[Experimental effects of air pollutants on healthy probands and asthmatic patients]

We investigated the acute airway response to nitrogen dioxide (NO2) and ozone in healthy and asthmatic subjects. A) 12 subjects with mild bronchial asthma and 8 healthy subjects were studied to determine the effects of shortterm exposure to NO2 on lung function, bronchoalveolar lavage cells and mediators, and bronchial mucosal biopsy specimens. The asthmatic subjects exhibited changes in prostanoid and leukotriene mediators but no changes in differential cell numbers after NO2 exposure, whereas the normal subjects showed no consistent effects. These results indicate that changes in mediator profile induced by NO2 may be found without concomitant alterations in differential cell numbers. B) Ozone has been demonstrated to induce deterioration of lung function and bronchial responsiveness but it is not clear whether subjects with asthma or rhinitis are more susceptible than normals. We studied the effect of a short-term exposure to ozone on lung function and airway responsiveness to methacholine in 12 subjects with atopic asthma, 18 subjects with allergic rhinitis, and 38 healthy subjects. There was a large interindividual variability in the airway response to ozone but no statistically significant difference between study groups with respect to changes of lung function and airway responsiveness. Our data indicate that an intrinsic variability in ozone sensitivity is of higher relevance than a pre-existing airway disease such as asthma or rhinitis. By comparing both studies we suggest that the relationship between airway disease and airway responsiveness to oxidant pollutants is not homogeneous over substances.