TIME COURSE OF LUNG INFLAMMATION AND CARDIAC OXYGEN METABOLISM IN A MICE MODEL OF CONTINUOUS EXPOSURE TO URBAN AIR POLLUTION

MARCHINI, TIMOTEO; GARCES, MARIANA; CALABRO, VALERIA; PAZ, MARIELA; LAGO, NESTOR; CACERES, LOURDES; VICO, TAMARA; GUAGLIANONE, ALEJANDRO; VANASCO, VIRGINIA; GONZALEZ MAGLIO, DANIEL; BERRA, ALEJANDRO; ALVAREZ, SILVIA; EVELSON, PABLO

Congreso; Reunión Conjunta de Sociedades de Biociencias.; 2017

The exposure to air pollution leads to increased morbidity and mortality rates from cardiorespiratory diseases. In has been suggested that local and systemic oxidative stress and inflammation play a central role in this scenario. The aim of this work was to characterize a mice model of continuous exposure to urban air pollution, by the assessment of different markers of pulmonary, systemic, and cardiac oxygen metabolism and inflammation. 8-week-old balb/c male mice were exposed to urban or filtered air (control) inside a chamber located in a highly populated area of Buenos Aires City. Animals were exposed for 8 h/day, 5 days/week, for up to 3 months. After 2 months, mice exposed to urban air pollution showed a 53% increase in total leucocytes in bronchoalveolar lavage (BAL) samples in comparison with the control group (control: 1.0±0.2 x105 cells, p<0.001), together with a 104% increase in BAL protein concentration (control: 0.15±0.03 mg/mL, p<0.05). Both BAL leucocytes and protein concentration were still significantly increased after 3 months in exposed mice in comparison with the control group. NADPH oxidase activity was increased in lung homogenates by 25% (control: 1.33±0.03 AU/mg protein, p<0.05) after 2 months. While no differences were observed in total lung oxygen consumption at any evaluated time point, cardiac oxygen consumption decreased by 37% in exposed mice in comparison with the control group after 2 months (control: 980±50 nmol O2/min g tissue, p<0.05), and by 32% after 3 months (control: 1100±90 nmol O2/min g tissue, p<0.01). A slight, yet not significant increase was observed in plasma TNF-α and IL-6 levels in exposed mice. The present data suggest that a continuous exposure to urban air leads to lung inflammation and decreased cardiac oxygen metabolism, which may explain some of the adverse health effects associated with the exposure to air pollution.