Pulmonary arachidonic acid metabolism following acute exposures to ozone and nitrogen dioxide

Ozone (O3) and nitrogen dioxide (NO2) are common air pollutants, and exposure to these gases has been shown to affect pulmonary physiology, biochemistry, and structure. This study examined their ability to modulate arachidonic acid metabolites (eicosanoids) in the lungs. Rabbits were exposed for 2 h to O3 at 0.1, 0.3, or 1 ppm; NO2 at 1, 3, or 10 ppm; or to a mixture of 0.3 ppm O3 and 3 ppm NO2. Groups of animals sacrificed either immediately or 24 h after each exposure underwent broncho-pulmonary lavage. Selected eicosanoids were assessed in lavage fluid by radioimmunoassay. Increases in prostaglandins E2 (PGE2) and F2 alpha (PGF2 alpha) were found immediately after exposure to 1 ppm O3. Exposure to 10 ppm NO2 resulted in a depression of 6-keto-PGF1 alpha, while thromboxane B2 (TxB2) was elevated after exposure to 1 ppm NO2 and depressed following 3 and 10 ppm. The O3/NO2 mixture resulted in synergistic increases in PGE2 and PGF2 alpha, with the response appearing to be driven by O3. This study has demonstrated that acute exposure to either O3 or NO2 can alter pulmonary arachidonic acid metabolism and that the responses to these oxidants differ, both quantitatively and qualitatively.