目的:本研究旨在调查妊娠期暴露于环境细颗粒物(PM2.5)及其成分对早产(PTB)患病率的影响。此外,我们试图确定易感暴露窗口。此外,我们探讨了血液分析和综合代谢小组在污染物暴露与PTB发病率之间的潜在中介作用.
方法:这项出生队列研究在2021年1月至2023年6月期间从福建省妇幼保健院招募了139名PTB结局的参与者和1713名对照。收集参与者首次怀孕期间的社会人口统计学特征和临床治疗数据。利用卫星遥感数据,通过组合地理统计模型估算了怀孕期间对污染物的暴露水平。分布滞后非线性模型用于评估怀孕期间污染物暴露与PTB患病率之间的关联。加权分位数回归用于确定与妊娠期PM2.5和PTB相关的关键成分。此外,进行了中介效应分析以评估血液分析的作用.代谢谱用于筛选与PTB相关的差异丰富的代谢物,并探索它们与空气污染物和PTB发生率的相对表达。
结果:调整潜在混杂变量后,PM2.5的每周平均敏感性窗为7-10,16-19和22-28周;无机硫酸盐为8-10和15-19周;硝酸盐为6-10和15-28周;铵(NH4+)为6-12和15-28周;有机物为7-9,18-20和22-36周.在混合暴露于PM2.5成分期间,关键成分是NH4+。在混合暴露于PM2.5成分中,NH4+成为一个关键的贡献者。调解分析的结果显示,血红蛋白发挥了中介作用,占环境污染物暴露与PTB患病率之间关联的21.53%。值得注意的是,未观察到其他变量的中介效应.此外,非靶向代谢组学鉴定出17种与PTB相关的代谢物.在这些因素中,磷酸氢盐可能影响代谢途径,如氧化磷酸化,影响PTB的风险。环境污染物和代谢物之间的相互作用,特别是通过氧化磷酸化途径,可能有助于PTB的发病率。
结论:证据表明,怀孕期间暴露于PM2.5及其成分是PTB的重要危险因素。值得注意的是,在怀孕期间确定了特定的每周污染物暴露窗口.在PM2.5成分中,在暴露于组分和PTB的混合物之间的关联分析中,NH4+表现出最显著的权重。此外,我们的中介分析显示,血红蛋白在妊娠期暴露于污染物与PTB患病率之间的关系中起部分中介作用.此外,孕妇血清代谢谱在早产组和对照组之间存在差异.值得注意的是,涉及磷酸氢盐和混合暴露于PM2.5组分的综合作用进一步促进了PTB的发展。氧化磷酸化途径可能在这种复杂的关联中起关键作用。
OBJECTIVE: This study aimed to investigate the influence of exposure to ambient fine particulate matter (PM2.5) and its components during pregnancy on the prevalence of preterm birth (PTB). Additionally, we sought to identify the susceptible exposure window. Furthermore, we explored the potential mediating role of blood analysis and a comprehensive metabolic panel in the association between pollutant exposure and PTB incidence.
METHODS: This birth cohort study recruited 139 participants with PTB outcomes and 1713 controls from Fujian Maternal and Child Health Hospital between January 2021 and June 2023. Sociodemographic characteristics and clinical treatment data during participants\' first pregnancies were collected. The exposure levels to
pollutants during pregnancy were estimated via a combined geographic-statistical model utilising satellite remote sensing data. The distributional lag nonlinear modelling was employed to assess associations between pollutant exposure during pregnancy and the prevalence of PTB. Weighted quantile regression was used to identify key components associated with PM2.5 and PTB during pregnancy. Additionally, a mediating effect analysis was conducted to evaluate the role of blood analysis. The metabolic profile was used to screen for differentially abundant metabolites associated with PTB and explore their relative expression in relation to air pollutants and PTB incidence.
RESULTS: Following the adjustment for potential confounding variables, the mean weekly susceptibility windows for PM2.5 were identified as 7-10, 16-19, and 22-28 weeks; 8-10, and 15-19 weeks for inorganic sulfate; 6-10, and 15-28 weeks for nitrate; 6-12, and 15-28 weeks for ammonium (NH4+); and 7-9, 18-20, and 22-36 weeks for organic matter. During mixed exposure to PM2.5 components, the key component is NH4+. In the mixed exposure to PM2.5 components, NH4+ emerged as a key contributor. The results of the mediation analysis revealed that haemoglobin played a mediating role, accounting for 21.53 % of the association between exposure to environmental
pollutants and the prevalence of PTB. It is noteworthy that, no mediating effects were observed for the other variables. Furthermore, non-targeted metabolomics identified 17 metabolites associated with PTB. Among these factors, hydrogen phosphate may impact metabolic pathways such as oxidative phosphorylation, influencing the risk of PTB. The interplay between environmental
pollutants and metabolites, particularly through oxidative phosphorylation pathways, may contribute to PTB incidence.
CONCLUSIONS: The evidence indicates that exposure to PM2.5 and its components during pregnancy were a significant risk factor for PTB. Notably, specific weekly exposure windows were identified for
pollutants during pregnancy. Among the PM2.5 components, NH4+ exhibited the most substantial weight in the association analysis between exposure to the mixture of components and PTB. Furthermore, our mediation analysis revealed that haemoglobin serves as a partial mediator in the relationship between exposure to
pollutants during pregnancy and the prevalence of PTB. Additionally, maternal serum metabolic profiles differed between the preterm and control groups. Notably, a combined effect involving hydrogen phosphate and mixed exposure to PM2.5 fractions further contributed to the development of PTB. Oxidative phosphorylation pathways may play pivotal roles in this intricate association.