Document XRBBnB4YLG14Z4DOyE09nLyow

CHEMICAL MANUFACTURERS ASSOCIATION November 18, 1985 \ TO : FROM : SUBJECT: Vinylidene Chloride Program Panel Robert R. Romano, Ph.D. \ f ' I ] / I i' * EPA's Health Advisory on VDC CMA is attempting to comment on the numerous Health Advisories presented to us from EPA. The Agency will use these advisories as the basis for proposing RMCLs and MCLs, and ulti mately will issue final RMCLs and MCLs. Enclosed is an EPA news release which explains this Drinking Water Act action. I have also enclosed EPA's health advisory on VDC. Please review the advisory and provide your comments/tJj^becember 5, 198S,, directly to: Safe vv-- J, McDade Dow Chemical USA Inorganic Chemicals Department 2020 Willard H. Dow Center Midland, MI 48640 (517) 636-1321 Mr. McDade is coordinating all VDC comments to eventu ally become part of the official CMA comment package. If you have any questions, please do not hesitate to call me at (202) 887-1198. cc: J. McDade Ann Mason, CMA NOTE: The November 13, 1985 Federal Register has EPA's final RMCLs, proposed MCLs and the new proposed RMCLs. -o-"ier y Mar.-sc'r y ner":s:s A=s&o:at;or- -- 5erviag Cnermca: '"au = "y S.r,c '872 lit," M \ v\ * /; _( z,Dr I'C i -0c7 * ""J1 "r2"0tt* 2Lv' 867 " 1 0C * e ftx 896' " 'CWA WS^i SL 063103 *EPA Uwt*d StatM Environment*! Protection Agency Offica of Public Affairs (A-107) Washington DC 20400 Environmental News EPA ANNOUNCES DRINKING WATER STANDARDS AND MONITORING REQUIREMENTS R-185 FOR RELEASE: FRIDAY, OCTOBER 11, 1985 Mike O'Reilly 382-5590 The U.S. Environmental Protection Agency announced today recommended maximum contaminant levels (RMCLs) and proposed maximum contaminant levels (MCLs) for a group of eight chemical compounds that could cause health problems if they are found in drinking water supplies at significant levels. The agency also proposed monitoring requirements for 51 additional compounds for public water systems* Quantities of all of these conpounds have be n found at very low levels in about one-fifth of drinking water supplies. However, they are sometimes found in groundwater at much higher levels. The agency's major concern is to control current and future conta mination of groundwater. Chemical conpounds covered by the proposal are benzene, carbon tetrachloride, p-dichlorobenzene, 1,2-dichloroethane, 1,1-dichloroethylene, 1,1,1-trichloroethane, trichloroethylene and vinyl chloride. These chemicals are members of a group known as volatile synthetic organic chemicals (VOCs), which are manufactured in hundreds of millions of pounds per year.They are industrial chemicals, degreasing agents, and dry cleaning fluids. The recommended maximum contaminant levels (RMCLs) are nonenforceable health goals. Under the Safe Drinking Water Act this is the first step in setting standards. Under the law, recommended levels must be set at a point that presents no risk to public health. This action sets RMCLs for the chemicals based on the evidence indicating possible human cancer riskRMCLs of zero are set for five of the chemicals which have sufficient human or animal vidence to b consider as probable carcinogens. The other thr e compounds-- (more) 063104 1,l-dichloroethylene, 1,1,1-trichloroethane and p-dichlorobenzene are not carcinogen* and ara *et at level* of .007, .2, and .75 milligrams per liter, respectively, based upon their chronic toxicity. EPA's proposed maximum contaminant levels for the eight compounds will lead to enforceable standards. The MCLs are set as close to the RMCLs as possible based on health considerations, treatment technologies, cost, and other factors. Four of the eight confounds -- trichloroethylene, carbon t trachloride, 1,2-dichloroethane and benzene are proposed at levels of .005 milligrams per liter (5 parts per billion)r vinyl chloride is set at .001 milligrams per liter. The other three, 1,1-dichloroethylene, 1,1,1trichloroethane, and p-dichlorobenzene are proposed at the same levels as the r commended maximum contaminant levels. Approximately 1,300 community water systems would be expected to exceed th proposed MCLs. EPA estimates the capital cost to the nation for treatment would be $280 million. Annual operating costs for treatment to comply with the proposed rules is estimated at $21 million per year. Effective and economical water treatment methoc are available to control VOCs. The treatment techniques include aeration and filtration through granular activated carbon. In addition to RMCLs and MCLs for the eight VOCs, this rule also proposes monitoring procedures for other currently unregulated VOCs. Because similar analytical procedures for the eight VOCs can also measure numerous other chemicals at a small additional cost, monitoring regulations for approximately 51 other VOCs are included in this proposed rule. Public comment on tetrachloroethylene, which was included in EPA's origin al RMCL proposal, was extended in order to strengthen that standard based on new scientific data. EPA will set the RMCL and propose MCL levels for this compound in the near future after public comments have been reviewed on the new data. These chemicals constitute Phase I of EPA's four part program for re vised drinking water regulations. Phase II, which is also being announced today, covers synthetic organic chemicals, inorganic chemicals and micro biological contaminants. Phase III regulations will ccver radionuclides which will include limitations for the amounts of radioactive substances found in drinking water such as radon and uranium. Phase IV regulations will cover limit* for the byproducts from the disinfection of water supplies such as produced through chlorination. Once completed, this four phase program will represent the most comprehensive, scientific-bas d regulatory program for drinking water to date. The final RMCLs and the proposed MCLs will be published in the Federal Register in the near future. A 90 day comment period on the proposed MCLs will begin with the publication of the rule in the Federal Register. R-185 *#* MCL for the VOCs o The MCLs are proposed as follows: Compound Trichloroethylene Carbon tetrachloride Vinyl chloride 1,2-Diehloroethane Benzene 1.1-Dichloroethylene 1.1.1-Trichloroethane p-Dichlorobenzene Proposed MCL (mg/1) ppb 0.005 0.005 0.001 0.005 0.005 0.007 0.200 0.750 5 5 1 5 5 7 200 750 o Comment period is 90 days from publication. o A public hearing will be held in Washington, D.C. in December, 1985. FOR FURTHER INFORMATION CONTACT: Joseph A. Cotruvo, Ph.D., Director, Criteria and Standards Division, Office of Drinking Water (WH-550), Environmental Protection Agency, 401 M Street, S.w., Washington, D.C. 20460, telephone (202) 382-7575. R-18 5 RMCL for the synthetic organic chemical* are proposed as follows Acrylamide Alachlor Aldicarb. aldicarb sulfoxide and aldicarb sulfone Carbofuran Chlordane cis-1,2-Dichloroethylene DBCP 1,2-Dichloropropane o-Dichlorobenzene 2,4-D EDB Epichlorohydrin Ethylbenzene Heptachlor Heptachlor epoxide Lindane Methoxychlor Monochlorobenzene PCBs Pentachlorophenol Styrene Toluene 2,4,5-TP Toxaphene trans-1,2-Dichloroethylene Xylene Proposed RMCL (mg/1) zero zero 0.009 0.036 zero 0.07 zero 0.006 0.62 0.07 zero zero 0.68 zero zero 0.0002 0.34 0.06 zero 0.22 0.14 2.0 0.052 zero 0.07 0.44 o Comment period is 120 days from publication. o A public hearing will be held in Washington. D.C. in January 1986. FOR FURTHER INFORMATION CONTACT: Joseph A. Cotruvo, Ph.D., Director, Criteria and Standards Division, Office of DrinXing Water (WH-550), Environmental Protection Agency, 401 M Street, S.W., Washington, D.C. 20460, telephone (202) 382-7575. SL 063107 / o RMCLs for non-carcinogens ere set baaed upon chronic toxicity data using Acceptable Daily Intake Levels (ADIs). o RMCLs consider the total exposure from air, food and drinking water when data are available. Typically 20% of the ADI is allocated to drinking water. o RMCLs have been proposed for Giardia and viruses in order to control for waterborne infectious disease which is still a significant problem in some water supplies that are inadequately treated. More than 80,000 cases have been reported between 1971 and 1980 and most of them are caused by viruses and Giardia. o RMCLs for the inorganic chemicals are proposed as follows: Contaminant Propose Arsenic Barium Cadmium Chromium Copper Lead Mercury Nitrate Nitrite Selenium 0.050 1.5 0.005 0.12 1.3 0.020 0.003 10 1 0.045 Asbestos 7.1 mmi illion long fibers per liter o RMCLs for the microbiological parameters are sero for total coliforms, Giardia and viruses and 0.1 Nephelometric Turbidity Unit (NtU) for turbidity. R-1B4 SL 063108 SEPA UnitwJ StatM Environments! Protection Agency Office of Public Affairs (A-10/) Washington DC 20400 Environmental News EPA PROPOSES NEW DRINKING WATER GOALS 10 4 FOR RELEASE: FRIDAY, OCTOBER 11, 1985 Mike O'Reilly 382-5590 The U.S. Environmental Protection Agency announced today it is proposing recommended maximum contaminant levels (RMCLs) for 37 chemical (plus 2 by-products) and 4 microbiological contaminants that could be harmful if found in the drinking water supplies at significant levels. The proposed goals are the first step in re stricting levels of chemical and biological contaminant: sometimes found in drinking water sources. Twenty-six synthetic organic chemicals are covered in this proposal including PCB's (polychlorinated biphenyls) and numerous pesticides including aldicarb. PCB's are used as liquid coolant and insulating material in electrical equipment. Aldicarb is a highly toxic pesticide that has been found in some ground water in agricultural areas. The proposed rule also covers 11 inorganic chemicals including lead and mercury. The four microbiological contaminants covered by the proposed rule are coliforms, turbidity, Giardia and other viruses. These relate to bacteria and other organisms which may cause infection and disease from contaminated and inadequately treated drinking water. "The proposed goals are a significant step in the process of protecting the nation's public h alth from drinking water contamination," said EPA Adminis trator Lee M. Thomas. "The quantities of these chemicals found in drinking water have generally been at very low levels, but they are sometimes found in surface waters and groundwaters at high levels. Our major cone rn is to control current contamination of groundwater and prevent futur contamination." SL 063109 2. Waterborn inf ctious disease is still a significant problem in some water supplies that are inadequately treated. More than 80,000 cases have been reported between 1971 and 1982 and most of them are caused by viruses or Giardia, a parasite. EPA's major goal is to use proper treatment or other protections in all public water supplies to assure safety. The recommended maximum levels are nonenforceable goals. Under the Safe Drinking Water Act this is the first step in setting standards. The law requires that recommended levels be set at a point which would r suit in no known or anticipated adverse health effects with an adequate margin of safety. The chemicals atfe grouped according to the strength of the evidence that they cause cancer or other health risks. The three categories include: (1) known or probable human carcinogens, (2) possible human carcinogens and (3) non-carcinogens. RMCLs for probable human carcinogens are being proposed at zero. The level for the second category are higher than zero, but are set at low levels in case future information increases the evidence of possible carcinogenicity The RMCLs for the third group are based upon chronic toxicity. In determining RMCLs, contamination from the chemicals in the air and the food chain is also taken into consideration. Final standards would come later in the process with the setting of maximum contaminant levels (MCLs) if EPA decides they are needed based upon health considerations , treatment technologies, cost and other factors. The proposed rule also contains health advisory type information on 28 chemicals for which RMCLs are proposed and 10 which are not being proposed. A treatment advisory is proposed for Legionella,(legionnaire's disease organism) although an RMCL for Legionella is not proposed at this t ime. Effective water treatment methods are available to control the chemicals and contaminants covered by this proposed rule. The treatment techniques include aeration and filtration through granular activated carbon and other processing depending on the chemical. The four biological contaminants can be controlled through filtration and disinfection. These chemicals and biological agents are Phase II in EPA's four part program for revised drinking water regulations. Phase I, which is also being announced today, covers eight volatile synthetic organic chemicals and monitoring requirements for an additional 51 unregulated VOCs. Phase III regulations will cover radionuclides which will include limitations for the amounts of radioactive substances found in drinking water such as radon and uranium. Phase IV regulations will cover limits for the byproducts from the disinfection of water supplies such as produced through chlori nation. Once completed, this four phase program will represent the most comprehensive, scientific-based regulatory program for drinking wat r to date. The proposed RMCLs will be published in the Federal Register in the near futur . A 120 day comment period will b gin with the publica tion of the proposed rule in the Federal Register. R-184 ## # SL 063110 1,l-Dichloroethylene September 30, 1985 -15- Siirmon, V.F., K. Kauhanen and R.G- TardiEf. 1977. Mutagenic activity of chemicals identified in drinking water. Dev. Toxicol. Environ. Sci. 2:249-258. U.S. EPA. 1979. U.S. Environmental Protection Agency. Water Related Environ mental Fate of 129 Priority Pollutants. Office of Water Planning and Standards, EPA-440/4-79-029, December. U.S. EPA. 1980. U.S. Environmental Protection Agency. Ambient water quality criteria for dichloroethylenes. Office of Water Regulations and Standards. Criteria and Standards Division. Washington, D.C. EPA 440/5-80-041. U.S. EPA. 1983. U.S. Environmental Protection Agency. Vmylidine chloride occurrence in drinking water, food, and air. Office of Drinking Water. U.S. EPA. 1984a. U.S. Environmental Protection Agency. Draft criteria document for the dichloroethylenes. Criteria and Standards Division, Office of Drinking Water, Washington, DC. U.S. EPA. 1984b. U.S. Environmental Protection Agency. Proposed guidelines for carcinogenic risk assessment; Request for comments- Federal Register 49(227): 46294-46301. No1' ouer 23. U.S. EPA. 1984c. U.S. Environmental Protection Agency. National primary drinking water regulations; Volatile synthetic organic chemicals; Proposed rulemaking. Federal Register 49(114):24330-24355, June 12. U.S. EPA. 1984d. i.S. Environmental Protection Agency. Method 501.1, Volatile halogenated organic confounds in water by purge and trap gas chromatography. Environmental Monitoring and Support Laboratory, Cincinnati, Ohio 45268. June. U.S. EPA. 1985. U.S. Environmental Protection Agency. Method 524.1. Volatile organic compounds in water by purge and trap gas chromatography/mass spectraitttry. Environmental Monitoring and Support Laboratory, Cincinnati. Ohio. June. U.S. rrc. 1982. United States International Trade Commission. Synthetic organic chemicals United States production. 1983 USITC Publication 1422, Washington, D-C. 20436. Van IXiuren, B.L., B.M. Goldsclimidt, G. Loewengart, A.C. Smith, S. Melchionne, I. Seldman and D. Roth. 1979. Carcinogenicity of halogenated olefinic and aliphatic hydrocarbons in mice. J. Natl. Cancer Inst. 63:1433-1439, WHO. 1984. world Health Organization. Guidelines for drinking water quality. Volume 1. Recotrmendations. Geneva, Switzerland. Windholz, m., ed. 1933. The Merck Index. 10th edition. Merck and Co., Inc. Rahway, NJ. SL 0631H 1,l-Dichloroethylene -13- September 30, 1985 IARC. 1983. International Agency for Research on Cancer. IARC Monog r^phs on the evaluation of carcinogenic risks of chemicals to humans. Chemical-;, industrial processes and industries associated with cancer in humans. IARC Monographs, Volumes 1-19. Supplement 4. pp. 262-264. Irish, D.D. 1963. Vinylidene chloride. In: F.A. Patty (ed.), Industrial Hygiene and Toxicology. 2nd. ed. Vol. II. John Wiley and Sons, Inc* New York. pp. 1305-1309. Jaeger, R.J., L.G. Shoner and L.J. Coffman. 1977. 1,1-Dichloroethylene hej^totoxicity: Proposed mechanism of action of distribution and binding of radioactivity following inhalation exposure in rats. Environ. Health Perspect. 21:113. Jenkins, L.F., Jr., M.J. Trabulus and S.D. Murphy. 1972. Biochemical effects of 1,1-dichloroethylene in rats: Ccnparison with carbon tetrachloride and 1,2-dichloroethylene. Toxicol. Appl. Pharmacol. 23:501-510. Jones, 3.K. and D.E. Hathway. 1978a. The biological 'ate of vinylidene chloride in rats. Qiem. Biol. Interactions. 20:27-41- Jones, B.K., and D.E. Hathway. 978b. Differences in metabolism of vinylidene chloride betvejen mice and rats. Brit. J. Cancer. 37:411-417. Lieblec, Q.C., and F.P. Guengerich. 1983. Olefin oxidation by cytochrome )P*450: Evidence for group migration in catalytic intermediates formed with vinylidf.-.- chloride and trans-l-pheny1-1-butene. Biochemistry 22:5482-5489. Liebler, D.C., M.J. Meredith and F.P, Guengerich* 1984. Reactive metabolite of vinylidene chloride: Characterization of covalent adducts farmed with proteins and glutathione in microsomes and isolated hepatocytes. Cancer Res., In Press. Maltoni, C. 1977. Recent findings on the carcinogen'city of chlorinated olfeins. Environ. Health Perspect. 21:1-5. Maltoni, C., G. Lefemine, G. Cotti, P. Chieco and V. Patella. 1935. Experimental research on vinylidene chloride carcinogenesis. In: Archives of Research on Industrial Carcinogenesis. Volume III. C. Maltoni and M.A. Mehlman, eds. Princeton Scientific Publishers, Princeton, NJ. (In press). McKenna, M.J., P.G. Watanabe and P.J. Gehring. 1977. Pharmacokinetics of vinylidene chloride in the rat. Environ. Health Perspect. 21:99-105. McKenna, M.J., J.A. 2empel, E.O. Madrid and P.J. Gehring. 1978a. The pharmacokinetics of ( ^C) vinylidene chloride in rats following inhalation exposure. Toxicol. Appl. Pharmacol. 45:699-710. McKenna, M.J., J.A. Zempel, E.C. Madrid, W.H. Braun and P.J. Gehr.no. 1978b. Metabolism and pharmacokinetic profile of vinylidene chloride n rats following oral administration. Toxicol. Appl. Pharmacol. 49:189-202. SL 063112 1-Dichloroethylene -14- September 30, 1985 Murr^y, F.J., K.D. Nitschke, L.W. Rampy and B.A. Schwetz. 1979. Embryotoxicity and et itoxicity of inhaled or ingested vinylidene chloride in rats and rabbits. Toxicol. Appl. Pharmacol. 49:189-202. NAS. 1983. National Academy of Sciences. Drinking Water and Health. Volume 5. National Academy Press, Washington, DC. NIOSH. 1978. National Institute for Occupational Safety and Health. I,L-Dichioroethylene. Registry of toxic effects of chemical substances, p. 563. NIOSH. 1979. [ C.D. for Occupational Standard] NT?. 1982. National Toxicology Program. Carcinogenesis bioassay of vinylidene chloride (CAS No. 75-35-4) in F344 rats and B6C3F1 mice (gavage study). U.S. HHS. PHS. NIH NTP-80-2 NIH Publication No. 82-1784. Poncmarkov, V., and L. Tcmatis. 1980. Long-term testing of vinylidene chloride and chloroprene for carcinogenicity in rats. Oncology 37:136-141. Prendergast, J.A., R.A. Jones, L.J. Jenkins, Jr. and J. Siegel. 1967. Effects on experimental animals of long-term inhalation of trichloro ethylene, carbon tetrachloride, 1,1,1-trichloroethane, dichlorodifluoromethane, and 1,1-dichloroethylene. Toxicol. Appl. Pharmacol. 10:270-289. toast, J.F., C.G; Humiston, C.E. Wade, J. Ballard, J.E. Beyer, R.W. Schwetz and J.M. Norris. 1983. A chronic toxicity and oncogenicity study in rats and subchronic toxicity study in dogs on ingested vinylidene chloride. Fund. Appl. Toxicol. 3:55-62. Rampy, L.W., J.F. toast, C.G. Humiston, M.F. Blamer and B.A. Schwetz. 1977. Interim results of two-year toxicological studies in rats of vinylidene chloride incorporated in the drinking water or administered by repeated inhalation. Environ. Health Perspect. 21:33-43. Reitz, R.H., P.G. Watanabe, M.J. McKenna, J.F. toast and P.J. Gehring. 1980. Effects of vinylidene chloride on DNA synthesis and DMA repair in the rat and mouse: A comparative study with dimethylnitrosamine. Toxicol. Appl. Pharmacol. 52:357-370. Reynolds, E.S., M.T. Moslen, S. Szabo, R.J. Jaeger and S.D. Murphy. 1975. Hepatotoxicity of vinyl chloride and l^l-dichloroethylene. Amer. Jour. Pathol. 81:219. Short, R.D., J.L. Minor, J.M. Winston and C.C. Lee. 1977. A dominant lethal study in male rats after repeated exposure to vinyl chloride or vinylidonw chloride. J. Toxicol. Environ. Health 3:965-968. 063113 1, l-Dichloroethylene -11- September 30, 1985 of 1,1-dichloroethylene over a concentration range of 0.03 to 1500 ' ug/l. Conficrotory analysis for 1,1-dichloroethylene is by mass spectrometry (Method 524.1. Volatile organic compounds in water oy purge and trap gas chromatography/mass spectometry. U.S. EPA, 1985b) The detection limit for confirmation by mass spectometry is 0.2 ug/L. VIII. TREATMENT 0 Granular activated carbon. (GAC) adsorption and aeration treatment technologies are available for the removal of 1,1-DCE from water and have been reported to be effective. Selection of individual or combinations of technologies to achieve chemical reduction rmst be based on a case-by-case technical evaluation and an assessment of the economics involved. 0 Aeration has been shewn to be effective in removing 1,1-DCE from water, based upon its carbon adsorption isotherm (Henry's Law Constant = 498 atm) and pilot and full-scale testing. The chemical was removed successfully from contaminated ground water at 12-14C in an EPA pilot packed tower aerator containing 18 feet of l-inch plastic saddle packing (KSE, 19?*4). The average percent removal varied with air-to-water volume r . o, from 90.6% to 99.99% at ratios of 5 to 30, respectively. Similarly, the concentration of 1,1-DCE in contaminatec well water decreased from 122, ug/L to 4 ug/L (97%) using diffused aeration (ESE, 1934). Aeration was conducted in a pilot (1.5 inch diameter, 4-foot long) countercurrent glass column, using a 10-minute contact time and an air-to-water ratio of 4. Air stripping is an effective, siirple and relatively inexpensive process for removing 1,1-DCE and other organics from water. However, the use of this process transfers the contaminant directly to the air stream. When considering use of air stripping as a traetment process, it is suggested that careful consideration be given to the overall environs occurrence, fate, route of exposure and various hazards associated with the chemical. SL 063114 i, l-Di-.uoroethylene -12- September 30, 1985 X. REFERENCES ACGIH. 1982. American Conference of Govt- iient Industrial Hygienists. TLVs. Threshold limit values for c mical substances in work air. \ndersun, M.E., and L.R. Jenkins, Jr. 1977. Oral toxicity of 1,1-dichloroethylene in the rat: Effects of sex, age and fasting. Environ. Health Perspect. 21:157-163. Andersen, M.E., O.E. Thomas, M.L. Gargas, R.A. Jones and L.J. Jenkins, Jr. 1980. The significance of multiple detoxification pathways for reactive metabolites in the toxicity of 1,1-dichloroethylene. Anderson, 0. 1977. Dominant lethal studies with the halogenated olefins vinyl chloride and vinylidene chloride in male CD-I mice. Environ. Health Perspect. 21:71. Bartsch, H., C. Malaveille, R. Montesano and L. Tcmatis. 1975. Tissuemediated mutagenicity of vinylidene chloride and 2-chlocobutadiene in Salmonella typhimurium. Nature 255:641-643. CEH. L983. Chemical Economics Handbook, Stanford Research Iastitute, Menlo Park, California. Chieco, P., M.T. Moslen and E.S. Reynolds. 1982. Histocheraical evidence that plasma and mitochondrial membranes are primary foci of hepato cellular injury caused by 1,1-dichloroethylene. Lab. Invest. 46:413-421. Dobbs, R.A., and J.M. Cohen. 1980. Carbon adsorption isotherms for toxic organics. EPA 600/80-02: MERL, Cincinnati, OH. Drevon, C., and T. Kuroki. 1979. Mutagenicity of vinyl chloride, vinyli dene chloride and chloroprune in V79 Chinese hamster cells. Mutat. Res. 67:173-182, ESE. 1984. Environmental Science and Engineering. Draft technologies and costs for the removal of volatile organic chemicals from potable water supplies. ESE No. 84-912-0300. Prepared for the U.S. EPA, Science and Technology Branch, CSD, OCW, Washington, DC. Greim, H., G. Bohse, Z. Radwan, D. Reichert and D. Henschler. 1975. Mutagenicity in vitro and potential carcinogenicity of chlorinated ethylenes as a function of metabolic oxirane formation. Biochem. Pharmacol. 24:2013-2017. Hess, A.F., J.s. Dykesen and G-C. Cline. 1981. Case studies involving removal of organic chemical compounds from ground water. Presented at the Preconference seminar concerning organic chemical contaminants in ground water at the 1981 annual conference of the ,WWA, June 7-U, 1981, St. Louis, MO. SL 063115 1,1-Dichloroethylene September 30, 1985 Where; 10 mg/kg/day * LOAEL 100 = uncertainty factor, appropriate for use with animal study 10 = uncertainty factor, conversion of LDAEL to 'JOAEL *RRfD = Risk Reference Dose: estimate of daily exposure to the human population which appears tg,-be without appreciable risk of deleterious nonTcaretrtoqenic effects over a lifetime of exposure Step 2: Determination of Lifetime Health Advisory Lifetime HA = (0.01 mg/kg/day) (70 kg) S 0.35 nc/L = 350 ug/L (2 L/day) V Where; 0.01 mgA'. day = RRff) 70 kg assumed weight of protected individual 2 L/day = assumed volume of water ingested by 70 kg adult . The Lifetime Health Advisory of 350 ug/L derived above reflects an assumption that 100% of the exposure to 1,1-dichloroethylene is via the drinking water. It has been shown, however, that exposure might well occur via other routes. Since compound-specific data on actual relative source contribution are lacking, it may assumed that drinking water contributes 20% of an adult's daily exposure to this substance. The Lifetime Health Advisory for the 70 kg adult,would be_70 ug/1, taking this relative source contribution into account. V ^------ Evaluation of Carcinogenic Potential Qualitative and quantitative assessment of tne carcinogenic potential of 1,1-dichloroethylene is complicated by the fact that the only positive data - manmary tumors in fenale rats and mice and kidney adenocarcinomas in mice-(Maltoni, 1977) have become finalized only recently. They have not yet been published, although they have been submitted for oublication (Malf.ni et al., 1985). On ti;e basis of the preliminary data from the study using mice (Mai ton i, 1977), the EPA Carcinogen Assessment Croup calculated estimated incremental excess cancer risk associated with exposure to 1,1-dichloroethylene in drinkin water (U.S. EPA, 1934a,c) Assuming consumption of 2 liters of water by a 70 kg individual, ic was estimate! th\'r exposure to 0.2t ug/1 i,l-diuhloroethvlen SL 063116 1, 1-Dichioroethylene -10- September JU, over 3 lifetime would result in a one in a million risk rate (10"). Risks of 10"5 and 10"4 were estimated if exposure occurred at 2.4 or 24 ug/1, respectively. IARC (1983) reported that the data were inadequate to assess the '.-ircinojenic ;>->tential in humans, but that it would reevaluate this assessrent ;i i. r it liad the opportunity to review the rat drinking water study (Rampy, et al., 1977; Quast, et al., 1983) and the NTP gavage bioassays (NTP, 1982). Applying the gri^ria" descirTBetKin EPA's guidelines for assessment of cargincgeniq risk (U.S. EPA, 1984b), J., 1-dichloroethylene may be classified irf^Group C: PossiblelSuTOrr carclnoqen. Group C includes agents with limited (evidence of carcinogenicity in aninals in the absence of human data. -T. OTHER CRITERIA, GUIDANCE AND STANDARDS In June, 1984, EPA proposed a Recorrmended Maximum Contaminant L?vol (RMCL) of zero for 1,1-dichloroethylene in drinking water (U.S. EPA, 1984c). Promulgation of an RMCL is expected in late 1985. In 1980, EPA estimated a range of excess cancer risks for lifetime exposure to 1,1-dichloroethylene when developing ambient water quality criteria (U.S. EPA, 1980a). This range was 23 ug/1, 2.3 ug/1 and ',0,23 ug/1^respectively, for risks of 10"^, 10"^ and 10", assuming conSunption of 2 liters of water and 6.5 grams of contaminated fish per day by 70 kg adult. o The National Academy of Sciences-calculated a chronic SNARL (SuggestedNo-Adverse-Response-Leve il (of 100 ug/L, Jbased upon nog-carc inoganic ... effects only (NAS, 1983), identifiedrA NOAEL of 2 mg/kg '"j frcro the 1982 NTP bioassay in mice. An uncertainty"factor-of toO was applied; it was assumed that a 70 kg adult consumes 2 liters of water daily and 20% of the exposure of most individuals would be from drinking water; in addition, a factor of 5/7 to correct from 5- to 7-day/week exposure. -- o "\ The World Health Organization has established a guideline for 1,1-dichloroethylene in drinking water of 0.3 ug/1, set on evidence of carcinogenicity (WHO, 1984). \ o V The threshold limit TLV) for occupational settings is 5 ppm (20 mg/W3) (ACGIH,(1982), V, VII. ANALYSIS * Analysis of 1,1-dichloroethylene is by a purge-and-trap gas chromato graphic procedure used for the determination of volatile organohalides in drinking water (Method 502.1. Volatile halogenated organic compounds in water by purge and trap gas chromatography. U.S. EPA, 1985a). Tins method calls for the bubbling of an inert gas through the sample md trapping 1,1-dichloroethylene on an adsorbant material. The adsorbant: material is heated to drive off the 1,1-dichloroethylene onto a gas chromatographic column. This method is applicable to the measurement SL 063117 1,l-Dichloroethylene -7- September 30, 1985 UF(s) * uncertainty factors, based upon quality and nature of data L/day * assumed daily water consumption (1 or 2) in liters One-dav Health Advisory The Jenkins, et al. (1972) study in which five liver or plasma enzyme activities were nuasured is considered to be appropriate for calculation of the One-day HA. Single oral doses of 100 , 300 or 500 mg 1,1-DCEAg in com oil were administered to adult rats. Twenty-two to 46 hours after dosing with 100 mg/kg, liver glucose-6-phosphatase (G-6-P) was reduced to 80% of control; liver alkaline phosphatase (AP) was doubled. At 300 mg/kg, liver G-6-P was reduced to 53% of control, liver AP nearly quintupled, liver tyrosine transami'..a ~a quadrupled and plasma alkaline transaminase was elevated 150 percent. At 500 mgAg all four enzymes were affected further; in addition, plasma alkaline phosphatase was elevated more than 400 percent above control. The lowest dose -administered (100 mgAg) was identified as a tDAEL. The one-day HA for tne 10 kg child is calculated Iowsj____ _____ One-day HA = (100 mu Kg/riay) (10 kg) (iOd) (IQi (l L/day) ^ i.o nu/L = 1000 ug/L Where: TOO my, kg/day = LOAEL 10 kg a assumed weight of protected individual 100 = uncertainty factor, appropriate for use with animal study 10 * uncertainty factor, appropriate for use in -t- fjOAEL to NOAEL l L/day - assumed volume of drinking water consumed by 10 kg child Ten-day Health Advisory Appropriate studies for the calculation of the Ton-day HA are not available. However, evaluation of all toxicological data for 1,1-DCE suggests that the Longer-term Health Advisory for the 10 kg child would provide sufficient protection over a ten-day period as well. Thus, the Ten-day HA is 1000 ug/L. Longer-term Health .Advisory A longer-term HA can be calculated from a 90-day subchronic study in whic rats of both saxes wore giver 1,1-DCE at nominal concentrations of 0, 50, 100 or 200 ppm (0 to 25,6 mg/kg bw,bay) in their drinking water (Rampv, et al., i977). Except for a decrease i -.dr-.,-/ v;dy weight ratio in m > le-^ t^e low dose, there were no statistical ly - .oni - icant differences in organ vey;ht in organ:body wiyht ratios at the l-mination of th<a study. The or.ij <. .-'t' SL 063118 1,1-Dichloroethylene September 30, 1985 pathology noted was an increased cytoplasmic vacuolization of hepatocytes in the livers of both sexes exposed to the highest dose. A NOAEL of 100 ppn {10 to 12.6 mg/kg) was identified. A Longer-term HA for the 10 kg child is calculated as follows: Longer-term HA = (10 mq/kq/day) (10 kg) * 1.0 ng/1 * 1000 ug/L (100) (1 L/day) Where: 10 mg/kg/day 10 kg = NOAEL = assumed weight of protected individual 100 1 L/day uncertainty factor, appropriate for use with animal data * assumed volume of water consumed by 10 kg chili A Longer-term HA for the 70 kg adult is calculated as follows: Longer-term HA * (10 mqAd/day) (70 kg) . * 3.5 mg/L * 3500 ug/L (100) (2 L/day) Where: all factors are the same except, 70 kg * assumed weight of protected.individual 2 L/day = assumed volume of water consumed per day by 70 kg adult Lifetime Health Advisory The Lifetime HA can be calculated from the 2-year chronic study in rats (Quast, et al., 1983). 1,1-Dichloroethylene, at nominal concentrations of 0, 50, 100 or 200 ppm (0 to 20 mg/kg/day) in drinking water, was adninistered to animals of both sexes. No consistent treatment-related changes were observed in any parameter measured. The only histopathology observed was in the livers of both sexes receiving the highest dose, changes characterized by a minimal amount of mid-zonal fatty accunulation. No liver degeneration was noted. A LQAEL of 100 ppm (10 mgAg) was identified, based upon a trend towards increased fatty deposition in the liver. The Lifetime HA for the 70 kg adult is calculated as follows: Step 1: Determination of RRfD* RRfD = (10 mqAq/dav) (100) (10) 0.01 mg/kg/day SL 063119 1,1-Dichloroethylene -5- September 30, 1985 # Reports of effects on workers exposed to this chemical in canbination with other vinyl compounds include liver function abnormalities, headaches, vision problems, weakness, fatigue and neurological sensory disturbances (NIOSH, 1979). Animals Short-term Exposure 0 Reported oral LDjq's in adult rats, range from 200 to 1800 mgAg (NIOSH, 1978;Poncnarkov and Tcmatis,1980). Young or fasted rats are more sensitive to the acute effects of administration, with LDsq's of approximately 50 mg/kg (Andersen and Jenkins, 1977). The oral tiro's in the mouse and the doy were reported to be 200 mg/kg (Jones and Hathway, 1978b) and 5750 mg/kg (NIOSH, 1978), respectively. # The most sensitive end-point of 1,1-0CE toxicity is liver damage, ranging from fatty infiltration to necrosis, although the mechanism appears to be different from that of other halogensted ethylenes (Reynolds, et al., 1975;Chieco, et al., 1982). The liver toxicity of 1,1-dichloroethylene follows a comkm pattern of dose-response, with a threshold level, a concentration of rapid increase and an extended plateau where increase Joses cause little further increase in effect (Andersen and Jen*ins, 1977). * Kidney lesions a Is., have been datmstrated following exposure to 1,1- dichloroethylene at doses similar to those affecting the liver (Prendecgast, et al., 1967). 0 The acute toxicity of the chemical is probably tlie result of a toxic metabolite rather than the parent compound (Andersen, et al., 1980). Longer-term Exposure 0 As with acute exposure, the liver appears to be the principal target of 1,1-dichloroethylene toxicity following extended periods of exposure. Chronic exposure of rats to levels up to 200 ppm ( 22 mgAg) in drinking water resulted in fatty changes and hypertrophy of liver cells in fenwles .t all doses anti in males at the highest dose (Ranpy, et al., 1977;\>.iast, et al., 1983). Teratogenic/Reproductive Effects 8 1,1-Dichloroethylene did not produce teratogenic effects in rats or rabbits following inhalation or drinking water exposure of dams during organogenesis (Murray, et al., 1979). Potential effects of 1,'.-IXE on reproductive capacity have not been studied. Mutagenicity 8 1,1-Dichloroethylene w. '"ut : .'nic to bacteria In tk- 5aImonella test (Bartsch, et al., ..`75, kmnon, et al., 1977) dnd E. nolT (Greim, et al., 1975) 1, the p: :once, but not the absence, 3t' a metabolic activation sy--m. SL 063120 1,1-Dicnloroethylene -6- September 30, 1985 0 Mutation has not been confirmed in manmalian systems using V79 Chinese hamster ovary cells (Drevon and Kuroki, 1979) or dominant lethal tests in rats and mice (Anderson,1977; Andersen and Jenkins, 1977; * Short, et al., 1977). 9 1,1-Dichloroethylene binds with ENA to a slight degree in the liver and kidneys oE both rats and mice after inhalation exposure to 10 or 50 ppm for 6 hours (Reitz, et al., 1980). However, massive tissue damage also occurred. 9 The International Agency for Research on Cancer (IARC) concluded that there is sufficient evidence to state that 1,1-dichloroethylene is mutagenic (IARC, 1983). Carcinogenicity O The results of most studies of the carcinogenic potential of this substance fail to support a significant, treatment-related increase in tumor incidence (U.s. EPA, 1984a). No oral study has resulted in a significant tumor response (NTP, 1982;Quast, et al., 1983). Some, but not all, of the inhalation studies have reported significant tumor increases (e.g., manmary tumors in female rats and mice and kidney adenocarcinomas in mice) (Maltoni, 1977; Maltoni, et al., in press). * 1,1-Dichloroethylene was inactive as a whole mouse skin carcinogen when administered subcutaneously (Van Duuren, et al., 1979). It was active as a skin tumor initiator following several applications of phorbol ester as a premotor. V. QUANTIFICATION OF TOXICOLOGICAL EFFECTS Health Advisories are based upon the identification of adverse health effects associated with the most sensitive and meaningful non-carcinogenic end-point of toxicity. The induction of this effect is related to a particular exposure dose over a specified period of time, most often determined frcm the results of an experimental animal study. Traditional risk characterization methodology for threshold toxicants is applied in HA development. The general formula is as follows: (NQftEL or LOAEL) (BW) ,, __uq/L (UF(s)) (_L/day) Where: NOAEL or LOAEL a No-Observed-Mverse-Effect-Level or Lewest-Observed-Adverse-Effect-Leve1 (the exposure dose in mg/kg bw) BW = assumed body weight of protected individual in kg (10 or 70) 1,l-Dichloroethylene -3- September 30, 1985 Occurrence 1,l-Dichloroethylene (1,1-DCE) is a synthetic chemical with no natural sources (U.S. EPA, 1983). 0 Approximately 200 million pounds of 1,1-dichloroethylene were produced in 1980. the major use of 1,1-dichloroethylene is as a co-monomer in the production of a number of polymers. Polymers of 1, t-dichloroethyl.*ne and vinyl chloride are used as food wrap (CEH, 1983). * The major releases of 1,1-dichloroethylene to the environment are during its production and its use in the manufacture of polymers. IXe to its volatile nature, the majority of releases are expected to be to air. Small amounts of 1,1-dichloroethylene may be released to water and land in industrial effluents and from the disposal of solid wastes (U.S. EPA, 1983), 1,l-Dichloroethylene may be a degradation product of trichloroethylene and perchloroethylene. While laboratory studies ace currently inconclusive, 1,1-dichloroethylene has been foun l to co-occur in ground water with trichloroethylene and tetrachloroethylene ami their other degradation products, cis- and trans-1,2-dichloroethylene and vinyl chloride- 8 there is relatively 11: tie information on the behavior of 1,1-dichloroethylene in the environment- However, the behavior of tills chemical has been estimated based upon the information on similar chlorinated compounds (U.S. EPA, 1979). 1,l-Dichloroethylene released to the atmosphere is expected to chemically degrade in a matter of hours; when released to surface waters, 1,1,-DCS is expected to volatilize rapidly tc air. 1,l-Dichloroethylene is chemically stable in water and mobile in soils. Once released to land, 1,1-dichloroethylene is expected to migrate with ground water. 1,l-Dichloroethylene is net teLieved to bioaccunulate in plants or animals. 8 Available data suggest that 1,1-dichloroethylene is not a comnon contaminant of drinking water. It has not been refxirted to occur at levels higher than 0.1 ug/L in surface water. However, i,l-dichloro ethylene has been reported to occur at levels up to 40 uy/L in w-*!ls contaminated with other chlorinated solvents. 8 No information is available on the occurrence of 1,l-dichloroethylene in food. While 1,1-dichloroethylene is used in the manufacture of food wrap, residual levels are expected to be very low because of its high volatility. Little or no contamination of food is expected frtm this use. Because of limited release, rapid degradation and high volatility, 1,1-DCE is not expected to be a curenon contaminant in food. 8 1,l-Dichloroethylene contamination of air has been reported to occur in urban and suburban areas in the low ppt range. Levels in the ppb range have t>;en reported in the areas where 1,1-DCE and its polymers are manufactured (U.S. EPA, 1983). SL 063122 1, 1-Dichloroethyiene -4- September 30, 1985 I. PHARMACOKINETICS Absorption Administration of a single oral dose of 1,1-dichloroethylene in the range of 0.5 to 50 mg/kg resulted in rapid and complete absorption in rats and mice (Jones and Hathway, 1978a;McKenna, et al., 1978b). Distribution 0 Distribution in rats following a single oral dose of 25 mg 1,1-DCEAg resulted in high concentrations in the liver and kidneys after 30 minutes with more general distribution throughout other soft tissues after 1 hour (Jones and Hathway, 1978a). Single oral doses of ^^C-1,1-DCE at l or 50 mg/kg were administer*! to rats (McKenna, et al., 1978a,b). At 72 hours after dosing, the greatest percentage of radioactivity was found in the liver- Metabolism 0 The netabolic end products of chlorinated ethylenes are predominately alcohols and carboxylic acids. The known metabolites of 1,i-dichloroethylene are chloroacetic acid and dichloroacetaldehyde (Liebler and Guengerich, 1983;Liebler, et al., 1984). Tbxic intermediates that are formed may interact with tissue macronolecules. * Metabolism is readily saturable at higher doses (McKenna, et al., 1978a,b), but presumably not so at levels expected to lie encountered in contamination incidents. Excretion The rate of excretion is relatively rapid, since most of a dose is eliminated within the first 24-72 hixirs after administration (Jaeger, et al., 1977). At lew doses, most of the metabolites are eliminated via renal and biliary excretion. Carbon dioxide formed during metabolism is expired through the lungs. 0 At higher dose levels, as metabolism reaches saturation, less of the compound is removed from the blood as it passes through the liver. As a result, increasing amounts of unchanged 1,1-dichloro ethylene are eliminated via the lungs (McKenna, et al., 1977). IV. HEALTH EFFECTS Humans 0 At high concentrations (>_ 4000 ppm), inhalation of 1,1-dichloro ethylene results in rapid onset of G4S depression, with unconsciousness following if exposure is continued (Irish, 1963). SL 063123 September 30, 1985 1,1-DICHLDFOETHYLENE Health Advisory Office of Drinking Water S. environmental Protection Agency ng Water's non-regulatory Health Advisory Program provides :ects, analytical1 methodology and treatment technology that vg with contamination of drinking water. Health Advisories .ns of contaminants in drinking water at which adverse .cipated to ocftir* A margin of safety is included to ; of the populatione not legally enforceable Federal standards. They are and better information becomes available. The Advisories guidance to assist Federal, State and local officials n of the public health. numbers are developed from data describing non-carcinogen They do not Incorporate quantitatively any potential .ch exposurS. '^Wr those chemicals which are known or s according to the proposed Agency classification scheme, and Longer-term Health Advisorios may he derived, with n Advisories for lifetime exposures may not be reconmende-: cancer n'sks are provided to give an estimate of contaminant vrfich may pose a carcinogenic risk to al estimates usually are presented as upper 95% confidence inearized multistage model which is considered to be the probabletrue risk. ia SL 063124 1,1-Dichloroethylene September 30, 1985 This Health Advisory (HA) is based upon information presented in the Office of Drinking Water's Health Effects Criteria Document (CD) for the Dichloroethylenes (U.S. EPA, 1984a). The HA and CD formats are similar for easy reference, Individuals desiring further information on the toxicological iata base or rationale for risk characterization should consult the CD. The C'J is available for review at each EPA Regional Office of Drinking Water counterpart (e.g.. Water Supply Branch or Drinking Water Branch), or for a tee from the National Technical Information Service, U.S. Department of Commerce, 5285 Port Royal Rd:, Springfield, VA., 22161, PB #, 5The toll free number is (800) 336--4700; in Washirviton, D.C. area; (701) 437-4650. iI. General Information and Properties Synonyms Vinylidene chloride, 1,L-0CE, dichloroethene Uses Chemical intermediate Manufacture of polyvinylidene copolymers Properties CAS # Chemical formula Molecular weight Physical state (room tenp,) siting point uling point x>r pressure ^cific gravity cer solubility Octanol/water partition coefficient Taste threshold (water) Odor threshold (water) Odor threshold (air) 75-35-4 clear, colocless liquid -122.2 C n.5 C 591 torr (20C) 1.3 250,000 ug/L (20*C) 5.37 2000-5500 ng/m3 Structural formula Cl Cl-C-C-H H (Irish, 1963; Windholz, et al., 1976) SL 063125