title: Baseline airway inflammation may be a determinant of the response to ozone exposure in asthmatic patients.
abstract: BACKGROUND
  It is well known that ozone exposure decreases lung function and increases airway neutrophilia, but large variability has been observed among asthmatic patients.
  
  
  OBJECTIVE
  To find possible predictors of functional and inflammatory airway response to ozone in asthmatic patients.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors: Cardio-Thoracic and Vascular Department, University of Pisa, Pisa, Italy. m.bartoli@ao-pisa.toscana.it
authors: Maria Laura
authors: ML
authors: Bartoli
authors: Barbara
authors: B
authors: Vagaggini
authors: Laura
authors: L
authors: Malagrinò
authors: Elena
authors: E
authors: Bacci
authors: Silvana
authors: S
authors: Cianchetti
authors: Federico L
authors: FL
authors: Dente
authors: Federica
authors: F
authors: Novelli
authors: Francesco
authors: F
authors: Costa
authors: Pierluigi
authors: P
authors: Paggiaro
mesh_terms: D000328:Adult; D001249:Asthma / Q000139:chemically induced* / Q000276:immunology / Q000503:physiopathology; D001273:Atmosphere Exposure Chambers; D005260:Female; D005541:Forced Expiratory Volume / Q000502:physiology; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000503:physiopathology*; D019570:Inhalation Exposure; D008297:Male; D016210:Methacholine Chloride; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology; D010083:Oxidants, Photochemical / Q000009:adverse effects*; D010126:Ozone / Q000009:adverse effects*; D013183:Sputum / Q000166:cytology / Q000276:immunology
chemical_list: D005938:Glucocorticoids; D010083:Oxidants, Photochemical; D016210:Methacholine Chloride; D010126:Ozone