Maria Laura Bartoli, Barbara Vagaggini, Laura Malagrinò, Elena Bacci, Silvana Cianchetti, Federico L Dente, Federica Novelli, Francesco Costa, Pierluigi Paggiaro
Cardio-Thoracic and Vascular Department, University of Pisa, Pisa, Italy. m.bartoli@ao-pisa.toscana.it
Inhalation toxicology 2013 FebIt is well known that ozone exposure decreases lung function and increases airway neutrophilia, but large variability has been observed among asthmatic patients. To find possible predictors of functional and inflammatory airway response to ozone in asthmatic patients. We studied 120 patients with mild-to-moderate asthma, randomly exposed to either air or ozone (0.3 ppm for 2 h) in a challenge chamber. Symptoms and pulmonary function test (PFT) were measured before and immediately after exposure. Six hours after exposure, induced sputum was collected. Patients were evaluated according to their functional (FEV₁ responders) or neutrophilic (neutrophil responders) response to ozone. We considered, as possible predictors of response: age, baseline FEV₁, previous treatment with inhaled corticosteroids (ICS), baseline sputum neutrophils, baseline sputum eosinophils, methacholine responsiveness, atopy and smoking habit. FEV₁ responders had lower baseline FEV₁, and a lower percentage of these had received ICS treatment. Neutrophil responders were younger, with lower baseline sputum inflammation and greater methacholine responsiveness. These results were confirmed by multivariate logistic analysis. Patients not previously treated with ICS and patients with lower FEV₁ are more prone to functional response to ozone. Lower baseline airway inflammation and greater bronchial hyperresponsiveness may predict neutrophilic airway response to ozone in asthmatic patients. Thus, determinants of functional and inflammatory responses to ozone are different.
Maria Laura Bartoli, Barbara Vagaggini, Laura Malagrinò, Elena Bacci, Silvana Cianchetti, Federico L Dente, Federica Novelli, Francesco Costa, Pierluigi Paggiaro. Baseline airway inflammation may be a determinant of the response to ozone exposure in asthmatic patients. Inhalation toxicology. 2013 Feb;25(3):127-33
PMID: 23421484
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