Johnson & Bell Shareholders, D. Patterson Gloor and Stephen P. Ellenbecker, along with Law Clerk, Stephanie Flowers, have developed this primer on the burgeoning area of genetics and its interplay in litigation. The article touches on the considerations plaintiffs and defendants should factor into genetic litigation strategies, and the court’s familiarity with genetic issues.
Genetics: The Future is Now
Introduction
Toxic tort litigation involves a plaintiff who alleges he or she suffered an injury as a result of an exposure to a toxic substance.1 These cases typically hinge on whether the plaintiff meets the burden of proving proximate cause. Proximate cause includes general and specific causation. General causation is evidence that the substance in question is capable of causing Plaintiff’s disease.2 Specific causation is evidence proving that the substance in question did cause Plaintiff’s disease. Prior to genomic science, experts typically opined on the general risk of injury posed by the alleged exposure. For years, experts relied exclusively upon epidemiological studies to show or disprove causation.
Most courts accept epidemiological studies and ratios as evidence of causation in the absence of another method more capable of identifying specific causation. Courtrooms are lagging behind advancements in genetic science which promise to be a powerful tool in proving or debunking causation in complex exposure cases.
Courts are, however, familiar with genetic evidence. Genetic evidence, like DNA, has been routinely introduced since the mid-1980s. Its admissibility in early years faced similar pushback from courts as being a novel science. However, DNA transformed the criminal justice system. DNA evidence is critical in identifying the true perpetrator of a crime. It is asserted as grounds for re-trying criminal cases and for exonerating wrongly convicted individuals. Aside from the criminal arena, courts regularly order DNA testing in paternity disputes. This type of genetic evidence can be critical in contested inheritance cases.
Genomic science is now capable of specifying certain genes and gene mutations that cause certain conditions or diseases. With constant technological advances, genetic testing is more accessible at lower costs and higher speeds than ever before. Genomic evidence has the potential to be the new weapon in mass tort litigation.
In this article, we forego a genetics tutorial and skip to taking a pragmatic look at how both plaintiffs and defendants might use genomic science in litigation and discuss the hurdle of FRE 35 and other admissibility challenges either party might face. Finally, we describe the current state of genomic science in the courtroom by analyzing recent cases in which litigants either successfully admitted genetic evidence or were denied the opportunity to use it.
Applying Genetic Science to the Litigation
Genetic evidence can be useful for all parties in toxic tort litigation. In addition to the ordinary epidemiologist, plaintiffs may use geneticists to bolster their causation proofs by introducing evidence of genetic susceptibility. For example, a genetic test that shows a person having a mutated CYP2E1 gene may indicate his susceptibility to benzene’s toxic effects. Where there is clear evidence of exposure, this could be fatal to the defense. Plaintiffs have also attempted to introduce synergy theories where genetic testing shows a person having a genetic predisposition to the alleged injury. Exposure to a toxic substance may heighten the already increased risk of developing a disease for an individual carrying a predisposing genetic variant, like BRCA1.3
The defense should articulate that a genetic predisposition is no more dispositive than risk ratios. Individuals with the mutated gene are only members of genetic subpopulations and any relative risk associated with this class does not translate to particularistic or individualistic causation.4 Furthermore, defendants may challenge synergy theories for failing to offer anything more than mere conjecture.
Genetics will also be subject to Daubert and Frye challenges prior to trial in toxic tort cases. An expert must consider all possible causes before coming to his/her conclusion. Genetics are one possible cause of or gateway to disease. If an epidemiologist rules in exposure to an alleged toxin, but fails to rule in genetics, the expert’s method is clearly unreliable. Without appropriately ruling in genetics, the expert is incapable of ruling out genetics as a cause.5 Defense attorneys should routinely check whether plaintiffs’ experts adequately consider genetics before opining that genes played no role in causing the disease.
If the plaintiff did not submit to genetic testing for his or her own case theory, defendants can request such testing during discovery under Federal Rule of Civil Procedure 35, or your state equivalent.6 Genetic testing, in many cases, can be done by taking a saliva swab or drawing blood, rather than an invasive or painful procedure. So long as plaintiff put his or her health at issue, genetic testing should be permitted during discovery as it may produce highly probative evidence of causation. Defendants should argue that plaintiff’s genes, rather than the alleged exposure, are the actual cause. In the alternative, genetic testing may expose the absence of necessary “cause and effect” biomarkers.7 The presence or absence of these biomarkers may ultimately implicate the alleged toxin or some alternative cause in plaintiff’s disease.
Although genetic testing has potential for high rewards, there are also high risks involved in unfavorable results from the tests. Bringing up genetics as an alternative cause opens the door for plaintiffs to argue they are genetically susceptible to the disease. Any risk plaintiffs can bring up at trial in combination with the alleged exposure may assist plaintiffs in meeting their burden. Moreover, if certain biomarkers of effect are present in the results, plaintiffs will surely use that ‘smoking gun’ as qualitative evidence that the alleged toxin caused the injuries. Regardless of the potential risks involved, genetic evidence may provide clearer explanation of the actual cause of injuries.
Current State of Genomic Science in the Courtroom
As we indicated earlier, genomic evidence is no stranger to the courtroom. Since the early 2000s, litigants sought to use genetics as support for causation theories in products liability, toxic tort, and vaccination cases. Genetic evidence is utilized as an alternative cause, to show susceptibility to toxic effect, and in showing the presence of absence of biomarkers of exposure and/or effect.
Alternative Causation
The most prominent advocate of using genetics as an alternative cause is the United States government in defending claims under the Childhood Vaccine Injury Act of 1986.8 See e.g., Hopkins v. Sec’y of HHS, 84 Fed. Cl. 530, 540-41 (2008); Deribeaux v. Sec’y of HHS, 717 F.3d 1363 (Fed. Cir. 2013); Snyder v. Sec’y of HHS, 553 Fed. Appx. 994(Fed. Cir. 2014). In Snyder, the plaintiffs brought claims under the Vaccine Act, 42 U.S.C. § 300aa-1 – 300aa-34, alleging they suffered from Severe Myoclonic Epilepsy of Infancy (“SMEI”) as a result of receiving the DTaP vaccine. Id. at 995. Plaintiffs submitted to genetic testing which identified a mutated SCN1A gene in each child. This gene provides instructions for making sodium ion channels; abnormal function of these channels may cause seizures. Id. at 996. There, compensation was denied after experts stated the SCN1A gene mutation identified in each plaintiff was the sole cause of their seizure disorders. Id. at 997. Snyder highlights the importance of using up to date science and experienced experts. Ultimately, the judge weighed the Secretary’s experts’ evidence more heavily and discredited the plaintiffs’ expert who lacked in experience and could not explain how the DTaP vaccine actually affected the children. Id. at 1000-1003.9
Newly discovered gene mutations were introduced in Bowen v. E. I. Du Pont de Numours & Co. Plaintiffs alleged their children suffered from serious birth defects as a result of prenatal exposure to the fungicide Benlate. The defense argued that the children suffered from genetically determined developmental abnormalities; plaintiffs contested that diagnosis with epidemiology. In the midst of Daubert challenges, a new genetic test became available which could identify a particular gene mutation found to cause the disorder. Id. at 18-20. The defense requested plaintiffs submit to genetic testing. The tests revealed the children had a mutated CHD7 gene, which geneticists believed was a cause of CHARGE Syndrome. Id. at 19. The defense asserted plaintiffs suffered from CHARGE, caused by the CHD7 mutation and not exposure to Benlate. Id. After the tests were done, plaintiffs’ own experts admitted that Benlate did not cause the genetic mutation itself. Some argued Benlate acted together with the gene mutation to cause the condition. Id. at 19-20. However, because the experts were not qualified in the areas of teratology or toxicology the court excluded their testimony. As a result, the court granted the defendants motion for summary judgment. Id. at 48.10
In 2009, the 8th Circuit dealt with genetic testing in In re Prempro Products Liability Litigation. In that case, plaintiffs argued that their use of hormone replacement therapies resulted in breast cancer. Those therapies had been linked to increased risk of breast cancer; but, a number of genetic variations, including the notable BRCA1 and BRCA2 genes are associated with varying degrees of heightened risk of breast cancer. The defense appealed the trial court’s decision after it allowed an expert to testify that the hormone replacement therapies were the only possible source of hormones essential to the growth of plaintiff’s tumor. The defense argued that the expert wholly failed to consider genetic causes, like family history of breast cancer and other risk factors. However, because the plaintiff submitted to every available genetic test and each came back negative for the most common breast cancer genes, the court affirmed the decision. See id. at 566. The defense experts maintain that genetics caused the plaintiff’s breast cancer, but the jury decided otherwise.11
In re Prempro shows how genetic testing could fare in plaintiff’s favor. The absence of a particular gene, but presence of certain exposure supported finding the hormones were the cause of her breast cancer. This case highlights the risks involved with requesting genetic testing where there is an equally heightened risk from either genetics or exposure. Bowen, on the other hand, highlights the benefits of requesting genetic testing. In that particular case, there was reasonable certainty before requiring testing that the children suffered from CHARGE and that a particular gene was the cause of that disorder. Without such certainty, genetic testing would be riskier and potentially less useful. The genetic testing served as scientific confirmation of the defense expert’s opinion that the children suffered from the disorder and bolstered the alternative cause theory.
Genetic Susceptibility and Synergy
Aside from its use in alternative causation theories, genetic evidence is utilized by plaintiffs who argue they are part of a class of people with a heightened risk of injury due to their genetic makeup. Recently, plaintiffs involved in the talc litigation asserted that they belong to a class of a particular genotype that has a heightened risk of developing ovarian cancer. The individuals were genetic susceptibility to developing ovarian cancer after exposure to talc. The theory was flawed because talc has yet to be conclusively linked to causing ovarian cancer. Thus, defendants argued alleged exposure to talc could not have a synergistic effect. Defendants can utilize the genetic predisposition as an alternative cause of the disease by arguing any alleged exposure did not increase the plaintiff’s already heightened risk of developing cancer. Any additive effect talc allegedly caused could not, to any degree of certainty, overpower or negate the fact that plaintiffs were already genetically predisposed to ovarian cancer which would have developed with or without exposure.12
Genetic susceptibility can be useful for defendants in product liability litigation. Ordinarily, a product manufacturer has a duty to warn consumers of foreseeable potential hazards posed by their products. Failing to adequately warn consumers often results in civil liability. If the results of plaintiff’s genetic testing show a particular genetic susceptibility to disease, defendant product manufacturers may argue that there is no duty to protect individual consumers with rare genetic susceptibilities to the product at issue. This argument runs parallel to an alternative cause defense whereby the plaintiff suffered from an “idiosyncratic response” to the product.13 See Presbrey v. Gillette Co., 105 Ill. App. 3d 1082, 1091, 435 N.E.2d 513, 520, 61 Ill. Dec. 816 (1982) (“. . . the plaintiff's own idiosyncrasy or allergy is the proximate cause of his injury, not the failure to warn.”); Adelman-Tremblay v. Jewel Cos., 859 F.2d 517, 522 (7th Cir. 1988); Bingham v. Terminix Int’l Co., 896 F. Supp. 642, 645 (S.D. Miss. 1995); Friedman v. Merck & Co., 107 Cal. App. 4th 454, 131 Cal. Rptr. 2d 885 (2003).
Biomarkers of Exposure and Effect
Certain diseases, referred to as “signature diseases,” easily and notably implicate their cause. Asbestosis, for example, is caused by exposure to asbestos. Other conditions, however, may have numerous potential causes or may fall into the category of diseases with no known cause. See Henrickson v. Conoco Phillips Co., 605 F. Supp. 2d 1142, 1149 (E.D. Wash. 2009). Acute myelogenous leukemia, or AML, is one of the most common types of leukemia in adults in the United States. Despite being a widespread disease affecting thousands of people of all ages, cultures, and with various toxic exposures, the majority of AML cases have no known cause. Id. Cases of the disease are categorized as either idiopathic, or de novo, (“onset without external or environmental stimulus”), or secondary events which could be related to exposure to various cancer treatments in addressing preexisting hematologic disorders or exposure to environmental toxins. Id. The underlying biology of these two categories, as the court noted in Henrickson, is usually distinct. See id.
The Eastern District of Washington relied on the absence of putative biomarkers of exposure or affect in Henrickson v. Conoco Phillips Co., where a former gasoline truck driver sued the gasoline company alleging his AML was caused by occupational exposure to benzene. The defendant filed several Daubert motions to exclude plaintiffs’ causation experts because they could not opine that plaintiff’s exposure to gasoline was a substantial factor in his development of AML. In nearly 90% of all secondary AML cases, including benzene exposure cases, cytogenetic or distinct patterns of chromosomal aberrations were considered characteristic findings. The same abnormalities were only observed in about 50% of de novo AML cases. Mr. Henrickson lacked chromosomal abnormalities. Id. at 1150. Defense experts asserted that there was no way to scientifically separate the plaintiff’s AML from idiopathic or de novo AML occurring in people with no particular exposure to chemicals. Id. at 1150. The court agreed and reasoned that the presence of a known risk factor, like benzene exposure, standing alone is insufficient for ruling out idiopathic origins of disease. Id. at 1162-63. Without particularistic biomarker information, the experts’ testimony was deemed speculative conjecture. As such, the court excluded the experts and granted summary judgment in favor of Conoco Phillips Co.14
Also, in Tompkin v. Philip Morris USA, Inc., several defense experts introduced both epidemiological and genetic evidence to defend the tobacco company in a product liability suit where a former smoker alleged cigarettes caused his lung cancer. 362 F.3d 882 (6th Cir. 2004). First, a medical professor testified about the plaintiff’s exposure to various carcinogens, including cigarettes and asbestos. He opined that plaintiff was exposed to asbestos and other carcinogens while working and the most significant exposure inducing his lung cancer was his asbestos exposure. Id. at 889. Next, a biostatician testified about the epidemiological association between lung cancer and exposure to asbestos and smoking. He concluded that plaintiff’s cancer was not associated with smoking, but rather was associated with asbestos exposure. He explained the relative risk from smoking was 1.59 and the relative risk from smoking combined with asbestos exposure was 1.56. The relative risk from asbestos exposure alone, however, was between 2.65 and 5.91. Id. at 890. Based on those figures, he concluded that plaintiff’s smoking did not increase the risk beyond the already heightened risk posed by asbestos exposure alone. Id. He stated that smoking and asbestos exposure had an additive effect, but not a synergistic effect. Finally, an anatomic pathologist testified about the genetic characteristics of plaintiff’s tissue samples. Mutations in the p53 and k-ras cancer suppressor genes are common characteristics of normal smoking-related changes. Plaintiff lacked those specific mutations. Id. The pathologist opined that his testing revealed no pathological or biochemical evidence of an effect from smoking. Ultimately, he concluded that plaintiff’s lung cancer was caused by occupational exposure to asbestos. Id.15 A jury found for the defendants.
Conclusion
While recorded opinions discussing genetic evidence are few right now, the use of genetics is important to consider in a variety of practice areas. Pharmaceutical companies include genetic information on their labeling for certain drugs. Physicians should consider genetics when prescribing medications or determining treatment plans. Malpractice attorneys may find genetic based arguments in suits against doctors for failures to diagnose or negligent care. Labor lawyers may consider genetics when informing clients of legal risks associated with certain workplace conditions or chemicals. Product liability defendants should utilize genetics to determine whether a duty to warn even arises with various plaintiffs who may have a genetic predisposition to certain diseases or conditions. Even litigation regarding food borne illnesses should utilize genetic evidence to pinpoint the cause of outbreaks. Clearly, genetic evidence is not something to put on the backburner. The potential rewards associated with genetics are overwhelming for plaintiffs and defendants. Keep in mind the risks associated with opening the door to genetic evidence that may help your opponent. Consulting with experts who specialize in genetics is strongly encouraged to determine what genetic information is relevant and what the best course of action is in bringing or defending lawsuits.
1 See Rimbert v. Eli Lilly and Co., No. CIV 06-0874, 2009 WL 2208570 (D. N.M. July 21, 2009)
2 Susan E. Brice, Dr. Whitney V. Christian, “The Use of Genetic Evidence to Defend Against Toxic Tort Claims” 29 No. 9 Intell. Prop. & Tech. L.J. 3, 3-4 (2017).
3 Steve C. Gold, “The Holy Grail? The Potential of Genomics to Shape Toxic Tort Litigation,” p. 8, Toxic Tort and Environmental Law (March 2016)
4 Steve C. Gold, “The Holy Grail? The Potential of Genomics to Shape Toxic Tort Litigation,” p. 8, Toxic Tort and Environmental Law (March 2016)
5 Joseph G. Eaton, Kara M. Kapke, and Apryl E. Underwood, “MEDICAL GENETICS IN CHEMICAL EXPOSURE CASES: Genetic Testing of a Plaintiff – The Pros and Cons” 54 No. 1 DRI For Def. 58, 63 (January 2012)
6 See Fed. R. Civ. Pro. Rule 35(1),
The court where the action is pending may order a party whose mental or physical condition—including blood group—is in controversy to submit to a physical or mental examination by a suitably licensed or certified examiner. The court has the same authority to order a party to produce for examination a person who is in its custody or under its legal control.
7 Steve C. Gold, “The Holy Grail? The Potential of Genomics to Shape Toxic Tort Litigation,” p. 6, Toxic Tort and Environmental Law (March 2016)
8 Steve C. Gold, “The Holy Grail? The Potential of Genomics to Shape Toxic Tort Litigation,” p. 6, Toxic Tort and Environmental Law (March 2016)
9 Snyder v. Sec’y of HHS, 553 Fed. Appx. 994 (Fed. Cir. 2014)
10 Bowen v. E. I. Du Pont de Numours & Co., 2005 Del. Super. LEXIS 239 (Del. Super. Ct. Aug. 5, 2005), aff’d, 906 A.2d 787 (Del. 2006)
11 In re Prempro Products Liab. Litig., 586 F.3d 547 (8th Cir. 2009)
12 See Charmaine Lloyd, et al. v. Johnson & Johnson, et al., Superior Court of California, County of Los Angeles, Case No. BC628228 (October 20, 2017).
13 Gary Marchant, “Genetic Data In Toxic Tort Litigation,” 14 J.L. & Pol'y 7, 14-15 (2006)
14 Henrickson v. Conoco Phillips Co., 605 F. Supp. 2d 1142 (E.D. Wash. 2009)
15 Tompkin v. Philip Morris USA, Inc., 362 F.3d 882 (6th Cir. 2004)
