AAAR 31st Annual Conference
October 8-12, 2012
Hyatt Regency Minneapolis
Minneapolis, Minnesota, USA
Abstract View
Pro-inflammatory Responses of Diesel Engine Exhaust Particles - Impact of Organic Compounds
ANNIKE IRENE TOTLANDSDAL, Alena Kubatova, Johan Øvrevik, Richard Cochran, Jan Inge Herseth, Anette Kocbach Bølling, Per E Schwarze, Flemming R Cassee, Edel Lilleaas, Magne Refsnes, Jørn A Holme, Marit Låg, Norwegian Institute of Public Health, Norway
Abstract Number: 57 Working Group: Combustion
Abstract Exposure to diesel engine exhaust particles (DEPs), representing a complex and variable mixture of components, has been linked to adverse cardiopulmonary effects. The biological mechanisms involved are currently not clarified, but inflammation is considered a key event. In this study we characterize and explore which components of DEPs that may initiate pro-inflammatory responses.
Human bronchial epithelial cells (BEAS-2B) were exposed to either native DEPs, corresponding methanol DEP-extract or residual DEPs, and investigated with respect to cytotoxicity and expression and release of multiple inflammation-related mediators. In order to further investigate the potency of different groups of organics to induce these pro-inflammatory responses, cells were also exposed to fractionated methanol extracts, which were prepared by using solid phase extraction with hexane and 20% dichloromethane (DCM) in hexane and methanol.
Both native DEPs and DEP-extract, but not residual DEPs, induced marked mRNA expression of COX-2, IL-6 and IL-8, as well as cytotoxicity and release of IL-6. However, CYP1A1 was primarily induced by the native and residual DEPs. Gas chromatography with mass spectrometry (GC/MS) analysis of DEP-extracts indicated that the majority of the analysed polycyclic aromatic hydrocarbons (PAHs) and PAH-derivatives were extracted from the particles, but that certain PAH-derivatives, possibly their carboxylic isomers, tended to be retained on the residual DEPs. Notably, certain cytokine-inducing components of the methanol extract may suppress CYP1A1 expression. Chemical analyses of fractionated extracts indicated that the methanol-soluble fraction containing hydroxy-PAHs may be responsible for the pro-inflammatory response induced by the DEP extracts. Interestingly, the same fraction seemed to be important for similar polarity fractions of wood smoke particles. These results suggest that hydroxy-PAHs may represent a group of compounds that may be of particular interest to study in further research of inflammatory responses induced by exposure to particulate air pollution.