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 Rosmarie A. Faust, Ph.D, Chemical Hazard Evaluation Group in the Biomedical and Environmental Information Analysis Section, Health Sciences Research Division, Oak Ridge National Laboratory*.
Prepared for: Oak Ridge Reservation Environmental Restoration Program.
*Managed by Martin Marietta Energy Systems, Inc., for the U.S. Department of Energy under Contract No. DE-AC05-84OR21400.
1,1,2-Trichloroethane (CAS Reg. No. 79-00-5), also known as vinyl trichloride, is a nonflammable liquid that is used in the manufacture of 1,1-dichloroethene; as a solvent for fats, waxes, resins, and alkaloids; and in organic synthesis (Budavari et al. 1989, EPA 1980).
1,1,2-Trichloroethane is released to the environment as a result of anthropogenic activity. The chemical has been identified in the United States at 45 of 1177 hazardous waste sites on the National Priorities List. Based on release patterns of related chemicals, it is estimated that 70-90% of the total release is to air, 10-30% to land, and a few percent to water. Removal of 1,1,2-trichloroethane from the atmosphere is thought to occur by reaction with photochemically produced hydroxyl radicals (estimated half-life 49 days) and from washout by precipitation; however, most of the 1,1,2-trichloroethane removed by washout is expected to reenter the atmosphere by volatilization. If released to soil, 1,1,2-trichloroethane is expected to partially leach into groundwater and to partially volatilize. In surface water, volatilization is the primary removal process (ATSDR 1989).
1,1,2-Trichloroethane is rapidly absorbed, widely distributed in organs and tissues, and extensively metabolized. Major metabolites include chloroacetic acid, S-carboxymethylcysteine, and thiodiacetic acid. 1,1,2-Trichloroethane and/or its metabolites are primarily excreted through the lungs and urine (Morgan et al. 1970, 1972; Kronevi et al. 1977; Mitoma et al. 1985).
Very limited human data were available to evaluate the toxicity of 1,1,2-trichloroethane. The chemical exerts a narcotic action at "low" concentrations and is irritating to the eyes and mucous membranes of the respiratory tract. When in contact with skin, 1,1,2-trichloroethane may cause cracking and erythema (IARC 1979).
The oral LD50 for mice (378-491 mg/kg) (White et al. 1985) indicates that in animals the acute oral toxicity of 1,1,2-trichloroethane is moderate. 1,1,2-Trichloroethane is a central nervous system depressant, inducing sedation in mice at oral doses of 378 mg/kg (White et al. 1985) and drowsiness, incoordination, and narcosis in dogs at 289 mg/kg (Wright and Schaffer 1932). Male and female CD-1 mice ingesting 384 mg/kg in drinking water for 90 days exhibited alterations in serum enzyme and hepatic microsomal enzyme activities, indicating adverse liver effects. In addition, depressed immune function in both sexes and decreased hemoglobin and hematocrit values in females were noted (Sanders et al. 1985, White et al. 1985). Decreased survival was reported in female B6C3F1 mice exposed to 195 or 390 mg/kg/day for 78 weeks (NCI 1978).
Bonnet et al. (1980) reported an inhalation LC50 of 1654 ppm for rats exposed to 1,1,2-trichloroethane for 6 hours, while another study found that a single 7-hour exposure to 250 or 500 ppm resulted in the death of more than half of the exposed female rats, with surviving animals exhibiting marked liver and kidney damage (Torkelson 1994). As noted previously, 1,1,2-trichloroethane is a central nervous system depressant inducing narcosis; death results from respiratory arrest (ACGIH 1991). In mice, a concentration of 3750 ppm for 30 minutes produced central nervous system depression and significantly increased liver enzyme activity within 18 minutes and death in half the animals within 10 hours (Gehring 1968). No adverse effects were observed in rats, guinea pigs, and rabbits exposed to 15 ppm for 7 hours/day, 5 days/week for 6 months, but female rats exposed to 30 ppm (16 exposures; 7 hours/day, 5 days/week) exhibited minor hepatic effects (Torkelson 1994). Repeated topical applications of 0.1 mL 1,1,2-trichloroethane produced erythema, edema, fissuring, and scaling of rabbit and guinea pig skin (Wahlberg 1984b).
An oral reference dose of 0.04 mg/kg/day for subchronic exposure (EPA 1995b) and 0.004 mg/kg/day for chronic exposure (EPA 1995a) to 1,1,2-trichloroethane was calculated based on a no observed adverse effects level (NOAEL) of 3.9 mg/kg/day and a lowest observed adverse effects level (LOAEL) of 44 mg/kg/day from a 90-day drinking water study with mice (White et al. 1985, Sanders et al. 1985). Clinical chemistry alterations indicative of liver damage were identified as critical effects. An inhalation reference concentration for 1,1,2-trichloroethane is under review by EPA (EPA 1995a).
No epidemiologic studies or case reports addressing the carcinogenicity of 1,1,2-trichloroethane in humans were available. In a rodent bioassay, 1,1,2-trichloroethane was administered by gavage to Osborne-Mendel rats (46 or 92 mg/kg/day) and B6C3F1 mice (195 or 390 mg/kg/day), 5 days/week for 78 weeks (NCI 1978). No effects on tumor development were noted in rats. Treated mice had significantly (p<0.01) increased incidences of hepatocellular carcinomas. The tumor incidences in treated males were 37% and 76% in the low- and high-dose groups, respectively, compared with 10% in vehicle controls, and 33% and 89% in females, respectively, compared to no observed tumors in vehicle controls. An increased incidence of adrenal pheochromocytomas was also observed in male and female mice. In a cancer initiation/promotion study with rats, 1,1,2-trichloroethane did not exhibit tumor initiating or promoting activity (Story et al. 1986).
Based on United States Environmental Protection Agency (EPA) guidelines, 1,1,2-trichloroethane was assigned to weight-of-evidence group C, possible human carcinogen. For oral exposure, the slope factor is 5.7E-2 (mg/kg/day)-1 and the unit risk for drinking water is 1.6E-6 (µg/L)-1 (EPA 1995a). The inhalation slope factor and unit risk are 5.7E-2 (mg/kg/day)-1 (EPA 1995b) and 1.6E-5 (µg/m3)-1, respectively (EPA 1995a).Retrieve Toxicity Profiles Formal Version
Last Updated 2/13/98