <0.9% APFO, with most containing approximately 0.3% APFO. B. Information on the Exposure Levels of Washington Works Employees Since most of the processing done in the L'S with APFO and APFO containing intermediates and products is done at Washington Works, DuPont's airborne industrial hygiene data is concentrated at that site. The limited measurements of airborne APFO concentrations at the other sites where APFO containing products are used have shown much lower levels (mostly non-detectable) levels of APFO. The data in the table below Confidential Business Information Redacted E ID 1 14207 000 Page 7 Voluntary CLIP, A m m onium I'ciiliini'ouctaiinnte Revised .January 2001 reflect monitoring done over the last 5 years at Washington Works. The sample results are a combination of chemical operator and maintenance worker personal samples. Year Sample Type 1999 1998 1997 1996 1995 Partial Shift (mostly 6-8 hours) # of Samples 100 83 100 73 32 Minimum Concentration fmpb7) <0.01 .001 <0.01 N/D N/D Maximum Concentration (mpb) 0.58 0.78 2.4 0.29 0.16 Mean (mpb) 0.061 0.103 0.146 0.055 0.067 Standard ' Deviation 0.151 0.145 0.378 0.069 0.063 ! 1 ! Partial shift air samples are taken at the rate of 200 mL/min using a Tenax collection tube that has been pretreated with sodium hydroxide/ethylene glycol/methanol. The APFO is desorbed from the tubes using meihanolic hydrogen chloride, which also serves as a derivatizing reagent, converting the APFO to its methyl ester. After workup, the methyi ester is quantified using a gas chromatograph equipped with an electron capture detector. The methyl ester of perfluorodecunoic acid is used as an internal standard, and at least three calibration samples are prepared to cover the concentration range of interest. Precision is estimated to be +/- 1 0 relative. The data above show averages consistently below the AGCHI TLV of 0.01mg/m3, with only a very few samples above the TLV. Where results are above or near to the TLV, the event is investigated and corrective action (additional personal protective equipment or engineering controls) to reduce the exposure levels is undertaken. Older data from the 1980's show higher levels of exposure. In the early 1990's, Washington Works switched from receiving the APFO as a powder to receiving it as an aqueous solution. This change was done to reduce the potential for exposure during handling of the dry powder. It should be noted that in the 1997 time period, the site was starting up new APFO recoverv facilities. Operating and maintenance difficulties associated with the start-up of these facilities may have contributed to the higher levels of APFO in the persona! samples during that year. Task specific monitoring data and wipe monitoring data exist. However, these data are not indicative of employee exposure and are not presented here. These samples are taken to identify areas where additional exposure controls may be necessary. Engineering controls to reduce exposure consist of the follow mg: > Reaction systems are closed systems with continuous ambient monitoring for monomer concentrations s- Ventilation systems are installed where airborne concentrations are significant > The polymer dryers operate under negative pressure to contain APFO and other materials. > Recovery systems are in place to reduce airborne emissions. 7 mpb= moles per b illio n . Q.56rnpb is equivalent to the A C G IH T L V o f 0 01 m g/m 1 b/.(>:i)i)d>i Confidential Business Information Redacted f 14208 Page 3 \ oltint-.iry Utili*, Ammonium l'erfluornoctanontc Revised .Jumiarv 21)01 Personal protective equipment that workers regularly wear consist of the following: > Safety shoes and side-shield safety glasses in all areas. > Impervious gloves when handling APFO solutions or aqueous dispersion products. > Chemical protective coveralls and goggles or face shields when the possibility of splashes of APFO containing solutions is present. > Airline respirators or cartridge respirators where monitoring has shown to have high exposure potential. At Washington Works, blood serum levels of APFO have been measured since 1981. Measurements of blood fluoride levels have been taken prior to 1981, but are of limited value in assessing exposure to APFO. A summary of results of employees with identified APFO exposure potential the 1995. 1989-90, 1985,und 1984 volunteer sampling events m in the table below. Due to significant job assignment movement during this period of time, analysis of trends of data are difficult. The data in the table below prior to 1995 are for employees included in the 1995 sampling data so that comparisons of relative levels ' of APFO in blood serum can be compared. The entire data set of blood concentrations is available upon requesr.i Year 1995 1989-90 1985 1984 # of Samples 73 23 21 19 j Minimum Concentration : ippmi i 1 2 1 04 i 6* ; 0.07' Maximum Concentration (ppm) 4.5 8.5 189 24* Mean Concentration (ppm) 1.57 3.13 2.44 3.82 i This individual was working in a job that has APFO exposure potemial at the time o f the sample. '' This individual consistently has iiad the highest blood concentration of APFO since APFO specific samples were taken. This employee left an APFO exposure potemial assignment in 1991. In 1995 this employee's hlood serum level was 4.4ppm. Confidential Business Information Redacted EID114209 <?Of) Page > 1/ 23/01 Public Copy DuPont US APFO Balance / 1 -- .. . I Captured and i Seni lo Waste M Waler Treatment j oli-site i ' ..................... _ . y C-8 used for Polymer Processing V -' . N Captured and Recycled to Supplier ' .> Contained in Dispeision Products DuPont Use tor Producing Teflon Finishes Exports EIDU4210 i? Residual C-8 in Dry Resins i 'JP c.n c? -- External Sales to Industrial Customers Received in NonDuPont i generated t wastewater f ~ ""S I Contained In Product/ Applied 1 to Substrate ----------- , Contract Processing . _____/ A i