TY - JOUR
T1 - Prenatal air pollution, maternal immune activation, and autism spectrum disorder
AU - Yu, Xin
AU - Mostafijur Rahman, Md
AU - Carter, Sarah A.
AU - Lin, Jane C.
AU - Zhuang, Zimin
AU - Chow, Ting
AU - Lurmann, Frederick W.
AU - Kleeman, Michael J.
AU - Martinez, Mayra P.
AU - van Donkelaar, Aaron
AU - Martin, Randall V.
AU - Eckel, Sandrah P.
AU - Chen, Zhanghua
AU - Levitt, Pat
AU - Schwartz, Joel
AU - Hackman, Daniel
AU - Chen, Jiu Chiuan
AU - McConnell, Rob
AU - Xiang, Anny H.
N1 - Publisher Copyright:
© 2023
PY - 2023/9
Y1 - 2023/9
N2 - 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 (PM2.5) 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 PM2.5 or major PM2.5 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 PM2.5 and four PM2.5 components, black carbon (BC), organic matter (OM), nitrate (NO3–), and sulfate (SO42-), 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 PM2.5 [1.07; 1.03–1.12 per interquartile (3.73 μg/m3) increase] and with all four PM2.5 components. However, there were no interactions of each category of MIA-related conditions with PM2.5 or its components on either multiplicative or additive scales. Conclusions: MIA-related conditions and pregnancy PM2.5 were independently associations with ASD risk. There were no statistically significant interactions of MIA conditions and prenatal PM2.5 exposure with ASD risk.
AB - 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 (PM2.5) 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 PM2.5 or major PM2.5 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 PM2.5 and four PM2.5 components, black carbon (BC), organic matter (OM), nitrate (NO3–), and sulfate (SO42-), 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 PM2.5 [1.07; 1.03–1.12 per interquartile (3.73 μg/m3) increase] and with all four PM2.5 components. However, there were no interactions of each category of MIA-related conditions with PM2.5 or its components on either multiplicative or additive scales. Conclusions: MIA-related conditions and pregnancy PM2.5 were independently associations with ASD risk. There were no statistically significant interactions of MIA conditions and prenatal PM2.5 exposure with ASD risk.
KW - Autism spectrum disorders
KW - Interaction
KW - PM
KW - PM chemical components
KW - Susceptibility
UR - https://www.scopus.com/pages/publications/85168010130
U2 - 10.1016/j.envint.2023.108148
DO - 10.1016/j.envint.2023.108148
M3 - Article
C2 - 37595536
AN - SCOPUS:85168010130
SN - 0160-4120
VL - 179
JO - Environment International
JF - Environment International
M1 - 108148
ER -