Towards the regulation of aerosol emissions by their potential health impact: Assessing adverse effects of aerosols from wood combustion and ship diesel engine emissions by combining comprehensive data on the chemical composition and their toxicological effects on human lung cells

Wednesday, 17 December 2014
Ralf Zimmermann1, Thorsten Streibel1, Gunnar Dittmar2,3, Tamara Kanashova2,3, Jeroen Buters3,4, Sebastian Öder3,4, Hanns Rudolf Paur5, Marco Dilger3,5, Carsten Weiss3,5, Horst Harndorf1,3, Benjamin Stengel1,3, Maija-Riita Hirvonen3,6, Jorma Jokiniemi3,6, Karsten Hiller3,7, Sean Sapcariu3,7, Olli Sippula3,6, Jürgen Orasche8, Laarnie Müller3,8, Ahmed Rheda3,8, Johannes Passig1,3, Christian Radischat1,3, Hendryk Czech1,3, Petri Tiita6, Pasi Jalava6, Stefanie Kasurinen6, Theo Schwemer1, Pasi Yli-Prilä6, Jarkko Tissari6, Heikki Lamberg6 and Jürgen Schnelle-Kreis1, (1)University of Rostock, Rostock, Germany, (2)Max-Delbrück-Centrum, Berlin, Germany, (3)HICE - Helmholtz Virtual Institute of Complex Molecular Systems in Environmental Health, Munich, Germany, (4)Technical University Munich, Center of Allergy and Environment (ZAUM), Munich, Germany, (5)Karlsruhe Institute of Technology, Karlsruhe, Germany, (6)University of Eastern Finland, Kuopio, Finland, (7)University of Luxembourg, Luxembourg, Luxembourg, (8)Helmholtz Center Munich, Oberschleissheim, Germany
Ship engine emissions are important regarding lung and cardiovascular diseases in coastal regions worldwide. Bio mass burning is made responsible for adverse health effects in many cities and rural regions. The Virtual Helmholtz Institute-HICE (www.hice-vi.eu) addresses chemical & physical properties and health effects of anthropogenic combustion emissions. Typical lung cell responses to combustion aerosols include inflammation and apoptosis, but a molecular link with the specific chemical composition in particular of ship emissions has not been established. Through an air-liquid interface exposure system (ALI), we exposed human lung cells at-site to exhaust fumes from a ship engine running on common heavy fuel oil (HFO) and cleaner-burning diesel fuel (DF) as well as to emissions of wood combustion compliances. A special field deployable ALI-exposition system and a mobile S2-biological laboratory were developed for this study. Human alveolar basal epithelial cells (A549 etc.) are ALI-exposed to fresh, diluted (1:40-1:100) combustion aerosols and subsequently were toxicologically and molecular-biologically characterized. Advanced chemical analyses of the exhaust aerosols were combined with transcriptional, proteomic and metabolomic profiling to characterise the cellular responses. The HFO ship emissions contained high concentrations of toxic compounds (transition metals, organic toxicants) and particle masses. The cellular responses included inflammation and oxidative stress. Surprisingly, the DF ship emissions, which predominantly contain rather “pure” carbonaceous soot and much less known toxicants, induced significantly broader biological effects, affecting essential cellular pathways (e.g., mitochondrial function and intracellular transport). Therefore the use of distillate fuels for shipping (this is the current emission reduction strategy of the IMO) appears insufficient for diminishing health effects. The study suggests rather reducing the particle emissions by secondary measures (filters) than shifting the fuel. In the case of wood combustion the reduction of soot and carcinogenic aromatic compounds is suggested. However, for both sources (wood and ship diesel) we found that effects of the gaseous pollutants (e.g. aldehydes) are potentially problematic.