Associations between prenatal PMexposures and intellectual disability: Are there differential impacts based on co-occurrence of autism spectrum disorder?

This study looked at air pollution exposure during pregnancy and its link to intellectual disability with and without autism. Researchers found that higher levels of fine particles in the air during the months before conception and first three months of pregnancy increased the risk of both conditions. Children with both intellectual disability and autism seemed more sensitive to higher pollution levels during early pregnancy.

This study examined prenatal fine particulate matter (PM₂.₅) exposure and its association with intellectual disability (ID) alone versus ID co-occurring with autism spectrum disorder (ID + ASD). Using Utah birth data with matched controls, researchers analyzed PM₂.₅ exposure across four prenatal periods using long-term averages and WHO/US air quality threshold exceedances. Results showed increased PM₂.₅ during preconception and first trimester elevated risk for both ID-only and ID + ASD. Notably, ID + ASD appeared particularly sensitive to US threshold exceedances during early pregnancy periods, while ID-only showed greater sensitivity to WHO threshold exceedances during preconception.

The findings suggest differential timing and magnitude effects of air pollution on neurodevelopmental outcomes.

Findings support the importance of air quality monitoring and protection during preconception and early pregnancy. Results suggest need for targeted interventions based on diagnostic profiles and highlight critical exposure windows for neurodevelopmental risk prevention strategies.

Sample size not reported. Study design unclear from abstract. Observational design cannot establish causation. Limited to Utah population which may affect generalizability. No information provided about confounding variables controlled for in the analysis.

Prenatal fine particulate matter (PM) 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 PMexposure 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.

PMexposure 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 PMduring preconception and first trimester was associated with increased odds of ID-only and ID + ASD.

Exceedances of the WHO 24-h threshold (15 μg/m) 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/m) exceedances during preconception and first trimester were associated with ID + ASD. Results reveal that long-term PMexposure 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 PMexposure differentially influence neurodevelopmental risk. They also highlight the need for targeted public health interventions and stronger air quality regulations to protect early neurodevelopment.