Science as Adversarial Process versus Group Think

Climate scientists, at least those scientists who believe that climate change is both real and an existential threat to human civilization, have invoked their consensus as an evidentiary ground for political action. These same scientists have also used their claim of a consensus to shame opposing points of view (climate change skeptics) as coming from “climate change deniers.”

Consensus, or “general acceptance” as it is sometimes cast in legal discussions, is rarely more than nose counting. At best, consensus is a proxy for data quality and inferential validity. At worst, consensus is a manifestation of group think and herd mentality. Debates about climate change, as well as most scientific issues, would progress more dependably if there were more data, and less harrumphing about consensus.

Olah’s Nobel Speech

One Nobel laureate, Professor George Olah, explicitly rejected the kumbaya view of science and its misplaced emphasis on consensus and collaboration. In accepting his Nobel Prize in Chemistry, Olah emphasized the value of adversarial challenges in refining and establishing scientific discovery:

“Intensive, critical studies of a controversial topic always help to eliminate the possibility of any errors. One of my favorite quotation is that by George von Bekessy (Nobel Prize in Medicine, 1961).

‘[One] way of dealing with errors is to have friends who are willing to spend the time necessary to carry out a critical examination of the experimental design beforehand and the results after the experiments have been completed. An even better way is to have an enemy. An enemy is willing to devote a vast amount of time and brain power to ferreting out errors both large and small, and this without any compensation. The trouble is that really capable enemies are scarce; most of them are only ordinary. Another trouble with enemies is that they sometimes develop into friends and lose a good deal of their zeal. It was in this way the writer lost his three best enemies. Everyone, not just scientists, needs a few good enemies!’”

George A. Olah, “My Search for Carbocations and Their Role in Chemistry,” Nobel Lecture (Dec. 8, 1994), quoting George von Békésy, Experiments in Hearing 8 (N.Y. 1960); see also McMillan v. Togus Reg’l Office, Dep’t of Veterans Affairs, 294 F. Supp. 2d 305, 317 (E.D.N.Y. 2003) (“As in political controversy, ‘science is, above all, an adversary process.’”) (internal citation omitted).

Carl Sagan expressed similar views about the importance of skepticism in science :

“At the heart of science is an essential balance between two seemingly contradictory attitudes — an openness to new ideas, no matter how bizarre or counterintuitive they may be, and the most ruthless skeptical scrutiny of all ideas, old and new. This is how deep truths are winnowed from deep nonsense.”

Carl Sagan, The Demon-Haunted World: Science as a Candle in the Dark (1995); See also Cary Coglianese, “The Limits of Consensus,” 41 Environment 28 (April 1999).

Michael Crichton, no fan of Sagan, agreed at least on the principle:

“I want to . . . talk about this notion of consensus, and the rise of what has been called consensus science. I regard consensus science as an extremely pernicious development that ought to be stopped cold in its tracks. Historically, the claim of consensus has been the first refuge of scoundrels; it is a way to avoid debate by claiming that the matter is already settled. Whenever you hear the consensus of scientists agrees on something or other, reach for your wallet, because you’re being had.

Let’s be clear: the work of science has nothing whatever to do with consensus. Consensus is the business of politics. Science, on the contrary, requires only one investigator who happens to be right, which means that he or she has results that are verifiable by reference to the real world. In science consensus is irrelevant. What is relevant is [sic] reproducible results. The greatest scientists in history are great precisely because they broke with the consensus.  There is no such thing as consensus science. If it’s consensus, it isn’t science. If it’s science, it isn’t consensus. Period.34

Michael Crichton, “Lecture at California Institute of Technology: Aliens Cause Global Warming” (Jan. 17, 2003) (describing many examples of how “consensus” science historically has frustrated scientific progress).

Crystalline Silica, Carcinogenesis, and Faux Consensus

Clearly, there are times when consensus in science works against knowledge and data-driven inferences. Consider the saga of crystalline silica and lung cancer. Suggestions that silica causes lung cancer date back to the 1930s, but the suggestions were dispelled by data. The available data were evaluated by the likes of Wilhelm Heuper[1], Cuyler Hammond[2] (Selikoff’s go-to-epidemiologist), Gerrit Schepers[3], and Hans Weill[4]. Even etiologic fabulists, such as Kaye Kilburn, disclaimed any connection between silica or silicosis and lung cancer[5]. As recently as 1988, august international committees, writing for the National Institute of Occupational Safety and Health, acknowledged the evidentiary insufficiency of any claim that silica caused lung cancer[6].

IARC (1987)

So what happened to the “consensus”? A group of activist scientists, who disagreed with the consensus, sought to establish their own, new consensus. Working through the International Agency for Research on Cancer (IARC), these scientists were able to inject themselves into the IARC working group process, and gradually raise the IARC ranking of crystalline silica. In 1987, the advocate scientists were able to move the IARC to adopt a “limited evidence” classification for crystalline silica.

The term “limited evidence” is defined incoherently by the IARC as evidence that provides for a “credible” causal explanation, even though chance, bias, and confounding have not been adequately excluded. Despite the incoherent definition that giveth and taketh away, the 1987 IARC reclassification[7] into Group 2A had regulatory consequences that saw silica classified as a “regulatory carcinogen,” or a substance that was “reasonably anticipated to be a carcinogen.”

The advocates’ prophecy was self-fulfilling. In 1996, another working group of the IARC met in Lyon, France, to deliberate on the classification of crystalline silica. The 1996 working group agreed, by a close vote, to reclassify crystalline silica as a “known human carcinogen,” or a Group 1 carcinogen. The decision was accepted and reported officially in volume 68 of the IARC monographs, in 1997.

According to participants, the debate was intense and the vote close. Here is the description from one of the combatants;

“When the IARC Working Group met in Lyon in October 1996 to assess the carcinogenicity of crystalline silica, a seemingly interminable debate ensued, only curtailed by a reminder from the Secretariat that the IARC was concerned with the identification of carcinogenic hazards and not the evaluation of risks. The important distinction between the potential to cause disease in certain circumstances, and in what circumstances, is not always appreciated.

*   *   *   *   *

Even so, the debate in Lyon continued for some time, finally ending in a narrow vote, reflecting the majority view of the experts present at that particular time.”

See Corbett McDonald, “Silica and Lung Cancer: Hazard or Risk,” 44 Ann. Occup. Hyg. 1, 1 (2000); see also Corbett McDonald & Nicola Cherry, “Crystalline Silica and Lung Cancer: The Problem of Conflicting Evidence,” 8 Indoor Built Env’t 8 (1999).

Although the IARC reclassification hardly put the silica lung cancer debate to rest, it did push the regulatory agencies to walk in lockstep with the IARC and declare crystalline silica to be a “known human carcinogen.” More important, it gave regulators and scientists an excuse to avoid the hard business of evaluating complicated data, and of thinking for themselves.

Post IARC

From a sociology of science perspective, the aftermath of the 1997 IARC monograph is a fascinating natural experiment to view the creation of a sudden, thinly supported, new orthodoxy. To be sure, there were scientists who looked carefully at the IARC’s stated bases and found them inadequate, inconsistent, and incoherent[8]. One well-regarded pulmonary text in particular gives the IARC and regulatory agencies little deference:

“Silica-induced lung cancer

A series of studies suggesting that there might be a link between silica inhalation and lung cancer was reviewed by the International Agency for Research on Cancer in 1987, leading to the conclusion that the evidence for carcinogenicity of crystalline silica in experimental animals was sufficient, while in humans it was limited.112 Subsequent epidemiological publications were reviewed in 1996, when it was concluded that the epidemiological evidence linking exposure to silica to the risk of lung cancer had become somewhat stronger.113 but that in the absence of lung fibrosis remained scanty.113 The pathological evidence in humans is also weak in that premalignant changes around silicotic nodules are seldom evident.114 Nevertheless, on this rather insubstantial evidence, lung cancer in the presence of silicosis (but not coal or mixed-dust pneumoconiosis) has been accepted as a pre­scribed industrial disease in the UK since 1992.115 Some subsequent studies have provided support for this decision.116 In contrast to the sparse data on classic silicosis, the evidence linking carcinoma of the lung to the rare diffuse pattern of fibrosis attributed to silica and mixed dusts is much stronger and appears incontrovertible.33,92

Bryan Corrin[9] & Andrew Nicholson, Pathology of the Lungs (3d ed. 2011).

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Cognitive biases cause some people to see a glass half full, while others see it half empty. Add a “scientific consensus” to the mix, and many people will see a glass filled 5% as 95% full.

Consider a paper by Centers for Disease Control and NIOSH authors on silica exposure and morality from various diseases. Geoffrey M. Calvert, Faye L. Rice, James M. Boiano, J. W. Sheehy, and Wayne T. Sanderson, “Occupational silica exposure and risk of various diseases: an analysis using death certificates from 27 states of the United States,” 60 Occup. Envt’l Med. 122 (2003). The paper was nominated for the Charles Shepard Award for Best Scientific Publication by a CDC employee, and was published in the British Medical Journal’s publication on occupational medicine. The study analyzed death certificate data from the U.S. National Occupational Mortality Surveillance (NOMS) system, which is based upon the collaboration of NIOSH, the National Center for Health Statistics, the National Cancer Institute, and some state health departments. Id. at 122.

From about 4.8 million death certificates included in their analysis, the authors found a statistically decreased mortality odds ratio (MOR) for lung cancer among those who had silicosis (MOR = 0.70, 95% C.I., 0.55 to 0.89). Of course, with silicosis on the death certificates along with lung cancer, the investigators could be reasonably certain about silica exposure. Given the group-think in occupational medicine about silica and lung cancer, the authors struggled to explain away their finding:

“Although many studies observed that silicotics have an increased risk for lung cancer, a few studies, including ours, found evidence suggesting the lack of such an association. Although this lack of consistency across studies may be related to differences in study design, it suggests that silicosis is not necessary for an increased risk of lung cancer among silica exposed workers.”

Well this statement is at best disingenuous. The authors did not merely find a lack of an association; they found a statistically significance inverse or “negative” association between silicosis and lung cancer. So it is not the case that silicosis is not necessary for an increased risk; silicosis is antithetical to an increased risk.

Looking at only death certificate information, without any data on known or suspected confounders (“diet, hobbies, tobacco use, alcohol use, or medication,” id. at 126, or comorbid diseases or pulmonary impairment, or other occupational or environmental exposures), the authors inferred low, medium, high, and “super high” silica exposure from job categories. Comparing the ever-exposed categories with low exposure yielded absolutely no association between exposure and lung cancer, and subgroup analyses (without any correction for multiple comparisons) found little association, although two subgroups were nominally statistically significantly increased, and one was nominally statistically significantly decreased, at very small deviations from expected:

Lung Cancer Mortality Odds Ratios (p-value for trend < 0.001)

ever vs. low/no exposure:                0.99 (0.98 to 1.00)

medium vs. low/no exposure:         0.88 (0.87 to 0.90)

high vs. low/no exposure:                 1.13 (1.11 to 1.15)

super high vs. low/no exposure:      1.13 (1.06 to 1.21)

Id. at Table 4, and 124.

On this weak evidentiary display, the authors declare that their “study corroborates the association between crystalline silica exposure and silicosis, lung cancer.” Id. at 123. In their conclusions, they elaborate:

“Our findings support an association between high level crystalline silica exposure and lung cancer. The statistically significant MORs for high and super high exposures compared with low/no exposure (MORs = 1.13) are consistent with the relative risk of 1.3 reported in a meta-analysis of 16 cohort and case-control studies of lung cancer in crystalline silica exposed workers without silicosis”

Id. at 126. Actually not; Calvert’s reported MORs exclude an OR of 1.3.

The Calvert study thus is a stunning example of authors, prominent in the field of public health, looking at largely exculpatory data and declaring that they have confirmed an important finding of silica carcinogenesis. And to think that United States taxpayers paid for this paper, and that the authors almost received an honorific award for this thing!


[1] Wilhelm Hueper, “Environmental Lung Cancer,” 20 Industrial Medicine & Surgery 49, 55-56 (1951) (“However, the great majority of investigators have come to the conclusion that there does not exist any causal relation between silicosis and pulmonary or laryngeal malignancy”).

[2] Cuyler Hammond & W. Machle, “Environmental and Occupational Factors in the Development of Lung Cancer,” Ch. 3, pp. 41, 50, in E. Mayer & H. Maier, Pulmonary Carcinoma: Pathogenesis, Diagnosis, and Treatment (N.Y. 1956) (“Studies by Vorwald (41) and others agree in the conclusion that pneumoconiosis in general, and silicosis in particular, do not involve any predisposition of lung cancer.”).

[3] Gerrit Schepers, “Occupational Chest Diseases,” Chap. 33, in A. Fleming, et al., eds., Modern Occupational Medicine at 455 (Philadelphia 2d ed. 1960) (“Lung cancer, of course, occurs in silicotics and is on the increase. Thus far, however, statistical studies have failed to reveal a relatively enhanced incidence of pulmonary neoplasia in silicotic subjects.”).

[4] Ziskind, Jones, and Weill, “State of the Art: Silicosis” 113 Am. Rev. Respir. Dis. 643, 653 (1976) (“There is no indication that silicosis is associated with increased risk for the development of cancer of the respiratory or other systems.”); Weill, Jones, and Parkes, “Silicosis and Related Diseases, Chap. 12, in Occupational Lung Disorders (3d ed. 1994) (“It may be reasonably concluded that the evidence to date that occupational exposure to silica results in excess lung cancer risk is not yet persuasive.”).

[5] Kaye Kilburn, Ruth Lilis, Edwin Holstein, “Silicosis,” in Maxcy-Rosenau, Public Health and Preventive Medicine, 11th ed., at 606 (N.Y. 1980) (“Lung cancer is apparently not a complication of silicosis”).

[6] NIOSH Silicosis and Silicate Disease Committee, “Diseases Associated With Exposure to Silica and Nonfibrous Silicate Minerals,” 112 Arch. Path. & Lab. Med. 673, 711b, ¶ 2 (1988) (“The epidemiological evidence at present is insufficient to permit conclusions regarding the role of silica in the pathogenesis of bronchogenic carcinoma.”)

[7] 42 IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans at 22, 111, § 4.4 (1987).

[8] See, e.g., Patrick A. Hessel, John F. Gamble, J. Bernard L. Gee, Graham Gibbs, Francis H. Y. Green, W. Keith C. Morgan, and Brooke T. Mossman, “Silica, Silicosis, and Lung Cancer: A Response to A Recent Working Group,” 42 J. Occup. Envt’l Med. 704, 718 (2000) (“The data demonstrate a lack of association between lung cancer and exposure to crystalline silica in human studies. Furthermore, silica is not directly genotoxic and has been to be a pulmonary carcinogen in only one animal species, the rat, which seems to be an inappropriate carcinogenesis in humans.”)

[9] Professor of Thoracic Pathology, National Heart and Lung Institute, Imperial College School of Medicine; Honorary Consultant Pathologist, Brompton Hospital, London, UK.

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