When it comes to vaping, it's relatively unknown. There's no hard data on how much of each chemical is absorbed when we vape an e-liquid with X amount of Y chemical or how the amount of each or a single chemical in the vapor will affect us. The data that we do have is from lab studies on lab rats and the rare cases of BO which falls back to the popcorn industry. That does not mean that the data holds no merit, it does, though the recommended exposures are based off of these studies from what I can tell.
That being said, the documented effects of each chemical, from available studies I've read, are generally in concentrated form. Meaning they are testing diacetyl, acetoin and acetyl proprionyl in their pure form; not in an e-liquid, not in a solvated blend. We may see this in the future, especially if AEMSA and other parties begin to play a larger role in the production and manufacturing of e-liquids, though it's not to that point just yet.
As far as the chemicals go, Acetyl Proprionyl (2,3-Pentanedione) caused proliferation of fibrous connective tissue in the walls of airways and projections of fibrous connective tissue sometimes extended into the air passageways and that repeated exposures to either Acetyl Proprionyl (2,3-pentanedione) or diacetyl can cause airway fibrosis in rats (source - CDC). Essentially, they can cause airway damage.
As an alternative comparison, drinking alcohol can cause liver damage, especially if consumption is excessive. It may damage the liver of one person in only a few years time, while another may not see the effects for 20-40 years of hardcore consumption; some may never see it at all. Everyone is different and the effects are going to be drastically different for everyone. This is not meant to downplay the seriousness of a potential issue, but provide a comparison of what happens over time.
There's a lot of unknowns with vaping and with each passing year we're learning more and more, albeit, on our own. With the help of Dr. Farsalinos, hopefully we'll learn more and more and yet, even more as he's been a big contributor to the industry as a whole and hopefully will continue to be for some time.
That being said, the documented effects of each chemical, from available studies I've read, are generally in concentrated form. Meaning they are testing diacetyl, acetoin and acetyl proprionyl in their pure form; not in an e-liquid, not in a solvated blend.
What available studies are you reading? The one's we've read are clearly NOT done with these chemicals in their "pure form" and the ppm (which is far less than pure) is clearly noted. A couple of examples:
Respiratory toxicologic pathology of inhaled ... [Toxicol Pathol. 2008] - PubMed - NCBI
In rats, we investigated the toxicity of inhaled diacetyl at concentrations of up to 365 ppm (time weighted average), either as six-hour continuous exposures or as four brief, intense exposures over six hours. A separate group inhaled a single pulse of ~1800 ppm diacetyl (92.9 ppm six-hour average). Rats were necropsied 18 to 20 hours after exposure. Diacetyl inhalation caused epithelial necrosis and suppurative to fibrinosuppurative inflammation in the nose, larynx, trachea, and bronchi. Bronchi were affected at diacetyl concentrations of 294.6 ppm or greater; the trachea and larynx were affected at diacetyl concentrations of 224 ppm or greater...
http://toxsci.oxfordjournals.org/content/103/1/169.full.pdf
Male C57Bl/6 mice were
exposed to inhaled diacetyl across several concentrations and
duration profiles, or by direct oropharyngeal aspiration. Effects of
diacetyl on the respiratory tract were evaluated by histopathology
and BALF analyses. Effects of
diacetyl on the respiratory tract were evaluated by histopathology
and BALF analyses. Subacute exposure to 200 or 400 ppm
diacetyl for 5 days caused deaths, necrotizing rhinitis, necrotizing
laryngitis and bronchitis.
Reducing the exposure to 1 h/day (100,
200, 400 ppm) for 4 weeks resulted in less nasal and laryngeal
toxicity, but led to peribronchial and peribronchiolar lymphocytic
inflammation.
A similar pattern was observed with intermittent
high-dose exposures at 1200 ppm (15 min, twice a day, 4 weeks).
Subchronic exposures to 100 ppm (6 h/day, 12 weeks) caused
moderate nasal injury, and peribronchial lymphocytic inflamma-
tion accompanied by epithelial atrophy, denudation, and re-
generation.
In rats, we investigated the toxicity of inhaled diacetyl at concentrations of up to 365 ppm (time weighted average), either as six-hour continuous exposures or as four brief, intense exposures over six hours. A separate group inhaled a single pulse of ~1800 ppm diacetyl (92.9 ppm six-hour average). Rats were necropsied 18 to 20 hours after exposure. Diacetyl inhalation caused epithelial necrosis and suppurative to fibrinosuppurative inflammation in the nose, larynx, trachea, and bronchi. Bronchi were affected at diacetyl concentrations of 294.6 ppm or greater; the trachea and larynx were affected at diacetyl concentrations of 224 ppm or greater...
http://toxsci.oxfordjournals.org/content/103/1/169.full.pdf
Male C57Bl/6 mice were
exposed to inhaled diacetyl across several concentrations and
duration profiles, or by direct oropharyngeal aspiration. Effects of
diacetyl on the respiratory tract were evaluated by histopathology
and BALF analyses. Effects of
diacetyl on the respiratory tract were evaluated by histopathology
and BALF analyses. Subacute exposure to 200 or 400 ppm
diacetyl for 5 days caused deaths, necrotizing rhinitis, necrotizing
laryngitis and bronchitis.
Reducing the exposure to 1 h/day (100,
200, 400 ppm) for 4 weeks resulted in less nasal and laryngeal
toxicity, but led to peribronchial and peribronchiolar lymphocytic
inflammation.
A similar pattern was observed with intermittent
high-dose exposures at 1200 ppm (15 min, twice a day, 4 weeks).
Subchronic exposures to 100 ppm (6 h/day, 12 weeks) caused
moderate nasal injury, and peribronchial lymphocytic inflamma-
tion accompanied by epithelial atrophy, denudation, and re-
generation.
As an alternative comparison, drinking alcohol can cause liver damage, especially if consumption is excessive. It may damage the liver of one person in only a few years time, while another may not see the effects for 20-40 years of hardcore consumption; some may never see it at all. Everyone is different and the effects are going to be drastically different for everyone. This is not meant to downplay the seriousness of a potential issue, but provide a comparison of what happens over time.
Wethinks a better "alternative comparison" would be the affects & risks of alcohol on the liver to people that already have liver compromise....because most all of us already have some level of lung compromise from smoking. The worst part is that when we quit smoking, we feel & discern the relief from the absence of hot smoke & scorching tar...hence we don't feel whatever (lesser?/different?) compromise that we may be experiencing from vaping. That's why it's SO important to avoid the chemicals that have been shown to cause compromise.
With the help of Dr. Farsalinos, hopefully we'll learn more and more...
We feel it's essential to point out that Dr. Farsalinos work is not necessarily "conclusive" as to how these chemicals affect the lungs in humans or animals. Currently (as we understand it) the majority of his work is not on live animals at all, but rather 'cells in a petri dish'. More on that in the copy/post below.
We are NOT complaining or in any way criticizing the work of Dr. F., ClearStream or FA - it's all very good for what it is. But from what we've seen, it's almost all "comparisons to cigarettes"...and just because something can be proven to be safer than cigarettes, doesn't prove it is safe.
'Don't want to start a huge debate here (and we're not trying to discredit FA in any way) - but we do want to point out...
There are nearly 50 different/distinct cells in the lungs & bronchia (a VERY good overview on the anatomy & physiology of the lungs Anatomy, development, and physiology of the lungs : GI Motility online)...and they each are dependent on a myriad of factors within the lungs (and outside the lungs) for their health & function. ClearStream testing tests one type of cell (mammalian fibroblasts) in vitro (which literally means "in glass" - many times referred to as a "test tube" or "petri dish" test).
So while the tests tell us how one type of lung cell reacts to the specific vapor blend when the cells are outside of body, well, that's all it really tells usAnd just like in this study (that vapers typically assume "proves" that e-vapor is safer than cig smoke http://www.gwern.net/docs/nicotine/2013-romagna.pdf)...we see this very integral sentence at the end of the 'results section': These results should be validated by clinical studies. (as in, studies inside real lungs).
Again, we're not trying to discredit was is being done by ClearStream. These tests are valid and offer good information...but they are not conclusive, as they do not show what happens in actual lungs - and wethinks this is very important for people to know.
Because, (of course!) absolutely no in vitro test is proof of what will actually happen inside the body - and all researchers know this.
Last edited: