Background: Passive smoking is widespread, and environmental tobacco smoke contains many potent respiratory irritants. This analysis aimed to estimate the effect of passive smoking on respiratory symptoms, bronchial responsiveness, lung function, and total serum IgE in the European Community Respiratory Health Survey. Methods: This analysis included data from 7882 adults (age 20-48 years) who had never smoked, from 36 centres in 16 countries. Information on passive smoking, respiratory symptoms, asthma, and allergic rhinitis was gathered through a structured interview. Spirometry and methacholine challenge were carried out, and total and specific IgE were measured. The effect of passive smoking was estimated by means of logistic and multiple linear regression for each country and combined across countries by random-effects meta-analysis. Findings: In 12 of the 36 centres, more than half the participants were regularly involuntarily exposed to tobacco smoke. The prevalence of passive smoking in the workplace varied from 2.5% in Uppsala, Sweden, to 53.8% in Galdakao, Spain. Passive smoking was significantly associated with nocturnal chest tightness (odds ratio 1.28 [95% CI 1.02 to 1.60]), nocturnal breathlessness (1.30 [1.01 to 1.67]), breathlessness after activity (1.25 [1.07 to 1.47]), and increased bronchial responsiveness (effect -0.18 [-0.30 to -0.05]). Passive smoking in the workplace was significantly associated with all types of respiratory symptoms and current asthma (odds ratio 1.90 [95% CI 0.90 to 2.88]). No significant association was found between passive smoking and total serum IgE. Interpretation: Passive smoking is common but the prevalence varies widely between different countries. Passive smoking increased the likelihood of experiencing respiratory symptoms and was associated with increased bronchial responsiveness. Decreasing involuntary exposure to tobacco smoke in the community, especially in workplaces, is likely to improve respiratory health.
Bibliographical noteFunding Information:
The coordination of this work was supported by the European Commission. We thank Colette Baya and Manuel Hallen for their help during the study and K Vuylsteek and the members of the COMAC for their support. The following grants helped to fund the local studies: Allen and Hanbury's, (Australia); Belgian Science Policy Office, National Fund for Scientific Research (Belgium); Estonian Scientific Foundation (grant 1088), Glaxo Wellcome (Estonia); Ministere de la Santé, Glaxo France, Institut Pneumologique d'Aquitaine, Contrat de Plan Etat-Région Languedoc-Rousillon, CNMATS, CNMRT (90MR/10, 91AF/6), Ministre delegué de la santé, RNSP (France); GSF, and the Bundesminister für Forschung und Technologie, Bonn (Germany); Ministero dell'Università e della Ricerca Scientifica e Tecnologica, CNR, Regione Veneto grant RSF number 381/05·93 (Italy); Asthma Foundation of New Zealand, Lotteries Grant Board, Health Research Council of New Zealand (New Zealand); Norwegian Research Council project number 101422/310 (Norway); Ministero Sanidad y Consumo FIS grants 91/0016060/00E-05E, 92/0319, 93/0393, Hospital General de Albacete, Hospital General Juan Ramón Jiménez, Consejeria de Sanidad Principado de Asturias (Spain); Swedish Heart Lung Foundation, Swedish Medical Research Council, Swedish Association against Asthma and Allergy (Sweden); Swiss National Science Foundation grant 4026–28099 (Switzerland); National Asthma Campaign, British Lung Foundation, Department of Health, South Thames Regional Health Authority (UK); United States Department of Health, Education and Welfare Public Health Service Grant 2 S07 RR05521-28 (USA).