Perinatal exposure to hazardous air pollutants and autism spectrum disorders at age 8

Abstract

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.

FIGURE

Odds ratios (circles) and 95% confidence intervals (bars) for ambient concentrations of hazardous air pollutants and autism spectrum disorders versus speech and language impairment estimated using different logistic regression models. ORs compare a high exposure (80th percentile) to a low exposure (20th percentile), as shown in Table 3. Single-pollutant estimates include each pollutant in a separate model. Multipollutant models include all listed pollutants except for coke oven emissions. The unadjusted model (n = 3212; 383 cases) controls for surveillance year and state. Adjusted and semi-Bayes models (n = 3177; 374 cases) also include a priori confounders: race (non-Hispanic white, black, other), maternal education (