The aim of this study was to evaluate genotoxicity and oxidative stress in workers who formulate organophosphorus (OP) pesticides. In this survey, blood leukocytes and erythrocytes of a group of 21 pesticide formulating workers and an equal number of control subjects were examined for genotoxicity and oxidative stress parameters. The mean comet tail length and mean comet length were used to measure DNA damage. Lipid peroxidation level, catalase, superoxide dismutase (SOD) and glutathione peroxidase activities in erythrocytes were analysed as biomarkers of oxidative stress. In addition, the acetylcholinesterase activity was measured as a biomarker of toxicity. The average duration of employment of workers in the factory was 97 months. Results indicated that chronic exposure (multiple5dose, greater than or equal to 6 months duration) to OP pesticides was associated with increased activities of catalase, SOD and glutathione peroxidase in erythrocytes. The level of lipid peroxidation and acetylcholinesterase activity did not show any significant differences between the two groups. The results also indicated that chronic exposure to OP pesticides was associated with increased DNA damage. It is concluded that human chronic exposure to OP pesticides may result in stimulated antioxidant enzymes and increased DNA damage in the absence of depressed acetylcholinesterase levels. Routine genotoxicity monitoring concomitant to acetylcholinesterase activity in workers occupationally exposed to OP insecticides is suggested.

The majority of poisoning cases in adults occur intentionally and in children accidentally.

Adult male Sprague-Dawley rats were irradiated to the right hemithorax with a range of total doses delivered in 10 equal daily fractions of 4 MeV X rays. Half of each dose group consumed control feed, and half consumed feed containing the angiotensin-converting enzyme inhibitor captopril (50 mg/kg/day) continuously after the last irradiation. High-resolution computed tomography (CT) of the entire thorax was performed at 4 and 8 weeks after the last irradiation, and the findings with CT were correlated with hemodynamic data, heart weight, and pulmonary histopathology. Rats exposed to 20 or 40 Gy in 10 fractions exhibited no acute changes in right lung density. After 60 Gy in 10 fractions, however, right lung density in rats on the control diet increased significantly at 4 weeks, and then returned to normal at 8 weeks. Captopril-treated rats exposed to 60 Gy/10 fractions did not exhibit this transient increase in right lung density. After 80 Gy/10 fractions, right lung density increased to 0.60-0.65 g/cm3 at 4 weeks regardless of diet. At 8 weeks after 80 Gy/10 fractions, right lung density increased further in rats given the control diet, but decreased to near normal levels in captopril-treated animals. The density of the shielded left lung based on the CT was independent of both contralateral radiation dose and diet. Histological examination of the irradiated lungs indicated that these acute changes detected by CT were associated with the exudative and edematous phases of radiation pneumonitis, and that captopril reduced the severity of these changes. Irradiated (40-80 Gy/10 fractions) animals fed the control diet exhibited a significant increase in central venous and pulmonary artery pressure, and cardiac right ventricular hypertrophy. Captopril prevented or attenuated these hypertensive reactions. These data demonstrate that high-resolution CT can detect radiation reactions in rat lung within 4 weeks after 60 Gy/10 fractions, and that captopril spares these acute changes detected by CT. The mechanism of captopril action is not clear, but may be due in part to a reduction in pulmonary arterial pressure, resulting in less severe edema in the irradiated lung.

Aim: To describe the treatment and successful outcome of a patient who had taken an amount of aluminium phosphide that would normally be lethal. Case report: A 47‐year‐old woman was admitted two hours after ingesting 16.8 g of aluminium phosphide with suicidal intent. Treatment consisted of: gastric lavage with potassium permanganate solution; intravenous bicarbonate, magnesium and calcium; and oral bicarbonate and coconut oil. Supportive therapy in intensive care was also provided. Her clinical course included hypotension, metabolic acidosis and liver dysfunction. Discussion: Aluminium phosphide produces phosphine gas and is used to control rodents in grain storage facilities. This patient had apparently ingested what would normally be a lethal amount of aluminium phosphide and had signs and symptoms of severe toxicity. She survived following rapid treatment and supportive care. Recommended measures to limit absorption and phosphine toxicity may have contributed to survival.

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