1. INTRODUCTION: Toward a Sociology of Health Hazards in Daily Life
1. P. Slovic, ed., The Perception of Risk (London, UK: Earthscan, 2002); C. R. Sunstein, Risk and Reason: Safety, Law, and the Environment (Cambridge: Cambridge University Press, 2002); N. Pidgeon, R. E. Kasperson and P. Slovic (eds), The Social Amplification of Risk (Cambridge: Cambridge University Press, 2003).
2. In addition to the rise of epidemiology and environmentalism, it is also likely that the countercultural critique of capitalism of the 1960s made possible a novel critique of corporate practices, including those with harmful effects on health and the environment.
3. In the area of cancer, in addition to cigarette smoking and lung cancer, these include heavy alcohol consumption and cancers of the upper respiratory and alimentary tracts, exposure to solar radiation and skin cancer, exposure to estrogen replacement therapy as a cause of endometrial cancer, exposure to ionizing radiation and certain chemicals as causes of specific cancers, as well as the role of specific viruses and bacteria. In addition, epidemiology played a critical role in identifying a variety of risk factors for coronary heart disease. A listing of some of the major achievements of epidemiology is given by Kuller (L. Kuller, “Is Phenomenology the Best Approach to Health Research?” American Journal of Epidemiology 166 (2007): 109–1115).
4. G. Kolata, “Environment and Cancer: The Links Are Elusive,” New York Times, December 13, 2005. This article provides one of the clearest and most insightful discussions of this issue that I have seen.
5. J. P. A. Ioannidis, “Why Most Published Research Findings Are False,” PLoS Medicine 2 (August 2005): e124.
6. G. Taubes, “Epidemiology Faces Its Limits,” Science 269 (July 14, 1995): 164–169.
7. J. Niederdeppe and A. G. Levy, “Fatalistic Beliefs About Cancer Prevention and Three Prevention Behaviors,” Cancer Epidemiology Biomarkers and Prevention 16, 5 (May 1, 2007): 988–1003, doi:10.1158/1055-9965.EPI-06-0608.
8. Of course, “benefits”—whether of pharmaceutical products, diet supplements, or other health products—are also routinely hyped, in what would appear to be the “flip side” of the hyping of dangers.
9. Thomas S. Kuhn, The Structure of Scientific Revolutions (2nd ed.) (Chicago: University of Chicago Press, 1970); Paul Feyerabend, Against Method (London: Verso, 2002); Robert K. Merton, The Sociology of Science: Theoretical and Empirical Investigations (Chicago: University of Chicago Press, 1973); Michel Foucault, Power/Knowledge: Selected Interviews and Other Writings, 1972–77, ed. Colin Gordon (New York: Pantheon, 1980).
10. K. M. Cummings, A. Brown, and R. O’Connor, “The Cigarette Controversy,” Cancer Epidemiology Biomarkers and Prevention (June 2007): 1070–1076; Richard Kluger, Ashes to Ashes: America’s Hundred-Year Cigarette War, the Public Health, and the Unabashed Triumph of Philip Morris (New York: Random House, 1997); Gerald Markowitz and David Rosner, Deceit and Denial: The Deadly Politics of Industrial Pollution (Berkeley: University of California Press, 2002).
11. D. Michaels and C. Monforton, “Manufacturing Uncertainty: Contested Science and the Protection of the Public’s Health and Environment,” American Journal of Public Health Supplement 95 (2005): S39–S48.
12. A. C. Revkin, “Bush vs. the Laureates: How Science Became a Partisan Issue,” New York Times, October 19, 2004; Chris Mooney, The Republican War on Science (New York: Basic Books, 2005); K. M. Rest and M. H. Halpern. “Politics and the Erosion of Federal Scientific Capacity: Restoring Scientific Integrity to Public Health Science,” American Journal of Public Health 97 (2007): 1939–1944.
13. L. Hardell et al., “Secret Ties to Industry and Conflicting Interests in Cancer Research,” American Journal of Industrial Medicine 50 (2007): 227–233. M. Newton and A. L. Young. “The Story of 2,4,5-T: A Case Study of Science and Societal Concerns,” Environmental Science and Pollution Research 11 (2004): 207–208; P. Cole et al., “Dioxin and Cancer: A Critical Review,” Regulatory Toxicology and Pharmacology 38 (2003): 378–388; J. D. Boice Jr. and J. K. McLaughlin, “Epidemiologic Studies of Cellular Telephones and Cancer Risk: A Review,” SSI Report (Statens Strålskyddsinstitut) 16 (2002); R. L. Barnes, S. K. Hammond, and S. A. Glantz, “The Tobacco Industry’s Role in the 16 Cities Study of Second-hand Tobacco Smoke: Do the Data Support the Stated Conclusions?” Environmental Health Perspectives 114 (2006): 1890–1897; C. V. Phillips, “Warning: Anti-Tobacco Activism May Be Hazardous to Epidemiologic Science,” Epidemiologic Perspectives and Innovations 4 (2007), doi:10.1186/1742-5573-4-13.
14. To give just a few examples restricted to the United States, the auto industry has effectively stymied progress on pollution control; the mining industry has almost entirely done away with health and safety enforcement; the food industry has brought about tremendous limitations in agriculture inspection, especially of meat; and the Food and Drug Administration is “so overwhelmed by the flood of imports that it is incapable of protecting the public from unsafe drugs, medical devices and food” from abroad, and particularly from China (G. Harris, “For F.D.A., A Major Backlog Overseas,” New York Times, January 29, 2008.
15. J. D. Graham, K. Clemente, and R. Glass, “Breast Cancer: What Are the Perceived Risk Factors?” Harvard Center for Risk Analysis 4 (1996): 1–2.
16. Slovic, The Perception of Risk, 264–274.
19. J. M. Last, A Dictionary of Epidemiology (4th ed.) (New York: Oxford University Press, 2001); P. Boffetta et al. “‘Environment’ in Cancer Causation and Etiological Fraction: Limitations and Ambiguities,” Carcinogenesis 28 (May 2007): 913–915.
20. H. Harris and A. O’Connor, “On Autism’s Cause, It’s Parents vs. Research,” New York Times, June 25, 2005.
21. The power of these movies stems in no small part from the deep-seated fear of a deadly toxin seeping into our environment and imperceptibly causing disease. Even though the science often cannot provide clear-cut evidence of cause and effect in such situations, there is a larger truth behind these stories and the associated fear, and this is that there is always the potential for the gradual accumulation of toxins that could lead to disease. And some disease clusters due to a “point source” of pollution undoubtedly go undetected.
22. Phillips, “Warning: Anti-Tobacco Activism”; D. T. Levy, E. A. Mumford, K. M. Cummings, E. A. Gilpin, G. Giovino, A. Hyland, D. Sweanor, and K. E. Warner. “The Relative Risks of a Low-Nitrosamine Smokeless Tobacco Product Compared with Smoking Cigarettes: Estimates of a Panel of Experts,” Cancer Epidemiology Biomarkers and Prevention 13 (2004): 2035–2042.
23. Kolata, “Environment and Cancer.”
24. B. N. Ames and L. S. Gold. “Paracelsus to Parascience: The Environment and Cancer Distraction,” Mutation Research 447 (2000): 3–13.
25. M. L. Wald, “With New Data, A Debate on Low-Level Radiation,” New York Times, July 7, 2005; G. Kolata, “For Radiation, How Much Is Too Much?” New York Times, November 27, 2001.
26. E. L. Wynder, I. T. T. Higgins, and R. E. Harris, “The Wish Bias,” Journal of Clinical Epidemiology 43 (1990): 619–621; Ioannidis, “Why Most Published Research Findings Are False,” 2005.
27. Cited in Taubes, “Epidemiology Faces Its Limits.”
28. To give just one example of what I have in mind, it has been widely accepted that roughly 50,000 deaths from heart disease a year are due to exposure to secondhand tobacco smoke. Review articles and agency reports that attempt to make a case for secondhand smoke being an important cause of heart disease are unlikely to mention, no less to give weight to, certain highly relevant facts. First, active smoking is one of a number of risk factors for heart disease and is associated with less than a doubling of the risk. Second, exposure to secondhand smoke is orders of magnitude more dilute that the smoke the active smoker inhales. Third, since the 1950s the death rate from heart disease has declined dramatically in both smokers and nonsmokers, by about 50–60 percent. These would seem to be pertinent facts to mention when considering a possible effect of secondhand smoke exposure on heart disease risk. However, giving these facts due consideration would have the effect of reducing the importance of the factor under study.
29. The Oxford epidemiologist Sir Richard Peto is quoted as saying, “Epidemiology is so beautiful and provides such an important perspective on human life and death, but an incredible amount of rubbish is published.” G. Taubes, “Unhealthy Science: Why Can’t We Trust Much of What We Hear About Diet, Health, and Behavior-Related Diseases?” New York Times Magazine, September 16, 2007, 52–80.
30. S. Shane, “Debating the Evidence of Gulf War Illnesses,” New York Times, November 16, 2004.
31. L. A. Cole, Element of Risk: The Politics of Radon (New York: Oxford University Press, 1993), 101.
33. Grady, D. “Pregnancy Problems Tied to Caffeine.” New York Times, January 21, 2008.
34. M. Douglas and A. Wildavsky, Risk and Culture: An Essay on the Selection of Technological and Environmental Dangers (Berkeley: University of California Press, 1982).
35. B. N. Ames, M. Profet, and L. S. Gold, “Dietary Pesticides (99.99% All Natural),” Proceedings of the National Academy of Sciences USA 87 (1990): 7777–7781.
36. D. Kahneman and A. Tversky, “Judgment Under Uncertainty: Heuristics and Biases,” Science 185 (September 1974): 1124–1131.
37. D. Ropeik and G. Gray, Risk! A Practical Guide for Deciding What’s Really Safe and What’s Really Dangerous in the World Around You (Boston: Houghton Mifflin, 2002).
2. EPIDEMIOLOGY: Its Uses, Strengths, and Limitations
1. The many achievements of epidemiology need publicizing because epidemiology has come in for a good deal of criticism (G. Taubes, “Epidemiology Faces Its Limits,” Science 269 (July 14, 1995), 164–169; G. Taubes, “Unhealthy Science: Why Can’t We Trust Much of What We Hear About Diet, Health, and Behavior-Related Diseases?” New York Times Magazine (September 16, 2007)). While Taubes makes some valid and important points, his assessment of epidemiology is, I believe, misinformed.
2. K. J. Rothman, Epidemiology: An Introduction (New York: Oxford University Press, 2002).
3. For further reading, I strongly recommend Leon Gordis’ textbook Epidemiology (3rd ed.), Philadelphia: Saunders, 2004. This comes as close to a beginner-friendly yet comprehensive introduction to the field as one can find.
4. K. M. Flegal et al. “Cause-Specific Excess Deaths Associated with Underweight, Overweight, and Obesity,” Journal of the American Medical Association 298 (November 7, 2007), 2028–2037.
5. K. A. Matthews et al., “Prior Use of Estrogen Replacement Therapy, Are Users Healthier Than Nonusers?” American Journal of Epidemiology 143 (May 15, 1996): 971–978; C. A. Derby et al., “Correlates of Postmenopausal Estrogen Use and Trends Through the 1980s in Two Southeastern New England Communities,” American Journal of Epidemiology 137 (1993): 1125–1135; C. B. Johannes et al., “Longitudinal Patterns and Correlates of Hormone Replacement Therapy Use in Middle-Aged Women,” American Journal of Epidemiology 140 (1994): 439–452.
6. Unlike the situation of smoking, where we have people who never smoked as the unexposed group, when studying diet, for example, there is no unexposed group, so we can only examine contrasts between different degrees of exposure to a given dietary factor.
7. R. P. Beasley, “Hepatitis B Virus: The Major Etiology of Hepatocellular Carcinoma,” Cancer 61 (1988): 1942–1956.
8. N. Muñoz et al., “HPV in the Etiology of Human Cancer,” Vaccine 24, S3 (2006), S1–S10.
9. Beasley, “Hepatitis B Virus.”
10. J. E. Enstrom and G. C. Kabat, “Environmental Tobacco Smoke and Tobacco Related Mortality in a Prospective Study of Californians, 1960-98,” BMJ 326 (May 17, 2003), 1057–1066.
11. International Agency for Research on Cancer (IARC), IARC Monograph 44: Alcohol Drinking (Lyon, France: IARC, 1988), 169.
12. G. A. Colditz et al., “Family history, age, and risk of breast cancer: prospective data from the Nurses’ Health Study,” Journal of the American Medical Association 270 (1993): 338–343.
13. C. W. Bain et al., “Early Age at First Birth and Decreased Risk of Breast Cancer,” American Journal of Epidemiology 114 (1981): 705–709.
14. Enstrom and Kabat, “Environmental Tobacco Smoke.”
15. N. R. Shah, J. Borenstein, and R. W. Dubois, “Postmenopausal Hormone Therapy and Breast Cancer: A Systematic Review and Meta-analysis,” Menopause 12 (2005): 653–655.
16. Z. A. Stein, “Silicone Breast Implants: Epidemiological Evidence of Sequelae,” American Journal of Public Health 89 (April 1999), 484–487.
17. A. K. Hackshaw, M. R. Law, and N. J. Wald, “The Accumulated Evidence on Lung Cancer and Environmental Tobacco Smoke,” BMJ 315 (1997): 980–988.
18. G. Pershagen et al., “Residential Radon Exposure and Lung Cancer in Sweden,” New England Journal of Medicine 330 (1994): 159–164.
19. S. Greenland et al., “A Pooled Analysis of Magnetic Fields, Wire Codes, and Childhood Leukemia,” Epidemiology 12 (2001): 472–474.
20. C. A. Pope III et al., “Particulate Air Pollution as a Predictor of Mortality in a Prospective Study of U.S. Adults,” American Journal of Respiratory and Critical Care Medicine 151 (1995), 669–674.
21. F. Laden et al., “Plasma Organochlorine Levels and the Risk of Breast Cancer: An Extended Follow-Up in the Nurses’ Health Study,” International Journal of Cancer 91 (2001): 568–574.
22. Stein, “Silicone Breast Implants.”
23. U.S. Environmental Protection Agency, Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders (Washington, D. C.: U.S. Department of Health and Human Services, 1992); K. Steenland, “Passive Smoking and the Risk of Heart Disease,” Journal of the American Medical Association 267 (January 1992), 94–99; National Research Council, Health Effects of Exposure to Radon: BEIR VI (Washington, D. C.: National Academy Press, 1999).
24. K. J. Rothman and S. Greenland, “Causation and Causal Inference in Epidemiology,” American Journal of Public Health (supplement) 95, S1 (2005): S144–S150.
27. C. V. Phillips and K. J. Goodman, “The Missed Lessons of Sir Austin Bradford Hill,” Epidemiologic Perspectives & Innovations 1 (October 2004): 3, doi:10.1186/1742-5573-1-3.
28. A. B. Hill, “The Environment and Disease: Association or Causation?” Proceedings of the Royal Society of Medicine 58 (1965): 295–300.
29. U.S. Public Health Service. Smoking and Health: Report of the Advisory Committee to the Surgeon General of the Public Health Service, PHS Publication 1103, U.S. Department of Health, Education, and Welfare, Public Health Service, Center for Disease Control, 1964.
30. A. Morabia, “On the Origins of Hill’s Causal Criteria,” Epidemiology 2 (1991): 367–369.
31. R. M. Lucas and A. J. McMichael, “Association or Causation: Evaluating Links Between ‘Environment and Disease,’” Bulletin of the World Health Organization 83 (2005): 792–795.
32. M. Susser, Causal Thinking in the Health Sciences: Concepts and Strategies of Epidemiology (New York: Oxford University Press, 1973).
33. Morabia, “On the Origins of Hill’s Causal Criteria.”
34. Enstrom and Kabat, “Environmental Tobacco Smoke.”
35. J. M. Elwood, et al., “Alcohol, Smoking, and Social and Occupational Factors in the Aetiology of Cancer of the Oral Cavity, Pharynx and Larynx,” International Journal of Cancer 34 (1984): 603–612.
36. D. Grady et al., “Hormone Replacement Therapy and Endometrial Cancer Risk: A Meta-analysis,” Obstetrics and Gynecology 85 (1995): 304–313.
37. Enstrom and Kabat, “Environmental Tobacco Smoke.”
38. G. A. Colditz, “Relationship Between Estrogen Levels, Use of Hormone Replacement Therapy, and Breast Cancer (Review),” Journal of the National Cancer Institute 90 (1998): 814–823.
39. M. Egger, M. Schneider, and G. Davey Smith, “Spurious Precision? Meta-analysis of Observational Studies,” BMJ 316 (1998): 140–144.
40. S. Shapiro, “Meta-analysis/Shmeta-analysis,” American Journal of Epidemiology 140 (1994): 771–778.
41. Egger et al., “Spurious Precision? Meta-analysis of Observational Studies.”
42. Shapiro, “Meta-analysis/Shmeta-analysis.”
43. A. Morabia, “Risky Concepts: Methods in Cancer Research,” American Journal of Public Health 91 (March 2001): 355–357.
45. L. M. Schwartz et al., “Ratio Measures in Leading Medical Journals: Structured Review of Accessibility of Underlying Absolute Risks,” BMJ 333 (October 2006), 1248, doi:10.1136/bmj.38985.564317.7C.
47. Schwartz et al., “Ratio Measures in Leading Medical Journals.”
48. Morabia, “Risky Concepts.”
49. M. Marmot, The Status Syndrome: How Social Standing Affects Our Health and Longevity (London: Bloomsbury, 2005).
3. DOES THE ENVIRONMENT CAUSE BREAST CANCER?
1. Barbara Balaban, interview with author, January 20, 2005.
2. T. R. Holford et al., “Changing Patterns in Breast Cancer Incidence Trends,” Journal of the National Cancer Institute Monographs No. 36 (2007): 19–25.
3. P. M. Ravdin et al., “The Decrease in Breast-Cancer Incidence in 2003 in the United States,” New England Journal of Medicine 356 (April 19, 2007): 1670–1674.
4. The most likely source of the 30 percent figure is a reported 27 percent higher breast cancer mortality rate in Nassau and Suffolk compared to the United States rate based on data from the National Center for Health Statistics. This figure was routinely cited as incidence, rather than mortality. Susan Jenks, “Researchers to Comb Long Island for Potential Cancer Factors,” Journal of the National Cancer Institute 86 (January 19, 1994): 88–89.
5. G. Kolata, “The Epidemic That Wasn’t,” New York Times, August 29, 2002.
6. Regina Santella, interview with author, January 20, 2005.
7. J. D. Graham, K. Clemente, and R. Glass, “Breast Cancer: What Are the Perceived Risk Factors?” Harvard Center for Risk Analysis 4 (1996), 1–2.
8. Marilie Gammon, interview with author, January 20, 2004; follow-up interview, January 19, 2005.
9. S. R. Sturgeon et al., “Geographic Variation in Mortality from Breast Cancer Among White Women in the United States,” Journal of the National Cancer Institute 87 (December 20, 1995): 1846–1853; M. Kulldorff et al., “Breast Cancer Clusters in the Northeast United States: A Geographic Analysis,” American Journal of Epidemioliology 146 (July 15, 1997): 161–170.
10. For a number of reasons, a higher number of people with a history of a disease like breast cancer in a particular community may not be evidence of any shared common environmental exposure. Apparent cancer clusters are more likely to have a common underlying cause if the cancer involved is rare and if it manifests itself in a group that does not usually develop this cancer. Neither of these conditions held for breast cancer on Long Island. Most investigations of cancer clusters turn out not to have an identifiable common cause. See Atul Gawande, “The Cancer Cluster Myth,” the New Yorker, February 8, 1999.
11. Balaban, interview with author.
12. Davis’ claims about increased cancer rates due to environmental pollution came in for harsh criticism from eminent epidemiologists, such as Richard Doll and Richard Peto. See Karen Wright, “Going by the Numbers,” New York Times Magazine, December 15, 1991.
13. Mary Wolff, interview with author, July 20, 2004.
16. Dr. Samuel Broder, who was director of the National Cancer Institute at time, commented that, “I don’t think it’s a good idea for the Congress, in general terms, to identify a scientific problem and then issue detailed instructions to an institute.” Brodeur identified the rush to enact the legislation and the lack of give-and-take between the politicians and the cancer institute as having seriously compromised the study. “It’s not an optimal situation when the Congress doesn’t allow time for dialogue, or doesn’t even want dialogue,” he said. “If you have dialogue at the beginning, you can come to an understanding about the scope, the limits and the expectations of a project.” Dan Fagin, “Tattered Hopes: A $30-million federal study of breast cancer and pollution on LI has disappointed activists and scientists.” Newsday, July 28, 2002.
17. D. Fagin, “So Many Things Went Wrong: Costly Search for Links Between Pollution and Breast Cancer Was Hobbled from the Start,” Newsday, July 29, 2002.
18. In an interview with Newsday in 2000, Dr. Ellen Heineman, the National Cancer Institute official overseeing the GIS project, gave a more realistic appraisal of the utility of the GIS for identifying the causes of breast cancer: “A ‘beginning’ is also how Ellen Heineman . . . described the system. She emphasized that the data will allow researchers to test their hypotheses and spark further research, but it won’t lead them to definite conclusions. ‘It’s a starting point, a jumping board. People who are putting all their hopes in this system will be terribly disappointed,’ she told the audience.” Heather Sokoloff, Cancer map of LI unveiled. Newsday, September 21, 2000.
19. T. Coborn, D. Dumanoski, and J. P. Myers, Our Stolen Future: Are We Threatening Our Fertility, Intelligence, and Survival? (New York: Plume Books, 1996).
20. H.-O. Adami et al., “Organochlorine Compounds and Estrogen-Related Cancers in Women,” Cancer Causes and Control 6 (1995): 551–566; U. G. Ahlborg et al., “Organochlorine Compounds in Relation to Breast Cancer, Endometrial Cancer, and Endometriosis: An Assessment of the Biological and Epidemiological Evidence,” Critical Reviews in Toxicology 25 (1995): 463–531.
21. T. Key and G. Reeves, “Organochlorines in the Environment and Breast Cancer,” BMJ 308 (June 11, 1994): 1520–1521.
22. S. H. Safe, “Is There an Association Between Exposure to Environmental Estrogens and Breast Cancer?” Environmental Health Perspectives 105, Supplement 3 (April 1997): 675–678.
23. D. H. Phillips, “DNA Adducts as Markers of Exposure and Risk,” Mutation Research 577 (2005): 284–292.
24. S. Jenks, “Researchers to Comb Long Island for Potential Cancer Factors,” Journal of the National Cancer Institute 86 (1994): 88–89.
25. R. Ochs, “The LI Breast Cancer Study,” Newsday, December 10, 1996.
27. M. S. Wolff et al., “Blood Levels of Organochlorine Residues and Risk of Breast Cancer,” Journal of the National Cancer Institute 85 (1993): 648–652.
29. D. J. Hunter and K. T. Kelsey, “Pesticide Residues and Breast Cancer: The Harvest of a Silent Spring?” Journal of the National Cancer Institute 85 (April 21, 1993): 598–599.
30. E. E. Calle, et al., “Organochlorines and Breast Cancer Risk,” CA A Cancer Journal for Clinicians 52 (2002): 301–309.
32. M. Lopez-Cervantes et al., “Dichlorodiphenyldichloroethane Burden and Breast Cancer Risk: A Meta-analysis of the Epidemiologic Evidence,” Environmental Health Perspectives 112 (2004): 207–214.
33. M. S. Wolff et al., “Risk of Breast Cancer and Organochlorine Exposure,” Cancer Epidemiology Biomarkers Prevention 9 (2000): 271–277.
34. M. D. Gammon et al., “Environmental Toxins and Breast Cancer on Long Island. II. Organochlorine Compound Levels in Blood,” Cancer Epidemiology Biomarkers & Prevention 11 (2002): 686–697.
35. M. D. Gammon and R. M. Santella, “Reply to F. Perrera,” Cancer Epidemiology Biomarkers & Prevention 12 (2003): 75–76.
36. B. MacMahon et al., “Coffee and Cancer of the Pancreas,” New England Journal of Medicine 304 (1981): 630–633.
37. V. L. Ernster et al., “Effects of Caffeine-Free Diet on Benign Breast Disease: A Randomized Trial,” Surgery 91 (1982), 263–267.
38. W. C. Willett, “Prospective Studies of Diet and Breast Cancer,” Cancer 74, 3 Supplement (1994): 1085–1089.
39. In response to the advocates’ desire to see a wider range of compounds included in the study, Gammon and colleagues drafted a report tabulating available evidence for thirty-six additional compounds, including both evidence of carcinogenicity in laboratory experiments and the availability of an adequate biological marker. “LIBCSP Year 2 Progress Report: Other Chemicals of Community Interest.”
40. D. Fagin, “Tattered Hopes; A $30-Million Dollar Federal Study of Breast Cancer and Pollution on LI Has Disappointed Activists and Scientists,” Newsday, July 28, 2002; “So Many Things Went Wrong: Costly Search for Links Between Pollution and Breast Cancer Was Hobbled from the Start, Critics Say,” Newsday, July 29, 2002; “Still Searching: A Computer Mapping System Was Supposed to Help Unearth Information About Breast Cancer and the Environment,” News-day, July 30, 2002.
41. Kolata, “The Epidemic That Wasn’t.”
44. Marilie Gammon, interview with author, January 20, 2004.
47. Steven Stellman, interview with author, October 13, 2004.
48. Institute of Medicine. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides. Veterans and Agent Orange: Health Effects of Herbicides Used in Vietnam. (Washington, D.C.: National Academy of Sciences Press, 1994), 283.
50. Mary Wolff, interview with author, July 7, 2004.
51. G. Kolata, “Reversing Trend, Big Drop Is Seen in Breast Cancer,” New York Times, December 15, 2006; P. M. Ravdin et al., “The Decrease in Breast-Cancer Incidence,” 2007.
52. C. McNeil, “Breast Cancer Decline Mirrors Fall in Hormone Use, Spurs Both Debate and Research,” Journal of the National Cancer Institute 99 (February 21, 2007): 266–267.
53. V. C. Jordan, “SERMs: Meeting the Promise of Multifunctional Medicines,” Journal of the National Cancer Institute 99 (March 7, 2007): 350–356.
54. G. Kolata, “Hormones and Cancer: Assessing the Risks,” New York Times, December 26, 2006.
4. ELECTROMAGNETIC FIELDS: The Rise and Fall of a “Pervasive Threat”
1. L. I. Kheifets et al., “Electric and Magnetic Fields and Cancer: Case Study,” American Journal of Epidemiology 154 (supplement) (2000): S50–S59.
2. N. Wertheimer and E. Leeper, “Electrical Wiring Configurations and Childhood Cancer,” American Journal of Epidemiology 109 (1979): 273–284.
3. D. A. Bromley, The President’s Scientist: Reminiscences of a White House Science Advisor (New Haven: Yale University Press, 1994); R. L. Park, Voodoo Science: The Road from Foolishness to Fraud (New York: Oxford University Press, 2000).
4. Wertheimer and Leeper, “Electrical Wiring Configurations,” 283.
5. L. Tomenius, “50-Hz Electromagnetic Environment and the Incidence of Childhood Tumors in Stockholm County,” Biolectromagnetics 7 (1986): 191–207.
6. For a review of the early occupational studies, see D. A. Savitz and E. E. Calle, “Leukemia and Occupational Exposure to Electromagnetic Fields: Review of Epidemiologic Surveys,” Journal of Occupational Medicine 29 (1987): 47–51.
7. David Savitz, interview with author, January 21, 2004.
8. D. A. Savitz, H. Wachtel, F. A. Barnes, E. M. John, and J. G. Tvrdik, “Case-Control Study of Childhood Cancer and Exposure to 60-Hz Magnetic Fields,” American Journal of Epidemiology 128 (1988): 21–38.
9. D. A. Savitz, N. E. Pearce, and C. Poole, “Methodological Issues in the Epidemiology of Electromagnetic Fields and Cancer,” Epidemiologic Reviews 11 (1989): 59–78.
12. C. Poole and D. Trichopoulos, “Extremely Low-Frequency Electric and Magnetic Fields and Cancer,” Cancer Causes and Control 2 (1991): 267–276.
14. ORAU Panel on Health Effects of Low-Frequency Electric and Magnetic Fields, “EMF and Cancer (Letter),” Science 260 (April 2, 1993): 14–16.
16. P. Brodeur, Currents of Death: Power Lines, Computer Terminals, and the Attempt to Cover Up Their Threat to Your Health (New York: Simon and Shuster, 1989).
17. E. R. Adair, “Currents of Death” rectified. A paper commissioned by the IEEE-USA Committee on Man and Radiation in Response to the book by Paul Brodeur (New York: IEEE-USA, 1991).
18. R. G. Stevens, “Electric Power Use and Breast Cancer: A Hypothesis,” American Journal of Epidemiology 125 (1987): 556–561; G. C. Brainard, R. Kavet, and L. I. Kheifets, “The Relationship Between Electromagnetic Field and Light Exposures to Melatonin and Breast Cancer Risk: A Review of the Relevant Literature,” Journal of Pineal Research 26 (1999): 65–100.
19. R. K. Adair, “Constraints on Biological Effects of Weak Extremely-Low-Frequency Electromagnetic Fields,” Physical Review A 43 (1991): 1039–1048. This first paper by Adair on electromagnetic fields built to some extent on a highly influential paper by two physicists that had appeared in 1990: J. C. Weaver and R. D. Astumian, “Response of Cells to Very Weak Electric Fields,” Science 247 (1990): 459–462.
20. Robert K. Adair, email message to author, November 22, 2004.
21. R. K. Adair, “Fear of Weak Electromagnetic Fields,” Scientific Review of Alternative Medicine 3 (1999): 22–23.
22. R. K. Adair, “Static and Low-Frequency Magnetic Fields: Health Risks and Therapies,” Reports on Progress in Physics 63 (2000): 415–454. Adair had this to say about experimental research on ELF-EMF: “There is strong evidence that fields between 1–10 mV m-1 affect biology. However, after a quarter century of intense experimentation and more than 200 results that report biological effects of fields smaller than 50 T at 50-60 Hz, fields that generate induced currents less than 1 mA m-1, no persuasive result showing effects of such weak fields has been forthcoming. “Is the rejection of so large a set of results—albeit none that are definitive—quite unusual? No! Other areas of science have experienced the phenomenon of having large sets of invalid results purporting to establish pathological science. Recently, there have been several hundred reports of experiments that demonstrated ‘cold fusion’; but there is no cold fusion.” (p. 437).
23. U.S. Department of Health and Human Services, “Findings of Scientific Misconduct,” NIH Guide (June 18, 1999).
24. R. K. Adair, “Measurements Described in a Paper by Blackman, Blanchard, Bename, and House Are Statistically Invalid,” Bioelectromagnetics 17 (1996): 510–511.
25. W. R. Bennett Jr., “Cancer and Power Lines,” Physics Today (April 1994): 23–29.
26. R. K. Adair, “Biological Responses to Weak 60-Hz Electric and Magnetic Fields Must Vary as the Square of the Field Strength,” Proceedings of the National Academy of Sciences USA 91 (1994): 9422–9425.
27. National Research Council, Possible Health Effects of Exposure to Residential Electric and Magnetic Fields (Washington, D. C.: National Academy Press, 1997).
29. The makeup of a committee can have a decisive effect on the tenor of its conclusions. In this regard, the background to the formation of the National Research Council’s EMF committee is worth noting. According to Adair, the original chairman-designate was David Savitz, who by then was chairman of the epidemiology department at the University of North Carolina. Owing to complaints from Adair and other physicists, first to Frank Press, president of the National Academy of Sciences, and then to Bruce Alberts, his successor, Stevens was appointed as chairman, and Savitz became deputy chairman. In addition, Adair was concerned that “about 40 percent” of the committee members had a bias in favor of health effects from EMF due to their own work. To ensure what he saw as balance, he succeeded in persuading Alberts to add the physicist Richard Garwin to the committee.
30. S. J. London et al., “Exposure to Residential Electric and Magnetic Fields and Risk of Childhood Leukemia,” American Journal of Epidemiology 134 (1991): 923–937.
31. M. Feychting and A. Ahlbom, “Magnetic Fields and Cancer in Children Residing near Swedish High-Voltage Power Lines,” American Journal of Epidemiology 138 (1993): 467–481.
32. R. Wilson and A. Shlyakhter, “Re: Magnetic Fields and Cancer in Children Residing near Swedish High-Voltage Power Lines,” American Journal of Epidemiology 141 (1995): 378–379.
33. M. S. Linet et al., “Residential Exposure to Magnetic Fields and Acute Lymphoblastic Leukemia in Children,” New England Journal of Medicine 337 (1997): 1–7.
34. National Institute of Environmental Health Sciences, NIEHS Report on Health Effects from Exposure to Power-Line Frequency Electric and Magnetic Fields, NIH Publication 99-4493, Washington D.C., 1999.
36. Clearly outraged by the biases operating in the NIEHS working group, Adair drafted a ten-page, detailed inventory of biases and errors in the report ranging from the composition of the committee to the interpretation of specific experiments. This was submitted to NIEHS during the public comment period on the document. (R. K. Adair, “A Critique of the NIEHS Working Group Report on Assessment of Health Effects from Exposure to Power-Line Frequency Electric and Magnetic Fields,” September 17, 1998).
37. M. B. Bracken et al., “Correlates of Residential Wiring Code Used in Studies of Health Effects of Residential Electromagnetic Fields,” American Journal of Epidemiology 148 (1998): 467–474; E. Hatch et al., “Do Confounding or Selection Factors of Residential Wiring Codes and Magnetic Fields Distort Findings of Electromagnetic Fields Studies?” Epidemiology 11 (2000): 189–198.
38. S. Greenland et al., “A Pooled Analysis of Magnetic Fields, Wire Codes, and Childhood Leukemia,” Epidemiology 11 (2000): 624–634.
39. A. Ahlbom et al., “A Pooled Analysis of Magnetic Fields and Childhood Leukemia,” British Journal of Cancer 83 (2000): 692–698.
40. Greenland et al., “A Pooled Analysis of Magnetic Fields, Wire Codes,” 632.
41. Ahlbom et al., “A Pooled Analysis of Magnetic Fields and Childhood Leukemia,” 697–698.
42. S. Davis, D. K. Mirick, and R. G. Stevens, “Residential Magnetic Fields and the Risk of Breast Cancer,” American Journal of Epidemiology 155 (2002): 446– 454; E. R. Schoenfeld et al., “Electromagnetic Fields and Breast Cancer on Long Island: A Case-Control Study,” American Journal of Epidemiology 158 (2003): 47– 58; S. J. London et al., “Residential Magnetic Field Exposure and Breast Cancer Risk: A Nested Case-Control Study from a Multiethnic Cohort in Los Angeles County, California,” American Journal of Epidemiology 15 (2003): 158: 969–980.
43. The NIEHS final report issued in 1999 concluded that the accumulated evidence provided “little support that exposure to ELF-EMF is altering melatonin levels in humans” (p. 19).
44. D. P. Sandler, “On Blankets and Breast Cancer (Editorial),” Epidemiology 14 (2003): 509.
45. E. W. Campion, “Power Lines, Cancer, and Fear (Editorial),” New Eng- land Journal of Medicine 337 (1997): 44–46.
46. D. A. Savitz, “Health Effects of Electric and Magnetic Fields: Are We Done Yet?” Epidemiology 14 (2003): 15–17.
47. M. Feychting and A. Ahlbom, “Childhood Leukemia and Residential Exposure to Weak Extremely Low Frequency Magnetic Fields,” Environmental Health Perspectives, Supplement 2 (1995): 59–62.
48. A. B. Hill, “The Environment and Disease: Association or Causation?” Proceedings of the Royal Society of Medicine 58 (1965): 295–300.
49. Kheifets, “Electric and Magnetic Fields and Cancer.”
5. THE SCIENCE AND POLITICS OF RESIDENTIAL RADON
1. J. H. Lubin and J. D. Boice Jr., “Lung Cancer Risk From Residential Radon: Meta-analysis of Eight Epidemiologic Studies,” Journal of the National Cancer Institute 89 (January 1, 1997): 49–57.
2. L. Alderson, “A Creeping Suspicion About Radon,” Environmental Health Perspectives 102 (October 1994): 826–831.
3. National Research Council. Health Effects of Exposure to Radon. BEIR VI. (Washington, D. C.: National Academy Press, 1999).
4. National Research Council. Health Risks of Radon and Other Internally- Deposited Alpha-Emitters. BEIR IV (Washington, D.C.: National Academy Press, 1988).
5. National Research Council, Health Effects of Exposure, 20.
6. National Research Council, Health Risks of Radon, 445.
9. L. A. Cole, Element of Risk: The Politics of Radon (New York: Oxford University Press, 1993), 11.
10. Cole, Element of Risk, 11; R. N. Proctor, Cancer Wars: How Politics Shapes What We Know and Don’t Know About Cancer (New York: Basic Books, 1995), 216.
11. Proctor, Cancer Wars, 203–204.
13. J. D. Boice Jr., “Ionizing Radiation,” in Cancer Epidemiology and Prevention, eds. D. Schottenfeld and J. F. Fraumeni Jr. (Oxford: Oxford University Press, 2006), 259–293.
14. P. Shabecoff, “Radioactive Gas in Soil Raises Concern in Three-State Area,” New York Times, May 19, 1985.
15. Cole, Element of Risk, 12–13. According to Anthony Nero, a physicist at Lawrence Berkeley Laboratory, as quoted in the New York Times, “It is fairly clear that the real incentive for activity was that a single area in eastern Pennsylvania was found to contain homes with radon levels that were truly astounding. It finally shook local and national regulators into taking regulatory action. Before they had been only doing research and thinking about the problem.” P. Shabecoff, “Issue of Radon: New Focus on Ecology,” New York Times, September 10, 1986.
16. P. Shabecoff, “Drive to Locate Risk Areas for Radioactive Gas Urged,” New York Times, May 24, 1985; P. Shabecoff, “E.P.A. Proposes 5-Year Program Aimed at Radioactive Radon Gas,” New York Times, October 10, 1985.
17. R. Pear, “Safety Standard is Set on Radon in U.S. Homes,” New York Times, August 15, 1986; “U.S. Says Radon Gas Is States’ Fight,” New York Times, August 16, 1986.
18. U.S. Environmental Protection Agency. Technical support document for the 1992 Citizen’s Guide to Radon, EPA 400-R-92-011 (Washington, D.C.: U.S. Environmental Protection Agency, 1992).
19. Atlanta Constitution, July 15, 1985.
20. Newsweek, August 18, 1986, 60–61.
21. P. Shabecoff, “Radioactive Gas in Soil Raises Concern in Three-State Area,” New York Times, May 19, 1985.
22. K. E. Warner, D. D. Mendez, and P. N. Courant. “Toward a More Realistic Appraisal of the Lung Cancer Risk from Radon: The Effects of Residential Mobility,” American Journal of Public Health 86 (September 1, 1996): 1222–1227.
23. Cole, Element of Risk, 1.
24. Ibid., 150. Cole asks why media attention to radon declined after 1987, when the EPA and the U.S. Surgeon General’s office ratcheted up their message in the late eighties. A partial explanation, he argues, is that radon became just another in a long succession of trumpeted health hazards and that saturation set in. But he also proposes that EPA’s extremist radon policy coupled with problems of obtaining accurate testing results and effective remediation, as well as the bungled handling of landfill contamination in places like Montclair, New Jersey, undermined the public’s confidence in the agency’s policy (Cole, 151–152).
27. Ibid., 17–19, 82; Proctor, Cancer Wars, 214.
28. Cole, Element of Risk, 93; S. S. Epstein, “A Straw Man” (letter), New York Times, October 22, 1988; Proctor, Cancer Wars, 199, 211; “Cancer Risk from Domestic Radon,” Lancet 1 (January 14, 1989): 93.
29. U.S. Environmental Protection Agency. A Citizen’s Guide to Radon: What It Is and What to Do About It (Washington, D.C.: U.S. Environmental Protection Agency, August 1986).
31. Cole, Element of Risk, 13–14.
35. P. H. Abelson, “Radon Today: The Role of Flimflam in Public Policy,” Regulation (Fall 1991).
38. Cole, Element of Risk, 15–16.
40. UNSCEAR (United Nations Scientific Committee on the Effects of Atomic Radiation), Sources and Effects of Ionizing Radiation (New York: United Nations, 1994).
41. Slovic, “Perception of Risk from Radiation,” in Perception of Risk, ed. Slovic, 264–274.
42. M. deCourcy Hinds, “Radon: Making the Public Pay Attention,” New York Times, September 24, 1988.
43. W. E. Leary, “13,000 Deaths a Year Indicated by Science Academy Radon Study,” New York Times, January 6, 1988.
44. J. H. Lubin et al., “Lung Cancer in Radon-Exposed Miners and Estimation of Risk from Indoor Exposure,” Journal of the National Cancer Institute 87 (June 7, 1995): 817–827; S. Darby, D. Hill, and R. Doll, “Radon: A Likely Carcinogen at All Exposures (review),” Annals of Oncology 12 (October 2001): 1341–1351; D. Krewski et al., “Residential Radon and Risk of Lung Cancer: A Combined Analysis of 7 North American Case-Control Studies,” Epidemiology 16 (March 2005): 137–145.
45. Cole, Element of Risk, 170.
46. E. Eckholm, “Radon: The Threat Is Real, but Scientists Argue over Its Severity,” New York Times, September 2, 1986.
47. Cole, Element of Risk, 73–75.
48. Eckholm, “Radon: The Threat Is Real.”
51. Warner et al., “Toward a More Realistic Appraisal.”
52. W. W. Nazaroff and K. Teichman, “Indoor Radon: Exploring U.S. Federal Policy for Controlling Human Exposures,” Environmental Science and Technology 24 (1990): 774–782.
54. Abelson, “Radon Today”; Cole, Element of Risk, 12–17.
55. Abelson, “Radon Today.”
56. National Research Council, Health Risks of Radon, 446-454.
61. Ibid., Table VII-9, 528.
62. Ibid., Table VII-9, 528.
63. T. Reynolds, “Experts Debate Radon’s Cancer Risks,” Journal of the National Cancer Institute 83 (June 19, 1991): 810–812.
64. National Research Council, Health Effects of Exposure, 18.
67. Lubin et al., “Lung Cancer in Radon-Exposed Miners”; J. H. Lubin and J. D. Boice, Jr., “Lung Cancer Risk from Residential Radon: Meta-analysis of Eight Epidemiologic Studies,” Journal of the National Cancer Institute 89 (January 1997): 49–57.
68. Lubin et al., “Lung Cancer in Radon-Exposed Miners.”
69. Lubin and Boice, “Lung Cancer Risk.”
71. Lubin et al., “Lung Cancer in Radon-Exposed Miners.”
73. Lubin and Boice, “Lung Cancer Risk.”
74. National Research Council, Health Effects of Exposure, 19.
75. Lubin et al., “Lung Cancer in Radon-Exposed Miners.”
76. Krewski et al., “Residential Radon.”
77. Alderson, “A Creeping Suspicion.”
78. Krewski et al., “Residential Radon”; Lubin et al., “Lung Cancer in Radon-Exposed Miners.”
79. Alderson, “A Creeping Suspicion”; J. H. Lubin, J. M. Samet, and C. Weinberg, “Design Issues in Epidemiologic Studies of Indoor Exposure to Rn and Risk of Lung Cancer,” Health Physics 59 (December 1990): 807–817.
80. Abelson, “Radon Today”; P. H. Abelson, “Uncertainties About Health Effects of Radon,” Science 250 (October 19, 1990): 353.
81. Abelson, “Radon Today.”
82. M. Upfal, G. Divine, and J. Siemiatycki, “Design Issues in Studies of Radon and Lung Cancer: Implications of the Joint Effect of Smoking and Radon,” Environmental Health Perspectives 103 (January 1995): 58–63; J. S. Neuberger and T. F. Gesell, “Residential Radon Exposure and Lung Cancer: Risk in Nonsmokers,” Health Physics 83 (2002): 1–18.
83. Neuberger and Gesell, “Residential Radon Exposure.”
84. Lubin et al., “Design Issues in Epidemiologic Studies.”
87. R. E. Thompson et al., “Case-Control Study of Lung Cancer Risk from Residential Radon Exposure in Worcester County, Massachusetts,” Health Physics 94 (2008): 228–241.
88. Krewski et al., “Residential Radon”; S. Darby et al., “Radon in Homes and Risk of Lung Cancer: Collaborative Analysis of Individual Data from 13 European Case-Control Studies,” BMJ 330 (January 29, 2005): 223–228.
89. Dale Sandler, interview with author, August 5, 2006.
90. Neuberger and Gesell, “Residential Radon Exposure.”
92. D. P. Sandler et al., “Indoor Radon and Lung Cancer Risk in Connecticut and Utah,” Journal of Toxicology and Environmental Health, Part A 69 (2006): 633–654.
95. Krewski et al., “Residential Radon.”
96. Sandler et al., “Indoor Radon.”
97. J. S. Neuberger, interview with author, August 16, 2006.
99. Sandler, interview with author.
100. U.S. Environmental Protection Agency, A Citizen’s Guide to Radon: The Guide to Protecting Yourself and Your Family from Radon (Washington, D.C., 2005).
102. Stat Bite, “Causes of Lung Cancer in Nonsmokers,” Journal of the National Cancer Institute 98 (May 17, 2006): 664. The American Cancer Society is credited as the source of the estimates used in the pie chart. But the original source of the number of lung cancer deaths in never smokers due to radon exposure is the National Research Council (Health Effects of Exposure). However, ACS selected the higher of two figures; furthermore, the number is used without any reference to the many attending assumptions and uncertainties due to the extrapolation from the miner data to exposure in homes. In this way, what is a highly uncertain estimate can take on the status of fact.
103. Neuberger and Gesell, “Residential Radon Exposure.”
104. P. Boffetta and D. Trichopoulos, “Cancer of the Lung, Larynx, and Pleura,” in Textbook of Cancer Epidemiology, eds. H.-O. Adami et al. (New York: Oxford University Press, 2002), 248–280.
105. R. C. Brownson et al., “Epidemiology and Prevention of Lung Cancer in Nonsmokers,” Epidemiologic Reviews 20 (1998): 218–236.
106. J. D. Boice Jr., “Ionizing Radiation,” in Cancer Epidemiology and Prevention (3rd ed.), eds. D. Schottenfeld and J. F. Fraumeni Jr. (New York: Oxford University Press, 2006), 259–293.
6. THE CONTROVERSY OVER PASSIVE SMOKING: A Casualty of the “Tobacco Wars”
1. R. Kluger, Ashes to Ashes: America’s Hundred-Year Cigarette War, the Public Health, and the Unabashed Triumph of Phillip Morris (New York: Vintage Books, 1997), 737–739; M. Crichton, “Aliens Cause Global Warming,” Michelin Lecture (Pasadena: Caltech, January 17, 2003); P. L. Bernstein, Against the Gods: The Remarkable Story of Risk (New York: Wiley, 1996), 211–213.
2. E. L. Wynder and G. C. Kabat, “Environmental Tobacco Smoke and Lung Cancer: A Critical Assessment,” in Indoor Air Quality, ed. H. Kasuga (Berlin: Springer-Verlag, 1990), 5–15; N. Mantel, “What Is the Epidemiologic Evidence for a Passive Smoking–Lung Cancer Association?” in Indoor Air Quality, ed. H. Kasuga (Berlin: Springer-Verlag, 1990), 341–347; J. C. Bailar, “Passive Smoking, Coronary Heart Disease, and Meta-analysis,” New England Journal of Medicine 340 (March 1999): 958–959.
3. My account of the background to the nonsmokers’ rights movement in the 1970s relies heavily on R. Bayer and J. Colgrove (“Science, Politics, and Ideology in the Campaign Against Environmental Tobacco Smoke,” American Journal of Public Health 92 (June 2002): 949–954) and Richard Kluger (Ashes to Ashes).
4. Quoted in Bayer and Colgrove, “Science, Politics, and Ideology.”
5. R. Taylor, F. Najafi, and A. Dobson, “Meta-analysis of Studies of Passive Smoking and Lung Cancer: Effects of Study Type and Continent,” International Journal of Epidemiology 36 (2007): 1048–1059, doi:10.1093/1je/dym158.
6. T. Hirayama, “Nonsmoking Wives of Heavy Smokers have a Higher Risk of Lung Cancer: A Study from Japan,” BMJ 282 (January 1981): 183–185.
7. L. Garfinkel, “Time Trends in Lung Cancer Mortality Among Nonsmokers and a Note on Passive Smoking,” Journal of the National Cancer Institute 66 (June 1981): 1061–1066.
8. J. E. Enstrom, “Rising Lung Cancer Mortality Among Nonsmokers,” Journal of the National Cancer Institute 62 (April 1979): 755–760.
9. O. Auerbach, E. C. Hammond, and L. Garfinkel, “Changes in Bronchial Epithelium in Relation to Cigarette Smoking, 1955-1960 vs. 1970-1977,” New England Journal of Medicine 300 (February 1979): 381–385.
10. Garfinkel, “Time Trends in Lung Cancer.”
13. L. Garfinkel, “Passive Smoking and Cancer—American Experience,” Preventive Medicine 13 (November 1984): 691–697.
14. National Research Council, Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects (Washington, D.C., 1986); U.S Department of Health and Human Services, The Health Consequences of Involuntary Smoking, A Report of the Surgeon General (Rockville, Md., 1986); International Agency for Research on Cancer (IARC), Monographs on the Evaluation of the Carcinogenic Risks of Chemicals to Humans: Tobacco Smoking, vol. 38 (Lyon, France: IARC, 1986).
15. IARC Monograph, “Evaluation of the Carcinogenic Risks.”
16. U.S. Department of Health and Human Services, “The Health Consequences.”
17. U.S. Environmental Protection Agency, Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders (Washington, D.C.: U.S. Department of Health and Human Services, 1992). My view of the EPA report was shaped both by having served on the committee convened by the EPA to critically review the draft document and by my familiarity with the scientific literature concerning smoking and lung cancer and the occurrence of lung cancer occurring in never smokers. By 1992, I had published three articles on the topic of ETS and lung cancer, and a fourth appeared in 1995: G. C. Kabat and E. L. Wynder, “Lung Cancer in Nonsmokers,” Cancer 53 (March 1984): 1212–1221; E. L. Wynder and G. C. Kabat, “Environmental Tobacco Smoke”; G. C. Kabat, “Epidemiologic Studies of the Relationship Between Passive Smoking and Lung Cancer,” Toxicology Forum (February 20, 1990): 187–201; G. C. Kabat, S. D. Stellman, and E. L. Wynder, “Relation Between Environmental Tobacco Smoke and Lung Cancer in Lifetime Nonsmokers,” American Journal of Epidemiology 142 (July 1995): 141–148.
18. This was clear from the EPA staff’s presentation of the background of the report at the hearings in 1990. In addition, in July 1992, after the second meeting of the committee, I telephoned the chairman Dr. Morton Lippman to express my misgivings that the EPA had essentially marshaled the evidence in support of a predetermined conclusion that ETS was a “known human carcinogen.” Lippman responded that he would not disagree with my formulation.
19. For example, see pages 1–2, 2–8, 2–9, 5–67, 6–30, 6–31 of the EPA report (Respiratory Health Effects).
20. Garfinkel, “Passive Smoking and Cancer”; M. J. Thun et al., “Trends in Smoking and Mortality from Cigarette Use in Cancer Prevention Studies I (1959 through 1965) and II (1982 through 1988),” in Changes in Cigarette-Related Disease Risks and their Implication for Prevention and Control, Smoking and Tobacco Control Monograph, vol. 8 (Washington, D. C.: National Cancer Institute, 1996), 318.
21. Another important point concerns the reliance on levels of cotinine (and other tobacco-specific compounds) in body fluids to compare nonsmokers’ exposure to ETS with that incurred by active smokers. This approach has been used, in addition to the results of epidemiologic studies, to estimate the risk in nonsmokers. Studies carried out in the 1980s were interpreted as indicating that nonsmokers exposed to ETS had an exposure (uptake of tobacco smoke) equivalent to a smoker of one cigarette per day, and this figure was used to estimate the risk of nonsmokers. However, it appears that nonsmokers may metabolize cotinine, and perhaps other compounds in tobacco smoke, differently than active smokers. Specifically, nonsmokers may metabolize these products less efficiently than smokers, presumably because smokers have to adapt to coping with much higher levels. For this reason, it appears that comparisons between nonsmokers with exposure to ETS and active smokers may overstate the formers’ exposure if they do not take into account the difference in metabolism. The EPA acknowledged this problem but then went on to make the comparison anyway and to accept the claim that the average passive smoker is exposed to the equivalent of 1 cigarette per day.
22. Although I submitted many of these points to the committee (all members were required to hand in written comments on the draft of the document), none made their way into the final version of the report.
23. G. B. Gori and J. C. Luik, Passive Smoke: The EPA’s Betrayal of Science and Policy (Vancouver: The Fraser Institute, 1999).
24. “The idea that secondhand smoke is a deadly health hazard dovetails so well with the goal of discouraging smoking that tobacco’s opponents generally have not been inclined to scrutinize it very closely.” J. Sullum, For Your Own Good: The Anti-Smoking Crusade and the Tyranny of Public Health (New York: The Free Press, 1998), 160.
25. Bayer and Colgrove, “Science, Politics, and Ideology.”
26. P. Brennan et al., “Secondhand Smoke Exposure in Adulthood and Risk of Lung Cancer Among Never Smokers: A Pooled Analysis of Two Large Studies,” International Journal of Cancer 109 (2004): 125–131.
27. B. Meier, “Judge Voids Study Linking Cancer to Secondhand Smoke,” New York Times, July 20, 1998. Gori and Luik, Passive Smoke, contains a complete transcript of the legal decision.
28. R. C. Brownson et al., “Environmental Tobacco Smoke: Health Effects and Policies to Reduce Exposure,” Annual Review of Public Health 18 (1997): 163–185.
29. Stat Bite, “Exposure to Secondhand Smoke Among Nonsmokers, 1988–2002,” Journal of the National Cancer Institute 98 (March 2006): 302.
30. W. C. Hinds and M. W. First, “Concentrations of Nicotine and Tobacco Smoke in Public Places,” New England Journal of Medicine 292 (April 1975): 844–845.
31. Melvin First, interview with author, November 21, 2003.
32. R. A. Jenkins et al., “Exposure to Environmental Tobacco Smoke in Sixteen Cities in the United States as Determined by Personal Breathing Zone Air Sampling,” Journal of Exposure Analysis and Environmental Epidemiology 6 (October–December 1996): 473–502; R. A. Jenkins and R. W. Counts, “Personal Exposure to Environmental Tobacco Smoke: Salivary Cotinine, Airborne Nicotine, and Nonsmoker Misclassification,” Journal of Exposure Analysis and Environmental Epidemiology 9 (July–August 1999): 352–363.
33. M. R. Guerin, R. A. Jenkins, and B. Tomkins, The Chemistry of Environmental Tobacco Smoke: Composition and Measurement (2nd ed.), Indoor Air Research Series (Boca Raton, Fla.: CRC Press, 2000).
34. Roger Jenkins, interview with author, September 30 and November 21, 2003.
36. K. Phillips et al., “Assessment of Personal Exposures to Environmental Tobacco Smoke in British Nonsmokers,” Environment International 20 (1994): 693–712.
37. Roger Jenkins, interview with author.
39. C. S. Fox et al., “Temporal Trends in Coronary Heart Disease Mortality and Sudden Cardiac Death from 1950 to 1999: The Framingham Heart Study,” Circulation 110 (2004): 522–527.
40. M. R. Law, J. K. Morris, and N. J. Wald, “Environmental Tobacco Smoke Exposure and Ischaemic Heart Disease: An Evaluation of the Evidence,” BMJ 315 (October 18, 1997): 973–980; M. Thun, J. Henley, and L. Apicella, “Epidemiologic Studies of Fatal and Nonfatal Cardiovascular Disease and ETS Exposure from Spousal Smoking,” Environmental Health Perspectives 107 (Supplement 6) (December 1999): 841–846; J. He et al., “Passive Smoking and the Risk of Coronary Heart Disease—A Meta-analysis of Epidemiologic Studies,” New England Journal of Medicine 340 (March 25, 1999): 920–926.
41. K. Steenland, “Passive Smoking and the Risk of Heart Disease,” Journal of the American Medical Association 267 (January 1992): 94–99.
42. Bailar, “Passive Smoking.”
43. M. E. LeVois and M. W. Layard, “Publication Bias in the Environmental Tobacco Smoke/Coronary Heart Disease Epidemiologic Literature,” Regulatory Toxicology and Pharmacology 21 (February 1995): 184–191.
44. K. Steenland et al., “Environmental Tobacco Smoke and Coronary Heart Disease in the American Society CPS II Cohort,” Circulation 94 (August 1996): 622–628.
45. M. J. Thun et al., “Trends in Tobacco Smoking and Mortality from Cigarette Use in Cancer Prevention Studies I (1959 through 1965) and II (1982 through 1988),” in Changes in Cigarette-Related Disease Risks and Their Implication for Prevention and Control, Smoking and Tobacco Control Monograph 8 (Washington, D. C.: National Cancer Institute, 1996), 311.
46. J. E. Enstrom and G. C. Kabat, “Environmental Tobacco Smoke and Coronary Heart Disease Mortality in the United States—A Meta-analysis and Critique,” Inhalation Toxicology 18 (March 2006): 199–210.
47. Law et al., “Environmental Tobacco Smoke Exposure.”
48. J. E. Enstrom and G. C. Kabat, “Environmental Tobacco Smoke and Tobacco Related Mortality in a Prospective Study of Californians, 1960–98,” BMJ 326 (May 17, 2003): 1057–1066.
49. Enstrom, “Rising Lung Cancer Mortality.”
52. The published correspondence regarding the Enstrom and Kabat paper is to be found in BMJ 327 (August 30, 2003): 501–505.
53. Richard Smith, “Comment from the Editor,” BMJ 327 (August 30, 2003): 505.
54. In our 2006 paper, we presented data from five large surveys showing that, in fact, not all nonsmokers back in the 1960s were exposed to ETS.
55. Enstrom and Kabat, “Environmental Tobacco Smoke.”
57. In contrast to the attention directed at our 2003 BMJ paper, this attempt to perform a rigorous and transparent meta-analysis of ETS and heart disease is rarely cited.
58. International Agency for Research on Cancer, Tobacco Smoke and Involuntary Smoking. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, vol. 83 (Lyon, France: IARC, 2003); California Environmental Protection Agency, Proposed Identification of Environmental Tobacco Smoke as a Toxic Air Contaminant (draft) (Air Resources Board, California Environmental Protection Agency, June 2005), www.arb.ca.gov/toxics/ets/dreport/dreport.htm; U.S. Department of Health and Human Services, The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General (Washington, D.C.: Department of Health and Human Services; 2006), at http://www.surgeongeneral.gov/library/secondhandsmoke.
59. Bailar, “Passive Smoking.”
61. As Roger Jenkins pointed out to me, the most glaring instance of the report’s failure to put things in perspective is its estimate of the amount of nicotine emitted into the California air by smokers—40 tons per year—but does not mention the amount emitted by the growing of all the solanaceous vegetables in the Central Valley (these include tomatoes, eggplants, and green peppers). That nicotine would be emitted from the leaves of the plants, as they sit out in the hot sun in the cloudless Central Valley. As Jenkins put it, “Everything has a vapor pressure, and nicotine’s, especially if it is in the free base form, is fairly high.” Similarly, the report gives a figure of 1,907 tons per year of carbon monoxide due to ETS emissions but fails to give any indication of how this compares with other sources. It turns out that all California’s cigarette smokers emit, to a first approximation, about the same amount of carbon monoxide as 7,500 cars. This sounds like a lot, until you realize that there are at least 15 million cars in the state of California. Of course, this leaves out other sources of carbon monoxide, such as power plants, forest fires, wood-burning stoves, volcanoes, etc. Thus, to think of cigarettes as a significant contributor to carbon monoxide pollution is ludicrous. The estimates of 40 tons of nicotine and 1,907 tons of carbon monoxide per year are numbers without any context and thus uninformative.
62. L. A. Bero, S. Glantz and M. K. Hong, “The Limits of Competing Interest Disclosure,” Tobacco Control 14 (April 2005): 118–126; M. J. Thun, “More Misleading Science from the Tobacco Industry,” BMJ 327 (2003): E237–238E; UPI, 2003; J. A. Francis, A. K. Shea, and J. M. Samet, “Challenging the Epidemiologic Evidence on Passive Smoking: Tactics of Tobacco Industry Expert Witnesses,” Tobacco Control 15, Supplement IV (2006): iv68–iv76, doi:10.1136/tc.2005.014241; R. L. Barnes, S. K. Hammond, and S. A. Glantz, “The Tobacco Industry’s Role in the 16 Cities Study of Secondhand Tobacco Smoke: Do the Data Support the Stated Conclusions? Environmental Health Perspectives 114 (December 2006): 1890–1897.
63. For a detailed account of the attacks directed at James Enstrom, see J. E. Enstrom, “Defending Legitimate Epidemiologic Research: Combating Lysenko Pseudoscience,” Epidemiologic Perspectives and Innovations 4 (2007): 11.
64. K. J. Rothman, “Conflict of Interest: The New McCarthyism in Science,” Journal of the American Medical Association 269 (June 1993): 2782–2784.
65. K. J. Rothman, “Conflict of Interest Policies: Protecting Readers or Censoring Authors? In Reply,” Journal of the American Medical Association 270 (December 8, 1993): 2684.
66. S. Ungar and D. Bray, “Silencing Science: Partisanship and the Career of a Publication Disputing the Danger of Secondhand Smoke,” Public Understanding of Science 14 (2005): 5–23.
68. Economic Affairs Committee, House of Lords, 2006.
69. S. Sun, J. H. Schiller and A. F. Gazdar, “Lung Cancer in Never Smokers—A Different Disease,” Nature 7 (October 2007): 778–790.
CONCLUSION
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