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3 times greater in mice; mice experienced a higher body burden than rats, but were able to metabolize the same percentage of it. The inherent ability of mice to metabolize 1,1,2-trichloroethane at a higher rate than rats may contribute to the greater susceptibility of mice to 1,1,2-trichloroethance cytotoxicity and carcinogenity. It is not known how the rate of 1,1,2-trichloroethane metabolism in humans compares to that in mice and rats. Metabolism in humans is likely to be qualitatively similar to that in animals, however.

Cloudy swelling and congestion of the kidney were found by histopathological examination in dogs given 1,1,2-trichloroethane orally (vehicle not specified) at doses of 144 mg/kg or above (Wright and Schaffer 1932). There was a significant, low-level depression of in vitro organic ion uptake in renal cortical slices taken from rats given single oral doses of 1,1,2-trichloroethane in corn oil at 72 to 505 mg/kg (Watrous and Plaa 1972a). There was no clear dose-response relationship in this study, however.

1985, Morgan et al. 1972, Sato and Nakajima 1979). This indicates that 1,1,2-trichloroethane could be easily distributed and retained in fat, liver, and brain in both animals and humans. 2 Oral Exposure No studies were located regarding distribution in humans or animals following oral exposure to 1,1,2-trichloroethane. One study showed that 1,1,2-trichloroethane was distributed to the liver following oral exposure in animals (Mitoma et al. 1985). In this study, 1,1,2-trichloroethane was extensively metabolized (presumably by the liver), and was also found to bind hepatic protein.

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Toxicological profiles - 1,1,2-trichloroethane by Agency for Toxic Substances and Disease Registry

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