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Diesel exhaust augments allergen-induced lower airway inflammation in allergic individuals: a controlled human exposure study
  1. Chris Carlsten1,2,
  2. Anders Blomberg3,
  3. Mandy Pui1,
  4. Thomas Sandstrom3,
  5. Sze Wing Wong1,
  6. Neil Alexis4,
  7. Jeremy Hirota1,2
  1. 1Division of Respiratory Medicine, Department of Medicine, Chan-Yeung Centre for Occupational and Environmental Respiratory Disease, University of British Columbia, Vancouver, British Columbia, Canada
  2. 2Centre for Heart Lung Innovation, Institute for Heart and Lung Health, University of British Columbia, Vancouver, British Columbia, Canada
  3. 3Division of Medicine/Respiratory Medicine, Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden
  4. 4Department of Pediatrics, University of North Carolina, Chapel Hill, North Carolina, USA
  1. Correspondence to Dr Chris Carlsten, Gordon and Leslie Diamond Health Care Centre, The Lung Center, Vancouver General Hospital (VGH), 2775 Laurel Street, 7th floor, Vancouver, BC, Canada V5Z 1M9; carlsten{at}mail.ubc.ca

Abstract

Rationale Traffic-related air pollution has been shown to augment allergy and airway disease. However, the enhancement of allergenic effects by diesel exhaust in particular is unproven in vivo in the human lung, and underlying details of this apparent synergy are poorly understood.

Objective To test the hypothesis that a 2 h inhalation of diesel exhaust augments lower airway inflammation and immune cell activation following segmental allergen challenge in atopic subjects.

Methods 18 blinded atopic volunteers were exposed to filtered air or 300 µg PM2.5/m3 of diesel exhaust in random fashion. 1 h post-exposure, diluent-controlled segmental allergen challenge was performed; 2 days later, samples from the challenged segments were obtained by bronchoscopic lavage. Samples were analysed for markers and modifiers of allergic inflammation (eosinophils, Th2 cytokines) and adaptive immune cell activation. Mixed effects models with ordinal contrasts compared effects of single and combined exposures on these end points.

Results Diesel exhaust augmented the allergen-induced increase in airway eosinophils, interleukin 5 (IL-5) and eosinophil cationic protein (ECP) and the GSTT1 null genotype was significantly associated with the augmented IL-5 response. Diesel exhaust alone also augmented markers of non-allergic inflammation and monocyte chemotactic protein (MCP)-1 and suppressed activity of macrophages and myeloid dendritic cells.

Conclusion Inhalation of diesel exhaust at environmentally relevant concentrations augments allergen-induced allergic inflammation in the lower airways of atopic individuals and the GSTT1 genotype enhances this response. Allergic individuals are a susceptible population to the deleterious airway effects of diesel exhaust.

Trial registration number NCT01792232.

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