Jane G. Gravelle

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Jane G Gravelle was an economist who worked on tax problems for the Congressional Research Service (CRS). Her position was as an Economics Policy analyst. She occasionally worked with an associate, C. Stephen Redhead who was a physiologist. Individually and jointly they produced a number of reports on the tobacco industry and the problem of second-hand smoke, most of which took a favorable line from the viewpoint of the cigarette companies.

Documents & Timeline

1994 Mar 8 A CRS Report for Congress. Cigarette Taxes to Fund Health Care R¢form: An Economic Analysis by Jane G. Gravelle, Senior Specialist in Economic Policy, at the Office of Senior Specialists (CRC), and Dennis Zimmerman, Specialist In Public Finance, Economics Division stated on, p.47 charged the EPA with manipulating its results:

"One thing EPA did in its assessment is change the standard for statistical significance from the usual standard [95% confidence intervals], and the one generally used in the original studies . "Admittedly, it is unusual to return to a study after the fact, lower the required significance level [to 90%], and declare its results to be supportive rather than unsupportive of the effect one's theory suggests should be present."

A week later, in an appearnace before a Senate Sub-committee on Clean Air and Nuclear Regulation (Committee on Environment and Public Works), Jane Gravelle stated outright:

" .. .our evaluation was that the statistical evidence does not appear to support a conclusion that there are substantial health effects of passive smoking ."[2]


1994 June 9: The Department of Health and Human Services immediately contradicted her claim.
Extract from HHS submission to Senate Committee hearing on H.R. 3434, the Smokefree Environment Act.

Statement by Centers for Disease Control and Prevention

In its report, "Cigarette Taxes to Fund Health Care Reform: An Economic Analysis," the Congressional Research Service (CRS), assesses the health risks of environmental tobacco smoke (ETS) and disputes well-documented scientific evidence that exposure to ETS is a cause of disease. The CRS report concludes that the link between passive smoking and disease is uncertain, and that epidemiologic studies suggesting a link are scientifically flawed. In reaching these conclusions, the CRS report regrettably has discounted the fundamental principles and scientific rigor of epidemiology, as well as the immense body of research on ETS exposure.

It would not be appropriate to consider the CRS report a review or analysis of the evidence relating to tne health effects of ETS exposure. Hundreds of studies, including the 1986 Report of the Surgeon General, The Health Consequences of Involuntary Smoking, document the relationship between ETS and health outcomes. The CRS report directly cites only two studies, and based on these two references, reaches conclusions unsupported by the preponderance of scientific evidence.

In testimony before the United States Senate, the authors acknowledge limitations in their qualification to conduct a valid epidemiologic analysis. They note that, as economists, their area of expertise is "economic analysis and the associated areas of statistical inference and quantification of effects for purposes of cost-benefit analysis and related economic policies," rather than the "physiological and biological transmission mechanisms of disease causing agents."

Most importantly, the CRS report challenges the EPA risk assessment on lung cancer and ETS exposure. The EPA report was written and reviewed by many reputable scientists trained in the causation and prevention of disease. The Department of Health and Human Services fully supports this report as an accurate assessment of the health risks of ETS exposure. Accepting conclusions on issues of disease causation by any but the consensus of medical and epidemiologic scientists would be a serious mistake.

The following are the most important areas of public health concern in the CRS report on the health risks of exposure to ETS:

1. On page 45, the report raises questions about whether there is a dose-response relationsnip between tobacco smoke exposure and adverse health effects over the wide range of ETS levels to which nonsmokers are exposed. The epidemiologic data in this regard, however, are clear. The weight of the evidence shows that the risk of lung cancer rises as ETS exposure levels increase.

2. On page 45, the report suggests that there may be a threshold level below which there is no biological damage from ETS exposure. The existence of a threshold for tobacco smoke in lung cancer is theoretically possible, but there are no empirical data to support the threshold concept and most scientists argue against a threshold for any carcinogen. Indeed, the data that do exist clearly lavor the non-threshold hypothesis. Virtually every one of the thousands of studies evaluating lung cancer among smokers shows that risks increase in proportion to level of smoking, with demonstrable increases in risk even among the very lightest smokers.

3. On page 45, the report suggests that the relationship between tobacco smoke exposure and health effects at the level of passive smoke exposure is such that the effects would be minor. The CRS report refers to the 1989 Surgeon General's report citation (page 44) of a cohort study of lung cancer and smoking among about 34,000 British physicians. This study estimated that risk of lung cancer rose in proportion to the square of the number of cigarettes smoked per day. The CRS states that this implies that the relation is "strongly nonlinear.' This statement is questionable, since the departure from linearity with the quadratic model may not be great. More importantly, the CRS report disregards data presented on page 45 of the same Surgeon General's report. There, a graph is presented showing a clearly linear relation between the number of cigarettes smoked per day and lung cancer risk. The data on page 45 derive from a much larger cohort study of nearly 250,000 American veterans.

4. On pages 47 and 48, the report expresses concerns about the use of a one-tailed test of significance (approximately equivalent to using a 90 percent confidence interval to test the chance that a relative risk differs from 1.0), even though it offers no plausible reason to believe that exposure to ETS may decrease lung cancer risk. Although 95 percent confidence limits are commonly used, 90 percent confidence intervals are often used in health studies, and are in fact standard in epidemiologic studies of agents such as radiation, which like tobacco, is a strong lung carcinogen. In putting a large emphasis on this rather minor part of the analysis, the report ignores the importance of other factors used by epidemiologists in causal inference, such as consistency of association, strength of association, temporality of the association, dose-response relationship and biologic plausibility.

5. On page 48, the report suggests that recall bias may invalidate the conclusion of an adverse health effect of ETS exposure. This ignores the fact that there is a consistent association between ETS exposure and disease even in four cohort studies, in which recall bias cannot occur, because exposure is ascertained before disease has occurred.

6. On page 48, the report suggests that confounding factors may explain the observed association between ETS exposure and lung cancer. However, it does not suggest a single factor that could plausibly explain the association. Specifically, it does not point out any factor that is a strong independent risk factor for lung cancer that is also strongly related to ETS exposure. Moreover, the consistency of results across a wide variety of study designs and populations argues against confounding as an explanation of the consistent study findings. A wealth of data on cigarette smoking indicates that it is an independent cause of several chronic diseases.

7. In their testimony, she authors of the CRS report suggest that the presence of a consistent dose-response relationship in the epidemiologic studies should not have increased confidence in the conclusion of a causal relationship between ETS and lung cancer. This statement is in direct conflict with one of the most basic principles of epidemiology.

8. In their testimony, the authors suggest that the findings of two recent studies, published too late to be included in the EPA review, cast doubt on the relationship between ETS and lung cancer. On the contrary, in combination these studies are entirely consistent with the body of epidemiologic evidence on the issue, and they add additional support for the conclusion that ETS increases lung cancer risk. The authors of the CRS report ignored the published conclusions of botn of these studies. Specifically, in the Brownson study, the authors found an elevated lung cancer risk for adults with more than 40 pack-years of exposure to ETS from household members, and concluded that "exposure to high levels of environmental tobacco smoke in adulthood increases the risk of lung cancer in nonsmokers."

In the Stockwell study, the authors found that the risk of lung cancer more than doubled for women with more than 40 pack-years of household ETS exposure and conclude that "long-term exposure to environmental tobacco smoke increases the risk of lung cancer in women who have never smoked."

9. The authors attempt to determine the risk of passive smoking by extrapolating from urinary cotinine levels in active compared to passive smokers. They conclude that the average exposure is 0.1 cigarette equivalents per day. However, using this same approach, Guerin et al. have shown that 0.1 cigarette equivalents of exposure to nicotine in inhaled air implies exposure to 60 cigarette equivalents of pyridine and 56 cigarette equivalents of ammonia. The concentrations of many of the carcinogenic components of tobacco smoke are much higher in sidestream than in mainstream smoke. But it is exposure to these components, and not to nicotine, that is likely to determine the lung cancer risk among exposed nonsmokers.

See original document: [3]


1995 Jun 13 Peggy Carter at RJ Reynolds is writing to the top misinformation team in the company, Tom Griscom, Chuck Blixt and Dan Donahue about her observations at a recent Manhattan Institute seminar on "Junk Science and the Law".

Walter Olson and Peter Huber at the Manhattan Institute were both in the pay of Philip Morris and promoting their junk-science propaganda.

She comments on some in attendance:

  • Michael Fumento: Mike authored the Investor's Business Daily piece on the EPA's ETS risk assessment that we've been sending out for some time. He told me that piece generated more reaction than anything he's ever done. He's clearly keeping his distance from the industry to preserve his neutral position. Matt Swetonic advises on the QT that work is in progress to nationally syndicate Mike as a science columnist.
  • Steve Milloy: Milloy included in his remarks a recap of the problems with the EPA's ETS risk assessment, and told me privately that we're really getting "screwed" on this issue. He asked me if I knew CRS was working on an evaluation of the EPA's assessment; seems he and Steve Redhead (the CRS official who contacted us) are good friends. He characterized Redhead as an "anti." Dr. Redhead told Milloy last week that their report was going to require "significant rewrite."
    In response to my question about why, he indicated Redhead felt the only issue was in homes with high exposures over long periods of time. He clearly did not want to be more precise, and apparently felt that was clue enough. Perhaps Chris Coggins can tea-leaf read if - that means CRS was convinced to reevaluate their position on high exposures.
    [4]
C. Stephen Redhead was a physiologist who worked for the Congressional Research Center who became embroiled in controversy over the Gravelle CRS report which attacked the EPA's anti-tobacco stance (she was actually an Economics Policy analyst). [5] Redhead had already, reported on Mortality and Economic Costs Attributable to Smoking and Alcohol Abuse in April 1993. [6]

References

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