Eleven studies were included in this large review of air pollution and its contribution to autism. Harvard scientists looked at results that included 313,301 children. There was a 64% increase in autism during early childhood for each 10 microgram per cubic meter increase in 2.5 particulate matter air pollution. Primary sources include coal-fired power plants, incineration and vehicle traffic. When exposure occurred during the third trimester of pregnancy, there was a 31% increase in autism for each 10 microgram/m3 increase in exposure. Increased rates of autism were also detected at very low levels of only 8 micrograms/m3. As there was a strong dose/response effect, this study provides credibility to the increasing link between air pollution and autism, and stresses the importance of reducing fossil fuel air pollution immediately. As PM2.5 is also a major component of car and truck exhaust, higher rates of autism would be expected for families living close to busy traffic roadways, especially if less than 300 feet.
ABSTRACT
The impact of prenatal and early childhood exposure of ambient particulate matters (PMs) on the risk of autism spectrum disorder (ASD) in children remained inconclusive, particularly at low levels below current National Ambient Air Quality Standards. The study summarizes the epidemiological association between PM exposure and risks of ASD in children. PubMed, Embase, Web of Science, Cochrane Library, Compendex, Biosis Previews, and Agricultural & Environmental Science Databases for studies published before February 2020. Original studies with the following information were included: (a) exposure of ambient PM (including PM2.5 and/or PM10); (b) ASD as the outcome of interest in children; (c) effect estimates of relative risk (RR), odds ratio (OR), or hazard ratio. The risks of ASD are summarized at different exposure windows (i.e. first, second, third trimesters, and early childhood period) by using a random-effects model. Exposure-response meta-regression was performed across various background levels of PM2.5. We used Newcastle–Ottawa Scale for quality assessment. Eleven studies (two cohort and nine case-control studies) and 313 301 children were enrolled. Overall, the risk of ASD increased by 64% (pooled RR = 1.64, 95% CI = 1.16–2.34) and 31% (pooled RR = 1.31, 95% CI = 1.08–1.58), with exposure to 10 μg m−3 increment of PM2.5 during early childhood and prenatal periods, respectively. Stratifying by three trimesters of prenatal period, the risk of ASD increased 35% per 10 μg m−3 difference of PM2.5 exposure during the third trimester (pooled RR = 1.35, 95% CI = 1.18–1.55), but not during the first and second trimesters. The risks of ASD persisted at the background PM2.5 levels from 8 μg m−3 (pooled RR = 1.30, 95% CI = 1.02–1.66) and onward. Our findings suggested an association between PM2.5 exposure and risks of ASD, particularly within specific exposure windows, even at low background levels of PM2.5.