Brain Inflammation and Alzheimer's-Like Pathology in Individuals Exposed to Severe Air Pollution

Author： CALDERóN-GARCIDUEñAS LILIAN REED WILLIAM MARONPOT ROBERT HENRÍQUEZ-ROLDÁN CARLOS DELGADO-CHAVEZ RICARDO CALDERóN-GARCIDUEñAS ANA DRAGUSTINOVIS IRMA FRANCO-LIRA MARICELA ARAGóN-FLORES MARIANA SOLT ANNA ALTENBURG MICHAEL TORRES-JARDÓN RICARDO SWENBERG JAMES

Publisher： Ashgate Publishing Ltd

ISSN： 0192-6233

Source： Toxicologic Pathology, Vol.32, Iss.6, 2004-11, pp. : 650-658

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Abstract

Air pollution is a complex mixture of gases (e.g., ozone), particulate matter, and organic compounds present in outdoor and indoor air. Dogs exposed to severe air pollution exhibit chronic inflammation and acceleration of Alzheimer's-like pathology, suggesting that the brain is adversely affected by pollutants. We investigated whether residency in cities with high levels of air pollution is associated with human brain inflammation. Expression of cyclooxygenase-2 (COX2), an inflammatory mediator, and accumulation of the 42-amino acid form ofβ-amyloid (Aβ42), a cause of neuronal dysfunction, were measured in autopsy brain tissues of cognitively and neurologically intact lifelong residents of cities having low (n:9) or high (n:10) levels of air pollution. Genomic DNA apurinic/apyrimidinic sites, nuclear factor-κB activation and apolipoprotein E genotype were also evaluated. Residents of cities with severe air pollution had significantly higher COX2 expression in frontal cortex and hippocampus and greater neuronal and astrocytic accumulation of Aβ42 compared to residents in low air pollution cities. Increased COX2 expression and Aβ42 accumulation were also observed in the olfactory bulb. These findings suggest that exposure to severe air pollution is associated with brain inflammation and Aβ42 accumulation, two causes of neuronal dysfunction that precede the appearance of neuritic plaques and neurofibrillary tangles, hallmarks of Alzheimer's disease.