Featured Article: Available for free download (http://ajplung.physiology.org/) even by those with no subscription to APS journals
Kelly S Schweitzer , Steven X Chen , Sarah Law , Mary J Van Demark , Christophe Poirier , Matthew J Justice , Walter C Hubbard , Elena S Kim , Xianyin Lai , Mu Wang , William D. Kranz, Clinton J. Carroll , Bruce D. Ray , Robert Bittman , John Goodpaster , Irina Petrache
American Journal of Physiology - Lung Cellular and Molecular Physiology Published 15 May 2015 Vol. no. , DOI: 10.1152/ajplung.00411.2014
It is well known that cigarette smoking is the primary cause of chronic obstructive lung disease and contributes to the development of atherosclerosis and cardiovascular disease. During the last two years, AJP-Lung has published about 60 papers documenting the potential mechanisms by which cigarette smoke damage every components of the respiratory system by a variety of mechanisms (PubMed search: Am J Physiol Lung Cell Mol Physiol. AND cigarette smoke AND (2012 OR 2013 OR 2014 OR 2015). The classical studies of Church and Pryor (see Environ Health Perspect. 1985 Dec; 64: 111–126) showed that the vapor phase of cigarette smoke contains a large number of highly reactive oxygen, nitrogen and carbon centered radicals (generated by the combustion of tobacco leaves; Indoor Air. 2005 Apr;15(2):135-40.) while the tar phase contains quinone/hydroquinone which is capable of reducing oxygen to generate reactive oxygen and nitrogen species. In addition cigarette smoke contains a mixture of more than 5,000 toxic chemicals, including nicotine and acrolein; Int J Environ Res Public Health. 2011 Feb; 8(2): 613–628).
However, the possible hazards of electronic-cigarette smoke have not been documented. A lot of young people, enamored with the electronic age, are frequent smokers of e-cigarettes which were thought to be less harmful than regular cigarettes of even safe. Dr. Petrache’s (an Associate Editor of AJP-Lung) and her colleagues demonstrate that e-cigarette smoke damages not only epithelial cell (the first cells to come into contact with the injurious agents in smoke) but also endothelial cells causing decreased resistance of the endothelial barrier, increased permeability and lung inflammation. Although nicotine was responsible for the lion’ share of this injury (independent of its ability to generate reactive intermediates), even nicotine free e-smoke could cause significant injury due to the presence of other damaging compounds including acrolein. The investigators proceeded in identifying the signaling events associated with an increase in endothelial permeability which are succinctly summarized in Figure 8 of their article (please read the article for the whole story). Furthermore, they showed that enhancement of S1P1 (sphingosine-1 phosphate) lung levels prevented the deleterious effects of e-smoke most likely by reinforcing the tethering forces holding the endothelial cells together.
Clearly a lot more work has to be done to document the long term effects of e-cigarette smoke on the development of chronic lung and cardiovascular disease. However, it is safe to say that this article clearly demonstrates that e-cigarette smoke is not safe.