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

journal contribution
posted on 2019-06-01, 00:00 authored by Annalicia Vaughan, Svetlana StevanovicSvetlana Stevanovic, Mohammad Jafari, Rayleen V Bowman, Kwun M Fong, Zoran D Ristovski, Ian A Yang
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.

History

Journal

Toxicology in vitro

Volume

57

Pagination

67-75

Location

Amsterdam, The Netherlands

ISSN

0887-2333

eISSN

1879-3177

Language

eng

Publication classification

C1.1 Refereed article in a scholarly journal

Copyright notice

2019, Elsevier Ltd.

Publisher

Elsevier