BIOACCUMULATIVE POTENTIAL AND TOXICITY OF ENDOSULFAN INSECTICIDE TO NONTARGET ANIMALS

1. Endosulfan insecticide is a polychlorinated compound used for contr olling a variety of insects; it is practically water-insoluble, but re adily adheres to clay particles and persists in soil and water for sev eral years. Its mode of action involves repetitive nerve-discharges po sitively correlated to increase in temperature. This compound is extre mely toxic to most fish and can cause massive mortalities. In fish, it causes marked changes in Na and K concentrations, decrease in blood C a2+ and Mg levels and inhibits Na, K and Mg-dependent ATPase (in brain ), 2. Bioaccumulation of endosulfan is reported for marine animals; ho wever, freshwater animals (e.g. crayfish) accumulate it to some extent , but they lose the compound rapidly during depuration. Endosulfan is generally less toxic to aquatic invertebrates than fish. However, it c auses decreases in adenylate energy charge, oxygen consumption, hemoly mph amino acids, succinate dehydrogenase, heart-beat (mussel) and alte red osmoregulation. 3. Generally, mammals are less susceptible to endo sulfan's toxicity than aquatic animals. The majority of studies conduc ted on laboratory mammals can be summarized. (a) Neurotoxicity: male r ats are more sensitive than females to endosulfan, which decreases bra in and plasma acetylcholinesterase activity. Endosulfan I (a metabolit e) causes a significant change in norepinephrine, 5-HT and GABA. (b) R enal toxicity: inhibition of MFOs activity was noticed in rats; other effects included changes in proximal convoluted tubules and necrosis o f the tubular epithelium. (c) Hepatotoxicity: chemically-induced amino pyrine N-demethylase and aniline hydrolase were found in rat liver, an d reduction in the glycogen level occurred. (d) Hematologic toxicity: endosulfan exposure resulted in a significant decrease in the erythroc yte glutathione reductase, hemoglobin amount, RBC number and mean corp uscular volume. 4. Respiratory toxicity: involved dyspnea, acute emphy sema, cyanosis and hemorrhages in the interalveolar partitions of rat' s lungs. 5. Biochemical: in rats, endosulfan caused increased glucose- 6-phosphate dehydrogenase activity, blood glucose level, phospholipid contents of the microsomal and surfactant system, and profoundly induc ed the activity of alcohol dehydrogenase and cytosolic glutathione S-t ransferases. It also decreased significantly Na+, K+ and Mg2+ ATPases, plasma calcium level and alkaline phosphatase in the intestinal epith elium. 6. Immunologic toxicity: rat serum antibody titer to tetanus to xin, IgG, IgM and gammaglobulins were significantly reduced. 7. Reprod uctive toxicity: degenerative changes in the seminiferous epithelium, induction of the rate-limiting in testosterone production (3beta-hydro xysteroid transferase and 17beta-hydroxysteroid transferase), histolog ical changes in reproductive organs, testicular atrophy and the occurr ence of ovarian cysts were noticed in rat. Reduction in the weight of secondary sex organ was also observed. 8. Developmental, teratogenic a nd genotoxicity: this insecticide caused a significant increase in the fetal resorption of rats. Skeletal abnormalities included underweight fetuses, small 4th and 5th unossified sternabrae. No fetotoxic or ter atogenic activity was found in rabbits; however, in chickens, egg-hatc hability and sterility occurred due to antimitotic activity. Endosulfa n caused significant chromosomal aberrations in mouse and hamster bone -marrow cells and damage to spermatozoa cells. In Drosophila, sex-link ed recessive lethals were noticed. In mice, dominant lethal mutations occurred; increase in abnormal sperm and decrease in count occurred. 9 . Carcinogenic toxicity: not reported to be carcinogenic in B6C3F mice or humans by any route of exposure. 10. Toxicity to humans: endosulfa n exposure has exhibited epileptic effects, hyperactivity, irritabilit y, tremors, convulsions and paralysis in humans. A suicidal attempt by a 20-year old male who ingested 30% endosulfan caused hypoxia, follow ed by recurrent aspiration pneumonia, episodes of tachycardiogenic sho ck which was preceded by tachycardia and hypertension.