UC Davis researcher opens window to environment, autism link

By Rachel Zamzow


Hertz-Picciotto presents her research at the MU Life Sciences & Society Symposium. Photo by Roger Meissen/Bond LSC

COLUMBIA, Mo. – Humans are resilient creatures. We are equipped to withstand insults to our system, from genetic mutations to environmental risks, such as exposure to toxins. But when these insults collide, certain problems can arise.

This is the case for autism, a developmental disorder that affects an individual’s ability to communicate and engage in social interactions. Early twin studies led scientists to think autism was driven primarily by genetics. In these studies, if one child of a set of identical twins had autism, the chance of the other also having autism was up to 90 percent.

But when environmental epidemiologists like Irva Hertz-Picciotto joined autism research in the 2000s, the focus of the field broadened to include factors outside the genome.

“Instead of thinking about genes versus the environment, I like to think about it as genes and the environment,” Hertz-Picciotto said during her talk at the University of Missouri Life Sciences & Society Symposium, March 13 – 15. This year’s iteration of the annual symposium explored the topic of epigenetics — factors that can alter gene expression without affecting the genetic code.

Hertz-Picciotto, a professor of public health sciences at the University of California, Davis, studies these factors in the context of the environment: what we eat, breathe and experience both before and after birth. And she’s linking several of these factors to the risk of having autism.

In an extensive investigation that launched in 2003, Hertz-Picciotto and her team have assessed more than 1,800 families whose children have autism, developmental delay or are typically developing with hopes of identifying environmental influences that increase the risk of autism.

This study focuses on modifiable environmental factors that may inform interventions, Hertz-Picciotto said. For example, she has studied nutrition during pregnancy, such as the intake of folic acid, which is known to reduce the risk of spina bifida and other neural tube defects.

She found that lower intake of folic acid during pregnancy was associated with a greater risk of having a child with autism. But this effect was present even before conception, as mothers with autistic children were less likely to have taken folic acid supplements three months before pregnancy.

Environmental effects can extend beyond the womb, according to Hertz-Picciotto, who has also explored exposure to air pollution as it relates to autism. In one study, families who lived less than two tenths of a mile from a freeway had an almost two-fold increase in the risk of having a child with autism. And this link remained when Hertz-Picciotto’s group accounted for potential confounds like socio-economic status.

Hertz-Picciotto hopes to find environmental factors that point to an underlying set of biological pathways that are perturbed in autism. Her efforts may also lead to a more refined understanding of why autism’s prevalence appears to be increasing in the U.S. Though there are many possible explanations for this trend, other conditions with environmental roles, such as obesity and asthma, are also on the rise.

“I hope I get to see the day when the rates stop climbing and really fall,” she said.

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