Abstract
BackgroundThe discrepancy between functional and inflammatory airway response to ozone has been reported in normal subjects, but few data are available for stable asthmatics regularly treated with inhaled corticosteroids.MethodsTwenty-three well controlled, regularly treated, mild-to-moderate asthmatic patients underwent two sequential randomised exposures to either filtered air or ozone (0.3 ppm for 2 hours) in a challenge chamber. Pulmonary function (PF) was monitored, and patients with FEV1 decrease greater than 10% from pre-challenge value were considered as responders. Immediately after each exposure, exhaled breath condensate (EBC) was collected to measure malondialdehyde (MDA). Six hours after each exposure, PF and EBC collection were repeated, and sputum was induced to measure inflammatory cell counts and soluble mediators (IL-8 and neutrophil elastase). The response to ozone was also evaluated according to the presence of polymorphism in oxidative stress related NQO1 and GSTM1 genes.ResultsAfter ozone exposure, sputum neutrophils significantly increased in responders (n = 8), but not in nonresponders (n = 15). Other markers of neutrophil activation in sputum supernatant and MDA in EBC significantly increased in all patients, but only in nonresponders the increase was significant. In nonresponders, sputum eosinophils also significantly increased after ozone. There was a positive correlation between ozone-induced FEV1 fall and increase in sputum neutrophils. No difference in functional or inflammatory response to ozone was observed between subjects with or without the combination of NQO1wt- GSTM1null genotypes.ConclusionsMarkers of neutrophilic inflammation and oxidative stress increase also in asthmatic subjects not responding to ozone. A greater functional response to ozone is associated with greater neutrophil airway recruitment in asthmatic subjects.
Highlights
The discrepancy between functional and inflammatory airway response to ozone has been reported in normal subjects, but few data are available for stable asthmatics regularly treated with inhaled corticosteroids
Many studies have reported an increase in markers of neutrophilic activation in induced sputum or in bronchoalveolar lavage (BAL) after ozone exposure in healthy ad asthmatic subjects [6,7], as well as an increase in markers of oxidative stress in lung tissue and BAL fluid of animals exposed to high ozone concentrations [8]
Sputum neutrophils significantly increased in responders, but not in nonresponders
Summary
The discrepancy between functional and inflammatory airway response to ozone has been reported in normal subjects, but few data are available for stable asthmatics regularly treated with inhaled corticosteroids. Many studies have reported an increase in markers of neutrophilic activation in induced sputum or in bronchoalveolar lavage (BAL) after ozone exposure in healthy ad asthmatic subjects [6,7], as well as an increase in markers of oxidative stress in lung tissue and BAL fluid of animals exposed to high ozone concentrations [8]. Most experimental studies in humans have reported no correlation between functional response and severity of inflammatory response measured in induced sputum or bronchoalveolar lavage fluid [12,13,14]. Very few data have been reported in asthmatic subjects
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