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Philip Morris

Overview of the Crs Report on Ets and Lung Cancer Risk

Date: 1995 (est.)
Length: 2 pages
2048280340-2048280341
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Type
REPT, REPORT, OTHER
Area
WORLDWIDE REG AFFAIRS/LIBRARY
Site
N403
Characteristic
MARG, MARGINALIA
Document File
2048280245/2048280868/Ets Congressional Research Svce. (Crs)@ 2048280246/2048280600/Ets Crs Compilation 940000 - 960000
Master ID
2048280248/0599

Related Documents:
Litigation
Stmn/Produced
Named Person
Brownson
Fontham
Request
Stmn/R1-048
Named Organization
Congressional Research Service
Epa, Environmental Protection Agency
OSHA, Occupational Safety & Health Administration
Senate
Date Loaded
05 Jun 1998
UCSF Legacy ID
qiq92e00

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Page 1: qiq92e00
I I OVERVIEW OF THE CRS REPORT ON ETS AND LUNG CANCER RISK "The statistical evidence does not appear to support a conclusion that there are substantial health effects of passive smoking." So reported the Congressional Research Service (CRS) in testimony before a Senate Committee in May of 1994. CRS has subsequently conducted a detailed examination of the environmental tobacco smoke (ETS) issue. The CRS document "Environmental Tobacco Smoke and Lung Cancer Risk," raises serious issues about reports by EPA and OSHA that serve as the basis of anti smoking measures. CRS repeatedly notes instances of substantial uncertainties and unverified assumptions that call into question those agencies' handling ETS issues. For example" • On the EPA's 1993 classification of ETS as a "Group A" carcinogen, CRS notes: "For a variety of reasons, EPA's conclusions have been controversial. While many in the scientific community have accepted the EPA conclusions, others have criticized them. First, the, findings on the studies were mixed, and of the 30 studies examined by the EPA ( one Japanese study could not be used because of the presentation data), 24 found an increased risk, though only five were statistically significant at the 95 percent level, and six actually found a negative risk (with one statistically significant). Of the eleven U.S. studies, eight found a positive risk and three found a negative risk, though none was statistically significant." (p. 23) • Reviewing the four recent studies published since the EPA report, the CRS indicates "the new studies, including the very large Brownson study, did not clarify the existence of a risk. Indeed, they complicated the interpretation of the evidence since the two largest U.S. studies - Fontham and Brownson - found in once case a positive risk that was barely statistically significant and the other no risk at all." (p. 25) • CRS notes that even under the questionable approach EPA used (meta- analysis to combine a range of studies), the ETS risk is "very small": "Even when overall risk is considered, it is a very small risk and is not statistically significant at a conventional 95 percent level. (p. 25) • CRS challenges critical assumptions by OSHA to support its proposed smoking ban in all U.S. workplaces: "If, on average, workplace exposure is lower than residential exposure, then it is likely that many workers would not be exposed to sufficient ETS to be at increased risk for lung cancer. More extensive workplace exposure data are required before this issue can be resolved." (p. 4) I I I I I I I I I I I I I I r4 , ~ 00 , I a
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I I I I I I I I I I I I I I I I I • In addition, CRS notes that if OSHA has conducted an analysis of all of the available studies on smoking in the workplace, it would likely have found no increased cancer risk due to ETS. The report states, "had OSHA performed a meta-analysis, it seems likely that it would have found no increased lung cancer from occupational ETS exposure." (p. 62) • The CRS report makes similar observations with respect to ETS and heart disease. The report notes discrepancies in the data and cites two recent large studies which reported _no increased risk of heart disease from passive smoking. In addition, CRS acknowledges the importance of confounding factors, particularly for heart disease studies, and notes that most of the studies on ETS and heart disease failed to control for most, if not all, of the 18 potential heart disease confounders. (p. 68) , I

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