At least 25 anti-smoking and health groups have joined Action on Smoking and Health (ASH), SmokeFreeOhio (SFO), and Americans for Nonsmokers' Rights (ANR) in making fallacious claims about the acute cardiovascular health effects of secondhand smoke exposure.
These public communications, which are (with one exception) still being made on these groups' web sites, inaccurately claim that an acute, transient exposure to secondhand smoke (30 minutes) causes hardening of the arteries in nonsmokers, increases the heart attack risk in nonsmokers to the level observed in smokers, increases heart attack risk in otherwise healthy nonsmokers, reduces coronary blood flow putting nonsmokers at risk of suffering a heart attack, causes heart damage, and/or increases otherwise healthy nonsmokers' risk of suffering some other fatal or catastrophic cardiac event.
All of these claims are inaccurate because there is no evidence that a single transient exposure to secondhand smoke poses any severe or fatal cardiovascular risk to any individual, other than someone who has existing severe coronary artery disease. Moreover, it is medically impossible for a person to develop atherosclerosis in only 30 minutes (it takes years), so evidence supporting the claims being made by these groups would defy medical science.
And furthermore, there is evidence which documents that coronary blood flow is not reduced in nonsmokers exposed to 30 minutes of secondhand smoke and that nonsmokers can exercise vigorously on a treadmill under such conditions without necessarily even experiencing a decline in their exercise tolerance, much less any serious or catastrophic consequences.
Here are the groups making the claims and the specific claims being made (this appears to be a partial and not entirely inclusive accounting of the extent of the problem):
Tobacco Free Coalitions of Clark County and Skamania County: "As little as 30 minutes of secondhand smoke can lead to hardening of the arteries in nonsmokers."
British Heart Foundation: "Just 30 minutes exposure to tobacco smoke can affect the cells lining the coronary arteries and this can contribute to the development of atheroma narrowing the coronary arteries and reducing blood flow to the heart."
Coalition for a Tobacco-Free Hawaii: "Thirty minutes of secondhand smoke compromises a non-smoker'’s coronary arteries to the same extent as in smokers. ... All of these effects not only increase the long term risks of developing heart disease, but also increase the immediate risk of heart attack."
Action on Smoking and Health (London): "Short term exposure to tobacco smoke also has a measurable effect on the heart in non-smokers. Just 30 minutes exposure is enough to reduce coronary blood flow."
Campaign for Tobacco-Free Kids: "as little as 30 minutes of exposure to secondhand smoke can trigger harmful cardiovascular changes, such as increased blood clotting, that increase the risk of a heart attack."
Heart Foundation South Africa: "Only 30 minutes of exposure can damage a non-smoker's heart and increases the risk of heart disease by 30%."
Clearing the Air Scotland: "30 minutes exposure to second hand smoke is sufficient to reduce coronary blood flow in otherwise healthy adults."
Americans for Nonsmokers' Rights: "Even a half hour of secondhand smoke exposure causes heart damage similar to that of habitual smokers. Nonsmokers'’ heart arteries showed a reduced ability to dilate, diminishing the ability of the heart to get life-giving blood."
DuPage County Health Department: "30 minutes exposure = stiffened, clogged arteries"
Tobacco Public Policy Center: " A recent study completed by Japanese researchers concluded that just 30 minutes of exposure to secondhand smoke can lead to hardening of the arteries in nonsmokers."
American Lung Association of Oregon: "As few as 30 minutes of secondhand smoke exposure can impair coronary circulation in a non-smoker."
Tobacco-Free Coalition of Oregon: "The journal article points out that even 30 minutes of exposure to secondhand smoke increases blood platelet '‘stickiness,'’ which can lead to blood clots. In addition, arteries narrow after exposure to secondhand smoke, so smaller clots cause more damage, and there is an increase in heart rhythm problems associated with heart attacks."
Health Sponsorship Council (New Zealand): "After 30 minutes --– arteries affected. Non-smokers usually have arteries that can dilate and boost blood flow to the heart more efficiently than a smoker'’s arteries. But exposure to second-hand smoke compromises that advantage after 30 minutes, to the same degree as for a pack-a-day smoker."
University of North Carolina Department of Family Medicine: "30 minutes of exposure = stiffened, clogged arteries"
Michigan Smoke-Free Dining Petition Drive: "A half hour of exposure to secondhand smoke dramatically increases a person'’s short-term risk of heart attack."
Tobacco-Free Iowa (no longer an active link - this is the cached page): "Nonsmokers exposed to secondhand smoke for just 30 minutes experience hardening of the arteries."
Tobacco Technical Assistance Consortium (TTAC): "Short exposure to secondhand smoke hardens arteries: According to Japanese researchers who presented at a recent American Heart Association meeting, as little as 30 minutes of exposure to secondhand smoke can cause the arteries of nonsmokers to harden."
Maricopa County Department of Public Health: "Nonsmokers exposed to secondhand smoke for just 30 minutes experience hardening of the arteries."
Action on Smoking and Health: "Even for people without such respiratory conditions, breathing drifting tobacco smoke for even brief periods can be deadly. For example, the Centers for Disease Controls [CDC] has warned that breathing drifting tobacco smoke for as little as 30 minutes ( less than the time one might be exposed outdoors on a beach, sitting on a park bench, listening to a concert in a park, etc.) can raise a nonsmoker'’s risk of suffering a fatal heart attack to that of a smoker."
SmokeFreeOhio: "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. 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. 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. ... 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."
TobaccoScam: "30 minutes exposure = stiffened, clogged arteries"
Citizens Against Unhealthy Smoke-Filled Environments: "Just 30 minutes exposure to secondhand smoke can compromise the cardiovascular system of nonsmokers by reducing blood flow to the heart."
Smokefree Islington (UK): "A study published in the Journal Of The American Medical Association found that just 30 minutes' exposure is enough to reduce coronary blood flow."
New York City Department of Health and Mental Hygiene: "Just 30 minutes of exposure to second-hand smoke produces some of the same physical reactions that would occur from long-term smoking, and increases the risk of heart disease in non-smokers."
Clean Air for Everyone (C.A.F.E.) Iowa: "Nonsmokers exposed to secondhand smoke for just 30 minutes experience hardening of the arteries."
Washington State Department of Health: "Only 30 minutes of secondhand smoke exposure may cause heart damage similar to that of regular smokers. This exposure can reduce the ability of the arteries close to the heart to expand, which reduces the ability of the heart to receive life-giving blood."
Campaign for a Healthy and Responsible Tennessee : "The Journal of the American Medical Association reports that just 30 minutes of exposure to secondhand smoke changes blood chemistry and increases the risk of heart disease in non-smokers."
Smoke-free Bristol (UK): "Short-term exposure to second-hand smoke has a measurable effect on the heart in non-smokers -– 30 minutes exposure is enough to reduce blood flow to the heart muscle."
The Rest of the Story
Note that most of these communications claimed that 30 minutes of secondhand smoke exposure causes heart damage, narrowing of the coronary arteries, clogged coronary arteries, or reduced coronary blood flow, even though the Otsuka studied (which is cited for many of these claims) actually documented that there is no reduction in coronary blood flow in nonsmokers exposed to secondhand smoke for 30 minutes.
It is, in fact, medically impossible for someone to develop coronary atherosclerosis in 30 minutes. Atherosclerosis is a gradual process that takes years to occur.
I have already attempted, on multiple occasions, to explain why these claims are completely fallacious (occasion 1; occasion 2; occasion 3; occasion 4; occasion 5; occasion 6; occasion 7; occasion 8).
I will not repeat the entire discussion here, but instead, refer readers to these prior commentaries.
The fallacious claims appear to stem from an exceedingly flawed extrapolation from a study by Otsuka and colleagues (see Otsuka R, Watanabe H, Hirata K, et al. Acute effects of passive smoking on the coronary circulation in healthy young adults. JAMA 2001), which reported that 30 minute of secondhand smoke exposure causes endothelial dysfunction in nonsmokers. The relevant study reported 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.
But endothelial dysfunction is a far cry from hardening of the arteries, stiffened and clogged arteries, and a heart attack.
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 an otherwise healthy nonsmoker could suffer a heart attack as a result of a 30 minute exposure to secondhand smoke, and it certainly does not mean that a nonsmoker's risk of a heart attack approaches that of a smoker's after 30 minutes of exposure to secondhand smoke.
It is important to note that eating a single high-fat meal can cause significant endothelial dysfunction. Plotnick et al., writing in the Journal of the American Medical Association, reported that: "A single high-fat meal transiently reduces endothelial function for up to 4 hours in healthy, normocholesterolemic subjects, probably through the accumulation of triglyceride-rich lipoproteins." (see Plotnick GD, Corretti MC, Vogel RA. Effect of antioxidant vitamins on the transient impairment of endothelium-dependent brachial artery vasoactivity following a single high-fat meal. JAMA 1997; 278:1682-86).
The exact same reasoning and the same extrapolation that the above anti-smoking groups are using to claim that 30 minutes of secondhand smoke exposure is potentially fatal could also be used to argue that eating a hamburger raises the risk of a heart attack in an otherwise healthy individual. Or that a brief exposure to air pollution could do so. These examples show how meaningless the relevant studies are in terms of documenting any acute heart attack risk in healthy individuals.
The possible acute cardiovascular risk of secondhand smoke exposure is the slight possibility that in people with existing severe coronary artery disease, the endothelial dysfunction, platelet activation, or other physiologic changes caused by acute exposure to secondhand smoke might be enough to trigger a coronary event (i.e., a heart attack). There is very little evidence that this is actually a substantial, clinically-observed risk, but it is possible, and I would agree with recommending that nonsmokers with coronary artery disease should try to minimize or eliminate their exposure to secondhand smoke.
Unfortunately, all of the above scientific claims go far beyond simply suggesting an increased risk of myocardial infarction in patients with severe coronary artery disease who are exposed acutely to secondhand smoke.
The bottom line is that a large number of anti-smoking organizations are making grossly inaccurate scientific claims in order to support policies to ban smoking in certain public places. This has gone far beyond simply one or two organizations that are making errant claims. It is now essentially a movement-wide misrepresentation of the science of secondhand smoke.
I think what we have here is a movement that is entering a crisis situation: it is at risk of losing its scientific credibility. Something has gone wrong in the movement's ability to exercise critical scientific judgment. Its mechanisms of "checks and balances" to ensure some measure of critical evaluation of scientific claims before they are made publicly have somehow gone awry.
How it responds to this crisis will determine whether the tobacco control movement is able to retain its credibility and reputation as being purveyors of solid science in support of a public health agenda.
I think there will clearly need to be an apology and a correction or clarification if not a retraction of these claims on the part of a large number of anti-smoking groups. I also think that there needs to be a much greater concern on the part of anti-smoking groups about the accuracy of their public statements in support of the agenda. The agenda has simply become the driving force for the interpretation and communication of the science, rather than the science driving the policy, as it should in public health.
Finally, I want to make it clear that I would not be publicly exposing this crisis (and calling it to the attention of the tobacco companies) if I did not truly believe that in the long run, the effectiveness of the tobacco control movement, dependent upon its credibility in the eyes of the public and the media, was seriously at stake and at great risk of being undermined.
But as a public health scientist and conscientious tobacco control advocate, I cannot let something of this magnitude slip by unnoticed. It is simply not appropriate to use fallacious scientific health claims to advance our agenda, no matter how important that agenda is in terms of saving lives and promoting the public's health. The ends do not justify the means. And the means need a lot of work, urgently, if the tobacco control movement is to be able to continue to save lives and promote the public's health into the future.
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