Second-hand science

Editorial
Copyright 1999 Washington Times
March 30, 1999



Last week the New England Journal of Medicine published findings from Tulane University researchers that purported to show passive smoking caused an increase of coronary heart disease in nonsmokers. Like a controversial Environmental Protection Agency study that linked it to as many as 3,000 premature deaths each year, the Tulane research relied on a meta-analysis that attempted to combine the results of earlier studies on passive smoking and coronary heart disease.

The results? On average, nonsmokers exposed to passive smoke had a relative risk of 1.25 - an increase of 25 percent - compared to nonsmokers who weren't exposed. Passive smoking is associated with a small increase in the risk of coronary heart disease, the researchers concluded. "Given the high prevalence of cigarette smoking," they said, "the public health consequences of passive smoking with regard to coronary heart disease may be important."

Or it may not. When researchers found a few years ago that a woman who had an abortion faced a 50 percent increase in breast cancer (relative risk 1.5), a spokesman for the American Cancer Society hustled out to downplay the news. Epidemiological studies in general, she told The Washington Post, are probably not able to identify with any confidence any relative risks lower than 1.3. A relative risk of 1.5 is "modest," she said.

But even the much smaller risk of 1.25 that the Tulane researchers found is questionable. In an editorial accompanying publication of the article, John Bailar of the University of Chicago said there is "broad evidence that the results of meta-analyses are often not very reliable."

Part of the problem is that studies of one group of nonsmokers may not combine easily with studies of another group. If the rate of one disease among men is 5 percent and its rate among women is 1 percent, asked Mr. Bailar, does that mean that 3 percent is the rate for a person of "average" sex?

Another problem is the quality of the data itself. If someone participating in a study of the effects of passive smoking is looking for some external cause of his health problem (such as smoking by a spouse or coworker), if someone doesn't really know the amount of smoke to which he was exposed, or if he isn't forthcoming about the fact that at one time he himself smoked, his answers may skew the study's findings. The Tulane researchers, said Mr. Bailar, gave little consideration to such problems.

Perhaps most troubling of all, the 25-percent increase in risk for coronary heart disease from passive smoke is surprisingly large given that there is only a 75 percent increase in risk for active smokers. Mr. Bailar said he finds it hard to understand how diluted, second-hand smoke could constitute as much as a third of the risk of smoke inhaled directly into the lungs.

"I regretfully conclude," wrote Mr. Bailar, "that we still do not know, with accuracy, how much or even whether exposure to environmental tobacco smoke increases the risk of coronary heart disease." Repeated exposure to second-hand science of the kind Mr. Bailar found in the Tulane study can be hazardous to public policy. That too is news.


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