Prenatal exposure to fine particulate matter components and autism risk in childhood

Importance — Prenatal and early-life exposure to fine particulate matter (PM2.5) has been associated with autism spectrum disorder (ASD), but the role of individual components and timing of exposure remains unclear.

Objective — To examine associations between prenatal and first-year-of-life exposure to PM2.5 components and ASD diagnosis, and identify potentially sensitive periods during pregnancy.

Design, setting, and participants — This cohort study conducted in Ontario, Canada, used administrative health data covering approximately 98% of births in the province. The cohort included singleton live births from Ontario hospitals between April 1, 2002, and December 31, 2022, with gestational age 36 to 42 weeks, birth weight 500 to 6800 g, maternal age 15 to 55 years, complete residential history, and provincial health insurance coverage. At least 18 months of follow-up was required for postnatal exposure analyses.

Exposures — Biweekly concentrations of PM2.5 components (black carbon, dust, ammonium, nitrate, organic matter, sulfate, sea salt) and weekly NO2 and O3 from conception to age 36 weeks. Prenatal models were adjusted for postnatal exposure using annual averages. Pollutant levels were estimated using satellite data, chemical transport models, and ground-based measurements.

Main outcomes and measures — ASD diagnosis by age 5 years. Cox proportional hazards models were used to assess associations, and distributed lag nonlinear models identified sensitive exposure windows.

Results — Among 2 183 324 births (mean [SD] maternal age, 30.5 [5.4] years; mean [SD] gestational age at birth, 39.2 [1.1] weeks; 1 152 040 female infants [48.9%]), prenatal exposure to PM2.5, sulfate (SO42−), and ammonium (NH4+), and postnatal exposure to ozone (O3), were associated with ASD. Hazard ratios (HRs) per 1-IQR increase for SO42− were 1.15 (95% CI, 1.06-1.25) and for NH4+ was 1.12 (95% CI, 1.01-1.23). PM2.5 mass excluding SO42− and NH4+ during their respective critical windows was not associated with ASD (HR, 1.04; 95% CI, 0.92-1.19). O3 exposure during weeks 26 to 30 (HR, 1.03; 95% CI, 1.00-1.05) and over the first year (HR, 1.09; 95% CI, 1.01-1.17) was also associated with ASD.

Conclusions and relevance — In this large cohort study, prenatal exposure to specific PM2.5 components and postnatal O3 exposure were associated with ASD risk. The second and third trimesters may represent sensitive exposure windows. These findings support further research on air pollution’s role in ASD etiology.