Centre for Molecular, Environmental, Genetic, and Analytical Epidemiology, University of Melbourne, Victoria, Australia.
Am J Respir Crit Care Med. 2013 Jan 1;187(1):42-8. doi: 10.1164/rccm.201205-0788OC. Epub 2012 Nov 15.
The contribution by asthma to the development of fixed airflow obstruction (AO) and the nature of its effect combined with active smoking and atopy remain unclear.
To investigate the prevalence and relative influence of lifetime asthma, active smoking, and atopy on fixed AO in middle age.
The population-based Tasmanian Longitudinal Health Study cohort born in 1961 (n = 8,583) and studied with prebronchodilator spirometry in 1968 was retraced (n = 7,312) and resurveyed (n = 5,729 responses) from 2002 to 2005. A sample enriched for asthma and chronic bronchitis underwent a further questionnaire, pre- and post-bronchodilator spirometry (n = 1,389), skin prick testing, lung volumes, and diffusing capacity measurements. Prevalence estimates were reweighted for sampling fractions. Multiple linear and logistic regression were used to assess the relevant associations.
Main effects and interactions between lifetime asthma, active smoking, and atopy as they relate to fixed AO were measured. The prevalence of fixed AO was 6.0% (95% confidence interval [CI], 4.5-7.5%). Its association with early-onset current clinical asthma was equivalent to a 33 pack-year history of smoking (odds ratio, 3.7; 95% CI, 1.5-9.3; P = 0.005), compared with a 24 pack-year history for late-onset current clinical asthma (odds ratio, 2.6; 95% CI, 1.03-6.5; P = 0.042). An interaction (multiplicative effect) was present between asthma and active smoking as it relates to the ratio of post-bronchodilator FEV(1)/FVC, but only among those with atopic sensitization.
Active smoking and current clinical asthma both contribute substantially to fixed AO in middle age, especially among those with atopy. The interaction between these factors provides another compelling reason for atopic individuals with current asthma who smoke to quit.
哮喘对固定气流阻塞(AO)的发展的贡献以及其与主动吸烟和特应性结合的性质尚不清楚。
研究一生中哮喘、主动吸烟和特应性对中年固定 AO 的患病率和相对影响。
基于人群的塔斯马尼亚纵向健康研究队列于 1961 年出生(n = 8583),并于 1968 年进行了支气管扩张剂前肺量测定(n = 7312),并于 2002 年至 2005 年进行了再调查(n = 5729 份回复)。一个哮喘和慢性支气管炎丰富的样本进行了进一步的问卷调查、支气管扩张剂前和后肺量测定(n = 1389)、皮肤点刺试验、肺容积和弥散量测量。对抽样分数进行了重新加权以获得患病率估计值。采用多元线性和逻辑回归来评估相关关联。
测量了一生中哮喘、主动吸烟和特应性之间的主要作用和相互作用,以及它们与固定 AO 的关系。固定 AO 的患病率为 6.0%(95%置信区间 [CI],4.5-7.5%)。它与早发性当前临床哮喘的关联与 33 包年吸烟史相当(比值比,3.7;95%CI,1.5-9.3;P = 0.005),而晚发性当前临床哮喘的 24 包年吸烟史(比值比,2.6;95%CI,1.03-6.5;P = 0.042)。在哮喘和主动吸烟与支气管扩张剂后 FEV1/FVC 比值的关系中存在相互作用(乘法效应),但仅存在于特应性敏感的人群中。
主动吸烟和当前临床哮喘都对中年固定 AO 有很大贡献,尤其是在特应性人群中。这些因素之间的相互作用为吸烟的特应性哮喘患者提供了另一个强烈的戒烟理由。