Wednesday, May 07, 2008

30 Minute Tobacco Smoke Study Authors Continue to Claim that Research Proves Brief Exposure Causes Heart Attacks; Media Reporting the Same

Although their study relates to mechanisms for the effects of chronic exposure to secondhand smoke, researchers who published last week's article in the Journal of the American College of Cardiology are insisting that their research demonstrates an increased risk of heart attacks from brief tobacco smoke exposure.

In a press release issued by the University of California, San Francisco (home to several of the study authors), the authors indicate that their findings demonstrate an effect of brie tobacco smoke exposure not only on endothelial function, but also on heart attack risk.

According to the press release: "The public health implications of the study findings are significant, according to Yeghiazarians [a study author]. 'Our study helps explain why there is about a 20 percent drop in hospital admissions for heart attacks when cities and states pass laws mandating smokefree workplaces, restaurants and bars.'"

The media has apparently picked up on the authors' interpretation of their findings, as evidenced by the leading paragraph of this Metro (UK) story about the article: "Inhaling second-hand smoke for as little as half-an-hour damages blood vessels and can lead to heart attacks and strokes, a study has found."

The Rest of the Story

It is blatantly misleading to state that these study results support the conclusion that 30 minutes of secondhand smoke exposure can lead to heart attacks and strokes. What the study shows is that brief tobacco smoke exposure causes endothelial injury. This injury, if repeated over and over through the course of many years, could lead to the process of atherosclerosis, and eventually (after many years), to heart disease and heart attacks.

However, the study provides absolutely no evidence that a mere 30 minutes of tobacco smoke exposure increases the risk of an individual suffering a heart attack.

There are many exposures and factors which can cause endothelial dysfunction similar to that observed in the recent study. For example, mental stress has, like secondhand smoke exposure, been found to cause transient endothelial dysfunction (see: Spieker et al. Mental stress induces prolonged endothelial dysfunction via endothelin-A receptors. Circulation 2002; 105:2817-2820 and Ghiadoni et al. Mental stress induces transient endothelial dysfunction in humans. Circulation 2000; 102;2473-2478).

The authors of these studies of the effects of mental stress interpreted and reported the results of their studies properly. They explained that their results suggest a mechanism for the observed effects of chronic mental stress on heart disease. For example, Ghiadoni et al. conclude as follows: "These findings suggest that brief episodes of mental stress, similar to those encountered in everyday life, may cause transient (up to 4 hours) endothelial dysfunction in healthy young individuals. This might represent a mechanistic link between mental stress and atherogenesis."

Note that the authors' conclusion is that brief episodes of mental stress may, if repeated over time, lead to the atherosclerotic process. The authors do not conclude that their study demonstrates that an individual exposed to brief mental stress is at a risk of suffering a heart attack.

It is especially misleading to make an unqualified claim that 30 minutes of secondhand smoke exposure can cause a heart attack in an otherwise healthy person. Unfortunately, many anti-smoking groups are making precisely such a claim.

One such example is the Canadian Lung Association, which claims on its website: "Just 30 minutes' exposure to second-hand smoke hardens your arteries (arteriosclerosis)."

This is obviously not just a misleading statement, but an inaccurate and absurd one. There is no way that 30 minutes of secondhand smoke exposure can cause the arteries to harden. Atherosclerosis is a process which takes more than just 30 minutes. It takes many years.

While the intention of the researchers and groups making these misleading and unsupported statements is to promote the passage of smoking bans, I believe that this exaggeration and distortion of the science is actually going to hurt the cause. There is only so much that the public is going to take. When they realize that anti-smoking groups are actually stating that 30 minutes of secondhand smoke is enough to cause hardening of the arteries, a process that takes many years, the public is going to come to believe that the anti-smoking movement is a joke, or at least that its science leaves a lot to be desired.

(Thanks to Rose, Bill Gibson, Gian Turci, and Ann W. for tips leading to this post)

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