Air Pollution and Brain Damage

DOI Web Site 被引用文献5件
  • 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
  • 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

抄録

<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>

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