A continuous exposure to urban air pollution aggravates myocardial infarction in mice: the role of lung inflammation and impaired cardiac mitochondrial function

MARCHINI T; MAGNANI ND; GARCÉS M; KELLY J; PAZ ML; LAGO N; MARGIOTTIELLO NAVARRO D; CÁCERES L; CALABRÓ V; VICO T; VANASCO V; ALVAREZ S; GONZÁLEZ MAGLIO DH; BERRA A; GELPI RJ; EVELSON PA

Congreso; Reunión Conjunta SAIC SAI SAFIS; 2018

The exposure to air pollution leads to increased morbidity and mortality rates from cardiorespiratory diseases, largely due to myocardial infarction (MI). It has been suggested that pulmonary and systemic oxidative stress and inflammation play a central role in this scenario. In order to address this hypothesis, 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 lung, blood, and cardiac oxygen metabolism and inflammation, and to study its contribution over experimental MI. 8-week-old BALB/c male mice were exposed to filtered air (control) or urban air in whole-body inhalation chambers located in a highly populated area of Buenos Aires City. Animals were exposed during 8 hours/day, 5 days/week, for up to 3 months. After 2 months, mice breathing urban air showed a 53% increase in total leucocyte count in bronchoalveolar lavage (BAL) samples in comparison with the control group (control: 1.0±0.2 x105 cells, p