In an all-too-familiar refrain, the Daily Fail has once again thrown journalistic integrity out of the window (as if they had any to begin with) to boldly tell the world that “e-cigs are bad mmkay”. Regular readers will of course remember a similar “study” – these things seem to come out at regular intervals – that claimed e-cigs have the potential to have severe adverse effects on the heart. It was a festering pile of fetid dingo kidneys then and, guess what, it still is.
Of course, you could easily be forgiven for the headline:
E-cigs: The incendiary truth… Just 10 puffs increases your risk of heart disease and they may even make smokers LESS likely to quit
Just ten puffs eh?
But how accurate (snork) is the Daily Fail in this case? I think we can guess at that. So instead, let’s look at the study this article is derived from.
Cigarette smoking impairs vascular repair, enhances platelet activation and induces endothelial dysfunction. We have previously demonstrated that healthy volunteers smoking just one cigarette exhibited increased levels of circulating EPCs as well as MVs from endothelial cells, leukocytes and platelets. We concluded that this increase in EPCs and MVs may have been generated by acute endothelial dysfunction, inflammation and possible vascular injury. Based on these findings, we hypothesized that e-cigarette inhalation would give a similar response in regards to EPC and MV release.
Before the introduction is over, these researchers are already thinking that e-cigs are cigarettes, so you can guess how this is going to go.
Sixteen healthy seldom smokers (maximum of 10 cigarettes/month) were recruited. We have specifically chosen to recruit sporadic smokers as they would better tolerate exposure to ECV than cigarette smoke-naïve individuals, thus minimizing the probability of developing sickness or nausea that are usually associated with smoke inhalation.
So a large sample then. Good grief, and they are going to call this conclusive?
All subjects were required to abstain from caffeine consumption, heavy exercise and alcohol for 24 hours and tobacco or marijuana usage 7 days prior to exposure.
Aha, remember the previous post on aortic stiffening (which some believe is an indicator of risk for heart disease)? Well, the vast majority of potential triggers have been excluded (with the exception of watching scary movies and other high-stress activities). As a mild stimulant, both caffeine and nicotine exhibit very similar reactions on a biological level.
In accordance to the protocol proposed by Flouris et al., we adjusted the nicotine concentration and inhalation frequency to achieve comparable effects to a combustible cigarette containing 1 mg nicotine.
Another “tell” here. In order for cigarette-like effects to be recorded, nicotine concentration and inhalation frequency were adjusted. This isn’t a case of observing vapers in the wild, this is a case of deliberately emphasising a particular result.
A popular second-generation electronic cigarette device (eGo XL, 1100 mAh, operating at 3,7V) with a dual-coil CE5 atomizer was used.
Of course. Another study using a CE5. Look, the CE5 isn’t a terribly bad tank – for a starter, but the top coil and wick arrangement is a major problem when it comes to research. The CE tanks had no end of wicking problems – especially with higher than 50% VG ratio. In this scenario, where the device is going to be used just like a cigarette it’ll have another problem. Dry hits.
So what did they actually find?
- Cotinine – well, of course they would (they did exclude two of the 16 as those two broke the rules and likely had a smoke prior to the study commencing)
- Endothelial progenitor cells – elevated levels. Which in itself indicates a whole lot of nothing. The term endothelial progenitor cell is a term applied to multiple cell types that play a role (or roles) in the regeneration of the endothelial (interior surface) lining of blood vessels
- Microvesicles – (Microvesicles are small membrane-enclosed sacs that are thought to be shed from a variety of cell types 1.) – they found these at all time points in both groups, control and vaper. Not much to see there
- FeNo – (Fractional exhaled Nitric oxide) – a measurement of airway inflammation – again, so significant differences in either group
All in all, they didn’t find a lot – no airway inflammation, elevated levels of progenitor cells (which doesn’t mean that much), so where did the Fail get its headline from? From the discussion – and likely their friendly anti-ecig buffoon.
These findings suggest that a very short exposure to ECV caused a rapid EPC mobilization in blood, which may indicate an impact on vascular integrity leading to future atherosclerosis.
Which “may impact” integrity and lead to clogging of the arteries. Where on earth did the researchers get that from?
It has been suggested that EPCs play a crucial role in vascular repair. Following endothelial injury, EPCs are recruited from the bone marrow, spleen or vascular wall where they reside
Having had a quick read on the subject of endothelial progenitor cells, I would tend to agree that they do have a role in repair. This is hardly likely to cause acute vascular problems, unless…. oh:
ECV particles are primarily liquid in composition and seem to dissipate faster than those produced during combustible processes. Nevertheless, ECV contains high amounts of fine and ultrafine particles. Of particulate matter, ultrafine particles are considered to generate the most adverse health effects due to their vast number and great surface area that enable transportation of toxic components
I wondered when that would show up. The researchers claim – not without some basis – that e-cig aerosol contains a host of toxic components.
The same toxicants, although in higher concentrations, were demonstrated to be present in cigarette smoke as well as in combustion-derived air pollution, both of which are strongly associated with detrimental cardiovascular effects .
So, the dose makes the poison then.
Our healthy volunteers were exposed to ECV for only 10 minutes and had to inhale 10 puffs of e-liquid (nicotine 12 mg/ml). The calculations we used had projected that such an exposure level would result in a similar plasma cotinine level to that obtained from smoking a traditional cigarette (with a nicotine content of 1 mg).
Except that they didn’t.
However, we observed significantly lower cotinine levels after e-cigarette inhalation in comparison to our previous study following cigarette smoking, which could be due to insufficient exposure. Another factor that could influence nicotine absorption is the inhalation technique. Our subjects were not used to ECV inhalation, which could have affected nicotine absorption.
So, 10 puffs of 1.2% over 10 minutes doesn’t produce levels comparable to cigarette smoking. Who knew? *facepalm*
Might as well add this to the “utter useless tripe” pile. It’ll be a good candidate for the Golden Turd award.
(Image credit Marc Bruxelle/shutterstock.com)