ets exposure, lung cancer - Legacy Tobacco Documents Library

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312 . LL•VOfS AND t.+.YARt)
er al., 1988 ; Lc Marchand c1 al., 1991), and such corrclations could account for appareuc
dose-responsc trends .
As part of its justiflcation for concluding thrt ETS should be classificd as a Group
A careinogen, the EPA claimed that the proportion of spousal smoking studies reporting
a lung cancer risk elevation is improbably high and cannot be attributed to chance
alone. However, this argument is meaningless, since it depends on the dubious assumption
that the spousat smokinZ study design is essentially free of uncontrolled
influences, and produces att unbiased estimate of an ETS effcc :t . The opposite assutnption,
that the spousal smoking design is subject to positive bias and confounding,
is more likely to be true, so weak spousal smoking-lung cancer risk elevations in the
individual studies may well be the result of anifact alotte . Givcn the large number oi'
studies, all using the llawcd spousal smoking study design, a statistical u :sl of association
based on the proportion of positive studies will with high probability detect the influcncc
of bias and confounding inherent in that design ; that is, such a test will likciy be
significant simply due to anifact .
3. WORKPLACE ETS-1 .UNG CANCER STUDIES
Having estimated an ETS-lung cancer risk from fcmale spousal smoking studies,
the EPA extrapolated that risk to males, to exsmokers, and to workplace and other
nonspousal. ETS exposure. A suhstantial majority of thc EPA's estimatcd ETS-attributable
annual U .S . lung cancer deaths, 2200 of 30G0 total deaths (71 .9So), were ascribed
to nonspousat exposure sources, primarily workplace ETS exposurc . Rcmarkably, the
EPA did not use available information front nine U .S, studies of workplace ETS
exposure to estimate workplacc ETS-lung canccr risk . Instead, the agency axsumcd
that workplace l3TS risk can be axtrapolated from the spousal risk estimate .
However, a comparison bctwcen the workplace BTS-lung cancer dttta and the
spousal smoking data indicates that the workplacc data are not consistent with even
the weak risk elevations roponed iu some spousal smoking studies, and indeed the
combined workplacc studies exhibit no ETS-lung cancer association .
To make this comparison, we performed, using the summarization method employed
by the EPA, a meta-analysis of the rt,-sults of 12 studies that have reportcd lutts
caneer relative risks for workplace exposure to L•-1'S (Table 2) . In most of these studies
the exposure index was sclf-reponed exposure to ETS at work, and the comparison
group was porsons not exposed at work . Of the 12 studies, 7 were conducted in the
United States, 3 in Asia, and 2 in Europe . L•levcn studies, including 6 U .S . studies,
reported results for women, 4 studies, including 3 U .S . studies, reportcd results for
men, and one U .S . study rcported results for rncn and women combined . Reported
sex-specific relative risks ranged from 0 .68 to 3 .27, with 9 of 16 being above 1 .0 and
the remaining 7 being 1 .0 or bclow . The authors of two U .S . femalc studies, IIrownson
er al. (1992) and Stockwell er aL (1992), considered workplace ETS oxposure and
reported no sigtti6cant increase in lung cancer risk, but did not present numerical
results . Of the 16 reponed relative risks, we combined 15 by computing a weighted
average of their logarithms, the wcights being the inverses of the variances of the log
relative risks (the Butler rclutive risk of 0 .0 for males could not be ittcludcd in the
mcta-analysir). The sunttnary relative risk for 12 of the 14 worldwide studies was 1 .01,
with 95% confidence interval (0 .92, 1 .11) . The summary rr,.lative risk for 7 of the 9