AAAR 36th Annual Conference October 16 - October 20, 2017 Raleigh Convention Center Raleigh, North Carolina, USA
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Comparison of Airway Responses Induced in a Mouse Model by the Gas and Particulate Fractions of Gasoline Direct Injection Engine Exhaust
CAITLIN MAIKAWA, Naomi Zimmerman, Manuel Ramos, Mittal Shah, James S. Wallace, Krystal Godri Pollitt, University of Massachusetts Amherst
Abstract Number: 281 Working Group: Health Related Aerosols
Abstract Exposure to environmental pollutants can exacerbate asthmatic symptoms as well as induce airway inflammation and mucus production. Whilst exposure to diesel exhaust has been associated with asthma exacerbations, the response to other engine type emissions is not clear. The increasing prevalence of vehicles with gasoline direct injection (GDI) engines motivated this study. The objective of this study was to evaluate the pulmonary responses induced by acute exposure to gasoline direct injection engine exhaust in an allergic asthma murine model. Balb/c mice were sensitised with an allergen (Dermatophagoides pteronyssinus) to induce airway hyperresponsiveness or treated with saline as the control group. Saline- and allergen-sensitised mice were challenged for two hours to engine-out exhaust from a laboratory GDI engine operated at conditions equivalent to vehicle highway cruise conditions. Exhaust was filtered to assess particulate and gas fractions. Lung mechanics and mRNA production were evaluated post-exposure as well as the inflammatory airway response through histology examination. Particulate matter released from GDI engine exhaust induced upregulation of a genes related to polycyclic aromatic hydrocarbon (PAH) metabolism (Cyp1b1), inflammation (Tnfα, Cxcl1) and remodelling (Vegf) in the lungs of naïve mice. High molecular weight PAHs dominated the particulate fraction of the exhaust and were likely attributable to this response. Mice with airway hyperresponsiveness exhibited elevated basal levels of airway inflammation, compared to naïve animals, such that no differences were found between GDI engine exhaust and HEPA filtered air exposure scenarios as noted by mRNA production and histology examination. Exposure to particle fraction of GDI engine exhaust by allergen-sensitised mice was further found to enhance resistance in the central airway and dampening in the peripheral tissues in response to methacholine. As GDI engines become more predominant in the global vehicle fleet, understanding the impacts of their tailpipe emissions on respiratory health becomes increasingly important. Short-term exposure to particulate PAHs released from GDI engine exhaust exacerbates airway inflammation and remodelling in naïve mice. The particle fraction of GDI engine exhaust further contributed to enhanced methacholine responsiveness in the central and peripheral tissues in animals with airway hyperresponsiveness.