Prenatal Internal Exposure to Polycyclic Aromatic Hydrocarbons, Maternal Genetic Susceptibility, and Child Growth Trajectories: Evidence from a Prospective Cohort Study

Abstract

Prenatal exposure to polycyclic aromatic hydrocarbons (PAHs) is a widespread environmental health concern, yet its impact on early childhood growth trajectories remains poorly understood. In a prospective birth cohort in China (PKUBC-T), we identified distinct growth trajectories from birth to age 3 years using K-means clustering for longitudinal data (N = 1467) and measured 16 plasma PAHs in first-trimester maternal samples (N = 333). Twenty maternal single nucleotide polymorphisms (SNPs) related to PAHs metabolism were genotyped. Modified Poisson and weighted quantile sum regression showed that higher prenatal PAHs exposure was associated with increased risk of rapid higher growth trajectory, with phenanthrene, pyrene, and fluoranthene contributing most. This trajectory is characterized by a marginally higher BMI Z-score at birth, followed by rapid growth during infancy and sustained high levels thereafter. Furthermore, the AHR rs2066853 variant significantly modified the association, with the positive association being observed only among mothers carrying GA/AA genotypes (RR, 2.44; 95% CI, 1.51–3.97) but not among those with GG homozygotes (P for interaction is 0.049). We provide evidence that prenatal PAHs exposure may alter early childhood growth patterns, with effects modified by maternal genetic susceptibility. If confirmed, these findings highlight the mechanistic importance of AHR signaling in environmental developmental toxicity and underscore the need for exposure reduction and targeted maternal monitoring.