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The potential role of airborne particulates from air pollution in causing autism spectrum disorder through impacts on the developmental process

Although autism spectrum disorder (ASD), which remains incurable, is an idiopathic disorder, it has been associated with an assortment of both environmental and genetic factors for pathogenesis despite the fact that the exact pathogenic factors of ASD remain undetermined. One such environmental factor with a potential impact on ASD development is air pollution via early stage exposure to airborne particles, i.e., particulate matter (PM) with 2.5 or 10 microns diameters (PM2.5 or PM10). While a number of studies have identified the impact air pollutants has on ASD, this thesis investigates the potential roles of the particle concentration, timing of exposure, and chemical type of particle have on inducing ASD. The central rationale is that exposure to small particles, including but not limited to PM2.5 and PM10, in high concentrations during development may be associated with an increase in the rates of ASD. To examine this possibility, published literature has been analytically reviewed to assess the impacts of PM2.5 and PM10 on the brain and mechanisms through which the particles act to influence brain cells. In particular, there is a strong association between small particle exposure, especially during 2nd and 3rd trimester of pregnancy, and autism spectrum disorder prevalence. Overall, the data suggest that PM-triggered oxidative stress and neuroinflammation in the developing brain may be partially responsible for the pathophysiological onset of ASD. However, additional investigations are needed in order to determine whether early life exposure to PM2.5 and PM10 can be specifically linked ASD-like brain pathology, behavioral evolvement, and ASD onset. Furthermore, the exact mechanisms underlying the ASD pathogenic effect of airborne particles have to be uncovered before effective preventive and therapeutic interventions can be devised.

Identiferoai:union.ndltd.org:bu.edu/oai:open.bu.edu:2144/48358
Date07 March 2024
CreatorsPaul, Jacob
ContributorsMcKnight, C. James
Source SetsBoston University
Languageen_US
Detected LanguageEnglish
TypeThesis/Dissertation

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