Biological effects of co-exposure to Tajogaite volcano (La Palma, Spain) ash and sulphur dioxide gas in human lung cells
Ines Tomašek1,2,3, Julia Eychenne1,2, Fanny Henrioux2, David E. Damby4, Matthieu Jabaudon2,5, Lucie Sauzéat1,2, Gaëlle Uzu6, Loïc Blanchon2, Vincent Sapin2,7
Affiliations: 1Laboratoire Magmas et Volcans (LMV), CNRS, IRD, OPGC, Université Clermont Auvergne, Clermont-Ferrand, France. 2Institute of Genetic Reproduction and Development (iGReD), CNRS, INSERM, Université Clermont Auvergne, Clermont-Ferrand, France. 3Istituto Nazionale di Geofisica e Vulcanologia (INGV), Osservatorio Etneo, Catania, Italy. 4Volcano Science Center, U.S. Geological Survey (USGS), Menlo Park, CA, USA. 5Centre Hospitalier Universitaire (CHU) Clermont-Ferrand, Department of Perioperative Medicine, France. 6Université Grenoble Alpes, IRD, CNRS, INRAE, INP-G, IGE (UMR 5001), Grenoble, France. 7CHU Clermont-Ferrand, Department of Biochemistry and Molecular Genetics, Clermont-Ferrand, France.
Presentation type: Poster
Presentation time: Monday 16:30 - 18:30, Room Poster Hall
Poster Board Number: 19
Programme No: 6.6.7
Abstract
Volcanic emissions are an important source of natural air pollutants, including, but not limited to, sulphur dioxide (SO2) gas and fine particulate matter, that can degrade air quality in populated areas. Short-term exposure to these pollutants has been associated with acute respiratory symptoms, such as irritation and cough. However, the potential lung injury from combined exposure to multiple volcanic pollutants is still poorly understood, as biological investigations to date have focused primarily on volcanic ash. In this study, we investigated the biological impact of acute co-exposure to volcanic ash and SO2 gas on human alveolar epithelial cells (A549) to evaluate whether combined exposure poses a greater hazard than inhaling them separately. In the experiments, we used sub-10 µm ash from Tajogaite volcano, representative of resuspension material. We exposed A549 cells cultured at the air-liquid interface to ash (100 µg/cm2) and SO2 gas (50 ppm for 1 h, 2 h or 3 h), individually and concomitantly, using a sophisticated cell exposure system (CelTox Sampler). Subsequently, we assessed cellular responses, including cytotoxicity (LDH release) and release of pro-inflammatory markers (IL-6, IL-8 and MCP-1, at gene and protein levels). The results indicate that exposure to volcanic ash alone had limited impact on A549 cells. However, prolonged SO2 exposure appeared to impair the cellular response, and co-exposures increased the release of pro-inflammatory markers. These findings suggest that combined exposures to volcanic pollutants could potentially affect the normal inflammatory response. These data could also help explain responses not necessarily captured by single-pollutant experiments.