Sebastian Oeder , Tamara Kanashova , Olli Sippula , Sean C. Sapcariu , Thorsten Streibel , Jose Manuel Arteaga-Salas , Johannes Passig , Marco Dilger, Hanns-Rudolf Paur, Christoph Schlager, Sonja Mülhopt, Silvia Diabaté, Carsten Weiss, Benjamin Stengel, Rom Rabe, Horst Harndorf, Tiina Torvela, Jorma K. Jokiniemi, Maija-Riitta Hirvonen, Carsten Schmidt-Weber, Claudia Traidl-Hoffmann, Kelly A. BéruBé, Anna J. Wlodarczyk, Zoë Prytherch, Bernhard Michalke, Tobias Krebs, André S. H. Prévôt, Michael Kelbg, Josef Tiggesbäumker, Erwin Karg, Gert Jakobi, Sorana Scholtes, Jürgen Schnelle-Kreis, Jutta Lintelmann, Georg Matuschek, Martin Sklorz, Sophie Klingbeil, Jürgen Orasche, Patrick Richthammer, Laarnie Müller, Michael Elsasser, Ahmed Reda, Thomas Gröger, Benedikt Weggler, Theo Schwemer, Hendryk Czech, Christopher P. Rüger, Gülcin Abbaszade, Christian Radischat, Karsten Hiller, Jeroen T. M. Buters , Gunnar Dittmar , Ralf Zimmermann
Exposition of Heavy Fuel Oil and Diesel Fuel Shipping Emissions on human lung cells in the air-liquid interface exposure system for advanced chemical analysis combined with transcriptional, proteomic and metabolomic profiling and isotope labelling methods.
Ship engine emissions are important with regard to lung and cardiovascular diseases especially in coastal regions worldwide. Known cellular responses to combustion particles include oxidative stress and inflammatory signalling.
To provide a molecular link between the chemical and physical characteristics of ship emission particles and the cellular responses they elicit and to identify potentially harmful fractions in shipping emission aerosols.
Through an air-liquid interface exposure system, we exposed human lung cells under realisticin vitro conditions to exhaust fumes from a ship engine running on either common heavy fuel oil (HFO) or cleaner-burning diesel fuel (DF). Advanced chemical analyses of the exhaust aerosols were combined with transcriptional, proteomic and metabolomic profiling including isotope labelling methods to characterise the lung cell responses.
The HFO emissions contained high concentrations of toxic compounds such as metals and polycyclic aromatic hydrocarbon, and were higher in particle mass. These compounds were lower in DF emissions, which in turn had higher concentrations of elemental carbon (“soot”). Common cellular reactions included cellular stress responses and endocytosis. Reactions to HFO emissions were dominated by oxidative stress and inflammatory responses, whereas DF emissions induced generally a broader biological response than HFO emissions and affected essential cellular pathways such as energy metabolism, protein synthesis, and chromatin modification.
Despite a lower content of known toxic compounds, combustion particles from the clean shipping fuel DF influenced several essential pathways of lung cell metabolism more strongly than particles from the unrefined fuel HFO. This might be attributable to a higher soot content in DF. Thus the role of diesel soot, which is a known carcinogen in acute air pollution-induced health effects should be further investigated. For the use of HFO and DF we recommend a reduction of carbonaceous soot in the ship emissions by implementation of filtration devices.
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