Trichloroethylene (TRI) and perchloroethylene (PER) are chlorinated hydrocarbons with similar chemical and toxicological properties. Cancer bioassay results with TRI and PER have shown increased incidence of liver tumors in B6C3F1 mice. Though the exact mechanism of tumor induction caused by TRI or PER is unknown, metabolic activation is strongly implicated. The major metabolite, trichloroacetic acid (TCA), induces peroxisomal proliferation (PP) in livers of rodents. Evidence suggests that PP in the liver is linked to the development of hepatic carcinomas. Whether PP is causative or just a by-product of liver cancer is unknown, but results establish that human cells do not react to TCA as rodent cells do. The current information on pharmacokinetics and mechanism-of-action for TRI and PER do not support a concern for carcinogenicity of exposed persons, based on findings of cancer in rodents. Moreover, the findings do not suggest a need for quantitative risk assessment.
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