Associations between prenatal PM2.5 exposures and intellectual disability: Are there differential impacts based on
Roger A Renteria1, Sara E Grineski1, Jacqueline Gomez2
1University of Utah, Department of Sociology, 380 S. 1530 E., Rm. 301, Salt Lake City, UT 84112, USA.
Abstract:
Prenatal fine particulate matter (PM2.5) has been associated with intellectual disability (ID) and autism spectrum disorder (ASD), separately. Its role in co-occurring ID with ASD (ID + ASD) is less understood. To address this gap, this study uniquely disaggregates ID-only from ID + ASD to assess the associations between prenatal PM2.5 exposure and odds of ID-only and ID + ASD across multiple exposure windows and measures. For children born in Utah, U.S.A., children with ID (ID-only and ID + ASD) were matched 1:3 with non-ID affected controls. PM2.5 exposure was estimated across four prenatal periods (i.e., preconception, 1st, 2nd, and 3rd trimester) using long-term averages and exceedances of WHO and U.S. NAAQS 24-h thresholds and assigned to children. Associations were examined using multilevel multinomial logistic regressions. Results show that increase in long-term PM2.5 during preconception and first trimester was associated with increased odds of ID-only and ID + ASD. Exceedances of the WHO 24-h threshold (15 μg/m3) during preconception were linked to ID-only, while first trimester WHO 24-h exceedances were linked to both ID-only and ID + ASD. U.S. NAAQS 24-h threshold (35 μg/m3) exceedances during preconception and first trimester were associated with ID + ASD. Results reveal that long-term PM2.5 exposure during preconception and the first trimester elevates risk for both ID-only and ID + ASD. ID + ASD appears particularly sensitive to preconception and first trimester exceedances of the U.S. NAAQS 24-h threshold, whereas ID-only may be more sensitive to exceedances of the WHO 24-h threshold during preconception. By distinguishing these neurodevelopmental outcomes, these results underscore timing and magnitude of prenatal PM2.5 exposure differentially influence neurodevelopmental risk. They also highlight the need for targeted public health interventions and stronger air quality regulations to protect early neurodevelopment.
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