28 ELR 10293 | Environmental Law Reporter | copyright © 1998 | All rights reserved

Separating the Scientist's Wheat From the Charlatan's Chaff: Daubert's Role in Toxic Tort Litigation

Editors' Summary: In the wake of Daubert v. Merrell Dow Pharmaceuticals, Inc., it has become increasingly important for the judicial system to discern the reliability of scientific evidence offered by experts in toxic tort cases. In this Article, the authors offer practical guidance on the application of the rule established in Daubert to toxic tort litigation. From the general acceptance test established in Frye v. United States to the refinements of the Daubert test outlined in the recently decided General Electric Co. v. Joiner case, the authors trace the evolution of the rule governing the admissibility of scientific evidence. They then examine the application of the Daubert rule to toxic tort cases by evaluating the various types of scientific evidence that can be used to prove causation. Last, they analyze the application of the Daubert rule in cases where a plaintiff has alleged development of a multiple chemical sensitivity.

Mr. Buckley is a partner in the Washington, D.C. office of the law firmof Gibson, Dunn & Crutcher LLP, and he chairs the firm's Environment and Natural Resources Practice Group. Mr. Haake is an associate in the firm's Irvine, California, office, and he also is a member of the firm's Environment and Natural Resources Practice Group.

[28 ELR 10293]

The toxic tort is a new species of tort action and is an outgrowth of our industrialized society. Simply put, the toxic tort plaintiff attempts to establish that exposure to a particular substance caused an injury. Causation, however, has proven to be an extremely contentious issue in toxic tort litigation. In contrast to a traditional tort, where causation can be established with little or no difficulty (it should not be difficult to show that a blow to the face caused a broken nose), it may be impossible for a toxic tort plaintiff to show that exposure to a particular substance caused a particular disease, or for a defendant to show that its product did not cause the injury complained of. Expert testimony, therefore, plays a pivotal role in toxic tort litigation. A plaintiff will bring forth a cadre of experts purporting to show that the defendant's releases of pollutants caused the injuries, while the defendant will counter with its own experts to refute such testimony. In the end, the jury will be faced with the seemingly insurmountable task of discerning which of the two groups of experts is "correct."

Often, however, the real battle will be waged and won well before the case gets to the jury. In the preliminary stages of the case, the attorneys for the defendant will attempt to have the testimony of the plaintiff's experts excluded on the ground that it lacks a proper scientific foundation. If the trial court agrees, and excludes the testimony of the plaintiff's expert, it will almost assuredly dismiss the plaintiff's case, as the plaintiff will not be able to make the requisite showing of causation. If, on the other hand, the court overrules the defendant's objection and admits the testimony, the defendant may settle, fearing the uncertainty of a trial and the prospect of a large verdict.

This Article examines how federal courts address the admissibility of scientific evidence in the context of a toxic tort case. It begins by examining the former "general acceptance" test set forth in the seminal case of Frye v. United States¹ and explaining how the enactment of the Federal Rules of Evidence brought the continued validity of the test into question. Next, the Article describes how the U.S. Supreme Court case of Daubert v. Merrell Dow Pharmaceuticals, Inc.² expressly overruled the Frye "general acceptance" test in favor of a more liberal approach in which the trial judge acts as a "gate-keeper" to ensure that the proffered expert testimony is both reliable and relevant. It then addresses how a court applying the Daubert factors examines expert medical testimony purporting to establish causation in a toxic tort case. Finally, the Article examines how courts address the admissibility of evidence concerning clinical ecology, a field that is increasingly common in the toxic tort context.

The Rise and Fall of Frye

The Genesis of the "General Acceptance" Test

For over 70 years the "general acceptance" test of Frye v. United States³ was the cornerstone of admissibility of scientific [28 ELR 10294] evidence. Frye was a short and citation-free decision dealing with the admissibility of evidence derived from an old version of the lie detector, known as the blood pressure deception test, which the defendant sought to introduce to establish his innocence. In what has become the most famous passage of that opinion, the U.S. Court of Appeals for the D.C. Circuit stated:

Just when a scientific principle or discovery crosses the line between the experimental and demonstrable stages is difficult to define. Somewhere in this twilight zone the evidential force of the principle must be recognized, and while courts will go a long way in admitting expert testimony deduced from a well-recognized scientific principle or discovery, the thing from which the deduction is made must be sufficiently established to have gained general acceptance in the particular field in which it belongs.⁴

Applying this test, the court held that the deception test had not yet gained general acceptance in the scientific community and thus was inadmissible. In the years that followed, the Frye "general acceptance" test became the standard in almost every court in the country by which the admissibility of scientific evidence was weighed.⁵

The Advent of the Federal Rules of Evidence

In 1975, Congress enacted the Federal Rules of Evidence. Rule 702 provides, "if scientific, technical or other specialized knowledge will assist the trier of fact to understand the evidence or to determine a fact in issue, a witness qualified as an expert by knowledge, skill, experience, training, or education, may testify thereto in the form of an opinion or otherwise."⁶ The enactment of the Federal Rules "reflect[s] a liberal attitude toward the admission of evidence and vest[s] trial court judges with broad discretion in screening evidence."⁷ The Federal Rules, however, did not specifically mention the Frye test or discuss how it would be affected by the new standard. Was that test incorporated into Rule 702, or did Rule 702 supersede it? In the years following the enactment of the Federal Rules, the circuit courts split on this issue, some concluding that the "general acceptance" test did not survive the enactment of the Federal Rules of Evidence,⁸ and others holding that the Frye test did survive the Rules' enactment.⁹

The Daubert Rule

The Supreme Court effectively put an end to this debate when it handed down its decision in Daubert v. Merrell Dow Pharmaceuticals, Inc.¹⁰ Daubert was one in a long series of cases alleging that the antinausea drug, Bendectin, caused birth defects in children whose mothers ingested the drug. In order to establish causation, plaintiff's experts relied primarily on in vivo and in vitro animal tests, chemical structural analyses, and reanalysis of epidemiologic studies. Merrell Dow countered with the testimony of its own experts, backed by over 30 published epidemiologic studies that purported to show that there was no statistically significant association between Bendectin and birth defects. Citing the "general acceptance" test, the district court held that the evidence proffered by plaintiff's experts was inadmissible. Because of the overwhelming body of epidemiologic data refuting any link between Bendectin and birth defects, the court held that any expert opinion to the contrary that was not backed up by statistically significant epidemiological data was inadmissible.¹¹ The Ninth Circuit affirmed, also relying on the "general acceptance" test.¹²

The Supreme Court reversed. The Court held that the Frye "general acceptance" test had been superseded by the Federal Rules of Evidence and further held that the trial judge must assume a gate-keeping role in assessing the admissibility of scientific evidence, rather than deferring to a consensus of the scientific community.

That the Frye test was displaced by the Rules of Evidence does not mean, however, that the Rules themselves place no limits on the admissibility of purportedly scientific evidence. Nor is the trial judge disabled from screening such evidence. To the contrary, under the Rules the trial judge must ensure that any and all scientific testimony or evidence admitted is not only relevant, but reliable.¹³

Daubert was a significant departure from the Frye regime. Under the old rule, a trial judge was to defer to the scientific community in assessing the admissibility of scientific evidence. Indeed, many courts and commentators viewed that task of the trial judge as nothing more than "nose counting."¹⁴ Daubert, on the other hand, envisions an active role on the part of the trial judge in making an independent assessment of the scientific reliability of the proffered evidence. As the opinion states, "the Rules of Evidence — especially Rule 702 — do assign to the trial judge the task of ensuring that an expert's testimony both rests on a reliable foundation and is relevant to the task at hand."¹⁵ This is the task Justice Rehnquist refers to as the trial judge's "gate-keeping responsibility."¹⁶

The Requirements of Daubert

In Daubert, the Supreme Court enumerated a two-part test to determine the reliability of proffered scientific evidence: "Faced with a proffer of expert scientific testimony, then, the trial judge must determine at the outset … whether the [28 ELR 10295] expert is proposing to testify to (1) scientific knowledge that (2) will assist the trier of fact to understand or determine a fact in issue."¹⁷ These two factors have become known as the "reliability prong" and the "fit prong."

The Reliability Prong. In assessing the admissibility of scientific evidence, the first inquiry is whether the proffered scientific evidence is reliable. In order to aid trial courts in making this assessment, the Supreme Court outlined a non-exclusive list of four factors to be considered. These factors are (1) whether the technique or scientific knowledge can be and has been tested, (2) whether the theory or technique has been subject to the strictures of peer review and publication, (3) what the known or potential rate of error is, and (4) whether the theory or technique is generally accepted.

Testability is an important factor in determining scientific reliability. The Supreme Court noted this fact in Daubert:

[A] key question to be answered in determining whether a theory or technique is scientific knowledge that will assist the trier of fact will be whether it can be (and has been) tested. Scientific methodology today is based on generating hypotheses and testing them to see if they can be falsified ….¹⁸

Although decided before Daubert, DeLuca ex rel. DeLuca v. Merrell Dow Pharmaceuticals, Inc.¹⁹ is an example of how this factor may be applied. There, one of the plaintiff's experts reanalyzed existing epidemiologic studies to show that Bendectin causes birth defects. However, none of the other expert epidemiologists testifying, including the plaintiff's other experts, were able to replicate this methodology or result. Since the court was unable to ascertain the precise techniques or methodology employed by this expert, and thus could not assess the reliability of the expert's reanalysis, the court held that the evidence was inadmissible.²⁰

As a second factor, the Supreme Court noted that peer review would be an important consideration in the assessment of scientific reliability. Although peer review is not a sine qua non of admissibility, the Court held that "submission to the scrutiny of the scientific community is a component of 'good science,' in part because it increases the likelihood that substantive flaws in methodology will be detected."²¹ As is discussed later in this Article, this factor is becoming increasingly relevant where experts seek to testify concerning new or controversial diagnoses such as multiple chemical sensitivities.

The third factor, and the one that has been construed the least by courts applying the Daubert test, is the rate of error. The Court noted that in the case of a particular scientific technique, the trial court should consider the known or potential rate of error and the existence of standards controlling the technique's operation.

Finally, the Court found that general acceptance can still have a bearing on the inquiry: "Widespread acceptance can be an important factor in ruling particular evidence admissible, and a known technique that has been able to attract only minimal support within the community … may properly be viewed with skepticism."²² This factor has been most relevant in those cases in which a party seeks to introduce evidence concerning a new field of scientific study.²³

After the Supreme Court remanded Daubert to the Ninth Circuit, that court added that an additional factor to be considered in assessing the scientific validity of an expert's opinion is "whether the experts are proposing to testify about matters growing naturally and directly out of research they have conducted independent of litigation, or whether they have developed their opinions expressly for the purposes of testifying."²⁴ The court reasoned that "an expert testifying based on research he has conducted independent of the litigation provides important, objective proof that the research comports with the dictates of good science."²⁵ After all, "experts whose findings flow from existing research are less likely to have been biased toward a particular conclusion by the promise of remuneration …."²⁶ Thus, in again rejecting the plaintiff's expert testimony based on the dictates of the Supreme Court, the court in Daubert II found it significant that none of the plaintiff's experts based his or her findings on independent pre-litigation research.²⁷

The Fit Prong. After considering the reliability of the proposed scientific evidence, the trial court must consider the "fit" that the proposed evidence has with the ultimate issue to be decided. The Supreme Court stated that "Rule 702 further requires that the evidence or testimony 'assist the trier of fact to understand the evidence or to determine a fact in issue ….' Expert testimony which does not relate to any issue in the case is not relevant and, ergo, nonhelpful."²⁸ The Court used the following example to illustrate this fit requirement:

The study of the phases of the moon, for example, may provide valid scientific "knowledge" about whether a certain night was dark, and if darkness is a fact in issue, the knowledge will assist the trier of fact. However (absent creditable grounds supporting such a link), evidence that the moon was full on a certain night will not assist the trier of fact in determining whether an individual was unusually likely to have behaved irrationally on that night.²⁹

As the Ninth Circuit in Daubert II explained, in order to fulfill the "fit" requirement, the testimony must "logically advance[] a material aspect of the proposing party's case."³⁰

Analytically, the distinction between the reliability prong and the fit prong may not always be too clear, and the two tests will often overlap. For example, a published theory or study may purport to prove A; yet from this study an expert [28 ELR 10296] may attempt to conclude B. Even though the study on which the expert purports to rely may be valid, it may be that the expert's reliance on the study for his conclusion is not.³¹ A court could decide that the evidence is inadmissible because there is not a "fit" between the study and the science at issue in the case, or because the expert's reliance on the study is methodologically flawed, and his testimony is thus unreliable.³²

Daubert Applies to Each Step of an Expert's Analysis

Often scientific evidence will involve a multistep analysis that ultimately leads to the conclusion offered by the witness (i.e., if a then b; if b then c; therefore, if a then c). This situation will often arise in a toxic tort case where a toxicologist seeks to establish causation based on animal studies. Such studies, which usually involve exposing animals to high doses of a known or suspected toxin, require extrapolation from the high dose to a lower dose and, then, from the animal to humans.³³ Courts have held that in order for such a causal chain to withstand scrutiny under Daubert, each individual link in that chain must satisfy the Daubert test. As the court stated in In re Paoli Railroad Yard PCB Litigation,³⁴ "Daubert's requirement that the expert testify to scientific knowledge — conclusions supported by good grounds for each step in the analysis — means that any step that renders the analysis unreliable under the Daubert factors renders the expert's testimony inadmissible."³⁵

The Ninth Circuit used this reasoning to exclude proffered expert testimony in Schudel v. General Electric Co.³⁶ In that case, the plaintiff sought to establish that his exposure to two industrial solvents, trichloroethane (TCA) and perchloroethylene (Perc or TCE), caused him to suffer from toxic encephalopathy. The court noted that plaintiff's expert's testimony was based on (1) extrapolation from studies involving substances other than TCA or Perc; and (2) extrapolation from studies involving long-term exposure at relatively low chemical concentrations or short-term exposure at very high concentrations, rather than the short-term moderate level exposure sustained by the plaintiff in that case.³⁷ The court noted that while the extrapolations were necessary to make the studies relevant, there was no showing that the necessary extrapolations were scientifically acceptable. Thus, since the expert had not adequately connected the causal chain with scientifically valid evidence, the court held that the evidence was inadmissible.³⁸

The Methodology/Conclusion Debate

There has been a recurring question in the literature about the extent to which a court applying Daubert should look at the conclusions of an expert witness, as opposed to focusing solely on the methodology. This debate revolves around the passage in Daubert that states:

The inquiry envisioned by Rule 702 is, we emphasize, a flexible one. Its overarching subject is the scientific validity — and thus the evidentiary relevance and reliability — of the principles that underlie a proposed submission. The focus, of course, must be solely on principles and methodology, not on the conclusions that they generate.³⁹

Courts, however, have held that this requirement is not as strict as it sounds. For example, the court in Paoli stated:

Plaintiffs are correct, of course, that Daubert requires the judge's admissibility decision to focus not on the expert's conclusions but on his or her principles and methodology. But we think that this distinction has only limited practical import. When a judge disagrees with the conclusions of an expert, it will generally be because he or she thinks that there is a mistake at some step in the investigative or reasoning process of that expert. If the judge thinks that the conclusions of some other expert are correct, it will likely be because the judge thinks that the methodology and reasoning process of the other expert are superior to those of the first expert. This is especially true given that the expert's view that a particular conclusion "fits" a particular case must itself constitute scientific knowledge — a challenge to "fit" is very close to a challenge to the expert's ultimate conclusion about the particular case, and yet it is part of the judge's admissibility calculus under Daubert.⁴⁰

This view has gathered support in the legal literature. For example, one commentator has pointed out:

When Daubert forbids courts to examine an expert's conclusions, it is obviously alluding to the Frye rule. Some courts used Frye to exclude novel expert testimony if it conflicted with the established view in the scientific community, regardless of the soundness of the expert's methodology and reasoning. That is no longer permissible after Daubert.

But Daubert does demand that courts assess the scientific validity of the expert's testimony. Daubert demands that in reviewing the expert's principles and methodology, a court should determine whether "the principle supports what it purports to show." Daubert therefore not only allows, but requires, courts to determine whether an expert's extrapolation from underlying studies or data is proper, or whether the expert has committed scientific or mathematical errors.⁴¹

In the recent case of Lust v. Merrell Dow Pharmaceuticals, Inc.,⁴² the Ninth Circuit threw its support behind this conclusion. In that case, the court acknowledged that a district court need not ignore an expert's anomalous conclusions in [28 ELR 10297] determining the admissibility of evidence under Rule 702. There, plaintiff's expert proposed to testify that the drug Clomid causes a substantial increase in the probability of all birth defects. He based this conclusion on the ground that human epidemiologic studies and animal studies show an association between the drug and a wide variety of other problems. Defense experts, however, indicated that this premise was not even espoused by a relevant minority of scientists in the field. The Ninth Circuit held that the district court properly excluded the expert's testimony. Responding to the charge that the court was violating Daubert's command that the inquiry must be on methodology and not conclusions, the court stated:

When a scientist claims to rely on a method practiced by most scientists, yet presents conclusions that are shared by no other scientist, the district court should be wary that the method has not been faithfully applied. It is the proponent of the expert who has the burden of proving admissibility. To enforce this burden, the district court can exclude the opinion if the expert fails to identify and defend the reasons that his conclusions are anomalous.⁴³

Thus, as the Ninth Circuit has made clear, it is appropriate for a court to scrutinize the conclusions of an expert in order to determine whether the expert's methodology is sound.

In a decision handed down this last term, the Supreme Court agreed that an analysis of the scientific reliability of an expert's opinion cannot be divorced from an examination of the conclusions. In General Electric Co. v. Joiner,⁴⁴ the plaintiff, Joiner, sued General Electric alleging that his exposure to polychlorinated biphenyls (PCBs) "promoted" his contracting small cell lung cancer. To support his claim, Joiner relied on the testimony of experts to establish causation. The experts based their opinions in part on studies involving infant mice that had developed cancer after having massive doses of PCBs injected directly into their stomachs. The Supreme Court held that the district court did not abuse its discretion in finding that these studies were too dissimilar to the facts presented in the litigation to support the experts' conclusions. Joiner was an adult human who had been indirectly exposed to much lower concentrations of PCBs and had developed a different kind of cancer.⁴⁵

Joiner's experts also relied on several epidemiologic studies that purported to show an increased rate of lung cancer in individuals exposed to PCBs in an occupational setting. Again, the Supreme Court held that it was not an abuse of discretion for the district court to hold that these reports were not a sufficient basis for the experts' opinions. Two of the reports specifically stated that there was no reason to associate the increased rate of cancer with PCB exposure, the third report dealt with chemicals other than PCBs, and the fourth involved subjects who had been exposed to numerous other carcinogens.⁴⁶

In what is perhaps the most significant portion of the decision, the Supreme Court held that it was not error for the district court to examine whether the conclusions offered by the experts were supported by the studies they cited:

Respondent points to Daubert's language that the "focus, of course, must be solely on principles and methodology, not on the conclusions that they generate." 509 U.S., at 595. He claims that because the District Court's disagreement was with the conclusions that the experts drew from the studies, the District Court committed legal error and was properly reversed by the Court of Appeals. But conclusions and methodology are not entirely distinct from one another. Trained experts commonly extrapolate from existing data. But nothing in either Daubert or the Federal Rules of Evidence requires a district court to admit opinion evidence which is connected to the 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.⁴⁷

In other words, a district court need not blindly accept the opinion of an expert who professes to have relied on valid epidemiologic and animal studies to support his decision. Rather, the court may independently and critically examine those reports and determine whether they indeed provide the scientific support that the expert claims they do.

The Standard of Review

Evidentiary decisions are reviewed under an abuse of discretion standard. This has been the law since at least the 1879 case of Spring Co. v. Edgar,⁴⁸ wherein the Supreme Court stated that "cases arise where it is very much a matter of discretion with the court whether to receive or exclude the evidence; but the appellate court will not reverse in such a case, unless the ruling is manifestly erroneous."⁴⁹ The Frye test, however, represented a significant departure from this general rule. A determination of whether a test or technique was generally accepted in the scientific community did not require any discretion on the part of the trial judge. This was especially true in light of one of the policies behind the "general acceptance" test, which was to establish uniformity in decisions regarding scientific evidence.⁵⁰ Thus, whether a particular test or technique met the requirements of Frye became a question of law, which an appellate court would review de novo.⁵¹

When the Supreme Court decided in Daubert that the trial judge must independently assess the reliability and relevance of scientific evidence, it brought the discretion of the trial judge back into the picture. Whether a particular expert's scientific testimony is reliable and relevant to the case at bar became an inquiry more tailored to the facts of each particular case. Thus, appellate courts began reviewing decisions regarding the admissibility of scientific evidence under Daubert by using an abuse of discretion standard.⁵²

[28 ELR 10298]

This rule, however, was not uniformly applied. One of the first cases to address the issue of the standard of review under Daubert was Paoli where the court noted that the general rule is that a district court's decision regarding the admissibility of evidence is granted substantial deference.⁵³ The court concluded, however, that since the Federal Rules of Evidence display a preference for admissibility, an appellate court should apply a "hard look" standard where the trial judge decides to exclude scientific evidence, especially where such a decision results in summary judgment in favor of the defendant.⁵⁴

The only other circuit to adopt this rule was the Eleventh, in the case of Joiner v. General Electric Co.⁵⁵ There, the district court granted summary judgment in favor of the defendant after having excluded the testimony of the plaintiff's expert witnesses. On appeal, the Eleventh Circuit reversed. The court held that "because the Federal Rules of Evidence governing expert testimony display a preference for admissibility, we apply a particularly stringent standard of review to the trial judge's exclusion of expert testimony."⁵⁶ Applying its own "hard look" at the evidence introduced by the plaintiff, the court held that it was error for the trial court to exclude the proffered testimony and, thus, reversed the grant of summary judgment.

On appeal, a unanimous Supreme Court reversed. The Court held that abuse of discretion is the proper standard to apply to any evidentiary decision by the trial court, including decisions excluding scientific evidence.⁵⁷ The Court rejected the idea that in liberalizing the test for admitting scientific evidence, Daubert altered the general rule when a trial court decides to exclude scientific evidence.⁵⁸ The Court likewise held that the standard of review remains the same even where excluding the evidence necessarily leads to a judgment in favor of the defendant. Such an "outcome-determinative" decision does not warrant a more searching inquiry by the reviewing court.⁵⁹ Thus, the Supreme Court concluded that "in applying an overly 'stringent' review to [the district court's] ruling, [the circuit court] failed to give the trial court the deference that is the hallmark of abuse of discretion review."⁶⁰

The Application of Daubert to Toxic Tort Claims

In order to prevail in a toxic tort claim, the plaintiff must show that he or she has been exposed to a harmful substance and that the exposure has led to an injury. In order to make this showing, the plaintiff must establish two types of causation: general and specific. General causation assesses whether a substance is capable of causing the injury at issue. Specific causation assesses whether exposure to the substance did in fact cause the particular injury to the particular plaintiff.⁶¹

Before moving on to the issue of specific causation, a plaintiff in a toxic tort case may attempt to have the issue of general causation decided early in the case by asking the court to hold that the substance at issue is capable of causing a disease in humans. Such a finding can provide a plaintiff with several advantages. For example, a preliminary determination that the defendant's release of pollutants is harmful can provide the plaintiff with a strong springboard into settlement negotiations. A defendant may rather settle than have it widely reported that it is allegedly exposing the public to cancer-causing chemicals. Additionally, plaintiffs' attorneys will often seek to have the case certified as a class action. A class action means that there will be more claimants, greater liability and, thus, a larger pie from which the plaintiffs' attorneys will take a slice. Plaintiffs' attorneys will therefore claim that the issue of general causation is ripe for class certification, arguing that this issue is a question of fact common to the class.⁶²

Courts have correctly recognized, however, that the issue of general causation cannot be examined in a vacuum. Courts must consider the dose to which the plaintiff was allegedly exposed. After all, in sufficient quantities, just about any substance, including water, can be toxic.⁶³ Thus, in addressing the issue of causation, many courts will require the plaintiff to establish that levels of the substance comparable to those received by the plaintiff can cause the type of injury alleged. For example, the court in Mancuso v. Consolidated Edison Co. of New York, Inc.⁶⁴ stated:

Numerous courts have followed this method. It requires first that the expert determine the dosage of the toxin at issue to which the plaintiff was exposed …. Second, the expert must establish "general causation" by demonstrating that, according to scientific literature, levels of the toxin comparable to those received by the plaintiff can cause the specific types of injuries he alleges …. Third, the expert must establish specific causation, by demonstrating that, more likely than not, the toxin caused the plaintiff's injuries in this particular case.⁶⁵

[28 ELR 10299]

Thus, the issue of general causation may require a more particularized, fact-specific inquiry than is appropriate for summary adjudication early in the proceedings.

In order to establish causation, whether general or specific, a plaintiff must rely on expert testimony. Experts base their conclusions that a particular substance may be harmful on several methodologies: (1) epidemiologic studies; (2) case studies; (3) animal studies (both in vivo and in vitro); and (4) pharmacological studies. Each of these methodologies may play a pivotal role in the admission or exclusion of scientific evidence under Daubert.

Epidemiology

Epidemiology is a science devoted to determining the causes of diseases in human beings. "Epidemiologists compare control groups of unexposed individuals to groups of individuals exposed to a hypothetical cause of the disease being studied to determine whether exposed individuals have a greater risk of manifesting that disease."⁶⁶ Epidemiology is by its very nature a scientific endeavor. As one court has pointed out, "useful hypotheses are framed, tested, refined, and used in identifying relations between one event, such as the exposure to carcinogenic substance … and a subsequent event, such as the development of disease …."⁶⁷ Epidemiology focuses on the question of general causation rather than the issue of specific causation.⁶⁸

There are several types of epidemiologic studies. A "cohort study" involves comparisons of populations that have been exposed to a suspected agent with populations that have not. The two groups are then observed over a period of time, and the incidences of new cases of disease are calculated and compared.⁶⁹ Another type of study, called the "case control study," compares exposure histories of individuals with a particular disease with the exposure histories of individuals who do not have the disease.⁷⁰ Based on the results of an epidemiologic study, an epidemiologist will come up with a "relative risk ratio." The relative risk ratio compares the incidence of disease occurrence in exposed individuals to the incidence of disease occurrence in unexposed individuals. It is computed by simply dividing those two numbers. A relevant risk of 1.00 indicates that the disease occurs among the exposed population with the same frequency as it occurs among the unexposed population. A relative risk of 2.00 means that the disease occurs among the exposed population with twice the frequency as it occurs among the unexposed population. Epidemiologists take this to mean that there is a 50 percent chance that a particular case of the disease was associated with the exposure and a 50 percent chance that the disease was not associated with the exposure.⁷¹

Epidemiologic studies are considered to be the most helpful and relevant evidence in determining the toxicity of a substance to humans. Indeed, many courts have concluded that they are all but indispensable to proving causation in a toxic tort case. For example, in In re Agent Orange Product Liability Litigation,⁷² Judge Weinstein stated that "in a mass tort case such as Agent Orange, epidemiologic studies on causation assume a role of critical importance."⁷³ Thus, the court found that the plaintiffs' evidence purporting to establish that Agent Orange caused their injuries was insufficient as a matter of law because plaintiffs were unable to come forward with admissible epidemiologic evidence to establish the requisite causal connection.⁷⁴

Epidemiologic studies have proven to be most relevant in assessing the second prong of the Daubert analysis: the "fit" requirement. After the Supreme Court remanded Daubert, the Ninth Circuit observed that California tort law required a plaintiff to show not merely that a substance increased a likelihood of injury, but more likely than not caused her injuries. Seizing on this rule, the Court in Daubert II held:

In terms of statistical proof, this means that plaintiffs must establish not just that their mothers' ingestion of Bendectin increased somewhat the likelihood of birth defects, but that it more than doubled it — only then can it be said that Bendectin is more likely than not the source of their injury. Because the background rate of limb reduction defects is one per thousand births, plaintiffs must show that among children of mothers who took Bendectin the incidence of such defects was more than two per thousand.⁷⁵

In terms of epidemiologic proof, this meant that: "For an epidemiological study to show causation under a preponderance standard, 'the relative risk of limb reduction defects arising from the epidemiological data … will, at a minimum, have to exceed 2.'"⁷⁶

The court in Daubert II did, however, concede that a relative risk of greater than 2.0 is not a sine qua non of causation. A statistical study showing a relative risk of less than 2.0 could be combined with other epidemiologic and clinical data to show that it is more likely than not that the substance at issue is responsible for the particular plaintiff's injury.⁷⁷

[28 ELR 10300]

Case Studies Are Not an Acceptable Substitute for Epidemiologic Studies

Often, where full-blown epidemiologic studies are not available to establish an association between a particular agent and a disease, experts will attempt to use case studies to demonstrate such a link. Case studies simply describe reported phenomena in a group of patients without a comparison to the rate at which the phenomena occur in the general population.⁷⁸ In Casey v. Ohio Medical Products,⁷⁹ the plaintiff attempted to establish that her husband's exposure to halothane during his work as an anesthesiologist caused him to contract hepatitis. In order to establish causation, she proffered the testimony of an expert to establish a link between halothane and hepatitis based on a compilation of case reports. The court held that this testimony did not satisfy the requirements of Daubert:

Such case reports are not reliable scientific evidence of causation, because they simply describe[] reported phenomena without comparison to the rate at which the phenomena occur in the general population or in a defined control group; do not isolate and exclude potentially alternative causes; and do not investigate or explain the mechanism of causation.⁸⁰

Guidance Provided by the Reference Manual on Scientific Evidence

Daubert greatly expanded the responsibilities of the trial judge in determining whether expert scientific evidence is admissible at trial. With this new role as a gate-keeper, the judge can no longer defer to the judgment of the relevant scientific community. Rather, the judge is charged with the task of making an independent assessment of the scientific validity of the proffered evidence. In order to assist judges in making this determination, the Federal Judicial Center published the Reference Manual on Scientific Evidence (Reference Manual). The Reference Manual is designed to help judges understand the methods and reasoning of selected areas of scientific evidence and suggests a series of questions that will enable them to identify issues that are likely to be disputed at trial.

One portion of the Reference Manual deals with epidemiology. The "Reference Guide on Epidemiology" provides a detailed analysis of the questions and issues that the court must explore when presented with epidemiologic evidence. The next section of this Article identifies the main subissues raised by epidemiologic evidence and outlines the considerations relevant to each.

[] Sub-Issue One: Were the Research Methods Trustworthy? The first consideration to be addressed in assessing the reliability of an epidemiologic study is whether the research design was appropriate for answering the research question. The research question should be clearly outlined before data compilation begins, and the research method chosen should be constructed so as to minimize the potential for bias.⁸¹

Next, one should consider whether the study populations were well defined and samples adequately selected so as to allow for meaningful comparisons between study groups or between time periods. One important factor in this regard is whether the sample size was adequate to draw a valid conclusion.⁸² A second factor is whether the researcher was able to minimize the risk of selection bias. Three questions should be asked in assessing the risk of bias: (1) How were the cases and controls (in a case control study) or exposed and unexposed subjects (in a cohort study) identified and selected? (2) What percentage of those selected for the study agreed to participate? and (3) What proportion of the subjects dropped out of the study before it was completed?⁸³

A third consideration is whether exposure to the putative agent was measured using a standardized and reliable methodology. Four questions are relevant in this regard: (1) Were data collected from objective and reliable sources? (2) What types of procedures were instituted to control the quality of measurements of exposure? (3) Was information obtained from one group of the study population more accurate or complete than that obtained from the comparison group? and (4) Did the method of collecting data yield reliable information?⁸⁴

A fourth and final consideration is whether the health effects (i.e., disease or disability) were clearly defined and reliably measured. Precise definition of the health effects ensures that the same variable is being measured throughout the study.⁸⁵

[] Sub-Issue Two: Is Exposure to the Agent Associated With Disease? There are four considerations that are relevant to an inquiry into whether exposure is associated with disease: (1) What is the basis for concluding that the exposure is associated with an increased risk of disease? (2) What categories of error might have produced a false result? (3) What statistical methods exist to evaluate the likelihood that the result of an epidemiologic study was due to random sampling error? and (4) What biases may have existed that would result in an erroneous association?⁸⁶

[] Sub-Issue Three: If the Agent Is Associated With Disease, Is It a Causal Relationship? In making a determination as to whether a causal association exists between exposure and the onset of disease, there are three relevant considerations. First, one should consider whether a confounding factor could be responsible for the study result. Two questions should be asked in assessing the risks associated with confounding factors: (1) What techniques, if any, were used to identify confounding factors? and (2) What techniques, if any, were used to control confounding factors?⁸⁷

[28 ELR 10301]

The second consideration is whether application of the guidelines for causation supports a finding of causation.⁸⁸ The following seven factors should be considered by an epidemiologist in determining whether there is a causal relationship between exposure and disease: (1) How strong is the association between the exposure and disease? (2) Is there a temporal relationship? (3) Is the association consistent with other research? (4) Is the association biologically plausible (i.e., consistent with other knowledge)? (5) Have alternative explanations been ruled out? (6) Does the association exhibit specificity? and (7) Is there a dose-response relationship?⁸⁹

The third and final consideration is the type of causal association that has been demonstrated between exposure and disease. Is, for example, exposure to an agent necessary and sufficient to bring about the disease, sufficient but not necessary, or necessary but not sufficient?⁹⁰

Animal Studies

Scientists often use animal studies, also known as toxicological studies, to assess whether a particular substance is harmful to humans, and if so, in what amount. There are several types of animal studies. In a lethal dose 50 study ("LD50"), animal subjects are administered various doses of a suspected toxic substance in order to determine the dose at which half of the population will die. Since every substance, even water, is toxic at some dose, an LD50 study is most useful as an indicator of substances that deserve further study and as a method of identifying which organ systems are affected by the administration of the toxic dose.⁹¹

Subchronic, or short term, toxicity testing is used to determine the level at which some adverse affects, other than death, occur in test subjects so that a safe exposure level can be determined. Using this process, the scientists determine the highest dosage level at which no adverse effects occur in the animal study population. This is called the "no observed effect level" (NOEL). This process is repeated using different animal species, and the lowest NOEL is multiplied by a safety factor to determine a safe level for humans.⁹²

The most common form of toxicity study, the chronic or long-term toxicity study, is generally employed to determine the carcinogenic potential of a given substance. Using this methodology, very high but nonlethal doses of a suspected agent are administered to animal study groups for a prolonged period. After the animals die, they are studied to determine the incidence of tumor onset at the high-dose levels. Toxicologists then extrapolate a predicted incidence of cancer at more realistic and lower doses. Once the low-dose extrapolation has been completed, the toxicologist will translate the results of the animal experiments into an expression of human risk by using an extrapolation that is based on conversion factors, which are based on the body weight or surface area of the animals and humans.⁹³

Animal Studies Have Limited Value in Proving Causation

Courts have generally recognized the limited value animal studies have in proving causation in toxic tort cases. For example, in the extremely influential and often cited Agent Orange case, Judge Weinstein states: "The animal studies are not helpful in the instant case because they involve different biological species. They are of so little probative force and are so potentially misleading as to be inadmissible."⁹⁴

The problem that most courts have with animal studies is that in order to be probative of causation in a toxic tort case, the animal study must make two analytical connections. First, because animal studies are generally conducted using extremely high doses, the expert must extrapolate from the higher dose to a lower dose. Courts tend to be critical of the methodology used by toxicologists to make this extrapolation. For example, in the context of birth defects, the Wade-Greaux court noted that the field of teratology recognizes a principle known as Karnofsky's law, also known as "sledgehammer teratology." This principle recognizes that at some dosage level virtually all substances can cause malformations. Thus, the court found that the expert opinion based on a study showing the teratogenic effects of high doses of the substance in question in rabbits was non-probative of whether the substance could cause malformations at the lower dose to which the plaintiff was exposed, and ruled that the proffered testimony was inadmissible.⁹⁵

As a second connection, the expert must extrapolate from animals to humans. Courts have also looked at such extrapolations with a skeptical eye. For example, the court in Paoli noted that "animal studies may be methodologically acceptable to show that chemical X increases a risk of cancer in animals, but they may not be methodologically [28 ELR 10302] acceptable to show that chemical X increases the risk of cancer in humans."⁹⁶

Guidance Provided by the Reference Manual on Scientific Evidence

In order to assist judges in assessing causation based on animal studies, the "Reference Guide on Toxicology" divides the question into three sub-issues and identifies considerations that are relevant to each of them. These sub-issues and their corresponding considerations are discussed below, as well as case law, where available, that is relevant to each of the considerations.

[] Sub-Issue One: Demonstrating an Association Between Exposure and the Risk of Disease. In addressing this sub-issue, the "Reference Guide" identifies five considerations that are relevant.

(1) On which species of animals was the substance tested, and what is known about the biological similarities and differences between the tested animals and humans? The difference between the biological makeup of animals and humans may affect the ability to extrapolate from the animal data in assessing the risk to humans. Therefore, the expert needs to review similarities and differences in absorption, distribution, metabolism, and excretion in the animal species in which the substance was tested and in humans.⁹⁷ Thus, the Wade-Greaux court noted that mammalian studies are accorded more weight than nonmammalian studies, and primate studies are given greater weight than nonprimate studies.⁹⁸

This consideration can be especially important because there are vast differences in susceptibility to toxic substances between species. For example, arsenic has been known to cause cancer in humans but has not been demonstrated to be an animal carcinogen. Similarly, aflatoxin has been shown to be extremely harmful to rats and perhaps humans, but not to mice.⁹⁹ In Allen v. Pennsylvania Engineering Corp.,¹⁰⁰ the court examined this very type of inconsistency. In that case, the plaintiff tried to establish that ethylene oxide (ETO) had caused his brain cancer. His experts relied on two studies that found brain tumors in rats exposed to inhaled ETO. The court found, however, that:

Although in these particular studies, F-344 rats contracted brain cancer after being exposed to [ETO], Allen's experts concede that the same effect did not occur in mice studies …. Thus, the lack of capacity for the F-344 rat to predict how even the mouse model responds necessarily undercuts confidence that the rat will predict accurately how other species including humans will respond [to ]ETO[ exposure].¹⁰¹

(2) Does the research show that the substance affects a specific target organ, and will humans be affected similarly? Due to the manner in which the body absorbs, distributes, and metabolizes a chemical, certain organs may be affected by the chemical but not others.¹⁰² Thus, if a plaintiff seeks to establish that his exposure to an agent caused a disease in a particular organ, say, the liver, itwould be extremely relevant if the available animal studies indicate that the substance has only been shown to affect a different target organ, say, the lungs. For example, in Schmaltz v. Norfolk & Western Railroad Co.,¹⁰³ the plaintiff claimed that his exposure to certain herbicides containing atrazene caused his chronic respiratory disease. In order to establish causation, his expert relied on studies where high doses of atrazene caused eye irritation in rabbits. In excluding the expert's testimony under Daubert, the court observed that the record "fails to make clear why the incidence of eye irritation in rabbits exposed to high doses of atrazene could reasonably lead a doctor to conclude that indirect exposure to atrazene causes pulmonary or respiratory conditions in humans."¹⁰⁴

(3) Has the substance been the subject of in vitro research, and if so, can the findings be related to what occurs in vivo? Test tube research on specific organs and cells can be helpful in determining exactly how a toxic substance reacts with the body.¹⁰⁵ However, courts are skeptical as to whether in vitro research standing alone can be sufficient to establish causation. For example, the court in Wade-Greaux noted that the route of administration of a substance is often different in experimental animal studies from the route employed by humans. Thus, humans, on the one hand, will ingest and breathe an agent, thereby subjecting it to the body's processing and metabolism. In vitro tests, on the other hand, involve dripping the agent directly onto the cells or organs involved in the study. Thus, the agent is never subjected to the metabolism of the body, nor is it ever expelled.¹⁰⁶ This raises a serious question with respect to the application of in vitro research to the issue of human causation.

(4) What is known about the chemical structure of the compound and its relationship to toxicity? Structural activity relationships are employed to compare the chemical structure of compounds with known toxicity to chemical structures of compounds with unknown toxicity. Toxicity is then estimated based on molecular similarities between the two compounds. This is known as pharmacology.¹⁰⁷ This method, however, can lead to conflicting results. For example, in National Bank of Commerce, the court was presented with expert testimony that attempted to show that certain pesticides can cause birth defects based on structural comparisons with other organophosphates. The court found that while some organophosphates proved to be teratogenic, other similar organophosphates proved to be non-teratogenic. [28 ELR 10303] Thus, "once one knows that different organophosphates have teratogenic and non-teratogenic effects, their similar chemical structures can no longer be used to postulate with any degree of certainty either a teratogenic or non-teratogenic effect."¹⁰⁸

Additionally, Daubert would require that there be a scientifically valid basis for making such a comparison. For example, in Schudel, one basis for the plaintiffs' conclusion that TCA and Perc caused toxic encephalopathy was an extrapolation from studies that involved organic solvents other than TCA or Perc. The court found that the expert "did not establish it was scientifically acceptable to draw general conclusions about the neurotoxicity of TCA and Perc from studies of other chemicals; indeed, the testimony indicated small differences in molecular structure often have significant consequences."¹⁰⁹

(5) Is the association between exposure and disease biologically plausible? As the Reference Manual points out, "it is difficult to accept an association between a compound and a health effect where no mechanism can be ascribed by which the chemical exposure leads to the putative effect."¹¹⁰ This consideration has been important in cases considering the plausibility of the diagnosis of multiple chemical sensitivities, where the expert witnesses have been unable to identify the mechanisms by which the acute exposure to certain chemicals purportedly led to a sensitization of the body toward other chemicals.¹¹¹

[] Sub-Issue Two: Specific Causal Association Between an Individual's Exposure and the Onset of Disease. The second sub-issue in the overarching question of causation is the demonstration of a specific causal association between an individual's exposure and the onset of disease. The Reference Manual outlines six considerations that are relevant to this inquiry.

(1) Was the plaintiff exposed to the substance, and if so, did the exposure occur in a manner that can result in absorption into the body? Evidence of exposure is essential in determining the harmful effects of a toxic substance. Exposure can be measured directly by measuring the medium in question (i.e., the air, water, or soil); indirectly by using mathe-matical models to estimate the transport of the pollutant from the source to the receptor; or biologically through monitoring the amount of the substance in the blood or urine. Based on this information, the toxicologist will determine if the individual was exposed to the substance in a manner than can result in absorption into the body. Absorption is a function of the compound's physiochemical properties, its concentration, and the presence of other agents or conditions that assist or interfere with its uptake.¹¹²

(2) Were other factors present that can affect the distribution of the compound within the body? This consideration deals with the rate of distribution of the substance throughout the body by the bloodstream once the substance is absorbed into the body through the skin, lungs, or gastrointestinal tract.¹¹³ The toxicity of a substance, for example, is affected by the route by which it enters the body, the rate of blood flow to various organs and tissues, the solubility of the tissue, lymphatic supplies to the organ, and the individual's metabolism.¹¹⁴

(3) What is known about how the metabolism in the human body alters a toxic effect of the compound? Some substances are considered direct-acting agents, which means that they cause toxicity without any metabolic conversion in the body. Others are known as indirect-acting agents, which means that they require metabolic activation before they can produce adverse effects. Conversely, substances that are initially harmful may be broken down by the body into nonharmful agents. The toxicologist must explain how these mechanisms alter the effect an alleged toxic substance has on the body.¹¹⁵

(4) What excretory route does the compound take, and how does this affect its toxicity? Toxic substances do not remain in the body indefinitely. For example, many inhaled toxic substances may be immediately expelled through exhalation. The toxicologist should show how these excretory functions affect the way a substance reacts with the body.¹¹⁶

(5) Does the relationship between exposure and the onset of disease support a contradictory causation? For most acute injuries there is a short time period between the harm-causing event and its effect on the body. In some situations, however, biological processes require a longer period of time between the initial exposure and the onset of observable disease. For example, certain types of leukemia require one to two years from initial exposure to a harmful substance to the manifestation of a clinically recognizable case of leukemia. A tort claim alleging a shorter time period between cause and effect would be scientifically untenable.¹¹⁷

(6) If exposure to the substance is associated with a disease, is there a NOEL? And if so, was the individual exposed above the NOEL? The NOEL is the level of exposure below which a substance does not produce any observable toxic effect. The NOEL for humans is extrapolated from the animal NOEL using a conversion factor to ensure human safety.¹¹⁸ Assuming that an individual was exposed to a chemical, if the level of exposure was below the NOEL, a relationship between the exposure and the disease cannot be established.¹¹⁹

[] Sub-Issue Three: Medical History. The third and final sub-issue to be considered in assessing causation revolves around the medical history of the individual plaintiff. The Reference Manual lists seven considerations to be addressed when looking at the plaintiff's medical history.

(1) Is the medical history of the individual consistent with the toxicologist's expert opinion concerning injury? The patient's medical history is one of the most basic and useful [28 ELR 10304] tools in diagnosis and treatment of disease. A patient's medical history should include: (a) past and present occupational and environmental exposure to toxic agents; (b) life-style characteristics, such as use of nicotine or alcohol; (c) family medical history; and (d) personal medical history.¹²⁰

(2) Are the complaints specific or nonspecific? A myriad of nonspecific symptoms that can result from acute exposure to many toxic agents — including headache, nausea, lightheadedness, and fatigue — can also result from many other causes. These symptoms are almost impossible to quantify or document beyond a patient's report. Often these symptoms can be attributed mistakenly to an exposure to a toxic agent or conversely discounted as unimportant when, in fact, they reflect a significant exposure. Thus, a careful medical history should focus on the time pattern of symptoms in relation to any exposure, and on the constellation of symptoms, to determine causation.¹²¹

(3) Do laboratory tests indicate exposure to the compound? Routine or specialized tests, such as blood or urine tests, may be used to determine whether there is a presence of the chemical or physical agent in the patient's body.¹²²

(4) What other causes could lead to the given complaint? A careful medical history should examine the possibility of competing causes or confounding factors for any disease. This would lead the physician to a differential diagnosis.¹²³ A differential diagnosis may be especially important in a toxic tort case where the goal of the court is to determine whether the substance more likely than not caused the injuries of the plaintiff. As one court pointed out:

The process of differential diagnosis is undoubtedly important to the question of "specific causation." If other possible causes of an injury cannot be ruled out, or at least the probability of their contribution to causation minimized, then the "more likely than not" threshold for proving causation may not be met.¹²⁴

(5) Is there evidence of interaction with other chemicals? Simultaneous exposure to different substances may alter how the body responds to agents. The effect may be additive (the sum of the effects of the individual agents), synergistic (the effect of the multiple agents is greater that the sum of their individual effects), antagonistic (one agent causes a decrease in the effect of another agent), or potentiative (an agent by itself produces no effect, but causes an enhancement of the effect of another agent).¹²⁵

(6) Do humans differ in the extent of susceptibility to the particular compound in question, and are these differences relevant to the case at issue? Individual differences such as lifestyles affect how a substance reacts with the body. For example, a person who exercises will inhale more than a sedentary person, thus exposing him or her more to airborne toxins. Additionally, a person's age, sex, and genetic makeup will affect how the body processes a compound.¹²⁶

(7) Has the expert considered data that contradict his or her opinion? Often, animal studies, pharmacological research, in vitro tissue studies, and epidemiologic studies will offer differing conclusions regarding the toxicity of a substance. Where different research studies reach different conclusions regarding toxicity, the expert must be asked to explain how those results have been taken into account in the formulation of his or her opinion.¹²⁷ This is especially true where the toxicologist seeks to offer an opinion based upon animal research that is refuted by the available epidemiologic data.¹²⁸

How Daubert Applies to the Field of Clinical Ecology

Clinical ecology is a relatively new and controversial field of medicine. According to the Reference Manual on Scientific Evidence, "clinical ecologists claim that various kinds of environmental insults may depress a person's immune system so that the exposed person develops a multiple chemical sensitivity; that is, becomes hypersensitive to other chemicals and naturally occurring substances."¹²⁹ A common diagnosis reached by clinical ecologists is that of multiple chemical sensitivity (MCS). According to the American College of Occupational and Environmental Medicine, MCS is characterized by the following elements: (1) an initial identifiable environmental exposure resulting in an onset of symptoms; (2) symptoms occurring among multiple organ systems (e.g., nervous and respiratory systems); (3) symptoms recurring and abating in response to exposures to very low levels of diverse chemicals; and (4) symptoms that cannot be accounted for by other medical conditions.¹³⁰

Courts that have been faced with the question have held without exception that evidence regarding MCS does not withstand scrutiny under Daubert.¹³¹ The most important basis for holding that testimony regarding MCS is inadmissible is the fact that the existence of the disease has not been properly tested. For example, in Bradley v. Brown,¹³² the district court examined the plaintiffs' proffered evidence regarding MCS and held that "even relying wholly upon plaintiffs' own exhibits, plaintiffs fail to establish that the etiology of MCS, accepting arguendo that such a clinical entity exists, is known or tested at this point."¹³³ The court noted that the plaintiffs' own experts stated that MCS was at the early stage of scientific scrutiny. Thus, plaintiffs' own evidence established that the "'science' … of MCS's etiology has not progressed from the plausible; that is, the hypothetical, [28 ELR 10305] to knowledge capable of assisting a fact-finder, jury or judge."¹³⁴

In another case, Summers v. Missouri Pacific Railroad System,¹³⁵ the district court likewise held that the existence of MCS was too untested and hypothetical to pass muster under Daubert. For example, the court examined the transcript of one of the plaintiffs' experts in reaching this conclusion:

Q: Well, how are these unknown substances acting on Mr. Potts body to produce these symptoms at this present day?

A: Well, as I said, the mechanisms of the sensitivity are unknown. We know that the substances do cause changes in cellular function, but exactly how all that occurs is unknown at this point.

Q: Okay. What changes in cellular — are you saying that it is because of a change in cellular function that Mr. Potts has mental confusion, dizziness, or lack of concentration?

A: That is one of the theories, yes, on how that works.

Q: Okay. And that is a theory; is that not correct?

A: Yes.

Q: You haven't demonstrated specifically with respect to Mr. Potts that — that a cellular function is responsible for mental confusion, dizziness, or lack of concentration, have you?

A: Not to that correlation.¹³⁶

Thus, the court held that the theory behind MCS had not been properly tested and verified as required by Daubert.

Likewise, courts have found that a diagnosis of MCS is not generally accepted in the medical community. For example, the court in Summers noted that those medical societies that have issued informational reports and position papers on clinical ecology have reported that:

No scientific evidence supports the contention that MCS is a significant cause of disease or that the diagnostic tests or treatments used have any therapeutic value. Until such accurate, reproducible, and well-controlled studies are available, the American Medical Association Council on Scientific Affairs believes that multiple chemical sensitivity should not be considered a recognized clinical syndrome.¹³⁷

The field of clinical ecology has also been examined using the Frye "general acceptance" test. Not surprisingly, the less tolerant approach taken under that test also leads to the exclusion of such evidence. In Sterling v. Velsicol Chemical Corp.,¹³⁸ neighbors of a landfill successfully sued the owner of the landfill for damages allegedly caused by hazardous chemicals that leaked into their water supply. Among the damages awarded to the plaintiffs were those attributable to the impairment of their immune systems. On appeal, Velsicol argued that it was error to admit expert testimony that purported to show that Velsicol's chemicals harmed the plaintiffs' immune systems, because the principles on which the testimony was based were not "in conformity to a generally accepted explanatory theory."¹³⁹ The Court of Appeals agreed, finding that "the leading professional societies in the specialty of allergy and immunology, the American Academy of Allergy and Immunology (AAAI) and the California Medical Association (CMA), have rejected clinical ecology as an unproven methodology lacking any scientific basis in either fact or theory."¹⁴⁰ Additionally, the court noted in reaching its conclusions that the plaintiffs' experts neither personally examined nor interviewed the plaintiffs, nor did they perform the requisite medical tests. Rather, they based their opinions on blood tests and medical histories provided by plaintiffs' attorneys. Thus, the court held that this evidence should have been excluded under Frye.¹⁴¹

Conclusion

In a toxic tort case, millions of dollars can be won or lost depending on the opinions offered by expert witnesses. Thus, it is no surprise that expert witness referral bureaus have emerged that promise: "If the first doctor we refer doesn't agree with your legal theory, we will provide you with the name of a second."¹⁴² In the wake of Daubert, it is the responsibility of the trial judge to close the courthouse door to those so-called experts who would do little more than offer their unsupported, yet well paid for, speculation that exposure to the defendant's chemicals caused an injury to a plaintiff. As the litany of toxic tort cases decided since Daubert demonstrates, the American judicial system has proven itself quite capable of assessing the validity of expert testimony, and separating the scientific wheat from the charlatan chaff.

1. 293 F. 1013 (D.C. Cir. 1923).

2. 509 U.S. 579, 23 ELR 20979 (1993).

3. 293 F. 1013 (D.C. Cir. 1923).

4. Id. at 1014 (emphasis added).

5. See, e.g., Reed v. State, 391 A.2d 364, 368 (Md. 1978) (stating that the Frye test "has come to be the standard in almost all of the courts in the country which have considered the question of the admissibility of scientific evidence.") quoted in Developments in the Law: Confronting the New Challenges of Scientific Evidence, 108 HARV. L. REV. 1481, 1486 n.22 (1995).

6. FED. R. EVID. 702.

7. Developments in the Law, supra note 5, at 1486.

8. See, e.g., Viterbo v. Dow Chem. Co., 826 F.2d 420 (5th Cir. 1987).

9. See, e.g., United States v. Smith, 869 F.2d 348 (7th Cir. 1989).

10. 509 U.S. 579, 23 ELR 20979 (1993).

11. Daubert v. Merrell Dow Pharm., Inc., 727 F. Supp. 570, 575 (S.D. Cal. 1989), aff'd, 951 F.2d 1128 (9th Cir. 1991), vacated, 509 U.S. 579, 23 ELR 20979 (1993).

12. Daubert, 951 F.2d at 1128, vacated, 509 U.S. at 579, 23 ELR at 20979.

13. Id., 509 U.S. at 589, 23 ELR at 20981 (internal footnote omitted).

14. See, e.g., People v. Leahy, 882 P.2d 321, 329 (Cal. 1994) ("Amicus curiae … asserts that [the Frye test] emphasizes 'nose counting' of the scientific community ….").

15. Daubert, 509 U.S. at 597, 23 ELR at 20983.

16. Id. at 600, 23 ELR at 20984 (Rehnquist J., concurring in part and dissenting in part).

17. Id. at 592, 23 ELR at 20982 (internal footnote omitted).

18. Id. at 593, 23 ELR at 20982 (internal quotation omitted).

19. 791 F. Supp. 1042 (D.N.J. 1992).

20. Id. at 1056.

21. Daubert, 509 U.S. at 593, 23 ELR at 20982.

22. Id. at 594, 23 ELR at 20982 (internal quotation omitted).

23. See infra notes 121-32 and accompanying text.

24. Daubert v. Merrell Dow Pharm., Inc., 43 F.3d 1311, 1317, 25 ELR 20856, 20858 (9th Cir. 1995) ("Daubert II").

25. Id.

26. Id; see also National Bank of Commerce v. Dow Chem. Co., 965 F. Supp. 1490, 1516 (E.D. Ark. 1996) (discrediting the testimony of an expert who came off as an advocate because her research was in anticipation of litigation and she had served as a litigation consultant in some 8,000 cases).

27. Daubert II, 43 F.3d at 1317, 25 ELR at 20859.

28. Daubert v. Merrell Dow Pharm., Inc., 509 U.S. 579, 591, 23 ELR 20979, 20981 (1993) (internal quotation omitted).

29. Id. at 591, 23 ELR at 20982.

30. Daubert II, 43 F.3d at 1315, 25 ELR at 20857.

31. See National Bank of Commerce, 965 F. Supp. at 1496.

32. Compare In re Paoli R.R. Yard PCB Litig., 35 F.3d 717, 743, 25 ELR 20989, 20997 (3d Cir. 1994) (holding that the expert's extrapolation from animal studies to humans was inadmissible because it did not meet the fit requirement), with Joiner v. General Elec. Co., 864 F. Supp. 1310, 1323 (N.D. Ga. 1994), rev'd, 78 F.3d 524 (11th Cir. 1996), rev'd, 118 S. Ct. 512, 28 ELR 20227 (1997) (holding that the expert's opinion based in part on extrapolation from mice studies was inadmissible as there was no reliable basis for such an analytical leap).

33. See infra notes 91-125 and accompanying text.

34. 35 F.3d 717, 25 ELR 20989 (3d Cir. 1994).

35. Id. at 745, 25 ELR at 20998 (emphasis in original).

36. 120 F.3d 991, 27 ELR 21506 (9th Cir. 1997).

37. Id. at 997, 27 ELR at 21508.

38. Id; see also Allen v. Pennsylvania Eng'g Corp., 102 F.3d 194 (5th Cir. 1996) (holding that evidence linking a substance to lymphatic cancer was not probative of whether the substance caused brain cancer).

39. Daubert v. Merrell Dow Pharm., 509 U.S. 579, 594-95, 23 ELR 20979, 20982 (1993) (internal footnote omitted).

40. In re Paoli R.R. Yard PCB Litig., 35 F.3d 717, 746, 25 ELR 20989, 20998 (3d Cir. 1994) (internal citation omitted).

41. David E. Bernstein, The Admissibility of Scientific Evidence After Daubert v. Merrell Dow Pharmaceuticals, Inc., 15 CARDOZO L. REV. 2139, 2165-66 (1994).

42. 89 F.3d 594 (9th Cir. 1996).

43. Id. at 598.

44. 118 S. Ct. 512, 28 ELR 20227 (1997).

45. Id. at 518, 28 ELR at 20228.

46. Id. at 518-19, 28 ELR at 20229.

47. Id. at 519, 28 ELR 20229.

48. 99 U.S. 645 (1879).

49. Id. at 658 (quoted in General Elec. Co. v. Joiner, 118 S. Ct. at 517, 28 ELR at 20228).

50. See, e.g., People v. Leahy, 882 P.2d 321, 325 (1994) (noting that one of the advantages of the "general acceptance" test was "promoting uniformity of decision based on finding a consensus in the scientific community.")

51. See, e.g., Reed v. State, 391 A.2d 364, 367 (Md. 1978) ("The answer to the question about the reliability of a scientific technique or process does not vary according to the circumstances of each case. It is therefore inappropriate to view this threshold question of reliability as a matter within each trial judge's individual discretion.").

52. See, e.g., Bradley v. Brown, 42 F.3d 434, 436-37 (7th Cir. 1994) (applying an abuse of discretion standard to the district court's decision to exclude expert testimony under Daubert); Claar v. Burlington N. R.R., 29 F.3d 499, 500-01 (9th Cir. 1994) (same).

53. In re Paoli R.R. Yard PCB Litig., 35 F.3d 717, 743, 25 ELR 20989, 20100 (3d Cir. 1994).

54. Id. at 749-50, 25 ELR at 21001.

55. 78 F.3d 524, 26 ELR 20939 (11th Cir. 1996), rev'd, 118 S. Ct. 512 (1997).

56. Id. at 529, 26 ELR at 20940.

57. Even the plaintiff conceded that abuse of discretion was the proper standard of review, arguing insteadthat the appellate court had properly applied this standard. General Electric Co. v. Joiner, 118 S. Ct. 512, 517, 28 ELR 20227, 20228 (1997).

58. Id.

59. Id.

60. Id.

61. See Casey v. Ortho Medical Prods., 877 F. Supp. 1380, 1382 (N.D. Cal. 1995); Wade-Greaux v. White Hall Labs., Inc., 874 F. Supp. 1441, 1448 (D.V.I. 1994).

62. FED. R. CIV. P. 23(a).

63. Bernard D. Goldstein & Mary Sue Henifin, Reference Guide on Toxicology, in REFERENCE MANUAL ON SCIENTIFIC EVIDENCE 185 (Federal Judicial Center 1994).

64. 967 F. Supp. 1437 (S.D.N.Y. 1997).

65. Id. at 1445-46; see also Wright v. Willamette Indus. Inc., 91 F.3d 1105, 1107-08 (8th Cir. 1996) (stating that dose is necessary to address the issue of general causation); Cavallo v. Star Enter., 892 F. Supp. 756, 764 (E.D. Va. 1995)

First an evaluation is made of the chemicals to which the individual might have been exposed, and of the concentrations of these chemicals in air breathed by the individual …. The second step involves an evaluation, based on the published scientific literature, of the exposures necessary to produce the adverse effects associated with the chemicals to which the individual may be exposed.

aff'd in part, rev'd in part on other grounds, 100 F.3d 1150 (4th Cir. 1996), cert. denied, 1998 WL 6290 (U.S. Jan. 12, 1998); Chikovsky v. Ortho Pharm. Corp., 832 F. Supp. 341, 345 (S.D. Fla. 1993) (concluding that since "the dose of a particular substance is relevant in determining whether it acts as a teratogen," plaintiffs' expert could not opine as to causation without the requisite information regarding dose).

66. Hall v. Baxter Healthcare Corp., 947 F. Supp. 1387, 1403 (D. Or. 1996).

67. In re Joint Eastern & Southern Dist. Asbestos Litig., 827 F. Supp. 1014, 1027 (S.D.N.Y. 1993), rev'd on other grounds, 52 F.3d 1124, 25 ELR 20828 (2d Cir. 1995).

68. Linda Bailey et al., Reference Guide on Epidemiology, in REFERENCE MANUAL ON SCIENTIFIC EVIDENCE 126 (Federal Judicial Center 1994).

69. Id. at 134-36; see also J.K. McLaughlin & R. Brookmeyer, Epidemiology and Biostatistics, in A PRACTICAL APPROACH TO OCCUPATIONAL AND ENVIRONMENTAL MEDICINE 347-48 (Robert J. McCunney ed., 1994).

70. Bailey et al., supra note 68, at 136-38; see also McLaughlin & Brookmeyer, supra note 69, at 348-49.

71. See Wade-Greaux v. White Hall Labs., Inc., 874 F. Supp. 1441, 1452 (D.V.I. 1994); In re Joint Eastern & Southern Dist. Asbestos Litig., 52 F.3d 1124, 1128, 25 ELR 20828, 20830 (2d Cir. 1995).

72. 611 F. Supp. 1223 (E.D.N.Y. 1985).

73. Id. at 1239.

74. See also Asbestos Litig., 52 F.3d at 1128, 25 ELR 20829 ("Epidemiological evidence is indispensable in toxic and carcinogenic tort actions where direct proof of causation is lacking."); Brock v. Merrell Dow Pharm., Inc., 874 F.2d 307 (5th Cir. 1989) (deciding the case on sufficiency of evidence reasons, the court concluded that a Bendectin plaintiff must proffer a statistically significant epidemiologic study before satisfying her burden on proof of causation); Lynch v. Merrell-National Labs., 830 F.2d 1190, 1194 (1st Cir. 1987) (holding that nonepidemiologic studies used singly or in combination do not have the capability of proving causation in human beings in the absence of any confirmatory epidemiologic data).

75. Daubert v. Merrell Dow Pharm., Inc., 43 F.3d 1311, 1320, 25 ELR 20856, 20860 (9th Cir. 1995).

76. Id. at 1321, 25 ELR at 20860 (quoting DeLuca ex rel. DeLuca v. Merrell Dow Pharm., Inc., 911 F.2d 941, 958 (3d Cir. 1990)).

77. Id. at 1321 n.16, 25 ELR at 20861 n. 16.

78. See Casey v. Ohio Med. Prods., 877 F. Supp. 1380, 1385 (N.D. Cal. 1995).

79. Id.

80. Id. at 1385; see also Hall v. Baxter Healthcare Corp., 947 F. Supp. 1387, 1411 (D. Or. 1996) ("case reports and case studies are universally regarded as an insufficient scientific basis for a conclusion regarding causation because case reports lack controls.")

81. Bailey et al., supra note 68, at 131.

82. Id. at 139.

83. Id. at 138-39.

84. Id. at 143-45.

85. Id. at 146.

86. Id. at 147-57.

87. Id. at 158-60.

88. The district court in In re Joint Eastern & Southern Dist. Asbestos Litig. undertook a review of five substantially similar "sufficiency criteria" in its assessment of the epidemiologic studies proffered by the plaintiff. 827 F. Supp. 1014 (S.D.N.Y. 1993). The court ultimately found that the studies, though admissible, were insufficient to support a jury finding of causation since they did not satisfy any of thecriteria. On appeal, however, the Second Circuit held that the district court overstepped its bounds by impermissibly crossing the line from determining evidentiary reliability to usurping the role of the jury. 52 F.3d 1124 (2d Cir. 1995).

89. Bailey et al., supra note 68, at 160-64.

90. Id. at 164-66.

91. Jack L. Landau & W. Hugh O'Riordan, Of Mice and Men: The Admissibility of Animal Studies to Prove Causation in Toxic Tort Litigation, 25 IDAHO L. REV. 521, 535 (1989).

92. Id. at 535-36.

93. Id. at 536-37.

94. In re Agent Orange Prod. Liab. Litig., 611 F. Supp. 1223, 1241 (E.D.N.Y. 1985); see also National Bank of Commerce v. Dow Chem. Co., 965 F. Supp. 1490, 1527 (E.D. Ark. 1996) ("There are millions of different species of animals. Each has its own physiological, biochemical and metabolic systems. One cannot scientifically conclude from a determination that a chemical agent has a teratogenic effect in one species that will have such effect in other species."); Landau & O'Riordan, supra note 91 at 523 ("Use of animal toxicity studies to prove causation in toxic tort trials is dangerous and improper.").

95. Wade-Greaux v. White Hall Labs., Inc., 874 F. Supp. 1441, 1480 (D.V.I. 1994); see also Schudel v. General Elec. Co., 120 F.3d 991, 997, 27 ELR 21506, 21508 (9th Cir. 1997)

As to differences in length and intensity of exposure, the district court erroneously reasoned that because there was evidence that acute exposure to TCA and Perc can cause toxic encephalopathy, whether Williams' exposure was sufficient to cause her symptoms was a question of fact for the jury …. Extrapolation was necessary to make the studies relevant, and there was no showing that the necessary extrapolation was scientifically acceptable.

96. In re Paoli R.R. Yard PCB Litig., 35 F.3d 717, 743, 25 ELR 20989, 20997 (3d Cir. 1994); see also National Bank of Commerce, 965 F. Supp. at 1527 ("Because of the difference in animal species, the methods and routes of administration of the suspect chemical agent, maternal metabolism and other factors, animal studies, taken alone, are unreliable predictors of causation in humans.").

97. Goldstein & Henifin, supra note 63, at 201-02.

98. Wade-Greaux, 874 F. Supp. at 1454.

99. Landau & O'Riordan, supra note 91, at 544.

100. 102 F.3d 194 (5th Cir. 1996).

101. Id. at 197.

102. Goldstein & Henifin, supra note 63, at 202.

103. 878 F. Supp. 1119 (N.D. Ill. 1995).

104. Id. at 1112. The fact that a substance has only been shown to affect a specific target organ can also be relevant in assessing the probative value of epidemiologic studies. See Allen, 102 F.3d at 197 ("Evidence has been found that suggests a connection between [ETO] exposure and human lymphatic and hematopoietic cancers, but this is not probative on the causation of brain cancer.").

105. Goldstein & Henifin, supra note 63, at 203.

106. Wade-Greaux v. White Hall Labs., Inc., 874 F. Supp. 1441, 1454 (D.V.I. 1994).

107. Goldstein & Henifin, supra note 63, at 203.

108. National Bank of Commerce v. Dow Chem. Co., 965 F. Supp. 1490, 1526 (E.D. Ark. 1996).

109. Schudel v. General Elec. Co., 120 F.3d 991, 997, 27 ELR 21506, 21508 (9th Cir. 1997).

110. Goldstein & Henifin, supra note 63, at 204.

111. See Bradley v. Brown, 852 F. Supp. 690 (N.D. Ind. 1994); see also Schudel, 120 F.3d at 997 (rejecting plaintiff expert's testimony where the expert "acknowledged that the biochemical mechanism of neurotoxicity from TCA and Perc has not been demonstrated").

112. Goldstein & Henifin, supra note 63, at 206.

113. Id.

114. Id. at 207.

115. Id.

116. Id.

117. Id.

118. Landau & O'Riordan, supra note 91, at 536.

119. Goldstein & Henifin, supra note 63, at 208.

120. Id. at 209.

121. Id.

122. Id. at 210.

123. Id.

124. Cavallo v. Star Enter., 892 F. Supp. 756, 771 (E.D. Va. 1995); see also Claar v. Burlington N. R.R. Co., 29 F.3d 499 (9th Cir. 1994) (upholding the exclusion of plaintiff's expert testimony in part because the expert made no attempt to rule out other possible causes of the injuries sustained by the plaintiff).

125. Goldstein & Henifin, supra note 63, at 211.

126. Id.

127. Id. at 212.

128. See, e.g., Lynch v. Merrell-National Labs., 830 F.2d 1190, 1194 (1st Cir. 1987) (holding that in vivo and in vitro animal studies could not provide the basis for an expert's opinion regarding causation when they were contradicted by the available epidemiologic data.)

129. Margaret A. Berger, Evidentiary Framework, in REFERENCE MANUAL ON SCIENTIFIC EVIDENCE 37, 73 (Federal Judicial Center 1994).

130. E.E. Sikorski et al., Roundtable Summary: The Question of Multiple Chemical Sensitivity, 24 FUNDAMENTAL AND APPLIED TOXICOLOGY 22, 28 (1995).

131. The issue of how courts apply the Frye "general acceptance" test to expert testimony regarding MCS will be discussed below. See infra notes 135-38 and accompanying text.

132. 852 F. Supp. 690 (N.D. Ind. 1994).

133. Id. at 698.

134. Id. at 700.

135. 897 F. Supp. 533 (E.D. Okla. 1995).

136. Id. at 537-38.

137. Id. at 536; see also Sanderson v. International Flavors & Fragrances, Inc., 950 F. Supp. 981, 1001 (C.D. Cal. 1996) ("As defendants point out, every recognized medical organization that has studied this alleged condition has concluded that MCS has not been demonstrated to constitute a physiological, as opposed to purely psychological, illness").

138. 855 F.2d 1188, 19 ELR 20404 (6th Cir. 1988).

139. Id. at 1207, 19 ELR at 20414.

140. Id. at 1208, 19 ELR at 20414.

141. Id. at 1207-09, 19 ELR 20414.

142. Peter Huber, Junk Science in the Courtroom, 26 VAL. U. L. REV. 723, 750 (1992).

28 ELR 10293 | Environmental Law Reporter | copyright © 1998 | All rights reserved