Division of Pulmonary, Critical Care and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, NY.
Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY; Department of Pediatrics, Kravis Children's Hospital, Icahn School of Medicine at Mount Sinai, New York, NY.
J Allergy Clin Immunol. 2018 May;141(5):1880-1886. doi: 10.1016/j.jaci.2017.07.017. Epub 2017 Aug 8.
The impact of prenatal ambient air pollution on child asthma may be modified by maternal stress, child sex, and exposure dose and timing.
We prospectively examined associations between coexposure to prenatal particulate matter with an aerodynamic diameter of less than 2.5 microns (PM) and maternal stress and childhood asthma (n = 736).
Daily PM exposure during pregnancy was estimated using a validated satellite-based spatiotemporally resolved prediction model. Prenatal maternal negative life events (NLEs) were dichotomized around the median (high: NLE ≥ 3; low: NLE < 3). We used Bayesian distributed lag interaction models to identify sensitive windows for prenatal PM exposure on children's asthma by age 6 years, and determine effect modification by maternal stress and child sex.
Bayesian distributed lag interaction models identified a critical window of exposure (19-23 weeks' gestation, cumulative odds ratio, 1.15; 95% CI, 1.03-1.26; per interquartile range [1.7 μg/m] increase in prenatal PM level) during which children concomitantly exposed to prenatal PM and maternal stress had increased risk of asthma. No significant association was seen in children born to women reporting low prenatal stress. When examining modifying effects of prenatal stress and fetal sex, we found that boys born to mothers with higher prenatal stress were most vulnerable (19-21 weeks' gestation; cumulative odds ratio, 1.28; 95% CI, 1.15-1.41; per interquartile range increase in PM).
Prenatal PM exposure during sensitive windows is associated with increased risk of child asthma, especially in boys concurrently exposed to elevated maternal stress.
产前环境空气污染对儿童哮喘的影响可能会受到母体应激、儿童性别以及暴露剂量和时间的影响。
我们前瞻性地研究了产前细颗粒物(PM)和母体应激与儿童哮喘(n=736)之间的共暴露与儿童哮喘之间的相关性。
使用经过验证的基于卫星的时空分辨率预测模型来估计怀孕期间的每日 PM 暴露。将产前母体负性生活事件(NLEs)围绕中位数(高:NLE≥3;低:NLE<3)分为两类。我们使用贝叶斯分布式滞后交互模型,确定产前 PM 暴露对 6 岁儿童哮喘的敏感窗口,并确定母体应激和儿童性别对其的影响。
贝叶斯分布式滞后交互模型确定了暴露的关键窗口(19-23 周妊娠,累积优势比,1.15;95%置信区间,1.03-1.26;每增加 1.7μg/m 产前 PM 水平),在此期间,同时暴露于产前 PM 和母体应激的儿童哮喘风险增加。在报告产前压力较低的女性所生的儿童中,没有发现明显的关联。当检查产前应激和胎儿性别对影响的修饰作用时,我们发现,母体应激较高的母亲所生的男孩最易受影响(19-21 周妊娠;累积优势比,1.28;95%置信区间,1.15-1.41;每增加 1.7μg/m 产前 PM)。
在敏感窗口期间,产前 PM 暴露与儿童哮喘风险增加有关,尤其是在同时暴露于母体应激的男孩中。