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Main Title Effects of Phosgene Exposure on Lung Arachidonic Acid Metabolism.
Author Madden, M. C. ; Friedman, M. ; Keyes, L. L. ; Koren, H. S. ; Burleson, G. R. ;
CORP Author North Carolina Univ. at Chapel Hill. Center for Environmental Medicine and Lung Biology. ;North Carolina Univ. at Chapel Hill. Center for Environmental Medicine and Lung Biology. ;Health Effects Research Lab., Research Triangle Park, NC.
Publisher c1991
Year Published 1991
Report Number EPA-68-02-4450; EPA/600/J-91/007;
Stock Number PB91-177352
Additional Subjects Phosgene ; Toxicity ; Lung ; Arachidonic acids ; Metabolism ; Bronchoalveolar lavage fluid ; Macrophages ; Pulmonary alveoli ; Eicosanoids ; Leukotrienes ; Prostaglandins ; In vitro analysis ; High pressure liquid chromatography ; Statistical analysis ; Radioimmunoassay ; Dose-response relationships ; Reprints ;
Library Call Number Additional Info Location Last
NTIS  PB91-177352 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 20p
Phosgene is a pulmonary toxicant that can produce lung edema, bronchoconstriction, and immune suppression following an acute exposure. In the report, the effects of acute in vivo and in vitro phosgene exposure on lung arachidonic acid metabolism were examined. Fischer-344 rats were exposed either to air or to phosgene (0.05-1.0 ppm) for 4 hr and the lungs lavaged at 0.4, 20, and 44 hr post exposure. Leukotriene B4 (LTB4), leukotrienes C4, D4, and E4 (LTC4/D4/E4), and prostaglandin E2 (PGE2) were measured in lavage fluid by radioimmunoassay. With the exception of the LTC4/D4/E4 concentration in 1.0 ppm phosgene-exposed rats, in vivo phosgene exposure at > or = 0.1 ppm produced significant decreases in the concentrations of PGE2, LTB4, and LTC4/D4/E4 in the lavage fluid collected immediately after exposure. Temporally associated with the decreased eicosanoid production was a smaller number of alveolar macrophages recovered in the lavage fluid of phosgene-exposed rats. Dose response studies were performed. Phosgene exposure in vitro of rat and human alveolar macrophages was then performed to determine if the toxicant could directly inhibit the formation of eicosanoids by alveolar macrophages.