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DDT and Related Chlorinated Hydrocarbon Insecticides: Pharmacological Basis of Their Toxicity in Mammals

1975; Elsevier BV; Linguagem: Inglês

10.1016/s1054-3589(08)60219-7

1557-8925

Pavel D. Hrdina, Radhey L. Singhal, George M. Ling,

Pesticide Exposure and Toxicity

This chapter discusses the pharmacological basis of DDT and related chlorinated hydrocarbon insecticides toxicity in mammals. In mammals, the administration of acute large doses of DDT and related chlorinated hydrocarbon insecticides produces a variety of toxic effects and invariably leads to death. Methoxychlor, that appears to be replacing DDT in certain countries, exhibits toxicity that is about 30 times less than that seen with DDT. The major routes of DDT metabolism in mammals are (1) oxidation to DDA, (2) dehydrochlorination to DDE, and (3) reductive dechlorination to DDD. In vertebrates, the major metabolite of DDT in feces and urine is DDA. Of DDT-derived, ether-soluble material in the rat bile, DDT constitutes about 3%, DDE 1%, and free DDA 25-35%; the remaining consists of complexes of DDA or a closely related material. DDE is the principal storage form of ingested DDT in man. However, while men stores about 60% of DDT-derived material in the form of DDE, rats store only about 22-29% of DDE, and monkeys convert little or no DDT to DDE.