TY - JOUR
T1 - Particulate matter from both heavy fuel oil and diesel fuel shipping emissions show strong biological effects on human lung cells at realistic and comparable in vitro exposure conditions
AU - Oeder, Sebastian
AU - Kanashova, Tamara
AU - Sippula, Olli
AU - Sapcariu, Sean C.
AU - Streibel, Thorsten
AU - Arteaga-Salas, Jose Manuel
AU - Passig, Johannes
AU - Dilger, Marco
AU - Paur, Hanns-Rudolf
AU - Schlager, Christoph
AU - Mülhopt, Sonja
AU - Diabaté, Silvia
AU - Weiss, Carsten
AU - Stengel, Benjamin
AU - Rabe, Rom
AU - Harndorf, Horst
AU - Torvela, Tiina
AU - Jokiniemi, Jorma K.
AU - Hirvonen, Maija-Riitta
AU - al, et
PY - 2015
Y1 - 2015
N2 - Background: 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. Objectives: 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. Methods: Through 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. Results: 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. Conclusions: 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.
AB - Background: 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. Objectives: 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. Methods: Through 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. Results: 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. Conclusions: 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.
U2 - 10.1371/journal.pone.0126536
DO - 10.1371/journal.pone.0126536
M3 - Article
SN - 1932-6203
VL - 10
JO - PLoS ONE
JF - PLoS ONE
IS - 6
M1 - e0126536
ER -