NOTE: Although the toxicity values presented in these toxicity profiles were correct at the time they were produced, these values are subject to change. Users should always refer to the Toxicity Value Database for the current toxicity values.
Prepared by Dennis M. Opresko, Ph.D., Chemical Hazard Evaluation Group, Biomedical and Environmental Information Analysis Section, Health Sciences Research Division, *, Oak Ridge, Tennessee.
Prepared for OAK RIDGE RESERVATION ENVIRONMENTAL RESTORATION PROGRAM
*Managed by Lockheed Martin Energy Systems, Inc., for the U.S. Department of Energy under Contract No. DE-AC05-84OR21400.
Acetone (CAS No. 67-64-1) is a clear, colorless, highly flammable liquid with a vapor pressure of 182 mm Hg at 20C (Morgott, 1993). It is completely miscible in water and soluble in organics such as benzene and ethanol (ATSDR, 1994). Its log Kow has been estimated to be -0.24 (ATSDR, 1994). Acetone is used primarily as a solvent and chemical intermediate, and it is also found in some consumer products such as nail polish remover (Inoue, 1983; Kumai et al., 1983).
Acetone may be released into the environment as stack emissions and/or fugitive emissions and in waste water effluents from facilities involved in its production and use as a chemical intermediate and solvent (HSDB, 1995). Acetone is also a natural metabolic byproduct found in and released from plants and animals. Much of the acetone released into the environment will volatilize into the atmosphere where it will be subject to photo-oxidation (average half-life is 22 days). Volatilization from surface waters is moderately rapid (estimated half-life about 20 hours from a model river). If released onto the ground, acetone will both volatilize and leach into the soil and relatively little will be adsorbed to soil particles (HSDB, 1995). Acetone has been detected in groundwater and drinking water.
Acetone can be absorbed through the lungs, digestive tract, and the skin (Morgott, 1993). It is rapidly transported throughout the body and is not preferentially stored in any body tissue (Morgott, 1993). The liver is the major organ of acetone metabolism, and excretion occurs mainly through the lungs and in the urine.
Acute toxic effects following ingestion of 50 mL or more may include ataxia, sedation, and coma; respiratory depression; gastrointestinal disorders (vomiting and hematemesis); hyperglycemia and ketonemia; acidosis; and hepatic and renal lesions (Krasavage et al., 1982). Ingestion of 10-20 mL (7.9-15.8 g) generally is not toxic (HSDB, 1995), and consumption of 20 g/day for several days resulted in only slight drowsiness (Morgott, 1993). The minimum lethal dose for a 150-lb man is estimated to be 100 mL (79.1 g). No information is available on the subchronic or chronic oral toxicity to humans. In animal studies, subchronic oral exposures were associated with kidney damage and hematological changes.
The reference dose (RfD) for chronic oral exposures, 0.1 mg/kg/day (EPA, 1995), is based on increased liver and kidney weights and nephrotoxicity in rats (EPA, 1986). The subchronic oral RfD of 1 mg/kg/day (EPA, 1994) is based on the same rodent study.
Information on the inhalation toxicity of acetone to humans is derived from occupational and laboratory studies. Typical symptoms of inhalation exposure are central nervous system depression and irritation of the mucous membranes of the eyes, nose, and throat (Morgott, 1993). Central nervous system effects can range from subtle neurobehavioral changes to narcosis depending on the magnitude and length of exposure. Neurobehavioral changes have been reported at concentrations as low as 237 ppm (574 mg/m3) (Dick et al., 1989). Irritant effects have been reported at concentrations of 500 ppm (1210 mg/m3) and higher. Transient effects were reported in workers exposed to 600-2150 ppm (1452-5203 mg/m3) (EPA, 1995). Extremely high concentrations (> 29 g/m3) can cause dizziness, confusion, unsteadiness, and unconsciousness (ATSDR, 1994). Prolonged occupational exposures to acetone vapors have not been associated with chronic systemic disorders (Morgott, 1993).
Studies have shown that acetone vapor concentrations in excess of 8000 ppm (19.36 mg/m3) are generally required to produce signs of central nervous system depression in animals, but concentrations as low as 500 ppm (1210 mg/m3) may cause subtle behavioral changes (Morgott, 1993; ATSDR, 1994). Little information is available on subchronic or chronic inhalation toxicity in animals.
An inhalation reference concentration (RfC) has not been derived for acetone (EPA, 1995).
Animal data indicate that acetone is not teratogenic; however, adverse reproductive effects may occur at high concentrations. Drinking water concentrations equal to doses >3 g/kg/day during pregnancy were associated with spermatogenic effects, reduced reproductive index, and decreased pup survival of rodents (Larsen et al., 1991; EHRT, 1987). Inhalation exposure to 11,000 ppm resulted in reduction in maternal body weight gain, a decrease in uterine and extragestational weight gain, and a significant reduction in fetal weight of rats but no adverse effects on reproduction or development (Mast et al., 1988). In the latter study, the incidence of malformations was not increased by exposure to acetone.
No evidence is available that suggests acetone is carcinogenic in humans or animals (Morgott, 1993). Negative results have been reported in occupational exposure studies and in rodent skin painting studies. Although acetone has not been tested in a 2-year rodent bioassay, in vitro tests for mutagenicity, chromosome damage, and DNA interaction indicate that acetone is not genotoxic except under severe conditions (Morgott, 1993). Acetone is classified by EPA in weight-of-evidence Group D, not classifiable as to human carcinogenicity (EPA, 1995). Retrieve Toxicity Profiles Formal Version
Last Updated 8/29/97