The prevalence of autism spectrum disorders (ASDs) has been increasing during the last 10 years with increasing burden on society. While genetic risk factors are widely implicated in ASDs, the current increase is not likely to result from genetic factors alone and it is possible that environmental factors may augment known genetic risks. Current research examining biomarkers of oxidative stress and inflammation in children with an ASD suggests that these pathways may play a role in etiology. We propose to examine the association of air pollution, a common exposure that induces inflammation and oxidative stress, with autism. Using data collected as part of the Childhood Autism Risks from Genetics and the Environment Study (CHARGE) we will assess the role of traffic related air pollutants in autism risk based on monthly exposure at each child's home during prenatal, perinatal and postnatal time points. We plan to genotype 384 single nucleotide polymorphisms (SNPs) in 17 candidate genes and to examine SNP-air pollution interactions. This work may provide important insight into the etiology of ASDs and evidence for risk due to a common environmental exposure.
In this study we seek to examine if air pollution due to traffic, a common environmental exposure, increases risk for ASD. We will also examine genes that process pollutants in the body to determine if they are different in children with and without autism, and to see if these genes interact with air pollution to increase autism risk. We believe that this work may provide important insight into what causes ASDs and evidence for risk due to a common exposure increasing in the environment (traffic related air pollution).
