www.rivkinradler.com April 2004   Reprinted with permission from the April 2004 issue of Mealey's Litigation Report   Mold Taking the "Toxic" Out of Mold [1]   By: Eric S. Strober     [Author Bio: Eric S. Strober is an Associate of Rivkin Radler LLP concentrating in the defense of toxic tort, medical malpractice and general liability cases.]   [Editor's Note: The contents of this article are not necessarily reflective of the positions of Rivkin Radler LLP or our clients.]   It is difficult to overstate the claims that are being made by some plaintiffs as a result of exposure to various molds. The news media have, in fact, sounded some very loud alarms that have added to the perception that molds are "toxic" and therefore, extremely hazardous to humans. In truth, various molds have always been known to be allergenic to certain people. Recently, however, claims have been made that go well beyond the claims of simple allergic reactions to those of much more serious injuries. Over the last few years, plaintiffs have filed suit against building owners, contractors and others alleging, among other things, permanent lung injury, permanent damage to immune system, neurological injury, brain damage and cognitive deficits, as well as an increased risk of cancer. Ed McMahon even claimed that "toxic" mold killed his dog. The most commonly cited "toxic" molds include Stachybotrys, Aspergillus, Trichoderma, Cladosporium, Penicillium and Fusarium. It is generally agreed that the human body can have three different types of reactions to an exposure: allergic, immune or toxic. Plaintiffs alleging toxic effects of the molds cited above generally attribute their symptoms not the molds themselves, but rather to potential mold byproducts called mycotoxins. The most commonly cited are aflatoxins, which can be produced by some Penicillium species; ochratoxins, associated with Stachybotrys and Fusarium; and tricothecenes, which can be produced by Stachybotrys and Trichoderma. It should be noted that while certain mycotoxins have been associated with certain molds, they are not necessarily present concurrently with these molds. Indoor air can be tested for the presence of mycotoxins just as it can for mold spores. Thus, even if the testing shows elevated concentrations of mold spores, one should not, and in fact cannot, conclude that mycotoxins are also in the air. While there has been a general medical consensus regarding the allergic reactions and asthmatic implications of mold exposure, there is generally no such agreement regarding the toxic effects, if any, of environmental mold exposure, especially under the conditions that have been the basis for most mold related lawsuits. In the pages that follow, I will take a closer look at the toxicological analysis that should be satisfied as part of showing toxic injury caused by alleged mold exposure. In fact, as part of the overall inquiry into scientific validity, a specific set of scientific criteria should be evaluated in every alleged toxic mold exposure case to evaluate whether a case of toxic causation exists. A careful and detailed examination of these specific toxicological criteria may be a useful component of a Daubert challenge to determine if the opinions proffered by a plaintiff's expert are based on sound and reliable information and supported by sound scientific methodology. In such an analysis, the toxicological causation must be proven by the plaintiff's experts to be reliable at every step.[2] The inquiry may also apply in a Frye[3] challenge where the examination of "general acceptence" is the rule. Of course, scientific challenges to environmental testing and fact specific challenges to the claimed medical damages also remain available to the defense in addition to the toxicological causation challenge analyzed here. Here is how the toxicological challenge on causation works. Beginning in 1965 with Sir Bradford Hill, toxicologists have set forth specific criteria for the evaluation and establishment of determining medical causation from an alleged toxic exposure. The establishment of these criteria was later reiterated by the World Health Organization[4], and the National Academy of Sciences.[5] The epidemiological criteria include the following: · Strength and significance of association · Specificity of Association · Consistency of Association · Temporal relationship · Dose response relationship, and · Plausibility and Coherence Therefore, any injury or illness allegedly caused by exposure to a "toxic" substance should be analyzed using the above framework in order to have scientific and epidemiologic validity. If not, the opinion on causation should be excluded. This is especially true under a Daubert analysis that will examine, among other things, the quality of the scientific method used to arrive at an expert's opinion on causation. If the plaintiff cannot establish that their expert's causation opinions are based on sound scientific methodology, which in the field of toxicology is defined as the Bradford-Hill Criteria, the gate-keeping role of the trial court requires preclusion of that expert under Daubert. With that said, let's take a closer look at the application of the criteria to an alleged "toxic" mold case. The first criteria, Strength of Association is an examination of whether more intense exposure leads to more frequent or more severe effects. It is measured in epidemiological studies as the magnitude of the measure of effect.[6] In the mold exposure setting, one must therefore look for evidence of a consistent and proven increase in the alleged health effects related to, and consistent with, a measured increase in either the intensity or frequency of exposure. In other words, do the symptoms get worse when the mold levels are higher? In answering this question, one would look to seasonal changes in the ambient air mold content as well as any variations in the results of air quality testing and compare them to the documented complaints or symptoms contained in the medical records. Only where there is a demonstrated worsening of medical symptoms as the mold exposure increases is the Strength of Association demonstrated. The Specificity of the Association means that similar signs and symptoms are not observed in the absence of the suspected agent.[7] This is an evaluation of whether the person experiences the suspect adverse health effects when not exposed to the suspected agent. One would therefore have to look to whether the exposed person experienced the claimed symptoms when known to be in an environment with no, or at least greatly diminished, levels of mold. Due to the ubiquitous nature of molds in the environment, it is extremely unlikely to ever be in an environment completely free of all mold spores or hyphae. Establishing the Consistency of Association requires that an association be found regularly in a variety of medically valid and scientifically supported studies.[8] The results of the studies must be positive and the differences in measured effects must be within the range expected on the basis of types of error, including sampling, selection bias, misclassification, confounding, and differences in actual exposure levels. In essence, there must be published, scientifically valid medical studies that show consistent health effects from the same molds across the tested population. This is especially important in the mold exposure dynamic. It is not disputed that there are literally hundreds of species of molds, not all of which are even suspected or claimed of being a health hazard. It is therefore of paramount importance to identify the mold, down to its species, that is alleged to have caused an adverse health effect. It is not possible to make this type of inquiry at the genus level as, for example, there are over two hundred species of penicillium and many species of aspergillus, some of which are used for beneficial or innocuous purposes, such as making penicillin or Roquefort cheese. Once one or more specific species are identified, one must look for studies that are directly applicable to the claimed agent or agents. A study on Stachybotrys for example is not relevant to an inquiry into the toxicity of Fusarium. While the examination of epidemiological studies is but one of many factors in a Daubert analysis using the Bradford Hill criteria, it may be more prominent in a Frye challenge, given the importance of the applicable peer-reviewed literature and its "general acceptance" into the base of knowledge. In such a challenge, the court will look to see if the opinion of plaintiff's expert has gained acceptance in the field and should review all pertinent literature. If there are no scientifically valid studies regarding the mold or molds that are the subject of the lawsuit, it will be difficult to prove general acceptance. Under the Bradford Hill evaluation, if there is no pertinent supporting literature as defined above, the criteria are not satisfied and the expert's opinion should be found unreliable and therefore precluded. There are numerous studies of the mycotoxic effects of molds that go back many years. When evaluating these studies, it is important to take the route of exposure into account. Thus, a study of humans who repeatedly ingested mold or mycotoxin contaminated foods, or a study of animals that were injected with mycotoxins will not show a consistency of association that will be relevant to a person claiming airborne exposure. Most significantly, to date, no valid peer reviewed study has been put forth establishing toxic causation as a result of the inhalation of mycotoxins by humans.[9] Thus, any claim of such a toxic causation should fail the Bradford-Hill analysis, as it cannot satisfy the Consistency of Association requirement. Dr. Stephen Redd of the Centers for Disease Control highlighted the difference between ingestion and inhalation and the lack of evidence on the effects of the latter in his testimony before a Congressional Subcommittee on Oversight and Investigations and Housing and Community Opportunity.[10] In his testimony, Dr. Redd noted that the only evidence of tumors being connected to mycotoxin exposure was as a result of chronic ingestion of toxin contaminated foods. While acknowledging the reactive airway and asthmatic effects of inhalation exposure to mold, he went on to state that there is simply an absence of evidence linking inhalation exposure with pulmonary hemorrhage, memory loss or lethargy. The epidemiological studies of the effects of ingestion exposure should not, on their own, suffice to show consistency of association in a case of inhaled or other type of exposure. Only when a study shows consistency of association in the same manner of exposure will this aspect of the epidemiological criteria be satisfied. The next criteria, the Temporality of Relationship means that the symptoms or effects of the exposure are present at the time of exposure, and not present when there is no exposure. This also means that the initial exposure must precede the initial onset of symptoms. If, for instance, some or all of the claimed symptoms predate the first known exposure, a temporal relationship does not exist. In the mold plaintiff, this requires a thorough examination of all of the medical records that predate the time of the first known or alleged exposure. If, for instance, the plaintiff was a long-standing asthma sufferer, then the asthma cannot be said to have been caused by the exposure alleged in the case -- exacerbated perhaps, but not caused. The Dose-Response Relationship, or Biologic Gradient, is similar to the Strength and Significance of Association criteria in that it is essentially a measure of whether an increase in the dose will cause an increase in the severity or frequency of exposure. Seasonal variations in environmental molds as well as variations in available indoor air quality tests should be examined and compared to the timing and severity of the plaintiff's claimed adverse health effects. Once again, the specific agent and the exact level and route of exposure must be known. The Plausibility and Coherence criteria ask whether there is a reasonable basis to conclude that the proposed agent/response association fits into existing biologic or medical knowledge. This also requires an examination of the actual mechanism that is claimed or suspected of linking the cause and effect and determining if it makes medical sense. In other words, "how would an inhaled mycotoxin cause a tumor, brain damage or damage to the immune system?" The existence of a possible mechanism of cause and effect will increase the likelihood of exposure-disease association. Likewise, the absence of a plausible causative mechanism will make the association less likely. Finally, as part of the Plausibility evaluation as to whether a medical opinion on causation is based on sound scientific methodologies, a supportable epidemiological inquiry requires the formulation of a differential diagnosis for each adverse health effect claimed. The formulation of a differential diagnosis requires and accounting of all of the possible causes for a given sign or symptom and eliminating those which are found to be inapplicable. If there is more than one plausible or suspected cause of the given effect, more investigation and the elimination of other alternatives are needed to determine if causation can be established. The application of the Bradford Hill criteria in evaluating the reliability of the opinions of a plaintiff's expert was illustrated in detail in Amorgianos v. Nat'l R.R. Passenger Corporation, 137 F. Supp 2d 147 (S.D.N.Y. 2001), aff'd on appeal 303 F. 3d 256 (2d Cir. 2002). Here, using the Bradford Hill criteria in a Daubert analysis, the court determined that various opinions expressed by the plaintiffs' experts that permanent illness due to xylene exposure did not satisfy the established criteria. The court found that there was insufficient support in the medical literature for the plaintiffs claim of exposure related chronic neurological condition and therefore precluded any testimony on the matter. The court also noted that defects in the calculations of the concentration of exposure would undermine the validity of the dose-response relationship criteria. The plaintiff's claims that did not satisfy the Bradford Hill criteria were dismissed. The Bradford Hill criteria have also been applied in federal cases in Pennsylvania, Vermont, New Jersey, Illinois and Texas, among others. This methodological framework has also now been applied under the Daubert standard in a federal case of alleged mold poisoning. In Roche v. Lincoln Property Co., (No. 02-1390 E.D.Va, July 25, 2003.), the District Court for the Eastern District of Virginia, Judge Gerald Bruce Lee, evaluated the claims by plaintiffs expert physician that exposure to Stachybotrys, Cladosporium, Penicillium and Aspergillus caused chronic headaches, nasal stuffiness, shortness of breath, sinus congestion and chest congestion. Citing Cavallo v. Star Enterprise, 892, F. Supp. 756, the Court confirmed that the principles and methodologies of toxicology, as set forth by the World Health Organization, National Academy of Sciences, and other agencies of the United States government, had to be applied to the opinions set forth by plaintiffs expert to aid in determining reliability, and thus, admissibility. In summing up the above criteria, the Roche court stated that the methodology requires: "First an evaluation is made of the [molds] to which the individual might have been exposed, and of the concentrations of these [molds] in air breathed by the individual. The second step involves an evaluation, based upon published scientific literature, of the exposures necessary to produce the adverse effects associated with the [molds] to which the individual may have been exposed. These two evaluations are then combined in the final step of the risk assessment to provide an estimate of the likelihood that any of the harmful properties of any or all of the [molds] might have been expressed in the exposed individual." In the opinion of plaintiffs' expert, the above symptoms were due to exposure to the various molds found in their apartment. Plaintiffs' expert did not, however, develop a differential diagnosis to rule out other possible causes of the plaintiffs' symptoms. He could not rule in or rule out the impact that the other allergies for which the plaintiffs tested positive had on their health. In fact, the only one of the methodological criteria plaintiffs could satisfy was the temporal relationship between exposure and symptoms. The court found that temporality, on its own, is insufficient to satisfy the scientific inquiry to Daubert satisfaction. The Court then dismissed all claims of injury and thus, granted summary judgment, as there were no provable damages. In sum, for every claimed mold exposure there are several variables that must be examined including: the species of mold, the presence or absence of mycotoxins, the degree of exposure (in both concentration and duration), the prior health of the plaintiff, the condition of the plaintiff during the exposure and the injuries alleged as a result. A complex evaluation must be made in the context of the accepted epidemiological and toxicological methodologies to determine if a cause and effect relationship can be established. If not, the proposed causal connection should not withstand scientific challenge in court. Unless and until there is solid epidemiological evidence specifically showing that certain species of molds, inhaled by humans at certain levels of exposure, cause the toxic effects such as neurological damage, memory loss or an increased risk of cancer, as claimed by some plaintiffs, the accepted toxicological criteria will not be satisfied and there should be no "toxic" in mold. - top - NOTES: [1] In addition to the references cited, information included in this article was taken from consultations and depositions of expert toxicologists, physicians and industrial hygienists involved in pending mold litigation. [2] Daubert v. Merrell Dow Pharm., Inc., 509 U.S. 579, 589, 125 L. Ed. 2d 469, 113 S. Ct. 2786 (1993), Amorgianos v. Nat'l R.R. Passenger Corporation, 137 F. Supp 2d 147 (S.D.N.Y. 2001), aff'd on appeal 303 F. 3d 256 (2d Cir. 2002). [3] See Frye v. U.S., 54 App. D.C. 46; 293 F. 1013; Robert Selig et al., v. Pfizer, Inc., 290 A.D.2d 319; 735 N.Y.S.2d 549; (2002). [4] Environmental Health Criteria 72, Principles of Studies on Diseases of Suspected Chemical Etiology and Their Prevention. World Health Organization, Geneva, 1987. [5] Clearing The Air: Asthma and Indoor Air Exposures, Chapter 2. Methodological Considerations in Evaluating the Evidence. National Academy Press, 2000. [6] Id at 46. [7] Environmental Health Criteria 72, Principles of Studies on Deseases of Suspected Chemical Etiology and Their Prevention. World Health Organization, Geneva, 1987. [8] Clearing The Air: Asthma and Indoor Air Exposures, Chapter 2. Methodological Considerations in Evaluating the Evidence. National Academy Press, 2000. Pg 47. [9] Nordness ME, Zacharisen MC, Fink JN,.Toxic and other non-IgE-mediated effects of fungal exposures. Curr Allergy Asthma Rep. 2003 Sep;3(5):438-46. [10] State of the Science on Molds and Human Health, Dr. Stephen C. Redd, Statement for the Record. Released July 18, 2002.