Study Finds Prenatal DEHP Exposure Linked to Autism‑ and ADHD‑Like Symptoms in Early Childhood

A new observational study published in Med (a Cell Press journal) reports an association between estimated prenatal exposure to the plasticizer DEHP and later autism- and ADHD‑related behaviours in early childhood. The research combines maternal urine measurements late in pregnancy with DNA methylation analysis from newborn umbilical cord blood and behavioural screening at ages two and four.

What the Study Did

The researchers used data from the Barwon Infant Study in Australia, enrolling 847 mothers and their babies, with 589 mother–infant pairs providing complete data for the analyses. Mothers supplied a single urine sample at about 36 weeks’ gestation. Scientists measured specific DEHP metabolites in these samples as proxies for maternal DEHP intake and estimated fetal exposure. At birth, DNA from umbilical cord blood was analysed for methylation patterns. Children’s behaviour was assessed using parent-completed questionnaires at ages two and four to capture autism- and ADHD‑related traits.

Key Findings

The team identified a coordinated methylation signature involving 531 genes that appeared to mediate roughly 21% of the association between higher estimated prenatal DEHP exposure and later autism- and ADHD‑related behaviours. A complementary analysis across 1,000 genomic sites produced consistent results. The observed associations were stronger and more consistent in boys than in girls.

“Our study found infants exposed to higher levels of DEHP before birth showed distinctive changes in DNA methylation — an epigenetic switch that turns genes on or off — in their umbilical cord blood at birth,”

said Sam Tanner, the study’s lead author and a bioinformatics analyst at the University of Melbourne.

Limitations And What This Does Not Prove

Experts and the authors emphasize important limitations. The study is observational and cannot establish causation. A single urine sample late in pregnancy may not reflect long-term maternal exposure, and maternal urine metabolites are an indirect proxy for fetal exposure rather than a direct measurement in the fetus, placenta, or uterus. Behavioural outcomes were based on parent-reported screening questionnaires rather than clinical diagnoses, which can be subjective and provide limited information about clinical autism or ADHD.

“Chemical exposure levels are mainly determined at the population level and are not easily a matter of personal choice,”

notes Anne-Louise Ponsonby, a neuroepidemiologist at the University of Melbourne, pointing to the policy relevance of stronger regulation of food processing and packaging to protect pregnant people and infants.

Mirko Uljarevic, a medical researcher not involved in the study, also cautions: the work could not test the full causal chain from chemical exposure to brain changes to behaviour — it examined only parts of that pathway.

What Comes Next

While the findings add to evidence that prenatal chemical exposures may relate to epigenetic changes and later behaviour, the authors call for replication and more comprehensive studies. Future research should use repeated exposure measurements across pregnancy, direct fetal biomarkers when possible, longer follow-up with clinical assessments, and investigation of sex-specific mechanisms to better understand any causal relationships.

In short, the study highlights a plausible biological pathway linking estimated prenatal DEHP exposure to later neurodevelopmental traits, but it does not prove DEHP causes autism or ADHD. The results suggest priorities for further research and for policymakers to consider as evidence accumulates.