Strange Story of Popcorn Lung

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jesrf

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If it makes anyone feel better I started using njoy back in March of 2009. I’ve been puffing away ever since using a variety of ecigs and do it all day from morning till sleep (was previously two packs a day for 23 years). I feel completely fine I breathe as well or better as I did in 2008.
 

DPLongo22

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My personal opinion of The Great Diacetyl Ruse of 2014 was/is somewhat inconsistent with many vapers (at the time/today).

I'm actually in a similar position with another "scare" that's currently permeating some vapers' minds. I'm clearly in the minority though, so I've decided to leave all research to the many experts and puritan-ex-smokers that exist.

The many studies we've already seen, such as the recent one below, give me much comfort in my decision to switch from smoking to vaping, so many moons ago.

Landmark Long-Term Study on Vaping by Never-Smokers Finds No Negative Health Impacts - American Vaping Association

To make myself obsessed with every element of every move would be counter-productive to my life, and would likely result in more harm than good for my overall being. I figure that I could always just quit, but I don't want to. If something emerges that makes me change that mind, I'll deal with it then. So far, not even close.

I am not chasing perfection, instead just trying to do the best that I can. Vaping, unlike smoking before it, has now been moved to the back of my personal line of concerns.

Now I need to go wash & prepare my scarlet letter for the coming weekend. :blink:

Where the flip did I put my popcorn??? :eek:
 

Kent C

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To make myself obsessed with every element of every move would be counter-productive to my life, and would likely result in more harm than good for my overall being.

:thumbs:

That's the type of thinking that kills puritanism.

“Puritanism: The haunting fear that someone, somewhere, may be happy.”
H.L. Mencken
 

DPLongo22

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:thumbs:

That's the type of thinking that kills puritanism.

“Puritanism: The haunting fear that someone, somewhere, may be happy.”
H.L. Mencken

LOL! Truth.

Can I interest you in a scarlet letter? :cool:

d-400.png
 

BigEgo

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I am not one who buries my head in the sand and refuses to acknowledge any news that's potentially negative about vaping. On the other hand, this case smacks of the old lipoid pneumonia cases we heard about a few years ago. I read one of the case studies written by the lipoid pneumonia patient's physician and this physician said in his report that glycerin is an oil (it's not -- it's an alcohol). While that doctor probably is an expert in his field (I forget his specialty), it's a classic case of a physician stepping outside his area of expertise. His case study write-up obviously was not peer reviewed like you'd see in a proper medical journal. If it was, he would have been corrected by chemists and toxicologists before it was published (he was only corrected after he published). This is why I don't put much stock in "case study" write-ups -- they are informal and not rigorously reviewed before publication. They are more of a "here's what I saw in a patient in my practice, tell me if I am right or wrong." While they can be helpful and spark further research, they are by no means intended to be some sort of conclusive decree on the subject. For that you need properly designed studies with large sample sizes.

Like those cases, this one is severely lacking in detail.

1) What were this guy's other potential exposures to airborne diketones? Or did he have exposure to other airborne chemicals associated with B.O? (Diketones are only one of a myriad of potential causes).

2) How much and how long did he smoke?

3) Who are his doctors? Why aren't they named? One would think they'd be willing to put their names on this report, especially if they are "world renown."

4) Are they even sure it's B.O? From my understanding, it is a hard condition to even diagnose. During the popcorn factory cases in the 90's, numerous workers went to pulmonologists and those doctors completely missed it. One of them just happened to diagnose it through persistence and a bit of luck.

5) Why does smoking not cause B.O. even though cigarettes have higher levels of diacetyl than most vape liquids? Is it possible that many smokers DO have B.O but it's being misdiagnosed as COPD? I find this hard to believe because, even though the symptoms are similar, there is a clear distinction between COPD and B.O. from a diagnostic perspective. (That is to say they present on the cellular level much differently and any pulmonologist would be able to tell the difference once he looked at cell cultures, x-rays, biopsies, etc.).

6) Where is ANTZ? Why aren't they publicizing this? They would like nothing more than to make it headline news worldwide. This tells me that even the ANTZ scientists know it's a load of crap (or at least not verifiable at this time).
 

zoiDman

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...

4) Are they even sure it's B.O? From my understanding, it is a hard condition to even diagnose. During the popcorn factory cases in the 90's, numerous workers went to pulmonologists and those doctors completely missed it. One of them just happened to diagnose it through persistence and a bit of luck.

5) Why does smoking not cause B.O. even though cigarettes have higher levels of diacetyl than most vape liquids? Is it possible that many smokers DO have B.O but it's being misdiagnosed as COPD? I find this hard to believe because, even though the symptoms are similar, there is a clear distinction between COPD and B.O. from a diagnostic perspective. (That is to say they present on the cellular level much differently and any pulmonologist would be able to tell the difference once he looked at cell cultures, x-rays, biopsies, etc.).

...

Doesn't #5 kinda Contradict #4?

Or #4 supports #5 depending on the point being made.
 
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BigEgo

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Doesn't #5 kinda Contradict #4?

Or #4 supports #5 depending on depending on the point being made.

#5 was just me trying to reconcile the fact that cigarette smoke contains lots of diacetyl yet we never hear about B.O. cases in smokers. Moreover, I have read in some of the literature that the popcorn workers who smoked were LESS likely to contract B.O. than the non-smoking workers. Perhaps it was coincidence or perhaps there were other confounding factors, but it's interesting nonetheless. To quote a paper published in the NEJM about the popcorn workers:

The prevalence ratios were higher among workers who had never smoked than among current or former smokers and were higher among younger workers (those 17 to 39 years old) than among older workers (those 40 to 69 years old). The prevalences of self-reported, physician-diagnosed asthma and chronic bronchitis among the current workers were 1.8 and 2.1 times the expected rates, respectively, but there was no evidence of a disproportionate prevalence of hay fever (data not shown). Overall, current employees had 3.3 times the expected rate of airway obstruction. The prevalence of airway obstruction increased with increasing age in both current and former smokers at the plant and especially in workers who had never smoked.

So we see that airway obstruction was more prevalent in non-smokers and younger people.

Furthermore, some of the workers took years to contract the condition while others were there for less than a year and were diagnosed. (One guy was in his early 30's, never smoked, in good shape, and he got it after like 9 months working at the plant).

Some have speculated that perhaps B.O. does happen in smokers but is misdiagnosed as COPD. This makes sense on the face of it, but it seems unlikely. After all these years of studying smokers, I am confident someone -- either a research scientist or a practicing physician -- would have been able to distinguish COPD from B.O. They have similar symptoms upon presentation, but once you dig into it with biopsies, x-rays, CT scans, etc. the distinction becomes more evident.

At the end of the day, it seems likely there are other factors than just pure diacetyl inhalation. Perhaps there is a genetic factor. Perhaps there are other chemicals that in conjunction with diacetyl cause the condition. Perhaps it only occurs comorbidly with other conditions (for instance people with rheumatoid arthritis sometimes get B.O. and I am pretty sure no one understands exactly why). A lot of unknowns here.

I am not saying diacetyl has nothing to do with it, as I think the evidence clearly shows it does. For instance, it has been known since at least the 70's that people working in bakeries sometimes came down with debilitating lung conditions. What is in the air in bakeries? Diacetyl. Same goes for coffee roasters and perhaps even beer breweries.
 

zoiDman

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#5 was just me trying to reconcile the fact that cigarette smoke contains lots of diacetyl yet we never hear about B.O. cases in smokers. Moreover, I have read in some of the literature that the popcorn workers who smoked were LESS likely to contract B.O. than the non-smoking workers. Perhaps it was coincidence or perhaps there were other confounding factors, but it's interesting nonetheless. To quote a paper published in the NEJM about the popcorn workers:



So we see that airway obstruction was more prevalent in non-smokers and younger people.

Furthermore, some of the workers took years to contract the condition while others were there for less than a year and were diagnosed. (One guy was in his early 30's, never smoked, in good shape, and he got it after like 9 months working at the plant).

Some have speculated that perhaps B.O. does happen in smokers but is misdiagnosed as COPD. This makes sense on the face of it, but it seems unlikely. After all these years of studying smokers, I am confident someone -- either a research scientist or a practicing physician -- would have been able to distinguish COPD from B.O. They have similar symptoms upon presentation, but once you dig into it with biopsies, x-rays, CT scans, etc. the distinction becomes more evident.

At the end of the day, it seems likely there are other factors than just pure diacetyl inhalation. Perhaps there is a genetic factor. Perhaps there are other chemicals that in conjunction with diacetyl cause the condition. Perhaps it only occurs comorbidly with other conditions (for instance people with rheumatoid arthritis sometimes get B.O. and I am pretty sure no one understands exactly why). A lot of unknowns here.

I am not saying diacetyl has nothing to do with it, as I think the evidence clearly shows it does. For instance, it has been known since at least the 70's that people working in bakeries sometimes came down with debilitating lung conditions. What is in the air in bakeries? Diacetyl. Same goes for coffee roasters and perhaps even beer breweries.

Gotcha.

:)
 

Kent C

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side notes:

Judge rules against workers in ‘popcorn-lung’ lawsuit | 2017-10-20 | The Indiana Lawyer

http://www.tandfonline.com/doi/full/10.3109/10408444.2014.930093?src=recsys

... 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. [Dr. F has agreed in this forum with the Critical Reviews in Toxicology, conclusion - “smoking has not been shown to be a risk factor for bronchiolitis (popcorn lung).]

Akpinar-Elci and Elci claim that “A cluster of such a rare disease as bronchiolitis obliterans indicates a possible risk factor related to the work environment”. As U.S. Supreme Court Justice Louis Brandeis noted when referring to the benefits of transparency, “sunlight is said to be the best of disinfectants”. Let us shed some sunlight onto the above claim. First, they failed to note that only three of their alleged nine cases of bronchiolitis obliterans underwent lung biopsy to allow for confirmation of the suspected diagnosis. Of these, only one had findings that supported a possible diagnosis of bronchiolitis obliterans. Second, although bronchiolitis obliterans is a fixed obstructive disease, there was no difference in the prevalence of obstruction between the diacetyl-exposed workers versus controls in either of the Akpinar-Elci et al. (2005 Akpinar-Elci M, Stemple KJ, Enright PL, Fahy JV, Bledsoe TA, Kreiss K, Weissman DN. (2005). Induced sputum evaluation in microwave popcorn production workers. Chest, 128, 991–7.[Crossref], [PubMed], [Web of Science ®], [Google Scholar], 2006 Akpinar-Elci M, Stemple KJ, Elci OC, Dweik RA, Kreiss K, Enright PL. (2006). Exhaled nitric oxide measurement in workers in a microwave popcorn production plant. Int J Occup Env Health, 12, 106–10. [Google Scholar]) studies of GML workers. Oddly, in neither study do they note that these findings completely contradict those of Kreiss et al. (2002) Kreiss K, Gomaa A, Kullman G, Fedan K, Simoes E, Enright P. (2002). Clinical bronchiolitis obliterans in workers at a microwave-popcorn plant. N Engl J Med, 347, 330–8.[Crossref], [PubMed], [Web of Science ®], [Google Scholar], who claimed to have observed a significant relationship between diacetyl exposure and obstruction prevalence in workers at the same facility. Given the fact that Kreiss et al. (2002) Kreiss K, Gomaa A, Kullman G, Fedan K, Simoes E, Enright P. (2002). Clinical bronchiolitis obliterans in workers at a microwave-popcorn plant. N Engl J Med, 347, 330–8.[Crossref], [PubMed], [Web of Science ®], [Google Scholar] is considered by Akpinar-Elci et al. to be a seminal study, failure to replicate the results of Kreiss et al. (2002) Kreiss K, Gomaa A, Kullman G, Fedan K, Simoes E, Enright P. (2002). Clinical bronchiolitis obliterans in workers at a microwave-popcorn plant. N Engl J Med, 347, 330–8.[Crossref], [PubMed], [Web of Science ®], [Google Scholar] in their studies should warrant some mention in their papers. Similarly, in neither study do the authors inform the reader that in the original GML cohort (Kreiss et al. 2002 Kreiss K, Gomaa A, Kullman G, Fedan K, Simoes E, Enright P. (2002). Clinical bronchiolitis obliterans in workers at a microwave-popcorn plant. N Engl J Med, 347, 330–8.[Crossref], [PubMed], [Web of Science ®], [Google Scholar]), 57% of the cohort claimed to have had off-site (mostly farming-related) exposures to “other possible causes of lung disease”, including known inducers of bronchiolitis obliterans, such as nitrogen oxides (silo gas).

Furthermore, the authors are mistaken in suggesting that had we “more carefully” reviewed the findings of their analyses, our conclusions would have been different. We have reviewed their studies at length, and believe that their claim of “findings that strongly indicate a relationship between occupational butter flavoring exposure and respiratory diseases among popcorn production workers” is desperately over-reaching. In fact, their own papers provide substantially more evidence to the contrary. For example, they found that:

(1)
Sputum characteristics were not related to pulmonary function.

(2)
There were no significant differences in spirometric values between highly exposed workers and the internal reference group.

(3)
The mean FEV1 and FEV1/FVC percent of predicted were both greater than 95% among all popcorn production workers (indicating a healthy workforce).

We find it disingenuous that Akpinar-Elci and Elci would attempt to cloak themselves in the Hippocratic oath. One could easily argue that a rush to judgment on diacetyl has ushered in the heavy use of replacement chemicals which NIOSH scientists themselves are now claiming appear to be similar to or even more potent than diacetyl (NIOSH 2011 NIOSH. (2011). Occupational exposure to diacetyl and 2,3-pentanedione. Draft criteria for a recommended standard: Department of Health and Human Services, National Institute for Occupational Safety and Health (NIOSH). [Google Scholar], Morgan et al. 2012 Morgan DL, Jokinen MP, Price HC, Gwinn WM, Palmer SM, Flake GP. (2012). Bronchial and bronchiolar fibrosis in rats exposed to 2,3-pentanedione vapors: implications for bronchiolitis obliterans in humans. Toxicol Pathol, 40, 448–65.[Crossref], [PubMed], [Web of Science ®], [Google Scholar], Zaccone et al. 2013 Zaccone EJ, Thompson JA, Ponnoth DS, Cumpston AM, Goldsmith WT, Jackson MC, et al. (2013). Popcorn flavoring effects on reactivity of rat airways in vivo and in vitro. JTEH A, 76, 669–89. [Google Scholar]).

In summary, we stand by our original premise, which is supported by Akpinar-Elci et al.'s own published findings: (1) all the food/flavoring cohorts had significant smoking histories, (2) cigarette smoke contains very high diacetyl levels, (3) none of the diacetyl exposure–response evaluations to date have accounted for this very large non-occupational source of diacetyl, therefore, (4) all such evaluations are inherently flawed (though unintentionally) and should be revisited.
 

Letitia

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I had some popcorn at the movies the other day, and I woke up coughing this morning.

Should I change my vape?
No, change your popcorn. Garlic, chive, and balsamic works well for me. Trying to come up with a plum wine juice recipe to vape with it.
 
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