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PROLONGED EXPOSURE OF HUMANS TO AMBIENT LEVELS OF OZONE CAUSES CELLULAR AND BIOCHEMICAL CHANGES IN THE LUNG
Citation:
Devlin, R., W. McDonnell, D. House, K. Koren, D. Screinemachers, S. Becker, AND R. Mann. PROLONGED EXPOSURE OF HUMANS TO AMBIENT LEVELS OF OZONE CAUSES CELLULAR AND BIOCHEMICAL CHANGES IN THE LUNG. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/J-91/119 (NTIS PB91207126).
Description:
An acute (2h) exposure of humans to 0.4 ppm ozone initiates biochemical changes in the lung resulting in the production of components which mediate inflammation and acute lung damage as well as components which have the potential to lead to long term effects such as fibrosis. owever, many people are exposed to lower levels of ozone than this, but for periods of several hours. herefore, it is important to determine if a prolonged exposure to low levels of ozone is also capable of causing cellular and biochemical changes in the lung. on-smoking males were randomly exposed to filtered air and either 0.10 ppm ozone or 0.08 ppm ozone for 6.6 h with moderate exercise (40 I/min). ronchalveolar lavage (BAL) was performed 18 h after each exposure, add cells and fluid analyzed. he BAL fluid of volunteers exposed to 0.10 ppm ozone had significant increases in neutrophils (PMNs), protein, PGE2, fibronectin, interleukin-6 (IL-6), and lactate dehydrogenase (LDH) compared with BAL fluid from the same volunteers exposed to filtered air. n addition, there was a decrease in the ability of alveolar macrophages to phagocytize yeast via the complement receptor. xposure to 0.08 ppm ozone resulted in significant increases in PMNs, PGE2, LDH, IL-6, a-l antitrypsin, and decreased phagocytosis via the complement receptor. owever, BAL fluid protein and fibronectin were no longer significantly elevated. e conclude that exposure of humans to low levels of ozone is sufficient to initiate an inflammatory reaction in the lung.