WED AM: Dixon on Physiology of Smoking and Tar Compensation

March 9, 2005 1:27 pm by Gene Borio

This morning BATCos Bruce Sheffler questioned British physiologist Dr. Michael Dixon (Senior Scientific Advisor to British American Tobacco (Investments) Limited) on the physiology of smoking — from the first puff of smoke into the mouth, to inhalation down the throat into the lungs, to absorption and transmission through the bloodstream to the brain.

A key part of his testimony involved “impact” which apparently is limited to a set of nerves at a specific area in the back of the throat. “Impact” is not achieved until the soft palate is opened to allow the smoke to enter that region during inhalation. But once hit by a puff of smoke–and this area can apparently discern the difference between low-tar puffs and high-tar puffs of equal volume–the nerve endiings can signal the brain in a fraction of a second.

BATCo’s studies of puff volume and variations of nicotine/tar levels seem to indicate that smokers can and do control their puff volume in response to “impact,” not in response to nicotine.

Are they reacting to nicotine?

Nicotine is primarily in smoke’s particulate phase. When more air enters the mouth for the inhalation process, diluting the smoke, the “free” nicotine is released into the gaseous phase in the mouth and upper airways, while the bound nicotine is delivered to the lung.

The gaseous nicotine released in the mouth has a longer, more circuitous route to the brain–through the unoxygenated venous system to the heart, then to the lungs to get oxygen, then back through the heart to be delivered to the brain. The nicotine that remains bound to the particulates in smoke reaches down into the gas-exchange region of the “deep lung,” where it is released into gas that is absorbed by the blood stream as it is gathering oxygen. Then it is travels with the oxygenated blood the short distance to the heart to be delivered by the arterial system right to the brain. This route takes only about 10 seconds.

The point of this testimony is that if you increased pH (via ammonia as DOJ has charged), you would not increase the rate or amount of nicotine sent to the brain, as the free nicotine released in the mouth and absorbed in the mouth and upper throat tissues would take a longer path to the brain, and along that path would have attendant distribution losses.

Dr. Dixon stated that in his opinion, based on BATCo’s puff volume experiments, nicotine had nothing to do with whatever compensation may occur among switchers to lower yield cigarettes.

While these experiments seemed to involve a very small number of subjects–I think I heard 12– they had a number of interesting aspects.

While people generally take smaller puffs at the end of a cigarette than at the beginning, one experiment gave people new cigarettes for every puff, to see if there was a nicotine titration, or satiation effect, ie, once the smoker had enough nicotine for now, he or she would begin to take smaller puffs.

This experiment found smokers taking the same puff volume for all ten puffs, even rising at the 10th puff(!)

The researchers also secretly varied the nicotine and/or the tar values for each puff, to see if that influenced puff volume as smoker’s puff volume. The smokers’ ability to instantaneously change their puff volume bespoke a far faster reaction that the arrival of nicotine to the brain. In fact, puff volume, probably controlled by the “impact” area of the throat, seemed to respond dramatically and exclusively to tar levels, and seemed completely independent of nicotine levels.

Dr. Dixon’s research and experiments have led him to the conclusion that for most switchers there is partial compensation, but in the main, smokers of lower yield cigarettes receive lower levels of tar and nicotine than if they had stayed with their regular cigarettes.

In fact, Dr. Dixon testified that it seems “some component of tar is driving force for the mechanism” of compensation.

Much of the research Dr. Dixon talked about has not yet been published.

DOJ attorney Sharon Eubanks has begun her cross.

[Gotta go back to the courtroom–Hope this entry makes sense, I always need an editor; will revise this entry this evening.]

3 Responses to “WED AM: Dixon on Physiology of Smoking and Tar Compensation”

  1. krueger Says:

    Dixon’s testimony is interesting, and of course highly technical. But it’s also consistent with the industry’s public PR on ammonia: oh gosh, that’s not why we add it.

    But in private, the industry says otherwise.

    “The secret of Marlboro is ammonia” concluded B&W in 1989. “Ammonia technology provides improved nicotine transfer”. Among “key desirables” are “free nicotine/nicotine transfer”.…

    Or take the 1991 B&W leaf blenders handbook:

    “Ammonia, when added to a tobacco blend, reacts with the indigenous nicotine salts and liberates free nicotine. As a result of such change the ratio of extractable nicotine to bound nicotine in the smoke may be altered in favor of extractable nicotine. As we know, extractable nicotine contributes to impact in cigarette smoke and this is how ammonia can act as an impact booster.”

    That’s what the industry says in private.

    In public, it’s all carefully worded denial. E.g. Philip Morris protests “There is no indication that ammonia compounds in our cigarettes alter the amount of nicotine the smoker inhales.” B&W cries “the use of ammonia in the processing [of tobacco] does not increase the amount of nicotine absorbed by the smoker.” Dixon’s testimony is entirely consistent with industry public denails.

    But not with what the industry says in private.

  2. tobacco observer Says:

    Krueger, I don’t think you fully understand what it is you just posted. There is no contradiction between what the industry says in public and private inherent to your quotes.

    There are multiple forms of nicotine released from burning cigarettes. Assuming that the “private” quote you attributed to B&W is correct, the purpose of adding ammonia is simply to change one form to another.

    Specifically the added ammonia may convert some of the particle-bound nicotine in the smoke into the “free” (aka “unprotonated”, “unbound”, “extractable”, etc) form that is absorbed a bit more quickly, giving (as B&W puts it) more “impact” to the smoker.

    So again, even given that B&W’s “private” quote is correct and that ammonia does have this effect (and there is even some internal doubt about that expressed in the quote you gave from the leaf binder’s manual) both Philip Morris’s and B&W’s public pronouncements are still correct. There is no contradiction. Ammonia does NOT alter the amount of nicotine the smoker inhales from smoking. It just makes the smoker absorb some of it faster, giving more “kick” (”impact”, etc) to a puff.

    Now given all of this, it is probably reasonable to conclude that tobacco isn’t being completely forthright about why it adds ammonia to cigarettes in its public statements. But based on what you posted, they don’t seem to be lying about it either.

  3. krueger Says:

    I’m not sure you read what I wrote. I wrote “carefully worded” denials. I meant it.

    Indeed, I’d say industry wording reaches high art here. Literally true yet consummately misleading, it pushes a distinction without a difference as if it were critical, while carefully avoiding the real issue.

    But then, this industry is very good at word games.

    If you want to play word games, you could likewise say that freebasing cocaine doesn’t alter the amount of cocaine delivered. It would be equally misleading, but you could say it.

    What Big Tobacco’s carefully worded denials stay well away from: its purpose. Concealing the nicotine, enhancing the effect of nicotine, increasing the “kick” of the nicotine, manipulating a product to fool FTC tests and misinform the public and the customer, creating and sustaining addiction, engineering a drug delivery device:

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