1 Allergy and Lung Health Unit, University of Melbourne, Melbourne, Victoria, Australia.
2 Institute for Breathing and Sleep, Heidelberg, Victoria, Australia.
Ann Am Thorac Soc. 2018 Sep;15(9):1057-1066. doi: 10.1513/AnnalsATS.201806-374OC.
Childhood risk factors for long-term lung health often coexist and their specific patterns may affect subsequent lung function differently.
To identify childhood risk factor profiles and their influence on lung function and chronic obstructive pulmonary disease (COPD) in middle age, and potential pathways.
Profiles of 11 childhood respiratory risk factors, documented at age 7, were identified in 8,352 participants from the Tasmanian Longitudinal Health Study using latent class analysis. We investigated associations between risk profiles and post-bronchodilator lung function and COPD at age 53, mediation by childhood lung function and adult asthma, and interaction with personal smoking.
Six risk profiles were identified: 1) unexposed or least exposed (49%); 2) parental smoking (21.5%); 3) allergy (10%); 4) frequent asthma, bronchitis (8.7%); 5) infrequent asthma, bronchitis (8.3%); and 6) frequent asthma, bronchitis, allergy (2.6%). Profile 6 was most strongly associated with lower forced expiratory volume in 1 second (FEV) (-261; 95% confidence interval, -373 to -148 ml); lower FEV/forced vital capacity (FVC) (-3.4; -4.8 to -1.9%) and increased COPD risk (odds ratio, 4.9; 2.1 to 11.0) at age 53. The effect of profile 6 on COPD was largely mediated by adult active asthma (62.5%) and reduced childhood lung function (26.5%). Profiles 2 and 4 had smaller adverse effects than profile 6. Notably, the effects of profiles 2 and 6 were synergistically stronger for smokers.
Profiles of childhood respiratory risk factors predict middle-age lung function levels and COPD risk. Specifically, children with frequent asthma attacks and allergies, especially if they also become adult smokers, are the most vulnerable group. Targeting active asthma in adulthood (i.e., a dominant mediator) and smoking (i.e., an effect modifier) may block causal pathways and lessen the effect of such established early-life exposures.
儿童时期的健康风险因素通常并存，其特定模式可能会对以后的肺功能产生不同的影响。
确定儿童时期的风险因素特征及其对中年肺功能和慢性阻塞性肺疾病（COPD）的影响，并探讨潜在的途径。
使用潜在类别分析，在塔斯马尼亚纵向健康研究中的 8352 名参与者中，确定了 11 种儿童时期呼吸道风险因素在 7 岁时的特征。我们研究了风险特征与支气管扩张剂后肺功能和 53 岁时 COPD 之间的关系，以及儿童肺功能和成年哮喘的中介作用，以及与个人吸烟的相互作用。
确定了 6 种风险特征：1）未暴露或暴露最少（49%）；2）父母吸烟（21.5%）；3）过敏（10%）；4）频繁的哮喘、支气管炎（8.7%）；5）不频繁的哮喘、支气管炎（8.3%）；6）频繁的哮喘、支气管炎、过敏（2.6%）。特征 6 与用力呼气量（FEV）降低（-261；95%置信区间，-373 至-148 ml）、FEV/FVC 降低（-3.4；-4.8 至-1.9%）和 COPD 风险增加（比值比，4.9；2.1 至 11.0）关系最密切。特征 6 对 COPD 的影响主要通过成年期活动性哮喘（62.5%）和儿童期肺功能下降（26.5%）来介导。特征 2 和 4 的不良影响小于特征 6。值得注意的是，特征 2 和 6 的影响对于吸烟者的协同作用更强。
儿童时期呼吸道风险因素的特征预测中年时的肺功能水平和 COPD 风险。特别是频繁发生哮喘发作和过敏的儿童，尤其是那些成年后成为吸烟者的儿童，是最脆弱的群体。针对成年期的活动性哮喘（即主要的中介因素）和吸烟（即效应修饰剂）可能阻断因果途径，减轻这些既定的早期暴露的影响。
