ACUTE, SUB-CHRONIC, AND CHRONIC TOXICITY OF CHLORDECONE

Oral LD50 values were 132 mg/kg for male rats, 126 mg/kg for female rats, 71 mg/kg for male rabbits, and approximately 250 mg/kg for dogs. The percutaneous LD50 for male rabbits was 410 mg/kg. Deaths were preceded by the development of severe tremors. Gross autopsy findings were essentially negative. Rats were fed chlordecone in concentrations of 1, 5, 10, 25, and 80 ppm for up to 2 years. All rats on 50 and 80 ppm died during the first 6 months. Depressed growth occurred at concentrations at low as 10 ppm for females and 25 ppm for males. Food consumption tended to increase as the dietary concentration of chlordecone became greater. This effect was associated with a measured increase in the metabolic rate. Concentrations of 5 ppm and higher accelerated and intensified the rate of development of proteinuria. Increased liver-to-body weight ratios were consistently observed. Elevated ratios for other organs measured (kidney, heart, spleen, and testes) were found at certain periods, but at higher chlordecone concentrations than required for liver. Principal histopathologic findings in rats were degenerative changes in liver cells (fatty changes, hyperplasia), kidney lesions (primarily glomerulosclerosis), and testicular atrophy. Hematocrit and hemoglobin values were reduced in rats receiving concentrations of 25 ppm and above. There was no evidence of a clotting defect, although some rats receiving 50 and 80 ppm showed a bleeding tendency. Beagle dogs fed chlordecone at concentrations of 1,5, and 25 ppm for periods up to 127 weeks exhibited few gross or histopathologic signs of toxicity. © 1979 Academic Press, Inc. All rights reserved.