DEHP Exposure in Pregnancy Tied to ADHD, Autism Symptoms in Children

A recent Australian study has found an association between prenatal exposure to the chemical DEHP—di(2-ethylhexyl) phthalate—and increased symptoms related to autism spectrum disorder and attention-deficit/hyperactivity disorder (ADHD) in children.

How DEHP enters the body

DEHP is used in the production of certain plastic products. Human exposure can occur through food ingestion, inhalation, or skin contact.

Epigenetic mechanisms under investigation

Researchers examined how prenatal DEHP exposure affects fetal brain development, focusing on epigenetic programming—a biological process that alters gene activity without changing the underlying DNA sequence.

The team analyzed urine samples from 847 pregnant women collected at week 36 of gestation, alongside umbilical cord blood samples obtained after birth. They assessed DNA methylation patterns, a key epigenetic mechanism involved in regulating gene expression.

Child behavioral follow-up

Children’s behavior was tracked at ages two and four using parent-completed questionnaires covering domains including attention, hyperactivity, and social difficulties.

Results showed that higher maternal DEHP exposure during pregnancy correlated with increased hyperactivity, inattention, and peer interaction problems in offspring. The strongest associations were observed among children in the top 2% of exposure levels.

A gene network tied to brain development

The researchers identified a network of 531 genes named Co-MN1. This network was linked both to DEHP exposure and to critical neurodevelopmental processes—including attention regulation and social behavior.

Several genes within the Co-MN1 network overlapped with those previously associated with autism and ADHD, including FOXP1 and SHANK2.

Causal claims not supported

The study does not establish that DEHP exposure directly causes autism or ADHD. Its observational design precludes causal inference. Both conditions are understood to arise from multiple genetic and environmental factors.

Dietary counter-effects observed

In a separate finding, greater maternal consumption of whole, unprocessed foods during pregnancy was associated with epigenetic changes in the same Co-MN1 gene network—but in the opposite direction to those linked with DEHP exposure. This dietary pattern also correlated with reduced attention-related difficulties and improved social behavior in children.

The research adds to the growing body of evidence examining how environmental chemicals affect prenatal brain development. It underscores the need for further investigation into safe exposure thresholds for phthalates—particularly during pregnancy.