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Prenatal Environmental Determinants of Aromatase Brain-Promoter Methylation in Cord Blood: Chemical, Airborne, Pharmacological, and Nutritional Factors
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Researchers found that a mix of everyday exposures during pregnancy, including BPA (a chemical in plastics), phthalates, air pollution, household mould, low sunlight, and low folate intake, was linked to changes in a gene that helps balance hormones in a developing baby's brain. This matters because that gene has previously been tied to autism risk, suggesting these common exposures might work together to affect brain development in ways science is only beginning to understand. It's an early finding, not proof of cause and effect, but it adds to growing concerns about how plastic-related chemicals and pollution during pregnancy could influence a baby's long-term
Abstract Aromatase, an enzyme encoded by the gene CYP19A1, plays central roles in neurodevelopment. In the brain, its function is to convert androgens into neuroestrogens, ensuring balanced hormonal signalling. Both animal experiments and human studies have shown that, in males, disruption of aromatase, either genetically or epigenetically, can increase symptoms of autism. Prenatal exposure to bisphenol A (BPA), a common plastic chemical, can increase levels of DNA methylation—a key epigenetic modification—at the brain-specific CYP19A1 promoter, P1.f, reducing CYP19A1 expression. However, the extent to which other neurodevelopmentally relevant environmental exposures influence P1.f methylation remains unclear. Here, in the Barwon Infant Study (BIS) birth cohort (N = 906), we analysed the association between 25 prenatal exposures (from five classes previously linked to neurodevelopmental outcomes: manufactured chemicals, air pollution, and pharmacological, nutrition and sunlight-related factors) and methylation of the CYP19A1 P1.f promoter using Weighted Quantile Sum (WQS) regression. We found that the WQS mixture index, a weighted combination of the prenatal exposures, was positively associated with higher P1.f methylation (Adjusted Mean Difference (AMD) = 0.71 (95% CI 0.11, 1.32), p = 0.021), indicating reduced brain aromatase activity. Prenatal exposures with the strongest contribution to the mixture effect included bisphenols (including BPA), reduced sunlight, household mould, phthalates, low folate intake, and air pollution. These findings highlight epigenetic modification of the aromatase gene as a biologically plausible, convergent mechanism through which multiple environmental risk factors for autism may exert effects.
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