1 Department of Preventive and Social Medicine, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
2 Department of Psychology, University of Otago, Dunedin, New Zealand; and.
Am J Respir Crit Care Med. 2016 Aug 1;194(3):276-84. doi: 10.1164/rccm.201512-2492OC.
Life-course persistent asthma and tobacco smoking are risk factors for irreversible airflow obstruction. It is often assumed that smoking and asthma have additive or multiplicative effects on the risk for airflow obstruction, but this has not been demonstrated in prospective studies of children with persistent asthma.
To investigate the effects of smoking and asthma on the development of airflow obstruction in a population-based birth cohort followed to age 38 years.
Reports of childhood asthma from ages 9, 11, and 13 and self-reports of adult asthma at ages 32 and 38 years were used to define childhood-onset persistent asthma (n = 91), late-onset asthma (n = 93), asthma in remission (n = 85), and nonasthmatic (n = 572) phenotypes. Cumulative tobacco smoking histories and spirometry were obtained at ages 18, 21, 26, 32, and 38 years. Analyses were by generalized estimating equations adjusting for childhood spirometry, body mass index, age, and sex.
Smoking history and childhood-onset persistent asthma were both associated with lower FEV1/FVC ratios. Associations between smoking and FEV1/FVC ratios were different between asthma phenotypes (interaction P < 0.001). Smoking was associated with lower prebronchodilator and post-bronchodilator FEV1/FVC ratios among subjects without asthma and those with late-onset or remittent asthma, but smoking was not associated with lower FEV1/FVC ratios among those with childhood-onset persistent asthma.
Childhood-onset persistent asthma is associated with airflow obstruction by mid-adult life, but this does not seem to be made worse by tobacco smoking. We found no evidence that smoking and childhood-persistent asthma have additive or multiplicative effects on airflow obstruction.
终身性哮喘和吸烟是不可逆气流阻塞的危险因素。通常认为,吸烟和哮喘对气流阻塞的风险具有相加或相乘作用,但在持续性哮喘儿童的前瞻性研究中尚未得到证实。
在一项随访至 38 岁的基于人群的出生队列中,研究吸烟和哮喘对气流阻塞发展的影响。
使用 9、11 和 13 岁时的儿童哮喘报告以及 32 和 38 岁时的成人哮喘自我报告来定义儿童起病持续性哮喘(n=91)、迟发性哮喘(n=93)、哮喘缓解(n=85)和非哮喘(n=572)表型。在 18、21、26、32 和 38 岁时获取累积吸烟史和肺活量测定值。分析采用广义估计方程,调整儿童期肺活量、体重指数、年龄和性别。
吸烟史和儿童起病持续性哮喘均与较低的 FEV1/FVC 比值相关。吸烟与 FEV1/FVC 比值之间的关联在哮喘表型之间存在差异(交互 P<0.001)。在无哮喘、迟发性或缓解性哮喘患者中,吸烟与未使用支气管扩张剂和使用支气管扩张剂后的 FEV1/FVC 比值降低相关,但在儿童起病持续性哮喘患者中,吸烟与 FEV1/FVC 比值降低无关。
儿童起病持续性哮喘与中年时的气流阻塞相关,但吸烟似乎不会使病情恶化。我们没有发现证据表明吸烟和儿童持续性哮喘对气流阻塞具有相加或相乘作用。