The dramatic increase in prevalence rates of Autism Spectrum Disorders (ASDs) over recent decades likely reflects the influence of multiple factors. In the current paper, it is argued ASDs can result from an interaction between genetic susceptibilities and environmental exposures. Specifically, we hypothesize that fetal or infantile exposure to methyl mercury containing pollution by individuals with biologically inhibited antioxidant functions contributes to development of autism. Correlational data reveal that ASD rates are higher in areas of greater pollution levels, and autistic individuals exhibit biological evidence of mercury toxicity. Further, oxidative stress and decreased antioxidant activities are manifested in individuals with ASDs, specifically autism. Taken together, available evidence supports a methyl mercury-induced oxidative stress model of the disorders for at least some sufferers. Consequently, legislative efforts should focus on preventing exposures to methyl mercury and other toxicants that can adversely impact neurodevelopment. [ABSTRACT FROM AUTHOR]