Published ahead of print on July 14, 2005, doi:10.1164/rccm.200503-323OC
© 2005 American Thoracic Society doi: 10.1164/rccm.200503-323OC An Increase in Bronchial Responsiveness Is Associated with Continuing or Restarting SmokingDepartment of Public Health Sciences, King's College London, London, United Kingdom; Institute of Social and Preventive Medicine, University of Basel, Basel, Switzerland; Medical Research Institute (IMIM) and Universitat Pompeu Fabra (UPF), Barcelona, Spain; Division of Respiratory Diseases, IRCCS "San Matteo" Hospital, University of Pavia, Pavia, Italy; University of Verona, Department of Medicine and Public Health, Division of Epidemiology and Statistics, Verona, Italy; Department Allergy, Respiratory Medicine and Sleep, University Hospital (E7), Reykjavik, Iceland; Institute of Epidemiology, GSF—National Research Center for Environment and Health, Neuherberg, Germany; Respiratory Medicine and Allergology, University of Uppsala, Uppsala, Sweden; Keck School of Medicine, University of Southern California, Los Angeles, California; INSERM—The French Institute of Health and Medical Research, Epidemiology, Faculty of Medicine, Paris, France; University of Groningen, Department Epidemiology and Bioinformatics, University Medical Center Groningen, Groningen, The Netherlands; and Department of Thoracic Medicine, Haukeland Hospital, Bergen, Norway Correspondence and requests for reprints should be addressed to Professor S. Chinn, Department of Public Health Sciences, 5th floor Capital House, 42 Weston Street, London SE1 3QD, UK. E-mail: sue.chinn{at}kcl.ac.uk Rationale: Bronchial responsiveness (BHR) has been found to be associated with smoking, atopy, and lower lung function in cross-sectional studies, but there is little information on determinants of change in adults. Objectives: To analyze change in bronchial responsiveness in an international longitudinal community study. Methods: The study was performed in 3,993 participants in the European Community Respiratory Health Survey who had bronchial responsiveness measured in 1991–1993, when aged 20 to 44 yr, and in 1998–2002. Measurements: Bronchial responsiveness was assessed by methacholine challenge. Serum samples were tested for total IgE, and for specific IgE to four common allergens. Smoking information was obtained from detailed administered questionnaires. Change in bronchial responsiveness was analyzed by change in IgE sensitization, smoking, and lung function, with tests of interaction terms with age and sex. Main Results: Continuing and restarting smokers had increasing bronchial responsiveness, approximately equivalent to a mean reduction in PD20 of 0.68 and 0.75 doubling doses, respectively, over 10 yr, in addition to a small increase explained by decline in FEV1. No other risk factor for change in bronchial responsiveness was identified. Conclusions: Smoking is a risk factor for increasing bronchial responsiveness over and above the effect of decreasing lung function. Neither baseline IgE sensitization nor change in sensitization was shown to be a risk factor for increasing BHR, the latter possibly due to little overall increase or decrease in sensitization.
Key Words: asthma • atopy • bronchial hyperreactivity • immunoglobulin E • pulmonary disease, chronic obstructive This article has been cited by other articles:
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