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include online databases, unpublished EPA information, government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              -138.8C                     CHEMFATE 1994
Boiling Point              -50.2C                      Verschueren 1983
Water Solubility           1220 mg/L @ 25C             CHEMFATE 1994
Specific gravity           1.24 @ -87C                 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 @ 25C          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 
                           @ 25C (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 @ 25C & 
                           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 = -50.2C (HSDB 1994); vapor pressure, 9412.3 mm Hg 
        @ 25C (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 @ 25C 
        (Chemfate 1994)] and estimated Henry's Law constant (4.9 x 10-2 atm 
        m3/mol @ 25C) 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.