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Exposure to components of fine particulate matter is associated with risk of autism spectrum disorder
1. In this cohort of singleton births in Ontario, prenatal exposure to specific components of Fine particulate matter (PM2.5), specifically sulfate (SO42-) and ammonium (NH4+), was associated with an increased autism spectrum disorder (ASD) risk, while overall PM2.5 was not.
2. The greatest risk occurred during the second and third trimesters for PM2.5 components, and the first year of life for ozone (O3).
Evidence Rating Level: 2 (Good)
Study Rundown: Fine particulate matter (PM2.5) is a known pollutant associated with many health issues and remains a large public health concern. Fetal exposure to these toxins in pre-natal or early post-natal periods has been associated with neurodevelopmental conditions such as autism spectrum disorder (ASD), potentially through mechanisms such as inflammation, oxidative stress, and epigenetic changes. However, most previous studies have investigated PM2.5 as a whole, overlooking the distinct aspects of its chemical composition that may have varying effects. To address these gaps, this retrospective cohort study examined the associations between prenatal and early postnatal exposure to PM2.5 components, nitrogen dioxide (NO2), and ozone (O3) and the risk of ASD diagnosis.
Concentrations of PM2.5 components, such as black carbon, dust, and ammonium, were assigned biweekly, while NO2 and O3 were assigned weekly from conception to 36 weeks of age. Follow-up took place from birth until age 5 years or ASD diagnosis, if that occurred sooner. Prenatal exposure to PM2.5 was only significantly associated with ASD when not accounting for the specific components. Among PM2.5 components, NH4+ was consistently associated with ASD risk across adjusted models. Several limitations exist, including decreased generalizability due to differences in socioeconomic status and excluding individuals without OHIP coverage. Despite the limitations, this study provided new evidence that PM2.5 components were associated with increased ASD risk, highlighting the importance of implementing public health strategies to reduce harmful air pollution.
Click here to read the study in JAMA Network Open
In-Depth [retrospective cohort study]: This population-based retrospective cohort study was designed to assess if exposure to environmental pollutants ASD diagnosis are associated. A total of 2,183,324 singleton live births were included (mean [SD] maternal age at delivery 30.5 [5.4], mean [SD] gestational age at birth, 39.2 [1.1] weeks). During the first year of life, there was a significant association between prenatal PM2.5 exposure and increased risk of ASD (HR, 1.15; 95% CI, 1.07-1.23; per 1-IQR increase, 3.5 μg/m3 increase). However, after adjusting for NH4+ and SO42- during their critical periods, the association was no longer significant. Prenatal exposure to NH4+ was associated with an elevated risk of ASD in PM2.5 residual variation-adjusted (HR, 1.13; 95% CI, 1.05-1.23, per 1-IQR [0.60 μg/m3]) and postnatal exposure models (HR, 1.12; 95% CI, 1.01-1.23). O3 exposure was initially associated with increased ASD risk (HR, 1.10; 95% CI, 1.06-1.15; per 1-IQR [19.14 ppb]) in PM2.5 adjusted models; however, this association weakened after adjusting for first year exposure. Among exposure periods, only the first year of O3 exposure demonstrated a significant association with ASD. In summary, prenatal exposure to specific components of PM2.5 (NH4+ and SO42-), and postnatal O3 were associated with increased risk of ASD.
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