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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