Ozone exposure enhances mast-cell inflammation in asthmatic airways despite inhaled corticosteroid therapy.Show others and affiliations
2010 (English)In: Inhalation Toxicology, ISSN 0895-8378, E-ISSN 1091-7691, Vol. 22, no 2, p. 133-139Article in journal (Refereed) Published
Abstract [en]
Asthmatics are recognised to be more susceptible than healthy individuals to adverse health effects caused by exposure to the common air pollutant ozone. Ozone has been reported to induce airway neutrophilia in mild asthmatics, but little is known about how it affects the airways of asthmatic subjects on inhaled corticosteroids. We hypothesised that ozone exposure would exacerbate the pre-existent asthmatic airway inflammation despite regular inhaled corticosteroid treatment. Therefore, we exposed subjects with persistent asthma on inhaled corticosteroid therapy to 0.2 ppm ozone or filtered air for 2 h, on 2 separate occasions. Lung function was evaluated before and immediately after exposure, while bronchoscopy was performed 18 h post exposure. Compared to filtered air, ozone exposure increased airway resistance. Ozone significantly enhanced neutrophil numbers and myeloperoxidase levels in airway lavages, and induced a fourfold increase in bronchial mucosal mast cell numbers. The present findings indicate that ozone worsened asthmatic airway inflammation and offer a possible biological explanation for the epidemiological findings of increased need for rescue medication and hospitalisation in asthmatic people following exposure to ambient ozone.
Place, publisher, year, edition, pages
Informa Healthcare , 2010. Vol. 22, no 2, p. 133-139
Keywords [en]
Airway inflammation, air pollution, BAL, bronchial mucosa, myeloperoxidase, neutrophil
National Category
Respiratory Medicine and Allergy
Research subject
Lung Medicine
Identifiers
URN: urn:nbn:se:umu:diva-35692DOI: 10.3109/08958370903005736ISI: 000273643300009PubMedID: 20044881Scopus ID: 2-s2.0-75449109364OAI: oai:DiVA.org:umu-35692DiVA, id: diva2:346308
2010-08-312010-08-312024-07-02Bibliographically approved