Exposure to second hand smoke is a major cause of chronic obstructive pulmonary disease (COPD) in the non-smoker. In this review we explore the use of animal smoke exposure models and their insight into disease pathogenesis. The methods of smoke exposure, including exposure delivery systems, are described. Key findings from the acute and chronic smoke exposure models are outlined, including descriptions of the inflammation processes, proteases involved, oxidative stress, and apoptosis. Finally, alternatives to rodent models of lung disease are presented.
Keywords: emphysema, COPD, animal models, cigarette smoke, inflammation, apoptosis, proteases
Citation: Goldklang MP, Marks SM and D'Armiento JM (2013) Second hand smoke and COPD: lessons from animal studies. Front. Physiol. 4:30. doi: 10.3389/fphys.2013.00030
Received: 24 November 2012; Paper pending published: 08 January 2013;
Accepted: 07 February 2013; Published online: 27 February 2013.
Edited by:Laima Taraseviciene-Stewart, University of Colorado Denver, USA
Copyright © 2013 Goldklang, Marks and D'Armiento. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.
*Correspondence: Jeanine M. D'Armiento, Department of Medicine, Division of Molecular Medicine, Columbia University, 630 West 168th Street, P&S 9-449, New York, NY 10032, USA. e-mail: email@example.com