Department of Public Health Sciences, University of Rochester Medical Center, Rochester, NY, USA.
Department of Pediatrics, University of Rochester Medical Center, Rochester, NY, USA.
Environ Res. 2024 Nov 1;260:119639. doi: 10.1016/j.envres.2024.119639. Epub 2024 Jul 19.
Air pollution exposure during pregnancy has been associated with numerous adverse pregnancy, birth, and child health outcomes. One proposed mechanism underlying these associations is maternal immune activation and dysregulation. We examined associations between PM and NO exposure during pregnancy and immune markers within immune function groups (TH1, TH2, TH17, Innate/Early Activation, Regulatory, Homeostatic, and Proinflammatory), and examined whether those associations changed across pregnancy.
In a pregnancy cohort study (n = 290) in Rochester, New York, we measured immune markers (using Luminex) in maternal plasma up to 3 times during pregnancy. We estimated ambient PM and NO concentrations at participants' home addresses using a spatial-temporal model. Using mixed effects models, we estimated changes in immune marker concentrations associated with interquartile range increases in PM (2.88 μg/m) and NO (7.82 ppb) 0-6 days before blood collection, and assessed whether associations were different in early, mid, and late pregnancy.
Increased NO concentrations were associated with higher maternal immune markers, with associations observed across TH1, TH2, TH17, Regulatory, and Homeostatic groups of immune markers. Furthermore, the largest increases in immune markers associated with each 7.82 ppb increase in NO concentration were in late pregnancy (e.g., IL-23 = 0.26 pg/ml, 95% CI = 0.07, 0.46) compared to early pregnancy (e.g., IL-23 = 0.08 pg/ml, 95% CI = -0.11, 0.26).
Results were suggestive of NO-related immune activation. Increases in effect sizes from early to mid to late pregnancy may be due to changes in immune function over the course of pregnancy. These findings provide a basis for immune activation as a mechanism for previously observed associations between air pollution exposure during pregnancy and reduced birthweight, fetal growth restriction, and pregnancy complications.
孕期暴露于空气污染与多种不良妊娠、分娩和儿童健康结局有关。这些关联的一个潜在机制是母体免疫激活和失调。我们研究了孕期 PM 和 NO 暴露与免疫功能群（TH1、TH2、TH17、先天/早期激活、调节、平衡和促炎）内免疫标志物之间的关系，并研究了这些关系在孕期是否发生变化。
在纽约罗切斯特的一项妊娠队列研究（n=290）中，我们在孕期最多 3 次测量了母亲血浆中的免疫标志物（使用 Luminex）。我们使用时空模型估计了参与者家庭住址的环境 PM 和 NO 浓度。使用混合效应模型，我们估计了与血液采集前 0-6 天内 PM（2.88μg/m）和 NO（7.82ppb）的四分位距增加相关的免疫标志物浓度的变化，并评估了这些关联在妊娠早期、中期和晚期是否不同。
NO 浓度的升高与较高的母体免疫标志物相关，这种关联在 TH1、TH2、TH17、调节和平衡免疫标志物组中都存在。此外，与每增加 7.82ppb 的 NO 浓度相关的最大免疫标志物增加出现在晚期妊娠（例如，IL-23=0.26pg/ml，95%CI=0.07，0.46），而不是早期妊娠（例如，IL-23=0.08pg/ml，95%CI=-0.11，0.26）。
结果提示存在与 NO 相关的免疫激活。从妊娠早期到中期到晚期，效应大小的增加可能是由于孕期免疫功能的变化。这些发现为免疫激活作为孕期暴露于空气污染与降低出生体重、胎儿生长受限和妊娠并发症之间已观察到的关联的机制提供了依据。
