EPA 749-F-94-004a
           CHEMICAL SUMMARY FOR ACETONITRILE (CAS NO. 75-05-8)
                               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include online databases, unpublished EPA information, government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 acetonitrile 
are summarized in Table 1.
             TABLE 1.  CHEMICAL IDENTITY AND CHEMICAL/PHYSICAL 
                           PROPERTIES OF ACETONITRILE
__________________________________________________________________________
Characteristic/Property            Data                    Reference
__________________________________________________________________________
CAS No.                  75-05-8                  
Common Synonyms          methyl cyanide, cyanomethane, 
                         ethylnitrile                  Budavari et al. 1989
Molecular Formula        C2H3N                    
Chemical Structure         H
                           |
                         H-C-CN
                           |    
                           H                   
Physical State           colorless liquid              Verschueren 1983
Molecular Weight         41.05                         Budavari et al.1989
Melting Point            -45C                         Budavari et al.1989
Boiling Point            81.6C at 760 mm Hg           Budavari et al.1989
Water Solubility         miscible                      Budavari et al.1989
Density                  d20/4, 0.79 g/mL              Verschueren 1983
Vapor Density (air = 1)  1.42                          HSDB 1994
KOC                      16                            CHEMFATE 1994
Log KOW                  -0.34                         CHEMFATE 1994
Vapor Pressure           91.1 mm Hg at 25C            CHEMFATE 1994
Reactivity               contact with strong oxidizers 
                         may result in fire            Keith & Walters 1985
Flash Point              12.8C                        Budavari et al.1989
Henry's Law Constant      3.46 x 10-5 atm m3/mol       CHEMFATE 1994
Fish Bioconcentration 
  Factor                 <1 (estimated) HSDB 1994
Odor Threshold           1143 ppm (in air)             Verschueren 1983;
                                                       HSDB 1994
Conversion Factors       1 ppm = 1.71 mg/m3
                         1 mg/m3 = 0.59 ppm            Verschueren 1983
___________________________________________________________________________
 II. PRODUCTION, USE, AND TRENDS
     A. Production
        There are four producers of acetonitrile in the United States: 
        BP Chemicals; Dupont; J.T. Baker Chemical; and Sterling Chemicals.
        In 1992, 14.7 million kilograms (32.3 million pounds) were
        produced in the United States. (U.S. International Trade
        Commission 1994).
     B. Use
        Acetonitrile has a number of uses, primarily as an extraction
        solvent for butadiene; as a chemical intermediate in pesticide
        manufacturing; and as a solvent for both inorganic and organic
        compounds.  Uses also include use as a starting material for the
        production of acetophenone, alpha-naphthalenacetic acid, thiamine,
        and acetamidine; to remove tars, phenols, and coloring matter
        from petroleum hydrocarbons not soluble in acetonitrile; in the 
        production of acrylic fibers; and in pharmaceuticals, perfumes, 
        nitrile rubber, and ABS (acrylonitrile-butadiene-styrene) resins 
        (HSDB 1994).
     C. Trends
        Because it is a byproduct of acrylonitrile production, production 
        trends for acetonitrile should follow trends in acrylonitrile
        production, which are expected to generally mirror trends in
        United States economic growth (Mannsville, "Acrylonitrile," 1992.)
III. ENVIRONMENTAL FATE
     A. Environmental Release
        Of the total acetonitrile released to the environment in 1992,
        11.3 million pounds were into the atmosphere, 20 million pounds
        were into underground sites, 50 thousand pounds were into surface 
        water, and only 29 pounds were onto the land (TRI92 1994).  
        Acetonitrile has been detected in air near ground levels, ranging 
        from 2 to 7 ppb in both urban and rural areas (HSDB 1994).  The 
        chemical occurs naturally in coal tar and cigarette smoke (HSDB 
        1994).
     B. Transport
        Acetonitrile is expected to adsorb weakly to soils as predicted
        by its KOC value; removal occurs primarily by volatilization and
        leaching into groundwater (HSDB 1994).  Volatilization from
        surface waters is slow due to the high water solubility, moderate 
        vapor pressure (91.1 mm Hg), and low Henry's law constant (3.46 x 
        10-5 atmm3/mole) of the chemical (HSDB 1994).  The water
        solubility of acetonitrile suggests that dissolution into clouds
        and raindrops may occur leading to possible removal in rainfall
        (U.S. EPA 1985).
     C. Transformation/Persistence
        1. Air - Degradation occurs by reaction with hydroxyl radicals and
           ozone.  Estimated half-lives for reaction with hydroxyl radicals
           range from 0.6 days (CHEMFATE 1994) to about 20 days (U.S. EPA 
           1985).  Reaction with ozone is slower with estimated half-lives 
           of 54 days (U.S. EPA 1985) and 76.4 days (CHEMFATE 1994).
        2. Soil - Acetonitrile is removed from soil by microbial
           degradation (U.S. EPA 1985).  Nocardia rhodochrus LL100-21 and
           Aeromonas sp. BN 7013 isolated from soils are capable of
           utilizing acetonitrile as a sole carbon and nitrogen source
           (CHEMFATE 1994; U.S. EPA 1985).  The chemical is enzymatically
           hydrolyzed by a strain of the fungus Fusarium solani (U.S. EPA
           1985).  Evaporation and leaching are also important in removing
           acetonitrile from soils (U.S. EPA 1985).
        3. Water - Acetonitrile is removed from water by biodegradation, 
           with decomposition occurring about five times faster following 
           acclimation of the microorganisms (U.S. EPA 1985; CHEMFATE
           1994).  Decomposition of the chemical in the Ohio River (0.1 to
           25 mg/L) was 20% in 5 days and 40% in 12 days (HSDB 1994).  
           Degradation occurs by Corynebacterium nitrilophilus isolated
           from activated sludge (U.S. EPA 1985; CHEMFATE 1994).  Enzymatic
           hydrolysis is accomplished by Pseudomonas sp. capable of
           utilizing acetonitrile as a sole carbon source (U.S. EPA 1985). 
           Calculated volatization half-lives from a typical pond and river
           are 11 days and 6 days, respectively (U.S. EPA 1985).  Although
           slow, loss by volatilization may become more important in
           shallow waters (HSDB 1994).
        4. Biota - Based on the high water solubility and very low
           calculated bioconcentration factor (0.3) of acetonitrile,
           bioaccumulation in aquatic organisms is not expected to be
           significant (U.S. EPA 1985; HSDB 1994).
IV. HUMAN HEALTH EFFECTS
    Acetonitrile is metabolized in the body to hydrogen cyanide and
    thiocyanate; these chemicals are thought to be responsible for the
    adverse effects of acetonitrile.
    A. Pharmacokinetics
       1. Absorption - Absorption of acetonitrile occurs after oral,
          dermal, or inhalation exposure.  Although no quantitative
          absorption data were found for oral exposure, signs of acute
          toxicity, observed after oral exposure, indicate that absorption 
          occurs (U.S. EPA 1987).  In humans, 74% of acetonitrile was 
          absorbed from cigarette smoke held in the mouth for 2 seconds; 
          when inhaled into the lungs, absorption increased to 91% (U.S. 
          EPA 1985; 1987).  Dogs exposed by inhalation to 16,000 ppm for 
          4 hours appeared to reach steady-state blood concentrations 
          within 3-4 hours (U.S. EPA 1985; 1987).
      2. Distribution - Acetonitrile and its metabolites are transported
         throughout the body in the blood (U.S. EPA 1985).  After oral or 
         inhalation exposures to experimental animals, parent compound or 
         metabolites were found in the brain, heart, liver, kidney,
         spleen, blood, stomach, and muscle (U.S. EPA 1985).  After a fatal
         human inhalation exposure, metabolites were also found in those
         organs as well as skin, lungs, intestine, testes, and urine (U.S.
         EPA 1985).
      3. Metabolism - Acetonitrile is metabolized to hydrogen cyanide
         and thiocyanate which are responsible for the toxic effects
         of the chemical (HSDB 1994; U.S. EPA 1985).  Metabolism is
         mediated by the cytochrome P-450 system (U.S. EPA 1985).
      4. Excretion - Acetonitrile is excreted as the parent chemical in 
         expired air and as parent or metabolite in urine (U.S. EPA 1985). 
         Urinary excretion of thiocyanate following oral exposure in rats 
         ranged from 11.8% (U.S. EPA 1985) to 37% (HSDB 1994) of 
         administered dose.  Concentrations of acetonitrile of 2.2-20 
         microgram/100 mL of urine have been found for heavy smokers 
         (U.S. EPA 1985).
    B. Acute Toxicity
       Acetonitrile liquid or vapor is irritating to the skin, eyes, and 
       respiratory tract.  At high enough doses, death can occur quickly 
       from respiratory failure.  Lower doses cause typical symptoms of 
       cyanide poisoning such as salivation, nausea, vomiting, anxiety, 
       confusion, hyperpnea, dyspnea, rapid pulse, unconsciousness, and 
       convulsions.  
       1. Humans - Liquid or vapor acetonitrile is irritating to eyes,
          skin, nose, and throat (Keith and Walters 1985). Concentrations 
          of acetonitrile vapor up to 500 ppm cause irritation of mucous 
          membranes (HSDB 1994).  Volunteers were exposed to 40, 80, or 
          160 ppm for 4 hours; several hours after exposure one person had 
          tightness of the chest after exposure to 40 ppm and another 
          experienced flushing of the face and bronchial tightness after 
          exposure to 160 ppm (ACGIH 1991).  The concentration of 160 ppm 
          is roughly equivalent to a total of 19.5 mg/kg over the 4 hour 
          period (see end note 1).  One photographic laboratory worker 
          died after "massive" exposure to acetonitrile vapor; gastric 
          distress and nausea began about 4 hours after exposure followed 
          by hypersalivation, conjunctivitis, low urine output, low blood 
          pressure, albumin in urine and cerebrospinal fluid, coma, and 
          death due to cardiac and respiratory failure (HSDB 1994).  
          Similar signs and symptoms, including death, occurred in a worker
          painting the interior of a tank with a resin containing 30-40% 
          acetonitrile (HSDB 1994).
       2. Animals - Oral LD50 values for acetonitrile in the rat range
          from 2.46 to 6.5 g/kg (U.S. EPA 1985).  The 4-hour inhalation 
          LC50 varies with species from 2828 ppm in the rabbit to 16,000 
          ppm in the rat; dermal LD50 values of 3.9 and 1.25 g/kg have been
          reported for the rabbit (U.S. EPA 1985).  Deaths occurred in dogs
          exposed by inhalation to 16,000 or 32,000 ppm; necropsy indicated
          pulmonary hemorrhage and vascular congestion (ACGIH 1991).
   C. Subchronic/Chronic Toxicity
      Limited information was found on the adverse effects of long term 
      human exposure to acetonitrile.  Animals exposed chronically by 
      inhalation have liver vacuolization, cerebral hemorrhage, lung 
      lesions including focal emphysema and proliferation of alveolar 
      septa, and decreases in hematological parameters.  EPA has derived an 
      oral reference dose (RfD) (see end note 2) of 0.006 mg/kg/day for 
      acetonitrile, based on adverse blood effects observed in animal 
      inhalation studies.  Confidence in this RfD is low; it may be changed 
      in the near future, pending results of further review now being 
      conducted by EPA. 
      1. Humans - No information was found on the adverse effects of
         long term human exposure to acetonitrile.  Brief references
         appear in HSDB (1994), suggesting that chronic exposure to
         acetonitrile may cause headache, anorexia, dizziness, weakness, 
         and macular, papular, or vesicular dermatitis.  No additional 
         information was provided in support of these statements.
      2. Animals - Female mice exposed to 100, 200, or 400 ppm, 6
         hours/day, 5 days/week for 90 days had thymic atrophy at the
         middle and high doses and hepatic vacuolization at the high dose;
         dose-related decreases were observed in hematocrit, blood
         hemoglobin concentration, and erythrocyte and leucocyte counts
         (U.S. EPA 1994).  A no-observed-adverse effect level (NOAEL) for
         this study was 100 ppm (equivalent to 19.3 mg/kg/day).  Based on
         these inhalation data the U.S. EPA (1994) calculated an oral
         reference dose for acetonitrile of 0.006 mg/kg/day.  Similar
         hepatic and blood profile changes were observed in mice exposed to
         200 or 400 ppm 6.5 hours/day, 5 days/week for 13 weeks (ACGIH
         1991).
         Rats exposed by inhalation to 166, 330, or 655 ppm acetonitrile 
         7 hours/day, 5 days/week for 90 days had a dose-responsive
         increase in the severity of lung lesions.  Animals in the low and
         middle dose groups had "histiocytic clumps in alveoli,
         atelectasis, bronchitis or pneumonia"; high dose animals had
         alveolar congestion and focal edema, bronchial inflammation,
         desquamation, and excess mucus as well as swelling of the liver
         and kidneys and cerebral hemorrhage (U.S. EPA 1985; 1987).  Dogs
         and monkeys exposed to 350 ppm, 7 hours/day, 5 days/week for 91
         days had pulmonary lesions including focal emphysema, atelectasis
         and proliferation of alveolar septa; transient depression in 
         hematocrit and hemoglobin values also occurred in dogs, and brain 
         hemorrhages were observed in monkeys (U.S. EPA 1985; 1987).  
         Male and female mice (groups of 10/sex) were exposed to 25, 50, 
         100, 200, or 400 ppm, 6 hours/day for 65 days. Decreased BUN, red 
         blood cell counts, and hematocrit occurred in females exposed to 
         the two highest doses, and increased liver weights were observed 
         in males at 400 ppm and females at 100 and 200 ppm (U.S. EPA
         1987).
   
   D. Carcinogenicity
      No information was found on the carcinogenicity of acetonitrile
      in the secondary sources search.
      1. Humans - No information was found in the secondary sources
         searched regarding the carcinogenicity of acetonitrile to humans.
      2. Animals - No information was found in the secondary sources
         searched regarding the carcinogenicity of acetonitrile to animals. 
         A 2-year study conducted by the National Toxicology Program is 
         currently scheduled for peer review (NTP 1994).
   E. Genotoxicity
      Acetonitrile was negative for mutations in Chinese hamster ovary
      cells and Salmonella strains TA98, TA100, TA1535, and TA1537
      when assayed with or without metabolic activation (HSDB 1994).
 
   F. Developmental/Reproductive Toxicity
      Acetonitrile causes a dose-related increase in early resorptions
      and fetal death in hamsters, rats, and rabbits.  Neural tube defects 
      also occur in hamsters after a single oral or inhalation exposure 
      during early gestation.
      1. Humans - No information was found in the secondary sources
         searched regarding the developmental or reproductive toxicity of 
         acetonitrile to humans.
      2. Animals - Hamsters (6 to 12/group) were administered a single oral 
         dose of acetonitrile of 100, 200, 300, or 400 mg/kg on day 8 of 
         gestation.  At the 2 highest doses, increases in exencephaly, 
         encephalocele, and rib malformations were observed; decreased 
         fetal body weight occurred at all doses and an increase in 
         resorptions occurred at 200 and 400 mg/kg (U.S. EPA 1987).  
         The same malformations occurred when hamsters were exposed by 
         inhalation to 5000 or 8000 ppm for 1 hour on day 8 of gestation 
         (U.S. EPA 1985).  An increase in early resorptions also occurred 
         in rats receiving 375 mg/kg/day by gavage on gestation days 6-19; 
         no adverse effects were observed at 200 mg/kg/day (U.S. EPA 1987).
         Rabbits given 2, 15, or 30 mg/kg/day acetonitrile by gavage on 
         gestation days 6-18 had an increase in fetal death at the highest
         dose (U.S. EPA 1987).  No effects in sperm motility and morphology
         or in vaginal cytology was observed in rats or mice exposed to 
         400 ppm, 6 hours/day, 5 days/week for 13 weeks (U.S. EPA 1987).
   G. Neurotoxicity
      Exposure to high concentrations of acetonitrile causes death by
      respiratory failure and has been shown to cause brain lesions in
      animals.
     
      1. Humans - The nervous system is a major target for acetonitrile 
         acute toxicity.  Acute exposure may cause salivation, nausea, 
         vomiting, anxiety, confusion, hyperpnea, dyspnea, rapid pulse, 
         unconsciousness, and convulsions followed by death from
         respiratory failure.  Chronic exposure may cause headache,
         anorexia, dizziness, and weakness (HSDB 1994).
      2. Animals - Acetonitrile inhalation caused cerebral hemorrhages in 
         rats exposed to 655 ppm 7 hours/day, 5 days/week, for 90 days and 
         monkeys exposed to 350 ppm 7 hours/day, 5 days/week, for 91 days 
         (U.S. EPA 1987).
        
V. ENVIRONMENTAL EFFECTS
   A. Toxicity to Aquatic Organisms
      Acetonitrile has low acute toxicity to aquatic organisms; toxicity 
      values are greater than 100 mg/L.  The 96-hour TLm values 
      (see end note 3) for Pimephales promelas (fathead minnow) in hard 
      and soft water are 1020 mg/L and 1000 mg/L, respectively (Verschueren
      1983).  For Lepomis macrochirus (bluegill) and Lebistes reticulatus 
      (guppy), the TLm values in soft water are 1850 mg/L and 1650 mg/L, 
      respectively (Verschueren 1983).
   B. Toxicity to Terrestrial Organisms
      No information was found in the secondary sources searched regarding 
      the toxicity of acetonitrile to terrestrial organisms.  Based on the 
      range of inhalation LC50 values, from 2828 ppm in the rabbit to 
      16,000 ppm in the rat, and the range of oral LD50 values in the rat 
      from 2.46 to 6.5 g/kg, it is unlikely that acetonitrile would be 
      lethal to terrestrial animals at levels normally found in the 
      environment.  However, developmental toxicity (see Section IV.F.2) 
      may occur in terrestrial animals if the level of a single exposure 
      were abnormally high, for example, after a spill.
  C. Abiotic Effects
     According to the definition provided in the Federal Register (1992), 
     acetonitrile is a volatile organic compound (VOC) substance.  As a 
     VOC, acetonitrile can contribute to the formation of photochemical 
     smog in the presence of other VOCs.
VI. EPA/OTHER FEDERAL/OTHER GROUP ACTIVITY
     The Clean Air Act Amendments of 1990 list acetonitrile as a hazardous 
     air pollutant.  Occupational exposure to acetonitrile is regulated 
     by the Occupational Safety and Health Administration.  The permissible
     exposure limit (PEL) is 40 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 acetonitrile are listed in Tables 3 and 4.
                  TABLE 3.  EPA OFFICES AND CONTACT NUMBERS 
                      FOR INFORMATION ON ACETONITRILE
________________________________________________________________________
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 &         Comprehensive Environmental
 Emergency Response    Response, Compensation, and
                       Liability Act (Superfund)/
                      Resource Conservation and Recovery
                       Act / EPCRA (Sec. 304/311/312)    (800) 424-9346
_________________________________________________________________________
         TABLE 4.  OTHER FEDERAL OFFICES/OTHER GROUP CONTACT NUMBERS 
                       FOR INFORMATION ON ACETONITRILE
__________________________________________________________________________
Other Agency/Department/Group                          Contact Number
__________________________________________________________________________
                                                                          
American Conference of Governmental 
   Industrial Hygenists
   (Recommended Exposure Limit 
   (see end note 4): 40 ppm)
   (Recommended 15-Minute Exposure Limit: 60 ppm)      (513) 742-2020
National Institute for Occupational Safety & Health
  (Recommended Exposure Limit 
  (see end note 4): 20 ppm)                            (800) 356-4674
Occupational Safety & Health Administration            Check local phone
  (Permissible Exposure Limit                          book for phone
  (see end note 5): 40 ppm)                            number under
                                                       Department of Labor
__________________________________________________________________________
VII. END NOTES
1. Calculated using the factor 1.706 (Verschueren 1983) to convert 160
ppm to 272.96 mg/m3 which is multiplied by 0.071 (the 4-hour breathing
rate, 5 m3 [from the occupational standard 8-hour breathing rate, 10 m3]
divided by the assumed adult body weight, 70 kg) to obtain the dose in
mg/kg (U.S. EPA 1988).
2. 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.
3. TLm is often used interchangeably with aquatic LC50 (U.S. EPA 1977).
4. The ACGIH/NOISH exposure limits are time-weighted average (TWA) 
concentrations for a normal 8-hour workday (ACGIH) or up to a 10-hour 
workday (NIOSH) during a 40-hour workweek.
5.The OSHA exposure limits are time-weighted average (TWA) concentrations 
that must not be exceeced during any 8-hour work shift of a 40-hour 
workweek.
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Index, 11th ed. Rahway, NJ: Merck & Co., Inc., p. 11.
CHEMFATE. 1994. Syracuse Research Corporation's Environmental Fate Data
Bases, retrieved 8/15/94. Syracuse Research Corporation, Syracuse, NY.
Federal Register.  1992.  Part 51 - Requirements for Preparation,
Adoption, and Submittal of Implementation Plans. Fed. Reg. 57:3945.
HSDB. 1994. Hazardous Substances Data Bank. MEDLARS Online Information
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Keith LH, Walters DB. 1985. Compendium of Safety Data Sheets for Research 
and Industrial Chemicals, Part I. Deerfield Beach: VCH Publishers, 
p. 42-43.
Mannsville.  1992.  Chemical Products Synopsis, Acrylonitrile. Mannsville 
Chemical Products Corporation.  January 1992. 
NTP. 1994. National Toxicology Program. Management Status Report
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TRI92. 1994. 1992 Toxics Release Inventory. Office of Pollution
Prevention and Toxics, U.S. EPA, Washington, D.C., p. 86.
U.S. EPA. 1977. U.S. Environmental Protection Agency. Multimedia
Environmental Goals for Environmental Assessment, Vol. 1. Office of
Research and Development, U.S. EPA, Washington, D.C., p. H-30.
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Development, U.S. EPA, Washington, D.C., 67 pp. ECAO-CIN-P137.
U.S. EPA. 1987. Health Effects Assessment for Acetonitrile. Office of
Research and Development, U.S. EPA, Washington, D.C., 28 pp. 
ECAO-CIN-H104.
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,
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U. S. EPA. 1994. U.S. Environmental Protection Agency. Integrated Risk
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U. S. International Trade Commission.  1994.  Needs full citation (EETD)
Verschueren K (Ed.). 1983. Handbook of Environmental Data on Organic
Chemicals, 2nd ed. New York: Van Nostrand Reinhold Company, pp. 151-152.
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