BACKGROUND: No epidemiological studies have systematically evaluated the associations between prenatal exposure to organophosphate esters and polychlorinated biphenyls and the risk of congenital heart disease (CHD) in offspring. Moreover, the potential modifying role of maternal B-vitamin status in persistent organic pollutants (POPs)-CHD associations has not been examined. We therefore investigated the cardiotoxic effects of prenatal POPs exposure and evaluated effect modification by maternal B-vitamin levels. METHODS: A multicenter case-control study was conducted in China from 2016 to 2021, including 425 participants. Thirty POPs and seven plasma B vitamins were quantified using high-resolution mass spectrometry. Single-exposure associations were examined by logistic regression, while multipollutant effects were assessed through Bayesian kernel machine regression (BKMR) and Weighted Quantile Sum (WQS) models. Potential effect modification by B vitamins was systematically evaluated. RESULTS: Prenatal exposure to p-cresyl diphenyl phosphate was associated with an increased risk of CHD (odds ratio OR = 1.36, 95% confidence interval CI: 1.08, 1.71). Mixture analyses consistently showed an increasing trend in CHD risk with higher exposure to the POPs mixture, with the WQS model yielding a statistically significant association (OR = 1.20, 95% CI: 1.03, 1.40). Higher concentrations of pyridoxamine, pyridoxal, and vitamin B12 were inversely associated with CHD risk, and mixture analyses using both BKMR and WQS regression further demonstrated a significant negative association between the overall B-vitamin mixture and CHD risk. In the interaction analysis, B vitamins significantly modified the association between prenatal POPs exposure and CHD risk (OR = 0.14, 95% CI: 0.04, 0.52). CONCLUSIONS: This study provides the first population evidence that prenatal POPs exposure is associated with increased CHD risk and adequate maternal B-vitamin levels may attenuate the developmental cardiotoxicity of emerging flame retardants, highlighting the importance of maternal nutritional status in modifying environmental risk factors for CHD.
Li et al. (Mon,) studied this question.