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1 Dept of Respiratory Medicine and Allergy, University Hospital, and 4 Energy Technology and Thermal Process Chemistry, Umeå University, Umeå, Sweden. 2 Respiratory Cell and Molecular Biology Research Division, Southampton General Hospital, Southampton, and 3 Lung Biology, Pharmacology and Therapeutics, Pharmaceutical Sciences Research Division, Franklin-Wilkins Building, King's College London, London, UK, 5 Centre for Environmental Health Research, National Institute of Public Health and the Environment (RIVM), Bilthoven, The Netherlands. 6 Equal contribution to first authorship.
CORRESPONDENCE: T. Sandström, Dept of Respiratory Medicine and Allergy, University Hospital, SE-901 85 Umeå, Sweden. Fax: 46 90141369. E-mail: thomas.sandstrom{at}lung.umu.se
Keywords: Air pollution, airway inflammation, antioxidants, diesel exhaust, glutathione, particulate matter
Received: November 30, 2004
Accepted September 15, 2005
Pulmonary cells exposed to diesel exhaust (DE) particles in vitro respond in a hierarchical fashion with protective antioxidant responses predominating at low doses and inflammation and injury only occurring at higher concentrations. In the present study, the authors examined whether similar responses occurred in vivo, specifically whether antioxidants were upregulated following a low-dose DE challenge and investigated how these responses related to the development of airway inflammation at different levels of the respiratory tract where particle dose varies markedly.
A total of 15 volunteers were exposed to DE (100 µg·m–3 airborne particulate matter with a diameter of <10 µm for 2 h) and air in a double-blinded, randomised fashion. At 18 h post-exposure, bronchoscopy was performed with lavage and mucosal biopsies taken to assess airway redox and inflammatory status.
Following DE exposure, the current authors observed an increase in bronchial mucosa neutrophil and mast cell numbers, as well as increased neutrophil numbers, interleukin-8 and myeloperoxidase concentrations in bronchial lavage. No inflammatory responses were seen in the alveolar compartment, but both reduced glutathione and urate concentrations were increased following diesel exposure.
In conclusion, the lung inflammatory response to diesel exhaust is compartmentalised, related to differing antioxidant responses in the conducting airway and alveolar regions.
This article has been cited by other articles:
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