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History of Silica Litigation – the Lung Cancer Angle

February 3rd, 2019

In the late 1990s, the litigation industry attempted a revival of mass-tort silicosis claiming, by initiating unlawful, unethical radiological screenings. This effort was the plaintiffs’ bar’s “Field of Dreams,” based upon its glib assumption that “if you build it, they will come.” They were the thousands of imaginary silicosis victims who somehow were not getting access to legal redress in the courts.

In large part, the litigation industry’s confidence was based upon plausible belief that a then recent classification of crystalline silica as a Category I human carcinogen by the International Agency for Research on Cancer would sex up their litigation claims. Dozens of plaintiffs’ and defense lawyers weighed in by asking whether silica was the new asbestos.1

This recrudescence of silica litigation ultimately failed, and the overwhelming number (but not all) of the specious medical claims have been wiped away.2 Why did silicosis fail as a mass tort, when other claims gained recognition? Surely, the lack of real, valid silicosis diagnoses from mass screenings helped sink many claims. Plaintiffs also faced up an uphill battle on legal liability, given the widespread common knowledge about how, why, and when silica causes silicosis, among industry, organized and unorganized labor, government scientists and regulators, and academics. Even when the so-called sophisticated intermediary was not a complete legal defense, the realities of employer-purchaser knowledge of silica hazards, and prevalent state and federal regulation of silica in the workplace made silicosis claims unattractive.

Finally, the sex appeal of silica as a cause of lung cancer dissipated. Every dogma has its day, but the IARC was quickly losing credibility as a disinterested voice in debates about cancer causation. The 1996 working group vote on silica was closely decided by a slim majority. The head of the working group exhibited a serious conflict of interest, by promoting his own study as the rationale for the working group’s decision. Although the regulatory agencies and the litigation industry’s consultants quickly jumped on the cancer bandwagon, the IARC ruling was itself qualified and hedged:

“In making the overall evaluation, the Working Group noted that carcinogenicity in humans was not detected in all industrial circumstances studied. Carcinogenicity may be dependent on inherent characteristics of the crystalline silica or on external factors affecting its biological activity or distribution of its polymorphs. Crystalline silica inhaled in the form of quartz or cristobolite from occupational sources is carcinogenic to humans. (Group 1).”3

The 1997 IARC monograph on silica provoked a scholarly debate on the correctness of the IARC analysis and decision. Two prominent pathologists weighed:

“Whether an increased lung cancer risk also exists in the absence of asbestosis is a matter of considerable debate (177). In rats, crystalline silica is clearly a lung carcinogen and tumors again arise in close spatial relationship to silicotic nodules, whereas strains of mice and hamsters that do not develop fibrotic lesions after exposure to silica also do not show an in-creased incidence of cancers (178). The International Agency for Research on Cancer (IARC) recently classified crystalline silica as a definite human carcinogen (179). This classification is controversial, but the association between silica exposure and lung cancer in humans appears to be on much firmer ground in those with silicosis than in those without (5, 25).”4

In 2000, just a few years after the IARC published its silica monograph, Colin A. Soutar, a scientist at the Institute of Medicine in Edinburgh, described the science behind the IARC decision as uncertain:

“Descriptive studies frequently though not invariably suggest an excess lung cancer risk in silica-exposed workers compared with the general population, but exposure-response studies consistently fail to confirm that the cause is exposure to quartz. A single exposure-response study of cristobalite suggests a positive relation. Both sets of evidence have weaknesses. There are uncertainties on whether the excess risks in the descriptive studies are related to silica exposure or to lifestyle, including smoking habits. There are doubts on whether the exposure estimates in some of the exposure-response studies were sufficiently reliable to detect a small risk or weak association, though they are unlikely to have missed a strong effect.”5

In 2000, a group of seven scientists criticized the IARC determination for its biased selectivity in excluding important “negative” studies, as well as for other analytical flaws:

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.”6

Another important aspect to the silica lung cancer debate differentiated silica litigation from asbestos cases. In the evolution of knowledge about the carcinogenicity of asbestos, there were important voices in the scientific community who suggested or claimed that asbestosis caused lung cancer, well before any scientific consensus emerged, and well before 1964, when many companies begin to label its asbestosconsumer products with warnings. The “state of the art” with respect to knowledge of silica and its alleged carcinogenicity was very different from the asbestos history. Up until the IARC 1997 silica monograph, virtually all experts in the field expressed views that silica did not cause lung cancer. Among these experts were many of the experts lauded by the litigation industries’ expert witnesses on asbestos history. Furthermore, much of the silica sand industry began to warn about a lung cancer hazard, despite the lack of a reasonable conclusion of carcinogenicity, back in the 1980s, when claims of carcinogenicity were being made only by a few zealots. Unlike the asbestos litigation, which received a huge boost from the negligence failure-to-warn about cancer claims, the silica claims were bereft of this moral grievance.7

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1 See, e.g., Robert D. Chesler, James Stewart, and Geoffrey T. Gibson, “Is Silica the Next Asbestos? Silica litigation will present similar insurance issues and raise many of the same controversies as asbestos litigation,” 177 N. J. L. J. (June 28, 2004); Melissa Shapiro, “Is Silica the Next Asbestos? An Analysis of Silica Litigation and the Sudden Resurgence of Silica Lawsuit Filings,” 32 Pepperdine L. Rev. 983 (2005); Chris Michael Temple, “A Case for Why Silica Litigation Is Not the ‘Next Asbestos’,” Product Liab. Law & Strategy 1, 6-7 (Nov. 2004); Peter A. Antonucci & Jason Marino, “Silicosis Litigation: Here We Go Again,” Toxic Torts & Envt’l Law Comm. News 10 (Summer 2004); Sharon L. Caffrey, Kenneth M. Argentieri & Julie S. Greenberg, “Another Wave Of Silicosis Claims May Be On The Horizon,” Law360 (Oct. 3, 2012); Lawrence G. Cetrulo & Lawrence J. Sugarman, “The Re-emergence of Silica Litigation and the Theories of Liability Under Which it is Litigated,” HarrisMartin (Feb. 24, 2004); Thomas A Gilligan, Jr., “Is Silica The Next Asbestos? The Defendants’ Perspective,” 1 Mealey’s Litig. Rep. 19 (Jan. 2003). See alsoThe Unreasonable Success of Asbestos Litigation” (July 25, 2015).

2 See Kimberley A. Strassel, “He Fought the Tort Bar — and Won; Thanks to a CEO’s persistence, a federal judge discovers massive lawsuit fraud,” Wall St. J. (May 3, 2009).

3 68 IARC Monograph 210-11 (1997) (emphasis in original).

4 Brooke Brookman & Andrew Churg, “Mechanisms in the Pathogenesis of Asbestosis and Silicosis,” 157 Am. J. Respir. Critical Care Med. 1666, 1676 (1998)

5 Colin A. Soutar, “Epidemiological Evidence on the Carcinogenicity of Silica: Factors in Scientific Judgement,” 44 Ann. Occup. Hyg. 3 (2000).

6 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 Report,” 42 J. Occup. & Envt’l Med. 704, 718 (2000).

7 A brief review of who was saying what, when about silica and lung cancer, is helpful to make the point.

Arthur J. Vorwald (1938)

“Inhaled dusts, therefore, except those containing recognized carcinogenic substances such as radium and tar, cannot in general be considered as etiological factors in the development of primary pulmonary carcinoma.”

Vorwald & Karr, “Pneumoconiosis and Pulmonary Carcinoma,” 14 Am. J. Path. 49, 57 (1938)

Sir Ernest Laurence Kennaway & Nina Marion Kennaway (1947)

“The general indication of these results is that the factors which lead to silicosis are not very active in producing cancer of the lung or larynx.”

(Kennaway & Kennaway, “A Further Study of the Incidence of Cancer of the Lung and Larynx,” Br. J. Cancer 260 (1947))

Madge Thurlow Macklin (1948)

“If silicosis is being considered as a causative agent in lung cancer, the control group should be as nearly like the experimental or observed group as possible in sex, age distribution, race, facilities for diagnosis, other possible carcinogenic factors, etc. The only point in which the control group should differ in an ideal study would be that they were not exposed to free silica, whereas the experimental group was. The incidence of lung cancer could then be compared in the two groups of patients.

This necessity is often ignored; and a ‘random’ control group is obtained for comparison on the assumption that any group taken at random is a good group for comparison. Fallacious results based on such studies are discussed briefly.”

Madge Thurlow Macklin, “Pitfalls in Dealing with Cancer Statistics, Especially as Related to Cancer of the Lung,” 14 Diseases Chest 525 532-33, 529-30 (1948).

Alexander Thom Doig (1949)

“Some ten years ago a number of cases of lung cancer occurring in men suffering from silicosis were reported and an impression arose that silica might play an etiological part in producing malignant lung disease. This has not been borne out by further enquiry but evidence is accumulating that cancer of the lung is unduly frequent in asbestos workers usually associated with asbestosis.”

A. T. Doig, “Other Lung Diseases Due to Dust,” 25 Postgrad. Med. J. 639, 645 (1949) [His Majesty’s Inspector of Factories]

Wilhelm Hueper (1951)

“Since silicotic pneumoconiosis is characterized by a chronic granulomatous inflammatory reaction, and thus seems to fulfill remarkably well the basic requirements of the chronic irritation theory of cancerigenesis, several investigators have incriminated this frequent type of occupational pneumoconiosis in the development of cancer of the lung (Fine & Jaso; Anderson & Dible; Charr; Klotz; Dible). There are in fact some 50 cases on record in which cancer of the lung or larynx and silicosis were co-existing (Dible; Fine & Jaso; Klotz & Simpson; Maxwell; Sladden; Middleton; Sweany, Porsche & Douglass; Vorwald & Karr; Allen; Sokoloff; Pancoast & Pendergrass; Simmons; Schnurer; Charr; Harris). 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 (Vorwald & Karr; Allen; Feil; Harris; Pancoast & Pendergrass; Saupe; Schulte; Schulz; Berblinger). Schulte and Schultz noted that coal miners in the Ruhr district, among whom silicosis is frequent, have no unusual frequency of lung cancer, while Allen recorded a similar observation for the coal miners of Pennsylvania. Corresponding negative observations were made by Vorwald and Karr on individuals who came to necropsy with silicosis at the Saranac Laboratory and have been reported by the Miner’s Phthisis Medical Bureau of South Africa based on studies made among the South African gold miners in the Johannesburg district.”

“These conclusions are supported by the results of experimental investigations, in which mice, rats, guinea pigs, rabbits, chickens and cats were exposed to the inhalation of silica dust (Cambell; Vorwald & Karr; Willis & Brutsaert). A fundamentally different situation, on the other hand, seems to prevail in regard to the causal relation between asbestosis and cancer of the lung.…

(Hueper, “Environmental Lung Cancer,” 20 Industrial Medicine & Surgery 49, 55-56 (1951))

Maxcy (1951)

“Thus, there is no evidence that lung cancer is related in any way to silicosis.”

Maxcy, ed., Rosenau Preventive Medicine and Hygiene 1051 (NY, 7th ed. 1951)

May Mayers, New York Dep’t of Labor (1952)

“Silica and asbestos are of special importance among the dusts which fall into this category. The environmental conditions for their development are essentially similar. Nevertheless, silicosis is not, apparently associated with, or productive of, lung cancer, whereas asbestosis very probably is.

(Mayers, “Industrial Cancer of the Lungs,” 4 Compensation Medicine 11, 12 (1952)). [Dr. May Mayers was Chief, Medical Unit, Division of Industrial Hygiene and Safety Standards, N.Y. Dep’t of Labor]

Behrens (1953)

Special mention is made of the association of asbestosis with carcinoma, which is contrary to experience in cases of silicosis. Post-mortem reports from the literature indicate that in 309 cases of asbestosis there were 44 lung carcinomas (14.2 per cent.) whereas in 2,204 cases of silicosis only 32 carcinomas were found (1.4 per cent.)”

(Behrens, “Über Klinik and Pathologic der Asbestosis,” 45 Zeitschrift fur Unfallmed and Berufskrankh 129-140, 179-189 (June 15, Sept. 15, 1952; abstracted at Bulletin of Hygiene 192 (March 1953))

Wilhelm Hueper (1954)

“Rather far-reaching, if not extravagant, claims recently have been advanced as to the important, if not predominant, role which cigarette smoking is alleged to have played in the production of lung cancer and its progressive rise in frequency during the past 50 years. A critical and sober analysis of the evidence offered in support of these assertions is in order not only for reasons of scientific accuracy but also for medicolegal reasons and especially for determining the direction of future epidemiologic research and of control activities in the field of lung cancer.”

* * *

“It may be concluded that the existing evidence neither proves nor strongly indicates that tobacco smoking, and especially cigarette smoking, represents a major or even predominating causal factor in the production of cancers of the respiratory tract and are the main reason for the phenomenal increase of pulmonary tumors during recent decades. If excessive smoking actually plays a role in the production of lung cancer, it seems to be a minor one if judged from the evidence on hand. However, it may be well to remember in this connection, the concluding statement of Doll and Kennaway, that ‘the study of the relation between the national consumption of tobacco and the national incidence of cancer of the lung has scarcely begun.’”

(Hueper, “Lung Cancer and the Tobacco Smoking Habit,” 23 Industrial Medicine & Surgery 13, 19 (1954)) [Hueper, Chief of Environmental Section, National Cancer Institute, U.S. Public Health Service, in Bethesda, MD]

Wilhlem Hueper (1955)

“The concept that members of occupations especially exposed to dust, particularly silica, have an unusual liability to cancer is an old one which is still held. Reliable epidemiologic data from various sources, however, show that pulmonary cancers are not excessively frequent among persons having occupational contact with coal and silica dust and affected with anthracosis, silicosis, and anthracosilicosis, such as gold and coal mines.

[Hueper, 25 Am. J. Clinical Path. 1388, 1388 (1955)]

Cuyler Hammond (1956)

“Pneumoconiosis. Any direct carcinogenic effect of the pneumoconiosis-producing dusts is extremely doubtful.

* * *

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.” (p. 50)

[As to asbestosis: “The data at present are suggestive but inference as to causal relationship is not warranted.” (p. 50)

“. . . in our opinion, the evidence for their causal role is insufficient.” (p. 57)]

[As to smoking: “There is a high degree of association between cigarette smoking and the occurrence of lung cancer. We are of the opinion that cigarette smoking acts as one of the causative factors for the development of lung cancer.”]

(Cuyler Hammond & W. Machle, “Environmental and Occupational Factors in the Development of Lung Cancer,” Ch. 3, pp. 41-61, in E. Mayer & H. Maier, Pulmonary Carcinoma: Pathogenesis, Diagnosis, and Treatment (NY 1956))

Wilhelm Hueper (1956)

“Although the data are in part contradictory, it seems that silicosis does not play any significant role as a direct or contributory cause of cancer of the lung among the radioactive-ore miners in Schneeberg and Joachimsthal. Whether it has an antagonistic affect upon the cancerization process or modifies the course of the established cancer remains problematical.”

(W. Hueper, “A Quest Into the Environmental Causes of Cancer of the Lung,” Public Health Service Publ. No. 452, 71 Public Health Reports, No. 1, at 42-43 (1956))

[As to smoking: “From these considerations, it is apparent that any final decision concerning the relative role of cigarette smoking in the causation of cancer of the human lung should be kept in abeyance until a great deal of (additional and more valid, and especially medically conclusive, evidence becomes available. The data on hand make it unlikely that cigarette smoking represents a major factor in the production of lung cancer and in its recent phenomenal rise in frequency. For these reasons, it would be most injudicious mainly to base the future preventive control of lung cancer hazards on a theory of such doubtful scientific merits and to concentrate the immediate epidemiological and experimental efforts on this over propagandized concept.]

Id. at 44-45.

Sir Richard Doll (1959)

“Some degree of pneumoconiosis is present in most forms of industrial lung cancer, but all investigators agree that there is no quantitative relationship between silicosis and the presence of the cancer.”

Richard Doll, “Occupational Lung Cancer: A Review,” 16 Brit. J. Indus. Med. 181, 188 (1959)

Gerret Schepers (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.”

(G. Schepers, “Occupational Chest Diseases,” Chap. 33, p. 455, ¶3, in A. Fleming, et al., eds., Modern Occupational Medicine (Philadelphia 2d ed. 1960))

Compare: “Pulmonary carcinoma has been observed with such high frequency in employees of the asbestos industry that a causal relationship has been accepted by most authorities.”

(Id. at 467, ¶5)

Herbert Spencer (1962)

“Silicosis and lung cancer inhaled silica, unlike asbestos, does not predispose to the development of lung cancer. Gardner (1939) investigated the incidence among employees of Rand gold mines in South Africia and found that the incidence of lung cancer in the silicotic miners amounted to 0.7 per cent; among a large comparable group of males employed on the surface outside the mines the incidence was 0.93 per cent. Similar findings have been reported amongst a group of silicotic South Wales coal miners by James (1995)

Herbert Spencer, Pathology of the Lung (Excluding Pulmonary Tuberculosis) (1962)

Joseph K. Wagoner (1963)

“Since epidemiologic studies have demonstrated that silicosis and occupational exposure to free silica dust do not predispose to the development of cancer of the respiratory tract7,18,19 attention must be paid to specific components of the ore that have been suspected of carcinogenic activity in man.”

Joseph K. Wagoner, Robert W. Miller, Frank E. Lundin, Jr., Joseph Fraumeni, and Marian E. Hai, “Unusual Cancer Mortality Among a Group of Underground Metal Miners,” 269 New Engl. J. Med. 284, 287 (1963)

“Attention was given to the possible explanations for the threefold increase in cancer of the respiratory system. This excess was not attributed to an effect of age, smoking, nativity, urbanization, socioeconomic status, heredity, diagnostic accuracy or silicosis.”

Id. at 288 (emphasis added)

Joseph K. Wagner (1965)

“In 1964 Wagoner and his co-workers9 reported a tenfold excess of respiratory cancer among long-term underground uranium miners in the United States. This excess was not attributable to age, smoking, nativity, heredity, urbanization, self-selection, diagnostic accuracy, prior hard-rock mining or nonradioactive-ore constituents, including silica dust.”

Joseph K. Wagoner, Victor E. Archer, Frank E. Lundin, Jr., Duncan A. Holaday, and William Lloyd, “Radiation as the Cause of Lung Cancer Among Uranium Miners,” 273 New Engl. J. Med. 181, 182 (1965)

Sir Richard Doll (1966)

“I should like to draw your attention to the absence of a risk, although one has been looked for very carefully, among men with silicosis. Irritation of the lungs of the type that is produced by silica is, therefore, not in itself a cause of lung cancer.”

Richard Doll, “The Statistical Approach to Industrial Lung Cancer,” in Douglas Teare & Joan Fenning, eds., Some Aspects of Carcinoma of the Bronchus and Other Malignant Diseases of the Lung 5, 14 (1966)

Wilhelm Hueper (1966)

“Silicosis has been in the past and to somewhat lesser extent still is a rather common occupational disease occurring among member of several large work groups, such as especially hard rock miners, foundry workers, anthracite miners, stone masons and granite cutters. The relationship of silicosis to cancer of the lung covers three aspects (HUEPER, WEISSMAN).

A. The occurrence of large densities observed on X-ray film of the chest in individuals suffering from tuberculosilicosis may be mistaken from carcinoma of the lung.

B. It has remained controversial whether silicosis favors the development of lung cancer, hinders it, or does not exert any influence on this process.

C. Since the exposure to several established or suspected carcinogens (radioactive substances, iron, arsenic) is complicated in some occupations by a simultaneous contact with silica, the role of silica and silicosis on the action of the specific carcinogens and on the cancerization process, respectively, has remained a subject of dispute.

* * * *

The bulk of the available epidemiologic evidence on the association of silicosis and lung cancer supports the view of a mere coincidental role of silicosis in this combination. Several large statistical analyses performed on autopsy material derived from several occupational groups with silicosis hazard confirm this conclusion (Table 1), which is, moreover, shard by many experienced investigators (VORWALD and KARR; SCHULZ; SCHULTE; KENAWAY and KENAWAY; MEREWETHER; FAULDS; MITTMANN; FRUEHLING and OPPERMANN; BRAUN; JAMES; MULLER, MARCHAND-ALPHAND, CUALLACCI, NADIRAS and MULLER; ALLEN; RUETTNER; SCHOCH; BERBLINGER; WEDLER; FISCHER; FISCHER-WASELS; HOLSTEIN; STAEMMLER, JOHNSTONE; CHARR; WAETJEN and others).

* * * *

From the evidence on hand, it appears that a well advanced silicosis does not seem to furnish a favorable soil for the development of cancer of the lung.”

(W. Hueper, Occupational and Environmental Cancers of the Respiratory System at 2-6 (N.Y. 1966))
Note: Dr. Hueper was chief of the National Cancer Institute in Bethesda, MD.

Harriet L. Hardy (1967)

“cancer of the lung is not a risk for the silicotic. It is a serious risk following asbestos exposure and for hematite, feldspar, and uranium miners. This means that certain dusts and ionizing radiation alone or perhaps with cigarette smoke act as carcinogens.”

Harriet L. Hardy, “Current Concepts of Occupational Lung Disease of Interest to the Radiologist,” 2 Sem. Roentgenology 225, 231-32 (1967)

W. Raymond Parkes (1974)

“Bronchial carcinoma occasionally occurs in silicotic lungs but there is no evidence of a causal relationship between it and silicosis; indeed the incidence of lung cancer in miners with silicosis is significantly lower than in non-silicotic males (Miners Phthisis Medical Bureau, 1944; Rüttner & Heer, 1969).”

W. Raymond Parkes, Occupational Lung Disorders 192 (London 1974)

NIOSH (1974)

In Section III, entitled “Biologic Effects of Exposure,” there is no mention of cancer (or of autoimmune disease).

[NIOSH, Criteria for a Recommended Standard: Occupational Exposure to Crystalline Silica (1974)] [In the Asbestos Criteria Document, cancer is a principal subject of concern.]

Morton Ziskind, Robert N. Jones, Hans Weill (1976)

There is no indication that silicosis is associated with increased risk for the development of cancer of the respiratory or other systems. When there is a combined exposure to silica and other substances such as arsenic, nickel, or chromate, the increased susceptibility to cancer appears to be related to the other material. There is no indication of a synergistic increase of susceptibility to cancer after exposure to such other dusts and silica.

(Ziskind, Jones, and Weill, “State of the Art: Silicosis” 113 Am. Rev. Respir. Dis. 643, 653b, ¶ 1 (1976)

Herbert Spencer (1977)

Inhaled silica, unlike asbestos, does not predispose to the development of lung cancer. Gardner (1939) investigated the incidence among employees of the Rand gold-miners in South Africa and found that the incidence of lung cancer in the silicotic miners amounted to 0.7 per cent; among a large comparable group of males employed on the surface outside the miners the incidence was 0.93 per cent. These findings were again confirmed by Chatgidakis (1963) among white South African miners. She found that although in recent times bronchogenic carcinoma had become the most common form malignant tumorer among these miners, the incidence was the same as among the non-miners. Similar findings in Great Britain were reported by James (1955) amongst a group of South Wales coal-miners showing silicotic changes.”

[H. Spencer, Pathology of the Lung, Vol. 1, p. 395 (3d ed. 1977)]

Kaye Kilburn, Ruth Lilis, and Edwin Holstein (1980)

Lung cancer is apparently not a complication of silicosis. In a substantial mortality experience from Hamburg, lung cancer was present in 2.3 per cent of 688 deaths from silicosis and 3.99 per cent of 212,827 control deaths in males over 20 years of age.

[Kaye Kilburn, Ruth Lilis, Edwin Holstein, “Silicosis,” in Maxcy-Rosenau, Public Health and Preventive Medicine, 11th ed., at 606 (N.Y. 1980)]

LEBOWITZ (1981)

“It is my opinion that no definitive etiological relationship has been proven between silicosis and lung carcinoma, although there is some data to support such a relationship.”

(Lebowitz, “The Relationship Among Silica, Silicosis, and Lung Carcinoma,” 38 Ariz. Med. 596, 598a, last ¶ (1981)). R. Lemen was one of the editors of Lebowitz’s article. (Id. at 596b – credits)

Raymond Parkes (1982)

Bronchial carcinoma occasionally occurs in silicotic lungs but there is no evidence of a causal relationship between it and silicosis or siliceous dusts; indeed, the incidence of lung cancer with silicosis is significantly lower than in non‑silicotic males (Miners Phthisis Medical Bureau, 1944; Ruttner & Heer, 1969).”

[R. Parkes, “Diseases Due To Free Silica,” Chap. 7, Occupational Lung Disorders 157 (2d ed. 1982)]

William Rom (1983)

“The weight of epidemiologic evidence is against the proposition that silicosis carries an increased risk of respiratory malignancy.”

[Robert N. Jones, “Silicosis,” Chap. 16, in William Rom, et al., eds., Environmental and Occupational Medicine at 205 (Boston 1983)]

Herbert Anderson (1985)

“There is no evidence that silica increases the risk of lung cancer, nor does it enhance tobacco‑induced carcinogenesis.”

(I Anderson’s Pathology at 910b (1985))

Alfred Gordon Heppleston (1985)

From this mass of evidence, pathological and epidemiological, it is thus reasonable to believe that primary carcinoma of the lung shows no demonstrable causal connection either with the accumulation of dust per se containing silica in high or low proportions, or with the prior existence of pneumoconiosis whether assuming the form of classical silicosis or of the distinct variety seen in coal workers. If selection enters into necropsy studies, this conclusion may even be emphasized.”

(Heppleston, “Silica, Pneumoconiosis, and Carcinoma of the Lung,” 7 Am. J. Ind. Med. 285, 291 ¶ 2 (1985))

Herbert Spencer (1985)

Inhaled silica, unlike asbestos, does not predispose to the development of lung cancer. Gardner (1939) investigated the incidence among employees of the Rand gold-miners in South Africa and found that the incidence of lung cancer in the silicotic miners amounted to 0.7 per cent; among a large comparable group of males employed on the surface outside the miners the incidence was 0.93 per cent. These findings were again confirmed by Chatgidakis (1963) among white South African miners. She found that although in recent times bronchogenic carcinoma had become the most common form malignant tumorer among these miners, the incidence was the same as among the non-miners. Similar findings in Great Britain were reported by James (1955) amongst a group of South Wales coal-miners showing silicotic changes.”

(H. Spencer, Pathology of the Lung, 4th ed., Vol. 1, 439 (Oxford 1985))

United States Surgeon General (1985)

1985 Surgeon General’s Report, Chapter 8 “Silica‑Exposed Workers”

Summary & Conclusions

* *

*

4. “A number of studies have demonstrated an increased risk of lung cancer in workers exposed to silica, but few of these studies have adequately controlled for smoking. Therefore, while the increased standardized mortality ratios for lung cancer in these populations suggest the need for further investigation of a potential carcinogenic effect of silica exposure (particularly in the combined exposure with other possible carcinogens), the evidence does not currently establish whether silica exposure increases the risk of developing lung cancer in men.”

5. “Smoking control efforts should be an important concomitant of efforts to reduce the burden of silica‑related illness in working populations.”

(1985 Surg. Gen. Report at 348)

In 1966, Dr. W.C. Hueper reviewed the evidence on this claim and “observed that the data support the idea that lung cancer is a coincidental finding among silicotics and that there is no etiological relationship.”

(1985 Surg. Gen. at 341, citing W. Hueper, “Recent Results in Cancer Research, in III Occupational and Environmental Cancers of the Respiratory System 1‑6 (1966))

“None of these studies [reviewed by Hueper] addressed the smoking status of the subjects, a crucial omission in any study of lung cancer. Furthermore, age was not adjusted, nor were there any quantitative estimates of the silica exposure or assessments of the severity of the silicotic lesions.”

(1985 Surg. Gen. Report at 341, last ¶) IARC (1987)

William Weiss (1986)

“A search of the Index Medicine for the years 1935-39 revealed three times as many cases of silicosis with lung cancer as cases of asbestosis with lung cancer. As a result of later studies designed to answer the question whether the frequency of lung cancer among people with silicosis or asbestosis is higher than in the general population, it has been shown that there is no association between silicosis and lung cancer, but there is an association between asbestosis and lung cancer.”

William Weiss, “History of hazards associated with asbestos,” 89 Penn. Med. 57, 57 (1986)

IARC (1987)

“Limited evidence” is a term defined specifically by the IARC Working Group:

“Limited evidence of carcinogenicity indicates that a causal interpretation is credible, but that alternative explanations, such as chance, bias or confounding could not adequately be excluded.”

(42 IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans at 22 (1987))

IARC concluded that:

There is limite devidence for the carcinogenicity of crystalline silica to humans.

(42 IARC at 111, § 4.4)

John E. Cotes & COTES (1987)

The inhalation of silica dust does not contribute to malignancy.”

J. Cotes & J. Steel, Work-Related Lung Disorders 156 (Oxford 1987)

W. K. C. Morgan & Antony Seaton (1987)

It is generally believed that silicosis does not predispose to lung cancer.”

On balance, it seems unlikely that silicosis itself predisposes to lung cancer.

[K. Morgan & A. Seaton, Occupational Lung Diseases at 266, ¶ 1 (2d ed. 1987)]

Graham Gibbs & Christopher Wagner in CHURG & GREEN (1988)

“Until recently, it has been denied that silicosis is associated with the development of lung cancer. However, several epidemiologic studies have claimed increased rates of lung cancer in occupations with high free‑silica exposure. These have included silicotic miners, iron and steel foundry workers, metal molders, sandblasters, and ceramic workers. Some support for this has come from animal studies that have shown that silica can function as a direct acting carcinogen or co‑carcinogen. However, this is species dependent. Heppleston has critically reviewed the literature linking silica and lung cancer and notes that published studies lackdetailed of smoking histories and have not excluded other possible atmospheric carcinogens. At the present time, the evidence linking silica exposure with lung cancer is not entirely convincing. Further epidemiologic and pathologic studies are required to support or refute the association.”

[Gibbs & Wagner, “Disease Due to Silica,” in A. Churg & F. Green, Pathology of Occupational Lung Disease at 165 1st ed. (1988)]

NIOSH COMMITTEE (1988)

“The epidemiological evidence at present is insufficient to permit conclusions regarding the role of silica in the pathogenesis of bronchogenic carcinoma.”

(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)) [cited as 1988 NIOSH]

Arthur Frank (1989)

“The question of the relationship of coal mining to the development of lung cancer has been frequently considered. Most evidence points to cigarette smoking among coal miners as the major causative factor in the development of lung cancer, and neither a recent84 nor a British study of lung cancer among coal miners has found any relationship to occupational exposure.”

Arthur Frank, “Epidemiology of Lung Cancer, in J. Roth, et al., Thoracic Oncology, Chap. 2, at p. 8 (Table 2-1), 11 (Phila. 1989) (omitting silica from table of lung carcinogens)

BAUM & WOLINSKY (1989)

There is little evidence that either exposure to silica or the presence of silicosis predisposes to the development of lung cancer. The SMR in workers exposed to silica has been reported to be elevated in a number of studies, but most of these studies have made no allowance for cigarette smoking habits and have been carried out retrospectively. In other instances, the exposure has not been to silica alone, but has included other agents, such as coal tar pitch, polycyclic hydrocarbons, or radiation. That an increased death rate from silicosis and tuberculosis in metal miners exposed to silica can be demonstrated in the absence of any concomitant increase from lung cancer militates against silicosis being associated with an increased risk of lung cancer.”

[1989 Morgan, in G. Baum & E. Wolinsky, Textbook of Pulmonary Diseases at 771b (1989)]

Corbett McDonald (1989)

“Evidence for the carcinogenicity of crystalline silica to man is indeed limited; although credible, alternative explanations such as chance, bias, or confounding have not been adequately excluded.”

“The credibility of the hypothesis rests largely on a few animal experiments that are themselves difficult to interpret (J.C. Wagner, personal communication).”

Without more and better evidence, it is premature to conclude that exposure to crystalline silica has caused lung cancer in man.”

(McDonald, “Editorial; Silica, Silicosis, and Lung Cancer,” 46 Brit. J. Indus. Med. 289, 290b, last ¶ (1989))

Hans Weill, Robert N. Jones, and Raymond Parkes (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.

[Weill, Jones, and Parkes, “Silicosis and Related Diseases, Chap. 12, in Occupational Lung Disorders (3d ed. 1994)]

HUNTER (1994)

“The IARC’s evaluation states that there is ‘limited evidence’ for the carcinogenicity of crystalline silica to humans, which has led some countries to treat it as a proven carcinogen. However, many workers in this field agree with Craighead that such action is premature, believing that concomitant exposure to other carcinogens and inadequate control for cigarette smoke probably accounts for most of the observed risk. In any event, the possible risk of cancer can be eliminated if silicosis is reduced by good dust control.”

Peter Elmes, “Inorganic Dusts,” chap. 20, at 424 (p. 410-457), in P. Raffle, et al., eds., Hunter’s Diseases of Occupations (London 1994)

Eva Hnizdo (1994)

“Although the respirable dust in South African gold is very fibrogenic, it is not certain whether the gold miners have an increased risk of lung cancer due to the effect of silica dust. The mortality studies showed an increased standardized mortality ratio, but the dose-response trend with silica dust is inconsistent, and in two case-control studies, no association with silica or silicosis was shown. As some of the gold miners were also uranium producing mines, radiation is a strong confounding factor. Smoking is also a confounding factor. A study done in the 1960s reported that in comparison to a non-mining male population of the same socio-economic status, the miners had a higher proportion of smokers [Sluis-Cremer et al., 1967].

[Hnizdo, “Letter: Risk of Silicosis,” 25 Am. J. Indus. Med. 771 (1994)]

History of Silicosis Litigation

January 31st, 2019

“Now, Silicosis, you’re a dirty robber and a thief;
Yes, silicosis, you’re a dirty robber and a thief;
Robbed me of my right to live,
and all you brought poor me is grief.
I was there diggin’ that tunnel for just six bits a day;
I was diggin’ that tunnel for just six bits a day;
Didn’t know I was diggin’ my own grave,
Silicosis was eatin’ my lungs away.”

Josh White, “Silicosis Is Killin’ Me (Silicosis Blues)” (1936)

Recently, David Rosner, labor historian, social justice warrior, and expert witness for the litigation industry, gave the Fielding H. Garrison Lecture, in which he argued for the importance of the work that he and his comrade-in-arms, Gerald Markowitz, have done as historian expert witnesses in tort cases.1 Although I am of course grateful for the shout out that Professor Rosner gives me,2 I am still obligated to call him on the short-comings of his account of silicosis litigation.3 Under the rubric of “the contentious struggle to define disease,” Rosner presents a tendentious account of silicosis litigation, which is highly misleading, for what it says, and in particular, for it omits.

For Rosner’s self-congratulatory view of his own role in silicosis litigation to make sense, we must imagine a counterfactual world that is the center piece of his historical narrative in which silicosis remains the scourge of the American worker, and manufacturing industry is engaged in a perpetual cover up.

Rosner’s fabulistic account of silicosis litigation and his role in it falls apart under even mild scrutiny. The hazards of silica exposure were known to Josh White and the entire country in 1936. Some silicosis litigation arose in the 1930s against employers, but plaintiffs were clearly hampered by tort doctrines of assumption of risk, contributory negligence, the fellow-servant rule. To my knowledge, there were no litigation claims against remote suppliers of silica before the late 1970s, when courts started to experiment with hyperstrict liability rules.

Eventually, the litigation industry, buoyed by its successes against asbestos-product manufacturers turned their attention to silica sand suppliers to foundries and other industrial users. Liability claims against remote suppliers of a natural raw material such as silica sand, however, made no sense in terms of the rationales of tort law. There was no disparity of information between customer and supplier; the customer, plaintiffs’ employer was not only the cheapest and most efficient cost and risk avoider, the employer was the only party that could control the risk. Workers and their unions were well aware of the hazards of working in uncontrolled silica-laden workplaces.

Although employer compliance with safety and health regulations for silica exposure has never been perfect, the problem of rampant acute silicosis, such as what afflicted the tunnel workers memorialized by Josh White, is a thing of the past in the United States. The control of silica exposures and the elimination of silicosis are rightly claimed to be one of the great public health achievements of the 20th century. See Centers Disease Control, “Ten Great Public Health Achievements — United States, 1900-1999,” 48 Morbidity & Mortality Weekly Report 241 (April 02, 1999).

Interestingly, after World War II, silicosis has been a much greater problem in the communist countries, such as China, the countries that made up the Soviet Union. Rosner and Markowitz, however, like the leftist intellectuals of the 1950s who could not bring themselves to criticize Stalin, seem blind to the sorry state of workplace safety in communist countries. Their blindness vitiates their historical project, which attempts to reduce occupational diseases and other workplace hazards to the excesses of corporate capitalism. A fair comparison with non-capitalist systems would reveal that silicosis results from many motives and conditions, including inattention, apathy, carelessness, concern with productivity, party goals, and labor-management rivalries. In the case of silicosis, ignorance of the hazards of silica is the least likely explanation for silicosis cases arising out of workplace exposures after the mid-1930s.

In the United States, silicosis litigation has been infused with fraud and deception, not by the defendants, but by the litigation industry that creates lawsuits. Absent from Rosner’s historical narratives is any mention of the frauds that have led to dismissals of thousands of cases, and the professional defrocking of any number of physician witnesses.  In re Silica Products Liab. Litig., MDL No. 1553, 398 F.Supp. 2d 563 (S.D.Tex. 2005).

Nor does Rosner deign to discuss the ethical and legal breaches committed by the plaintiffs’ counsel in conducting radiographic screenings of workers, in the hopes of creating lawsuits. With the help of unscrupulous physicians, these screenings were unnaturally successful not only in detecting silicosis that did not exist, but in some cases, in transmuting real asbestosis into silicosis.4

Many silicosis cases in recent times were accompanied by more subtle frauds, which turned on the “failure-to-warn” rhetoric implicit in the Restatement (Second) of Torts § 402A. Consider the outbreak of silicosis litigation in western Pennsylvania, in the mid-1980s. Many of the men who claimed to have silicosis had significant silica exposure at the Bethlehem and U.S. Steel foundries in the Johnstown areas. Some of the claimants actually had simple silicosis, although discovery of these claimants’ workplace records revealed that they had been non-compliant with workplace safety rules.

The Johnstown, Cambria County, cases were not the result of unlawful medical screenings, paid for by plaintiffs’ lawyers and conducted by physicians of dubious integrity and medical acumen. Instead, the plaintiffs’ lawyers found their claimants as a result of the claimants’ having had previous workers’ compensation claims for silicosis, which resulted after the workers were diagnosed by employer medical screening programs.

Cambria County Courthouse in Ebensburg, PA (venue for an outbreak of silicosis litigation in the 1980s and early 1990s5)

The first of the foundrymen’s cases was set for trial in 1989, 30 years ago, in Cambria County, Pennsylvania. The silica cases were on the docket of the President Judge, the Hon. Joseph O’Kicki, who turned out to be less than honorable. Just before the first silica trial, Judge O’Kicki was arrested on charges of corruption, as well as lewdness (for calling in his female staff while lounging in chambers in his panties).

As a result of O’Kicki’s arrest, the only Cambria Country trial we saw in 1989 was the criminal trial of Judge O’Kicki, in Northampton County. In April 1989, a jury found O’Kicki guilty of bribery and corruption, although it acquitted him on charges of lewdness.6 Facing a sentence of over 25 years, and a second trial on additional charges, O’Kicki returned to the land of his forebears, Slovenia, where he lived out his days and contributed to the surplus population.7

Whatever schadenfreude experienced by the defendants in the Cambria County silicosis litigation was quickly dispelled by the assignment of the silica cases to the Hon. Eugene Creany, who proved to be an active partisan for the plaintiffs’ cause. Faced with a large backlog of cases created by the rapacious filings of the Pittsburgh plaintiffs’ lawfirms, and Judge O’Kicki’s furlough from judicial service, Judge Creany devised various abridgements of due process, the first of which was to consolidate cases. As a result, the first case up in 1990 was actually three individual cases “clustered” for a single jury trial: Harmotta, Phillips, and Peterson.8 To poke due process in both eyes, Judge Creany made sure that one of the “clustered” cases was a death case (Peterson).

Jury selection started in earnest on April 2, 1990, with opening statements set for April 4. In between, the defense made the first of its many motions for mistrial, when defense lawyers observed one of the plaintiffs, Mr. Phillips, having breakfast with some of the jurors in the courthouse cafeteria. Judge Creany did not seem to think that this pre-game confabulation was exceptional, and admonished the defense that folks in Cambria County are just friendly, but they are fair. Trial slogged on for four weeks, with new abridgments of due process almost every day, such as forcing defendants, with adverse interests and positions, into having one direct- and one cross-examination of each witness. The last motion for mistrial was provoked by Judge Creany’s walking into the jury room during its deliberations, to deliver doughnuts.

At the end of the day, in May 1990, the jury proved to be much fairer than the trial judge. Judge Creany instructed the jury that “silica was the defect,” and on other novel points of law. Led by its foreman, a union organizer for the United Mine Workers, the jury returned a defense verdict in the Peterson case, which involved a claim that Mr. Peterson’s heart attack death case was caused by his underlying silicosis. In the two living plaintiffs’ cases, the jury found that the men had knowingly assumed the risk of silicosis, but at the judge’s insistence, the jury proceeded to address defendants’ liability, and to assess damages, in the amount of $22,500, in the two cases.

Pennsylvania’s appellate courts took a dim view of plaintiffs’ efforts to hold remote silica suppliers responsible for silicosis arising out of employment by large, sophisticated steel manufacturers. The Superior Court, Pennsylvania’s intermediate appellate court, reversed and remanded both plaintiffs’ verdicts. In Mr. Harmotta’s case, the court held that his action was collaterally estopped by a previous workman’s compensation judge’s finding that he did not have silicosis. In Mr. Phillip’s case, the court addressed the ultimate issue, whether a remote supplier to a sophisticated intermediary can be liable for silicosis that resulted from the intermediary’s employment and use of the supplied raw material. In what was a typical factual scenario of supply of silica to foundry employers, the Superior Court held that there was no strict or negligence liability for the employees’ silicosis.9 The Pennsylvania Supreme Court declined to hear Harmotta’s appeal on collateral estoppels, but heard an appeal in Phillips’ case. The Supreme Court pulled back from the sophisticated intermediary rationale for reversal, and placed its holding instead on the obvious lack of proximate cause between the alleged failure to warn and the claimed harm, given the jury’s special finding of assumed risk.10

One of plaintiffs’ counsel’s principal arguments, aimed at the union organizer on the jury, was that even if a warning to the individual plaintiffs might not have changed their behavior, a warning to the union would have been effective. The case law involving claims against unions for failing to warn have largely exculpated unions and taken them out of the warning loop. Given this case law, plaintiffs’ argument was puzzling, but the puzzlement turned to outrage when we learned after the first trial that Judge Creany had been a union solicitor, in which role, he had regularly written to U.S. Steel in Johnstown, to notify the employer when one of the local union members had been diagnosed with silicosis.

The next natural step seemed to list Judge Creany as a percipient fact witness to the pervasive knowledge of silicosis among the workforce and especially among the union leadership. Judge Creany did not take kindly to being listed as a fact witness, or being identified in voire dire as a potential witness. Still, the big lie about failure to warn and worker and labor union ignorance had been uncovered. Judge Creany started to delegate trials to other judges in the courthouse and to bring judges in from neighboring counties. The defense went on win the next dozen or so cases, before the plaintiffs’ lawyers gave up on their misbegotten enterprise of trying to use Pennsylvania’s hyperstrict liability rules to make remote silica suppliers pay for the fault of workers and their employers.

You won’t find any mention of the Cambria County saga in Rosner or Markowitz’s glorified accounts of silicosis litigation. The widespread unlawful screenings, the “double dipping” by asbestos claimants seeking a second paycheck for fabricated silicosis, the manufactured diagnoses and product identification do not rent space in Rosner and Markowitz’s fantastical histories.


2 See, e.g., Nathan A. Schachtman, “On Deadly Dust and Histrionic Historians: Preliminary Thoughts on History and Historians as Expert Witnesses,” 2 Mealey’s Silica Litigation Report Silica 1, 2 (November 2003); Nathan Schachtman & John Ulizio, “Courting Clio:  Historians and Their Testimony in Products Liability Action,” in: Brian Dolan & Paul Blanc, eds., At Work in the World: Proceedings of the Fourth International Conference on the History of Occupational and Environmental Health, Perspectives in Medical Humanities, University of California Medical Humanities Consortium, University of California Press (2012); Schachtman, “On Deadly Dust & Histrionic Historians 041904,”; How Testifying Historians Are Like Lawn-Mowing Dogs” (May 15, 2010)A Walk on the Wild Side (July 16, 2010); Counter Narratives for Hire (Dec. 13, 2010); Historians Noir (Nov. 18, 2014); Succès de scandale – With Thanks to Rosner & Markowitz” (Mar. 26, 2017). And of course, I have experienced some schadenfreude for when one of the Pink Panthers was excluded in a case in which he was disclosed as a testifying expert witness. Quester v. B.F. Goodrich Co., Case No. 03-509539, Court of Common Pleas for Cuyahoga Cty., Ohio, Order Sur Motion to Exclude Dr. Gerald Markowitz (Sweeney, J.).

3 “Trying Times” is the sixth Rosnowitz publication to point to me as a source of criticism of the Rosner-Markowitz radical leftist history of silicosis in the United States. See David Rosner, “Trying Times: The Courts, the Historian, and the Contentious Struggle to Define Disease,” 91 Bull. History Med. 473, 491-92 & n.32 (2017); Previously, Rosner and Markowitz have attempted to call me out in four published articles and one book. See D. Rosner & G. Markowitz, “The Trials and Tribulations of Two Historians:  Adjudicating Responsibility for Pollution and Personal Harm, 53 Medical History 271, 280-81 (2009); D. Rosner & G. Markowitz, “L’histoire au prétoire.  Deux historiens dans les procès des maladies professionnelles et environnementales,” 56 Revue  D’Histoire Moderne & Contemporaine 227, 238-39 (2009); David Rosner, “Trials and Tribulations:  What Happens When Historians Enter the Courtroom,” 72 Law & Contemporary Problems 137, 152 (2009); David Rosner & Gerald Markowitz, “The Historians of Industry” Academe (Nov. 2010); and Gerald Markowitz and David Rosner, Deceit and Denial: The Deadly Politics of Industrial Pollution at 313-14 (U. Calif. rev. ed. 2013). 

4 Nathan A. Schachtman, “State Regulators Impose Sanction Unlawful Screenings 05-25-07,” Washington Legal Foundation Legal Opinion Letter, vol. 17, no. 13 (May 2007); “Silica Litigation – Screening, Scheming, and Suing,” Washington Legal Foundation Critical Legal Issues Working Paper (December 2005); Medico-Legal Issues in Occupational Lung Disease Litigation,” 27 Seminars in Roentgenology140 (1992).

5 by Publichall – own work, CC BY-SA 3.0.

6 Assoc’d Press, “Pennsylvania County Judge Guilty of Corruption,” (April 18, 1989).

7 U.P.I., “Facing Prison, Convicted Judge Skips Bail,” (Mar. 8, 1993); “Judge O’kicki Declared Fugitive; May Be In Slovenia,” The Morning Call (April 20, 1993).

8 Harmotta v. Walter C. Best, Inc., Cambria Cty. Ct. C.P. No. 1986-128; Phillips v. Walter C. Best, Inc., Cambria Cty. Ct. C.P. No. 1987-434(b)(10); Peterson v. Walter C. Best, Inc., Cambria Cty. Ct. C.P. No. 1986-678.

9 Phillips v. A.P. Green Co., 428 Pa. Super. 167, 630 A.2d 874 (1993).

10 Phillips v. A-Best Products Co., 542 Pa. 124, 665 A.2d 1167 (1995).

Daubert Retrospective – Statistical Significance

January 5th, 2019

The holiday break was an opportunity and an excuse to revisit the briefs filed in the Supreme Court by parties and amici, in the Daubert case. The 22 amicus briefs in particular provided a wonderful basis upon which to reflect how far we have come, and also how far we have to go, to achieve real evidence-based fact finding in technical and scientific litigation. Twenty-five years ago, Rules 702 and 703 vied for control over errant and improvident expert witness testimony. With Daubert decided, Rule 702 emerged as the winner. Sadly, most courts seem to ignore or forget about Rule 703, perhaps because of its awkward wording. Rule 702, however, received the judicial imprimatur to support the policing and gatekeeping of dysepistemic claims in the federal courts.

As noted last week,1 the petitioners (plaintiffs) in Daubert advanced several lines of fallacious and specious argument, some of which was lost in the shuffle and page limitations of the Supreme Court briefings. The plaintiffs’ transposition fallacy received barely a mention, although it did bring forth at least a footnote in an important and overlooked amicus brief filed by American Medical Association (AMA), the American College of Physicians, and over a dozen other medical specialty organizations,2 all of which both emphasized the importance of statistical significance in interpreting epidemiologic studies, and the fallacy of interpreting 95% confidence intervals as providing a measure of certainty about the estimated association as a parameter. The language of these associations’ amicus brief is noteworthy and still relevant to today’s controversies.

The AMA’s amicus brief, like the brief filed by the National Academies of Science and the American Association for the Advancement of Science, strongly endorsed a gatekeeping role for trial courts to exclude testimony not based upon rigorous scientific analysis:

The touchstone of Rule 702 is scientific knowledge. Under this Rule, expert scientific testimony must adhere to the recognized standards of good scientific methodology including rigorous analysis, accurate and statistically significant measurement, and reproducibility.”3

Having incorporated the term “scientific knowledge,” Rule 702 could not permit anything less in expert witness testimony, lest it pollute federal courtrooms across the land.

Elsewhere, the AMA elaborated upon its reference to “statistically significant measurement”:

Medical researchers acquire scientific knowledge through laboratory investigation, studies of animal models, human trials, and epidemiological studies. Such empirical investigations frequently demonstrate some correlation between the intervention studied and the hypothesized result. However, the demonstration of a correlation does not prove the hypothesized result and does not constitute scientific knowledge. In order to determine whether the observed correlation is indicative of a causal relationship, scientists necessarily rely on the concept of “statistical significance.” The requirement of statistical reliability, which tends to prove that the relationship is not merely the product of chance, is a fundamental and indispensable component of valid scientific methodology.”4

And then again, the AMA spelled out its position, in case the Court missed its other references to the importance of statistical significance:

Medical studies, whether clinical trials or epidemiologic studies, frequently demonstrate some correlation between the action studied … . To determine whether the observed correlation is not due to chance, medical scientists rely on the concept of ‘statistical significance’. A ‘statistically significant’ correlation is generally considered to be one in which statistical analysis suggests that the observed relationship is not the result of chance. A statistically significant correlation does not ‘prove’ causation, but in the absence of such a correlation, scientific causation clearly is not proven.95

In its footnote 9, in the above quoted section of the brief, the AMA called out the plaintiffs’ transposition fallacy, without specifically citing to plaintiffs’ briefs:

It is misleading to compare the 95% confidence level used in empirical research to the 51% level inherent in the preponderance of the evidence standard.”6

Actually the plaintiffs’ ruse was much worse than misleading. The plaintiffs did not compare the two probabilities; they equated them. Some might call this ruse, an outright fraud on the court. In any event, the AMA amicus brief remains an available, citable source for opposing this fraud and the casual dismissal of the importance of statistical significance.

One other amicus brief touched on the plaintiffs’ statistical shanigans. The Product Liability Advisory Council, National Association of Manufacturers, Business Roundtable, and Chemical Manufacturers Association jointly filed an amicus brief to challenge some of the excesses of the plaintiffs’ submissions.7  Plaintiffs’ expert witness, Shanna Swan, had calculated type II error rates and post-hoc power for some selected epidemiologic studies relied upon by the defense. Swan’s complaint had been that some studies had only 20% probability (power) to detect a statistically significant doubling of limb reduction risk, with significance at p < 5%.8

The PLAC Brief pointed out that power calculations must assume an alternative hypothesis, and that the doubling of risk hypothesis had no basis in the evidentiary record. Although the PLAC complaint was correct, it missed the plaintiffs’ point that the defense had set exceeding a risk ratio of 2.0, as an important benchmark for specific causation attributability. Swan’s calculation of post-hoc power would have yielded an even lower probability for detecting risk ratios of 1.2 or so. More to the point, PLAC noted that other studies had much greater power, and that collectively, all the available studies would have had much greater power to have at least one study achieve statistical significance without dodgy re-analyses.


1 The Advocates’ Errors in Daubert” (Dec. 28, 2018).

2 American Academy of Allergy and Immunology, American Academy of Dermatology, American Academy of Family Physicians, American Academy of Neurology, American Academy of Orthopaedic Surgeons, American Academy of Pain Medicine, American Association of Neurological Surgeons, American College of Obstetricians and Gynecologists, American College of Pain Medicine, American College of Physicians, American College of Radiology, American Society of Anesthesiologists, American Society of Plastic and Reconstructive Surgeons, American Urological Association, and College of American Pathologists.

3 Brief of the American Medical Association, et al., as Amici Curiae, in Support of Respondent, in Daubert v. Merrell Dow Pharmaceuticals, Inc., U.S. Supreme Court no. 92-102, 1993 WL 13006285, at *27 (U.S., Jan. 19, 1993)[AMA Brief].

4 AMA Brief at *4-*5 (emphasis added).

5 AMA Brief at *14-*15 (emphasis added).

6 AMA Brief at *15 & n.9.

7 Brief of the Product Liability Advisory Council, Inc., National Association of Manufacturers, Business Roundtable, and Chemical Manufacturers Association as Amici Curiae in Support of Respondent, as Amici Curiae, in Support of Respondent, in Daubert v. Merrell Dow Pharmaceuticals, Inc., U.S. Supreme Court no. 92-102, 1993 WL 13006288 (U.S., Jan. 19, 1993) [PLAC Brief].

8 PLAC Brief at *21.

The Advocates’ Errors in Daubert

December 28th, 2018
Over 25 years ago, the United States Supreme Court answered a narrow legal question about whether the so-called Frye rule was incorporated into Rule 702 of the Federal Rules of Evidence. Plaintiffs in Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579 (1993), appealed a Ninth Circuit ruling that the Frye rule survived, and was incorporated into, the enactment of a statutory evidentiary rule, Rule 702. As most legal observers can now discern, plaintiffs won the battle and lost the war. The Court held that the plain language of Rule 702 does not memorialize Frye; rather the rule requires an epistemic warrant for the opinion testimony of expert witnesses.

Many of the sub-issues of the Daubert case are now so much water over the dam. The case involved claims of birth defects from maternal use of an anti-nausea medication, Bendectin. Litigation over Bendectin is long over, and the medication is now approved for use in pregnant women, on the basis of a full new drug application, supported by clinical trial evidence.

In revisiting Daubert, therefore, we might imagine that legal scholars and scientists would be interested in the anatomy of the errors that led Bendectin plaintiffs stridently to maintain their causal claims. The oral argument before the Supreme Court is telling with respect to some of the sources of error. Two law professors, Michael H. Gottesman, for plaintiffs, and Charles Fried, for the defense, squared off one Tuesday morning in March 1993. A review of Gottesman’s argument reveals several fallacious lines of argument, which are still relevant today:

A. Regulation is Based Upon Scientific Determinations of Causation

In his oral argument, Gottesman asserted that regulators (as opposed to the scientific community) are in charge of determining causation,1 and environmental regulations are based upon scientific causation determinations.2 By the time that the Supreme Court heard argument in the Daubert case, this conflation of scientific and regulatory standards for causal conclusions was fairly well debunked.3 Gottesman’s attempt to mislead the Court failed, but the effort continues in courtrooms around the United States.

B. Similar Chemical Structures Have the Same Toxicities

Gottesman asserted that human teratogenicity can be determined from similarity in chemical structures with other established teratogens.4 Close may count in horseshoes, but in chemical structural activities, small differences in chemical structures can result in huge differences in toxicologic or pharmacologic properties. A silly little methyl group on a complicated hydrocarbon ring structure can make a world of difference, as in the difference between estrogen and testosterone.

C. All Animals React the Same to Any Given Substance

Gottesman, in his oral argument, maintained that human teratogenicity can be determined from teratogenicity in non-human, non-primate, murine species.5 The Court wasted little time on this claim, the credibility of which has continued to decline in the last 25 years.

D. The Transposition Fallacy

Perhaps of greatest interest to me was Gottesman’s claim that the probability of the claimed causal association can be determined from the p-value or from the coefficient of confidence taken from the observational epidemiologic studies of birth defects among children of women who ingested Bendectin in pregancy; a.k.a. the transposition fallacy.6

All these errors are still in play in American courtrooms, despite efforts of scientists and scientific organizations to disabuse judges and lawyers. The transposition fallacy, which has been addressed in these pages and elsewhere at great length seems especially resilient to educational efforts. Still, the fallacy was as well recognized at the time of the Daubert argument as it is today, and it is noteworthy that the law professor who argued the plaintiffs’ case, in the highest court of the land, advanced this fallacious argument, and that the scientific and statistical community did little to nothing to correct the error.7

Although Professor Gottesman’s meaning in the oral argument is not entirely clear, on multiple occasions, he appeared to have conflated the coefficient of confidence, from confidence intervals, with the posterior probability that attaches to the alternative hypothesis of some association:

What the lower courts have said was yes, but prove to us to a degree of statistical certainty which would give us 95 percent confidence that the human epidemiological data is reflective, that these higher numbers for the mothers who used Bendectin were not the product of random chance but in fact are demonstrating the linkage between this drug and the symptoms observed.”8

* * * * *

“… what was demonstrated by Shanna Swan was that if you used a degree of confidence lower than 95 percent but still sufficient to prove the point as likelier than not, the epidemiological evidence is positive… .”9

* * * * *

The question is, how confident can we be that that is in fact probative of causation, not at a 95 percent level, but what Drs. Swan and Glassman said was applying the Rothman technique, a published technique and doing the arithmetic, that you find that this does link causation likelier than not.”10

Professor Fried’s oral argument for the defense largely refused or failed to engage with plaintiffs’ argument on statistical inference. With respect to the “Rothman” approach, Fried pointed out that plaintiffs’ statistical expert witness, Shanna swan, never actually employed “the Rothman principle.”11

With respect to plaintiffs’ claim that individual studies had low power to detect risk ratios of two, Professor Fried missed the opportunity to point out that such post-hoc power calculations, whatever validity they might possess, embrace the concept of statistical significance at the customary 5% level. Fried did note that a meta-analysis, based upon all the epidemiologic studies, rendered plaintiffs’ power complaint irrelevant.12

Some readers may believe that judging advocates speaking extemporaneously about statistical concepts might be overly harsh. How well then did the lawyers explain and represent statistical concepts in their written briefs in the Daubert case?

Petitioners’ Briefs

Petitioners’ Opening Brief

The petitioners’ briefs reveal that Gottesman’s statements at oral argument represent a consistent misunderstanding of statistical concepts. The plaintiffs consistently conflated significance probability or the coefficient of confidence with the civil burden of proof probability:

The crux of the disagreement between Merrell’s experts and those whose testimony is put forward by plaintiffs is that the latter are prepared to find causation more probable than not when the epidemiological evidence is strongly positive (albeit not at a 95% confidence level) and when it is buttressed with animal and chemical evidence predictive of causation, while the former are unwilling to find causation in the absence of an epidemiological study that satisfies the 95% confidence level.”13

After giving a reasonable fascimile of a definition of statistical significance, the plaintiffs’ brief proceeds to confuse the complement of alpha, or the coefficient of confidence (typically 95%), with probability that the observed risk ratio in a sample is the actual population parameter of risk:

But in toxic tort lawsuits, the issue is not whether it is certain that a chemical caused a result, but rather whether it is likelier than not that it did. It is not self-evident that the latter conclusion would require eliminating the null hypothesis (i.e. non-causation) to a confidence level of 95%.3014

The plaintiffs’ brief cited heavily to Rothman’s textbook, Modern Epidemiology, with the specious claim that the textbook supported the plaintiffs’ use of the coefficient of confidence to derive a posterior probability (> 50%) of the correctness of an elevated risk ratio for birth defects in children born to mothers who had taken Bendectin in their first trimesters of pregnancy:

An alternative mechanism has been developed by epidemiologists in recent years to give a somewhat more informative picture of what the statistics mean. At any given confidence level (e.g. 95%) a confidence interval can be constructed. The confidence interval identifies the range of relative risks that collectively comprise the 95% universe. Additional confidence levels are then constructed exhibiting the range at other confidence levels, e.g., at 90%, 80%, etc. From this set of nested confidence intervals the epidemiologist can make assessments of how likely it is that the statistics are showing a true association. Rothman, Tab 9, pp. 122-25. By calculating nested confidence intervals for the data in the Bendectin studies, Dr. Swan was able to determine that it is far more likely than not that a true association exists between Bendectin and human limb reduction birth defects. Swan, Tab 12, at 3618-28.”15

The heavy reliance upon Rothman’s textbook at first blush appears confusing. Modern Epidemiology makes one limited mention of nested confidence intervals, and certainly never suggests that such intervals can provide a posterior probability of the correctness of the hypothesis. Rothman’s complaints about reliance upon “statistical significance,” however, are well-known, and Rothman himself submitted an amicus brief16 in Daubert, a brief that has its own problems.17

In direct response to the Rothman Brief,18 Professor Alvin Feinstein filed an amicus brief in Daubert, wherein he acknowledged that meta-analyses and re-analyses can be valid, but these techniques are subject to many sources of invalidity, and their employment by careful practitioners in some instances should not be a blank check to professional witnesses who are supported by plaintiffs’ counsel. Similarly, Feinstein acknowledged that standards of statistical significance:

should be appropriately flexible, but they must exist if science is to preserve its tradition of intellectual discipline and high quality research.”19

Petitioners’ Reply Brief

The plaintiffs’ statistical misunderstandings are further exemplified in their Reply Brief, where they reassert the transposition fallacy and alternatively state that associations with p-values greater than 5%, or 95% confidence intervals that include the risk ratio of 1.0, do not show the absence of an association.20 The latter point was, of course irrelevant in the Daubert case, in which plaintiffs had the burden of persuasion. As in their oral argument through Professor Gottesman, the plaintiffs’ appellate briefs misunderstand the crucial point that confidence intervals are conditioned upon the data observed from a particular sample, and do not provide posterior probabilities for the correctness of a claimed hypothesis.

Defense Brief

The defense brief spent little time on the statistical issue or plaintiffs’ misstatements, but dispatched the issue in a trenchant footnote:

Petitioners stress the controversy some epidemiologists have raised about the standard use by epidemiologists of a 95% confidence level as a condition of statistical significance. Pet. Br. 8-10. See also Rothman Amicus Br. It is hard to see what point petitioners’ discussion establishes that could help their case. Petitioners’ experts have never developed and defended a detailed analysis of the epidemiological data using some alternative well-articulated methodology. Nor, indeed, do they show (or could they) that with some other plausible measure of confidence (say, 90%) the many published studies would collectively support an inference that Bendectin caused petitioners’ limb reduction defects. At the very most, all that petitioners’ theoretical speculations do is question whether these studies – as the medical profession and regulatory authorities in many countries have concluded – affirmatively prove that Bendectin is not a teratogen.”21

The defense never responded to the specious argument, stated or implied within the plaintiffs’ briefs, and in Gottesman’s oral argument, that a coefficient of confidence of 51% would have generated confidence intervals that routinely excluded the null hypothesis of risk ratio of 1.0. The defense did, however, respond to plaintiffs’ power argument by adverting to a meta-analysis that failed to find a statistically significant association.22

The defense also advanced two important arguments to which the plaintiffs’ briefs never meaningfully responded. First, the defense detailed the “cherry picking” or selective reliance engaged in by plaintiffs’ expert witnesses.23 Second, the defense noted that plaintiffs’ had a specific causation problem in that their expert witnesses had been attempting to infer specific causation based upon relative risks well below 2.0.24

To some extent, the plaintiffs’ statistical misstatements were taken up by an amicus brief submitted by the United States government, speaking through the office of the Solicitor General.25 Drawing upon the Supreme Court’s decisions in race discrimination cases,26 the government asserted that epidemiologists “must determine” whether a finding of an elevated risk ratio “could have arisen due to chance alone.”27

Unfortunately, the government’s brief butchered the meaning of confidence intervals. Rather than describe the confidence interval as showing what point estimates of risk ratios are reasonable compatible with the sample result, the government stated that confidence intervals show “how close the real population percentage is likely to be to the figure observed in the sample”:

since there is a 95 percent chance that the ‘true’ value lies within two standard deviations of the sample figure, that particular ‘confidence interval’ (i.e., two standard deviations) is therefore said to have a ‘confidence level’ of about 95 percent.” 28

The Solicitor General’s office seemed to have had some awareness that it was giving offense with the above definition because it quickly added:

“While it is customary (and, in many cases, easier) to speak of ‘a 95 percent chance’ that the actual population percentage is within two standard deviations of the figure obtained from the sample, ‘the chances are in the sampling procedure, not in the parameter’.”29

Easier perhaps but clearly erroneous to speak that way, and customary only among the unwashed. The government half apologized for misleading the Court when it followed up with a better definition from David Freedman’s textbook, but sadly the government lawyers were not content to let the matter sit there. The Solicitor General offices brief obscured the textbook definition with a further inaccurate and false précis:

if the sampling from the general population were repeated numerous times, the ‘real’ population figure would be within the confidence interval 95 percent of the time. The ‘real’ figure would be outside that interval the remaining five percent of the time.”30

The lawyers in the Solicitor General’s office thus made the rookie mistake of forgetting that in the long run, after numerous repeated samples, there would be numerous confidence intervals, not one. The 95% probability of containing the true population value belongs to the set of the numerous confidence intervals, not “the confidence interval” obtained in the first go around.

The Daubert case has been the subject of nearly endless scholarly comment, but few authors have chosen to revisit the parties’ briefs. Two authors have published a paper that reviewed the scientists’ amici briefs in Daubert.31 The Rothman brief was outlined in detail; the Feinstein rebuttal was not substantively discussed. The plaintiffs’ invocation of the transposition fallacy in Daubert has apparently gone unnoticed.


1 Oral Argument in Daubert v. Merrell Dow Pharmaceuticals, Inc., U.S. Supreme Court no. 92-102, 1993 WL 754951, *5 (Tuesday, March 30, 1993) [Oral Arg.]

2 Oral Arg. at *6.

3 In re Agent Orange Product Liab. Litig., 597 F. Supp. 740, 781 (E.D.N.Y.1984) (“The distinction between avoidance of risk through regulation and compensation for injuries after the fact is a fundamental one.”), aff’d in relevant part, 818 F.2d 145 (2d Cir. 1987), cert. denied sub nom. Pinkney v. Dow Chemical Co., 484 U.S. 1004 (1988).

4 Org. Arg. at *19.

5 Oral Arg. at *18-19.

6 Oral Arg. at *19.

7 See, e.g., “Sander Greenland on ‘The Need for Critical Appraisal of Expert Witnesses in Epidemiology and Statistics’” (Feb. 8, 2015) (noting biostatistician Sander Greenland’s publications, which selectively criticize only defense expert witnesses and lawyers for statistical misstatements); see alsoSome High-Value Targets for Sander Greenland in 2018” (Dec. 27, 2017).

8 Oral Arg. at *19.

9 Oral Arg. at *20

10 Oral Arg. at *44. At the oral argument, this last statement was perhaps Gottesman’s clearest misstatement of statistical principles, in that he directly suggested that the coefficient of confidence translates into a posterior probability of the claimed association at the observed size.

11 Oral Arg. at *37.

12 Oral Arg. at *32.

13 Petitioner’s Brief in Daubert v. Merrell Dow Pharmaceuticals, Inc., U.S. Supreme Court No. 92-102, 1992 WL 12006442, *8 (U.S. Dec. 2, 1992) [Petitioiner’s Brief].

14 Petitioner’s Brief at *9.

15 Petitioner’s Brief at *n. 36.

16 Brief Amici Curiae of Professors Kenneth Rothman, Noel Weiss, James Robins, Raymond Neutra and Steven Stellman, in Support of Petitioners, 1992 WL 12006438, Daubert v. Merrell Dow Pharmaceuticals, Inc., U.S. S. Ct. No. 92-102 (Dec. 2, 1992).

18 Brief Amicus Curiae of Professor Alvan R. Feinstein in Support of Respondent, in Daubert v. Merrell Dow Pharmaceuticals, Inc., U.S. Supreme Court no. 92-102, 1993 WL 13006284, at *2 (U.S., Jan. 19, 1993) [Feinstein Brief].

19 Feinstein Brief at *19.

20 Petitioner’s Reply Brief in Daubert v. Merrell Dow Pharmaceuticals, Inc., U.S. Supreme Court No. 92-102, 1993 WL 13006390, at *4 (U.S., Feb. 22, 1993).

21 Respondent’s Brief in Daubert v. Merrell Dow Pharmaceuticals, Inc., U.S. Supreme Court No. 92-102, 1993 WL 13006277, at n. 32 (U.S., Jan. 19, 1993) [Respondent Brief].

22 Respondent Brief at *4.

23 Respondent Brief at *42 n.32 and 47.

24 Respondent Brief at *40-41 (citing DeLuca v. Merrell Dow Pharms., Inc., 911 F.2d 941, 958 (3d Cir. 1990)).

25 Brief for the United States as Amicus Curiae Supporting Respondent in Daubert v. Merrell Dow Pharmaceuticals, Inc., U.S. Supreme Court No. 92-102, 1993 WL 13006291 (U.S., Jan. 19, 1993) [U.S. Brief].

26 See, e.g., Hazelwood School District v. United States, 433 U.S. 299, 308-312

(1977); Castaneda v. Partida, 430 U.S. 482, 495-499 & nn.16-18 (1977) (“As a general rule for such large samples, if the difference between the expected value and the observed number is greater than two or three standard deviations, then the hypothesis that the jury drawing was random would be suspect to a social scientist.”).

27 U.S. Brief at *3-4. Over two decades later, when politically convenient, the United States government submitted an amicus brief in a case involving alleged securities fraud for failing to disclose adverse events of an over-the-counter medication. In Matrixx Initiatives Inc. v. Siracusano, 131 S. Ct. 1309 (2011), the securities fraud plaintiffs contended that they need not plead “statistically significant” evidence for adverse drug effects. The Solicitor General’s office, along with counsel for the Food and Drug Division of the Department of Health & Human Services, in their zeal to assist plaintiffs disclaimed the necessity, or even the importance, of statistical significance:

[w]hile statistical significance provides some indication about the validity of a correlation between a product and a harm, a determination that certain data are not statistically significant … does not refute an inference of causation.”

Brief for the United States as Amicus Curiae Supporting Respondents, in Matrixx Initiatives, Inc. v. Siracusano, 2010 WL 4624148, at *14 (Nov. 12, 2010).

28 U.S. Brief at *5.

29 U.S. Brief at *5-6 (citing David Freedman, Freedman, R. Pisani, R. Purves & A. Adhikari, Statistics 351, 397 (2d ed. 1991)).

30 U.S. Brief at *6 (citing Freedman’s text at 351) (emphasis added).

31 See Joan E. Bertin & Mary S. Henifin, Science, Law, and the Search for Truth in the Courtroom: Lessons from Dauburt v. Menell Dow,” 22 J. Law, Medicine & Ethics 6 (1994); Joan E. Bertin & Mary Sue Henifin, “Scientists Talk to Judges: Reflections on Daubert v. Merrell Dow,” 4(3) New Solutions 3 (1994). The authors’ choice of the New Solutions journal is interesting and curious. New Solutions: A journal of Environmental and Occupational Health Policy was published by the Oil, Chemical and Atomic Workers International Union, under the control of Anthony Mazzocchi (June 13, 1926 – Oct. 5, 2002), who was the union’s secretary-treasurer. Anthony Mazzocchi, “Finding Common Ground: Our Commitment to Confront the Issues,” 1 New Solutions 3 (1990); see also Steven Greenhouse, “Anthony Mazzocchi, 76, Dies; Union Officer and Party Father,” N.Y. Times (Oct. 9, 2002). Even a cursory review of this journal’s contents reveals how concerned, even obsessed, the union was interested and invested in the litigation industry and that industry’s expert witnesses. 

 

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