1,1-Dichloroethylene-induced pulmonary injury.
Oral administration of 1,1-dichloroethylene (1,1-DCE) produces acute injury to the lungs of C57Bl/6 mice. The bronchiolar epithelium is most severely affected with damage selective for Clara cells. After a 100 mg kg/dose of 1.1-DCE. Clara cells show extensive dilatation of cisternae and degeneration of the endoplasmic reticulum. At 6 hr after administration of 200 mg 1,1-DCE/kg, both ciliated and Clara cells are necrotic, and bronchiolar epithelial lining exfoliates. By 24 hr. pulmonary edema, hemorrhage, and focal atelectasis are also present. Pulmonary injury, at 24 hr after the high dose, is associated with a significant hypoxia as demonstrated through a decrease in the partial pressure of oxygen in arterial blood. In spite of the severe injury, recovery occurs and airways display an intact epithelial lining with normal parenchymal elements by 7 days.
D000818:Animals; D001980:Bronchi / Q000187:drug effects* / Q000648:ultrastructure; D001982:Bronchial Diseases / Q000139:chemically induced* / Q000473:pathology; D002273:Carcinogens; D004000:Dichloroethylenes / Q000633:toxicity*; D004848:Epithelium / Q000648:ultrastructure; D006843:Hydrocarbons, Chlorinated / Q000633:toxicity*; D008168:Lung / Q000187:drug effects*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009153:Mutagens; D011654:Pulmonary Edema / Q000139:chemically induced* / Q000473:pathology
D002273:Carcinogens; D004000:Dichloroethylenes; D006843:Hydrocarbons, Chlorinated; D009153:Mutagens; C029297:vinylidene chloride