Air Pollution, Ultrafine Particles, and Your Brain: Are Combustion Nanoparticle Emissions and Engineered Nanoparticles Causing Preventable Fatal Neurodegenerative Diseases and Common Neuropsychiatric Outcomes?

Abstract

Exposure to particulate matter (PM) pollution damages the human brain. Fossil fuel burning for transportation energy accounts for a significant fraction of urban air and climate pollution. While current United States (US) standards limit PM ambient concentrations and emissions, they do not regulate explicitly ultrafine particles (UFP ≤ 100 nm in diameter). There is a growing body of evidence suggesting UFP may play a bigger role inflicting adverse health impacts than has been recognized, and in this perspective, we highlight effects on the brain, particularly of young individuals. UFP penetrate the body through nasal/olfactory, respiratory, gastrointestinal, placenta, and brain–blood barriers, translocating in the bloodstream and reaching the glymphatic and central nervous systems. We discuss one case study. The 21.8 million residents in the Metropolitan Mexico City (MMC) are regularly exposed to fine PM (PM2.5) above the US 12 μg/m3 annual average standards. Alzheimer’s disease (AD), Parkinson’s disease (PD), and TAR DNA-binding protein (TDP-43) pathologies and nanoparticles (NP ≤ 50 nm in diameter) in critical brain organelles have been documented in MMC children and young adult autopsies. MMC young residents have cognitive and olfaction deficits, altered gait and equilibrium, brainstem auditory evoked potentials, and sleep disorders. Higher risk of AD and vascular dementia associated with residency close to high traffic roadways have been documented. The US is not ready or prepared to adopt ambient air quality or emission standards for UFP and will continue to focus regulations only on the total mass of PM2.5 and PM10. Thus, this approach raises the question: are we dropping the ball? As research continues to answer the remaining questions about UFP sources, exposures, impacts, and controls, the precautionary principle should call us to accelerate and expand policy interventions to abate or eliminate UFP emissions and to mitigate UFP exposures. For residents of highly polluted cities, particularly in the developing world where there is likely older and dirtier vehicles, equipment, and fuels in use and less regulatory oversight, we should embark in a strong campaign to raise public awareness of the associations between high PM pollution, heavy traffic, UFP, NP, and neuropsychiatric outcomes, including dementia. Neurodegenerative diseases evolving from childhood in polluted, anthropogenic, and industrial environments ought to be preventable.

Alpha-Synuclein at the Interface between Depression, Parkinson’s Disease and Dementia: Evidence from Epidemiology, Population Genetics and Gene-Environment Interactions

“…These results are consistent with existing research on the shared pathogenic mechanisms for these disorders [55][56][57][58], as well as with the results of longitudinal research in individual countries demonstrating a prospective link between depressive disorders and neuro-degenerative disorders [59][60][61][62]. Prior evidence suggests that the links between depression, Parkinson's disease and Alzheimer's disease are mediated by both genetic vulnerability [63][64][65] and exposure to environmental risk factors, such as stress and environmental toxins [66][67][68]. These two sets of risk factors should not be seen in isolation; there is already preliminary evidence of gene-environment interactions between genetic risk and diabetes mellitus [69] and between genetic variants and pesticide exposure [70] in influencing the development of subsequent Parkinson's disease.…”

Evidence of Indoor Dust Acting as Carrier for Metal-Based Nanoparticles: A Study of Exposure and Oxidative Risks

“…In lung interstitial fluids, dust-borne MNPs exhibited instability and aggregation (e.g., ∼2.8-fold increase in the size of Fe-based MNPs), which may lead to MNPs being deposited in bronchioles and posing potential pulmonary health risks. Smaller bioavailable MNPs (down to 100 nm) reported in this study can be considered as the missing puzzle in the indoor environment assessment as previous studies mostly focused on dissolved metals. , Additionally, the oxidative assessment further revealed the peroxidase-like activity of MNPs in indoor dust, generating 1.5 times more ROS than the control, which correlates with some nasal and respiratory diseases, as well as neuropsychiatric outcomes . Our comprehensive assessment raises the flag on the presence of multielement MNPs in indoor dust and their potential health risks, particularly because people stay in indoor habitats for a long period (even longer during the COVID-19 epidemic) without intentional protection.…”

Effect of Short- to Long-Term Exposure to Ambient Particulate Matter on Cognitive Function in a Cohort of Middle-Aged and Older Adults: KoGES

“…Emission sources can provide valuable information on ambient PM. Emissions from non-combustion sources are prone to produce disproportionately large and coarse particles that are less likely to enter the deeper side of the lungs or bloodstream than smaller particles [ 54 , 55 ]. In contrast, combustion sources tend to generate large numbers of smaller particles that are biologically active.…”