Daubert v. Merrell Dow Pharmaceuticals Provides

Key Challenge to Mold Injury Causation Evidence

 

Walter J. Andrews, Lon A. Berk and David C. Ferro [1]

 

         Recent coverage of mold-related personal injury and property damage claims in the popular media, [2] unfortunately spurred by large jury awards and high profile cases, [3] typically ignores the fact that the science underlying the more significant personal injury claims remains elusive.  In fact, reliable epidemiological studies or peer-reviewed research tending to show a causal connection between mold exposure and significant illness, does not currently exist. [4]   Although plaintiffs' experts testify that exposure to mold and mycotoxins can cause injury, under the 1993 Supreme Court decision Daubert v. Merrell Dow Pharmaceuticals, Inc. [5] and similar state court decisions that require judges to exclude expert testimony that does not meet a standard of evidentiary reliability, defendants should rely on the absence of scientific evidence to exclude such causation testimony and defeat mold-related personal injury claims.

The Court's Role in

 Assessing Scientific Evidence

 

Until 1993, the standard for the admissibility of scientific evidence in federal courts was whether the evidence was based on a scientific technique generally accepted as reliable within the relevant scientific community. [6]   The Frye "general acceptance" test became the dominant standard for the admissibility of novel scientific evidence in most states as well. [7]   With the adoption of the Federal Rules of Evidence, however, some Circuits held that the Frye standard had been preempted, [8] while other courts continued to use the Frye test, even after the enactment of the Federal Rules. [9]

In Daubert v. Merrell Dow Pharmaceuticals, [10] the United States Supreme Court held that the adoption of the Federal Rules of Evidence superseded Frye, and that Rule 702 [11] requires judges to act as evidentiary "gatekeeper" and exclude expert scientific testimony that is not both relevant and reliable.  Assuming the testimony is relevant, a court must determine whether the testimony pertains to "scientific knowledge," which requires that the evidence be supported by "appropriate validation — i.e., Ôgood grounds,'" [12]   This is the "standard of evidentiary reliability." [13]   The Supreme Court held that Rule 702 requires that district courts undertake a "preliminary assessment of whether that reasoning or methodology underlying the testimony is scientifically valid and of whether that reasoning or methodology properly can be applied to the facts at issue." [14]

Under Daubert, to assess expert scientific testimony offered under Rule 702, district courts must "evaluate the methods, analysis, and principles relied upon in reaching the opinion. . . . ensure that the opinion comports with applicable professional standards outside the courtroom and that it will have a reliable basis in the knowledge and experience of the discipline." [15]   The Supreme Court set forth specific, but not exhaustive, criteria by which federal district courts may fulfill their Rule 702 responsibilities as evidentiary "gatekeeper:"

1.            Whether the proffered knowledge can be or has been tested empirically, i.e., whether it is "falsifiable;"

2.            Whether the theory or technique has been subjected to peer review and publication;

3.            Whether, in the case of a particularly scientific technique, the method contains a high known or potential rate of error; and

4.            Whether the methodology is generally accepted. [16]

Many states have adopted Daubert-style standards of scientific reliability for the admissibility of scientific evidence. [17]

More recently, the Supreme Court has protected the district court's judgment on the admissibility of expert testimony from appellate review, holding in General Electric Company v. Joiner that a district court's decision to admit or exclude expert scientific evidence is reviewable only for abuse of discretion. [18]   The "abuse of discretion" standard is the most deferential to a trial judge's determination of admissibility.  In addition to the procedural holding in Joiner, Chief Justice Rehnquist, writing for the Court, added to the Daubert analysis by explaining that "nothing in either Daubert or the Federal Rules of Evidence requires a district court to admit opinion evidence which is connected to existing data only by the ipse dixit of the expert.  A court may conclude that there is simply too great an analytical gap between the data and the opinion proffered." [19]

The Supreme Court unanimously expanded Daubert and the scope of Rule 702's "gatekeeping" function to apply to all "technical" or "specialized" — not strictly scientific — testimony in Kumho Tire Co. v. Carmichael. [20]   The Supreme Court also granted the district courts "considerable leeway" and "the same broad latitude when [the district court] decides how to determine reliability as it enjoys in respect to its ultimate reliability determination in deciding in a particular case how to go about determining whether particular expert testimony is reliable" [21]   As one Court explained, the Daubert factors provide a means to evaluate "whether the expert is a hired gun or a person whose opinion will withstand the same scrutiny that it would among his professional peers." [22]

With the DaubertÑJoinerÑKumho Tire rulings (and their state court analogues), and the subsequent revision to Rule 702 incorporating Daubert, defense counsel now have the analytic tools sufficient to guide courts, to reject, for failing to "assist the trier of fact to understand the evidence or to determine a fact in issue," unreliable causation testimony in mold-related personal injury cases. 

The Basis for

Personal Injury Mold Claims

 

The idea that mold might lead to personal injury claims is by now, especially in light of the recent widespread media coverage, well known. [23]   Mold spores are and have always been in the air we breathe, indoors and out, and exist almost everywhere on Earth.  Mold thrives in damp and dark environments, and a plumbing leak or burst, flood, rainwater intrusion, or other unintended water event in a building can give airborne mold a chance to colonize and flourish.  Ideal growth conditions for mold can occur in virtually any building humans occupy, including office buildings, apartment complexes, and single family dwellings.  Once afforded hospitable conditions, mold will grow wherever a source of food exists — under carpets, floorboards, in and behind sheetrock walls, under wallpaper or other wall covering, or on top of most any dark and damp building or furniture surface.

In addition to dramatic or chronic unintended water events, heating, ventilation, and air conditioning (HVAC) systems have been blamed for mold growth.  The energy crisis of the 1970s led to the construction of buildings with centralized HVAC systems and sealed windows, which may potentially restrict the flow of outside fresh air into the building and retain too much humidity.  In addition, HVAC system components have been themselves blamed for becoming locations of mold growth for various reasons.  Because HVAC systems are by design intended to remove mold spores from the air, spores collect within or on the air filters in the system.  In addition, HVAC systems occupy the dark locations within buildings, such as behind sheetrock walls and within the ceiling plenum.  Moreover, the operation of the air conditioning coils and condensate drain pans produces and collects moisture within the HVAC system.  Finally, improper maintenance, such as failure to replace air filters regularly and to ensure proper condensate drainage, and poor design, such as inaccessible air filters and condensate drains, may reduce the effectiveness of the HVAC system (i.e., a reduced ability to remove mold from the indoor air) and exacerbate the problem (i.e., the system may become an actual amplification site for mold growth).

Because the growth of some mold species can be odorous to varying degrees, and because the spores of some mold species can be allergens to which sensitized persons may experience atopic reactions, occupants of buildings with mold growth may experience discomfort or even health effects as mold growth develops.  Building occupants may complain about a variety of non-specific health-related effects including, for example, sneezing, wheezing, coughing, cognitive impairment, headaches, body aches, nausea, asthma, and allergic rhinitis.  Higher concentrations of mold spores, pollens, and other allergens may exacerbate existing asthma and allergic conditions.  Such discomfort and health symptoms should be transient, however, and should subside when the affected person leaves the affected building.  Such subsidence would be, not surprisingly, one factor in the ultimate identification of building conditions as the cause of the occupants' health symptoms.  If the adverse health systems persist outside the suspected building, the identification of the cause may be more difficult.

         Although relief from the transient health effects is, literally, just out the door, some building occupants may claim that their chronic exposure to molds and the toxins molds produce (i.e., mycotoxins) has caused a permanent disability. [24]   In these building occupants, their claims of nonspecific and often subjective health effects may transform into much more ominous sounding maladies, such as sick building syndrome (SBS), multiple chemical sensitivity (MCS), chronic fatigue syndrome (CFS), and fibromyalgia (FM), and even neuropsychological and cognitive deficits, to name a few.  Allegations of such permanent ailments have led to large jury awards. [25]   There is no exhaustive list of alleged mold-related conditions; litigants have attributed almost any physical, mental, or psychological symptom to excessive mold growth in an indoor environment. [26]

Right now, mold litigation threatens to be the next "the next asbestos."  Whether it actually becomes "the next asbestos" will depend largely on the extent to which the plaintiffs' bar and their experts demonstrate that the science and medicine underlying the conclusions that mold and mycotoxin exposure can cause permanent injury satisfies the threshold expectations of the law: Daubert, Joiner, Kumho Tire, and amended Rule 702 of the Federal Rules of Evidence.  To meet those expectations, a plaintiff in an mold-related personal injury case may employ several medical experts from different specialties, including allergists/immunologists, epidemiologists, toxicologists, neuropsychologists, and others.  These experts may each rely on their own examination of the plaintiff and perhaps volumes of the plaintiff's medical history, as well as each others' reports and opinions, to establish causation.  The experts may also rely on the investigations, reports, and opinions of non-medical experts such as certified industrial hygienists, mechanical and building engineers, and others.  The scope of a Daubert challenge to such a battery of witnesses is considerable, but by no means prohibitive.  Moreover, it is necessary, given that Daubert's requirements of scientific validity can prevent the admission of expert opinions attributing the cause of a personal injury to mold exposure.

The Scientific Barriers to Satisfying

the Mold-Injury Plaintiff's Burden of Proof

 

Daubert v. Merrell Dow Pharmaceuticals establishes the standard by which a court will determine whether expert testimony is sufficiently reliable to be admissible.  Daubert says nothing about the sufficiency of the substantive content of such opinions.  Thus, in a toxic tort case, to prove that an alleged injury was caused by exposure to a particular toxin (e.g., a mold or mycotoxin), a plaintiff typically must introduce sufficient evidence of "general causation" and "specific causation" of the alleged injury. [27]   This will undoubtedly require expert testimony.  To prove general causation, a plaintiff must demonstrate that the particular toxin at issue has been shown to cause the injury the plaintiff sustained.  Evidence of general causation answers the question, "is this toxin capable of causing the plaintiff's injury?"  To prove specific causation, a plaintiff must demonstrate that the plaintiff was in fact exposed to a dose — a concentration of the toxin over a specific period of time — sufficient to cause the injury, i.e., a "toxic" dose. [28]   Evidence of specific causation answers the question, "was the plaintiff exposed to a dose of the alleged toxin sufficient to cause the plaintiff's injury?"  Failure to provide sufficient evidence of both general and specific causation should be fatal to a plaintiff's case. [29]

Proof of causation of an alleged mold-related or toxic injury involves both epidemiological and toxicological evidence.  The "classic" epidemiological standard for assessing whether an association between exposure to an agent and a reaction or response thereto is in fact a causal relationship is known as the Hill criteria. [30]   The Hill criteria indicate that a causal relationship may be inferred when the association between exposure and reaction exhibits the following:

1.      Strength (high relative risk or correlation, e.g., smoking and lung cancer);

2.      Consistency (evidence of a similar association confirmed on multiple occasions);

3.      Specificity (causative agent and response are narrowly defined, not broad or variable);

4.      Temporal relationship (the exposure must precede the reaction, and the reaction                      should follow within a reasonable time);

5.      Biological gradient (intensity of responses should vary with that of exposure; also known as the "dose-response curve," this the domain of toxicologists);

6.      Coherence (similar responses are observed for similar exposures);

7.      Biological plausibility (a believable biological basis for the association);

8.      Experimental evidence (reproducible results under controlled conditions); and

9.      Analogy (similarity of association to other established causal associations). [31]

The greater an association of exposure and response can satisfy these criteria, the greater the scientific validity of a conclusion that the association is causal. [32]   None of the criteria, other than temporality, is essential, but a failure to address any of these criteria should be fatal to a plaintiff's expert causation opinion.  These criteria for causation have only briefly been discussed in the context of mold litigation. [33]   However, they should form the basis of any expert defense opinion used to counter a plaintiffs' offered opinion that mold exposure caused an injury.

The difficulty for mold-injury plaintiffs is that sufficient evidence that meets the Daubert criteria for reliability is unavailable.  Right now, science and medicine have not established a causal link between mycotoxins and disease: [34]

While there is general agreement that active mold growth in indoor environments is unsanitary and must be corrected, the point at which mold contamination becomes a threat to health is unknown. . . . Research and systematic field investigation are needed to provide an understanding of the health implications of mycotoxin exposures in indoor environments. [35]

 

Existing research simply is insufficient to reach valid conclusions about causation.  Much of the scientific studies on the effects of mycotoxins examine the effect of ingested mycotoxins on animals. [36]   The few studies that have examined the effects of inhaled mycotoxins provide conflicting or inconsistent results. [37]   In fact, animal inhalation studies support the conclusion that the toxicity of a mycotoxic dose decreases over time, suggesting that the body can "mitigate the effect of exposure at low doses." [38]   Mice who received nasal injections of mycotoxins produced health effects in the mice, but the value of the study is severely limited: the health effects were graded subjectively, the introduction of the mycotoxin by nasal injection was artificial and thus not analogous to human exposures, and the doses could not be extrapolated to typical human exposures. [39]   Case reports of human exposure exist and may suggest a need for additional study, but case reports have no value with respect to causation. [40]

[P]hysicians following scientific methodology would not examine a patient or several patients in uncontrolled settings to determine whether a particular drug has favorable effects, nor would they rely on case reports to determine whether a substance is harmful. [41]

Case reports amount to anecdotal or particularized data that accomplish no more than create a false appearance of direct and actual knowledge of a causal relationship.

Some epidemiological studies of mold effects in humans have been conducted, but they too are flawed.  For example, the Centers for Disease Control investigated a series of pulmonary illnesses in infants in Cleveland, Ohio, in 1994, and multiple reports of that investigation implicated the mold species Stachybotrys chartarum as a cause.  However, not long thereafter, citing the unscientific manner in which investigators conducted the mold sampling and the unjustifiable assumptions underlying the sampling, the CDC concluded that the association between mold and the infants' illness "was not proven." [42]   Other studies have relied on surveys or questionnaires of patients and are therefore skewed by self-reporting bias and outcome-directed methodology. [43]   Experts who opine about an alleged general cause of a plaintiff's alleged mold-related illness cannot rely upon legally reliable scientific knowledge; thus, their testimony should be excluded under Daubert.

In addition to the lack of scientific knowledge supporting a general causal link between mold and injury, admissible evidence of the specific causal link between mold exposure and a particular plaintiff is equally non-existent.  Every personal injury mold exposure case will involve the expert analysis of one or many samples of air or material collected from inside the building in which the plaintiff was allegedly exposed to mold.  Indoor air sampling is common, as is bulk sampling of suspected mold-harboring materials from the building.  A qualified laboratory will then analyze and quantify any mold contained in the sample. [44]   The laboratory report containing the analysis of the sample can be useful to a certified industrial hygienist and mechanical engineer, who wish to understand, gauge, and optimize the indoor air environment and the performance of the HVAC system. Such reports, with neatly ordered charts indicating with apparent precision the various types of molds, identified by scientific genus and species name, the lab detected in each sample, have all the appearance of conclusive scientific evidence.  But a sample analysis report is of no use in establishing medical causation of a plaintiff's condition. 

"Large gaps remain in the knowledge base needed to conduct quantitative risk assessments for inhaled mycotoxins." [45]   The sampling and analysis represents merely a "snapshot" look at the mold present in an indoor environment at the time of sampling; the sampling does not address the actual level of exposure of a particular person in that environment to molds or mycotoxins.  Sampling and analysis reports may provide dramatic numbers that portray an ominously contaminated  environment, but mere numbers are largely meaningless.  There are no standards that address acceptable concentrations of mold or mycotoxins — or any biological matter — in indoor environments (other than specific manufacturing environments). [46]   As a baseline, industrial hygienists typically compare indoor results with sampling results from outside to determine whether there is an "amplification site" for mold growth indoors, and, if so, to take appropriate remedial action to eliminate such a site. [47]   But even reports of indoor levels of mold exceeding outdoor levels fall well short of the required evidence of the dose of mold or mycotoxin to which the plaintiff was exposed.  Reports of such excessive indoor mold levels may indicate that mold is growing, even thriving, somewhere indoors, but such reports alone do not address specific causation. [48]   The snapshot reports don't indicate the dose — i.e., the concentration over time — of mycotoxin a plaintiff allegedly received.  Experts who opine about an alleged specific cause of a plaintiff's alleged mold-related illness cannot rely upon legally reliable scientific knowledge; thus, their testimony should be excluded under Daubert.

Daubert-Based Outcomes

 

The result of the lack of scientific support for mold claims is that, under Daubert, and based on the current state of scientific knowledge about mold and disease, plaintiffs should not be able to introduce evidence, let alone establish, that mold or mycotoxin caused their alleged illness.  Although the popular media may perpetuate the seemingly unjust plight of allegedly injured but uncompensated plaintiffs, the fairness of the system derives from the fact that this result is consistent with the standard of negligence to which the law holds all defendants.  Absent scientific evidence of causation, plaintiffs cannot meet their ultimate burden of proof:  that the defendant knew or should have known of the danger mold presented to the plaintiff.  Individuals who are injured may continue to blame mold, but until a scientific methodology that satisfies the requirements of Daubert can demonstrate a causal connection, holding defendants liable for such an unforeseeable injury is unfair and antithetical to the concepts on which the legal system exists. 

Several recent federal and state cases illustrate both the difficulty plaintiffs face in establishing that mold exposure can cause permanent illness or disability, as well as the rewards of plaintiffs' persistence — and the associated risks to defendants — in overcoming that difficulty.

         Ballard v. Fire Ins. Exchange

In a widely publicized and closely watched Texas case, Ballard v. Fire Insurance Exchange, [49] a judge in Austin excluded the plaintiffs' proffered causation testimony necessary to prove that the undisputed mold infestation in their home caused alleged permanent cognitive impairments.  The mold, among which was the same S. chartarum implicated in the Cleveland infant studies, resulted from numerous water leaks throughout the house.  Although the plaintiffs had received some indemnification for the property damage, the plaintiffs sued their insurers when their claims for personal injuries resulting from exposure to the mold and mycotoxins were denied.  Although the subsequent jury trial resulted in a $32 million verdict against the plaintiffs' insurers for improper claims handling [50] — not personal injury caused by mold — the defendants successfully employed a Daubert-type attack on the scientific validity of the key tests and studies underlying the causation opinions of the plaintiffs' experts.  The power of that Daubert attack is evidenced by the fact that the defendant's motion in limine succeeded despite, if the popular press accounts are accurate, impressive anecdotal evidence of causation:

Straus [a professor of microbiology and immunology at Texas Tech University Health Sciences Center] barely lasted 30 minutes.  "Walking into that house was one of the biggest mistakes I ever made," he says.  "None of us were wearing any protection.  I was standing on that Tara staircase, and all of a sudden I didn't feel very good."  Strauss spent the next four hours lying in Holder's truck, crawling out only to vomit.  He lost 25 percent of the hearing in one ear, and the damage seems to be permanent.  "I don't go into Stachy houses anymore." [51]

However, Professor Strauss' experience is merely anecdotal, not scientific evidence.  The Ballard plaintiffs' experts must rely on something more scientifically reliable to assist the trier of fact in determining the fact in issue — whether the mold in their home injured them.

         To establish the general causation of their injuries — that mold and mycotoxins are capable of causing their cognitive impairments — the Ballard plaintiffs relied upon an epidemiological survey, conducted by plaintiffs' expert witness Dr. Eckhardt Johanning, of a group of people who were exposed to mold while working in a museum.  The defendants argued that the study lacked scientific validity under Merrell Dow Pharmaceuticals v. Havner, [52] and could not support the conclusion that mold or mycotoxins are capable of causing cognitive injuries. 

Havner establishes the criteria by which litigants may rely upon epidemiological data in Texas courts as scientifically valid.  These criteria include that the epidemiological data be the result of a properly designed study free from bias, that the data demonstrate an increased risk of injury, and that the data satisfy the Hill criteria. [53]   The Havner court observed that the "limits of science" must, at some point, enter the courtroom and guide the outcome: 

[T]he law must balance the need to compensate those who have been injured by the wrongful actions of another with the concept deeply imbedded in our jurisprudence that a defendant cannot be found liable for an injury unless the preponderance of the evidence supports cause in fact." [54]

 

         Although the museum study Dr. Johanning relied upon in Ballard drew conclusions about symptoms, duration of exposure in the museum, and location in the museum, the study made no attempt to link exposure to mycotoxins and cognitive difficulties.  The study consisted only of a survey conducted of the museum employees, some of whom were already patients of plaintiffs' expert.  Thus Dr. Johanning's study collected self-reported (and therefore biased) data, failed to demonstrate an increased risk, and largely failed to meet any of the Hill criteria.  The Ballard court's ultimate exclusion of Dr. Johanning's causation testimony was consistent with the current state of scientific literature on mold science and, therefore, Havner and Daubert.

         Because reliable scientific methodologies cannot establish that mold or mycotoxin generally causes the permanent type of injuries about which the Ballard plaintiffs complained, a fortiori the Ballard plaintiffs could not establish that their exposure to the molds or mycotoxins in their home specifically caused their injuries as a matter of law.  Nonetheless, they did attempt to establish specific causation of their injuries — that they were in fact exposed to a toxic does of mycotoxins in their home, which caused their cognitive impairments.  The Ballard plaintiffs relied upon tests of air and material samples collected from their house, which purported to establish that the mold in their house was toxic, and upon the deaths of mice placed in the house as a test by one of the plaintiffs. 

The defendants argued that the plaintiffs' evidence fell well short of that necessary to demonstrate specific causation.  For example, the deaths of the mice were inconclusive proof of causation because the deaths were not part of a scientifically derived and designed methodology that was free from the bias of the plaintiffs themselves.  More importantly, the defendants argued successfully, the results of testing the samples taken in the house were inconclusive proof of causation: the tests failed to rule out that non-mold toxins caused the plaintiffs' injuries, and the tests showed toxicity in the non-Ballard control samples.  Thus, the test results did not provide the trier of fact with any basis for concluding that the Ballards' claims were either true or false, and the court properly, under Havner and Daubert, excluded testimony based on those results.

         The Ballard plaintiffs, who needed to prove by a preponderance of the evidence that mycotoxins were present in their home in a concentration capable of causing their injuries, and that they were exposed to those mycotoxins in a dose sufficient to cause their injuries, and which caused their injury, eventually had to face the "limits of science." [55]   They could not demonstrate that any link in the entire causal chain they proposed was anything more than a series of assumptions. [56]   Nonetheless, the Ballard plaintiffs won a $32 million verdict based on their insurers' handling of their claims.  The Daubert "victory," then, may seem like small consolation to the defendants.  Yet defense counsel remarked that the prospect of admissible causation testimony, which may have netted the plaintiffs an additional $10-20 million in lost future earnings and mental anguish, "scares me to death." [57]

         Minner v. American Mortgage & Guaranty Co.

In another recent case, three plaintiffs who worked for a credit card company in Delaware claimed to have suffered permanent disabilities, including cognitive deficits, as a result of long-term, low-dose exposure to mold, mycotoxins, and other toxins at their office workstations. [58]   The plaintiffs in Minner v. American Mortgage & Guaranty offered the opinions of a battalion of alleged medical, psychological, and scientific expert witnesses, whose testimony would have supported the position that the plaintiffs' exposure to, inter alia, mold and mycotoxins at their workplace caused such permanent injuries as MCS, SBS, CFS, FM, Reactive Airways Dysfunction Syndrome ("RADS"), Toxic Encephalopathy ("TE"), cognitive impairment and neuropsychological deficits.

The defendant owner of plaintiff's office building in Minner launched a Daubert-style attack on the admissibility of all causation opinions. [59]   Echoing the Havner court's "limits of science," the Minner court recognized that "[t]his is one of those cases where it is possible that the precepts of science have not caught up with all the claims of the Plaintiffs." [60]   With respect to MCS and SBS, the defendant successfully argued that medical science does not agree on whether either malady exists or on a definition of either malady.  In light of that, no scientifically reliable methodology could support a conclusion under M.G. Bancorporation or Daubert about the cause of the plaintiffs' MCS or SBS.  With respect to CFS and FM, both of which are recognized ailments within their respective medical specialties with recognized diagnostic criteria, the defendant successfully argued that the etiology of both ailments is entirely unknown.  In light of that, no scientifically valid methodology could support a conclusion under M.G. Bancorporation or Daubert about the cause of the plaintiffs' CFS or FM.  With respect to RADS and TE, the defendant argued that medical science had identified only very high-dose, acute exposures to chemicals as potential causes, and that any conclusion that the plaintiffs' low-dose, chronic exposure caused RADS and TE could not satisfy M.G. Bancorporation or Daubert.  The court disagreed, and allowed the testimony, explaining that, given the existence of a known cause, whether the conclusion that the plaintiffs' ailments were caused in some other manner bore on the weight of the evidence, not its admissibility. [61]   The methodology of the conclusions may produce incorrect results, but the methodology was not unsound, "by a bare minimum," according to the Minner court. [62]  

The Minner court believed that its middle-of-the-road decision was "consistent with the healthy skepticism with which the Courts have historically greeted expert testimony.  The fringe has been eliminated.  At the same time, the Opinion does not foreclose a case on the frontier of medical exploration." [63]

         National Bank of Commerce v. Associated Milk Producers

The plaintiff in National Bank of Commerce v. Associated Milk Producers blamed his laryngeal cancer on exposure to mycotoxins while he worked on the production line in a cheese factory. [64]   He sued one of the cheese factory's suppliers, whose employees had previously pleaded guilty to federal charges including distribution of, and conspiracy to distribute, contaminated milk in interstate commerce. [65]   The plaintiff claimed that, because he inhaled aerosol milk particles produced during the cheese making process, he was exposed to aflatoxin M-1 from the defendant's contaminated milk.  The defendant challenged the admissibility of the plaintiff's expert testimony that the plaintiff's exposure to contaminated milk caused his cancer.

Aflatoxin B-1 is produced by mold that can be found in cattle feed, and aflatoxin M-1 is a bovine metabolite of B-1 that cows excrete in their milk. [66]   The National Bank court found that neither party had identified any publication, study, or direct scientific evidence demonstrating that exposure to either aflatoxin M-1 or B-1 at any level caused laryngeal cancer in humans.  In addition, the court found an absence of any indirect scientific evidence, such as epidemiological studies, in vitro studies,  or animal studies, demonstrating that exposure to either toxin could cause laryngeal cancer. [67]   Note that in the absence of such evidence, the plaintiff could not have established that he had been exposed to a toxic dose of aflatoxin M-1.  As a result, the court determined that granting the defendant's Daubert motion regarding plaintiff's causation testimony was justified.

Recognizing the "draconian" consequence of such a ruling — dismissal — the National Bank court engaged in an extended and detailed discussion of the state of scientific knowledge about aflatoxin B-1 and M-1.  And although this mold case atypically involves cancer, that discussion highlights the Daubert-style analysis in a mold-related personal injury case.  The court observed that, despite considerable research into aflatoxins, and reported connections to liver and kidney diseases, including cancer, "[t]here have been no epidemiological associations reported in the 35 years of study of aflatoxins between aflatoxin B1 and M1 and laryngeal cancer." [68]   The court also considered two other bases on which plaintiff sought to bolster his claim — the theory that exposure to just a single carcinogenic molecule could have caused his cancer (the "no threshold" theory), and the testimony of his expert witnesses that they had considered and ruled out other possible causes (the "differential diagnosis" methodology (see below)).  Consistent with the expectations of Daubert, the National Bank court held that even testimony of a valid differential diagnosis combined with the "no-threshold" theory "cannot obviate the need for some scientific proof that at some level of exposure aflatoxin M-1 can and does cause laryngeal cancer [-general causation-] and [the plaintiff] was exposed to at least that level [-specific causation-]." [69]  

The National Bank plaintiff could not demonstrate that his exposure to aflatoxins in the aerosol milk exceeded his ordinary exposure to aflatoxins from other sources (such as food), or that his cancer was not the result of other exposures to known carcinogens that could have caused his cancer. [70]   Although the plaintiff's experts testified that in their opinion the cancer was caused by the plaintiff's exposure to aflatoxin M-1 in aerosol milk particles at his workplace, the court instead relied upon an effective critique of those causation opinions by one of the defendant's experts based on the Hill criteria.  Using the plaintiff's expert's assumptions about the dose of aflatoxin M-1 the plaintiff received in the aerosol milk, the defendant's expert determined that the plaintiff faced no "excessive risk" of cancer from his purported exposure to aflatoxin at work, and in the absence of any excessive risk from that exposure, there was no basis for concluding "that there was any likelihood that, in fact, [the plaintiff's] cancer was caused as a result of exposure to the aflatoxin, because you couldn't eliminate the other sources of aflatoxin." [71]   Based on that analysis, the court agreed with the defendant's expert that the plaintiff's experts did not use an appropriate scientific methodology "and that there is no scientific basis by which one could come to an opinion that aflatoxin causes laryngeal cancer to a standard of a reasonable scientific probability." [72]

The National Bank court recognized, consistent with other courts that follow Daubert, that its duty was not to rely merely on the claims of the plaintiff's expert — i.e., the expert's ipse dixit [73] — that the opinion was valid and reliable, but to function as a "gatekeeper" and assess the scientific reliability of the testimony for itself:

[S]omething doesn't become "scientific knowledge" just because it's uttered by a scientist; nor can an expert's self-serving assertion that his conclusions were "derived by the scientific method" be deemed conclusive, else the [Daubert] opinion could have ended with footnote two ... [I]t is our responsibility to determine whether those experts' proposed testimony amounts to "scientific knowledge," constitutes "good science," and was "derived by the scientific method." [74]

 

Under Daubert, a court must subject the conclusions of a testifying expert to the same scrutiny such conclusions would face in the community, scientific or otherwise, of the witness' peers:

A physician, even a treating physician, or other expert who has seen a skewed data sample, such as one of a few infants who has a birth defect, is not in a position to infer causation.  The scientific community would not accept as methodologically sound a "study" by such an expert reporting that the ingestion of a particular drug by the mother caused the birth defect.  Similarly, an expert's assertion that a physical examination confirmed causation should not be accepted at face value. [75]

 

Much like the Ballard plaintiffs, the National Bank plaintiff could not demonstrate that the basis for his expert's causation opinion was anything more than speculation, which is precisely the sort of expert testimony Daubert seeks to exclude.

                  Mondelli v. Kendel Homes Corp.

         In light of the foregoing cases, all decided in the last three years, a Nebraska case decided in July 2001 is particularly interesting.  In Mondelli v. Kendel Homes Corp. [76] the plaintiffs sought to recover for alleged injuries household mold exposure injuries, in this case asthma.  Applying the Frye standard, [77] the trial court excluded the testimony the plaintiffs' expert causation witnesses, an environmental toxicologist employed by the state department of health, and a biologist who worked as a director of the laboratory that had analyzed air samples taken from the Mondelli home, for their failure to demonstrate "general acceptance" of their opinions in the relevant scientific community.  The Supreme Court of Nebraska reversed the trial court decision, holding that the plaintiffs' experts testimony satisfied the Frye standard.  The Supreme Court also reversed the trial court's directed verdict for the defendants, and ordered a new trial.  Although the Mondelli decision now carries little precedential value in light of Nebraska's decision to follow Daubert, the decision remains relevant to a discussion of expert testimony on mold causation.

         Having held that the trial court abused its discretion in excluding plaintiffs' expert testimony, the Mondelli court reversed the trial court's directed verdict for the defendants.  The court determined that had the expert testimony been admitted, "the record would have contained evidence about which reasonable minds could differ," thus precluding the entry of directed verdict." [78]   The Supreme Court of Nebraska, however, came to this conclusion summarily, without indicating whether and how the evidence would have sufficiently established general or specific causation.  In fact, the plaintiffs' expert's testimony is to the contrary: the toxicologist "stated that no industry standards exist to determine the acceptable level of mold in an indoor area; only guidelines and recommendations exist." [79]   The experts apparently would have testified that the measured levels of mold inside the house exceeded outdoor levels, but that alone fails to indicate that the plaintiffs received a dose sufficient to cause their illness.  As noted above, air sampling results, about which the plaintiffs' biologist expert planned to testify, merely present a snapshot look at mold levels at the time the sampling was performed, and do not address the level of exposure that someone who lives in such an environment actually received.  Although admissible under the Frye standard — according to the Supreme Court of Nebraska — as having "general acceptance" in the relevant field, how reasonable minds could have differed about the sufficiency of the plaintiffs' evidence of causation remained unspoken.

Stroot: A Daubert Loophole?

         A testifying expert witness, however, need not rely upon published studies or peer-reviewed research to reliably testify about causation.  Under Daubert, the methodology leading to the expert's conclusion is paramount to admissibility.  This may permit the use of a single-patient methodology such as "differential diagnosis," which, as applied to a single patient is not susceptible to peer review or publication but which, as a methodology, is recognized in medicine as reliable. [80]   Differential diagnosis is a process whereby a physician examines a patient, takes a medical history of the patient, conducts laboratory tests as indicated from the exam and history, and considers and eliminates alternative causes of illness. [81]   The physician is not required to rule out all possible alternative causes, and the use of differential diagnosis to arrive at a novel conclusion is not grounds for excluding testimony under Daubert. [82]   As a methodology, a differential diagnosis breaks down only when the defendant can proffer a plausible alternative cause and plaintiff's expert cannot provide the basis for eliminating that alternative cause in the differential diagnosis. [83]   Given its recognition for reliability in medicine, a properly conducted differential diagnosis may satisfy Daubert.

         Another recent Delaware state case contrasts with the scientific Daubert analysis that, for example, the National Bank court performed in detail, and illustrates how differential diagnosis may impact mold-related litigation.  In Stroot v. New Haverford Partnership, the defendant landlord appealed the admission of the plaintiff tenants' expert's opinions that the plaintiffs' injuries were caused by mold in their apartments. [84]   The landlord argued that air sampling was insufficient to establish a baseline level of mold in the apartments and, absent a baseline level of mold, plaintiffs' experts' opinion that levels of mold in the plaintiffs' apartments were "excessive" was not methodologically sound. [85]   The landlord also argued that the plaintiffs' experts failed to rule out other potential causes of the plaintiffs' injuries, such as smoking and dog allergies. [86]

         The Stroot court was unpersuaded by the defendants, at least in part because the defendants' burden on appeal was quite high, requiring that the defendants demonstrate that the trial judge abused his discretion in admitting the evidence.  However, the court also found that the methodology underlying plaintiff's expert's causation opinion supported the trial court's decision to admit the testimony under M.G. Bancorporation v. Le Beau.  That methodology — a differential diagnosis — appears to have insulated the expert's opinion from Daubert challenge:

[Dr.] Johanning testified that he followed the scientifically accepted procedure of obtaining a medical history and a detailed questionnaire from the plaintiffs.  He then ruled out other possible causes of plaintiffs' health problems by reviewing that information together with the blood test results and the data collected from the apartment buildings.  The foundation for an expert's causation opinion need not be established with the precision of a laboratory experiment. [87]

 

The Stroot court is probably correct that, to be admissible, Daubert requires less precision of an expert's opinion than of, for example, a laboratory experiment underlying it, but not much less, because the methodological expectations of Daubert are the same.  In this context, however, the court's comparison only serves to suggest that the Daubert bar is lower for opinions based on a differential diagnosis: in the end, differential diagnosis as a methodology does rely to an extent on the expert's ipse dixit.  The Stroot decision is the first case involving differential diagnosis in a mold related personal injury case, and may provide a basis for plaintiffs to skirt the Daubert requirements.

         Two other cases, however, indicate that the Daubert loophole that differential diagnosis may provide is not as broad as it may appear.  In Turner v. Iowa Fire Equip. Co., [88] a non-mold toxic exposure case, the United States Court of Appeals for the Eighth Circuit distinguished between a differential diagnosis performed to determine the cause of a plaintiff's illness and a differential diagnosis performed to determine the plaintiff's condition.  The court excluded the expert's testimony on causation, because the expert acknowledged that he conducted a differential diagnosis to determine the only the plaintiff's condition, not the cause of the plaintiff's condition. [89]  

         Without recognizing it, the court's distinction is consistent with at least one medical authority's notion of differential diagnosis.  Steadman's Medical Dictionary defines "differential diagnosis" as "the determination of which of two or more diseases with similar symptoms is the one from which the patient is suffering, by a systematic comparison and contrasting of the clinical findings." [90]   This indicates that the physician's role is to differentiate and identify which disease underlies (or "causes") the symptoms that the physician observes in a patient — a biological or physiological inquiry — rather than differentiate which of a variety of events or exposures has caused the disease underlying the symptoms — a toxicological inquiry.  Indeed, this medical understanding of differential diagnosis indicates that the Turner distinction between cause and condition is superfluous, and that the plaintiff-proffered notion of a "differential diagnosis" of the cause of a plaintiff's alleged injury is susceptible to a Daubert attack: in the absence of evidence of a general and specific cause of mold-related illness, a physician's "differential diagnosis" that mold caused a plaintiff's alleged illness lacks sufficient scientific reliability. 

         Next, the United States Court of Appeals for the Fifth Circuit has rejected the use of differential diagnosis to render an admissible causation opinion under Daubert. [91]   In Moore v. Ashland Chemical, the Fifth Circuit affirmed the district court's exclusion of an opinion based on a differential diagnosis.  This decision is significant in Texas, where mold-related claims are rising dramatically.  Unfortunately, Moore remains the decidedly minority view among the Circuit Courts. [92]

Conclusion

         Each of the cases discussed above, including the approval of differential diagnosis in Stroot, underscores the necessity of challenging plaintiffs' experts' mold injury causation opinions under Daubert effectively and systematically as early as possible in litigation.  By rigorously applying the Hill criteria, defendants' experts should be able to undermine the scientific validity of plaintiffs' experts causation opinions for the foreseeable future.  Until additional scientific research and study is complete, there is a sound legal basis for challenging proffered expert opinions that attribute injury to exposure to mold or mycotoxins.