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DOI: 10.1080/01926230601059985 © 2007 Society of Toxicologic Pathology Pediatric Respiratory and Systemic Effects of Chronic Air Pollution Exposure: Nose, Lung, Heart, and Brain PathologyInstituto Nacional de Pediatría, Mexico City 14410, Mexico, The Center for Structural and Functional Neurosciences, University of Montana, Missoula, MT 59812, USA
Escuela Médico Militar, Universidad del Ejército y Fuerza Aérea, Mexico City 11649, Mexico
Centro de Ciencias de la Atmósfera, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico
Departmento de Estadística, Universidad de Valparaíso 327-0168, Chile
Instituto Nacional de Pediatría, Mexico City 14410, Mexico
Pediatric private practice, Mexico City 04510, Mexico
Instituto Nacional de Pediatría, Mexico City 14410, Mexico
Instituto Nacional de Pediatría, Mexico City 14410, Mexico
EPSCoR undergraduate student at The Center for Structural and Functional Neurosciences, University of Montana, Missoula, MT 59812, USA
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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