AAAR 37th Annual Conference October 14 - October 18, 2019 Oregon Convention Center Portland, Oregon, USA
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The Toxicity of Gasoline Automobile Engine Emissions Depends on Fuel Type (Gasoline and Ethanol) and Driving Cycle: A Combined Biological and Aerosol Composition Study
Sebastian Oeder, J. Candeias, Tamara Kanashova, Benjamin Stengel, M. Dilger, S. Murugadoss, Olli Sippula, Sebastiano di Bucchianico, S. Bauer, Thorsten Streibel, Martin Sklorz, Jürgen Orasche, Toni Miersch, Hendryk Czech, C. Rüger, Bert Buchholz, C. Weiss, Jorma Jokiniemi, Maija-Riitta Hirvonen, Gunnar Dittmar, C. Schmidt-Weber, Jeroen Buters, RALF ZIMMERMANN, HICE Consortium, University of Rostock and Helmholtz Zentrum Munich, Germany
Abstract Number: 607 Working Group: Health-Related Aerosols
Abstract Car engine emissions are relevant for local air pollution and contribute to the greenhouse gas-burden. Therefore, the change from fossil- to renewable fuel-sources is promoted. The impact of the changing emission on human health, however, is widely unknown. Our study compares lung cell responses towards the exposure to diluted car engine emissions from engine-operation with conventional versus bio-fuel (ethanol). Also different driving cycles are considered. A standard 2.0 litre flexi-fuel engine with 132 kW/320 Nm was operated with gasoline containing either ~10% (E10) or ~85% (E85) ethanol. The NEDC and a high-speed driving cycles were used to simulated chassis dyno tests by operating the test bench engine with correlating speed/torque patterns. A lung epithelium cell line (A549) was directly exposed at the air-liquid-interface (ALI) to diluted (1:10, 1:40) emissions. After 4h of exposure cells were lysed, RNA extracted and analysed by whole-genome gene expression arrays. Using clean air treated cells as control, aerosol-induced gene regulation was calculated. Gene ontology (GO) and canonical pathway analysis was performed using at least 1.5-fold regulation and p<0.05 in t-test with multiple testing correction. The cells reacted to the E85 emissions with a 2-fold increase in regulated genes compared to conventional fuel emissions. In the high-speed cycle (gasoline) the number of affected genes increased by 28% with respect to the standard NEDC cycle. All tested aerosols caused general cell-stress, affected the cell-cycle and inflammatory responses (GO term analysis). Canonical pathway analysis revealed additionally aerosol specific effects: Emissions from conventional gasoline caused higher levels of oxidative stress and fibrosis-related changes, whereas E85 emissions induced stronger DNA-damage responses (likely due to higher aldehyde concentrations in E85-emissions). We conclude that addition of higher amounts of ethanol may increase the emission’s toxicity.