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Repeated exposure to ozone increases alveolar macrophage recruitment into asthmatic airways
Journal article   Peer reviewed

Repeated exposure to ozone increases alveolar macrophage recruitment into asthmatic airways

M Arjomandi, A Witten, E Abbritti, K Reintjes, I Schmidlin, W Zhai, Colin Solomon and J Balmes
American Journal of Respiratory and Critical Care Medicine, Vol.172(4), pp.427-432
2005
url
https://doi.org/10.1164/rccm.200502-272OCView
Published Version

Abstract

Cardiovascular Medicine and Haematology airway inflammation alveolar macrophage asthma multiday exposure ozone
Rationale: Repeated, short-term exposures to ozone (O3) lead to attenuation of the acute lung function and airway inflammatory responses seen after a single exposure in healthy subjects, but it is unclear whether these acute responses also attenuate in subjects with asthma. Objective: To address this question by exposing 14 subjects with asthma to 0.2 ppm O3 for either 4 hours on a single day or 4 hours on 4 consecutive days (multiday [MD]). At least 3 weeks later, subjects underwent the alternate exposure. Methods: Spirometry was performed immediately pre- and postexposure and bronchoalveolar lavage (BAL) was obtained 18 hours after each exposure. Main Results: The decrease in FEV1 was greatest across Day 2 of the MD (MD2) exposure and then gradually declined on successive days of the MD exposure (mean ± SD decrease in FEV1 of 25.4 ± 18.0% across MD2 compared with 4.2 ± 6.5% across MD4). Respiratory symptoms followed a similar pattern to that of FEV1. Although the concentration of neutrophils in BAL after the MD4 exposure was not significantly different from that after the single-day exposure (1.7 ± 1.3 x 104 cells/ml vs. 1.2 ± 0.8 x 104 cells/ml, p = 0.20), the concentration of alveolar macrophages did significantly increase in BAL after the MD exposure (19.9 ± 9.7 x 104 cells/ml after MD4 vs. 12.1 ± 6.4 x 104 cells/ml after the single day). Conclusions: Alveolar macrophages are recruited to the airways of subjects with asthma with repeated short-term exposures to O3, suggesting a possible role for these cells in the chronic response to oxidant-induced injury.

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