Thorax · 1997
Smoking and bronchial responsiveness in nonatopic and atopic young adults. Spanish Group of the European Study of Asthma.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Sunyer J, Antó J M, Kogevinas M, Soriano J B, Tobias A, Muñoz A
Аннотация
BACKGROUND: Smoking may influence the response of the lungs to other inhaled substances. A study was undertaken to assess the effect of the interaction between smoking and the immunoresponse to common aeroallergens (atopy) on bronchial responsiveness.
METHODS: A random sample was selected from the general population census of five areas of Spain (Albacete, Barcelona, Galdakao, Huelva, and Oviedo). A total of 1169 (35%) subjects completed a face-to-face respiratory questionnaire, a methacholine bronchial responsiveness challenge, and underwent measurements of total and specific serum IgE levels to mites, pets and moulds. A survival model (Weibull) was used to examine the methacholine dose-response relation, adjusting for bronchial obstruction.
RESULTS: Smokers showed greater bronchial responsiveness than never smokers (p < 0.05) at any dose of methacholine, but only among non-atopic individuals. Atopy had a large effect on responsiveness at low levels of methacholine, but smoking did not increase responsiveness in atopic subjects. There were no differences in intensity or cessation of smoking between atopic and non-atopic subjects, suggesting that smoking self-selection does not fully explain these results.
CONCLUSIONS: The association between smoking and bronchial responsiveness varies with atopy, which may be explained by different immunological and/or inflammatory effects of smoking on atopy.
METHODS: A random sample was selected from the general population census of five areas of Spain (Albacete, Barcelona, Galdakao, Huelva, and Oviedo). A total of 1169 (35%) subjects completed a face-to-face respiratory questionnaire, a methacholine bronchial responsiveness challenge, and underwent measurements of total and specific serum IgE levels to mites, pets and moulds. A survival model (Weibull) was used to examine the methacholine dose-response relation, adjusting for bronchial obstruction.
RESULTS: Smokers showed greater bronchial responsiveness than never smokers (p < 0.05) at any dose of methacholine, but only among non-atopic individuals. Atopy had a large effect on responsiveness at low levels of methacholine, but smoking did not increase responsiveness in atopic subjects. There were no differences in intensity or cessation of smoking between atopic and non-atopic subjects, suggesting that smoking self-selection does not fully explain these results.
CONCLUSIONS: The association between smoking and bronchial responsiveness varies with atopy, which may be explained by different immunological and/or inflammatory effects of smoking on atopy.