Appeal from the Order of the Superior Court entered April 30, 2010 at No. 1058 WDA 2006, reversing the Order of the Court of Common Pleas of Allegheny County entered May 10, 2006 at No. GD 05-4662 and remanding.
The opinion of the court was delivered by: Mr. Justice Saylor
The civil action underlying this appeal was selected as a test case for the admissibility of expert opinion evidence to the effect that each and every fiber of inhaled asbestos is a substantial contributing factor to any asbestos-related disease. The inquiry has proceeded under principles derived from Frye v. United States, 293 F. 1013 (D.C. Cir. 1923).
In February 2005, Charles Simikian commenced a product liability action against Allied Signal, Inc., Ford Motor Company ("collectively Appellants"), and others, asserting causes of action grounded on multiple theories including strict liability. Mr. Simikian alleged that, throughout a forty-four year career as an automotive mechanic, his exposure to asbestos-containing friction products, such as brake linings, caused his mesothelioma. Upon Mr. Simikian's death, his wife, acting as executrix ("Appellee"), substituted as the plaintiff.
Appellee's action was among a number of similar ones pending in the court of common pleas. Two of the common defendants in these cases anticipated that the plaintiffs would rely on expert opinion that each and every exposure to asbestos -- no matter how small -- contributes substantially to the development of asbestos-related diseases. This opinion often is referred to as the "any-exposure," "any-breath," or "any-fiber" theory of legal (or substantial-factor) causation. See generally Summers v. Certainteed Corp., 606 Pa. 294, 316, 997 A.2d 1152, 1164-65 (2010) (discussing the requirement for a plaintiff to prove that a defendant's product was a substantial factor in causing injury).
Seeking to preclude such opinion testimony, these defendants filed global motions challenging its admissibility under the litmus of general acceptance in the relevant scientific community applicable to novel scientific evidence.*fn1 See Pa.R.C.P. No. 207.1; Commonwealth v. Topa, 471 Pa. 223, 231-33, 369 A.2d 1277, 1281-82 (1977) (confirming Pennsylvania's adherence to the Frye test; explaining that it bars novel scientific evidence from the courtroom until it has achieved general acceptance in the relevant scientific community; and indicating that strict application of the test is required to ensure fairness). The defendants referenced a litany of techniques used for various purposes in science (e.g., chemical structure analysis; anecdotal case reporting; reliance on animal studies; and extrapolation to a cause-and-effect relationship), arguing that none of these -- alone or in combination -- supports the any-exposure theory. See, e.g., Amended Global Frye Motion of June 3, 2005, In re Toxic Substance Cases, No. A.D. 03-319 (C.P. Allegheny). Highlighting the trial court's role in screening scientific evidence for reliability before permitting such evidence to be put before a jury, see, e.g., Grady v. Frito-Lay, Inc., 576 Pa. 546, 557, 839 A.2d 1038, 1044-45 (2003), the defendants contended that the methodology underlying the any-exposure theory is novel and scientifically invalid. Thus, they urged that the any-exposure theory should be deemed inadmissible at all trials of asbestos cases against them.
The common pleas court, per the Honorable Robert J. Colville, directed the parties to designate test cases through which to address the Frye challenge, among which the present one was selected. The court also required an exchange of expert reports, which were to identify, in particular, the opinions and methodology supporting the plaintiffs' theory that exposure to friction products was a proximate cause of asbestos-related disease. See Order of June 23, 2005, In re Toxic Substance Cases, No. A.D. 03-319 (C.P. Allegheny). The plaintiffs identified a pathologist as their primary causation expert -- John C. Maddox, M.D. -- and submitted his report. As relevant here, the core explanation Dr. Maddox provided for his opinion as to specific and proximate causation is as follows:
Asbestos-related mesothelioma, like other diseases induced by toxic exposures, is a dose response disease: each inhalation of asbestos-containing dust from the use of products has been shown to contribute to cause asbestos-related diseases, including mesothelioma. Each of the exposures to asbestos contributes to the total dose that causes mesothelioma and, in so doing, shortens the period necessary for the mesothelioma to develop. . . . [E]ach exposure to asbestos is therefore a substantial contributing factor in the development of the disease that actually occurs, when it occurs.
Affidavit of John C. Maddox, M.D., of Aug. 4, 2005, at 12 (emphasis added). In his report, Dr. Maddox did not provide an assessment of the individual exposure histories for the test plaintiffs, presumably as this was thought to be unnecessary, given the breadth of the any-exposure theory.
In response, the defendants proffered a report from M. Jane Teta, Dr.P.H., M.P.H., an occupational environmental epidemiologist, who couched Dr. Maddox's any- exposure opinion as nothing more than a mere assumption. See Expert Report of M. Jane Teta, Dr.P.H., M.P.H., of Aug. 16, 2005 ("Teta Report"), at 9. According to Dr. Teta, Dr. Maddox did not follow the scientific method in proceeding from hypothesis through scientific proof in support of his conclusions. Rather, she asserted, the pathologist ignored an established hierarchy of scientific evidence; employed a selective approach to the scientific literature; and, in particular, disregarded a wealth of epidemiological evidence to the effect that those who work with automotive friction products do not suffer from a higher incidence of mesothelioma than is found in the general population. See supra note 1. Additionally, Dr. Teta observed that the any-exposure opinion is inconsistent with the common understanding that the context and circumstances of exposure to toxic substances -- including the critical component of dose -- matter greatly in terms of determining the risk of disease. See generally Bernard D. Goldstein, Toxic Torts: The Devil Is In the Dose, 16 J.L. & POL'Y 551, 551 (2008) ("Dose is a central concept in toxicology -- 'the dose makes the poison' is the oldest maxim in the field."). Furthermore, she found that Dr. Maddox exceeded the range of his expertise in rendering a broad-scale opinion concerning the theoretical impact of a single asbestos fiber. See Teta Report at 10-11.
In ensuing arguments before Judge Colville, the plaintiffs contended that a Frye challenge was inapposite. In their view, Dr. Maddox's methodology in forming his any-exposure opinion was in no way novel, but rather, resided within the scientific mainstream.*fn2 The plaintiffs pointed to the wealth of scientific information developed over time concerning the hazards of asbestos, see N.T., Aug. 17, 2005, at 84-85 (reflecting the plaintiffs' observation that "[t]he medical literature has been talking about the effects of asbestos chrysotile since the 1920s"), and to government regulatory responses to protect human health. See, e.g., id. at 88-89 ("Now, the Environmental Protection Agency, their stance on this issue is that asbestos causes asbestos diseases, specifically chrysotile causes asbestos diseases and, more specifically, brake linings cause asbestos disease."). Downplaying the necessity for epidemiological evidence, see, e.g., id. at 99 ("[E]pidemiology studies are not the sine qua non as to whether there is cause and effect."), the plaintiffs asserted that conclusions favorable to their position could be drawn from such evidence in any event. Furthermore, they emphasized that their position was consistent with the admission of opinion evidence reflecting the any-exposure theory in other cases, most notably, Smalls v. Pittsburgh-Corning Corp., 843 A.2d 410 (Pa. Super. 2004). See id. at 414 (indicating that "this type of opinion evidence is not only admissible, it is sufficient to demonstrate a prima facie case of liability against an asbestos manufacturer if believed by the fact finder").
Based on the any-exposure theory, a plaintiff's attorney couched the plaintiffs' position with regard to specific causation as follows:
[Y]ou don't have to look at each individual, you don't have to look at Mopar brakes and then look at Bendix brakes. You don't look at that. You don't even look at whether it is brakes or gaskets. You don't even look whether it is brakes or pipe covering. It doesn't matter. As a matter of law, you just say, hey, you breathed asbestos from a product, oh, you are going to the jury. Just as a matter of law, the courts, as a matter of law, you do not distinguish between products.
N.T., Aug. 17, 2005, at 75-76; see also id. at 83. Thus, from the plaintiffs' point of view, any questions concerning the any-exposure theory were credibility matters to be addressed by a jury. See id. at 80 ("This is not novel stuff. Any kind of problems they have with this is for cross-examination."). Finally, the plaintiffs highlighted a desire, on the part of courts, to limit the range of cases in which a Frye-type inquiry would be necessary. See id. at 84 ("The Trach case also says that, [']Our Supreme Court does not intend that trial courts be required to apply the Frye standard every time scientific experts are called to render an opinion at trial, a result that is nothing short of Kafkaesque to contemplate.[']" (quoting Trach v. Fellin, 817 A.2d 1102, 1110 (Pa. Super. 2003) (en banc))).
The defendants, on the other hand, argued that the concept of "novelty," as applied to scientific evidence, does not necessarily mean "new," but, rather, applies where there is a colorable challenge to whether the methodology used by an expert enjoys general support in the relevant scientific community. From their perspective, this is the only approach that would allow trial judges to fulfill their screening function to assure sufficient reliability and thus lessen the possibility for jurors to be misled by expert witnesses. On the merits, the defendants' position was consistent with their motion and Dr. Teta's report.
Judge Colville felt the defendants had raised sufficient questions about Dr. Maddox's methodology to warrant further inquiry. He did not question the pathologist's opinion in terms of general causation, but he expressed circumspection concerning how that opinion translated to substantial-factor causation. See N.T., Aug. 17, 2005, at 105. For example, he remarked:
The vast majority of what [Dr. Maddox] says seems to be based in long-standing traditional scientific principles, understood quantities and characteristics of asbestos generally, but that portion of what he says relates only to . . . the general risks associated with asbestos. Where Maddox' opinion becomes . . . novel in that it is new, original or striking is when he attempts to extrapolate down to the position that each and every fiber contributes to the disease process. . . . Without that statement, I have no causation as to any of the specific plaintiffs. You need that element of Maddox' report to prove causation to each plaintiff.
Id. at 105-06 (emphasis added).
Accordingly, the common pleas court centered its focus on the use of extrapolation, which it found to be a linchpin of Dr. Maddox's methodology and opinion supporting a finding of proximate cause. See N.T., Aug. 17, 2005, at 107-08. Along such lines, the court expressed concern with an "analytical gap" between the scientific proofs and the pathologist's conclusion. N.T., Oct. 17, 2005 (a.m.), at 21-22. A Frye hearing ensued, which was supplemented by other testimonial and documentary evidence.
In his direct testimony, Dr. Maddox discussed the chrysotile asbestos fibers which were integrated into automotive friction products in relevant time periods, finding them to be carcinogenic along the lines of other, more potent varieties of such fibers. See, e.g., N.T., Oct. 17, 2005 (a.m.), at 64-66.*fn3 The pathologist discussed the different activities of automotive mechanics that can create dust from automotive friction products, such as opening boxes containing brake parts, sanding or grinding brake linings, and using compressed air to blow dust from friction product parts. See id. at 89-91, 101; N.T., Oct. 17, 2005 (p.m.), at 16-17. He also highlighted the long latency period between asbestos exposure and the manifestation of disease, with the minimum time lapse being about ten years. See id. at 15-16. As pertains to the risk of developing mesothelioma, Dr. Maddox indicated that no safe level of exposure has ever been determined for any type of asbestos. See N.T., Oct. 17, 2005 (a.m.), at 69.
As a component of this testimony in support of the plaintiffs' claim of general causation, Dr. Maddox frequently indicated that each and every exposure "should be considered," "contributes to" and "increase[s] the risk of" asbestos-related diseases. See, e.g., N.T., Oct. 17, 2005 (a.m.), at 80-81, 87, 93. According to his opinion, "it is the total and cumulative exposure that should be considered for causation purposes." Id. at 80-81; accord N.T., Oct. 17, 2005 (p.m.), at 89 (indicting that incremental exposure "would always have to be considered a contributing factor").
Dr. Maddox testified that he used generally accepted methodology in reaching his conclusion that exposure to asbestos fibers by automobile mechanics causes mesothelioma. See, e.g., Oct. 17, 2005 (a.m.), at 71; N.T., Oct. 17, 2005 (p.m.), at 12, 28. By way of further explanation, the pathologist explained that his reasoning followed a series of "small bridges," from "chrysotile is carcinogenic, to the product containing chrysotile, the product releasing chrysotile, people breathing chrysotile, and people developing tumors." N.T., Oct. 17, 2005 (a.m.), at 103; N.T., Oct. 17, 2005 (p.m.), at 11-12.
Dr. Maddox also said that he drew his conclusions from case reports, animal studies, government regulatory assessments, and other scientific and medical literature. See, e.g., N.T., Oct. 17, 2005 (a.m.), at 69-70, 71-82, 85, 94, 103-09; N.T., Oct. 17, 2005 (p.m.), at 7-15, 18. In various passages of his testimony, the pathologist indicated that his opinion was supported by epidemiological science, see, e.g., N.T., Oct. 17, 2005 (a.m.), at 67; N.T., Oct. 17, 2005 (p.m.), at 159, albeit he couched the particular studies directed to automotive workers as "inconclusive," id. at 12, and he did not consider epidemiology appropriate to low-dose exposures, see id. at 13 ("So instead of the broad stroke to make the call from an epidemiologic study, I think one is forced to take the small steps to link together all the parts of the chain."); see also id. at 132. Additionally, while claiming some support in epidemiological science, the witness sought to avoid deeper discussion of the subject matter. See id. at 112 ("I am not really prepared to discuss epidemiology with you.").*fn4 Dr. Maddox did agree that epidemiology is "one branch" of science that addresses the cause and effect of disease in human populations, id. at 92, and that scientists in the field test causation hypotheses; conduct human health studies; accumulate research; publish studies in journals to be reviewed by disinterested peers; and thereby work toward achieving scientific consensus regarding disease causation. See id. at 92-93.
In his methodology, Dr. Maddox acknowledged that he "picked and chose" among studies in support of his opinion, although he didn't believe his selection process necessarily reflected bias. See N.T., Oct. 17, 2005 (p.m.), at 73-74. The following passage from Dr. Maddox's cross-examination reflects some further explanation of his approach to the literature in forming his opinion:
Q. So to summarize your methodology on the specific issue of asbestos exposure and risk associated with being a vehicle mechanic, . . . you chose to both not discuss and ignore numerous conclusions reached by scientist after scientist in the epidemiological field and industrial hygiene field that were consistent as showing no increased risk; correct?
A. It was not a deliberate choice. It was simply an attempt to keep this paper of manageable size and directed at the issue of chrysotile exposure in general.
Q. Dr. Maddox, is one of the reasons why you chose to ignore the epidemiological studies because of your -- I don't mean this condescendingly -- because you didn't understand the role of epidemiology and did not understand those studies? Is that the reason why you didn't include it?
A. No, that is not really the reason. I made no conscious choice to exclude them for any particular reason. It is just that I had plenty of material upon which to base my decision and I used what I had.
N.T., Oct. 17, 2005 (p.m.), at 117-18.
Dr. Maddox found particular support in reports of a 1997 conference of scientists conducted in Helsinki, Finland, which, he related, indicated that an occupational history of asbestos exposure should be enough to establish a causal link to asbestos-related diseases. See N.T., Oct. 17, 2005 (a.m.), at 83-84; N.T., Oct. 17, 2005 (p.m.), at 32-33. According to the pathologist, the conference concluded:
[T]he likelihood that asbestos exposure has made a substantial contribution increases when the exposure increases. Cumulative exposure, on a probability basis, should thus be considered the main criterion for the attribution of a substantial contribution by asbestos to lung cancer risk.
N.T., Oct. 17, 2005 (a.m.), at 84-85.*fn5
Dr. Maddox also offered several analogies to illustrate his opinions, as follows:
[T]he more common analogy that has been used is the example of a glass of water. One drops marbles into the glass of water until the water finally overflows from the glass.
Is it the first marble or the last marble that causes the glass to overflow? Well, both, all of them. The marbles cause the glass to overflow. That's a cumulative effect. Likewise, on another analogy, who won the war? Was it General Eisenhower or every troop in the field?
A third analogy that's been used is the analogy of the boxer who goes nine rounds and finally loses the fight. Was it every blow that the boxer took, or just the last blow that the boxer took? Well, the cumulative effect of all the blows would be the cause of the boxer finally going down.
Once [a fiber] enters the body through the nose, then it doesn't matter where it came from. Then everything becomes equal. That is Ellis Island. You are an American then.
N.T., Oct. 17, 2005 (a.m.), at 85-86; N.T., Oct. 17, 2005 (p.m.), at 141. Indeed, the pathologist expressed the same opinion relative to cigarette smoking, namely, that "[a]ll the cigarettes that one smokes are considered to be contributory to the development of the lung cancer." N.T., Oct. 17, 2005 (a.m.), at 86.*fn6 Accordingly, in his estimation, in terms of asbestos disease causation, it makes no difference if the plaintiff merely worked infrequently on a family vehicle or was a shipyard worker frequently exposed to friable asbestos of the most carcinogenic form. See N.T., Oct. 17, 2005 (p.m.), at 36.
In his testimony, Dr. Maddox frequently couched his role in general terms, namely, to render an opinion that chrysotile asbestos contributes to disease. See, e.g., N.T., Oct. 17, 2005 (p.m.), at 37. Indeed, with regard to the test cases, the pathologist's testimony reflected his unfamiliarity with the test-case plaintiffs' or decedents' history of exposure to asbestos. See id. at 51-52. The witness maintained, however, that exposure to a single asbestos fiber of any type was sufficient to establish causation. See id. at 154.
Nevertheless, Dr. Maddox also gave testimony which is in sharp tension with the any-exposure theory as applied to substantial-factor causation. Among other things, he said:
Now, individual exposures differ in the potency of the fiber to which an individual is exposed, to the concentration or intensity of the fibers to which one is exposed, and to the duration of the exposure to that particular material. So those are the three factors that need to be considered in trying to estimate the relative effects of different exposures. But all exposures have some effect.
N.T., Oct. 17, 2005 (p.m.), at 37 (emphasis added).*fn7
Upon cross-examination, Dr. Maddox agreed that scientists presently do not know the mechanism by which asbestos causes mesothelioma. See N.T., Oct. 17, 2005 (p.m.), at 46, 81, 83 ("The hypothesis of individual mechanisms of mesothelioma formation remains uproven[.]"). Additionally, he recognized that his opinions were not based on any sort of direct attribution, but rather, were grounded entirely upon an assessment of risk. See, e.g., id. at 136-37 ("I believe that once an individual develops a mesothelioma, the risk becomes the cause."). The pathologist further conceded that he was unaware of the guidelines for health assessments offered by a regulatory agency upon which he relied. See id. at 120-21. He also did not wish to agree with the defendants' position that his methodology entailed extrapolation from scientific findings concerning high-dose asbestos exposure (relating to trades such as asbestos mining, insulating, and ship working) to a scenario entailing low-dose exposure (automotive maintenance). See, e.g., id. at 81-83. Instead, Dr. Maddox preferred the word "interpolation" to describe his manner of thinking. Id. at 82.
Judge Colville attempted to engage Dr. Maddox on the topic of specific causation in the following discussion:
THE COURT: . . . [Y]our statement that you can generalize regarding the causation issues once the fiber enters the body is related to what I characterize as general causation issues, not specific causation issues? Not the specific causation of disease in a specific individual, but generally the general causation of positive properties of fiber in a human being generally?
Here is what I am drawing at. A fiber can enter my body and sit for a week, a month, a year and do nothing, or it may cause a disease process. You have ...