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.
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.
Authors: Frank D Gilliland; Talat Islam; Kiros Berhane; W James Gauderman; Rob McConnell; Edward Avol; John M Peters Journal: Am J Respir Crit Care Med Date: 2006-09-14 Impact factor: 21.405
Authors: M H Brutsche; S H Downs; C Schindler; M W Gerbase; J Schwartz; M Frey; E W Russi; U Ackermann-Liebrich; P Leuenberger Journal: Thorax Date: 2006-05-02 Impact factor: 9.139