I may have been a bit misleading when I suggested that Action on Smoking and Health (ASH) went off the deep end by claiming that 30 minutes of exposure to drifting tobacco smoke increases a nonsmoker's risk of a fatal heart attack to that of a smoker's.
In fact, ASH appears to be somewhat conservative, if you can believe it.
It turns out that another anti-smoking group - SmokeFreeOhio - is claiming that just 20 minutes of exposure to secondhand smoke increases a nonsmoker's risk of suffering a heart attack.
According to a SmokeFreeOhio "fact" sheet entitled "The Dangers of Secondhand Smoke":
"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."
Elsewhere in the "fact" sheet, SmokeFreeOhio claims that:
"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."
Elsewhere, SmokeFreeOhio claims that:
"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."
And still elsewhere, SmokeFreeOhio claims that:
"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."
The Rest of the Story
I find each of these four claims to be scientifically inaccurate.
Let's take each of the claims, one by one:
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, how do you get from a little platelet stickiness to a reduced ability of the heart to pump and an elevated risk of heart attack?
You simply can't equate a transient increase in platelet stickiness with an elevated heart attack risk. And you certainly 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 inaccurate.
The fact sheet backs up this claim by citing a study which shows that brief exposure to secondhand smoke decreases platelet sensitivity to prostacyclin.
But you can't 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.
Rather than documenting SmokeFreeOhio's claim, this study actually shows why the claim is inaccurate.
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."
This is completely inaccurate. You simply 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 a far cry from 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 fact sheet backs up this claim by citing 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.
Far from 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.
Just think about it. 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 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 fact sheet backs up this claim by citing 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 warn the public 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).
To be clear, I am not accusing SmokeFreeOhio of lying or intentionally deceiving the public. I don't know their beliefs or intentions. It is possible that they simply misinterpreted the results of these studies. What I am simply saying is that what they are disseminating is wrong. It is scientifically inaccurate.
Conclusion
The rest of the story is that another anti-smoking group is making an inaccurate scientific claim in order to support its policy agenda of promoting smoking bans. This one, more aggressive than the first (Action on Smoking and Health) is claiming that just 20 minutes of secondhand smoke exposure (rather than 30) increases the risk of a heart attack in nonsmokers.
In addition to being wrong because it is, I believe, unethical, inappropriate, and irresponsible to be disseminating scientifically invalid information, these actions are going to harm the credibility of the anti-smoking movement simply because they are so completely implausible and seemingly taken out of nowhere. The extrapolations being made are so extreme that they threaten to undermine the public's perception of the anti-smoking movement's ability to interpret and report the results of scientific studies at all, even when that reporting is appropriate.
The problem is - the public and policy makers will not necessarily know the difference. They will not be able to differentiate easily between when the claims we are making are legitimate and when they are extreme and errant extrapolations. They will just begin to question everything that we say.
So as we stand today, the claim that 30 minutes of secondhand smoke exposure increases heart attack risk among nonsmokers is a conservative one. Now we're down to 20 minutes. Does any anti-smoking group care to go for 10 minutes? Anybody? Anybody?
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