Through with Chew Week: Don’t Be Fooled

Chewers and Dippers: It’s the third week in February, which means it’s time for you to be badgered by the annual Through with Chew public relations campaign.  Across the nation, tobacco prohibitionists are publishing unscientific and unsubstantiated claims about smokeless tobacco.  Here are recent examples from Fallon County, Montana and Boone County, Iowa, followed by the facts

Claim 1: “chew products deliver a higher dose of nicotine than cigarettes, making the product more habit forming.”

The Facts: The amount of nicotine that smokeless tobacco “delivers” is irrelevant, because chewers and dippers use products in ways that satisfy them.  In fact, there is evidence from one of the world’s foremost authorities on nicotine addiction that smokeless tobacco is less habit-forming than cigarettes (here and here).  Most Americans are badly misinformed about the absence of significant health effects of nicotine (here).  

Claim 2: “Smokeless ‘Spit’ tobacco contains over 2,000 chemicals.”

The Facts: Every natural product, including coffee contains thousands of chemicals (here).  A product’s chemical composition is unimportant if it carries little or no risk.  Like coffee, smokeless tobacco fits in that category.

Claim 3: “Chew contains at least 28 chemicals that have been found to cause cancer…”

The Facts: Almost everything we eat contains cancer-causing chemicals, but they are in trace levels that present no risk.  Again, coffee is a prime example (here).  Numerous scientific studies prove that there are vanishingly small levels of carcinogens in modern smokeless tobacco products (here, here, here, here, here). 

Claim 4: “Harmful effects of smokeless tobacco include mouth, tongue, esophageal, and throat cancer…stomach and pancreatic cancer”

The Facts: According to dozens of published epidemiologic studies (reviewed here), the risks for these cancers are not elevated.

Claim 5: “Harmful effects of smokeless tobacco include increased risk of heart disease, heart attacks and stroke.”

The Facts: Among the many risk factors for heart disease and stroke, smoking is one of the biggest.  That is not the case with smokeless tobacco.  When the American Heart Association conducted an extensive investigation of smokeless tobacco and heart disease, it found almost nothing (here).  Large studies from Sweden show that snus users do not have risk for heart attacks (here) and strokes (here), and snus use may even offer benefits for heart attack survival (here).

Claim 6: “Harmful effects of smokeless tobacco include leukoplakia (white sores in the mouth that can become cancer).”

The Facts: White patches are common in chewers and dippers, but they are nearly always benign.  The link with mouth cancer is virtually zero (here).

Claim 7: “Harmful effects of smokeless tobacco include receding gums, bone loss around the roots of the teeth, abrasion (wearing down) of teeth.”

The Facts: There is virtually no scientific evidence that smokeless tobacco is a risk factor for any dental problem (here, here).  In fact, one study shows that snus and moist snuff (dip tobacco) might be protective against cavities (here).

Don’t be fooled by bogus smokeless tobacco health claims.

How Dangerous is Swedish Snus? Don’t Ask The New York Times

The New York Times has published (here) a reasonably accurate portrayal of the Swedish snus experience that I have chronicled for over a decade (here,  here,  and here).  Reporters Matt Richtel and David Jolly examined Swedish Match’s FDA application to remove the federally mandated mouth cancer and not-safe-alternative warnings from snus products.  I have discussed this landmark filing previously (here). 

In a companion piece (here) the paper tried to answer two important questions about snus and mouth cancer: “How accurate is the current warning? How dangerous is Swedish snus?” 

Despite a wealth of available information, the Times unfortunately failed to nail the answers, even after acknowledging that “Many studies have been done on the question (sic),..." but fretting that "...but as in many fields that involve complex questions and human subjects, the research is imperfect.” 

How is the research imperfect?  “For instance, some research concluding virtually no oral cancer risk from snus was funded by Swedish Match itself.”  The Times fell back on the old canard – the funder influenced the finding, despite total disclosure and high-quality peer review.  The paper failed to note that numerous studies, regardless of funding, show “virtually no oral cancer risk” for Swedish snus and American chew and dip.

The Times asked Kristin L. Sainani, a Stanford epidemiologist not involved in tobacco research, to examine the science.  She was remarkably indecisive:   “‘The weight of the evidence suggests a small increase’ in the risk of oral cancer with snus.  In Sweden, users of Swedish snus see virtually no increase in the rates of lip and oral cancer.”  In the end she made the correct call: virtually no increase. 

Dr. Sainani attempted to provide an anti-snus slant using double negatives: she said that “it is inconsistent with the evidence” to suggest that there is “absolutely no harm to an individual” from snus.  In essence, she repeated the no-win argument that snus can’t be proven absolutely safe.  That’s an irrational standard that many common foods couldn’t meet.

Dr. Sainani was asked by the Times to resolve the mouth cancer question, yet she is quoted on an entirely different matter: “In fact, she said, Swedish snus users face a doubling of risk of pancreatic cancer…”  It appears that Dr. Sainani exclusively used a 2008 review by Boffetta et al., which has been exposed as relying on cherry picked data (here). 

Is a snus pancreas cancer risk real?  No.  Five years ago I detailed how Boffetta fabricated the risk in 2008 (here), and, in 2011, Boffetta acknowledged that his earlier finding was wrong (here).  Sainani would have discovered this if she had compared the faulty Boffetta analysis with the most authoritative and comprehensive meta-analysis by Peter Lee and Jan Hamling (here), which found no pancreas cancer risk, in addition to no mouth cancer risk.

 

The Times article ended with Dr. Deborah Winn, deputy director of the division of cancer control at the National Cancer Institute.  Readers of this blog know that Dr. Winn launched the smokeless tobacco mouth cancer scare in 1981 (here and here).  While she is the NCI’s top authority on smokeless tobacco and cancer, she demonstrated an appalling disregard of facts in a 2010 congressional hearing (here).  In the Times article, her obfuscation continued:  “[Winn] considered Swedish snus to be ‘a form of smokeless tobacco,’ which, in general, she said, is generally ‘linked to mouth cancer…Swedish snus in the past has given you cancer, and at the current low levels, I don’t know,’ she said. ‘There could be some risk there.’”

The one data point Winn provided to the Times is false.  “She said studies done in the 1990s showed that users of Swedish snus in the 1970s faced a twofold increase in the risk of oral cancer.”  There were two studies of Swedish snus and mouth cancer published in 1998.  They concluded:

1.  “[Snus] was not found to be a risk factor for oral cancer in our study.” (here)

2.  “No increased risk [for head and neck cancer, including oral cancer] was found for the use of Swedish [snus].” (here)

The Times and their quoted experts did a major disservice to their audience; they failed to report the simple truth, that mouth cancer risk for Swedish snus is next to nil. 

New Study: Smokeless Tobacco is NOT Associated with Pancreatic Cancer

A new study documents that smokeless tobacco use is not associated with increased risk for pancreatic cancer. The study, from the International Pancreatic Cancer Case-Control Consortium and lead author Paolo Bertuccio of Milan, Italy, was published in Annals of Oncology (abstract here). It is a collaborative analysis of 6,000 cases of pancreatic cancer from 11 studies in North America and Europe.

With only 130 pancreatic cancer cases among ever smokeless tobacco users, the odds ratio (OR) is 0.98 (95% Confidence Interval, CI = 0.75 – 1.27). Twenty-three cases among exclusive users of smokeless tobacco produced an OR of 0.62 (CI = 0.37 – 1.04), which was almost significant for a PROTECTIVE EFFECT. Smokeless users who were also cigarette smokers had an OR of 1.36, which was not statistically significant (CI = 0.94 – 1.96) but confirms other studies that showed higher pancreatic cancer risks for smokers.

(The odds ratio is the measure used for case-control studies. Its interpretation is similar to that used for relative risks, which was discussed in this post.)

The importance of this study is hard to overestimate. First, it provides additional evidence that smokeless tobacco users are not at risk for pancreatic cancer. More importantly, it directly addresses a persistent question about the integrity of previous studies.

In September 2009, I described in detail the results of two meta-analyses of cancer risks among smokeless tobacco users (read my description here). The first report, published in 2008 by Paolo Boffetta and colleagues in Lancet Oncology, concluded that smokeless users had an increased risk for pancreatic cancer (RR = 1.6, CI = 1.1 – 2.2). But that study used cherry-picked data in an unscientific manner to artificially raise the cancer risks. The second study, by Peter Lee and Jan Hamling, using a more scientifically credible and valid approach, reported an RR for pancreatic cancer of 0.99 (CI = 0.71 – 1.60).

The results from the current study are in close agreement with the Lee-Hamling estimate, and at odds with the Boffetta estimate, which Bertuccio clearly acknowledges:

“Our results on smokeless tobacco use are in broad agreement with a recently published meta-analysis of all published data on the issue [Lee-Hamling], which reported NO EXCESS RISK OF PANCREATIC CANCER in case-control studies. They are, however, at variance with those from another meta-analysis [Boffetta], based mainly on data from two Nordic cohort studies, which suggested that smokeless tobacco is associated with an increased risk of pancreatic cancer.” (emphasis added)

Bertuccio actually cited a different Lee-Hamling publication (abstract here), but the data from this study is identical to the Lee-Hamling meta-analysis.

The Bertuccio study is significant because it endorses the Lee-Hamling analysis and clearly refutes the Boffetta analysis. But there is another, profound aspect to this report: Paolo Boffetta is a co-author. Thus, Dr. Boffetta is finally acknowledging that his 2008 meta-analysis was wrong.

American consumers have been deceived for decades by the myth that smokeless tobacco confers high risk for oral cancer (here ). Because of the misguided 2008 Boffetta meta-analysis, smokeless tobacco opponents have built a second unscientific line of attack around the issue of pancreatic cancer.

Regulatory authorities worldwide should now acknowledge that use of modern American and Swedish smokeless tobacco products is not a risk factor for cancers of the oral cavity or pancreas.

New Study Documents the Health Effects from Snus Use: Almost Zero

A detailed review of epidemiologic studies regarding snus use has just been published online by Regulatory Toxicology and Pharmacology (abstract here). Author Peter Lee, a UK epidemiologist, concludes: “Using snus is clearly much safer than smoking. While smoking substantially increases the risk of cancer and cardiovascular diseases, any increase from snus use is undemonstrated, and if it exists is probably about 1% of that from smoking.”

Dr. Lee confirms what I have been asserting since 1994: Smokeless tobacco use is 99% less hazardous than smoking, and the magnitude of risk, if it exists, is difficult to measure using modern epidemiologic methods.

Lee reviewed the evidence from over 150 studies covering many diseases. Previously, he published separate meta analyses involving smokeless tobacco use and all cancers (abstract here), dental problems (abstract here), pancreas cancer (here), oral cancer (here), and circulatory diseases (here).

The hallmark of Lee’s analytic approach is to use all of the published evidence in a systematic and unbiased manner. This is in direct contrast to anti-tobacco advocates like Dr. Paolo Boffetta, who cherry pick the data and use only numbers that confirm their pre-existing belief that smokeless tobacco causes disease. Pancreas cancer is an excellent example.

In 2008, Boffetta published a meta analysis (abstract here) in which he claimed that snus use is a risk factor for pancreas cancer. He cited two studies, one from Norway (here) and another from Sweden (here). The Norway study reported a risk increase among all snus users (Relative Risk = 1.7, Confidence Interval = 1.1 – 2.5) but not for a subset of snus users who were never smokers (RR = 0.9, CI = 0.2 – 3.1). The Swedish study reported exactly the opposite: There was virtually no risk among all snus users (RR = 0.9, CI = 0.7 – 1.2), but the subset of snus users who never smoked had an increased risk (RR = 2.0, CI = 1.2 – 3.3).

Dr. Boffetta chose only to use the elevated risks, even though they were from different groups. As Lee points out, “For pancreatic cancer, Boffetta cited only the increases for never smokers from the [Swedish] study and for the whole population from the [Norwegian] study, not mentioning the lack of increase for the whole population for the construction workers and for never smokers for the Norway cohorts.”

It is important to note Dr. Boffetta was an author of both studies; that makes his selective use of data from them even more objectionable.

Another issue raised by Lee about another Boffetta meta analysis (here) claiming that snus use is a risk factor for fatal – as opposed to non-fatal – heart attack and stroke. In a 2009 blog post, I noted that Boffetta’s claim was questionable (here): “Boffetta found that smokeless users had no significant risk for all heart attacks and strokes but had elevated risks for fatal cases. It logically follows that smokeless users probably had LOWER risks for NON-FATAL heart attacks and strokes.” Lee echoes my concern: “Anyway, an association for fatal cases but not for all cases seems unlikely unless implausibly snus protects against non-fatal cases.”

Finally, Lee reviewed epidemiologic studies to answer this question: Does snus encourage initiation of smoking or discourage quitting? His conclusion: “There is no good evidence that introducing snus in a population would encourage smoking initiation or discourage cessation.”

This is an especially important point, because RJ Reynolds has just launched a campaign encouraging smokers to switch completely to Camel Snus (article here). While apparently in full compliance with FDA tobacco regulations, the ads have enraged prohibitionists like Matt Myers, who said that Reynolds should “stop its insidious marketing of tobacco products in ways that seek to discourage smokers from quitting and keep them hooked on nicotine...The ads are trying to take advantage of people trying to end all uses of tobacco.”

Myers is wrong about many things. Most smokers are not trying to achieve abstinence, but they are interested in enjoying tobacco in a safer manner. As Dr. Lee documents, snus is a vastly safer cigarette substitute.

Mayo Clinic Misinformation About Smokeless Tobacco

For many years, tobacco “experts” at the Mayo Clinic have tarnished the institution’s name by fabricating misinformation about smokeless tobacco. In a 2004 article about such tactics (available here), I noted that the Mayo website contained this irresponsible, unprofessional and demonstrably false statement: “…smokeless tobacco, also called spit tobacco, has health risks just as severe or even more severe as those associated with cigarette smoking.”

Last week, Jennifer A. Kern, a Mayo Clinic behavioral counselor and former smoker, published a quit-smoking blog entry for the official Mayo Clinic web site, in which she invented new health risks related to smokeless tobacco use (here).

Ms. Kern begins with an explicit acknowledgment that smokeless tobacco is an effective substitute for cigarettes: “Those of us who live in the north are moving into the cooler seasons…it's not uncommon to see people switching tobacco products in order to stay indoors while still getting their nicotine fix. Some folks put down cigarettes and pick up smokeless tobacco products such as chewing tobacco and snuff instead.”

Ms. Kern doesn’t like smokers switching to vastly safer smokeless products, so she tries to convince them not to do so by invoking a “just-as-harmful” theme: “Smokeless tobacco products carry carcinogens, or cancer-causing chemicals, just like cigarettes do.”

Next, Ms. Kern turns to outright fabrication: “In fact, a variety of cancers that can be caused by smokeless tobacco use include: mouth and gum, larynx (voice box), esophagus, and salivary gland, as well as non-oral cancers like pancreas, kidney and penile cancer.”

My readers know that a comprehensive meta-analysis published in 2009 found that smokeless tobacco use is not associated with cancers of the mouth and gum, larynx, esophagus, pancreas or kidney (for a full discussion, click here). But what about salivary gland and penile cancer?

For salivary gland cancer, Ms. Kern may have misread a story involving Tony Gwynn, a former major league baseball player. In early October, Gwynn was diagnosed with cancer of the parotid salivary gland (described here), and he commented that “I haven't discussed that with the doctors yet, but I'm thinking it's related to dipping.” Apparently Gwynn and Ms. Kern are unaware that no epidemiologic studies have linked smokeless tobacco use and salivary gland cancer.

Ms. Kern’s most bizarre claim is that smokeless tobacco use causes penile cancer. According to the National Cancer Institute, penile cancer is extremely rare, occurring in only 1,250 American men each year (here). Penile cancer is strongly related to human papillomavirus infections and lack of circumcision (here). Maybe Ms. Kern was referring to a 1995 report linking penile cancer and smokeless use in India (here), but Swedish and American products have not been implicated in numerous epidemiologic studies.

Someone should counsel Ms. Kern and her employer about the public health imperative of sticking to the facts.

Snus Users and Smokers in Stockholm

A new study published in Biomed Central Public Health (available here) describes the socioeconomic and lifestyle characteristics of snus users and smokers in Stockholm County, Sweden. Based on a 2006 survey of 35,000 residents, it was authored by Karin Engström and colleagues at the Department of Public Health Sciences at the Karolinska Institute. In addition to providing interesting information about snus users, this study has important implications for Karolinska Institute claims about the link between snus use and cancer.

Among men, 17% were exclusive snus users, 11% smoked and 2.4% were dual users. Among women, cigarette smoking was dominant (15%), while snus use and dual use were only 3.1% and 0.5% respectively. Given this, I will focus on the findings for men.

It is noteworthy that the prevalence of snus use was highest among men less than 35 years old. This means that young men in Stockholm strongly prefer snus, a lifestyle choice that will have little or no effect on their health as they age.

Snus users were somewhat more likely to have lower education levels than nonusers of tobacco, a trend that was even stronger among smokers. Smokers were also more likely to be unskilled and skilled workers in the very low income group, while snus users were more evenly distributed among all occupational classes and across all income levels.

One of the more interesting results concerned alcohol consumption. Risky alcohol consumption was defined as 14 standard drinks per week; the survey also asked about weekly or monthly binge drinking. Snus users and smokers were more likely to practice risky consumption than nonusers (odds ratios = 1.8 – 1.9), and they were more likely to have weekly binge-drinking episodes (ORs around 3.1).

This information on alcohol abuse among snus users is important, because a Karolinska epidemiology group, led by Olof Nyrén, published studies suggesting that snus use is associated with a small risk of pancreatic, stomach and esophageal cancer (abstracts here and here) among workers in the Swedish construction industry. Alcohol abuse is a strong risk factor for esophageal cancer and may be linked to stomach and pancreas cancer; this makes it a confounder with respect to snus use. In other words, if snus users are more likely to be alcohol abusers, then some of the cancers attributed to snus might instead be caused by alcohol. In many modern epidemiologic studies, standard procedures are used to account for confounders. In this case, to accurately separate the risks due to snus use from those due to alcohol abuse.

But the construction worker studies had no information on alcohol consumption, so alcohol abuse could not be ruled out as a competing risk factor. The lack of information about alcohol in these studies is a serious deficiency that raises questions about the validity of Nyrén’s claims.

In summary, men in Stockholm from all income levels and all occupations prefer snus over cigarettes. The impact of this preference on their health is so small that it is barely measurable by modern epidemiologic methods. Furthermore, snus users, like smokers, are more likely to abuse alcohol, which may be a distinct risk factor for some cancers that has not been evaluated in previous Karolinska Institute reports on snus use.

Magnifying Smokeless Tobacco Risks By Cherry Picking Data: A Case Study

A month ago, I discussed in this blog the definitive study of cancer risks among smokeless tobacco users. This comprehensive meta-analysis, which produced a series of summary relative risks for cancer among smokeless tobacco users by systematically combining all of the primary epidemiologic studies, was completed by Peter Lee and Jan Hamling. They concluded that there is very little evidence that smokeless tobacco use is associated with any cancer.

The results in the Lee-Hamling study were surprisingly different from an earlier meta-analysis performed by Paolo Boffetta, an epidemiologist at the International Agency for Research on Cancer, and co-authors, which was published in the journal Lancet Oncology. The Boffetta team had produced relative risk estimates for cancers of the oral cavity and pharynx, esophagus and pancreas that were considerably higher than those from Lee and Hamling, as illustrated in the following table:

Cancer Site	Boffetta Relative Risk Estimate (95% CI)	Lee-Hamling Relative Risk Estimate (95% CI)
Oral cavity/pharynx	1.8 (1.1 – 2.9)	1.36 (1.04 – 1.77)
Esophagus	1.6 (1.1 – 2.3)	1.13 (0.95 – 1.36)
Pancreas	1.6 (1.1 – 2.2)	0.99 (0.71 – 1.60)

Why did the Boffetta meta-analysis always produce higher risk estimates than the Lee-Hamling study if both were using essentially the same data? A commentary published by Lee and Hamling in the journal BMC Cancer provides the answer to that question. The answer is simple and disturbing.

First, let me give you some background information. Most primary epidemiologic studies report results for many different sets of circumstances. For example, a study about smokeless tobacco might report risk estimates for all users and these subgroups: current users, former users, exclusive users who never smoked, and users who also smoked. So it is important for investigators conducting meta-analyses to develop specific rules for combining estimates from different studies. Lee and Hamling developed rules and followed them systematically in their meta-analyses. In contrast, Boffetta did not specify any rules but appears to have followed one: Use only the highest risk estimate.

The Lee/Hamling commentary focused on the inherent contradictions in Boffetta’s approach, the best example of which is illustrated in the table below. There are two important primary epidemiologic studies on pancreatic cancer among smokeless tobacco users, one published in the Lancet and the other in the International Journal of Cancer. Each study provided risk estimates for exclusive smokeless users (i.e., those who never smoked) and for users who might also have smoked, as seen in this table:

Primary Study Journal, Year	Risk Among Exclusive Users (95% CI)	Risk Among Users +/- Smoking
Lancet, 2007	1.8 (1.1 – 2.9)	0.9 (0.7 – 1.2)
Int J Cancer, 2005	0.85 (0.24 – 3.07)	1.67 (1.12 – 2.50)

Lee and Hamling make it clear that they produced their summary estimates by either combining risks for exclusive users (i.e. 1.8 and 0.85), or risks for users who might have smoked (0.9 and 1.67). This is both logical and scientifically valid. But which estimates did Boffetta use? The highest, of course. For the Lancet study he used the estimate of 1.8 in exclusive users, but for the International Journal of Cancer study he used the estimate of 1.67 in smokeless users who might have smoked. His goal was to maximize the health risks from smokeless tobacco use, thereby feeding scaremongers who portray smokeless tobacco as deadly, despite decades of research to the contrary. The scientific term for this epidemiologic method is cherry picking.

This is just one example of the unscientific manner in which the Boffetta meta-analysis was conducted. The Lee/Hamling commentary describes many others.

According to its website, the International Agency for Research on Cancer places emphasis on “elucidating the role of environmental and lifestyle risk factors” in cancer development. The IARC should not condone the fabrication of estimates misrepresenting the scientific evidence that cancer risks from smokeless tobacco use in Sweden and the U.S. are minimal to nonexistent. Kudos to Peter Lee and Jan Hamling for documenting this travesty.