In Vitro Ozone Exposure Increases Release of Arachidonic Acid Products from a Human Bronchial Epithelial Cell Line

Eicosanoids released after ozone exposure of a human bronchial epithelial cell line, BEAS-S6, were analyzed by high-pressure liquid chromatography (HPLC) of supernatants from exposed cells prelabeled with [ 3H]arachidonic acid. BEAS cells released thromboxane B 2 (TxB 2), prostaglandin E 2(PGE 2), leukotriene C 4 (LTC 4), LTD 4, LTE 4, and 12-hydroxyheptadecatrienoic acid (HHT) after exposure to ozone at concentrations of 0.1, 0.25, 0.5, and 1.0 ppm. The eicosanoids were identified by coelution with authentic standards. The largest product from ozone-exposed BEAS cells was the most polar peak, designated Peak I. Release of cyclooxygenase products such as TxB 2, PGE 2, and HHT was inhibited by acetylsalicylic acid. Peaks that migrated with authentic standards for LTB 4, LTC 4, and LTD 4 were inhibited by the lipoxygenase inhibitor nordihydroguaiaretic acid. The leukotrienes LTB 4 and LTC 4/D 4 could also be detected by immunoassay of concentrated peak fractions. Thus BEAS cells released eicosanoids from cyclooxygenase and lipoxygenase pathways of arachidonic acid metabolism following exposure to ozone. Airway epithelial cells may he an important source of eicosanoids following ozone stimulation in humans.