Prenatal exposure to nonpersistent endocrine disruptors and early childhood BMI: single pollutant and mixture analyses from the ECHO Program.

Background

Exposure to non-persistent endocrine-disrupting chemicals (EDCs), including phenols and phthalates, has been linked to obesity risk. While many studies focus on single-chemical exposures, mixture effects on child adiposity remain unclear.

Objectives

To assess associations of prenatal phenol and phthalate exposures, singly and as mixtures, with early childhood BMI in the U.S. Environmental influences on Child Health Outcomes (ECHO) Program.

Methods

We included 586 mother-child pairs from three ECHO sites with 23 phenols and phthalate metabolites measured in maternal urine during pregnancy, and child BMI z-scores (BMIZ) at 2-5 years. Associations were estimated using covariate-adjusted single-pollutant linear regression and two mixture methods: Bayesian Weighted Quantile Sum (BWQS) and Bayesian Kernel Machine Regression (BKMR). Sex-specific effects were examined in stratified models.

Results

No associations were observed between the overall prenatal EDC mixture and BMIZ. In single-pollutant models, MBzP (highest tertile) was inversely associated with BMIZ (β = -0.36, 95% CI: -0.63, -0.08), while MEP (second tertile) was positively associated (β = 0.27, 95% CI: 0.01, 0.53). Among boys, MBP (second tertile) was positively associated (β = 0.45, 95% CI: 0.11, 0.79).

Conclusions

We found no strong evidence for mixture effects, though some individual compounds showed non-linear and sex-specific associations. IMPACT Using a 23-analyte panel of phenols and phthalate metabolites, and complementary (BKMR, BWQS) alongside single-pollutant and sex-stratified models, this study strengthens inference and addresses limitations of prior research. Prenatal exposure to ubiquitous, short-lived endocrine-disrupting phthalates showed non-monotonic, sex-specific associations with early childhood BMI in single-pollutant models. These findings contribute to the limited evidence base on mixture effects of endocrine-disrupting chemicals in early-life obesity risk.