EPA 749-F-94-012a CHEMICAL SUMMARY FOR FREON 113 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 These sources include online databases, unpublished EPA information, government publications, review documents, and standard reference materials.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 freon 113 are summarized in Table 1. TABLE 1. CHEMICAL IDENTITY AND CHEMICAL/PHYSICAL PROPERTIES OF FREON 113 __________________________________________________________________________ Characteristic/Property Data Reference __________________________________________________________________________ CAS No. 76-13-1 Common Synonyms CFC-113; UCON-113; 1,1,2-trichloro- 1,2,2-trifluoroethane HSDB 1994 Molecular Formula C2Cl3F3 Chemical Structure Cl F | | F - C - C - Cl | | Cl F Physical State colorless liquid Verschueren 1983 Molecular Weight 187.38 Verschueren 1983 Melting Point -35øC Verschueren 1983 Boiling Point 48øC Verschueren 1983 Water Solubility 170 mg/L CHEMFATE 1994 Density 1.5635 at 25øC HSDB 1994 Vapor Density (air = 1) 6.5 Verschueren 1983 KOC 372 CHEMFATE 1994 Log KOW 1.66 HSDB 1994 Vapor Pressure 284 mm Hg at 20øC HSDB 1994 Reactivity Flash Point nonflammable HSDB 1994 Henry's Law Constant 5.3 x 10-1 atm m3/mol HSDB 1994 Fish Bioconcentration Factor 10 to 30 (estimated) HSDB 1994 Odor Threshold 135 ppm (in air) Verschueren 1983 Conversion Factors 1 ppm = 7.79 mg/m3 1 mg/m3 = 0.13 ppm Verschueren 1983 _______________________________________________________________________ II. PRODUCTION, USE, AND TRENDS A. Production Freon 113, also called trichlorotrifluoroethane or CFC-113, is produced in the U.S. by 2 companies. Table 2 lists producers, plant locations, and plant capacities. Annual capacity is estimated to be 300 million pounds, though production was limited to 177 million pounds in 1993 (Mannsville 1993). B. Use Freon 113 is used primarily as a chlorofluorocarbon (CFC) cleaning solvent. It also has applications as a refrigerant in commercial/industrial air conditioning and industrial process cooling; as a chemical intermediate in the manufacture of high- temperature lubricants; as a foaming or blowing agent; as an intermediate in the manufacture of fluorocarbon resins; and as a solvent or active ingredient in aerosol formulations. C. Trends A ban of the production of CFCs is scheduled to take effect at the end of 1995. One freon 113 producer DuPont has announced plans to cease production of CFCs by the end of 1994. TABLE 2. U.S. PRODUCERS OF FREON 113 _______________________________________________________________________ Company Plant Location Plant Capacity (Allowance) (in millions of pounds) _______________________________________________________________________ Allied-Signal Baton Rouge, LA 100(48) DuPont Corpus Christi, TX 200(129) _______________________________________________________________________ Source: Mannsville 1993. III. ENVIRONMENTAL FATE A. Environmental Release Greater than 99% of the 24.6 million pounds of freon 113 released in 1992, was into the atmosphere (TRI92 1994). Only 1916 pounds and 9028 pounds were released to surface and ground waters combined and to land, respectively (TRI92 1994). Due to the high volatility of the chemical, the small amount released to land or ground or surface waters would be expected to enter the atmosphere quickly. Once in the atmosphere, freon 113 diffuses from the troposphere into the stratosphere (U.S. EPA 1983; HSDB 1994). Between 1973 and 1980, freon 113 concentrations in rural and urban areas of the U.S. ranged from 28 ppt to 220 ppt, respectively (HSDB 1994). B. Transport Freon 113's water solubility and vapor pressure indicate rapid volatilization to the atmosphere from surface waters. An estimated half-life for freon 113 in a model river is 4 hours (HSDB 1994). If released to soils, the chemical would rapidly volatalize or leach to ground waters. Once in the atmosphere, freon 113 is relatively inert in the troposphere and is transported slowly to the stratosphere (HSDB 1994; U.S. EPA 1983). The half- life for diffusion out of the troposphere is 20 years (HSDB 1994). C. Transformation/Persistence 1. Air - Freon 113 is relatively inert in the troposphere; however, once in the stratosphere, the chemical is degraded by direct photolysis or reaction with excited atomic oxygen (U.S. EPA 1983). Photolytic degradation accounts for 84-89% of breakdown with a stratospheric half-life ranging from 63 to 122 years (U.S. EPA 1983). Photodissociation releases atomic chlorine which reacts with ozone to yield chlorine oxide and oxygen. This can, in theory, lead to a chain reaction resulting in continual destruction of ozone (U.S. EPA 1983). 2. Soil - If released to soil, freon 113 will rapidly volatalize to the atmosphere or leach into ground water (HSDB 1994). 3. Water - Because freon 113's water solubility and vapor pressure, the chemical will quickly enter the atmosphere (HSDB 1994). 4. Biota - Based on bioconcentration factors of 11 - 34, freon 113 is not expected to accumulate in aquatic organisms (HSDB 1994). IV. HUMAN HEALTH EFFECTS A. Pharmacokinetics 1. Absorption - Freon 113 is rapidly absorbed after inhalation or dermal exposure. Absorption after ingestion is estimated to be 35 - 48 times lower than after inhalation (HSDB 1994). Absorp- tion is biphasic with an initial rapid increase in blood levels followed by a slower increase to maximum (U.S. EPA 1983). A concentration of 12 ppm was detected within 20 minutes in the expired air of individuals exposed to freon 113 on their hands, forearms, and scalp (U.S. EPA 1983); but no account was given for possible inhalation of vapors. 2. Distribution - The main factor affecting distribution of freon 113 in an individual is body fat. Freon 113 can be concentrated in body fat before being released to the blood. The chemical is also partitioned to brain, liver, and lung (HSDB 1994). 3. Metabolism - After human volunteers were exposed to 247 ppm or 494 ppm freon 113, only 2.6 - 4.3% of the dose was recovered in expired air after termination of exposure. The report suggests some metabolism may have occurred (U.S. EPA 1983), but no data were presented. Rats exposed to 2000 ppm 6 hours/day, 5 days/ week, for 2 weeks had decreased cerebral glutathione and glutathione peroxidase levels as well as decreased hepatic cytochrome P-450. Freon 113 appeared to bind to microsomal cytochrome P-450 (U.S. EPA 1983) but no metabolites were reported. 4. Excretion - Experiments in dogs given similar chemicals by various routes of exposure indicate that chlorofluorocarbons are eliminated entirely by the respiratory tract (U.S. EPA 1983). In humans exposed dermally, the concentration of freon 113 in expired air declined from a peak of 12.7 ppm to 0.5 ppm within 90 minutes (U.S. EPA 1983). B. Acute Toxicity Adverse acute human health effects of freon 113 include irregular heartbeat and adverse effects on psychomotor performance. A no- observed-effect level (NOEL) for acute effects for freon 113 is in the range of 1500 to 2000 ppm. 4-Hour inhalation LC50 values for rats are greater than 52,000 ppm. 1. Humans - Inhalation of freon 113 for 2.75 hours resulted in no effect on psychomotor performance at 1500 ppm, slight deterioration at 2500 ppm, and increasing decrement at 4500 ppm (U.S. EPA 1983). Cardiac arrhythmias have been associated with inhalation exposure to freon 113 (HSDB 1994). Based on these data, a no-observed-adverse-effect level (NOAEL) for short-term exposure to freon 113 is in the range of 1500 to 2000 ppm (U.S. EPA 1983). Accidental ingestion of approximately 1 liter of the chemical produced immediate but transient cyanosis and severe rectal irritation and diarrhea for 3 days (U.S. EPA 1983; HSDB 1994). No adverse toxicity or dermal irritation resulted from application of freon 113 to the scalp and forehead for up to 30 days (U.S. EPA 1983). 2. Animals - The 4 hour inhalation LC50's for rats range from 52,000 to 68,000 ppm. For rats, guinea pigs, mice, and rabbits, 2 hour lethal concentrations range from 50,000 to 120,000 ppm (HSDB 1994). Anesthetized monkeys exposed to 25,000 ppm or 50,000 ppm for 5 minutes had cardiac arrhythmias including tachycardia and decreased contractility (U.S. EPA 1983). Rats exposed to 1000 or 2000 ppm freon 113 for 1 and 2 weeks had proliferation and vacuolization of the smooth endoplasmic reticulum of the liver (U.S. EPA 1983). Liver alterations were also seen in rats exposed to 5000 ppm for 30 days (HSDB 1994). No signs of toxicity were observed in rabbits or dogs exposed to 12,500 ppm for 3.5 hours/day for 20 days (U.S. EPA 1983). Dermal application to rabbits greater than 11 g/kg caused only drying of the skin at the site of application (U.S. EPA 1983). C. Subchronic/Chronic Toxicity No adverse human health effects have been reported for workers exposed to freon 113. Based on a NOEL of 697 ppm for workers, EPA has derived an oral RfD of 30 mg/kg/day for freon 113. 1. Humans - No effects have been reported for workers occupationally exposed to 65 ppm for 11 years or 697 ppm for 2.77 years. Therefore, a NOAEL for chronic freon 113 exposure is listed as 697 ppm with the oral RfD (reference dose), calculated from the inhalation study, of 30 mg/kg/day (see end note 1) (U.S. EPA 1994). Epidemiological studies of men and women with greater than 1 year of occupational exposure to freon 113 showed no alterations in blood chemistry or urinalysis; one case of dermatitis was observed in males (U.S. EPA 1983). 2. Animals - Gross and microscopic pathology evaluations of rats exposed to freon 113 for 90 days or 1 year show no evidence of toxicity up to 20,000 ppm (U.S. EPA 1983). D. Carcinogenicity No information was found on the carcinogenicity of freon 113. One study has reported no carcinogenicty in rats exposed by inhalation to concentrations up to 20,000 ppm for two years. 1. Humans - No information was found in the secondary sources searched concerning the carcinogenicity of direct exposure to freon 113. However, in the stratosphere, freon 113 photo- catalytically destroys ozone allowing more ultraviolet radiation to reach the earth's surface. Theoretically this effect could result in an increase in the incidence of non- malignant skin cancers, although to date, there is no empirical data to support this hypothesis (U.S. EPA 1983). 2. Animals - No cancers were seen in rats exposed to 2000, 10,000, or 20,000 ppm freon 113 for 2 years (U.S. EPA 1983). E. Genotoxicity Freon 113 was negative for gene reversion in 4 strains of Salmonella typhimurium (U.S. EPA 1983). F. Developmental/Reproductive Toxicity No information was found concerning the developmental or reproductive toxicity of freon 113 to humans. No developmental/ reproductive effects have been reported in laboratory animal studies of freon 113. 1. Humans - No information was found in the secondary sources searched concerning the developmental or reproductive toxicity of freon 113 to humans. 2. Animals - Rats were exposed to 5000, 12,500, or 25,000 ppm freon 113 for 6 hours/day on days 6-15 of gestation. Maternal toxicity as indicated by decreased weight gain and feed consumption occurred at the highest dose, but no evidence of developmental toxicity was seen in pups from any exposure group (U.S. EPA 1983). No teratogenicity was seen in offspring of rabbits exposed either orally (up to 5 g/kg) or by inhalation (up to 20,000 ppm); EPA has concluded that niether of these studies was adequate for use in assessing the developmental toxicity of freon 113 (U.S. EPA 1983). G. Neurotoxicity Available evidence from human and laboratory animal studies indicates that freon 113 adversely affects the psychomotor performance at high inhalation doses. The threshold concentration of freon 113 for impairment of psychomotor performance (loss of concentration ability, mild lethargy) is about 2500 ppm. 1. Humans - The threshold concentration of freon 113 for impairment of psychomotor performance (loss of concentration ability, mild lethargy) is about 2500 ppm. Humans limited to exposures for 2.75 hours showed no impairment of psychomotor performance at 1500 ppm, slight impairment at 2500 ppm, and increased decrement at 4500 ppm (HSDB 1994). One case of sensorimotor neuropathy was reported in a woman who worked in a laundry for several years; recovery occurred after removal from exposure (HSDB 1994). 2. Animals - Guinea pigs exposed to 50,000 ppm freon 113 have loss of coordination after 30 minutes and die within 1 hour (HSDB 1994). V. ENVIRONMENTAL EFFECTS A. Toxicity to Aquatic Organisms No information was found concerning the toxicity of freon 113 to aquatic organisms. Due to its water solubility (170 mg/L), its high vapor pressure (284 mm Hg), and its estimated low bioconcen- tration factors (10-30), freon 113 is not likely to accumulate in aquatic organisms to toxic levels (HSDB 1994). Aquatic organisms, such as phytoplankton, zooplankton, and the larval stages of many insects and fishes, that inhabit the surface of the water column may be susceptible to increased ultraviolet radiation (TRI92 1994) due to ozone depletion as a result of freon 113 degradation and release of chlorine atoms in the upper atmosphere (see Section V.C). B. Toxicity to Terrestrial Organisms No information was found in the secondary sources searched for toxicity of freon 113 to terrestrial organisms. Due to its volatility, freon 113 is not expected to accumulate to toxic concentrations in soils or surface waters. The range of inhalation LC50 values (52,000 - 68,000 ppm) in laboratory animals is orders of magnitude higher than any measured atmospheric concentration in the US (220 ppt in urban areas) (HSDB 1994). C. Abiotic Effects Freon 113 moves slowly through the lower atmosphere into the stratosphere. Photodegradation of freon 113 in the upper atmosphere releases chlorine atoms which react with ozone. Stratospheric depletion of ozone increases the amount of ultraviolet-B radiation that reaches the earth's surface (U.S. EPA 1983). Increased, surface UV radiation can adversely affect human health and the environment. VI. EPA/OTHER FEDERAL/OTHER GROUP ACTIVITY The EPA is interested in Freon 113 because of its ozone depleting properties. A ban on the production of chlorofluorocarbons (CFCs) is scheduled to take effect at the end of 1995 (Mannsville 1993). Occupational exposure to Freon 113 is regulated by the Occupational Safety and Health Administration. The permissible exposure limit (PEL) is 1,000 parts per million parts of air (ppm) (29 CFR 1910.1000). Federal agency and other group activities for freon 113 are summarized in Tables 3 and 4. TABLE 3. EPA OFFICES AND CONTACT NUMBERS FOR INFORMATION ON FREON 113 ________________________________________________________________________ EPA OFFICE LAW PHONE NUMBER ________________________________________________________________________ Pollution Prevention Toxic Substances Control Act & Toxics (Sec. 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 & Resource Conservation and Recovery Emergency Response Act / EPCRA (Sec. 311/312) (800) 424-9346 ________________________________________________________________________ TABLE 4. OTHER FEDERAL OFFICE/OTHER GROUP CONTACT NUMBERS FOR INFORMATION ON FREON 113 _________________________________________________________________________ Other Agency/Department/Group Contact Number _________________________________________________________________________ Agency for Toxic Substances & Disease Registry (404) 639-6000 American Conference of Governmental Industrial Hygienists (513) 742-2020 (Recommended Exposure Limit (see end note 2): 1000 ppm) (Recommended Short Term Limit (see end note 3): 1250 ppm) Consumer Product Safety Commission (301) 817-0994 National Institute for Occupational Safety & Health (Recommended Exposure Limit (see end note 2): 1000 ppm) (800) 356-4674 Occupational Safety & Health Administration (Permissible Exposure Limit (see end note 4): 1000 ppm) (Check local phone book for phone number under Department of Labor) _________________________________________________________________________ VII. END NOTES 1. The RfD is an estimate (with uncertainty spanning perhaps an order of magnitude) of the daily 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. 2. The ACGIH/NIOSH exposure limits are time-weighted average (TWA) concentrations for an 8-hour workday (ACGIH) and up to a 10-hour workday (NIOSH) for a 40-hour workweek. 3. This is a recommended 15-minute exposure limit that should not be exceeded any time during an 8-hour workday. 4. The OSHA exposure limit is a time-weighted average (TWA)concentration that must not be exceeded during any 8-hour workshift of a 40-hour workweek. VIII. CITED REFERENCES CHEMFATE. 1994. Syracuse Research Corporation's Environmental Fate Data Bases, retrieved 7/25/94. Syracuse Research Corporation, Syracuse, NY. HSDB. 1994. Hazardous Substances Data Bank. MEDLARS Online Information Retrieval System, National Library of Medicine. Retrieved May 1994. Mannsville. 1993. Chemical Products Synopsis, Fluorocarbon Solvents. Mannsville Chemical Products Corporation. January, 1993. TRI92. 1994. 1992 Toxics Release Inventory. Office of Pollution Prevention and Toxics, U.S. EPA, Washington, D.C., p.90. U.S. EPA. 1983. U.S. Environmental Protection Agency. Health Assessment Document for 1,1,2-Trichloro-1,2,2-Trifluoroethane (Chlorofluorocarbon CFC-113). Office of Research and Development, U.S. EPA, Washington, D.C., 71 pp. EPA-000/8-82-002F. U.S. EPA. 1994. Integrated Risk Information System (IRIS) Online. Cincinnati, OH: Office of Health and Environment Assessment. Verschueren K, Ed. 1983. Handbook of Environmental Data on Organic Chemicals, 2nd ed. Van Nostrand Reinhold Company, New York, p.1147. 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. Clayton GD, Clayton FE. 1981-1982. Patty's Industrial Hygiene and Toxicology, 3rd ed., Vol. 2C. 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 Enviornmental 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.