Plastic Exposure Before Birth Linked to ADHD And Autism Symptoms (Sep 2026, n=847) Prenatal exposure to the plasticizer DEHP increases the likelihood of early-life autism and ADHD symptoms through epigenetic programming Study

[Michael Harrop]

• https://www.sciencealert.com/plastic-exposure-before-birth-linked-to-adhd-and-autism-symptoms-heres-what-you-need-to-know
• https://www.cell.com/med/fulltext/S2666-6340(26)00294-1

Context and significance​

Prenatal exposure to DEHP, a common plasticizer, is linked to neurodevelopmental disorders, yet the biological pathways remain poorly understood. This study investigated whether DEHP affects the developing brain through “epigenetic programming”, a process in which genes can be turned on or off without changing the DNA sequence.

Analyzing a large birth cohort, the researchers identified specific epigenetic signatures of DEHP exposure in umbilical-cord blood that indicate disturbances in critical neurodevelopmental pathways. These epigenetic changes provide a biological link between prenatal DEHP exposure and early-life autism and ADHD symptoms.

This study provides a molecular explanation for phthalate-related risks using real-world human data and suggests that current regulatory limits for DEHP exposure during pregnancy may need reassessment to protect child brain health and support healthy development.

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Highlights​

• Prenatal DEHP exposure relates to increased autism and ADHD symptoms
• Child DNA methylation, a key epigenetic marker, mediates these neurotoxic effects
• Affected gene networks are enriched for neurodevelopmental genes
• Identified epigenetic signatures replicate in independent blood and brain datasets

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Summary​

Background​

Growing evidence implicates prenatal exposure to di-(2-ethylhexyl) phthalate (DEHP), a common endocrine-disrupting plasticizer, in the development of autism and attention-deficit/hyperactivity disorder (ADHD). Yet underlying mechanisms remain unclear.

Methods​

Here, we examined whether cord blood DNA methylation, a key epigenetic marker, mediates the association between prenatal DEHP exposure and autism and ADHD symptoms in 847 children from the Barwon Infant Study. Autism and ADHD are complex phenotypes driven by alterations in higher-level gene networks and neuronal circuits, where diverse genetic and environmental risk factors converge. Accordingly, rather than a gene-by-gene approach, we employed a data-driven strategy to elucidate broader functional epigenetic signatures of autism and ADHD elicited by DEHP exposure. This included (1) a methylation profile score for DEHP exposure (MPSDEHP), and (2) a targeted analysis of DEHP-associated co-methylated gene networks.

Findings​

Causal mediation analysis showed that both MPSDEHP and a network of 531 co-methylated genes mediated the effect of DEHP on increased autism and ADHD symptoms at ages 2 and 4 years (proportion mediated: 0.21–0.80). The co-methylation network was enriched for neural cell-type markers, autism and ADHD risk genes (including FOXP1, SHANK2, and PLXNB1), and targets of endocrine receptors previously linked to DEHP (including estrogen and glucocorticoid receptors), providing biological plausibility. We validated key results in independent blood (n = 66) and postmortem-brain (n = 40) DNA methylation datasets.

Conclusion​

These findings provide mechanistic evidence linking DEHP to adverse neurodevelopment and reinforce mounting concerns regarding the risks of prenatal exposure.

Funding​

Funding was obtained from the NHMRC, the Minderoo Foundation, and additional sources (detailed in acknowledgments).

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