Associations between prenatal exposure to phenols, epigenetic age acceleration, and child neurodevelopment at two years of age in a South African birth cohort Restricted; Files Only
Zhou, Terry (Spring 2024)
Abstract
There is little research on the effects of phenol exposure mixtures on child neurodevelopment. Previous studies have identified DNA methylation as a mediator between prenatal environmental exposures and child neurodevelopment. We analyzed associations between prenatal phenol exposures and cognitive neurodevelopment at age two among 545 children from the South African Drakenstein Child Health Study. Furthermore, we investigated if associations between prenatal phenol exposure and cognitive neurodevelopment at age 2 were mediated by gestational epigenetic age acceleration (ΔGA).
We measured maternal urine phenol concentrations (BP1, BP3, BPA, BPS, ETPB, MEPB, PCP, PRPB, TCS) during the second trimester and assessed cognitive neurodevelopment at age two using the Bayley Scales of Infant and Toddler Development, third edition. DNA methylation was measured using the Illumina HumanMethylation450K BeadChip and Infinium MethylationEPIC BeadChip arrays. Gestational epigenetic age acceleration was calculated using the Knight-Clock gestational age predictor. We examined individual exposure effects using linear regression models adjusted for maternal HIV status, maternal age, ethnicity, maternal smoking, child sex, and socioeconomic status (SES). We utilized four mixture methods to investigate the joint effects of multiple phenol exposures: self-organizing maps, Bayesian kernel machine regression, quantile-based G-computation, and weighted quantile sum regression to explore joint effects of the exposure mixture. We assessed effect modification by SES, sex, smoking, and ethnicity. We used linear regression models to examine individual phenol exposure effects on ΔGA and the effects of ΔGA on cognitive neurodevelopment.
We found no association between individual phenol exposures or the exposure mixture with cognitive neurodevelopment. Smoking modified the association between PCP and cognitive neurodevelopment (interaction p-value=0.012), with non-smokers having a significant adverse association (beta=- 2.17; 95% CI: -3.85, -0.49). Sex modified the association between BPA and cognitive neurodevelopment (interaction p-value=0.021), with males having a significant adverse association (beta=-1.39; 95% CI: -2.54, -0.23). We also found no associations between ΔGA and the individual phenol exposures or ΔGA and cognitive neurodevelopment.
While we found no main effects of prenatal phenol exposure on cognitive neurodevelopment, the associations with PCP and BPA were more pronounced among certain subgroups. Furthermore, we did not find associations between ΔGA with prenatal phenol exposure and cognitive neurodevelopment.
Table of Contents
Chapter 1: Associations between prenatal exposure to phenols and child
neurodevelopment at two years of age …..………………………………………………...... 1
Introduction
Methods
Results
Discussion
Figures
Chapter 2: Potential mediation by epigenetic age acceleration …………………..……… 27
Introduction
Methods
Results
Discussion
Figures
References ………………………………………………………………………..…………… 36
Supplemental Figures …………………………………………………………..…………… 43
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