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Lethal acute lung injury and hypoglycemia after subcutaneous administration of monochloroacetic acidDepartment of Hygiene and Public Health, Osaka Medical College, 2-7 Daigakumachi, Takatsuki City, Osaka 569-8686, Japan, in1073{at}poh.osaka-med.ac.jp
Department of Hygiene and Public Health, Osaka Medical College, 2-7 Daigakumachi, Takatsuki City, Osaka 569-8686, Japan
Department of Hygiene and Public Health, Osaka Medical College, 2-7 Daigakumachi, Takatsuki City, Osaka 569-8686, Japan
Department of Hygiene and Public Health, Osaka Medical College, 2-7 Daigakumachi, Takatsuki City, Osaka 569-8686, Japan
Department of Hygiene and Public Health, Osaka Medical College, 2-7 Daigakumachi, Takatsuki City, Osaka 569-8686, Japan
Department of Hygiene and Public Health, Osaka Medical College, 2-7 Daigakumachi, Takatsuki City, Osaka 569-8686, Japan Hypoglycemia is suspected in the acute lethal toxicity induced by cutaneous exposure to monochloroacetic acid (MCA). Although it has been shown that hepato-renal dysfunction is involved, the mechanism and the target organs that directly affect mortality remain to be determined. We suspected respiratory failure as a main cause of death in some reported cases. We investigated dose-response effects, hypoglycemia, and lung injury in rats exposed to MCA. Serum glucose, blood gases, and parameters of alveolar injury in bronchoalveolar lavage fluid (BALF) were analysed 2 and 4 h after subcutaneous administration of MCA (108, 135 or 163 mg/kg). Apparent pulmonary injury and hypoglycemia were not identified 2 h after administration, but lactate dehydrogenase (LDH) and total cells in BALF were dose-dependently increased; and severe hypoglycemia was identified 4 h after administration. Blood gas analysis showed remarkable alveolar gas dysfunction as exchange in the 163 mg/kg group. Thus, hypoglycemia and lung injury appear to cause death in response to MCA exposure.
Toxicology and Industrial Health, Vol. 22, No. 5,
203-209 (2006) |
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