Air pollution and brain damage.

Exposuretocomplexmixturesofairpollutantsproducesineammationintheupperandlowerrespiratorytract. Becausethenasalcavityisacommon portal of entry, respiratory and olfactory epithelia are vulnerable targets for toxicological damage. This study has evaluated, by light and electron microscopy andimmunohistochemical expressionof nuclear factor-kappa beta (NF-j B) and inducible nitric oxide synthase (iNOS), the olfactory and respiratorynasal mucosae, olfactory bulb, andcortical and subcortical structures from 32 healthy mongrel canineresidents inSouthwest 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-j B and iNOS in cortical endothelial cells occurred at ages 2 and 4 weeks; subsequent damage included alterations of theblood‐brain barrier (BBB), degeneratingcortical neurons, apoptotic glial white matter cells, depositionof apolipoprotein E (apoE)-positivelipiddropletsinsmoothmusclecellsandpericytes,nonneuriticplaques,andneuroebrillarytangles.Persistentpulmonaryineammation 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.