In his response to my commentary on the deception of the public by anti-smoking groups, Dr. Glantz cites several articles which he implies rebut my argument that anti-smoking groups are deceiving the public when they suggest that secondhand smoke exposure can cause heart attacks in healthy nonsmokers. These articles, he suggests, show that I don't know what I'm talking about when I argue that it is inaccurate to tell the public that acute secondhand smoke exposure can put healthy nonsmokers at risk of a heart attack.
The most important article - a comprehensive review of the acute cardiovascular effects of secondhand smoke - was published this year in the European Heart Journal (see: Raupach T, Schafer K, Konstantinides S, Andreas S. Secondhand smoke as an acute threat for the cardiovascular system: a change in paradigm. European Heart Journal 2006; 27:386-392).
I recently re-reviewed this article, thinking that possibly I might have missed some evidence presented by the authors to support the contention that secondhand smoke may pose an increased risk of acute coronary events (heart attacks) among healthy nonsmokers.
The Rest of the Story
Raupach et al. present 4 lines of evidence - 4 different types of acute cardiovascular effects of secondhand smoke: (1) impairment of endothelial function; (2) effects on platelet activation; (3) oxidative stress, lipoprotein modification, and inflammation; (4) stimulation of sympathetic nervous system activity; and (5) effects on oxygen-carrying capacity.
Here is a summary of what they have to say about each of these effects. I focus here on their conclusions regarding the clinically meaningful effects of each.
1. Impairment of endothelial function
Brief secondhand smoke exposure impairs the ability of the endothelial cells (those which line the coronary arteries) to regulate vascular tone. Normally, in response to certain stresses, these cells release substances such as nitric oxide which relax the smooth muscle in the artery wall, leading to vasodilation and increased blood flow through the vessel. This response is impaired by secondhand smoke, as well as by a high-fat meal, diabetes, and high cholesterol. In addition, secondhand smoke has a direct adverse effect on the viability of endothelial cells.
These effects "result in the migration of monocytes into the vessel wall, their transformation into lipid-laden macrophages, and the subsequent growth and destabilization of lesions due to local inflammatory activity."
In summary, "impairment of endothelial function predicts the initiation and progression of atherosclerosis [hardening of the arteries]."
In other words, the effects of secondhand smoke on the endothelium have 2 clinically meaningful implications: (1) these effects may promote atherosclerosis; and (2) in an individual with severe existing coronary artery disease, it is possible that these effects could trigger a heart attack.
In order to develop atherosclerosis, years and years of exposure are necessary. In order to trigger a heart attack, the individual in question would have to be severely compromised to begin with. He or she would need severely narrowed coronary arteries with existing artery lesions. In other words, he or she would have to have severe existing coronary artery disease.
2. Effects on platelet activation
Secondhand smoke exposure increases platelet activity, leading to platelet aggregation and enhanced coagulability (clotting ability) of the blood. The clinically significant meaning of this effect, as summarized by the study authors, is that: "Platelet activation and thrombosis [clot formation] at sites of vascular injury or atheromatous plaque disruption play a crucial role in the pathophysiology of acute coronary events."
In other words, this effect of secondhand smoke exposure could potentially trigger a heart attack in someone with severe pre-existing coronary artery disease.
3. Oxidative stress, lipoprotein modification, and inflammation
Secondhand smoke exposure causes oxidative stress and impairs anti-oxidant functions in nonsmokers. It also enhances lipid [fat] accumulation in the artery wall and if repeated over time, causes a persistent inflammatory state. The long-term consequence of these effects (if exposure is sustained) is the development of atherosclerotic plaques.
The clinical meaning of these effects is that if "passive smoking occurs on a regular basis...it is very likely to contribute to a persistent inflammatory response which promotes atherothrombosis."
Once again, the evidence for an increased risk of heart attack applies only to, and specifically to, individuals with chronic exposure or with severe existing coronary artery disease.
4. Stimulation of sympathetic nervous system activity
Secondhand smoke exposure increases sympathetic nervous system activity. One manifestation of this is increased cardiac autonomic tone, which leads to decreased heart rate variability. The clinical significance of this effect is that "autonomic dysfunction is linked to higher mortality rates in patients with chronic heart failure."
Thus, this effect would not have clinical meaning for healthy individuals. It would be potentially significant only for individuals with severe existing heart disease and chronic heart failure.
5. Reduced oxygen-carrying capacity
Secondhand smoke, because it contains carbon monoxide which binds to hemoglobin, can impair the ability of red blood cells to carry oxygen. At the cellular level, the decreased oxygen delivery can be significant. Specifically, it "lowers the threshold for cardiac arrhythmias in patients with coronary artery disease. Moreover, exposure to SHS shortens the symptom-free interval in patients with stable angina."
Thus, any effect on the risk of an acute coronary event is restricted to individuals with severe existing coronary artery disease.
In summary, this article (which is consistent with the overall literature) provides evidence that secondhand smoke exposure has a number of physiologic effects which could potentially trigger an acute coronary event (heart attack or arrhythmia) in an individual with severe existing coronary artery disease.
But importantly, the article presents no evidence that there is any acute heart attack, arrhythmia, decreased coronary blood flow, or other adverse clinical event risk in a healthy individual. It also presents no evidence that brief secondhand smoke exposure can cause atherosclerosis.
The rest of the story, then, is that this article strongly supports, rather than refutes, my argument that a large number of anti-smoking groups are deceiving the public by stating that brief exposure to secondhand smoke reduces coronary blood flow in healthy adults, increases heart attack risk in nonsmokers in general, presents clinically meaningful effects that are equivalent to that observed in active smokers, and/or causes hardening of the arteries.
I stand by all of my previous commentaries.
The only aspect of my previous commentaries which I am having some trouble with is my belief that the deception of the public may be inadvertent, due to simple, innocent mistakes. I no longer feel that is a viable explanation for what is going on. My opinion now is that this is basically a deliberate attempt to mislead the public into thinking that secondhand smoke is far more dangerous, on an acute level, than it actually is.
While I share the concern about educating people about the hazards of secondhand smoke and promoting policies to protect them from these hazards, I do not share the conviction that the ends justify the means and that misleading people is acceptable as long as the ultimate goal is a noble one. Deceiving people, with the intention of promoting a favored policy, is wrong. What we are observing is unethical behavior within the anti-smoking movement.
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