Primary human bronchial epithelial cell responses to diesel and novel biodiesel emissions

Introduction: Diesel particulate matter can cause inflammation and oxidative stress in the airways. A strategy to reduce adverse effects associated with particulate matter in diesel emissions is the use of biodiesels and fuel additives such as triacetin, but very little is known about the health effects of these alternative emissions. The aim of this study is to evaluate the effects of biodiesel and triacetin/biodiesel emissions on primary human bronchial epithelial cells (pHBECs) in comparison to conventional diesel emissions. Methods: Primary HBECs were differentiated at air-liquid interface and exposed to diesel (D100), biodiesel (B20, B50 and B100: 20%, 50% and 100% biodiesel derived from waste cooking oil, respectively) and triacetin/biodiesel (B96 and B90: 4% and 10% triacetin in biodiesel, respectively) emissions for 30 minutes. Indicators of cell viability, inflammation, antioxidant production and xenobiotic metabolism were measured. Results: Biodiesel and triacetin substitution altered the particulate matter composition of the diesel emissions. B50, B90 and B100 significantly increased percentage cell death (75%, 60.9 and 49%, respectively). B50 and B90 significantly increased HO-1 mRNA expression (16.9-fold and 18.3-fold increase, respectively). B90 and B100 significantly increased IL-8 secretion (6.9-fold and 3-fold increase, respectively). Conclusions: Biodiesel fuels and fuel additives (triacetin) reduce particulate matter in diesel emissions, but have adverse effects on bronchial epithelial cell viability, metabolism and antioxidant production, compared to conventional diesel emissions. Further studies of the effect of diesel fuel alternatives on pHBECs are required.