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CO-EXPOSURE OF HUMAN AIRWAY EPITHELIAL CELLS TO OZONE AND PARTICULATE MATTER: EFFECTS ON ARACHIDONIC ACID METABOLISM
Citation:
Stamm, D., L. A. Dailey, AND M. C. Madden. CO-EXPOSURE OF HUMAN AIRWAY EPITHELIAL CELLS TO OZONE AND PARTICULATE MATTER: EFFECTS ON ARACHIDONIC ACID METABOLISM. Presented at UNC-CH MC/PHD Student Research Program Annual Meeting, Chapel Hill, NC, October 15, 2001.
Description:
Co-exposure of human airway epithelial cells to ozone and particulate matter: effects on arachidonic acid metabolism.
D. Stamm1, L. Dailey2, M.C. Madden2
1 University of North Carolina-Chapel Hill, School of Medicine
2 U.S. EPA, ORD, NHEERL, HSD, Chapel Hill, NC, USA
ABSTRACT
Many epidemiological studies have reported increased mortality and morbidity due to cardiopulmonary problems in response to high levels of airborne particulate matter (PM). Ozone, a ubiquitous oxidant air pollutant, may exacerbate PM effects. Metabolites of arachidonic acid, such as prostaglandin E2 (PGE2), may mediate the observed responses. In this study we investigated the combined effect of PM and ozone exposure on the responses of normal human bronchial epithelial (NHBE) cells. Residual oil fly ash (ROFA) PM was used as the PM source. We found that PGE2 production increased in cells pretreated with ROFA, and subsequently exposed to ozone. Viability was decreased in ROFA treated cells in a dose dependent manner. Immunohistochemical studies showed an increase in COX-2 expression, an enzyme involved with PGE2 production, after ROFA exposure for 24 hr. These data suggest that co-exposures of PM and ozone can increase inflammatory lipids. These inflammatory lipids may play a role in PM-induced morbidity and mortality. [This is an abstract of a proposed presentation, and does necessarily reflect EPA policy.]