Ozone-induced human respiratory dysfunction and disease.

Exercising volunteers exposed in chambers to as little as 80 ppb O3 for several hours exhibit impaired lung function and irritative lower airway symptoms. Comparable changes occur among children and young adults exposed to summer smog containing O3. Intensity of the response is reproducible but varies widely among individuals. The (reversible) decrements in vital capacity are due to involuntary inhibition of deep inspiration probably mediated by nociceptive bronchial C-fibers that may be stimulated by local prostaglandin release, and can be modulated by appropriate pharmacologic agents. A second characteristic response to low O3 levels is mucosal neutrophilic inflammation probably mediated by phospholipid-derived products and by epithelial cell-derived chemokines and cytokines, but poorly correlated with lung function changes. Fluctuations in ambient O3 levels are associated with acute respiratory health effects in exposed populations but concomitant acid aerosol pollution is an important confounder. Whether irreversible impairment of lung function occurs among residents of chronically high ozone-pollution areas is debated.