ets exposure, lung cancer - Legacy Tobacco Documents Library

http://legacy.library.ucsf.edu/tid/wyk81f00/pdf
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U .S. studies was 0 .98 with 95''ro confidencc interval (0 .89, 1 .09) . Although we could
not include the Arownsou ci al . (1992) and Stockwcil rr al . (1992) studies in the mctaanalyscs,
since they did not report relative risk esumatrs for workplacc exposure, the
authors' cotnutents, noted iu Tablc 2, indicate tha : including them would not change
the conclusion that there is no epidetniologic evidence of an association between
workplace ETS exposure and lung catlcer .
In most of these studies, the referencc "nonexposed" group consisted of subjects
who reportedly were not exposed to ETS at work, but may have b .:ccn czposed clsrwhere,
such as in the homc . Subjects in the workplacc•cxposed group also may have been
exposed to ETS elsewluru. 1f there werc an GTS-Jung eancer association, camParison
betwecn these groups would tcnd to produce lower reported relative risks for F."15
• workplace exposurc than would a comparison between groups having no natworkplace
ETS exposure. Howcver, ttonoccuPational ETS exposure could not climittate the cffect
of workplace exposure if a real association existed, so tlu combined results of the 12
studies, showing no lung cancer risk elevation, stand as cvidcnce against tlte existence
of a link between lung cattcer risk and E7S exposure .
The fact that, with the cxccption of Chiua, summary relative risks from spousal
stnoking lung cancer studies are higher than that from -orkplace ETS studies suppoRs
the arguments of Section 2 that tlu rcponed spousal smoking risk elevation is a con•
sequcnce of bins and confounding factors that are introduced by the spousal smoking
study design . Workplace studies would not be subjeet to bias and confounding due to
spousal concordance, and this is a likely explanation for the inconsistency between
workplace and spousal smoking findings .
The EPA (Farland, 1993) took the position that workplacc L•TS studies ean be
disregarded for several reasons: (1) thcre arc fewer worldwidc workplace studies than
spousal ETS exposure studies ; (2) workplaco exposures arc much more variable over
time than spousal cxposures, sinee study subjects and their co-wurkers typic :ally changc
jobs severnl times during a lifetime, while ETS exposure fratU spousal smoking is
relatively stable over time ; (3) presence of ha :e.ardous chemicals in somc workplaces
can make interpretation of study results lnorc difficult than for spousal studics ; and
(4) it can be inferred that if home b?S exposure can cause lung cancer, exposure "at
comparable levels from other sources" can also incrcasc risk . These arguments do not
withstand close examination . Iirst, 14 workplace E'i'S studies comprise an important,
and relatively large, database that cannot be ignored . Second, the notion that workplace
rTS exposures are much more variable than "relativcly stable" spousal exposures is
unsupported spcculatiotl, In fact, the opposite may well be the case : it is hardly uncommon
for people's smokius habits to change and for cohabiting partners to change,
while there is no particular reason to suppose that subjects' workplace ETS exposure
would be markedly difCerent even if they changed jobs, particularly since the type of
job and work environtnent are likely to be similar . Third, the proportion of subjccu
in the workplace ETS studies who arc exposed to occupational lung carcinogens is
likely to bc quite small, since 111c studies arc population-bascd, so it is hard to understand
how workplaae ehcmicals could substantially bias an ETS-lung cancer association in
these studics. In any case, if there wcrz such a bias, it %++ould surely tend to inflate an
observed ETS risk, rather than tlu opposite . One would expcct smoking prevalences
to be higher, not lower, in hazardous workplaces than in others since such vvorkplaces
tend to employ bluc.collar workers . The I:PA's fourth point, that ETS exposure in
workplaces is comparable to home exposure, and therefore if home exposurc can
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