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Two spraymen working in public health occupations in Alexandria, Egypt, experienced acute toxicity resulting from exposure to diazinon. Symptomatology was similar to that previously reported for exposure to parathion or other organophosphorus insecticides. Plasma and red blood cell cholinesterase activity values were determined in blood samples obtained from both individuals at various times after the incident. Cholinesterase activity showed a marked reduction up to 18 days after exposure. Blood cholinesterase activity recovered to approximately 90% of the normal level of activity 28 days after the poisoning incident in one individual. This activity recovered to about the same level in the other individual, but after only 20 days from the poisoning date. Experimental results suggested that this acute toxicity resulted from unsuitable storage conditions of the emulsifiable concentrate formulation of diazinon. The diazinon that was applied was stored in "tin" containers made of tin-plated sheet steel. The emulsifiable concentrate (60%) was not in compliance with the World Health Organization's standard specifications regarding the emulsion stability tests because of the presence of crystals in the emulsifiable concentrate. A sample of this crystalline material was analyzed. Gas chromatographic analysis combined with mass spectrometric techniques failed to identify intact diazinon in samples of that material. The sample represented virtually complete conversion of diazinion into transformation products. Sulfotepp and monothiono-TEPP were two of the identified products in the sample, both of which are much more toxic than diazinon.

The delayed neurotoxic effects of tri-o-cresyl-phosphate (TOCP), O-methyl-O-(4-bromo-2,5-dichlorophenyl) phenylphosphonothioate (leptophos), and O-ethyl O-(4-nitrophenyl) phenylphosphonothioate (EPN) at 5, 5, and 1 mg/kg/day, respectively, on male sheep were studied during 6 months of daily oral treatment under field conditions. A vehicle-control group of sheep given corn oil (0.1 ml/kg/day) only was used for comparison. All sheep were killed 24 h after the 180th daily treatment. Blood, brain, spinal cord, and sciatic nerve tissues were taken for histological and/or biochemical examinations. The results indicated that leptophos induced severe ataxia and paralysis in sheep following about 4 months of treatment. TOCP produced either mild ataxia or lameness in two of four sheep during the last week of experiment. On the other hand, none of the EPN-treated sheep showed clinical signs of neurotoxicity during the course of the experiment at the dosage tested. These clinical results were supported by histological findings and also by biochemical results with neurotoxic esterase (NTE) measurements. In the case of leptophos-treated sheep, numerous prominent degenerative lesions of axons were observed in spinal cords and brains. Similar but somewhat less numerous lesions were noted in sheep treated with TOCP. No histological changes were observed in similar tissues taken from EPN-treated sheep. The results also indicated that, for chronic exposure to these neurotoxic organophosphorus compounds in sheep, a threshold in excess of 60-70% prolonged inhibition of brain NTE, or 50-60% inhibition of spinal cord NTE must be exceeded to initiate clinical and/or histological neurotoxic effects.

Although the use of arsenical herbicides in both crop and non-crop areas has been widely accepted, the use of certain formulations of these chemicals may have a disastrous effect on wildlife. The following incident emphasizes the sometimes tragic effects of the indiscriminate use of these herbicides by qualified and/or non-qualified persons.

Tri-o-cresyl phosphate (TOCP) and O-ethyl O-(4-cyanophenyl) phenylphosphonothioate (cyanofenphos, Surecide) were found to be delayed neurotoxicants. They were administered to chickens by gavage at 100 and 30 mg/kg . d for 15 d, respectively. In CD-1 mice neither TOCP nor cyanophenphos induced any of the usually recognized clinical symptoms of neuropathy when administered daily by gavage at 262 or 31.25 mg/kg . d for 30 d, respectively. In the chickens, TOCP and cyanofenphos produced about 98 and 90% in vivo inhibition of brain neurotoxic esterase (NTE) activity. In the mice, 24 h after the last daily dose, TOCP and cyanofenphos produced only about 50 and 40% in vivo inhibition of the brain NTE activity. Parathion [O,O-diethyl O-(4-nitrophenyl) phosphorothioate], at 2 or 6.75 mg/kg . d for 15 or 30 d, did not induce neuropathy in either chicken or mice and produced no significant in vivo inhibition of brain NTE activity at the end of the dosing regimen. The specific activity of NTE in control chicken brain crude homogenate was much higher than that in mouse brain homogenate. These results suggest that the differences between chickens and mice in susceptibility to neurotoxic organophosphates may be attributed to (1) inhibitor specificity of NTE forms in the brain in these two different animal species and/or (2) inability of the active metabolites of these neurotoxic compounds to reach the site of action.

Diets containing the herbicide dinoseb (2-sec- butyl 4,6-dinitrophenol) were fed to adult male Sherman rats for 11 weeks. One-half the survivors were killed for terminal studies during the eleventh week and the remainder bred to untreated females during posttreatment, and then killed for terminal studies. Interim sacrifices were made in groups fed 0 and 300 ppm. In rats fed 300 ppm, differential classification of spermatozoa from the cauda epididymidis indicated 90% of the cells were atypical by 20 days of treatment. By 30 days, bizarre and amorphous forms were observed and epididymal sperm counts were decreased. Histologic changes in the testes included abnormal spermatozoa and spermatids and multinucleated spermatogenic cells at 20 and 30 days and severe damage to spermatogenic cells by 50 days. Dietary levels of 225 and 300 ppm produced marked oligospermia and extensive loss of spermatogenic cells in rats fed dinoseb for 11 weeks. Evidence of necrotic spermatogenic cells was seen in some tubules, and in many tubules, only Sertoli cells remained. Reproductive failure occurred at 225 and 300 ppm, although mating behavior and libido were unaffected. There was little or no remission of these effects during the 16-week post-treatment period. Decreased epididymal sperm counts, atypical epididymal spermatozoa, and minimal testicular changes were seen in rats fed 150 ppm, but reproduction was unaffected and the anomalies were reversible. No effects were detected in animals fed 75 ppm.

Clinical symptoms and gross autopsy findings in two cases of dieldrin poisoning are presented. Studies in one child suggest that redistribution of the insecticide into fat is slow and that the more rapid redistribution of dieldrin is from brain to muscle, which may account for termination of seizures. Concentrations fall to population levels with a first-order decay rate which had, in this case, a half-life of 50 days. Electroencephalograms, helpful for diagnosis, may reflect the brain load of poison. Evidence for liver toxicity was found both acutely and more than one year after poisoning.