Diacetyl exposure graphed.

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skoony

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Rossum

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Using the "average" is a bit misleading. Most of the e-cigs tested had zero or trace amounts. Nobody is worried about trace amounts (except of course those trying to advance an anti-vaping agenda). But when we look at some of the worst offending liquids that have as much as 1000µg/ml of diketones and multiply that by the 20-30 ml/day that some people vape, then we do get a total exposure that's "worse than smoking" when it comes to diketones. Is that dangerous? I don't know, but I prefer not to be the guinea pig that finds out. ;)
 

LaraC

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VNeil, I just want to say that I was impressed with the way you and Shawn Avery (author of the article) went about discussing and correcting the error. It was nice to see you both working it out together, the way scientists who are interested in accuracy should.

The civil, rational exchange you two had in the comments section below the article was a pleasure to read.

Soooo different from the defensive, hostile reaction of the Portland bunch when problems with their "formaldehyde" study (and with their conclusions) were pointed out to them some months ago.

skoony's original link, now showing the corrections:
Everybody is talking about vaping and "popcorn lung" again, so here's a graph
 

Rossum

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But you're okay being the guinea pig on all the other potentially dangerous aspects of vaping? Please explain that to me.
Compared to smoking? Yes. What's in our vape?
  • Nicotine. I want that. I'm not very pleasant to be around without it; just ask my wife (who has never smoked or vaped). I'm willing to accept whatever negative consequences nicotine may have in exchange for its benefits to me -- my wife not leaving me being one of them.

  • VG. Generally considered benign, even when inhaled as vapor/aerosol.

  • PG. Generally considered benign, even when inhaled as vapor/aerosol. May even be beneficial due to its bactericidal / virucidal properties. I've not had a single cold in the (few days shy of) two years I've been vaping. I've woken up on a few mornings with symptoms that I previously would have taken to indicate I had a cold coming on. I started vaping as usual and those symptoms were gone in an hour or less.

  • Flavorings. This component is optional. That means not essential. This component may or may not include substances that have been shown both in vitro and in vivo to be anything but benign. It makes sense to try to minimize one's exposure to such substances.

You keep trying to frame this as through diketones are essential to vape. They are not. One does not need to give up vaping, or even flavors, in order to avoid diketones.

The damage diketones can cause to lung tissue is permanent and irreversible. There is no argument that exposure to sufficient quantities of them WILL cause such damage. The only argument is whether the quantities in our vapes are sufficient to do that. Me, I'm not willing to risk that for a particular flavor profile, there are plenty of flavors I find entirely acceptable outside of that profile -- in moderation. Is it possible that other substances are in flavorings are less than benign? Yes, it is. But none have been identified as causing permanent and irreversible damage. If some were, I'd avoid those too.

Keep in mind, this is a personal decision on my part. I'm by no means trying to tell anyone else what they should or shouldn't vape. It's your body. You own it. Do as you please with it.

What I object to is when people try to sweep this issue under the rug, because I do think that vapers should be educated and be able to make informed decisions.
 

VNeil

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VNeil, I just want to say that I was impressed with the way you and Shawn Avery (author of the article) went about discussing and correcting the error. It was nice to see you both working it out together, the way scientists who are interested in accuracy should.

The civil, rational exchange you two had in the comments section below the article was a pleasure to read.

Soooo different from the defensive, hostile reaction of the Portland bunch when problems with their "formaldehyde" study (and with their conclusions) were pointed out to them some months ago.

skoony's original link, now showing the corrections:
Everybody is talking about vaping and "popcorn lung" again, so here's a graph
All the credit goes to Shawn, who quickly recognized the error and corrected it (improving on my suggested value).
 

Rossum

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I see your point Rossum. That's still based still based on the NOISH safe exposure limits that are admittedly arbitrarily low.
Huh? I didn't mention NIOSH limits. I compared the numbers from a high-diketone juice to the numbers given for cigarettes in the article you posted.

I for one would think a 20 to 30 ml per day usage would have to be on the uber high end of the consumption rate for vapers. How many at that rate are actually using diketones in their juice. Its my impression high end users tend to be shying away from flavors in general as they seem to be more interested in vapor production. A lot of flavors are PG or alcohol based which tends to negate said vapor production.
Mass consumption of any adult related product usually has negative results associated with
it and as such I believe one should look more towards the average usage of a product or, at
least make sure extreme usage doesn't skew the results.
OK, I consider myself reasonably average, at least among the folks here at ECF. I vape around 6ml a day. If I were to use a juice that had 1000µg/ml of diketones, I'd still be getting as much as a pack-a-day smoker. I'll pass on that, thanks. :)
 

Kent C

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Diacetyl is found in very common areas every day but discussed minimally. The coffee industy is produces a fair amount and is the focus of studies, I wonder when the FDA will shut down Starbucks.

Not likely...

For example, coffee processing workers can be exposed to natural diacetyl levels well above the OELs [22], yet the respiratory status of coffee processing workers has been evaluated in many studies [21], [26], [27], [29], [33], [43], [50], [51], [52], [54], [55], [58] and [59] and the most consistent adverse effects are allergic respiratory responses to specific allergens in respirable green coffee dusts [21], [26], [27], [29], [30], [50], [54], [55] and [59]. To the best of our knowledge, there are no reports of bronchiolitis obliterans or other serious, obstructive diseases occurring at elevated rates in coffee processing workers handling unflavored coffee beans or ground coffee. Similarly, although retail coffee workers may be exposed to naturally occurring diacetyl at levels exceeding the recommended OELs (as suggested by the present analysis), we are not aware of any epidemiology studies suggesting an increased risk of obstructive disorders in coffee shop workers, nor are there any published case reports of bronchiolitis obliterans occurring in coffee shop employees. Finally, cigarette smoke contains naturally occurring diacetyl concentrations in the hundreds of parts per million, and the resulting exposures to smokers are much higher than those typically experienced by workers handling diacetyl-containing flavorings in food processing facilities. However, smoking has not been associated with an increased risk of bronchiolitis obliterans [48].

Characterization of naturally occurring airborne diacetyl concentrations associated with the preparation and consumption of unflavored coffee
 

Kent C

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"They can also be inhaled in the form of a powder if airborne dust is created in the production process. Many of these chemicals are highly irritating to the eyes, respiratory tract, and skin."
CDC - Flavorings-Related Lung Disease: Exposures to Flavoring Chemicals - NIOSH Workplace Safety and Health Topic
"we assessed diacetyl emissions and airborne dust levels from butter flavorings used by several microwave popcorn manufacturing companies."
Diacetyl emissions and airborne dust from butter flavorings used in microwave popcorn production. - PubMed - NCBI
regards
mike

Yeah, Rossum's right. Any liquid in any factory can be similarly carried by dust - but that doesn't make it into a 'powder form' of the substance.
 

Mazinny

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I see a glaring discrepancy. The factor of 0.99 g/ml is the density of water, not air. The correct number is 0.0012 g/ml. So his result should be divided by 820, resulting in a number more like 927. Everyone is free to check my math too, for discrepancies :)
This makes sense. I was wondering that if Dr. F extrapolated 5 ppb in ambient air to 65 ppm per day, correctly , there is no way that the op figures can be correct as well. 0.2 ppm is only 40 times as high as 5 ppb. There is no way the factory workers could be exposed to the 760,000 number the op cites.
 

Kent C

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ok so popcorn factory workers are exposed to more diacetyl than cigarette smokers who in turn are exposed to more diacetyl than starbucks workers !?

According to the OP post, yes. However..... The other study that is cited elsewhere in this forum from the daily caller article:

How The Media Totally Exaggerated Study On Risk Of ‘Popcorn Lung’ From E-Cigarettes

... also cites the "Critical Reviews in Toxicology" study. That deals with the diketones - diacetyl/AP in cigarettes.

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(as pointed out in the other thread - this 'error' still gets you to the study abstract :- )

They also found what the coffee study found:

"We found that diacetyl and 2,3-pentanedione exposures from cigarette smoking far exceed occupational exposures for most food/flavoring workers who smoke."

Their conclusion as a result of not finding OB in cigarettes is:

"This suggests that previous claims of a significant exposure-response relationship between diacetyl inhalation and respiratory disease in food/flavoring workers were confounded, because none of the investigations considered or quantified the non-occupational diacetyl exposure from cigarette smoke, yet all of the cohorts evaluated had considerable smoking histories".

IOW, their findings call into question any link between diacetyl and bronchiolitis obliterans, including the earlier popcorn factory (BML) studies, and they fully acknowledge this:

"Further, because smoking has not been shown to be a risk factor for bronchiolitis obliterans, our findings are inconsistent with claims that diacetyl and/or 2,3-pentanedione exposure are risk factors for this disease."
 

Kent C

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here's the response from Muge Akpinar :
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And in keeping with the 'dueling science' theme, here was Pierce's response to Akpinar-Elci and Elci.

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"Akpinar-Elci and Elci suggest that we “falsely” claimed that “all of the cohorts evaluated had considerable smoking histories”. To support their assertion, they offer a non- sequitur: of the nine alleged cases of bronchiolitis obliterans in their cohort, a majority (6/9) were current or former smokers. Unfortunately, they seem to have confused the terms “cohort” and “case”. To reiterate, all food/flavoring cohorts studied to date had a significant fraction of current/former smokers, and indeed in the Akpinar-Elci et al. analyses of the Gilster-Mary Lee (GML) workers, nearly 50% of the study participants were current smokers.

They also appear to believe that, because most of the alleged cases of bronchiolitis obliterans in their cohort (8/9) were not current smokers, then smoking was not a confounder in their study. They have unintentionally reinforced our point. Cigarette smoke contains high levels of diacetyl, therefore workers who smoke have much higher diacetyl exposures than the non-smoking food/flavoring workers. More importantly, even though smokers arguably have the highest peak and cumulative diacetyl exposures of any definable cohort, smoking is not a risk factor for bronchiolitis obliterans. These observations argue against a relationship between diacetyl exposure and bronchiolitis obliterans. Finally, they have confused “controlling for the effects of smoking on respiratory function” (which they did do) versus “accounting for the relatively large diacetyl exposure from smoking when assessing the exposure-response relationship between diacetyl inhalation and respiratory function in food/flavoring workers” (which they certainly did not do)."

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Kent C

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My concerns regarding diacetyl and and acetylpropionyl just decreased significantly.
Not entirely, but significantly.

For some reason (I think I know why - gov't schools, gov't lapdog media and Hollywood) people tend to think that businesses are responsible for all that is bad in the world, when in fact, governments of all kinds throughout history, have a corner on that market.

That doesn't stop juries from taking junk science as "truth". So whether it is the popcorn factory, Dow Chemical (breast implants), second hand smoke studies, diacetyl in cigarettes or coffee or any flavoring, there is a built in bias (by brainwashing) that tends to prejudices science and court cases against business. This is not to say that some businesses have been culpable, but the bias continues despite having found, subsequently the science brought forth in some of these cases is junk. The breast implant info is just one of many - discussed in this article:

The Decade of 'Junk Science'

... from a few decades back but the practice is still going strong....

" A four-member expert panel appointed by U.S. District Court judge Samuel Pointer reached a similar conclusion last December. It reported that “No association was evident between breast implants and any of the individual connective tissue diseases, all definite connective diseases combined, or the other autoimmune heumatic conditions.” None of this means that many, if not most, plaintiffs were not ill. But there is no evidence that implants are at fault. As Dr. Angell puts it: Women have “been told they might get sick because of the implants. They’ve developed symptoms that any women over 25 could develop.” Because the evidence was so overwhelming, the vast majority of court cases have gone for the defendants. But that doesn’t mean justice was done. As Bernstein points out, “sometimes a lawyer can win just by getting the game in play. Deterred by the possibility of large awards by unpredictable juries, high legal costs, and the notoriety of a trial, many defendants can be induced to offer huge settlements.” In the United States, it is too late to undo the damage suffered by implant makers. But judicial and legislative reform could prevent a repeat performance in another industry."

------
The: 'none of this means... the patients were not ill' points to the 'confounding factors' that have been brought up by Pierce's studies in diacetyl, and many others that have more correlation than causation, with even the correlation suspect. And the last line (underlined) was more hopeful that is warranted - as we have seen.

The fact is, that despite overwhelming evidence to the contrary, I'm guessing few know the eventual medical outcome of the implants. If you'd ask 10 people on the street today, 10 may still be under the impression that they are harmful. Which points to exactly what the Harvard study may do to ecigarettes - not just now, but decades from now. I also think that they rely on that.
 
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VNeil

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Just a note to say that the linked article was modified to use the correct computation of density in air. That should resolve the debate we had last night over that matter. He used a different number than I suggested here, to account for the actual density of airborne diacetyl I guess.
 

Jman8

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Not likely...

For example, coffee processing workers can be exposed to natural diacetyl levels well above the OELs [22], yet the respiratory status of coffee processing workers has been evaluated in many studies [21], [26], [27], [29], [33], [43], [50], [51], [52], [54], [55], [58] and [59] and the most consistent adverse effects are allergic respiratory responses to specific allergens in respirable green coffee dusts [21], [26], [27], [29], [30], [50], [54], [55] and [59]. To the best of our knowledge, there are no reports of bronchiolitis obliterans or other serious, obstructive diseases occurring at elevated rates in coffee processing workers handling unflavored coffee beans or ground coffee. Similarly, although retail coffee workers may be exposed to naturally occurring diacetyl at levels exceeding the recommended OELs (as suggested by the present analysis), we are not aware of any epidemiology studies suggesting an increased risk of obstructive disorders in coffee shop workers, nor are there any published case reports of bronchiolitis obliterans occurring in coffee shop employees. Finally, cigarette smoke contains naturally occurring diacetyl concentrations in the hundreds of parts per million, and the resulting exposures to smokers are much higher than those typically experienced by workers handling diacetyl-containing flavorings in food processing facilities. However, smoking has not been associated with an increased risk of bronchiolitis obliterans [48].

Characterization of naturally occurring airborne diacetyl concentrations associated with the preparation and consumption of unflavored coffee

Guinea pigs.

Is what my cynical side would say. My more mature, scientific side would say this is such a minute level of concern (across any industry) that it warrants harsh and strong rebuttal for those who dare to make it out to be a significant issue.
 

VNeil

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Here's an article from Daily Drip. The graph compares exposures for e-cigs to cigarettes
and, factory workers. The author requests that his math be checked. I didn't find any
glaring discrepancies.
Everybody is talking about vaping and "popcorn lung" again, so here's a graph

Regards
Mike
I see a glaring discrepancy. The factor of 0.99 g/ml is the density of water, not air. The correct number is 0.0012 g/ml. So his result should be divided by 820, resulting in a number more like 927. Everyone is free to check my math too, for discrepancies :)
 
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VNeil

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...There is no argument that exposure to sufficient quantities of them WILL cause such damage. The only argument is whether the quantities in our vapes are sufficient to do that.
I'm not sure that is true at all. My understanding of the science is that OSHA, for example, is reluctant to put a workplace limit on airborne diacetyl because they are not convinced the studies have proven the case that diacetyl is the cause of OB in the popcorn and coffee factories. There appear to be many questions remaining, including why other smokers do not get OB, nor are smokers more at risk in those factories because of their combined exposure.
One study or a series of studies chained on each other do not always amount to "there is no remaining argument...". Nor does the opinion of a gov't body, such as the FDA do that, especially around here :eek:
 

Mazinny

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Their conclusion as a result of not finding OB in cigarettes is:

"This suggests that previous claims of a significant exposure-response relationship between diacetyl inhalation and respiratory disease in food/flavoring workers were confounded, because none of the investigations considered or quantified the non-occupational diacetyl exposure from cigarette smoke, yet all of the cohorts evaluated had considerable smoking histories".

IOW, their findings call into question any link between diacetyl and bronchiolitis obliterans, including the earlier popcorn factory (BML) studies, and they fully acknowledge this:

"Further, because smoking has not been shown to be a risk factor for bronchiolitis obliterans, our findings are inconsistent with claims that diacetyl and/or 2,3-pentanedione exposure are risk factors for this disease."

I believe the people who were cited for the bold part, claimed that this false. They wrote a response to the study you are citing. Let's see if i can find it. I believe Dr. F also wrote a response to the Pierce study you are citing.

And this from their conflict of interest statement :

All the authors are employed by Cardno ChemRisk, a consulting firm that provides scientific advice to the government, corporations, law firms and various scientific/professional organizations. Cardno ChemRisk has been engaged by several manufacturers and suppliers of diacetyl and diacetyl-containing flavorings in various litigation matters, and two of the authors (Drs. Pierce and Finley) have served as experts in diacetyl litigation. However, no external funding was received for the study, the research supporting the analysis, nor the time needed to prepare the article.
 

Mazinny

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And in keeping with the 'dueling science' theme, here was Pierce's response to Akpinar-Elci and Elci.

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"Akpinar-Elci and Elci suggest that we “falsely” claimed that “all of the cohorts evaluated had considerable smoking histories”. To support their assertion, they offer a non- sequitur: of the nine alleged cases of bronchiolitis obliterans in their cohort, a majority (6/9) were current or former smokers. Unfortunately, they seem to have confused the terms “cohort” and “case”. To reiterate, all food/flavoring cohorts studied to date had a significant fraction of current/former smokers, and indeed in the Akpinar-Elci et al. analyses of the Gilster-Mary Lee (GML) workers, nearly 50% of the study participants were current smokers.

They also appear to believe that, because most of the alleged cases of bronchiolitis obliterans in their cohort (8/9) were not current smokers, then smoking was not a confounder in their study. They have unintentionally reinforced our point. Cigarette smoke contains high levels of diacetyl, therefore workers who smoke have much higher diacetyl exposures than the non-smoking food/flavoring workers. More importantly, even though smokers arguably have the highest peak and cumulative diacetyl exposures of any definable cohort, smoking is not a risk factor for bronchiolitis obliterans. These observations argue against a relationship between diacetyl exposure and bronchiolitis obliterans. Finally, they have confused “controlling for the effects of smoking on respiratory function” (which they did do) versus “accounting for the relatively large diacetyl exposure from smoking when assessing the exposure-response relationship between diacetyl inhalation and respiratory function in food/flavoring workers” (which they certainly did not do)."
lol ... is there a response to this response !
 
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