A certain gene mutation and exposure to air pollution can interact to heighten the risk for autism, finds a groundbreaking study that will be published in Epidemiology.

The lead author of the study, Heather Volk, at the Keck School of Medicine of USC, had already drawn a link between autism and certain levels air pollution exposure during pregnancy and early infancy. Additionally, work done by study co-author, Daniel Campbell (also at USC), furthered evidence that autism is more likely to occur when people carry a certain form of the so-called MET gene. The current study aimed to explore whether these seperate factors could combine and augment the chances for autism, especially since animal studies showed that pollution could interfere with the MET gene.

The researchers assessed children participating in California’s Childhood Autism Risk from Genetics and the Environment study. The 408 children in the study were between the ages of 2 and 5, and more than half of them had a form of autism spectrum disorder. The presence of MET gene mutations were detected via blood samples while the residential history of the children and their mothers and the respective traffic patterns and air quality readings of these areas provided an estimate of pollution exposure.

Nothing stood out when the authors compared children based on variation of the MET gene nor when there was a MET mutation but low level of pollution exposure. But when the authors looked at children who carried the altered MET gene and who were also prenatally exposed to high levels of pollution, they discovered that the likelihood for autism tripled compared to those who experienced neither of these risk factors.

“Although gene-environment interactions are widely believed to contribute to autism risk, this is the first demonstration of a specific interaction between a well-established genetic risk factor and an environmental factor that independently contribute to autism risk,” Campell explained in Autism Daily Newscast.

The MET gene variant, Campbell explained, controls expression of the MET protein in both the brain and the immune system, and predicts altered brain structure and function. “It will be important to replicate this finding and to determine the mechanisms by which these genetic and environmental factors interact to increase the risk for autism,” he said.

The study’s multifaceted takeaway corroborates with an extensive amount of research showing that the causes of autism are numerous and complex, with various factors usually interacting and ultimately altering the course of a child’s development. “The results may argue that research on autism’s genetic and environmental risk factors should not be done in isolation,” Alycia Halladay, senior director of environmental and clinical research at Autism Speaks, noted on the organization’s website. “We need further research to confirm the findings and determine the mechanisms underlying the gene-environment interaction.”