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<title lang=en>0461 : Comparison of cardiovascular responses to nitrogen dioxide and diesel exhausts. An experimental study with controlled exposures to air pollutants</title>
<creator>Karoui, Ahmed</creator>
<creator>Crochemore, Clément</creator>
<creator>Mekki, Malik</creator>
<creator>Préterre, David</creator>
<creator>Cazier, Fabrice</creator>
<creator>Dewaele, Dorothée</creator>
<creator>Vaugeois, Jean-Marie</creator>
<creator>Corbière, Cécile</creator>
<creator>Lecureur, Valérie</creator>
<creator>Richard, Vincent</creator>
<creator>Mulder, Paul</creator>
<creator>Monteil, Christelle</creator>
<contributor>Centre commun de mesure, Dunkerque, France ; Université du Littoral Côte d'Opale</contributor>
<contributor>Centre de recherche en neurosciences de Lyon ; Université Claude Bernard Lyon 1 (UCBL) - Université Jean Monnet [Saint-Étienne] (UJM) - Université de Lyon - Institut National de la Santé et de la Recherche Médicale (INSERM) - Centre National de la Recherche Scientifique (CNRS)</contributor>
<contributor>Unité de neuropsychopharmacologie expérimentale (UNE) ; Université de Rouen Normandie (URN) ; Normandie Université (NU) - Normandie Université (NU) - Centre National de la Recherche Scientifique (CNRS)</contributor>
<contributor>Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>Unité d'Epidémiologie [Antananarivo, Madagascar] (IPM) ; Institut Pasteur de Madagascar - Réseau International de Instituts Pasteur</contributor>
<contributor>Nouvelles Cibles Pharmacologiques de la Protection Endothéliale et de l'Insuffisance Cardiaque (EnVI) ; CHU Rouen - Université de Rouen Normandie (URN) ; Normandie Université (NU) - Normandie Université (NU) - Institut National de la Santé et de la Recherche Médicale (INSERM)</contributor>
<description>International audience</description>
<source>Archives of Cardiovascular Diseases Supplements</source>
<coverage>Toulouse, France</coverage>
<identifier>hal-01150495</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01150495</identifier>
<source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01150495</source>
<source>Archives of Cardiovascular Diseases Supplements, Apr 2015, Toulouse, France. 7, pp.142, 2015, Printemps de la Cardiologie : Recherche Fondamentale et Clinique - Centre de Congrès Pierre Baudis, Toulouse, 2-3 avril 2015. 〈10.1016/S1878-6480(15)30036-7〉</source>
<identifier>DOI : 10.1016/S1878-6480(15)30036-7</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1016/S1878-6480(15)30036-7</relation>
<language>en</language>
<subject>[SDV] Life Sciences [q-bio]</subject>
<type>info:eu-repo/semantics/conferenceObject</type>
<type>Conference papers</type>
<description lang=en>Traffic air pollution is a major health problem and is recognized as an important risk factor for cardiovascular disease. Even so the role of particles-induced adverse health effects is well established, recent studies outlined the contribution of nitrogen dioxide (NO2) in these effects, in particular on the cardiovascular function. The main sources of this pollutant are oxidation catalysts used to reduce emissions of carbon monoxide and non-methane hydrocarbons from the exhaust of diesel engines and also to facilitate filter regeneration. However, the contribution of NO2 compared to other gaseous and particulate pollutants remains unknown. Consequently, the main objective of this study was to analyze the specific contributions of NO2 in the traffic-related air pollution-induced cardiovascular adverse effects. For this, Wistar rats were exposed for 3 weeks (3h/day, 5 days/week) to either a continuous flow of catalyzed diesel exhaust (DE), particle free or whole DE (particles concentration 2mg/m3), either to a continuous flow of NO2 used at a concentration identical to that measured in the exhaust line. The composition of the emission and the NO2 analyses were monitored on-line during the whole experiment. We evaluated cardiac function and biological effects after 16h recovery in clean air. DE or NO2 exposures induced a modest cardiac dysfunction characterized by an increase in left ventricular diameters and a decrease in fractional shortening. In the case of DE, the presence of particles did not worsen the impairment of cardiac function. In parallel to this effect, mitochondrial function was altered as illustrated by the reduction of the oxygen consumption and of the ATP production. Mitochondrial reactive oxygen species was increased only by the NO2 exposure. In conclusion, these results suggest that DE-induced cardiac dysfunction is due to, at least in part, to NO2 present in DE.</description>
<date>2015-04-02</date>
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