OZONE-INDUCED HUMAN RESPIRATORY DYSFUNCTION AND DISEASE

Exercising volunteers exposed in chambers to as little as 80 ppb O-3 f or several hours exhibit impaired lung function and irritative lower a irway symptoms. Comparable changes occur among children and young adul ts exposed to summer smog containing O-3. Intensity of the response is reproducible but varies widely among individuals. The (reversible) de crements in vital capacity are due to involuntary inhibition of deep i nspiration probably mediated by nociceptive bronchial C-fibers that ma y be stimulated by local prostaglandin release, and can be modulated b y appropriate pharmacologic agents. A second characteristic response t o low O-3 levels is mucosal neutrophilic inflammation probably mediate d by phospholipid-derived products and by epithelial cell-derived chem okines and cytokines, but poorly correlated with lung function changes . Fluctuations in ambient O-3 levels are associated with acute respira tory health effects in exposed populations but concomitant acid aeroso l pollution is an important confounder. Whether irreversible impairmen t of lung function occurs among residents of chronically high ozone-po llution areas is debated.