Genotoxicity by rapeseed methyl ester and hydrogenated vegetable oil combustion exhaust products in lung epithelial (A549) cells

Research output: Contribution to journalJournal articleResearchpeer-review

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Genotoxicity by rapeseed methyl ester and hydrogenated vegetable oil combustion exhaust products in lung epithelial (A549) cells. / Rothmann, Monika Hezareh; Møller, Peter; Essig, Yona J; Gren, Louise; Malmborg, Vilhelm B; Tunér, Martin; Pagels, Joakim; Krais, Annette M; Roursgaard, Martin.

In: Mutagenesis, Vol. 38, No. 4, 2023, p. 238–249.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Rothmann, MH, Møller, P, Essig, YJ, Gren, L, Malmborg, VB, Tunér, M, Pagels, J, Krais, AM & Roursgaard, M 2023, 'Genotoxicity by rapeseed methyl ester and hydrogenated vegetable oil combustion exhaust products in lung epithelial (A549) cells', Mutagenesis, vol. 38, no. 4, pp. 238–249. https://doi.org/10.1093/mutage/gead016

APA

Rothmann, M. H., Møller, P., Essig, Y. J., Gren, L., Malmborg, V. B., Tunér, M., Pagels, J., Krais, A. M., & Roursgaard, M. (2023). Genotoxicity by rapeseed methyl ester and hydrogenated vegetable oil combustion exhaust products in lung epithelial (A549) cells. Mutagenesis, 38(4), 238–249. https://doi.org/10.1093/mutage/gead016

Vancouver

Rothmann MH, Møller P, Essig YJ, Gren L, Malmborg VB, Tunér M et al. Genotoxicity by rapeseed methyl ester and hydrogenated vegetable oil combustion exhaust products in lung epithelial (A549) cells. Mutagenesis. 2023;38(4):238–249. https://doi.org/10.1093/mutage/gead016

Author

Rothmann, Monika Hezareh ; Møller, Peter ; Essig, Yona J ; Gren, Louise ; Malmborg, Vilhelm B ; Tunér, Martin ; Pagels, Joakim ; Krais, Annette M ; Roursgaard, Martin. / Genotoxicity by rapeseed methyl ester and hydrogenated vegetable oil combustion exhaust products in lung epithelial (A549) cells. In: Mutagenesis. 2023 ; Vol. 38, No. 4. pp. 238–249.

Bibtex

@article{c5fd401184db44539d56fc918c426c66,
title = "Genotoxicity by rapeseed methyl ester and hydrogenated vegetable oil combustion exhaust products in lung epithelial (A549) cells",
abstract = "Biofuel is an attractive substitute for petrodiesel because of its lower environmental footprint. For instance, the polycyclic aromatic hydrocarbons (PAH) emission per fuel energy content is lower for rapeseed methyl ester (RME) than for petrodiesel. The present study assesses genotoxicity by extractable organic matter (EOM) of exhaust particles from combustion of petrodiesel, RME and hydrogenated vegetable oil (HVO) in lung epithelial (A549) cells. Genotoxicity was assessed as DNA strand breaks by the alkaline comet assay. EOM from combustion of petrodiesel and RME generated the same level of DNA strand breaks based on equal concentration of total PAH (i.e. net increases of 0.13 [95% confidence interval (CI): 0.002, 0.259 and 0.12 [95% CI: 0.01, 0.24] lesions per million base pairs, respectively). In comparison, the positive control (etoposide) generated much higher level of DNA strand breaks (i.e. 0.84, 95% CI: 0.72, 0.97) lesions per million base pairs). Relatively low concentrations of EOM from RME and HVO combustion particles (<116 ng/ml total PAH) did not cause DNA strand breaks in A549 cells, whereas benzo[a]pyrene and PAH-rich EOM from petrodiesel combusted using low oxygen inlet concentration were genotoxic. The genotoxicity was attributed to high molecular weight PAH isomers with 5-6 rings. In summary, the results show that EOM from combustion of petrodiesel and RME generate the same level of DNA strand breaks on equal total PAH basis. However, the genotoxic hazard of engine exhaust from on-road vehicles is lower for RME than petrodiesel because of lower PAH emission per fuel energy content.",
author = "Rothmann, {Monika Hezareh} and Peter M{\o}ller and Essig, {Yona J} and Louise Gren and Malmborg, {Vilhelm B} and Martin Tun{\'e}r and Joakim Pagels and Krais, {Annette M} and Martin Roursgaard",
note = "{\textcopyright} The Author(s) 2023. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.",
year = "2023",
doi = "10.1093/mutage/gead016",
language = "English",
volume = "38",
pages = "238–249",
journal = "Mutagenesis",
issn = "0267-8357",
publisher = "Oxford University Press",
number = "4",

}

RIS

TY - JOUR

T1 - Genotoxicity by rapeseed methyl ester and hydrogenated vegetable oil combustion exhaust products in lung epithelial (A549) cells

AU - Rothmann, Monika Hezareh

AU - Møller, Peter

AU - Essig, Yona J

AU - Gren, Louise

AU - Malmborg, Vilhelm B

AU - Tunér, Martin

AU - Pagels, Joakim

AU - Krais, Annette M

AU - Roursgaard, Martin

N1 - © The Author(s) 2023. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

PY - 2023

Y1 - 2023

N2 - Biofuel is an attractive substitute for petrodiesel because of its lower environmental footprint. For instance, the polycyclic aromatic hydrocarbons (PAH) emission per fuel energy content is lower for rapeseed methyl ester (RME) than for petrodiesel. The present study assesses genotoxicity by extractable organic matter (EOM) of exhaust particles from combustion of petrodiesel, RME and hydrogenated vegetable oil (HVO) in lung epithelial (A549) cells. Genotoxicity was assessed as DNA strand breaks by the alkaline comet assay. EOM from combustion of petrodiesel and RME generated the same level of DNA strand breaks based on equal concentration of total PAH (i.e. net increases of 0.13 [95% confidence interval (CI): 0.002, 0.259 and 0.12 [95% CI: 0.01, 0.24] lesions per million base pairs, respectively). In comparison, the positive control (etoposide) generated much higher level of DNA strand breaks (i.e. 0.84, 95% CI: 0.72, 0.97) lesions per million base pairs). Relatively low concentrations of EOM from RME and HVO combustion particles (<116 ng/ml total PAH) did not cause DNA strand breaks in A549 cells, whereas benzo[a]pyrene and PAH-rich EOM from petrodiesel combusted using low oxygen inlet concentration were genotoxic. The genotoxicity was attributed to high molecular weight PAH isomers with 5-6 rings. In summary, the results show that EOM from combustion of petrodiesel and RME generate the same level of DNA strand breaks on equal total PAH basis. However, the genotoxic hazard of engine exhaust from on-road vehicles is lower for RME than petrodiesel because of lower PAH emission per fuel energy content.

AB - Biofuel is an attractive substitute for petrodiesel because of its lower environmental footprint. For instance, the polycyclic aromatic hydrocarbons (PAH) emission per fuel energy content is lower for rapeseed methyl ester (RME) than for petrodiesel. The present study assesses genotoxicity by extractable organic matter (EOM) of exhaust particles from combustion of petrodiesel, RME and hydrogenated vegetable oil (HVO) in lung epithelial (A549) cells. Genotoxicity was assessed as DNA strand breaks by the alkaline comet assay. EOM from combustion of petrodiesel and RME generated the same level of DNA strand breaks based on equal concentration of total PAH (i.e. net increases of 0.13 [95% confidence interval (CI): 0.002, 0.259 and 0.12 [95% CI: 0.01, 0.24] lesions per million base pairs, respectively). In comparison, the positive control (etoposide) generated much higher level of DNA strand breaks (i.e. 0.84, 95% CI: 0.72, 0.97) lesions per million base pairs). Relatively low concentrations of EOM from RME and HVO combustion particles (<116 ng/ml total PAH) did not cause DNA strand breaks in A549 cells, whereas benzo[a]pyrene and PAH-rich EOM from petrodiesel combusted using low oxygen inlet concentration were genotoxic. The genotoxicity was attributed to high molecular weight PAH isomers with 5-6 rings. In summary, the results show that EOM from combustion of petrodiesel and RME generate the same level of DNA strand breaks on equal total PAH basis. However, the genotoxic hazard of engine exhaust from on-road vehicles is lower for RME than petrodiesel because of lower PAH emission per fuel energy content.

U2 - 10.1093/mutage/gead016

DO - 10.1093/mutage/gead016

M3 - Journal article

C2 - 37232551

VL - 38

SP - 238

EP - 249

JO - Mutagenesis

JF - Mutagenesis

SN - 0267-8357

IS - 4

ER -

ID: 357730967