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Air Pollution and Brain Damage

Curriculum in Toxicology, University of North Carolina at Chapel Hill, North Carolina 27599-7310, USA, liliancalderon888{at}hotmail.com, Instituto Nacional de Pediatria, Mexico City, 14410, Mexico

Biagio Azzarelli

Pathology Department, Indiana University, Indianapolis, Indiana 46202-5120, USA

Hilda Acuna

Instituto Nacional de Pediatria, Mexico City, 14410, Mexico

Raquel Garcia

Instituto Nacional de Pediatria, Mexico City, 14410, Mexico

Todd M. Gambling

Center for Environmental Medicine and Lung Biology, University of North Carolina at Chapel Hill, North Carolina 27599-7310, USA

Norma Osnaya

Instituto Nacional de Pediatria, Mexico City, 14410, Mexico

Sylvia Monroy

Instituto Nacional de Pediatria, Mexico City, 14410, Mexico

Maria Del Rosario Tizapantzi

Instituto Nacional de Pediatria, Mexico City, 14410, Mexico

Johnny L. Carson

Center for Environmental Medicine and Lung Biology, University of North Carolina at Chapel Hill, North Carolina 27599-7310, USA

Anna Villarreal-Calderon

Instituto Nacional de Pediatria, Mexico City, 14410, Mexico

Barry Rewcastle

Pathology Department, Foothills Hospital, Calgary, Alberta, T2S0R3, Canada

Exposure to complex mixtures of air pollutants produces infl ammation in the upper and lower respiratory tract. Because the nasal cavity is a common portal of entry, respiratory and olfactory epithelia are vulnerable targets for toxicological damage. This study has evaluated, by light and electron microscopy and immunohistochemica l expression of nuclear factor-kappa beta (NF-B) and inducible nitric oxide synthase (iNOS), the olfactory and respiratory nasal mucosae, olfactory bulb, and cortical and subcortical structures from 32 healthy mongrel canine residents in Southwest Metropolitan Mexico City (SWMMC), a highly polluted urban region. Findings were compared to those in 8 dogs from Tlaxcala, a less polluted, control city. In SWMMC dogs, expression of nuclear neuronal NF-B and iNOS in cortical endothelial cells occurred at ages 2 and 4 weeks; subsequent damage included alterations of the blood—brain barrier (BBB), degenerating cortical neurons, apoptotic glial white matter cells, deposition of apolipoprotein E (apoE)-positive lipid droplets in smooth muscle cells and pericytes, nonneuritic plaques , and neurofi brillary tangles. Persistent pulmonary infl ammation and deteriorating olfactory and respiratory barriers may play a role in the neuropathology observed in the brains of these highly exposed canines. Neurodegenerative disorders such as Alzheimer's may begin early in life with air pollutants playing a crucial role.

Key Words: Air pollution • Mexico City • canines • Alzheimer's • nasal epithelia • BBB • NFB • iNOS.

Toxicologic Pathology, Vol. 30, No. 3, 373-389 (2002)
DOI: 10.1080/01926230252929954


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