Schachtman Law

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

Litigation-Driven Access to Underlying Data and Materials

October 23rd, 2013

On Monday, October 21, 2013, the Center for Public Integrity published an editorial criticizing Georgia-Pacific Corporation for its “secretive research program.” See “Facing lawsuits over deadly asbestos, paper giant launched secretive research program.”

Georgia-Pacific (GP) commissioned several studies to help advance its defenses in asbestos litigation. Given that plaintiffs, plaintiffs’ counsel, proxies for the plaintiffs, and self-appointed public health zealots have commissioned and conducted research designed to advance interests of the litigation industry (a/k/a the plaintiffs’ bar) and to undermine GP’s defenses, GP’s actions seem perfectly appropriate. GP’s attempt to claim an attorney-client and work-product privilege in the communications with investigators, however, raises serious concerns by casting a shadow over industry sponsorship generally.

In response to publication of GP’s sponsored research, plaintiffs’ counsel Jerry Kristal sought discovery of some of the studies and GP’s role in instigating, planning, conducting, and interpreting the studies. Again, these discovery requests seem perfectly reasonable, but GP reacted by asserting that its lawyers had been involved in the communication loop between GP and the scientists who conducted and published the research, and therefore, the requested evidence was protected by the attorney-client privilege. As I have argued previously, GP’s position was a serious mistake, and it has opened itself up to a good deal of justified criticism for “secretive research.” See, e.g., Noah S. Seixas, “Protecting Our Science,” 57 Ann. Occup. Hyg. 963 (2013) (emphasizing that there was no evidence that GP’s research was in fact fraudulent, and that the papers published in the Annals of Occupational Hygiene had appropriate disclosures). See also “A Cautionary Tale on How Not to Sponsor a Scientific Study for Litigation” (June 21, 2013); “Using the Rule 45 Subpoena to Obtain Research Data” (July 24, 2013).

One measure of the lapse in judgment by GP in questionably asserting an attorney-client privilege is the ammunition that it gives to idealogues and zealots such as the Center for Public Integrity (CPI). The CPI editorial quotes Harvard University Professor Sheila Jasanoff, as noting that:

“There’s something extremely smelly about claiming attorney-client privilege for something that is being claimed at the same time as good science. … Legal confidentiality protections should not be placed around good science.”

Professor Jasonoff is absolutely correct, but interestingly, her olfactory sense has been remarkably inconsistent. Back in October 2007, Dr. Brad Racette and I were invited by the Committee on Science, Technology, and Law of the National Academies of Science to discuss, and debate, litigation and compelled access to underlying research data. Dr. Racette moaned and groaned about how disruptive subpoenas were into the operation of his research. Some members of the Committee seemed sympathetic until I reminded them that Racette’s research grew out of medico-legal screenings organized, conducted, and paid for by plaintiffs’ lawyers, and that it had been over 30 years since the National Research Council urged scientists to plan proactively for sharing data from their research, and that current National Institutes of Health guidelines require such a plan. See National Institutes of Health, Final Statement on Sharing Research Data (Feb. 26, 2003); Stephen E. Fienberg, et al., eds. Committee on National Statistics, National Research Council, Sharing Research Data (1985); Eleanor Singer, chair, Panel on Data Access for Research Purposes, National Research Council, Expanding Access to Research Data: Reconciling Risks and Opportunities (2005). See also National Academy of Sciences Committee on Ensuring the Utility and Integrity of Research Data in a Digital Age, Ensuring the Integrity, Accessibility, and Stewardship of Research Data in the Digital Age (2009). Most members of the Committee expressed their reassurance that nothing untoward had occurred with the subpoena of Dr. Racette’s underlying data, but at the time, Professor Jasanoff maintained her opposition to the approach.

Jasanoff’s selective sniffing reflects the hypocrisy and asymmetry that pervades current discussions of conflicts of interest (COI) and access to data. COI accusations are directed at industry, but not at the litigation industry, staffed by the plaintiffs’ bar and advanced by eco-zealots. Access to data is a rallying cry against pharmaceutical industry clinical trials, and industry-sponsored studies, but when stakeholders want access to non-industry study data, suddenly privacy interests and researchers’ privileges become paramount, and researchers “feel harrassed.” It really is time to choose: either we stop our insistence upon seeing the data themselves, or we formulate rules that apply across the board, independent of study sponsorship.

We are becoming, by fits and starts, a data-driven and evidence-based world. The time has come and gone to rely upon authors’ own interpretation of the data, and to realize that there is a public trust, interest, and need for data sharing. GP’s capital mistake was the same made by Dr. Racette, when he asserted various privileges to argue against disclosure of his underlying data. (Had GP paid attention to prior disputes, it would have learned that the attorney-client privilege has been uniformly rejected, as it was in Racette’s case.) Jasanoff’s capital mistake is to attribute stench to GP for asserting a privilege, but excusing it when done by scientists funded or supported by the “litigation industry.”

The CPI reported that a GP spokesman refused to answer questions, but referred a reporter to GP’s court filings, where GP maintained that it “properly commissioned studies to explore scientific issues that repeatedly arise in joint compound litigation, disclosed its role in the studies themselves, and submitted them to the technical rigors of scientific peer review by qualified scientists who were neither affiliated with nor selected by Georgia-Pacific.”

Sounds good, but then why try to assert an attorney-client privilege and an attorney-work product confidentiality? Plaintiffs’ counsel, having relied upon some rather poorly conducted studies would likely known that peer review is not a very good filter for sound science, and they would press for access to the inner workings of the studies and the possible influence that the sponsor had on any aspect of the studies. Furthermore, faced with the prospect of GP’s succeeding in its claim of privilege, the plaintiffs were surely warranted in trying to explore exceptions to the privilege, such as the crime-fraud exception, weak though the evidence may be to support such an exception.

Now Look Who Is Manufacturing Doubt!

In the GP case, the New York Appellate Division did not hold that GP had engaged in a fraudulent scheme, only that plaintiffs’ allegations were serious enough to support an order that the trial judge review, in camera, the supposedly privileged materials. The CPI, however, has used the decision to support its overwrought generalization of charges against all industry-sponsored studies.

The CPI has used the commonplace smear tactic of analogizing every company’s defensive strategies against litigation, even against unwarranted claims, as a manifestation of the same tactics used by Big Tobacco. Unfortunately, GP advanced the attorney-client privilege theory, which had been asserted previously, and unsuccessfully, by tobacco companies. This legal misstep, however, does not justify CPI’s smear campaign against the scientists who conducted the studies at issue. There is nothing stated or suggested in CPI’s editorial that raises any meaningful question about the validity of the research sponsored by GP.

COI and Access to Data – Two-Way Street

GP’s misguided assertion of the attorney-client privilege opened itself and industry generally to the CPI charges of using “well-paid experts to minimize the hazards of toxic chemicals and fend off liability, regulation, or both.” Indeed, the CPI’s editorial is little more than a sustained ad hominem attack on industry’s efforts to protect itself from liability and regulation, without any acknowledgement that often the attempts to impose liability or regulation are based upon dubious science or imprudent policy. Some liability claims are corrupt, and must be defended, including many frivolous and fraudulent claims in the asbestos litigation.

While the CPI rails against industry experts, it is suspiciously silent about so-called public interest groups or claimants, using well-paid experts, or worse, over-zealous experts, to obtain litigation or regulation results. To be sure, there are many instances of plaintiffs’ expert witnesses failing to disclose their potential conflicts, as well as failing to disclose their funding or support from plaintiffs’ counsel, plaintiffs, or plaintiffs’ proxies. Mr. Kristal’s strategy of claiming fraud in failing to disclose potential conflicts of interest will lead to a regime that will be uncomfortable for many scientists and physicians who fail to make appropriate disclosures. See, e.g., “Conflicts of Interest in Asbestos Studies – the Plaintiffs’ Double Standard” (Sept. 18, 2013); “The Mt. Sinai Catechism” (June 7, 2013).

The CPI’s complaint that GP hired experts who were aligned with their cause is curious given the history of the plaintiffs’ counsel to hire expert witnesses who were aligned with their clients’ labor unions and the like. Irving Selikoff, who was engaged by the insulators’ union to conduct a study of their cancer mortality, had testified in worker compensation proceedings and in some of the early civil actions involving claims of asbestos-related injuries. The CPI quotes plaintiffs’ lawyer Alan Golanski as alleging that GP had tried to “seed” the medical literature with “methodologically skewed, litigation-driven research.” Of course, this is exactly what plaintiffs’ expert witnesses have done over the last half century.

It really is time to stop. COI disclosures cannot be a full, satisfactory answer because the most potent conflicts arise out of intellectual and political commitments, not money. Increasing transparency and access to study protocols, data, analyses may perhaps help.

Posted in Data Sharing, Underlying Data | Comments Off on Litigation-Driven Access to Underlying Data and Materials

Expiation of Guilt by Expert Witnessing – The Strange Case of Gerrit Schepers

October 19th, 2013

Expert witnesses come in all sizes, colors, shapes, races, ethnicities, and personalities. More interestingly, expert witnesses have various motives for becoming involved in the litigation process. Most expert witnesses, I believe, become involved because they find the issues interesting, and intellectually challenging. After looking at the claims and defenses put forward by the parties, these expert witnesses believe that one side or the other has the better warrant, or perhaps the only warrant, for its contentions.

Some witnesses sign up to “change the world.” They are advocates, and they see the courtroom as an extension of the laboratory or the university. They may want acceptance for their theories or beliefs, and they hope that favorable jury verdicts and judgments based upon those verdicts will elevate their theories in the world of science or policy.

Other expert witnesses are motivated by “white-hat bias.” They see a verdict for the side for which they testify as promoting retributive, distributive, or social justice. They may be deontological or utilitarian or Aristotelian in their assessments of the issues, but they are motivated by considerations that often transcend the facts of the particular case.

Of course, there are expert witnesses who see litigants and litigation as an ATM to aid their personal fisc.

I have known only one expert witness who was motivated by guilt.

* * * * * *

Robert B. Anderson kindly alerted me to an interesting historical wiki on Saranac Lake, New York, with some interesting entries for some of the protagonists of the asbestos litigation: Leroy Upson Gardner, Arthur Vorwald, Gerrit Schepers, and others.

Dr. Edward Livingston Trudeau founded the Saranac Laboratory for the Study of Tuberculosis, in 1884, as a center for research and treatment of tuberculosis. The Laboratory, later became known as the Trudeau Institute, was also one of the leading pneumoconiosis research facilities in the 20th century. Many companies engaged the Laboratory to test their products, or the materials within their products; and Saranac Lake was the natural venue for various symposia and research meetings on industrial dust diseases.

As its director from 1927, until his death in 1946, Dr. Gardner helped put the Saranac Laboratory on the intellectual world map. His directorship coincided with the period in which the pneumoconioses were becoming important topics in industrial medicine, and in labor-industry battles. After Dr. Gardner’s death, Dr. Vorwald became the Director of Laboratories at Saranac. He held the position from 1947, until 1954, when he left to organize a new medical school department, of Industrial Medicine and Hygiene, in Wayne State University, in Michigan.

In 1954, the Laboratories fell into the hands of Dr. Schepers, who oversaw its passing into irrelevancy as research moved into the major universities. Schepers left Saranac in 1958.

Dr. Schepers used his supposed personal knowledge of dealings with various companies to create a livelihood in later life, when he testified extensively for plaintiffs’ counsel in asbestos personal injury litigation. As the litigation matured, so did Dr. Schepers, who became deaf and daft, and fantasized and testified to conversations with people, long dead, who could not contradict him. Schepers thus used his longevity to good advantage.

After Dr. Schepers adopted the catechism of Mt. Sinai, his publications, from the early 1980s until his death, became particularly unreliable, and these typically are the only ones cited now by plaintiffs’ counsel and plaintiffs’ expert witnesses. Fortunately, Dr. Schepers memorialized his contemporaneous observations, which frequently contradicted him when he was confronted by well-prepared defense counsel, in court or deposition examination. Under the Federal Rules of Evidence, and most state evidentiary law, Schepers’ prior statements are admissible as they bear on his credibility and the truth of his later, scurrilous writings:

“When a hearsay statement … has been admitted in evidence, the declarant’s credibility may be attacked, and then supported, by any evidence that would be admissible for those purposes if the declarant had testified as a witness. The court may admit evidence of the declarant’s inconsistent statement or conduct, regardless of when it occurred or whether the declarant had an opportunity to explain or deny it. If the party against whom the statement was admitted calls the declarant as a witness, the party may examine the declarant on the statement as if on cross-examination.”

Federal Rule of Evidence 806. See, e.g., “Gerrit W. H. Schepers, MD, RIP” (2011).

The Saranac Wiki also notes that Schepers was “an experienced anthropologist and neurologist.” Most scientists, however, have been probably all too happy to forget Dr. Schepers’ work in this area. See, e.g., G.W.H. Schepers, “The Corpus Callosum and Related Structures in the South African Negro Brain,” 24 Am. J. Physical Anthropology 161 (1938).

The Wiki points to a hagiographic obituary that quotes an anonymous friend who called Schepers “the Old War Horse, the record holder for longevity in the struggle against corporate crime.” Laurie Kazan-Allen and Barry Castleman, “The Passing of a Great Man” (Sept. 13, 2011). Schepers lived to 97, but his struggle was with his own past, not with alleged corporate crime.

Labor historian Jock McCulloch wrote about Schepers’ role in documenting silicosis disability among South African miners, but even Schepers’ good deeds came with a dubious shadow. McCulloch describes a South African investigator who described “Dr Schepers as a man whose outstanding intellect was compromised by an ‘inexcusable scientific dishonesty’.” Jock McCulloch, “Hiding a Pandemic: Dr G.W.H. Schepers and the Politics of Silicosis in South Africa,” 35 J. Southern African Studies 835, 838 (2009) (citing to South African National Archives, Pretoria, F 33\671, Supplementary Confidential Report of the Departmental Committee of Enquiry into the Relation between Silicosis and Pulmonary Disability. Departmental Committee to Inquire into the Definition of Silicosis & Chest Diseases (Oosthuizen) Departmental Committee at 23 (1954)).

Contrary to the fantasy “state of the art” that made Schepers so much in demand for plaintiffs’ lawyers, and endeared so to Kazan, Castleman, and McCulloch, Schepers’ publications tell a different story. Schepers’ very first publication on asbestos and cancer came in 1963, after the work by Dr. Christopher Wagner and others, from South Africa. At that time, he wrote about pulmonary cancers:

“Neoplasia occurs in two forms: alveolar and bronchiole carcinoma, and pleural mesothelioma. The latter is particularly common in crocidolite workers, and has been mainly reported from South Africa.”

G. Schepers, ““Lung Disease Caused by Inorganic and Organic Dust” 44 Chest 133, 136 (1963). This statement came after his South Africa and Saranac experiences, but before senescence set in. Schepers also noted that “neoplasia has not yet resulted” from asbestos in experimental models. Id. at 136.

American College of Chest Physicians (1964)

In 1964, Schepers helped prepare a position paper on asbestosis for the American College of Chest Physicians. This report noted that the enhanced prevalence of pulmonary neoplasia did not appear to apply for the chrysotile industry in North America:

“In the medical literature, there are more articles favoring a positive relationship between cancer of the lung and asbestosis than denying it. While it has been reported that there may be an enhanced prevalence of pulmonary neoplasia in some asbestos industries (e.g. crocidolite or amosite), or in some locations (e.g. South Africa, England), this does not appear to apply for the chrysotile industry in North America. This comment applies both with respect to intrapulmonary new growths and to pleural mesothelioma.”

Peter A. Theodos, John W. G. Hannon, Paul Cartier, Ross K. Childerhose, David T. Dubow, G. W. H. Schepers, Reginald H. Smart, and Roy E. Whitehead, “Asbestosis: Report of the Section on Nature and Prevalence Committee on Occupational Diseases of the Chest,” 45 Chest 107, 109b (1964). This report also put pleural plaques into proper historical and physiological perspective:

“In many individuals and perhaps even the majority of cases, these pleural plaques do not present any histologic lesions of asbestosis and contain no asbestos fibers. *** These plaques, though apparent on X‑ray, are not associated with any disability.”

Id. at 109a.

New York Academy of Science Conference on Asbestos (1964)

Also in 1964, Schepers was a significant presence at Dr. Selikoff’s 1964 conference of the New York Academy of Science, where he commented upon others’ presentations. Here Schepers continued to express his doubts about the carcinogenicity of North American chrysotile:

“Finally, there is the question of whether inhalation of chrysotile is associated with neoplasia. On critically reviewing the work histories of eleven cases of lung cancer in chrysotile workers, I find that all of these had at one time or another also been exposed to other forms of asbestos, mainly amosite or crocidolite. Their predominant exposure was to chrysotile, but since there is strong evidence incriminating amosite as a carcinogen, the fact that these men also had been exposed to amosite is disruptive of a theory of carcinogenicity per se.”

Schepers, “Discussion,” in Biological Effects of Asbestos 132 Ann. N. Y. Acad. Sci. 589, 596 (1965). Schepers paved the way on manufacturing uncertainty when he suggested at the 1964 conference, an alternative hypothesis to crocidolite as a cause of mesothelioma; he suggested that some of the mesotheliomas in South Africa might have been caused by a native grass known as Klitsgras.

Talc Symposium (1973)

In May 1973, Schepers participated in a written presentation at a symposium on talc, sponsored by the United States Department of Interior. At the time, Schepers was an employee of the United States government, the Chief of the Medical Service, Veterans Administration, in Lebanon, Pennsylvania:

“There are marked differences between the capacities of the individual classes of silicate minerals to provoke responses in human and animal tissues. There also are major misconceptions as to what these substances can do when inhaled by man or other mammals. Two of the most extreme of these are

(1) that all siliceous minerals are equally pathogenic and

(2) that there is even the least semblance between the effects of the asbestiform and the non-asbestiform silicates.”

Gerrit W. H. Schepers, “The Biological Action of Talc and Other Silicate Minerals,” at 54, in Aurel Goodwin, Proceedings of the symposium on talc: U.S. Bureau of Mines; Information Circular 8639 (1974). This view was directly opposed to the Mt. Sinai gospel about to be delivered in another government proceeding. See U.S. Environmental Protection Agency v. Reserve Mining Co., 514 F.2d 492 (8th Cir. 1975) (en banc). Schepers, however, had not yet gotten the memo, or perhaps his loyalty was still to his employer, the United States government. Schepers was not, however, under the influence of any company or corporate interest, when he wrote:

“Is chrysotile a carcinogen? This is a very perplexing question. A crescendo of popular opinion has sought to incriminate chrysotile. This author remains unconvinced. The main premise for carcinogenicity stems from epidemiological observation of employees of the insulation and shipbuilding industries. In both these industries there has been in the past considerable exposure of pipe laggers to asbestos dust. Only in recent decades, however, have these insulation bats been composed predominantly of chrysotile. In former years crocidolite and amosite were important components.

***

Finally, it should be pointed out that the role of cigarette smoking has not been satisfactorily discounted in the referenced epidemiological studies of lung cancer among insulation workers. In some groups reported an excess prevalence of lung cancer was not demonstrable when cigarette smoking was taken into consideration. Epidemiological surveys of chrysotile workers in Quebec showed no excess of lung cancer. A review of pleural mesothiliomatosis in Canada also failed to focus attention on Quebec or any other center where chrysotile industries are concentrated.”

Gerrit W. H. Schepers, “The Biological Action of Talc and Other Silicate Minerals,” at 70. Unlike Dr. Selikoff, Schepers was not a crocidolite denier.

OSHA Proceedings 1976

In 1970, the Williams-Steiger Act created a new federal agency, the Occupational Safety and Health Administration, and one of its first missions was to address an asbestos problem that emerged in the 1960s. The new agency held extensive hearings and engaged in factfinding, which was dominated by Dr. Selikoff and other proxies for the labor unions.

In 1976, Schepers was not yet under the influence of the Mt. Sinai crowd; indeed, he was an employee of the United States. Here are the contemporaneous views of Dr. Schepers, as he attempted to influence the OSHA investigation of the asbestos fiber controversy. In a letter dated July 19, 1976, Schepers wrote Grover Wrenn, Chief, Division of Health Standards Development, OSHA:

“This is a follow-up on our recent meeting with the Assistant Secretary of Labor at which we discussed the question of asbestosis and berylliosis and the relationship of exposure of various industrial substances to lung cancer.

I promised to help you place items in the record which you appeared not have available.”

***

“As you can see my researches cast considerable doubt on the proposition that American fibrous minerals are carcinogenic. I am not one of those that deny the carcinogenicity of everything. To the contrary, I believe that I have helped prove that some environmental pollutants are carcinogenic. For this reason you may perhaps accept the credibility of my findings when I state that I could detect no evidence of carcinogenicity for either chrysotile, talc or fiberglass.”

Asbestos Litigation – The Gathering Storm (1978)

By the late 1970s, asbestos litigation was swamping American courtrooms. The United States Navy in particular was threatened by the potential expense of compensating its large civilian shipyard workforce. Schepers sought out the role of testifying witness, in a letter dated March 10, 1978, Dr Schepers wrote to Captain Hoeffler, of the Navy’s Bureau of Medicine and Surgery, in Washington D.C. Schepers shamelessly took credit for discovering the connection between mesothelioma and amphibole asbestos, in 1949. Of course, if this self-aggrandizing claim were true, Schepers would have been involved in a much more devastating cover-up than any American company. Here is the substance of Schepers’ 1978 solicitation letter:

“Here is a CV and some reprints which will possibly be helpful. Since I have been involved with so many things, my expertise with respect to asbestosis is somewhat hidden among the rest. For emphasis therefore let me summarize that my clinical and research involvement with asbestosis and thus also lung cancer spans some thirty years. I commenced this work in South Africa, where as a …. Medical director for the pneumoconiosis Bureau we researched the working conditions and health of all employees of that countries [sic] extensive crocidolite and amosite mines and industries. The fact that mesothelioma can be associated with asbestos dust was first discovered by me during 1949 at the Penge Egnep mines in the Eastern Transvaal. It is also important to know that only one out of three persons who develop mesothelioma ever was exposed to asbestos dust. The Institute for Pneumoconiosis Research which I started there has abundant evidence about this.

In the USA I next studied the asbestos problem for the Quebec Government and the Johns Mansville Company and also for various asbestos producing companies. This embraced research on human subjects, lung tissue and experimental animals. The net result of my fifteen years of work in this field has been to convince me that chrysotile, which is the North American type of asbestos, is relatively innocuous as compared to the African and Russian varieties. I have never seen a case of lung cancer develop on any person exposed to chrysotile only. However I have seen plenty of lung cancers in asbestos workers.

This is because most asbestos workers are exposed to carcinogenic materials other than asbestos and all the cases with lung cancer also were chronic lung self-mutilators through cigarette smoking. In a rather major set of experiments of mine, I exposed animals to the most potent known carcinogenic (beryllium sulphate) and then exposed them to asbestos (chrysotile) dust. These animals had fewer cancers than those exposed to the beryllium sulphate. So chrysotile is not even a significant co-carcinogen. I reversed the order of the exposure – namely asbestos (chrysotile) first and the the BeSO4. The result was the same. The animals exposed only to chrysotile never developed any lung cancers.

I probably have the largest collection of asbestosis case materials, having been a consultant to hundreds of physicians. I have a very detailed knowledge of what various types of asbestos can and cannot do to the lungs. If my command of this subject can be of use to the Navy in the current law suit, please feel to use my services as consultant as you deem fit.”

Schepers Reinvented

As we can see from his 1978 correspondence, Dr. Schepers was not shy about touting his expertise, or his opinions about the innocuousness of chrysotile asbestos. Castleman’s revisionist history has some support only from Scheper’s own later attempts to reinvent his past. See, e.g., Gerrit W.H. Schepers, “Chronology of Asbestos Cancer Discoveries: Experimental Studies of the Saranac Laboratory,” 27 Am. J. Indus. Med. 593-606 (1995). The contemporaneous history of Schepers’ views is, however, completely at odds with words written only after decades of consulting with, and testifying for, plaintiffs’ counsel in asbestos litigation.

Like many other defense lawyers, I confronted Dr. Schepers in cases in which he testified both on state-of-the-art issues and on the causation of mesothelioma. Towards the end of his testifying career, he likened his courtroom performances to that of “performing seal for lawyers in the courtroom.” Testimony of Gerrit W. Schepers, in Hill v. Carey Canada, New Jersey Superior Court, Law Division for Camden County, Docket No. L-051429-84, 48-50 (July 24, 1990) (before Judge Supnick and a jury).

The interviews he gave for the media were even more of a performance. In one interview that Schepers gave about a year or so before his death, he cut even more grandiose poses of a whistleblower and crusader. See Lorraine Mallinder, “Deadly Secret: A 1940s whistle-blower uncovers hidden evidence linking asbestos to cancer,” 91 Canada’s History 33 (April 2011).

Why did Schepers commit himself in retirement to the plaintiffs’ bar and their relentless prosecution of asbestos cases? Marxist historians and writers such as McCulloch and Castleman, who see every societal ill as the result of corporate influence will not likely discern Schepers’ true motivations. By the time I encountered Schepers he was no longer a needy former civil servant. He was trying to rewrite history because he was personally responsible for the continued use of South African crocidolite in the United States, for decades after he claimed to have discovered its causal relation to mesothelioma. He was a man tormented by guilt, and his ritualistic participation in trials of mesothelioma claims was expiation for his role in the tragedy.

It is sad that the asbestos litigation is still with us. Dean Wellington’s pipedream of turning the asbestos litigation feeding frenzy into an administrative routine is long gone. The bankruptcies of dozens of companies, with the losses of jobs and income for many thousands of American workers is a great tragedy; but so is the loss of historical perspective.

Posted in Historian Testimony | Comments Off on Expiation of Guilt by Expert Witnessing – The Strange Case of Gerrit Schepers

British Labor Historians Belaboring American Labor History – Gauley Bridge

October 14th, 2013

Jock McCulloch and Geoffrey Tweedale are labor historians, which means mostly they write about the issues of interest to industrial workers, from an unremittingly pro-labor and anti-management perspective. Recently, these British writers have weighed in on American labor history, and the role of Dr. Anthony Lanza in the litigation that followed the Gauley Bridge tunnel construction. See Jock McCulloch and Geoffrey Tweedale, “Anthony J. Lanza, Silicosis and the Gauley Bridge ‘Nine’,” 26 Social History of Medicine (2013), in press [cited as M&T]

Here is the authors’ abstract:

“Gauley Bridge was the scene of America’s biggest industrial disaster, in which hundreds of workers died from silicosis in the aftermath of the drilling in 1930–31 of a hydro-electric tunnel at Hawk’s Nest. This article scrutinises for the first time the role of Dr A. J. Lanza (a medical director of Metropolitan Life Insurance Company) in hiding the extent of acute silicosis amongst the tunnellers. Lanza and his allies in the medical profession were able to impose their own interpretation on events at Gauley Bridge. Their analysis of nine autopsies ignored the evidence of acute silicosis, in favour of one which emphasised tuberculosis, racial susceptibility, syphilis, the supposed negligence of the workforce and alleged racketeering by lawyers. The result was that acute silicosis largely disappeared from medical discourse and Gauley Bridge was denied a place in America’s national consciousness.”

McCulloch & Tweedale’s investigation into Lanza’s role in the litigation is interesting, but hardly surprising. He was, after all, a medical director of a large insurance company, and no doubt that the Gauley Bridge litigation, which started in 1932, threatened Met Life’s interests and his own. These British authors, however, do a much less convincing job of investigating the bias of the physicians who testified for some of the Gauley Bridge victims, and of the plaintiffs’ lawyers, who had a substantial interest in passing off tuberculosis, pneumonia, and other respiratory illnesses as silicosis.

Was Gauley Bridge Denied A Place in America’s National Consciousness?

McCulloch and Tweedale claim that the Gauley Bridge disaster hardly registered in the nation’s memory. Their claim is demonstrably false. M&T at 2. These authors appear to make their claim to advance a conspiratorial labor view of history that fails to account for evidence from many other walks of life. They write:

“The neglect of Hawk’s Nest—which is indicative of the way that risks in the workplace and silicosis in particular have been underplayed or ignored by historians and social scientists—is unfortunate.”

M&T at 3. While their suggestion that Hawk’s Nest, another name for the Gauley Bridge locale, has been ignored by social historians until recently has some plausibility, their implication of more widespread neglect cannot be sustained. Furthermore, their suggestion that Gauley Bridge fits into their Marxist paradigm of corporate corruption of science (citing similar works by Michaels, Castleman, Rosner, et al.) ignores the robust debate from all sectors of society, including the scientific community, organized labor, political actors, industry, government, and academia.

The Gauley Bridge disaster, and disaster it was, was memorialized in song, in literature, and most important, in a refined understanding of how extreme silica exposures can lead to rapid onset of silicosis. These “non-labor” sources are generally ignored in the authors’ “tunnel vision.” McCulloch and Tweedale’s indictment against Lanza asserts that Lanza:

“did not seek to find a truthful explanation for the premature deaths of these men(and countless others), but instead hijacked the medical agenda to serve powerful business interests. In doing so, they certainly proved to be accomplices, but hardly unknowing ones.”

M&T at 3-4.

The historical evidence may support Lanza’s work behind the scenes in the Gauley Bridge trials, but the authors broad, overwrought implications are non-sequiturs:

“As a result, for almost half a century Hawk’s Nest was denied a place in the national consciousness and silicosis was elided as a major public health issue in the USA.”

M&T at 4.

In Song

In 1936, Josh White wrote and sang a labor protest song, “Silicosis is Killing Me”:

I said silicosis, you made a mighty bad break of me.
Awww, silicosis made a mighty bad break of me.
You robbed me of my youth and health;
All you brought poor me was misery.

Now silicosis, you’re a dirty robber and a thief.
Awww silicosis, dirty robber and a thief.
Robbed me of my right to live and all you brought poor me was grief.

I was there digging that tunnel for six bits a day;
I was there digging that tunnel for six bits a day;
Didn’t know I was digging my own grave, silicosis eating my lungs away.

I says mama, mama, mama, cool my fevered head.
I says mama, mama, come and cool my fevered head.
I’m going to meet my Jesus, God knows I’ll soon be dead.

Six bits I got for digging, digging that tunnel hole.
Six bits I got for digging, digging that tunnel hole.
Takes me away from my baby, it sure done wrecked my soul.

Now tell all my buddies, tell all my friends you see;
Now tell all my buddies, tell all my friends you see.
I’m going way up yonder, please don’t grieve for me.

In Cinema

Silicosis was addressed in the emerging art form of cinema, but perhaps most notably in The Citadel (1938), which featured Robert Donat as a physician trying to treat and prevent silicosis. The movie was nominated for an Academy Award, for best picture in 1939; King Vidor was nominated for his directing of the movie.

Perhaps less artistic, but no less compelling than King Vidor, in 1937, Secretary of Labor Frances Perkins declared war on silicosis, toured mines, convened national conferences on the problem, and issued a film entitled, “Stop Silicosis.”

Secretary Perkins as she appeared in “Stop Silicosis.”

In Media

The Gauley Bridge disaster and aftermath were covered widely in newspapers and magazines through the mid- to late-1930s. McCulloch and Tweedale concede the existence “extensive national media coverage.” M&T at 14. They complain, however, that “press interest subsided.” Id. Before we advert to conspiracy theories and suggestions of mass attention deficit disorder, we need only remind ourselves that soon after the Congressional hearings, and the National Silicosis Conference, of the 1930s, Hirohito and Hitler occupied center stage. Press interest is, almost by definition, ephemeral.

In Legislative Action

In 1936, Congress reacted angrily to the media coverage of the Gauley Bridge tunnel workers’ developing and dying of acute silicosis.

A contemporaneous account described the congressional hearings and quoted from the Committee’s official report:

“In a two hundred printed page report the Committee on Labor of the House of Representatives at Washington furnishes the ‘Hearings’ on House Joint Resolution 449 – the legislative vehicle which rudely trundled into the light of publicity the secrets of the silicosis tragedy at Gauley Bridge, West Virginia. This Committee of the Congress presents the testimony of many specialists, including several from the United States Bureau of Mines and the Public Health Service, as well as of special investigators and several surviving victims of the occupational disease from this now notorious tunnel operation. The official report of the investigation

concludes:

‘That the whole driving of the tunnel was begun, continued, and completed with grave and inhuman disregard of any consideration for the health, lives, and future of the employees.

That as a result many workmen became infected with silicosis; that many died of the disease and many not yet dead are doomed to die from the ravages of the disease as a result of their employment and the negligence of the employing contractor. That such negligence was either willful or the result of inexcusable and indefensible ignorance there can be no doubt on the face of the evidence presented to the committee.’

The record presents a story of a condition that is hardly conceivable in a democratic government in the present century. It would be more representative of the middle ages. It is the story of a tragedy worthy of the pen of a Victor Hugo–the

story of men in the darkest days of the depression, with work hard to secure, driven by despair and the stark fear of hunger to work for a mere existence wage under almost intolerable conditions.”

26 Am. Labor Legis. Rev. 66 (1936)

Francis Perkins, Roosevelt’s Secretary of Labor, in 1938 convened a National Silicosis Conference, which brought together organized labor, industry, government, and academics to address the outstanding safety and health issues in industries that gave rise to unsafe silica exposures among their workers. The National Silicosis Conference published its proceedings in a series of reports, which in turn were memorialized in textbooks of the time. See, e.g., Jewett V. Reed & A.K. Harcourt, The Essentials of Occupational Disease 162 & n. 15 (1941) (citing National Silicosis Conference, Report on Medical Control. United States Dep’t of Labor Bull. No. 21, Part 1 (1938)).

LITIGATION: plus ça change, plus c’est la même chose

Jock McCulloch and Geoffrey Tweedale deplore Dr. Lanza’s participation in the silicosis litigation that followed the Gauley Bridge disaster. They go to great lengths to suggest that Lanza suppressed the diagnostic entity of “acute silicosis,” and that he was motivated by race prejudice against the African American tunnel workers and bias in favor of the insurance company for which he worked.

Their narrative of the Gauley Bridge litigation, however, is selective and fatally incomplete. They report that the first case to go to trial in 1933, Raymond Johnson v. Rinehart & Dennis Company, resulted in a hung jury, and they offer multiple hearsay to suggest that the defense bribed several members of the jury. Perhaps there is something to the innuendo, but these historians ignore the contemporaneous accounts that described the circus atmosphere created by the histrionics of the plaintiffs’ counsel. Newsweek described the “legal pyrotechnics”: the plaintiffs’ lawyers

“threw handfuls of white silica dust into the air to show jurors how it hung like an ectoplasmic pall. The plaintiffs’ legal team arranged a court room procession of doomed silicosis sufferers — the parade of the living dead.”

“Silicosis Tunneling Through an Atmosphere of Deadly Dust” Newsweek 33, 34 (Jan. 25, 1936). Rinehart & Dennis settled 200 cases in the aftermath of the hung jury. The plaintiffs’ lawyers filed additional cases, but McCulloch and Tweedale fail to report that the next jury, sitting in Charleston, rejected the worker’s claim. Id.

In 1949, the U. S. Supreme Court, following the lead of the New York Court of Appeals, declared it to be a matter of common knowledge that breathing silica dust “is injurious to the lungs and dangerous to health,” a fact the plaintiff’s employer “was bound to know.” Urie v. Thomas, 337 U.S. 163, 180 (1949), citing Sadowski v. Long Island R.R., 292 N.Y. 448, 456 (1944).

In Occupational Medicine

Before the Gauley Bridge disaster, acute silicosis was not a well-defined diagnostic condition. A paper published in the Journal of the American Medical Association, in 1932, states that “acute silicosis” did not gain recognition until 1929. Earle M. Chapman, “Acute Silicosis,” 98 J. Am. Med. Ass’n 1439 (1932). The author described cases arising out of the abrasive soap manufacturing industry, where silica exposures were confounded by exposure to alkali soap powder.

Two papers in 1933, in the American Journal of Public Health, gave tentative recognition to acute silicosis, and cautiously labeled the condition, “so-called acute silicosis.” Homer L. Sampson, “The Roentgenogram in So-Called ‘Acute’ Silicosis, 23 Am. J. Pub. Health 1237 (1933); and Leroy U. Gardner, “Pathology of So-Called Acute Silicosis,” 23 Am. J. Pub. Health 1237 (1933).

Unfortunately for McCulloch and Tweedale’s thesis, the recognition of acute silicosis, and the assessment of the prevalence of all varieties of silicosis, were confounded by the wide-spread prevalence of tuberculosis (TB). The radiographic appearance of TB often consists of nodular opacities, which physicians, using early, unsophisticated chest radiography, could easily confuse with silicosis. Often workers had both TB and silicosis, and the severity of the patients’ conditions could not easily be attributed to one or the other condition.

Reading the medical literature of the day is a healthful antidote to the glib generalizations that unfairly import present-day knowledge into the discussion of silicosis in the 1930s. In 1934, Dr. John Hawes, in the New England Journal of Medicine, noted that:

“Our ideas concerning silicosis have undergone radical changes during the past ten to fifteen years.”

John B. Hawes, II & Moses Stone, “The Effect of Acute Respiratory Tract Infections Upon Latent Silicosis,” 211 New Engl. J. Med. 1147, 1147 (1934). Tuberculosis and tuberculosilicosis were major confounders in the clinical, diagnostic picture confronted by physicians in the 1930s and 1940s. See, e.g., Louis Benson, “Tuberculosilicosis,” 223 New Engl. J. Med. 398 (1940); H. K. Taylor & H. Alexander, “Silicosis and Silico-Tuberculosis,” 111 J. Am. Med. Ass’n 400 (1938); G. Ornstein & D. Olmar, “Tuberculosis and Silicosis,” 2 Quarterly Bulletin Seaview Hospital 28 (1936).

An editorial in the New England Journal of Medicine, in 1936, presented a balanced view of the issues, and noted that both labor and management had important work to do to bring the safety issues under control. Editorial, “The Problem of Silicosis,” 214 New Engl. J. Med. 794 (1936).

Effective therapies for TB became available in the 1950s. During the 1930s, silicotuberculosis was often called “complicated” silicosis; i.e., silicosis was complicated by mycobacterial infection. In the 1950s, with the advent of antiobiotic therapies for TB, “complicated silicosis” changed meaning to refer to advanced chronic silicosis in which small silicotic nodules had coalesced into large nodules.

Even after antibiotics became available for TB, silicosis was hardly forgotten. Of course, the medical profession and the citizenry had other pressing issues in the 1950s: polio, an emerging epidemic of tobacco-related lung cancer, the threat of war and nuclear holocaust. Still, silicosis remained part of the larger discussion of occupational and environmental hazards. See, e.g., Harriet L. Hardy, “Medical Progress: Occupational Medicine,” 247 New Engl. J. Med. 473 (1951). See also Schachtman, “Conspiracy Theories: Historians, In and Out of Court” (2013) (discussing the quantitation of publication rates about silicosis in both PubMed and in Google labs, both of which show continuing interest in, and publication about, silicosis throughout the 1950s and 1960s, into the OSHA era).

The Gauley Bridge litigation was a short-lived side show in the history of silicosis. Contrary to the McCulloch and Tweedale’s narrative, however, acute or rapid-onset silicosis became a well-accepted diagnostic entity. See, e.g., Lewis Gregory Cole & William Gregory Cole, Pneumoconiosis (Silicosis) – The Story of Dusty Lungs – A Preliminary Report (N.Y. 1940); Jewett V. Reed & A.K. Harcourt, The Essentials of Occupational Disease 164 (1941); Rutherford T. Johnstone, Occupational Medicine and Industrial Hygiene 337 (1948); Donald Hunter, Diseases of the Occupations 837, 849 (1955).

Prevalent Racketeering

McCulloch and Tweedale concede that accurate diagnoses of silicosis require a chest X-ray (which labor radicals and plaintiffs’ lawyers in the 1930s disputed), as well as well as careful clinical examination and full occupational and personal medical histories. M&T at 5. Although they note the diagnostic difficulties, the authors miss the lack of specialization and experience among many general practice physicians to make an accurate diagnosis of silicosis. They acknowledge that the use of X-rays in diagnosis was still contested in the early 1930s. M&T at 11. The situation in the 1930s was thus ripe for specious claiming.

What McCulloch and Tweedale also seem to miss in their focus on a few compelling Gauley Bridge cases is that the diagnostic difficulties and confounders were a prescription for fraud and scamming on the wider stage. In deploring management’s lobbying for workmen compensation laws, they ignore that many labor unions concurred. In the context of silicosis hazards, plaintiffs faced serious legal hurdles against their employers, in the form of limitations, assumption of risk, fellow worker, and contributory negligence defenses.

In 1936, in the pages of the New England Journal of Medicine, Dr. Hawes commented upon the widespread scamming and racketeering that accompanied the serious silicosis cases in West Virginia.

“Very few physicians are aware of the extent to which claims for alleged injury and disease due to dust are being brought before courts and industrial accident boards in this country. The situation in this regard amounts to a ‘racket’ compared with which others, notorious in New York, Chicago and elsewhere, fade into insignificance. Unscrupulous lawyers have their ‘runners’ on the lookout for any employee who is exposed to dust in the course of his work, no matter what the nature of the dust nor however harmless it may be, who happens to come down with a cough or a cold or indeed with almost any other illness and then and there try to persuade him to bring suit. Unfortunately, in too many instances, physicians partly through ignorance and partly through an honest desire to help their patients and perhaps on the general theory of ‘soaking the insurance company’ are willing to testify that the dust to which this individual had been exposed was entirely responsible for his condition. In nearly 100 per cent of such cases the doctor takesat its face value the word of the worker and his friends as to the dust hazard without any real knowledge of the situation obtained from a personal inspection of the plant or at least by interviewing those in a position to know.”

John B. Hayes, II, MD, “Silicosis,” 215 New Engl. J. Med. 143 (1936).

Although the medical understanding of silicosis has advanced tremendously, the racketeering, alas, is still with us to this day. See In re Silica Products Liab. Lit., 398 F. Supp. 2d 563 (S.D. Tex. 2005) (Jack, J.) (describing the attorneys’ manufacturing fraudulent silicosis claims in MDL 1553). Of course, there are real silicosis cases, but overwhelmingly they are “simple” silicosis cases, typically unaccompanied by impairment or disability. Tuberculosis is now rarely a confounder, but histoplasmosis and coccidioidomycosis are important confounders of simple silicosis in some areas of the United States.

The Charge of Racism

McCulloch and Tweedale point out that Lanza formed an opinion that black workers were more prone to TB and silica-related disease because of their race and prevalent syphilis. To be sure, there was (and still is) much race, ethnic, and religious prejudice in the United States. Lanza’s views on race, however, are irrelevant to the ultimate acceptance of acute or rapid-onset silicosis as an occupational hazard of extremely high-levels of occupational silica exposure. The race theory appeared to play no role in the civil litigation in West Virginia, and it receives no mention in the many textbooks that describe and accept acute silicosis as a diagnostic entity. As for the continuing existence of race prejudice, McCulloch and Tweedale might have noted that Dr. Gerrit Schepers, who testified for plaintiffs in asbestos and silica cases in the United States for decades, described young black African children as “pickaninnies.” See Gerrit Schepers, “Discussion,” 132 Annals N. Y. Acad. Sci. 246, 247 (1965). It is a relatively easy, ad hominem game to play, to dismiss a scientist’s views because of his irrational race prejudices. Lanza may have been influenced by his racial theories in acting behind the scenes of the Gauley Bridge litigation, but McCulloch and Tweedale would be hard pressed to find them articulated in Lanza’s textbooks or articles.

The Rosner-Markowitz Hypothesis

The authors note that Lanza, with Metropolitan Life, helped to form the Air Hygiene Foundation (later the IHF), and they insinuate that these organizations were involved in various nefarious actions:

“The AHF (later named the Industrial Hygiene Foundation) was an enduring and powerful industry group, which helped defuse the silicosis crisis by helping companies defend compensation claims, by conducting industry-sponsored industrial hygiene studies and by assuaging public fears. This organisation, in effect, took the dust problem away from the trade unions and the public and sequestered it inside laboratories and private gatherings, where health issues could be mediated by experts and government, safe from untoward publicity. Industry lobbying was able to influence the shaping of state compensation laws for silicosis, which protected big business.”

M&T at 15-16. These insinuations are borrowed, with attribution, from fellow labor historians, David Rosner and Gerald Markowitz. The claims are a mixed lot. For instance, why would not an industry work to help companies defend compensation claims? Organized labor worked to help its members prosecute claims. Surely McCulloch and Tweedale do not believe that every claim made was valid or that every defense frivolous.

Assuming that the AHF/IHF had some role in pressing for state workman compensation laws, then it was aligned with many labor unions that pushed for similar reforms. As noted above, plaintiffs were often at a serious disadvantage in litigation against employers, and they frequently were turned out of court on grounds of limitations, contributory negligence, fellow-worker rule, or assumption of risk. Plaintiffs needed certainty in coverage for occupational disease, not a jury lottery system, and employers needed some reasonable limits on the extent of liability. Workman’s compensation was a compromise, bound not to satisfy everyone.

As for helping companies institute industrial hygiene measures and conduct hygiene studies, the AHF/IHF was helping industry live up to its obligations to provide a safe workplace. The United States government, under the Presidency of Franklin Roosevelt, was involved in similar measures in the 1930s. See, e.g., United States Dep’t of Labor, Silicosis Prevention: Dust Control in Foundries (1939).

McCulloch and Tweedale’s accusation that the AHF/IHF “in effect, took the dust problem away from the trade unions and the public and sequestered it inside laboratories and private gatherings, where health issues could be mediated by experts and government, safe from untoward publicity,” is, of course, borrowed directly from the writings of Rosner and Markowitz. The accusation does not gain any credibility from being repeated. Involving scientists and competent laboratories that would study the issues and publish their results was a responsible step for industry to take. Much of the early political rhetoric about silicosis was driven by personal, subjective anecdotes and uncontrolled observations. The involvement of scientists was a step followed by labor unions, as in the example of the asbestos insulation workers union hiring Dr. Irving Selikoff in the 1950s to investigate their concerns about occupational cancer risk.

There was much to be gained by de-escalating the emotion and vitriol of the labor-management conflicts of the 1930s, although the de-escalation was unsatisfactory to radicals on both sides. The fact is that the labor unions remained interested in, and concerned about, silicosis, both before and after World War II. Labor unions had their own private gatherings, and engaged in rent-seeking from state and federal agencies, as did industry. After the passage of the Occupational Health and Safety Act of 1970, labor’s interests generally prevailed at the agency level.

“The result was that acute silicosis largely disappeared from medical discourse and Gauley Bridge was denied a place in America’s national consciousness.” M&T at Abstract. This causal conclusion is demonstrably wrong. If you like conspiracy theories, McCulloch and Tweedale’s history might well be self-referentially labeled, Deceit and Denial, after the work of their American counterparts, Rosner and Markowitz.

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Christopher Bryson and the Problem of Political Science

October 12th, 2013

Fluoridation of water has long been a “political science” issue, with radical libertarians and anarchists viewing fluoridation as the high-water mark of state paternalism. The motive to misstate and misrepresent the science may at times be obvious, but individual statements, standing alone, may be difficult to judge.

Fluorine chemistry and toxicology are sufficiently advanced that misrepresentations should be easy to detect. Fluorine is a halogen; the lightest in the series. As a gas, fluorine is extremely reactive and toxic, as are other halogen gases, such as chlorine. Fluorine gas was used for uranium enrichment in the Manhattan project, and project scientists conducted research on fluorine toxicity to help them set exposure limits in a new manufacturing process.

As devotees of Breaking Bad no doubt have learned, hydrogen fluoride is extremely toxic and corrosive. Other halogen-based acids are, of course, toxic and corrosive, such as hydrogen chloride.

Compounds of fluorine are generically fluorides, and the properties of the salts and compounds varies considerably with the cation and the chemical structures involved. Many modern medications, such as atorvastatin and fluoxetine contain fluorine in their chemical structures. The toxicology of the fluorine compounds must, therefore, take into account the variability of structure and function of fluorine. Toxicity of fluorine gas or of hydrogen fluoride cannot be “extrapolated” to a simple sodium salt, and more than the toxicity of chlorine gas can be imply the toxicity or ordinary table salt, sodium chloride. The allergenicity of a compound such as potassium aluminumtetrafluoride cannot be the basis for asserting the immunogenicity of a simple alkali salt.

Recently, I came across a YouTube video of a journalist, Christopher Bryson, holding forth on his perception of a vast conspiracy to poison people by the fluoridation of drinking water. Bryson’s passion and selectivity in making his case resembles the deep flaws of our tort system, which allows lawyers and expert witnesses to overwhelm judges and juries with emotion, selectivity, and overstatement. Bryson refers to all fluorine chemicals, whether the elemental gas, the acid, or the many complex and variable salts as “fluoride.” Occupational and environmental exposures to hydrogen fluoride are equated with micromolar levels of sodium fluoride in drinking water. Never once does he actually quantitate the exposures he labels as “toxic.” Largely, Bryson proceeds by ad hominems, ad nauseam. If scientists have industry connections, they are bad, and their science is corrupt. If a scientist has ever done something productive (e.g., George L. Waldbott), and he opines that water fluoridation is bad, then that scientist must be correct. Apparently, Bryson has never heard of Linus Pauling and his Vitamin C fiasco. See K. Frank Austen, M. Dworetzky, Richard S. Farr, G.B. Logan, S. Malkiel, E. Middleton Jr., M.M. Miller, Roy Patterson, C.E. Reed, S.C. Siegel, and P.P. Van Arsdel Jr., “A statement on the question of allergy to fluoride as used in the fluoridation of community water supplies,” 47 J. Allergy & Clinical Immunology 347 (1971) (“no”).

Bryson makes for an interesting case study in hysteria. He is also very much a public example of the tone and substance of many of the plaintiffs’ theories that clog the civil dockets of our court system. Bryson’s passion and intensity — heat without illumination — are reminiscent of the courtroom antics in many a so-called “toxic tort” case. Bryson’s video is thus a good place to start to try to understand science in the courtroom, and the need for strong gatekeeping. The potential for inflammatory advocacy, distortion, and misrepresentation have always been part of legal proceedings, but when it comes to advocacy about claims that turn on “scientific” evidence, there is a difference. Juries in common law cases, in 1789, were not confronted with the abuses of the sort that Bryson so well exemplifies.

The Bryson video led me to look at Bryson’s book, The Fluoride Deception. The book starts with “Notes on Terminology,” which warns that

“THE TERMS fluorine and fluoride should not be confused in a book about chemical toxicity.”

* * *

“In these pages I’ve tried to be clear when I’m referring to the element fluorine or to a compound, a fluoride. And because different fluoride compounds often have unique toxicities, where relevant or possible, I have also given the compound’s specific name.”

So far so good, but then Bryson, having baited, switches:

“Mostly, however, for simplicity’s sake, I have followed convention and used the shorthand fluoride when referring to the element and its multiple manifestations, a procedure approved and used by the U.S. National Academy of Sciences.”

Christopher Bryson, The Fluoride Deception at xi (2004).

Fluoride deception indeed Mr. Bryson. The cited source for the indiscriminate use of fluoride makes clear that it uses “fluoride” as a general term when differentiation is not necessary for its discussion. It is not, however, a basis for conflating or confusing the toxicities of fluorine species or doses. National Research Council, Biological Effects of Atmospheric Pollutants: Fluorides 3 (1971). Bryson provides an apt example of how science communication works in politicized contexts, such as the courtroom or the legislature.

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Harkonen’s Appeal Updated

October 9th, 2013

The Solicitor General’s office has obtained yet another extension in which to file its opposition to Dr. Harkonen’s petition for a writ of certiorari. The new due date is November 8, 2013.

This week, Nature published a news article on the Harkonen case. See Ewen Callaway, “Uncertainty on trial,” 502 Nature 17 (2013). Mr. Calloway’s story accurately recounts that Thomas Fleming, a biostatistician at the University of Washington, chaired the data safety monitoring board for the InterMune trial, and that he had told Dr. Harkonen and others at InterMune that he, Fleming, believed that the press release was misleading. But this “fact” simply represents that Fleming disagreed with the causal inference of efficacy. His opinion might well have been correct, but it did not make Dr. Harkonen’s press release “demonstrably” false. Overstating confidence in a conclusion may be the occasion for disputing the evidentiary warrant for the conclusion, but it does not make the speaker a liar.

Calloway also reports that the government believed that documents suggested that there had been off-label promotion of interferon γ-1b, but of course, the jury acquitted Dr. Harkonen of mislabeling. Calloway’s recitation of these discredited allegations, however, provide important context for why the federal government continues to overreach by pressing its opposition to Dr. Harkonen’s appeal on the conviction for criminal wire fraud.

Mr. Calloway notes that there were “statisticians, clinical researchers and legal scholars” who criticized the judgment of conviction on grounds that it rested upon misinterpretations and misunderstandings of statistics, and that it could criminalize much expert witness testimony, grant applications, and article submissions. But Mr. Calloway’s presentation is subtly biased. He fails to identify those “statisticians, clinical researchers and legal scholars,” other than a few whom he then impugns as having been “compensated” by the defense.

He quotes Stanford Professor Steven Goodman as filing a brief stating that:

“You don’t want to have on the books a conviction for a practice that many scientists do, and in fact think is critical to medical research… .”

Calloway errs in suggesting that Professor Goodman was a brief writer rather than an affiant. Dr. Zibrak, a pulmonary physician is quoted, with the note that he was compensated to tell other physicians about his clinical experience with interferon γ-1b in patients with idiopathic pulmonary fibrosis. By playing the “compensation card,” Calloway tries to diminish the force of Goodman’s and Zibrak’s substantive arguments. This sly attempt, however, is blunted by the significant number of legal scholars and scientists who filed amicus briefs without compensation. More important, the attempt is irrelevant to the issues in the case.

MISLEADING REPORTING

Calloway described the trial as showing that only “slightly fewer” patients had died on interferon γ-1b than on placebo, but that the difference was not statistically significant “because the probability that it was not due to the drug was greater than 5%, a widely accepted statistical threshold.” Well, the p-value was 0.08 on the intent-to-treat analysis, and 0.055 on the per-protocol analysis. When the investigators published a more sophisticated time-to-event analysis in the New England Journal of Medicine, their reported “hazard ratio for death in the interferon gamma-1b group, as compared with the placebo group, was 0.3 (95 percent confidence interval, 0.1 to 0.9).” Raghu et al. N. Engl. J. Med. 350, 125–133; 2004 (for the entire trial, not the “controversial” subgroup). Calloway notes the publication of the results, but fails to inform the Nature readers of this hazard ratio or the confidence interval. Some might say that Mr. Calloway misled readers by inaptly describing this hazard ratio as “slightly fewer” deaths on interferon γ-1b than placebo, and by failing to provide all the pertinent information.

Oh; wait. Is failure to present all the facts, fraud???

TRANSPOSITION FALLACY

Perhaps more ironic was that Mr. Calloway’s interpretation of statistical significance is wrong. The p-value is not the “probability that it was not due to the drug” or the probability that the null hypothesis is true. Good thing that Mr. Calloway does not live in the United States where statistical errors of this sort can be a criminal offense.

The Nature news story quoted Gordon Guyatt, from McMaster University, who thinks that Dr. Harkonen skewed the findings:

“This guy gave a very unbalanced presentation; whether it is sufficiently unbalanced that you should send him to jail, I don’t know… .”

But the data were all accurately presented; it was the use of the verb “demonstrate,” which triggered the prosecution. And it was hardly a “presentation”; it was a press release, which clearly communicated that a presentation was forthcoming within a couple of weeks at a scientific conference.

The story also cites Patricia Zettler, a former FDA attorney, who now teaches at Stanford Law School, for her doubts that the case will matter to most scientists. See also Zettle, “U.S. v. Harkonen: Should Scientists Worry About Being Prosecuted for How They Interpret Their Research Results?” (Oct. 7, 2013). If her prediction is correct, then this is a sad commentary on the scientific community. Ms. Zettler suggests that the Supreme Court is likely to deny the petition, and leave Dr. Harkonen’s conviction in place, and that this denial will not seriously affect scientific discourse. If this suggestion is true, then courts will have acquiesced in a very selective prosecution, given the widespread prevalence of the statistical reporting practices that were on trial here.

As much as everyone would like to see editors, scientists, governments, companies, and universities held to higher standards in science reporting, criminalizing the commonplace because the speaker is an unpopular scientist who has a commercial, as well as a scientific, interest is profoundly disturbing. Ultimately, all scientists, from private or public sectors, from academic or non-academic institutions, have financial or reputational interests to be advanced in their communication of scientific results.

The irony is that many federal judges would not exclude an expert witness who would testify under oath to a conclusion based upon much weaker evidence than Dr. Harkonen presented in a press release, and which announced a much fuller discussion at an upcoming scientific conference in a couple of weeks. If Ms. Zettler is correct, it will be much more difficult for federal and state trial judges to reject challenges to expert witness testimony based upon statistically “non-significant” results, with the old “goes to the weight, not the admissibility” excuse.

Posted in Conflicts of Interest, Scientific Evidence, Scientific Misconduct | Comments Off on Harkonen’s Appeal Updated

Professor Rachel Maines on Historians as Expert Witnesses

October 1st, 2013

Professor Rachel P. Maines, an historian in Cornell University recently presented on “Historians as Experts,” in an American Law Institute webcast continuing legal education program on “Finding and Developing New Expert Witnesses in Litigation” (Sept. 26, 2013). Of course, historians are experts of sorts, or they aspire to be, but Professor Maines addressed historians as expert witnesses in court, a special breed of expert.

Professor Maines’ contributions to the history of technology, and to asbestos in particular, are impressive, and so I appreciated her noting my blog post, “How testifying historians are like lawn-mowing dogs,” (May 2010), as one of my more entertaining “diatribes against testifying historians.” I don’t believe that historians are unnecessary in all cases, only in most cases.

Professor Maines also provided an important practice pointer by emphasizing the value of local historical societies as repositories of documents that may be important to litigation issues. Indeed, recently, I had the pleasure of working with an archivist at the Onondaga County Historical Society, in Syracuse, New York, not far from the hallowed halls of Cornell. A plaintiff, who worked at Syracuse China, in Syracuse, sued on a claim that he developed silicosis from workplace exposure. The crystalline silica and clay suppliers provided warnings on bags and on Material Safety Data Sheets, but the defendants wanted to show the depth and the duration of the employer’s knowledge of silica hazards.

The works of historians and archivists proved to be very important in the favorable resolution of this upstate New York silicosis case. The plaintiff worked at a chinaware factory owned by Syracuse China. A chinaware collector’s history of Syracuse China contained several statements that the employer had longstanding knowledge of silicosis hazards, as do virtually all responsible employers in the United States, from the early 1930’s forward. See Cleota Reed & Stan Skoczen, Syracuse China (Syracuse Univ. Press 1997). Several internet sources alerted me to the existence of the Onondaga Historical Association and its potential as a source of important documents about Syracuse China, and its predecessor, Onondaga Pottery. See, e.g., Tom Huddleston Jr., “Onondaga Historical Association unveils Syracuse China exhibit for two fundraisers,” (Mar. 22, 2010). A few phone calls later, I had an appointment to visit the Onondaga Historical Association and meet its very helpful staff.

Syracuse China closed its doors and ceased manufacturing a few years before the law suit was filed, and discovery of the employer for evidence of its sophistication was slow going. As luck would have it, the company had provided a room full of documents going back to the first decades of the 20th century. Among these documents were original pleadings in lawsuits, brought by employees who claimed to have developed silicosis in the 1930s. The management clearly followed not only litigation developments, but also technical aspects of dust measurement and control. In reviewing the Syracuse China archive at the Onondaga Historical Association, I found, among other things:

pre-OSHA New York state regulations for workplace safety for use of crystalline silica;

correspondence with silica expert, Dr. Leonard Greenberg, then at Yale University in the 1930s, and later an official in the New York Department of Labor; and

American Ceramic Society publications and documents on crystalline silica health hazards and environmental controls.

Personnel records allowed me to establish that Onondaga Pottery had hired a young scientist, Edward Schramm, in the 1930’s, from the United States Bureau of Standards. Schramm served as one of the company’s representative to the American Ceramic Society. In 1933, Schramm published an article “Dust Elimination in the Pottery Industry” in 16 J. Am. Ceramics Soc’y 205 (1933), a journal of the American Ceramics Society. The sophistication of the plaintiff’s employer with respect to silica hazards and their control was indisputable, from the 1930’s forward.

The “treasure trove” of historical documents from the local historical society allowed the defendants to file an extremely strong motion for summary judgment on the issue of sophisticated intermediary and proximate causation. See Affirmation of Counsel for U.S. Silica Co. in Support of Motion for Summary Judgment, in Irwin v. Alcoa, Inc. et al., New York Supreme Court (Onondaga County) Index No. 2010-1098 (Oct. 1, 2012).

Professor Maines’ advice is an important reminder of the utility of informal discovery through historical archives as a supplement to the more typical lawyerly tools of subpoenas and document requests.

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LNT in Milward v. Acuity Specialty Products Group

September 28th, 2013

Professor Edward J. Calabrese previously has written about the shadowy origins of the linear no threshold (LNT) model of cancer causation. See The Dubious Origins of the Linear No Threshold Model of Carcinogenesis (Jan. 10, 2013). Recently, Calabrese has deepened his historical scholarship with two additional, interesting articles. See “Toxicologist Says NAS Panel ‘Misled the World’ When Adopting Radiation Exposure Guidelines” (Aug. 13, 2013).

These articles, now available online, are important tools in the work chest of lawyers who litigate health effect claims. Edward J. Calabrese, “How the US National Academy of Sciences misled the world community on cancer risk assessment: new findings challenge historical foundations of the linear dose response,” 87 Arch. Toxicol. (2013) (in press); Edward J. Calabrese, “Origin of the linearity no threshold (LNT) dose–response concept,” 87 Arch. Toxicol. 1621 (2013). Professor Calabrese illuminates the exaggerations and ipse dixit in the origins of the linear-no threshold model, first applied to radiogenic cancers, and later to human carcinogenesis more generally.

On remand from the First Circuit, the trial judge in Milward, now the Hon. Douglas Woodlock, faced a renewed Rule 702 motion directed to Milward’s specific causation expert witnesses. Milward v. Acuity Specialty Products Group, Inc., Civil Action No. 07–11944–DPW, 2013 WL 4812425 (D. Mass. Sept. 6, 2013). Plaintiffs attempted to invoke the dubious LNT concept to argue that benzene should be in the “differential” for ascertaining the specific cause of Mr. Milward’s APL. In performing a careful Rule 702 analysis, Judge Woodlock rule that, “[t]o the extent Butler [Milward’s expert witness] seeks to establish specific causation based on the argument that any level of benzene is sufficient to cause leukemia—a so-called “no safe level,” “no threshold,” or “linear” model—her opinion is inadmissibly unreliable.” Id. at *8.

In recognizing Dr. Butler’s reliance upon LNT concepts in civil litigation as unreliable, Judge Woodlock followed the lead of other courts, within the First Circuit, which have previously rejected expert witness opinion testimony founded upon the LNT model. See, e.g., Whiting v. Boston Edison Co., 891 F.Supp. 12, 25 (D.Mass.1995) (“[t]he linear non-threshold model cannot be falsified, nor can it be validated. To the extent that it has been subjected to peer review and publication, it has been rejected by the overwhelming majority of the scientific community. It has no known or potential rate of error. It is merely an hypothesis.” ); Sutera v. Perrier Group of America Inc., 986 F.Supp. 655, 666 (D.Mass.1997) (“Accordingly, although there is evidence that one camp of scientists … believes that a non-linear model is appropriate basis for predicting the risks of low-level exposures to benzene, there is no scientific evidence that the linear no-safe threshold analysis is an acceptable scientific technique used by experts in determining causation in an individual instance.”). Strong precedent outside the First Circuit also supports Judge Woodlock’s holding. See Allen v. Pennsylvania Eng’g Corp., 102 F.3d 194, 198 (5th Cir.1996); Henricksen v. ConocoPhillips Co., 605 F.Supp. 2d 1142, 1166 (E.D.Wash.2009) (“[Plaintiffs’ expert witness’s] theory that any amount of exposure more than negligible should be considered substantial risk factor for AML flies in the face of the scientific literature reviewed and other expert testimony in this case that there is a threshold or dose below which you do not see a statistically significant risk of developing AML.”); In re W.R. Grace & Co. 355 B.R. 462, 476 (Bankr. D. Del. 2006) (the “no threshold model . . . flies in the face of the toxicological law of dose-response . . . doesn’t satisfy Daubert, and doesn’t stand up to scientific scrutiny”); Cano v. Everest Minerals Corp., 362 F. Supp. 2d 814, 853–54 (W.D. Tex. 2005) (even accepting the linear, no-threshold model for uranium mining and cancer, it is not enough to show exposure, you must show causation as well). See also McClain v. Metabolife Int’l, Inc., 401 F.3d 1233, 1244 (11^th Cir. 2005) (“in evaluating the reliability of the experts’ opinions on general causation, it would help to know how much additional risk for heart attack or ischemic stroke Metabolife consumers have over the risks the general population faces”). National Bank of Commerce v. Assoc. Milk Producers, 22 F. Supp. 2d 942, 960 (E.D. Ark. 1998), aff’d, 191 F.3d 858 (8th Cir.1999). See generally Federal Judicial Center, Reference Manual on Scientific Evidence, at 643 n. 28 (3d ed.2011).

The district court in Milward held that because Dr. Butler “did not and could not quantify a threshold exposure level for benzene, Milward cannot posit that his cumulative exposure level crossed a relevant threshold.” Milward, 2013 WL 4812425, at 8. In addressing Milward’s reliance upon LNT, Judge Woodlock rejected three specious arguments, which frequently recur in Rule 702 litigation.

First, the district saw through the argument that the claimed benzene-APL LNT model was good science because the United States Environmental Protection Agency (EPA) relies upon it. The EPA applies the LNT model for benzene

“due to uncertainty about the shape of the dose-response curve below 40 ppm-years.”

Id. at 8[1]. The district court recognized that the EPA’s reasoning was a “classic example of a cautious prophylactic administrative rule” that “does not support the reliability of the linear, no-threshold model in establishing specific causation.” Id. In so ruling, the Milward district court joins a long line of courts that have distinguished administrative rulemaking from civil litigation standards for causation. See, e.g., Allen v. Pa. Eng’g Corp., 102 F.3d 194, 198 (5th Cir. 1996)(“This methodology results from the preventive perspective that the agencies adopt in order to reduce public exposure to harmful substances. The agencies’ threshold of proof is reasonably lower than that appropriate in tort law, which traditionally makes more particularized inquiries into cause and effect.”)

Second, the Milward district court also saw through plaintiffs’ argument that the First Circuit’s embrace of its “weight of the evidence” general causation approach, which appears to enjoy support among federal bureaucrats, required approval of plaintiffs’ attempt to use a LNT prophylactic or precautionary approach. Milward, 649 F.3d at 18 & n. 9. Plaintiffs have the burden of showing reliability of the LNT model, and the EPA’s acknowledged uncertainty about the model for benzene was an insuperable barrier to their success. Milward, 2013 WL 4812425, at 8 & n.4.

Third, the district court rejected Dr. Butler’s attempt to “bait and switch,” by pointing to a study on hematotoxicity as opposed to carcinogenicity. Butler argued that there was “no clear evidence of a threshold below which benzene does not cause hematotoxicity in humans.”[2] The court recognized that the study referred to the lack of a hematotoxicity threshold for low average doses of benzene. Hematotoxicity is not necessarily induction of APL; nor was the lack of clear evidence for a threshold evidence against a threshold.

Even in the regulatory realm, the LNT model is losing traction. See Chlorine Chemistry Council v. EPA, 206 F.3d 1286, 1287 (D.C. Cir. 2000) (invalidating EPA regulation under the Safe Drinking Water Act, when the EPA persisted in using an LNT model, after it had concluded that chloroform, a contaminant in drinking water from chlorination exerted a “a nonlinear mode of carcinogenic action”). In the scientific realm, researchers can merely watch in amazement at the “political science” that proceeds under a mistaken, outdated model of carcinogenesis. See, e.g., Brant A. Ulsh, “Checking the Foundation: Recent Radiobiology and the Linear No-Threshold Theory,” 99 Health Physics 747 (2010) (“However, a large and rapidly growing body of radiobiological evidence indicates that cell and tissue level responses to this damage, particularly at low doses and/or dose-rates, are nonlinear and may exhibit thresholds. To the extent that responses observed at lower levels of biological organization in vitro are predictive of carcinogenesis observed in vivo, this evidence directly contradicts the assumptions upon which the microdosimetric argument is based.”); Bernard L. Cohen, “The Linear No-Threshold Theory of Radiation Carcinogenesis Should Be Rejected,” 13 J. Am. Physicians & Surgeons 70, 75 (2008) (“The conclusion from the evidence reviewed in this paper and more extensively elsewhere is that the linear-no threshold theory (LNT) fails very badly in the low-dose region, grossly overestimating the risk from low-level radiation. This means that the cancer risk from the vast majority of normally encountered radiation exposures is much lower than given by usual estimates, and may well be zero or even negative.”); Maurice Tubiana, Ludwig E. Feinendegen, Chichuan Yang, and Joseph M. Kaminski, “The Linear No-Threshold Relationship Is Inconsistent with Radiation Biologic and Experimental Data,” 251 Radiology 13, 13, 15-16, 18 (2009) (noting that LNT model is obsolete in view of known upregulation of cellular protective mechanisms against cancer; “LNT was a useful model half a century ago. But current radiation protection concepts should be based on facts and on concepts consistent with current scientific results and not on opinions. Preconceived concepts impede progress; in the case of the LNT model, they have resulted in substantial medical, economic, and other societal harm.”).

[1] The court EPA Office of Research and Development, Carcinogenic Effects of Benzene: An Update, at 38–39 (April 1998).

[2] Dr. Butler cited Richard B. Hayes, et al., “Benzene and Lymphohemaptopoietic Malignancies in Humans,” 40 Am. J. Indus. Med. 117, 120 (2001).

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Differential Diagnosis in Milward v. Acuity Specialty Products Group

September 26th, 2013

Graffiti on the bathroom wall in the building that housed my undergraduate college’s philosophy department:

How does a philosopher treat constipation?

By using iterative disjunctive syllogism.

The joke is that this variety of syllogism is nothing other than reasoning by the process of elimination.

A or B or C

~A

B or C

~B

∴C

The syllogism works as a valid form of argument if the premises are all true. So, if we start with three possible causes, A, B, and C, and we know that one or more of them caused an outcome, then we might proceed by the process of elimination to show that we can rule out all the others but the alleged cause. The first line of the syllogism is true if at least one of the disjuncts is true. As we rule out particular disjuncts upon learning that they are in fact false, we are left we a smaller set of disjuncts. If we can proceed until we are left with the disjunct of interest, we may actually have succeeded in identifying a cause in fact of the particular case.

In the syllogistic argument above, we must be able to show that A and B are false before we can then conclude that C is true.

In differential etiology, we start with known causes, exposures or conditions that are known to be capable of causing a disease or disorder. We do not know whether the potential causes were actually in play in a given case. If we can use this syllogistic reasoning to conclude that the defendant’s product was a cause of the of the plaintiff’s harm, we might actually have shown specific causation in a reliable fashion. If, however, we cannot proceed to a conclusion that unequivocally includes the defendant’s product, we are left with an indeterminate outcome, and the plaintiff must take nothing.

The Milward case was recently back in the news. On remand from the First Circuit, the district judge, now the Hon. Douglas Woodlock, faced a renewed Rule 702 motion directed to Milward’s specific causation expert witnesses. Milward v. Acuity Specialty Products Group, Inc., Civil Action No. 07–11944–DPW, 2013 WL 4812425 (D. Mass. Sept. 6, 2013).

Judge Woodlock wryly commented upon the First Circuit’s ignoring the statutory mandate of Rule 702, by its embracing caselaw that predated the 2000 statutory amendment of the Rule:

“While a 2000 amendment to Fed.R.Evid. 702 codified a rigorous reliability test, the Daubert line of cases has been read by the First Circuit as “demand[ing] only that the proponent of the evidence show that the expert’s conclusion has been arrived at in a scientifically sound and methodologically reliable fashion.” Ruiz–Troche v. Pepsi Cola of Puerto Rico Bottling Co., 161 F.3d 77, 85 (1st Cir.1998). “So long as an expert’s scientific testimony rests upon good grounds based on what is known, it should be tested by the adversarial process, rather than excluded for fear that jurors will not be able to handle the scientific complexities.” Milward, 639 F.3d at 15 (internal quotation and citation omitted).”

Milward, at *3. After noting the statute’s “rigorous reliability test,” and the First Circuit’s having diluted the statutory standard by drawing from pre-statute caselaw, Judge Woodlock got down to the business of gatekeeping, by examining the facts of record before him.

The defense’s first challenge was to Milward’s industrial hygienist’s opinion that quantified his benzene exposure. The industrial hygienist, James Stewart, estimated Milward’s benzene exposure, both total and from individual products. The defense challenge was interesting, given that plaintiffs have challenged defendants’ use of similar exposure recreations to advance apportionments that will defeat joint and several liability. The district court denied the defense challenge, and turned its attention to the specific causation issue, which proved to be a good example of patho-epistemology .

The plaintiffs relied upon Dr. Sheila Butler, who was board certified in occupational medicine, pathology, and hematology, to opine that Brian Milward’s exposure was responsible for causing his Acute Promyelocytic Leukemia (“APL”), a rare subtype of Acute Myeloid Leukemia (“AML”). Butler’s opinion was simple if not simpistic:

“there is a ‘reasonable medical probability that there is a direct causal association between Mr. Milward’s APL and his excessive occupational exposure to benzene containing substances’ based primarily on

(1) the fact that his exposure to benzene preceded his development of APL, and

(2) a survey of studies showing increased AML risk following low average dose exposures to benzene.”

Milward at *6.

Simplistic and simply wrong. Butler had equated exposure and some risk, unquantified, with specific causation, an empty and unsupported assertion. Judge Woodlock did not dignify this subjective opinion with further discussion, but turned his attention to Butler’s “differential diagnosis” analysis by which Butler claimed to have eliminated other potential causes of Milward’s APL such that she could say that benzene was a specific cause.

The district court started from the premise that so-called differential diagnosis is useful and accepted for assessing causation. Id. at *7 (citing Baker v. Dalkon Shield Claimants Trust, 156 F.3d 248, 253 (1st Cir.1998). For some reason, however, the court emphasized that the differential etiology was particularly appropriate when the expert witness’s opinion lacks a foundation of epidemiologic studies or a “well-established threshold exposure levels at which disease occurs.” The district court did not explain what it possibly could have meant by this emphasis, and I doubt that there is any basis for the court’s statement.

The real issue in Milward, on remand, was whether Dr. Butler applied the differential etiology in a reliable manner. The defense argued that Dr. Butler failed to rule out competing risk factors, Milward’s prior smoking, and his morbid obesity, as causes of Milward’s APL. The court dismissed this challenge with the recognition that plaintiffs might still prevail if Milward’s disease resulted from either benzene and smoking or benzene, smoking, and obesity. Sadly, the court did not address the quality or quantity of the evidence for smoking, or for obesity, and APL; nor did it address the magnitude of the associations that were being claimed by the defense, or by the plaintiffs. The court did not explore the evidentiary base for the defense assertion that smoking or obesity causes APL such that it should be in the first line of the iterative disjunctive syllogism.

The problem, of course, was not the plaintiffs’ failure to rule out obesity or smoking, but their failure to rule out the unknown factors, which account for the solid majority of APL cases. Indeed, in the first round of Rule 702 briefings and hearings, plaintiffs’ expert witness, Dr. Martin Smith, opined that between 70 and 80 percent of APL cases are idiopathic; that is, they have no known cause. Id. at *7. The syllogism thus becomes very difficult because one proposition in the first line of the argument is that the cause is unknown, and the plaintiff cannot arrive at the conclusion that his APL was caused by benzene unless and until he provides reliable evidence that more likely than not, his APL disease was not caused by one or more of the unknown causes. In other words, plaintiffs must show that the APL was not a background case that would have occurred regardless of occupational benzene exposure, and perhaps regardless of occupational exposure with obesity and smoking. Judge Woodlock, relying heavily upon the Restatement (Third) of Torts expressed the matter this way:

“When a disease has a discrete set of causes, eliminating some number of them significantly raises the probability that the remaining option or options were the cause-in-fact of the disease. Restatement (Third) of Torts: Phys. & Emot. Harm § 28, cmt. c(4) (2010) (‘The underlying premise [of differential etiology] is that each of the[] known causes is independently responsible for some proportion of the disease in a given population. Eliminating one or more of these as a possible cause for a specific plaintiff’s disease increases the probability that the agent in question was responsible for that plaintiff’s disease.’). The same cannot be said when eliminating a few possible causes leaves not only fewer possible causes but also a high probability that a cause cannot be identified. Id. (‘When the causes of a disease are largely unknown … differential etiology is of little assistance’.).”

In the face of this irrefutable logic of this part of comment c, Butler argued that she had “ruled out” idiopathic APL by “ruling in” benzene. Of course, benzene had to be postulated as a general cause in order for it to be placed into the first line of the syllogism, but Butler’s assertion about ruling in benzene as a specific cause is truly an ipse dixit, a non sequitur, and a petitio principii, all rolled into one opinion. After all, the APL case may have arisen out of benzene exposure and the unknown causes, or only the unknown (idiopathic) causes. Butler cannot rule in benzene until she rules out idiopathic causes as the sole specific causes in this case. To be fair, the prevalence of idiopathic cases cited by Martyn Smith might be lower in a population with heavy benzene exposure, assuming Smith’s general causation were true, but again, such an acknowledgment would only raise the question of what the prevalence of idiopathic cases is in a population of exposure that looked like Mr. Milward’s.

Dr. Butler argued that Martyn Smith had previously ruled in benzene, but that was only as a general cause that can then be represented as one disjunct in the first line of the syllogism. Here Judge Woodlock identified another gap between Smith’s general causation opinion and Dr. Butler’s attempt to use Smith’s opinion to place benzene into the differential etiology for Mr. Milward. On this remand, the plaintiffs had to show that “the levels of exposure that are hazardous to human beings generally as well as the plaintiff’s actual level of exposure.” Id. (citing Westberry v. Gislaved Gummi AB, 178 F.3d 257, 263-64 (4th Cir.1999) (talcum powder undisputedly could cause sinus problems, and plaintiff was exposed at levels known to be causative). The court suggested that Milward had not yet shown that exposure at the levels he experienced could cause APL. Of course, even if Milward sustained cumulative exposures capable of causing APL, this fact sufficed only to place benzene into the differential diagnosis, and it did not advance the iterative disjunctive syllogism to a conclusion of either a single or multiple disjuncts that included benzene.

Judge Woodlock did a good job of saving the First Circuit from the notoriety of its general causation decision in the Milward case. The new trial court decision is a strong reminder that risk does not equal causation. Differential etiology cannot rule out idiopathic cause(s) as the sole specific cause of a plaintiff’s disease unless there is a fingerprint of causation that makes the risk identifiable as a cause in a specific case. Such a fingerprint or biomarker was apparently absent in the Milward case. Similarly, the differential etiology might rule out putative specific causes on a probabilistic basis if the idiopathic cases made up a small number of all the cases in relation to the number of cases that arise from the exposure that is the subject of the litigation.

The Milward decision joins other soundly decided differential diagnosis cases coming out of the First Circuit. See, e.g., Plourde v. Gladstone, 190 F. Supp. 2d 708, 722-723 (D. Vt. 2002) (excluding testimony where expert failed to rule out causes of plaintiff’s illness other than exposure to herbicides); Whiting v. Boston Edison Co., 891 F. Supp. 12, 21 n.41 (D. Mass. 1995) (noting that differential diagnosis cannot be used to support conclusion of specific causation when 90% disease cases are idiopathic).

But lest anyone get too comfortable with the notion that this issue has been mastered by the federal judiciary, keep in mind that there are some really poorly reasoned cases out there. See, e.g., Allen v. Martin Surfacing, 263 F.R.D. 47, 56 (D. Mass. 2008) (admitting general and specific causation testimony to be tested by adversary process, rather than excluded altogether, despite paucity of epidemiologic evidence and general acceptance that there are no known causes of amyotrophic lateral sclerosis).

The limits of the “process of elimination” approach has been addressed by some scientific organizations, such as the Teratology Society, in the particularly demanding context of determining a cause for a child’s congenital malformation:

“Biologic plausibility includes a consideration of alternative explanations for the outcome in an individual plaintiff. For example, if a plaintiff has a birth defect syndrome caused by a known genetic disorder, chemical exposure becomes implausible as a cause of the abnormality in that particular individual. The consideration of alternative explanations is sometimes misused by expert witnesses to mean that failure to find an alternative explanation for an outcome is proof that the exposure at issue must have caused the outcome. A conclusion that an exposure caused an outcome is, however, based on positive evidence rather than on lack of an alternative explanation.”

The Public Affairs Committee of the Teratology Society, “Teratology Society Public Affairs Committee Position Paper Causation in Teratology-Related Litigation,” 73 Birth Defects Research (Part A) 421, 423 (2005).

A brief, partial survey of differential etiology cases is set out below.

SECOND CIRCUIT

McCullock v. H.B. Fuller Co., 61 F.3d 1038, 1044 (2d Cir. 1995) (defining differential etiology as an analysis “which requires listing possible causes, then eliminating all causes but one”)

Prohaska v. Sofamor, S.N.C., 138 F. Supp. 2d 422, 439 (W.D.N.Y. 2001) (excluding expert’s opinion and granting summary judgment where expert “was unable to rule out, to a reasonable degree of medical certainty, [plaintiff’s] pre-existing condition, scoliosis, as a current cause of her pain”)

Zwillinger v. Garfield Slope Hous. Corp., 1998 WL 623589, at *20 (E.D.N.Y. Aug. 17, 1998) (excluding testimony and granting summary judgment where expert failed to rule out alternative causes of plaintiff’s immunotoxicity syndrome)

THIRD CIRCUIT

Magistrini v. One Hour Martinizing Dry Cleaning, 180 F. Supp. 2d 584, 608-610 (D.N.J. 2002) (excluding testimony of expert who sought to testify that dry cleaning fluid caused leukemia, but failed to rule out smoking as an alternative cause), aff’d, 68 F. App’x 356 (3d Cir. 2003)

In re Paoli R.R. Yard PCB Litig., 2000 WL 274262, at *5 (E.D. Pa. March 1, 2000) (expert’s opinion should be excluded “because she failed to rule out alternative causes” of plaintiff’s injuries)

Kent v. Howell Elec. Motors, 1999 WL 517106, at * 5 (E.D. Pa. July 20, 1999) (excluding expert testimony and granting summary judgment because expert could “not rule out reasonable alternative theories of what caused the retaining ring to fail”);

O’Brien v. Sofamor, 1999 WL 239414, at *5 (E.D. Pa. Mar. 30, 1999) (excluding expert’s testimony and granting summary judgment where plaintiff “offer[ed] no evidence that [plaintiff’s experts] performed a differential diagnosis, or even considered other potential causes” of plaintiff’s back condition)

Schmerling v. Danek Med., Inc., 1999 WL 712591, at *9 (E.D. Pa. Sept. 10, 1999) (excluding expert’s testimony and granting summary judgment on the grounds that expert’s failure to rule out alternative causes “alone warrants a determination that the expert’s methodology is unreliable”);

Turbe v. Lynch Trucking Inc., 1999 WL 1087026, at *6 (D.V.I. Oct. 7, 1999) (excluding expert’s testimony where expert “expressed awareness of obvious alternative causes” yet “did not investigate any other possible causes”);

Reiff v. Convergent Technologies, 957 F. Supp. 573, 582-83 (D.N. J. 1997) (excluding expert’s testimony and granting summary judgment where expert failed to rule out alternative causes of plaintiff’s carpal tunnel syndrome)

Rutigliano v. Valley Bus. Forms, 929 F. Supp. 779, 787 (D.N.J. 1996) (excluding expert’s testimony and granting summary judgment where the “record is replete with evidence, including [the expert’s] own admissions, that [plaintiff’s] symptoms could be attributable to medical conditions other than formaldehyde sensitization”)

Diaz v. Matthey, Inc., 893 F. Supp. 358, 376-377 (D.N.J. 1995) (excluding testimony and granting summary judgment where expert failed to rule out alternative causes for plaintiff’s asthma) (Irenas, J.)

Wade-Greaux v. Whitehall Labs., Inc., 874 F. Supp. 1441 (D.V. I.), aff’d, 46 F.3d 1120 (3d Cir. 1994) (excluding testimony of expert who failed to rule out alternative causes of plaintiff’s birth defects)

FOURTH CIRCUIT

Westberry v. Gislaved Gummi AB, 178 F.3d 257, 262-263 (4th Cir. 1999) (“Differential diagnosis, or differential etiology, is a standard scientific technique of identifying the cause of a medical problem by eliminating the likely causes until the most probable one is isolated”)

Shreve v. Sears, Robuck & Co., 166 F. Supp. 2d 378, 397-98 (D. Md. 2001) (excluding testimony where expert failed to rule out other causes of plaintiff’s injury other than an alleged defect in snow thrower)

Fitzerald v. Smith & Nephew Richards, Inc., 1999 WL 1489199 (D. Md. Dec. 30, 1999) (excluding expert’s testimony and granting summary judgment where expert “failed to rule out what could have been another cause of [plaintiff’s] condition”)

Aldridge v. Goodyear Tire & Rubber Co., 34 F. Supp. 2d 1010, 1024 (D. Md. 1999), vacated on other grounds, 223 F.3d 263 (4th Cir. 2000) (excluding testimony of plaintiffs’ experts where they “failed to adequately address possible alternative causes of plaintiffs’ illnesses”)

Oglesby v. General Motors Corp., 190 F.3d 244, 250 (4th Cir. 1999) (affirming exclusion of testimony where “as a matter of logic, [the expert witness] could not eliminate other equally plausible causes” of cracked plastic inlet);

Driggers v. Sofamor, S.N.C., 44 F. Supp. 2d 760, 765 (M.D.N.C. 1998) (excluding expert’s testimony and granting summary judgment where “expert failed to rule out other possible causes of [plaintiff’s back] pain”);

Higgins v. Diversey Corp., 998 F. Supp. 598, 603 (D. Md. 1997), aff’d, 135 F.2d 769 (4th Cir. 1998) (excluding expert’s testimony that the accidental inhalation of a bleach caused plaintiff’s injuries, where expert “admit[ted] that he [could] not rule out several other possible causes”)

FIFTH CIRCUIT

Michaels v. Avitech, Inc., 202 F.3d 746, 753 (5th Cir. 2000) (excluding testimony when “plaintiff’s experts wholly fail[ed] to address and rule out the numerous other potential causes” of an aircraft disaster)

Black v Food Lion, Inc, 171 F3d 308 (5th Cir 1999) (expert witness, purporting to use a differential diagnosis, testified that plaintiff’s slip in the supermarket caused fibromyalgia, which is largely idiopathic) (“This analysis amounts to saying that because [the physician] thought she had eliminated other possible causes of fibromyalgia, even though she does not know the real ‘cause,’ it had to be the fall at Food Lion. This is not an exercise in scientific logic but in the fallacy of post-hoc propter-hoc reasoning, which is as unacceptable in science as in law.”)

Conger v. Danek Med., Inc., 1998 WL 1041331, at *5-6 (N.D. Tex. Dec. 14, 1998) (excluding expert’s testimony and granting summary judgment when expert “had not attempted to rule out [other potential sources] as causes for [plaintiff’s back] pain”);

Leigh v. Danek Med., Inc., 1998 WL 1041329, at *4-5 (N.D. Tex. Dec. 14, 1998) (excluding expert’s testimony and granting summary judgment where expert failed to rule out alternative causes of plaintiff’s back pain)

Bennett v. PRC Public Sector, 931 F. Supp. 484, 492 (S.D. Tex. 1996) (excluding testimony of expert who failed to consider and rule out alternative causes of plaintiff’s repetitive motion disorders)

SIXTH CIRCUIT

Nelson v. Tennessee Gas Pipeline Co., 1998 WL 1297690, at *6 (W.D. Tenn. Aug. 1, 1998) (excluding testimony of expert who “failed to engage in adequate techniques to rule out alternative causes and offers no good explanation as to why his opinion is nevertheless reliable in light of other potential causes of the alleged injuries”);

Downs v. Perstorp Components, 126 F. Supp. 2d 1090, 1127 (E.D. Tenn. 1999) (excluding expert testimony as to whether exposure to chemicals caused plaintiff’s injuries where expert failed to rule out alternative causes)

EIGHTH CIRCUIT

Jisa Farms, Inc. v. Farmland Indus., No. 4:99CV3294, 2001 U.S. Dist. LEXIS 26084 (D. Neb. 2001)

Thurman v. Missouri Gas Energy, 107 F. Supp. 2d 1046, 1058 (W.D. Mo. 2000) (expert’s opinion “that the pipeline failed because of corrosion” was excluded and summary judgment granted where expert reached the conclusion “without eliminating other causes”)

Bruzer v. Danek Med., Inc., 1999 WL 613329, at *8 (D. Minn. Mar. 8, 1999) (excluding expert’s testimony and granting summary judgment where expert did “not attempt to rule out any alternative potential causes for [plaintiff’s] continuing and increasing [back] pain”)

National Bank of Commerce v. Assoc. Milk Producers, 22 F. Supp. 2d 942, 963 (E.D. Ark. 1998), aff’d, 191 F.3d 858 (8th Cir.1999) (excluding testimony and granting summary judgment where expert did “not successfully rule out other possible alternative causes” for cancer)

TENTH CIRCUIT

In re Breast Implant Lit., 11 F. Supp. 2d 1217, 1234 (D. Colo. 1998) (excluding expert testimony where expert failed to “explain what alternative causes he considered, or how he ruled out other possible causes” of plaintiffs’ auto- immune disease)

Stover v. Eagle Products, 1996 WL 172972, at *11 (D. Kan. Mar. 19, 1996) (excluding testimony of expert who “[did] not explain in any meaningful detail how he [was] able to exclude the numerous multiple alternative causes” of injury to plaintiff’s dogs)

ELEVENTH CIRCUIT

Rink v. Cheminova, Inc., 400 F.3d 1286, 1295 (11th Cir. 2005) (“[I]n the context of summary judgment . . . differential diagnosis evidence by itself does not suffice for proof of causation.”)

STATE COURT CASES

Blanchard v. Goodyear Tire & Rubber Co., 2011 Vt. 85, 30 A.3d 1271 (2011) (holding that plaintiff’s claim that his NHL was caused by benzene was not reliably supported by differential diagnosis when a large percentage of NHL cases have no known cause)

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Bradford Hill on Statistical Methods

September 24th, 2013

I am indebted to the article by Dr. Frank Woodside and Allison Davis on the so-called Bradford Hill criteria, for reminding me about the distorted view that some plaintiffs’ counsel advance in litigation about Bradford Hill’s view of statistical testing. Frank C. Woodside, III & Allison G. Davis, “The Bradford Hill Criteria: The Forgotten Predicate,” 35 Thomas Jefferson L. Rev. 103 (2013). Dr. David Schwartz has also written an insightful blog post on Bradford Hill. See David Schwartz, “5 Reasons to Apply the Bradford Hill Criteria in Your Next Case” (Sept. 20, 2013).

Here is where Bradford Hill postulates the position of a research question before his famous nine factors come into the analysis:

“Disregarding then any such problem in semantics we have this situation. Our observations reveal an association between two variables, perfectly clear-cut and beyond what we would care to attribute to the play of chance. What aspects of that association should we especially consider before deciding that the most likely interpretation of it is causation?”

Austin Bradford Hill, “The Environment and Disease: Association or Causation?” 58 Proc. Royal Soc’y Med. 295, 295 (1965).

The starting point, before the Bradford Hill nine factors come into play, requires a “clear-cut” association, which is “beyond what we would care to attribute to the play of chance.” What is “clear-cut” association? The most reasonable interpretation of Bradford Hill is that the starting point is an association that is not the result of chance, bias, or confounding.

I parted company with Woodside and Davis over whether Bradford Hill was somehow dismissive of the role of assessing chance in explaining an association. In acknowledging any validity in the plaintiffs’ interpretation of Bradford Hill’s 1965 paper, Woodside and Davis, do an injustice, in my view, to Bradford Hill’s careful articulation of his position.

The starting position, quoted above, seems very clear, but Woodside and Davis note that later on in his speech, Bradford Hill suggested that tests of significance do not contribute to proof of the hypothesis. Bradford Hill’s actual words are, however, fairly precise:

“No formal tests of significance can answer those questions. Such tests can, and should, remind us of the effects that the play of chance can create, and they will instruct us in the likely magnitude of those effects. Beyond that they contribute nothing to the ‘proof’ of our hypothesis.”

Bradford Hill at 299.

Plaintiffs’ counsel sometimes argue that this passage means that significance testing contributes “nothing” to proving the hypothesis, but this ignores two key points. First, the argument ignores where in the text the passage occurs: after Bradford Hill’s discussion of the nine factors. Bradford Hill’s statement can be understood only as a reflection back on the nine factors. The phrase “those questions” refers back to the nine factors, and this is the limitation that Bradford Hill is placing upon “formal tests of significance.” The starting point, before the nine factors are examined, is, after all, a “clear-cut” association, “beyond what we would care to attribute to the play of chance.”

Second, plaintiffs’ counsel’s argument ignores the clear meaning of the “[b]eyond that” phrase. Beyond what? Well, the limited role is nothing other than quantifying the play of chance in the observed results. This role is hugely important, and of course, is incorporated into the starting point before the nine factors are examined. In modern analyses, the role of random variability would actually be explored in the analysis of the exposure-outcome gradient, and perhaps in some of the other nine factors as well. Bradford Hill implied that a statistically significant association was a preliminary step, after which the really hard work began.

It would be unfair to Bradford Hill to read into his statement much about “strict” testing versus a more flexible inferential approach in selecting or interpreting a Type I error rate. By the time he presented his Presidential Address to the Royal Society of Medicine in 1965, much fur had flown in the disputes between Neyman and Fisher. Resolving Bradford Hill’s view on the dispute is not a pressing issue because on either account, the quantification of the p-value is an extremely important step in evaluating scientific data.

In his textbook on medical statistics, Bradford Hill expands on the role of statistical analysis in medicine:

“Are simple methods of the interpretation of figures only a synonym for common sense or do they involve an art or knowledge which can be imparted? Familiarity with medical statistics leads inevitably to the conclusion that common sense is not enough. Mistakes which when pointed out look extremely foolish are quite frequently made by intelligent persons, and the same mistakes, or types of mistakes, crop up again and again. There is often lacking what has been called a ‘statistical tact, which is rather more than simple good sense’. That tact the majority of persons must acquire (with a minority it is undoubtedly innate) by a study of the basic principles of statistical method.”

Austin Bradford Hill, Principles of Medical Statistics at 2 (4th ed. 1948) (emphasis in original).

Even in this early work though, Bradford Hill acknowledges the limits of statistical methods:

“It is a serious mistake to rely upon the statistical method to eliminate disturbing factors at the completion of the work. No statistical method can compensate for a badly planned experiment.”

Id. at 4 (emphasis in original). That statistical method cannot save a poorly planned experiment (or observational study) does not, however, imply that statistical methods are not needed to interpret a properly planned experiment or study.

In the summary section of the first chapter, Bradford Hill removes any doubt about his view of the importance, and the necessity, of statistical methods:

“The statistical method is required in the interpretation of figures which are at the mercy of numerous influences, and its object is to determine whether individual influences can be isolated and their effects measured.”

Id. at 10 (emphasis added).

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Conflicts of Interest in Asbestos Studies – the Plaintiffs’ Double Standard

September 18th, 2013

Conflicts of interest disclosures have become the stuff of “criminal” accusations. In Weitz & Luxenberg P.C. v. Georgia–Pacific LLC, 2013 WL 2435565 (N.Y. App. Div., 1st Dep’t June 6, 2013), the court recited a defense expert witness’s failure to disclose his expert witness status in articles as part of a determination that a prima facie showing of “crime-fraud” had been made to justify the trial court’s in camera review of materials claimed to be protected from discovery under the attorney-client privilege:

“Nor did the articles reveal that Dr. Bernstein has been disclosed as a GP expert witness in NYCAL since 2009, that he had testified as a defense expert for Union Carbide Corporation in asbestos litigation, or that he had been paid by, and spoken on behalf of, the Chrysotile Institute, the lobbying arm of the Quebec chrysotile mining industry.”

Id. at *2. In “A Cautionary Tale on How Not to Sponsor a Scientific Study for Litigation,” I wrote about how the First Department of the New York Appellate Division went off the rails in considering the crime-fraud exception without first determining that the privilege applied in the first place. The appellate court’s reasoning as to why the trial court should look for an exception was equally vacuous. If failure to disclose consulting or testifying for attorneys is a “crime” or a “fraud,” then the playing field should be level and the indictment should apply to all sides.

Steve Markowitz is a physician with Queens College, City University of New York. Dr. Markowitz testifies for plaintiffs, both here in New York City, and abroad, in asbestos personal injury cases. See, e.g., Wannall v. Honeywell International Inc., 2013 WL 1966060 (D.D.C. May 14, 2013) (excluding Markowitz’ testimony as unreliable). So the plaintiffs’ bar, which would equate failure to disclose consulting with “crime” or “fraud,” should be on the alert that Dr. Markowitz does not disclose his consulting arrangements in publications that bear on the issues covered by his testimony.

I blogged previously about an in-press version of Markowitz’s publication of an update of the epidemiologic study of North American insulators. See “The Mt. Sinai Catechism” (June 7, 2013). The paper is now out in final form, although behind a paywall. Steven B. Markowitz, Steven M. Levin, Albert A. Miller, and Alfred Morabia, “Asbestos, asbestosis, smoking, and lung cancer. New findings from the North American insulator cohort,” 188 Am. J. Respir. Crit. Care Med. 90 (2013). What is publicly available, however, are the disclosure statements for each of the authors. Lo, and behold, Dr. Markowitz declared no consultations that could be a potential conflict of interest.

This is a remarkable double standard. Consulting for a defendant is a “crime,” if not disclosed, but plaintiffs’ testifying expert witnesses do not feel the need to disclose their consultancies at all. What is more remarkable, however, is that the authors of this article strained and stretched their data to try to save their synergy theory. Even the editorial that accompanied the article, while generally reciting the Mt. Sinai catechism, noted that the synergistic, multiplicative interaction was no longer so clear: “asbestos exposure and smoking together are associated with an at least additive increased risk. …” John R. Balmes, “Asbestos and Lung Cancer: What We Know,” 188 Am. J. Respir. Crit. Care Med. 8,9 (2013).

The only reason that I harp on conflicts is that the Third Edition of the Reference Manual on Scientific Evidence (2011) improvidently started down this road, as have several federal district and state court judges, including the judges who sat on the First Department panel, which decided Weitz & Luxenberg P.C. v. Georgia–Pacific LLC. I believe that the focus should be on the data and the analysis, not on the speaker. If the courts insist upon creating this toxic environment for scientists who “consult,” then the toxicity should be visited on all parties’ expert witnesses equally.

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