TORTINI

For your delectation and delight, desultory dicta on the law of delicts.

Palavering About P-Values

August 17th, 2019

The American Statistical Association’s most recent confused and confusing communication about statistical significance testing has given rise to great mischief in the world of science and science publishing.[1] Take for instance last week’s opinion piece about “Is It Time to Ban the P Value?” Please.

Helena Chmura Kraemer is an accomplished professor of statistics at Stanford University. This week the Journal of the American Medical Association network flagged Professor Kraemer’s opinion piece on p-values as one of its most read articles. Kraemer’s eye-catching title creates the impression that the p-value is unnecessary and inimical to valid inference.[2]

Remarkably, Kraemer’s article commits the very mistake that the ASA set out to correct back in 2016,[3] by conflating the probability of the data under a hypothesis of no association with the probability of a hypothesis given the data:

“If P value is less than .05, that indicates that the study evidence was good enough to support that hypothesis beyond reasonable doubt, in cases in which the P value .05 reflects the current consensus standard for what is reasonable.”

The ASA tried to break the bad habit of scientists’ interpreting p-values as allowing us to assign posterior probabilities, such as beyond a reasonable doubt, to hypotheses, but obviously to no avail.

Kraemer also ignores the ASA 2016 Statement’s teaching of what the p-value is not and cannot do, by claiming that p-values are determined by non-random error probabilities such as:

“the reliability and sensitivity of the measures used, the quality of the design and analytic procedures, the fidelity to the research protocol, and in general, the quality of the research.”

Kraemer provides errant advice and counsel by insisting that “[a] non-significant result indicates that the study has failed, not that the hypothesis has failed.” If the p-value is the measure of the probability of observing an association at least as large as obtained given an assumed null hypothesis, then of course a large p-value cannot speak to the failure of the hypothesis, but why declare that the study has failed? The study was perhaps indeterminate, but it still yielded information that perhaps can be combined with other data, or help guide future studies.

Perhaps in her most misleading advice, Kraemer asserts that:

“[w]hether P values are banned matters little. All readers (reviewers, patients, clinicians, policy makers, and researchers) can just ignore P values and focus on the quality of research studies and effect sizes to guide decision-making.”

Really? If a high quality study finds an “effect size” of interest, we can now ignore random error?

The ASA 2016 Statement, with its “six principles,” has provoked some deliberate or ill-informed distortions in American judicial proceedings, but Kraemer’s editorial creates idiosyncratic meanings for p-values. Even the 2019 ASA “post-modernism” does not advocate ignoring random error and p-values, as opposed to proscribing dichotomous characterization of results as “statistically significant,” or not.[4] The current author guidelines for articles submitted to the Journals of the American Medical Association clearly reject this new-fangled rejection of evaluating this new-fangled rejection of the need to assess the role of random error.[5]


[1]  See Ronald L. Wasserstein, Allen L. Schirm, and Nicole A. Lazar, “Editorial: Moving to a World Beyond ‘p < 0.05’,” 73 Am. Statistician S1, S2 (2019).

[2]  Helena Chmura Kraemer, “Is It Time to Ban the P Value?J. Am. Med. Ass’n Psych. (August 7, 2019), in-press at doi:10.1001/jamapsychiatry.2019.1965.

[3]  Ronald L. Wasserstein & Nicole A. Lazar, “The ASA’s Statement on p-Values: Context, Process, and Purpose,” 70 The American Statistician 129 (2016).

[4]  “Has the American Statistical Association Gone Post-Modern?” (May 24, 2019).

[5]  See instructions for authors at https://jamanetwork.com/journals/jama/pages/instructions-for-authors

Link-a-lot, right and left

March 1st, 2019


The right-wing of American politics, with its religious enthusiams, has long shown a willingness to ignore and subvert science to advance its policy agendas. The left wing of American politics, however, is not immune from ignoring evidence-based scientific conclusions in its policy agenda. When it comes to World-Trade Center (WTC) attack, the hostility to evidence-based conclusions appears to be bipartisan.

The attack on the WTC by evil Muslim religious extremists was deplorable, and the September 11th rescue workers deserve our respect and gratitude. They may even deserve compensation for fortuitous, un-related chronic diseases experienced a decade or so later. Dressing up our gratitude in the language of causality and victimhood, however, undermines basic respect for scientific evidence and leads to specious claiming.

The New York Times, no slouch when it comes to specious claiming on scientific issues, provided a great example with its editorial this morning, advocating for increased federal funding for the WTC compensation fund. Editorial Board, “Give Sept. 11 Survivors the Help They Deserve: A fund to aid the thousands sickened from the toxic dust of the World Trade Center attack is running out of money,” N.Y. Times (Feb. 28, 2019). The Times’ editors pictured a retired federal worker as one “who suffers from illnesses like leukemia related to recovery work at ground zero.” The editorial tells us that this man, in 2015, “was told he had leukemia linked to his work there, “like many who had been at the site.” The editors went on to bemoan how this man, and others like him, might receive much less than what had been promised by the federal WTC compensation fund.

The passive voice can be very revealing for the deception and misrepresentations it hides. Who told this man such a thing, about a “link,” whatever that is? And on what evidence was the “link” supposedly established?

Of course, there were toxic materials disseminated by the Muslim terrorist attack, and scientists have studied health outcomes among both the rescue workers and responders, as well as among civilians who joined the effort to look for survivors and victims. One study that was published shortly after the 10-year anniversary of the WTC attack, failed to show any “link” between respiratory or physical exposure to WTC dusts and materials and leukemia.1 In the authors’ words, “”Using within-cohort comparisons, the intensity of World Trade Center exposure was not significantly associated with cancer of the lung, prostate, thyroid, non-Hodgkin lymphoma, or hematological cancer in either group.”

Table 3 of their paper reported specifically on leukemia, using standardized incidence ratios (SIR), in two time windows:

Early Period (with enrollment through 2006, n = 21,218.

SIR 0.73 (95% C.I., 0.20 to 1.87)

and

Later Period (enrollment 2007-2008, n = 20,991)

SIR = 1.25 (95% C.I., 0.46 to 2.72)

A later paper by many of the same authors updated the cohort through 2011. Again, the results overall were equivocal in terms of standardized incidence ratios, but quite “null” for leukemia:

“RESULTS: All-cancer SIR was 1.11 (95% confidence interval (CI) 1.03-1.20) in RRWs, and 1.08 (95% CI 1.02-1.15) in non-RRWs. Prostate cancer and skin melanoma were significantly elevated in both populations. Thyroid cancer was significantly elevated only in RRWs [rescue workers] while breast cancer and non-Hodgkin’s lymphoma were significantly elevated only in non-RRWs. There was a significant exposure dose-response for bladder cancer among RRWs, and for skin melanoma among non-RRWs [civilians].”2

Table II of this later report provides the evidence that the New York Times’ anonymous “linker” was mostly likely full of soup:

Rescue/recovery workers (RRW) (N=24,863)

Leukemia: 16 observed; 17 expected

SIR = 0.95 (95% C.I., 0.54 – 1.54)

Enrollees not involved in rescue and recovery (non-RRW) (N = 35,476)

Leukemia: 18 observed, 22 expected

SIR = 0.81 (95% C.I., 0.48 – 1.29)

An article reporting on the results of multiple cohorts in the American Journal of Industrial Medicine (“red journal”) makes clear that causal conclusions or “linking” is not appropriate on the available evidence:

Conclusions. The presence of three cohorts strengthens the effort of identifying and quantifying the cancer risk; the heterogeneity in design might increase sensitivity to the identification of cancers potentially associated with exposure. The presence and magnitude of an increased cancer risk remains to be fully elucidated. Continued long-term follow up with minimal longitudinal dropout is crucial to achieve this goal.”3

These authors’ point about continued, long-term follow up is of course true, but immaterial to the validity of the present compensation schemes. The evidence for the relevant time window has been collected and analyzed. Whether compensation for longer latency period manifestations of chronic disease is appropriate is a separate issue. There is just no link in the New York Times’ linking. Evidence-based policy needs evidence, not editorial opinion.

1Jiehui Li, James E. Cone, Amy R. Kahn, Robert M. Brackbill, Mark R. Farfel, Carolyn M. Greene, James L. Hadler,Leslie T. Stayner, and Steven D. Stellman, “Association between World Trade Center exposure and excess cancer risk,” 308 J. Am. Med. Ass’n 2479 (2012).

2Mark R. Farfel, James L. Hadler, Amy R. Kahn, Kevin J. Konty, Leslie T. Stayner, and Steven D. Stellman, “Ten-year cancer incidence in rescue/recovery workers and civilians exposed to the September 11, 2001 terrorist attacks on the World Trade Center,” 59 Am. J. Indus. Med. 709 (2016).

3Paolo Boffetta, Rachel Zeig-Owens, Sylvan Wallenstein, Jiehui Li, Robert Brackbill, James Cone, Mark Farfel, William Holden, Roberto Lucchini, Mayris P. Webber, David Prezant, and Steven D. Stellman, “Cancer in World Trade Center responders: Findings from multiple cohorts and options for future study,” 59 Am. J. Indus. Med. 96, 96 (2016) (emphasis added).

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

——————————————————————————————————————–

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)]

Stranger to the Contract and to the World

March 10th, 2018

It Was a Dark and Stormy Night

All around the country, first year law students are staring at the prospect of their final examination in contracts, one of the required courses in the law school curriculum in the United States. So here is a practice question.

A lawyer for David Dennison drafts a memorandum of agreement between Mr Dennison and Stephanie Clifford. The memorandum calls for Ms Clifford to remain silent about a sexual liaison between Mr Dennison and her, in return for payment of $130,000, in “hush money.”

Mr Dennison never signed the putative contract, and he never provided the consideration for Ms Clifford’s silence. The lawyer for Mr Dennison, however, wired Ms Clifford the money, although he apparently was never given the money by his client, or reimbursed for the payment, later1.

Mr Dennison’s lawyer also represents the President of the United States (POTUS). POTUS may well be Mr Dennison, but he has never acknowledged that Dennison was a name he used. Mr Dennison’s lawyer has publicly acknowledged that he provided the money to Ms. Clifford, and that his client Mr Dennison or whoever Mr Dennison is, did not reimburse him2.

The putative contract calls for arbitration and penalties. A company, EC, LLC, obtained a temporary restraining order (TRO) from the designated alternative dispute resolution company. EC, LLC v Peterson, ADR Services TRO (Feb. 27, 2018)3. A week later, Stephanie Clifford sued POTUS (a.k.a. David Dennison) for declaratory relief, in California Superior Court, Los Angeles County, after the TRO was entered. Clifford v. Trump, Calif. Super. Ct., Los Angeles Cty. Complaint (Mar. 06, 2018)4.

Prepare a bench memorandum for the trial court judge who has been assigned the declaratory judgment action. Make sure you address all issues of contract formation and enforcement, affirmative defenses such as the statute of frauds5, as well as professional ethics of the lawyers involved. Address the ethical propriety of POTUS’s lawyer’s paying consideration for a hush contract out of his own pocket and then claiming the benefit of the bargain for his client, as well as the legal consequences of his public disclosure on the enforceability of the putative contract. If you come up with a negotiation strategy for the wife of POTUS to vitiate her pre-nuptial agreements with POTUS, you will receive extra credit.

Watch the upcoming issues of the New York Times for the answer to this practice question.


1 Amy Davidson Sorkin, “Does Stormy Daniels Have a Case Against Donald Trump?” New Yorker (Mar. 7, 2018).

2 Debra Cassens Weiss, “Stormy Daniels sues Trump, says confidentiality deal is void because he didn’t sign it,” Am. Bar. Ass’n J. (Mar. 7, 2018).

3 Jim Rutenberg & Peter Baker, “Trump Lawyer Obtained Restraining Order to Silence Stormy Daniels,” N.Y. Times (Mar. 7, 2018).

4 Rebecca R. Ruiz & Matt Stevens, “Stormy Daniels Sues, Saying Trump Never Signed ‘Hush Agreement’,” N.Y. Times (Mar. 6, 2018).