Perinatal exposure to hazardous air pollutants and autism spectrum disorders at age 8.
BACKGROUND
Hazardous air pollutants are plausible candidate exposures for autism spectrum disorders. They have been explored in recent studies for their role in the development of these disorders.


METHODS
We used a prevalent case-control design to screen perinatal exposure to 35 hazardous air pollutants for further investigation in autism etiology. We included 383 children with autism spectrum disorders and, as controls, 2,829 children with speech and language impairment. All participants were identified from the records-based surveillance of 8-year-old children conducted by the Autism and Developmental Disabilities Monitoring Network in North Carolina (for children born in 1994 and 1996) and West Virginia (born in 1992 and 1994). Exposures to ambient concentrations of metal, particulate, and volatile organic air pollutants in the census tract of the child's birth residence were assigned from the 1996 National Air Toxics Assessment annual-average model. We estimated odds ratios (ORs) for autism spectrum disorders and corresponding 95% confidence intervals (CIs), comparing across the 20th and 80th percentiles of log-transformed hazardous air pollutant concentration among the selected controls, using semi-Bayes logistic models and adjusting for sampling variables (surveillance year and state), a priori demographic confounders from the birth certificate and census, and covarying air pollutants.


RESULTS
We estimated many near-null ORs, including those for metals, established human neurodevelopmental toxicants, and several pollutants that were elevated in a similar study in California. Hazardous air pollutants with more precise and elevated OR estimates included methylene chloride, 1.4 (95% CI = 0.7-2.5), quinoline, 1.4 (1.0-2.2), and styrene, 1.8 (1.0-3.1).


CONCLUSIONS
Our screening design was limited by exposure misclassification of air pollutants and the use of an alternate developmental disorder as the control group, both of which may have biased results toward the null. Despite these limitations, methylene chloride, quinoline, and styrene emerged (based on this analysis and prior epidemiologic evidence) as candidates that warrant further investigation for a possible role in autism etiology.
Kalkbrenner
Amy E
AE
Department of Epidemiology, University of North Carolina, Chapel Hill, NC 27599, USA. amyk@unc.edu
Daniels
Julie L
JL
Chen
Jiu-Chiuan
JC
Poole
Charles
C
Emch
Michael
M
Morrissey
Joseph
J
D000393:Air Pollutants / Q000009:adverse effects* / Q000032:analysis; D001499:Bayes Theorem; D016022:Case-Control Studies; D002648:Child; D002659:Child Development Disorders, Pervasive / Q000139:chemically induced* / Q000453:epidemiology / Q000209:etiology; D016001:Confidence Intervals; D004781:Environmental Exposure / Q000009:adverse effects*; D005260:Female; D006801:Humans; D016015:Logistic Models; D008297:Male; D009657:North Carolina / Q000453:epidemiology; D016017:Odds Ratio; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced*; D014903:West Virginia / Q000453:epidemiology
D000393:Air Pollutants