Kannan Jennifer A, Brokamp Cole, Bernstein David I, LeMasters Grace K, Hershey Gurjit K Khurana, Villareal Manuel S, Lockey James E, Ryan Patrick H
Division of Immunology, Allergy and Rheumatology, Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Division of Biostatistics and Epidemiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
Pediatr Allergy Immunol Pulmonol. 2017 Mar 1;30(1):31-38. doi: 10.1089/ped.2016.0681.
The objective of this study was to determine whether atopy and other clinical and environmental variables predict the risk of childhood habitual snoring (HS) in a birth cohort born to atopic parents. Participants completed clinical evaluations and questionnaires at ages 1-4 and age 7. HS was defined as snoring ≥3 nights/week. Traffic-related air pollution (TRAP) exposure was estimated using land-use regression. The association between early (≤age 4) and current (age 7) allergic disease, environmental exposures, and snoring at age 7 was examined using adjusted logistic regression. Of the 609 children analyzed the prevalence of HS at age 7 was 21%. Early tobacco smoke exposure [environmental tobacco smoke (ETS)] [odds ratio (OR) 1.79, 95% CI (confidence interval) 1.12-2.84], rhinitis (OR 1.74, 95% CI 1.06-2.92), wheezing (OR 1.63, 95% CI 1.05-2.53), maternal HS (OR 2.08, 95% CI 1.36-3.18), and paternal HS (OR 1.83, 95% CI 1.14-3.00) were significantly associated with HS at age 7. Current TRAP (OR 1.93, 95% CI 1.13-3.26), respiratory infections (OR 1.16, 95% 1.03-1.35), maternal HS (OR 2.86, 95% CI 1.69-4.84), and paternal HS (OR 3.01, 95% CI 1.82-5.09) were significantly associated with HS at age 7. To our knowledge, this is the largest birth cohort examining longitudinal predictors of snoring in children born to atopic parents. Parental HS was the only variable consistently associated with childhood HS from ages 1 to 7. Early rhinitis, early ETS exposure, and concurrent traffic pollution exposure increased the risk of HS at age 7, while aeroallergen sensitization did not. Children with these characteristics should be considered for screening of sleep disorders.
本研究的目的是确定特应性以及其他临床和环境变量是否能预测父母为特应性的出生队列中儿童习惯性打鼾(HS)的风险。参与者在1至4岁和7岁时完成了临床评估和问卷调查。HS被定义为每周打鼾≥3晚。使用土地利用回归估计与交通相关的空气污染(TRAP)暴露情况。采用校正逻辑回归分析7岁时早期(≤4岁)和当前(7岁)过敏性疾病、环境暴露与打鼾之间的关联。在分析的609名儿童中,7岁时HS的患病率为21%。早期接触烟草烟雾[环境烟草烟雾(ETS)][比值比(OR)1.79,95%置信区间(CI)1.12 - 2.84]、鼻炎(OR 1.74,95% CI 1.06 - 2.92)、喘息(OR 1.63,95% CI 1.05 - 2.53)、母亲打鼾(OR 2.08,95% CI 1.36 - 3.18)和父亲打鼾(OR 1.83,95% CI 1.14 - 3.00)与7岁时的HS显著相关。当前的TRAP(OR 1.93,95% CI 1.13 - 3.26)、呼吸道感染(OR 1.16,95% CI 1.03 - 1.35)、母亲打鼾(OR 2.86,95% CI 1.69 - 4.84)和父亲打鼾(OR 3.01,95% CI 1.82 - 5.09)与7岁时的HS显著相关。据我们所知,这是研究父母为特应性的儿童打鼾纵向预测因素的最大出生队列。父母打鼾是1至7岁儿童HS唯一始终相关的变量。早期鼻炎、早期ETS暴露和同时期的交通污染暴露增加了7岁时HS的风险,而吸入性变应原致敏则不然。具有这些特征的儿童应考虑进行睡眠障碍筛查。