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

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.