Abstract
BackgroundShip 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.ObjectivesTo 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.MethodsThrough an air-liquid interface exposure system, we exposed human lung cells under realistic in 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.ResultsThe 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.ConclusionsDespite 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.
Highlights
Epidemiological studies provide compelling evidence that pollution by airborne particulate matter (PM) derived from fossil fuel combustion is an important cause of morbidity and premature death [1, 2]
Reactions to heavy fuel oils (HFOs) emissions were dominated by oxidative stress and inflammatory responses, whereas diesel fuel (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
For the use of HFO and DF we recommend a reduction of carbonaceous soot in the ship emissions by implementation of filtration devices
Summary
Epidemiological studies provide compelling evidence that pollution by airborne particulate matter (PM) derived from fossil fuel combustion is an important cause of morbidity and premature death [1, 2]. Current regulations target HFO use by limiting their sulphur content In this context, the maximum sulphur content in shipping fuel is internationally regulated by the International Maritime Organisation (IMO) at 3.5%; in most European and US coastal areas, the maximum allowed sulphur content is 1% (Sulphur Emission Control Areas, SECA) [12, 13]. In 2015, a 0.1% sulphur fuel limit will be implemented in the Baltic and North Sea SECAs [14] To comply with these new sulphur limits, highly refined distillate fuels are necessary (diesel fuel, DF, or marine gas oil, MGO). In 2011, 170 million tons of HFO and 43 million tons of MGO and DF were consumed by ship diesel engines worldwide [15, 16] This volume corresponds to approximately 21% of global fuel consumption [17]. Known cellular responses to combustion particles include oxidative stress and inflammatory signalling
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have