Air Pollution and Brain Damage
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- Lilian Calderón-Garcidueñas
- Curriculum in Toxicology, University of North Carolina at Chapel Hill, North Carolina 27599-7310, USA, , Instituto Nacional de Pediatria, Mexico City, 14410, Mexico
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- Biagio Azzarelli
- Pathology Department, Indiana University, Indianapolis, Indiana 46202-5120, USA
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- Hilda Acuna
- Instituto Nacional de Pediatria, Mexico City, 14410, Mexico
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- Raquel Garcia
- Instituto Nacional de Pediatria, Mexico City, 14410, Mexico
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- Todd M. Gambling
- Center for Environmental Medicine and Lung Biology, University of North Carolina at Chapel Hill, North Carolina 27599-7310, USA
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- Norma Osnaya
- Instituto Nacional de Pediatria, Mexico City, 14410, Mexico
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- Sylvia Monroy
- Instituto Nacional de Pediatria, Mexico City, 14410, Mexico
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- Maria Del Rosario Tizapantzi
- Instituto Nacional de Pediatria, Mexico City, 14410, Mexico
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- Johnny L. Carson
- Center for Environmental Medicine and Lung Biology, University of North Carolina at Chapel Hill, North Carolina 27599-7310, USA
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- Anna Villarreal-Calderon
- Instituto Nacional de Pediatria, Mexico City, 14410, Mexico
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- Barry Rewcastle
- Pathology Department, Foothills Hospital, Calgary, Alberta, T2S0R3, Canada
Description
<jats:p>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- κB) 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- κB 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.</jats:p>
Journal
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- Toxicologic Pathology
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Toxicologic Pathology 30 (3), 373-389, 2002-04
SAGE Publications
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Details 詳細情報について
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- CRID
- 1362825894447527296
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- NII Article ID
- 30016887790
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- ISSN
- 15331601
- 01926233
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- Data Source
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- Crossref
- CiNii Articles