We’ve been searching for triggers of autism with a microscope; we need a wider lens.
The rise of autism has sent scientists deep into the genome, searching for answers in DNA sequence. Yet the harder they look, the clearer it becomes that the answer isn’t hidden in the genome. Rare mutations account for only a fraction of cases, and the common variants we keep cataloging are—by definition—common. If they alone dictated destiny, nearly everyone would meet the diagnostic checklist. Something outside the genome is nudging children’s brains off course.
A web of factors
That “something” is not a single villain but a web of factors. Prenatal air pollution impairs the fetal brain; organophosphate pesticides sabotage synapse formation; and phthalates disrupt hormones just when they should choreograph growth. Combine pesticide exposure with inadequate folate, Bisphenol A with the aromatase gene, or air pollution and the MET gene, and risk increases substantially. These findings don’t cancel genetics; they reveal its contingency.
We have been slow to accept this because toxic chemicals and pollutants are messy and political. Genes are tidy: you can sequence them in a lab and implicate no one. Pollution points to factories, zoning laws, and weak regulation. That invites accountability. Yet evidence is evidence: children downwind of highways or born near pesticide-treated fields reveal dose-related increases in autistic traits. By contrast, folic-acid supplementation—cheap, safe, and proven—cuts risk for some children.
A repeating pattern
The pattern echoes an older story. Lead once lurked in paint and gasoline. Industry insisted low doses were harmless until researchers widened the frame—tracking IQ, attention, and crime. We phased lead out, and children’s blood levels plummeted. Autism research stands at a similar crossroads: cling to genetic determinism or chart the exposome—the sum of lifetime environmental exposures—and act on what we learn.
Action doesn’t demand certainty. We already know how to reduce exposures: enforce clean-air rules, ban neurotoxic pesticides, replace hormone-disrupting plastics, and fortify diets with folate. These are population strategies—unflashy but high-return—like the sanitation and vaccination drives that once tamed infectious killers.
Across autism, ADHD, and learning disorders, studies converge on a core insight: brain development lies on a spectrum shaped by many influences—genetic coding, nutrient supply, and an ever-changing mix of environmental chemicals. Some exposures adjust the melody; others throw the orchestra out of tune. When the discord grows, a child’s developmental path can shift in ways we are only beginning to map. What we do know is that toxic chemicals and synthetic chemicals exert a powerful pull on that trajectory.
Understanding this interplay is no longer optional; it is central to preventing disability and promoting lifelong health.
Contact the author for references at blanphear@sfu.ca. This article first appeared in the Summer/Fall issue of the San Franscisco Marin Medicine journal (Volume 98, Number 3) in a special section on children's environmental health. This and previous issues of the SF/Marin Med Society journal featuring articles from CHE are available in our Resource Library.
Bruce Lanphear, MD, MPH, is a preventive medicine physician and professor at Simon Fraser University in Vancouver. For over 30 years, he’s studied how toxic chemicals—like lead, fluoride, and pesticides—impact human health, especially children. His research helped set federal standards for lead and sparked the landmark conclusion that no level of lead is safe. To reach a wider audience, Bruce launched Little Things Matter, a project that produces sharp, engaging videos revealing how invisible chemical exposures shape our health—and how we can prevent harm before it starts. On his Substack, Bruce shares the stories behind the science: what we’ve learned, what we’ve overlooked, and what’s needed to protect future generations.