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.