Increased Hepatic Microsomal Enzyme Activity from Occupational Exposure to Certain Organochlorine Pesticides

Abstract

THERE is increasing concern about the possible harmful effects resulting from accumulation of organochlorine pesticides in soil, water and in the food of animals and man. DDT, the first organochlorine pesticide (introduced in 1941), has been supplemented by the cyclodiene group, which includes aldrin, dieldrin and endrin ^*. These compounds, like DDT, accumulate in fat and are only excreted slowly. Their toxic effects are also similar, large doses causing convulsions and hepatic damage. The blood concentrations currently found in the general population of Europe are unlikely to be directly toxic, although present levels of environmental exposure have been claimed to be harmful to fish¹ and predatory birds². Doses of these pesticides below those at which direct toxic effects are observed have, however, been shown to induce hepatic microsomal enzymes in animals³, and in the rat this occurs with as little as 10 p.p.m. of DDT in the body fat⁴. Whether current levels of environmental exposure to organochlorine pesticides are sufficient to produce enzyme induction in man is uncertain: Kolmodin et al.⁵ found a decrease in the half life of injected antipyrine in the plasma of men manufacturing pesticides, and Poland et al.⁶ reported changes in cortisol and phenylbutazone metabolism in factory workers with heavy exposure to DDT. In studies of workers engaged in the manufacture of pesticides, hepatic microsomal enzyme activity was assessed from changes in the urinary excretion of D-glucaric acid (an end product of the glucuronic acid pathway of the liver⁷) and related to blood pesticide levels.