PDF(Pubmed)
Abstract：
BACKGROUND: Prenatal air pollution exposure has been associated with individual inflammatory, cardiovascular, and metabolic biomarkers in mothers and neonates. However, studies of air pollution and a comprehensive panel of biomarkers across maternal and cord blood samples remain limited. Few studies used data-driven methods to identify biomarker groupings that converge biomarkers from multiple biological pathways. This study aims to investigate the impacts of prenatal air pollution on groups of biomarkers in maternal and cord blood samples.
METHODS: In the Maternal And Developmental Risks from Environmental and Social Stressors (MADRES) cohort, 87 biomarkers were quantified from 45 trimester 1 maternal blood and 55 cord blood samples. Pregnancy and trimester 1-averaged concentrations of particulate matter ≤2.5 μm and ≤10 μm in diameter (PM2.5 and PM10), nitrogen dioxide (NO2), and ozone (O3) were estimated, using inverse distance squared weighted spatial interpolation from regulatory air monitoring stations. Traffic-related NOx was assessed using California Line Source Dispersion Model: freeway/highway roads, non-freeway major roads, non-freeway minor roads, and their sum as total NOx. Elastic Net (EN) regression within the rexposome R package was used to group biomarkers and assess their associations with air pollution.
RESULTS: In maternal samples, trimester 1-averaged PM10 was associated with elevated inflammation biomarkers and lowered cardiovascular biomarkers. NO2 exhibited positive associations with cardiovascular and inflammation markers. O3 was inversely associated with inflammation, metabolic, and cardiovascular biomarkers. In cord blood, pregnancy-averaged PM2.5 was associated with higher cardiovascular biomarkers and lower metabolic biomarkers. PM10 was associated with lower inflammation and higher cardiovascular biomarkers. Total and major road NOx was associated with lower cardiovascular biomarkers.
CONCLUSIONS: Prenatal air pollution exposure was associated with changes in biomarkers related to inflammation, cardiovascular, metabolic, cancer, and neurological function in both mothers and neonates. This study shed light on mechanisms by which air pollution can influence biological function during pregnancy.
METHODS: In the Maternal And Developmental Risks from Environmental and Social Stressors (MADRES) cohort, 87 biomarkers were quantified from 45 trimester 1 maternal blood and 55 cord blood samples. Pregnancy and trimester 1-averaged concentrations of particulate matter ≤2.5 μm and ≤10 μm in diameter (PM2.5 and PM10), nitrogen dioxide (NO2), and ozone (O3) were estimated, using inverse distance squared weighted spatial interpolation from regulatory air monitoring stations. Traffic-related NOx was assessed using California Line Source Dispersion Model: freeway/highway roads, non-freeway major roads, non-freeway minor roads, and their sum as total NOx. Elastic Net (EN) regression within the rexposome R package was used to group biomarkers and assess their associations with air pollution.
RESULTS: In maternal samples, trimester 1-averaged PM10 was associated with elevated inflammation biomarkers and lowered cardiovascular biomarkers. NO2 exhibited positive associations with cardiovascular and inflammation markers. O3 was inversely associated with inflammation, metabolic, and cardiovascular biomarkers. In cord blood, pregnancy-averaged PM2.5 was associated with higher cardiovascular biomarkers and lower metabolic biomarkers. PM10 was associated with lower inflammation and higher cardiovascular biomarkers. Total and major road NOx was associated with lower cardiovascular biomarkers.
CONCLUSIONS: Prenatal air pollution exposure was associated with changes in biomarkers related to inflammation, cardiovascular, metabolic, cancer, and neurological function in both mothers and neonates. This study shed light on mechanisms by which air pollution can influence biological function during pregnancy.
摘要：
背景：产前空气污染暴露与个体炎症有关，心血管,以及母亲和新生儿的代谢生物标志物。然而,关于空气污染的研究以及跨母体和脐带血样本的全面生物标志物组的研究仍然有限.很少有研究使用数据驱动的方法来识别融合来自多个生物途径的生物标志物的生物标志物分组。这项研究旨在调查产前空气污染对母体和脐带血样本中生物标志物组的影响。
方法：在来自环境和社会压力源（MADRES）的孕产妇和发育风险队列中，从45个三个月1日的母体血液和55个脐带血样品中量化了87个生物标志物。妊娠和妊娠1个月平均颗粒物浓度直径≤2.5μm和≤10μm（PM2.5和PM10），二氧化氮(NO2),和臭氧(O3)进行了估算，使用来自管制空气监测站的反距离平方加权空间插值。使用加利福尼亚线源分散模型评估与交通相关的NOx：高速公路/高速公路，非高速公路主要道路，非高速公路小路,以及它们的总和作为总NOx。使用rexposomeR包中的ElasticNet（EN）回归对生物标志物进行分组，并评估其与空气污染的关联。
结果：在母体样本中，妊娠1个月平均PM10与炎症生物标志物升高和心血管生物标志物降低相关.NO2与心血管和炎症标志物呈正相关。O3与炎症呈负相关，新陈代谢，和心血管生物标志物。在脐带血中，妊娠平均PM2.5与较高的心血管生物标志物和较低的代谢生物标志物相关.PM10与较低的炎症和较高的心血管生物标志物相关。总道路和主要道路NOx与较低的心血管生物标志物相关。
结论：产前空气污染暴露与炎症相关生物标志物的变化有关，心血管,新陈代谢，癌症,母亲和新生儿的神经功能。这项研究揭示了空气污染可能影响怀孕期间生物学功能的机制。
方法：在来自环境和社会压力源（MADRES）的孕产妇和发育风险队列中，从45个三个月1日的母体血液和55个脐带血样品中量化了87个生物标志物。妊娠和妊娠1个月平均颗粒物浓度直径≤2.5μm和≤10μm（PM2.5和PM10），二氧化氮(NO2),和臭氧(O3)进行了估算，使用来自管制空气监测站的反距离平方加权空间插值。使用加利福尼亚线源分散模型评估与交通相关的NOx：高速公路/高速公路，非高速公路主要道路，非高速公路小路,以及它们的总和作为总NOx。使用rexposomeR包中的ElasticNet（EN）回归对生物标志物进行分组，并评估其与空气污染的关联。
结果：在母体样本中，妊娠1个月平均PM10与炎症生物标志物升高和心血管生物标志物降低相关.NO2与心血管和炎症标志物呈正相关。O3与炎症呈负相关，新陈代谢，和心血管生物标志物。在脐带血中，妊娠平均PM2.5与较高的心血管生物标志物和较低的代谢生物标志物相关.PM10与较低的炎症和较高的心血管生物标志物相关。总道路和主要道路NOx与较低的心血管生物标志物相关。
结论：产前空气污染暴露与炎症相关生物标志物的变化有关，心血管,新陈代谢，癌症,母亲和新生儿的神经功能。这项研究揭示了空气污染可能影响怀孕期间生物学功能的机制。
