Comparison of Airway Responses Induced in a Mouse Model by the Gas and Particulate Fractions of Gasoline Direct Injection Engine Exhaust

Caitlin L. Maikawa, Naomi Zimmerman, Manuel Ramos, Mittal Shah, James S. Wallace and Krystal J. Godri Pollitt
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Caitlin L. Maikawa: Environmental Health Sciences, University of Massachusetts, 686 North Pleasant Street, Goessmann Laboratory Room 175, Amherst, MA 01003, USA
Naomi Zimmerman: Mechanical Engineering, University of British Columbia, Vancouver, BC V6T 1Z4, Canada
Manuel Ramos: Mechanical and Industrial Engineering, University of Toronto, Toronto, ON M5S 3G8, Canada
Mittal Shah: Institute of Orthopaedics and Musculoskeletal Sciences, University College London, Royal National Orthopaedic Hospital, Stanmore HA7 4LP, UK
James S. Wallace: Mechanical and Industrial Engineering, University of Toronto, Toronto, ON M5S 3G8, Canada
Krystal J. Godri Pollitt: Environmental Health Sciences, University of Massachusetts, 686 North Pleasant Street, Goessmann Laboratory Room 175, Amherst, MA 01003, USA

IJERPH, 2018, vol. 15, issue 3, 1-14

Abstract: Diesel exhaust has been associated with asthma, but its response to other engine emissions is not clear. The increasing prevalence of vehicles with gasoline direct injection (GDI) engines motivated this study, and the objective was to evaluate pulmonary responses induced by acute exposure to GDI engine exhaust in an allergic asthma murine model. Mice were sensitized with an allergen to induce airway hyperresponsiveness or treated with saline (non-allergic group). Animals were challenged for 2-h to exhaust from a laboratory GDI engine operated at conditions equivalent to a highway cruise. Exhaust was filtered to assess responses induced by the particulate and gas fractions. Short-term exposure to particulate matter from GDI engine exhaust induced upregulation of genes related to polycyclic aromatic hydrocarbon (PAH) metabolism ( Cyp1b1 ) and inflammation ( TNFα ) in the lungs of non-allergic mice. High molecular weight PAHs dominated the particulate fraction of the exhaust, and this response was therefore likely attributable to the presence of these PAHs. The particle fraction of GDI engine exhaust further contributed to enhanced methacholine responsiveness in the central and peripheral tissues in animals with airway hyperresponsiveness. As GDI engines gain prevalence in the vehicle fleet, understanding the health impacts of their emissions becomes increasingly important.

Keywords: gasoline direct injection engine exhaust; polycyclic aromatic hydrocarbons; inflammation; Cyp1b1; TNFα; in vivo (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2018
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