Bioaccumulative potential and toxicity of endosulfan insecticide to non-target animals

Abstract

1. Endosulfan insecticide is a polychlorinated compound used for controlling a variety of insects; it is practically water-insoluble, but readily adheres to clay particles and persists in soil and water for several years. Its mode of action involves repetitive nerve-discharges positively correlated to increase in temperature. This compound is extremely toxic to most fish and can cause massive mortalities. In fish, it causes marked changes in Na and K concentrations, decrease in blood Ca 2+ and Mg levels and inhibits Na, K and Mg-dependent ATPase (in brain). 2. Bioaccumulation of endosulfan is reported for marine animals; however, 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 causes decreases in adenylate energy charge, oxygen consumption, hemolymph amino acids, succinate dehydrogenase, heart-beat (mussel) and altered osmoregulation. 3. Generally, mammals are less susceptible to endosulfan's toxicity than aquatic animals. The majority of studies conducted on laboratory mammals can be summarized, (a) Neurotoxicity: male rats are more sensitive than females to endosulfan, which decreases brain and plasma acetyleholinesterase activity. Endosulfan I (a metabolite) causes a significant change in norepinephrine, 5-HT and GABA. (b) Renal toxicity: inhibition of MFOs activity was noticed in rats; other effects included changes in proximal convoluted tubules and necrosis of the tubular epithelium, (c) Hepatotoxicity: chemically-induced aminopyrine N-demethylase and aniline hydrolase were found in rat liver, and reduction in the glycogen level occurred, (d) Hematologic toxicity: endosulfan exposure resulted in a significant decrease in the erythrocyte glutathione reductase, hemoglobin amount, RBC number and mean corpuscular volume. 4. Respiratory toxicity: involved dyspnea, acute emphysema, 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 induced the activity of alcohol dehydrogenase and cytosolic glutathione S-transferases. It also decreased significantly Na +, K + and Mg 2+ ATPases, plasma calcium level and alkaline phosphatase in the intestinal epithelium. 6. Immunologic toxicity: rat serum antibody titer to tetanus toxin, IgG, IgM and gammaglobulins were significantly reduced. 7. Reproductive toxicity: degenerative changes in the seminiferous epithelium, induction of the rate-limiting enzyme in testosterone production (3β-hydroxysteroid transferase and 17β-hydroxysteroid transferase), histological changes in reproductive organs, testicular atrophy and the occurrence of ovarian cysts were noticed in rat. Reduction in the weight of secondary sex organ was also observed. 8. Developmental, teratogenic and genotoxicity: this insecticide caused a significant increase in the fetal résorption of rats. Skeletal abnormalities included underweight fetuses, small 4th and 5th unossified sternabrae. No fetotoxic or teratogenic activity was found in rabbits; however, in chickens, egg-hatchability and sterility occurred due to antimitotic activity. Endosulfan caused significant chromosomal aberrations in mouse and hamster bone-marrow cells and damage to spermatozoa cells. In Drosophila, sex-linked 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: endosulfan exposure has exhibited epileptic effects, hyperactivity, irritability, tremors, convulsions and paralysis in humans. A suicidal attempt by a 20-year old male who ingested 30% endosulfan caused hypoxia, followed by recurrent aspiration pneumonia, episodes of tachycardiogenic shock which was preceded by tachycardia and hypertension.