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Pediatric Respiratory and Systemic Effects of Chronic Air Pollution Exposure: Nose, Lung, Heart, and Brain Pathology

Instituto Nacional de Pediatría, Mexico City 14410, Mexico, The Center for Structural and Functional Neurosciences, University of Montana, Missoula, MT 59812, USA

Maricela Franco-Lira

Escuela Médico Militar, Universidad del Ejército y Fuerza Aérea, Mexico City 11649, Mexico

Ricardo Torres-Jardón

Centro de Ciencias de la Atmósfera, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico

Carlos Henriquez-Roldán

Departmento de Estadística, Universidad de Valparaíso 327-0168, Chile

Gerardo Barragán-Mejía

Instituto Nacional de Pediatría, Mexico City 14410, Mexico

Gildardo Valencia-Salazar

Pediatric private practice, Mexico City 04510, Mexico

Angelica González-Maciel

Instituto Nacional de Pediatría, Mexico City 14410, Mexico

Rafael Reynoso-Robles

Instituto Nacional de Pediatría, Mexico City 14410, Mexico

Rafael Villarreal-Calderón

EPSCoR undergraduate student at The Center for Structural and Functional Neurosciences, University of Montana, Missoula, MT 59812, USA

William Reed

Center for Environmental Medicine, Asthma and Lung Biology, and Department of Pediatrics, University of North Carolina, Chapel Hill, NC 27599-7310, USA, william_reed{at}med.unc. edu

Exposures to particulate matter and gaseous air pollutants have been associated with respiratory tract inflammation, disruption of the nasal respiratory and olfactory barriers, systemic inflammation, production of mediators of inflammation capable of reaching the brain and systemic circulation of particulate matter. Mexico City (MC) residents are exposed to significant amounts of ozone, particulate matter and associated lipopolysaccharides. MC dogs exhibit brain inflammation and an acceleration of Alzheimer's-like pathology, suggesting that the brain is adversely affected by air pollutants. MC children, adolescents and adults have a significant upregulation of cyclooxygenase-2 (COX2) and interleukin-1 β (IL-1β) in olfactory bulb and frontal cortex, as well as neuronal and astrocytic accumulation of the 42 amino acid form of β -amyloid peptide (Aβ42), including diffuse amyloid plaques in frontal cortex. The pathogenesis of Alzheimer's disease (AD) is characterized by brain inflammation and the accumulation of Aβ42, which precede the appearance of neuritic plaques and neurofibrillary tangles, the pathological hallmarks of AD. Our findings of nasal barrier disruption, systemic inflammation, and the upregulation of COX2 and IL-1β expression and Aβ 42 accumulation in brain suggests that sustained exposures to significant concentrations of air pollutants such as particulate matter could be a risk factor for AD and other neurodegenerative diseases.

Key Words: Children • particulate matter • systemic inflammation • beta-amyloid • nasal epithelial barrier • air pollution • Alzheimer disease early risk factors.

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