Abstract
Exposure to metals is ubiquitous and emission sources include gasoline, diesel, smoke from wildfires, contaminated soil, water and food, medical implants, waste recycling facilities, subway exposures, and occupational environments. PM2.5 exposure is associated with impaired cognitive performance, neurobehavioral alterations, incidence of dementia, and Alzheimer's disease (AD) risk. Heavy-duty diesel vehicles are major emitters of metal-rich PM2.5 and nanoparticles in Metropolitan Mexico City (MMC). Cognitive impairment was investigated in 336 clinically healthy, middle-class, Mexican volunteers, age 29.2 ± 13.3 years with 13.7 ± 2.4 years of education using the Montreal Cognitive Assessment (MoCA). MoCA scores varied with age and residency in three Mexican cities with cognition deficits impacting ~74% of the young middle-class population (MoCA ≤ 25). MMC residents ≥31 years (46.2 ± 11.8 y) had MoCA 20.4 ± 3.4 vs. low pollution controls 25.2 ± 2.4 (p < 0.0001). Formal education years positively impacted MoCA total scores across all participants (p < 0.0001). Residency in PM2.5 polluted cities impacts multi-domain cognitive performance. Identifying and making every effort to lower key pollutants impacting neural risk trajectories and monitoring cognitive longitudinal performance are urgent. PM2.5 emission control should be prioritized, metal emissions targeted, and neuroprevention interventions implemented early.
Highlights
Brain metal homeostasis is critical at all stages of development [1–4]
We have recently described in 202/203 consecutive forensic autopsies of Metropolitan Mexico City (MMC) 25.3 ± 9.2 years old, including 44 children, age 12.9 ± 4.9 years, the presence of neuropathological markers of Alzheimer’s disease (AD): hyperphosphorylated tau (P-tau) and amyloid-β (Aβ) starting in 11-month-old babies [19], along with frontal cortex upregulation of gene clusters IL1, NFκB, TNF, IFN, and TLRs and downregulation of the prion-related protein [PrP(C)] [20]
In a 517 cohort of young individuals, age 21.60 ± 5.88 years, with lifetime exposures to PM2.5 [22], we described cognitive impairment in 55% of the population screened with the Montreal Cognitive Assessment (MoCA)
Summary
Brain metal homeostasis is critical at all stages of development [1–4]. Intoxication with heavy metals is a global health problem [5] as is the extensive environmental Al pollution [2] and the metal exposures associated with outdoor and indoor particulate matter (PM) in urban environments [6, 7]. Exposures to air pollutants, including fine particulate matter (PM2.5) and their metal content [7, 9, 11] negatively impact cognitive abilities across ages, in the short and long term [14–17]. Residents in Metropolitan Mexico City (MMC) are chronically exposed to complex emission mixtures of fine particulate matter (PM2.5) containing toxic combustion and industrial metals [18]. In an olfactory bulb and frontal cortex autopsy study of 12 low air pollutant controls vs 47 MMC children and young adults of age 33.06 ± 4.8 years, inductively coupled plasma mass spectrometry and real-time PCR to evaluate COX2, IL1β, and DNA repair genes, highly exposed residents had higher concentrations of manganese (p = 0.003), nickel and chromium (p = 0.02) along with higher frontal COX2 mRNA (p = 0.008) and IL1β (p = 0.0002), and olfactory bulb COX2 (p = 0.005) indicating neuroinflammation [18]. In a 517 cohort of young individuals, age 21.60 ± 5.88 years, with lifetime exposures to PM2.5 [22], we described cognitive impairment in 55% of the population screened with the Montreal Cognitive Assessment (MoCA)
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