滞后
分布滞后
怀孕
医学
混淆
内科学
内分泌学
生理学
生物
数学
计算机网络
计算机科学
计量经济学
遗传学
作者
Chen Gong,Mengyu Chu,Junnan Yang,Xian Gong,Bin Han,Li Chen,Bai Zhang,Jianmei Wang,Yujuan Zhang
标识
DOI:10.1016/j.envpol.2022.120446
摘要
The effect of fine particulate matter (PM2.5) on human early maternal-fetal interface is unknown. We explored the association between maternal exposure to ambient PM2.5 and inflammation in placental villus of 114 women with clinically recognized early pregnancy loss (CREPL) and 114 women with normal early pregnancy (NEP). Temporally-adjusted land use regression models were used to estimate maternal daily PM2.5 exposure during pregnancy. Villus interleukin-1beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were measured using multiplex cytokines detection platform. Single-day lag effect of PM2.5 exposure within ten days before early placental villus collection was estimated using multivariable linear regression model. Distributed lag and net cumulative effects of PM2.5 exposures within ten and 30 days before villus collection, as well as five single weeks during the periovulatory period, were estimated using distributed lag non-linear models. In all 228 subjects, after adjusting for group (CREPL or NEP), temporal confounders, and demographic characteristics, both single-day and distributed lag effects of PM2.5 exposure at lag 8 significantly increased villus IL-6; distributed lag effects of PM2.5 exposure in the first and second weeks before ovulation increased IL-1β, and PM2.5 exposure in the third week after ovulation increased IL-6 and TNF-α. In CREPL, single-day lag effect significantly increased IL-1β (at lag 1), IL-6 (at lag 8), and TNF-α (at lag 5); distributed lag effect increased IL-6 (at lag 4-lag 8) and TNF-α (at lag 4-lag 6); and cumulative effect within ten days before villus collection increased IL-6. There was no statistically significant cumulative effect in NEP. In summary, maternal PM2.5 exposure was associated with placental inflammation in human early pregnancy, particularly with increased villus IL-6 in CREPL. Whether maternal-fetal interface inflammation related to PM2.5 exposure during the periovulatory period or later contributes to CREPL or other adverse pregnancy outcomes requires further study.
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