Abstract
We appraise newly accumulated evidence of the impact of particle pollution on the brain, the portals of entry, the neural damage mechanisms, and ultimately the neurological and psychiatric outcomes statistically associated with exposures. PM pollution comes from natural and anthropogenic sources such as fossil fuel combustion, engineered nanoparticles (NP ≤ 100 nm), wildfires, and wood burning. We are all constantly exposed during normal daily activities to some level of particle pollution of various sizes—PM2.5 (≤2.5 µm), ultrafine PM (UFP ≤ 100 nm), or NPs. Inhalation, ingestion, and dermal absorption are key portals of entry. Selected literature provides context for the US Environmental Protection Agency (US EPA) ambient air quality standards, the conclusions of an Independent Particulate Matter Review Panel, the importance of internal combustion emissions, and evidence suggesting UFPs/NPs cross biological barriers and reach the brain. NPs produce oxidative stress and neuroinflammation, neurovascular unit, mitochondrial, endoplasmic reticulum and DNA damage, protein aggregation and misfolding, and other effects. Exposure to ambient PM2.5 concentrations at or below current US standards can increase the risk for TIAs, ischemic and hemorrhagic stroke, cognitive deficits, dementia, and Alzheimer’s and Parkinson’s diseases. Residing in a highly polluted megacity is associated with Alzheimer neuropathology hallmarks in 99.5% of residents between 11 months and ≤40 y. PD risk and aggravation are linked to air pollution and exposure to diesel exhaust increases ALS risk. Overall, the literature supports that particle pollution contributes to targeted neurological and psychiatric outcomes and highlights the complexity of the pathophysiologic mechanisms and the marked differences in pollution profiles inducing neural damage. Factors such as emission source intensity, genetics, nutrition, comorbidities, and others also play a role. PM2.5 is a threat for neurological and psychiatric diseases. Thus, future research should address specifically the potential role of UFPs/NPs in inducing neural damage.
Highlights
We live surrounded by environmental hazards including toxic compounds in air, water, soil, and food
Neurotoxic organic and inorganic compounds come from fossil fuel combustion, engineered nanoparticles, nanoplastics, and compounds resulting from disasters such as forest wildfires
NPs can travel anterograde, retrograde, and trans-synaptically from any portal of entry, altered proteins are capable of moving in all directions [14,15,17]; (3) protein misfolding, aggregation, and fibrillation take place in neural cells and follow the NP path’s initial portal of entry [17,22,23,24]; and (4) neuroinflammation, damage to the neurovascular unit, oxidative stress, and magnetic effects all potentially contribute to neural damage [22,23,24,25,26]
Summary
We live surrounded by environmental hazards including toxic compounds in air, water, soil, and food. Our discussion covers the current policy landscape in the US regarding particle pollution, internal combustion engine PM emissions, the differences in ambient air quality standards between the US and WHO 2021 guidelines, the recent expert suggestions of an Independent Particulate Matter Review Panel, and the importance of UFPs and NPs for the mechanistic neural damaging pathways linked to exposure to them. Of utmost importance for this Review, wildfire PM2.5 concentrations are on average 150.0 μg/m3 with recorded concentrations above 500 μg/m3 and with spatial patterns that do not follow traditional socioeconomic pollution exposure gradients [9,10] These are key pieces of information to keep in mind for future data collection on incidence and prevalence of major neurological and psychiatric diseases in the most affected regions (Figure 1). Much remains to be discovered about the explicit role that human exposure to UFP pollution plays in the well-documented morbidity and mortality effects of exposure to PM2.5
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: International Journal of Environmental Research and Public Health
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
