State Supreme Court Issues Significant Asbestos Ruling

The Pennsylvania Supreme Court last week issued a potentially highly significant decision in the long-standing asbestos mass tort. See Betz v. Pneumo Abex LLC et al., No. J-87-2011 (Pa. May 23, 2012).

The issue is causation.  Readers know that a tort plaintiff has to establish cause in fact and proximate cause.  Cause in fact can mean "but for" the defendant's conduct, the plaintiff would not have been injured, or, in some cases, that the conduct was a "substantial factor" in causing the harm.  In toxic tort cases, cause in fact includes general causation (the product can cause this type of disease) and specific causation (the product did cause this plaintiff's disease). Often, epidemiological proof is used to establish causation in a toxic tort context, but there are strengths and limitations to that type of evidence, which can show an association between the product and the disease, and which typically demonstrates that there is some specific relationship between the amount of exposure to the product and the amount of disease seen in the exposed population (a dose-response relationship).  What may be unknown from the epidemiology (and other relevant scientific evidence) is whether there is a threshold of exposure below which there is no risk of disease, or whether any level of exposure carries a measurable increased risk of disease.  Plaintiffs' experts often assume there is no safe level of exposure, and regulatory agencies may assume the same as a matter of public health policy; these latter assumptions do not establish legal causation given their cautionary, prophylactic nature. But what proof a plaintiff has that an extremely low level of exposure to a given defendant's product can or did cause his disease is a crucial issue in many toxic tort contexts.

In asbestos, the grandfather of all mass torts, plaintiffs' experts often seek to testify that "one fiber can kill," meaning there is no safe level of exposure to asbestos, and from that to conclude that that any exposure to any amount of asbestos from any defendant was a substantial factor contributing to the asbestos disease the plaintiff has.  They say this even as they admit, as the epidemiology shows, that at all the measurable levels of exposure (no one can find a plaintiff exposed to just one fiber) asbestos-related disease demonstrates a clear dose-response relationship.

Back in 2005, plaintiff Simikian commenced a product liability action against several defendants, asserting causes of action grounded on multiple theories including strict liability. Mr. Simikian
alleged that, throughout a forty-four year career as an automotive mechanic, his exposure to asbestos-containing friction products, such as brake linings, caused his mesothelioma. Plaintiff indicated he would rely on expert opinion that each and every exposure to asbestos -- no
matter how small -- contributed substantially to the development of his asbestos-related
diseases: the the “any-exposure,” “any-breath,” or “any fiber” theory of legal (or substantial-factor) causation. See generally Summers v. Certainteed Corp., 606 Pa. 294, 316, 997 A.2d 1152, 1164-65 (2010) (discussing the requirement for a plaintiff to prove that a defendant’s product was a substantial factor in causing injury). Seeking to preclude such opinion testimony, defendants filed a motion under the Frye test (PA is a general acceptance jurisdiction), arguing that it barred this "novel" scientific evidence from the courtroom until it has achieved general acceptance in the relevant scientific community.

Plaintiffs relied on a Dr. Maddox, who provided for his opinion as to specific and proximate
causation that asbestos-related mesothelioma, like other diseases induced by toxic exposures, is a dose-response disease; that each inhalation of asbestos-containing dust from the use of
products has been shown to contribute to cause asbestos-related diseases, including  mesothelioma. Each of the exposures to asbestos allegedly contributes to the total dose that causes mesothelioma and, in so doing, shortens the period necessary for the mesothelioma to develop. Plaintiff further argued that each exposure to asbestos is therefore a substantial contributing factor in the development of the disease that actually occurs; a court need not look at individual exposures or the identity of the product or the manufacturer. "As a matter of law, you just say, hey, you breathed asbestos from a product, oh, you are going to the jury."

The trial court requested expert reports, and then held an evidentiary hearing. The Common Pleas court centered its focus on the use of extrapolation, from high doses down to a single finer, which it found to be a linchpin of Dr. Maddox’s methodology and opinion supporting a finding of proximate cause. The court expressed concern with an “analytical gap” between the scientific proofs and the expert's conclusion. At the hearing, the expert admitted he did not consider epidemiology appropriate to consult regarding low-dose exposures, offering an "analogy" that has been used in the example of a glass of water. One drops marbles into the glass of water until the water finally overflows from the glass; is it the first marble or the last marble that causes the glass
to overflow? Well, both, or all of them, said the plaintiff expert.

The expert testified, however, that individual exposures differ in the potency of the fiber to
which an individual is exposed, to the concentration or intensity of the fibers to which one is exposed, and to the duration of the exposure to that particular material. Dr. Maddox agreed that scientists presently do not know the mechanism by which asbestos causes mesothelioma. Additionally, he recognized that his opinions were not based on any sort of direct attribution, but rather, were grounded entirely upon an assessment of increased risk.

The trial court sustained the Frye challenge and precluded the plaintiffs from adducing the any-exposure opinion. Overall, Judge Colville could find no credible explanation for how it was that Dr.
Maddox was able to determine if it was exposure to a particular defendant’s friction product that
caused a plaintiff’s mesothelioma, and not some other exposure to asbestos material. Even if one accepts that a single fiber may possibly increase the risk of developing disease, it did not accept that an unquantified (and potentially infinitesimal) increase in risk could serve as proof that a defendant’s product was a substantial cause of a plaintiff’s or decedent’s disease. Generally accepted scientific methodology may well establish that certain “high dose” asbestos exposure causes, or contributes to, a specific hypothetical plaintiff’s disease, but the plaintiffs had not proffered any generally accepted methodology to support the contention that a single exposure or an otherwise vanishingly small exposure has, in fact, in any case, ever caused or contributed to any specific individual’s disease, or even less so, that in this case such a small exposure did, in fact, contribute to this specific plaintiff’s disease.

Plaintiff appealed, and the Superior Court reversed, basically disagreeing with every aspect of the trial court's analysis. It relied on Ferebee v. Chevron Chemical Co., 736 F.2d 1529 (D.C. Cir. 1984), essentially for the proposition that, so long as an expert is willing to testify to an extrapolation, courts should permit its admission. (The notion that courts have no screening function is at odds with the last couple decades of federal court evidence law, just as it was at odds with most federal circuits at the time the DC CIrcuit opinion was written, and with states that have adopted Daubert and also those that still adhere to Frye.) Defendants then appealed.

Appellants (and their amici) offered extensive critiques of Dr. Maddox’s methodology from both scientific and logical perspectives, with the bottom line that the any-exposure opinion remains a hypothesis or assumption, and stressing Dr. Maddox’s inability to identify any peer-reviewed scientific support undergirding the opinion. While plaintiffs offered much argument on the effects of high doses of asbestos, they did not squarely address appellants’ arguments concerning differences in potency among asbestos fibers, or the potential that exposure to asbestos from a defendant’s product might be minimal in comparison to others.

The state Supreme Court noted that this case was selected among test cases for the any-exposure opinion as a means, in and of itself, to establish substantial-factor causation. The plaintiff's efforts to invoke case reports, animal studies, and regulatory standards to support the theory were ineffectual in terms of substantial-factor causation, since the most these can do is suggest that there is underlying risk from the defendants’ products, a proposition with which the trial court did not disagree.  What was more of concern was the assessment of substantiality.
In this regard, Dr. Maddox’s any-exposure opinion was in irreconcilable conflict with itself. Simply put, one cannot simultaneously maintain that a single fiber among millions is substantially causative, while also conceding that a disease is dose-responsive. The any-exposure opinion, as
applied to substantial-factor causation, did not consider the three factors which Dr. Maddox himself explained needed to be considered in trying to estimate the relative effects of different exposures: potency, intensity, duration.

The court took on directly the analogy offered by Dr. Maddox in support of his position: the marbles-in-a-glass illustration changes materially upon the recognition that to be a fair comparison one must include the factors that the marbles are all non-uniform in size and shape, and microscopic so that millions are needed to fill the glass. From this frame of reference, it is very difficult to say that a single one of the smallest of microscopic marbles is a substantial factor in causing a glass of water to overflow.  

Superior Court reversed; trial court affirmed.

Beverage Maker Not Liable for Alleged Failure to Warn

The maker of  a drink containing alcohol and caffeine was not liable to a woman allegedly injured when the driver of the motorcycle on which she was a passenger crashed, after the driver consumed the beverage.  See Cook v. MillerCoors LLC, No. 11-1488 (M.D. Fla., 10/28/11).

The operator of the motorcycle in the accident was killed, and plaintiff Cook, who was a passenger, was injured.  Prior to the crash, the driver allegedly had consumed several “Sparks”
alcoholic beverages containing caffeine and other stimulants, manufactured by defendant.

Cook argued that alcoholic beverages such as Sparks containing stimulants are “uniquely dangerous” because they appeal to younger drinkers and because the addition of caffeine enables one to drink more alcohol without feeling as intoxicated as one normally would. Thus, she alleged, consumers of these beverages are more likely to “engage in dangerous behavior such as driving.”  She asserted the driver did not appear impaired, even though toxicology reports from his autopsy revealed that his blood alcohol level was 0.10 at the time of the crash.

Defendant responded that the risks associated with operating a motor vehicle while under the influence of alcohol are well known; therefore, it could not be held responsible for the operator's choice to consume Sparks then illegally operate his motorcycle. The addition of other ingredients to the beverage did not lessen his responsibility to refrain from operating his motorcycle after having consumed the alcohol, and his actions, not the manufacture of Sparks,
proximately caused Cook’s injuries.  The crux of the defense motion to dismiss thus was that there is no cause of action against a manufacturer of alcoholic beverages for injuries resulting from their consumption because the effects of alcohol consumption are well known. With a response from plaintiff that the legion of such holdings in courts everywhere apply to “conventional” alcoholic beverages, not to an alcoholic beverage mixed with stimulants which allegedly suppress the consumer’s subjective awareness of alcohol’s well-known effects.

Regarding the failure to warn theory, a plaintiff must establish the existence of a duty. A manufacturer’s duty to warn arises when there is a need to inform consumers of dangers of which they are unaware.  The effects of alcohol and the need to not drink and drive are universally known.  While plaintiff argued about the unconventionality of this product, plaintiff did not and could not allege that the driver was unaware that he was drinking alcohol. His alleged subjective awareness of the speed or impact of those effects did not alter the legal reasoning of precedent that holds that there is no duty to warn because of the universal recognition of all potential dangers associated with alcohol. 

Plaintiff also failed to adequately allege how the product was unreasonably dangerous for the design defect claim. The effects of alcohol are universally and objectively well known, irrespective of the operator's alleged subjective awareness of them. The defectiveness of a design is determined based on an objective standard, not from the viewpoint of any specific user, said the court.

Moreover, plaintiff's theories failed as to proximate cause. Plaintiff alleged that the manufacturer's negligence caused the driver to become intoxicated to the point of impairment,
causing the crash and Cook’s injuries. In Florida, however, voluntary drinking of alcohol is the proximate cause of an injury from an intoxicated driver, rather than the manufacture or sale of those intoxicating beverages to that person.  This doomed the negligence claim.

Readers can readily see why the court was reluctant to make an exception to the rule for the "unconventional" beverage.  There are hundreds of alcohol-containing products that are not "conventional" in one way or another, by taste, ingredients, color, manufacturing process, advertising... To shift responsibility from the person who over-consumes one of these and then drives impaired is to send the absolutely wrong policy message.

Courts have typically recognized no duty on the maker, regardless of plaintiff's attempt to differentiate either themselves or the product. See, e.g., Malek v. Miller Brewing Co., 749 S.W.2d 521 (Tex. App. 1988) (finding no duty to warn despite claim that advertising led plaintiff to believe that “Lite” beer was less intoxicating than other beer); Pemberton v. Am. Distilled Spirits Co., 664 S.W.2d 690 (Tenn. 1984); Greif v. Anheuser-Busch Cos., Inc., 114 F. Supp. 2d 100 (D. Conn. 2000)(particular, alleged tolerance of an individual consumer); MaGuire v. Pabst Brewing Co., 387 N.W.2d 565 (Iowa 1986).


 

Proof of General Causation in Drug Case Not Automatic

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.

Failure to Warn Even When You Warn? Court Rejects Plaintiff's Theory

One of the fascinating and disturbing things about failure to warn claims is the endless supply of creative, far-fetched, fantastic, implausible, fanciful, incredible, questionable, even bizarre theories that plaintiff lawyers sometimes come up with to support this type of claim.

Last week, a Pennsylvania appeals court rejected just such a theory. Specifically, plaintiff alleged that a failure to warn caused her injury -- nothing strange there.  But the manufacturer DID warn specifically of the condition she developed.  So, what was the plaintiff's failure to warn theory?  That a drug maker may be liable for failure to warn despite warning of the condition plaintiff developed, because a warning about a different medical issue —one that she did not develop— would somehow have caused her doctor to not prescribe the drug.  Cochran v. Wyeth Inc., 2010 WL 2902717 (Pa. Super. Ct., 7/27/10).

Plaintiff ingested the prescription weight-loss drug dexfenfluramine, which was manufactured by Wyeth and sold under the brand name Redux. Wyeth informed the prescriber that Redux may cause primary pulmonary hypertension (“PPH”). The doctor, in turn, warned plaintiff of the risk of PPH prior to prescribing her Redux. At the time of his decision, however, the prescriber claimed he was unaware of the risk that Redux may cause valvular heart disease (“VHD”).  Later, plaintiff was diagnosed with PPH, which she had been warned about.  But she claimed that the doctor would not have prescribed Redux to her had he been warned that Redux could cause VHD.

Proximate cause is an essential element in a failure to warn case.  A proximate, or legal cause, is defined under Pennsylvania law as a substantial contributing factor in bringing about the harm in question. That is, a plaintiff must establish proximate causation by showing that had defendant issued a proper warning to the learned intermediary, he would have altered his behavior and the injury would have been avoided.   Wyeth argued that even if its warnings with regard to VHD were inadequate, its failure to warn of VHD was not the proximate cause of plaintiff's PPH.  To establish proximate causation, plaintiff must prove that the warnings failed to disclose the risk of her particular injury (PPH).

The trial court agreed. On appeal, the court found an absence of clear authority on the issue, but strong guidance in those cases that have addressed a plaintiff's burden of proving proximate causation in the informed consent context.  Finding the torts of informed consent and failure to warn analogous, the superior court was persuaded by those jurisdictions that have concluded a plaintiff cannot establish proximate causation where the non-disclosed risk never materialized into an injury.

Here, the risk of VHD did not develop into the actual injury of VHD. Although the prescriber testified in deposition that he would not have prescribed Redux had he known of the risk of VHD, this does not alter the fact that while Wyeth allegedly failed to disclose the risk of VHD the plaintiff suffered from PPH. In these circumstances, the relationship between the legal wrong (the alleged failure to disclose the risk of VHD) and the injury (PPH) was  "not directly correlative and is too remote" for proximate causation.

Summary judgment for defendant affirmed.