Search

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 (PM 2.5 and PM 10 ), nitrogen dioxide (NO 2 ), and ozone (O 3 ) were estimated, using inverse distance squared weighted spatial interpolation from regulatory air monitoring stations. Traffic-related NO x 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 PM 10 was associated with elevated inflammation biomarkers and lowered cardiovascular biomarkers. NO 2 exhibited positive associations with cardiovascular and inflammation markers. O 3 was inversely associated with inflammation, metabolic, and cardiovascular biomarkers. In cord blood, pregnancy-averaged PM 2.5 was associated with higher cardiovascular biomarkers and lower metabolic biomarkers. PM 10 was associated with lower inflammation and higher cardiovascular biomarkers. Total and major road NOx was associated with lower cardiovascular biomarkers., Conclusion: 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., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Background: Air pollution has been associated with gestational hypertension (GH) and preeclampsia, but susceptible windows of exposure and potential vulnerability by comorbidities, such as prenatal depression, remain unclear., Methods: We ascertained GH and preeclampsia cases in a prospective pregnancy cohort in Los Angeles, CA. Daily levels of ambient particulate matters (with a diameter of ≤10 μm [PM 10 ] or ≤2.5 μm [PM 2.5 ]), nitrogen dioxide, and ozone were averaged for each week from 12 weeks preconception to 20 gestational weeks. We used distributed lag models to identify susceptible exposure windows, adjusting for potential confounders. Analyses were additionally stratified by probable prenatal depression to explore population vulnerability., Results: Among 619 participants, 60 developed preeclampsia and 42 developed GH. We identified a susceptible window for exposure to PM 2.5 from 1 week preconception to 11 weeks postconception: higher exposure (5 µg/m 3 ) within this window was associated with an average of 8% (95% CI, 1%-15%) higher risk of GH. Among participants with probable prenatal depression (n=179; 32%), overlapping sensitive windows were observed for all pollutants from 8 weeks before to 10 weeks postconception with increased risk of GH (PM 2.5 , 16% [95% CI, 3%-31%]; PM 10 , 39% [95% CI, 13%-72%]; nitrogen dioxide, 65% [95% CI, 17%-134%]; and ozone, 45% [95% CI, 9%-93%]), while the associations were close to null among those without prenatal depression. Air pollutants were not associated with preeclampsia in any analyses., Conclusions: We identified periconception through early pregnancy as a susceptible window of air pollution exposure with an increased risk of GH. Prenatal depression increases vulnerability to air pollution exposure and GH., Competing Interests: Disclosures None.

In Beijing, particulate matter (PM) in the atmosphere, especially PM 2.5 and PM 10 , have attracted public attention because of its adverse effects. A series of studies have investigated the sources and spatial-temporal variation of PM. Wetland has been reported to own the capacity of resolving air problem. To examine the characteristics of the particulate matter in wetlands, the diurnal variation of PM 2.5 and PM 10 concentrations with respect to two heights (i.e. 1.5 and 10 m, respectively) and three meteorological factors (i.e. wind speed, temperature, and relative humidity, respectively) was monitored in the Cuihu National Wetland Park in Beijing, and the dry deposition velocity and flux were analysed using the above-mentioned data. Results indicated that (1) As for diurnal variation, the PM concentration constantly decreased at 07:00-16:00 and gradually increased at 16:00-18:00. The maximum instantaneous concentration was observed at 07:00-10:00, while the minimum instantaneous concentration was observed at 13:00-16:00. (2) The annual concentration variation of PM followed the order of dry period > wet period > normal period. (3) The particulate concentrations at 10 m were always greater than those at 1.5 m. (4) The PM concentration was positively correlated to the relative humidity and negatively correlated to the temperature. Wind speed exhibited a complex effect on PM concentration. (5) The regulation of dry deposition efficiency followed the order of spring > winter > summer. (6) Wind speed strongly and positively affected the dry deposition velocity of PM10. The effects of temperature and relative humidity on dry deposition were uncertain.