重庆市孕产期PM2.5成分对子代先天性心脏病风险的共同影响

IF 7.3 2区环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES

Environmental Pollution Pub Date : 2025-08-11 DOI:10.1016/j.envpol.2025.126973

Yi Li , Xiao Zhang , Jie Zhang , Jun Liu , Linjin Di , Deqiang Mao , Zihao Wang , Yunyun Wu , Qunying Li , Xinzhi Xiang , Huadong Zhang , Qi Zhang

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引用次数: 0

摘要

虽然PM2.5暴露与先天性心脏病（CHD）之间的关联已被广泛报道，但组分特异性效应、关键暴露窗口期和多组分协同效应仍不清楚。本研究采用病例对照设计。在我们的研究中，我们评估了从重庆市出生缺陷监测系统收集的9152例孕妇孕前和妊娠早期PM2.5及其成分暴露浓度。采用多因素logistic回归分析PM2.5及其成分对子代冠心病患病率的影响。基于分位数的g计算也用于分析混合暴露于这些成分的风险。所有参与者在孕前和妊娠早期的PM2.5日均暴露量分别为31.26和32.59μg/m3。在单一污染模型中，黑碳（）和未形成物质与整体冠心病、室间隔缺损（SPD）和动脉导管未闭（PDA）风险显著相关。硫酸盐（）和有机物（）分别增加了孕前和妊娠早期PDA的风险。在前三个月，共暴露于PM2.5成分与冠心病总风险增加17% （OR = 1.17, 95% CI: 1.03-1.33）相关，SPD增加22% (OR = 1.22, 95% CI: 1.00-1.50)， PDA增加29% (OR = 1.29, 95% CI: 1.05-1.59)，其他冠心病亚型增加33% （OR = 1.33, 95% CI: 1.03-1.72）。在孕前期，PDA的风险增加38% （OR = 1.38, 95% CI: 1.07-1.78）。孕前和妊娠早期各成分综合影响的边际混合优势比（MM-ORs）高于PM2.5单独影响的边际混合优势比，突出了考虑成分混合的重要性。本研究表明，PM2.5的毒性可能是由其成分的协同作用驱动的。在孕前和妊娠前三个月可能通过不同的机制干扰后代心脏发育。这些结果提倡制定针对特定成分的空气质量法规，以降低冠心病风险。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Joint effects of PM2.5 components during periconception on offspring congenital heart disease risk in Chongqing, China

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Joint effects of PM2.5 components during periconception on offspring congenital heart disease risk in Chongqing, China

Although the association between particulate matter(PM_2.5) exposure and congenital heart disease (CHD) has been widely reported, the component-specific effects, critical exposure window period, and multicomponent synergistic effects remain unknown. This study used a case-control design. In our study, we assessed PM_2.5 and its components exposure concentrations during preconception and first trimester of 9152 pregnancies collected from the Chongqing Municipal Birth Defects Surveillance System. Multivariate logistic regression was used to analyse the effect of PM_2.5 and its components on offspring CHD prevalence. A quantile-based g-computation was also used to analyse the risk of mixed exposure to the components. For all participants, mean daily PM_2.5 exposure was 31.26 and 32.59 μg/m³ during preconception and first trimester, respectively. Black carbon (

B C

),and unspeciated matter

(U M)

were significantly associated with overall CHD, Septal Defects (SPD), and Patent Ductus Arteriosus (PDA) risk in the single-pollution model. Sulfates(

{SO}_{4}^{2 -}

), and organic matter (

O M

) specifically increased the risk of PDA during preconception and first-trimester, respectively. During the first trimester, co-exposure to PM_2.5 components was associated with a 17 % increase (OR = 1.17, 95 % CI: 1.03–1.33) in the overall risk of CHD, a 22 % increase (OR = 1.22, 95 % CI: 1.00–1.50) in SPD, a 29 % increase (OR = 1.29, 95 % CI: 1.05–1.59) in PDA, and a 33 % increase (OR = 1.33, 95 % CI: 1.03–1.72) in other CHD subtypes. In the preconception period, the risk of PDA increased by 38 % (OR = 1.38, 95 % CI: 1.07–1.78). The Marginal Mixture Odds Ratios (MM-ORs) for the combined effects of components during both the preconception and first-trimester periods were higher than those for PM_2.5 alone, highlighting the importance of considering component mixtures. This study suggests that the toxicity of PM_2.5 may be driven by the synergistic effects of its components.

B C

{S O}_{4}^{2 -}

O M

, and

U M

may interfere with offspring cardiac development through distinct mechanisms during both preconception and the first trimester of pregnancy. These results advocate for component-specific air quality regulations to mitigate CHD risk.

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来源期刊

Environmental Pollution 环境科学-环境科学

CiteScore

16.00

自引率

6.70%

发文量

2082

审稿时长

2.9 months

期刊介绍： Environmental Pollution is an international peer-reviewed journal that publishes high-quality research papers and review articles covering all aspects of environmental pollution and its impacts on ecosystems and human health. Subject areas include, but are not limited to: • Sources and occurrences of pollutants that are clearly defined and measured in environmental compartments, food and food-related items, and human bodies; • Interlinks between contaminant exposure and biological, ecological, and human health effects, including those of climate change; • Contaminants of emerging concerns (including but not limited to antibiotic resistant microorganisms or genes, microplastics/nanoplastics, electronic wastes, light, and noise) and/or their biological, ecological, or human health effects; • Laboratory and field studies on the remediation/mitigation of environmental pollution via new techniques and with clear links to biological, ecological, or human health effects; • Modeling of pollution processes, patterns, or trends that is of clear environmental and/or human health interest; • New techniques that measure and examine environmental occurrences, transport, behavior, and effects of pollutants within the environment or the laboratory, provided that they can be clearly used to address problems within regional or global environmental compartments.