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

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.