Development and testing of treatments for battlefield phosgene poisoning. Midterm report, 1 August 1994-30 April 1995

The aim of the first phase of this project has been to characterize changes in microvascular endothelial cells and alveolar epithelial cells after exposure to phosgene in vitro, so that proposed prophylactic and therapeutic interventions can be evaluated in the second phase. In the first months, we showed that an anti-neutrophil antibody reduces both neutrophil infiltration into the lungs and the late-onset protein leak into the alveolar space after exposure of rats to phosgene. We have now characterized the time course of release of arachidonic acid metabolites from human lung microvascular endothelial cells in vitro: levels of the cyclooxgyenase pathway products, 6-keto-PGF1(alpha) (a stable product of prostacyclin) and thromboxane B2 both increase -2 h after exposure to 900 ppm/min phosgene.