Prenatal air pollution, maternal immune activation, and autism spectrum disorder.

BACKGROUND

Autism Spectrum Disorder (ASD) risk is highly heritable, with potential additional non-genetic factors, such as prenatal exposure to ambient particulate matter with aerodynamic diameter < 2.5 µm (PM) and maternal immune activation (MIA) conditions. Because these exposures may share common biological effect pathways, we hypothesized that synergistic associations of prenatal air pollution and MIA-related conditions would increase ASD risk in children.

OBJECTIVES

This study examined interactions between MIA-related conditions and prenatal PM or major PM components on ASD risk.

METHODS

In a population-based pregnancy cohort of children born between 2001 and 2014 in Southern California, 318,751 mother-child pairs were followed through electronic medical records (EMR); 4,559 children were diagnosed with ASD before age 5. Four broad categories of MIA-related conditions were classified, including infection, hypertension, maternal asthma, and autoimmune conditions. Average exposures to PM and four PM components, black carbon (BC), organic matter (OM), nitrate (NO), and sulfate (SO), were estimated at maternal residential addresses during pregnancy. We estimated the ASD risk associated with MIA-related conditions, air pollution, and their interactions, using Cox regression models to adjust for covariates.

RESULTS

ASD risk was associated with MIA-related conditions [infection (hazard ratio 1.11; 95% confidence interval 1.05-1.18), hypertension (1.30; 1.19-1.42), maternal asthma (1.22; 1.08-1.38), autoimmune disease (1.19; 1.09-1.30)], with higher pregnancy PM [1.07; 1.03-1.12 per interquartile (3.73 μg/m) increase] and with all four PM components. However, there were no interactions of each category of MIA-related conditions with PM or its components on either multiplicative or additive scales.

CONCLUSIONS

MIA-related conditions and pregnancy PM were independently associations with ASD risk. There were no statistically significant interactions of MIA conditions and prenatal PM exposure with ASD risk.