Trichloroethylene (TCE) produced bronchiolar damage when administered to mice. Administration of 2000 mg/kg caused injury in Clara cells of the bronchiolar epithelium, which was observed at 24 h following TCE treatment; increase of the dosage to 2500 mg/kg induced additionally, alterations in alveolar Type II cells of the parenchyma. Specifically, lamellar bodies were reduced in number and microvilli displayed distorted protrusions. The increase in severity of cellular injury with higher dosages of TCE coincided with increased accumulation of pulmonary calcium and lengthened anesthesia recovery times following TCE-induced anesthesia. Time-course studies conducted with 2000 mg/kg demonstrated rapid and marked reduction in pulmonary microsomal cytochrome P-450 content and aryl hydrocarbon hydroxylase activity. Significant decreases were observed as early as 1 h, and the levels were still depressed at 24 h following TCE treatment. Hepatic necrosis was relatively mild at the dosages of TCE examined. These results demonstrate that TCE is pneumotoxic and affects Clara and alveolar Type II cells.