Mass Tort Defense : Mass Tort Defense Lawyer & Attorney : Sean P. Wajert : Dechert Law Firm : Products Liability, Class Actions, Pharmaceutical Litigation

The Vermont Supreme Court recently held that a plaintiff's evidence that exposure to benzene allegedly caused his cancer was insufficient to get to the jury.  Blanchard v. Goodyear Tire & Rubber Co.,  No. 2010-250 (Vt. 8/5/11).

Plaintiff was diagnosed with non-Hodgkin's lymphoma, and he attributed the onset of the disease to benzene exposure that allegedly occurred between 1968 and 1973 while he was a teenager playing on a ball field on the grounds of the former Goodyear rubber manufacturing plant. That  plant operated in Windsor, Vermont from 1936 to 1986. He sued, alleging that the field itself was polluted and that there was a gully in the outfield that transported foul-smelling and oily stormwater discharge away from the manufacturing plant.

Defendants moved for summary judgment. The lower court concluded that plaintiff was not entitled to present his case to a jury because he had provided insufficient evidence to support an inference that he had been exposed to benzene in any amount, let alone an amount that could have caused his illness, nor sufficient expert testimony sufficient to eliminate other potential causes of his disease. On appeal, plaintiff argued that his circumstantial evidence of causation was sufficient to present his case to the jury.

The state Supreme Court noted that the plaintiff could not survive the motion for summary judgment on his toxic tort claim unless he was able to point to evidence suggesting a probability, rather than a mere possibility, that (1) he was exposed to the specified chemical at a level that could have caused his physical condition (general causation); and (2) the exposure to that chemical did in fact result in the condition (specific causation).  In a toxic tort case, general causation addresses whether a substance is capable of causing a particular injury or condition in a population, while specific causation addresses whether a substance caused a particular individual's alleged injury. E.g., King v. Burlington Northern Santa Fe Ry. Co., 762 N.W.2d 24, 34 (Neb. 2009). General causation is typically shown through epidemiological studies, and plaintiffs in toxic exposure cases in Vermont generally must demonstrate specific causation by submitting evidence concerning the amount, duration, intensity, and frequency of exposure. Citing  Henricksen v. ConocoPhillips Co., 605 F. Supp. 2d 1142, 1157 (E.D. Wash. 2009) (citing several appellate court cases holding that experts testifying as to specific causation must pay careful attention to amount, intensity, and duration of exposure).

The court recognized that in some toxic tort cases it is impossible to quantify exposure with hard proof, such as the presence of the alleged toxic substance in the plaintiff's blood or tissue and the precise amount of the toxic substance to which an individual plaintiff was exposed. Plourde v. Gladstone, 190 F. Supp. 2d 708, 721 (D. Vt. 2002).  Therefore, expert testimony on toxic injuries may be admissible where dosage or exposure levels have been established through sufficient reliable circumstantial evidence. While it is not always necessary for a plaintiff to quantify exposure levels precisely, the courts generally preclude experts from testifying as to specific causation without having any some measurement or reasonable estimate of a  plaintiff's exposure to the allegedly harmful substance. Finally, a defendant's concession that its product contains a carcinogen, say benzene, does not excuse a plaintiff from having to show the benzene contained in defendant's product is capable of causing the illness at issue.

When direct evidence of the precise amount of exposure to a toxic substance is limited, some courts have allowed expert witnesses to use a differential diagnosis process as a method of proving specific causation. We have posted before about the mis-use and mischaracterization of this process.  Differential diagnosis is a scientific analysis entailing the weighing of relevant evidence, listing all likely explanations of the patient's observed symptoms or injury, then eliminating all but one.  Some courts have made the leap from allowing the process designed to arrive at a diagnosis (what disease caused the symptoms) to arrive at a cause (what substance caused the disease). However, said the state court, even the courts that do recognize differential diagnosis are reluctant to admit causation testimony based on a differential diagnosis where the proffered expert possesses only weak circumstantial evidence that some exposure occurred and makes insufficient effort to scientifically evaluate or estimate the degree of exposure or dosage. Also, and significantly, standing alone, the presence of a known risk factor is not a sufficient basis for ruling out idiopathic origin in a particular case, particularly where most cases of the disease have no known cause. In such cases, analysis beyond a differential diagnosis is required.

Here, plaintiff pointed to three bits of circumstantial evidence. First, he offered statements made by himself and boyhood friends concerning their alleged exposure to chemicals from the Goodyear plant when they were teenagers playing ball on a field adjoining the plant.  Second, plaintiff relied on the testimony of the project manager for an environmental firm hired by Goodyear in 2007 to conduct a site investigation in response to a clean-up agreement reached by Goodyear and the State of Vermont. The 2009 report stemming from the investigation listed contaminants of concern, including petroleum products containing benzene, that could have been released into the environment. Third, plaintiff relies upon the testimony of his two experts, who testified that occupational exposure to benzene is generally associated with a risk of non-Hodgkin's lymphoma, and that plaintiff's cancer was not caused by an immunodeficiency disorder, one of the known causes of that form of cancer.

That evidence "falls well short" of what plaintiff would be required to show in order to prevail in a jury trial. Indeed, if a jury were to find in favor of plaintiff on the evidence relied upon by plaintiff, said the court, "we would have to overturn the verdict." In the end, plaintiff's suspicion that his cancer was caused by exposure to benzene on the Goodyear ball field when he was a teenager was purely speculative. There was no way to know whether any benzene-containing product actually contaminated the ball field.  And there was no evidence indicating the amount or concentration of benzene that was present, even assuming some was. Nor was there any evidence indicating plaintiff's level of exposure to any benzene that may have been present on the field. Nor was plaintiff able to point to studies indicating a risk of cancer posed by exposure to limited amounts of benzene from petroleum products in an outside environment.  

Further, plaintiff could not rely upon differential diagnosis to overcome the complete lack of evidence as to the level of any exposure to benzene. A large percentage of cases of plaintiff's type of lymphoma are of unknown origin. Thus plaintiff's experts could not rule out all other causes, an essential part of the differential diagnosis.  E.g., Whiting v. Boston Edison Co., 891 F. Supp. 12, 21 n.41 (D. Mass. 1995) (concluding that differential diagnosis cannot be used to explain disease where 90% of cases of disease are of unknown origin).
 

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The Third Circuit last week affirmed the exclusion of expert testimony in a toxic tort suit in which plaintiff alleged defendants' insecticide products gave him non-Hodgkin's lymphoma. Pritchard v. Dow AgroSciences, et al., No.10-2168 (3d Cir. 2011).

Plaintiff claimed that he contracted cancer from a pesticide produced by defendant Dow AgroSciences. His wife claimed to have suffered derivative injuries. In support of their complaint, the Pritchards solicited the expert testimony of Dr. Bennet I. Omalu, who provided the District Court with a report and, later, a declaration, stating that Dursban caused the cancer.  Although the trial court found Dr. Omalu to be a qualified expert, it ruled (on Dow's motion) that his proposed testimony was unreliable and therefore inadmissible at trial under Daubert v. Merrell Dow Pharmaceuticals, 509 U.S. 579 (1993). The exclusion of Dr. Omalu's testimony doomed the lawsuit, because plaintiffs had no other evidence of causation.  Plaintiffs appealed.

The appeal tried to raise the issues surrounding the intersection of federal law, rules of evidence underlying Daubert, and state law, which supplies the elements of a claim (including causation) in a diversity case. Plaintiffs argued that in the course of finding that Dr. Omalu's testimony was unreliable, the District Court erroneously relied on principles that were supposedly at odds with state (Pennsylvania) substantive law governing the level of certainty required to establish causation, having to do with idiopathic disease and epidemiological studies.

It is true that the trial court noted that Dr. Omalu did not rule out unknown or idiopathic causes; that the court considered the fact that the epidemiological study on which the doctor wished to rely showed only a relative risk of 2.0; and that the court observed that the proposed testimony was not grounded in science as Dr. Omalu has not presented any statistically significant evidence showing an association between the chemical agent at issue and non-Hodgkins lymphoma. See Pritchard v. Dow Agro Sciences, 705 F. Supp. 2d 471, 492, 486, 493 (W.D. Pa. 2010).

However, the trial court considered these factors among “a host of other deficiencies,” as components of a determination that the proffered testimony failed to satisfy the admissibility standard. The trial court did not adopt any bright-line rules, but instead evaluated the plaintiffs' proffer using a flexible approach as directed by the Court of Appeals in Heller v. Shaw Industries, 167 F.3d 146 (3d Cir. 1999).  This was an evidentiary ruling, separate and distinct from any substantive question regarding causation (which the court never had reason to reach).

Plaintiffs also argued that the court had engaged in some kind of improper balancing of plaintiffs' scientific evidence vs. defendants'. But the district court engaged in no such balancing. Instead, it rightly concluded that Dr. Omalu's proposed testimony was unreliable due to numerous cracks in its scientific foundation.  He cited only one specific study in support of his general causation conclusion that Dursban causes cancer — and in fact, he relied not on the study itself but on his own reinterpretation of the study's findings using a lower confidence interval. (That is, he recalculated the study's conclusions so as to serve plaintiff's litigation needs, said the court.)   Moreover, the plaintiffs offered no clear explanation of the methods through which he recalculated the study's results, leaving the court unable to evaluate the reliability of his methodology.

And the expert's specific causation conclusion that Dursban had caused Mr. Pritchard's illness was not supported by evidence in the medical records, discovery responses, deposition testimony, application records, or any other information regarding Mr. Pritchard's exposure to pesticides.  Significantly, Dr. Omalu also failed to adequately address possible alternative causes of the cancer.

Accordingly, the trial committed no error in excluding the expert testimony, and in the absence of proof of causation, the case was properly dismissed. Affirmed.

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A West Virginia federal court has granted summary judgment against a plaintiff alleging that the heartburn drug metoclopramide caused her tardive dyskinesia.  Meade v. Parsley, et al., 2010 WL 4909435 (S.D.W.Va.,  11/24/10).

Since its approval by the Food and Drug Administration in 1980, metoclopramide has been widely used to treat gastroesophageal reflux disease (“GRD”), nausea, and gastroparesis.  Plaintiff's treater, Dr. Deidre Parsley, prescribed metoclopramide to Mrs. Meade in order to treat her
GRD, nausea, and loss of appetite. Plaintiff  never read any written materials accompanying her metoclopramide prescriptions, which included a statement that therapy longer than 12 weeks has not been evaluated and cannot be recommended.  Dr. Parsley likewise did not read the metoclopramide package insert or any other written materials produced by PLIVA before prescribing the drug to Mrs. Meade. After the drug usage, the FDA added a black box warning about tardive dyskinesia.  But, save for the placement of the warning in a black box, the previous warning seemed not too different.

Plaintiffs contended that the warnings were inadequate in that they misleadingly invited long term use that has never been approved by the FDA, despite the fact that the warning did state that therapy longer than 12 weeks has not been evaluated and cannot be recommended. In addition,
plaintiffs claim that the warnings downplayed the seriousness and potential irreversibility of the risk of tardive dyskinesia in long term use, but the warning did state that the risk is highest among the elderly, especially elderly women (like this plaintiff), and that the likelihood of irreversibility is believed to increase with the duration of treatment and the total cumulative dose. 

Defendant moved for summary judgment, contending that there were no genuine issues of material fact inasmuch as (1) plaintiffs could not establish causation; (2) Dr. Parsley was aware of the risks of using metoclopramide when she prescribed the drug to Mrs. Meade; (3) PLIVA satisfied any alleged duty to warn by providing a package insert explaining potential side effects of
metoclopramide.  The court never had to reach the third argument.

In a pharmaceutical products liability action, a plaintiff must initially establish both general and specific causation for his injuries. Bourne ex rel. Bourne v. E.I. Dupont de Nemours & Co., 189 F. Supp. 2d 482, 485 (S.D. W. Va. 2002).  General causation is whether a substance is capable of causing a particular injury or condition in the general population, while specific causation is whether a substance caused a particular individual's injury. In re Rezulin Prods. Liab. Litig., 369 F.
Supp. 2d 398, 402 (S.D.N.Y. 2005); In re Hanford Nuclear Reservation Litig., 292 F.3d 1124, 1129 (9th Cir. 2002). General causation is established by demonstrating, often through a review of scientific and medical literature, that exposure to a substance can cause a particular disease.

In addition to general and specific causation, plaintiffs must establish proximate causation.To
show proximate causation in a failure-to-warn case based on an allegedly inadequate drug label, a plaintiff must show that a different label or warning would have avoided the plaintiff’s injuries. The court noted that the West Virginia Supreme Court has not had occasion to clarify whether a drug manufacturer must warn both the patient and the physician, or just the patient.  But it did not need to resolve this issue in evaluating proximate causation, however, because the undisputed evidence shows that an adequate warning would not have changed either Mrs. Meade’s or Dr. Parsley’s behavior in a manner which would have avoided Mrs. Meade’s injury.  Rather than merely showing that “adequate warnings would have changed behavior,”  as plaintiff argued, plaintiffs must
establish that an adequate warning would have changed behavior in a manner which would have avoided the plaintiff’s injury.  Mrs. Meade testified that she never read the package insert or any other documents accompanying her metoclopramide prescription.  Dr. Parsley likewise testified that she did not read the metoclopramide warning. And while Dr. Parsley did read the PDR for
the brand name version of the drug, it is undisputed that the defendant did not create that PDR.

The more interesting part of the opinion for our readers is the treatment of the issue of general causation.  It seems that none of plaintiffs’ retained experts offered any opinions regarding general
causation. So plaintiffs were left to argue that several of Mrs. Meade’s treating physicians (whom plaintiffs began referring to as “non-retained experts”) testified regarding the causal link between metoclopramide and tardive dyskinesia. None of these non-retained experts provided written
reports, and in deposition none of these physicians testified directly as to general causation. They assumed causation as a prelude to a specific causation opinion, but this mere assumption does not establish general causation. The law is clear that a mere possibility of causation and, more
specifically, indeterminate expert testimony on causation that is based solely on possibility is not sufficient to allow a reasonable juror to find causation. 

As an alternative basis for general causation, plaintiffs tried to rely on the fact that defendant's own package inserts and brand name warnings refer to a "causal link” between metoclopramide and tardive dyskinesia. Plaintiffs could cite no authority for the proposition that a plaintiff in a pharmaceutical products liability case can satisfy his or her burden of proving general causation by relying on the defendant manufacturer’s drug label warnings. Moreover, this contention was undermined by the general principle that causation evidence in toxic tort cases must be in the form of expert scientific testimony.  PLIVA’s drug label, which merely warns of metoclopramide’s potential side-effects without explaining the scientific basis for the warning, was no substitute for expert testimony that establishes causation in terms of reasonable probability.

Third, plaintiffs also tried to cite, as evidence of general causation, the subsequent FDA directive requiring drug manufacturers to insert a black box warning on metoclopramide labels to convey a
greater risk of tardive dyskinesia. The court, as have several other courts have, however, rejected reliance on agency determinations as a basis for general causation. Inasmuch as the cost-benefit balancing employed by the FDA differs from the threshold standard for establishing causation in tort actions, this court likewise concluded that the FDA-mandated tardive dyskinesia warning cannot establish general causation.

 Summary judgment granted.

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A federal court last week dismissed consolidated toxic tort suits brought against Alcoa Inc. and other defendants brought by employees of Lockheed Martin Corp. who claimed they were exposed to beryllium used in the manufacture of airplanes. Neal Parker et al. v. Brush Wellman Inc. et al., No. 04-cv-606; Timothy Berube et al. v. Brush Wellman Inc. et al., No. 08-cv-2725(N.D. Ga. 9/17/10).

The dozen plaintiffs in the cases were current or former employees of Lockheed Martin Corp.at its Marietta, Georgia plant site; plaintiffs alleged they had a variety of job responsibilities, time periods of employment, and work areas at the Lockheed facility. Lockheed’s Marietta Facility was purchased by the U.S. Government in 1942 and is leased and operated by Lockheed. Since 1952, Lockheed has produced the beryllium-containing C-130 Hercules airlifter, the C-5 Galaxy, the C-141 Starlifter, and the F/A-22 Raptor Air Dominance Fighter at its Marietta location. Each defendant was alleged to have manufactured component parts for Lockheed using copper-beryllium or aluminum-beryllium alloys.  Plaintiffs alleged that defendants failed to provide Lockheed with sufficient and accurate warnings pertaining to the beryllium contained in the manufactured products. Specifically, plaintiffs asserted a failure to warn claim, arguing that the warning materials that the defendants provided did not adequately communicate the health risks associated with the use of beryllium nor did they describe the methods that would reduce such risks.

Defendants filed a Daubert motion to exclude the testimony of Dr. John Martyny, plaintiffs' causation expert, and a companion motion for summary judgment. The Court ordered a Daubert hearing to clarify the evidentiary and factual background for the expert witness’s opinion and an evidentiary hearing regarding the motions to compel and summary judgment.

Since beryllium is generally recognized in the medical community as being able to cause the type of harm plaintiffs alleged –beryllium-related sickness– the Daubert analysis here focused on specific or individual causation to the plaintiffs, the plaintiff-specific questions: was plaintiff exposed to the toxin, was plaintiff exposed to enough of the toxin to cause the alleged injury, and did the toxin in fact cause the injury? The Eleventh Circuit has recognized that in order to carry
this causation burden in a toxic tort case, a plaintiff must demonstrate the levels of exposure that are hazardous to human beings as well as the plaintiff’s actual level of exposure to the defendant’s toxic substances before he or she may recover.

Here, the link between the expert’s opinion and the dose relationship was a key element of the analysis. Indeed, the hallmark of the science of toxic torts is the dose-response  relationship.  Exposure is only the opportunity for contact. Dose is what enters the body. While Dr. Marytny indicated, based on his experience and anecdotal evidence, that plaintiffs may have been exposed to beryllium at the plant, he did not indicate the level, frequency, duration or particle size of this exposure which would indicate the dose from these defendants’ products.  Importantly, Dr. Marytny did not produce any evidence that even a low-dose exposure resulted from defendants’ products. In fact, Dr. Martyny admitted that he could not opine as to the individual product or products that were the source of the alleged exposure.

Secondly, Dr. Martyny’s theory had not been appropriately tested.  The company itself did some sampling, and every air sample indicated that airborne beryllium concentrations were below the analytical reporting limit (<0.001 μg/sample) and thus also less than the OSHA PEL for beryllium.  Theoretically, defendants’ products could have been placed in an environmental chamber and the various machining procedures could have been reenacted to determine the particle production and size. While clearly this would not be as conclusive as personal sampling data for each plaintiff, this evidence would at least minimally indicate that bio-available beryllium from defendants’ products was possible, said the court.  But plaintiffs did no such testing.  Furthermore, no published studies documented levels of beryllium released by workers working with beryllium-aluminum in the aircraft industry.

Without such data, the expert's opinion merely assumed that plaintiffs’ injuries must have been caused by defendants’ products because the defendants produced  beryllium parts which were sold to Lockheed. However, nothing in his opinion linked these products to the alleged exposure of the plaintiffs nor ruled out other manufacturers’ products that were also present at the Marietta facility. 

Thus, the expert's opinion was excluded, and absent a reliable causation opinion, summary judgment was also appropriate.

The court the offered an alternative basis for the summary judgment on the failure to warn claim -- the sophisticated user doctrine. If a sophisticated user’s employees have knowledge that a particular risk of harm exists and yet allow the harm to occur, this knowledge may bar other employees’ claims against the product manufacturer. The supervising employees’ knowledge –the knowledge of the sophisticated user– can bar other employee’s claims against the product manufacturer. And the user’s knowledge does not need to encompass the precise, physical nature of the hazard presented by his use of the product; it is sufficient if he is aware generally that the use being made of the product is dangerous.

Here, Lockheed was a sophisticated user of beryllium alloys. Lockheed, as a part of the beryllium
industry, had as much access to information regarding beryllium safety as anyone else. For more than forty years, Lockheed  used the Department of Defense’s “Handbook for Metallic Materials and Elements for Aerospace Vehicle Structures” which provides guidelines for proper beryllium use. Lockheed issued its own “Safety and Industrial Hygiene Standard" which recognized that beryllium dust and vapors can cause respiratory problems. Lockheed recognized that it should order “medical monitoring” for those within the exposed worker population. The record made clear that the employer was a sophisticated user; summary judgment was appropriate on this basis as well.

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The Sixth Circuit last week vacated one of the rare plaintiff verdicts in the welding rod litigation.  Tamraz  v. Lincoln Electric Co., et al., 2010 WL  3489002 (6th Cir. 9/8/10).  The key issue in the appeal was the trial court's decision to allow a causation expert, Dr. Walter Carlini, to testify on behalf of the plaintiff Jeff Tamraz over defendants' Daubert challenge.

From roughly 1979 to 2004, Jeff Tamraz worked as an independent-contracting welder in California, on bridges and buildings.  Plaintiffs contended that Mr. Tamraz suffers from manganese-induced Parkinsonism as a result of exposure to manganese-containing welding fumes on these jobs.

The case went to trial in 2007, and the jury in the Northern District of Ohio (plaintiffs are from Oregon) returned a plaintiff verdict, awarding $17.5 million to Jeff Tamraz in compensatory damages and $3 million to his wife, Terry Tamraz, for loss of consortium.

Defendants, including Lincoln Electric, Hobart Brothers Co. and ESAB Group Inc., appealed on various grounds, including the trial court's decision to permit the testimony of Dr. Carlini on causation issues despite the Daubert challenge.

The opinion offers a number of useful observations for toxic tort litigation, especially on the almost-always central issue of causation.

It begins with a nice overview of the science on the spectrum of movement disorders often termed "parkinsonism" that have different causes and different but overlapping symptoms.  No one disputed that plaintiff here suffered from parkinsonism; the questions were what kind and from what cause. Apparently, every doctor to examine Tamraz reached a different conclusion about one or both of those issues.  Plaintiff's expert concluded that Tamraz suffers from “manganese-induced parkinsonism,” but not in the sense of a manifestation of the disease "manganism," as that phrase is sometimes used in these welding cases. Rather, he believed that manganese exposure caused something closely akin to traditional Parkinson's Disease in Tamraz.  Dr. Carlini hypothesized that Tamraz might have a genetic predisposition to Parkinson's Disease, and that manganese in lower levels than necessary to cause true manganism might nevertheless “trigger” the symptoms of Parkinson's Disease, like “the straw that broke the camel's back.” He did not believe that Tamraz has Parkinson's Disease in the strict medical sense, but manganese caused a disease that he believed to be otherwise similar to Parkinson's Disease. 

Defendants disputed this conclusion that manganese exposure caused the illness; that is, they challenged Dr. Carlini's etiology (what caused the disorder diagnosed?), not the methodology to arrive at his general spectrum diagnosis (what disorder caused the set of symptoms observed?).  And the Sixth Circuit agreed there were serious issues here. The problem here was that, when Dr. Carlini testified that manganese exposure caused Tamraz's condition, he went beyond the boundaries of allowable testimony under Rule 702.

The opinion was at most a working hypothesis, not admissible scientific “knowledge.” Fed.R.Evid. 702. His theory was a "plausible hypothesis. It may even be right. But it is no more than a hypothesis."  For example, the expert admitted that the literature hypothesizing a link between environmental toxins and latent genetic Parkinson's Disease was “all theoretical.”  He also conceded there were no studies finding a link between manganese and true Parkinson's Disease.  He further he conceded that he was speculating that Tamraz had an underlying predisposition to Parkinson's Disease, even though Tamraz had no family history of Parkinson's Disease. 

And finally, even if manganese could cause Parkinson's Disease in someone like Tamraz, that did not show that manganese did cause Tamraz's Parkinson's Disease. Parkinson's Disease occurs commonly in the general population and usually without any known cause. Any given case of Parkinson's Disease thus might have occurred regardless of the manganese exposure, making it hard to attribute one case to manganese exposure over all of the other possible causes.

Plaintiffs stressed on appeal that Dr. Carlini opined “with a reasonable degree of medical certainty,” but the court of appeals correctly noted that the phrase --the conclusion by itself-- does not make a causation opinion admissible. The “ipse dixit of the expert” alone is not sufficient to permit the admission of an opinion. General Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997). Minus that one phrase, nothing in this testimony took the opinion beyond speculation, theory, hypothesis. 

Plaintiffs, understandably, also tried to bolster the opinion by emphasizing areas of agreement among experts on the general diagnosis of some parkinsonism disorder.  But in conflating “manganese-induced parkinsonism” with manganism, plaintiff conflated diagnosis with etiology, erasing the distinction between Tamraz's disease and what caused it. Diagnosis and etiology, however, both were in play in this case. Because Dr. Carlini diagnosed Tamraz with something akin to Parkinson's Disease, not manganism, and because Parkinson's Disease unlike manganism has no standard etiology and lots of idiopathic cases, Dr. Carlini's etiology opinion had to rise or fall on its own.

Plaintiffs also trotted out the standard "differential diagnosis" argument, the tent that supposedly (and too often does) covers all kinds of unreliable causation opinions from medical experts.  The court here made some very useful observations about this issue. 

1) Most treating physicians have more training in and experience with diagnosis than etiology. See D. Faigman, Judges as “Amateur Scientists”, 86 B . U. L.Rev. 1207, 1221-22 (2006); E. Imwinkelried, The Admissibility and Legal Sufficiency of Testimony About Differential Diagnosis (Etiology), 56 Baylor L.Rev. 391, 405 (2004); M. Henefin, Reference Guide on Medical Testimony, in Reference Manual on Scientific Evidence 439, 471-72 (2d ed.2000). 

2) When physicians think about etiology in a clinical setting, moreover, they may think about it in a different way from the way judges and juries think about it in a courtroom. 

3) Getting the diagnosis right matters greatly to a treating physician, as a bungled diagnosis can lead to unnecessary procedures at best and death at worst. See Bowers v. Norfolk S. Corp., 537 F.Supp.2d 1343, 1361 (M.D.Ga.2007). But with etiology, the same physician may often follow a precautionary principle: If a particular factor might cause a disease, and the factor is readily avoidable, why not advise the patient to avoid it? Such advice  --telling a worker, say, to use a respirator-- can do little harm, think the doctors, and might do some good. See J. Hollingsworth & E. Lasker, The Case Against Differential Diagnosis: Daubert, Medical Causation Testimony, and the Scientific Method, 37 J. Health L. 85, 98 (2004). A lower threshold for making a causation decision serves well in the clinic but not in the courtroom, said the court. 

Of course, some courts permit the physician to testify as to etiology using this methodology, e.g., Hardyman v. Norfolk & W. Ry. Co., 243 F.3d 255, 260-67 (6th Cir.2001), but even these courts must apply the Daubert principles carefully in considering it. The ability to diagnose medical conditions is not remotely the same as the ability to deduce, in a scientifically reliable manner, the causes of those medical conditions. Gass v. Marriott Hotel Servs., Inc., 501 F.Supp.2d 1011, 1019 (W.D.Mich.2007), rev'd on other grounds, 558 F.3d 419 (6th Cir.2009). Doctors thus may testify to both, at least in the Sixth Circuit, but the reliability of one does not guarantee the reliability of the other. 

Thus, whether plaintiffs described Dr. Carlini's causation methodology as “differential etiology” or “differential diagnosis,” that label does not make it reliable. Using the differential diagnosis method is not some "incantation that opens the Daubert gate.”  The issues remain, did the expert make an accurate diagnosis of the nature of the disease? Did the expert reliably rule in the possible causes of it? Did the expert reliably rule out the rejected causes? If the court answers “no” to any of these questions, the court must exclude the ultimate conclusion reached. See Best v. Lowe's Home Ctrs., Inc., 563 F.3d 171, 179 (6th Cir .2009).

Here, Dr. Carlini's opinion failed the last two prongs because his efforts to “rule in” manganese exposure as a possible cause, or to “rule out” other possible causes, turned on speculation and theory and hypothesis, not a valid methodology. 

While expressing sympathy for the plaintiffs, the court observed that ignoring Rule 702 — allowing the law to "get ahead of science" — would be just as unfair. Such an approach eventually would destroy jobs and stifle innovation unnecessarily, because it would impose liability on business based on speculation, not science.

Case remanded for new trial, with different evidence obviously. 

(The dissent would have found the challenge going to the weight, not admissibility of the testimony, and the trial court's decision not an abuse of discretion.)

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A federal judge has issued an opinion explaining her Daubert and summary judgment rulings in a case brought by a consumer who alleged he contracted lung disease from the fumes of microwave popcorn. Newkirk et al. v. ConAgra Foods Inc., No. 2:08-cv-00273 (E.D. Wash. 7/2/2010).

Readers of MassTortDefense may be familiar with the so-called "popcorn lung" litigation in which plaintiffs have alleged they contracted a series of diseases, including Bronchiolitis obliterans, from inhaling the chemical diacetyl which had been used in the artificial butter on microwave popcorn.  Most of the claims have been made by workers with alleged industrial-level exposures on a daily basis in popcorn factories several years ago.  There are, however, a handful of cases by consumers claiming they somehow had sufficient exposure in their homes to have the same respiratory injuries.  These latter cases raise significant issues of general and specific causation, arising from the central tenet of toxicology: the dose makes the poison.  The studies relied on by plaintiffs noted that the cumulative exposure to diacetyl was correlated with chronic effects on lung function in plant workers.

Plaintiff Newkirk claimed that the natural and artificial butter flavoring in ConAgra's Act II Butter and Act II Butter Lovers popcorn products caused him severe and progressive damage to the respiratory system, extreme shortness of breath, and reduced life expectancy.  He claimed that he ate between five and seven bags of ConAgra's popcorn every day for more than a decade.

The motions centered around plaintiff's burden to prove causation. Plaintiffs in toxic tort cases must establish both general and specific causation. Golden v. CH2M Hill Hanford Group, Inc., 528 F.3d 681, 683 (9th Cir.2008). Evidence supporting general causation addresses “whether the substance at issue had the capacity to cause the harm alleged.” In re Hanford Nuclear Reservation Litigation, 292 F.3d 1124, 1133 (9th Cir.2002). Specific causation, by contrast, concerns whether a particular individual suffers from a particular ailment as a result of exposure to the substance. Defendants challenged plaintiff's proof of both under Daubert.

Plaintiffs retained Dr. Egilman to offer an opinion on general causation, as well as to examine Mr. Newkirk, diagnose him, and offer an opinion regarding the specific cause of his condition. The expert opinion testimony of Dr. Egilman was the plaintiffs’ primary evidence supporting general causation. (All of the Newkirks’ other causation expert witnesses assumed that general causation already has been established.)  He opined that,  “There is no known safe level of diacetyl exposure. Existing scientific studies also suggest that levels of diacetyl exposure below and around 1 ppm can cause BO and other respiratory illnesses.”

The court found, however, that Dr. Egilman's attempt to analogize kitchen to industrial exposures failed. He offered no sufficient basis or methodology for support for the conclusion that there is no important (medically relevant) qualitative difference between the vapor from butter flavoring slurry in a mixing vat in a popcorn plant and the vapor from butter flavoring that is emitted from microwave popcorn in the home. There was nothing to support Dr. Egilman’s conclusions that were at the heart of this case: that the vapors emitted from a microwave popcorn bag contain the same proportion of chemicals or in sufficient doses or that all of the substances in the two instances are identical. In other parts of his reports and testimony, the court found, Dr. Egilman relied on some existing data, mostly in the form of published studies, but drew conclusions far beyond what the study authors concluded.

Or, Dr. Egilman manipulated the data from those studies to reach misleading conclusions of his own. Slip opin. at 25. For example, he relied on statements by a Dr. Cecile Rose, on a patient (and another consumer plaintiff), Mr. Watson, who allegedly contracted disease from popcorn fumes. But this was in the nature of a single case report, and in it even Dr. Rose did not assert that her conclusions could be extrapolated to other consumers in the absence of publication or peer review; Dr. Egilman acknowledged that Dr. Rose did not publish the exposure levels measured in Mr. Watson’s home -- so no such comparison was possible.  Dr. Rose herself qualified her conclusions: “It is difficult to make a causal connection based on a single case report. We cannot be sure that this patient’s exposure to butter flavored microwave popcorn from daily heavy preparation has caused his lung disease.” 
 

The expert also relied on testing conducted by Dr. John Martyny in a kitchen (not of a consumer), despite that doctor's own reflections that the methodology underlying the work could not support extrapolating to general causation for a broader group of consumers.  The expert also relied on animal studies. Expert opinion relying on animal studies to reach an opinion on causation in humans is usually admissible only when the expert explains how and why the results of the animal toxicological study can reliably be extrapolated to humans. General Electric Co. v. Joiner, 522 U.S. 136, 143-45 (1997).  Dr. Egilman offered no such analytical bridge between the animal studies finding harm from high levels of diacetyl exposure to lab rats and his conclusion that those studies demonstrate that diacetyl exposure causes decreased lung function in humans. He offered no sufficient explanation for how and why the results of those studies could be extrapolated to humans, let alone low-dose consumer contexts.

Without Dr. Egilman's testimony to support causation, the plaintiffs' other expert witnesses couldn't establish this element either.

Note also that the court excluded Dr. Egilman's "legal conclusions" from his expert report and affidavits, since the witness was no more capable than the fact-finder to draw such a conclusion. See Nationwide Transp. Fin. v. Cass Info. Sys., 523 F.3d 1051, 1059-60 (9th Cir.2008) (expert witness cannot give an opinion as to her legal conclusion, i.e., an opinion on an ultimate issue of law). For example, Dr. Egilman tried to opine that about what the defendant "knew" and "failed to warn" consumers. This is another useful precedent against plaintiffs' mis-use of the conduct "expert" who provides mere legal conclusions and invades the province of the jury.

(Dechert is involved in the diacetyl litigation, but not this case.)

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The Eleventh Circuit recently  affirmed a judgment for defendant Evenflo Co. in a suit by a plaintiff who had alleged that the car seat manufacturer was responsible for her son's autism. Hendrix v. Evenflo Co., 2010 WL 2490760 (11th Cir., 6/22/10).

Plaintiff alleged that her son sustained traumatic brain injuries when a child restraint system manufactured by Evenflo allegedly malfunctioned during a minor traffic accident. Hendrix further alleged that those brain injuries caused the son to develop autism spectrum disorder (“ASD”). The district court excluded testimony from two of Hendrix's expert witnesses that the accident caused the ASD, concluding that the methods used by Hendrix's experts were not sufficiently reliable under Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579 (1993). See Hendrix v. Evenflo Co., Inc., 255 F.R.D. 568 (N.D.Fla. 2009). The lower court then granted partial summary judgment to Evenflo on Hendrix's ASD claim, determining that without the excluded testimony there was no reliable evidence to support Hendrix's theory that the accident caused the ASD. Hendrix voluntarily dismissed, with prejudice, her remaining damages claims and filed a notice of appeal.

Hendrix's experts relied primarily on the controversial differential etiology method to link the child's traumatic brain injury to his ASD diagnosis. Differential etiology, said the court, is a medical process of elimination whereby the possible causes of a condition are considered and ruled out one-by-one, leaving only one cause remaining. It is a questionable extension of the method by which doctors diagnose a disease into the area of what caused the disease.

The Eleventh Circuit has previously held that, when applied under certain circumstances that it thinks will ensure reliability, the differential etiology method can provide a valid basis for medical causation opinions. The reliability of the method must be judged by considering the reasonableness of applying the differential etiology approach to the facts of this case and the validity of the experts' particular method of analyzing the data and drawing conclusions therefrom. According to the court, a reliable differential etiology analysis is performed in two steps. First, the expert must compile a comprehensive list of hypotheses that might explain the set of salient clinical findings under consideration; the issue at this point in the process is which of the competing causes are generally capable of causing the patient's symptoms. See Clausen v. M/V New Carissa, 339 F.3d 1049, 1057-58 (9th Cir.2003). Second, the expert must eliminate all causes but one.

With regard to the first step, the district court must ensure that, for each possible cause the expert “rules in” at the first stage of the analysis, the expert's opinion on general causation is derived from scientifically valid methodology.  Hollander v. Sandoz Pharm. Corp., 289 F.3d 1193, 1211 (10th Cir.2002); Siharath v. Sandoz Pharms. Corp., 131 F.Supp.2d 1347, 1362-63 (N.D.Ga.2001). This is because a fundamental assumption underlying differential etiology is that the final, suspected cause must actually be capable of causing the injury. Thus, here, the experts' purported use of the differential etiology method will not overcome a fundamental failure to lay the scientific groundwork for the theory that traumatic brain injury can, in general, cause autism.

The Eleventh Circuit has distinguished cases in which the medical community generally recognizes that a certain chemical or product can cause the injury the plaintiff alleges from those in which the medical community has not reached such a consensus. In the second category of cases, the district court must apply the Daubert analysis not only to the expert's methodology for figuring out whether the agent caused the plaintiff's specific injury, but also to the question of whether the drug or chemical or product can, in general, cause the harm plaintiff alleges. Thus, the district court must assess the reliability of the expert's opinion on general, as well as specific, causation.  In this regard, the court (like most) rejects the “post hoc ergo propter hoc fallacy" which assumes causality from temporal sequence; a mere temporal relationship between an event and a patient's disease or symptoms does not allow an expert to place that event on a list of possible causes of the disease or symptoms. Case studies and clinical experience, used alone and not merely to bolster other evidence, are also insufficient to show general causation.

Here, none of the medical textbooks and epidemiological studies submitted by the expert came close to providing useful evidence of a definitive causal link between traumatic head injuries and autistic disorders, and none provided even marginal support for plaintiff's theory of a relationship between abnormal cerebral spinal fluid pressure and problems with cerebellum pressure, leading to autism. For example, the text chapter listing the known etiological factors involved in ASD does not mention acquired trauma in the perinatal brain.

Plaintiff also attempted to sidestep the deficiencies in the medical literature by focusing on the expert's experience and training. Merely demonstrating that an expert has experience, however, does not automatically render every opinion and statement by that expert reliable. The witness must explain how that experience leads to the conclusion reached, why that experience is a sufficient basis for the opinion, and how that experience is reliably applied to the facts. The trial court's gatekeeping function requires more than simply “taking the expert's word for it.”

Judgment for defendant affirmed.

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A federal appeals court recently affirmed a judgment for the maker of a drug used to treat Parkinson's disease in litigation alleging that the drug caused plaintiff's compulsive gambling.  Wells v. SmithKline Beecham Corp., 2010 WL 1010591 (5th Cir. 2010).

Wells sued GlaxoSmithKline, the manufacturer of Requip, alleging that GSK had failed to warn patients about the alleged side effect of pathological gambling.  For Wells to win under Texas law,  he had to show that the failure to warn caused his injury.  Causation has two levels, general and specific, and a plaintiff must prove both. General causation is whether a substance is capable of causing a particular injury or condition in the general population, while specific causation is whether a substance caused a particular individual's injury. Sequence matters, said the 5th Circuit: a plaintiff must establish general causation before moving to specific causation. Without the predicate proof of general causation, the tort claim fails.

Wells engaged three expert witnesses to address general causation, that the drug supposedly could cause pathological gambling. In reaching their conclusions, the experts relied upon: (1) published articles documenting case-specific correlations between Requip and gambling; (2) a single unpublished study allegedly showing a nexus between Parkinson's medicines generally and gambling; (3)  internal data supposedly revealing case-specific associations between Requip and gambling; and (4) the fact that GSK has since changed the Requip label to warn about possible gambling side-effects. (Of course, on the last point a regulatory agency can require a warning based on a lesser level of proof than is required to recover in a tort action.) Defendant challenged the evidence under Daubert, and the district court granted summary judgment.  Plaintiff appealed.

Readers know that Daubert requires admissible expert testimony to be both reliable and relevant.  This entails a preliminary assessment of whether the reasoning or methodology underlying the testimony is scientifically valid and of whether that reasoning or methodology properly can be applied to the facts in issue.  Although there are “no certainties in science,” the expert must present conclusions grounded in the methods and procedures of science.  In short, the expert must employ in the courtroom the same level of intellectual rigor that characterizes the practice of an expert in the relevant field.

The court of appeals found that each of the three experts had, in deposition, in essence conceded that there exists no scientifically reliable evidence of a cause-and-effect relationship between Requip and gambling, that the state of the art was mere association, not cause.  That alone would doom the plaintiff's case.

But more interesting for readers is when the court went on, in the alternative, to address the methodologies and fit. 

The studies relied on were, each expert conceded, not statistically significant epidemiology. They were, in fact, case studies. Although case-control studies are not per se inadmissible evidence on general causation,  the courts have frowned on causative conclusions bereft of statistically significant epidemiological support. While the court agreed that in epidemiology hardly any single study is ever conclusive, and it did not suggest that an expert must back his or her opinion with multiple published studies that unequivocally support his or her conclusions, here there was simply too great an analytical gap between the data and the opinion proffered.  Bottom line-- the bases for the experts' conclusions passed none of the applicable Daubert factors: that Requip causes problem gambling is not generally accepted, has not been subjected to peer review and publication, and is not backed by studies meeting requisite scientific standards.

Without the expert testimony, Wells could not prove general causation.  Here's a useful quote:  "Wells urges the law to lead science -- a sequence not countenanced by Daubert."  See also Rosen v. Ciba-Geigy Corp., 78 F.3d 316, 319 (7th Cir.1996) (“Law lags science; it does not lead it.”).

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A New Jersey appellate court recently affirmed a trial court's decision that an Accutane plaintiff's expert's study must be excluded as unreliable. See Palazzolo v. Hoffmann La Roche Inc., 2010 WL 363834 (N.J. Super. Ct., 2/3/10).

Plaintiffs filed a product liability and consumer fraud complaint against defendants claiming that Accutane, a drug used to treat acne, caused their family member to develop depression which led to his suicide. They contended that at the time of his death in 1997, Accutane should have carried a warning label concerning the possibility that the drug could cause depression and suicide.

As one element of their product liability cause of action, plaintiffs needed to establish “general causation,” by showing that Accutane can cause depression and suicide. See Kemp v. State, 174 N.J. 412, 417 (2002); Coffman v. Keene Corp., 133 N.J. 581, 594 (1993). On that issue, plaintiffs retained Dr. James Bremner, as an expert.  Plaintiffs paid Bremner to undertake a study of the issue; there was no dispute that the study was commissioned specifically for use in this litigation.

In the study at issue, Bremner and a team of other scientists used positron emission tomography (PET) technology to compare changes in brain metabolism between two groups of subjects being treated for acne. One group was receiving antibiotic treatment and the other group was being treated with Accutane.  According to Bremner, the PET study demonstrated that the subjects treated with Accutane showed decreased metabolism in the orbital frontal cortex, a portion of the brain associated with depression. He published an article about the study in a scientific journal, describing his methodology and his conclusions. Based largely but not entirely on the PET study, he issued an expert report opining that Accutane can cause depression and suicide.

Defendants challenged the evidence. In deposition and at a hearing, Bremner was repeatedly confronted with potential problems in the PET study, including missing data, inaccurate data, and deviations from the methodology he claimed to have followed. As a result, in the middle of the Rule 104 hearing, the court permitted Bremner to re-work his study data and issue a supplemental expert report and allowed defendant to re-depose him. The trial court then excluded the evidence.

The court of appeals affirmed. First, Bremner did not actually use the methodology he claimed to have used. Although his PET scan article was peer-reviewed, he admitted that he did not in fact follow the steps described in the article. Significantly, contrary to representations made in the article, he did not get before-and-after questionnaires from many of the subjects.  Those questionnaires were designed to elicit the extent to which the subjects might be worried about their acne. This was relevant because some scientists were of the view that worrying, as well as depression, could affect activity in the orbital frontal cortex.

Secondly, Bremner also could not document much of the data on which his published results were based. Third, he admitted that some of the statistical analysis was inaccurate. For example, in the hearing session, Bremner admitted that, for each study participant, comparing the activity in the orbital frontal cortex with the activity in the whole brain revealed no difference between the subjects who took Accutane and those who took antibiotics.

The court noted that an expert's scientific peers cannot fairly judge the expert's written work, including whether it is worthy of publication, if his article does not accurately represent either the underlying data or what the author did to produce his results. In essence, Bremner's study was not  soundly and reliably generated.

There also was no error in precluding Bremner from providing supplemental reports or information after the Rule 104 hearing record closed. The judge allowed Bremner multiple opportunities to correct errors in his study before the record closed. The orderly conduct of litigation demands that expert opinions reach closure. See Miller v. Pfizer, Inc., 356 F.3d 1326, 1334 (10th Cir.), cert. denied, 543 U.S. 917 (2004).

The court of appeals remanded the case for consideration whether, even without the PET study, Dr. Bremner can still offer an opinion that Accutane can affect the brain and produce depression.

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The 11th Circuit has affirmed a trial court’s exclusion of key expert causation proof in a suit against the manufacturer of Remicade, finding the expert evidence was not adequately supported by scientific studies or literature. Goldstein v. Centocor Inc., 2009 WL 275322 (11th Cir. 2/05/09).

Plaintiff-appellant contended that the prescription medication Remicade caused his pulmonary fibrosis, requiring a bilateral lung replacement. The trial court excluded plaintiff’s expert testimony on general causation, pursuant to Fed.R.Evid. 702 and Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579 (1993). The court of appeals reviews a trial court's Daubert rulings under an abuse of discretion standard. McClain v. Metabolife Intern'l, Inc., 401 F.3d 1233, 1238 (11th Cir.2005).

Plaintiff’s expert did not rely on any epidemiological studies that connect Remicade with pulmonary fibrosis. This is not necessarily fatal, said the 11th Circuit, but it makes a plaintiff’s task to show general causation more difficult. See Rider v. Sandoz Pharmaceuticals Corp., 295 F.3d 1194, 1198 (11th Cir.2002).

In the absence of epidemiological studies, the expert reviewed four sources to make his general causation assessment. The first category, plaintiff's lung and bowel pathology reports, was not relevant to general causation; its focus on the plaintiff made it relevant to specific causation. See McClain, 401 F.3d at 1239 (“General causation is concerned with whether an agent increases the incidence of disease in a group and not whether the agent caused any given individual's disease.”). The second category, MedWatch case reports submitted by doctors who observed possible reactions to Remicade, have a limited weight. Such reports are made without medical controls or scientific assessment, and while they may support other proof of causation, alone they cannot prove causation. Id. at 1199. (putting aside an expert’s reliance on such reports, they are hearsay and do not fall within any of the exceptions to the hearsay rule; also, the prejudicial effect of these reports outweighs their probative value.)

The third category, a review of medical textbooks, revealed no relevant general causation information, only extended analogies. The fourth category, a review of abstracts of four articles linking Remicade with pulmonary fibrosis, is relevant to general causation but provided only very limited information.

A court may conclude that there is simply too great an analytical gap between the data and the opinion proffered. General Elec. Co. v. Joiner, 522 U.S. 136, 146, (1997). The district court did so here, and the 11th Circuit found no abuse of discretion in its determination.
 

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