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

Abstract

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 (eico‐sanoids) in the lungs. Rabbits were exposed for 2h 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 radioimmu‐noassay. Increases in prostaglandins E₂ (PGE₂) and F_2α (PGF_2α) were found immediately after exposure to 1 ppm O₃. Exposure to 10 ppm NO₂ resulted in a depression of 6‐keto‐PCF_1α, 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 PGF_2α, 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.