I had planned to wait until Friday to report back on responses I received to my post criticizing certain claims made by three prominent anti-smoking groups regarding the acute cardiovascular effects of secondhand smoke. However, the first response I received is too important to pass up.
TobaccoScam responded yesterday with the following statement, which was sent to thousands of tobacco control advocates worldwide:
"The finding of similar changes in endothelial function with a high cholesterol load is not new. It just shows that the high oxidant load has effects similar to SHS (which is probably also acting, at least in part through the oxidant load in the smoke). We published the first paper on this over ten years ago, when I was an associate editor of the Journal of the American College of Cardiology. (The "intervention" there was an Egg McMuffin.)
In addition to the acute effects, the associated insult to the vascular endothelium is important for the long-run development of atherosclerosis.
Mike's comments are further evidence that he just does not understand modern vascular biology."
The Rest of the Story
The issue at hand, however, is not vascular biology. The issue is the clinical significance of that vascular biology.
I am not contesting the vascular biology itself, which is quite clear: brief exposure to secondhand smoke, like eating a high-fat meal, induces endothelial dysfunction, as measured by a reduction in endothelial-dependent flow-mediated dilatation.
What I am contesting is the conclusion that this transient alteration of endothelial dysfunction caused by a brief exposure to secondhand smoke results in clogged arteries, narrowed arteries, heart disease, stroke, and heart attacks.
Certainly, with respect to the endothelial dysfunction caused by eating a high-fat meal, we do not conclude that eating a meal at McDonalds results in clogged arteries, narrowed arteries, heart disease, stroke, and heart attacks. So how can we make the same claim with respect to secondhand smoke?
Actually, I agree completely with TobaccoScam that there are similar changes in endothelial function that occur with a high cholesterol load and with brief secondhand smoke exposure. I also agree that the high oxidant load presented by a high-fat meal has effects similar to secondhand smoke, which is probably also acting, at least in part, through the oxidant load in the smoke. And further, I agree that the associated insult to the vascular endothelium is important for the long-run development of atherosclerosis.
However, the point of contention here is not whether secondhand smoke impairs endothelial dysfunction or whether it causes heart disease. The point of contention is whether 30 minutes of exposure to secondhand smoke clogs arteries, causes hardening of the arteries, results immediately in heart disease, and causes strokes and heart attacks.
And rather than address these critical issues, TobaccoScam has chosen instead to attack me and my knowledge of medicine, rather than to discuss and defend its claims that brief secondhand smoke exposure clogs arteries, inducing heart attacks and strokes.
In fact, anyone familiar with my commentaries or research will know that I have clearly stated my belief that chronic secondhand smoke exposure is a cause of heart disease. I think the evidence on this point is quite strong. I also think the evidence that there is acute impairment of endothelial dysfunction (as well as activation of platelets and other adverse physiologic changes) is also strong.
However, what is not strong is the evidence that the transient impairment of endothelial dysfunction induced by brief exposure to secondhand smoke results in clogging of the arteries which therefore causes heart attacks and strokes.
In fact, it is not only the case that there is not strong evidence that the transient impairment of endothelial dysfunction results in clogged arteries and heart attacks, but it is medically implausible that such an effect could happen in a healthy person. As I have pointed out repeatedly, the process of artery clogging (atherosclerosis) does not occur quickly. It cannot happen after a single 30 minute exposure to secondhand smoke. It takes many years of exposure. Just as it takes many years of eating high-fat foods before a person develops atherosclerosis. You don't drop dead of a heart attack after eating a single Big Mac. If you did, you would see a long line of stretchers being carted off from McDonalds.
If we're not going to communicate that eating a high-fat meal is equivalent to clogged arteries, then we shouldn't communicate the same thing with respect to brief secondhand smoke exposure. And the same goes with heart disease and heart attack and stroke risk.
As I've also said before, I'm not even contesting a statement that a brief exposure to secondhand smoke could have severe consequences for an individual with severe, pre-existing coronary artery disease. But that's not even the statement that's being made by these anti-smoking groups. In every case, what I've taken issue with is an unqualified statement that applies to all individuals, not just those with severe, pre-existing disease.
Even for individuals with severe coronary artery disease, we wouldn't take the evidence that a high-fat meal causes endothelial dysfunction and platelet activation and communicate to people that eating a Big Mac might cause a fatal heart attack.
I think it's time for a serious discussion in the tobacco control movement about the validity of the actual claims that are being made publicly by numerous anti-smoking groups. Whether such a discussion is even possible is not clear to me. There seems to be no interest in discussing the substance of these scientific and ethical issues, merely a desire to discredit and blackball the person who is pointing out these scientific flaws in the tobacco control movement's communications.
I apologize for my apparent complete ignorance of vascular biology. I guess I was out touring the beautiful sights of New Haven when the rest of my medical school class was attending our vascular biology lectures, discussing vascular biology research and its clinical implications, and diagnosing and treating patients with vascular disease. If anyone has a copy of "Vascular Biology for Dummies," I'd greatly appreciate a copy.
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