Researchers found that prenatal exposure to the widely used plastic additive DEHP was associated with childhood ADHD and autism-related traits and with changes involving hundreds of genes important to brain development.
By yourNEWS Media Newsroom.
A chemical widely used in plastics was associated with signs of ADHD and autism in young children and with changes involving hundreds of genes tied to brain development, according to new research examining exposure during pregnancy.
The study focused on Di-(2-ethylhexyl) phthalate, or DEHP, a plastic additive to which people can be exposed through numerous consumer products and materials.
Researchers compared biological samples collected from pregnant women with behavioral assessments of their children at ages 2 and 4, looking for relationships between maternal DEHP exposure and later neurodevelopmental characteristics.
Higher levels of DEHP were associated with more symptoms related to ADHD and autism in the children, according to the research.
Investigators then examined blood collected from the mothers’ placental cords to explore a possible biological explanation for the association. Their epigenetic analysis found a strong relationship between DEHP levels and approximately 500 genes involved in brain development.
The findings suggest that exposure during pregnancy may influence how certain genes involved in neurodevelopment are regulated. They do not establish that DEHP causes either ADHD or autism.
One of the researchers emphasized that distinction.
“The current study offers important avenues for future research,” the researcher said.
“However, 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.”
Nearly all of the women participating in the Australian study had detectable DEHP in their bodies, illustrating how widespread exposure to the chemical can be.
DEHP belongs to a class of chemicals known as phthalates, which are commonly added to plastics to alter properties such as softness and flexibility. Concerns about prenatal exposure have attracted particular attention because fetal brain development involves tightly coordinated genetic and biological processes that can be sensitive to environmental influences.
The latest work adds an epigenetic component to that research.
Epigenetic changes affect how genes operate without changing the underlying DNA sequence itself. By examining umbilical cord blood, researchers were able to investigate whether maternal exposure was associated with altered regulation of genes during a critical period of development.
The identification of roughly 500 brain-development-related genes associated with DEHP exposure gives researchers potential biological pathways to examine in future studies.
The study nevertheless remains observational. An association between a chemical exposure and later behavioral characteristics cannot prove that the exposure produced those outcomes, particularly with conditions as complex as autism and ADHD.
Both involve combinations of genetic, developmental and environmental factors, and researchers cautioned against treating DEHP as a single explanation.
The findings come as autism diagnoses have increased substantially in the United States. About one in 31 U.S. children is now diagnosed with autism, compared with approximately one in 150 in 2000.
That increase has intensified scientific interest in understanding the full range of genetic and environmental factors that may influence neurodevelopment.
Environmental exposures have become one area of federal attention as well. Health Secretary Robert F. Kennedy Jr. has made investigating potential environmental contributors to autism part of the Make America Healthy Again health agenda. HHS has publicly identified understanding autism’s causes and examining potentially harmful chemical exposures as agency priorities.
Kennedy announced an investigation into autism causes in April 2025 and initially said findings were expected later that year.
In September 2025, Kennedy discussed a possible association involving acetaminophen use during pregnancy and autism. He subsequently emphasized that autism is multifactorial and later described the evidence involving acetaminophen as “not sufficient to say it definitely causes autism” but “very suggestive.” The relationship between acetaminophen and autism has remained the subject of scientific dispute, and an association does not itself demonstrate causation.
The new DEHP research similarly stops short of a causal conclusion.
Its significance lies instead in the combination of exposure measurements, childhood behavioral assessments and epigenetic evidence suggesting a possible pathway connecting prenatal chemical exposure with neurodevelopment.
Researchers measured DEHP exposure through blood and urine samples obtained during pregnancy, later comparing those data with assessments conducted when the children were 2 and 4 years old.
The subsequent cord-blood analysis allowed investigators to look beyond a statistical relationship and identify biological changes associated with the exposure.
Finding a relationship involving hundreds of genes central to brain development provides researchers with specific targets for additional investigation, including studies designed to determine whether the observed epigenetic changes persist as children grow and whether they have measurable effects on brain function.
Future research will also be needed to determine how DEHP interacts with genetics and other environmental exposures, whether particular periods of pregnancy carry greater vulnerability and what levels of exposure may be most significant.
For now, the study adds to evidence that environmental chemicals may be one component in the complicated biological processes associated with neurodevelopmental conditions.
The researchers cautioned, however, that neither autism nor ADHD can be attributed to a single chemical exposure. The findings identify DEHP as a factor warranting further investigation rather than establishing it as a cause of either condition.
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