Ozone exposure enhances mast-cell inflammation in asthmatic airways despite inhaled corticosteroid therapy.

TitleOzone exposure enhances mast-cell inflammation in asthmatic airways despite inhaled corticosteroid therapy.
Publication TypeJournal Article
Year of Publication2010
AuthorsStenfors N, Bosson J, Helleday R, Behndig AF, Pourazar J, Törnqvist H, Kelly FJ, Frew AJ, Sandström T, Mudway IS, Blomberg A
JournalInhal Toxicol
Volume22
Issue2
Pagination133-9
Date Published2010 Feb
ISSN1091-7691
KeywordsAdministration, Inhalation, Adrenal Cortex Hormones, Adult, Asthma, Bronchoalveolar Lavage Fluid, Cell Count, Female, Forced Expiratory Flow Rates, Forced Expiratory Volume, Humans, Inflammation, Male, Mast Cells, Middle Aged, Oxidants, Photochemical, Ozone, Peroxidase, Respiratory Function Tests, Vital Capacity, Young Adult
Abstract

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.

DOI10.3109/08958370903005736
Alternate JournalInhal Toxicol
PubMed ID20044881