Primary human bronchial epithelial cell responses to diesel and biodiesel emissions at an air-liquid interface.

Vaughan, A; Stevanovic, S; Jafari, M; Bowman, RV; Fong, KM; Ristovski, ZD; Yang, IA

Primary human bronchial epithelial cell responses to diesel and biodiesel emissions at an air-liquid interface.

Vaughan, A

Stevanovic, S Jafari, M Bowman, RV Fong, KM Ristovski, ZD Yang, IA

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Publisher:: PERGAMON-ELSEVIER SCIENCE LTD
Publication Type:: Journal Article
Citation:: Toxicol In Vitro, 2019, 57, pp. 67-75
Issue Date:: 2019-06

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Field	Value	Language
dc.contributor.author	Vaughan, A https://orcid.org/0000-0001-5890-7877
dc.contributor.author	Stevanovic, S
dc.contributor.author	Jafari, M
dc.contributor.author	Bowman, RV
dc.contributor.author	Fong, KM
dc.contributor.author	Ristovski, ZD
dc.contributor.author	Yang, IA
dc.date.accessioned	2022-09-26T02:02:10Z
dc.date.available	2019-02-05
dc.date.available	2022-09-26T02:02:10Z
dc.date.issued	2019-06
dc.identifier.citation	Toxicol In Vitro, 2019, 57, pp. 67-75
dc.identifier.issn	0887-2333
dc.identifier.issn	1879-3177
dc.identifier.uri	http://hdl.handle.net/10453/162063
dc.description.abstract	INTRODUCTION: Diesel emissions have a high level of particulate matter which can cause inflammation and oxidative stress in the airways. A strategy to reduce diesel particulate matter and the associated adverse effects is the use of biodiesels and fuel additives. However, very little is known about the biological effects of these alternative emissions. The aim of this study is to compare the effect of biodiesel and triacetin/biodiesel emissions on primary human bronchial epithelial cells (pHBECs) compared to diesel emissions. METHODS: pHBECs were exposed to diesel, biodiesel (20%, 50% and 100% biodiesel derived from coconut oil) and triacetin/biodiesel (4% and 10% triacetin) emissions for 30 min at air-liquid interface. Cell viability (cellular metabolism, cell death, CASP3 mRNA expression and BCL2 mRNA expression), inflammation (IL-8 and IL-6 secretion), antioxidant production (HO-1 mRNA expression) and xenobiotic metabolism (CYP1a1 mRNA expression) were measured. RESULTS: Biodiesel emissions (B50) reduced cell viability, and increased oxidative stress. Triacetin/biodiesel emissions (B90) decreased cell viability and increased antioxidant production, inflammation and xenobiotic metabolism. Biodiesel emissions (B100) reduced cell viability, and increased IL-8 secretion and xenobiotic metabolism. CONCLUSIONS: Biodiesel substitution in diesel fuel and triacetin substitution in biodiesel can increase the adverse effects of diesel emissions of pHBECs. Further studies of the effect of these diesel fuel alternatives on pHBECs are required.
dc.format	Print-Electronic
dc.language	eng
dc.publisher	PERGAMON-ELSEVIER SCIENCE LTD
dc.relation.ispartof	Toxicol In Vitro
dc.relation.isbasedon	10.1016/j.tiv.2019.02.005
dc.rights	info:eu-repo/semantics/closedAccess
dc.subject	1115 Pharmacology and Pharmaceutical Sciences
dc.subject.classification	Toxicology
dc.subject.mesh	Air Pollutants
dc.subject.mesh	Biofuels
dc.subject.mesh	Bronchi
dc.subject.mesh	Caspase 3
dc.subject.mesh	Cell Survival
dc.subject.mesh	Cells, Cultured
dc.subject.mesh	Cytochrome P-450 CYP1A1
dc.subject.mesh	Epithelial Cells
dc.subject.mesh	Gasoline
dc.subject.mesh	Heme Oxygenase-1
dc.subject.mesh	Humans
dc.subject.mesh	Interleukin-6
dc.subject.mesh	Interleukin-8
dc.subject.mesh	Proto-Oncogene Proteins c-bcl-2
dc.subject.mesh	Vehicle Emissions
dc.subject.mesh	Bronchi
dc.subject.mesh	Cells, Cultured
dc.subject.mesh	Epithelial Cells
dc.subject.mesh	Humans
dc.subject.mesh	Cytochrome P-450 CYP1A1
dc.subject.mesh	Proto-Oncogene Proteins c-bcl-2
dc.subject.mesh	Interleukin-8
dc.subject.mesh	Interleukin-6
dc.subject.mesh	Air Pollutants
dc.subject.mesh	Gasoline
dc.subject.mesh	Vehicle Emissions
dc.subject.mesh	Cell Survival
dc.subject.mesh	Heme Oxygenase-1
dc.subject.mesh	Caspase 3
dc.subject.mesh	Biofuels
dc.title	Primary human bronchial epithelial cell responses to diesel and biodiesel emissions at an air-liquid interface.
dc.type	Journal Article
utslib.citation.volume	57
utslib.location.activity	England
utslib.for	1115 Pharmacology and Pharmaceutical Sciences
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
utslib.copyright.status	closed_access	*
dc.date.updated	2022-09-26T02:02:07Z
pubs.publication-status	Published
pubs.volume	57

Abstract:

INTRODUCTION: Diesel emissions have a high level of particulate matter which can cause inflammation and oxidative stress in the airways. A strategy to reduce diesel particulate matter and the associated adverse effects is the use of biodiesels and fuel additives. However, very little is known about the biological effects of these alternative emissions. The aim of this study is to compare the effect of biodiesel and triacetin/biodiesel emissions on primary human bronchial epithelial cells (pHBECs) compared to diesel emissions. METHODS: pHBECs were exposed to diesel, biodiesel (20%, 50% and 100% biodiesel derived from coconut oil) and triacetin/biodiesel (4% and 10% triacetin) emissions for 30 min at air-liquid interface. Cell viability (cellular metabolism, cell death, CASP3 mRNA expression and BCL2 mRNA expression), inflammation (IL-8 and IL-6 secretion), antioxidant production (HO-1 mRNA expression) and xenobiotic metabolism (CYP1a1 mRNA expression) were measured. RESULTS: Biodiesel emissions (B50) reduced cell viability, and increased oxidative stress. Triacetin/biodiesel emissions (B90) decreased cell viability and increased antioxidant production, inflammation and xenobiotic metabolism. Biodiesel emissions (B100) reduced cell viability, and increased IL-8 secretion and xenobiotic metabolism. CONCLUSIONS: Biodiesel substitution in diesel fuel and triacetin substitution in biodiesel can increase the adverse effects of diesel emissions of pHBECs. Further studies of the effect of these diesel fuel alternatives on pHBECs are required.

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http://hdl.handle.net/10453/162063