In a number of previous posts, I have explained why anti-smoking groups' claims that a brief exposure to secondhand smoke can cause heart attacks are misleading, because they do not qualify their statements by pointing out that such a risk pertains only to individuals with severe, existing coronary artery disease.
Here, I argue that there is simply not evidence to support a claim that there is any substantial heart attack risk from a brief exposure to secondhand smoke, even among those with coronary artery disease.
The assertion that a brief secondhand smoke exposure can trigger a heart attack in someone with coronary artery stenosis is based on the observations that:
(1) tobacco smoke exposure causes platelet activation, which increases the clotting tendency of the blood and could lead to heart attack through the formation of platelet aggregates in the coronary microcirculation or through clot formation in the coronary arteries around areas of an existing atherosclerotic plaque; and
(2) tobacco smoke impairs endothelium-dependent vasodilation, thus reducing the coronary arteries' ability to deliver adequate blood to the heart under a circumstance of extreme stress, which could be enough to trigger a heart attack in someone with existing coronary artery stenosis.
The Rest of the Story
The rest of the story is that the effects of a brief tobacco smoke exposure on platelet activation are extremely short-lived and thus may not present a real and substantial threat of triggering a heart attack. Even the effects of active smoking on platelet activation are short-lived.
In Law et al.'s meta-analysis of studies relating secondhand smoke exposure and heart disease (in which they conclude there is a 23% increased risk of coronary artery disease due to chronic secondhand smoke exposure), the authors acknowledge that the effects of smoking on platelet activation are transient, and thus they exclude cross-sectional studies of platelet aggregation in smokers and nonsmokers (see: Law MR, Morris JK, Wald NJ. Environmental tobacco smoke exposure and ischaemic heart disease: an evaluation of the evidence. BMJ 1997; 315:973-980).
As the authors state: "We did not use cross sectional studies of platelet aggregation in smokers and non-smokers because...the effects of smoking are short term and may not be apparent in smokers who had not smoked for a few hours before blood was collected."
So the effects of tobacco smoke on platelet activation are so short-term that even in a chronic active smoker, one may not detect any effects if the person has not smoked for a few hours before his or her blood is tested.
In fact, evidence (cited by Law et al. to support their claims) shows that the effects of tobacco smoke on platelet activation are quite transient. Schmidt and Rasmussen found that the effect of tobacco smoke on platelet aggregation essentially disappears one hour after exposure (see: Schmidt KG, Rasmussen JW. Acute platelet activation induced by smoking: In vivo and ex vivo studies in humans. Thrombosis and Haemostasis 1984; 51: 279-282).
Even if the observed short-term effect of platelet activation in nonsmokers did substantially increase heart attack risk among those with coronary artery stenosis, the heart attack would pretty much have to occur instantly after the exposure, as the effects are gone within about an hour. So if this were a true, substantial effect, we would see nonsmokers keeling over from heart attacks when they are eating out in smoky bars or restaurants.
Similarly, the effects of tobacco smoke on endothelium-dependent vasodilation appear to be short-lived. There is no evidence that these effects are anything but transient. Moreover, while one study (the Otsuka et al. study) showed evidence of an acute effect of brief tobacco smoke exposure on endothelial dysfunction, another study failed to find such an effect, and in fact concluded that the observed differences in endothelial function between secondhand smoke-exposed nonsmokers and non-exposed nonsmokers are due to chronic, rather than acute exposure (see: Kato M, Roberts-Thomson P, Phillips BG, et al. The effects of short-term passive smoke exposure on endothelium-dependent and independent vasodilation. Journal of Hypertension 1999; 17: 1395-1401).
As the authors state: "Our data demonstrate that acute exposure to passive smoke does not alter either endothelium-dependent or independent vasodilatory responses in healthy nonsmoking individuals. Hence, impaired endothelial vasodilatory responses in nonsmokers chronically exposed to passive smoke most likely reflect chronic functional changes and/or structural changes in responses to cigarette smoke, rather than the acute effects of cigarette smoke toxicity on endothelial function."
This study contradicts the statements of anti-smoking groups that brief exposure to secondhand smoke can increase heart attack risk by impairing endothelial-dependent vasodilation.
My point, however, is not that the evidence is definitive that there is no real and substantial increase in heart attack risk in a nonsmoker with coronary artery disease who is exposed briefly to secondhand smoke. My point is simply that there is no conclusive evidence that there is any real and substantial risk, and thus, that it is premature (and not solid science) for anti-smoking groups to be making such claims widely to the public based purely on speculation, but not on any actual documentation of a substantial risk.
Beyond the lack of documentation to support the claim that brief secondhand smoke exposure presents a real and substantial risk of heart attack among individuals with coronary artery disease, it is important to understand that a number of behaviors in which people typically engage are equally likely to induce a pro-thrombotic state because of platelet activation or other effects.
For example, eating a single high-fat meal has been shown to temporarily increase the clotting tendency of the blood (see: Mutanen M, Freese R. Fats, lipids and blood coagulation. Current Opinions in Lipidology 2001; 12:25-29).
Eating butter is also well-known to increase the clotting tendency of blood, also potentially triggering a heart attack in people with coronary artery disease (following the logic of the anti-smoking groups): "The addition of butter to plasma shortened the Stypven clotting time of human plasma by over 75% and butter was more active than any other fat tested" (see: Billimoria JD, Curtis RG, Maclagan NF. The phospholipids of butter and their effect on blood coagulation. Biochemistry Journal 1961; 78:185-194).
This body of research prompted Hodgson et al. to conclude that: "Postprandial lipaemia is recognized as a procoagulant state..." (see Hodgson JM, Puddey IB, Burke V, et al. Acute effects of ingestion of black tea on postprandial platelet aggregation in human subjects. British Journal of Nutrition 2002; 87: 141-145).
The reasoning and scientific "evidence" being used by anti-smoking groups to support their assertion that a brief secondhand smoke exposure increases heart attack risk [among individuals with existing coronary artery disease] could just as easily support an assertion that eating butter or any high-fat meal causes heart attacks.
I guess there is some truth, then, to the claim that eating a Big Mac could give you a heart attack.
The point is that we do not make claims in medicine that a particular brief exposure will cause heart attacks simply because there is evidence that the exposure causes endothelial dysfunction and/or platelet activation. Without documenting that such an exposure actually causes people to have heart attacks, we would not make such a claim. It would essentially be based on speculation. However, this has not stopped anti-smoking groups from making the precise type of claim for secondhand smoke under the precise scientific evidence.
Essentially, it appears to me that the entire heart attack risk from brief secondhand smoke exposure claim is little more than a gimmick, apparently conjured up to try to increase the emotional appeal of the secondhand smoke message by scaring people into thinking that merely breathing in secondhand smoke for a few minutes could cause them to keel over from a heart attack.
If this is the basis for supporting bans on smoking in bars and restaurants, then I'm afraid we're on very weak grounds. First, because the claim is scientifically weak. Second, because under similar conditions, no one is arguing that we should ban the sale of high-fat foods or require restaurants to only serve meals that have been shown not to increase the clotting tendency of the blood.
Obviously, those who read this blog know that I believe there is plenty of evidence to support the protection of nonsmokers from secondhand smoke exposure in the workplace. But the risk of suffering a heart attack from a brief exposure is not one of them. And to continue to rely heavily upon this unsupported claim does not strengthen our case, it greatly weakens it. Because it calls our credibility into question, which could lead some to wonder whether any of our health claims are worth trusting.
While there might be a perception by anti-smoking groups that they can increase support for smoke-free laws by scaring people into thinking they will have heart attacks from a brief exposure to secondhand smoke, the truth is that these kind of scientifically weak claims are only going to serve, eventually, to erode the public's trust in our movement, destroy our credibility, and reduce (not enhance) our effectiveness in protecting the public from secondhand smoke.