How the Use of an Atmospheric Smog Chamber Allows Us to Investigate the Impact of Urban Air Pollution on the Exacerbation of Pulmonary Fibrosis
AMBRE DELATER, Zakaria Maakoul, Elie Al Marj, Aline Gratien, Lucy Gerard, Juan Camilo Macias Rodriguez, Mathieu Cazaunau, Edouard Pangui, Antonin Berger, Cécile Gaimoz, Bénédicte Picquet-Varrault, Dominique Marchant, Jean-François Bernaudin, Emilie Boncoeur, Clément Buissot, Audrey Der Vartanian, Sophie Lanone, Patrice Coll, Carole Planes, Nicolas Voituron,
Université Paris Cité and Univ Paris Est Creteil, CNRS, LISA Abstract Number: 165
Working Group: Health-Related Aerosols
AbstractSeveral epidemiological studies suggest that air pollution promotes the incidence and acute exacerbation (AE) of idiopathic pulmonary fibrosis, although the mechanisms involved are not fully understood. In this context, our aim is to evaluate the biological impact of urban atmospheric pollution (low- and middle- levels) on different cell types of the normal and fibrotic lung, and the subsequent effects on lung fibrosis progression. To this end, we exposed mice presenting or not progressive pulmonary fibrosis (induced by repeated bleomycin treatment) to realistic atmospheres generated at the laboratory, representative of atmospheric episodes observed in a city, for one week. The targeted atmospheres were the ones of the Paris metropolis (France) i) during summer and ii) during winter. These atmospheres were simulated at the laboratory, starting from Air Quality survey networks data and from literature data, using the PolluRisk platform. The platform consists of a smog chamber (CESAM - a national instrument in France dedicated to study the multiphase atmospheric processes) where primary pollutants (gas and particles) are injected and aged to form secondary products, before being injected into exposure devices where mice are placed. The simulation of the atmosphere of Paris in summer is characterized by low concentration of particles and gases in comparison with the atmosphere of Paris in winter, where biomass burning organic aerosols from wood heating (tubular furnace) were added, as well as higher NO2 concentrations to simulate the low atmospheric dispersity of species in winter. In the exposed mice, histopathological and biological approaches were conducted to document acute alveolar damage and quantify pulmonary fibrosis. We will also define a gene expression profile and a molecular signature, and thus understand the physiopathology, the signaling pathways, and deduce possible therapeutic targets.
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