Chronic urban air pollution exposure aggravates myocardial infarction in mice. The role of altered lung redox metabolism, inflammation and impaired cardiac mitochondrial function

MAGNANI, NATALIA; PAZ, MARIELA; LAGO, NESTOR; CALABRÓ, VALERIA; TRIPODI, VALERIA; GONZÁLEZ MAGLIO, DANIEL; EVELSON, PABLO; GARCÉS, MARIANA; CALTANA, LAURA; CÁCERES, LOURDES; VICO, TAMARA; ALVAREZ, SILVIA; BERRA, ALEJANDRO; MARCHINI, TIMOTEO; KELLY, JAZMÍN; CONTÍN, MARIO; MARGIOTTIELLO, DANIEL; VANASCO, VIRGINIA; BUCHHOLZ, BRUNO; GELPI, RICARDO J

Breisach am Rhein

Jornada; 5th Atherothrombosis Winter School; 2020

Sociedad Alemana de Cardiología (DGK)

Background: Every year, air pollution exposure accounts for 2.4 million deaths from myocardial infarction (MI), which represents 25% of the total global burden for this disease. Fine particulate matter (PM2.5) ? airborne particles < 2.5 µm in diameter that mainly arises from diesel exhaust in urban areas ? has been pointed out as the main responsible. It has been suggested that, following PM2.5 inhalation, lung and systemic oxidative stress and inflammation worsen MI progression. However, the underlying mechanisms are still an intensive area of research. Herein, we aim to test this hypothesis in a combined biologically-relevant real-life mice model of continuous exposure to urban polluted air and experimental MI.Methods & Results: Male eight-week-old BALB/c mice were exposed to filtered air (FA) or urban air (UA) inside whole-body inhalation chambers located in Buenos Aires City downtown (12 to 37 µg PM2.5/m3). After 8 weeks, mice breathing UA showed a 56% increase in total leucocyte count in bronchoalveolar lavage (BAL) samples (FA: 1.0±0.2 x105 cells, p