Monthly Archives: March 2014

Allow e-cig and allow proper information on Harm reduction products in Canada

Quoted from Montreal Gazette march 24th

I am writing on behalf of a group of doctors, professors and health advocates to say that we believe the time has come for the federal government to authorize the sale in Canada of electronic cigarettes containing nicotine.

These devices, which basically heat a propylene glycol or glycerine solution containing nicotine, offer a safer and more acceptable alternative for smokers to appease their addiction, compared to regular cigarettes.

No doubt, tremendous strides have been made over the years to impose a strict regulatory framework on regular cigarettes. More, though, obviously can be done. Unfortunately, it is wishful thinking that one day we will completely eradicate nicotine use. The vast majority of smokers want to quit. Unfortunately, only 10 per cent of them, when surveyed, are still abstinent after trying to quit in the past year.

In such a context, we believe that the time has come for tobacco control to move beyond the usual approaches of education, total nicotine cessation and prevention. In a landmark report published in 2007, the Royal College of Physicians makes a compelling case why harm reduction should no longer be ignored by health authorities to lower the death and disease caused by tobacco use. In the report the college says:

Conventional preventive measures focus entirely on preventing uptake of smoking and helping smokers to quit smoking.

This approach will be ineffective for the millions of smokers who, despite best efforts to persuade and help them to quit, will carry on smoking.

Tobacco-control policy needs to be radically extended to address the needs of these smokers with implementation of effective harm reduction strategies.

Harm reduction in smoking can be achieved by providing smokers with safer sources of nicotine that are acceptable, and effective cigarette substitutes.

There is a moral and ethical duty to provide these products to addicted smokers.

Electronic cigarettes are such a substitute.

First, they cannot even remotely be as toxic as regular cigarettes because there is simply no combustion of tobacco which produces the smoke containing, for example, the carbon monoxide and the bronchopulmonary irritants that are among the 7,000 chemical substances responsible for causing cardiovascular diseases, chronic obstructive lung diseases and at least 10 different cancers.

Secondly, sales data show that these products are widely accepted by smokers. In fact, there has never been a product that has generated so much enthusiasm on their part. Such interest is not surprising since electronic cigarettes deliver nicotine much quicker than existing nicotine-replacement therapies and provide a similar behavioural experience as smoking.

Opponents view the fact that electronic cigarettes are well accepted by consumers as a threat because they fear they will be a gateway to regular smoking. Such a claim has yet to be confirmed, since current tobacco consumption trends are still dropping in countries such as France, the United Kingdom and United States, where electronic cigarettes containing nicotine are sold legally.

This is not to say that there are no risks of unintended consequences. But as with other health-policy interventions, there is a strong preponderance of evidence in favour of electronic cigarettes. The death rates from continued smoking are simply too high to accept a continued nicotine-abstinence policy orientation.

Electronic cigarettes need to be appropriately regulated so that good manufacturing practices are followed to protect consumers and that sales to minors are forbidden. However, any excessive regulations that could make it too difficult to communicate about the reduced risks of these products or to access them should be avoided.

What are the health effects of smokeless tobacco – CASAA – Befrits

What are the health effects of smokeless tobacco?

Contrary to popular belief, smokeless tobacco is not a major health hazard. In fact, it has not been definitively linked to any deadly disease. More important, to the extent that it causes any risks, the scientific evidence clearly shows that the risks are very small (See Lee & Hamling 2009).

This might surprise you. We will admit that it surprised every one of us when we first learned it. Because there is so much misinformation about ST, much of it spread by otherwise legitimate health authorities, it can be difficult to find the truth. Below, we take up the question of how to sort out truth, lies, and genuine scientific uncertainty. Here, we present what the scientific evidence actually shows. (Reading list.)

Doesn’t smokeless tobacco cause oral cancer (cancer of the mouth)?

-If so, very rarely.

There is overwhelming evidence that any risk for oral cancer (cancer of the mouth) from ST is very low.

This is an important question in the ST debate, so here is a little background first. Oral cancer (cancer of the mouth and surrounding areas) is a fairly rare disease in Western countries, and in most cases is caused by smoking. Smoking can increase your risk of oral cancer by eight or ten times, much more than even the worst-case-scenario estimate for ST. The American government attributes about 75% of all oral cancer deaths in that country to smoking combined with drinking. In other words, the best thing you can do to reduce the risk for oral cancer is not to smoke.

Even if ST did cause a measurable increase in oral cancer risk, the total risk would still be small. The “baseline” risk for oral cancer (the risk for people who do not smoke or drink a lot of alcohol) is quite low. So even if ST multiplied that risk by 2 or even 4, the total risk of dying from it would still be very small compared to the risks of the lung and heart diseases caused by smoking. (Consider if you had a choice between doubling your chances of dying by getting hit by lightning versus doubling your chances of dying in a car crash. Doubling your risk from lightning would hardly matter because it is so rare in the first place; two times a very small number is still a very small number. But doubling your risk from a car crash would be a lot more worrisome.)

In one of the most remarkable marketing successes ever, anti-ST activists have convinced people that, “if I switch from smoking to dipping, I will just trade lung cancer for mouth cancer.” In reality, switching from cigarettes to ST will dramatically reduce your oral cancer risk (and your risk of lung disease, heart disease, and many other diseases), and even if that were not true, the tradeoff would still be a good one because the risk of oral cancer for non-smokers is so low in the first place.

Having said all that, what is the answer to the original question? What does the scientific evidence say about the risk for oral cancer from smokeless tobacco?

It turns out that the evidence clearly shows there is very little risk. When looking at scientific research, it is necessary to look at all of it, not just one or two particular studies. As with most things we study in health science, the results vary. A few studies find that people who use ST have a higher risk for oral cancer but most studies have found that the risk is very low. Some even show a negative association. This is the same to say, if someone just picked out those studies and ignored the rest, they might conclude that using ST protects you against getting oral cancer. Of course, picking just a few studies with extreme results is just bad science.

When we look at the all the scientific evidence, it averages out to there being either no risk or very little risk (it is impossible to tell the difference between those two conclusions because health science methods are always imperfect). By “very little”, we mean that using smokeless tobacco might cause a 10% or 20% increase in the risk for oral cancer compared to not smoking or not drinking heavily. The evidence shows it is extremely unlikely that the increase in risk is as high as 50%(which is still much less than the risk from smoking). (Oral cancer reading list.)

If you do not want to delve into the technical details, the previous points and our calculation of thecomparative risk of smoking and smokeless tobacco are all you need to know.

But doesn’t smokeless tobacco cause oral lesions which can become cancerous? – If so, very rarely.

Much of the following is taken from Rodu and Godshall’s Tobacco harm reduction: an alternative cessation strategy for inveterate smokers. See the original for further reading or for details on the research behind the conclusions.

Oral leukoplakia is an ominous sounding term used frequently in discussions about oral lesions resulting from ST use. The term literally means “white plaque,” and it is used to describe areas of the mouth lining that become thickened by ST use or smoking. The World Health Organization has determined that leukoplakias resulting from ST use are considerably different from those resulting from smoking. The distinctions are based on the frequency of occurrence, the location in the mouth, and how often these leukoplakias result in mouth cancer.

The condition is rare, occurring in less than 1% of the general population, primarily in long-time smokers 40 to 60 years old. Smoking-related leukoplakias most commonly involve the undersurface of the tongue and throat area, locations that account for 75% of oral cancer in the U.S..

Oral leukoplakias occur in up to 60% of ST users, within 6 months to 3 years of starting ST use. They primarily occur at the site of ST use and are largely a result of local irritation. The frequency of appearance depends on the type of ST that is used. Moist snuff, which is more alkaline than chewing tobacco, more often leads to leukoplakia. However, moist snuff in pre-portioned pouches (like snus) causes fewer cases of leukoplakia than does the loose form.

There are distinct differences in how often ST and smoking leukoplakias show pre-cancerous changes called dysplasia. Dysplasia is seen infrequently in ST leukoplakias (less than 3%). Furthermore, even when dysplasia is present in ST leukoplakia, it usually is found in earlier stages than in leukoplakias among smokers, where it is seen in about 20% of cases.

ST leukoplakias only rarely progress to cancer. For example, one study found no case of cancer in 1,550 ST users with leukoplakia who were followed for 10 years, and a second study reported no case of oral cancer among 500 regular ST users followed for six years. A retrospective study of 200,000 male snuff users in Sweden found only one case of oral cancer per year, an extremely low frequency. In comparison, a follow-up study reported that 17% of smoking leukoplakias transformed into cancer within seven years.

In conclusion, oral leukoplakia occurs commonly in ST users, but it primarily represents irritation and only very rarely progresses to oral cancer.

Does smokeless tobacco cause other cancers?
– If so, very rarely.

Again, the answer has to be that there is no conclusive evidence that it does, but it is certainly possible that it does at some very low level. There is no clear evidence that ST causes any cancer. Hence, the evidence indicates that if there is any risk, it is small.

Other than oral cancer, the cancers that seem most likely to be associated with ST are laryngeal, esophageal (throat), and gastric (stomach), since those are the other parts of the body that come in contact with the tobacco. For these sites, along with a few others, there is plenty of scientific evidence that there is no substantially elevated risk. As with oral cancer, researchers have looked for an association and have failed to find one. For other cancer sites there are few or no studies, so we do not have any evidence one way or the other. However, studies that look at all cancers combined have failed to find an increase among smokeless tobacco users, so there cannot be a very big increase for any particular cancer.

Does smokeless tobacco cause heart disease or stroke? – The risk is probably quite small.

There may be some small risk, though there is no definitive evidence. Most studies of cardiovascular diseaseand smokeless tobacco have found no increased risk. However, because nicotine is a mild stimulant, it might increase the risk of certain cardiovascular outcomes, such as stroke. Many stimulants have been linked to some risk for fatal cardiovascular events. This does not prove that nicotine causes such risk, but it suggests that it is plausible.

The available evidence shows that if there is any risk from smokeless tobacco, it is low, less than a 20% increase (for comparison, smoking is estimated to roughly double this risk, a 100% increase). This is potentially more important than a similar percentage increase in oral cancer risk, since cardiovascular disease is a lot more common. If the risk of cardiovascular disease increases by as much as 20% then smokeless tobacco might cause 3% or 4% of the risk associated with smoking. That is still a lot better than smoking, of course, but worse than one percent. Fortunately, most of the evidence suggests that nicotine without the smoke is not actually quite that bad. But it would be useful to do more research to find out more. Unlike with oral cancer, there is not enough available research about cardiovascular disease for us to feel entirely comfortable in our conclusions.

What does this all mean for the total risk compared to smoking? – Using smokeless tobacco is much safer than smoking.

It means that the risk is tiny compared to smoking. You might hear other estimates but as far as we know, we are the only ones who have actually done the calculation. Our calculations show that if we take a worst case scenario and assess the risks for cancer and cardiovascular disease, the total risk from ST is only a few percent of that from smoking.

Due to the limitations of health science, we cannot be sure exactly how the risks compare. But we can be very sure that the total risk of dying from ST use is less than 1% of that from smoking. That is, for any plausible levels of risk for disease from ST, any values that are not clearly ruled out by the science, the total risk is less than 1/100th that from smoking. There is no legitimate scientific doubt that someone’s risk drops by at least 99% by using ST instead of smoking.

So why do so many people say “smokeless tobacco is not a safe alternative to cigarettes”?
The main reason that this phrase is so common is that the U.S. and Canadian governments require a version of it to be printed on packages of ST products. This is unfortunate, since most people interpret the phrase “not safe” to mean “dangerous”. The phrase “not a safe alternative to cigarettes” is understood as “just as bad as cigarettes”.

Strictly speaking, the statement is true. If we interpret “safe” to mean “100% safe; creating no health risk at all” then smokeless tobacco is not “safe” (and neither is anything else. Chances are that somewhere, sometime, somehow, broccoli has killed someone). Smokeless tobacco may not be a “safe” alternative, but neither are any of the other products used to help people stop smoking. Certainly trying to quit and failing, or smoking for another year or two before quitting are not “safe” either. ST is much safer, however, and that is what matters.

Think about this: Driving safely and properly is not a safe alternative to speeding while drunk and not wearing a seatbelt. But it is very close. It might even reduce the risk by as much as 95%. Somehow, there seems to be no confusion about which of those options we think someone should choose. There should be no confusion about tobacco products either. Smokeless tobacco is much less harmful, and the fact that it is not 100% safe does not change this.

Are you saying that smokeless tobacco is harmless? – No.

As far as we know, no one is saying that. As we noted, it is possible that smokeless tobacco causes cancer or other deadly diseases at some very low level. We know that the nicotine has short-term cardiovascular effects which may be a little bit harmful. Nothing is 100% harmless, and this includes smokeless tobacco. This does not change the fact that it is a much less harmful alternative to smoking. (Reading list.)

What about all the chemicals in smokeless tobacco that I hear about?

Sometimes people who are opposed to harm reduction or any use of ST present a list of potentially harmful constituents. What they do not tell you is that many of those chemicals are in other plants, including the healthy vegetables that you eat. A little bit of all the metals on Earth,including cadmium, polonium, and others that are quite bad for you in large quantities, end up in everything. They are in tobacco, carrots, wheat, and even the water you drink. There are also organic molecules like formaldehyde in most every life form on Earth, including tobacco. Again, concentrated in large quantities, you would certainly want to stay away from some of these chemicals, but the amount that naturally occurs in plants (and in your own body) is not a problem. We are lucky that there are not a lot of anti-broccoli advocates out there trying to trick you into not eating it because it contains some cadmium.

One set of chemicals that are talked about a lot in the science are nitrosamines, or tobacco-specific nitrosamines (TSNAs). Nitrosamines are a class of chemicals that we are exposed to in food and through other pathways. Some of these are known to be carcinogens in some quantities. Whether the TSNAs might be carcinogens is the subject of debate. Fortunately, it does not matter whether these chemicals might cause cancer since we have evidence about whether ST itself causes cancer. The evidence shows that people who use ST do not have measurable increases in cancer rates or mortality. So it does not really matter what chemicals are there.

Think about this: If you met a thin person who always ate huge amounts of food, would you tell him that eating all that food is making him overweight? Obviously not, since you can directly observe that he is not overweight. All this talk about chemicals is like that. If all you knew about a person was that he always overeats, it might suggest that he would be overweight. Similarly, if you only knew about the chemicals and had never observed the actual health effect of the products, the chemical analysis could suggest that there might be a health effect. But once you observe that someone is thin (or observe that smokeless tobacco users do not have elevated disease rates), the suggestive evidence is no longer informative. It can only be used to trick you into thinking there is a health effect when the evidence actually says otherwise.

Doesn’t smokeless tobacco contain fibreglass? – No.

The fiberglass thing is a complete myth. There is no evidence for this, though it gets repeated by many anti-ST activists. We have heard the claim that fiberglass creates little cuts which allows absorption of nicotine. However, nicotine is absorbed quite well through the intact and healthy inside surface of your mouth, so there is no reason to do this. Creating holes in the surface, thus causing bleeding, might well interfere with absorption.

The only legitimate reference we have been able to find for the use of fibreglass in tobacco products is in some cigarette filters.

I know someone (or read about someone) who got cancer from using smokeless tobacco. How do you explain that?

We offer our sympathy if someone in your life got cancer, but it wasn’t necessarily caused by smokeless tobacco. The same is true for the various oral cancer victims whose stories are used in the anti-smokeless-tobacco literature. Just because two things coincide does not mean that one caused the other. These cases are almost certainly coincidences.

You can understand the reasoning behind this point without needing much math. In a large population (like North America), even if we are talking about something that relatively few people do (such as use ST) and a fairly rare disease (e.g., oral cancer), there will still be quite a few people who fall into both categories just by chance. For example, if 1-in-100 people are exposed to a substance, and 1-in-1000 people get a disease, then by chance (coincidence) alone we would expect about 1-in-100,000 people to both have that exposure and get the disease (1/100 x 1/1000 = 1/100,000).

That does not seem like a lot, until you realize that there are over 300,000,000 people in North America. So it is not strange then that you will find someone with oral cancer who used ST. There will be quite a few such people, just by chance. In our example above, 3000 people would have both the exposure and the disease by chance alone. That is why epidemiology (the science that explores whether a disease is caused by an exposure) always uses a “comparison group” (people who do not have the exposure) to see if those with the exposure have more cases of the disease. The evidence does not show that ST users have more cases of various diseases than the regular population, but of course they will have some cases.

Consider this analogy: Some people read a lot of mystery novels (the exposure); some people get pancreatic cancer. If we told a scary story about a mystery fan dying of pancreatic cancer, and posted gory pictures on the web, would that be evidence that the novels caused the disease?

Since oral cancer is usually caused by smoking, finding someone who never smoked who has oral cancer means looking for something unusual and misleading. It is as if someone collected pictures of people who had died in car crashes while wearing seatbelts and argued that seatbelts are bad for you. We know that wearing a seatbelt is much better than not wearing one, but there will still be people who die even when they choose the safer option. It is completely irresponsible to emphasize those people and discourage people from making the safer choice.

But what about cases where someone, perhaps a doctor, said that ST caused a particular disease? Well, there is a strong human tendency to look for a specific cause, especially for highly traumatic events, even when such a determination is impossible to make. Causes for some diseases are easy to see (if you break your arm while falling down, it is pretty easy to figure out why), but this is not true for cancer and cardiovascular disease. So, when people have been repeatedly told that ST is a terrible health hazard, it is not surprising that they end up thinking that it caused a disease.

For a few diseases and exposures, we can conclude that it is likely that the exposure caused the disease. If someone who has smoked for fifty years gets lung or oral cancer, we know that it is quite likely that this was caused by smoking. But we know that because when we compare smokers to non-smokers, the disease rates for smokers are much higher. If smokers have 9 times the risk of non-smokers for a particular disease, when one of them gets that disease there is a 90% chance it was caused by the smoking (and a 10% chance that it would have happened anyway).

As a final, more technical note, most of the oral cancer victims who are exploited in the anti-smokeless-tobacco propaganda suffered from tongue cancer at a fairly young age. To the extent that any evidence suggests there is a link between Western smokeless tobacco and oral cancer, the related cancer occurs at ages greater than 60, after many decades of use, (and it is not cancer of the tongue). In developed countries, almost all oral cancer occurs at age 60 or older. By contrast, there are a small number of young people, generally under 30, who get tongue cancer (in the range of one to two hundred per year in North America, which has increased over the last three or four decades). These cancers do not appear to be associated with smoking and heavy drinking nor with smokeless tobacco use. We do not know what causes these cancers, other than knowing that it does not seem to be any of the usual suspects. Of course, by coincidence, one or two of these victims every year will be smokeless tobacco users (and about 40 of them smokers, some heavy drinkers, and so on). Taking scary pictures of one of those unfortunate individuals provides absolutely no evidence about the dangers of smokeless tobacco, and for a health related initiative, is highly inappropriate.

Reblogged in its entirety from you Clive



Cease and desist: making false claims about the gateway effect


Gateway effect: maybe… but is it an entrance or exit?

I am totally exasperated by nonsensical spin about the so-called gateway effect from pseudo-scientists, misguided officials, prohibitionists and propagandists.

Unable to take any more, I decided to write to Professor Stanton Glantz and Dr Lauren Dutra, the authors of an analysis of teenage smoking and e-cigarette use based on the US National Youth Tobacco Survey:  Dutra LM, Glantz SA. Electronic Cigarettes and Conventional Cigarette Use Among US Adolescents. JAMA Pediatrics  online 6 March 2014. I hope the letter is self-explanatory.


____________ LETTER TEXT _____________

Dear Professor Glantz, Dr Dutra

Misleading use of survey data has no place in professional public health practice

I had intended to blog about your recent paper, but decided instead to write an open letter and to put these concerns to you directly. So, I write to express dismay at the false, misleading and damaging conclusions you have drawn from your recent paper in JAMA Pediatrics and related media communications. The errors of reasoning are elementary, but have been used to draw conclusions that are relentlessly hostile to e-cigarettes and the important public health concept of ‘tobacco harm reduction’.  

It should be stressed that misleading information in this arena can cause actual harm to real people if they react to misplaced concerns in ways that cause them to continue to smoke. Further dangers arise as physicians and other trusted professionals give bad advice based on false information. Finally, there is the danger that policy-makers and legislators will be misled into making excessively restrictive regulations that protect cigarette sales from competition from much safer and better alternatives.  I believe your study and the subsequent media work owe more to misguided activism than to responsible academic investigation, and as such they have no place in professional public health practice or a reputable university.

I would like to address the claims made in three documents.

Document 1: Published article in JAMA Pediatrics

JAMA Pediatrics published article Electronic Cigarettes and Conventional Cigarette Use Among US Adolescents.  From the abstract:

Conclusions and Relevance  Use of e-cigarettes was associated with higher odds of ever or current cigarette smoking, higher odds of established smoking, higher odds of planning to quit smoking among current smokers, and, among experimenters, lower odds of abstinence from conventional cigarettes. Use of e-cigarettes does not discourage, and may encourage, conventional cigarette use among US adolescents

All of these findings stated in the first sentence can be explained by the idea that e-cigarettes appeal more to smokers – hardly a surprise given they both provide nicotine – and that smokers are trying them more than non-smokers because smokers have an intent to quit, cut down or otherwise protect their health, or that whatever causes someone to smoke also causes them to try e-cigarettes.  None of this is surprising, but somehow you have managed to position this study as showing there is a gateway from e-cigarette use to smoking. NOTHING in the study or the underlying data suggests this.  You would need information on how smoking, e-cigarette use and abstinence evolved over time to test these hypotheses, but your study does not have that.

There is no basis in this data to claim categorically that ‘use of e-cigarettes does not discourage […] conventional cigarette use among US adolescents‘.  In fact, despite the moral panic hyped up by CDC and FDA officials over this survey, there was a significant fall in current smoking among school-age adolescents in this survey between 2011 and 2012 (see CDC data: here and here). The relevant data are plotted below and are available to download [XLS]  ( done in association with Brad Rodu).

 US NYTS data

The data show a pronounced decline in cigarette smoking and in combined e-cigarette and cigarette prevalence between 2011 and 2012, as e-cigarette use increased (roughly as expected and in line with the growth in adult use). Of course, we cannot conclude from this that e-cigarettes are contributing to the reduction in smoking, but you certainly cannot rule it out in the way you have done.  It is quite possible, and consistent with the data, that e-cigarettes are being used to quit smoking and nicotine use altogether, to cut down on smoking or to convert smokers to vapers. It is possible also that dual users are on a path to either exclusive use of e-cigarettes or to complete nicotine cessation, and this is a snapshot of the early stages of a migration out of smoking.  The available data cannot demonstrate this is happening, but contrary to your unqualified assertion, it certainly does not demonstrate that: “use of e-cigarettes does not discourage, […] conventional cigarette use among US adolescents“. Nor is there any basis in your analysis to believe e-cigarettes ‘may encourage conventional cigarette use‘  any more than they discourage it.  So why has this statement been included?

You have included a caveat in the article, but then ignored it…

While the cross-sectional nature of our study does not allow us to identify whether most youths are initiating smoking with conventional cigarettes and then moving on to (usually dual use of) e-cigarettes or vice versa, our results suggest that e-cigarettes are not discouraging use of conventional cigarettes. (emphasis added)

This rather important qualification regarding the limits of the study is included in the full text of the article, not the abstract, but has not stopped you drawing causal inferences that the data and survey simply do not support for these reasons given above. In fact the caveat in the first part of this sentence should stop you making the assertion in the second part.  How do you justify both the caveat and the assertion within a single sentence?

Document 2: JAMA Pediatrics press release

E-Cigarette Use by Adolescents Associated With Higher Odds of Smoking. I will focus only on one part of this, as it otherwise mostly follows the abstract.

Background: E-cigarettes are marketed in much the same way cigarette manufacturers marketed conventional cigarettes in the 1950s and 1960s, including on TV and the radio where cigarette advertising has been banned for more than 40 years. Studies have shown that exposing young people to cigarette advertising can cause them to start smoking. E-cigarettes also are sold in flavors (e.g. strawberry, licorice and chocolate) that are banned in conventional cigarettes because they appeal to young people.

This is a one-sided and contentious framing of the issue, and none of it relates to the study in question.  Its most useful, and unintended, function is to reveal the bias of the authors.  You could equally have said: “E-cigarettes are eroding the market for cigarettes by helping smokers to switch to vaping, cut down smoking or stop using nicotine completely.  The edgy and skilful advertising of these products and imaginative range of flavours are essential to encourage as many smokers as possible to switch to low risk products.  These products may completely change the market for tobacco and become one of the most significant public health innovations of the century. However, policymakers need to be mindful of unintended consequences“.  But you didn’t. You chose to frame the issue in a way that suggests a strong predetermined belief, and not a that of a neutral investigator.

Document 3: UCSF press release

E-Cigarettes: Gateway to Nicotine Addiction for U.S. Teens, Says UCSF Study 

Given what the study says and the token attempt at a caveat in the published paper, the UCSF press release headline and most of the text of release is shockingly misleading.

E-Cigarettes: Gateway to Nicotine Addiction for U.S. Teens, Says UCSF Study.

There is no basis for drawing this unequivocal ‘gateway’ conclusion from the data presented in the study.  None whatsoever – and the published study even makes this clear. In fact the data are consistent with the opposite hypothesis – that e-cigarettes are primarily used by smokers interested in quitting or cutting down. Indeed the observation  that users have a higher intention to quit smoking lends support to that hypothesis more than to your preferred explanation.  This headline error is compounded and elaborated thus:

But the authors noted that about 20 percent of middle school students and about 7 percent of high school students who had ever used e-cigarettes had never smoked regular cigarettes – meaning that some kids are introduced to the addictive drug nicotine through e-cigarettes, the authors said.

This is highly misleading. In an alternative situation in which e-cigarettes were not available, then the small proportion of kids that “are introduced to the addictive drug nicotine through e-cigarettes” may simply have started to smoke cigarettes and got their introduction via the much more dangerous and addictive route.  In that case it may be a good thing that their smoking onset has been diverted into e-cigarette use – please see my posting: We need to talk about the children – the gateway effect examined for more discussion on the likelihood that gateway effects will be positive for health, or exits from smoking.

In one situation where low risk nicotine products have radically eroded the market for cigarettes, that being snus use in Sweden and Norway, we see snus acting as alternative to smoking onset, diverting young people away from smoking,  with greatly reduced risks that follow from that.  If you are unaware of this experience, this paper might help: Ramstrom L., Foulds J. Role of snus in initiation and cessation of tobacco smoking in Sweden. Tob Control 2006; 15:210–4. I can provide further citations if you are interested in gaining a better understanding of the practical experience of market-based tobacco harm reduction and real-world gateway ‘exits’ from smoking.

Also, to note the insight offered by Carl Phillips, it is not the order in which initial use occurs that determines whether one behaviour causes another and there is a ‘gateway effect’.  We are interested in what determines whether someone becomes a smoker (i.e. adopts an enduring pattern of cigarette use), not what causes someone to use their first cigarette – these effects are obviously different and can have different causes.  It is theoretically possible for people to take their first nicotine through smoking, but only to continue to regular smoking because of the availability of e-cigarettes to provide ancillary support their smoking habit.  In that (unlikely) event, e-cigarettes would be the cause of the smoking behaviour, but not the cause of the first cigarette.   Equally, people who have smoked first may use e-cigarettes to quit.  People who first use e-cigarettes, may go on to smoke and then use e-cigarettes to to quit smoking.  The point is that your study has no data that can illuminate which, if any, of the these pathways is being followed, and by how many people.  However, that has not stopped you choosing the most negative and damaging (and unlikely) interpretation over all others for no credible reason, and then making a headline message of it.

I would like to draw out one further statement:

“Despite claims that e-cigarettes are helping people quit smoking, we found that e-cigarettes were associated with more, not less, cigarette smoking among adolescents,” said lead author Lauren Dutra, a postdoctoral fellow at the UCSF Center for Tobacco Control Research and Education.

The reasoning for claiming e-cigarettes do not help people quit smoking amounts to a crude non sequitur: “e-cigarettes were associated with more, not less, cigarette smoking among adults“.  More, not less… but compared to what? The study found that more smokers were using e-cigarettes than non-smokers. However, this banal observation does not confirm that e-cigarettes do not help quitting any more than finding that NRT is used more by smokers would suggest NRT is not used for quitting. The real test of the impact of e-cigarettes is hard to gauge because it requires knowledge of what would have happened in the absence of e-cigarettes.  If you could show there is “more, not less” smoking than there otherwise would have been had e-cigarettes not become available, then that would definitely be a concern.  But of course the study does not and cannot do this, given the limitations of its methods and the available data.That doesn’t stop you claiming the following, which as far as I can see,is based on nothing at all:

“E-cigarettes are likely to be gateway devices for nicotine addiction among youth, opening up a whole new market for tobacco”

Reaction from tobacco control and public health experts

The tobacco control community is often reluctant to challenge its priesthood and can be supine or complicit in supporting junk science that justifies its preferred policies. However, the distortions in this study and its media communications are so egregious that it has provoked criticism from public health establishment figures.  The New York Times report on the study contained the following welcome rejection of the key assertions by Tom Glynn of the American Cancer Society:

“The use of e-cigarettes does not discourage, and may encourage, conventional cigarette use among U.S. adolescents,” the study concluded. It was published online in the journal JAMA Pediatrics on Thursday. But other experts said the data did not support that interpretation. They said that just because e-cigarettes are being used by youths who smoke more and have a harder time quitting does not mean that the devices themselves are the cause of those problems. It is just as possible, they said, that young people who use the devices were heavier smokers to begin with, or would have become heavy smokers anyway. “The data in this study do not allow many of the broad conclusions that it draws,” said Thomas J. Glynn, a researcher at the American Cancer Society.

… and David Abrams of Legacy Foundation also ridiculed the reasoning:

But David Abrams, executive director of the Schroeder Institute for Tobacco Research and Policy Studies at the Legacy Foundation, an antismoking research group, said the study’s data do not support that conclusion. “I am quite certain that a survey would find that people who have used nicotine gum are much more likely to be smokers and to have trouble quitting, but that does not mean that gum is a gateway to smoking or makes it harder to quit,” he said.

David Abrams elaborates further in the Huffington Post

The problem with Dutra’s conclusion, said Abrams, is that causality could run the other way; kids who smoke (because of genetics, or parents who smoke) could simply be more likely to engage in other risky behaviors as well, such as alcohol, marijuana or e-cigarettes.

“One does not lead to the other [in this study],” said Abrams. “The behaviors just travel together in vulnerable kids.” The only way to establish causality is a rigorous longitudinal study that follows a large number of people over a long period of time — something that would take decades. In the mean time, said Abrams, “the science doesn’t support panic or fear [of e-cigarettes] — yet.”

Best known for its “Truth Campaign” ads, Legacy’s vision is a society free of the death and disease caused by tobacco. And according to Abrams, e-cigarettes could be the key to achieving that society. “They are the first product in 100 years that might make cigarettes obsolete,” said Abrams. “That would literally wipe out the death cause to 5.6 million kids alive today, as well as 480,000 adults every year.”

Would you care to explain if you think Glynn and Abrams are incorrect in their assessment?  

Other commentators

There are several robust analyses of this study, all of which I have benefited from.  All of them are unflinching in their criticism:

Sadly, this is not the first time such irresponsible over-interpretation of data has been used as part of a media propaganda offensive against e-cigarettes.  The same model was used in this study of Korean school age adolescents (Lee S, Grana RA, Glantz SA. Electronic Cigarette Use Among Korean Adolescents: A Cross-Sectional Study of Market Penetration, Dual Use, and Relationship to Quit Attempts and Former Smoking. J Adolesc Health 22 November 2013).

The failings in the Korean analysis and media approach were bluntly pointed out at the time, and it is therefore all the more troubling that they have been repeated in the new paper.

An approach that abuses and erodes trust

It appears there is a malign system at work here. The original paper has a modestly phrased, but incorrect and unsupported, statement suggesting that e-cigarettes do not reduce smoking and may increase it. This is surrounded a barrage of statistics and protected by what appears to be a responsible caveat, though that is actually ignored in practice.  This gets past the inattentive journal peer reviewers and into a publication with an important sounding name. Caveats are then jettisoned and hype is developed in the JAMA press release and, above all, in the UCSF press release. The media work seems to be free of any academic integrity and aimed at creating a media storm irrespective of the quite dull and predictable findings of the actual analysis.   The media, which is still used to trusting famous universities and well known public health academics, obliges and repackages the hype relentlessly –including, annoyingly, in the UK.  The distinction between association and causation is lost, as journalists read the press release and quite reasonably assume that the association must be causal or there would be no point or justification in making the ‘gateway’ headline with it.

Once in the news media, and widely propagated via wire services, it is uncritically repeated in maybe hundreds of regional and local outlets and goes world wide.  Then it enters the political sphere.  Here is an example – no doubt one of many – of an elected representative, Philadelphia City Councilman and Majority Deputy Whip, Bill Greenlee being mislead by the study and press release, and so tweeting the bogus story:

Greenlee tweet

You are responsible for this, and it is not something to be proud of. It is not the proper role of a university to introduce this sort of propaganda into democratic debate on public health, nor is it right for you and UCSF to abuse the trust of citizens, journalists and politicians like Mr Greenlee.  Will you contact Mr Greenlee and explain that he has been misled?

Please put this right and reconsider your approach

I really hope you will reconsider your approach – it does not serve public health or the public interest.  It is wrong simply to assume that e-cigarettes will play no part in reducing the expected one billion 21st Century deaths from smoking.  The evidence that there is, taken as a whole, is actually very encouraging, and certainly not a reason to mount a ‘dirty tricks campaign’ against these products.  In any event, there is never a case to mislead the public, policy-makers and legislators  even if you are convinced the end justifies the means, which in this case it does not. 

I would welcome your responses to the points raised in this letter.   If I have misunderstood your work I will of course acknowledge and correct.  I trust you would wish to do the same for false or misleading statements in your own work.  As you know, UCSF expects adherence to the highest standards of integrity in proposing, conducting and reporting research.  I do not think the highest standards have been met in this case, do you?  Do you agree that you should now withdraw the paper from JAMA Pediatrics and circulate a substantial correction to the UCSF press notice?  If not, what is the alternative?

Yours sincerely

Clive Bates
London, UK

New York Times march 7th

But David Abrams, executive director of the Schroeder Institute for Tobacco Research and Policy Studies at the Legacy Foundation, an antismoking research group, said the study’s data do not support that conclusion.

“I am quite certain that a survey would find that people who have used nicotine gum are much more likely to be smokers and to have trouble quitting, but that does not mean that gum is a gateway to smoking or makes it harder to quit,” he said.

He argued that there were many possible reasons that students who experimented with e-cigarettes were also heavier smokers — for example, living in a home where people smoke, belonging to a social circle where smoking is more common, or abusing drugs or alcohol.

The study did have a bright spot: Youths who used e-cigarettes were more likely to plan to quit smoking. Dr. Abrams highlighted that finding, but said it was impossible to tell whether students who planned to quit actually did, because the data did not track this.


New England Journal of Medicine

Furthermore, we need to communicate intelligently about harm reduction: not all nicotine-containing products are equal, and the public health focus should be on eliminating combustible tobacco products, even if some people who give up combustibles will continue using FDA-approved medications, e-cigarettes, or smokeless tobacco products indefinitely.

Email to Czech MEP Ouzky this morning on Snus, Dumansiz Tütün

Dear Honorable MEP Ouzky,

My name is Atakan Befrits and I am a Swedish European as well as a Harm Reduction entrepreneur and activist based entirely outside the EU.

I am writing to you for information purposes only. I am intensely curious as to why the Czech republic had such a diametrically opposed total voting behaviour on the TPD compared to other countries.

As you know, Sweden is the only country in the EU where snus is freely sold and used as an alternative to cigarette smoking. Sweden is also an EU country that already has a blanket ban on e-cigarettes. (Very curious in itself)

I also know for a fact that Swedish snus “derivative” products are sold in the Czech Republic. (By derivative I mean in a format designed to “avoid” the EU snus ban)

Can you give me any insight as to why so extremely many Czech MEP’s didn’t vote at all, abstained or voted NO to the TPD?

Is the general feeling in the Czech Republic that Harm Reduction products are a good thing or is the voting behaviour from your fellow MEP’s and yourself based on some other “important” consideration for your country? Such as a large internal tobacco production industry or something like that?

For your information the Swedish MEP’s voted 1 abstain, 1 NO, and 19 yes to the TPD. That means that approximately 90% of Swedish MEP’s actually voted to DENY the rest of Europe the free choice to use a 99% less harmful form of tobacco.

Isn’t that very very strange coming from a country that has 13% smokers compared to Europe’s 28%, but the same percentage of tobacco users. At the same time Sweden’s tobacco related disease levels are approximately 50% lower than the rest of Europe.

I thank you very much in advance for your insight and input on this highly controversial issue on tobacco, ethics and morals.

I salute you for your vote!

Atakan Befrits