Rubanick v. Witco Chemical Corp.

The opinion of the Court was delivered by

In this case, the Court must determine the standard governing the admissibility of expert evidence relating to the causation of cancer in toxic-tort litigation. The survivors of two men who had worked at a chemical plant where they had been exposed to a toxic substance, polychlorinated biphenyls (PCBs), claim that their decedents’ fatal colon cancer was caused by that exposure. The Law Division conducted a hearing to determine whether plaintiffs’ expert testimony that PCBs had caused the fatal colon cancer of the victims was admissible. *425 Applying the conventional rule for determining the admissibility of such testimony, the court found that the expert’s theory of causation was not sufficiently reliable because it had not been “accepted by at least a substantial minority of the applicable scientific community,” and granted summary judgment for defendants. See 225 N.J.Super. 485, 542 A.2d 975 (1988).

A divided panel of the Appellate Division reversed the trial court. It determined that the conventional “general acceptance” test of reliability for theories of causation that are novel and controversial is inadequate in toxic-tort cases. It concluded that a different test of testimonial reliability, one focusing on the soundness of the foundation for the novel scientific theory of causation, is required in toxic-tort litigation. Finding plaintiffs’ expert testimony admissible under that standard, it remanded the case to trial. See 242 N.J.Super. 36, 576 A.2d 4 (1990).

I

Ronald G. Rubanick worked for the Witco Chemical Corporation (Witco) at its plant in Perth Amboy from 1974 through 1979. In 1979 he was diagnosed as suffering from colon cancer. He died of the cancer on July 23, 1980, at the age of twenty-nine. About three-and-one half years after Rubanick’s death, Anthony DeMaio, a thirty-year Witco employee, was also diagnosed as suffering from colon cancer. He died of the disease on June 29, 1984, at the age of fifty-two.

Plaintiffs, survivors of Rubanick and DeMaio, brought separate actions, which were heard together in the Appellate Division. Each complaint alleged that the individual decedent’s exposure to PCBs caused the decedent’s colon cancer and ultimate death. Defendant Monsanto Company (Monsanto) had. sold Witco PCB fluids, under the trade-name Therminal, beginning in 1969 and continuing until some time prior to 1976.

Before the Rubanick trial, the court granted Monsanto’s motion for an Evidence Rule 8 hearing to assess the qualifica *426 tions and competence of plaintiffs expert in the case, Dr. Earl Balis. The hearing consumed three days. The court put the burden on Monsanto, the moving party, to present sufficient evidence to call into question the admissibility of the proffered testimony. The court therefore first received testimony from Monsanto’s three experts (who were already familiar with Dr. Balis’s theory, apparently from deposition testimony). Dr. Balis then testified as plaintiff’s sole witness.

Dr. Balis holds a doctorate in biochemistry. Although recently retired at the time of the Evidence Rule 8 hearing, Dr. Balis had been a primary cancer researcher at the Sloan-Kettering Cancer Center in New York City for over thirty-seven years. He had headed a research group primarily concerned with investigating the cause, diagnosis, and treatment of colon cancer. He had also served as chairman of the Department of Biochemistry of the Cornell University Medical College. He was a member of the National Large Bowel Cancer Committee, and an associate editor of the publication General Cancer Research. He has personally authored or participated in the publication of approximately 170 scientific articles, of which approximately fifteen concern carcinogenesis. Dr. Balis was also part of a research team with Dr. Nancy Keminey, Rubanick’s treating physician, who was not offered as a witness in this case. Dr. Balis never personally examined Rubanick. This was the first time that Dr. Balis had testified as an expert witness (he told the court he hoped it would be his last).

Dr. Balis’s opinion that exposure to PCBs caused Rubanick’s colon cancer was essentially based on the following factors: (1) the extremely low incidence of cancer in males under thirty; (2) Rubanick’s personal history, e.g., his diet, the fact that he was a non-smoker, and that he did not come from a “cancer family” (i.e., a family whose members are at'a high risk of cancer due to genetic predisposition to the disease); (8) the fact that 5 out of 105 employees at Witco developed some kind of cancer during the relevant period; (4) “a very large body of evidence” showing that PCBs produce cancer in experimental animals; *427 and (5) thirteen articles on the effects of exposure to PCBs on animals and human beings that, according to Dr. Balis, supported his opinion that PCBs are human carcinogens. Dr. Balis also summarized the evidence concerning the quantity of PCBs to which Rubanick had been exposed as follows:

that there was some thirty-five thousand parts per million PCBs in the soil around there, that he would come home covered with this stuff and the material was oozing out of his clothes, according to I guess it was his wife’s testimony, it was something, and I think that report that he lifted these heavy drums and slopping around in this muddy PCB mix, and you also showed me some document about the State of New Jersey, some agency complaining about contamination from that stuff.

The trial court asked Dr. Balis whether his theory that PCBs cause cancer in human beings finds support in the scientific community. Answering that most of the scientific community “pays [no] attention to PCBs whatsoever,” Dr. Balis noted that thirteen of the thirty-nine papers he had reviewed on the subject supported his opinion.

Monsanto’s first witness was Dr. Thomas Fahey, a licensed physician and board certified internist. At the time of the hearing, Dr. Fahey was the deputy physician in charge of the Memorial Hospital at the Sloan-Kettering Cancer Institute and Associate Dean of Medicine at Cornell University Medical College. He had also served as associate chairman of the Department of Medicine at Memorial Hospital, where his responsibilities included overview of the hospital’s oncology services. As an internist at the hospital, he had been directly involved in the care of patients suffering from different types of cancer, including colon cancer. Dr. Fahey, although familiar with epidemiological principles and their scientific uses, did not purport to be an expert in the field of epidemiology. He had done no primary research on carcinogenesis, nor had he ever conducted or participated in research involving the effects of PCBs on humans.

Although he acknowledged that a biochemist with primary research responsibilities would be more conversant with carcinogenesis literature than a treating clinical physician, Dr. Fa- *428 hey testified that he was nonetheless familiar with the literature. He testified that there are no published scientific studies to suggest that colon cancer has any relationship to PCB exposure, and that there is very little in the literature suggesting that PCBs are directly related to carcinogenesis in humans. Reviewing the studies and data on which Dr. Balis had based his conclusion that PCBs caused Rubanick’s colon cancer, Dr. Fahey asserted that that conclusion was “really untenable from the scientific standpoint.” He stated that

there is no evidence that I have seen to this date that would definitively suggest that the individual actually did have extensive exposure to PCBs, and there’s no evidence to suggest that his disease was different in any way from the usual ordinary run-of-the-mill colon cancer that we see in over a hundred forty thousand individuals a year in this country.

He found particularly objectionable Dr. Balis’s use of studies showing that PCBs had caused cancer in animals, testifying that “it’s well accepted now in the cancer field that you cannot extrapolate findings in one species to that of another.” In response to the court’s question whether there is “a substantial body of scientific thought that accepts as a proposition that human exposure to PCBs will give rise to any form of cancer,” Dr. Fahey responded that there was not.

Monsanto’s next witness was Dr. Raymond Harbison, who holds a Ph.D. in toxicology, as well as a degree in pharmacology. At the time of the hearing, Dr. Harbison was Director of Toxicology at the University of Arkansas in conjunction with the National Center for Toxicological Research. He had served as a consultant to the National Institute of Health on the toxicological effects of various environmental pollutants, as well as to the United States Environmental Protection Agency on the toxic effects on humans of exposure to PCBs. He had been directly involved with a medical and toxicological study of employees of a PCB disposal company in Arkansas. Dr. Harbison had testified on behalf of Monsanto on at least one prior occasion, in a case (Amorello v. Monsanto Corp., 186 Mich. App. 324, 463 N.W. 2d 487 (1990)) in which the issue was, as here, whether PCBs had caused the plaintiffs’ injuries.

*429 Dr. Harbison testified that there were many types of PCBs, and that their toxicity varied according to their chlorine content — the greater the chlorination, the greater the toxicity. He testified further that the types of PCBs manufactured by Monsanto had a relatively low chlorine content, and that he was aware of no studies indicating that PCBs of similar chlorine content were carcinogenic to animals. According to Dr. Harbison, there are approximately seventeen studies that have been conducted on the effects on humans of exposure to PCBs. He testified that none of those studies identified an increase in colon cancer, or for that matter, any kind of cancer, as a result of exposure to PCBs. On cross-examination, Dr. Harbison testified that he believed that exposure to PCBs actually reduced tumors.

Dr. Harbison was also asked by the court whether he was “aware of any substantial minority acceptance in the scientific community of the conclusion that Dr. Balis has reached on the evidence ... before him.” Dr. Harbison answered that he was not. He further testified that Dr. Balis had not used the “scientific method” in arriving at his opinion. Harbison explained that what distinguishes scientists from other observers is “rigorous evaluation and methodology,” and that an extremely high level of proof is required before scientists will accept a given theory.

Monsanto’s last witness was Dr. Philip Cole, who testified as an expert epidemiologist. Dr. Cole is a licensed medical doctor and holds a Ph.D. from the Harvard School of Public Health, at which he also taught for ten years, reaching the position of full professor. At the time of the hearing, he was chairman of the Department of Epidemiology at the University of Alabama. He had served as the chairman of the National Cancer Institute committee on the causes of human cancer. He had also spent a year in the Department of Epidemiology of the International Agency for Research of Cancer.

*430 Dr. Cole testified that there had been relatively few studies done on the effects of PCB exposure on human beings, and that the results of the studies had not been highly consistent. However, although he was unwilling to say that PCBs definitely do not cause cancer in human beings, he testified that the studies are “in the aggregate ... persuasive to the effect that there is little or no increase[d] risk of cancer among human beings” due to exposure to PCBs. Dr. Cole also testified that based on the manner in which Dr. Balis had apparently analyzed the data, he did not believe Balis to be qualified to interpret epidemiological evidence. Dr. Cole, too, was asked by the court whether he was “aware of any recognized valid scientific opinion, either as a consensus or as a substantial minority opinion, which would recognize PCBs as a causative factor in human cancer.” Like Monsanto's other two witnesses, he answered that he was not. Dr. Cole acknowledged, however, that the committee of the International Agency for Research of Cancer on which he had sat had listed PCBs as a probable human carcinogen over his dissenting vote.

At the close of the hearing, the court determined that the expert testimony of Dr. Balis was inadmissible. It made the following findings: (1) that Dr. Balis was qualified to offer an opinion on human carcinogenesis generally; (2) that as a non-physician he was not qualified to offer an opinion on a specific patient’s cancer and its possible causal relationship to PCBs; and (3) that the theory of causation Dr. Balis offered had not been generally accepted by the scientific community. 225 N.J.Super, at 492-503, 542 A.2d 975. The court accordingly granted defendant’s motion to exclude Dr. Balis’s testimony, and subsequently granted defendant’s summary judgment motions against Rubanick and DeMaio, whose cause of action was based on the same theory of causation supported by the same expert.

The Appellate Division, in reversing the trial court, issued three separate opinions. 242 N.J.Super. 36, 576 A.2d 4. Judge Petrella, in the court’s lead opinion, believed that the scope of *431 the Evidence Rule 8 hearing had been far too broad and voted to remand for trial. He wrote that a Evidence Rule 8 hearing should address only the issue of the expert’s qualifications; other issues concerning the expert’s testimony go to its weight and therefore should be determined by the jury. Id. at 47-48, 576 A.2d 4. Judge Stern also voted to remand for trial. Although he concluded that the record as presented at the Evidence Rule 8 hearing did not support Dr. Balis’s conclusion that PCBs caused Rubanick’s cancer, he believed that a fuller record developed at trial might provide grounds for its admissibility. Id. at 59, 576 A.2d 4. Judge Havey dissented, finding that the expert testimony was without support, and that the trial court judgment was therefore proper. Id. at 63, 576 A.2d 4. All three of the Appellate Division judges agreed, however, that the conventional standard for admissibility of evidence of causation applied by the trial court was too strict. Id. at 44, 576 A.2d 4 (Petrella, J.A.D.); id. at 58, 576 A.2d 4 (Stern, J.A.D., concurring); id. at 65, 576 A.2d 4 (Havey, J.A.D., dissenting).

Defendants appealed to this Court as of right. R. 2:2-1.

II

Resolution of the issues in this case is dictated by our rules governing the admissibility of expert evidence. Evidence Rule 56(2) provides:

A witness qualified pursuant to Rule 19 as an expert by knowledge, skill, experience, training or education may testify in the form of opinion or otherwise as to matters requiring scientific, technical or other specialized knowledge if such testimony will assist the trier of fact to understand the evidence or determine a fact in issue. The facts or data in the particular case upon which an expert bases an opinion or inference may be those perceived by or made known to him at or before the hearing. If of a type reasonably relied upon by experts in the particular field in forming opinions or inferences upon the subject, the facts or data need not be admissible in evidence.

In State v. Kelly, 97 N.J. 178, 208, 478 A.2d 364 (1984), the Court explained that in determining admissibility of expert testimony, the field of science “must be at a state of the art *432 such that an expert’s testimony could be sufficiently reliable.” Reliability can be established by demonstrating “general acceptance” of the expert’s opinion or theory within the scientific or professional community. Id. at 210, 478 A. 2d 364. “There are,” we stated in Windmere, Inc. v. International Ins. Co., 105 N.J. 373, 379, 522 A.2d 405 (1987), “generally three ways in which a proponent of expert testimony or scientific results can prove the required reliability in terms of its general acceptance within the scientific community: (1) the testimony of knowledgeable experts; (2) authoritative scientific literature; (3) persuasive judicial decisions which acknowledge such general acceptance of expert testimony.” We have followed that approach for determining reliability of expert evidence in a variety of contexts. E.g., ibid, (reliability of spectrography, or voiceprint analysis); State v. Kelly, supra, 97 N.J. 178, 478 A.2d 364 (theory of “battered woman’s syndrome”); Romano v. Kimmelman, 96 N.J. 66, 474 A.2d 1 (1984) (breathalyzer test); State v. Cavallo, 88 N.J. 508, 443 A.2d 1020 (1982) (diagnosis of tendency to commit rape on basis of rapist profile); State v. Hurd, 86 N.J. 525, 432 A.2d 86 (1981) (hypnotically refreshed testimony).

The trial court, here, relying primarily on Windmere, Inc., determined that plaintiff’s theory of causation was inadmissible because it had not been accepted by “at least a substantial minority of the applicable scientific community.” 225 N.J.Super. at 498-500, 542 A.2d 975. All three Appellate Division judges, however, thought that the conventional “general acceptance” test of reliability is too stringent for determining the reliability of expert theories of causation in toxic-tort litigation because scientific knowledge of carcinogenesis is still evolving. Hence, the question posed by the several decisions of the lower courts is whether the Court must adhere to the conventional test of admissibility of expert testimony relating to new or developing theories of causation in toxic-tort litigation, because, in the terms used by State v. Kelly, supra, 97 N.J. at 208, 478 A.2d 364, that scientific knowledge is not “at a state of the art *433 such that an expert’s testimony could be sufficiently reliable.” Alternatively, the issue is whether the Court should fashion a broader standard for assessing the reliability of such evidence in this type of litigation.

We do not easily depart from the traditional test governing the admissibility of expert testimony. We have recognized the dangers of allowing the jury to consider expert testimony the reliability of which has not been sufficiently demonstrated. “[W]hen unreliable evidence is labeled ‘expert,’ juries might not accurately assess its weight.” Ryan v. KDI Sylvan Pools, 121 N.J. 276, 285, 579 A.2d 1241 (1990) (citing State v. Cavallo, supra, 88 N.J. 508, 443 A.2d 1020). We have particularly emphasized the need for this reliability when a machine is used to displace the human functions in determining criminal guilt. Romano v. Kimmelman, supra, 96 N.J. 66, 474 A.2d 1. At the same time, we have recognized the extraordinary and unique burdens facing plaintiffs who seek to prove causation in toxic-tort litigation. See Ayers v. Jackson Tp., 106 N.J. 557, 580-87, 525 A.2d 287 (1987). In Ayers, for example, a large class of plaintiffs had been exposed to toxic pollutants due to the township’s negligent operation of a landfill. We recognized that

[b]y far the most difficult problem for plaintiffs to overcome in toxic tort litigation is the burden of proving causation. In the typical tort case, the plaintiff must prove tortious conduct, injury and proximate cause. Ordinarily, proof of causation requires the establishment of a sufficient nexus between defendant’s conduct and the plaintiff’s injury. In toxic tort cases, the task of proving causation is invariably made more complex because of the long latency period of illnesses caused by carcinogens or other toxic chemicals. The fact that ten or twenty years or more may intervene between the exposure and the manifestation of disease highlights the practical difficulties encountered in the effort to prove causation. Moreover, the fact that segments of the entire population are afflicted by cancer and other toxically-induced diseases requires plaintiffs, years after their exposure, to counter the argument that other intervening exposures or forces were the “cause” of their injury. [Id. at 585, 525 A.2d 287 (citations omitted).]

We recognize, too, that because of the extremely high level of proof required before scientists will accept a new theory, and particularly because of the current inability of science to fully *434 comprehend carcinogenesis, see Brennan, Causal Chains and Statistical Links: The Role of Scientific Uncertainty in Hazardous-Substance Litigation, 73 Cornell L.Rev. 469, 474-75 (1988), plaintiffs in toxic-tort litigation, despite strong and indeed compelling indicators that they have been tortiously harmed by toxic exposure, may never recover if required to await general acceptance by the scientific community of a reasonable, but as yet not certain, theory of causation.

Each of the judges of the Appellate Division reached the conclusion that the conventional standard for determining the reliability of scientific knowledge was inappropriate in the context of toxic-tort litigation. Judge Petrella wrote:

The question here is not the acceptance of the “general acceptance” standard but whether there are sufficient factual and scientific underpinnings to the expert’s causation theory, recognizing that in experimentation and study of known or suspected cancer causing agents as a rule they are not intentionally administered to humans because of the risks involved. [242 NJSuper. at 44, 576 A.2d 4 (citation omitted).]

Judge Havey, in dissent, expressed essentially the same view on this issue:

A simple mechanistic application of the “general acceptance” standard is not appropriate when the issue, as here, is whether a specific chemical has probably caused a particular disease____ [T]he question is whether there are sufficient factual and scientific underpinnings to the expert’s causation theory. [Id. at 65, 576 AM 4.]

Judge Stern was in “full agreement with [his] colleagues that we are free to employ a broader standard when the issue concerns an expert opinion relating to the question of causation.” Id. at 58, 576 A.2d 4.

The Appellate Division’s unanimous recognition that there must be a different standard for determining the reliability of scientific theories of causation in toxic-tort litigation finds growing and impressive authoritative support. In recent years, a number of commentators have suggested that a broadened standard for determining the admissibility of causation theories in toxic-tort litigation is needed. See, e.g., Delgado, Beyond Sindell: Relaxation of Cause-in-Fact Rules for Indeterminate Plaintiffs, 70 Calif.L.Rev. 881 (1982); Farber, Toxic *435 Carnation, 71 Minn.L.Rev. 1219 (1987); King, Causation, Valuation, and Choice in Personal Injury Torts Involving Preexisting Conditions and Future Consequences, 90 Yale L.J. 1353 (1981); Robinson, Probabilistic Causation and Compensation for Tortious Risk, 14 J.Legal Stud. 779 (1985); Rosenberg, The Causal Connection in Mass Exposure Cases: A ‘Public Law’ Vision of the Tort System, 97 Harv.L.Rev. 851 (1984); Note, Pursuing a Cause of Action in Hazardous Waste Pollution Cases, 29 Buffalo L.Rev. 533 (1980); Note, The Inapplicability of Traditional Tort Analysis to Environmental Risks: The Example of Toxic Waste Pollution Victim Compensation, 35 Stan.L.Rev. 575 (1983); Note, Trans-Science in Torts, 96 Yale L.J. 428 (1986); Note, Tort Actions for Cancer: Deterrence, Compensation, and Environmental Carcinogenesis, 90 Yale L.J. 840 (1981). See also Brennan, Helping Courts with Toxic Torts: Some Proposals Regarding Alternative Methods for Presenting and Assessing Scientific Evidence in Common Law Courts, 51 U.Pitt.L.Rev. 1- (1989) (discussing the difficulties in proving causation in toxic-tort litigation and proposing alternatives to litigation). Those authorities agree that both the delayed effects in toxic-tort cases — effects that may not manifest themselves for years after the occurrence of the responsible act or events — «as well as the inability of current science to identify precisely the causes of cancer, create the need for a reasonable alternative to the traditional requirement of general acceptance as the primary measure of reliability of scientific knowledge for use in the tort system.

The imprecision of estimating the impact of environmental and occupational carcinogens derives from the central uncertainty surrounding the nature of carcinogenesis. Like the study of toxicology in general, the lack of clear insights into the disease’s molecular basis hampers the study of carcinogenicity. ********

Given this central uncertainty regarding the cause of cancer, any given statement about the role of any agent as a carcinogen is hedged with assumptions and hypotheses. Because scientists do not yet understand the molecular model of carcinogenesis, it is impossible to state that a given carcinogen caused *436 any individual tumor. [Brennan, supra, 73 Cornell L.Rev. at 474, 475 (footnote omitted).]

Recovery in toxic-tort cases has typically been granted “only after a statistically significant number of deaths and injuries were incurred, allowing experts to quantify the hazard.” Note, supra, 96 Yale L.J. at 429. The commentators therefore argue that the admissibility of a scientific theory of causation in toxic-tort litigation should not necessarily turn on its general acceptance by the scientific community. That acceptance entails the strict application of the scientific method, which requires an extraordinarily high level of proof based on prolonged, controlled, consistent, and validated experience. In the words of Dr. Harbison, “without that rigorous form of evaluation one has not used the scientific method, and the importance of the scientific method is to make certain that the observations that we make as scientists aren’t in error.” 1 The scientific method, *437 however, fails to address or accommodate the needs and goals of the tort system. Chief Judge Markey of the United States Court of Appeals for the Federal Circuit has stated:

The differences between the judicial and the scientific-technological processes are profound and pervasive. Failure to recognize that difference has led to judicial expressions of frustration and an unfortunate tendency to rest judicial decisions on current, and often transient, “truths” and “facts” of science and technology. The purpose and function of science is to learn physical facts____

The purpose and function of law is to resolve disputes and to facilitate a structure for the organization of a just society — in a word, to provide justice. [Markey, Needed: A Judicial Welcome for Technology — Star Wars or Stare Decisis?, 79 F.R.D. 209, 210 (1979).]

See also Handler, The Judicial Pursuit of Knowledge: Truth and/or Justice, 41 Rutgers L.Rev. 1, 26 (1988) (“[T]here are areas in which judicial need for certain facts equals or exceeds the scientific community’s ability to establish them. Many cases present issues with respect to which courts have been forced intuitively to make assumptions on the basis of available knowledge____”).

Judge Havey, dissenting below and drawing on our views expressed in Ayers v. Jackson Tp., supra, 106 N.J. at 585, 525 A.2d 287, observed:

Plaintiffs face complex and unique practical difficulties in their effort to prove causation because of long latency periods between exposure and illness, as well as the countervailing proofs that the plaintiffs have encountered other intervening exposures or forces which may have been the “cause” of their injury or disease. 7n my view, an epidemiological study of recent vintage may stand alone in establishing a causal relationship between a specific chemical and human cancer. [Id. 242 N.J.Super. at 65, 576 A.2d 4 (citation omitted).]

*438 Expressing similar concerns, several courts have taken a more flexible approach to the admission of causation theories in toxic-tort litigation. Those courts have looked not to whether the theories have been generally accepted by the scientific community, but rather to whether the scientific knowledge is sufficiently founded or based on a sound methodology, leaving the decision to credit the theory to the finder of fact.

In Ferebee v. Chevron Chemical Co., 736 F.2d 1529, cert. denied, 469 U.S. 1062, 105 S.Ct. 545, 83 L.Ed.2d 432 (1984), the Court of Appeals for the District of Columbia Circuit took an approach similar to that of the Appellate Division below. In Ferebee, the plaintiffs, children of an agricultural worker who died of pulmonary fibrosis, brought survival and wrongful death actions against the defendant paraquat manufacturer, claiming that the worker died as a result of exposure to paraquat for a period of approximately ten years. The jury found for the plaintiffs after considering the sharply divided theories of causation proffered by each side. Id. at 1532.

On appeal, the defendant argued that the plaintiffs’ theory of causation had not been generally accepted by the scientific community and was therefore inadmissible. The court rejected that argument, distinguishing between the test applied to “evidence based on novel scientific techniques or methodologies,” and that applied to “such evidence ... involved in the admission of scientific opinion testimony that, while controversial in its conclusions, is based on well-founded methodologies.” Id. at 1535 (citing Reed v. State, 283 Md. 374, 381, 391 A.364, 368 (1978)). Judge Mikva, writing for a unanimous court of appeals, counselled judicial humility and neutrality with respect to assessing the reliability of a complex theory of causation in toxic-tort litigation:

Judges, both trial and appellate, have no special competence to resolve the complex and refractory causal issues raised by the attempt to link low-level exposure to toxic chemicals with human disease. On questions such as these, which stand at the frontier of current medical and epidemiological inquiry, if *439 experts are willing to testily that such a link exists, it is for the jury to decide whether to credit such testimony. [Id. at 1534.]

Judge Mikva continued:

[A] cause-effect relationship need not be clearly established by animal or epidemiological studies before a doctor can testify that, in his opinion, such a relationship exists. As long as the basic methodology employed to reach such a conclusion is sound, such as the use of tissue samples, standard tests, and patient examination, products liability law does not preclude recovery until a “statistically significant” number of people have been injured or until science has had the time and resources to complete sophisticated laboratory studies of the chemical. In a courtroom, the test for allowing a plaintiff to recover in a tort suit of this type is not scientific certainty but legal sufficiency; if reasonable jurors could conclude from the expert testimony that paraquat more likely than not caused Ferebee’s injury, the fact that another jury might reach the opposite conclusion or that science would require more evidence before conclusively considering the causation question resolved is irrelevant. [Id. at 1535-36.]

A similar approach was taken by the court in Wells v. Ortho Pharmaceutical Corp., 615 F.Supp. 262 (N.D.Ga.1985), aff'd, 788 A.2d 741, reh’g denied, 795 A.2d 89 (11th Cir.), cert. denied, 479 U.S. 950, 107 S.Ct. 437, 93 L.Ed.2d 386 (1986). There, the plaintiffs, an infant and her parents, contended that the infant’s birth defects were caused by a spermicide manufactured by the defendant. At a bench trial, the plaintiffs presented a number of experts, including the child’s treating physicians, who testified that the defects were caused by the spermicide, as well as several epidemiological studies generally indicating an association between spermicide use and deleterious effects on the fetus. Id. at 269-79. The defense presented their own experts who testified that no causal link between spermicide use and congenital defects had been established; they assailed the studies submitted by the plaintiffs, as well as the application of the studies to the present case, noting that an advisory committee of the Food and Drug Administration had deemed the product “safe and effective.” Id. at 279-91.

The district court judge stated at the outset of his opinion that the court’s task

was not to presume the expertise to resolve, once and for all, the dispute within the scientific community about the safety of spermicides. Rather, the Court’s fu