IJE Advance Access published online on September 18, 2008
International Journal of Epidemiology, doi:10.1093/ije/dyn198
Book Review |
Hyping Health Risks: Environmental Hazards in Daily Life and the Science of Epidemiology. Kabat GC.
E-mail: n.e.pearce{at}massey.ac.nz
Hyping Health Risks: Environmental Hazards in Daily Life and the Science of Epidemiology. GC. Kabat New York: Columbia University Press, 2008
I wanted to like this book, and tried hard, but ultimately failed. I have recently written several papers on inappropriate corporate influences on the funding and conduct of epidemiological research, and have discussed several examples of hazards where the epidemiologic findings were strongly, and unethically, opposed by industry and by academic epidemiologists funded by industry.1–3 This book provides the other side of the coin and discusses in depth four examples (environmental causes of breast cancer, electromagnetic fields and cancer, residential radon exposure and lung cancer and passive smoking) where, in the author's opinion, the health risks were low or non-existent, but were hyped by researchers and policy makers thus resulting in unnecessary research, inappropriate funding decisions and unjustified public concern.
Such things certainly happen, and we need books like this which attempt to discuss them objectively, and which point out that academic researchers may also be affected by a range of influences including career and funding opportunities, even if they only accept peer-reviewed government funding and do not accept corporate funding. Thus, they may have incentives to overstate the evidence, just as industry and industry-funded epidemiologists may have incentives to negate or understate the evidence of health risks from environmental exposures.
The book states its case well, is clearly written and discusses complicated issues in a relatively simple and readable way. It makes the case that each side tends to cite the evidence that supports its point of view in order to influence public policy (p. 6) and that the tendency to overstate the evidence, for whatever purpose, actually strengthens the opposing party's hand. It sanctions the partisan use of science that should be rejected, no matter who is engaging in it. (p. 7)
The book also makes the important points that: (i) we have to some extent reached the limits of risk factor epidemiology and have identified the strong risks (e.g. active smoking and lung cancer) and are now trying to assess weak risks (e.g. passive smoking and lung cancer), which are much more difficult to assess and much more prone to be overwhelmed by bias; (ii) for many of these risks (e.g. residential radon exposure and lung cancer) it is not possible to directly estimate the risks from low exposures, and it is necessary to make theoretical assumptions to interpolate from the findings of studies of highly exposed occupational populations (e.g. miners exposed to radon); and (iii) many of these risks are very small and have received perhaps excessive funding and scientific attention in comparison with other public health risks.
So far so good. I agree with all of the above statements, and started reading the book in a positive frame of mind, with the expectation that it was an important book that would be an essential antidote to the writings of myself and others who have tended to emphasize the hazards of corporate influences. However, I became more frustrated and less impressed as I worked my way through the book, particularly when coming to discussions of issues that I had been involved in (e.g. electromagnetic fields and cancer). This probably reflects my own influences and prejudices. However, it became increasingly difficult, as I worked my way through the book, to avoid the conclusion that the discussions of these issues were, for want of a better word, biased, as well as being rather grumpy and unpleasant in parts. It seems that no one can get it right. No single study is good enough or big enough, but meta-analyses should be discouraged because they combine studies from different exposure settings and with different methodologies. Researchers are criticized for arguing that one must rely upon the evaluation of the data as a whole using expert judgement and the meta-analyses as a guide (p. 101), because this simply reflects their vested interests to continue researching a topic when an individual study is inconclusive. The findings of individual studies are dismissed because they are not statistically significant, even if they are consistent with previous findings. Significant associations are dismissed because they involved multiple comparisons, even if the specific associations were the a priori reason for the study and had been found previously [e.g. the reported association [of EMFs with childhood] leukaemia was one of a very large number of comparisons made by the researchers and hence could well have arisen by chance (p. 100)]. Studies that show interesting dose-response associations verging on statistical significance, such as the National Cancer Institute childhood leukaemia study,4 are not only dismissed, but also researchers are condemned for not accepting the findings as proof of lack of risk (it is hard to escape the impression that the reluctance of the NIEHS working group to close the door on the possibility of EMF as a cause of leukaemia had more to do with its members stake in this area of research than with scientific rigor (p. 101). While every academic researcher who wants to study these issues apparently has a vested interest, even if their university salary is already funded, critics of the research are apparently unbiased, reasonable and objective, even if their criticisms are directly or indirectly funded by industry. Researchers into radon and lung cancer are biased because they do not repeatedly emphasize that tobacco smoking is the major cause of lung cancer, and that most cases of radon-induced lung cancer involve joint effects with smoking (the corollary that some cases of lung cancer in smokers are due to joint effects with radon exposure is never mentioned, nor is it mentioned that the same arguments could be applied to many other important lung carcinogens such as asbestos).
The book gives particular emphasis to issues of biological plausibility, even though there are many historical examples of associations that were not biologically plausible when they were first discovered by epidemiologists, and the aetiological mechanisms involved were only subsequently discovered in laboratory-based studies. This is why, for example, all of the 30–40 known occupational causes of cancer (as classified by the International Agency for Research on Cancer) were first discovered in epidemiological studies, not in the laboratory. If it had been plausible that these substances caused cancer, then they would not have been used in the workplace. So epidemiology will always be in front of mechanistic research with regards to discovering new environmental and occupational causes of disease. The book also fails to mention that there are many historical examples of risks (dioxin and cancer is one example) where the evidence was initially weak and inconsistent but has strengthened over time (leading to the classification of dioxin as a carcinogen by the International Agency for Research on Cancer in 1997).
So what are we supposed to do about ubiquitous environmental exposures that may carry weak risks, but which may account for a substantial number of cases of disease on a population level? Kabat's solution is nihilistic, namely that we simply should not study such exposures, or at least not attempt to quantify their effects: it is entirely plausible that in some cases exposure to ETS may account for a few cases of lung cancer in nonsmokers, but ... it is not possible to quantify the excess risk with any certainty (p. 150). The argument is essentially that the risks are too small to quantify accurately, and therefore should not be studied, or at least should not be estimated quantitatively. We are never told how we should decide if a risk is too small to be concerned about if we do not first attempt to estimate its magnitude. And how are we supposed to tell the public that the risks are small (and their concerns are unimportant) without attempting to estimate them? And who decides what is a small risk?
The book finishes, literally on the last page, by advocating a broader/integrative vision of epidemiology—one that can accommodate social, economic, and ecological/environmental realities ... as well as rapidly evolving knowledge of the mechanisms of disease at the molecular level (p. 186).5–8 Such developments are to be encouraged, but they are intended to be inclusive, not exclusive, and we will have to continue to grapple with problems of studying weak risks from ubiquitous environmental exposures, even if they receive less attention than they have in the past. It is important to consider the influences on such research, including influences on academic researchers with regards to career opportunities and funding, even though these will continue to be relatively minor compared with the massive and pervasive influences of corporate funding of research and of critics of research.1–3 This book could have made a major contribution in this regard, but its lack of balance means that it fails to make such a contribution.
References
1 Pearce N. The rise and rise of corporate epidemiology and the narrowing of epidemiology's vision. Int J Epidemiol (2007) 36:713–17.
2 Pearce N. Corporate influences on epidemiology. Int J Epidemiol (2008) 37:46–53.
3 Pearce N. Response: the distribution and determinants of epidemiologic research. Int J Epidemiol (2008) 37:65–68.
4 Linet MS, Hatch EE, Kleinerman RA, et al. Residential exposure to magnetic fields and acute lymphoblastic leukemia in children. N Engl J Med (1997) 337:1–7.
5 Davey Smith G, Ebrahim S. Epidemiology - is it time to call it a day? Int J Epidemiol (2001) 301:1–11.
6 Krieger N. Epidemiology and the web of causation: has anyone seen the spider? Soc Sci Med (1994) 39:887–903.[CrossRef][Web of Science][Medline]
7 March D, Susser E. The Eco- in eco-epidemiology. Int J Epidemiol (2006) 35:1379–83.
8 McMichael AJ. Prisoners of the proximate: loosening the constraints on epidemiology in an age of change. Am J Epidemiol (1999) 149:887–97.
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