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 These sources include online databases, unpublished EPA information, government publications, review documents, and standard reference materials.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-CðN | H Physical State colorless liquid Verschueren 1983 Molecular Weight 41.05 Budavari et al.1989 Melting Point -45øC Budavari et al.1989 Boiling Point 81.6øC 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 25øC CHEMFATE 1994 Reactivity contact with strong oxidizers may result in fire Keith & Walters 1985 Flash Point 12.8øC 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 atmùm3/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 ò54 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 ó400 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. VIII. 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