A study published yesterday in PLOS ONE reports that mouse respiratory epithelial cells exposed to e-cigarette vapor showed signs of oxidative stress and inflammation and that mice exposed to e-cigarette aerosol experienced impaired pulmonary bacterial clearance.
It didn't take long for the conclusion that e-cigarettes can cause pneumonia to be disseminated across the world. For example, a WKYC news article headline told readers: "Study Links E-Cigarettes to Increased Risk of Viral Infections."
In this article, one of the study authors was quoted as stating:
"We have provided strong evidence that the liquid used in
e-cigarettes, whether it contains nicotine or not, has negative effects
on the airways and on the lungs. The problem is,
these products aren't regulated and there are no standards to control
how much nicotine or other chemicals they contain. I think e-cigarettes
could prove dangerous, especially with long-term consumption."
The Rest of the Story
There's just one problem with the alarmist conclusion from the study and the alarmist headlines being spread by the media: they are inadequately supported by scientific evidence.
This study was conducted on mice, and we know that there are severe problems with extrapolating from findings in mice to clinically meaningful findings in humans.
All the study really demonstrated was something we already knew: that e-cigarette aerosol can cause respiratory irritation. We've known that for years. The question of whether that irritation could translate into clinically meaningful lung disease remains unanswered, and there certainly is no evidence at the current time to suggest that there are any clinically significant adverse lung effects, at least acutely.
In fact, the only existing clinical evidence is that switching from smoking to e-cigarettes can actually reverse one form of obstructive airways disease (i.e., asthma). That study concluded: " This small retrospective study indicates that regular use of e-cigs to
substitute smoking is associated with objective and subjective
improvements in asthma outcomes. Considering that e-cig use is
reportedly less harmful than conventional smoking and can lead to
reduced cigarette consumption with subsequent improvements in asthma
outcomes, this study shows that e-cigs can be a valid option for
asthmatic patients who cannot quit smoking by other methods."
The danger in extrapolating from this finding in mice to clinically meaningful effects in man is demonstrated by a nearly identical study which found that mice treated with aspirin exhibit impaired clearance of bacteria from their lungs. The study concluded: "When challenged with a sublethal inoculum [of aspirin], pretreated and immediately treated animals
demonstrated significant impairments in their ability to clear viable
pneumococci from the lungs; the inefficient pulmonary clearance was
associated with a marked attenuation in the ability of aspirin-treated mice to recruit granulocytes and macrophages into the bronchoalveolar spaces. Survival in mice administered aspirin
6 h after pneumococcal challenge was not adversely affected; however,
the pulmonary clearance and cellular response were significantly
impaired. We conclude that aspirin can disrupt host defense against pneumococci by blunting the normal pulmonary inflammatory reaction to organisms deposited into the lower respiratory tract."
Based on that study, would researchers conclude that aspirin causes pneumonia in humans? Should the author of that study have warned the public that based on his findings, aspirin could be dangerous? Should the media have disseminated to the public the widespread conclusion that "Study Links Aspirin to Increased Risk of Bacterial Infections?"
Clearly, such conclusions would have been premature (and, as it turns out, wrong). Thus, the dangers of extrapolating from mice to men.