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special to the national law journal Thomas P. Redick is a member of, and Angela Loehr is an associate at, St. Louis’ Gallop, Johnson & Neuman. Redick is vice chair of the American Bar Association’s Committee on Toxic Tort and Environmental Litigation. Recent developments allow a peek at the future trajectory of medical-causation proof in mold litigation. Two recent state supreme court decisions allowing plaintiffs’ experts to testify in cases alleging personal injury from mold tell part of the story. This article will also try to predict future challenges to experts in mold litigation in jurisdictions allowing defendants to plead an “idiosyncratic reaction” defense. This can be a second line of defense should experts for the plaintiff be permitted to testify-and scientifically prove-an idiosyncratic or allergic reaction. Evidence of an idiosyncratic susceptibility to mold could provide a complete bar to recovery in most states. Lastly, this article discusses the emerging medico-legal field of “toxicogenomics,” or the use of genetic evidence to prove a genetic susceptibility. Such genetic evidence might surface in mold cases, which could implicate challenges to expert testimony and also raise the idiosyncratic-reaction defense. Junk science, continued The scientific validity of expert testimony about medical causation can be challenged in the mold litigation context as junk science under Daubert v. Merrell Dow Pharmaceuticals, 509 U.S. 579 (1993). The U.S. Supreme Court established the Daubert doctrine to guard against unreliable expert testimony in federal courts. Before an expert witness can testify to a judge or jury that a plaintiff has sustained injuries from mold exposure, a motion in limine to exclude the testimony can be brought. Jurisdictions applying Daubert make judges into gatekeepers who ensure that scientifically sound methodology supports the opinion. However, not all state courts have adopted Daubert, and many other states apply Frye v. United States, 293 F. 1013 (D.C. Cir. 1923) (using a “general acceptance” test for expert methodology). Under the Frye test, medical diagnosis is often left for the jury to evaluate, with a sympathetic doctor testifying to unproven associations between toxin and injury. While mold may produce mycotoxins, scientific data show no long-term injury from typical residential doses and exposure pathways. Since the data necessary to make this determination remains hypothetical, no uniform standards have been developed defining what an acceptable level of mold would be in an indoor environment. State court developments Two recent state court decisions have allowed plaintiffs’ experts to testify to mold-related injuries using current science. An award of $1 million for hypothetical neurological injuries was affirmed in New Haverford Partnership v. Stroot, 772 A.2d 792 (Del. 2001). In New Haverford, the plaintiffs alleged asthma and neurological injuries allegedly resulting from mold exposure. Before trial, the defendant challenged the method of sampling done by the plaintiffs’ experts, but not medical causation. After the jury awarded $1 million, the defendant appealed the decision, arguing that there was no sound scientific basis for the award. Applying Daubert principles, the New Haverford court found that the method used for collecting mold samples “was reviewed by peers and generally accepted in the scientific community.” Id. at 79. The plaintiffs’ experts were allowed to testify that mold readings within the plaintiffs’ apartments were excessive, without determining what was normal in Delaware’s air. This baseline comparison to outside air helps to determine if abnormally high levels of mold are present inside the home. By failing to sample surrounding buildings, the experts had not excluded other causes for the complaints (dog dander, smoking, etc.). The court exercised its gatekeeping function by letting the jury decide, stating that “the failure to conduct baseline testing goes to the weight of the experts’ opinions, not their admissibility.” As a result, the Delaware Supreme Court held that expert testimony about mold-related sampling methods and resulting injuries was properly admitted. A similarly plaintiff-oriented outcome resulted in Mondelli v. Kendall Homes Corp., 262 Neb. 262 (2001), in which the plaintiffs alleged that negligent home construction caused significant water damage and mold growth. The plaintiffs complained that mold exposure in their home caused headaches, nasal congestion and asthma triggered by excessive mold exposure. They hired an allegedly qualified toxicologist to prove that mold caused asthma and allergic rhinitis. Evidence excluded However, the trial court excluded the plaintiffs’ expert from testifying that mold specifically caused the plaintiffs’ injuries because “no standards existed in the scientific community concerning the level of mold which is acceptable in a house.” Id. at 268. The trial court also excluded evidence of laboratory sampling because it was flawed and lacked foundation. Id. The Nebraska Supreme Court, applying the Frye standard, reversed the trial court’s exclusion of expert testimony in Mondelli. The court noted that although the plaintiffs’ expert testified that there was no established standard to determine acceptable levels of mold, “the scientific community has generally accepted the principle that a connection exists between the presence of mold and health.” Id. at 273. Because the plaintiffs complained of typical allergic reactions, this decision may be distinguished from cases allowing recovery for neurological injuries. While these two high-profile decisions may indicate how difficult it is to exclude “junk science” in mold cases, defense attorneys report some success in excluding experts. In the landmark case of Ballard v. Farmers, No. 99-05252 (Texas Dist. Ct. 2001), the plaintiffs’ attorneys succeeded in defeating the Daubert motion, but lost a summary judgment motion on epidemiological grounds under the Texas analog to Daubert ( Merrell Dow Pharmaceuticals v. Havner, 953 S.W.2d 706 (Texas 1997), cert. denied, 118 S. Ct. 1799 (1998). As a result, Melinda Ballard’s expert testimony about her husband’s alleged brain damage was excluded from trial on the ground that epidemiology did not show general causation. The jury awarded $32 million for emotional distress and property damage; both sides appealed. General-causation issues relate to the lack of scientific knowledge and general acceptance-e.g., statistically significant epidemiology linking dose to symptom. Even if general causation has been shown, the courts will require specific causation (i.e., evidence specific to the plaintiff, including dose, timing of onset or “temporal relationships”and biological plausibility). For example, the noted mold toxicologist Dr. Ronald Gots reports that mold-associated mycotoxins (the “trichothecenes”) are only neurotoxic in extraordinarily high doses in experimental animals. Moreover, the onset of neurotoxicity depends upon serious symptoms such as pulmonary hemorrhage, hemolylsis (breaking apart of red blood cells) and similar trauma. Since typical “toxic encephalopathy” mold plaintiffs lack such dramatic symptoms, specific trichothecene toxicity cannot be shown. Reacting to reactions When Daubert gatekeeping fails, products liability provides a second line of defense in mold litigation: the idiosyncratic-reaction defense. For example, if a product manufacturer or builder of a home can demonstrate that a plaintiff’s particular reaction to mold is idiosyncratic (i.e., unique to that individual or a small subgroup), recovery may be barred by the idiosyncratic-reaction defense. See, e.g., Oakes v. E.I. du Pont de Nemours & Co. Inc., 272 Cal. App. 2d 645 (1969) (defendant not liable if it could not reasonably have foreseen that weed killer would trigger this allergic reaction). The new Restatement Third, Torts: Products Liability § 2, retained the idiosyncratic-reaction defense. Under the Restatement, a manufacturer may feel compelled to warn of a potential allergic reaction if the harm-causing ingredient will produce an adverse reaction to a number of possible users. Id. at comment K. In the mold context, genetic screening or allergy “patch testing” may provide evidence that a plaintiff possesses a particular sensitivity to certain molds that is not shared by a substantial portion of the population. If a plaintiff’s reaction is unique and not shared by a substantial number of persons, the injury is a result of the plaintiff’s idiosyncrasy and is not foreseeable enough to support liability. This idiosyncratic-reaction defense may not apply in mold cases in which a plaintiff complains of rhinitis, nasal congestion or asthma, if the jury or judge were to find that these reactions could foreseeably occur in a substantial number of people. However, this defense may work when the plaintiff’s complaints are only hypothetically linked to mold, such as cognitive impairment or digestive disorders. Duty to warn However, some jurisdictions impose a duty to warn when a manufacturer or supplier has unequal knowledge, actual or constructive, and knew or should have known that harm could occur if no warning was provided. See Goldman v. Walco Tool & Engineering Co., 614 N.E.2d 42 (Ill. App. Ct. 1993). As a result, potential defendants may find that the newly foreseeable genetic information arising from research into mold exposure merits monitoring. Since the foreseeability of a susceptible subgroup is nearly always an issue of fact, the idiosyncratic-reaction defense is best presented at trial, in the context of expert testimony about mold’s physical impact. In Morson v. Superior Court, 90 Cal. App. 4th 775 (2001), the court held that allergic reactions are “a complex biological and medical phenomenon, subject to dispute, that requires expert knowledge to understand and explain, for example, to a lay jury.” The defendants, latex glove manufacturers, were sued for allergic reactions that, the plaintiffs contended, could have been prevented with a better design or a warning about possible allergic reactions. The defendants argued that the plaintiffs suffered “idiosyncratic” injuries that were not due to a design defect. Id. at 782. Collision of cases and science The steady increase in mold-related personal-injury litigation is arriving as medical science may be changing its approach to proving medical causation in cases involving “idiosyncratic” reactions. The ability to identify genetically susceptible subclasses could permanently alter a substantial part of the landscape of mass tort liability. This change will occur in any instance in which a toxin’s interaction with genes can be documented to the satisfaction of a state or federal court, including compounds hypothetically associated with mold toxicity. This new development in medical evidence could implicate both Daubert motions and the use of the idiosyncratic-reaction defense at trial. The National Institute of Environmental Health Sciences has launched the Environmental Genome Project to hunt for genetic susceptibilities to toxins. See www.niehs.nih.gov. Natural compounds, like the alleged toxins associated with mold organisms (e.g., volatile organic compounds, mycotoxins), are presumably within the national institute’s mandate. As genetic linkages surface, experts in toxic tort lawsuits, including mold litigation, may use genetics to reassess scientific studies and prove hypothetical links to the “statistically significant” level of proof that scientific methodology would require. Some experts are already promoting genetic methodologies for establishing medical causation. With genetic susceptibility evidence, an expert can employ “genotype stratification” and separate those plaintiffs who are allegedly “genetically susceptible” into their own subclass. See, Sander Greenland and James M. Robins, Epidemiology, Justice and the Probability of Causation, 40 Jurimetrics 321 at 335, Spring 2000 (“genotype stratification” to establish medical causation for susceptible groups). Over time, the genotype-stratification approach could become commonplace, as the environmental genome project produces more genomic evidence to link to particular compounds or disorders caused by environmental toxins. Defense counsel may use this evidence to prove an idiosyncratic reaction, but plaintiffs’ counsel may one day use genetic evidence to prove medical causation for a “foreseeable” subgroup of susceptible people and counter this idiosyncratic-reaction defense. Before attorneys recommend testing for a genetic susceptibility, they should carefully consider the pros and cons of finding genetic susceptibility. Counsel should consider retaining an expert consultant (not subject to disclosure) to do research on genetic theories. The genetic expert may require specialized, sensitive discovery (e.g., patch tests, blood tests for genetic susceptibilities or family medical records) to reach his or her opinion. The 21st century will probably bring genetic-susceptibility theories that push the boundaries of junk science. Mold injuries are so inherently idiosyncratic that both plaintiffs and defendants may attempt to exploit genetic susceptibility. Defense counsel should be alert to the role of genetic evidence in resolving disputes, using the idiosyncratic-reaction defense as a last bulwark to mold liability should a Daubert challenge fail. Plaintiffs’ counsel may find themselves defending allegations that a proven genetic susceptibility is merely an idiosyncratic reaction. Counsel on both sides should recognize, however, that one side’s sword of an allegedly foreseeable genetic susceptibility can turn into the other side’s shield. Defense counsel may prove a genetic idiosyncrasy but risk providing the plaintiff with medical-causation evidence; the plaintiff’s counsel may decide to use genetic evidence to hurdle over Daubert, only to encounter the idiosyncratic-reaction defense. The future will hold plenty of surprises for both sides in toxic tort litigation, and mold litigation could be fertile ground for battles over genetically predetermined idiosyncratic reactions.

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