首頁(yè) 資訊關(guān)注嬰兒早期糖代謝，預(yù)防孕期空氣污染相關(guān)的神經(jīng)發(fā)育遲緩

關(guān)注嬰兒早期糖代謝，預(yù)防孕期空氣污染相關(guān)的神經(jīng)發(fā)育遲緩

來(lái)源：泰然健康網(wǎng) 時(shí)間：2024年11月23日 23:40

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

產(chǎn)前空氣污染、胎兒β細(xì)胞功能障礙和神經(jīng)發(fā)育遲緩

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

背景新證據(jù)報(bào)道孕期空氣污染暴露與子代神經(jīng)發(fā)育遲緩的顯著關(guān)聯(lián)，但是暴露敏感窗口期和潛在的修飾因素仍是不清楚的。

目的識(shí)別孕期空氣污染暴露與神經(jīng)發(fā)育遲緩關(guān)聯(lián)的敏感窗口期，并探討臍帶血C肽是否介導(dǎo)這種關(guān)聯(lián)。

方法本研究納入2015-2021年中國(guó)合肥市7438對(duì)母嬰對(duì)。污染物水平基于合肥市空氣監(jiān)測(cè)站點(diǎn)PM2.5、PM10、NO2和CO的周暴露量進(jìn)行估算。采用丹佛發(fā)育篩查試驗(yàn)第二版和Gesell發(fā)育量表評(píng)估6-36月齡兒童的神經(jīng)發(fā)育遲緩。采用分布滯后非線(xiàn)性模型識(shí)別孕期空氣污染暴露的敏感時(shí)間窗。通過(guò)中介分析評(píng)估臍血C肽的中介作用。

結(jié)果 孕期PM2.5、PM10、NO2和CO暴露與子代神經(jīng)發(fā)育遲緩顯著相關(guān)，其敏感暴露窗口期貫穿整個(gè)孕期。孕期空氣污染物周暴露水平與較高的神經(jīng)發(fā)育延遲風(fēng)險(xiǎn)相關(guān)[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)]。中介分析顯示臍血C肽的中介比例為18.3%[平均中介效應(yīng):0.04(0.01.0.06);平均直接效應(yīng):0.15(0.07.0.25)]。

結(jié)論 孕期空氣污染暴露與神經(jīng)發(fā)育遲緩的顯著關(guān)聯(lián)部分由胎兒β細(xì)胞功能異常介導(dǎo)。篩查和治療嬰兒糖代謝異常有助于預(yù)防空氣污染相關(guān)的神經(jīng)發(fā)育遲緩。