Gogna Priyanka, King Will D, Villeneuve Paul J, Kumarathasan Premkumari, Johnson Markey, Lanphear Bruce, Shutt Robin H, Arbuckle Tye E, Borghese Michael M
Department of Public Health Sciences, Queen's University, Kingston, Ontario.
Environmental Health Science and Research Bureau, Health Canada, Ottawa, Ontario.
Environ Epidemiol. 2021 Sep 7;5(5):e168. doi: 10.1097/EE9.0000000000000168. eCollection 2021 Oct.
Epidemiologic studies have consistently reported associations between air pollution and pregnancy outcomes including preeclampsia and gestational diabetes. However, the biologic mechanisms underlying these relationships remain unclear as few studies have collected relevant biomarker data. We examined relationships between ambient PM and NO with markers of inflammation during pregnancy in a prospective cohort of Canadian women.
We analyzed data from 1170 women enrolled in the Maternal-Infant Research on Environmental Chemicals study. Daily residential PM and NO exposures during pregnancy were estimated using satellite-based and land-use regression models and used to create 14-day and 30-day exposure windows before blood-draw. Inflammatory markers C-reactive protein, interleukin-6, interleukin-8, and tumor necrosis factor-α were measured in third trimester plasma samples. Multivariable linear regression was used to estimate associations for an interquartile range (IQR) increase in PM and NO and markers of inflammation, while adjusting for individual-level confounders.
Fourteen-day (IQR: 6.85 µg/m) and 30-day (IQR: 6.15 µg/m) average PM exposures before blood-draw were positively associated with C-reactive protein after adjustment for covariates (24.6% [95% CI = 9.4, 41.9] and 17.4% [95% CI = 1.0, 35.0] increases, respectively). This association was found to be robust in several sensitivity analyses. Neither PM nor NO exposures were associated with interleukin-6, interleukin-8, or tumor necrosis factor-α.
Exposure to ambient PM is positively associated with maternal inflammatory pathways in late pregnancy. This may contribute to positive associations between ambient PM and risk of adverse pregnancy outcomes.
流行病学研究一直报告空气污染与包括先兆子痫和妊娠期糖尿病在内的妊娠结局之间存在关联。然而,由于很少有研究收集相关生物标志物数据,这些关系背后的生物学机制仍不清楚。我们在一组加拿大女性前瞻性队列中研究了孕期环境细颗粒物(PM)和氮氧化物(NO)与炎症标志物之间的关系。
我们分析了1170名参与母婴环境化学物质研究的女性的数据。利用基于卫星和土地利用回归模型估算孕期每日居住环境中的PM和NO暴露量,并用于创建采血前14天和30天的暴露窗口。在孕晚期血浆样本中测量炎症标志物C反应蛋白、白细胞介素-6、白细胞介素-8和肿瘤坏死因子-α。使用多变量线性回归来估计PM和NO四分位间距(IQR)增加与炎症标志物之间的关联,同时调整个体水平的混杂因素。
在调整协变量后,采血前14天(IQR:6.85微克/立方米)和30天(IQR:6.15微克/立方米)的平均PM暴露量与C反应蛋白呈正相关(分别增加24.6%[95%CI=9.4,41.9]和17.4%[95%CI=1.0,35.0])。在多项敏感性分析中发现这种关联是稳健的。PM和NO暴露均与白细胞介素-6、白细胞介素-8或肿瘤坏死因子-α无关。
孕期暴露于环境PM与孕晚期母体炎症途径呈正相关。这可能有助于解释环境PM与不良妊娠结局风险之间的正相关关系。