A Systematic Review and Meta-Analysis of Multiple Airborne Pollutants and Autism Spectrum Disorder

Abstract

BackgroundExposure to ambient air pollution is widespread and may be detrimental to human brain development and a potential risk factor for Autism Spectrum Disorder (ASD). We conducted a systematic review of the human evidence on the relationship between ASD and exposure to all airborne pollutants, including particulate matter air pollutants and others (e.g. pesticides and metals).ObjectiveTo answer the question: “is developmental exposure to air pollution associated with ASD?”MethodsWe conducted a comprehensive search of the literature, identified relevant studies using inclusion/exclusion criteria pre-specified in our protocol (registered in PROSPERO, CRD # 42015017890), evaluated the potential risk of bias for each included study and identified an appropriate subset of studies to combine in a meta-analysis. We then rated the overall quality and strength of the evidence collectively across all air pollutants.ResultsOf 1,158 total references identified, 23 human studies met our inclusion criteria (17 case-control, 4 ecological, 2 cohort). Risk of bias was generally low across studies for most domains; study limitations were related to potential confounding and accuracy of exposure assessment methods. We rated the quality of the body of evidence across all air pollutants as “moderate.” From our meta-analysis, we found statistically significant summary odds ratios (ORs) of 1.07 (95% CI: 1.06, 1.08) per 10-μg/m3 increase in PM10 exposure (n = 6 studies) and 2.32 (95% CI: 2.15, 2.51) per 10-μg/m3 increase in PM2.5 exposure (n = 3 studies). For pollutants not included in a meta-analysis, we collectively evaluated evidence from each study in rating the strength and quality of overall evidence considering factors such as inconsistency, imprecision, and evidence of dose-response. All included studies generally showed increased risk of ASD with increasing exposure to air pollution, although not consistently across all chemical components.ConclusionAfter considering strengths and limitations of the body of research, we concluded that there is “limited evidence of toxicity” for the association between early life exposure to air pollution as a whole and diagnosis of ASD. The strongest evidence was between prenatal exposure to particulate matter and ASD. However, the small number of studies in the meta-analysis and unexplained statistical heterogeneity across the individual study estimates means that the effect could be larger or smaller (including not significant) than these studies estimate. Our research supports the need for health protective public policy to reduce exposures to harmful airborne contaminants among pregnant women and children and suggests opportunities for optimizing future research.

Pre‐natal brain development as a target for urban air pollution

“…In mice, the central nervous system could be a direct or indirect target (via the olfactory or lung pathway, respectively) of particles that elicit a neuroinflammatory response in various brain regions . In human beings, our group and others have shown that exposure to air pollution in utero is associated with increased risk of neurodevelopmental delay and autism . We also found that air pollution exposure during childhood is inversely associated with brain executive trajectories, and others have found an inverse association with academic achievement and higher risk of pathological changes associated with Alzheimer's disease .…”

Autism genes are selectively targeted by environmental pollutants including pesticides, heavy metals, bisphenol A, phthalates and many others in food, cosmetics or household products

“…Meta-analysis studies support the involvement of particulate matter or ambient air pollution in relation to autism in North American [81,309] but not European studies [87] and for the prenatal uses of SSRI's [310] or Vitamin D deficiency in autistic patients [311] but the diverse methodologies used to measure timing and exposure have rendered clear conclusions difficult for these and others such as phthalate esters [312]. These problems are confounded by the gene/environment interactions raised in this study (i.e.…”

Acute effects of fine particulate matter constituents on mortality: A systematic review and meta-regression analysis

“…Therefore, we assessed the risk of bias within each study based on the Office of Health Assessment and Translation (OHAT) tool by the National Institutes of Environmental Health Sciences-National Toxicology Program (NIEHS-NTP), and the Navigation Guide by the University of California, San Francisco (OHAT, 2015; Lam et al, 2016). Both of these tools assess the risk of bias of individual studies based on several risk of bias domains (e.g., selection bias, confounding, measurement, missing data, reporting) in a similar way.…”