title: Airway inflammatory responses to diesel exhaust in allergic rhinitics.
abstract: BACKGROUND
  Proximity to traffic, particularly to diesel-powered vehicles, has been associated with inducing and enhancing allergies. To investigate the basis for this association, we performed controlled exposures of allergic rhinitics to diesel exhaust (DE) at a dose known to be pro-inflammatory in healthy individuals.
  
  
  OBJECTIVE
  We hypothesized that diesel-exhaust exposure would augment lower airway inflammation in allergic rhinitics.
  
  
  METHODS
  Fourteen allergic rhinitics were exposed in a double-blinded, randomized trial to DE (100 μg/m³ PM₁₀) and filtered air for 2 h on separate occasions. Bronchoscopy with endobronchial mucosal biopsies and airway lavage was performed 18 h post-exposure, and inflammatory markers were assessed.
  
  
  RESULTS
  No evidence of neutrophilic airway inflammation was observed post-diesel, however, a small increase in myeloperoxidase was found in bronchoalveolar lavage (p = 0.032). We found no increases in allergic inflammatory cells. Reduced mast cell immunoreactivity for tryptase was observed in the epithelium (p = 0.013) parallel to a small decrease in bronchial wash stem cell factor (p = 0.033).
  
  
  CONCLUSIONS
  DE, at a dose previously shown to cause neutrophilic inflammation in healthy individuals, induced no neutrophilic inflammation in the lower airways of allergic rhinitics, consistent with previous reports in asthmatics. Although there was no increase in allergic inflammatory cell numbers, the reduction in tryptase in the epithelium may indicate mast cell degranulation. However, this occurred in the absence of allergic symptoms. These data do not provide a simplistic explanation of the sensitivity in rhinitics to traffic-related air pollution. The role of mast cells requires further investigation.
authors: Division of Medicine, Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden.
authors: Nirina
authors: N
authors: Larsson
authors: Joanna
authors: J
authors: Brown
authors: Nikolai
authors: N
authors: Stenfors
authors: Susan
authors: S
authors: Wilson
authors: Ian S
authors: IS
authors: Mudway
authors: Jamshid
authors: J
authors: Pourazar
authors: Annelie F
authors: AF
authors: Behndig
mesh_terms: D000328:Adult; D000393:Air Pollutants / Q000633:toxicity*; D015415:Biomarkers / Q000378:metabolism; D001706:Biopsy; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology / Q000276:immunology; D001999:Bronchoscopy; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D004311:Double-Blind Method; D005260:Female; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D008297:Male; D008407:Mast Cells / Q000187:drug effects / Q000201:enzymology; D009504:Neutrophils / Q000187:drug effects / Q000473:pathology; D009195:Peroxidase / Q000032:analysis / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D020545:Respiratory Mucosa / Q000187:drug effects* / Q000473:pathology; D065631:Rhinitis, Allergic; D012221:Rhinitis, Allergic, Perennial / Q000139:chemically induced* / Q000276:immunology / Q000378:metabolism; D019089:Stem Cell Factor / Q000032:analysis; D053802:Tryptases / Q000378:metabolism; D001335:Vehicle Emissions / Q000633:toxicity*; D055815:Young Adult
chemical_list: D000393:Air Pollutants; D015415:Biomarkers; D016207:Cytokines; D012333:RNA, Messenger; D019089:Stem Cell Factor; D001335:Vehicle Emissions; D009195:Peroxidase; D053802:Tryptases