关注婴儿早期糖代谢，预防孕期空气污染相关的神经发育迟缓

Prenatal air pollution, fetal β-cell dysfunction and neurodevelopmental delay

产前空气污染、胎儿β细胞功能障碍和神经发育迟缓

Authors: Lin Wu 1, Haixia Wang 1, Lei Zhang 2, Wanjun Yin 2, Ruixue Tao 3, Fangbiao Tao 1, Peng Zhu 4

Source：Ecotoxicol Environ Saf. 2023 Nov 16:268:115705.

Doi: 10.1186/s12916-023-03173-2.

Abstract

Background:Emerging evidence has reported significant associations of prenatal air pollution exposure with neurodevelopmental delay in offspring. Sensitive exposure windows and the modifiable factor remain elusive.

Objective:We aim to identify sensitive windows of air pollution during pregnancy on neurodevelopmental delay, and examine whether cord blood C-peptide mediates the relationship.

Methods:This study included 7438 mother-newborn pairs in Hefei, China, from 2015 to 2021. Weekly exposure to particulate matter of aerodynamic diameter

Results:The sensitive PM2.5, PM10, NO2, and CO exposure windows associated with neurodevelopmental delay were throughout pregnancy. Weekly air pollutants exposure was related to higher neurodevelopmental delay risks [cumulative odds ratio (OR): 1.40(1.29,1.53) in PM2.5 (per 10 μg/m3), 1.40(1.28,1.53) in PM10 (per 10 μg/m3), 1.41(1.30,1.52) in CO (per 0.1 mg/m3), and 1.49(1.29,1.72) in NO2 (per 5 μg/m3)]. Mediation analysis indicated 18.3 % contributions of cord C-peptide to the relationship [average mediation effect: 0.04(0.01.0.06); average direct effect: 0.15(0.07.0.25)].

Conclusions:Exposure to air pollution throughout pregnancy is linked to neurodevelopmental delay mediated by poorer fetal β-cell function. Screening and treatment of abnormal glucose metabolism in infants could benefit the prevention of air pollution-associated neurodevelopment delay.

Keywords: Air pollution; C-peptide; Fetal β-cell function; Neurodevelopmental delay.

摘要

背景 新证据报道孕期空气污染暴露与子代神经发育迟缓的显著关联，但是暴露敏感窗口期和潜在的修饰因素仍是不清楚的。

目的 识别孕期空气污染暴露与神经发育迟缓关联的敏感窗口期，并探讨脐带血C肽是否介导这种关联。

方法 本研究纳入2015-2021年中国合肥市7438对母婴对。污染物水平基于合肥市空气监测站点PM2.5、PM10、NO2和CO的周暴露量进行估算。采用丹佛发育筛查试验第二版和Gesell发育量表评估6-36月龄儿童的神经发育迟缓。采用分布滞后非线性模型识别孕期空气污染暴露的敏感时间窗。通过中介分析评估脐血C肽的中介作用。

结果 孕期PM2.5、PM10、NO2和CO暴露与子代神经发育迟缓显著相关，其敏感暴露窗口期贯穿整个孕期。孕期空气污染物周暴露水平与较高的神经发育延迟风险相关[PM2.5每增加10 μg/m3，OR: 1.40(1.29,1.53)，PM10每增加10 μg/m3 OR: 1.40(1.28,1.53)，CO每增加0.1 mg/m3, OR: 1.41(1.30,1.52)，NO2每增加5 μg/m3), OR: 1.49(1.29,1.72)]。中介分析显示脐血C肽的中介比例为18.3%[平均中介效应:0.04(0.01.0.06);平均直接效应:0.15(0.07.0.25)]。

结论 孕期空气污染暴露与神经发育迟缓的显著关联部分由胎儿β细胞功能异常介导。筛查和治疗婴儿糖代谢异常有助于预防空气污染相关的神经发育迟缓。

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