Asbestos litigation has now entered the modern era. Namely, the first case involving testimony related to BAP1 mutations has gone to trial in California: the Ortwein case. The trial involved a 50-year-old woman with pleural mesothelioma, represented by the Kazan firm.
Asbestos litigation has now entered the modern era. Namely, the first case involving testimony related to BAP1 mutations has gone to trial in California: the Ortwein case. The trial involved a 50-year-old woman with pleural mesothelioma, represented by the Kazan firm. The defendant at trial was CertainTeed, a building manufacturer, and the case settled shortly before it would have gone to the jury.
But does the Ortwein trial matter when it is only one case out of thousands filed every year? We believe it does matter. Why? For one, the ultimate issues for trial require thoughtful, intelligent, and efficient discovery requests to frame the proper issues for trial. Mutation analyses do not grow on trees, so to speak, and so the usual discovery approaches will be ineffective for the cases where the mutation possibilities do matter. The trial also matters because it illustrates some (but not all) of the types of cases in which the presence or absence of a germline mutation will matter. In short, the Ortwein trial marks a transformation point in the world of asbestos litigation, a transformation that has already been felt in other types of litigation. For a little context, it is important to delve into the past, and then to move beyond the realm of asbestos.
For decades, the harsh reality of asbestos litigation was that most people died relatively quickly of their diseases, and much attention was focused on which defendant(s) were involved with the source of disease. Once the cases moved past “state-of-the-art” issues, science received relatively little attention in asbestos litigation. However, that era is now ending as molecular knowledge increases.
For the past decade or so, molecular science has undergone a revolution, fueled mostly by spectacular advances in technology as well as a precipitous drop in the cost for genetic sequencing. With regard to mesothelioma, molecular science was brought to the forefront in a 2011 publication providing a look at genetic factors relevant to why some asbestos-exposed individuals developed mesotheliomas, but others do not.
The 2011 publication arose from the work of a team of scientists led by Michele Carbone (i.e. a lead researcher involved with the erionite village in Turkey) and Joseph Testa (a prominent cancer researcher with a focus on genetics and cancer). In the paper, Carbone and Testa reported on data from two U.S. families with a high incidence of mesothelioma as well as other cancers, including uveal melanomas. Members of both families were not exposed to erionite and had no identifiable occupational exposures to asbestos. They did, however, have germline (i.e., inherited) mutations of the BAP1 gene.
This report on the presence of BAP1 gene mutations in families with high rates of mesothelioma raised questions about the role of familial genetic inheritance in the development of mesothelioma and other cancers. The research team concluded that a BAP1–familial cancer syndrome was identifiable mostly through development of mesotheliomas and uveal melanomas. The researchers concluded their data could be interpreted in two ways: (1) BAP1 mutations could somehow have some sort of predisposing effect on asbestos-exposed individuals; or (2) BAP1 mutations alone could potentially be sufficient to cause mesothelioma independent of asbestos exposure. The investigators summarized their overall conclusions as follows:
“In summary, we demonstrate the existence of a BAP1-related cancer syndrome characterized by mesothelioma, uveal melanoma and possibly other cancer types. We hypothesize that when individuals with BAP1 mutations are exposed to asbestos, mesothelioma predominates. Alternatively, BAP1 mutation alone may be sufficient to cause mesothelioma.”
Since the publication of the Testa and Carbone article, research on BAP1 has accelerated and multiple studies have been published to support the view that germline mutations of BAP1 (and potentially numerous other genes) increase susceptibility for the development of several types of cancer, including mesothelioma (see here, here and here for examples).
Why do the molecular findings matter? In short, proof of the existence of BAP1 mutations brings into some asbestos cases new concepts and questions regarding the broad topic of familial cancer syndromes and questions regarding individual susceptibility. Plaintiff and/or defense attorneys may increasingly try to utilize genetic susceptibility as an argument for or against a causative role of a “toxin.”
For plaintiffs, counsel may seek to apply the “eggshell” plaintiff doctrine. For defendants, various potential arguments may be made depending on the nature of the specific case. If a plaintiff was born with a mutated gene, the defense may argue the mutation is the cause of the disease (as opposed to the alleged “toxic” exposure). In other instances, manufacturers may seek to argue that a duty to warn does not extend to individuals who are more susceptible to a potential toxin because of their genetic make-up, and therefore, might be affected at lower exposure levels than the general population. Those arguments cannot be asserted effectively or properly by persons who lack knowledge of historic developments in various branches of science.
For attorneys who “live and breathe” asbestos litigation, it is certainly worth taking a look at how molecular science has permeated other types of “toxic torts.” We previously addressed this topic in an interview with Gary Marchant, Ph.D. which is posted on our blog. In Actos bladder cancer litigation, molecular science apparently played a meaningful part in why a group of inter-related defendants recently offered over $2 billion to settle thousands of bladder cancer claims. The offer went on the table after a federal MDL judge denied a defense Daubert motion, and held instead that plaintiff’s world-class molecular science experts had offered plausible molecular evidence to show that the Actos drug (also known as pioglitazone) could cause bladder cancer in less than one year.
The impact of molecular science is also increasingly evident in benzene litigation. There, appellate and trial courts have made dozens of rulings about molecular and genetic evidence, and the rulings and evidence have cut both ways. On one hand, every major defense group tried – but failed – to convince SCOTUS to review the First Circuit’s Milward ruling allowing admission of molecular evidence regarding benzene causing certain forms of blood cancer. As a result, some defendants with some particular products or places of work now will pay to settle some claims involving some particular types of blood cancer with certain patterns of molecular alterations. On the other hand, some of the same defendants also have sought and used genetic testing in an attempt to exonerate their products.
The bottom line? Science goes where it goes, and may create risks and rewards for plaintiffs and defendants alike. Maintaining an awareness of current scientific developments can help you assess potential implications of new findings, and reduce the risk of being ambushed by your opponent at deposition of trial.
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