A new study has drawn a connection between prenatal exposure to a common plasticizer and the likelihood of autism and ADHD symptoms in early childhood. Published in Med, a peer-reviewed journal owned by Cell Press, the research adds another piece to the ongoing puzzle of why autism and ADHD diagnoses are rising and what role environmental chemicals might play in brain development.
But while the findings are noteworthy, they come with important caveats about what this kind of study can and cannot tell us.
What the Study Examined
The research focused on children’s behavioral traits at ages two and four, and how those traits correlate with potential prenatal exposure to DEHP (di-(2-ethylhexyl) phthalate), a synthetic chemical used to make plastics more flexible. DEHP is commonly found in vinyl furniture upholstery, garden hoses, shower curtains, medical tubing, and vegan leathers. It is also known to leach out of these materials easily, which is how it can end up in food, water, and ultimately the human body.
“Chemical exposure levels are mainly determined at the population level and are not easily a matter of personal choice,” explains Anne-Louise Ponsonby, a neuroepidemiologist at the University of Melbourne in Australia. “Plastic chemicals like DEHP are often ingested, so government safety regulations around food processing and packaging are very important. Global plastic control efforts should take into consideration recent evidence as it emerges on the need for health protection, particularly for vulnerable populations such as pregnant women and young babies.”
Previous animal experiments and human observational studies have picked up links—correlation, not causation—between in-utero DEHP exposure and neurodevelopmental issues, including symptoms generally associated with ADHD and autism. The new study probes deeper into this association, with a particular focus on epigenetic factors that some suspect could be involved in a causal link, if one exists.
Epigenetics and DNA Methylation
Epigenetics is the study of how environmental factors—such as DEHP exposure—can affect the way genes function without changing the underlying DNA sequence. One way this happens is through DNA methylation, in which methyl groups attach to genes and either increase or decrease their expression.
“What we have found is a possible biological explanation and one that provides new evidence that exposure to DEHP in pregnancy may contribute to autism and ADHD,” says the study’s lead author Sam Tanner, a bioinformatics analyst at the University of Melbourne. “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. Children who carried this ‘epigenetic signature’ went on to show more autism- and ADHD-related symptoms at ages two and four, with clearer effects in males than females.”
How the Research Was Conducted
This observational study drew on data from 847 Australian mothers and their babies who participated in the Barwon Infant Study. Of these, 589 mother-infant pairs provided a complete set of data points. Researchers began collecting data before the children were born.
At 36 weeks of pregnancy, each mother provided a single urine sample. In these samples, researchers looked for metabolites that would help estimate how much DEHP a mother was likely taking into her body daily. These metabolites are reliable indicators of DEHP exposure because they are the byproducts our bodies produce when breaking down this specific phthalate.
After birth, DNA was extracted from the babies’ umbilical cord blood and analyzed for epigenetic signatures that might be linked to DEHP exposure. A group of 531 genes, affected by methylation patterns that seemed to occur together, appeared to mediate 21 percent of the link between estimated DEHP exposure and the autism and ADHD symptoms measured when the children reached ages 2 and 4. Another test for methylation, based on 1,000 sites across the genome, pointed to the same conclusion, adding some weight to the possibility that DEHP could be contributing to the symptoms. Importantly, these links were only really significant among boys.
Limitations and Expert Caution
Several aspects of the methodology warrant caution. A single urine sample may not represent a person’s typical exposure over the long term. Also, the developing baby’s potential DEHP exposure was based on an estimate derived from a proxy measurement (urine), not a direct measurement of actual DEHP levels in the fetus, placenta, or uterus.
As medical researcher Mirko Uljarevic reiterates, this study is observational, not experimental, so it cannot prove cause and effect. “Autism and ADHD are complex conditions; however, the measures used by the authors were not developed for the purpose of comprehensively assessing autism or ADHD; rather, they provide very limited information,” says Uljarevic, who was not involved in the research.
He points out that the behavioral symptoms measured in the study—based on questionnaires filled out by the children’s parents—are not clinical diagnoses of ADHD or autism. They highlight behaviors that might warrant further investigation for a diagnosis when the child reaches school age, but they are not conclusive and are also fairly subjective.
“Crucially, the authors could not test the full chain from chemical exposure to brain changes to symptoms, only part of it,” Uljarevic adds. Together, the findings present interesting patterns, but it remains impossible to say DEHP has any specific health effect based on these results.
“The current study offers important avenues for future research; however, autism, ADHD, and other neurodevelopmental conditions are multifactorial conditions that arise from many genetic and environmental factors together,” Uljarevic concludes. “No single exposure like this is likely, on its own, to meaningfully change an individual child’s risk.”
The research was published in Med.
