Hazlehurst Marnie F, Carroll Kecia N, Loftus Christine T, Szpiro Adam A, Moore Paul E, Kaufman Joel D, Kirwa Kipruto, LeWinn Kaja Z, Bush Nicole R, Sathyanarayana Sheela, Tylavsky Frances A, Barrett Emily S, Nguyen Ruby H N, Karr Catherine J
Department of Epidemiology, University of Washington, Box 357236, Seattle WA, USA 98195-7236.
Division of General Pediatrics, Department of Pediatrics, Vanderbilt University Medical Center, 2146 Belcourt Avenue, Nashville TN, USA, 37212.
Environ Epidemiol. 2021 Apr;5(2). doi: 10.1097/ee9.0000000000000130.
Increasingly studies suggest prenatal exposure to air pollution may increase risk of childhood asthma. Few studies have investigated exposure during specific fetal pulmonary developmental windows.
To assess associations between prenatal fine particulate matter exposure and asthma at age 4.
This study included mother-child dyads from two pregnancy cohorts-CANDLE and TIDES-within the ECHO-PATHWAYS consortium (births in 2007-2013). Three child asthma outcomes were parent-reported: ever asthma, current asthma, and current wheeze. Fine particulate matter (PM) exposures during the pseudoglandular (5-16 weeks gestation), canalicular (16-24 weeks gestation), saccular (24-36 weeks gestation), and alveolar (36+ weeks gestation) phases of fetal lung development were estimated using a national spatiotemporal model. We estimated associations with Poisson regression with robust standard errors, and adjusted for child, maternal, and neighborhood factors.
Children (n=1469) were on average 4.3 (standard deviation 0.5) years old, 49% were male, and 11.7% had ever asthma; 46% of women identified as black and 53% had at least a college/technical school degree. A 2 μg/m higher PM exposure during the saccular phase was associated with 1.29 times higher risk of ever asthma (95% CI: 1.06-1.58). A similar association was observed with current asthma (RR 1.27, 95% CI: 1.04-1.54), but not current wheeze (RR 1.11, 95% CI: 0.92-1.33). Effect estimates for associations during other developmental windows had confidence intervals that included the null.
Later phases of prenatal lung development may be particularly sensitive to the developmental toxicity of PM.
越来越多的研究表明，产前暴露于空气污染中可能会增加儿童患哮喘的风险。很少有研究调查过在特定胎儿肺部发育窗口期的暴露情况。
评估产前细颗粒物暴露与4岁时哮喘之间的关联。
本研究纳入了ECHO-PATHWAYS联盟中两个妊娠队列（CANDLE和TIDES）的母婴对子（2007 - 2013年出生）。儿童哮喘的三个结局由家长报告：曾患哮喘、当前哮喘和当前喘息。使用国家时空模型估计胎儿肺发育的假腺期（妊娠5 - 16周）、小管期（妊娠16 - 24周）、囊泡期（妊娠24 - 36周）和肺泡期（妊娠36周及以后）的细颗粒物（PM）暴露情况。我们使用稳健标准误的泊松回归估计关联，并对儿童、母亲和邻里因素进行了调整。
儿童（n = 1469）平均年龄为4.3岁（标准差0.5），49%为男性，11.7%曾患哮喘；46%的女性为黑人，53%至少拥有大学/技术学校学位。囊泡期PM暴露每增加2 μg/m³，曾患哮喘的风险高1.29倍（95%置信区间：1.06 - 1.58）。当前哮喘也观察到类似关联（风险比1.27，95%置信区间：1.04 - 1.54），但当前喘息未观察到（风险比1.11，95%置信区间：0.92 - 1.33）。其他发育窗口期关联的效应估计值的置信区间包含无效值。
产前肺部发育的后期阶段可能对PM的发育毒性特别敏感。
