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
disease, 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.
