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By Daniella Gray
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Every day, people come into contact with plastics designed to make products softer and more flexible.
These chemicals are found in everything from food packaging to household items, and for years scientists have debated what effect they might have on developing babies.
Now researchers in Australia say they may have uncovered an important clue.
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In a study of more than 800 children, scientists found evidence that prenatal exposure to a common plasticizer called DEHP may leave detectable biological changes at birth that are linked to autism- and ADHD-related symptoms in early childhood.
The findings, published in Med, offer what researchers describe as a possible mechanism connecting exposure in the womb to later neurodevelopment.
DEHP, short for di-(2-ethylhexyl) phthalate, belongs to a family of chemicals known as phthalates, which are added to plastics to improve flexibility.
Previous studies have linked prenatal exposure to DEHP with autism and ADHD symptoms, but exactly how that relationship might occur has remained unclear.
To investigate, researchers analyzed data from 847 children enrolled in the Barwon Infant Study, a long-running Australian birth cohort.
The team measured DEHP exposure during pregnancy, examined DNA methylation patterns in umbilical cord blood collected at birth and then followed children through the ages of 2 and 4 years.
DNA methylation is an epigenetic process that can influence whether genes are switched on or off without changing the underlying DNA sequence.
The researchers found that higher prenatal DEHP exposure was associated with specific DNA methylation signatures in cord blood.
Those alterations, they said, appeared to help explain links between DEHP exposure and higher levels of autism- and ADHD-related symptoms later in childhood.
The affected gene networks included genes previously associated with neurodevelopment and contained markers linked to brain regions involved in attention, social behavior and emotional processing.
The researchers also found evidence that some of these epigenetic signatures could be detected in independent blood and brain datasets.
Professor Anne-Louise Ponsonby, the author of the study and a researcher at the Florey Institute of Neuroscience and Mental Health, said the findings should be viewed within the broader context of autism's complex origins.
"Autism is a complex multifactorial disease," Ponsonby told Newsweek. "Some risk factors are potentially modifiable and others are not. If we can understand modern environmental drivers, we may be more likely to understand then mitigate the factors driving severity and symptom load."
However, an expert cautioned that the findings should not be interpreted as proof that DEHP causes autism or ADHD.
Professor Mirko Uljarevic, a senior principal research fellow at The Kids Research Institute, said the work was methodologically sophisticated and helped address a longstanding question about how prenatal phthalate exposure might influence neurodevelopment.
"This study adds to the previously inconsistent research on prenatal phthalate exposure and neurodevelopmental outcomes by testing a specific biological mechanism and doing so in a methodologically sophisticated way," he said in a Scimex news release.
But he noted several important limitations.
"The effects observed were modest, and, like almost all research in this area, the study is observational rather than experimental, so it cannot prove cause and effect," he said.
Uljarevic also pointed out that the validation datasets were very small and that researchers could not directly test the entire pathway from chemical exposure to brain changes to symptoms.
In addition, some epigenetic patterns appeared in opposite directions when comparing blood and brain tissue.
"Autism and ADHD are complex conditions," he said. "Autism, ADHD and other neurodevelopmental conditions are multifactorial conditions that arise from many genetic and environmental factors together, so no single exposure like this is likely, on its own, to meaningfully change an individual child's risk."
The authors acknowledge similar limitations, noting that they assessed autism- and ADHD-related symptoms rather than formal diagnoses and that the study, while designed to strengthen causal inference, remains observational.
Ponsonby said the new research nevertheless provides stronger evidence than previous studies that simply identified an association between DEHP exposure and later neurodevelopmental outcomes.
Looking ahead, she argued that more responsibility should fall on industry and regulators when introducing chemicals that may become widespread in the environment.
"Ideally, the precautionary principle would come into play," Ponsonby said. "The onus would be on those introducing populations to widespread chemical exposures, often for business profit, to provide evidence first that they did not cause human health harm."
Reference
Tanner, S., Eisner, A., Novakovic, B., Holland, L., Mansell, T., England-Mason, G., Merrill, S., Dewey, D., Martin O’Hely, Christos Symeonides, Saffery, R., Mimi L.K. Tang, Sly, P.D., Vuillermin, P., Jung, C.-H., Park, D. and Ponsonby, A.-L. (2026). Prenatal exposure to the plasticizer DEHP increases the likelihood of early-life autism and ADHD symptoms through epigenetic programming. Med, [online] 0(0). doi:10.1016/j.medj.2026.101291.
Contact Newsweek editors on this story: Marc Vargas and Emma Lee-Sang
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