Toxic Tort Litigation Blog : Toxic Tort Lawyer & Attorney : Epstein Becker Green Law Firm : Product Liability, Contamination, Pollution

A Sixth Circuit case, Moeller v. Garlock Sealing Technologies, LLC, 2011 U.S.App.Lexis 19987 (6^th Cir. Sept. 28, 2011), is the most recent in a series of judicial decisions that have rejected the opinions of plaintiffs’ experts in asbestos cases who espouse the “any exposure” or “any fiber” or “single fiber” theory of causation.  Pursuant to this specious line of reasoning, asbestos disease is a cumulative dose response process. Each and every exposure to asbestos during a person’s lifetime, no matter how small or trivial – even a single fiber – substantially contributes to the disease, whether it be asbestosis, lung cancer or mesothelioma. Using this theory of causation, plaintiffs have initiated a wave of new lawsuits against defendants far removed from the production of asbestos containing products.  As defense practitioners are well aware, successfully challenging weak causation expert opinions is key to winning any toxic exposure case, whether it involves asbestos or some other substance.

In a “must read” column in the New York Law Journal, dated October 19, 2011 titled "Courts Shoot Down Asbestos Causation Theory", Michael Hoenig, whose law firm defends asbestos case litigation, describes how plaintiff experts are promoting the “any fiber” or “any exposure” theory in courtrooms across the country and how a series of notable judicial decisions have begun to reject these theories as the underlying scientific methodology is subjected to scrutiny. In a recent amicus curiae brief filed by eleven distinguished scientists in a Pennsylvania asbestos case, none of whom received funding from or testified as experts for any of the parties in the case, the scientists attacked the methodological errors of the “any exposure” expert for:  (1) failing to consider the dose level of exposure and minimum threshold of asbestos fiber levels; (2) failing to consider the physical chemical and toxicological differences between various types of asbestos; (3) failing to distinguish between general causation and specific causation (and not even establishing general causation for chrysotile asbestos); (4) for suggesting that “every exposure” and “cumulative risk” theories are generally accepted when they are not; and (5) ignoring the large body of toxicological studies demonstrating that chrysotile asbestos is not potent as a cancer-causing agent. 

The Pennsylvania Supreme Court observed in Gregg v. V-J Auto Parts Co., 943 A.2d, 216, 223 (Pa. Sup. Ct. 2007), that although it was “common for plaintiffs to submit expert affidavits attesting that any exposure to asbestos, no matter how minimal, is a substantial contributing factor in asbestos disease,” such opinions are not “not couched within accepted scientific methodology.”  The court called the “willingness on the part of some experts” to offer such opinions “one of the difficulties” courts face in the mass tort cases.

As the plaintiff bar continues to look further and further afield in its “endless search for a solvent bystander,” as one well-known plaintiff’s lawyer described the litigation, successful challenges under Daubert and Frye should only increase.  The author thanks Mr. Hoenig for his thoughtful treatment of this important topic.

From a risk management perspective, peripheral toxic tort defendants often decline to mount  Daubert challenges due to the cost and time involved and the uncertainty of the result, particularly when the plaintiff presents them with seemingly  reasonable settlement demands.  As a result, hundreds of peripheral defendants continue to be named in these cases and often pay their "penny in tribute" just to get out of the case.  Unfortunately, in many jurisdictions, judges responsible for large asbestos dockets are unwilling to give appropriate consideration to motions by "shade tree" defendants who might otherwise challenge plaintiffs' experts'  theories of causation.  Cynically, these judges know that the cases will most likely settle out if this type of motion is given short shrift.  There is little incentive for a peripheral defendant to risk an adverse  judgment at trial merely to earn the right to bring an appeal, no matter how strong the grounds may be.  Hopefully, cases like Moeller will have a trickle down effect and motivate the trial judges responsible for the asbestos dockets to re-think their approach. 

Consumer Reports, among others, reported this week that the International Agency for Research on Cancer ("IARC"), which is part of the World Health Organization ("WHO"), has classified low-level radiation from cell phones as "possibly carcinogenic to humans" based on limited evidence linking cell phone use to glioma, a type of brain cancer.  Although Consumer Reports concluded in its article that IARC's action was based on "limited evidence" and doesn't "convincingly" link typical cell phone use with cancer, an American public that often skims only headlines of articles, may be susceptible to appeals of sympathy by plaintiff lawyers representing long-time cell phone users with brain cancers.  Throughout the 1980's the utility industry battled spurious claims, premised upon junk science, that electromagnetic field radiation was responsible for "cancer clusters" of child leukemias and other dreaded diseases.  Although virtually every major EMF toxic tort claim was successfully defended by industry over a period of years, tens of millions of dollars was spent defending these lawsuits, which were brought in courts all  across the country.  As in the case of low dose radiation from cell phone use, there were  millions of millions of potential plaintiffs in the EMF cases and all of the prospective utility industry defendants had deep pockets. Following issuance of the IARC release, a spokeswoman for the Federal Communications Commission ("FCC") stated that FCC currently requires that all cell phones meet safety standards based upon the advice of federal health and safety agencies.  Moreover, according to the National Cancer Institute's Surveillance Epidemiology and End Results Program ("SEER"), the incidence of brain cancer in the United States has actually declined over recent years as cell phone use has skyrocketed.  Despite these reassuring pronouncements, well-heeled plaintiff lawyers may bring some cases as trial balloons to test industry resolve based upon other equally ambiguous pronouncements, such as the contention that cell phone use can affect "brain function".  As in the cases brought against chemical manufacturers in the 1980's,  which alleged that chemicals cause generic  "immune system dysfunction", enterprising plaintiffs may attribute any number of injuries to purported "brain function" impacts.  Hopefully, courts will continue to exercise their gatekeeper roles to maintain some semblance of scientific rigor in the courtroom to exclude inconclusive science  if these cases are brought. 

Guest Blogger M.C. Sungaila, one of California's most best known appellate advocates,  briefed and successfully argued the Molina appeal discussed here on behalf of Shell and Chevron. 

A Californiia appeals court rejected the lenient increased risk causation standard used to establish causation in asbestos cases in a toxic tort case not involving asbestos.  The Second Appellate District of the California Court of Appeal in Los Angeles upheld a defense verdict last month, in  Molina v. Shell OIl Company et al, determining that the trial court correctly refused to charge the Rutherford “increased risk” instruction applicable in asbestos cases because the ability of a product to cause the type of harm suffered by the plaintiff was hotly contested.

After a five-week trial and four days of deliberations in the trial court, a jury concluded that William Molina – who suffered from a variety of cancers and other ailments -- was not entitled to damages for his alleged exposure to defendants’ solvents during his 17-year career at a Firestone tire plant. The jury found that neither the solvents’ design nor any warning associated with them was a substantial factor in causing Molina’s non-Hodgkins lymphoma (NHL). Molina appealed, claiming among other things that the causation instruction used in California's asbestos litigation should have been given to the jury.

The appeals court court stopped short, however, of holding that the more liberal  Rutherford causation standard can never apply outside the asbestos context. Nevertheless, the Court of Appeal addressed a question repeatedly posed to trial courts throughout the state over the last five years: should a more lenient causation standard adopted by the California Supreme Court in the asbestos context be extended to other types of toxic tort cases like benzene? The appellate court’s answer was a qualified "no".

Causation, of course, is an essential element of a tort action. California has definitively adopted the substantial factor test of the Restatement Second of Torts for cause-in-fact determinations. Implicit in the substantial factor causation standard in a toxic tort case is the requirement of proving both that a chemical can cause a particular adverse health effect and that it did cause that effect in the plaintiff.  In other words, proof of causation necessarily includes a threshold determination whether, in reasonable medical probability, a particular chemical is capable of causing in humans the type of harm suffered by the plaintiff (i.e., “general causation”).　 If the chemical does not possess that capacity, the chemical cannot have caused the particular plaintiff’s claimed harm.　 But if the chemical does have that capacity, then the causation inquiry shifts to whether the plaintiff’s exposure to the chemical in question was, in reasonable medical probability, a substantial factor in causing this particular plaintiff’s harm (i.e., “specific causation”).　Toxic tort causation also involves a threshold element of exposure. In order to determine whether an exposure is a possible contributing factor to a plaintiff’s injury, ‘[f]requency of exposure, regularity of exposure, and proximity of the . . . product to [the] plaintiff are certainly relevant.” (Lineaweaver v. Plant Insulation Co. (1995) 31 Cal.App.4th 1409, 1416.)

Molina contended that California Civil Jury Instruction (CACI) No. 435, a relaxed “increased risk” causation instruction, should have been given because of the difficulties of proving cancer causation. The defendants successfully urged that the increased risk instruction under Rutherford should not apply where, as in Molina’s case, the ability of a chemical to cause a particular type of cancer is hotly disputed and far from well-established.

In Rutherford v. Owens-Illinois, Inc. (1997) 16 Cal.4th 953, 960, at the end of the first phase of trial, the jury concluded that exposure to asbestos fibers proximately caused the decedent’s lung cancer and awarded damages. After this phase, several defendants settled. In a second phase of trial, the jury was asked to apportion damages and allocate fault to the remaining defendant, Owens-Illinois. Owens-Illinois objected to the use of an instruction in the second phase of trial which stated that, once the plaintiff had established both that he was exposed to defendants’ asbestos and that his injuries were legally caused by asbestos exposure generally, the burden then shifted to the defendant to establish that its product was not a legal cause of the plaintiff’s harm.

The California Supreme Court rejected the use of the burden-shifting instruction as too “fundamental” a departure from traditional substantial factor causation. However, the Court concluded that, rather than be required to “trace the unknowable path of a given asbestos fiber,” a “plaintiff[] may prove causation in [an] asbestos-related cancer case[] by demonstrating that the plaintiff’s exposure to defendant’s asbestos-containing product in reasonable medical probability [fn. omitted] was a substantial factor in contributing to the aggregate dose of asbestos the plaintiff or decedent inhaled or ingested, and hence to the risk of developing asbestos-related cancer, without the need to demonstrate that fibers from the defendant’s particular product were the ones, or among the ones, that actually produced the malignant growth.”

Thus, in Rutherford, “it was already determined what caused the plaintiff’s illness—asbestos. The only remaining issue before the Court was the proper standard for determining who manufactured or supplied the asbestos that caused the plaintiff’s illness.” (Loewen, Causation in Toxic Tort Cases: Has the Bar Been Lowered? (Spring 2003) 17 Nat. Res. & Env’t 228, 229 (hereafter Loewen).) As one commentator observed: “This is undoubtedly the reason that the Rutherford court consistently and repeatedly limited its holding to ‘asbestos-related cancer cases’: its language linking risk to cause was expressly limited to cases where it has been determined that the cancer was ‘asbestos-related.’” (Ibid.) Accordingly, Rutherford does not apply in a case like this, where the ability of the defendants’ products to cause the plaintiff’s type of cancer is hotly disputed.

In Molina’s case, defendants’ toxicology expert testified that solvents do not cause NHL.  While one plaintiffs’ expert asserted that solvents could cause NHL, another plaintiffs’ expert testified that the evidence of a causal link between benzene and NHL was “weak” and therefore he could not state to a reasonable degree of medical probability that benzene could cause NHL.  Moreover, one of plaintiffs’ experts admitted that NHL is frequently idiopathic or of unknown origin.

The Court of Appeal agreed that the trial court correctly refused the Rutherford “increased risk” instruction applicable in asbestos cases. Rutherford involved a very different situation: in that case, a jury had already determined that the asbestos had caused the plaintiff’s lung cancer. The only remaining question was which manufacturers were responsible. The cause of Mr. Molina’s NHL, however, was not established.  In fact, the capability of defendants’ products to cause Mr. Molina’s injury was one of the most critical and hotly disputed issues in the case.

Guest Blogger M.C. Sungaila  is a partner in the appellate law firm of Horvitz & Levy in Los Angeles. Her appellate work has helped shape toxic tort law in California, including the scope of the duty to warn sophisticated users of product hazards and the guidelines for admitting expert testimony at trial.

Toxic Tort Litigation Blog’s post earlier this year about a Michigan appellate court’s affirmance of an award to residents of a home overrun with mold – without any expert testimony to prove causation – raises the question: what would happen to such a claim in a more famously liberal state like California? In this instance at least, California seems more likely to come to a more ‘conservative’ conclusion than Michigan.

Expert Testimony

California not only requires expert testimony for complex causation questions; it tests the foundation for that testimony and requires trial courts to exclude expert opinions that are unsupported. See an early article describing the development of these standards by M.C. Sungaila and David M. Axelrad published in California Lawyer. The California courts of appeal have specifically considered the admissibility of expert testimony in mold cases and ruled in favor of the defendants. Most recently, in Dee v. PCS Property Management, one of the appellate divisions in Los Angeles confirmed the trial court’s ability to exclude unfounded expert testimony in a residential mold case. Darcee Dee lived in an apartment for slightly over four months. She sued her landlord and property management company for alleged physical injuries, as well as fear of cancer, from living in an apartment that purportedly had toxic mold in it. After hearing the plaintiff’s experts testify over several days concerning their opinions and the foundation for them, the trial court granted the defendants’ motions in limine to exclude most of the experts’ testimony based on a lack of foundation. The remaining portions of Dee’s claims were tried to a jury, and the jury rejected her claims. The appellate court affirmed the judgment in Dee, concluding that the trial court did not abuse its discretion by excluding plaintiff’s experts for lack of an adequate foundation.  Each of Dee’s experts sought to testify that her exposure to mold mycotoxins caused her symptoms and her susceptibility to cancer, without any evidence that she was exposed to potentially harmful mycotoxins at her residence. The court relied on the decision in another mold case, Geffcken v. D’Andrea,  and distinguished its own prior decision in Roberti v. Andy’s Termite, the only published opinion to have rejected the trial court’s authority under the California Evidence Code to thoroughly analyze the foundation for expert testimony in order to determine its admissibility.  For another take on the Geffcken and Dee mold decisions, see an article on the Kring & Chung LLP website.

Toxic Tort Causation Standards

While California appellate courts would be certain to require expert testimony on causation, it is not as clear how they would analyze causation in a toxic tort case.  In toxic tort cases, a plaintiff must generally prove not only that a chemical or substance can cause a particular adverse health effect but also that it did cause the harm to the plaintiff.  Proof of causation therefore necessarily includes a threshold determination whether, as a matter of reasonable medical probability, a particular chemical is capable of causing in humans the type of harm suffered by the plaintiff (i.e., “general causation”). If the answer is that the chemical does not possess that capacity, then the chemical cannot have been a cause of plaintiff’s harm. But if the chemical does have that capacity, then the causation inquiry (in jurisdictions like California which apply a substantial factor causation standard) becomes whether the plaintiff’s exposure to the chemical in question was as a matter of reasonable medical probability a substantial factor in causing the particular plaintiff’s harm (i.e., “specific causation”).   For a helpful analysis of causation in toxic tort cases, see the excellent discussion by David E. Bernstein, a Professor at the George Mason University School of Law, in an article  titled "Getting to Causation in Toxic Tort Cases".  This two-step general and specific causation framework is almost universally accepted by federal courts analyzing toxic tort causation (including the Ninth Circuit, see, e.g., Golden v. CH2M Hill Hanford Group, Inc. (9th Cir. 2008) 528 F.3d 681, 683).  Trial courts in California have analyzed proof of causation in toxic tort cases along general and specific causation lines as well. California appellate courts have not, however, expressly adopted the general and specific causation distinction in a published decision. This has led to some confusion, as plaintiffs have attempted to convince courts that such a “two-part”causation test is incompatible with California’s prevailing causation standards.  In Dee v. PCS Property Management, the plaintiff raised this argument on appeal, but the Court of Appeal declined to reach it because the jury had found no negligence, which made an argument about causation standards “irrelevant.” An opportunity to address the general and specific causation distinctions head-on may come later this year, however, when the Court of Appeal in Los Angeles is likely to hear argument in and decide the plaintiffs’ appeal of summary judgment in a high-profile benzene exposure case brought by former students at Beverly Hills High. The appellate docket for the case, Lee v. Venoco, is attached here. The original summary judgment decision ruled on the admissibility of expert opinion on both general causation and specific causation.

BNA Toxics Law Reporter reported on December 31, 2009, that a Michigan Appeals Court affirmed a mold exposure verdict for $303,260, finding that expert testimony was not necessary under Michigan State law to prove either general causation or specific causation.  In Genna v. Jackson, Mich. Ct. App., No. 285746, the Michigan Court Of Appeals (Oakland Circuit Court) affirmed the trial court's denial of defendant's post-judgment motion for judgment notwithstanding the verdict (JNOV) and for a new trial. Based upon a review of the decision, it is not disputed ( at least by this writer) that defendant's negligent conduct resulted in substantial  flooding in the plaintiffs' home and the gross mold contamination that resulted. Plaintiff's microbial expert identified two molds in the home--penicillum and aspergillus--which he testified at trial could affect human health and pose safety issues.  Plaintiffs' children began to experience what the court described as "flu-like symptoms including: diarrhea, vomiting, congestion and nosebleeds".  Over a period of months, these symptoms worsened and the symptoms did not respond to aggressive treatment.  Plaintiffs did not call an expert to testify that these symptoms were the result of the mold contamination. Nonetheless, the appeals court held that plaintiff did not have to demonstrate that the alleged toxin is "capable" of causing injuries like those suffered by the children, let alone requiring the plaintiffs to prove that these children's symptoms were caused by mold exposure. The court reasoned as follows: "This is not a complicated case: the children were removed from the home, the mold was discovered, and the children recovered".  Thus, the court based its decision on "circumstantial evidence that would 'facilitate reasonable inferences of causation, not mere speculation'."  With due respect to the appellate panel, which was obviously impressed with the graphic description of "patches of mold of all different colors all over the walls and ceilings in her kitchen, family room and dining area", this is a really bad decision and a potentially dangerous precedent in Michigan!  It is a mistake to base toxic tort causation on a temporal relationship,i.e., the "children were removed from the home, the mold was discovered, and children recovered."  Flu-like symptoms can be caused by......well, the flu.  That the children's symptoms went away could signify that they had recovered from a prolonged bout of the  flu. Based upon this court's reasoning, the children's illness could have been caused just as easily by lead paint poisoning, contamination of their drinking water, VOC's emanating from their carpeting,  formaldehyde in the walls....or just a really bad allergic reaction to the family's cats.  Did anyone check the family furnace for carbon monoxide gas?  It is not as if the symptoms that the children suffered from were unique to mold "poisoning". Moreover, no one appears to have apprised the trial court that it is not unusual that the antibiotics the children were administered did not cure a viral infection! We also suffer from flu-like symptoms all the time. It is not unusual, particularly in the frigid month of February in Royal Oak, Michigan, when this incident occurred, for these symptoms to occur and to persist in the absence of an exposure to toxic mold. The court faults the defendant for not submitting "any scientific evidence that the mold in her condominium could not have caused plaintiffs' injuries." (emphasis theirs).  And since when does the burden in a negligence case shift to the defendant, and to prove a negative no less?