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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The Sixth Circuit last week upheld the dismissal of a plaintiff''s claim that benzene exposure caused her cancer. Pluck v. BP Oil Pipeline Co., No. 09-4572 (6th Cir.,  5/12/11).  The central issue was the exclusion of plaintiff's causation expert's opinion based on a "differential diagnosis" that failed to reliably rule in benzene exposure as a potential cause of plaintiff's cancer, and to rule out some other potential exposures.

This case arose from benzene contamination allegedly caused by gas-pipeline releases allegedly resulting in the seepage of gasoline into the surrounding soil and groundwater. Benzene, a component of gasoline, is a known carcinogen in sufficient doses under certain exposure circumstances, and is also ubiquitous in the ambient air and is a component or constituent of vehicle exhaust and cigarette smoke, said the court. Plaintiffs purchased a home in the area,  and used well water to drink, wash, shower, and irrigate their yard and garden. In October,  1996, plaintiffs say they noticed a gasoline odor in their home and water, and benzene was first detected in the well on their property in the amount of 3.6 parts per billion (“ppb”).  They began drinking bottled water in lieu of tap water, although they claim to have resumed drinking tap water upon the drilling of a new, deeper well. Between 1997 and May 2002, the new well tested negative for benzene twenty-two times.

Mrs. Pluck was diagnosed with Non-Hodgkins lymphoma (“NHL”) in 2002 at age forty-eight. She filed suit, alleging claims of strict liability for hazardous activity, negligence, and loss of consortium. To support their claims, plaintiff and spouse retained Drs. Joseph Landolph and James Dahlgren as experts on causation to demonstrate that benzene is generally capable of causing NHL and specifically caused Mrs. Pluck’s NHL. Defendant filed motions in limine to exclude the testimony of Dahlgren and Landolph on the grounds that their testimony failed to satisfy the standard for reliability set forth in Daubert. In particular, BP argued that Dr. Dahlgren’s testimony on specific causation was unreliable because he formulated a specific causation opinion without evidence of dose, and subsequently performed an unreliable dose reconstruction in an attempt to support his opinion.  Dahlgren then submitted a supplemental declaration in which he evaluated Mrs. Pluck’s illness under a "differential-diagnosis" methodology. The district court granted the motions, and plaintiff appealed.

In a toxic tort case, as here, the plaintiff must establish both general and specific causation through proof that the toxic substance is capable of causing, and did cause, the plaintiff’s alleged injury.  As to specific causation, the plaintiff must show that she was exposed to the toxic substance and that the level of exposure was sufficient to induce the complained-of medical condition (based on a dose-response relationship). Both causation inquiries involve scientific assessments that must be established through the testimony of a medical expert. Without this testimony, a plaintiff’s toxic tort claim will fail.

The Plucks had to concede that the expert Dr. Dahlgren did not establish dose; they instead argued that Dahlgren used differential diagnosis to determine specific causation. Defendant argued that Dr. Dahlgren did not apply differential diagnosis in either his expert opinion or his deposition, but did so only in an untimely supplemental declaration filed five months after the deadline for expert reports. And in any event, his approach was flawed. The Sixth Circuit has recognized differential diagnosis, properly done, as an appropriate method for making a determination of causation for an individual instance of disease. Differential diagnosis -- originally a standard technique for determining what disease caused a patient's symptoms -- has been adapted in some courts as an acceptable scientific technique for identifying the cause of a medical problem by eliminating the likely causes until the most probable one is isolated. A physician who applies differential diagnosis to determine causation considers all ("rules in") relevant potential causes of the symptoms and then eliminates ("rules out") alternative causes based on a physical examination, clinical tests, and a thorough case history.

Even in courts that accept this adapted method, not every opinion that is reached via a differential-diagnosis method will meet the standard of reliability required by Daubert.  Calling something a “differential diagnosis” or “differential etiology” does not by itself answer the reliability question but prompts at least three more:

(1) Did the expert make an accurate diagnosis of the nature of the disease?

(2) Did the expert reliably rule in the possible causes of it?

(3) 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.

Here the court agreed that Dahlgren could not reliably “rule in” benzene exposure as the cause of Mrs. Pluck’s NHL. In recognition of the fact that benzene poses a health concern at certain levels of exposure, the EPA has stated that the maximum permissible contaminant level for benzene in
drinking water is 5 ppb. 40 C.F.R. § 141.61(a)(2). Dahlgren, however, did not ascertain Mrs. Pluck’s level of benzene exposure, nor did he determine even whether she was exposed to quantities of benzene exceeding the EPA’s safety regulations. The levels of benzene in the Plucks’ wells never exceeded the maximum permissible contaminant level of 5 ppb designated by the EPA.

Dahlgren’s opinion that Mrs. Pluck’s “low-level exposure” to benzene caused her NHL was thus not grounded in “sufficient facts or data,”  nor did it reflect the “reliable principles and methods” required by Rule 702. It was, instead, pure conjecture.  Although the Plucks argued that the district court required too much specificity regarding Mrs. Pluck’s dose, this argument was also without merit. The mere existence of a toxin in the environment is insufficient to establish causation without proof that the level of exposure incurred could cause the plaintiff’s symptoms. See also McClain v. Metabolife Int’l, Inc., 401 F.3d 1233, 1242 (11th Cir. 2005) (causation “requires not simply proof of exposure to the substance, but proof of enough exposure to cause the plaintiff’s specific illness”).

Finally, even if Dr. Dahlgren had properly “ruled in” benzene exposure as the cause plaintiff's NHL, he failed to “rule out” alternative causes of her illness, as is required under the differential-diagnosis methodology. See also Wills v. Amerada Hess Corp., 379 F.3d 32, 50 (2d Cir. 2004) (expert’s opinion suffered from a “fatal flaw” when he acknowledged that cigarettes and alcohol were risk factors for developing squamous-cell carcinoma but failed to account for these variables in concluding that decedent’s cancer was caused by exposure to toxic chemicals such as benzene and PAHs).  In this case, Dahlgren acknowledged in his deposition that Mrs. Pluck was
exposed to other sources of benzene, from her extensive smoking habit and from other organic solvents.  Yet, Dr. Dahlgren neither identified these other solvents nor determined Mrs. Pluck’s potential level of exposure to these other possible sources of benzene.Thus, Dahlgren failed to “rule out” alternative causes of Mrs. Pluck’s NHL.

The court of appeals determined that the district court did not abuse its discretion in concluding that the expert did not perform a reliable differential diagnosis.  And summary judgment properly followed.

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Insecticide manufacturers held on to summary judgment as the Eight Circuit affirmed the lower court's causation ruling under Daubert.  Junk v. Terminix International Co., No. 08-3811 (8th Cir., 12/9/10).

The plaintiffs'  home had been infested with spiders during the mother's pregnancy, and she contacted Terminix about the problem.  Defendant thereafter sprayed a pesticide inside and outside the Junks' home, approximately 20 times, the last occurring two years after her son's birth. Junk alleged that the child's multiple medical conditions were caused by exposure to ingredients in Dursban, an insecticide manufactured by Dow, distributed by Terminix.

The defendants moved to exclude the causation testimony of plaintiffs' two medical experts, and for summary judgment.  The trial court first excluded the testimony of Dr. Richard Fenske, who had been retained to determine whether the son had been exposed to an unsafe level of the insecticide during his mother's pregnancy and after his birth. Dr. Fenske testified that when making toxic exposure and dosage estimates he usually relied on a "deterministic modeling" method in which he creates an exposure model that accounts for numerous variables. In this case, however, he did not have sufficient data to perform such an analysis. Instead, he compared what he knew about the circumstances of the child's exposure with those in published studies. This comparative analysis led him to conclude that plaintiff had been exposed to an unsafe level. Observing that Dr. Fenske had not followed his own usual methodology and concluding that he had relied on a number of ungrounded assumptions in his comparative approach, the district court excluded his opinion on the ground that his methodology was not sufficiently reliable.

Dr. Cynthia Bearer's testimony was also excluded. She was a neonatologist and board certified pediatrician whom Junk retained to give her opinion on general and specific causation.  Because Dr. Bearer's opinion on specific causation relied on Dr. Fenske's conclusions, after the court excluded Dr. Fenske's testimony, it found Dr. Bearer's opinion on specific causation also lacked a scientific factual basis and declined to admit it.

Plaintiffs appealed.

The court of appeals agreed that Dr. Fenske's comparative analysis depended on various unsupported assumptions. He did not account for differences between conditions in the Junk household and those described in the articles he consulted. In one instance, his only basis for comparison was the fact that the Junk household and those in a particular study were all treated with the Dursban ingredient chlorpyrifos. In another, he relied on a study where the only common variable between the Junks' experience and the homes studied was the total amount of chlorpyrifos applied. Dr. Fenske thus disregarded other important variables such as where and how chlorpyrifos was applied in the household and whether the homes in a comparison study were the same size as the Junks' home.

While Dr. Fenske was not required to produce a mathematically precise table equating levels of exposure with levels of harm, he was required to have a "scientifically valid" method to estimate that plaintiff's exposure exceeded a safe level. The expert's failure to follow his own general practice and his reliance on unfounded assumptions in his comparative method created "too great an analytical gap" between his opinion and the data on which it relied.

Because Dr. Bearer's differential diagnosis depended on Dr. Fenske's opinion on exposure, the district court did not abuse its discretion in excluding it. A differential diagnosis begins with an expert's "ruling in" plausible causes of an injury. See Kudabeck v. Kroger Co., 338 F.3d 856, 860–61 (8th Cir. 2003). Then the expert "rules out" less likely causes until the most likely cause remains. Without a scientific basis for including unsafe chlorpyrifos exposure in her differential, her opinion amounted to speculation.

To succeed in her claims, Junk needed to present expert testimony showing that the chlorpyfiros could have caused the son's injuries and that it did in fact cause those injuries. Junk's  experts did not survive the district court's Daubert analysis. After the court properly excluded Dr. Bearer's
testimony, Junk could not prove specific causation as required under Iowa law. As there was no longer a genuine issue of material fact as to that necessary element, Dow and Terminix were entitled to judgment.

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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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A while back we posted about an interesting toxic tort case involving important causation issues. See Zandi v. Wyeth, 2009 WL 2151141 (Minn.App.).  A Minnesota appeals court recently refused to rehear its prior affirmance of summary judgment for defendants in a suit by a woman who alleged hormone replacement drugs caused her breast cancer.  2009 Minn. LEXIS 648. 

Plaintiff alleged that between approximately 1981 and 2001, she ingested hormone replacement therapy (HRT) drugs manufactured, designed, packaged, marketed, and distributed by defendants. In November 2001, Zandi alleges she was diagnosed with "hormone-dependent breast cancer." She contended that the HRT drugs caused her cancer. 

The trial court found that plaintiff's specific causation evidence did not satisfy Minnesota's standard for admissibility of expert testimony. Zandi offered testimony from Dr. Lester Layfield and Dr. Gail Bender to try to prove that HRT drugs caused her cancer. Minnesota courts use the Frye standard to determine the admissibility of novel scientific evidence. Zandi's claims were based on the following propositions: 1) it is supposedly generally accepted that HRT causes hormone-dependent breast cancer, and 2) there is a generally accepted method of diagnosing the cause of hormone-dependent breast cancer in an individual. The appellate issues revolved around the second.

Plaintiff's experts based their specific causation opinions in part on "differential diagnosis."  As readers of MassTortDefense know,  differential diagnosis, sometimes called “differential etiology”  is a process through which all the scientifically plausible causes of an injury are “ruled in,” and the expert then “rules out” the less plausible causes until reaching the one that theoretically cannot be ruled out.  If you've watched "House" on TV, you have seen the use of differential diagnosis to discover what disease a patient is suffering from.  Less traditional, and more questionable, is the use of the technique to discover what is the cause of the disease in the patient.  Most doctors don't care as much about the cause of the disease as getting the right disease and treating it.  As used by toxic tort plaintiffs, differential diagnosis adopts a process of elimination to identify not just the injury (which may be debated) but also the cause; in theory, it seeks to eliminate the possibility of competing causes or confounding factors. 

Again, in performing a differential diagnosis, a physician begins by ruling in all scientifically plausible causes of the patient's injury. The physician then rules out the least plausible causes of injury until the most likely cause remains. Yet, breast cancer does not lend itself to such a differential diagnosis because the scientific community has not accepted that breast cancer has a limited number of discrete and recognized possible causes such that ruling out one or a few causes would necessarily implicate another. For differential diagnosis to be sufficiently reliable to even come close to proving causation, even assuming one accepts the method in this context, the diagnostician should rule out all other hypotheses, or at least explain why the other conceivable causes are excludable. But additional risk factors that plaintiff failed to adequately account for here in this case included family history. When faced with this dilemma, as is common when a disease has many idiopathic cases, plaintiff's experts simply suggest that it is possible to conduct a reliable differential diagnosis without ruling out other hypotheses, as long as "major" or "most" explanations are ruled out.  Courts should be wary of this.

Courts generally recognize that the proffered expert must have a sufficient basis to “rule in” the drug or toxic substance at issue as a plausible cause of plaintiff’s injury. E.g., Jazairi v. Royal Oaks Apts., 217 Fed. Appx. 895 (8th Cir. 2007).  But this case is a good reminder that the plaintiff's expert testimony must also reliably “rule out” the other plausible causes of the injury--  again, especially difficult when its causes are largely unknown.  On this record, the court said, “We conclude that there is not a method of diagnosing the specific cause of a particular woman's breast cancer that is generally accepted in the relevant scientific community. This reality leaves Zandi without a legally sufficient ability to prove specific causation.”  See also Perry v. Novartis, 564 F. Supp.2d 452 (E.D. Pa. 2008).

This clear reasoning can be contrasted with the inexplicable finding of the 8th Circuit in Scroggin v. Wyeth, 2009 WL 3518245 (8th Cir. Nov. 2, 2009), which accepted plaintiff's carefully constructed circular reasoning.  Unable to prove that the breast cancer was caused by hormone therapy drugs, plaintiff's expert simply re-diagnosed the disease as hormone-induced breast cancer.  This allowed the expert to engage in a so-called differential diagnosis to determine the cause of the breast cancer simply by ruling out the two possible sources of these hormones: (1) plaintiff produced the hormones herself, or (2) they came from the hormone replacement therapy she had allegedly taken for the past eleven years.  Under this circular reasoning, any form of cancer can easily be linked to the defendant's product because it will be re-characterized as the sub-type of disease caused by the substance at issue. 
 

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Zyprexa is a mature mass tort, as the defendant has settled approximately 31,000 individual product liability lawsuits over the drug, which was widely used in the treatment of psychiatric disorders. The federal court overseeing the multidistrict litigation over Eli Lilly and Co.'s product has made an important ruling on a Daubert challenge to a plaintiff expert in 13 cases involving 20 of the remaining claimants. In re Zyprexa Products Liability Litigation, MDL No. 1596 (E.D.N.Y. May 12, 2009).

Plaintiffs proposed to call an expert to establish the specific causal relationship between the Zyprexa taken and the onset or worsening of their diabetes. After briefing and an extensive evidentiary hearing, Senior Judge Jack B. Weinstein granted Eli Lilly's motion to disqualify Dr. Stephen J. Hamburger, M.D. While the expert met the necessary educational and experiential qualifications warranting the admissibility of his expert opinions, the court found his testimony lacked sufficient scientific reliability.

The court noted that in longstanding and highly complex litigation (read mass tort), particular emphasis must be placed on the reliability and scientific validity of the expert's opinions. Particularly in a mature mass tort ("advanced stage" described the court) when the issues of the benefits and risks of the drug have been a focus of the scientific community for some time, precision with respect to the relevant scientific knowledge and its application to the facts of the individual cases is expected, said the court.

The record demonstrated to the court that this expert's opinions relied on "a subjective methodology, a fast and loose application of his scientific theories to the facts, and conclusion-driven assessments on the issues of causation in the cases on which he proposes to testify,” the order said. In particular, the court pointed to the opinion that Zyprexa supposedly has a direct adverse effect on cells essential to the body's production of insulin, even in cases in which there was no documented weight gain. This opinion was not based on sufficient facts or data, nor was it the product of a reliable method.

In applying this theory to the facts of the cases (the "fit" required by Daubert), the expert had been, in the view of the court, “shockingly careless” about the scientific facts in these cases, including whether weight gain preceded or followed the plaintiffs' use of Zyprexa, and whether there was any weight gain at all. When confronted with these issues, he merely "shrugged off" factual discrepancies in his analyses or shifted to new theories on the fly.

Significantly, the court correctly observed that other mass torts had been subject to a kind of junk science, and it it could not "permit a major pharmaceutical litigation to become the subject of the kind of 'rubber-stamp' expert opinions that have so marred mass litigations such as those involving asbestos and breast implants.”

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