In a finding that points to a link between environmental toxins and autism, a new study shows that children who were exposed to the highest levels of traffic-related air pollution during gestation and in early infancy were three times more likely to be diagnosed with the neurodevelopmental disorder than were those whose early exposure to such pollutants was very low.
The study, published Monday in the Archives of General Psychiatry, found that early exposure to high levels of air pollution in general was linked to an increased likelihood of autism in a group of more than 500 children followed for several years from birth. The researchers gathered regional air quality data and used detailed calculations to estimate the air quality around the residence in which a child's mother spent her pregnancy and the resulting child spent his or her first year.
Their findings suggest that the link between air pollution and autism is evident largely at the highest levels of exposure, and slightly higher when the exposure comes later in a woman's pregnancy. The strongest link was found between exposure to nitrogen dioxide -- a pollutant found plentifully around freeways -- and autism, while exposure to particulates was less strongly linked to autism.
The abstract: of "Traffic-Related Air Pollution, Particulate Matter, and Autism," by Heather E. Volk, PhD, MPH; Fred Lurmann; Bryan Penfold; Irva Hertz-Picciotto, PhD; Rob McConnell, MD
Context Autism is a heterogeneous disorder with genetic and environmental factors likely contributing to its origins. Examination of hazardous pollutants has suggested the importance of air toxics in the etiology of autism, yet little research has examined its association with local levels of air pollution using residence-specific exposure assignments.
Objective To examine the relationship between traffic-related air pollution, air quality, and autism.
Design This population-based case-control study includes data obtained from children with autism and control children with typical development who were enrolled in the Childhood Autism Risks from Genetics and the Environment study in California. The mother's address from the birth certificate and addresses reported from a residential history questionnaire were used to estimate exposure for each trimester of pregnancy and first year of life. Traffic-related air pollution was assigned to each location using a line-source air-quality dispersion model. Regional air pollutant measures were based on the Environmental Protection Agency's Air Quality System data. Logistic regression models compared estimated and measured pollutant levels for children with autism and for control children with typical development.
Setting Case-control study from California.
Participants A total of 279 children with autism and a total of 245 control children with typical development.
Main Outcome Measures Crude and multivariable adjusted odds ratios (AORs) for autism.
Results Children with autism were more likely to live at residences that had the highest quartile of exposure to traffic-related air pollution, during gestation (AOR, 1.98 [95% CI, 1.20-3.31]) and during the first year of life (AOR, 3.10 [95% CI, 1.76-5.57]), compared with control children. Regional exposure measures of nitrogen dioxide and particulate matter less than 2.5 and 10 μm in diameter (PM2.5 and PM10) were also associated with autism during gestation (exposure to nitrogen dioxide: AOR, 1.81 [95% CI, 1.37-3.09]; exposure to PM2.5: AOR, 2.08 [95% CI, 1.93-2.25]; exposure to PM10: AOR, 2.17 [95% CI, 1.49-3.16) and during the first year of life (exposure to nitrogen dioxide: AOR, 2.06 [95% CI, 1.37-3.09]; exposure to PM2.5: AOR, 2.12 [95% CI, 1.45-3.10]; exposure to PM10: AOR, 2.14 [95% CI, 1.46-3.12]). All regional pollutant estimates were scaled to twice the standard deviation of the distribution for all pregnancy estimates.
Conclusions Exposure to traffic-related air pollution, nitrogen dioxide, PM2.5, and PM10 during pregnancy and during the first year of life was associated with autism. Further epidemiological and toxicological examinations of likely biological pathways will help determine whether these associations are causal.