© 1982 Oxford University Press
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Studies on the Carcinogenicity of Pentachloroethane in Rats and Mice1
National Toxicology Program, Research Triangle Park, NC, Gulf South Research Institute New Iberia, LA; Tracor-Jitco, Inc. Rockville, MD
Studies on the Carcinogenicity of Pentachloroethane in Rats and Mice. Mennear, J.H., Haseman, J.K., Sullivan, D.J., Bernal, E. and Hildebrandt, P.K. (1982). Fundam. Appl. Toxicol. 2:82–87. The carcinogenicity of chronically administered (41 to 103 weeks) technical-grade pentachloroethane (PCE) was assessed in groups of 50 male and female Fischer 344 rats and B6C3F1 mice. The major contaminant in the PCE sample used for the chronic study was hexachloroethane (4.2%). Prechronic studies (two and 13 weeks repeated dose) employing gavage doses of from 5.0 to 1000 mg/kg/day of PCE failed to reveal specific target organ toxicity in these species. In the absence of treatment-related pathological changes during the prechronic tests, the doses for the chronic studies were set on the basis of survival and body weight gains during the 13-week repeated dose study. During the chronic studies dose levels of 75 and 150 mg/kg for rats and 250 and 500 mg/kg for mice were administered, by gavage, five days per week. The survival of high-dose rats (both sexes) was significantly reduced as compared to the survival of control animals and that of the low-dose males was slightly, but not significantly, reduced. Although the administration of PCE to rats did not increase the incidence of primary tumors, it did produce a significant dose-related increase in the incidence of chronic renal inflammation among males. The survival times of all treated groups of mice were significantly shortened by PCE administration. Despite this reduced survival time, the incidence of hepato-cellular carcinoma was significantly increased in all treated groups. With the exception of a dose-related increase in the incidence of hepatocellular adenoma among females, there were no other significant increases in primary tumor incidence in mice. Neither renal lesions in rats nor hepatocellular carcinoma in mice were considered to be adequate explanations for the decreased survivals. Complete histopathological examinations failed to reveal the cause of decreased survival. The results of the study show that technical-grade PCE, like numerous other chlorinated ethanes, is an hepato-carcinogen for B6C3F1 mice. This interpretation for PCE per se, however, must be tempered because the major contaminant, hexachloroethane, has been shown to produce hepatocellular carcinoma in mice. While the results obtained in rats suggest a species difference in susceptibility, the reduced survival in this species may have contributed to the absence of a carcinogenic effect.