Effects of Ozone Exposure on Lipid

examine the possibility that these mediators may account for some of the pathophysiologic alterations seen in the lung after ozone (03) exposure, human AM were collected by bronchoalveolar lavage of normal subjects, plated into tissue culture dishes, and the adherent cells were incubated with [H]AA or [H!lysoPAF. Human AM exposed to 1.0 ppm 03 for 2 hr released 65 ? 12% more tritium, derived from [3HJAA, than paired, air-exposed controls into media supernatants. In other studies using a similar O3 exposure protocol, there was also a significant increase in human AM prostaglandin E2 production (2.0 0.5-fold increase above air-exposure values, p < 001, n = 17). In additional studies, using a similar O3 exposure protocol (1.0 ppm for 1 hr), there was also a significant increase in human AM PAF content (1.7 ? 0.2-fold increase above air-exposure values, p < 0.02, n = 5). These potent lipid mediators, originally derived from human AM, may play an important role in the mechanisms of 03 lung toxicity.