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DNA Damage in Nasal and Brain Tissues of Canines Exposed to Air Pollutants Is Associated with Evidence of Chronic Brain Inflammation and NeurodegenerationEnvironmental Pathology Program, University of North Carolina at Chapel Hill, North Carolina 27599-7310, USA, liliancalderon888{at}hotmail.com, Instituto Nacional de Pediatría, Mexico City 14410, Mexico
National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
Centro de Ciencias de la Atmósfera, Universidad Nacional Autónoma de México, Mexico City
Departamento de Estadística, Universidad de Valparaíso, Chile
Department of Environmental Sciences and Engineering, University of North Carolina at Chapel Hill, North Carolina 27599-7310, USA
Instituto Nacional de Pediatría, Mexico City 14410, Mexico
Facultad de Medicina, NUCE, Universidad Nacional Autónoma de México, Mexico
Department of Environmental Sciences and Engineering, University of North Carolina at Chapel Hill, North Carolina 27599-7310, USA
RTI International, Research Triangle Park, North Carolina 27709, USA
Department of Pediatrics and Center for Environmental Medicine, Asthma, and Lung Biology, University of North Carolina at Chapel Hill 27599-7310, USA
Pathology Department, Indiana University, Indianapolis, Indiana 46202-5120, USA
Department of Environmental Sciences and Engineering, University of North Carolina at Chapel Hill, North Carolina 27599-7310, USA
Acute, subchronic, or chronic exposures to particulate matter (PM) and pollutant gases affect people in urban areas and those exposed to fires, disasters, and wars. Respiratory tract inflammation, production of mediators of inflammation capable of reaching the brain, systemic circulation of PM, and disruption of the nasal respiratory and olfactory barriers are likely in these populations. DNA damage is crucial in aging and in age-associated diseases such as Alzheimer's disease. We evaluated apurinic/apyrimidinic (AP) sites in nasal and brain genomic DNA, and explored by immunohistochemistry the expression of nuclear factor NF
Key Words: Urban pollution • Alzheimer's disease • ozone • ultrafine particulate matter • brain inflammation • combustion metals • nasal and olfactory pathology • blood—brain barrier • DNA oxidative damage.
Toxicologic Pathology, Vol. 31, No. 5,
524-538 (2003) This article has been cited by other articles:
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B p65, inducible nitric oxide synthase (iNOS), cyclo-oxygenase 2 (COX2), metallothionein I and II, apolipoprotein E, amyloid precursor protein (APP), and beta-amyloid1-42 in healthy dogs naturally exposed to urban pollution in Mexico City. Nickel (Ni) and vanadium (V) were measured by inductively coupled plasma mass spectrometry (ICP-MS). Forty mongrel dogs, ages 7 days—10 years were studied (14 controls from Tlaxcala and 26 exposed to urban pollution in South West Metropolitan Mexico City (SWMMC)). Nasal respiratory and olfactory epithelium were found to be early pollutant targets. Olfactory bulb and hippocampal AP sites were significantly higher in exposed than in control age matched animals. Ni and V were present in a gradient from olfactory mucosa > olfactory bulb > frontal cortex. Exposed dogs had (a) nuclear neuronal NF
