Lung Oxidative Stress after in vivo Exposure to Buenos Aires Urban Air particles

DEBORAH RUTH TASAT (1,2), Susana Martin (2), Pablo Evelson (3), Eugenio Fernandez-Alanis (2), Veronica Delfosse (2), Juan Sebastian Yakisich (4)

(1) School of Dentistry, University of Buenos Aires, Argentina. (2) CESyMA, School of Science and Technology, National University of San Martín, Buenos Aires, Argentina. (3) PRALIB-CONICET, School of Pharmacy and Biochemistry, University of Buenos Aires,Argentina. (4) Department of Clinical Neuroscience, Karolinska Huddinge Hospital, Karolinska Institute, Stockholm, Sweden

     Abstract Number: 96
     Last modified: October 30, 2009

Abstract
Air pollution consists of a wide range of chemicals and particulates. Some pollutants present in this ambient mix, including particulate matter (PM), have the ability to generate reactive oxygen species (ROS) which overwhelming the antioxidant protection, may cause lung oxidative stress. The mechanisms by which PM causes oxidative stress comprise among others: generation of oxidants, release of metals or organic components from the particle and depletion of antioxidants. Previously, we have morphologically and chemically characterized Urban Air Particles from downtown Buenos Aires (UAP-BA) and reported them as spherical ultrafine particles coated with organic polycyclic aromatic hydrocarbons (PAHs) and polychlorinated biphenils (PCBs). Moreover, UAP-BA intranasal instillation was able to induce lung inflammation in a sub acute animal model. Herein we studied the possible UAP-BA mechanism of action assessing: cell viability, total cell number (TCN) and cell differential (CD) on bronchoalveolar lavages (BAL), the oxidative metabolism in lung by means of tert-butyl hydroperoxide-initiated chemiluminescence (CL), thiobarbituric reactive substances (TBARS), total antioxidant potential (TRAP), reduced glutathione (GSH) and apoptosis. We found that UAP-BA increases total cell number, modifies cell differential and decreases cell viability in the BAL. In lung homogenates TBARS and CL rose while TRAP and GSH showed no alteration when compared to controls. Occurrence of apoptosis markedly augmented for UAP-BA exposed animals. These data point to oxidative stress as one of the mechanisms responsible for the adverse respiratory effect of UAP-BA, and propose that instillation of ambient particulate air pollution from downtown Buenos Aires, streets with high automobile traffic, represents a biological hazard.