The Risk Assessment Information System

Toxicity Profiles

Condensed Toxicity Summary for 1,1,1-TRICHLOROETHANE

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.

September 1995 Prepared by M. W. Daugherty, M.S., and Carol S. Forsyth, Ph.D., Biomedical and Environmental Information Analysis Section, Health Sciences Research Division, *, Oak Ridge, Tennessee.


*Managed by Martin Marietta Energy Systems, Inc., for the U.S. Department of Energy under Contract No. DE-AC05-84OR21400

1,1,1-Trichloroethane is absorbed via the inhalation, oral, and dermal exposure routes (ATSDR 1995). After cessation of exposure, clearance of the chemical from the blood is rapid; 60 to 80% is eliminated within 2 hours, and greater than 95% is eliminated within 50 hours (Monster et al. 1979, Nolan et al. 1984). A large fraction of the absorbed dose is excreted unchanged in exhaled air, regardless of route of exposure (Torkelson 1994).

The distribution of absorbed 1,1,1-trichloroethane is similar for all routes of exposure. The chemical has been detected in the fat, liver, lung, and muscle of humans and in the fat, liver, kidney, brain, muscle, and skin of animals (Alles et al. 1988, Holmberg et al. 1977, Savolainen et al., 1977, Schumann et al. 1982, Takahara 1986). Humans and animals metabolize less than 10% of a dose of 1,1,1-trichloroethane regardless of the route of exposure; the major urinary metabolites are trichloroethanol and its glucuronide conjugate, trichloroacetic acid, and volatile carbon dioxide (ATSDR 1995, Nolan et al. 1984). These urinary metabolites are excreted slowly in comparison to the rate of expiration of 1,1,1-trichloroethane in the breath (elimination half-times, 10 to 27 and 70 to 85 hours, respectively), and may accumulate with repeated exposure, such as in the workplace (Nolan et al. 1984).

Few data were found for the oral toxicity of 1,1,1-trichloroethane. One case study reported gastrointestinal and hepatic effects in an individual who accidentally ingested approximately 600 mg/kg of the chemical (Stewart and Andrews 1966). In animals, oral LD50 values range from 5660 mg/kg (rabbits) to 12,300 mg/kg (rats) (Torkelson et al. 1958). Death in most cases has been attributed to central nervous system depression resulting from anesthesia. Chronic oral doses of $1500 mg/kg reduced body weight gain and increased the effects of aging in rats and reduced body weight gain and decreased survival in mice (NCI 1977). No other effects were noted in either species.

In both humans and animals, the first and primary response to acute, high concentrations of inhaled 1,1,1-trichloroethane is central nervous system depression. The chemical also can sensitize the heart to epinephrine at high levels but has little effect on other organs. Accidental exposures to concentrations ranging from 6000 to 20,000 ppm have been fatal to humans (ATSDR 1995, Torkelson 1994).

The effects of subchronic and chronic inhalation exposure to 1,1,1-trichloroethane are generally mild, characterized by growth reduction in guinea pigs (650 ppm) (Adams et al. 1950) and minimal hepatic effects in mice (247 ppm, continuous exposure) and rats (1500 ppm, intermittent exposure) (McNutt et al. 1975, Quast et al. 1988). At 1000 ppm for 7 hours/day, 5 days/week for 6 months, female guinea pigs had fatty liver changes and increased liver weights; the no observed adverse effects level was 500 ppm (Torkelson et al. 1958). Fatty liver in humans has been associated with exposure to 1,1,1-trichloroethane (Hodgson et al. 1989).

One epidemiology study and several animal studies did not establish a relationship between exposure to 1,1,1-trichloroethane and adverse developmental or reproductive effects (Wrensch et al. 1990, Riddle et al. 1981, Verschuuren and de Rooij 1990).

The subchronic and chronic oral RfD values for 1,1,1-trichloroethane were withdrawn from the Integrated Risk Information System database on August 1, 1991 (EPA 1995a) and from Health Effects Assessment Summary Tables (EPA 1995b). A provisional chronic inhalation reference concentration value of 1 mg/m3 has been recommended (EPA 1995c) based on fatty liver changes in guinea pigs.

Regarding the carcinogenicity of 1,1,1-trichloroethane, oral bioassays were inconclusive and inhalation studies were negative (NCI 1977, Maltoni et al. 1986, Rampy et al. 1977, Quast et al. 1988). No epidemiological data for 1,1,1-trichloroethane and inadequate carcinogenicity data for animals place the chemical in the United States Environmental Protection Agency's weight-of-evidence group D, not classifiable as to human carcinogenicity (EPA 1995a).

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Last Updated 02/13/98

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