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can still be considered plausible if their usual role relates to brain function in some way . Environmental factors aren ’ t as well catalogued , measured and tracked . But the better epidemiological studies do look for correlations with credible and pre-identified factors of interest ( so , not Scripps Spelling Bee words ).

For feasibility ’ s sake , work on environmental factors in autism has tended to focus on inputs that have broad effects on brain development . Robinson points to extreme preterm birth , which is related to many kinds of neurodevelopmental disorders — autism among them .

Eventually , studies can add up to connect dots and arrive at a plausible story of cause and effect . For example , along with preterm birth , air pollution also has been linked to autism risk . Another recent study found that when oil and power plants close down , preterm births in the region drop . It ’ s therefore a reasonable hypothesis that very preterm birth operates as an intermediate between air pollution exposure and autism .

Lyall believes that prenatal exposures to environmental pollutants that can behave like hormones are particularly strong candidates for involvement in autism risk .

These chemicals , collectively known as endocrine-disrupting compounds , include pesticides and even heavy metals , and they are pretty much everywhere — in air , land , water , food and us .

Some research suggests , for example , that exposure to the endocrine disruptor mercury in air pollution raises autism odds . The studies are few and the data haven ’ t overwhelmingly showed increases in risk , Lyall acknowledges , “ but I think that it ’ s an interesting and important area for future research given the lack of regulation around these chemicals , their ubiquity in the environment and their known adverse effects on broader neurodevelopment .”

Researchers have also homed in on plausible biological bases for a couple of other potential environmental effects . Gozzi points to animal studies , mostly in mice , that bolster human work linking autism in a child with prenatal exposure to a mother ’ s ramped-up immune responses as a result of infections . Again , Gozzi stresses that the findings are far from definitive , and most studies involving humans have focused on infections severe enough to require hospitalization .

Another unearthed link is to paternal age at conception :

Studies find that autism risk increases with the age of the father , usually starting in the thirties or forties , although the age range and magnitude of the increase vary among different studies . The cells that give rise to sperm tend to accumulate new mutations over the years , so the sperm contain sequence changes that pass to offspring but aren ’ t present in the father ’ s own body cells . Some of these changes involve regions or genes already implicated in autism risk . Sperm also show changes in the chemical tagging of DNA that controls the activity of genes .

Establishing environmental cause unequivocally is almost impossible , because of ethical constraints . It ’ s one thing to examine blood or tissue samples for genetic variants that track with autism diagnoses . It ’ s another thing entirely to manipulate factors to see if they induce autism or not . No one ’ s going to deliberately infect a pregnant woman or have a group of men specifically delay fatherhood just to test how these factors influence autism odds .

Researchers instead are stuck finding correlations between these factors and then looking at available measures , such as changes in gene activity , accrual of mutations over the

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