Arogbokun Knutson Olufunmilayo C, Luben Thomas J, Stingone Jeanette A, Engel Lawrence S, Martin Chantel L, Olshan Andrew F
Department of Health and Exercise Science, Morrison Family College of Health, University of St. Thomas, St. Paul, MN, United States.
United States Environmental Protection Agency, Office of Research and Development, Center for Public Health and Environmental Assessment, Research Triangle Park, NC, United States.
Am J Epidemiol. 2025 Mar 4;194(3):709-721. doi: 10.1093/aje/kwae253.
Air pollution may be a potential cause of congenital heart defects (CHDs), but racial disparities in this association are unexplored. We conducted a statewide population-based cohort study using North Carolina birth data from 2003 to 2015 (n = 1 225 285) to investigate the relationship between air pollution and CHDs (specifically pulmonary valve atresia/stenosis, tetralogy of Fallot [TOF], and atrioventricular septal defect [AVSD]). Maternal exposure to particulate matter ≤ 2.5 μm in diameter (PM2.5) and ozone during weeks 3 to 9 of pregnancy were estimated using the Environmental Protection Agency's Downscaler Model. Single- and co-pollutant log-binomial models were created for the entire population and stratified by race to investigate disparities. Positive associations between PM2.5 and CHDs were observed. An increasing concentration-response association was found for PM2.5 and TOF in adjusted, co-pollutant models (quartile 4 prevalence ratio: 1.46; 95% CI, 1.06-2.03). Differences in the effect of PM2.5 on CHD prevalence were seen in some models stratified by race, although clear exposure-prevalence gradients were not evident. Positive associations were also seen in adjusted, co-pollutant models of ozone and AVSD. Study results suggest that prenatal PM2.5 and ozone exposure may increase the prevalence of certain CHDs. A consistent pattern of differences in association by race/ethnicity was not apparent. This article is part of a Special Collection on Environmental Epidemiology.
空气污染可能是先天性心脏病(CHD)的一个潜在病因,但这种关联中的种族差异尚未得到探讨。我们利用北卡罗来纳州2003年至2015年的出生数据(n = 1225285)进行了一项全州范围的基于人群的队列研究,以调查空气污染与CHD(特别是肺动脉瓣闭锁/狭窄、法洛四联症[TOF]和房室间隔缺损[AVSD])之间的关系。使用美国环境保护局的降尺度模型估算了孕妇在怀孕第3至9周期间接触直径≤2.5μm的颗粒物(PM2.5)和臭氧的情况。为整个人口创建了单污染物和共污染物对数二项式模型,并按种族进行分层以调查差异。观察到PM2.5与CHD之间存在正相关。在调整后的共污染物模型中,发现PM2.5与TOF之间存在浓度 - 反应增加的关联(四分位数4患病率比:1.46;95%CI,1.06 - 2.03)。在一些按种族分层的模型中,观察到PM2.5对CHD患病率影响的差异,尽管明显的暴露 - 患病率梯度并不明显。在调整后的臭氧与AVSD的共污染物模型中也观察到正相关。研究结果表明,产前接触PM2.5和臭氧可能会增加某些CHD的患病率。种族/民族在关联方面的差异模式并不一致。本文是环境流行病学特刊的一部分。