There appears to be a lot of smoke spewing around Ohio these days - and I'm not talking about the smoke coming from the Cinergy plant in New Richmond.
It's coming from the seemingly most unlikely of places: a public health group that is trying to fight the lies and deception of the tobacco industry and set the record straight about misleading communications to the public.
If you're trying to blast your opponents for using misleading public communications that deceive people about the facts, it's probably not too wise to be using the same tactic yourself.
But that's exactly what SmokeFreeOhio, a broad coalition of anti-smoking and public health groups in Ohio, is doing to promote a state initiative that would eliminate smoking in workplaces, including bars and restaurants.
On its web site, SmokeFreeOhio is claiming that 30 minutes of secondhand smoke exposure is enough to cause narrowing of blood vessels and hardening of the arteries, that just 30 minutes of secondhand smoke exposure is also enough to cause fat deposits that increase heart disease and stroke risk, that 2 hours of secondhand smoke exposure increase the risk of a catastrophic or fatal heart arrhythmia, and that just 20 minutes of secondhand smoke exposure reduces the ability of the heart to pump and thus puts a nonsmoker at increased risk of suffering a heart attack.
On March 21 of this year, exactly 3 months ago, I wrote to SmokeFreeOhio noting my concerns about the scientific inaccuracy of these statements and providing detailed reasoning, including scientific citations, for why I believed that these claims were fallacious (see text of letter below). The organization is clearly aware of who I am as well as my scientific qualifications to comment on this issue, and apparently thinks enough of my scientific abilities to cite my research findings and conclusions in the same fact sheet (reference 32).
However, to this day, the organization has not corrected, clarified, retracted, or otherwise altered its fallacious claims. Since a quarter of a year has gone by, I think it is not unreasonable to draw the conclusion that SmokeFreeOhio has no intention of fixing its inaccurate and misleading public claims and that the group either doesn't agree that these statements are inaccurate, agrees that they are inaccurate but doesn't care, agrees that they are inaccurate and does care, but is intentionally misleading the public in order to garner more support for the agenda it is promoting, or doesn't really care enough about my concern in the first place to review their public statements in any reasonable length of time.
The Rest of the Story
I have already explained, in some detail, why I believe that each of the 4 major statements above are fallacious, and I will not repeat that commentary here.
The important point is that these scientific claims are so wildly misleading and inaccurate that they completely fly in the face of pure common sense. It doesn't take a rocket cardiologist to understand that it takes more than 30 minutes for narrowing of the arteries to occur, and to such a degree that it restricts blood flow and contributes to hardening of the arteries. And there simply isn't any scientific support for any of these four claims. In fact, the scientific evidence demonstrates that these claims are untrue.
The second important point is that SmokeFreeOhio has now had 3 full months to review these statements and to correct or clarify them. This is not particularly complicated material and it shouldn't take 3 months to review. But allowing the benefit of the doubt, by now the claim should have been corrected if it was found to be misleading or inaccurate.
So we are left with the 4 possibilities, none of which are particularly attractive for the anti-smoking movement. Obviously, if the organization is intentionally misleading the public or doesn't care enough to correct the claim, then it isn't a pretty story. And if SmokeFreeOhio doesn't particularly care about these concerns, then it is a shame, because we in tobacco control should take pride in our scientific integrity, especially when we spend much of our time attacking others for their lack of such.
The final possibility, that the group has concluded that there is nothing wrong with these claims, may seem more benign, but unfortunately, if true, it would spell the end of the viability of the anti-smoking movement in my view. Because if we are unable to interpret science to any reasonably accurate extent, then we really have no business communicating science to the public. If we truly believe that 20 minutes of secondhand smoke impairs the heart's ability to pump, then why should we be trusted to make any statements about the effects of secondhand smoke?
These same comments apply, I'm sure, to many of the more than 80 organizations that have made similar claims. I'm not trying to suggest that SmokeFreeOhio is any worse than these other examples; it just happens to be the group with which I had the most direct communication, and so I'm absolutely sure that they are well aware of my concerns.
This story also illustrates why I have not spent countless hours of my time contacting the 80+ groups individually. The response I received from each of the few groups that I did contact was uniform: they did nothing.
Unless you're a fan of irony and hypocrisy, the rest of the story - that an anti-smoking group that is trying to convince the public that its opposition is blowing smoke but is blowing smoke itself - is not particularly pleasing.
It is only a question of time before the media picks up on this. Already, a letter to the editor appeared in the Athens News which called SmokeFreeOhio on the accuracy of its claims. The damage that is being done to SmokeFreeOhio's credibility is certainly important, but it's time for us to realize that the damage being done applies to all of us in tobacco control and public health.
Letter to SmokeFreeOhio (sent March 21, 2006)
Here are the specific statements on the fact sheet that I feel are inaccurate, and a brief description of my reasoning:
1. "After twenty minutes of exposure to secondhand smoke, a nonsmoker's blood platelets become as sticky as a smoker's, reducing the ability of the heart to pump and putting a nonsmoker at an elevated risk of heart attack."
I agree that there is evidence that after 20 minutes of secondhand smoke exposure, platelet aggregation increases and that it may increase to the level of that seen in an active smoker. Thus, it is fine to say that a nonsmoker's platelets become as sticky as a smoker's after 20 minutes of secondhand smoke exposure.
However, you can't make the jump from a little platelet stickiness to a reduced ability of the heart to pump and an elevated risk of heart attack. You can't equate a transient increase in platelet stickiness with an elevated heart attack risk. And you can't equate it with reducing the ability of the heart to pump.
If someone were exposed to secondhand smoke repeatedly for a long period of time, then the constant and prolonged effects of secondhand smoke on platelets, along with the effects on endothelial dysfunction, could initiate and maintain the process of atherosclerosis. But it cannot occur in just 20 minutes.
And even chronic exposure to secondhand smoke does not reduce the ability of the heart to pump. What reduces the ability of the heart to pump is injury to the cardiac muscle, such as occurs in a heart attack, with cardiomyopathy, with certain arrhythmias, with myocardial disease, with cardiac tamponade, or with ventricular hypertrophy or valvular disease. But secondhand smoke exposure does not reduce the ability of the heart muscle to pump. Chronic exposure could lead to a heart attack, and that could certainly reduce the heart's ability to pump. But this claim that only 20 minutes of secondhand smoke exposure can reduce the heart's ability to pump is not accurate.
The reference used to back up this claim is a study which shows that brief exposure to secondhand smoke decreases platelet sensitivity to prostacyclin.
But I don't think it's accurate to go from a study that showed that brief exposure to secondhand smoke decreases platelet sensitivity to prostacyclin to a claim that it reduces the ability of the heart to pump and increases the risk of a heart attack.
In fact, what the study showed was that the effects of brief exposure to secondhand smoke on platelet sensitivity to prostacyclin are transient, such that in passive smokers, a measurable decline in this sensitivity can be detected. However, in chronic smokers, there is no observed decline in platelet sensitivity, because presumably, the chronic and repeated nature of the exposure creates a condition under which platelets are constantly activated (see: Burghuber OC, Punzengruber C, Sinzinger H, Haber P, Silberbauer K. Platelet sensitivity to prostacyclin in smokers and non-smokers. Chest 1986; 90:34-38).
As the study concluded: "This study indicates that platelets of chronic smokers are less sensitive to exogenous PGI2 than platelets of non-smokers. In addition, active as well as passive smoking decreases platelet sensitivity to PGI2 in non-smokers, whereas chronic smokers exhibit no further decline."
Thus, the study actually demonstrates just why it is that a brief exposure to secondhand smoke does not cause atherosclerosis, while a prolonged and chronic exposure may.
The study actually uses the sensitivity to prostacyclin of briefly exposed nonsmokers to provide support for the hypothesis that altered platelet function in smokers plays a role in the development of atherosclerosis in these individuals.
2. "Only 30 minutes of secondhand smoke exposure can cause narrowing of blood vessels, restricting the flow of blood and contributing to hardening of the arteries."
You cannot develop atherosclerosis in 30 minutes. If that were the case, you would see lots of young people dying from smoking as well as from secondhand smoke.
Why is it that most smokers who develop coronary artery disease don't show evidence of this disease until they are at least 40 years old?
The answer is that it takes many years to develop atherosclerosis. It is not a process that happens overnight, and certainly not in 20 minutes.
In fact, it usually takes something on the order of a 90% stenosis (i.e., narrowing) of the coronary arteries before the blood flow is restricted enough to cause a heart attack. Obviously, that cannot happen in 20 minutes.
The fact sheet backs up this claim by citing a study which shows that 30 minutes of exposure to secondhand smoke can cause endothelial dysfunction, as measured by coronary flow velocity reserve (CFVR), in nonsmokers to the same degree as seen in smokers (see Otsuka R, Watanabe H, Hirata K, et al. Acute effects of passive smoking on the coronary circulation in healthy young adults. JAMA 2001; 286:436-441).
But endothelial dysfunction is not the same thing as narrowing of blood vessels, restricted blood flow, and hardening of the arteries (atherosclerosis).
In fact, what endothelial dysfunction measures is the early process of atherosclerosis. As the authors (Otsuka et al.) concluded: "The present findings suggest that reduction of CFVR after passive smoking may be caused by endothelial dysfunction of the coronary circulation, an early process of atherosclerosis, and that this change may be one reason why passive smoking is a risk factor for cardiac disease morbidity and mortality in nonsmokers."
What this means is that acute exposure to secondhand smoke can result in endothelial dysfunction in nonsmokers that if prolonged and repeated over a long time, could eventually result in atherosclerosis and heart disease.
In other words, this study provides a potential mechanism for the observed increase in heart disease risk among passive smokers. It provides biologic plausibility for a causal relationship between exposure to secondhand smoke and heart disease. But it does not suggest that a nonsmoker could develop atherosclerosis as a result of a 30 minute exposure to secondhand smoke.
3. "In that same 30 minutes, changes to your blood boost your risk of building up fat deposits that could lead to heart attacks and strokes."
For the same reasons as above, this claim is also inaccurate. You simply cannot develop fat deposits that could lead to heart attacks and strokes from a 30 minute exposure.
The study the fact sheet cites to back up this claim is a study which shows that brief exposure to secondhand smoke causes cellular and biochemical changes that are seen in atherosclerosis. In other words, similar to the effect of passive smoking on endothelial dysfunction and platelet activation, the effects of passive smoking on low density lipoprotein (LDL) metabolism and cellular accumulation demonstrate a potential biologic mechanism by which chronic exposure to secondhand smoke could lead to atherosclerosis.
Instead of concluding that 30 minutes of secondhand smoke exposure increases the build-up of fat deposits that could lead to heart attacks and strokes, what the study actually concluded was that: "Exposure of nonsmoking subjects to secondhand smoke breaks down the serum antioxidant defense, leading to accelerated lipid peroxidation, LDL modification, and accumulation of LDL cholesterol in human macrophages." (see Valkonen M, Kuusi T. Passive smoking induces atherogenic changes in low-density lipoprotein. Circulation 1998; 97:2012-2016).
4. "After 120 minutes of exposure, your heart rate variability is reduced, increasing the chance of an irregular heart beat that can itself be fatal or trigger a heart attack."
While the first part of this statement is accurate, as there is evidence that acute exposure to secondhand smoke does reduce heart rate variability, the second part of the statement is false. This short-term decrease in heart rate variability does not increase the risk of an arrhythmia (irregular heart beat) that could be fatal or trigger a heart attack.
If this were true, you would see nonsmokers dropping dead all the time after acute exposure to secondhand smoke. If this were true, you would see nonsmokers suffering fatal arrhythmias induced by brief exposure to secondhand smoke. But in the sum total of my years of clinical experience, I have never heard of a nonsmoking patient suffering a fatal or catastrophic arrhythmia from acute exposure to secondhand smoke.
Also, if this were true, it would be unethical to do this type of research without doing cardiac monitoring of human subjects and having resuscitation equipment available. You couldn't just walk into the Salt Lake City airport (as was done in the relevant study) and ask subjects to spend 2 hours in a smoking area, measure a decrease in heart rate variability that could cause a fatal arrhythmia and then discharge those subjects.
The study cited by the fact sheet to back up this claim is a study of the effects of a 2 hour exposure in a smoking area at Salt Lake City Airport on heart rate variability and it does show that the exposure alters heart rate variability. However, the clinical significance of this finding with regards to an acute exposure is nil. The relevance is in terms of the effects of chronic exposure. Once again, this study provides a potential mechanism for the observed increase in heart disease risk among individuals chronically exposed to secondhand smoke (see Pope CA, Eatough DJ, Gold DR, et al. Acute exposure to environmental tobacco smoke and heart rate variability. Environmental Health Perspectives 2001; 109:711-716).
It is important to point out that air pollution also decreases heart rate variability, in a very similar way to the findings observed due to secondhand smoke. There are at least 3 studies which have documented that particulate air pollution changes heart rate variability, just like secondhand smoke; however, one wouldn't conclude that exposure to air pollution may trigger a fatal or catastrophic arrhythmia. (see Liao D, et al. Environmental Health Perspectives 1999; 197:521-525; Gold DR et al. Circulation 2000; 101:1267-1273; Pope CA et al. American Heart Journal 1999; 138:890-899).
If the fact sheet is corrected, please let me know and I would like to highlight that on my blog and praise the organization for fixing it.
Best regards,
Mike
Michael Siegel, MD, MPH
Professor
Boston University School of Public Health
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