Division of Pulmonary, Critical Care, and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, NY.
Department of Population Health, Science and Policy, Institute for Translational Epidemiology, Icahn School of Medicine at Mount Sinai, New York, NY.
Chest. 2018 Mar;153(3):630-637. doi: 10.1016/j.chest.2017.10.003. Epub 2017 Oct 14.
It has been difficult to determine the individual impact of prenatal and postnatal tobacco smoke exposure (TSE) on childhood lung function, as children are often exposed to both.
The goal of this study was to determine the association between current TSE and airflow obstruction while adjusting for self-reported prenatal TSE.
Children aged 6 to 11 years who participated in the National Health and Nutrition Examination Survey (2007-2012) who had serum cotinine levels measured and spirometry performed were included. Logistic regression was used to determine the association between log-transformed serum cotinine level and airflow obstruction while adjusting for confounders; the analysis was then stratified according to asthma status. The final model included both log-transformed serum cotinine level and prenatal exposure as covariates.
The sample consisted of 2,070 children; 9.6% had airflow obstruction. The association between cotinine levels and airflow obstruction was significant in an unadjusted analysis (OR, 1.12 [95% CI, 1.02-1.23]). In the multivariate analysis with both exposures included as covariates, serum cotinine level was not significantly associated with airflow obstruction (OR, 1.07 [95% CI, 0.94-1.21]), and no association was seen in children with asthma and nonasthmatic children. Prenatal smoking was associated with airflow obstruction in children with asthma (OR, 2.51 [95% CI, 1.08-5.79]) but not in nonasthmatic children (OR, 1.08 [95% CI, 0.53-2.18]).
Current TSE was not independently associated with airflow obstruction in school-aged children. Prenatal TSE was associated with airflow obstruction in children with asthma. Repeated studies into potential mediators and confounders of this relationship are needed.
由于儿童通常同时受到产前和产后烟草烟雾暴露（TSE）的影响，因此很难确定两者对儿童肺功能的个别影响。
本研究旨在确定当前 TSE 与气流阻塞之间的关联，同时调整自我报告的产前 TSE。
纳入了参加 2007-2012 年全国健康和营养检查调查（NHANES）且测量了血清可替宁水平并进行了肺功能检查的 6 至 11 岁儿童。使用逻辑回归来确定在调整混杂因素后，血清可替宁水平与气流阻塞之间的关联；然后根据哮喘状态对分析进行分层。最终模型将血清可替宁水平的对数变换和产前暴露作为协变量。
样本包括 2070 名儿童；9.6%有气流阻塞。在未调整分析中，可替宁水平与气流阻塞之间存在显著关联（OR，1.12[95%CI，1.02-1.23]）。在同时包含两种暴露作为协变量的多元分析中，血清可替宁水平与气流阻塞无显著关联（OR，1.07[95%CI，0.94-1.21]），在哮喘和非哮喘儿童中均未发现关联。产前吸烟与哮喘儿童的气流阻塞有关（OR，2.51[95%CI，1.08-5.79]），但与非哮喘儿童无关（OR，1.08[95%CI，0.53-2.18]）。
当前 TSE 与学龄儿童的气流阻塞无关。产前 TSE 与哮喘儿童的气流阻塞有关。需要进一步研究该关系的潜在介质和混杂因素。
