In a review of the literature regarding the relationship between smokeless tobacco use and cancer, a conflict of interest of one of the article's authors was initially not disclosed (see: Boffetta P, Hecht S, Gray N, Gupta P, Straif K. Smokeless tobacco and cancer. Lancet Oncology 2008; 9:667-675). The original article was published in July, 2008. That article stated: "The authors declare no conflicts of interest." After the editor of the journal was notified by a researcher with knowledge of a potential conflict of interest of Dr. Stephen Hecht (one of the study authors), an erratum was published in September 2008, which noted: "During the immediate months preceding submission of the review SH was acting in the capacity of an expert witness for the plaintiff in a future court case against a smokeless tobacco company. SH declares his participation in this case in no way influenced his writing or involvement in the review."
More recently, the researcher with knowledge of this conflict of interest made an inquiry to the journal Nicotine and Tobacco Research, in which appeared a December 2008 article co-authored by Dr. Hecht on toxin and carcinogen levels in various brands of smokeless tobacco without any declared conflict of interest. The article stated: "The authors do not have any competing interest pertaining to this work." (see: Stepanov I, Jensen J, Hatsukami D, Hecht SS. New and traditional smokeless tobacco: Comparison of toxicant and carcinogen levels. Nicotine and Tobacco Research 2008; 10:1773-1782).
Initially, the journal responded by stating: "We agree that it might have been more open to disclose Dr Hecht's involvement in this case. However, he argued that the data presented in this paper represented a scientific report which was in no way influenced by his acting as an expert witness in this case. Indeed, the request to him to act in this way reflected his expertise in the field. My senior editorial board unanimously agreed that there was no intention to deliberately mislead the readers in this instance and, indeed, the need to disclose that an author is serving as an expert witness is a moot point."
A later response from the journal stated: "Before responding to you, I contacted Dr Hecht again and took the views of my team of Deputy Editors. Our list of potential conflicts of interest includes specifically payments for providing expert opinion in court - one of my Deputy Editors reminded me of that. However, in this case it appears that Dr Hecht did not receive any payment - he waived the fee. The law firm involved, as I understand it, made an equivalent donation to a US cancer charity. Thus, we accept that there is no conflict of interest to declare."
The Rest of the Story
There are several interesting issues here that are worthy of discussion.
Q: Can serving as an expert witness represent a conflict of interest?
A: Most certainly. If an individual is being paid to be an expert witness in litigation and the research in question is directly related to the testimony to be given in the case, then there is a potential conflict of interest. Think about it the opposite way and it becomes clear. Suppose that a researcher who was testifying on behalf of the tobacco industry in a lawsuit regarding whether smoking causes cancer authored a paper on the causal relationship between smoking and cancer. We would expect that relationship to be disclosed in the paper. It is not less of a conflict just because the expert is testifying for the plaintiff.
Q: In what situations does being paid as an expert witness represent a conflict of interest?
A: Being paid to serve as an expert witness represents a conflict of interest when the research in question is directly related to the testimony to be given. The key question is whether the presence of the financial relationship between the researcher and the attorney/company could be perceived as having influenced the conduct or reporting of the research. If the research is directly related to the expert's testimony, then a reasonable person might question whether the fact of being paid to testify in the trial could have influenced the conduct or reporting of the research.
It is important to note that the research must be directly related to the testimony in order for their to exist a conflict of interest. If I am testifying that an individual's smoking caused his or her lung cancer, then there is no reason why all of my research related to smoking must include a conflict disclosure. However, if my research relates specifically to the issue of lung cancer causation by smoking, then a conflict disclosure would be in order.
In the above case, it is clear that a conflict of interest exists with respect to the Lancet Oncology article. That article reviews the relationship between smokeless tobacco and cancer. Since Dr. Hecht is presumably testifying about the causation of cancer by smokeless tobacco in the lawsuit, the research is directly related to the subject of his testimony, and the conflict should be disclosed. Here, I believe the journal acted correctly in publishing the erratum to note the conflict of interest.
Q: Does the argument that an investigator was not influenced by a significant financial relationship negate the existence of a conflict of interest?
A: This is perhaps the least understood aspect of conflict of interest in research. The answer is no. A conflict of interest is not defined on whether an investigator is influenced due to a financial relationship. A conflict of interest is defined on whether the investigator could be reasonably perceived as being influenced by that financial relationship.
So the initial response of the journal Nicotine and Tobacco Research is inappropriate because Dr. Hecht's argument that "the data presented in this paper represented a scientific report which was in no way influenced by his acting as an expert witness in this case" is not relevant. The relevant question is whether or not the conduct of the review or presentation of the results could be perceived to have been influenced by his being paid as an expert witness in the case. To determine the answer to that question, one does not interview the investigator to assess whether or not he sees himself as having been influenced or not. Instead, one must examine the nature and strength of the relationship between the research in question and the financial interest and assess whether it could reasonably be perceived that the expert testimony might influence the conduct or reporting of the research.
So if the journal is correct in declaring that there is no conflict of interest here, they are correct for the wrong reason. An appropriate reason to declare the lack of a conflict of interest would be a judgment that the subject of the research (the various levels of toxicity of different types of smokeless tobacco products) is not directly related to the testimony. I cannot make such a determination without knowing the expected nature of Dr. Hecht's testimony. If he intends to testify regarding the differing levels of toxicity of various smokeless tobacco brands, then a conflict of interest appears to exist. If that is beyond the scope of his testimony, then there may not be a conflict here - but not for the reason stated by the journal.
Even the erratum published by Lancet Oncology shows a misunderstanding of this central issue. The erratum noted that the investigator "declares his participation in this case in no way influenced his writing or involvement in the review." Again, that is irrelevant. An investigator never declares that his or her participation in a case influenced his work. An investigator never declares that a financial interest caused a bias in his research. If this were about investigators voluntarily coming forward when they believed that they had been influenced by a financial interest, we would be waiting for the cows to come home.
It is critical to recognize that in most situations, the influence of a conflict of interest on the conduct or reporting of research will not be conscious or intentional. The conflict most often works by having a subconscious effect on the research. This is why conflicts of interest should not be defined by whether the financial interest actually affected the research or not. The key issue, instead, is whether the financial interest could reasonably be perceived as having influenced the research or the reporting of its results.
When the journal writes that "there was no intention to deliberately mislead the readers in this instance and, indeed, the need to disclose that an author is serving as an expert witness is a moot point," it is demonstrating a misunderstanding of conflict of interest. It is not about whether there was an acknowledgment of a deliberate attempt to mislead readers. It is about whether or not there was a conflict of interest. If there is no conflict, there is no need to disclose it. If there is a conflict, it should be disclosed. The fact that an investigator is not trying to pull the wool over anyone's eyes does not negate the responsibility to report a conflict of interest if it exists.
Q: Does making a donation to charity in lieu of accepting payment for serving as an expert witness negate an otherwise relevant conflict of interest?
A: Simply, no. The individual is still essentially getting paid for his services. The fact that he chooses to do something with this money other than put it into his personal bank account is his own prerogative, but it does not make the financial interest go away.
Thus, the journal's essential reason for claiming that a conflict of interest does not exist in this case is fallacious. The journal is basically admitting that if Dr. Hecht were being paid for his testimony, a conflict would exist and should be disclosed. However, that is indeed the situation. Whether the money goes into his own bank account or is donated to charity, he is being paid for his testimony. Money is coming out of the law firm that would otherwise not be. And its use is being directed by the expert witness.
Now, let me close by noting that I am not arguing here that a conflict of interest exists with regards to the Nicotine and Tobacco Research article. That judgment depends upon the nature of Dr. Hecht's testimony in the lawsuit and whether or not the differential toxicity of various brands of smokeless tobacco is directly related to his testimony. But in either case, the journal's reason for declaring that there is no conflict of interest is faulty.
Researchers and scientific journals need to understand that conflict of interest is not a matter of wrongdoing. Declaring a conflict of interest does not mean that a researcher has done anything wrong. And the reverse of that is also true. Not doing anything wrong does not mean that a conflict of interest fails to exist.
Conflict of interest is simply about whether or not there is a reasonble perception that an investigator's work could be influenced by a significant financial interest. The disclosure of that conflict is important because it allows readers to take that into consideration in evaluating the research and its conclusions. The disclosure is not intended to alert readers of any wrongdoing. In fact, the only wrongdoing that is commonly present is the failure to disclose these conflicts of interest.
Wednesday, January 21, 2009
Tuesday, January 20, 2009
Author of Thirdhand Smoke Study Warns that Smokers are Contaminated and Emit Toxins; Suggests that Thirdhand Smoke Causes Lead Poisoning
Scientific American has published a review of the thirdhand smoke issue, including an interview with one of the authors of the study which brought the issue to national attention. In the article, that anti-smoking researcher warns that even when not actively smoking, smokers are contaminated and emit toxins that are hazardous to children. He also suggests that thirdhand smoke can result in lead poisoning among infants because of the presence of lead in tobacco smoke.
The article quotes the researcher as stating, in response to the question "Why is thirdhand smoke dangerous?": "The 2006 surgeon general's report says there is no risk-free level of tobacco exposure. There are 250 poisonous toxins found in cigarette smoke. One such substance is lead. Very good studies show that tiny levels of exposure are associated with diminished IQ."
It also quotes the researcher as stating: "Smokers themselves are also contaminated…smokers actually emit toxins [from clothing and hair]."
The Rest of the Story
While the claims made in this article make for interesting reading, they are not science. There simply isn't scientific support behind the assertions made by this researcher. In fact, Dr. Stanton Glantz himself acknowledges in the article that there is no scientific evidence to document that thirdhand smoke is hazardous to children and infants. According to the article, Dr. Glantz "is not aware of any studies directly linking third-hand smoke to disease."
So if there isn't scientific evidence linking thirdhand smoke with disease, then how can the anti-smoking researcher claim that thirdhand smoke causes lead poisoning?
The answer is that you don't need science behind you to make health claims in the tobacco control movement. You can make any claim you want and rest assured that virtually no one within the tobacco control movement is going to publicly question your statement. Sure, there may be some private discussions in which researchers whisper between themselves how unsupported the claim is. But there is no danger of the dissenting opinions becoming public, because dissent on issues like this is simply not allowed in this religious-like movement.
I am certainly not aware of any evidence that the levels of lead in household dust in homes with a smoker are high enough to cause lead poisoning in infants. For that matter, I am not aware of any evidence that the toxins in thirdhand smoke are ingested or inhaled to the level necessary to actually cause harm to children.
To be sure, speculation is reasonable. But if you're going to speculate, you need to make it clear that what you are doing is speculating. The Pediatrics article and this interview are not what I would characterize as speculation. Both make definitive health claims: that thirdhand smoke causes health damage to infants and children. And to the best of my knowledge, these health claims are not supported by any actual evidence.
It also seems rather obnoxious to call smokers "contaminated" and emphasize that they are "emitting toxins," without having any evidence that such "toxins" are actually causing health damage to nonsmokers. I may well have detectable levels of "toxins" from the smoke to which I am exposed from my pellet stove, but it would not be fair to say that I am contaminated and emitting toxins. (I did fall into a pile of metal hydroxide sludge once and I admit that at that moment I was contaminated.)
I also don't understand exactly what the point is. Is it to cast smokers as social outcasts who should be spurned from society and not allowed to have any contact with "the rest of us?" Is it to try to stimulate efforts to ban smokers from being child care providers or teachers? Because if it is true that smokers are contaminated and emitting toxins, then we certainly wouldn't want our children to be exposed to those toxins in day care centers or schools.
Another curious statement in the article is that "Studies in rats suggest that tobacco toxin exposure is the leading cause of sudden infant death syndrome (SIDS)." How could studies in rats possibly indicate the degree to which tobacco exposure is causing SIDS in humans? One would certainly need epidemiologic studies, not merely rat studies, to determine the extent to which tobacco smoke exposure is causing SIDS in humans.
While the article concludes by suggesting that the thirdhand smoke danger points to the need for all smokers to quit, I am afraid that the hysterical nature of the thirdhand smoke claims may actually do the opposite. It may convince many smokers that the anti-smoking folks are fanatics and that they should stop listening to this hysteria. It may also undermine the public's appreciation of the hazards of secondhand smoke and convince many smokers not to bother smoking outside of the home (since their children would be damaged anyway by the thirdhand smoke).
One final note. We've known about the offgassing of constituents from tobacco smoke that has absorbed on surfaces for a long time. What scientific evidence is new such that it would warrant a public education campaign about thirdhand smoke?
The most interesting aspect of this story to me is not that an anti-smoking researcher would make unsubstantiated and somewhat hysterical assertions like these, but that almost no one within the movement is willing to publicly challenge these assertions.
The article quotes the researcher as stating, in response to the question "Why is thirdhand smoke dangerous?": "The 2006 surgeon general's report says there is no risk-free level of tobacco exposure. There are 250 poisonous toxins found in cigarette smoke. One such substance is lead. Very good studies show that tiny levels of exposure are associated with diminished IQ."
It also quotes the researcher as stating: "Smokers themselves are also contaminated…smokers actually emit toxins [from clothing and hair]."
The Rest of the Story
While the claims made in this article make for interesting reading, they are not science. There simply isn't scientific support behind the assertions made by this researcher. In fact, Dr. Stanton Glantz himself acknowledges in the article that there is no scientific evidence to document that thirdhand smoke is hazardous to children and infants. According to the article, Dr. Glantz "is not aware of any studies directly linking third-hand smoke to disease."
So if there isn't scientific evidence linking thirdhand smoke with disease, then how can the anti-smoking researcher claim that thirdhand smoke causes lead poisoning?
The answer is that you don't need science behind you to make health claims in the tobacco control movement. You can make any claim you want and rest assured that virtually no one within the tobacco control movement is going to publicly question your statement. Sure, there may be some private discussions in which researchers whisper between themselves how unsupported the claim is. But there is no danger of the dissenting opinions becoming public, because dissent on issues like this is simply not allowed in this religious-like movement.
I am certainly not aware of any evidence that the levels of lead in household dust in homes with a smoker are high enough to cause lead poisoning in infants. For that matter, I am not aware of any evidence that the toxins in thirdhand smoke are ingested or inhaled to the level necessary to actually cause harm to children.
To be sure, speculation is reasonable. But if you're going to speculate, you need to make it clear that what you are doing is speculating. The Pediatrics article and this interview are not what I would characterize as speculation. Both make definitive health claims: that thirdhand smoke causes health damage to infants and children. And to the best of my knowledge, these health claims are not supported by any actual evidence.
It also seems rather obnoxious to call smokers "contaminated" and emphasize that they are "emitting toxins," without having any evidence that such "toxins" are actually causing health damage to nonsmokers. I may well have detectable levels of "toxins" from the smoke to which I am exposed from my pellet stove, but it would not be fair to say that I am contaminated and emitting toxins. (I did fall into a pile of metal hydroxide sludge once and I admit that at that moment I was contaminated.)
I also don't understand exactly what the point is. Is it to cast smokers as social outcasts who should be spurned from society and not allowed to have any contact with "the rest of us?" Is it to try to stimulate efforts to ban smokers from being child care providers or teachers? Because if it is true that smokers are contaminated and emitting toxins, then we certainly wouldn't want our children to be exposed to those toxins in day care centers or schools.
Another curious statement in the article is that "Studies in rats suggest that tobacco toxin exposure is the leading cause of sudden infant death syndrome (SIDS)." How could studies in rats possibly indicate the degree to which tobacco exposure is causing SIDS in humans? One would certainly need epidemiologic studies, not merely rat studies, to determine the extent to which tobacco smoke exposure is causing SIDS in humans.
While the article concludes by suggesting that the thirdhand smoke danger points to the need for all smokers to quit, I am afraid that the hysterical nature of the thirdhand smoke claims may actually do the opposite. It may convince many smokers that the anti-smoking folks are fanatics and that they should stop listening to this hysteria. It may also undermine the public's appreciation of the hazards of secondhand smoke and convince many smokers not to bother smoking outside of the home (since their children would be damaged anyway by the thirdhand smoke).
One final note. We've known about the offgassing of constituents from tobacco smoke that has absorbed on surfaces for a long time. What scientific evidence is new such that it would warrant a public education campaign about thirdhand smoke?
The most interesting aspect of this story to me is not that an anti-smoking researcher would make unsubstantiated and somewhat hysterical assertions like these, but that almost no one within the movement is willing to publicly challenge these assertions.
Monday, January 19, 2009
Anti-Smoking Advocate Tells Public that Thirdhand Smoke is Just as Lethal as First or Secondhand Smoke
An anti-smoking advocate who was a local coordinator of a state-funded anti-smoking group has communicated to the public, through a letter published in the Jamestown Post-Journal, that thirdhand smoke - the remnants of smoking that remain around smokers and on on surfaces - is just as lethal as active smoking or secondhand smoke exposure.
According to the letter: "Third-hand smoke is the toxic remnants of smoking that surround smokers and lingers in the air and on the surfaces exposed to second-hand smoke. It's just as lethal as first and second hand smoke, especially for kids."
The letter was written by Sam Vanstrom, who apparently was the coordinator of Chautauqua County Reality Check. According to a minor league baseball web site: "Reality Check is a youth-led action program that seeks to expose the manipulative and deceptive marketing tactics of the tobacco industry and to educate the community though civic action, engaging community members and leaders. It is part of a comprehensive tobacco control program developed by the New York State Department of Health." The Reality Check web site confirms that its mission is to challenge the deceptive practices of the tobacco companies and educate the community about the truth.
The Rest of the Story
It looks like the anti-smoking group and/or its advocate is the one who needs the reality check. There is no evidence that thirdhand smoke is as deadly as active smoking or secondhand smoke exposure. Nor is there any evidence that thirdhand smoke is lethal in the first place.
What the evidence actually shows is that thirdhand smoke produces very small levels of exposure and that these low levels of exposure have not been found to have any significant effect. There is absolutely no evidence that these very low levels of exposure are lethal -- i.e., that they can cause death.
I find it ironic that someone who coordinated a program whose goal is to challenge the deceptive practices of the tobacco industry would resort to deceptive practices to scare people about the effects of thirdhand tobacco smoke. The Reality Check organization is supposed to be about exposing the deception of the tobacco industry and telling the truth to the public. But its former coordinator is doing just the opposite.
How are Reality Check and similar organizations going to have any credibility when anti-smoking advocates who are part of these groups are spreading deception on very basic scientific issues, where they have no evidence to support their claims?
I think the tobacco control movement urgently needs a reality check of its own.
(Thanks to JustTheFacts for the tip.)
According to the letter: "Third-hand smoke is the toxic remnants of smoking that surround smokers and lingers in the air and on the surfaces exposed to second-hand smoke. It's just as lethal as first and second hand smoke, especially for kids."
The letter was written by Sam Vanstrom, who apparently was the coordinator of Chautauqua County Reality Check. According to a minor league baseball web site: "Reality Check is a youth-led action program that seeks to expose the manipulative and deceptive marketing tactics of the tobacco industry and to educate the community though civic action, engaging community members and leaders. It is part of a comprehensive tobacco control program developed by the New York State Department of Health." The Reality Check web site confirms that its mission is to challenge the deceptive practices of the tobacco companies and educate the community about the truth.
The Rest of the Story
It looks like the anti-smoking group and/or its advocate is the one who needs the reality check. There is no evidence that thirdhand smoke is as deadly as active smoking or secondhand smoke exposure. Nor is there any evidence that thirdhand smoke is lethal in the first place.
What the evidence actually shows is that thirdhand smoke produces very small levels of exposure and that these low levels of exposure have not been found to have any significant effect. There is absolutely no evidence that these very low levels of exposure are lethal -- i.e., that they can cause death.
I find it ironic that someone who coordinated a program whose goal is to challenge the deceptive practices of the tobacco industry would resort to deceptive practices to scare people about the effects of thirdhand tobacco smoke. The Reality Check organization is supposed to be about exposing the deception of the tobacco industry and telling the truth to the public. But its former coordinator is doing just the opposite.
How are Reality Check and similar organizations going to have any credibility when anti-smoking advocates who are part of these groups are spreading deception on very basic scientific issues, where they have no evidence to support their claims?
I think the tobacco control movement urgently needs a reality check of its own.
(Thanks to JustTheFacts for the tip.)
Thursday, January 15, 2009
New Study Advises that Practitioners Emphasize Effects of Smoking on Obesity; However, Study Doesn't Find Such Effects
A new study published in the just-released February issue of the American Journal of Public Health examines the relationship between adolescent smoking on obesity in early adulthood (see: Saarni SE, et al. Association of smoking in adolescence with abdominal obesity in adulthood: a follow-up study of 5 birth cohorts of Finnish twins. Am J Public Health 2009; 99:348-354).
This study was a prospective cohort study involving five different birth cohorts of Finnish twins, with a total sample size of more than 4,000. They were followed for approximately 11 years, between the ages of 16 and 27. The risk of abdominal obesity in young adulthood was related to whether the individual was a smoker in adolescence, while controlling for a number of potential confounding variables, including diet, physical activity, socioeconomic status, parental body mass index, and individual body mass index.
The study reports that without the confounding variables, there was a significant elevation of the odds ratio for obesity (OR = 1.77; 95% confidence interval, 1.39-2.26). After controlling for the potential confounders, there was no significant elevation of the odds ratio for obesity (OR = 1.34; 95% confidence interval, 0.95-1.88).
The study acknowledges that it failed to find a statistically significant relationship between smoking and obesity and that this may be explained by the hypothesis that it is other factors - not smoking itself - that lead smokers to tend to have a higher incidence of obesity. As the authors state: "The increase in the risk of abdominal obesity or overweight among the women was no longer statistically significant in the fully adjusted models. This may have been caused by insufficient statistical power. Another possible interpretation of our findings is that adolescent smoking is a proxy for other factors or is part of a cluster of factors predisposing to later abdominal obesity."
The authors conclude that: "Given the greater risk of overweight and abdominal obesity among girls who smoked daily and the fact that adolescent smoking is often associated with preoccupation with weight, emphasizing the deleterious effect of smoking on abdominal fat accumulation could be effective in smoking prevention among young women."
The Rest of the Story
Wait one second here. The study fails to find a significant relationship between adolescent smoking and obesity in young adulthood after confounding variables - such as diet, physical activity, parental BMI, and individual BMI - are accounted for. The study acknowledges that one interpretation of the findings is that smoking may simply be a proxy for other factors (such as other health behaviors) that actually are influencing obesity. But then the study concludes by advising readers that we should be telling the public (emphasizing to the public, no less) that one of the deleterious effects of smoking is to cause obesity later in life.
Do you mean to tell me that even though the study cannot conclude that smoking causes obesity, we should tell the public that smoking causes obesity because it might lead to a decrease in smoking initiation?
This is definitely an example of viewing the ends as justifying the means. Because reducing smoking initiation is a good thing, it doesn't matter if we lie to people about the effects of smoking or give them information which is not scientifically supported.
What's most odd is that this conflicting information appears in the very same paper. This suggests that the authors of the study are not concerned about the validity of the information that they are recommending be disseminated to the public.
When the study controlled for all the confounders, including body mass index at age 24, the association between smoking and obesity was no longer statistically significant. This suggests to me that the reason why smoking at an early age is associated with obesity later in life is most likely that smokers tend to have a constellation of poor health habits, including poorer diet and less physical activity. It is most likely that these factors, and not the smoking itself, is what is causing them to become obese.
This doesn't mean that smoking is not associated with obesity; it just means that the relationship is not a causal one. I think what this study really points to is the fact that smoking is just one of a constellation of health behaviors that tend to coincide, including smoking, poor diet, and inadequate physical activity. It is these other behaviors which are directly related to obesity. Smoking just happens to be associated with obesity because it is related to these other causal factors. But once you adequately control for these other factors, smoking is no longer significantly associated with obesity.
In fact, there is not a lot of biological plausibility for such an effect. The paper does not in fact outline any potential mechanisms by which smoking could cause obesity. There is some evidence that smoking may help keep a little bit of weight off, but not so much for the reverse. I think, again, that the most likely explanation here is not that smoking is causing obesity, but that smokers also tend to have poorer behaviors in other areas which lead to the obesity.
This research is still important, because it reinforces that smoking fulfills a need for teens. Teens who are less self-confident and lack self-esteem are more likely to smoke. But they are also more likely to engage in other unhealthy behaviors. This research suggests that public health practitioners may not want to treat smoking, diet, and physical activity separately, but that there may be a unifying cause for poor health behavior in general, and that perhaps we should try to focus more on the underlying reasons for youths to engage in poor health behaviors. There is too much compartmentalization in how we deal with adolescent health issues, and perhaps we need to take a more holistic approach.
But the one thing the paper does not demonstrate is that smoking during adolescence causes obesity or has deleterious efects on abdominal fat accumulation. The authors of the study themselves admit this. The authors themselves point out a plausible alternative explanation for the study findings - that "adolescent smoking is a proxy for other factors ... predisposing to later abdominal obesity." However, this does not stop them from recommending that public health practitioners should be "emphasizing the deleterious effect of smoking on abdominal fat accumulation...".
They could have made that recommendation without conducting the study. In fact, they would actually have been more justified in making that recommendation prior to conducting the study, because at that point there was reasonable speculation about the hypothesis. The study, however, suggests that the hypothesis is incorrect and it removes any justification for telling the public that smoking causes obesity.
As we saw with the thirdhand smoke issue, however, science doesn't appear to be necessary in tobacco control. Anti-smoking groups and advocates are communicating information to the public without any scientific evidence to back it up. Apparently, the attitude is that since this is all for a good cause, it is acceptable to lie or deceive the public.
Needless to say, I disagree. I think that as public health researchers and advocates, we have an ethical responsibility to communicate accurate information to the public and to be able to back up our communications with solid scientific evidence.
As I'm finding out, that's not happening in tobacco control.
This study was a prospective cohort study involving five different birth cohorts of Finnish twins, with a total sample size of more than 4,000. They were followed for approximately 11 years, between the ages of 16 and 27. The risk of abdominal obesity in young adulthood was related to whether the individual was a smoker in adolescence, while controlling for a number of potential confounding variables, including diet, physical activity, socioeconomic status, parental body mass index, and individual body mass index.
The study reports that without the confounding variables, there was a significant elevation of the odds ratio for obesity (OR = 1.77; 95% confidence interval, 1.39-2.26). After controlling for the potential confounders, there was no significant elevation of the odds ratio for obesity (OR = 1.34; 95% confidence interval, 0.95-1.88).
The study acknowledges that it failed to find a statistically significant relationship between smoking and obesity and that this may be explained by the hypothesis that it is other factors - not smoking itself - that lead smokers to tend to have a higher incidence of obesity. As the authors state: "The increase in the risk of abdominal obesity or overweight among the women was no longer statistically significant in the fully adjusted models. This may have been caused by insufficient statistical power. Another possible interpretation of our findings is that adolescent smoking is a proxy for other factors or is part of a cluster of factors predisposing to later abdominal obesity."
The authors conclude that: "Given the greater risk of overweight and abdominal obesity among girls who smoked daily and the fact that adolescent smoking is often associated with preoccupation with weight, emphasizing the deleterious effect of smoking on abdominal fat accumulation could be effective in smoking prevention among young women."
The Rest of the Story
Wait one second here. The study fails to find a significant relationship between adolescent smoking and obesity in young adulthood after confounding variables - such as diet, physical activity, parental BMI, and individual BMI - are accounted for. The study acknowledges that one interpretation of the findings is that smoking may simply be a proxy for other factors (such as other health behaviors) that actually are influencing obesity. But then the study concludes by advising readers that we should be telling the public (emphasizing to the public, no less) that one of the deleterious effects of smoking is to cause obesity later in life.
Do you mean to tell me that even though the study cannot conclude that smoking causes obesity, we should tell the public that smoking causes obesity because it might lead to a decrease in smoking initiation?
This is definitely an example of viewing the ends as justifying the means. Because reducing smoking initiation is a good thing, it doesn't matter if we lie to people about the effects of smoking or give them information which is not scientifically supported.
What's most odd is that this conflicting information appears in the very same paper. This suggests that the authors of the study are not concerned about the validity of the information that they are recommending be disseminated to the public.
When the study controlled for all the confounders, including body mass index at age 24, the association between smoking and obesity was no longer statistically significant. This suggests to me that the reason why smoking at an early age is associated with obesity later in life is most likely that smokers tend to have a constellation of poor health habits, including poorer diet and less physical activity. It is most likely that these factors, and not the smoking itself, is what is causing them to become obese.
This doesn't mean that smoking is not associated with obesity; it just means that the relationship is not a causal one. I think what this study really points to is the fact that smoking is just one of a constellation of health behaviors that tend to coincide, including smoking, poor diet, and inadequate physical activity. It is these other behaviors which are directly related to obesity. Smoking just happens to be associated with obesity because it is related to these other causal factors. But once you adequately control for these other factors, smoking is no longer significantly associated with obesity.
In fact, there is not a lot of biological plausibility for such an effect. The paper does not in fact outline any potential mechanisms by which smoking could cause obesity. There is some evidence that smoking may help keep a little bit of weight off, but not so much for the reverse. I think, again, that the most likely explanation here is not that smoking is causing obesity, but that smokers also tend to have poorer behaviors in other areas which lead to the obesity.
This research is still important, because it reinforces that smoking fulfills a need for teens. Teens who are less self-confident and lack self-esteem are more likely to smoke. But they are also more likely to engage in other unhealthy behaviors. This research suggests that public health practitioners may not want to treat smoking, diet, and physical activity separately, but that there may be a unifying cause for poor health behavior in general, and that perhaps we should try to focus more on the underlying reasons for youths to engage in poor health behaviors. There is too much compartmentalization in how we deal with adolescent health issues, and perhaps we need to take a more holistic approach.
But the one thing the paper does not demonstrate is that smoking during adolescence causes obesity or has deleterious efects on abdominal fat accumulation. The authors of the study themselves admit this. The authors themselves point out a plausible alternative explanation for the study findings - that "adolescent smoking is a proxy for other factors ... predisposing to later abdominal obesity." However, this does not stop them from recommending that public health practitioners should be "emphasizing the deleterious effect of smoking on abdominal fat accumulation...".
They could have made that recommendation without conducting the study. In fact, they would actually have been more justified in making that recommendation prior to conducting the study, because at that point there was reasonable speculation about the hypothesis. The study, however, suggests that the hypothesis is incorrect and it removes any justification for telling the public that smoking causes obesity.
As we saw with the thirdhand smoke issue, however, science doesn't appear to be necessary in tobacco control. Anti-smoking groups and advocates are communicating information to the public without any scientific evidence to back it up. Apparently, the attitude is that since this is all for a good cause, it is acceptable to lie or deceive the public.
Needless to say, I disagree. I think that as public health researchers and advocates, we have an ethical responsibility to communicate accurate information to the public and to be able to back up our communications with solid scientific evidence.
As I'm finding out, that's not happening in tobacco control.
Tuesday, January 13, 2009
New Study Shows that Nicotine Replacement Therapy is Ineffective for Gradual Smoking Cessation, But Concludes the Opposite
Severe Financial Conflicts of Interest are Present and the Resulting Bias is Apparent; Failure to Disclose Conflicts of Interest Also Appears to be a Problem
An article published in the February issue of the American Journal of Preventive Medicine concludes that nicotine replacement therapy - specifically, nicotine gum - is effective in achieving sustained smoking cessation (see: Shiffman S, Ferguson SG, Strahs KR. Quitting by gradual smoking reduction using nicotine gum: a randomized controlled trial. American Journal of Preventive Medicine, February 2009) (press release here).
This was a randomized placebo-controlled trial of nicotine gum for smokers who expressed a desire to quit using gradual reduction of smoking. The chief study finding was that the use of nicotine gum resulted in a three-fold increase in the proportion of subjects who achieved six-month continuous abstinence (OR = 2.86; 95% confidence interval, 1.93, 4.24). The study concludes that "smokers wanting to quit by gradual reduction can substantially increase their success by using nicotine gum to facilitate reduction and cessation. ... Offering this new way to use NRT may enhance the appeal and reach of a treatment that increases success, and thereby have positive public health impact."
The Rest of the Story
While the use of nicotine gum did result in a three-fold increase in the proportion of subjects who achieved six-month abstinence from smoking, the absolute proportion of these subjects was extremely low. Only 5.9% of subjects receiving nicotine gum achieved six-month abstinence, compared to 2.1% of those receiving placebo.
In my view, these results indicate that the use of nicotine replacement therapy was a dismal failure. The appropriate policy recommendation would be to encourage smokers who desire to quit to do so cold turkey. Cessation rates over six-months for cold turkey quitting are better than those observed here for quitting with the aid of nicotine gum. Thus, it is a very biased recommendation to encourage the national use of nicotine gum among subjects who express a desire to quit smoking gradually. From a policy perspective, it would be far more effective to encourage and stimulate smokers who desire to quit to do so cold turkey. This is what the scientific evidence, and the results of this paper itself, actually support.
The extreme bias in the conclusions of this paper would not be so problematic if it were not for the fact that two of the three authors have severe financial conflicts of interest with Big Pharma, and that at least three of the principal investigators in the study have financial relationships with pharmaceutical companies. More specifically, each of these authors and principal investigators have financial relationships with pharmaceutical companies that manufacture smoking cessation medications.
Two of the study authors - Dr. Saul Shiffman and Dr. Stuart Ferguson from the University of Pittsburgh - have financial conflicts of interest by virtue of their employment at a firm that consults for GlaxoSmithKline Consumer Healthcare on issues related to nicotine replacement medication. In addition, Dr. Shiffman has a financial conflict of interest because he has a financial interest in a venture to develop new nicotine replacement medications.
According to the article: "Through their work at Pinney Associates, Drs. Shiffman and Ferguson serve as consultants to GSKCH [GlaxoSmithKline Consumer Healthcare] on matters related to smoking control and/or nicotine replacement medications. Dr. Shiffman also has a financial interest in a venture to develop new nicotine replacement medications." These financial relationships are confirmed elsewhere.
Three of the principal investigators on the study at academic clinical sites also appear to have financial relationships with pharmaceutical companies:
Dr. David Gonzales (Oregon Health Sciences University): "Dr. Gonzales has received research contracts from Pfizer, Sanofi-Aventis, GlaxoSmithKline, Addex Pharmaceuticals, and Nabi Biopharmaceuticals and consulting fees and honoraria from Pfizer, Sanofi-Aventis, and GlaxoSmithKline and owns 5 shares of Pfizer stock."
Dr. Stephen Rennard (University of Nebraska Medical Center): "Dr. Rennard has had or currently has a number of relationships with companies who provide products and/or services relevant to outpatient management of chronic obstructive pulmonary disease. These relationships include serving as a consultant (for Adams, Almirall, Altana, Array Biopharma, AstraZeneca, Aventis, Biolipox, Centocor, Dey, Critical Therapeutics, GlaxoSmithKline, Johnson & Johnson, Merck, Novartis, Ono Pharma, Otsuka, RJ Reynolds, Roche, Sankyo, Schering-Plough, Scios, and Wyeth), advising regarding clinical trials (Altana, AstraZeneca, Aventis, Centocor, GlaxoSmithKline, Novartis, Pfizer, and Philip Morris), speaking at continuing medical education programs and performing funded research at both basic and clinical levels (Altana, AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline, and Novartis)."
Dr. Nancy Rigotti (Massachusetts General Hospital): "In the past 5 years, Dr Rigotti has received research grant funding from Pfizer, GlaxoSmithKline, Sanofi Aventis, and Nabi Biopharmaceuticals and has consulted for Pfizer and Sanofi Aventis. These companies have investigational or marketed smoking cessation medications."
There are a number of problems with the disclosure of these financial conflicts of interest. First, while the financial conflicts of interest of the study authors are revealed in the paper itself, they are not disclosed in the press release, so far as I can tell. Thus, reporters and members of the public who read these results and conclusions in the press release, but do not read the full article are not aware of the severe financial conflicts of interest of Dr. Shiffman and Dr. Ferguson.
Second, even in the article itself, the financial conflicts of interest of the study site principal investigators are not disclosed. I was able to find out about these financial conflicts only after hours of research using databases that are not publicly available. I think readers of this article would be shocked to find out, for example, that the principal investigator of this study at the University of Nebraska Medical Center has reported having consulted for GlaxoSmithKline, manufacturer of nicotine gum, as well as for 20 other pharmaceutical companies. This type of information, especially because it is not disclosed, really puts the validity of the study findings and conclusions in question.
The study does not even mention how smoking status was ascertained, who asked the question, who recorded the result, and whether the individual conducting the assessment was blinded as to the subject's intervention vs. placebo status. To have principal investigators of a clinical trial who are financially conflicted and not to reveal this in a manuscript summarizing the findings is extremely problematic. In my view, it violates ethical standards of conduct, since I believe all such financial relationships should be disclosed in the paper.
Beyond the apparent failure of disclosure of financial conflicts of interest of several of the study site principal investigators, an additional problem is the fact that principal investigators at academic institutions were allowed to serve in that capacity in the first place, given that this was a clinical trial in which an actual drug being marketed by the company of interest was being tested in human subjects, and among whom there was a risk of adverse events, which were monitored in the study.
At my institution, it would be extremely unlikely that we would allow an individual with this type of conflict of interest to serve as the principal investigator on a clinical trial such as this. When human subjects are involved in research, conflicted principal investigators are generally not acceptable, unless there is a major compelling reason to make an exception. It would be interesting to know whether conflict of interest advisory committees at the University of Pittsburgh, Massachusetts General Hospital, University of Nebraska Medical Center, and Oregon Health Sciences University reviewed these cases, and if so, what their justifications were for allowing individuals with financial relationships with pharmaceutical companies that manufacture smoking cessation products to serve as principal investigators on a clinical trial involving potential significant risks to human subjects.
It would also be of interest to know whether the human subjects at these institutions were informed of these conflicts of interest of their site principal investigators.
Also of interest would be knowing whether there were procedures in place to ensure that the conflicted principal investigator had no role in collecting or analyzing data in the study. This point, however, is almost moot since by definition, the principal investigator is the primary person with responsibility for the collection and analysis of the data, even if others are performing the primary tasks.
Readers may want to note that the fact that the study was funded by GlaxoSmithKline Consumer Healthcare is not of primary concern to me. My concern is over the financial conflicts of interest of study authors and principal investigators, not with the overall funding by a pharmaceutical company. The funding itself does not represent a financial conflict of interest. The conflict of interest comes from the fact that the study authors and some of the site principal investigators appear to have signficant financial relationships with pharmaceutical companies, including the company that manufacturers nicotine gum and others that manufacture other nicotine replacement therapy or smoking cessation medications.
I do find it problematic that the University of Pittsburgh apparently allowed Dr. Shiffman and Dr. Ferguson to serve as principal investigators of the overall study (which they appear to be since they are the authors of the summary article), since they have significant financial conflicts of interest and because this is human subjects research.
The conflict of interest calls into question the integrity of the process by which study site data were collected, combined, and analyzed. This is not because of any suspicion of anything less than honorable character and intent among the authors. It is because a financial conflict of interest can create an unconscious bias which may be perceived as affecting the conduct of the study and the reporting of the study results.
Let me also take this opportunity to emphasize that I am not accusing anyone of intentional wrongdoing or any lack of individual integrity. Bias related to conflicts of interest can be completely subconscious. But that is precisely why they need to be eliminated or managed properly.
There is little doubt in my mind that the financial conflicts of interest inherent in this research led to a bias (albeit unconscious) in the interpretation and presentation of the study findings and conclusions. Obviously, it led to a much more positive reporting of the findings than was warranted. In fact, I would go so far as to state that the study conclusion is unsupported by the study findings. Nicotine gum should not be recommended for these patients; they should be encouraged to quit smoking cold turkey.
While differences of opinion are appropriate and expected, when one opinion that is being widely disseminated with an eye towards affecting national policy is influenced by a financial conflict of interest - and especially when that conflict is not adequately disclosed - this is problematic.
Finally, while Dr. Shiffman's conflict of interest is disclosed in this article, it does not appear to be disclosed in another article he wrote about women's success in smoking cessation (see: Shiffman S. How when matters for quitting and relapse [commentary]. Addiction 2008; 103:822-823).
That article discusses factors that relate to the success of smoking cessation among women and treatment for smoking cessation and prevention of relapse. Thus, it would seem that Dr. Shiffman's conflict of interest by virtue of his consulting for GlaxoSmithKline and his venture to develop new smoking cessation medications would be relevant. However, this conflict of interest does not appear to be disclosed in the article. The declaration of interest statement says only: "The author is a co-founder of invivodata, inc., which provides electronic diaries for clinical trials."
If anything, I would think that the conflict of interest with a pharmaceutical company that manufacturers products for treatment of nicotine dependence and the interest in a venture to develop new such treatments would be of even more relevance than the interest in electronic diaries, which actually don't seem to be particularly relevant here. But the point is, if electronic diaries were thought to be relevant, then why weren't the pharmaceutical conflicts of interest disclosed?
It's always possible that I'm missing something here. I've examined the full text of the articles mentioned as well as the press release in detail.
The rest of the story is that this research appears to be an example of: (1) Failure to disclose relevant financial conflicts of interest in a study press release; (2) Failure to disclose some relevant conflicts of interest in the study itself; and (3) Inappropriate conflicts of interest among principal investigators on human subjects research.
That these issues are arising in tobacco control research does not come as a surprise to me.
For a previous discussion of the inappropriate role of conflicts of interest in tobacco control research and policy, see the following posts:
Executive Director of Campaign for Tobacco-Free Kids Violates President-Elect Obama's New Rules for Lobbyists on Transition Team
New Report Warns of Serious Risk Profile of Chantix; Recommendation of Chantix by Anti-Smoking Researchers with Conflicts of Interest is UnacceptableInternational Tobacco Control List-Serve and Discussion Site Now Sponsored by Big Pharma
Chantix Lawsuits Piling Up; Dangers from Severe Financial Conflicts of Interests of Tobacco Control Researchers and Institutions Revealed
With $50,000 in Annual Resources from GlaxoSmithKline, Chair of Expert Panel on Smoking Cessation Should Have Recused Himself, or Been Removed
Press Release on Smoking Cessation Guidelines Fails to Disclose Financial Conflict of Interest of Expert Panelists
NIH Expert Panel Recommends Smoking Cessation Pharmaceuticals for Every Smoking Patient; Panel Chair and 8 Members Have Financial Ties to Big Pharma Financial Conflict of Interest Not Disclosed in Article on Smoking Cessation; Another Example of Failed Disclosure in Tobacco Control Research
Weill Cornell Medical College Again Defends Researcher's Failure to Disclose Tobacco Funding and Financial Conflict of Interest
Monday, January 12, 2009
Original Study on Thirdhand Smoke Does Not Support Conclusion that Health Threat is Significant
It is important to evaluate the original study which is being used to support the idea that thirdhand smoke poses a significant risk to nonsmokers, especially to children and infants. That study appeared in Tobacco Control in 2004 (see: Matt GE, et al. Households contaminated by environmental tobacco smoke: sources of infant exposures. Tobacco Control 2004; 13:29-37).
The study compares airborne nicotine levels and urine cotinine levels in rooms and infants, respectively, in three settings:
1. Homes in which there are no smokers (referred to in the study as "no exposure").
2. Homes in which there are smokers, but they report making great efforts not to expose the infant (referred to in the study as "indirect exposure").
3. Homes in which there are smokers who do not report making great efforts not to expose the infant (referred to in the study as "direct exposure").
The major findings of the study are that air nicotine levels were 2-3 times higher in homes under the indirect exposure conditions as compared to the no exposure condition and that urine cotinine levels of infants living in indirect exposure conditions were about 8 times higher than among infants living in no exposure conditions. Based on these findings, the article (and subsequent articles which use this as a basis) concludes that thirdhand smoke is a significant health hazard.
The Rest of the Story
There are so many aspects of the rest of the story that it's difficult to know where to begin. To make it easier to follow, let me number each point.
1. Twice As High As a Miniscule Number is Also a Miniscule Number
While at first glance it may sound dangerous to have airborne nicotine levels that are twice as high as in a nonsmoking home, the level of nicotine in nonexposure homes is so low that even at twice this level, it does not appear to represent any substantial health threat. The average airborne nicotine level in nonexposure homes was about 0.1 ug/m3 (micrograms per cubic meter). In indirect exposure homes, the average nicotine level was between 0.2 and 0.3 ug/m3. These are extremely low levels; in fact, they are lower than levels which have been measured in many nonsmoking environments. So the simple fact that nicotine levels in indirect exposure conditions was twice as high as in direct exposure conditions does not necessarily mean that thirdhand smoke is a substantial health risk. In fact, based on the nicotine levels reported in the paper, it does not appear that thirdhand smoke results in airborne exposure to nicotine that is high enough to represent a significant health risk.
2. Some of the Indirect Exposure Homes in the Study Were Almost Certainly Direct Exposure Homes
The study relies upon self-report to determine whether parents smoke in the home or not. Almost certainly, parents are going to under-report smoking in the home. Given the societal scorn that is placed upon parents who expose their children to secondhand smoke (believe it or not, some anti-smoking groups and advocates go so far as to call them child abusers), it is not surprising that in a survey, parents are going to be hesitant to admit that they do smoke in the home around the child.
Thus, the indirect exposure condition almost certainly contains a number of homes in which the parents do smoke around the child. This misclassification severely biases the results of the study and makes it impossible to conclude that the levels of exposure of infants in "indirect" exposure homes is actually due to thirdhand smoke, rather than to secondhand smoke.
Ironically, one way to verify the presence of absence of smoking in the household would be to measure ambient nicotine levels, which would indicate whether smoking is taking place or not. So ironically, this study uses as an outcome measure a variable that actually should have been used as a verification of the parents' non-smoking status in the home.
To make matters worse, most of the homes had multiple smokers, so even if the parent interviewed was telling the truth, it may have been the case that another household member smoked inside the home. Even worse, a large proportion of these infants were exposed directly to smokers outside the home, which could well explain their elevated cotinine levels. In fact, in the indirect exposure group, one-third of the respondents reported that the infant had visited someone who smokes in the past 30 days. Thus, these subjects should not have been used in the study, especially for the measurement of cotinine levels, because it messes up the results.
While many parents in the indirect exposure group reported not smoking in the home in the past 30 days, 8% admitted to smoking in the home occasionally. These cannot be used as true indirect exposure homes, since the parent is admitting to smoking inside the home.
The bottom line is that this study is almost certainly not measuring the true exposure of infants who live in conditions in which parents never smoke in the home. These results therefore cannot be used reliably to evaluate the risk of thirdhand smoke.
3. Examining the Minimum Exposure Levels Appears to Confirm that if Stringently Adhered to, Smoking Outside the Home Results in No Significant Airborne Nicotine
Given the likelihood that many of the indirect exposure homes were actually direct exposure homes, it now becomes important to examine the minimum airborne nicotine levels in these homes. Importantly, the minimum airborne nicotine level in an indirect exposure home was about 0.1 ug/m3. This is no different from the airborne nicotine level in a nonexposure home. It therefore suggests that it is possible to smoke outside the home and to have the infant exposed to no significant airborne nicotine inside the home.
More provocatively, perhaps what the range of airborne nicotine levels indicates is the degree to which smoking is taking place inside the home, rather than the differences between homes, all of which represent the complete absence of any smoking.
The bottom line here is that it is possible for a smoker to protect the infant from any significant airborne nicotine exposure by smoking outside the home and perhaps taking other measures (such as ensuring that doors and windows are shut when smoking).
It is also interesting to note that the minimum level of nicotine in dust from the indirect exposure homes was 0. Again, this confirms that it is possible to have no infant airborne or dust nicotine exposure, even though the parent is a regular smoker.
This same pattern of results held for urine cotinine measurements as well.
4. The Study Does Not Acknowledge Any of These Limitations
Most concerning and worrisome to me is that the paper does not acknowledge as a limitation the possibility that parents are not being accurate in their reporting of smoking inside the home. We know that there is significant under-reporting even of just a person's smoking status. In other words, people are reluctant to even admit that they smoke, much less to admit that they smoke in the presence of infants. If there is significant under-reporting of smoking status, then the under-reporting of smoking in the presence of infants has to be very substantial.
That this is not even mentioned in the paper is concerning and has two important implications. First, it renders the conclusions of the study invalid. If researchers cannot defend their conclusions against the most plausible and likely limitation such as this, then there are plausible alternative explanations of the study findings, and the study conclusion cannot be accepted.
Second, it raises the spectre of investigator bias. One would not expect to see an omission of this magnitude in a situation where the researchers were free of substantial bias. Unfortunately, it raises the possibility that the researchers were trying to show that thirdhand smoke is harmful, rather than to objectively discover whether there is significant child exposure to tobacco smoke toxins when a parent is careful to never smoke in the home or around the child.
For further commentary on this study, see the insightful discussion of the study's conclusions and limitations over at Velvet Glove Iron Fist.
See also Dr. Alan Blum's take on the thirdhand smoke issue at The Birmingham News blog.
And here is Sandy Swarc's commentary on the issue over at her Junkfood Science blog.
The study compares airborne nicotine levels and urine cotinine levels in rooms and infants, respectively, in three settings:
1. Homes in which there are no smokers (referred to in the study as "no exposure").
2. Homes in which there are smokers, but they report making great efforts not to expose the infant (referred to in the study as "indirect exposure").
3. Homes in which there are smokers who do not report making great efforts not to expose the infant (referred to in the study as "direct exposure").
The major findings of the study are that air nicotine levels were 2-3 times higher in homes under the indirect exposure conditions as compared to the no exposure condition and that urine cotinine levels of infants living in indirect exposure conditions were about 8 times higher than among infants living in no exposure conditions. Based on these findings, the article (and subsequent articles which use this as a basis) concludes that thirdhand smoke is a significant health hazard.
The Rest of the Story
There are so many aspects of the rest of the story that it's difficult to know where to begin. To make it easier to follow, let me number each point.
1. Twice As High As a Miniscule Number is Also a Miniscule Number
While at first glance it may sound dangerous to have airborne nicotine levels that are twice as high as in a nonsmoking home, the level of nicotine in nonexposure homes is so low that even at twice this level, it does not appear to represent any substantial health threat. The average airborne nicotine level in nonexposure homes was about 0.1 ug/m3 (micrograms per cubic meter). In indirect exposure homes, the average nicotine level was between 0.2 and 0.3 ug/m3. These are extremely low levels; in fact, they are lower than levels which have been measured in many nonsmoking environments. So the simple fact that nicotine levels in indirect exposure conditions was twice as high as in direct exposure conditions does not necessarily mean that thirdhand smoke is a substantial health risk. In fact, based on the nicotine levels reported in the paper, it does not appear that thirdhand smoke results in airborne exposure to nicotine that is high enough to represent a significant health risk.
2. Some of the Indirect Exposure Homes in the Study Were Almost Certainly Direct Exposure Homes
The study relies upon self-report to determine whether parents smoke in the home or not. Almost certainly, parents are going to under-report smoking in the home. Given the societal scorn that is placed upon parents who expose their children to secondhand smoke (believe it or not, some anti-smoking groups and advocates go so far as to call them child abusers), it is not surprising that in a survey, parents are going to be hesitant to admit that they do smoke in the home around the child.
Thus, the indirect exposure condition almost certainly contains a number of homes in which the parents do smoke around the child. This misclassification severely biases the results of the study and makes it impossible to conclude that the levels of exposure of infants in "indirect" exposure homes is actually due to thirdhand smoke, rather than to secondhand smoke.
Ironically, one way to verify the presence of absence of smoking in the household would be to measure ambient nicotine levels, which would indicate whether smoking is taking place or not. So ironically, this study uses as an outcome measure a variable that actually should have been used as a verification of the parents' non-smoking status in the home.
To make matters worse, most of the homes had multiple smokers, so even if the parent interviewed was telling the truth, it may have been the case that another household member smoked inside the home. Even worse, a large proportion of these infants were exposed directly to smokers outside the home, which could well explain their elevated cotinine levels. In fact, in the indirect exposure group, one-third of the respondents reported that the infant had visited someone who smokes in the past 30 days. Thus, these subjects should not have been used in the study, especially for the measurement of cotinine levels, because it messes up the results.
While many parents in the indirect exposure group reported not smoking in the home in the past 30 days, 8% admitted to smoking in the home occasionally. These cannot be used as true indirect exposure homes, since the parent is admitting to smoking inside the home.
The bottom line is that this study is almost certainly not measuring the true exposure of infants who live in conditions in which parents never smoke in the home. These results therefore cannot be used reliably to evaluate the risk of thirdhand smoke.
3. Examining the Minimum Exposure Levels Appears to Confirm that if Stringently Adhered to, Smoking Outside the Home Results in No Significant Airborne Nicotine
Given the likelihood that many of the indirect exposure homes were actually direct exposure homes, it now becomes important to examine the minimum airborne nicotine levels in these homes. Importantly, the minimum airborne nicotine level in an indirect exposure home was about 0.1 ug/m3. This is no different from the airborne nicotine level in a nonexposure home. It therefore suggests that it is possible to smoke outside the home and to have the infant exposed to no significant airborne nicotine inside the home.
More provocatively, perhaps what the range of airborne nicotine levels indicates is the degree to which smoking is taking place inside the home, rather than the differences between homes, all of which represent the complete absence of any smoking.
The bottom line here is that it is possible for a smoker to protect the infant from any significant airborne nicotine exposure by smoking outside the home and perhaps taking other measures (such as ensuring that doors and windows are shut when smoking).
It is also interesting to note that the minimum level of nicotine in dust from the indirect exposure homes was 0. Again, this confirms that it is possible to have no infant airborne or dust nicotine exposure, even though the parent is a regular smoker.
This same pattern of results held for urine cotinine measurements as well.
4. The Study Does Not Acknowledge Any of These Limitations
Most concerning and worrisome to me is that the paper does not acknowledge as a limitation the possibility that parents are not being accurate in their reporting of smoking inside the home. We know that there is significant under-reporting even of just a person's smoking status. In other words, people are reluctant to even admit that they smoke, much less to admit that they smoke in the presence of infants. If there is significant under-reporting of smoking status, then the under-reporting of smoking in the presence of infants has to be very substantial.
That this is not even mentioned in the paper is concerning and has two important implications. First, it renders the conclusions of the study invalid. If researchers cannot defend their conclusions against the most plausible and likely limitation such as this, then there are plausible alternative explanations of the study findings, and the study conclusion cannot be accepted.
Second, it raises the spectre of investigator bias. One would not expect to see an omission of this magnitude in a situation where the researchers were free of substantial bias. Unfortunately, it raises the possibility that the researchers were trying to show that thirdhand smoke is harmful, rather than to objectively discover whether there is significant child exposure to tobacco smoke toxins when a parent is careful to never smoke in the home or around the child.
For further commentary on this study, see the insightful discussion of the study's conclusions and limitations over at Velvet Glove Iron Fist.
See also Dr. Alan Blum's take on the thirdhand smoke issue at The Birmingham News blog.
And here is Sandy Swarc's commentary on the issue over at her Junkfood Science blog.
Friday, January 09, 2009
Dr. Geoffrey Kabat's Take on the Thirdhand Smoke Issue
Dr. Geoffrey Kabat has published a commentary on the recent article warning of the dangers of thirdhand smoke. Dr. Kabat is a renowned epidemiologist and was a researcher for many years at the American Health Foundation in Valhalla. He is also the author of a recent book, entitled: " Hyping Health Risks: Environmental Hazards in Daily Life and the Science of Epidemiology."
As you will see, Dr. Kabat's take on the issue is very similar to my own.
As you will see, Dr. Kabat's take on the issue is very similar to my own.
Alex Beam on Thirdhand Smoke
I thought readers might be interested in seeing Alex Beam's column on thirdhand smoke, published today in the Boston Globe.
Thursday, January 08, 2009
Complete College Campus Smoking Ban Leading to Problems in Adjacent Neighborhoods
According to the Gazette (Montgomery County, MD), the all-out ban on smoking at Montgomery College has led to a problem of students going into adjacent neighborhoods to smoke and creating problems about which the neighbors have been complaining. A letter by the vice president of the college in yesterday's paper attempts to defend the policy.
The vice president writes: "Like many hospitals, schools and colleges, Montgomery College went tobacco-free to establish a clear and enforceable smoking policy, and to develop a healthy campus environment. At the Rockville campus, most students follow the "no smoking" policy and confine their smoking to off-campus locations along Mannakee Street and Rockville Pike. It is unfortunate that a small number of students have created problems by smoking, hanging out and littering on or near neighbors' properties. When the college first became aware of this issue, it took immediate action after talking with neighbors."
The Rest of the Story
It's not exactly clear to me how the Montgomery College becomes a healthy campus environment because the smokers who attend the college smoke on Mannakee Street or Rockville Pike rather than within the campus borders. How exactly does a student smoking on the opposite side of a street bordering the campus make the campus healthy, when if that same student smoked on the near side of the street, the campus would no longer be healthy? Frankly, this is stupidity.
It is kind of reminiscent of the logic beyond Boston's ban on the sale of tobacco by pharmacies. Somehow, it protects the public's health not to have pharmacies sell tobacco, but there's no problem if a convenience store or gas station sells tobacco. How exactly does it protect the public's health to make sure that people get their cigarettes at one type of establishment rather than another?
Yes, the anti-smoking movement is going too far. And it's going too far because it has lost its grounding in science. Moreover, it appears to have lost any semblance of reason as well.
The vice president writes: "Like many hospitals, schools and colleges, Montgomery College went tobacco-free to establish a clear and enforceable smoking policy, and to develop a healthy campus environment. At the Rockville campus, most students follow the "no smoking" policy and confine their smoking to off-campus locations along Mannakee Street and Rockville Pike. It is unfortunate that a small number of students have created problems by smoking, hanging out and littering on or near neighbors' properties. When the college first became aware of this issue, it took immediate action after talking with neighbors."
The Rest of the Story
It's not exactly clear to me how the Montgomery College becomes a healthy campus environment because the smokers who attend the college smoke on Mannakee Street or Rockville Pike rather than within the campus borders. How exactly does a student smoking on the opposite side of a street bordering the campus make the campus healthy, when if that same student smoked on the near side of the street, the campus would no longer be healthy? Frankly, this is stupidity.
It is kind of reminiscent of the logic beyond Boston's ban on the sale of tobacco by pharmacies. Somehow, it protects the public's health not to have pharmacies sell tobacco, but there's no problem if a convenience store or gas station sells tobacco. How exactly does it protect the public's health to make sure that people get their cigarettes at one type of establishment rather than another?
Yes, the anti-smoking movement is going too far. And it's going too far because it has lost its grounding in science. Moreover, it appears to have lost any semblance of reason as well.
Wednesday, January 07, 2009
IN MY VIEW: Why an Immediate Decrease in Heart Attacks Due to Reduced Secondhand Smoke Exposure is Implausible
For the sake of argument, let us assume that researchers at the CDC are correct and that a brief exposure to secondhand smoke, such as that experienced in a restaurant, can trigger a heart attack in someone who has severe, pre-existing coronary artery disease. Without even getting into the issue of how the CDC’s and Surgeon General’s statements (as well as those of hundreds of anti-smoking groups) fail to qualify their claims by making it clear that they apply only to those who severe coronary artery stenosis to begin with, let’s give them the benefit of the doubt for now and analyze the significance of the stipulated fact: a brief encounter with secondhand smoke can cause someone with severe coronary disease to suffer a heart attack by increasing the coagulation (clotting) potential of the blood platelets and causing endothelial dysfunction.
Anti-smoking researchers are touting studies like those in Helena, Pueblo and elsewhere – which they claim demonstrate a dramatic and immediate reduction in heart attacks caused by workplace/restaurant/bar smoking bans – as supporting the scientific claim that brief secondhand smoke exposure triggers a substantial number of heart attacks. The thinking is that if brief secondhand smoke exposure is triggering lots of heart attacks and that exposure is eliminated, then those heart attacks will be prevented.
The Rest of the Story
I think it is important to point out the flaw in this logic. First, readers should understand that in order for a brief tobacco smoke exposure to cause a heart attack, an individual must already have severe, pre-existing coronary artery stenosis. The coronary arteries do not go from completely patent (open) to closed off in a matter of minutes. However, if they are already severely compromised (say, more than 90% blocked), then it is possible that a small decrease in the artery diameter – such as that induced by formation of a clot on an existing plaque – could trigger a heart attack.
Second, readers should understand that there are a large number of acute “exposures” that can increase the coagulability of the blood and compromise endothelial function, thus potentially triggering a heart attack in someone with severe coronary artery narrowing. For example, eating a high-fat meal has been shown to cause endothelial dysfunction and to increase the stickiness of platelets to the same extent as secondhand smoke.
Importantly, even “exposures” such as stress can have the same effect. Researchers shows that stress – even the kind of mental stress induced by having an individual solve a difficult math problem – can cause the same kind of changes to the coronary circulation and the aggregation potential of platelets that acute exposure to secondhand smoke causes.
Third, it is important to note that the body does not know what is causing increased stickiness of blood platelets or endothelial dysfunction when it is occurring. In other words, there is nothing qualitatively different between changes induced by tobacco smoke exposure versus the same type of changes induced by stress or by eating a high-fat meal. There is nothing unique about the tobacco smoke exposure that distinguishes its effects from those precipitated by these other exposures.
Putting all of this together, the critical point is that someone who is at risk of having a heart attack triggered by a brief exposure to secondhand smoke has such brittle coronary artery disease that they are basically a heart attack waiting to happen. It is only a matter of time before some exposure puts them over the edge and triggers an inability of the coronary arteries to keep up with the oxygen demands of the heart and for a heart attack to therefore occur.
If the person is not exposed to tobacco smoke in a restaurant on Tuesday, who is to say that he or she will not eat a high-fat meal and have the final step of the heart attack pathway take place on Wednesday? Someone in such a brittle situation can simply not go around for a long time without experiencing cardiac ischemia. If they are so close to a heart attack that a 20-minute exposure to secondhand smoke could trigger such an attack by causing an increase in platelet aggregation, then the same degree of platelet aggregation caused by an acute stressful event is also going to trigger that heart attack.
The point is this: in such an individual, you cannot prevent a heart attack by eliminating all exposures that might increase the clotting ability of the blood or hamper endothelial function. Clinically, that would be be a crazy approach (and in fact would represent medical malpractice).
In such a situation, there are only two approaches that work. One is to prevent exposures from increasing the blood's clotting ability through medications such as aspirin (there are some other pharmaceutical approaches as well). The second is to repair the coronary artery stenosis through angioplasty or bypass surgery.
Any patient who has coronary artery stenosis so severe that a single acute exposure to secondhand smoke will trigger a heart attack needs to have a definitive procedure - such as angioplasty or coronary artery bypass surgery - immediately. You are simply not going to prevent a heart attack in that person by having them avoid secondhand smoke exposure. Something else is going to trigger that heart attack, and probably in short order. After all, the person cannot stop eating. She cannot eliminate all mental stress.
For this reason, it is implausible that reducing secondhand smoke exposure could result in a rapid 41% decline in heart attacks by eliminating cases of heart attacks triggered by acute secondhand smoke exposure in restaurants.
Let me say, also, that even if tobacco smoke were the sole trigger for heart attacks, the effects of eliminating exposure in restaurants alone is just not significant enough to explain a 41% reduction in heart attacks. But the reality is that tobacco smoke is just one of many potential triggers and even if occasionally tobacco smoke serves as a trigger, it is just not plausible that banning smoking in restaurants will substantially decrease heart attacks by putting an end to a common trigger for such attacks. They will simply be triggered by some other exposure.
I don't think the researchers who are using the studies of the Helena ilk to support the claim that brief exposures to secondhand smoke trigger heart attacks have thought this out to any extent.
By the way, if what these researchers are claiming is true, then it would actually be reasonable for a physician to tell a patient with severe coronary artery stenosis that he should simply avoid going to restaurants or other settings where there is smoking taking place. But such advice, we know, would be malpractice. If the patient's disease is that brittle, he is a heart attack waiting to happen and he needs definitive surgical intervention, probably with pharmaceutical intervention as well.
So even if we accept the claim that brief exposure to secondhand smoke is a common trigger for heart attacks among people with severe coronary artery stenosis, this would still not result in restaurant smoking bans causing any substantial decline in heart attacks in the short-term.
Note that smoking bans would still be expected to reduce heart attacks in the long-term, because over many years, the incidence of coronary artery disease would be reduced. But to posit that a heart attack decline on the order of 20% in one year or 40% in three years will occur in response to banning smoking in restaurants is simply implausible.
Finally, I would add that if it were true that exposure to tobacco smoke in restaurants was a common cause of heart attacks, would we not expect to occasionally observe someone in a restaurant keeling over from a heart attack? I've stipulated here, for the sake of argument, that the anti-smoking researchers' claim is true, but let's remember that it is merely a hypothetical or theoretical concern. There's no actual evidence that this is the case.
Anti-smoking researchers are touting studies like those in Helena, Pueblo and elsewhere – which they claim demonstrate a dramatic and immediate reduction in heart attacks caused by workplace/restaurant/bar smoking bans – as supporting the scientific claim that brief secondhand smoke exposure triggers a substantial number of heart attacks. The thinking is that if brief secondhand smoke exposure is triggering lots of heart attacks and that exposure is eliminated, then those heart attacks will be prevented.
The Rest of the Story
I think it is important to point out the flaw in this logic. First, readers should understand that in order for a brief tobacco smoke exposure to cause a heart attack, an individual must already have severe, pre-existing coronary artery stenosis. The coronary arteries do not go from completely patent (open) to closed off in a matter of minutes. However, if they are already severely compromised (say, more than 90% blocked), then it is possible that a small decrease in the artery diameter – such as that induced by formation of a clot on an existing plaque – could trigger a heart attack.
Second, readers should understand that there are a large number of acute “exposures” that can increase the coagulability of the blood and compromise endothelial function, thus potentially triggering a heart attack in someone with severe coronary artery narrowing. For example, eating a high-fat meal has been shown to cause endothelial dysfunction and to increase the stickiness of platelets to the same extent as secondhand smoke.
Importantly, even “exposures” such as stress can have the same effect. Researchers shows that stress – even the kind of mental stress induced by having an individual solve a difficult math problem – can cause the same kind of changes to the coronary circulation and the aggregation potential of platelets that acute exposure to secondhand smoke causes.
Third, it is important to note that the body does not know what is causing increased stickiness of blood platelets or endothelial dysfunction when it is occurring. In other words, there is nothing qualitatively different between changes induced by tobacco smoke exposure versus the same type of changes induced by stress or by eating a high-fat meal. There is nothing unique about the tobacco smoke exposure that distinguishes its effects from those precipitated by these other exposures.
Putting all of this together, the critical point is that someone who is at risk of having a heart attack triggered by a brief exposure to secondhand smoke has such brittle coronary artery disease that they are basically a heart attack waiting to happen. It is only a matter of time before some exposure puts them over the edge and triggers an inability of the coronary arteries to keep up with the oxygen demands of the heart and for a heart attack to therefore occur.
If the person is not exposed to tobacco smoke in a restaurant on Tuesday, who is to say that he or she will not eat a high-fat meal and have the final step of the heart attack pathway take place on Wednesday? Someone in such a brittle situation can simply not go around for a long time without experiencing cardiac ischemia. If they are so close to a heart attack that a 20-minute exposure to secondhand smoke could trigger such an attack by causing an increase in platelet aggregation, then the same degree of platelet aggregation caused by an acute stressful event is also going to trigger that heart attack.
The point is this: in such an individual, you cannot prevent a heart attack by eliminating all exposures that might increase the clotting ability of the blood or hamper endothelial function. Clinically, that would be be a crazy approach (and in fact would represent medical malpractice).
In such a situation, there are only two approaches that work. One is to prevent exposures from increasing the blood's clotting ability through medications such as aspirin (there are some other pharmaceutical approaches as well). The second is to repair the coronary artery stenosis through angioplasty or bypass surgery.
Any patient who has coronary artery stenosis so severe that a single acute exposure to secondhand smoke will trigger a heart attack needs to have a definitive procedure - such as angioplasty or coronary artery bypass surgery - immediately. You are simply not going to prevent a heart attack in that person by having them avoid secondhand smoke exposure. Something else is going to trigger that heart attack, and probably in short order. After all, the person cannot stop eating. She cannot eliminate all mental stress.
For this reason, it is implausible that reducing secondhand smoke exposure could result in a rapid 41% decline in heart attacks by eliminating cases of heart attacks triggered by acute secondhand smoke exposure in restaurants.
Let me say, also, that even if tobacco smoke were the sole trigger for heart attacks, the effects of eliminating exposure in restaurants alone is just not significant enough to explain a 41% reduction in heart attacks. But the reality is that tobacco smoke is just one of many potential triggers and even if occasionally tobacco smoke serves as a trigger, it is just not plausible that banning smoking in restaurants will substantially decrease heart attacks by putting an end to a common trigger for such attacks. They will simply be triggered by some other exposure.
I don't think the researchers who are using the studies of the Helena ilk to support the claim that brief exposures to secondhand smoke trigger heart attacks have thought this out to any extent.
By the way, if what these researchers are claiming is true, then it would actually be reasonable for a physician to tell a patient with severe coronary artery stenosis that he should simply avoid going to restaurants or other settings where there is smoking taking place. But such advice, we know, would be malpractice. If the patient's disease is that brittle, he is a heart attack waiting to happen and he needs definitive surgical intervention, probably with pharmaceutical intervention as well.
So even if we accept the claim that brief exposure to secondhand smoke is a common trigger for heart attacks among people with severe coronary artery stenosis, this would still not result in restaurant smoking bans causing any substantial decline in heart attacks in the short-term.
Note that smoking bans would still be expected to reduce heart attacks in the long-term, because over many years, the incidence of coronary artery disease would be reduced. But to posit that a heart attack decline on the order of 20% in one year or 40% in three years will occur in response to banning smoking in restaurants is simply implausible.
Finally, I would add that if it were true that exposure to tobacco smoke in restaurants was a common cause of heart attacks, would we not expect to occasionally observe someone in a restaurant keeling over from a heart attack? I've stipulated here, for the sake of argument, that the anti-smoking researchers' claim is true, but let's remember that it is merely a hypothetical or theoretical concern. There's no actual evidence that this is the case.
Jacob Sullum's Take on the Thirdhand Smoke Issue
I thought readers might be interested to see Jacob Sullum's take on the thirdhand smoke issue, which appeared yesterday over at Reason Online's Hit & Run blog.
Sullum nicely summarizes the recent research, which was published in Pediatrics, as follows: "The genius of the study is that it tries to stir up alarm about thirdhand smoke without bothering to show that such trace levels of toxins and carcinogens cause any measurable harm to children (or to anyone else). Instead the authors simply assume that thirdhand smoke is dangerous and then do a survey to see how many people are aware of this 'fact.'"
The Rest of the Story
Sullum is right. This study, while measuring people's knowledge of the "facts" about thirdhand smoke, failed to document what those facts are. It cited only one paper to support the notion that exposure to thirdhand smoke actually causes clinically meaningful health damage, and as I showed, that study was flawed and didn't demonstrate what the authors purport that it did.
The fact that tobacco smoke residue that settles during the smoking process can later be subject to offgassing, in which vapors that contain toxic constituents are released into the air, can occur is not being questioned here. What is being questioned is whether the very low levels of exposure that result from this offgassing are clinically meaningful and cause demonstrated harm.
I've seen no evidence for that. But it isn't stopping anti-smoking groups from communicating the dangers of thirdhand smoke to the public and calling for measures to protect people from having to be exposed to smokers, whose "breathe" is so toxic that we cannot allow nonsmokers in the same room.
Sullum nicely summarizes the recent research, which was published in Pediatrics, as follows: "The genius of the study is that it tries to stir up alarm about thirdhand smoke without bothering to show that such trace levels of toxins and carcinogens cause any measurable harm to children (or to anyone else). Instead the authors simply assume that thirdhand smoke is dangerous and then do a survey to see how many people are aware of this 'fact.'"
The Rest of the Story
Sullum is right. This study, while measuring people's knowledge of the "facts" about thirdhand smoke, failed to document what those facts are. It cited only one paper to support the notion that exposure to thirdhand smoke actually causes clinically meaningful health damage, and as I showed, that study was flawed and didn't demonstrate what the authors purport that it did.
The fact that tobacco smoke residue that settles during the smoking process can later be subject to offgassing, in which vapors that contain toxic constituents are released into the air, can occur is not being questioned here. What is being questioned is whether the very low levels of exposure that result from this offgassing are clinically meaningful and cause demonstrated harm.
I've seen no evidence for that. But it isn't stopping anti-smoking groups from communicating the dangers of thirdhand smoke to the public and calling for measures to protect people from having to be exposed to smokers, whose "breathe" is so toxic that we cannot allow nonsmokers in the same room.
Tuesday, January 06, 2009
Thirdhand Smoke: The Science Doesn't Matter; Look Out for Bans on Smokers in Childcare
The tobacco control movement's warnings to the public about the dangers of thirdhand smoke highlight once again that science is no longer driving the movement. Tobacco control practitioners are warning parents that even if they smoke outside the home, leaving a coat hanging on a door is going to expose their children to toxins and harm them due to offgassing of vapors from particulate matter that has settled on the coat during smoking. Yet there is no evidence that such very low levels of exposure to tobacco smoke residue constituents is harmful.
Several months ago, Action on Smoking and Health (ASH) called on measures to protect children from exposure to smokers - not merely from exposure to tobacco smoke - based on a study which purportedly showed that the breathe of smokers was toxic to children. But my analysis revealed that there was a fatal flaw in the study which invalidates the conclusion: it is highly likely that some smokers who claimed only to smoke outside the home actually do smoke in the home, at least on occasion. This would have completely explained the study result: that levels of smoke in homes with smokers who claim to only smoke outdoors are intermediate between levels in a smoke-free home and levels in a home with smokers who admit smoking inside the home.
The misinterpretation and misuse of these studies by anti-smoking groups and advocates endangers smokers because it will likely lead to efforts to bar smokers from the workplace and to prevent smokers from being around children, both of which would be tragic mistakes. If the Pediatrics study authors are correct and smokers are toxic to children even when not smoking, then this science can be used to justify measures to ban smokers from children's presence.
For example, if thirdhand smoke is toxic to children, then shouldn't child care workers be required to be nonsmokers? Shouldn't there be laws requiring that early childhood education teachers and staff be nonsmokers?
It would be a tragedy if "facts" like this were used to enact such measures when the truth is that the current science demonstrates no such harm.
If I thought that 2009 was going to be a year in which the anti-smoking movement would come back to its senses, the early returns suggest I was wrong. The movement seems even more dismissive of the science than it was in 2008.
Several months ago, Action on Smoking and Health (ASH) called on measures to protect children from exposure to smokers - not merely from exposure to tobacco smoke - based on a study which purportedly showed that the breathe of smokers was toxic to children. But my analysis revealed that there was a fatal flaw in the study which invalidates the conclusion: it is highly likely that some smokers who claimed only to smoke outside the home actually do smoke in the home, at least on occasion. This would have completely explained the study result: that levels of smoke in homes with smokers who claim to only smoke outdoors are intermediate between levels in a smoke-free home and levels in a home with smokers who admit smoking inside the home.
The misinterpretation and misuse of these studies by anti-smoking groups and advocates endangers smokers because it will likely lead to efforts to bar smokers from the workplace and to prevent smokers from being around children, both of which would be tragic mistakes. If the Pediatrics study authors are correct and smokers are toxic to children even when not smoking, then this science can be used to justify measures to ban smokers from children's presence.
For example, if thirdhand smoke is toxic to children, then shouldn't child care workers be required to be nonsmokers? Shouldn't there be laws requiring that early childhood education teachers and staff be nonsmokers?
It would be a tragedy if "facts" like this were used to enact such measures when the truth is that the current science demonstrates no such harm.
If I thought that 2009 was going to be a year in which the anti-smoking movement would come back to its senses, the early returns suggest I was wrong. The movement seems even more dismissive of the science than it was in 2008.
Monday, January 05, 2009
Welcome Back - 4 Posts Today
The holiday break was a busy time for tobacco control news. There are 4 posts today. I alert readers here so that they do not read the top story and fail to realize that there are 3 more blog posts. The 4 topics are:
1. A new study which concludes that the smoking ban in Pueblo, Colorado caused a 41% decline in heart attacks.
2. A new study which reports that "thirdhand" smoke is now a new health hazard to worry about.
3. A new book on the tobacco control movement which blasts the attorneys general and anti-smoking groups for their role in the public health disaster that is the Master Settlement Agreement.
4. The apparent 2009 theme of using cigarette tax increases to balance state budgets.
1. A new study which concludes that the smoking ban in Pueblo, Colorado caused a 41% decline in heart attacks.
2. A new study which reports that "thirdhand" smoke is now a new health hazard to worry about.
3. A new book on the tobacco control movement which blasts the attorneys general and anti-smoking groups for their role in the public health disaster that is the Master Settlement Agreement.
4. The apparent 2009 theme of using cigarette tax increases to balance state budgets.
CDC: Pueblo Smoking Ban Reduced Heart Attacks by 41%, Due Mostly to Decreased Secondhand Smoke Exposure; But Conclusions are Biased and Invalid
In a new study published in the current issue of MMWR (Morbidity and Mortality Weekly Reports), researchers from Colorado and from the Centers for Disease Control and Prevention (CDC) have concluded that the smoking ban in Pueblo, Colorado caused a 41% reduction in heart attacks during the three years following its implementation, primarily due to a reduction in secondhand smoke exposure associated with the ban (see: Alsever RN, et al. Reduced Hospitalizations for Acute Myocardial Infarction After Implementation of a Smoke-Free Ordinance --- City of Pueblo, Colorado, 2002--2006. MMWR 2009; 57(51);1373-1377).
The study compared the rate of hospitalizations for acute myocardial infarction (heart attacks) in the city of Pueblo with similar rates in Pueblo county (outside of Pueblo) and El Paso county (which includes Colorado Springs) for the 18-month period prior to the implementation of Pueblo's smoking ban and for the two 18-month periods following the smoking ban, which was implemented in July 2003. While there was no significant reduction in heart attack admissions for Pueblo or El Paso counties, there was a reduction in the heart attack rate of 19% and 41% from pre-implementation to the first and second post-implementation periods, respectively, in the city of Pueblo.
The study concludes: "These findings suggest that smoke-free policies can result in reductions in AMI [acute myocardial infarction] hospitalizations that are sustained over a 3-year period and that these policies are important in preventing morbidity and mortality associated with heart disease. This effect likely is mediated through reduced SHS [secondhand smoke] exposure among nonsmokers and reduced smoking, with the former making the larger contribution."
The Rest of the Story
Before you jump to any conclusions here (something the study did prematurely), consider this: let's accept the study's conclusion as correct - that smoking bans do lead to a dramatic, immediate reduction in heart attacks, in part because of a large reduction in smoking prevalence. Let's suppose that you want to demonstrate this "fact" by showing that compared to a similar city, heart attack rates in the city with the smoking ban fell substantially more after the ban was implemented.
Now you have to choose a comparison city. You have two choices, with the following information available about the smoking prevalence changes in those cities from pre-implementation to post-implementation:
City A - The smoking prevalence increased from 19% to 24%.
City B - The smoking prevalence remained relatively unchanged, dropping only from 24% to 23%.
Which city would you choose as the comparison city?
If you choose city B, you would be justified. There was little change in smoking prevalence, which mirrored the changes nationally during that time period, so one could argue that this is a reasonable comparison group.
If you choose city A, where there was a large increase in smoking prevalence, you are going to expect to see an increase in heart attacks due to the rise in smoking alone. This is going to artificially reduce any secular decline in heart attacks occurring in the comparison city and bias your results towards finding a larger decline in heart attacks in the city with the smoking ban.
A researcher who chose city A as the comparison city would certainly be suspected of having intentionally biased the results towards finding an effect of the smoking ban on heart attacks.
The last thing in the world that you want for a comparison city is one in which there was actually an increase in smoking prevalence, defying all odds about what the national trends in smoking are throughout the nation.
Unfortunately, this is exactly what this study does: it knowingly uses a comparison county in which it has been documented that the smoking prevalence over the study period has increased from 17.4% to 22.3%.
The study doesn't try to hide this fact. It openly acknowledges that the reported smoking prevalence in El Paso County (the comparison group) increased from 17.4% in 2002-2003 to 22.3% in 2004-2005.
Given this finding, El Paso County simply cannot be used as a comparison population. You can't take a population in which you know that smoking prevalence increased substantially and "pretend" that it represents a reasonable area in which to evaluate the baseline secular trends in heart attack admission rates that would have occurred in the smoking ban city in the absence of the smoking ban.
Of course you are going to find that the rate of heart attacks in El Paso County did not decline all that much, given the increase in smoking. El Paso County is clearly not going to give you a good, representative picture of what the actual secular trend in heart attack admissions is.
Now if smoking rates throughout the country had increased substantially during the same time period, one could argue that El Paso county is representative of the nation as a whole, or of Colorado as a whole. But clearly, the trends in smoking reported in El Paso are an anomaly - they are very different from the rest of the nation and from Colorado, where we know that smoking has continued to decline during the study period.
While I am not arguing here that the study intentionally used El Paso county in order to try to create the finding of a smoking ban effect on heart attacks, the fact that the study failed to even consider this problem suggests to me that there is a great deal of bias inherent in the paper. Yes, I do think that the study wanted to find an effect of the smoking ban and that it lost its neutrality somewhere in the process. It's natural to want to see the positive effects of a public health policy. But you have to separate your desires from the science itself. More about that later.
Another important problem is the other comparison group that was used: the rest of Pueblo county. Since this area is directly adjacent to Pueblo, which is the one city in this area, it would be expected that many residents of Pueblo county work in, and/or spend time in Pueblo, including eating in restaurants in the city. Thus, one would expect that if the smoking ban reduced heart attack rates, it would reduce rates among Pueblo county residents as well. It's not like those residents were somehow shielded from the intervention.
For this reason, the study should have combined the heart attack admissions from Pueblo and Pueblo county. Doing this, the reduction in the heart attack rate from pre-implementation to the second post-implementation period is 33%, rather than 41%.
Two logical comparison groups that one would want to consider are the state of Colorado as a whole and the nation as a whole. Heart attack admission rates for Colorado during the approximate period of the study (2002-2005) dropped by 18.4%. For the United States as a whole, the heart attack admission rate dropped by 17.2% during this period.
It is quite a different situation to claim that the smoking ban in Pueblo reduced heart attacks by 41% (because there was no significant decline in the inappropriate comparison county of El Paso) than it is to view the whole picture, and see that a 33% decline in heart attacks in Pueblo must be compared with about an 18% drop throughout the state of Colorado and a 17% decline nationally during the same time period.
The fact that these comparisons were not made is problematic, since the data are readily available (it took me about half hour to access and run the numbers). Why wouldn't the study want to look at the statewide trends in Colorado, rather than simply rely on the biased control group of El Paso county? In 30 minutes, the study could have determined that there was an impressive 18% decline in heart attacks in the whole state during the study period, thus making it clear that the present conclusion of the study is inaccurate.
The bottom line is that the study fails to appropriately determine the baseline secular trends in heart attacks in order to be able to judge the differences observed in Pueblo from the trends that would have been expected in the absence of the smoking ban. For this reason, the study cannot conclude that the observed changes in heart attacks are due to the smoking ban, rather than to other changes that took place over time, including changes in medications being used to treat heart disease, better diagnosis and more aggressive treatment of heart disease, and a substantial decline in smoking prevalence in Pueblo county during the study period, which may or may not be due to the smoking ban itself.
More troubling to me than the fact that the study draws a conclusion that is premature and inadequately supported by the data is the appearance of bias in the study. Not only in the choice of a comparison community where smoking prevalence dramatically increased during the study period, but also in the conclusion itself.
Even if we stipulate that the smoking ban did cause the decline in heart attacks, how can the study possibly conclude that the effect was due primarily to reduced secondhand smoke exposure? The study made no attempt to determine the smoking status of the heart attack victims, so there is no evidence that the reduction in heart attacks occurred primarily among nonsmokers. Neither did the study measure changes in population-based exposure to secondhand smoke.
Moreover, the study itself documents that there was a substantial decline in smoking prevalence in Pueblo county during the study period, from 25.9% to 20.6%. Wouldn't this documented decline in active smoking prevalence be the presumed major reason for the observed decline in heart attacks, as opposed to reductions in secondhand smoke exposure? At very least, wouldn't a study simply remark that both mechanisms may be operating, but that it can't be determined to what extent each is contributing?
The fact that the study concludes that it must primarily be the secondhand smoke reduction is curious. The fact that the editorial note of the study begins by claiming that evidence shows that brief secondhand smoke exposure can trigger a heart attack is revealing. If you look at the report to which that claim refers (the 2006 Surgeon General's report), you will not find any conclusion that brief secondhand smoke exposure triggers heart attacks. And you certainly won't find any evidence in that report that if we reduce secondhand smoke exposure, we can reduce heart attacks triggered by secondhand smoke exposure.
You may remember that I have previously called attention to the poor science by CDC and the Department of Health and Human Services in their communications regarding the acute cardiovascular effects of secondhand smoke, when they went out on a limb, against the advice of respected and expert scientists in the tobacco control field, and told the public that brief secondhand smoke exposure is enough to trigger heart attacks, cause heart disease, and cause lung cancer.
It seems odd that even if we stipulate that the overall conclusion of the study is valid (that the smoking ban caused a dramatic reduction in heart attacks in Pueblo), the study would emphasize that the effect must be primarily due to the reduction in secondhand smoke and thus a reduction in heart attacks among nonsmokers that would have otherwise been triggered by brief secondhand smoke exposures in restaurants or other public places.
Even if I were writing this editorial as a highly biased advocate, I would have simply concluded that the effect is likely due to the combination of a reduction in smoking prevalence and a reduction in secondhand smoke, but that the study provides no way of teasing out the degree to which these two phemomena are operating.
In fact, given the large decline in smoking prevalence reported in Pueblo county, even the above conclusion seems biased, since it is clear that if the effect were real, the smoking prevalence reduction would likely have been a major reason.
The study goes overboard not only in its overall conclusion, but in its attempt to paint these data as somehow proving that eating in a smoky restaurant for a half hour is causing lots of people to keel over from heart attacks. The study does nothing of the sort.
Let me finish by emphasizing that I would like nothing more than to have strong evidence presented that smoking bans are resulting in immediate and dramatic reductions in heart attacks. As I have devoted much of my life's work to promoting smoking bans, especially in bars and restaurants, it would bring a great sense of fulfillment to now that these policies are immediately saving lives and that we can document these acute effects.
However, I am first a scientist and I believe that in public health, our conclusions must be based on solid science, not just on conjecture or our deeply felt desire to see the success of our policies.
The study compared the rate of hospitalizations for acute myocardial infarction (heart attacks) in the city of Pueblo with similar rates in Pueblo county (outside of Pueblo) and El Paso county (which includes Colorado Springs) for the 18-month period prior to the implementation of Pueblo's smoking ban and for the two 18-month periods following the smoking ban, which was implemented in July 2003. While there was no significant reduction in heart attack admissions for Pueblo or El Paso counties, there was a reduction in the heart attack rate of 19% and 41% from pre-implementation to the first and second post-implementation periods, respectively, in the city of Pueblo.
The study concludes: "These findings suggest that smoke-free policies can result in reductions in AMI [acute myocardial infarction] hospitalizations that are sustained over a 3-year period and that these policies are important in preventing morbidity and mortality associated with heart disease. This effect likely is mediated through reduced SHS [secondhand smoke] exposure among nonsmokers and reduced smoking, with the former making the larger contribution."
The Rest of the Story
Before you jump to any conclusions here (something the study did prematurely), consider this: let's accept the study's conclusion as correct - that smoking bans do lead to a dramatic, immediate reduction in heart attacks, in part because of a large reduction in smoking prevalence. Let's suppose that you want to demonstrate this "fact" by showing that compared to a similar city, heart attack rates in the city with the smoking ban fell substantially more after the ban was implemented.
Now you have to choose a comparison city. You have two choices, with the following information available about the smoking prevalence changes in those cities from pre-implementation to post-implementation:
City A - The smoking prevalence increased from 19% to 24%.
City B - The smoking prevalence remained relatively unchanged, dropping only from 24% to 23%.
Which city would you choose as the comparison city?
If you choose city B, you would be justified. There was little change in smoking prevalence, which mirrored the changes nationally during that time period, so one could argue that this is a reasonable comparison group.
If you choose city A, where there was a large increase in smoking prevalence, you are going to expect to see an increase in heart attacks due to the rise in smoking alone. This is going to artificially reduce any secular decline in heart attacks occurring in the comparison city and bias your results towards finding a larger decline in heart attacks in the city with the smoking ban.
A researcher who chose city A as the comparison city would certainly be suspected of having intentionally biased the results towards finding an effect of the smoking ban on heart attacks.
The last thing in the world that you want for a comparison city is one in which there was actually an increase in smoking prevalence, defying all odds about what the national trends in smoking are throughout the nation.
Unfortunately, this is exactly what this study does: it knowingly uses a comparison county in which it has been documented that the smoking prevalence over the study period has increased from 17.4% to 22.3%.
The study doesn't try to hide this fact. It openly acknowledges that the reported smoking prevalence in El Paso County (the comparison group) increased from 17.4% in 2002-2003 to 22.3% in 2004-2005.
Given this finding, El Paso County simply cannot be used as a comparison population. You can't take a population in which you know that smoking prevalence increased substantially and "pretend" that it represents a reasonable area in which to evaluate the baseline secular trends in heart attack admission rates that would have occurred in the smoking ban city in the absence of the smoking ban.
Of course you are going to find that the rate of heart attacks in El Paso County did not decline all that much, given the increase in smoking. El Paso County is clearly not going to give you a good, representative picture of what the actual secular trend in heart attack admissions is.
Now if smoking rates throughout the country had increased substantially during the same time period, one could argue that El Paso county is representative of the nation as a whole, or of Colorado as a whole. But clearly, the trends in smoking reported in El Paso are an anomaly - they are very different from the rest of the nation and from Colorado, where we know that smoking has continued to decline during the study period.
While I am not arguing here that the study intentionally used El Paso county in order to try to create the finding of a smoking ban effect on heart attacks, the fact that the study failed to even consider this problem suggests to me that there is a great deal of bias inherent in the paper. Yes, I do think that the study wanted to find an effect of the smoking ban and that it lost its neutrality somewhere in the process. It's natural to want to see the positive effects of a public health policy. But you have to separate your desires from the science itself. More about that later.
Another important problem is the other comparison group that was used: the rest of Pueblo county. Since this area is directly adjacent to Pueblo, which is the one city in this area, it would be expected that many residents of Pueblo county work in, and/or spend time in Pueblo, including eating in restaurants in the city. Thus, one would expect that if the smoking ban reduced heart attack rates, it would reduce rates among Pueblo county residents as well. It's not like those residents were somehow shielded from the intervention.
For this reason, the study should have combined the heart attack admissions from Pueblo and Pueblo county. Doing this, the reduction in the heart attack rate from pre-implementation to the second post-implementation period is 33%, rather than 41%.
Two logical comparison groups that one would want to consider are the state of Colorado as a whole and the nation as a whole. Heart attack admission rates for Colorado during the approximate period of the study (2002-2005) dropped by 18.4%. For the United States as a whole, the heart attack admission rate dropped by 17.2% during this period.
It is quite a different situation to claim that the smoking ban in Pueblo reduced heart attacks by 41% (because there was no significant decline in the inappropriate comparison county of El Paso) than it is to view the whole picture, and see that a 33% decline in heart attacks in Pueblo must be compared with about an 18% drop throughout the state of Colorado and a 17% decline nationally during the same time period.
The fact that these comparisons were not made is problematic, since the data are readily available (it took me about half hour to access and run the numbers). Why wouldn't the study want to look at the statewide trends in Colorado, rather than simply rely on the biased control group of El Paso county? In 30 minutes, the study could have determined that there was an impressive 18% decline in heart attacks in the whole state during the study period, thus making it clear that the present conclusion of the study is inaccurate.
The bottom line is that the study fails to appropriately determine the baseline secular trends in heart attacks in order to be able to judge the differences observed in Pueblo from the trends that would have been expected in the absence of the smoking ban. For this reason, the study cannot conclude that the observed changes in heart attacks are due to the smoking ban, rather than to other changes that took place over time, including changes in medications being used to treat heart disease, better diagnosis and more aggressive treatment of heart disease, and a substantial decline in smoking prevalence in Pueblo county during the study period, which may or may not be due to the smoking ban itself.
More troubling to me than the fact that the study draws a conclusion that is premature and inadequately supported by the data is the appearance of bias in the study. Not only in the choice of a comparison community where smoking prevalence dramatically increased during the study period, but also in the conclusion itself.
Even if we stipulate that the smoking ban did cause the decline in heart attacks, how can the study possibly conclude that the effect was due primarily to reduced secondhand smoke exposure? The study made no attempt to determine the smoking status of the heart attack victims, so there is no evidence that the reduction in heart attacks occurred primarily among nonsmokers. Neither did the study measure changes in population-based exposure to secondhand smoke.
Moreover, the study itself documents that there was a substantial decline in smoking prevalence in Pueblo county during the study period, from 25.9% to 20.6%. Wouldn't this documented decline in active smoking prevalence be the presumed major reason for the observed decline in heart attacks, as opposed to reductions in secondhand smoke exposure? At very least, wouldn't a study simply remark that both mechanisms may be operating, but that it can't be determined to what extent each is contributing?
The fact that the study concludes that it must primarily be the secondhand smoke reduction is curious. The fact that the editorial note of the study begins by claiming that evidence shows that brief secondhand smoke exposure can trigger a heart attack is revealing. If you look at the report to which that claim refers (the 2006 Surgeon General's report), you will not find any conclusion that brief secondhand smoke exposure triggers heart attacks. And you certainly won't find any evidence in that report that if we reduce secondhand smoke exposure, we can reduce heart attacks triggered by secondhand smoke exposure.
You may remember that I have previously called attention to the poor science by CDC and the Department of Health and Human Services in their communications regarding the acute cardiovascular effects of secondhand smoke, when they went out on a limb, against the advice of respected and expert scientists in the tobacco control field, and told the public that brief secondhand smoke exposure is enough to trigger heart attacks, cause heart disease, and cause lung cancer.
It seems odd that even if we stipulate that the overall conclusion of the study is valid (that the smoking ban caused a dramatic reduction in heart attacks in Pueblo), the study would emphasize that the effect must be primarily due to the reduction in secondhand smoke and thus a reduction in heart attacks among nonsmokers that would have otherwise been triggered by brief secondhand smoke exposures in restaurants or other public places.
Even if I were writing this editorial as a highly biased advocate, I would have simply concluded that the effect is likely due to the combination of a reduction in smoking prevalence and a reduction in secondhand smoke, but that the study provides no way of teasing out the degree to which these two phemomena are operating.
In fact, given the large decline in smoking prevalence reported in Pueblo county, even the above conclusion seems biased, since it is clear that if the effect were real, the smoking prevalence reduction would likely have been a major reason.
The study goes overboard not only in its overall conclusion, but in its attempt to paint these data as somehow proving that eating in a smoky restaurant for a half hour is causing lots of people to keel over from heart attacks. The study does nothing of the sort.
Let me finish by emphasizing that I would like nothing more than to have strong evidence presented that smoking bans are resulting in immediate and dramatic reductions in heart attacks. As I have devoted much of my life's work to promoting smoking bans, especially in bars and restaurants, it would bring a great sense of fulfillment to now that these policies are immediately saving lives and that we can document these acute effects.
However, I am first a scientist and I believe that in public health, our conclusions must be based on solid science, not just on conjecture or our deeply felt desire to see the success of our policies.
New Study Warns of Dangers of "Thirdhand" Tobacco Smoke
A study published online ahead of print in the journal Pediatrics warns of the dangers, especially to children, of "thirdhand" tobacco smoke -- residual smoke which can cause exposure long after a smoker has stopped smoking. The study describes thirdhand smoke as "persistently high levels of tobacco toxins well beyond the period of active smoking. These toxins take the form of particulate matter deposited in a layer onto every surface within the home; in loose household dust; and as volatile toxic compounds that “off gas” into the air over days, weeks, and months. Smoking indoors on 1 day thus exposes people to tobacco toxins within that space in the future. We use the new term “thirdhand” smoke to name this complex phenomenon and define it as residual tobacco smoke contamination that remains after the cigarette is extinguished" (see: Winickoff JP, et al. Beliefs about the health effects of "thirdhand" smoke and home smoking bans. Pediatrics 2009; 123;e74-e79).
Regarding the risks posed by thirdhand smoke, the study concludes: "The toxicity of low levels of tobacco smoke constituents has been proved. ... Thirdhand smoke may remain inside even when smoking took place earlier. Similar to low levels of lead exposure, low levels of tobacco smoke markers have been associated with cognitive deficits among children. The highest tobacco exposure levels were associated with the lowest reading scores; however, the lowest levels of exposure were associated with the steepest slope in the decrement in reading levels. These facts underscore the possibility that compounds in tobacco smoke are neurotoxic at extremely low levels...".
The study also concludes that messages about the harms of thirdhand smoke, rather than those of secondhand smoke, should be used to help encourage smokers not to smoke at all in the home or to quit smoking altogether: "Thirdhand smoke health education campaigns might be more powerful motivators for these families than simply reiterating information about visible SHS [secondhand smoke] exposure that most families already know."
This message is already being used in an ad campaign to encourage parents to quit smoking altogether, warning them that there are serious risks of simply having clothing in the house that they wore when they were smoking, even it that smoking occurred outside of the home. One ad shows a picture of a coat hanging on a door hook and warns: "The toxins from cigarette smoke can hurt your children long after the cigarette is out."
The Rest of the Story
While I agree completely that parents should avoid smoking in the presence of their children and ideally, they should try to quit altogether, I am not convinced that the existing scientific evidence supports the conclusion that thirdhand smoke poses a significant public health hazard, even to children living in homes with a smoker.
While offgassing of toxic smoke constituents from surfaces onto which the smoke has settled has clearly been shown to occur, the resulting levels of exposure to these constituents in "thirdhand" smoke is extremely low. And there is no convincing scientific evidence that exposures of this magnitude produce any significant health harm, with the one possible exception being children who have asthma and are sensitive to tobacco smoke.
The Pediatrics article cites just a single study to support its contention that low levels of tobacco smoke exposure are associated with health harm: a study which purportedly showed that tobacco smoke exposure characterized by very low levels of cotinine causes children to have reduced cognitive function, as measured by math, reading, and block design scores (see: Yolton K et al. Exposure to environmental tobacco smoke and cognitive abilities among U.S. children and adolescents. Environmental Health Perspectives 2005; 113(1):98-103).
The rest of the story, however, is that this is a cross-sectional study which failed to consider two plausible alternative explanations why children with higher cotinine levels might have lower cognitive testing scores:
(1) These children are more likely to have been exposed to pre-natal tobacco smoke, which may have caused the observed impairment; and
(2) The parents of these children are more likely to have lower levels of cognitive testing scores and their children's scores are reflecting the parents' cognitive abilities and thus an inherited phenomenon.
Let's deal with alternative hypothesis #2 first. The study accounted for parental education, but it failed to account for parents' cognitive testing scores, which were not measured. Thus, the study cannot rule out the very plausible alernative explanation: the study is merely reflecting inherited similarities in cognitive function between parents and their children.
The study itself dealt with alternative hypothesis #1. For a subset of the sample, pre-natal exposure to tobacco smoke was measured and controlled for in the analysis (see Table 4). Interestingly, when pre-natal exposure was accounted for, the relationship between post-natal ETS exposure and math and block design scores disappeared, and the relationship between ETS exposure and reading scores was substantially reduced (by 30%).
Curiously, the study appears to hide or at least obscure the finding that the relationship between cotinine levels and cognitive function - as measured by math and block design scores - disappeared after controlling for pre-natal exposure and that the relationship between cotinine levels and reading scores was greatly reduced.
Part of the reason why the relationship between cotinine levels and reading scores may not have completely disappeared is because pre-natal exposure was based on parental self-report and was likely to be greatly under-reported. The authors acknowledge this, although it doesn't seem to alter their stated conclusions: "These prenatal data were obtained by parental report and may result in an underestimate of the intensity of tobacco smoke exposure. To confirm the causal role of ETS in diminished cognitive abilities among children, prospective birth cohort studies will be necessary."
The authors of the study acknowledge that because of its cross-sectional nature and these other issues, this study is not sufficient to draw a causal conclusion. They also acknowledge that there is no known biologic mechanism by which post-natal ETS exposure could lead to neurologic damage. Nevertheless, this acknowledgment does not appear to stop the authors from drawing such a causal conclusion anyway (an interesting statement about the bias which is now so apparent in tobacco control research).
The acknowledgment also does not stop the authors of the Pediatrics article from concluding that the effects of low levels of post-natal tobacco smoke exposure on children's cognitive function have been well-established (an interesting statement in itself about the bias of tobacco control researchers in reviewing the existing literature, not only in interpreting the results of their own studies).
Three other points deserve mention.
First, it's not clear to me why thirdhand smoke would be of any significant concern in the first place, since such exposure indicates that parents are smoking in the home and that children are therefore being exposed directly to secondhand smoke. Any health effects from the very low levels of exposure to thirdhand smoke will be dwarfed by the health risks from the substantial exposure to secondhand smoke, so why would we be concerned about the offgassing that is occurring?
It's kind of like telling a smoker to avoid exposure to secondhand smoke. In light of the active smoking, why worry about any small incremental effect of secondhand smoke? What the smoker needs to do is quit smoking if she wants to protect her health. Avoiding secondhand smoke seems to be almost a trivial concern in that situation. So why the emphasis on thirdhand smoke when we know these children are being exposed significantly to secondhand smoke because their parents are smoking in the home?
Second, if one were to counter my above point by arguing that smokers may not be smoking in the home, but may be exposing their children by virtue of residue left on clothing, then I would challenge the advocate of that position to produce evidence that such minimal exposure poses any significant health hazard. Based on my review of the literature, it is merely a theoretical concern.
Third, sending a message that smokers need to be worried about the effects of thirdhand smoke could well undermine efforts to encourage smokers not to smoke in their homes. If smokers are led to believe that even if they smoke outside the home, they will still be exposing their children to toxins, then many smokers may simply decide it is not worth the extra effort to smoke outside the home.
This all-or-nothing philosophy may undermine the harm reduction appraoch, and may actually result in smokers deciding not to bother to smoke outside the home. If their children are going to be exposed to toxins anyway, then why bother going through all that trouble?
Messages like the one in the ad campaign highlighted above could well backfire. Or at least, they might prove counterproductive for some smoking parents.
But most importantly, I question the accuracy and the scientific support behind such a health claim. It's not clear to me that if a smoker is careful never to smoke inside the home, that merely hanging up their coat on a hook inside the home will cause harm to his children from toxins that offgas from the coat. I just am not aware of any evidence that this represents a significant health risk.
Those who know my position understand that I believe the effects of secondhand smoke are enough. I do not believe that we need to invoke ever-so-shaky scientific evidence to try to now scare people about the effects of thirdhand smoke. Not only is this approach scientifically unsupported, but it may also backfire by undermining people's appreciation of the documented hazards of secondhand smoke.
Regarding the risks posed by thirdhand smoke, the study concludes: "The toxicity of low levels of tobacco smoke constituents has been proved. ... Thirdhand smoke may remain inside even when smoking took place earlier. Similar to low levels of lead exposure, low levels of tobacco smoke markers have been associated with cognitive deficits among children. The highest tobacco exposure levels were associated with the lowest reading scores; however, the lowest levels of exposure were associated with the steepest slope in the decrement in reading levels. These facts underscore the possibility that compounds in tobacco smoke are neurotoxic at extremely low levels...".
The study also concludes that messages about the harms of thirdhand smoke, rather than those of secondhand smoke, should be used to help encourage smokers not to smoke at all in the home or to quit smoking altogether: "Thirdhand smoke health education campaigns might be more powerful motivators for these families than simply reiterating information about visible SHS [secondhand smoke] exposure that most families already know."
This message is already being used in an ad campaign to encourage parents to quit smoking altogether, warning them that there are serious risks of simply having clothing in the house that they wore when they were smoking, even it that smoking occurred outside of the home. One ad shows a picture of a coat hanging on a door hook and warns: "The toxins from cigarette smoke can hurt your children long after the cigarette is out."
The Rest of the Story
While I agree completely that parents should avoid smoking in the presence of their children and ideally, they should try to quit altogether, I am not convinced that the existing scientific evidence supports the conclusion that thirdhand smoke poses a significant public health hazard, even to children living in homes with a smoker.
While offgassing of toxic smoke constituents from surfaces onto which the smoke has settled has clearly been shown to occur, the resulting levels of exposure to these constituents in "thirdhand" smoke is extremely low. And there is no convincing scientific evidence that exposures of this magnitude produce any significant health harm, with the one possible exception being children who have asthma and are sensitive to tobacco smoke.
The Pediatrics article cites just a single study to support its contention that low levels of tobacco smoke exposure are associated with health harm: a study which purportedly showed that tobacco smoke exposure characterized by very low levels of cotinine causes children to have reduced cognitive function, as measured by math, reading, and block design scores (see: Yolton K et al. Exposure to environmental tobacco smoke and cognitive abilities among U.S. children and adolescents. Environmental Health Perspectives 2005; 113(1):98-103).
The rest of the story, however, is that this is a cross-sectional study which failed to consider two plausible alternative explanations why children with higher cotinine levels might have lower cognitive testing scores:
(1) These children are more likely to have been exposed to pre-natal tobacco smoke, which may have caused the observed impairment; and
(2) The parents of these children are more likely to have lower levels of cognitive testing scores and their children's scores are reflecting the parents' cognitive abilities and thus an inherited phenomenon.
Let's deal with alternative hypothesis #2 first. The study accounted for parental education, but it failed to account for parents' cognitive testing scores, which were not measured. Thus, the study cannot rule out the very plausible alernative explanation: the study is merely reflecting inherited similarities in cognitive function between parents and their children.
The study itself dealt with alternative hypothesis #1. For a subset of the sample, pre-natal exposure to tobacco smoke was measured and controlled for in the analysis (see Table 4). Interestingly, when pre-natal exposure was accounted for, the relationship between post-natal ETS exposure and math and block design scores disappeared, and the relationship between ETS exposure and reading scores was substantially reduced (by 30%).
Curiously, the study appears to hide or at least obscure the finding that the relationship between cotinine levels and cognitive function - as measured by math and block design scores - disappeared after controlling for pre-natal exposure and that the relationship between cotinine levels and reading scores was greatly reduced.
Part of the reason why the relationship between cotinine levels and reading scores may not have completely disappeared is because pre-natal exposure was based on parental self-report and was likely to be greatly under-reported. The authors acknowledge this, although it doesn't seem to alter their stated conclusions: "These prenatal data were obtained by parental report and may result in an underestimate of the intensity of tobacco smoke exposure. To confirm the causal role of ETS in diminished cognitive abilities among children, prospective birth cohort studies will be necessary."
The authors of the study acknowledge that because of its cross-sectional nature and these other issues, this study is not sufficient to draw a causal conclusion. They also acknowledge that there is no known biologic mechanism by which post-natal ETS exposure could lead to neurologic damage. Nevertheless, this acknowledgment does not appear to stop the authors from drawing such a causal conclusion anyway (an interesting statement about the bias which is now so apparent in tobacco control research).
The acknowledgment also does not stop the authors of the Pediatrics article from concluding that the effects of low levels of post-natal tobacco smoke exposure on children's cognitive function have been well-established (an interesting statement in itself about the bias of tobacco control researchers in reviewing the existing literature, not only in interpreting the results of their own studies).
Three other points deserve mention.
First, it's not clear to me why thirdhand smoke would be of any significant concern in the first place, since such exposure indicates that parents are smoking in the home and that children are therefore being exposed directly to secondhand smoke. Any health effects from the very low levels of exposure to thirdhand smoke will be dwarfed by the health risks from the substantial exposure to secondhand smoke, so why would we be concerned about the offgassing that is occurring?
It's kind of like telling a smoker to avoid exposure to secondhand smoke. In light of the active smoking, why worry about any small incremental effect of secondhand smoke? What the smoker needs to do is quit smoking if she wants to protect her health. Avoiding secondhand smoke seems to be almost a trivial concern in that situation. So why the emphasis on thirdhand smoke when we know these children are being exposed significantly to secondhand smoke because their parents are smoking in the home?
Second, if one were to counter my above point by arguing that smokers may not be smoking in the home, but may be exposing their children by virtue of residue left on clothing, then I would challenge the advocate of that position to produce evidence that such minimal exposure poses any significant health hazard. Based on my review of the literature, it is merely a theoretical concern.
Third, sending a message that smokers need to be worried about the effects of thirdhand smoke could well undermine efforts to encourage smokers not to smoke in their homes. If smokers are led to believe that even if they smoke outside the home, they will still be exposing their children to toxins, then many smokers may simply decide it is not worth the extra effort to smoke outside the home.
This all-or-nothing philosophy may undermine the harm reduction appraoch, and may actually result in smokers deciding not to bother to smoke outside the home. If their children are going to be exposed to toxins anyway, then why bother going through all that trouble?
Messages like the one in the ad campaign highlighted above could well backfire. Or at least, they might prove counterproductive for some smoking parents.
But most importantly, I question the accuracy and the scientific support behind such a health claim. It's not clear to me that if a smoker is careful never to smoke inside the home, that merely hanging up their coat on a hook inside the home will cause harm to his children from toxins that offgas from the coat. I just am not aware of any evidence that this represents a significant health risk.
Those who know my position understand that I believe the effects of secondhand smoke are enough. I do not believe that we need to invoke ever-so-shaky scientific evidence to try to now scare people about the effects of thirdhand smoke. Not only is this approach scientifically unsupported, but it may also backfire by undermining people's appreciation of the documented hazards of secondhand smoke.
"Up in Smoke": A Scathing Critique of the Role of Anti-Smoking Groups, Attorneys General, and Private Tort Lawyers in Protecting Big Tobacco
I highly recommend to all my readers the book "Up in Smoke: From Legislation to Litigation in Tobacco Politics (2nd edition, copyright 2005, published by CQ Press). Written by Professor Martha Derthick, who was with the Department of Government and Foreign Affairs at the University of Virginia, where she was the Julia Allen Cooper Professor until her retirement in 1999, the book recounts in greater detail than ever before presented the history of the Master Settlement Agreement of 1998 and the events that led up to it.
The account is not only thorough, well-documented, and fresh, but it is the most unbiased presentation that you will find. Professor Derthick's primary interest and her experience are in government and policy, she is not directly involved in the tobacco wars, and thus her perspective is not only unbiased but very welcomed and needed.
Derthick provides a scathing critique of the role of anti-smoking groups, attorneys general, and private tort lawyers in creating unprecedented and possibly unconstitutional special protection for the tobacco companies at the expense of the protection of the public's health and at the cost of a probable violation of anti-trust principles, the Constitution, and the pocket books of smokers.
The following two excerpts summarize the conclusions of the book and will hopefully entice readers to obtain and read the whole book. It is a great way for readers to explore in detail "the rest of the story" regarding the role of the states and anti-smoking groups in defying the public's trust to protect their own pockets as well as those of Big Tobacco.
Summarizing the effects of the MSA, Derthick writes: "The industry received protection against competition, in defiance of state and federal antitrust laws, which are criminal statutes. This protection enabled it to raise prices even more than the settlement obligations required. ... Political allies and supporters of the attorneys ggeneral, including the relatively small number of private tort lawyers who helped prepare the cases, received billions of dollars in a breathtaking use of public power for private gain -- and a violation of the ethics of the legal profession, which supposedly limits fees to reasonable amounts. The cigarette companies in effect gained implicit partners in the state governments and tort lawyers, both of whom acquired a stake in the continuing profitability of the industry. The settlement was richly productive of perverse incentives."
She later writes: "The tobacco experience raises disturbing questions about how governments use their power. ... The lawyers' fees wildly surpassed any standard of reasonableness. No money went to smokers, who suffered the proximate harm from the cigarette manufacturers' products. Current smokers would pay higher prices for cigarettes -- a tax, in effect, imposed by a "public" process in which they were not represented. The legal instrument that resulted from the suits and settlement, the MSA, on its face flouts antitrust laws and may yet fall in federal court. It has also been challenged - so far, unsuccessfully - on constitutional grounds, most plausibly as a violation of the compact clause, which requires that interstate compacts and agreements be approved by Congress."
The Rest of the Story
I am glad to have been a vigorous opponent to this political power-creating and money-making scheme that has caused more public health harm than almost any government action purportedly intended to benefit the public in history.
Of note, however, the leading group in the anti-smoking movement - the Campaign for Tobacco-Free Kids - was a tacit supporter of this agreement, and in fact played a critical role in the early negotiations which eventually led to this bailout deal.
In many ways, the Campaign for Tobacco-Free Kids and the Attorneys General damaged the public health cause of tobacco control more than any non-tobacco-related entities in recent history.
The account is not only thorough, well-documented, and fresh, but it is the most unbiased presentation that you will find. Professor Derthick's primary interest and her experience are in government and policy, she is not directly involved in the tobacco wars, and thus her perspective is not only unbiased but very welcomed and needed.
Derthick provides a scathing critique of the role of anti-smoking groups, attorneys general, and private tort lawyers in creating unprecedented and possibly unconstitutional special protection for the tobacco companies at the expense of the protection of the public's health and at the cost of a probable violation of anti-trust principles, the Constitution, and the pocket books of smokers.
The following two excerpts summarize the conclusions of the book and will hopefully entice readers to obtain and read the whole book. It is a great way for readers to explore in detail "the rest of the story" regarding the role of the states and anti-smoking groups in defying the public's trust to protect their own pockets as well as those of Big Tobacco.
Summarizing the effects of the MSA, Derthick writes: "The industry received protection against competition, in defiance of state and federal antitrust laws, which are criminal statutes. This protection enabled it to raise prices even more than the settlement obligations required. ... Political allies and supporters of the attorneys ggeneral, including the relatively small number of private tort lawyers who helped prepare the cases, received billions of dollars in a breathtaking use of public power for private gain -- and a violation of the ethics of the legal profession, which supposedly limits fees to reasonable amounts. The cigarette companies in effect gained implicit partners in the state governments and tort lawyers, both of whom acquired a stake in the continuing profitability of the industry. The settlement was richly productive of perverse incentives."
She later writes: "The tobacco experience raises disturbing questions about how governments use their power. ... The lawyers' fees wildly surpassed any standard of reasonableness. No money went to smokers, who suffered the proximate harm from the cigarette manufacturers' products. Current smokers would pay higher prices for cigarettes -- a tax, in effect, imposed by a "public" process in which they were not represented. The legal instrument that resulted from the suits and settlement, the MSA, on its face flouts antitrust laws and may yet fall in federal court. It has also been challenged - so far, unsuccessfully - on constitutional grounds, most plausibly as a violation of the compact clause, which requires that interstate compacts and agreements be approved by Congress."
The Rest of the Story
I am glad to have been a vigorous opponent to this political power-creating and money-making scheme that has caused more public health harm than almost any government action purportedly intended to benefit the public in history.
Of note, however, the leading group in the anti-smoking movement - the Campaign for Tobacco-Free Kids - was a tacit supporter of this agreement, and in fact played a critical role in the early negotiations which eventually led to this bailout deal.
In many ways, the Campaign for Tobacco-Free Kids and the Attorneys General damaged the public health cause of tobacco control more than any non-tobacco-related entities in recent history.
Use of Cigarette Tax Revenue from Increased State Excise Tax to Fund Critical Government Programs Appears to Be Major Theme in 2009
The strategy of using increases in state cigarette excise taxes to fund critical government programs that would otherwise not be funded due to state budget shortfalls appears to be a major theme of 2009. Over just the past two weeks, for example, there have been proposals in Virginia and Arkansas to use cigarette tax increases to help balance the state budgets and allow funding for critical government programs.
Public health groups have cast these proposals as "win-win" policies that reduce cigarette consumption while producing needed revenue.
The Rest of the Story
There is another side to the picture, however. By tying critical government programs to cigarette tax revenues, policy makers are actually making these vital programs - and thus the state budget and economy - dependent upon continued high levels of cigarette consumption. The generation of this perverse incentive - which will discourage state policy makers from taking any action that would seriously threaten cigarette consumption - is, in my opinion, a public health disaster whose harms far outweigh any short-term benefits of the cigarette tax increase.
We have already seen the degree to which state governments will go to protect Big Tobacco once their budgets have become dependent upon continuing high levels of cigarettes sales. A large contingent of Attorneys General actually went to bat for Philip Morris in Illinois, filing an amicus brief to help the tobacco giant from having to pay the bond that would have otherwise been required for it to appeal its loss in a "lights" cigarette lawsuit. The Attorneys General thus helped save Philip Morris literally billions and billions of dollars -- all because the states were afraid that their payments under the Master Settlement Agreement might be threatened.
In Florida, state government officials and legislators went to bat for all the tobacco companies, changing the law to avoid them having to post billions of dollars of bond to appeal the $145 billion verdict against them in the Engle lawsuit. Once again, state lawmakers were acting to protect the state's financial interests, which were seen as being potentially threatened if tobacco settlement payments were to decline.
Making the government dependent upon cigarette revenue for critical programs that should be funded from other sources is the last thing in the world that we should want from a public health perspective. Doing so is truly creating a public health disaster. A healthy environment for tobacco control cannot flourish if these perverse incentives exist.
Moreover, these taxes are regressive and they put the burden of balancing state budgets on the very poorest of the state's citizens. An editorial in the Fredericksburg (Virginia) Free Lance-Star summarized this argument quite nicely, referring to Governor Kaine's proposal to increase the state cigarette excise tax by 30 cents per pack to balance the state budget:"let's recognize that Mr. Kaine's proposal represents a kind of classism. Cigarette smokers generally occupy the lower economic strata, which means that few of them inhabit the social sphere of governors and of the business and journalistic elites with whom the political class hobnobs. A cigarette tax, in short, is a tax on "them," not "us." Elites still like their microbrews, their merlots, and their double-malt Scotches, which is perhaps why Mr. Kaine isn't pushing higher taxes on another socially problematic substance, alcohol."
The editorial is right. If these government programs are so critical - and if they benefit all of society - then we should not be singling out smokers to bear the burden of paying for them. The reasons for burdening smokers are chiefly political - state politicians lack the guts to make the wealthier (and more politically powerful) segments of society pay their fair share. It's far easier to take advantage of smokers, who are quickly coming to represent an easily oppressed social class in American society.
So not only do these cigarette tax proposals represent poor public policy, they also represent political cowardice.
As I have argued before, if smokers are to be asked to shoulder the burden of a tax increase, then the revenues should be used for purposes related to smoking and smokers themselves should stand to potentially benefit directly from the programs and services offered. Using a "sin" tax on cigarettes to pay for anti-smoking education and prevention programs, research and treatment of smoking-related diseases, and smoking cessation services makes sense and represents fiscally sound policy that is also equitable. But asking smokers to shoulder the burden to balance our state budgets every time the economy takes a hit is neither fiscally sound nor is it fair.
A letter to the editor in this month's issue of the American Journal of Public Health argues that anti-smoking groups are misguided in promoting cigarette tax increases in order to coerce poor smokers to quit. David Ahrens of the Population Health Institute in Madison, Wisconsin argues that: "The Center for Tobacco Free Kids, an advocate of higher tobacco taxes, estimates that only 3% of the Master Settlement Agreement and tobacco excise taxes is used for tobacco control. Inclusion of the additional $7 billion from the federal excise tax would diminish the proportion spent on tobacco control to 2%. Furthermore, only a fraction of those funds are used to assist low-income smokers to help quit smoking. For tens of millions of smokers who want to quit, poorly funded tobacco control programs offer little assistance. Unfortunately, many of these same programs advocate for tobacco taxes under the misguided notion that high prices will economically coerce poor smokers to quit. If we are to believe our own science, that smoking is addictive, we must recognize the extent to which the primary result of highly priced tobacco products further impoverish a substantial portion of low-income tobacco users. This should be as much of a concern of public health advocates as the ongoing tobacco epidemic among the lower classes."
Thus, it could accurately be argued that cigarette tax increases have as a primary effect the further impoverishment of already low-income smokers. The policy will therefore exacerbate existing health disparities related to income, which is opposed to one of the main goals of the Healthy People 2010 objectives for the nation.
In Arkansas, state legislators and an anti-smoking group are apparently suggesting that the state increase its cigarette tax by 50 cents per pack to fund a new statewide trauma system. This would create an absurd situation in which treatment of trauma in the state of Arkansas would be done thanks to the generosity of smokers who choose to smoke rather than to quit. Quitting smoking would put the state's trauma treatment system in jeopardy!
I plan to test-market my newly designed T-shirts in Little Rock this week:
"I Support Treatment for Arkansas Trauma Victims: I Smoke and I'm Not Quitting."
Public health groups have cast these proposals as "win-win" policies that reduce cigarette consumption while producing needed revenue.
The Rest of the Story
There is another side to the picture, however. By tying critical government programs to cigarette tax revenues, policy makers are actually making these vital programs - and thus the state budget and economy - dependent upon continued high levels of cigarette consumption. The generation of this perverse incentive - which will discourage state policy makers from taking any action that would seriously threaten cigarette consumption - is, in my opinion, a public health disaster whose harms far outweigh any short-term benefits of the cigarette tax increase.
We have already seen the degree to which state governments will go to protect Big Tobacco once their budgets have become dependent upon continuing high levels of cigarettes sales. A large contingent of Attorneys General actually went to bat for Philip Morris in Illinois, filing an amicus brief to help the tobacco giant from having to pay the bond that would have otherwise been required for it to appeal its loss in a "lights" cigarette lawsuit. The Attorneys General thus helped save Philip Morris literally billions and billions of dollars -- all because the states were afraid that their payments under the Master Settlement Agreement might be threatened.
In Florida, state government officials and legislators went to bat for all the tobacco companies, changing the law to avoid them having to post billions of dollars of bond to appeal the $145 billion verdict against them in the Engle lawsuit. Once again, state lawmakers were acting to protect the state's financial interests, which were seen as being potentially threatened if tobacco settlement payments were to decline.
Making the government dependent upon cigarette revenue for critical programs that should be funded from other sources is the last thing in the world that we should want from a public health perspective. Doing so is truly creating a public health disaster. A healthy environment for tobacco control cannot flourish if these perverse incentives exist.
Moreover, these taxes are regressive and they put the burden of balancing state budgets on the very poorest of the state's citizens. An editorial in the Fredericksburg (Virginia) Free Lance-Star summarized this argument quite nicely, referring to Governor Kaine's proposal to increase the state cigarette excise tax by 30 cents per pack to balance the state budget:"let's recognize that Mr. Kaine's proposal represents a kind of classism. Cigarette smokers generally occupy the lower economic strata, which means that few of them inhabit the social sphere of governors and of the business and journalistic elites with whom the political class hobnobs. A cigarette tax, in short, is a tax on "them," not "us." Elites still like their microbrews, their merlots, and their double-malt Scotches, which is perhaps why Mr. Kaine isn't pushing higher taxes on another socially problematic substance, alcohol."
The editorial is right. If these government programs are so critical - and if they benefit all of society - then we should not be singling out smokers to bear the burden of paying for them. The reasons for burdening smokers are chiefly political - state politicians lack the guts to make the wealthier (and more politically powerful) segments of society pay their fair share. It's far easier to take advantage of smokers, who are quickly coming to represent an easily oppressed social class in American society.
So not only do these cigarette tax proposals represent poor public policy, they also represent political cowardice.
As I have argued before, if smokers are to be asked to shoulder the burden of a tax increase, then the revenues should be used for purposes related to smoking and smokers themselves should stand to potentially benefit directly from the programs and services offered. Using a "sin" tax on cigarettes to pay for anti-smoking education and prevention programs, research and treatment of smoking-related diseases, and smoking cessation services makes sense and represents fiscally sound policy that is also equitable. But asking smokers to shoulder the burden to balance our state budgets every time the economy takes a hit is neither fiscally sound nor is it fair.
A letter to the editor in this month's issue of the American Journal of Public Health argues that anti-smoking groups are misguided in promoting cigarette tax increases in order to coerce poor smokers to quit. David Ahrens of the Population Health Institute in Madison, Wisconsin argues that: "The Center for Tobacco Free Kids, an advocate of higher tobacco taxes, estimates that only 3% of the Master Settlement Agreement and tobacco excise taxes is used for tobacco control. Inclusion of the additional $7 billion from the federal excise tax would diminish the proportion spent on tobacco control to 2%. Furthermore, only a fraction of those funds are used to assist low-income smokers to help quit smoking. For tens of millions of smokers who want to quit, poorly funded tobacco control programs offer little assistance. Unfortunately, many of these same programs advocate for tobacco taxes under the misguided notion that high prices will economically coerce poor smokers to quit. If we are to believe our own science, that smoking is addictive, we must recognize the extent to which the primary result of highly priced tobacco products further impoverish a substantial portion of low-income tobacco users. This should be as much of a concern of public health advocates as the ongoing tobacco epidemic among the lower classes."
Thus, it could accurately be argued that cigarette tax increases have as a primary effect the further impoverishment of already low-income smokers. The policy will therefore exacerbate existing health disparities related to income, which is opposed to one of the main goals of the Healthy People 2010 objectives for the nation.
In Arkansas, state legislators and an anti-smoking group are apparently suggesting that the state increase its cigarette tax by 50 cents per pack to fund a new statewide trauma system. This would create an absurd situation in which treatment of trauma in the state of Arkansas would be done thanks to the generosity of smokers who choose to smoke rather than to quit. Quitting smoking would put the state's trauma treatment system in jeopardy!
I plan to test-market my newly designed T-shirts in Little Rock this week:
"I Support Treatment for Arkansas Trauma Victims: I Smoke and I'm Not Quitting."
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