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Published on: November 20, 2015
Prenatal air pollution, fetal β-cell dysfunction and neurodevelopmental delay
Peng Wang1, Lin Wu1, Haixia Wang1
1Department of Maternal, Child & Adolescent Health, School of Public Health, Anhui Medical University, Hefei, China; MOE Key Laboratory of Population Health Across Life Cycle, Hefei, China; NHC Key Laboratory of Study on Abnormal Gametes and Reproductive Tract, Hefei, China; Anhui Provincial Key Laboratory of Population Health and Aristogenics, Hefei, China; Center for Big Data and Population Health of IHM, Anhui Medical University, Hefei, Anhui, China.
Insights
Prenatal exposure to air pollution throughout pregnancy is linked to neurodevelopmental delay in children. This effect is mediated by impaired fetal beta-cell function, suggesting a potential intervention point.
Area of Science:
- Environmental Health
- Developmental Pediatrics
- Endocrinology
Background:
- Growing evidence links prenatal air pollution exposure to adverse neurodevelopmental outcomes in children.
- Specific exposure windows and modifiable factors contributing to this association require further investigation.
Purpose of the Study:
- To identify critical windows of prenatal air pollution exposure associated with neurodevelopmental delay.
- To investigate the mediating role of cord blood C-peptide in the relationship between air pollution and neurodevelopmental delay.
Main Methods:
- A cohort of 7438 mother-newborn pairs in Hefei, China (2015-2021) was analyzed.
- Weekly exposure to PM2.5, PM10, NO2, and CO was estimated. Neurodevelopmental delay was assessed using standardized tests in children aged 6-36 months.
- Distributed lag nonlinear models identified sensitive exposure windows, and mediation analysis assessed the role of cord blood C-peptide.
Main Results:
- Air pollution exposure throughout pregnancy was associated with increased risks of neurodevelopmental delay.
- Significant odds ratios were observed for PM2.5, PM10, CO, and NO2 exposure.
- Cord blood C-peptide mediated 18.3% of the association between air pollution and neurodevelopmental delay.
Conclusions:
- Prenatal air pollution exposure is linked to neurodevelopmental delay, with fetal beta-cell function impairment playing a mediating role.
- Screening and managing abnormal glucose metabolism in infants may help prevent air pollution-related neurodevelopmental delays.
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 <2.5 µm, 10 µm (PM2.5, PM10), nitrogen dioxide (NO2) and carbon monoxide (CO) was estimated at regulatory air monitoring stations in Hefei. Denver Developmental Screening Test-II and the Gesell Developmental Schedules were applied to assess the neurodevelopmental delay in children 6-36 mon of age. Distributed lag nonlinear models examined sensitive time windows of prenatal air pollutants exposure. Mediation analysis estimated the mediating role of cord blood C-peptide.
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.
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