The consensus on air pollution is that it increases late life mortality, largely via an increase in chronic inflammation in exposed tissues in the lung. Researchers here propose that uptake of iron from inhaled particulate matter can contribute to the age-related increase of iron that takes place in the brain, and thus cause pathology. The researchers demonstrate that this introduction of iron from airborne pollutants into the brain can occur in mice, but the question (as usual) is whether in humans this has an effect size large enough to be important versus the inflammatory consequences of air pollution.
Both excess brain iron (Fe) and air pollution (AP) exposures are associated with increased risk for multiple neurodegenerative disorders. Fe is a redox-active metal that is abundant in AP and even further elevated in U.S. subway systems. Exposures to AP and associated contaminants, such as Fe, are lifelong and could therefore contribute to elevated brain Fe observed in neurodegenerative diseases, particularly via nasal olfactory uptake of ultrafine particle AP. These studies tested the hypotheses that exogenously generated Fe oxide nanoparticles could reach the brain following inhalational exposures and produce neurotoxic effects consistent with neurodegenerative diseases and disorders in adult C57/Bl6J mice exposed by inhalation to Fe nanoparticles at a concentration similar to those found in underground subway systems (~150 µg/m3) for 20 days.
Inhaled Fe oxide nanoparticles appeared to lead to olfactory bulb uptake. Alzheimer's disease (AD) like characteristics were seen in Fe-exposed females including increased olfactory bulb diffusivity, impaired memory, and increased accumulation of total and phosphorylated tau, with total hippocampal tau levels significantly correlated with increased errors in the radial arm maze. Fe-exposed males showed increased volume of the substantia nigra pars compacta, a region critical to the motor impairments seen in Parkinson's disease (PD), in conjunction with reduced volume of the trigeminal nerve and optic tract and chiasm.
Link: https://doi.org/10.1186/s12989-025-00622-z
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