Full opinion text
OPINION SWEET, District Judge. Following a jury verdict rendered on February 10, 1993, in favor of the plaintiff Arlene Maiorana (the “Plaintiff’), certain defendants and third-party defendants (collectively, the “Defendants”) in this action have filed post-trial motions. The Plaintiff alleged and the jury found that the asbestos-containing products of certain of the Defendants were the proximate cause of the death of her husband, John Maiorana (“Maiorana”). After the verdict, Defendant and second third-party plaintiff United States Mineral Product Company (“USMP”), the sole remaining direct Defendant left in the trial, moved on March 10, 1993, pursuant to Rule 50(b), Fed.R.Civ.P., for judgment notwithstanding the verdict or, more properly, for judgment as a matter of law. USMP also moved for a new trial or, in the alternative, for remittitur pursuant to Rule 59, Fed.R.Civ.P., on the grounds that damages are excessive and that the Court failed to instruct the jury adequately pursuant to New York Labor Law § 200. Third-party Defendants Mario & DiBono Plastering Co. (“Mario & DiBono”), Castagna & Son, Inc. (“Castagna”), and Tishman Realty & Construction Co. of New York, Inc. (“Tishman”), have sought similar relief. Castagna moved for a stay of execution of judgment as well. Both Castagna and Tishman also have moved for judgment on their cross-claims for common law indemnity against Mario & DiBono, the Defendant who impleaded them. Finally, third-party Defendant the Port Authority of New York and New Jersey (the “Port Authority”), which was found not liable by the jury, has opposed the motion of USMP for a new trial pursuant to § 200, N.Y.Lab.L. For the following reasons, the motions for judgment as a matter of law are granted. In the event that this decision is appealed and overturned upon appeal, all motions filed by the parties are granted in part and denied in part. The Parties The Plaintiff is a natural person and is the widow of John Maiorana. She resides and is domiciled in the State of New York. Defendant and second third-party Plaintiff USMP is a corporation duly organized and existing under the laws of the State of New Jersey. Third-party Defendants Mario & DiBono, Castagna, and Tishman are corporations duly organized and existing under the laws of the State of New York. Third-party Defendant the Port Authority is a governmental entity duly organized and existing under and by virtue of the laws of the States of New York and New Jersey, with its principal place of business in New York. The Port Authority built and owns the World Trade Center (the “WTC”) in New York, New York. Prior Proceedings The Plaintiff filed her original complaint in this diversity action on July 28, 1987, as part of a case brought by sixteen plaintiffs on behalf of themselves and their deceased spouses, see In re Joint E. & S. Dist. Asbestos Litig., 758 F.Supp. 199 (S.D.N.Y.1991) (“Asbestos Litig. I”), rev’d, 964 F.2d 92 (2d Cir.1992) (“Asbestos Litig. II”). Defendant and second third-party plaintiff USMP filed its second third-party complaint on December 14, 1990. Certain Defendants, including USMP, moved for summary judgment alleging that the only evidence which the Plaintiff had set forth to prove that her husband’s colon cancer was caused by his exposure to asbestos was epidemiological evidence, and because this evidence did not indicate that asbestos exposure created at least a two-fold increase in the risks of getting colon cancer and thus the Defendants’ actions could not have been “more likely than not” the cause of his cancer, it was insufficient as a matter of law. The motion for summary judgment was granted on February 26, 1991. The Plaintiff appealed, and the Court of Appeals reversed the grant of súmmary judgment status on the grounds that the Plaintiff had presented clinical evidence of causation in addition to the epidemiological studies: “Maiorana’s own medical records and personal history were the clinical evidence upon which plaintiffs expert witnesses based their opinions that asbestos exposure was a significant factor in causing his colon cancer.” Asbestos Litig. II, 964 F.2d at 96. The Court found that the plaintiffs experts could testify that Maiorana’s exposure to asbestos was a “significant factor” and “a proximate cause, and a substantial factor” in the development of his colon cancer because: [t]hey based their conclusions on their review of Mr. Maiorana’s medical records, occupational and medical history, their knowledge as experts either in occupational medicine or epidemiology and their review of epidemiological studies. They also appropriately based their conclusions on the lack of other factors that could have caused Mr. Maiorana’s colon cancer. Granting plaintiff all favorable inferences, these statements are the equivalent of stating that asbestos exposure more probably than not caused the colon cancer. Medical experts need not invoke technical legal phrases in order to convey their medical opinions. Id. at 96-97. The case was tried to a jury from January 20 to February 10, 1993. The jury was charged on strict liability and negligence of manufacturers and on the negligence of all third party defendants. The jury, after allocating percentages of fault among the defendants and certain non-parties via special verdict, returned a verdict in favor of the plaintiff in the total amount of $4,510,000. The jury found USMP 50% responsible for the Plaintiffs’ damages and three of the third-parties approximately equally negligent (both contractors were assessed to be 14% responsible; subcontractor Mario & DiBono was assessed to be 15% responsible). The jury absolved the Port Authority of any liability. Oral argument was heard on the post-trial motions of USMP and the third-party Defendants on March 10, 1993, and these motions were considered fully submitted at that time. The Facts USMP was the manufacturer of Cafeo D, an asbestos-containing fireproof spray material used in the construction of both the WTC in Manhattan and Meadowbrook Hospital in Nassau County, New York. The Port Authority was the owner of the WTC. Tishman was the Port Authority’s prime or general contractor at the WTC job site and the Port Authority’s designated agent for dealing with the subcontractors and trade workers. Cas-tagna was the general contractor for Mea-dowbrook Hospital. Proof offered at trial established that both Castagna and Tishman had inspectors and workers on the site with direct control and authority over the various subcontractors and employees. Both Castagna and Tishman entered into contracts with the respective site owners which gave them certain authority and control over the job sites. These contracts were admitted into evidence at trial. One of these subcontractors was Mario & DiBono, the asbestos spray contractor for Meadowbrook and for interior work at the WTC. Maiorana worked at the WTC in 1969 and 1970 and at Meadowbrook from September 1969 until sometime in 1970 as a sheet metal worker for Alpine, a small sheet metal company no longer in operation, and another subcontractor. The Plaintiffs theory at trial was that the sheet metal workers, who worked alongside of and followed the work of the asbestos sprayers, were exposed to asbestos through contact with USMP’s sprayed insulation, Cafco D. Maiorana was exposed to asbestos-containing dust which hung in the air and accumulated on the floor after a session of spraying. Mario & DiBono began spraying Cafco D at the WTC in approximately August 1969. The Port Authority and Tishman banned the use of Cafco D at the "WTC in April of 1970. USMP shipped Cafco D to Meadowbrook in the fah of 1969. Maiorana was diagnosed as having colon cancer in January 1983, and he died from the disease six months later, on June 16, 1983. He was 40 years of age. Discussion I. The Standard for Judgment As a Matter of Law in the Second Circuit USMP and all the Defendants allege that they are entitled to judgment as a matter of law. A motion for judgment as a matter of law should be denied unless, viewed in the light most favorable to the nonmoving party, “the evidence is such that, without weighing the credibility of the witnesses or otherwise considering the weight of the evidence, there can be but one conclusion as the verdict that reasonable men could have reached.” Samuels v. Air Transport Local 504, 992 F.2d 12, 14 (2d Cir.1993) (quoting Simblest v. Maynard, 427 F.2d 1, 4 (2d Cir.1970)); accord Smith v. Lightning Bolt Prods., Inc., 861 F.2d 363, 367 (2d Cir.1988); Auwood v. Harry Brandt Booking Office, Inc., 850 F.2d 884, 889 (2d Cir.1988). There must be “such a complete absence of evidence supporting the verdict that the jury’s findings could only have been the result of sheer surmise and conjecture” that a reasonable and fair-minded jurors could not arrive at a verdict against him. Samuels, 992 F.2d at 14; see also Mattivi v. South African Marine Corp., “Huguenot,” 618 F.2d 163, 168 (2d Cir.1980). However, the court “ ‘cannot assess the weight of conflicting evidence, pass on the credibility of the witnesses, or substitute its judgment for that of the jury.’ ” Smith, 861 F.2d at 367 (quoting Katara v. D.E. Jones Commodities, Inc., 835 F.2d 966, 970 (2d Cir.1987)); see also Mattivi, 618 F.2d at 167. II. Sufficiency of the Evidence The standard for determining whether evidence is sufficient to create an issue of fact for the jury is a legal standard, but in determining it, the trial court must view the evidence in a light most favorable to the nonmovant and grant that party every reasonable inference that the jury might have drawn in its favor. See Samuels, 992 F.2d at 14. At issue here is the sufficiency of the evidence that Maiorana’s exposure to asbestos was the proximate cause of his colon cancer. That evidence was exclusively scientific in nature. A recent decision by the Supreme Court in Daubert v. Merrell Dow Pharmaceuticals, Inc., — U.S. -, 113 S.Ct. 2786, 125 L.Ed.2d 469 (1993), clarified the standards for admitting scientific evidence. While there is no question in this case that the testimony of both sides’ experts — all of whom possess impressive credentials — is admissible, certain passages in Daubert speak to the sufficiency required of scientific evidence and the gatekeeping role of the trial judge with regard to misleading evidence, — U.S. at -, 113 S.Ct. at 2798-99. In other words, although Daubert focuses on the admissibility of the evidence, dicta in that opinion about the methods by which a trial court may determine the reliability of the evidence are instructive as well. The recent decision in Daubert does not change the fundamental test of law, however. The evidence supplied by the Plaintiff at trial must be sufficient as a matter of law to show that Maiorana’s exposure to asbestos was a proximate cause of his colon cancer. To competently analyze the legal issues presented by this appeal, an understanding of the relevant scientific principles, albeit necessarily a rudimentary one drawn primarily from the relevant sources cited to by the parties, is essential. DeLuca v. Merrell Dow Pharmaceuticals, Inc., 911 F.2d 941, 945 (3d Cir.1990). For this reason, the scientific evidence presented by both the Plaintiff and the Defendants is summarized and analyzed below to determine if the plaintiff presented sufficient evidence in support of her claim. A. The Problem of Causation in Toxic and Carcinogenic Tort Actions Courts employ no fewer than three distinct concepts of “cause”: cause-in-fact, proximate cause, and causal linkage. Cause-in-fact is but-for causation: it is the particular necessary condition without which the event causing the injury would not have occurred, to wit, if event x qua cause-in-fact occurs, then event y will follow. Proximate cause is more important from the legal perspective because it is the cause whose proximity in time and.space qualifies it as the legally significant cause that is sufficient to sustain a cause of action in tort. Causal linkage, in contrast, asserts a causal relationship between events x and y on the basis of statistical probability: if x occurs, there is probability p that event y will follow. In the area of toxic and carcinogenic torts, the discussion. of causation is substantially complicated by the importance of scientific hypotheses and theories in determining whether a causal relationship exists between person A being exposed to carcinogen c and subsequently developing disease d. The most straightforward concept of causation is that used to frame universal laws of the form: ceteris paribus for all occurrences of an event of type x, then an event of type y will necessarily follow. Such universal causal relationships have been identified for certain “signature” diseases such as mesothelioma. The causal link between exposure to asbestos and mesothelioma has been demonstrated to such a high degree of probability, while at the same time few if any other possible causes have been identified, that if A is diagnosed as having mesothelioma and A was exposed to asbestos, A’s exposure to asbestos is recognized to be the cause of A’s mesothelioma. Of course, in order to assert such a universal connection between events x and y, it is necessary to have a thorough understanding of the relevant physical mechanisms involved in the relationship. Obvious difficulties emerge when those mechanisms are complex and imprecisely understood. Simply subjecting A to clinical evaluation will not be sufficient because of the difficulty involved in excluding other possible causes and confounding factors that'may be have caused or causally contributed to A’s disease. In these cases, the scientist is compelled to frame hypotheses in terms of laws asserting a statistical probability that if x, then y, rather than a universal connection between the two events. Thus, in addition to the aforementioned legal concepts of cause, the court is inevitably confronted with the myriad uses of the concept by scientists. B. Epidemiological Evidence Epidemiology is a scientific discipline that by the very nature of its subject matter employs the concept of cause qua statistical probability. Useful hypotheses are framed, tested, refined, and used in identifying relations between one event, such as the exposure to carcinogenic substance c, and a subsequent event, such as the development of disease d. However, because the physiological, biological, and chemical mechanisms involved with c and d and the interaction between them are not sufficiently well-known for any single individual to frame a universal law regarding the causal relationship between c and d, the epidemiologist focuses on a group of persons or a “cohort” and assesses the statistical probability that a percentage of individuals in a given cohort will develop d after being exposed to c. The Honorable Jack B. Weinstein has summarized the tasks and methods of the epidemiologist as follows: Epidemiological studies rely on “statistical methods to detect abnormally high incidence of disease in a study population and to associate these incidence with unusual exposures to suspect environmental factors.” In their study of diseases in human populations, epidemiologists use data from surveys, death certificates, and medical and clinical observations. Id. In re “Agent Orange” Prod. Liab. Litig., 611 F.Supp. 1223, 1231 (E.D.N.Y.1985) (“Agent Orange II”) (quoting Dore, A Commentary on the Use of Epidemiological Evidence in Demonstrating Cause-in-Fact, 7 Harv. Envtl.L.Rev. 429, 431 (1983)). The epidemiologist proceeds in two stages in analyzing the relationship between c and d: first, he determines whether a relationship between c and d is biologically possible; and second, if he concludes that it is, he then determines whether this relationship is causal in nature by considering whether there is a statistically significant association between the cohort’s exposure to c and the outbreak of d in the cohort. This association is determined by using a mathematical formula that produces a ratio for the relative risk of contracting the disease: The relative risk ratio is computed by dividing the observed number of eases of a particular disease for a particular time period (numerator data) by the expected number of cases of that disease for the same time period based on historical information not influenced by the event in question (denominator data). A relative risk of [1.0] is the expected rate of contracting a disease in a population not influenced by the event under investigation. A relative risk of [2.0] means that the disease occurs among the population not subject to the event under investigation. Phrased another way, a relative risk of [2.0] means that, on the average, there is & fifty percent likelihood that a particular case of the disease was caused by the event under investigation and a fifty percent likelihood that the disease was caused by chance alone. A relative risk greater than [2.0] means that the disease more likely than not was caused by the event. Manko v. United States, 636 F.Supp. 1419, 1434 (W.D.Mo.1986) (emphasis added), aff'd in part and rev’d in part, 830 F.2d 831 (8th Cir.1987); accord Asbestos Litig. I, 768 F.Supp. at 202-03. Once a statistically significant percentage of a cohort is determined to have developed d following exposure to c, the epidemiologist can then evaluate the nature and scope of the causal link between c and d. Nowhere is the imprecision confronting the epidemiologist clearer than that posed by the present state of scientific understanding of the causal relationships between environmental and occupational carcinogens and cancer. 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. Cancer biologists have developed useful hypotheses or carcinogenicity, some of which are now guiding potentially useful research. Nonetheless, the statement by a group of experts convened by the International Agency for Research on Cancer ... in 1980 remains true today: “the mechanisms by which chemicals induce cancer and the developmental stages from initial exposure to frank neoplasia are poorly understood.” Scientifically valid links, therefore, will not always demonstrate the connection between the causal event and the harmful effect to establish a legally cognizable proximate cause which is sufficient to sustain or succeed in a tort action. While an epidemiologist might be inclined to conclude that a causal relationship exists between c and d, despite the fact that the relative risk ratio is <2.0, the “more likely than not” test, which a plaintiff must satisfy to sustain a cause of action in tort, is not satisfied by epidemiological evidence alone unless the plaintiff establishes that the relative risk ratio or, in the case of epidemiological studies of asbestos, the standardized mortality ratio (“SMR”) between c and d is greater than 2.0. In other words, “at least a two-fold increase in incidence of the disease attributable to ... exposure [to asbestos] is required to permit recovery if epidemiological studies alone are relied upon.” In re “Agent Orange” Prod. Liab. Litig., 597 F.Supp. 740, 785 (E.D.N.Y.1984) (“Agent Orange I”). C. Clinical and Experimental Evidence A plaintiff need not rely exclusively on epidemiological studies in support of her causation proof. A plaintiff may rely on conclusions derived from experimental studies involving animals or discrete groups of persons, or from clinical evidence including the medical, personal, and family history of the individual suffering from the disease. On the issue of clinical evidence, Judge Weinstein considered that courts were divided between “strong” and “weak” versions of the preponderance of the evidence of causation, Agent Orange II, 611 F.Supp. at 1260. Under the “strong” version, a plaintiff must offer both epidemiologic evidence that the probability of causation exceeds 50% in the exposed population and “particularistic” proof that the conduct complained of caused his individual harm. See id. Judge Weinstein considered the law in New York to require “strong” evidence of causation, see Miller v. National Cabinet Co., 8 N.Y.2d 277, 204 N.Y.S.2d 129, 168 N.E.2d 811 (1960), where the Court of Appeals concluded that the plaintiffs expert’s unwillingness to say that plaintiffs exposure to benzene caused his leukemia as a matter of medical certainty, combined with the lack of statistical evidence of causation, was enough to dismiss the plaintiffs claim. In the case at bar, the Court of Appeals noted that: Maiorana’s own medical records and personal history were the clinical evidence upon which plaintiffs expert witnesses based their opinions that asbestos exposure was a significant factor in causing his colon cancer. Plaintiffs experts used epidemiological studies as one basis for an expert opinion but did not rely solely on epidemiological evidence. Thus, plaintiff did not need to provide epidemiological evidence of a certain magnitude to defeat a summary judgment motion because she did not rely on epidemiological studies alone. Asbestos Litig. II, 964 F.2d 92, 97 (2d Cir.1992). The Court of Appeals went on to conclude that it: agreed with the observation that a “physician or other such qualified expert may view the epidemiological studies and factor out other known risk factors such as family history, diet ... or other factors which might enhance the remaining recognized risks, even though the risk study fell short of the 2.0 correlation.” Grassis v. Johns-Manville Corp., 248 N.J.Super. 446, 591 A.2d 671, 675 (1991). Accordingly, an expert should be “permitted to testify respecting the bases for her causation opinion, including the epidemiological studies upon which she relied.” Id., 591 A.2d at 676. Asbestos Litig. II, 964 F.2d at 97. However, Grassis has been interpreted by the New Jersey courts to require more rigorous scientific evidence than the opinion itself seems to indicate is necessary. In Dafler v. Raymark Indus., Inc., 259 N.J.Super. 17, 611 A.2d 136 (N.J.Sup.1992), and Landrigan v. Celotex Corp., 127 N.J. 404, 605 A.2d 1079, 1086 (1992), both cases where the only clinical evidence that asbestos caused colon cancer was differential diagnosis (i.e., the ruling out of other known risk factors), the court found that the medical testimony about the particular plaintiff was not the compelling source of testimony about causation. In Landrigan, both witnesses reviewed specific evidence about the decedent’s medical and occupational histories, and: [b]oth witnesses also excluded certain known risk factors for colon cancer, such as excessive alcohol consumption, a high-fat diet, and a positive family history. From statistical population studies to the conclusion of causation in an individual, however, is a broad leap_ Nonetheless, proof of causation in toxic-tort cases depends largely on inferences derived from statistics about groups. Landrigan, 127 N.J. at 422, 605 A.2d 1079. Landrigan held that since a toxic tort victim might be compelled to report epidemiological evidence to prove causation, an expert’s testimony on such causation should be permitted provided the expert’s methodology was sound. Id. at 414, 422, 605 A.2d 1079. Other courts in New Jersey since Grassis have concluded the proof of causation in toxic tort cases rests essentially on the epidemiological evidence. See Dafler, 259 N.J.Super. at 36, 611 A.2d at 146 (citing Landrigan for the proposition that proof of causation may depend mostly upon inferences drawn from statistic evidence); Caterinicchio v. Pittsburgh Corning Corp., 127 N.J. 428, 433, 605 A.2d 1092 (1992) (referring to Landrigan standard where trial court must consider bases of and process by which expert witness reaches his conclusion, but reiterating proposition that epidemiological studies need not show a relative risk factor in excess of 2.0). These cases uphold Grassis in the sense that they do not create a strict threshold for statistical evidence below which the case will not be considered, as the federal courts did in most of the Bendectin cases. However, they do admit that where the clinical evidence is merely an elimination of other possible known sources of cancer, such evidence is less than compelling, and under those circumstances, the plaintiff may be forced to rely on epidemiological evidence in order to establish causation. It is also important to note that all three of the New Jersey cases concern summary judgment or the admissibility of testimony; they do not rule out the proposition that once the testimony is admitted, it may prove insufficient as a matter of law. Rather they support the proposition that epidemiological evidence should be admitted at trial because the plaintiff may be compelled to rely upon it, and they suggest that strictly clinical evidence would be insufficient for proof of causation as a matter of law. The question of sufficiency after all the evidence has been adduced is a different question from whether the evidence should be admitted or whether the action should be terminated through the mechanism of summary judgment. D. The “More Likely Than Not” Test Regardless of the kinds of evidence employed by a plaintiff in support of his causation proof in a carcinogenic tort action, the plaintiff must satisfy requirement of tort law that the purported cause was in fact more likely than not the actual cause of the injury in question. As Judge Weinstein has noted, A government administrative agency may regulate or prohibit the use of toxic substances through rulemaking, despite a very low probability of any causal relationship. A court, in contrast, must observe the tort law requirement that a plaintiff establish a probability of more than fifty percent that the defendant’s action injured him. Agent Orange I, 597 F.Supp. 740, 785. Therefore, even though epidemiological evidence regarding the relationship between exposure to c and the development of d may fall short of the 2.0 threshold of statistical significance, if this evidence is combined with clinical or experimental evidence which eliminates confounding factors and strengthens the connection between c and d specifically in the circumstances surrounding the plaintiffs case of d, then the plaintiffs causation proof may be sufficient to support a jury’s finding that it was more likely than not that the plaintiffs case of d was eased by his exposure to c. E. Battle of the Experts The traditional view was that determining whether scientific evidence was viable was a matter for the jury, not for the court. As long as the expert testimony was admissible under Rules 702 and 703, Fed.R.Evid., and not more prejudicial than probative under Rule 403, Fed.R.Evid., causation was an issue of weighing the evidence that was left to the jury. An example of the traditional approach can be found in a ease where the plaintiff alleged that a herbicide, paraquat, which he handled in liquid form at work, caused his injury: Plaintiffs’ theory of recovery was thus that paraquat, when absorbed through the skin, can attack the lungs in such a way as to cause chronic and self-perpetuating inflammation. Chevron argues that there has never been any evidence or any suggestion that paraquat can cause chronic injury of this sort_ The short answer to Chevron’s argument is that two expert witnesses refuted it and that the jury was entitled to believe those experts.... The experts on both sides relied on essentially the same diagnostic methodology; they differed solely on the conclusions they drew from the test results and other information. The case was thus a classic battle of the experts, a battle in which the jury must decide the victor. Ferebee v. Chevron Chem. Co., 736 F.2d 1529, 1535 (D.C.Cir.1984); cert. denied, 469 U.S. 1062, 105 S.Ct. 545, 83 L.Ed.2d 432 (1984). The D.C. Court of Appeals summarized the proper deference to be given a jury’s resolution of conflicting expert opinions in Ferebee: 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 experts are willing to testify that such a link exists, it is for the jury to decide whether to credit such testimony. 736 F.2d at 1634. Under this traditional view, provided the expert’s credentials have been established, courts have been understandably reluctant to evaluate such testimony: As a general rule, questions relating to the bases and sources of an expert’s opinion affect the weight to be assigned that opinion rather than its admissibility and should be left for the jury’s consideration. . Viterbo v. Dow Chem. Co., 826 F.2d 420, 422 (5th Cir.1987); see also Dixon v. International Harvester Co., 754 F.2d 573, 580 (5th Cir.1985); Graham v. Wyeth Lab., Div. Am. Home Prods. Corp., 906 F.2d 1399, 1404 (10th Cir.1990) (“the fact that Wyeth alleged that the evidence of causation was misconceived and that examined properly, the evidence would result in a finding of no causal connection between the DTP vaccine and [plaintiffs’] injury, is of no relevance”). Cf. Wilson v. Merrell Dow Pharmaceuticals, Inc., 893 F.2d 1149, 1155 (10th Cir.1990) (“When the evidence is in conflict, the jury alone has the power to weigh that evidence and assess the credibility of witnesses, and we will not retry the facts.”); McMahon v. Eli Lilly & Co., 774 F.2d 830, 834-35 (7th Cir.1985) (jury is to decide whether to credit expert testimony regarding causal link between toxic chemicals and human diseases). The courts’ fidelity to this traditional standard of deference has cracked in the face of huge cases and huge jury awards based on doubtful or nonexistent scientific evidence. Expert evidence in toxic tort cases has led courts to superimpose or replace the standard of deference "with a threshold of causation designed to eliminate a perceived abuse of expert testimony in the context of certain alleged toxins. Toxic tort litigation over Bendectin (a drug marketed until 1983 for morning sickness) alleged to cause birth defects, and over Agent Orange (sprayed as a defoliant in Vietnam) demonstrate the changes in the law. Even before the Supreme Court’s recent decision in Ddubert, — U.S. at -, 113 S.Ct. at 2789-90, the increasing criticism of expert witnesses together with the close scrutiny given expert testimony in Agent Orange and the Bendectin cases has had an influence on expert testimony in general. See, e.g., Peter Huber, Galileo’s Revenge: Junk Science in the Courtroom (1991). “The preliminary returns are in, and they are mixed. But a significant proportion of the cases accept Agent Orange and the Bendectin decisions as having tightened the evidentiary screws in toxic cases generally,” Michael D. Green, Expert Witnesses and Sufficiency of Evidence in Toxic Substances Litigation: The Legacy of Agent Orange and Bendectin Litigation, 86 Nw.U.L.Rev. 643, 671 (1992) [hereafter Green, Expert Witnesses ]. The question has recently been considered by the Supreme Court in Daubert, whose holding requires the judge to make his own assessment of whether the methodology underlying the expert’s opinion is fundamentally sound. Such a threshold evaluation of the expert’s methodology, even though it still leaves the evaluation of the weight of the evidence to the jury, limits the “battle of the experts.” 1. Agent Orange Litigation In Agent Orange II, Judge Weinstein found the plaintiffs’ evidence that the dioxin in Agent Orange caused their injuries insufficient as a matter of law because he found they needed epidemiological evidence to establish causal connections between dioxin and diseases in individual plaintiffs: In a mass tort case such as Agent Orange, epidemiologic studies on causation assume a role of critical importance. Cf. In re Swine Flu Immunization Prod. Liab. Litig., 508 F.Supp. 897, 907 (D.Colo.1981) (“(w)here ... the exact organic cause of a disease cannot be scientifically isolated, epidemiologic data becomes highly persuasive.”), aff'd sub nom. Lima v. United States, 708 F.2d 502 (10th Cir.1983). Confronted with the reality of mass tort litigation, courts have been forced to abandon their traditional reluctance, to rely upon epidemiological studies. Dore, A Commentary on the Use of Epidemiological Evidence in Demonstrating Cause-in-Fact, 7 Harv.Envtl.L.Rev. 429 (1983). 611 F.Supp. at 1240 (dismissing the claims of the opt-out plaintiffs on the merits). In order to assess the accuracy of the conclusions of the plaintiffs’ experts, Judge Weinstein reviewed in detail the major studies upon which the plaintiffs relied, after eliminating from his analysis those studies which did “not provide substantial support to plaintiffs because of their small size, self-selective nature and other defects.” Agent Orange I, 597 F.Supp. at 787. Instead, Judge Weinstein focused on what he considered to be the two most significant studies, described in his opinion as the Ranch Hand Study, conducted by the Air Force, and the CDC Birth Defect Study, conducted by the Center for Disease Control. The Ranch Hand Study compared 1024 matched pairs of men for analysis and studied essentially all the veterans who had participated in the fixed wing spraying in Vietnam and who could be located. See id. at 788. Although the “report concludes that there is insufficient evidence to support a cause and effect relationship,” Judge Weinstein noted that the study “offers no solace to either defendants or plaintiffs in the instant litigation. It simply seems inconclusive.” Id. at 788. Judge Weinstein analyzed the data compiled by the CDC Birth Defect Study in detail, including in his opinion tables which demonstrated that some indications of a slightly higher incidence of birth defects (such as cleft pallet or spina bifida) were counterbalanced by slightly lower incidence of others (such as cardiovascular defects). Judge Weinstein concluded that these “variations would not seem to be significant in a tort ease such as the one before us.” Id. at 790. An independent analysis of Australian veterans of the Vietnam war, also included in the CDC Birth Defects Study, revealed no increased risks of all types of birth defects. See Id. at 793. Independent reviews of the literature about dioxin prepared at the request of the Veterans’ Administration and other studies “leave the reader with the conclusion that there may be some causal connection between Agent Orange exposure and present diseases,” but nothing more. Id. at 794; see also In re “Agent Orange” Prod. Liab. Litig., 603 F.Supp. 239 (E.D.N.Y.1985) (claims of wives and children dismissed partly due to same lack of scientific evidence). In Agent Orange II, Judge Weinstein decided the fate of the opt-out members of the class of the Vietnam veteran plaintiffs. He considered a number of additional studies in this opinion, including at least two which apparently were released after Agent Orange I. See 611 F.Supp. at 1240. However, Judge Weinstein did not examine the reports themselves again, but merely noted that the new studies echoed the inconclusive results of the studies already on the record. Comparing the scientific proof with the testimony of the plaintiffs’ experts, however, led the court to conclude that in the absence of any direct proof of causation or of any medical examination of the plaintiffs, the plaintiffs’ physicians were not able to testify that the studies were evidence of causation. 2. Daubert, Bendectin, and the Admissibility of Scientific Evidence Agent Orange was filed and settled as a class action in the Eastern District of New York, and the plaintiffs’ claims never went to trial. Litigation over the drug Bendectin, by contrast, took place around the country, and unlike the actions arising from Agent Orange in which the experts never examined the plaintiffs, it involved cases in which treating physicians testified that the plaintiffs’ injuries were directly caused by the drug to a reasonable degree of medical certainty. The Supreme Court has recently decided one of these cases. See Daubert, — U.S. at -, 113 S.Ct. at 2789-90. The decision affirmed the role of the trial judge as “gatekeeper” on the question of the admissibility and effect of scientific evidence. Although it vacated the lower court decision on the standards for admitting evidence, the result of Daubert is a reflection of an emerging consensus in the courts, many of which are surveyed below. The lower court decision in Daubert v. Merrell Dow Pharmaceuticals, Inc., 951 F.2d 1128 (9th Cir.1991), relied upon the Frye test to determine that the plaintiffs expert’s rea-nalyses of epidemiological evidence on Bendectin was inadmissible evidence. The decision in Frye v. United States, 54 App.D.C. 46, 47, 293 F. 1013 (1923), accurately characterized by the Supreme Court as “short and citation-free,” Daubert, — U.S. at -, 113 S.Ct. at 2792-93, held the results of a test by an early lie-detector machine inadmissible. Frye created what became known as the “general acceptance” test for the admissibility of evidence: 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. Daubert, — U.S. at -, 113 S.Ct. at 2792-93 (quoting Frye, 54 App.D.C. at 47, 293 F. at 1014). The decision in Daubert kills Frye and then resurrects its ghost. The Supreme Court held that the Frye test for the admissibility of scientific evidence had been superseded by the enactment of the Federal Rules of Evidence, similar to the holding of the Second Circuit in United States v. Williams, 583 F.2d 1194 (2d Cir.1978), cert. denied, 439 U.S. 1117, 99 S.Ct. 1025, 59 L.Ed.2d 77 (1979). However, the court made it clear that the Federal Rules of Evidence themselves place certain limits on the admissibility of purportedly scientific evidence, for “under the Rules the trial judge must ensure that any and all scientific testimony or evidence admitted is not only relevant, but reliable.” Daubert, — U.S. at -, 113 S.Ct. at 2795. The trial judge’s function of determining the “reliability” of the evidence provides the mechanism for screening junk science. Faced with a proffer of expert scientific testimony, then, the trial judge must [make] ... a preliminary assessment of whether the reasoning or methodology underlying the testimony is scientifically valid and of whether that reasoning or methodology properly can be applied to the facts in issue- Many factors will bear on the inquiry, and we do not presume to set out a definitive checklist or test. But some general observations are appropriate. Daubert, — U.S. at -, 113 S.Ct. at 2796. The Court isolated four: whether the expert’s methodology had been tested, whether the theory or technique had been subjected to peer review and publication, whether the known or potential rate of error — here, the “confidence interval” — cast the results in doubt, and, finally, echoing Frye, whether the methodology meets with “general acceptance” in the scientific community. The opinion does address the question of the sufficiency of the evidence: [I]n the event the trial court concludes that the scintilla of evidence presented supporting a position is insufficient to allow a reasonable juror to conclude that the position more likely than not is true, the court remains free to direct a judgment.... These conventional devices, rather than wholesale exclusion under an uncompromising “general acceptance” test, are the appropriate safeguards where the basis of scientific testimony meets the standards of Rule 702. Daubert, — U.S. -, 113 S.Ct. at 2798. The Supreme Court cited Brock v. Merrell Dow Pharmaceuticals, Inc., 874 F.2d 307 (5th Cir.) (“Brock I ”), modified, 884 F.2d 166 (5th. Cir.1989) (“Brock II”), reh’g denied, 884 F.2d 167 (5th Cir.1989) (en banc) (“Brock III”), cert. denied, 494 U.S. 1046, 110 S.Ct. 1511, 108 L.Ed.2d 646 (1990), as an example of judgment appropriately granted as a matter of law based on insufficiency of the evidence. In Brock I, the Court of Appeals for the Fifth Circuit held: [o]ne certainly might infer from the evidence in the case that Bendectin causes birth defects, and further that Bendectin caused Rachel Brock’s limb reduction defect — in fact, the jury concluded that this very thing occurred. However, the court must determine whether this is a reasonable inference to be drawn from the evidence presented. 874 F.2d at 309. The court modeled its logic on Judge Weinstein’s opinion in Agent Orange II: “We are not without precedent in our approach to this problem. The case before us parallels in many respects the recently conducted Agent Orange Litigation.” Brock I, 874 F.2d at 310; see also id. at 310 n. 11. The Brocks’ major evidence was a reanalysis by their expert of a previously conducted study which had found no increase in risk of birth defects due to Bendectin. After the plaintiffs’ expert admitted that the confidence interval in his reanalysis made it statistically insignificant, the court noted that the plaintiffs’ expert had not published his results for peer criticism and review. While we do not hold that this failure, in and of itself, renders his conclusions inadmissible, courts must nonetheless be especially skeptical of medical and other scientific evidence that has not been subject to thorough peer review.... We find, in this case, the lack of conclusive epidemiological proof to be fatal to the Brock’s case. Id. at 313. The Brock court concluded that it hoped its decision would have the effect of encouraging district judges faced with medical and epidemiological proof in subsequent toxic tort cases to be especially vigilant in scrutinizing the basis, reasoning, and conclusiveness of studies presented by both sides. Id. at 315. Upon rehearing, the court replaced its use of the phrase “conclusiveness of studies” with “statistically significant studies.” Brock II, 884 F.2d 166, 167. Six of the judges dissented from the refusal of another rehearing en banc, maintaining that Brock I unavoidably changed the law: Six highly qualified and experienced experts testified that Bendectin is a human teratogen, i.e. capable of causing human birth defects. Three of them testified to the opinion that Bendectin was a cause of Rachel Brock’s deformation_ The panel's] characterization of this voluminous expert proof as “speculation” could just as well doom virtually all expert testimony. The panel ... [even] enters into the debate with Dr. Glasser on the statistical significance of the Heinonen study.... Brock III, 884 F.2d at 168. Brock I is an unusual case because it so broadly addressed the issue of toxic substances. Acknowledging the traditional deference afforded medical experts, the court, echoing Judge Weinstein in Agent Orange, contended that toxic substances litigation is different and requires a more critical analysis of expert witnesses. By relying on Agent Orange and broadly addressing toxic substances, the court expanded the potential scope of its decision beyond the prior Bendectin opinions.... The effect of the panels’ decision [in Brock III ] was to make insufficient any expert’s opinion not grounded in a statistically significant epidemiologic study. That may have been a meat-cleaver solution to expert witness abuse, but it surely is a solution, at least in the toxic substances arena. Green, Expert Witnesses, at 666 & n. 107. The Brock opinions were relied on by a district court granting judgment n.o.v. after a jury awarded $1,000,000 to a plaintiff who alleged the drug Accutane caused her seizures. See Thomas v. Hoffman-La Roche, Inc., 731 F.Supp. 224 (N.D.Miss.1989), aff'd, 949 F.2d 806 (5th Cir.1992). The trial court held that Brock required at least some “statistically significant epidemiological proof.” 731 F.Supp. at 228. In reaching his opinion that Accutane caused the 1984 seizures and neurological problems, it appears to the court that Dr. Mahalak relied primarily on his elimination of other causes.... In this regard the court must note that the opinion expressed [by four other doctors] that the seizures were viral in origin. Id. at 227. In the opinion of the court, the absence of any meaningful testimony either providing an explanation of how Accutane could cause the seizures or epidemiological evidence that it did warranted setting aside the jury verdict and entering judgment in favor of the defendant. The scrutiny recommended by the court in Brock I was extended by the Fifth Circuit to the admissibility of expert evidence in Christophersen v. Allied-Signal Corp., 939 F.2d 1106 (6th Cir.1991), cert. denied, — U.S. -, 112 S.Ct. 1280, 117 L.Ed.2d 506 (1992), where the plaintiffs expert had testified that the plaintiffs small-cell colon cancer (carcinoma) had to be the result of his exposure to toxic nickel and cadmium fumes because carcinoma of the lung was associated with such fumes. The court affirmed the trial court’s exclusion of this testimony, absent any proof of scientific evidence of causation, by holding that the methodology or reasoning that the expert uses to connect the facts to his conclusion must be generally acceptéd within the relevant scientific community, a conclusion which under Daubert is now only part of the test for the reliability of evidence. In the D.C. Circuit, which allowed the novel claim of injury due to paraquat in Ferebee, the validity of the scientific evidence was invoked in eases where the court refused to follow Ferebee for claims based on exposure to Bendeetin: Ferebee stands for the proposition that courts should be very reluctant to alter a jury’s verdict when the causation issue is novel and “stand[s] at the frontier of current medical and epidemiological inquiry.... The ease before us, however, is not like Ferebee. Indeed, we are at the other end of the spectrum, a great distance from the ‘frontier of current medical and epidemiological inquiry.’ And far from a paucity of scientific information on the oft-asserted claim of causal relationship of Bendeetin and birth defects, the drug has been extensively studied and a wealth of published epidemiological date has been amassed, none of which has concluded that the drug is teratogenic. Uniquely to this case, the law now has the benefit of twenty years of scientific study, and the published results must be given their just due. Richardson v. Richardson-Merrell, Inc., 857 F.2d 823, 832 (D.C.Cir.1988), cert. denied, 493 U.S. 882, 110 S.Ct. 218, 107 L.Ed.2d 171 (1989). The court in Richardson reviewed the epidemiological evidence in order to determine whether the plaintiff’s physician’s opinion had an adequate basis. After eliminating the chemical, in vitro, and invivo studies as inadequate (as Judge Weinstein had done in Agent Orange I, 597 F.Supp. at 782-95, and Agent Orange II, 611 F.Supp. at 1241) the court looked at the epidemiological studies showing the effects of Bendeetin and rejected the results as the Fifth Circuit had done in Brock I: [Thé plaintiffs expert] further admitted that no one who has published work on Bendeetin has concluded that there is a statistically significant association between Bendeetin and limb reduction defects of the type at issue in this case. Only by recalculating the data was [plaintiffs expert] able to obtain what he deems a statistically significant result. Moreover, the studies rejected by [plaintiffs expert] had been published in peer-reviewed scientific journals, while [the expert]' has neither published his recalculations nor offered them for peer review. Richardson, 857 F.2d at 831. After Richardson, in Ealy v. Richardson-Merrell, Inc., 897 F.2d 1159 (D.C.Cir.1990), cert. denied, 498 U.S. 950, 111 S.Ct. 370, 112 L.Ed.2d 332 (1990), the Court again distinguished Ferebee in overturning a jury award of $20,000,000 in compensatory damages and $75,000,000 in punitive damages to a plaintiff despite the complete lack of scientific proof that Bendeetin actually caused the type of harm alleged: The Richardson court concluded, as a matter of law, that the “wealth of published epidemiological data ... none of which has concluded that the drug is teratogenic ... must be given their just due.” ... [U]nder Rule 703, an opinion refuting this scientific consensus is inadmissible for lack of an adequate foundation, in the absence of other substantive probative evidence on which to base this opinion. It is this uncontroversial rale of evidence that is the ratio decidendi of Richardson and this case. Ealy, 897 F.2d at 1162. However, the D.C. Court has emphasized that the logic in the Bendectin cases applies only to cases where the science is “far from the frontier of current medical and epidemiological inquiry.” Richardson, 857 F.2d at 832. Experts who allege a factual basis for their conclusion must be allowed to testify as long as the trial court can verify that their methodology is sound. In Ambrosini v. Labarraque, 966 F.2d 1464 (D.C.Cir.1992), where the plaintiff alleged damages from Bendectin and another progesterone, Depo-Provera, and the Court held admissible expert testimony which the plaintiff had merely promised was based on “the available scientific epidemiological data concerning progestin and progesterone agents.” Id. at 1470. The Court held that the plaintiffs should be given their chance to prove causation, but it cautioned that “[t]he Ferebee court noted the difference between expert opinion based on controversial techniques or methods and expert opinion based on well-founded methods but which reaches a novel, and perhaps controversial, conclusion.” 966 F.2d at 1467. In Turpin v. Merrell Dow Pharmaceuticals, Inc., 959 F.2d 1349 (6th Cir.1992), cert. denied, — U.S. -, 113 S.Ct. 84, 121 L.Ed.2d 47 (1992), the Sixth Circuit affirmed summary judgment dismissing Bendectin litigation on the ground that the scientific evidence of causation was simply too insufficient as a matter of law, as the Fifth Circuit did in Brock: [Although judges should respect scientific opinion and recognize their own limited scientific knowledge, nevertheless courts have a duty to inspect the reasoning of qualified scientific experts to determine whether a ease should go to the jury. Based on the record before us, we also agree with Judge Siler that whether Ben-dectin caused the minor plaintiffs birth defects is not known and is not capable of being proved to the requisite degree of legal probability based on the scientific evidence currently available. Turpin, 959 F.2d at 1350. In arriving at its holding, the Sixth Circuit examined six representative studies of the more than 35 studies of Bendectin that it found in medical and scientific journals. The Court of Appeals repeated the relevant statistical information about each study in its opinion, including the sample size in each of the relevant studies, the names of the researchers and place of the publication of the research, confidence intervals, and whether the study was considered “statistically significant.” The Court of Appeals affirmed entry of summary judgement for the defendants because: the plaintiffs’ experts stop short of testifying that Bendectin more probably than not caused the birth defects in babies. They stop short because they have no factual or theoretical basis for a stronger hypothesis.... The analytical gap between the evidence presented and the inferences to be drawn on the ultimate issue of human birth defects is too wide. Under such circumstances, a jury should not be asked to speculate on the issue of causation. Id. at 1360-61. In Lynch v. Merrell-Nat’l Lab. Div. of Richardson-Merrell, Inc., 646 F.Supp. 856 (D.Mass.1986) (“Lynch I”), aff'd, 830 F.2d 1190 (1st Cir.1987) (“Lynch II”), the court examined eleven cohort studies and four ease control studies of epidemiological evidence, none of which demonstrated a statistically significant association between Bendectin and birth defects. These results were confirmed by epidemiological studies of population groups, including one which indicated that, while Bendectin usage declined from more than one million in 1979 to zero in 1984, there was no change in the incidence of limb reduction defects. Finally, a combined estimate of the relative risk for ten of the cohort studies found no statistical difference between the rate of birth defects among those exposed and those not exposed. The only epidemiological evidence offered by the plaintiffs is a re-analysis ... criticizing a study ... of the Center on Disease Control, and attempting to realign the data in the original study to demonstrate causal connection between Bendectin and birth defects.... Even if this Court were to find the methodology of ... re-analysis credible, this Court still could not accept result-oriented re-analysis of epidemiological studies and criticisms of others’ methodology ... as reliable data upon which to base on opinion on causation. The plaintiffs cannot merely rely on criticisms of the defendants’ studies to establish causation. Lynch I, 646 F.Supp. at 865. In affirming the decision, the First Circuit added: On the basis of the epidemiological evidence to date, Bendectin is as likely as aspirin to cause limb reduction.... The ignorance that prevails as to the etiology of most birth defects does not mean causation in a given case could not be proven; it does mean that there is a large terra in-cognita where gossip and guesswork abound, so that courts must carefully control the basis for testimony pointing to a particular cause.... The plaintiffs offered no new study [demonstrating that Bendectin caused their harm]. Lynch II, 830 F.2d at 1194. Against this background of the state of law and accepting as axiomatic that without more than credentials and a subjective opinion, an expert’s testimony that “it is so” is not sufficient to sustain a jury’s verdict, see Viterbo, 826 F.2d at 424, the epidemiological, clinical, and experimental studies testified to at trial by the Plaintiffs experts must be carefully scrutinized to determine whether they are, in fact, sufficient. III. The Plaintiff’s Causation Proof A. The Sufficiency Criteria: Evaluating The Sufficiency Of The Plaintiffs Epidemiological Evidence As has been noted, if an epidemiological study reveals that the SMR between exposure to carcinogen c and the subsequent development of disease din a cohort is greater than 2.0, that SMR is statistically significant and supports the conclusion that c and d are causally linked. This statistical conclusion also justifies the proposition that it is more likely than not that individual A’s exposure to c is the cause d in A. However, this is not the end of the analysis to determine whether the Plaintiffs causation proof is sufficient to withstand the Defendants’ motions for judgment as a matter of law. There are several additional criteria that have to be taken into consideration in assessing the conclusions of an epidemiological study to determine the soundness of an allegedly statistically significant SMR. In order to assess fully the accuracy of the conclusions offered in an epidemiological study regarding a purported causal relationship between exposure to c and the subsequent development of d, several factors must be considered. The SMR is only one of these factors, and it defines the strength of the possible association between exposure to c and the development of d. In addition to considering the SMR, the following five factors must be analyzed to assess accurately whether or not evidence has achieved the status of scientific knowledge (collectively, the “Sufficiency Criteria”): first, the consistency of the association between c and d, which raises the question, Is the SMR of a single epidemiological study addressing the relationship between c and d consistent with the SMRs derived in other epidemiological studies?; second, the dose-response relationship between c and d: What is the epidemiological response in a cohort to estimated doses of c?; third, the results of experimental studies: Have experimental studies been conducted on animals, for example, and if so, were they positive?; fourth, the plausibility of there being a biological link between c and d: Given the biological and chemical mechanisms involved, what is the degree of probability that exposure to c can give rise to the subsequent development of d,V, and fifth, the coherence between c and d: How many “confounding” or alternative factors or conditions can contribute to the development of d in A? And how difficult is it to exclude these confounding conditions thereby isolating A’s exposure to c as the statistically significant and “more likely than not” cause of d in A? While none of the Sufficiency Criteria is decisive by itself in determining the sufficiency of a plaintiffs epidemiological evidence in the context of a Rule 50(b) motion, sufficient epidemiological evidence will necessarily satisfy several of these criteria. More significantly, when epidemiological evidence fails to satisfy any of the Sufficiency Criteria, it cannot be relied on to support a jury verdict in the face of a motion for judgment as a matter of law. B. The Epidemiological Evidence When the Sufficiency Criteria are applied to the epidemiological evidence offered at trial by the Plaintiffs experts, the Plaintiffs causation proof only weakly satisfies the plausibility criterion and fails to satisfy any of the other Sufficiency Criteria. Therefore, the Plaintiffs proof fails to support the jury’s conclusion that Maiorana’s exposure to asbestos was the proximate cause of his colon cancer, and the Defendants’ Rule 50(b) motions must be granted. 1. Strength and Consistency of Association Of course, the stronger and more consistent an association, the more likely it represents a cause-and-effect relationship. Weak associations often turn out to be spurious and explainable by some known, or as yet unknown, confounding variable. In order for an association to be spurious, the underlying factor that explains it must have a stronger relationship to the disease than the suspected causal factor. When the causal factor under consideration is strongly related to the disease, it is likely, although not certain, that the underlying variable with the necessarily even stronger relationship to the disease would be recognizable. Strength of association is usually measured by the relative risk or the ratio of the disease rate in those with the factor to the rate in those without. The relative risk of lung cancer in cigarette smokers as compared to nonsmokers is on the order of 10:1, whereas the relative risk of pancreatic cancer is about 2:1. The difference suggests that cigarette smoking is more likely to be a causal factor for lung cancer than for pancreatic cancer. Landrigan, 127 N.J. at 416, 605 A.2d 1079. Consistency is measured by comparing the association between a purported cause and effect identified in one study with the results of other studies and with other relevant scientific knowledge. During the course of the trial, approximately 45 epidemiological studies and surveys of studies were discussed by the parties’ experts, by Drs. Steven Markowitz (“Markowitz”), Carl Shy (“Sh