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

Apportionment and Pennsylvania’s Fair Share Act

March 14th, 2019

In 2011, Pennsylvania enacted the Fair Share Act, which was remedial legislation designed to mitigate the unfairness of joint and several liability in mass, and other, tort litigation by abrogating joint and several liability in favor of apportionment of shares among multiple defendants, including settled defendants.1

Although the statute stated the general rule in terms of negligence,2 the Act was clearly intended to apply to actions for so-called strict liability:3

“(1) Where recovery is allowed against more than one person, including actions for strict liability, and where liability is attributed to more than one defendant, each defendant shall be liable for that proportion of the total dollar amount awarded as damages in the ratio of the amount of that defendant’s liability to the amount of liability attributed to all defendants and other persons to whom liability is apportioned under subsection.”

The intended result of the legislation was for courts to enter separate and several judgments against defendants held liable in the amount apportioned to each defendant’s liability.4 The Act created exceptions for for intentional torts and for cases in which a defendant receives 60% or greater share in the apportionment.5

In Pennsylvania, as in other states, judges sometimes fall prey to the superstition that the law, procedural and substantive, does not apply to asbestos cases. Roverano v. John Crane, Inc., is an asbestos case in which the plaintiff claimed his lung cancer was caused by exposure to multiple defendants’ products. The trial judge, falling under the sway of asbestos exceptionalism, refused to apply Fair Share Act, suggesting that “the jury was not presented with evidence that would permit an apportionment to be made by it.”

The Roverano trial judge’s suggestion is remarkable, given that any plaintiff is exposed to different asbestos products in distinguishable amounts, and for distinguishable durations. Furthermore, asbestos products have distinguishable, relative levels of friability, with different levels of respirable fiber exposure for the plaintiff. In some cases, the products contain different kinds of asbestos minerals, which have distinguishable and relative levels of potency to cause the plaintiff’s specific disease. Asbestos cases, whether involving asbestosis, lung cancer, or mesothelioma claims, are more amenable to apportionment of shares among co-defendants than are “red car / blue car” cases.

Pennsylvania’s intermediate appellate court reversed the trial court’s asbestos exceptionalism, and held that upon remand, the court must:

“[a]pply a non-per capita allocation to negligent joint tortfeasors and strict liability joint tortfeasors; and permit evidence of settlements reached between plaintiffs and bankrupt entities to be included in the calculation of allocation of liability.”

Roverano v. John Crane, 2017 Pa. Super. 415, 177 A.3d 892 (2017).

The Superior Court’s decision did not sit well with the litigation industry, which likes joint and several liability, with equal shares. Joint and several liability permits plaintiffs’ counsel to extort large settlements from minor defendants who face the prospect of out-sized pro rata shares after trial, without the benefit of reductions for the shares of settled bankrupt defendants. The Roverano plaintiff appealed from the Superior Court’s straightforward application of a remedial statute.

What should be a per curiam affirmance of the Superior Court, however, could result in another act of asbestos exceptionalism by Pennsylvania Supreme Court. Media reports of the oral argument in Roverano suggest that several of the justices invoked the specter of “junk science” in apportioning shares among asbestos co-defendants.6 Disrespectfully, Justice Max Baer commented:

“Respectfully, your theory is interjecting junk science. We’ve never held that duration of contact corresponds with culpability.”7

The Pennsylvania Justices’ muddle can be easily avoided. First, the legislature clearly expressed its intention that apportionment be permitted in strict liability cases.

Second, failure-to-warn strict liability cases are, as virtually all scholars and most courts recognize, essentially negligence cases, in any event.8

Third, apportionment is a well-recognized procedure in the law of Torts, including the Pennsylvania law of torts. Apportionment of damages among various causes was recognized in the Restatement of Torts (Second) Section 433A (Apportionment of Harm to Causes), which specifies that:

(1) Damages for harm are to be apportioned among two or more causes where

(a) there are distinct harms, or

(b) there is a reasonable basis for determining the contribution of each cause to a single harm.

Restatement (Second) of Torts § 433A(1) (1965) [hereinafter cited as Section 433A].

The comments to Section 433A suggest a liberal application for apportionment. The rules set out in Section 433A apply “whenever two or more causes have combined to bring about harm to the plaintiff, and each has been a substantial factor in producing the harm … .”

Id., comment a. The independent causes may be tortious or innocent, “and it is immaterial whether all or any of such persons are joined as defendants in the particular action.” Id. Indeed, apportionment also applies when the defendant’s conduct combines “with the operation of a force of nature, or with a pre-existing condition which the defendant has not caused, to bring about the harm to the plaintiff.” Just as the law of grits applies in everyone’s kitchen, the law of apportionment applies in Pennsylvania courts.

Apportionment of damages is an accepted legal principle in Pennsylvania law. Martin v. Owens-Corning Fiberglas Corp., 515 Pa. 377, 528 A.2d 947 (1987). Courts, applying Pennsylvania law, have permitted juries to apportion damages between asbestos and cigarette smoking as causal factors in plaintiffs’ lung cancers, based upon a reasonable basis for determining the contribution of each source of harm to a single harm.9

In Parker, none of the experts assigned exact mathematical percentages to the probability that asbestos rather than smoking caused the lung cancer. The Court of Appeals noted that on the record before it:

“we cannot say that no reasonable basis existed for determining the contribution of cigarette smoking to the cancer suffered by the decedent.”10

The Pennsylvania Supreme Court has itself affirmed the proposition that “liability attaches to a negligent act only to the degree that the negligent act caused the employee’s injury.”11 Thus, even in straight-up negligence cases, causal apportionment must play in a role, even when the relative causal contributions are much harder to determine than in the quasi-quantitative setting of an asbestos exposure claim.

Let’s hope that Justice Baer and his colleagues read the statute and the case law before delivering judgment. The first word in the name of the legislation is Fair.

1 42 Pa.C.S.A. § 7102.

2 42 Pa.C.S.A. § 7102(a)

3 42 Pa.C.S.A. § 7102(a)(1) (emphasis added).

4 42 Pa.C.S.A. § 7102(a)(2).

5 42 Pa.C.S.A. § 7102 (a)(3)(ii), (iii).

7 Id. (quoting Baer, J.).

8 See, e.g, Restatement (Third) of Torts: Products Liability § 2, and comment I (1998); Fane v. Zimmer, Inc., 927 F.2d 124, 130 (2d Cir. 1991) (“Failure to warn claims purporting to sound in strict liability and those sounding in negligence are essentially the same.”).

9 Parker v. Bell Asbestos Mines, No. 86-1197, unpublished slip op. at 5 (3d Cir., Dec. 30, 1987) (per curiam) (citing Section 433A as Pennsylvania law, and Martin v. Owens-Corning Fiberglas Corp. , 515 Pa. 377, 528 A.2d 947, 949 (1987))

10 Id. at 7.

11 Dale v. Baltimore & Ohio RR., 520 Pa. 96, 106, 552 A.2d 1037, 1041 (1989). See also McAllister v. Pennsylvania RR., 324 Pa. 65, 69-70, 187 A. 415, 418 (1936) (holding that plaintiff’s impairment, and pain and suffering, can be apportioned between two tortious causes; plaintiff need not separate damages with exactitude); Shamey v. State Farm Mutual Auto. Ins. Co., 229 Pa. Super. 215, 223, 331 A.2d 498, 502 (1974) (citing, and relying upon, Section 433A; difficulties in proof do not constitute sufficient reason to hold a defendant liable for the damage inflicted by another person). Pennsylvania law is in accord with the law of other states as well, on apportionment. See Waterson v. General Motors Corp., 111 N.J. 238, 544 A.2d 357 (1988) (holding that a strict liability claim against General Motors for an unreasonably dangerous product defect was subject to apportionment for contribution from failing to wear a seat belt) (the jury’s right to apportion furthered the public policy of properly allocating the costs of accidents and injuries).

ASA Statement Goes to Court – Part 2

March 7th, 2019

It has been almost three years since the American Statistical Association (ASA) issued its statement on statistical significance. Ronald L. Wasserstein & Nicole A. Lazar, “The ASA’s Statement on p-Values: Context, Process, and Purpose,” 70 The American Statistician 129 (2016) [ASA Statement]. Before the ASA’s Statement, courts and lawyers from all sides routinely misunderstood, misstated, and misrepresented the meaning of statistical significance.1 These errors were pandemic despite the efforts of the Federal Judicial Center and the National Academies of Science to educate judges and lawyers, through their Reference Manuals on Scientific Evidence and seminars. The interesting question is whether the ASA’s Statement has improved, or will improve, the unfortunate situation.2

The ASA Statement on Testosterone

“Ye blind guides, who strain out a gnat and swallow a camel!”
Matthew 23:24

To capture the state of the art, or the state of correct and flawed interpretations of the ASA Statement, reviewing a recent but now resolved, large so-called mass tort may be illustrative. Pharmaceutical products liability cases almost always turn on evidence from pharmaco-epidemiologic studies that compare the rate of an outcome of interest among patients taking a particular medication with the rate among similar, untreated patients. These studies compare the observed with the expected rates, and invariably assess the differences as either a “risk ratio,” or a “risk difference,” for both the magnitude of the difference and for “significance probability” of observing a rate at least as large as seen in the exposed group, given the assumptions that that the medication did not change the rate and that the data followed a given probability distribution. In these alleged “health effects” cases, claims and counterclaims of misuse of significance probability have been pervasive. After the ASA Statement was released, some lawyers began to modify their arguments to suggest that their adversaries’ arguments offend the ASA’s pronouncements.

One litigation that showcases the use and misuse of the ASA Statement arose from claims that AbbVie, Inc.’s transdermal testosterone medication (TRT) causes heart attacks, strokes, and venous thromboembolism. The FDA had reviewed the plaintiffs’ claims, made in a Public Citizen complaint, and resoundingly rejected the causal interpretation of two dubious observational studies, and an incomplete meta-analysis that used an off-beat composite end point.3 The Public Citizen petition probably did succeed in pushing the FDA to convene an Advisory Committee meeting, which again resulted in a rejection of the causal claims. The FDA did, however, modify the class labeling for TRT with respect to indication and a possible association with cardiovascular outcomes. And then the litigation came.

Notwithstanding the FDA’s determination that a causal association had not been shown, thousands of plaintiffs sued several companies, with most of the complaints falling on AbbVie, Inc., which had the largest presence in the market. The ASA Statement came up occasionally in pre-trial depositions, but became a major brouhaha, when AbbVie moved to exclude plaintiffs’ causation expert witnesses.4

The Defense’s Anticipatory Parry of the ASA Statement

As AbbVie described the situation:

Plaintiffs’ experts uniformly seek to abrogate the established methods and standards for determining … causal factors in favor of precisely the kind of subjective judgments that Daubert was designed to avoid. Tests for statistical significance are characterized as ‘misleading’ and rejected [by plaintiffs’ expert witnesses] in favor of non-statistical ‘estimates’, ‘clinical judgment’, and ‘gestalt’ views of the evidence.”5

AbbVie’s brief in support of excluding plaintiffs’ expert witnesses barely mentioned the ASA Statement, but in a footnote, the defense anticipated the Plaintiffs’ opposition would be based on rejecting the importance of statistical significance testing and the claim that this rejection was somehow supported by the ASA Statement:

The statistical community is currently debating whether scientists who lack expertise in statistics misunderstand p-values and overvalue significance testing. [citing ASA Statement] The fact that there is a debate among professional statisticians on this narrow issue does not validate Dr. Gerstman’s [plaintiffs’ expert witness’s] rejection of the importance of statistical significance testing, or undermine Defendants’ reliance on accepted methods for determining association and causation.”6

In its brief in support of excluding causation opinions, the defense took pains to define statistical significance, and managed to do so, painfully, or at least in ways that the ASA conferees would have found objectionable:

Any association found must be tested for its statistical significance. Statistical significance testing measures the likelihood that the observed association could be due to chance variation among samples. Scientists evaluate whether an observed effect is due to chance using p-values and confidence intervals. The prevailing scientific convention requires that there be 95% probability that the observed association is not due to chance (expressed as a p-value < 0.05) before reporting a result as “statistically significant. * * * This process guards against reporting false positive results by setting a ceiling for the probability that the observed positive association could be due to chance alone, assuming that no association was actually present.7

AbbVie’s brief proceeded to characterize the confidence interval as a tool of significance testing, again in a way that misstates the mathematical meaning and importance of the interval:

The determination of statistical significance can be described equivalently in terms of the confidence interval calculated in connection with the association. A confidence interval indicates the level of uncertainty that exists around the measured value of the association (i.e., the OR or RR). A confidence interval defines the range of possible values for the actual OR or RR that are compatible with the sample data, at a specified confidence level, typically 95% under the prevailing scientific convention. Reference Manual, at 580 (Ex. 14) (“If a 95% confidence interval is specified, the range encompasses the results we would expect 95% of the time if samples for new studies were repeatedly drawn from the same population.”). * * * If the confidence interval crosses 1.0, this means there may be no difference between the treatment group and the control group, therefore the result is not considered statistically significant.”8

Perhaps AbbVie’s counsel should be permitted a plea in mitigation by having cited to, and quoted from, the Reference Manual on Scientific Evidence’s chapter on epidemiology, which was also wide of the mark in its description of the confidence interval. Counsel would have been better served by the Manual’s more rigorous and accurate chapter on statistics. Even so, the above-quoted statements give an inappropriate interpretation of random error as a probability about the hypothesis being tested.9 Particularly dangerous, in terms of failing to advance AbbVie’s own objectives, was the characterization of the confidence interval as measuring the level of uncertainty, as though there were no other sources of uncertainty other than random error in the measurement of the risk ratio.

The Plaintiffs’ Attack on Significance Testing

The Plaintiffs, of course, filed an opposition brief that characterized the defense position as an attempt to:

elevate statistical significance, as measured by confidence intervals and so-called p-values, to the status of an absolute requirement to the establishment of causation.”10

Tellingly, the plaintiffs’ brief fails to point to any modern-era example of a scientific determination of causation based upon epidemiologic evidence, in which the pertinent studies were not assessed for, and found to show, statistical significance.

After citing a few judicial opinions that underplayed the importance of statistical significance, the Plaintiffs’ opposition turned to the ASA Statement for what it perceived to be support for its loosey-goosey approach to causal inference.11 The Plaintiffs’ opposition brief quoted a series of propositions from the ASA Statement, without the ASA’s elaborations and elucidations, and without much in the way of explanation or commentary. At the very least, the Plaintiffs’ heavy reliance upon, despite their distortions of, the ASA Statement helped them to define key statistical concepts more carefully than had AbbVie in its opening brief.

The ASA Statement, however, was not immune from being misrepresented in the Plaintiffs’ opposition brief. Many of the quoted propositions were quite beside the points of the dispute over the validity and reliability of Plaintiffs’ expert witnesses’ conclusions of causation about testosterone and heart attacks, conclusions not reached or shared by the FDA, any consensus statement from medical organizations, or any serious published systematic review:

P-values do not measure the probability that the studied hypothesis is true, … .”12

This proposition from the ASA Statement is true, but trivially true. (Of course, this ASA principle is relevant to the many judicial decisions that have managed to misstate what p-values measure.) The above-quoted proposition follows from the definition and meaning of the p-value; only someone who did not understand significance probability would confuse it with the probability of the truth of the studied hypothesis. P-values’ not measuring the probability of the null hypothesis, or any alternative hypothesis, is not a flaw in p-values, but arguably their strength.

A p-value, or statistical significance, does not measure the size of an effect or the importance of a result.”13

Again, true, true, and immaterial. The existence of other importance metrics, such as the magnitude of an association or correlation, hardly detracts from the importance of assessing the random error in an observed statistic. The need to assess clinical or practical significance of an association or correlation also does not detract from the importance of the assessed random error in a measured statistic.

By itself, a p-value does not provide a good measure of evidence regarding a model or hypothesis.”14

The Plaintiffs’ opposition attempted to spin the above ASA statement as a criticism of p-values involves an elenchi ignoratio. Once again, the p-value assumes a probability model and a null hypothesis, and so it cannot provide a “measure” or the model or hypothesis’ probability.

The Plaintiffs’ final harrumph on the ASA Statement was their claim that the ASA Statement’s conclusion was “especially significant” to the testosterone litigation:

Good statistical practice, as an essential component of good scientific practice, emphasizes principles of good study design and conduct, a variety of numerical and graphical summaries of data, understanding of the phenomenon under study, interpretation of results in context, complete reporting and proper logical and quantitative understanding of what data summaries mean. No single index should substitute for scientific reasoning.”15

The existence of other important criteria in the evaluation and synthesis of a complex body of studies does not erase or supersede the importance of assessing stochastic error in the epidemiologic studies. Plaintiffs’ Opposition Brief asserted that the Defense had attempted to:

to substitute the single index, the p-value, for scientific reasoning in the reports of Plaintiffs’ experts should be rejected.”16

Some of the defense’s opening brief could indeed be read as reducing causal inference to the determination of statistical significance. A sympathetic reading of the entire AbbVie brief, however, shows that it had criticized the threats to validity in the observational epidemiologic studies, as well as some of the clinical trials, and other rampant flaws in the Plaintiffs’ expert witnesses’ reasoning. The Plaintiffs’ citations to the ASA Statement’s “negative” propositions about p-values (to emphasize what they are not) appeared to be the stuffing of a strawman, used to divert attention from other failings of their own claims and proffered analyses. In other words, the substance of the Rule 702 application had much more to do with data quality and study validity than statistical significance.

What did the trial court make of this back and forth about statistical significance and the ASA Statement? For the most part, the trial court denied both sides’ challenges to proffered expert witness testimony on causation and statistical issues. In sorting the controversy over the ASA Statement, the trial court apparently misunderstood key statistical concepts and paid little attention to the threats to validity other than random variability in study results.17 The trial court summarized the controversy as follows:

In arguing that the scientific literature does not support a finding that TRT is associated with the alleged injuries, AbbVie emphasize [sic] the importance of considering the statistical significance of study results. Though experts for both AbbVie and plaintiffs agree that statistical significance is a widely accepted concept in the field of statistics and that there is a conventional method for determining the statistical significance of a study’s findings, the parties and their experts disagree about the conclusions one may permissibly draw from a study result that is deemed to possess or lack statistical significance according to conventional methods of making that determination.”18

Of course, there was never a controversy presented to the court about drawing a conclusion from “a study.” By the time the briefs were filed, both sides had multiple observational studies, clinical trials, and meta-analyses to synthesize into opinions for or against causal claims.

Ironically, AbbVie might claim to have prevailed in having the trial court adopt its misleading definitions of p-values and confidence intervals:

Statisticians test for statistical significance to determine the likelihood that a study’s findings are due to chance. *** According to conventional statistical practice, such a result *** would be considered statistically significant if there is a 95% probability, also expressed as a “p-value” of <0.05, that the observed association is not the product of chance. If, however, the p-value were greater than 0.05, the observed association would not be regarded as statistically significant, according to prevailing conventions, because there is a greater than 5% probability that the association observed was the result of chance.”19

The MDL court similarly appeared to accept AbbVie’s dubious description of the confidence interval:

A confidence interval consists of a range of values. For a 95% confidence interval, one would expect future studies sampling the same population to produce values within the range 95% of the time. So if the confidence interval ranged from 1.2 to 3.0, the association would be considered statistically significant, because one would expect, with 95% confidence, that future studies would report a ratio above 1.0 – indeed, above 1.2.”20

The court’s opinion clearly evidences the danger in stating the importance of statistical significance without placing equal emphasis on the need to exclude bias and confounding. Having found an observational study and one meta-analysis of clinical trial safety outcomes that were statistically significant, the trial court held that any dispute over the probativeness of the studies was for the jury to assess.

Some but not all of AbbVie’s brief might have encouraged this lax attitude by failing to emphasize study validity at the same time as emphasizing the importance of statistical significance. In any event, trial court continued with its précis of the plaintiffs’ argument that:

a study reporting a confidence interval ranging from 0.9 to 3.5, for example, should certainly not be understood as evidence that there is no association and may actually be understood as evidence in favor of an association, when considered in light of other evidence. Thus, according to plaintiffs’ experts, even studies that do not show a statistically significant association between TRT and the alleged injuries may plausibly bolster their opinions that TRT is capable of causing such injuries.”21

Of course, a single study that reported a risk ratio greater than 1.0, with a confidence interval 0.9 to 3.5 might be reasonably incorporated into a meta-analysis that in turn could support, or not support a causal inference. In the TRT litigation, however, the well-conducted, most up-to-date meta-analyses did not report statistically significant elevated rates of cardiovascular events among users of TRT. The court’s insistence that a study with a confidence interval 0.9 to 3.5 cannot be interpreted as evidence of no association is, of course, correct. Equally correct would be to say that the interval shows that the study failed to show an association. The trial court never grappled with the reality that the best conducted meta-analyses failed to show statistically significant increases in the rates of cardiovascular events.

The American Statistical Association and its members would likely have been deeply disappointed by how both parties used the ASA Statement for their litigation objectives. AbbVie’s suggestion that the ASA Statement reflects a debate about “whether scientists who lack expertise in statistics misunderstand p-values and overvalue significance testing” would appear to have no support in the Statement itself or any other commentary to come out of the meeting leading up to the Statement. The Plaintiffs’ argument that p-values properly understood are unimportant and misleading similarly finds no support in the ASA Statement. Conveniently, the Plaintiffs’ brief ignored the Statement’s insistence upon transparency in pre-specification of analyses and outcomes, and in handling of multiple comparisons:

P-values and related analyses should not be reported selectively. Conducting multiple analyses of the data and reporting only those with certain p-values (typically those passing a significance threshold) renders the reported p-values essentially uninterpretable. Cherrypicking promising findings, also known by such terms as data dredging, significance chasing, significance questing, selective inference, and ‘p-hacking’, leads to a spurious excess of statistically significant results in the published literature and should be vigorously avoided.”22

Most if not all of the plaintiffs’ expert witnesses’ reliance materials would have been eliminated under this principle set forth by the ASA Statement.

1 See, e.g., In re Ephedra Prods. Liab. Litig., 393 F.Supp. 2d 181, 191 (S.D.N.Y. 2005). See alsoConfidence in Intervals and Diffidence in the Courts” (March 4, 2012); “Scientific illiteracy among the judiciary” (Feb. 29, 2012).

3Letter of Janet Woodcock, Director of FDA’s Center for Drug Evaluation and Research, to Sidney Wolfe, Director of Public Citizen’s Health Research Group (July 16, 2014) (denying citizen petition for “black box” warning).

4 Defendants’ (AbbVie, Inc.’s) Motion to Exclude Plaintiffs Expert Testimony on the Issue of Causation, and for Summary Judgment, and Memorandum of Law in Support, Case No. 1:14-CV-01748, MDL 2545, Document #: 1753, 2017 WL 1104501 (N.D. Ill. Feb. 20, 2017) [AbbVie Brief].

5 AbbVie Brief at 3; see also id. at 7-8 (“Depending upon the expert, even the basic tests of statistical significance are simply ignored, dismissed as misleading… .”) AbbVie’s definitions of statistical significance occasionally wandered off track and into the transposition fallacy, but generally its point was understandable.

6 AbbVie Brief at 63 n.16 (emphasis in original).

7 AbbVie Brief at 13 (emphasis in original).

8 AbbVie Brief at 13-14 (emphasis in original).

9 The defense brief further emphasized statistical significance almost as though it were a sufficient basis for inferring causality from observational studies: “Regardless of this debate, courts have routinely found the traditional epidemiological method—including bedrock principles of significance testing—to be the most reliable and accepted way to establish general causation. See, e.g., In re Zoloft, 26 F. Supp. 3d 449, 455; see also Rosen v. Ciba-Geigy Corp., 78 F.3d 316, 319 (7th Cir. 1996) (“The law lags science; it does not lead it.”). AbbVie Brief at 63-64 & n.16. The defense’s language about “including bedrock principles of significance testing” absolves it of having totally ignored other necessary considerations, but still the defense might have advantageously pointed out at the other needed considerations for causal inference at the same time.

10 Plaintiffs’ Steering Committee’ Memorandum of Law in Opposition to Motion of AbbVie Defendants to Exclude Plaintiffs’ Expert Testimony on the Issue of Causation, and for Summary Judgment at p.34, Case No. 1:14-CV-01748, MDL 2545, Document No. 1753 (N.D. Ill. Mar. 23, 2017) [Opp. Brief].

11 Id. at 35 (appending the ASA Statement and the commentary of more than two dozen interested commentators).

12 Id. at 38 (quoting from the ASA Statement at 131).

13 Id. at 38 (quoting from the ASA Statement at 132).

14 Id. at 38 (quoting from the ASA Statement at 132).

15 Id. at 38 (quoting from the ASA Statement at 132).

16 Id. at 38

17  In re Testosterone Replacement Therapy Prods. Liab. Litig., MDL No. 2545, C.M.O. No. 46, 2017 WL 1833173 (N.D. Ill. May 8, 2017) [In re TRT]

18 In re TRT at *4.

19 In re TRT at *4.

20 Id.

21 Id. at *4.

22 ASA Statement at 131-32.

Link-a-lot, right and left

March 1st, 2019

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

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

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

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

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

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

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

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


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

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

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

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

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

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

Leukemia: 16 observed; 17 expected

SIR = 0.95 (95% C.I., 0.54 – 1.54)

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

Leukemia: 18 observed, 22 expected

SIR = 0.81 (95% C.I., 0.48 – 1.29)

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

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

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

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

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

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

History of Silica Litigation – the Lung Cancer Angle

February 3rd, 2019

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

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

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

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

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

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

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

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

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

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

The data demonstrate a lack of association between lung cancer and exposure to crystalline silica in human studies. Furthermore, silica is not directly genotoxic and has been to be a pulmonary carcinogen in only one animal species, the rat, which seems to be an inappropriate carcinogenesis in humans.”6

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


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

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

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

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

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

6 Patrick A. Hessel, John F. Gamble, J. Bernard L. Gee, Graham Gibbs, Francis H. Y. Green, W. Keith C. Morgan, and Brooke T. Mossman, “Silica, Silicosis, and Lung Cancer: A Response to a Recent Working Group Report,” 42 J. Occup. & Envt’l Med. 704, 718 (2000).

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

Arthur J. Vorwald (1938)

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

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

Sir Ernest Laurence Kennaway & Nina Marion Kennaway (1947)

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

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

Madge Thurlow Macklin (1948)

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

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

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

Alexander Thom Doig (1949)

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

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

Wilhelm Hueper (1951)

“Since silicotic pneumoconiosis is characterized by a chronic granulomatous inflammatory reaction, and thus seems to fulfill remarkably well the basic requirements of the chronic irritation theory of cancerigenesis, several investigators have incriminated this frequent type of occupational pneumoconiosis in the development of cancer of the lung (Fine & Jaso; Anderson & Dible; Charr; Klotz; Dible). There are in fact some 50 cases on record in which cancer of the lung or larynx and silicosis were co-existing (Dible; Fine & Jaso; Klotz & Simpson; Maxwell; Sladden; Middleton; Sweany, Porsche & Douglass; Vorwald & Karr; Allen; Sokoloff; Pancoast & Pendergrass; Simmons; Schnurer; Charr; Harris). However, the great majority of investigators have come to the conclusion that there does not exist any causal relation between silicosis and pulmonary or laryngeal malignancy (Vorwald & Karr; Allen; Feil; Harris; Pancoast & Pendergrass; Saupe; Schulte; Schulz; Berblinger). Schulte and Schultz noted that coal miners in the Ruhr district, among whom silicosis is frequent, have no unusual frequency of lung cancer, while Allen recorded a similar observation for the coal miners of Pennsylvania. Corresponding negative observations were made by Vorwald and Karr on individuals who came to necropsy with silicosis at the Saranac Laboratory and have been reported by the Miner’s Phthisis Medical Bureau of South Africa based on studies made among the South African gold miners in the Johannesburg district.”

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

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

Maxcy (1951)

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

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

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

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

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

Behrens (1953)

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

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

Wilhelm Hueper (1954)

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

* * *

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

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

Wilhlem Hueper (1955)

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

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

Cuyler Hammond (1956)

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

* * *

Studies by Vorwald (41) and others agree in the conclusion that pneumoconiosis in general, and silicosis in particular, do not involve any predisposition of lung cancer.” (p. 50)

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

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

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

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

Wilhelm Hueper (1956)

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

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

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

Id. at 44-45.

Sir Richard Doll (1959)

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

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

Gerret Schepers (1960)

Lung cancer, of course, occurs in silicotics and is on the increase. Thus far, however, statistical studies have failed to reveal a relatively enhanced incidence of pulmonary neoplasia in silicotic subjects.”

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

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

(Id. at 467, ¶5)

Herbert Spencer (1962)

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

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

Joseph K. Wagoner (1963)

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

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

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

Id. at 288 (emphasis added)

Joseph K. Wagner (1965)

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

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

Sir Richard Doll (1966)

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

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

Wilhelm Hueper (1966)

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

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

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

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

* * * *

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

* * * *

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

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

Harriet L. Hardy (1967)

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

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

W. Raymond Parkes (1974)

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

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

NIOSH (1974)

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

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

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

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

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

Herbert Spencer (1977)

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

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

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

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

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


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

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

Raymond Parkes (1982)

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

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

William Rom (1983)

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

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

Herbert Anderson (1985)

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

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

Alfred Gordon Heppleston (1985)

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

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

Herbert Spencer (1985)

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

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

United States Surgeon General (1985)

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

Summary & Conclusions

* *


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

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

(1985 Surg. Gen. Report at 348)

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

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

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

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

William Weiss (1986)

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

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

IARC (1987)

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

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

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

IARC concluded that:

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

(42 IARC at 111, § 4.4)

John E. Cotes & COTES (1987)

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

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

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

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

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

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

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

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

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


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

(NIOSH Silicosis and Silicate Disease Committee, “Diseases Associated With Exposure to Silica and Nonfibrous Silicate Minerals,” 112 Arch. Path. & Lab. Med. 673, 711b, ¶ 2 (1988)) [cited as 1988 NIOSH]

Arthur Frank (1989)

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

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


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

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

Corbett McDonald (1989)

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

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

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

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

Hans Weill, Robert N. Jones, and Raymond Parkes (1994)

It may be reasonably concluded that the evidence to date that occupational exposure to silica results in excess lung cancer risk is not yet persuasive.

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

HUNTER (1994)

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

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

Eva Hnizdo (1994)

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

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

The opinions, statements, and asseverations expressed on Tortini are my own, or those of invited guests, and these writings do not necessarily represent the views of clients, friends, or family, even when supported by good and sufficient reason.