Chronic Respiratory and Neurological Disorders Associated with Chronic Ultrafine Particle (UFP) Exposure in Urban Areas

Abstract Ultrafine particles (UFP), with their aerosol diameter smaller than 100 nm, are of increasing relevance to public health. Their small size, high surface area, and capacity to aggregate with other pollutants, metals, and some microorganisms can allow UFP to chronically disturb lung function, translocate across biological barriers, accumulate in the brain, and initiate molecular processes linked to neurological diseases such as Alzheimer’s, dementia, Parkinson’s disease, and multiple sclerosis. Due to their highly reactive properties, UFP, according to recent studies, can induce neuroinflammatory reactions, oxidative stress-associated-reactions, and apoptosis, leading to the development of several neurodegenerative disorders. The main objective of this review is to highlight the pathophysiological evidence of the chronic respiratory and neurological disorders associated with chronic UFP exposure, with a regional focus on urban populations. A narrative synthesis of recent epidemiological cohort data, in vivo and in vitro toxicological studies, and urban exposure assessments was conducted to provide a more comprehensive understanding of the translocation pathways of UFP through the blood-brain barrier or olfactory nerve, as well as cellular mechanisms (neuroinflammation, oxidative stress, protein aggregation) in the nervous system. Evidence suggests that chronic UFP exposure contributes to an increased risk not only for lung function disturbances but also for neurodegenerative diseases, including Alzheimer’s, Parkinson’s disease, multiple sclerosis, and cognitive deficits. The most affected individuals are often children and the elderly. According to findings presented in some studies, aggregated-UFP were detected in postmortem human brain tissue, supporting a causal pathway. Urban monitoring data indicate considerable regional and socioeconomic disparities in exposure across some cities.