EPA 749-F-94-009a CHEMICAL SUMMARY FOR CARBONYL SULFIDE 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 These sources include online databases, unpublished EPA information, government publications, review documents, and standard reference materials.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 from these databases or secondary sources. I. CHEMICAL IDENTITY AND PHYSICAL/CHEMICAL PROPERTIES The chemical identity and physical/chemical properties of carbonyl sulfide are summarized in Table 1. TABLE 1. CHEMICAL IDENTITY AND CHEMICAL/PHYSICAL PROPERTIES OF CARBONYL SULFIDE ________________________________________________________________________ Characteristic/Property Data Reference ________________________________________________________________________ CAS No. 463-58-1 Common Synonyms carbonoxysulfide Verschueren 1983 Molecular Formula COS Chemical Structure 0=C=S Physical State gas U.S. EPA 1990 Molecular Weight 60.07 Verschueren 1983 Melting Point -138.8øC CHEMFATE 1994 Boiling Point -50.2øC Verschueren 1983 Water Solubility 1220 mg/L @ 25øC CHEMFATE 1994 Specific gravity 1.24 @ -87øC Verschueren 1983 Vapor Density (air = 1) 2.1 Verschueren 1983 KOC 88 CHEMFATE 1994 Log KOW 0.80 CHEMFATE 1994 Vapor Pressure 9412.3 mm Hg @ 25øC CHEMFATE 1994 Reactivity Flammable; may be ignited by heat, sparks or flames. Container may explode in the heat of a fire. Forms explosive mixtures with air. When exposed to humidity or alkalies, decomposes to carbon monoxide and hydrogen sulfide. HSDB 1994 Flash Point No data Henry's Law Constant 4.92 X 10-2 atm-m3/mol @ 25øC (calculated) HSDB 1994 Fish Bioconcentration Factor 2-11 (estimated) HSDB 1994 Odor Threshold No information Conversion Factors 1 ppm = 2.45 mg/m3 1 mg/m3 = 0.41 ppm Calculated: 1 mg/m3=ppm x MW/24.5 @ 25øC & 760 mm Hg ___________________________________________________________________________ II. PRODUCTION, USE, AND TRENDS A. Production Carbonyl sulfide is normally produced as a by-product of the production of carbon disulfide. In 1977, production of carbonyl sulfide was estimated to be one million pounds. Based on information submitted to EPA under Toxic Release Inventory reporting (see section III.A), recent production may be signif- icantly higher than this. In 1992, over 16 million pounds of carbonyl sulfide were reported to have been released to air. B. Use Carbonyl sulfide is used as a non-isolated, site limited intermediate in the production of thiocarbamate herbicides. No other commercial uses of the substance are known. However, carbonyl sulfide appears as an impurity in some refinery and fuel gases, and in the combustion products of sulfur-containing fuels. III. ENVIRONMENTAL FATE A. Environmental Release Of the total carbonyl sulfide released to the environment almost all (16.2 million pounds) is released to air. Carbonyl sulfide is a gas [bp = -50.2øC (HSDB 1994); vapor pressure, 9412.3 mm Hg @ 25øC (Verschueren 1983)], and is released into the environment from industrial uses and natural sources. The largest man-made sources of carbonyl sulfide release include its primary use as a chemical intermediate; however, it is also released from automobiles, coal-fired power plants, biomass combustion, fish processing, combustion of refuse and plastics, petroleum manufacture, and manufacture of synthetic fibers, starch and rubber (HSDB 1994). Carbonyl sulfide is also released to the environment from deciduous and coniferous trees, volcanoes, salt marshes, and soil (HSDB 1994). The average total worldwide release of carbonyl sulfide to the atmosphere has been estimated at about 3 million tons/year of which less than one third was related to human activity (HSDB 1994). In 1992, releases of carbonyl sulfide to environmental media, as reported to the Toxic Chemical Release Inventory by certain types of U.S. industries, totaled about 16 million pounds. The total amount was released to the atmosphere (TRI92 1994). Levels of carbonyl sulfide in the atmosphere have been measured in rural and urban sites and near sites that are natural sources. In the United States, the reported concentration of carbonyl sulfide in the air in rural areas was 0.27-0.80 microgram/m3. Levels were 1.17 micrograms/m3 in Philadelphia, PA; 1.21 micrograms/m3 in Wallops Island, VA; and 1.37 micrograms/m3 in Lawton, OK. Reported concentrations of carbonyl sulfide over salt marshes, which are major natural sources, range from about 60 to 180 micrograms/m3, and 14 to 19 micrograms/m3 over the ocean (HSDB 1994). B. Transport Carbonyl sulfide is not expected to be retarded by adsorption to soils rich in organic material [Koc = 88 (Chemfate 1994)]; therefore, transport to ground water is not dependent on the soil composition. The high vapor pressure [9412.3 mm Hg @ 25øC (Chemfate 1994)] and estimated Henry's Law constant (4.9 x 10-2 atm m3/mol @ 25øC) indicate that it will rapidly volatilize from moist and dry soil (HSDB 1994). It is also expected to volatilize rapidly to the atmosphere when released to water (HSDB 1994). C. Transformation/Persistence 1. Air - The main degradation pathways for carbonyl sulfide in the atmosphere are reaction with singlet oxygen and photochemically produced hydroxyl radicals. Direct photolysis is not expected to occur in the troposphere but may occur in the stratosphere. Direct removal of carbonyl sulfide from the atmosphere by plants and soil microorganisms has been reported. The atmospheric half-life for carbonyl sulfide has been estimated at about 2 years (HSDB 1994). 2. Soil - In wet or dry soil, volatilization to air is the most important fate process for carbonyl sulfide (HSDB 1994). It is also highly mobile and may be leached from the soil by water (HSDB 1994). 3. Water - The most important fate process for carbonyl sulfide in water is volatilization (HSDB 1994). A half-life of 2.3 hours has been measured for the volatilization of carbonyl sulfide using a model river system. It is also hydrolyzed in water to hydrogen sulfide and carbon dioxide. It is not expected to be bound to sediment or suspended organic matter (HSDB 1994). 4. Biota - Carbonyl sulfide is not expected to bioconcentrate in fish or aquatic organisms (estimated range of bioconcentration factor between 2 and 11) (HSDB 1994). IV. HUMAN HEALTH EFFECTS Only limited information is available on the pharmacokinetics of carbonyl sulfide. It is likely that carbonyl sulfide is metabolized to hydrogen sulfide and carbon dioxide. Hydrogen sulfide is thought to be responsible for many of the reported adverse effects associated with exposure to carbonyl sulfide. A. Pharmacokinetics 1. Absorption - Limited studies in humans and in laboratory animals have demonstrated that carbonyl sulfide is primarily absorbed via the lungs; however, it can also be absorbed through the gastrointestinal system and through the skin (HSDB 1994). 2. Distribution - Carbonyl sulfide is known to be absorbed into the blood, but no information on its general distribution was found in the sources searched. Epidemiological studies have shown carbonyl sulfide to be present in the milk from nursing mothers located in urban centers in Pennsylvania, New Jersey, and Louisiana (HSDB 1994). 3. Metabolism - Carbonyl sulfide is metabolized to hydrogen sulfide and carbon dioxide apparently by carbonic anhydrase. The hydrogen sulfide is thought to be primarily responsible for the toxic effects (HSDB 1994). 4. Excretion - No information on excretion of carbonyl sulfide was found in the secondary sources searched. B. Acute Toxicity There is limited information on the acute toxicity of carbonyl sulfide in humans and in animals. Available information indicates that inhalation exposure to high (unspecified) concentrations of carbonyl sulfide can be fatal, presumably due to respiratory paralysis. 1. Humans - One of two workers died as a result of an accidental exposure to unknown concentrations of carbonyl sulfide; the authors reported sudden unconsciousness and fatal central respiratory paralysis practically without local irritation or olfactory warning (ITC 1983). The symptoms of poisoning are the same as those seen with hydrogen sulfide, but initial irritation to skin, eyes, and respiratory tract is less, resulting in less warning. Sublethal inhalation exposure can result in profuse salivation, nausea, vomiting, diarrhea, cardiac arrhythmia, albuminuria, weakness, and muscle cramps (HSDB 1994). 2. Animals - Results of acute inhalation exposures of carbonyl sulfide in rats and guinea pigs have been reported (ITC 1983). No deaths were reported when 6 rats were exposed to a concen- tration of 1000 ppm for 75 minutes. Three of 6 rats died at 1400 ppm for 90 minutes; and 3 of 6 rats died at 3000 ppm for 9 minutes. No deaths were reported when 4 guinea pigs were exposed to 1000 ppm for 90 minutes. C. Subchronic/Chronic Effects No information was found on the human health effects associated with long term exposure to carbonyl sulfide. Limited information from laboratory animal studies indicate that inhalation exposure to approximately 50 ppm carbonyl sulfide for up to 12 weeks does not adversely affect the lungs or the heart. 1. Humans - No information was found on the subchronic or chronic effects of carbonyl sulfide in the secondary sources searched. 2. Animals - Inhalation exposure of rabbits to 50 ppm carbonyl sulfide continuously for up to 12 weeks resulted in no histo- logical changes in the coronary arteries or the aorta (HSDB 1994). Continuous inhalation exposure of rabbits to 50 ppm carbonyl sulfide in another experiment was reported to result in increased serum cholesterol after 7 weeks; however, this was mainly due to observed decreases in control animals (ITC 1983). No histopathological changes in the lungs or coronary arteries were seen. D. Carcinogenicity No information was found on the carcinogenicity of carbonyl sulfide. 1. Humans - No information was found on the carcinogenicity of carbonyl sulfide in the secondary sources searched. 2. Animals - No information was found on the carcinogenicity of carbonyl sulfide in the secondary sources searched. E. Genotoxicity No information was found on the genotoxicity of carbonyl sulfide in the EPA GENETOX Program or in the other secondary sources searched. F. Developmental/Reproductive Toxicity No information was found on the developmental/reproductive effects of carbonyl sulfide. 1. Humans - No information was found on the developmental/repro- ductive toxicity of carbonyl sulfide in the secondary sources searched. 2. Animals - No information on the developmental/reproductive toxicity of carbonyl sulfide in the secondary sources searched. G. Neurotoxicity There is little information available on the neurotoxicity of carbonyl sulfide in humans and in animals. 1. Humans - High concentrations (>1000 ppm) can cause sudden collapse, convulsions, and death from respiratory paralysis (HSDB 1994). Non-lethal, inhalation exposure to carbonyl sulfide inhalationcauses giddiness, headache, vertigo, amnesia, confusion, and unconsciousness. 2. Animals - No information was found on the neurotoxicity of carbonyl sulfide in the secondary sources searched. V. ENVIRONMENTAL EFFECTS A. Toxicity to Aquatic Organisms No information on the toxicity of carbonyl sulfide to aquatic organisms was found in the secondary sources searched. Quantitative structure activity relationship (QSAR) estimates of acute toxicity for fish, daphnid, and algae are each greater than 1000 mg/L (Newsome 1994). Salt marshes, which are known for their high biological productivity, are a major natural source of the chemical (see section III.A.) resulting in atmospheric levels higher than those in urban areas. This suggests that adverse effects in aquatic organisms resulting from environmental levels of carbonyl sulfide are minimal. B. Toxicity to Terrestrial Organisms No information on the toxicity to terrestrial organisms of carbonyl sulfide was found in the secondary sources searched. However, the toxicity data reported for rats and rabbits (see sections IV.B.2. and IV.C.2.) suggest that no adverse effects would be likely to occur at normally low environmental concentrations. C. Abiotic Effects No information on the abiotic effects of carbonyl sulfide was found in the secondary sources searched. VI. EPA/OTHER FEDERAL ACTIVITY The Clean Air Act Amendments of 1990 list carbonyl sulfide as a hazardous air pollutant. Environmental Protection Agency offices that can provide additional information on carbonyl sulfide are listed in Table 2. No informa- tion has been found in the secondary sources searched to indicate that other federal agencies or departments or other groups regulate carbonyl sulfide. TABLE 2. EPA OFFICES AND CONTACT NUMBERS FOR INFORMATION ON CARBONYL SULFIDE ________________________________________________________________________ EPA OFFICE LAW PHONE NUMBER ________________________________________________________________________ Pollution Prevention Toxic Substances Control Act & Toxics (Sec. 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)/ EPCRA (Sec. 304/311/312) (800) 424-9346 VII. CITED REFERENCES CHEMFATE. 1994. Syracuse Research Corporation's Environmental Fate Data Bases. Syracuse Research Corporation, Syracuse, NY. Retrieved 8/15/94. HSDB. 1994. Hazardous Substances Data Bank. MEDLARS Online Information Retrieval system, National Library of Medicine. ITC. 1983. Information Review. Carbon oxide Sulfide. No. IR-364. Prepared for the Interagency Testing Committee by Dynamac Corporation, Rockville, MD. Newsome. 1994. Comments on the pilot OPPTS factsheets on ... carbonyl sulfide. Memorandum from Larry Newsome, Health and Environmental Review Division to Richard Wormell, Chemical Screening and Risk Assessment Division, Office of Pollution Prevention and Toxics, U.S. EPA, Washington, DC. September 14, 1994. TRI92. 1994. 1992 Toxics Release Inventory, Public Data Release. U.S. EPA, Office of Pollution Prevention and Toxics, Washington, D.C. Verschueren, K. 1983. Carbonyl sulfide. in: Handbook of Environmental Data on Organic Chemicals, Second Edition. Van Nostrand Reinhold Co., New York. pp: 1103-1108. APPENDIX A. SOURCES SEARCHED FOR FACT SHEET PREPARATION AQUIRE. 1994. IPA ERL-Duluth's Aquatic Ecotoxicology Data Systems. U.S. EPA, Duluth, MN. 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. 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 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.