Electronic cigarettes (e-cigs) are battery-operated devices which heat a liquid that contains nicotine, flavors, and additives and, in some cases, varying amounts of other unknown compounds, which are not regulated by the FDA. Aggressive advertising by e-cigs manufacturers implies these devices are less harmful and represent a “safe” alternative to conventional cigarette smoking. E-cigs reportedly contain less carcinogens than traditional cigarettes, with a predominance of nicotine in e-cig vapors that has led to them being variably called “nicotine delivery devices”. Thus, the assumption is that e-cigs cause less lung injury in the healthy user, and may help conventional cigarette users to quit smoking. Furthermore, e-cigs are viewed as being potentially safe for asthmatic smokers. Based on these purported safety profiles, e-cig use is increasing at an alarming rate.
In spite of the increasing use of e-cigs, data on their short- or long-term detrimental effects and toxicity are missing. In addition to the fact that the local heating and “vape” delivery by e-cigs has the potential to deliver substantially higher levels of nicotine to the upper and lower airways, e-cigs also contain formaldehyde, hemiacetals that can form formaldehyde, acrolein, and particulate matter, all of which can be potentially harmful. Furthermore, local delivery of e-cig products to the oropharynx and upper airways has the potential to substantially influence the oral and bronchial epithelium and salivary glands, thus influencing mucus membrane properties, barrier function, and immune responses and responsivity. Indeed, salivary gland dysfunction can lead to periodontal, gingivitis, bacterial colonization, and loss of enamel mineralization. These conditions are often encountered in conventional smokers and may be present in e-cig users as well. Similarly, higher nicotine or other product levels may adversely influence upper airway irritability, reflex bronchoconstriction and other key aspects of airway function. Finally, the influence of e-cig products on the alveolar epithelium and the pulmonary endothelium are still under exploration. In a recently article published in AJP-Lung and highlighted in a variety of electronic media, Dr. Petrache and her collaborators demonstrated that nicotine and other components present in e-cigs damaged endothelial cells and increase endothelial permeability in addition to damaging airway and alveolar epithelia: http://ajplung.physiology.org/content/early/2015/05/11/ajplung.00411.2014. Clearly additional research is needed on this very interesting topic
The American Journal of Physiology-Lung Cellular and Molecular Physiology is issuing a call for papers addressing key questions in the mechanisms and potentially toxic effects of e-cigs as it applies to the cardiopulmonary system and other organs that may be targeted. All manuscripts will be reviewed promptly, thoroughly, and fairly by members of the Editorial Board and guest reviewers who are recognized experts in this field. Accepted manuscripts will be published on line within two weeks after acceptance under a distinct heading and will receive special attention and handling. In addition, the Editor will solicit an annual perspective on this area to review seminal findings. Only those papers not requiring extensive revision will be published under this call for papers.
This call for papers is effective between August 1st, 2015 and October 1st, 2017.