PM2.5 and Neurodegenerative Diseases
Epidemiological human and animal studies support the notion that air pollution can affect the central nervous system (CNS)
and lead to CNS disorders [165,166,167].
PM2.5 and UFPM are of special concern as they can enter the systemic circulation and spread to the brain and other organs
, as well as obtain direct access to the brain via the nasal olfactory mucosa [168,169,170].
Decreased cognitive performance, olfactory problems, auditory impairments, depression symptoms, and other negative neuropsychological consequences have been reported in humans in highly polluted areas [171,172].
Controlled acute diesel exhaust (300 g/m3) exposure has been demonstrated to cause electroencephalogram (EEG) alterations [173].
Post-mortem examinations of highly exposed people have indicated elevations in the levels of indicators of oxidative stress and neuroinflammation [174]
. Furthermore, research suggests that young people may be especially vulnerable to air pollution-induced neurotoxicity [175].
Studies in Mexico City have found heightened levels of neuroinflammatory markers in the brains of children exposed to high levels of air pollution, as well as cognitive impairments and hyperactivity in 7-year-old children linked with early life exposure to traffic-related air pollution [176]
. A retrospective cohort study in Catalonia, Spain, discovered a link between air pollution (defined as residing 300 m from a highway) and the prevalence of attention deficit hyperactivity disorder (ADHD) [177].
In contrast, a major study including eight European population-based birth/child cohorts found no link between air pollution exposure and ADHD, similar to a Swedish investigation [178,179].
Experimental studies support the hypothesis that air pollution is a developmental neurotoxicant. A study by Ema, Naya, and Kato [180]
indicated that developmental exposure to diesel exhaust may produce toxicity and neurotoxicity. In male mice, in utero exposure to high doses of diesel exhaust (1.0 mg/m3) resulted in changes in motor activity and coordination, and impulsive behavior [181].
Further research in mice revealed that postnatal injection (PND 4–7 and 10–13, for 4 h/day) of diesel exhaust particulate matter (DE-PM) (100 g/m3) induced alterations in GFAP expression in numerous brain areas, whereas UFPM (45 g/m3) caused male-specific learning and memory dysfunctions [182].
Subsequent research has revealed that embryonic DE exposure in mice impacts motor activity, spatial learning and memory, and new object recognition abilities, and alters gene expression, causing neuroinflammation and oxidative damage [183].
The effects of air pollution on the nervous system and its possible role in neurodegenerative disorders are illustrated in Figure 5
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