EPA 749-F-94-014a CHEMICAL SUMMARY FOR METHYLCHLOROFORM prepared by OFFICE OF POLLUTION PREVENTION AND TOXICS U.S. ENVIRONMENTAL PROTECTION AGENCY August 1994 This summary is based on information retrieved from a systematic search limited to secondary sources (see Appendix A). These sources include online databases, unpublished EPA information, government publications, review documents, and standard reference materials. No attempt has been made to verify information in these databases and secondary sources. I. CHEMICAL IDENTITY AND PHYSICAL/CHEMICAL PROPERTIES The chemical identity and physical/chemical properties of methylchloroform are summarized in Table 1. TABLE 1. CHEMICAL IDENTITY AND CHEMICAL/PHYSICAL PROPERTIES OF METHYLCHLOROFORM _________________________________________________________________________ Characteristic/Property Data Reference _________________________________________________________________________ CAS No. 71-55-6 Common Synonyms 1,1,1-trichloroethane, chlorothene Budavari et al. 1989 Molecular Formula C2H3Cl3 Chemical Structure Cl H | | Cl- C - C - H | | Cl H Physical State colorless liquid Keith and Walters 1985 Molecular Weight 133.42 Budavari et al. 1989 Melting Point -32.5øC Budavari et al. 1989 Boiling Point 74.1øC Budavari et al. 1989 Water Solubility 1334 mg/L CHEMFATE 1994 Density d20/4, 1.3376 Budavari et al. 1989 Vapor Density (air = 1) 4.63 Verschueren 1983 KOC 152 U.S. Air Force 1989 Log KOW 2.49 U.S. Air Force 1989 Vapor Pressure 100 mm Hg at 20øC Verschueren 1983 Reactivity Flash Point nonflammable U.S. Air Force 1989 Henry's Law Constant 2.76 x 10-2 atm m3/mol U.S. Air Force 1989 Fish Bioconcentration Factor <9 (measured) HSDB 1994 Odor Threshold 100 ppm (in air) Torkelson and Rowe 1981 Conversion Factors 1 ppm = 5.54 mg/m3 1 mg/m3 = 0.18 ppm Verschueren 1983 ___________________________________________________________________________ II. PRODUCTION, USE, AND TRENDS A. Production Methylchloroform is produced by three companies in the United States. Table 2 lists the producers, along with plant locations and capacities. In 1991, US production was estimated to be 648 million pounds. During that same year, 162 million pounds of methyl chloroform were exported, and imports were negligible (Mannsville 1992). TABLE 2. United States Producers of Methylchloroform ________________________________________________________________________ Company Plant Location Plant Capacity (In Millions of Pounds) ________________________________________________________________________ Dow Chemical Freeport, TX 495 PPG Industries Lake Charles, LA 350 Vulcan Chemicals Geismar, LA 200 ________________________________________________________________________ Source: Mannsville 1992. B. Use Methylchloroform is most commonly used for metal cleaning, both cold cleaning and vapor degreasing. It is commonly used as a solvent in aerosol formulations, adhesives, coatings, inks, and electronics. It is also used as a lubricant in cutting oils and as a chemical intermediate for organic chemicals, such as vinylidene chloride (Mannsville 1992; HSDB 1994). Table 3 shows the estimated 1991 US end-use pattern for methyl chloroform. C. Trends Under current EPA regulations, production of methylchloroform will be permitted only for transformation and other uses to be defined by the EPA. Therefore, production is expected to decline to less than 50 million pounds per year after 1995 (Mannsville 1992). TABLE 3. Estimated 1991 United States End-Use Pattern of Methylchloroform ________________________________________________________________________ Use of Methyl Chloroform Percentage of US Methylchloroform Use (Typical Standard Industrial Classification (SIC) Code) (see end note 1) ________________________________________________________________________ Metal Cleaning (used in a variety of SICs) 50% Aerosols (production, SIC 2851; used in a variety of SICs) 11% Adhesives (production, SIC 2891; used in a variety of SICs) 11% Chemical Intermediate (production, SIC 2869; use, SIC 2869) 10% Coatings and Inks (production, SICs 2851, 2893; used in a variety of SICs) 8% Electronics (use, SIC 36) 4% Miscellaneous (no applicable SIC(s)) 6% ________________________________________________________________________ Source: Mannsville 1992. III. ENVIRONMENTAL FATE A. Environmental Release Of the methylchloroform (1,1,1-trichloroethane) released to the environment in 1992, as reported to the Toxic Chemical Release Inventory by certain types of U.S. industries, 114.9 million pounds were released into the atmosphere, 13.1 thousand pounds released into surface water, 500 pounds released to underground injection sites, and 76.4 thousand pounds released onto land (TRI92 1994). Concentrations of methylchloroform measured in untreated ground and surface waters samples from sites in over 100 U.S. cities range from 0.2 to 334 ppb (HSDB 1994). A range of 950 to 5440 ppb methylchloroform has been measured in samples of contaminated drinking water wells in New York, New Jersey, Connecticut, and Maine (HSDB 1994). Arctic sea water near Sweden contained 0.4 - 1.7 ng/L (parts per trillion) and concentrations of 0.6 - 69 parts per trillion have been measured in rain or snow at various locations around the globe (HSDB 1994). Atmospheric concentrations of methylchloroform ranged from 0.074 - 0.587 ppb, and 1.2 ppb has been measured in the workplace (HSDB 1994). The chemical has been detected in human mother's milk in urban areas (HSDB 1994). Due to the large output and slow degradation of the chemical, the atmospheric concentration is increasing by 4.8 -17% a year (HSDB 1994). B. Transport Methylchloroform volatilizes rapidly to the atmosphere from water and soil as predicted by its vapor pressure (100 mm Hg) and Henry's law constant (2.76 x 10-2 atmùm3/mol) (ATSDR 1993). Once in the atmosphere, the chemical is transported long distances, being found as distant as the South Pole (CHEMFATE 1994), but can be removed from the atmosphere in rain or snow (HSDB 1994). The chemical leaches into ground and surface waters from soil (U.S. Air Force 1989) due to its water solubility. C. Transformation/Persistence 1. Air - The estimated half-life for methylchloroform in air is 2.2 to 4.8 years (U.S. EPA 1984). Little degradation of methylchloroform occurs in the troposphere, but direct photolysis occurs in the stratosphere (CHEMFATE 1994; HSDB 1994). Degradation in the troposphere also occurs slowly by reaction with hydroxyl radicals (half-life, 3.7 years); however, the half-life is "drastically reduced" (to 26 weeks) in the presence of ozone or chlorine radicals (CHEMFATE 1994). 2. Soil - Evaporation and leaching are the major routes of removal of methylchloroform from soils (U.S. Air Force 1989). There is little evidence to suggest that biodegradation occurs except in acclimated soils, like those found in landfills (HSDB 1994; U.S. Air Force 1989). 3. Water - Volatilization of methylchloroform into the atmosphere is the main route of removal from water. The half-life in water ranges from hours to weeks (HSDB 1994). No photodegradation has been measured in water but slow to moderate biodegradation occurred after acclimatization (CHEMFATE 1994). 4. Biota - Bioconcentration of methylchloroform in aquatic organisms is not expected to be important based on the log bioconcentration factor of 0.95 in bluegill (CHEMFATE 1994). IV. HUMAN HEALTH EFFECTS A. Pharmacokinetics 1. Absorption - Methylchloroform is absorbed from both the lungs and the gastrointestinal tract (U.S. EPA 1984). The chemical was found in expired air (no quantities given) after accidental ingestion of 1 ounce (U.S. EPA 1984). The rate of absorption in human males exposed by inhalation to 72 or 213 ppm for 8 hours ranges from 26 - 32% (HSDB 1994). 2. Distribution - After exposure by inhalation to mice, methyl- chloroform was found in brain, kidney, and liver (IARC Monographs 1979). Following occupational exposures to humans of high concentrations (no levels given), the chemical has been found in blood, brain, liver. bile, skeletal muscle, and lungs (ACGIH 1991). The chemical is preferentially distributed to fatty tissue but cleared after cessation of exposure (ATSDR 1993). 3. Metabolism - Methylchloroform is metabolized to trichloroacetic acid and trichloroethanol (Torkelson and Rowe 1981). A "small percentage" will be metabolized to carbon monoxide (HSDB 1994). 4. Excretion - The majority of methylchloroform is eliminated unchanged in expired air. After exposure of humans by inhalation to 72 or 213 ppm for 8 hours, approximately 90% of the calculated dose was eliminated in expired air by 8 days; urinary excretion of glucuronide conjugated metabolites lasted about 12 days (HSDB 1994). Rats have been shown to eliminate greater than 98% of an absorbed dose in expired air with about 0.5% converted to CO2 and the remainder excreted in the urine as trichloroacetic acid or the glucuronide of trichloroethanol (IARC Monographs 1979). B. Acute Toxicity Inhalation exposure to high levels of methylchloroform can cause central nervous system depression with death due to respiratory failure and/or cardiac arrhythmia (see section IV.G for details on neurotoxicity). Non-lethal doses may cause headache and fatigue. The vapor is irritating to the eyes and nose. 1. Humans - Inhalation exposure to 1000 ppm causes eye and nasal irritation within 30 minutes (Torkelson and Rowe 1981). Hypotension, premature ventricular contractions, and cardiac arrest have been reported in patients exposed to 10,000 to 26,000 ppm methylchloroform as a surgical anesthetic (U.S. Air Force 1989). Transient liver and kidney dysfunction occurred in adolescents exposed to "large" concentrations of the chemical while sniffing glue; twenty-eight percent of sudden deaths in glue sniffers have been attributed to methylchloroform (HSDB 1994). Fatigue, irritation, and headache were the only effects reported in volunteers exposed to 500 ppm 7.5 hours/day, 5 days/ week for 3 weeks (U.S. EPA 1984). Accidental ingestion of 30 mL resulted in gastrointestinal disturbance but only minimal hepatic or renal damage; recovery was complete within 2 weeks (U.S. Air Force 1989). 2. Animals - Reported LD50 values for methylchloroform are greater than 5 g/kg for rats, mice, rabbits, and guinea pigs (ACGIH 1991). Methylchloroform is a skin irritant; application to guinea pigs of 1 mL liquid or repeated contact over 3 days caused edema, erythema, inflammation, and cellular degeneration (ACGIH 1991). Liquid methylchloroform caused only mild, transient irritation in the eyes of rabbits (Torkelson and Rowe 1981). Cardiac sensitiza- tion to epinephrine occurred in dogs exposed to 5000 or 10,000 ppm methylchloroform (no duration given) (ACGIH 1991). C. Subchronic/Chronic Toxicity Long-term worker inhalation exposure to methylchloroform has been reported to result in no observed permanent liver damage or adverse changes in cardiovascular function. Repeated dermal contact may cause transient dermatitis. Repeat dose laboratory animal studies have shown adverse liver and kidney effects after inhalation or oral exposure to high levels of methylchloroform. EPA is currently reviewing information to determine if an inhalation reference concentration (RfC)(see end note 2) can be derived for methylchloroform. 1. Humans - A no-observed adverse effect level for long-term occupational exposure is approximately 53 ppm (HSDB 1994). Epidemiological studies of workers exposed to methylchloroform for up to 6 years showed no effects on liver or cardiovascular function (Torkelson and Rowe 1981). "Prolonged or repeated contact with skin" may cause transient dermatitis (HSDB 1994). 2. Animals - Rats, rabbits, monkeys, and guinea pigs were exposed to 500 ppm methylchloroform by inhalation 7 hours/day, 5 days/ week for 6 months with no evidence of organ damage (ACGIH 1991). Continuous exposure for 14 weeks to 1000 ppm caused no adverse effects in dogs or monkeys but resulted in increased liver weight and fatty and necrotic changes in the livers of mice and rats (Torkelson and Rowe 1981). No adverse effects were seen in rats exposed to 875 or 1750 ppm 6 hours/day, 5 days/week, for 1 year (Torkelson and Rowe 1981). Animals were exposed to 650, 1500, 3000, or 5000 ppm 7 hours/day, 5 days/week, for 1-3 months. Slight reduction in growth rate at all doses and fatty liver changes at 5000 ppm were observed in guinea pigs but rats, rabbits, and monkeys were unaffected (U.S. EPA 1984). Rats and mice were given methylchloroform at doses of 0.5, 1, 2, 4, or 8% in feed (see end note 3) for 13 weeks (NTP 1994). Dose related systemic effects included hyaline degeneration and inflammation in kidneys of male rats, decreased body and heart weights in male mice, and decreased body and liver weights in female mice. D. Carcinogenicity Available evidence is inadequate to assess the carcinogenic potential of methylchloroform. There is no reported human cancer information, and animal studies have failed to demonstrate carcinogenicity. Based on no human and no animal cancer data, the U.S. EPA (1994) classified methylchloroform as class D, not classifiable as to human carcinogenicity. 1. Humans - No information was found in the secondary sources searched regarding the carcinogenicity of methylchloroform to humans. 2. Animals - No increase of tumors of any kind occurred in rats exposed by inhalation to 875 or 1750 ppm methylchloroform 6 hours/day, 5 days/week for 1 year, followed by a 19-month observation period (U.S. EPA 1984). No cancers were seen in rats or mice exposed to up to 1500 ppm 6 hours/day, 5 days/week, for 2 years (U.S. Air Force 1989). High mortality occurred in mice (time-weighted average doses, 2807 or 5615 mg/kg/day) and rats (750 or 1500 mg/kg/day) given methylchloroform by gavage 5 days/week for 78 weeks, precluding adequate carcinogenicity assessment (IARC Monographs 1979). Therefore, IARC classifies methylchloroform as Group 3, not classifiable as to its carcinogenicity to humans (IARC Monographs 1979). E. Genotoxicity Methylchloroform is positive for cell transformation with rat embryo cells (RLV/1706) and for sister chromatid exchange in mammalian cells; it was negative for alterations in mouse sperm morphology (GENETOX 1992). Methylchloroform has been tested for mutagenicity under Section 4 of the Toxic Substances Control Act (TSCA). The testing was to consist of a mouse micronucleus test and a dominant lethal test, the latter test being triggered by a positive response in the micronucleus assay. Methylchloroform was not a chromosome mutagen under conditions of the micronucleus test (Cimino 1990). F. Developmental/Reproductive Toxicity Results of testing, requested by and submitted to EPA under Section 4 of TSCA, indicate methylchloroform adversely affects the developing fetus at high concentrations in air. No evidence of reproductive toxicity has been seen in most species tested except in guinea pigs which showed testicular degeneration at high concentrations of methylchloroform in air. 1. Humans - No information was found in the secondary sources searched concerning the developmental or reproductive toxicity of methylchloroform in humans. 2. Animals - Developmental toxicity studies have been completed and submitted to EPA under the authority of Section 4 of TSCA (Troast 1989). Rats (30/group) and rabbits (24/group) were exposed by inhalation to 1000, 3000, and 6000 ppm methylchloroform on days 6-15 and 6-18 of gestation, respectively. Developmental toxicity (unossified/poorly ossified cervical centra, decreased fetal weight, and increased non viable implantations in rats; and an increase in bilateral extra 13th ribs in rabbits) was reported at 6000 ppm. The no-observed-adverse- effect level for developmental effects was 3000 ppm in both species. Maternal toxicity (reduced body weight gain and food consumption) occurred at each dose level in rats and at the two highest doses in rabbits. No maternal, fetal, or developmental toxicity was observed in rats or mice exposed by inhalation to 875 ppm methylchloroform, 7 hours/day on days 6-15 of gestation (U.S. EPA 1984). Rats were exposed to 2100 ppm, 6 hours/day, 7 days/week, beginning 2 weeks prior to mating and continuing throughout gestation (ACGIH 1991). Skeletal and soft tissue anomalies, observed in offspring sacrificed on gestation day 21, were attributed to developmental delays, andneurobehavioral and developmental delays in surviving offspring were no different from controls by 21 to 120 days of age. Successive generations of mice were exposed to 100, 300, or 1000 ppm methylchloroform in drinking water for 24 to 25 weeks (U.S. Air Force 1989). No effects on fertility, gestation, or viability indices were observed; no developmental toxicity was observed; and methylchloroform failed to produce dominant lethal mutations. Testicular degeneration was observed in guinea pigs exposed to 5000 ppm 7 hours/day, 5 days/week, for 1-3 months (U.S. EPA 1984). G. Neurotoxicity The nervous system is a major target for methylchloroform toxicity. High concentrations of methylchloroform in air are lethal in humans, occurring from its anesthetic effects and from its adverse effect on the heart (cardiac arrhythmia). 1. Humans - Deaths due to central nervous system depression and cardiac arrhythmia have occurred from inhalation of methylchloroform in poorly ventilated areas (ACGIH 1991) and from recreational glue sniffing (HSDB 1994). The anesthetic effects of methylchloroform increase with the duration of exposure and concentration of the chemical (Torkelson and Rowe 1981). Loss of equilibrium occurs by 60 minutes from exposure to 1000 ppm (Torkelson and Rowe 1981). For some individuals, the onset of anesthesia occurs at 500 ppm (Torkelson and Rowe 1981), but, 350 ppm for 2 hours is the apparent lowest-observed- adverse effect level for mental alertness (ACGIH 1991). The concentration of 350 ppm is roughly equivalent to 69.25 mg/kg for the 2 hour exposure period (see end note 4). Due to the effects on cardiac function and lack of efficacy, the chemical was abandoned as a surgical anesthetic (Torkelson and Rowe 1981). Accidental ingestion of 30 mL resulted in CNS depression (U.S. Air Force 1989). 2. Animals - Rats were exposed by inhalation to 5000 or 10,000 ppm methylchloroform 7 hours/day, 5 days/week for 1 month (Torkelson and Rowe 1981; U.S. Air Force 1989). At the high dose, animals showed a staggering gait and irregular respiration within 10 minutes progressing to semiconsciousness by 3 hours; at 5000 ppm, a mild narcotic effect was apparent within 1 hour. Cardiac sensitization to epinephrine occurred in dogs exposed to 5000 or 10,000 ppm (no duration given) (ACGIH 1991). V. ENVIRONMENTAL EFFECTS LC50 and EC50 values for methylchloroform in aquatic organisms range from approximately 30 to 130 mg/L; these values exceed measured concentration in untreated ground or surface waters by several orders of magnitude. The concentrations required for acute toxicity in laboratory animals are not likely to be reached in the environment. A. Toxicity to Aquatic Organisms Methylchloroform has moderate acute toxicity to aquatic organisms; toxicity values range between greater than 1 mg/L and 100 mg/L. Ninety-six hour LC50 values for Pimephales promelas (fathead minnow) under flow through or static test conditions are 52.8 mg/L and 105 mg/L, respectively (Verschueren 1983). Other reported 96-hour toxicity values for the fathead minnow include another LC50 (42.3 mg/L; flow through) and an EC50 for loss of equilibrium of 28.8 mg/L (HSDB 1994). The 7 day LC50 for Poecilia reticulata (guppy) is 133 mg/L (Verschueren 1983). B. Toxicity to Terrestrial Organisms No information was found in the secondary sources searched regarding the toxicity of methylchloroform to terrestrial organisms. However, due to the high volatility of the chemical (vapor pressure, 100 mm Hg), it is unlikely to accumulate to toxic concentrations in soils or surface waters. Also, based on the oral LC50 values of >5 g/kg for laboratory animals and the lack of developmental toxicity at high levels, it is unlikely that the chemical will be toxic to terrestrial animals at environmental levels. C. Abiotic Effects In the atmosphere, methylchloroform has a long half-life (2.2-4.8 years) and may transport through the troposphere and into the stratosphere where it can react with and destroy ozone (U.S.EPA 1984). The depletion of ozone in the upper atmosphere has been associated with increased levels of harmful, ultraviolet radiation reaching the Earth's surface. VI. EPA/OTHER FEDERAL/OTHER GROUP ACTIVITY Voluntary reduction of methylchloroform environmental releases has occurred since 1991, as a result of a joint industry/EPA pollution prevention initiative known as the 33/50 program. The Clean Air Act Amendments of 1990 list methylchloroform as a hazardous air pollutant. EPA has classified methyl chloroform as a "Class 1 Ozone Depleting Chemical." Production of methyl chloroform is required to cease by the end of 1995 for all uses other than transformation and essential uses, to be defined by the EPA (Mannsville 1992). Occupational exposure to methyl chloroform is regulated by the Occupational Safety and Health Administration. The permissible exposure limit (PEL) is 350 parts per million parts of air (ppm) as an 8-hour time-weighted average (TWA) (29 CFR 1910.1000). Federal agencies and other groups that can provide additional information on methylchloroform are listed in Tables 4 and 5. TABLE 4. EPA OFFICES AND CONTACT NUMBERS FOR INFORMATION ON METHYLCHLOROFORM ________________________________________________________________________ EPA OFFICE LAW PHONE NUMBER ________________________________________________________________________ Pollution Prevention Toxic Substances Control Act & Toxics (Sec. 4/8A/8D/8E) (202) 554-1404 Emergency Planning and Community Right-to-Know Act (EPCRA) Regulations (Sec. 313) (800) 424-9346 Toxics Release Inventory data (202) 260-1531 Air Clean Air Act (919) 541-0888 Solid Waste & Comprehensive Environmental Emergency Response Response, Compensation, and Liability Act (Superfund)/ Resource Conservation and Recovery Act / EPCRA (Sec. 304/311/312) (800) 424-9346 Water Clean Water Act (202) 260-7588 Safe Drinking Water Act (Drinking Water Standard: 0.2 mg/L) (800) 426-4791 ________________________________________________________________________ TABLE 5. OTHER FEDERAL OFFICE/OTHER GROUP CONTACT NUMBERS FOR INFORMATION ON METHYLCHLOROFORM ________________________________________________________________________ Other Agency/Department/Other Group Contact Number _________________________________________________________________________ Agency for Toxic Substances & Disease Registry (404) 639-6000 American Conference of Governmental Industrial Hygienists (Recommended Exposure Limit (see end note 5): 350 ppm) (Recommended Short-Term Exposure Limit: 450 ppm) (513) 742-2020 Consumer Products Safety Commission (301) 504-0994 Food & Drug Administration (301) 443-3170 National Institute for Occupational Safety & Health (Recommended Exposure Limit (see end note 6): 350 ppm) (800) 356-4674 Occupational Safety & Health Administration Check local (Permissible Exposure Limit phone book for (see endnote 7): 350 ppm) phone number under Department of Labor ________________________________________________________________________ VII. END NOTES 1.Standard Industrial Classification code is the statistical classification standard for all Federal economic statistics. The code provides a convenient way to reference economic data on industries of interest to the researcher. SIC codes presented here are not intended to be an exhaustive listing; rather, the codes listed should provide an indication of where a chemical may be most likely to be found in commerce. 2.An inhalation reference concentration is an estimate (with uncertainty spanning perhaps an order of magnitude) of the exposure level for the human population, including sensitive subpopulations, that is likely to be without an appreciable risk of deleterious effects during the time period of concern. 3.These doses are equivalent to 250, 500, 1000, 2000, or 4000 mg/kg/day for rats and 650, 1300, 2600, 5200, or 10,400 mg/kg/day for mice. Calculated using standard feed consumption estimates based on the fraction of body weight that is consumed each day as food: 0.05 and 0.13 for rats and mice, respectively (U.S. EPA 1988). 4. Calculated using the factor 5.54 (Verschueren 1983) to convert 350 ppm to 1939 mg/m3 which is multiplied by 0.036 (breathing rate for 2 hours, 2.5 m3 [standard occupational 8-hour breathing rate, 10 m3] divided by the assumed adult body weight, 70 kg) and assuming 100% absorption, to obtain the dose in mg/kg (U.S. EPA 1988). 5. The ACGIH exposure limit is a time-weighted average (TWA) concentration for an 8-hour workday during a 40-hour workweek.. 6.This is a 15-minute ceiling exposure limit value that should not be exceeded at any time. 7. The OSHA exposure limits are time-weighted average (TWA) concentrations that must not be exceeded during any 8-hour work shift of a 40-hour workweek. VIII. CITED REFERENCES ACGIH. 1991. American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices, 6th ed., pp. 958-964. ATSDR. 1993. Agency for Toxic Substances and Disease Registry. Toxicological Profile for 1,1,1-Trichloroethane. U.S. Department of Health and Human Services, ATSDR, Atlanta, GA. 213 pp. Budavari S, O'Neil MJ, Smith A, Heckelman PE (Eds.). 1989. The Merck Index, 11th ed. Merck & Co., Inc., Rahway, NJ, p. 1516. CHEMFATE. 1994. Syracuse Research Corporation's Environmental Fate Data Bases. Syracuse Research Corporation, Syracuse, NY, Retrieved 8/15/94. Cimino. 1990. Review of Micronucleus Study on 1,1,1-Trichloroethane. Memorandum from M. Cimino (Toxic Effects Branch) to G. Timm (Chemical Screening Branch), Office of Toxic Substances, USEPA, Washington D.C. Nov 19, 1990. GENETOX. 1992. U.S. EPA GENETOX Program, computerized data base. Retrieved August 1994. HSDB. 1994. Hazardous Substances Data Bank. MEDLARS Online Information Retrieval System, National Library of Medicine. Retrieved July 1994. IARC Monographs. 1979. IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans: Some Halogenated Hydrocarbons, Vol. 20. IARC, Lyon, France, pp. 515-525. Keith LH, Walters DB (Eds.). 1985. Compendium of Safety Data Sheets for Research and Industrial Chemicals, Part II. VCH Publishers, Deerfield Beach, pp. 1646-1647. Mannsville. 1992. Chemical Products Synopsis, 1,1,1-Trichloroethane. Mannsville Chemical roducts Corporation. January 1992. NIOSH. 1992. National Institute for Occupational Safety and Health. NIOSH Recommendations for Occupational Safety and Health Compendium of Policy Documents and Statements. NIOSH, Cincinnati, OH. p 128. NTP. 1994. National Toxicology Program. 13-Week Subchronic Dosed Feed Toxicity Study with 1,1,1-Trichloroethane (TCE) (C04626C) Administered by Microencapsulation to F344 Rats and B6C3F1 Mice. Pathology Working Group Review, National Institute of Environmental Health Sciences, Research Triangle Park, NC. OSHA. 1993. Occupational Safety and Health Administration. Air Contaminants Rule, Table Z-1, Limits for Air Contaminants. 29 CFR Part 1910, Part V, p 35346. Torkelson TR, Rowe VK. 1981. Halogenated Aliphatic Hydrocarbons. In: Patty"s Industrial Hygiene and Toxicology, 3rd ed. Vol. 2B, GD Clayton, FE Clayton, Eds. John Wiley & Sons, New York, pp. 3502-3510. TRI92. 1994. 1992 Toxics Release Inventory. Office of Pollution Prevention and Toxics, U.S. EPA, Washington D.C. Troast. 1989. Final Action on Section 4 Developmental Toxicity Study of 1,1,1-Trichloroethane. Memorandum from R. Troast (Test Rules Development Branch) to J. Merenda (Existing Chemicals Assessment Division), Office of Toxic Substances, USEPA, Washington D.C. August 23, 1989. U.S. Air Force. 1989. 1,1,1-Trichloroethane. In: The Installation Restoration Program Toxicology Guide, Vol. 1. Wright-Patterson Air Force Base, OH, pp. 10-1 through 10-37. U.S. EPA. 1984. U.S. Environmental Protection Agency. Health Effects Assessment for 1,1,1-Trichloroethane. Office of Research and Development, U.S. EPA, Cincinnati, OH. ECAO-CIN-H005. U.S. EPA. 1988. U.S. Environmental Protection Agency. Methodology for Evaluating Potential Carcinogenicity in Support of Reportable Quantity Adjustments Pursuant to CERCLA Section 102. Carcinogen Assessment Group, Office of Health and Environmental Assessment, U.S. EPA, Washington, D.C. OHEA-C-073. U.S. EPA. 1994. U.S. Environmental Protection Agency. Integrated Risk Information System (IRIS) Online. Coversheet for Methylchloroform. Office of Health and Environmental Assessment, U.S. EPA, Cincinnati, OH. Verschueren K (Ed). 1983. Handbook of Environmental Data on Organic Chemicals, 2nd ed. Van Nostrand Reinhold Co., New York, pp. 1129-1131. APPENDIX A: SOURCES SEARCHED FOR FACT SHEET PREPARATION AQUIRE. 1994. Aquatic Information Retrieval online data base. Chemical Information Systems, Inc., a subsidiary of Fein-Marquart Assoc. ATSDR. 1989-1994. Agency for Toxic Substances and Disease Registry. Toxicological Profiles. Chamblee, GA: ATSDR. Budavari S, O"Neil MJ, Smith A, Heckelman PE (Eds.). 1989. The Merck Index, 11th ed. Rahway, N.J.: Merck & Co., Inc. CHEMFATE. 1994. Syracuse Research Corporation"s Environmental Fate Data Bases. Syracuse Research Corporation, Syracuse, NY. Clayton GD, Clayton FE, Eds. 1981-1982. Patty"s Industrial Hygiene and Toxicology, 3rd ed. New York: John Wiley & Sons. GENETOX. 1994. U.S. EPA GENETOX Program, computerized database. HSDB. 1994. Hazardous Substances Data Bank. MEDLARS Online Information Retrieval System, National Library of Medicine. IARC. 1979-1994. International Agency for Research on Cancer. IARC Monographs on the Evaluation of Carcinogenic Risk of Chemicals to Man. Lyon: IARC. NIOSH (National Institute for Occupational Safety and Health). 1992. NIOSH Recommendations for Occupational Safety and Health. Compendium of Policy Documents and Statements. Cincinnati, OH: NIOSH. NTP. 1994. National Toxicology Program. Toxicology and Carcinogenesis Studies. Tech Rep Ser. NTP. 1994. National Toxicology Program. Management Status Report. Produced from NTP Chemtrack system. April 8, 1994. National Toxicology Program, Research Triangle Park, NC. OSHA. 1994. Occupational Safety and Health Administration. Table Z-2. Limits for Air Contaminants. RTECS. 1994. Registry of Toxic Effects of Chemical Substances. MEDLARS Online Information Retrieval System, National Library of Medicine. U.S. Air Force. 1989. The Installation Restoration Toxicology Guide, Vols. 1-5. Wright-Patterson Air Force Base, OH. U.S. EPA (U.S. Environmental Protection Agency). 1991. Table 302.4 List of Hazardous Substances and Reportable Quantities 40 CFR, part 302.4:3-271. U.S. EPA. Most current. Drinking Water Regulations and Health Advisories. Office of Drinking Water, U.S. Environmental Protection Agency, Washington, D.C. U.S. EPA. Most Current. Health Effects Assessment Summary Tables. Cincinnati, OH: Environmental Criteria and Assessment Office, U.S.EPA. U.S. EPA reviews such as Health and Environmental Effects Documents, Health and Environmental Effect Profiles, and Health and Environmental Assessments. U.S. EPA. 1994. Integrated Risk Information System (IRIS) Online. Cincinnati, OH: Office of Health and Environmental Assessment.