Suffering with autism spectrum disorder (ASD) or attention‑deficit/hyperactivity disorder (ADHD) as a child is difficult enough. Now, scientists tell us that those who suffer from ASD and ADHD also face higher vulnerability to common plastic pollutants.
A recent study found that their bodies detoxify bisphenol A (BPA) less efficiently than neurotypical peers, increasing the time their tissues are exposed to this chemical.
Dr. T. Peter Stein of Rowan‑Virtua School of Osteopathic Medicine led the study. Researchers measured urine glucuronidation, the liver process that adds a sugar molecule to BPA so it can be excreted.
Children with ASD and ADHD had reduced BPA detoxification efficiency compared to the control group.
BPA glucuronidation was about 11% lower in the ASD group and 17% lower in those with ADHD, while differences in phthalate DEHP detoxification followed the same trend but were not statistically significant.
Children with ASD and ADHD often have weaker detox systems, leaving them exposed to BPA in the body longer.
That doesn’t guarantee illness from BPA but raises concern. Stein noted that this was the “first hard biochemical evidence” linking impaired BPA clearance to neurodevelopmental disorders.
Individuals with ASD often face challenges in social communication and exhibit restricted or repetitive behaviors.
They might have difficulty interpreting social cues, maintaining eye contact, or adjusting to changes in routine.
Sensory sensitivities – such as heightened responses to light, sound, or textures – are also common. ASD presents across a wide spectrum, so the degree and nature of symptoms can vary greatly from person to person.
In contrast, ADHD primarily involves persistent patterns of inattention, hyperactivity, and impulsivity that interfere with daily functioning.
People with ADHD may struggle to focus, stay organized, or complete tasks, often acting without thinking or having trouble sitting still.
While ADHD and ASD are separate diagnoses, they can co-occur, and some traits overlap – such as difficulties with executive function and emotional regulation.
Glucuronidation converts toxins like BPA into water‑soluble compounds that exit via urine. In this study, mass spectrometry tracked both bound and unbound BPA.
A lower percentage of detoxification indicated less efficient excretion. Stein’s team confirmed the effect held true even when accounting for urine strength using creatinine levels.
Of twelve detox pathways tested, only BPA and DEHP stood out, suggesting a specific vulnerability rather than a broad weakness.
Comparing results with metabolomic profiles, ASD and ADHD children showed unique patterns tied to BPA metabolism that controls did not share.
BPA and DEHP act as endocrine disruptors, interfering with hormone signals. If detoxification is compromised, these chemicals linger longer in the body during critical phases of brain development.
Though genetic vulnerability may play a role, this adds a measurable biological mechanism to the environmental risk picture.
Sterile in lab animals, DEHP affects neurodevelopment via epigenetic changes such as DNA methylation. A recent analysis of prenatal exposure in 847 Australian children linked DEHP levels to later ASD and ADHD symptoms.
Methylation in key genes and neural cell networks showed mediation effects between 21% and 80%. These epigenetic footprints reinforce the idea that plastics can affect neurodevelopment through non-genetic pathways.
This study builds on a large body of research connecting neurodevelopmental disorders to environmental pollutants.
Epidemiological studies have associated prenatal exposure to air pollution, flame retardants, and pesticides with elevated ASD and ADHD risk.
The common thread in these findings is timing; exposure during pregnancy and early life seems to matter most.
Regulatory bodies have long debated what constitutes a “safe” exposure level for these chemicals.
The U.S. Food and Drug Administration and the European Food Safety Authority have reviewed BPA safety multiple times, but the growing evidence suggests current thresholds may not be low enough for sensitive populations, especially children with neurodevelopmental conditions.
This study doesn’t claim BPA or DEHP cause autism or ADHD. But it does show that children with these conditions often metabolize these chemicals less efficiently.
Because BPA exposure is widespread (found in everything from food can liners to thermal paper) this raises questions about safety thresholds for all kids, not just those with ASD or ADHD.
Reducing reliance on BPA and phthalates in daily life (choosing glass or stainless steel containers, fresh food over cans, and avoiding receipts) can help limit exposure.
Policy swings already reflect this concern: several countries are phasing out DEHP and tightening BPA regulations.
Future studies could investigate whether impaired detoxification is present from birth or develops over time. Longitudinal tracking of exposure, detox pathway function, and neurodevelopment could help answer this.
Researchers also recommend examining genetic variants in detox enzymes, which might identify individuals most at risk.
On the epigenetic side, researchers are starting to connect prenatal chemical exposure to long‑term DNA changes in specific brain regions, pointing to windows of vulnerability.
That knowledge could eventually guide nurse‑led intervention, dietary changes, or policies to protect early brain development.
Children with ASD and ADHD are at a double vulnerability: genetic and developmental differences and a slower ability to clear everyday pollutants.
While this study doesn’t offer advice on treatment or diagnosis, it certainly does ask parents and policymakers to seriously consider chemical exposure in early childhood and pregnancy as a significant factor in neurodevelopment.
The study is published in PLOS ONE.
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