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Pediatric Respiratory and Systemic Effects of Chronic Air Pollution Exposure: Nose, Lung, Heart, and Brain Pathology
1 Instituto Nacional de Pediatría, Mexico City 14410, Mexico Correspondence: Address correspondence to: William Reed, Center for Environmental Medicine, Asthma and Lung Biology, University of North Carolina, Chapel Hill, NC 27599-7310, USA; e-mail: williamreed{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-1β (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 Aβ42 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 Abbreviations: Aβ42, 42 amino acid form of β-amyloid • AD, Alzheimer’s disease • BBB, Blood-brain barrier • CO, Carbon monoxide • COX2, cyclooxygenase-2 • IL, interleukin • iNOS, inducible nitric oxide synthase • LPS, lipopolysaccharides • MC, Mexico City • NK, Natural killer • NO2, Nitrogen dioxide • O3, Ozone • PGE2, Prostagalandin E2 • PM, Particulate matter air pollution • PM2.5, PM < 2.5 µm in mean mass aerodynamic diameter • PM10, PM < 10 µm in mean mass aerodynamic diameter • RBC, red blood cell • ROS, reactive oxygen species • SO2, Sulphur dioxide
Toxicologic Pathology, Vol. 35, No. 1,
154-162 (2007) This article has been cited by other articles:
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