Document M86QvbdGMVjGQyqbYnwJz5nL

Environmental Working Group ||Policy Memo: DuPont, Teflon, Water, Contamination, ... Page 1 o f 3 f R jlji6 -- I IS'f ewg/science policy Critique of community briefings by West Virginia DEP >>l EWG Letter to West Virginia DEP >>| EWG Policy Memo The following is the text of the letter written to West Vli DEP stating EWG's findings: ^ O November 12, 2002 S Mr. Michael Callaghan Secretary West Virginia Department of Environmental Protection 1356 Hansford Street Charleston, WV 25301 Dear Secretary Callaghan: cn 13 3e Contamination of drinking water supplies by the toxic industrial chejm perfluorooctanoic acid (PFOA, or C8) is a continuing concern to the re! Parkersburg and surrounding areas of Wood County near the source o pollution, DuPont's manufacturing operation in Washington, West Virg As part of an ongoing assessment of human health and environmental by C8 and related compounds, researchers at the Environmental Work (EWG) examined materials on the subject prepared by the Departmen Environmental Protection (DEP) and presented by agency staff at seve meetings last summer. Our focus was on the science behind DEP's woi conclusions the Department presented to Wood County residents who exposed to C8 pollution from the DuPont Plant. EWG's over-arching conclusion is that the DEP's assessment Is serious numerous crucial -- and often very basic aspects of C8 science anti to: review of the science available at the time of the briefings shows that presentations made by the DEP did not accurately represent what was known about C8 toxicity. These shortcomings are compounded by the misinterpretation and misapplication of standard procedures for establ drinking water screening levels and contaminant limits. Last July, in the context of a controversy surrounding a review undert, DEP on the hazards posed by C8 contamination in the state, you state "If there is any reasonable question about the science behind the DEP's work, I welcome the input. Constructive criticism of a proc or result is part of science and it is our intent to assure citizens o Wood County that the work done regarding C8 has been accurati and reliable." (The Charleston Gazette, July 5, 2002) We have five major concerns with the scientific conclusions and stater by the DEP at these public meetings. Each of them is explained in gre; and fully referenced in the attached review by Dr. Kristina Thayer of o Specifically: 1. DEP materials assert that C8 does not cause developmental and reproductive effects or present a long-term risk to people who di in their tap water. This contention is not supported by industry st of C8 toxicity and is contradicted by high-ranking scientists and at US Environmental Protection Agency. 2. The DEP concludes that tumors caused by C8 in animals are irrel to humans. The US EPA, in contrast, considers C8 to be carcinog causing liver, pancreatic, testicular, and mammary gland tumors company documents, DuPont scientists assert that the testicular pancreatic tumors found in animals could be relevant to humans 3. The DEP fails to account for documented food and air exposures when setting the drinking water contaminant limit, and then fails the public of this omission, even though it constitutes a major de from standard US EPA protocols. Assuming that water is the only of exposure is a one big reason that the DEP arrived at a drinkim screening level that allows between 15 and 100 times more C8 ir water than would be normally permitted. In addition, the DEP die http://www.ewg.org/policymemo/20021113/wilesltr.php 000003 11/14/2002 Environmental Working Group ||Policy Memo: DuPont, Teflon, Water, Contamination,... Page 2 o f 3 account for bottle fed infants and children, who are likely more susceptible to the toxic effects of C8 and who certainly get a higt dose relative to their size than an adult when drinking a liter of C contaminated water. 4. DEP's public presentation materials assert that the allowable amt C8 contamination in drinking water is between 10 and 100 times protective than it actually is. If DEP staff had actually applied the factors they describe at the community meetings, the screening for C8 in drinking water would be between 1.5 and 15 parts per I (ppb), not 150 ppb. 5. The DEP review concludes that the allowable dose of C8 (the reft dose, or RfD) is five times more protective than that for the aver chemical. It is not. The reference dose for C8 is five times lower stringent) than the average RfD because C8 is five times more tc than the average chemical. The amount of protection provided b' C8 reference dose is equivalent to, or less than (see below) that provided for the average compound. Overall, in every important matter of scientific assessment and regulai judgment, the DEP appears consistently to have come down on the sic less protective of human health and the environment in Wood County highly favorable to the polluting company, DuPont. This tilt not only does a serious disservice to affected West Virginians, in marked contrast to the evolving regulatory posture towards C8 at u September 27, the agency initiated a rare, priority review of C8 out of about its developmental and reproductive effects, and because "addith sample analysis data indicate low level exposures to the general popui are unexplained at this time." Significantly, the EPA's motivating concern is with risks to the general population, where the potential for exposure is generally much lower t West Virginian's whose drinking water supplies have been directly con with C8 from manufacturing and disposal operations. The studies that instigated US EPA's priority review were available to i advance of your agency's public presentations earlier this year. A perf review of industry documents on file with the agency would have yield and scientific conclusions very much at odds with the "science behind on C8. EWG is aware of, but has not been party to, the controversy surround DEP's review of C8, specifically the procedures followed by the departi Science Advisor Dee Ann Staats, and her decision to include DuPont P' the DEP review panel. We are at a loss to explain how the weight of e> readily available from EPA and published sources about the serious ns could differ so dramatically from the conclusions the DEP reached, anc reassurances it communicated to the people of Wood County. In order to remove even the appearance of bias in the DEP process, f other reason, we urge you to impanel another, impartial group of sciei excluding industry-affiliated experts, to re-review C8 science and the application of drinking water regulation to the contamination problem County. It is our judgment that such a review would result in much sti regulatory action against C8, and vastly stricter protection for West vi whose tap water was once pure, but is now contaminated by a danger industrial chemical. Sincerely, [ signed ] Richard Wiles Senior Vice President Copyright 2002, Environmental Working Group. All Rights Reserved. 1436 U Street N.W., Suite 100 | Washington, DC 20009 || nfo@ewq.org http://www.ewg.org/policymemo/20021113/wilesltr.php 000004 11/ 1421)02 Environmental Working Group ||Policy Memo: DuPont, l etlon, Water, Contamination, ... Page l of 10 ew g/srience policy Critique of community briefings by West Virginia DEP 1 EWG Letter to West Virginia DEP >>| EWG Policy Memo A Critique of Community Briefings by The West \ Department of Environmental Protection on the I of Drinking Water Contaminated With C8 (perfluorooctanoic acid -- PFOA) Kristina Thayer Ph.D. Throughout the spring and summer of 2002, the West Virginia Departi Environmental Protection (DEP) conducted a series of community mee hazards of drinking tap water contaminated with perfluorooctanoic act C8) from DuPont's manufacturing operations in Washington, West Virc analysis of the content of the materials presented by the DEP at these finds them to be in conflict with positions of the U.S. Environmental Pr Agency (U.S. EPA), with studies in peer-reviewed scientific literature, industry-sponsored toxicity studies. The following analysis refers specifically to statements made, and slid* presentation made by DEP staff and expert consultants on May 15 anc In describing the health concerns associated with C8 and the safety st devised by the State, the DEP: 1. Clearly indicates that C8 does not cause developmental and reproductive effects or present a long-term risk to people who di in their tap water. This contention is not supported by industry si of C8 toxicity and is contradicted by high-ranking officials at U.S 2. Claims that tumors caused by C8 in animals are irrelevant to hur The U.S. EPA considers C8 to be carcinogenic -- causing liver, pancreatic, testicular, and mammary gland tumors [U.S. Environ Protection Agency (U.S. EPA) 2002b, p. 6]. In company documer DuPont scientists assert that the testicular and pancreatic tumor in animals could be relevant to humans. 3. Fails to account for documented food and air exposures to C8 wt setting the drinking water contaminant limit, and then fails to tei public of this omission, even though it constitutes a major deviat from standard US EPA protocols. DEP's method allows between l 100 times more C8 in tap water than would be allowed applying assumptions which account for other sources of exposure to C8 ; include protections for the fetus, infants and children from the ef suspected developmental toxins like C8 [Ammonium perfluorooci (C8) assessment of toxicity team (CATT) 2002, p. 34; Appendix 4. Asserts that the allowable amount of C8 contamination in drmkin is between 10 and 100 times more protective than it actually is DEP applied the safety factors described at the community meeti the screening level for C8 in drinking water would be between : 15 parts per billion (ppb), not 150 ppb. 5. Claims that the "safe" dose of C8 (the reference dose, or RfD) is times more protective than that for the average chemical. It is n> reference dose for C8 is five times lower than that for the averag chemical because C8 is five times more toxic than the average chemical. The amount of protection provided by the C8 reference is equivalent to, or less than (see below) that provided for the a\ compound. C8 and developmental/reproductive toxicity On May 15th or 16 th, 2002, DEP staff presented the following informa public [West Virginia Department of Environmental Protection (WVDEF Slide #3]: http://www.ewg.org/policymemo/20021113/policymemo.php 000005 11/14 20(12 Environmental Working Group ||Policy Memo: DuPont, Teflon, Water, Contamination, Page 2 o f 10 How toxic is C8? Not developmental^ toxic Not a reproductive toxicant [Excerpt I Full document! Far from considering C8 "not developmentally toxic," the U.S. EPA has "priority review" of C8 to determine whether expedited regulatory acti the compound is warranted under Section 4(f) of the Toxic Substance: Act (TSCA) due to concerns that the compound causes adverse develo and reproductive effects in animals. As characterized by Oscar Hernandez, the director of the U.S. EPA's O Prevention, Pesticides and Toxic Substances Risk Assessment Division "Toxicological studies in rodents and primates have shown that exposi (C8) can result in a variety of effects including developmental/reprodu toxicity, liver toxicity, and cancer" (U.S. EPA 2002c, p. 2:) [Excerpt I l document ! . According to Charles Auer, Director of the U.S. EPA's Office of Toxic Si the agency is taking this action because it has received data suggestir has "a potential for reproductive/developmental toxicity," and because blood sample analysis data indicate low level exposures to the genera! that are unexplained at this time" (U.S. EPA 2002d, p. 1) [Excerpt | Ft document] Our review of the studies available in the scientific literature shows th, findings are not new, and were available to the DEP well in advance ot presentations. For example, C8 causes numerous effects on male and female reprodi organs, such as testicular tumors (Biegel et al. 2001; Slbinski 1987), t sperm production (Sibinski 1987), mammary gland tumors (Sibinski l cellular effects in the ovary (Sibinski 1987). C8 also affects the prosta (York 2002) and increases estrogen levels (Biegel et al. 2001). In add causes a significant increase in low birth weight pups in animal studie: weight is recognized as a risk factor for insulin resistance or Type II di high blood pressure, and cardiovascular disease later in life (Godfrey t 2001, Hales and Barker 2001). Studies have also shown that health ri even for those low-birth weight children who achieve normal weight it childhood, including risks for high blood pressure, stroke, insulin resist glucose intolerance (Eriksson et ai. 2000a; Eriksson et al. 2002; Eriks2000b; Eriksson et al. 1999; Eriksson and Forsen 2002; Forsen et al. and Dunger 2002; Stettler et al. 2002). More recent work shows that C8 significantly increases mortality in developmentally-exposed rats at a dose that did not affect parent sur 2002). These findings suggest that fetuses, infants and children may t sensitive to C8 exposure than adults. Additional effects observed in developmentally-exposed male rats - at the lowest doses tested - me decreased body weight; increased liver, seminal vesicle (a part of the reproductive tract), and kidney weight; and decreased weight of the s important organ in the immune system. At higher doses, C8 delayed s maturation of male and female rat pups (York 2002). C8, cancer, and other long-term health risks Also, in Slide #3 from DEP's public presentation on May 15 or 16, 200 incorrectly represent the relevance to humans of C8 cancer studies m animals: How toxic is C8? Cancer -- rodents; mechanism not relevant to humans [Excerpt | Full document] http://www.ewg.org/policymemo/20021113/policymemo.php 000006 11/14 2<>(C Environmental Working Group |j Policy Memo: DuPont, Teflon, Water, Contamination, ... Page 3 ot 1U DEP implies that all types of tumors (liver, mammary gland, testicular pancreatic) caused by C8 in rodents are not relevant to humans. This is not supported by the science, nor has any regulatory body conclude Indeed, not even DuPont or 3M have attempted such a sweeping deni; health risk to humans. The manufacturers have argued that one of the mechanisms of action tumors in rats is a cellular process called peroxisome proliferation, a n generally thought to be much less relevant for humans than for rodem studies in primates, however, showed liver toxicity for C8 without perc proliferation. Primates are similar to humans in liver physiology and fu Specifically, C8 has been found to cause death In monkeys along with gastrointestinal tract toxicity, increased triglycerides levels and transit decreases in thyroid hormone even though "there was no evidence of proliferation... suggesting a different mode of action than observed in EPA 2002b, p.5, 53-56) [Excerpt | Full document]. In fact, the lowest administered to monkeys caused "liver toxicity and possible mortality'' 2002b, p.56) rExcerpt | Full document]. 3M and DuPont failed to persuade the European Union with this same proliferation argument when attempting to refute liver tumors caused chemical cousin to C8, known as PFOS. The EU review, which is the m definitive review of PFOS toxicity to date, concluded "there was no evi peroxisome proliferation in the livers of the treated animals" - even th animals had liver tumors (Organisation for Economic Co-operation ant Development 2002, p. 7) f Excerpt | Full document1 - indicating that li could be induced by a different mechanism that may well be relevant i According to the DEP's Dr. Staats in her May 15, 2002 presentation at Blennerhassett Jr. High School, one of the impetuses for the DEP Inve: C8 stems from the "toxicity of similar compound PFOS" (WVDEP 2002i (Excerpt | Full document], a chemical that 3M phased out of productio under pressure from U.S. EPA, when studies showed widespread hum; and fetal deaths in low-dose animal studies. Regardless of how the arguments for the C8-induced liver tumors evo also been shown to cause tumors in the mammary gland, testes, and (Biegel et al. 2001; Sibinski 1987; U.S. EPA 2002b, p.6). Scientists at have not concluded that a mechanism unique to rodents is responsible these tumors (U.S. EPA 2002b, p. 75-78). Even DuPont found that for and pancreatic tumors, "the mechanism of tumorigenesis is not compl understood, and therefore the relevance to humans can not be comple out" (DuPont 1997, p.25) [Excerpt | Full document]. DEP's "safe" C8 level in tap water is based on an < methodology that allows far more C8 in tap water the standard assumptions used by the U.S. EPA. In a May 9, 2002 press statement, DEP writes: "The team determined that a water level that contained less thar parts per billion of C8 would not cause harm to humans," said Dr Dee Ann Staats, West Virginia Department of Environmental Protection science adviser. "The team thoroughly reviewed the scientific studies and unanimously agreed to the human health protective levels for drinking water," Staats said. "We brought together some of the t scientists in the country. I am confident the human health protec levels established by the team are supported by the data." (WVC 2002d) [Read full press release on DuPont's website] What the DEP didn't tell the public is that in setting this standard, the deviated from its draft assessment and from standard assumptions us U.S. EPA when setting contaminant standards for drinking water. The http://wAvw.ewg.org/policymemo/2002l 113/policymemo.php 000007 11/14/2002 Environmental Working Uroup ||Policy Memo: DuPont, letlon, Water, Contamination, ... Page 4 oi 1U these omissions was to permit substantially more C8 in tap water thar allowed using standard assumptions. First, your Department stripped an important safety factor from its fin calculations of a drinking water safety limit, tripling the allowable leve WVDEP initially used this safety factor in draft calculations to account C8's unusual properties, including its long half-life in the human body persistence in the environment (WVDEP 2001) [Excerpt | Full Docume not known to ever break down in water, soil, air, or the human body, property that heightens public health concerns and that merited an ad safety factor in your Department's draft calculations. Not only did youi this safety factor from final calculations, but also they then presented the public implying that the safety factor had been left in place [Excer document). If this were true, the allowable level of C8 in drinking watt 50 ppb, not 150 ppb. Second, the state ignores potentially substantial background exposure from contamination in air and food. Water is not the only - and may n primary - route of exposure to C8. 3M reports that PFOA is present in beans, apples, bread, and ground beef at concentrations comparable t been found in drinking water supplies around DuPont's Washington w< (U.S. EPA 2001b, p. 1) [Excerpt | Full Document], Recent modeling of concentrations conducted by DuPont show significant levels of C8 in tf especially northeast of the Washington Works Plant across the Ohio Ri exceeding safety limits set by the WVDEP (DuPont 2002). For contaminants with multiple routes of exposure, U.S. EPA's standar assumption is that 20 percent of contaminant comes from drinking wa percent comes from other sources (EPA 19921. Had DEP used this star assumption, allowable amount of C8 in tap water for an adult would bi 30 ppb, not 150 (Appendix A). Adding back in the Department's safety persistence would bring the drinking water screening level to protect a to 10 ppb. In addition, the Department fails to set a protective level for infant exi Specifically, your Department did not account for the significant body difference between adults and infants. Bottle-fed infants fed formula reconstituted with C8-contaminated tap water are a population of high Bottle-fed infants receive the highest dose of all drinking water contan pound for pound, of any other segment of the population. This is beca an adult and an infant drink a liter of contaminated water, C8 will be r concentrated in the child -- resulting in a higher dose per unit of body A C8 level protective of bottle-fed infants would incorporate three mot factors your Department has ignored - a correction for infant body we safety factor for C8 persistence, and a factor to account for multiple rc exposure (such as air). Incorporating all three factors gives an allowai C8 in drinking water of 1.5 ppb (Appendix A), well within the range of found in the local drinking water sources. For instance, the peak C8 le springs that provide drinking water within one mile of the Washington facility were above 10 ppb (WVDEP 2002a, Slide 8) [Excerpt | Full Doc Average C8 levels in this same water were 4 parts per billion. During t 1990's, DuPont established its own Community Exposure Guideline (C in drinking water at 1 ppb (CATT 2002, p. 46) (Excerpt | Full Documei Considering that infants may be more vulnerable to C8, the standard i be more conservative than what we have outlined here. Animal studie C8 is more toxic to newborns; for example, it causes mortality in your doses that did not kill parent animals. Studies also show that the high' concentrations of C8 in non-worker populations occur in children (U S 2002b, p. 3) [Excerpt | Full Document] reinforcing the need for DEP tc C8 safety limits to protect infants. DEP implies that tap water safety limits of C8 are 100 times more protective than they actually are. In another public meeting presentation, on either May 15 or May 16, ; staff imply that they applied a large safety buffer when deriving the dr water safety limit for C8 (WVDEP 2002b, Slide 5) : http://www.ewg.or^policymemo/20021f 13/policymemo.php 000008 ll/14/20<>2 Environmental Working Group ||Policy Memo: DuPont, Teflon, Water, Contamination,... Page 5 o f 10 How are safe levels developed? No Observed Effect Level (NOEL) typically divided by at least 1,0 up to 10,000 Safety Factor Animals to humans Sensitive subpopulations Chronic lifetime exposure Other criteria such as biopersistence fExcerpt | Full document) The problem here is that the DEP did not apply the "typical" safety ma 10,000 -- or even 1000. Instead, DEP applied a safety factor of only 1 account for possible differences between small groups of rats In the la and large populations of humans exposed through contaminated drink Also, some of the listed criteria, such as biopersistence, were not take account at all. The most recent data from 3M shows that It takes hum. years to get rid of just half the amount of C8 in the body after all C8 e end (U.S. EPA 2002a, p. 2) (Excerpt | Full document]. If persistence v including when determining a safe dose of C8, the allowable amounts been much smaller, in part because there is no reason to believe the ( exposures are ending. DEP states, wrongly, that protections from C8 in c water are somehow more protective than protecti applied to other chemicals. During a May 15, 2002 public meeting at Blennerhassett Jr. High Schc staff presented the following slide: How does the C8 RfDo (reference dose, which means the daily "s dose) compare to that for other chemicals? The average EPA-developed oral RfD is 0.02 mg/kg-day which 15 times higher than C8's of 0.004 mg/kg-d. Therefore, C8's risk fa is more conservative or health protective than that for the avera' chemical. (WVDEP 2002c, Slide #15) [Excerpt l Full document] C8's reference dose is not more health protective than that for the avi chemical. C8 carries a lower reference dose than the average chemica Is more toxic than the average chemical, approximately 5 times more according to DEP's own calculations. C8's low reference dose simply re difference. In truth, far from being more protective than average, there are sever why the DEP risk factor may not be sufficiently protective. First, a dos causes no observed adverse effect level, or a NOAEL, was not identifie critical studies, the cancer study, and the reproduction study. The repi study was used by the DEP-led team to set a RfD for C8 . Typically, to> design animal studies with the expectation that the lowest dose testec produce adverse effects in laboratory animals. C8's manufacturers underestimated the toxicity of C8, and missed the no effect level in be studies -- even the lowest doses tested caused observable adverse efi not at all accurate to characterize a risk factor derived from studies th adverse effects at all doses as "more conservative or health protective average risk factor. Second, the study used to derive the RfD (a two-generation reproduct study) is not a chronic study, and Is not truly indicative of the hazards term consumption of C8 in tap water. In this study, animals exposed > followed, at a maximum, until they are young adults (about 4 months http://www.ewg.org/policymemo/2002l 113/policymemo.php 000009 11/ 14, 20(12 Environmental Working Group ||Policy Memo: DuPont, Teflon, Water, Contamination, ... Page 6 o f 10 design makes it impossible to address questions such as whether in ut life exposure to C8 can predispose an individual to cancer, degenerate system disorders, diabetes, or other diseases more prevalent at the er Third, C8 is an extremely biopersistent chemical, which was not taken account in setting the reference dose (see above). Biopersistence is a characteristic of C8, and must be explicitly considered in determining i faced by consumers of C8. Finally, the RfD assumes that the control animals in the critical studies directly administered C8 in the study) had no exposure to C8. This is r Control animals have been consistently shown to have significant liver levels of C8 (U.S. EPA 2002b, p. 48, 57-60) [Full document]. The fact RfD is based on studies with no true controls means that important to: may have been overlooked because they were also caused by C8 in th contaminated control animals. Conclusions On September 27, U.S. EPA initiated a priority review of C8 because o concerns about its developmental and reproductive effects, and becau "additional blood sample analysis data indicate low level exposures to population that are unexplained at this time" (U.S. EPA 2002d, p. l) [ Full document]. The EPA's concerns focus on exposures in the general population, amc who face lower overall potential for exposure than do the West Virgini, communities whose drinking water supplies have been directly contanr C8 from manufacturing and disposal operations. The studies that insti EPA's priority review were available to DEP well in advance of its publi presentations. In light of the federal government's position on the potential for C8 to reproduction and development, and its potential to cause cancer in hu appears that DEP's interpretation of C8's toxicity, and the drinking wai limits derived from that interpretation, fail to give the affected commu adequate margin of protection. REFERENCES: 1. Ammonium perfluorooctanoate (C8) assessment of toxicity team (CATT). 2002. Final Ammonium perfluorooctanoate (C8) assessrr toxicity team (CATT) report. Website 2. Biegel, L. B., M. E. Hurtt, S. R. Frame, J. C. O'Connor, and J. C i 2001. Mechanisms of extrahepatic tumor induction by peroxisom proliferators in male CD rats. Toxicol Sci 60 (l):44-55. 3. DuPont. 1997. Hazard characterization for human health C8 expc CAS registry no. 3825-26-1, Prepared by L.B. Biegel, Senior Res' Toxicologist. 4. DuPont. 2002. DuPont-Washington Works modeled C8 Ground L< Concentrations (Annual Averages). 5. Eriksson, ]., T. Forsen, J. Tuomilehto, C. Osmond, and D. Barker 2000a. Fetal and childhood growth and hypertension in adult life Hypertension 36 (5):790-4. 6. Eriksson, J. G., T. Forsen, J. Tuomilehto, V. W. Jaddoe, C. Osmoi D. J. Barker. 2002. Effects of size at birth and childhood growth . insulin resistance syndrome in elderly individuals. Diabetologia 4 (3) :342-8. 7. Eriksson, J. G., T. Forsen, J. Tuomilehto, C. Osmond, and D. J. B 2000b. Early growth, adult income, and risk of stroke. Stroke 31 (4) :869-74. 8. Eriksson, J. G., T. Forsen, J. Tuomilehto, P. D. Winter, C. Osmon D. J. Barker. 1999. Catch-up growth in childhood and death from coronary heart disease: longitudinal study. Bmj 318 (7181):427- 9. Eriksson, J. G., and T. J. Forsen. 2002. Childhood growth and cot http://www.ewg.org/policymemo/20021113/policymemo.php 000010 11/14 20. c Environmental Working Group ||Policy Memo: DuPont, Teflon, Water, Contamination, ... Page 7 o f 10 heart disease in later life. Ann Med 34 (3): 157-61. 10. Forsen, T., J. Eriksson, J. Tuomilehto, A. Reunanen, C. Osmond, Barker. 2000. The fetal and childhood growth of persons who de< type 2 diabetes. Ann Intern Med 133 (3): 176-82. 11. Godfrey, K. M., and D. J. Barker. 2001. Fetal programming and e health. Public Health Nutr 4 (2B):611-24. 12. Hales, C. N., and D. J. Barker. 2001. The thrifty phenotype hypo' Br Med Bull 60:5-20. 13. Organisation for Economic Co-Operation and Development (OECi 2002. Reviewed in: Draft Assessment of perfluorooctane sulfonat (PFOS) and its salts: Complete assessment. Full document 14. Ong, K. K., and D. B. Dunger. 2002. Perinatal growth failure: the to obesity, insulin resistance and cardiovascular disease in adults Pract Res Clin Endocrinol Metab 16 (2): 191-207. 15. Sibinski, L. J. 1987. Two-Year oral (diet) toxicity/carcinogenicity of fluorochemical FC-143 in rats, Reviewed by the US EPA in "Dr; Hazard Assessment of Perfluorooctanoic Acid (PFOA) and its Salts" (AR226-1079) p. 52-53. Report prepared for 3M, St. Paul, Minnesota by Riker Laboratories Inc. Study No. 0281CR0012. 16. Stettler, N., P. Bovet, H. Shamlaye, B. S. Zemel, V. A. Stallings, Paccaud. 2002. Prevalence and risk factors for overweight and ol in children from Seychelles, a country in rapid transition: the importance of early growth. Int J Obes Relat Metab Disord 26 (2' 9. 17. US Environmental Protection Agency (US EPA). 1992. Backgroun document 3: Office of Drinking Water Health Advisories. Website 18. US Environmental Protection Agency (US EPA). 2001a. 3M Environmental Laboratory Executive Summary: Environmental monitoring - multi-city study water, sludge, sediment, POTW effl and landfill leachate samples. U.S. EPA Administrative Record AR 1030a. Full document 19. US Environmental Protection Agency (US EPA). 2001b. Analysis < PFOS, FOSA, and PFOA from various food matrices using HPLC electrospray/mass spectrometry. U.S. EPA Administrative Record AR226-1030a. 3M study conducted by Centre Analytical Laboratc Inc. Full document 20. US Environmental Protection Agency (US EPA). 2002a. 3M subrm Interim report #2 Determination of serum half-lives of several fluorochemicals. U.S. EPA Administrative Record AR226-1086 Fi document 21. US Environmental Protection Agency (US EPA). 2002b. Revised c hazard assessment of PFOA and its salts. U.S. EPA Adm inistrate Record AR226 -in progress as of November 10, 2002. Full docum 22. US Environmental Protection Agency (US EPA). 2002c. Science a Board Proposed Project. U.S. EPA Administrative Record AR226 Full document 23. US Environmental Protection Agency (US EPA). 2002d. Memoran Revision of PFOA hazard assessment and next steps. U.S. EPA Administrative Record AR226 -1127. Full document 24. West Virginia Deparment of Environmental Protection (WVDEP) Draft: Development of provisional oral and inhalation reference c and preliminary screening levels for ammonium perfluorooctanoa document 25. West Virginia Department of Environmental Protection (WVDEP) CATT C-8 Groundwater Investigation steering team (GIST) prese by Dr. David Watkins at public meeting (Attach Ila); CATT repon presentation. Website 26. West Virginia Department of Environmental Protection (WVDEP) CATT C-8 presentation by Dr. Dee Ann Staats at public meeting i Ila). Website 27. West Virginia Department of Environmental Protection (WVDEP) CATT C-8 presentation by Or. Dee Ann Staats at public meeting ; lib). Website http://www.ewg.org/policymemo/20021113/policymemo.php OO0O11 u/H O O ": Environmental Working Group ||Policy Memo: DuPont, Teflon, Water, Contamination,... Page 8 o f 10 28. West Virginia Department of Environmental Protection (WVDEP). Press Release: Health Level for C8 announced by expert team. V\ 29. York, R. G. 2002. Oral (gavage) two-generation (one litter per generation) reproduction study of ammonium perfluorooctanoate (APFO) in rats, US EPA administrative record number AR226-109 Report prepared for 3M, St. Paul, Minnesota by Arguss Research. Sponsor's Study No. T-6889.6, Horsham, Pennsylvania. APPENDIX A WVDEP (C8 Assessment of Toxicity Team, or CAT! APPROACH: The approach used by WVDEP to calculate a drinking water screening is outlined below. Water Screening Level - THO x AT x BW EFx EDxllR/RfD,^) THQ = Target Hazard Quotient, assumed to be 1 RfDpEP = The oral reference dose estimated by DEP, 0.0042 (truncate mg/Kg-day BW = Body weight, assumed to by 70 kg for adults (children are hot c in DEP calculations) AT = Averaging time, 10950 days, the exposure duration expressed in EF = Exposure frequency, 350 days/year, the average number of day; people are exposed ED = Exposure duration, 30 years, the average number of years peop exposed IR = Ingestion rate, assumed to be 2 L/day for adults (children are no considered In DEP calculations) So, Water Screening Level - l \ lU^SQx 70_____ - 0 .14b me L (350 \ 30 x 12/0.1)041 U.S. EPA APPROACH: The standard U.S. EPA approach for developing drinking water safety presented below. U.S. EPA incorporates a factor called the Relative So Contribution in cases of chemicals like C8 associated with multiple rou exposure. Calculations below also reflect the safety factor of 3 that DE from its final calculations that were originally in place to account for C persistence and long half-life in the human body. Both of these chemii characteristics contributed to U.S. EPA's decision to conduct a priority C8. Adult Lifetime Drinking Water Health Advisory (DWHA): http://www.ewg.org/policymemo/20021113/policymemo.php 000012 11/14.2002 Environmental Working Group ||Policy Memo: DuPont, Teflon, Water, Contamination,... Page 9 o f 10 DVVHA - VVEL x RSC DWHA 50 pg/L x 0.2 = 10 |*g/L(ppb) PVVEL - RID x BVV IK DWEL - 0.0014(70) - 0.05 mg / L (ppm) or 50 to 2 KfD - Ki'D^/SF -0 .0 0 4 2 /3 -0 .0 0 1 4 mg/kg-da\ DWHA = Drinking Water Health Advisory; "safe" dose of C8 via drinkir DWEL = Drinking Water Equivalent Level; conversion of reference dos reference concentration RfD = The oral reference dose that accounts for persistence and long I the human body BW = Body weight, assumed to by 70 kg for adults, 10 - 15 kg for chi 5.2 for bottle fed kids IR = Water ingestion rate; 2 L/day for adults and 1 L for children and infants. RSC = Relative Source Contribution, which has a U.S. EPA default vali ( 0.2) SF = safety factor to account for persistence and long half-life in the h (3X) Bottle-fed Infant Drinking Water Health Advisory (DWHA): In this case, we assume that a bottle-fed infant weight 5.2 kg and dri L/day, consistent with the scientific literature and U.S. Department of formula consumption data. DW HA = 7.3 |ig/L x 0.2 = 1.5 ftgiL (ppb) DWtL - 0.0014(5.2) - 0.0073 itt^/L (ppm)or 7.3 u-'-l. 1 Drinking Water Health Advisory for a 10 or 15 kg (DWHA): For comparison against the limit derived for an exclusively bottle-fed i protective of a 10 or 15 kilogram child are presented below. http://www.ewg.org/policymemo/20021113/policymemo.php 000013 11/14.200: Environmental Working Group ||Policy Memo: DuPont, Teflon, Water, Contamination... Page 10 o f 10 For a 10 kg child: DWHA = 14 fig jl x 0.2 = 2.8/tf/L (ppb) DWEL - It.0 01 4HO) - 0.014 mg L (ppm) or 14 ug i For a lr> kg child: DWHA =21 v 0.2 = 4.2 /*?//. (}>}>{>) DWEL - (UX)14(15) - 0.021 mg L (ppm) or 21 ug l Copyright 2002, Environmental Working Group. All Rights Reserved. 1436 U Street N.W., Suite 100 | Washington, DC 20009 || info@ewa.ora http://www.ewg.org/policymemo/20021113/policymemo.php 000014 11/14 20' i2