3 research outputs found

    Effects Of Nitrogen Dioxide On Allergic Airway Responses In Subjects With Asthma

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    Objective: We sought to determine whether nitrogen dioxide (NO2) can enhance airway inflammation after allergen challenge in asthmatic subjects. Methods: Fifteen house-dust-mite (HDM)-sensitive asthmatic subjects were exposed for 3 hours to filtered air or 0.4 ppm NO2, followed by inhalational challenge with HDM allergen. Markers of inflammation were measured in sputum at 6 hours and 26 hours after allergen challenge. Results: After exposure to NO2, eosinophil concentration decreased significantly in the 6-hour postallergen sputum. No significant NO2-related difference was observed for other variables. Conclusions: Our results suggest that, in most asthmatic individuals, multihour exposure to a high ambient concentration of NO2 does not enhance the inflammatory response to subsequent inhaled allergen as assessed by cell distribution in induced sputum. Because the decrease in airway eosinophils has been reported in previous animal studies, future research should be directed toward the mechanism of this effect

    Repeated Exposure to Ozone Increases Alveolar Macrophage Recruitment into Asthmatic Airways

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    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 × 104 cells/ml vs. 1.2 ± 0.8 × 104 cells/ml, p = 0.20), the concentration of alveolar macrophages did significantly increase in BAL after the MD exposure (19.9 ± 9.7 × 104 cells/ml after MD4 vs. 12.1 ± 6.4 × 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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