Genotoxic potential of diesel exhaust particles from the combustion of first- and second-generation biodiesel fuels—the FuelHealth project

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Abstract

Epidemiological data indicate that exposure to diesel exhaust particles (DEPs) from traffic emissions is associated with higher risk of morbidity and mortality related to cardiovascular and pulmonary diseases, accelerated progression of atherosclerotic plaques, and possible lung cancer. While the impact of DEPs from combustion of fossil diesel fuel on human health has been extensively studied, current knowledge of DEPs from combustion of biofuels provides limited and inconsistent information about its mutagenicity and genotoxicity, as well as possible adverse health risks. The objective of the present work was to compare the genotoxicity of DEPs from combustion of two first-generation fuels, 7% fatty acid methyl esters (FAME) (B7) and 20% FAME (B20), and a second-generation 20% FAME/hydrotreated vegetable oil (SHB: synthetic hydrocarbon biofuel) fuel. Our results revealed that particulate engine emissions from each type of biodiesel fuel induced genotoxic effects in BEAS-2B and A549 cells, manifested as the increased levels of single-strand breaks, the increased frequencies of micronuclei, or the deregulated expression of genes involved in DNA damage signaling pathways. We also found that none of the tested DEPs showed the induction of oxidative DNA damage and the gamma-H2AX-detectable double-strand breaks. The most pronounced differences concerning the tested particles were observed for the induction of single-strand breaks, with the greatest genotoxicity being associated with the B7-derived DEPs. The differences in other effects between DEPs from the different biodiesel blend percentage and biodiesel feedstock were also observed, but the magnitude of these variations was limited.

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Most cited references 33

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Flap endonuclease 1.

Lata Balakrishnan, Robert A. Bambara (2012)

First discovered as a structure-specific endonuclease that evolved to cut at the base of single-stranded flaps, flap endonuclease (FEN1) is now recognized as a central component of cellular DNA metabolism. Substrate specificity allows FEN1 to process intermediates of Okazaki fragment maturation, long-patch base excision repair, telomere maintenance, and stalled replication fork rescue. For Okazaki fragments, the RNA primer is displaced into a 5' flap and then cleaved off. FEN1 binds to the flap base and then threads the 5' end of the flap through its helical arch and active site to create a configuration for cleavage. The threading requirement prevents this active nuclease from cutting the single-stranded template between Okazaki fragments. FEN1 efficiency and specificity are critical to the maintenance of genome fidelity. Overall, recent advances in our knowledge of FEN1 suggest that it was an ancient protein that has been fine-tuned over eons to coordinate many essential DNA transactions.

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Diesel exhaust: current knowledge of adverse effects and underlying cellular mechanisms

Sandro Steiner, Christoph Bisig, Alke Petri-Fink … (2016)

Diesel engine emissions are among the most prevalent anthropogenic pollutants worldwide, and with the growing popularity of diesel-fueled engines in the private transportation sector, they are becoming increasingly widespread in densely populated urban regions. However, a large number of toxicological studies clearly show that diesel engine emissions profoundly affect human health. Thus the interest in the molecular and cellular mechanisms underlying these effects is large, especially concerning the nature of the components of diesel exhaust responsible for the effects and how they could be eliminated from the exhaust. This review describes the fundamental properties of diesel exhaust as well as the human respiratory tract and concludes that adverse health effects of diesel exhaust not only emerge from its chemical composition, but also from the interplay between its physical properties, the physiological and cellular properties, and function of the human respiratory tract. Furthermore, the primary molecular and cellular mechanisms triggered by diesel exhaust exposure, as well as the fundamentals of the methods for toxicological testing of diesel exhaust toxicity, are described. The key aspects of adverse effects induced by diesel exhaust exposure described herein will be important for regulators to support or ban certain technologies or to legitimate incentives for the development of promising new technologies such as catalytic diesel particle filters.

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Measuring oxidative damage to DNA and its repair with the comet assay.

Samuel Collins (2014)

Single cell gel electrophoresis, or the comet assay, was devised as a sensitive method for detecting DNA strand breaks, at the level of individual cells. A simple modification, incorporating a digestion of DNA with a lesion-specific endonuclease, makes it possible to measure oxidised bases. With the inclusion of formamidopyrimidine DNA glycosylase to recognise oxidised purines, or Nth (endonuclease III) to detect oxidised pyrimidines, the comet assay has been used extensively in human biomonitoring to monitor oxidative stress, usually in peripheral blood mononuclear cells. There is evidence to suggest that the enzymic approach is more accurate than chromatographic methods, when applied to low background levels of base oxidation. However, there are potential problems of over-estimation (because the enzymes are not completely specific) or under-estimation (failure to detect lesions that are close together). Attempts have been made to improve the inter-laboratory reproducibility of the comet assay. In addition to measuring DNA damage, the assay can be used to monitor the cellular or in vitro repair of strand breaks or oxidised bases. It also has applications in assessing the antioxidant status of cells. In its various forms, the comet assay is now an invaluable tool in human biomonitoring and genotoxicity testing. This article is part of a Special Issue entitled Current methods to study reactive oxygen species - pros and cons and biophysics of membrane proteins. Guest Editor: Christine Winterbourn. Copyright © 2013 Elsevier B.V. All rights reserved.

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Author and article information

Contributors

Anna Lankoff: +48 41 349 62 96 , alankoff@gmail.com

Journal

Journal ID (nlm-ta): Environ Sci Pollut Res Int

Journal ID (iso-abbrev): Environ Sci Pollut Res Int

Title: Environmental Science and Pollution Research International

Publisher: Springer Berlin Heidelberg (Berlin/Heidelberg )

ISSN (Print): 0944-1344

ISSN (Electronic): 1614-7499

Publication date (Electronic): 9 September 2017

Publication date PMC-release: 9 September 2017

Publication date (Print): 2017

Volume: 24

Issue: 31

Pages: 24223-24234

Affiliations

[1 ]ISNI 0000 0001 2292 9126, GRID grid.411821.f, Department of Radiobiology and Immunology, Institute of Biology, , Jan Kochanowski University, ; 15 Swietokrzyska Str, 25-406 Kielce, Poland

[2 ]ISNI 0000 0001 2289 0890, GRID grid.418850.0, Center for Radiobiology and Biological Dosimetry, , Institute of Nuclear Chemistry and Technology, ; 16 Dorodna Str, 03-195 Warsaw, Poland

[3 ]ISNI 0000 0001 1955 7966, GRID grid.13276.31, Faculty of Human Nutrition and Consumer Science, , Warsaw University of Life Sciences, ; 166 Nowoursynowska Str, 02-787 Warsaw, Poland

[4 ]ISNI 0000 0001 1955 7966, GRID grid.13276.31, Faculty of Production Engineering, , Warsaw University of Life Sciences, ; 166 Nowoursynowska Str, 02-787 Warsaw, Poland

[5 ]ISNI 0000 0001 1541 4204, GRID grid.418193.6, Domain of Infection Control and Environmental Health, , Norwegian Institute of Public Health, ; P.O. Box 4404, Nydalen, 0403 Oslo, Norway

[6 ]GRID grid.414779.8, Department of Molecular Biology and Translational Research, , Institute of Rural Health, ; Jaczewskiego 2, 20-090 Lublin, Poland

[7 ]ISNI 0000 0001 1271 4615, GRID grid.445362.2, Faculty of Medicine, , University of Information Technology and Management in Rzeszow, ; Sucharskiego 2, 35-225 Rzeszow, Poland

Author notes

Responsible editor: Philippe Garrigues

Article

Publisher ID: 9995

DOI: 10.1007/s11356-017-9995-0

PMC ID: 5655577

PubMed ID: 28889235

SO-VID: 010f262f-5160-494d-9ec6-668f41a9fca7

License:

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

History

Date received : 3 April 2017

Date accepted : 22 August 2017

Funding

Funded by: Polish-Norwegian Research programm

Award ID: Pol-Nor/201040/72/2013

Award Recipient : Anna Lankoff

Custom metadata

ScienceOpen disciplines: General environmental science

Keywords: diesel exhaust particles,first- and second-generation biodiesel fuels,single- and double-strand breaks,oxidative dna damage,chromosomal damage

Data availability:

ScienceOpen disciplines: General environmental science

Keywords: diesel exhaust particles, first- and second-generation biodiesel fuels, single- and double-strand breaks, oxidative dna damage, chromosomal damage

Genotoxic potential of diesel exhaust particles from the combustion of first- and second-generation biodiesel fuels—the FuelHealth project

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Hydrology

Most cited references 33

Flap endonuclease 1.

Diesel exhaust: current knowledge of adverse effects and underlying cellular mechanisms

Measuring oxidative damage to DNA and its repair with the comet assay.

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