Brief exposures to NO sub(2) augment the allergic inflammation in asthmatics

Exposure to high ambient levels of nitrogen dioxide (NO sub(2)) enhances the airway reaction in humans to allergen, measured as decreased pulmonary function. We tested whether this NO sub(2) effect is associated with an increased inflammatory response to allergen in the airways. To mimic real-life c...

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Bibliographic Details
Published inEnvironmental research Vol. 97; no. 1; pp. 58 - 66
Main Authors Barck, C, Lundahl, J, Hallden, G, Bylin, G
Format Journal Article
LanguageEnglish
Published 01.01.2005
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Summary:Exposure to high ambient levels of nitrogen dioxide (NO sub(2)) enhances the airway reaction in humans to allergen, measured as decreased pulmonary function. We tested whether this NO sub(2) effect is associated with an increased inflammatory response to allergen in the airways. To mimic real-life conditions, in which exposure to high ambient levels of NO sub(2) occurs only during short periods of time but often several times a day, we used a repeated-exposure model. On day 1, 18 subjects with allergic asthma were exposed, in randomized order, to purified air or to 500 mu g/m super(3) NO sub(2) for 15min, and on day 2 for 2x15min. Allergen was inhaled 3-4h after the NO sub(2) exposures on both days. Symptoms, pulmonary function, and inflammatory response in sputum and blood were measured daily. Eosinophil cationic protein in both sputum and blood increased more from day 1 to day 3 after NO sub(2)+allergen than after air+allergen, whereas eosinophil counts did not differ. The change in myeloperoxidase was significantly greater after NO sub(2)+allergen than after air+allergen in blood but not in sputum. This finding was not accompanied by raised levels of neutrophils in sputum and blood. Symptoms and pulmonary function were equally affected by NO sub(2)+allergen and air+allergen. We conclude that two to three brief exposures to ambient levels of NO sub(2) can prime circulating eosinophils and enhance the eosinophilic activity in sputum in response to inhaled allergen. This might be an important mechanism by which air pollutants amplify the inflammatory reactions in the airways.
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ISSN:0013-9351
DOI:10.1016/j.envres.2004.02.009