Monday, April 17, 2006

Anti-Smoking Groups Reporting the Opposite of the Science On Acute Cardiovascular Effects of Secondhand Smoke

I have been actively reporting the fallacious claims being made by a large number of anti-smoking groups regarding the acute cardiovascular effects of secondhand smoke (post #1; post #2; post #3; post #4; post #5; post #6; post #7).

Lest readers obtain the impression that these fallacious claims merely represent exaggerations of scientific findings or overstating a case, I here discuss a number of cases where anti-smoking groups present scientific claims that I think communicate the opposite of the findings of the scientific studies upon which they are based.

Let's consider the following three claims:

1. This past Friday, SmokeFree Wisconsin publicly claimed that: "In five minutes of exposure to secondhand smoke, your body starts closing off arteries."

2. The Oregon Department of Human Services claims that: "Experts have found that just 30 minutes of secondhand smoke exposure can impair blood flow to and from the heart in non-smokers."

3. SmokeFreeOhio claims that: "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."

The Rest of the Story

1. The SmokeFree Wisconsin claim

The claim here is that 5 minutes of secondhand smoke exposure causes arteries to start to close off. Presumably, this claim is based on an errant interpretation of the study by Stefanidis et al., which showed that 5 minutes of exposure to secondhand smoke decreased aortic distensibility in patients with coronary artery disease (see: Stefanidis S, et al. Unfavorable effects of passive smoking on aortic function in men. Annals of Internal Medicine 1998; 128:426-434).

While this study did demonstrate that the aorta stiffens slightly in response to a brief secondhand smoke exposure, it certainly did not demonstrate that the aorta (or any other artery) starts to "close off."

In fact, the study showed that the aorta actually opened up a bit. The authors reported that: "The mean systolic and diastolic aortic diameters during the study are shown in Figure 5. Both diameters increased with passive smoking over time (peak at 4 minutes, 23.98 mm for systolic diameter [P = 0.04] and 22.53 mm for diastolic diameter [P = 0.001]."

In other words, this study showed that the aorta actually widened slightly in response to an acute secondhand smoke exposure. It did not close off, nor did it even start to close off.

The rest of the story here is that the very study upon which the scientific claim is based actually showed the exact opposite of the claim that is being made.

Now by no means am I suggesting that it would be accurate or scientifically honest to communicate to the public that secondhand smoke exposure improves blood flow by dilating the aorta slightly. This observed effect is not clinically meaningful in terms of the acute health of an individual without severe coronary artery disease. The point is that the acute clinical significance of this finding is essentially nil in an otherwise healthy individual.

The significance of the study's findings is that they demonstrate how an acute exposure affects the function of an artery , decreasing its elastic properties due primarily to increased smooth muscle tone. These changes are important because they explain why chronic exposure to secondhand smoke can result in atherogenic changes. Ultimately, the study helps to provide biologic plausibility for the observed finding of increased heart disease risk among adults chronically exposed to secondhand smoke.

What the study does not show, however, is that 5 minutes of secondhand smoke exposure causes the body to start closing off arteries.

It may also be important to point out that this study is really only relevant to individuals with existing coronary artery disease. As the authors themselves point out: "All participants were men, most of whom had coronary artery disease. Thus, we can only speculate about whether aortic function in other groups, such as women or persons without coronary artery disease, responds similarly to tobacco smoke exposure."

2. The Oregon Department of Health Services claim


The relevant claim here is that 30 minutes of secondhand smoke exposure impairs blood flow from the heart.

However, the scientific literature demonstrates that acute secondhand smoke exposure increases blood flow from the heart: specifically, it results in an increase in cardiac output (blood flow from the heart).

For example, Stefanidis et al. found that acute exposure to secondhand smoke increased cardiac output: "The mean heart rate and cardiac index increased over time in the passive smoking group ... Both passive and active smoking caused an increase in heart rate and cardiac output." (see: Stefanidis S, et al. Unfavorable effects of passive smoking on aortic function in men. Annals of Internal Medicine 1998; 128:426-434).

So again, the rest of the story here is that the very studies upon which the scientific claim is based actually showed the exact opposite of the claim that is being made.

Now again, by no means am I suggesting that it would be accurate or scientifically honest to communicate to the public that secondhand smoke exposure improves blood flow from the heart by increasing cardiac output. This observed effect is not clinically meaningful in terms of the acute health of an individual without severe coronary artery disease. Again, the point is that the acute clinical significance of this finding is essentially nil in an otherwise healthy individual.

The significance of the finding, again, is that it demonstrates a mechanism by which secondhand smoke could contribute to the diminishing of aortic elasticity, and ultimately (with repeated, chronic exposure) to disease.

What the evidence does not show, however, is that 30 minutes of secondhand smoke exposure impairs blood flow from the heart.

3. The SmokeFreeOhio claim

The claim here is that 20 minutes of secondhand smoke exposure reduces the ability of the heart to pump.

But here again, the scientific literature demonstrates that acute secondhand smoke exposure increases blood flow from the heart; it increases cardiac output (blood flow from the heart).

Once again, the rest of the story here is that the very studies upon which the scientific claim is based actually showed the exact opposite of the claim that is being made.

Conclusion

What I have shown is that the claims being made by many anti-smoking groups about the acute cardiovascular effects of secondhand smoke are not merely exaggerations or examples of overstating the findings of a scientific study. They are, in fact, complete misrepresentations of the science which in some ways communicate the exact opposite of what the scientific studies actually reported.

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