1998 WL 299925Only the Westlaw citation is currently available.
Superior Court of Arizona, Maricopa County.
LOFGRENv.
MOTOROLA
No. CV 93-05521. | June 1, 1998.
Attorneys and Law Firms
Robert L. Jennings, Jr., Goldberg, Persky, et al., Pittsburgh,PA, Garrett B. Johnson, Kirkland & Ellis, Chicago, IL, ScottP. DeVries, Nossaman, Gunther, et al., San Francisco, CA,Stanley M. Spracker, Weil, Gotshal & Manges, Washington,DC.
Opinion
SHELDON, J.
BACKGROUND
*1 This action arises out of claims for personal injuriesfiled on behalf of a number of plaintiffs. The actions havebeen separated out for trial and in this action, plaintiffs havefiled claims for injuries which they allege occurred as aresult of environmental exposure to trichloroethylene (TCE)in the East Phoenix area. The diseases which the plaintiffsclaim were caused by their exposures to TCE include:Hodgkin's disease (Motion # 3); leukemia (Motion # 6); non-Hodgkin's lymphoma (Motion # 7); brain tumors (Motion #4); rhabdomyosarcoma (Motion # 5); lupus (Motion # 8);congenital heart defect-bicuspid aortic valve defect (Motion# 9); and kidney disease (Motion # 10).
The plaintiffs have offered medical and scientific testimonyin support of the allegation that the TCE caused the plaintiffsvarious diseases. The “causation” opinion by plaintiffs'experts is built upon several layers. It appears that none ofplaintiffs' experts considered the actual exposures that anyof the individual plaintiffs incurred prior to submitting awritten opinion that linked each disease to TCE exposure.The plaintiffs' experts constructed what is referred to as a“modeling” opinion about the range of exposures that eachplaintiff may have incurred during the relevant periods of
time. The plaintiffs urged at the hearing in this matter andduring the arguments which followed, that their “causation”experts considered the exposures after the fact and none ofthem changed their opinions. Therefore, the Court assumesthat plaintiffs urge that their medical causation opinions canbe considered valid when made even though none of theexperts knew what the exposures were.
The plaintiffs also rely heavily on the expert opinion ofDr. David Ozonoff who opined on the link between TCEand a number of the various diseases at issue. Many of the“causation” experts testifying on behalf of plaintiffs reliedheavily on Dr. Ozonoff's “causation opinion” regarding TCEin forming their individual “causation” opinions regardingindividual, specific plaintiffs.
The exposures of individual plaintiffs are, obviously, at thisdate almost impossible to determine with certainty. However,the “modeling” experts would give their opinion about thenature and extent of exposures in water and air which theplaintiffs may have received during the relevant time periodin this case. The “relevant time period” generally refers totime periods which in many cases occurred 20 to 40 yearsago. (See Dr. Jerry Olshan affidavit, exhibit 11). Some of themore recent exposures occurred 10 to 15 years ago. However,with appropriate foundation, the “modeling” experts claim tobe able to determine potential exposure rates from the variousamounts of chemicals allegedly placed into the air or soil bythe various defendants.
The more troublesome issue in this case is the “standard” tobe applied by the Court in determining whether the “experts”for the plaintiffs can demonstrate the admissibility of theiropinions at trial.
CAUSATION
“But for”
*2 The “causation” inquiry actually proceeds on twodifferent bases. On the one hand, plaintiffs must demonstratethat the expert testimony satisfies the legal causationrequirements of Arizona tort law. Specifically, the defendantsargued that this state requires tort plaintiffs to show thattheir injuries would not have occurred “but for” the allegedlytortious conduct of the defendants. The plaintiffs have argued,however, that “but for” causation is not required and thattort plaintiffs need only show the defendant's conduct was
a “substantial factor” in bringing about the plaintiffs' harm.The defendants argue that the plaintiffs' failure to satisfythe legal standard for causation requires that summaryjudgment be entered in favor of the defendants even ifplaintiffs' expert opinions would be admissible at trial.The defendants argue that the plaintiffs must offer experttestimony that demonstrates that the plaintiffs' injuries wouldnot have occurred absent the defendants' alleged misconduct.Specifically, the Arizona Revised Jury Instruction containsthe following language on the issue of causation:
“Before you can find a defendant at fault, you must findthat defendant's negligence was a cause of plaintiff's injury.
Negligence causes an injury if it helps produce the injuryand if the injury would not have happened without thenegligence.”
The Arizona Supreme Court has stated that “as far ascausation-in-fact is concerned, the general rule is that adefendant may be held liable if his conduct contributed tothe result and if that result would not have occurred ‘but for’defendant's conduct.” Ontiveros v. Borak, 136 Ariz. 500, 667P.2d 200 (1983). Defendants argue that, additionally, in themedical context, plaintiff must satisfy the “but for” standardto a reasonable degree of medical probability (defense motion# 2, page 22). The defendants also argue that plaintiffsare simply incorrect in suggesting that the Arizona court'sadoption of the Restatement's “substantial factor” test haseliminated or replaced the “but for” causation test. Thedefendants argue that the “substantial factor” test and the“but for” causation test are not mutually exclusive but,in fact, are complementary. The defendants argue that thecomments to Restatements Section 431 and 432 make plainthat the substantial factor test is not satisfied unless thedefendant's conduct is also a “but for” cause of plaintiff'sharm. (Defendants' prehearing memorandum on the legalstandard for causation (page 3,4)). Finally, the defendantsargue that the plaintiffs' reliance on Restatement section 432is misplaced because the plaintiffs' experts have not opinedand cannot opine that plaintiffs' TCE exposure, by itself, wassufficient to bring about the harm at issue in this case. Tothe contrary, the defendants argue, the plaintiffs' experts havebeen willing to opine only that TCE was perhaps one ofseveral factors in bringing about the plaintiffs' illnesses. Thedefendants argue that the plaintiffs' experts must show thatplaintiffs would not have developed the illnesses of which
they now complain without their alleged exposures to TCEand that the experts have not made that showing.
*3 The defendants have set forth a number of examples inplaintiffs' experts' depositions wherein they assert the experts'failed to identify the TCE exposure, even if the dose had beenknown, as a “but for” causation of the diseases upon whichthey opined. For example, Dr. Kilburn responded when askedwhether it was his opinion that “but for” exposure to TCEthat one of the plaintiffs would not have developed a braintumor he responded, “I simply don't know .” (Defendants'prehearing memorandum on the legal standard for causation,page 8). Additionally, the deposition testimony and hearingtestimony of Dr. Miller clearly indicated that he lacked anybasis upon which to opine that the rhabdomyosarcoma caseswere caused by exposure to TCE. When asked, with respect toeach of the two plaintiffs, whether it was likely that “but for”their exposure to TCE that they would not have developedthe disease, Dr. Miller answered on each occasion, “I can'tanswer your question.”
Finally, with respect to the lupus victims, when Dr. Kilburnwas asked whether either of the lupus victims wouldhave developed their diseases without exposure to TCE,he responded, “When you get down to one patient, youknow, there is no real way of making statistical probabilitystatements; so I can't answer. I think that knowing thatTCE is a cause of lupus [an opinion which will be dealtwith separately later in this minute entry], knowing vinylchloride causes lupus and scleroderma and having, you know,reviewed all of this literature, that the absence of competingcauses makes the lupus in these two women more likely dueto vinyl chloride than anything else known at the moment. ButI can't say that that's a conclusive attribution. It isn't.” (Id.)Thus, these and other experts who testified on behalf ofplaintiffs simply could not, and probably were not willingon the state of the scientific knowledge at this time, to offeranything approaching a “but for” causation opinion.
“Medical Causation”
The defendants argue that in addition to failing to meet the“but for” standard for causation in Arizona, the plaintiffs'experts' testimony on causation fails the Frye standard andis not admissible. Defendants argue that plaintiffs' experts'novel theories as to a causal relationship between low-levelexposure to TCE and the various diseases which are thesubject of this suit are not generally accepted in any relevant
scientific community and are predicated on unscientific andflawed methodologies.
The defendants argue that the proof that plaintiffs' theories arenot generally accepted in the relevant medical and scientificcommunities is overwhelming. They point to the fact that notone “review article” or chapter in any authoritative textbookeven suggested that there is sufficient evidence to justify acredible scientist in agreeing that there is a causal relationshipbetween TCE and the diseases at issue in this case. Moreover,the defendants accurately note that not one plaintiffs' experttestified that the general causation theory upon which theyrelied had been generally accepted in any relevant scientificcommunity. To the contrary, numerous plaintiffs' expertsexpressly admitted that their general causation theories werenot, in fact, generally accepted in any scientific community.
*4 The defendants also argue that the evidence was clear thatthe plaintiffs' experts committed numerous methodologicalerrors that rendered their opinions unscientific andspeculative. The errors included: improper extrapolationsfrom studies involving other diseases; studies involving otherchemicals; reliance on unreliable animal studies; a failure toconsider any dose-response relationship between TCE anda causal relationship in the diseases at issue in this casesupported by any scientific literature or studies; ignoringthe fact that scientific literature in the area is “inconsistentat best,” and inappropriately applying and using a term,“differential diagnosis”, as a basis for purportedly finding“causation.”
The Court has concluded that because the expert opinionsin this case are based on the validity or accuracy ofscientific principles, they must be subjected to the Fryetest. None of the testimony in this case was based solelyon personal experience or common knowledge. Plaintiffs'experts generally had little (or in Dr. Olshan's case, NO) experience with TCE research or TCE exposed patients.Instead, plaintiffs' experts purported to rely extensively onscientific data, studies or reports of other scientists-in Dr.Olshan's case, he relied almost exclusively on the opinions ofDr. Ozonoff which were generated specifically for purposesof this litigation. (The Court is also concerned that Dr.Ozonoff's opinions in this case were essentially embodied ina letter to one of the plaintiffs' attorneys in July of 1993,before any exposure data was even available in this case.) The
test articulated in Frye v. United States, 293 F. 1013, 1014(D.C.Cir.1923) stated:
“Just when a scientific principle ordiscovery crosses the line between theexperimental and the demonstrable stagesis difficult to define. Somewhere in thistwilight zone the evidential force of theprinciple must be recognized, and whilecourts go a long way in admitting experttestimony deduced from a well-recognizedscientific principle or discovery, the thingfrom which the deduction is made mustbe sufficiently established to have gainedgeneral acceptance in the particular field inwhich it belongs.”
Although the plaintiffs argue that the holding in Baroldyv. Ortho Pharmaceutical Corp. 157 Ariz. 574, 760 P.2d574 (App.1988) suggests that toxic tort litigants in thisstate may find it easier to introduce expert testimony oncausation than litigants in other jurisdictions, the Court notesthat Baroldy, in fact, addressed the issue of admissibilityunder Frye and concluded that there was sufficient evidencepresented in that case to demonstrate that a “cross-section ofmedical experts [demonstrated] ... that the occlusion theoryis one accepted scientific hypothesis to explain the causalrelationship between diaphragms and TSS.” 157 Ariz. at 581,760 P.2d 574. Additionally, the holding in the case can bedistinguished on the basis that the expert was testifying on hisown general experience.
*5 Under Frye, expert scientific testimony is admissibleonly if the scientific principles or theories underlying thetestimony have been “generally accepted in the relevantscientific community.” State v. Johnson, 186 Ariz. 329,332, 922 P.2d 294 (1996). The party offering the experttestimony bears the burden of proving general acceptance.State v. Superior Court (Blake) 149 Ariz. 269, 278, 718P.2d 171 (1986). In this case, the experts generally agreethat the application of scientific principles of epidemiology,toxicology, biochemistry, biostatistics and other scientificfields applied to the information on TCE and its purportedrelationship to diseases caused by exposure to it.
Scientific evidence has always been a source of particularconcern to the judiciary. Because “science” is often acceptedin our society as synonymous with truth, the courts have
traditionally been concerned that a substantial risk exists thatthe jury would give undue weight to such evidence. See Statev. Superior Court ex rel. County of Cochise, 149 Ariz. 269,277, 718 P.2d 171 (1986). As noted in State v. Superior Court,Id. before expert opinion evidence based on a novel scientificprinciple can be admitted:
“the rule of Frye v. United States, supra requires that thetheory relied on be in conformity with a generally acceptedexplanatory theory.... The purpose of this requirementis to assure the reliability of the testimony ... Fryescreens out unreliable scientific evidence because under itsstandard it is not enough that a qualified expert, or evenseveral experts, testify that a particular scientific techniqueis valid; Frye imposes a specific burden-the techniquemust be generally accepted by the relevant scientificcommunity.”
Id. Finally, the court stated, “Recognizing that judges andjuries are not always in a position to assess the validity of theclaims made by an expert witness before making findings offact, Frye guarantees that reliability will be assessed by thosein the best position to do so; members of the relevant scientificfield who can dispassionately study and test the new theory.”Id.
The rule, of course, does not require that the explanatorytheory have universal acceptance. Id. at 279, 718 P.2d 171.However, if the validity of the new scientific theory “is incontroversy in the relevant scientific community or if it isgenerally regarded as merely experimental, expert testimonybased on its validity cannot be admitted into evidence.” Statev. Gortarez, 141 Ariz. 254, 263, 686 P.2d 1224 (1984); Statev. Zimmerman, 166 Ariz. 325, 802 P.2d 1024 (App.1990).The casting of the expert's opinions in terms of personalexperience does not necessarily comply with the Fryerequirement. See State v. Boles, 183 Ariz. 563, 905 P.2d 572(App.1995). In some instances, the court may find such anapproach to be “nothing more than a subtle evasion of Frye.”Id. The court found that if such testimony were admissible,then any expert could express an opinion regarding mattersnot generally accepted by the scientific community merely byframing it in terms of his or her own personal observations.Such a tactic has been rejected by the courts in Arizona. SeeState v. Boles, Id. It is interesting to note that in State v. Bible,175 Ariz. 549, 583-584, 858 P.2d 1152, the court examined atlength assumptions underlying the various experts' opinions
regarding random match frequency when the court concludedthat such testimony failed to meet the Frye standard.
*6 In State v. Johnson, 186 Ariz. 329, 922 P.2d 294 (1996),the court rejected the State's suggestion that the court abandonthe Frye test for determining when novel scientific evidence isready for the courtroom and to adopt in its place the standardarticulated in Daubert v. Merrell Dow Pharmaceuticals,Inc., 509 U.S. 579, 113 S.Ct. 2786, 125 L.Ed.2d 469(1992). The court noted that, “Under Frye, scientific evidencebased on a newly postulated theory is admissible whenthat theory has been generally accepted in the relevantscientific community.... In contrast, Daubert says the trialjudge in each case must make a ‘preliminary assessmentof whether the reasoning or methodology underlying thetestimony is scientifically valid and of whether that reasoningor methodology properly can be applied to the facts inissue.’ Daubert, 113 S.Ct. at 2796.” The court in Johnson, indeclining to adopt Daubert, found that the case left “manyquestions unanswered.” In deciding to continue to followFrye, the court stated that:
“Notwithstanding legitimate criticism of Frye, and ourdesire to preserve uniformity when possible [that] ... evenwere we to use Daubert 's reliability/scientific validityanalysis, we would still be left with the problem posed byFrye: precisely when ‘in [the] twilight zone the evidentialforce of the [scientific] principle must be recognized.’'
State v. Johnson, 186 Ariz. at 331, 922 P.2d 294.
In State v. Hummert, 188 Ariz., 119, 933 P.2d 1187 (1997),the court stated that, “Frye does not suggest that judgesmust become experts in the science behind the evidence.Rather, judges are to survey relevant scientific literature,not for substantive content, but to determine the level of
acceptance within the scientific community 1 .” Id. In thefootnote referenced at the end of that sentence, the courtstated that, “Frye does not ask judges to engage in a numbersgame. General acceptance is determined by considering ‘thequality, as well as quantity of the evidence supporting oropposing a new scientific technique. Mere numerical majoritysupport or opposition by persons minimally qualified to statean authoritative opinion is of little value.” Id. fn. 1
After the Daubert id. case was remanded, the lowercourt enunciated additional factors which trial judgesunder the Federal rules should apply in determining the
admissibility of scientific evidence. See Daubert v. MerrellDow Pharmaceuticals, Inc., 43 F.3d 1311 (9th Cir.1995)(Daubert II). Although it was clear that Frye was not thecontrolling standard, the court's analysis of the admissibilityof expert scientific evidence is helpful in resolving issues ofscientific methodology.
In Daubert II, the court was faced with the task of applyingthe Supreme Court's decision in Daubert. The court framedthe question as: “How do we figure out whether scientistshave derived their findings through the scientific methodor whether their testimony is based on scientifically validprinciples?” Id. The court rejected any facile conclusion thatan “expert's bald assurance of validity is [ ] enough.” Id.Rather, the court held that:
*7 “The party presenting the expert mustshow that the expert's findings are basedon sound science, and this will requiresome objective, independent validation ofthe expert's methodology.”
43 F.3d at 1316.
The court in Daubert II, recognized that whether the theoryor technique employed by the expert was generally acceptedin the scientific community was an important factor inevaluating the admissibility of the expert's testimony. Thecourt stated that, “yet something doesn't become ‘scientificknowledge’ just because it's uttered by a scientist; nor canan expert's self-serving assertion that his conclusions were‘derived by scientific method’ be deemed conclusive, elsethe Supreme Court's opinion could have ended with footnote2.” 43 F.3d at 1316. The court also noted that whether theexpert's testimony has been subjected to peer review andpublication was also important; whether it can be and hadbeen tested; whether the known or potential rate of errorwas acceptable. The court recognized that those factors wereillustrative rather than exhaustive; nor did it deem each ofthem to be equally applicable in every case. Id. at 1316-17.The court also recognized that:
“One very significant fact to be consideredis whether the experts are proposing totestify about matters growing naturallyand directly out of research they haveconducted independent of the litigation, orwhether they have developed their opinions
expressly for purposes of testifying. Thatan expert testifies for money does notnecessarily cast doubt on the reliability ofhis testimony, as few experts appear incourt merely as an eleemosynary gesture.But in determining whether proposed experttestimony amounts to good science, we maynot ignore the fact that a scientist's normalwork place is the lab or the field, not thecourtroom or the lawyer's office.”
43 F.3d at 1317. The court also observed that:
“Testimony proffered by an expert ... baseddirectly on legitimate, pre-existing researchunrelated to the litigation provides the mostpersuasive basis for concluding that theopinions he expresses were ‘derived by thescientific method’.”
43 F.3d at 1317.
The purpose of peer review and publication is to demonstrateflaws in methodology; therefore, the fact that defendants'experts and others independent of this litigation havecriticized the methodology of some of the epidemiologicalstudies upon which plaintiffs' experts relied is not ademonstration of bias or prejudice but rather evidence of thescientific community at work. As noted in Perry v. UnitedStates, 755 F.2d 888, 892 (11th Cir.1985), “The examinationof a scientific study by a cadre of lawyers is not the sameas its examination by others trained in the field of scienceor medicine.” A telling observation by the court in DaubertII illustrates the difficulty inherent in making determinationsabout the admissibility of complex, novel scientific evidence.In adopting a standard, the court stated:
*8 “One can conclude from this thatunfairness is inevitable when our toolsfor detecting causation are imperfect andwe must rely on probabilities rather thanmore direct proof. In any event, this is amatter to be sorted out by the states, whosesubstantive legal standards we are bound toapply.”
Finally, the court noted that the task before trial judgesdetermining the admissibility of scientific evidence, whetherunder Frye or Daubert, “is more daunting still when thedispute concerns matters at the very cutting edge of scientificresearch, where fact meets theory and certainty dissolves intoprobability.” Id. at 1316.
Of course, in applying the Frye test, the court mustfirst determine the relevant “scientific community” whoseacceptance must be ascertained. See State ex. rel. Collinsv. Superior Court, 132 Ariz. at 180, 199, 644 P.2d1266 (Supplemental Opinion, Feldman, J.). Generally,“acceptance” must be by those experts who are relativelydisinterested and impartial and whose livelihood, therefore,is not intimately connected with approval of the technique.Id. The requirement is not satisfied by testimony from asingle expert or group of experts “who personally believe thechallenged procedure is accepted or is reliable.” Id. The courtin State ex. rel. Collins stated that a court must be able tofind that the procedure is generally accepted as reliable bythe larger scientific community in which it originated. Id. Thecourt in Collins concluded:“That the Frye test is satisfied when the court isable to conclude that disinterested and impartial expertsknowledgeable in the scientific specialty which deals withand uses such procedures or techniques, have come torecognize the methodology as having sufficient scientificbasis to produce reasonably uniform and reliable results thatwill contribute materially to the ascertainment of the truth.”132 Ariz. at 180, 199, 644 P.2d 1266 (Supplemental opinion,Feldman, J.).
Finally, as noted in Collins in the supplemental opinionby Justice Feldman, “ideally resolution of the generalacceptance issue would require consideration of the views ofa typical cross-section of the scientific community, includingrepresentatives, if there are such, of those who oppose orquestion the new technique.” Id. Justice Feldman noted thatthe “general acceptance” issue can be addressed by permittingscientists to speak to the courts through their publishedwritings and scholarly treatises and journals and that courtsview such writings as “evidence” not of the actual reliabilityof the new scientific technique, but of its acceptance inthe scientific community. Justice Feldman noted that theburden is on the proponent of the new theory to show ascientific consensus supporting its use. Finally, in referring
to a California Supreme Court case on this issue, that courtnoted:
“If a fair overview of the literature disclosesthat scientists significant either in numberor expertise publicly oppose [the theory] ...as unreliable, the court may safely concludethat there is no such consensus at the presenttime.”
*9 132 Ariz. at 200, 644 P.2d 1266. (Quoting People v.Shirley, 31 Cal.3d at 55, 181 Cal.Rptr. 243, 723 P.2d 1354.)
Certainly, in this case, the affidavits presented prior tothe evidentiary hearing, the testimony at the hearing itself,and the pleadings submitted thereafter demonstrate that thescientific community, with respect to the specific chemicalat issue in this case, TCE, does not accept the theorythat it is causally linked to any of the specific diseases atissue in this case. Moreover, the plaintiffs have failed toprove that accepted scientific methodologies or techniquesgenerally accepted in the scientific community were utilizedby any of the plaintiffs' experts in reaching their conclusionsthat the plaintiffs' diseases were linked to their low-level,environmental exposures to the TCE allegedly disposed of bythe defendants.
The Court's evidentiary function under Frye will, on occasion,result in the exclusion of evidence at a trial. As succinctlynoted by the Supreme Court in Daubert v. Merrell DowPharmaceuticals, Inc., 113 S.Crt. 2786 (1993);
“there are important differences betweenthe quest for truth in the courtroom andthe quest for truth in the laboratory.Scientific conclusions are subject toperpetual revision. Law, on the other hand,must resolve disputes finally and quickly....[the consequence is that] a gatekeepingrule for the judge, no matter how flexible,inevitably on occasion will prevent thejury from learning of authentic insightsand innovations. That, nevertheless, isthe balance that is struck by Rules ofEvidence designed not for the exhaustivesearch for cosmic understanding, but for theparticularized resolution of legal disputes.”
Id. at 2798-99. Although the court's comments were made inthe context of the application of Rule 702 and 703 pursuant tothe Daubert guidelines, its observation is equally applicableto the consequences of the court's role and function pursuantto Frye. Under either standard, the objective is to ensure thefair and efficient resolution of legal controversies.
A substantial part of the plaintiffs' case relies on the field ofepidemiology. Clearly, this field of public health is intendedto assist scientists and doctors in better understandingcausation and to prevent disease in groups of individuals.See Reference Manual on Scientific Evidence (1994) p. 125(RMSE). Epidemiological evidence identifies agents thatmay be associated with increased risk of disease in groupsof individuals, may quantify the amount of excess diseasethat is associated with a particular chemical or environmentalagent and provides a profile of the type of individual whomay be likely to contract a certain disease after beingexposed to a chemical or environmental agent. Id. page 126.Epidemiology focuses on the general question of causationrather than on specific causation. Id. 126, 167. The issue of“specific causation” is beyond the domain of the science ofepidemiology. Id. page 167.
*10 The use of epidemiological studies raises a numberof issues regarding their utility, usefulness, and properconsideration in an accepted scientific methodology.Among those questions are: (1) Was the research methodtrustworthy?; (2) If so, was the exposure to the agentassociated with disease?; and (3) If the agent was associatedwith the disease, is it a causal relationship?” Id. 128.Association is not causation. Id., n. 7.
Scientists are very careful, generally, to avoid concludingthat because one thing occurs after another, it implies causaleffect. Such erroneous conclusions are generally referred toin writing and logic as coincidental correlation or “post-hoc ergo propter hoc.” The name, in Latin, means “afterthis therefore because of this.” This describes the fallacy. Aperson commits the fallacy when it is assumed that becauseone thing follows another that the one thing was caused by theother. Scientists use “causation” to describe the associationbetween two events when one event is a necessary link in achain of events that results in the effect. Id. 126. Generally,scientists recognize that there are a number of factors whichmust be considered before an association between an agentand a disease may be suggested to be “causal.”
Those factors are not only recognized in the ReferenceManual on Scientific Evidence (RMSE) but were alsoaddressed by all of the scientists testifying on behalf ofthe defendants. Id. Those factors guide scientists in makingjudgments about causation. They will be more fully discussedlater in this minute entry. The application of those guidelines,referred to generally as the Hill guidelines, assist scientists inavoiding making erroneous causation judgments. Scientistsconsider proper application of the factors for determiningcausation an important and intrinsic part of the methodologyin arriving at a generally accepted scientific opinion aboutcausation.
The relationship between cause and effect is a complex one.Scientists do not lightly draw it, nor do they generally ignorepervasive and persuasive scientific evidence contrary to theirhypothesis in order to simply arrive at a conclusion supportedby reliance on selected data which arguably supportstheir opinion. In the absence of a proper methodology orscientific technique explaining other substantial evidencewhich contradicts their theories, scientists do not generally“select” only data supporting their position.
The court's obligation to exclude unproven and potentiallymisleading scientific evidence is “especially sensitive incases where the plaintiff claims that exposure to a toxicsubstance caused his injury, [because a] jury may blindlyaccept an expert's opinion that conforms with their underlyingfears of toxic substances without carefully understanding orexamining the basis for that opinion.” Whiting v. BostonEdison Co., 891 F.Supp. 12, 24 (D.Mass.1995). Furthermore,the court in General Electric Co. v. Joiner. 522 U.S. 136, 118S.Ct. 512, 519, 139 L.Ed.2d 508 (1997) noted that:
*11 “[Conclusions] and methodology arenot entirely distinct from one another.Trained experts commonly extrapolatefrom existing data. But nothing in eitherDaubert or the Federal Rules of Evidencerequires a district court to admit opinionevidence which is connected to existingdata only by the ipse dixit of the expert. Acourt may conclude that there is simply toogreat an analytical gap between the data andthe opinion proffered.”
In a concurring opinion, Justice Breyer observed that thejudge's obligation to determine the admissibility of evidencein those cases where law and science intersect becomes evenmore critically important. He stated:
“today's toxic tort case provides an example. The plaintiffin today's case says that a chemical substance caused,or promoted, his lung cancer. His concern, and that ofothers, about the causes of cancer is understandable, forcancer kills over 1 in 5 Americans ... Moreover, scientificevidence implicates some chemicals as potential causes ofsome cancers ... yet modern life, including good healthas well as economic well-being, depends upon the use ofartificial or manufactured substances, such as chemicals.And it may prove particularly important to see that judgesfulfill their Daubert gate-keeping function, so that theyhelp assure that the powerful engine of tort liability, whichcan generate strong financial incentives to reduce, or toeliminate, production points towards the right substancesand does not destroy the wrong ones. It is, thus, essential inthis science-related area that the courts administer the rulesof evidence in order to achieve the ‘end[s]’ that the rulesthemselves set forth, not only so that the proceedings maybe ‘justly determined,’ but also so ‘that the truth may beascertained.’ Federal Rule Evidence 102.”
522 U.S. at ----, 118 S.Ct. at 521.
APPLICATION OF METHODOLOGIES GENERALLY
Although the plaintiffs have argued that their experts haverelied on and applied methods practiced by most scientists,as noted in Lust v. Merrell Dow Pharmaceuticals, Inc., 89F.3d 594, 598 (9th Cir.1996), “[when] a scientist claims torely on a method practiced by most scientists, yet presentsconclusions that are shared by no other scientist, the districtcourt should be wary that the method has not been faithfullyapplied.” As noted by the court in Hall v. Baxter Health CareCorp., 947 F.Supp. 1387, (D.Or.1996), a scientist's relianceupon a valid and established general causation theory (theHill or Koch criteria) is a critical step in the proper scientificmethodology applicable to determining specific causationof an individual's disease. Thus, the general acceptance inthe scientific community of the experts' general causationtheory is, in fact, an issue of methodology and not merelya difference of opinion between scientists regarding proper“conclusions.” As noted in Hall, “Courts and commentators
have wrestled with the methodology/conclusion distinction,concluding that the distinction is of limited practical import.”947 F.Supp. at 1399. As noted by the court:
*12 “There appears to be noclear demarcation between scientificmethodology and the conclusions itgenerates.... this court need not and shouldnot ignore any step in that process, but mustensure that in each step, from initial premiseto ultimate conclusion, the expert faithfullyfollowed valid scientific methodology. Inother words, this court need not accept,as scientifically reliable, any conclusionthat good science does not permit tobe drawn from the underlying data butwhich, instead, constitutes “unsupportedspeculation.” Accordingly, in resolvingthe pending issues before me, this courtwill examine the evidence to ensure ...that every step in the expert's reasoningprocess, including the expert's formulationof conclusions, are grounded in goodscience.
947 F.Supp. at 1401.
Such an analysis is not only applicable to the Daubert gate-keeping function for federal judges, but is also applicableto the determination under Frye. Whether the methodologiesrelied upon by the expert at arriving at a conclusion aregenerally accepted by the scientific community are ofprofound importance to the court. In this case, the novelscientific theory at issue is inextricably related to theconclusion. There are, it is clear from the motions as wellas the evidentiary hearing, no studies either epidemiologicalor animal that demonstrate TCE, in the absence of otherchemicals or in doses either similar to those at issue in thiscase or demonstrated through reliable scientific theory to bean appropriate extrapolation from existing studies, can belinked to any of the diseases at issue in this case at low level,environmental doses of TCE.
Of even more concern to the Court was the absence ofany valid scientific explanation supporting plaintiffs' experts'conclusions about the alleged non-applicability of TCEstudies in the industrial or occupational setting, where doseswere considerably higher than those at issue here, and the
absence of associations or causations to diseases causedby TCE. Dr. Tannenbaum's testimony on this aspect ofplaintiffs' case was particularly persuasive. Dr. Tannenbaum'stestimony was credible and persuasive in explaining thescientific unacceptability of making the simple, almost lay-person-like deduction, that because the family of chlorinatedhydrocarbons includes TCE and PCE that the chemicals andstudies related to them could be considered synonymously.The Court finds that Dr. Tannenbaum's expertise in thisarea is superior to that of Dr. Ozonoff who is, by trainingand experience, a medical doctor with a master's degree inpublic health. The issue related to oxidative metabolism ofchlorinated hydrocarbons appears to be an issue uniquelywithin the expertise of toxicologists-recognizing, of course,that others by training or experience could develop anexpertise in the area. However, the Court has concludedthat Dr. Tannenbaum's testimony regarding the generalacceptability of the underlying theory that PCE and TCE areequivalent for purposes of applying epidemiological studiesbased on either to a causation conclusion relating TCE to thediseases in this case is simply unsupported in the medicalor scientific community and lacks general acceptance. Dr.Tannenbaum testified that the breakdown metabolite believedto be associated with causing cancer in mice, TCAA, has notgenerally been recognized by the scientific community as acarcinogen in animals. He testified that it has only been seenas a cancer-causing agent in a specific mouse.
*13 Thus, it is clear that a key assumption to Dr. Ozonoff'stheories fails. As Dr. Tannenbaum noted, the plaintiffs'experts have attempted to use principles from toxicology but,“they didn't appear to understand them.” Dr. Tannenbaumhas worked with a number of organizations which utilize anddepend upon accurate toxicological evaluations of chemicalsto determine their potential carcinogenicity, including: IARC;EPA; and NTP. Dr. Tannenbaum noted that the NTP wasfirst involved with looking at TCE in 1983. At that time,Dr. Tannenbaum reviewed a number of animal studies andwas very familiar with this chemical substance. His testimonydemonstrated a distinct difference in the metabolism of thetwo chemicals and clearly supported his conclusion that it isnot appropriate scientific method to simply assume that bothchemicals react similarly in the body. Dr. Tannenbaum alsonoted that he is not aware of any agency, either in the UnitedStates or internationally, that has evaluated TCE's propertiesby utilizing studies on PCE to support their conclusions.He further stated that to evaluate the effects of TCE, a
“dose-response” is critical in making a proper analysis of itspotential effect on the human body.
In addition, Dr. Tannenbaum noted that IARC studies andothers looking at the genotoxicity of TCE have generallybeen negative. Furthermore, Dr. Tannenbaum testified that noone has demonstrated a “mutagenic” effect for TCE. In anyevent, Dr. Tannenbaum testified that it was not an appropriatescientific theory or conclusion to assume because a substanceis “genotoxic” it can cause cancer. Dr. Tannenbaum testifiedthat such a scientific conclusion would be “unequivocally notcorrect.”
Finally, Dr. Tannenbaum stressed in his testimony that theIARC's classification of TCE as a “probable” carcinogen isnot a dictionary definition and is “not intended to be one.”Dr. Tannenbaum testified that no scientist would accept sucha definition without qualifying it by the IARC's use of theterm and its defined classification system. Dr. Tannenbaumstressed that it is inappropriate to refer to the statement ina “vacuum” and that scientists consider it together with theterminology and definition utilized by the classifying agency.
The Court concludes that Dr. Tannenbaum's opinion thatplaintiffs' experts' opinions regarding the causal role TCEmay have played in the plaintiffs' disease by relying onanalogies to other chemicals are without general acceptancein the scientific community. This Court also finds that thereis no evidence to contradict Dr. Tannenbaum's conclusionand that there is no serious disagreement that all the dosesreceived by any of the plaintiffs are “remarkably small,both in absolute terms, and relative to the vastly largerdoses of TCE needed to observe even the subtlest of toxicresponses in controlled experiments.” Tannenbaum affidavitpage 4. Dr. Tannenbaum's affidavit and testimony constitutedpowerful evidence regarding the deficiencies in appropriatemethodology utilized by the plaintiffs' experts in this case. Asnoted in Dr. Tannenbaum's affidavit:
*14 “As discussed in my previous report,there are two and only two crediblemethods by which scientists outside oflitigation assess such risks [risk to healthassociated to low level exposure to TCE](paragraph 7) .... thus, to the extentthat working scientists outside of thecourtroom debate among themselves the“true” risks associated with tiny exposures
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to TCE, their quantitative disagreementsare limited to whether the actual risk iszero or, instead, some number very closeto zero (paragraph 12).... Fundamentally,is this why the “method” applied byProfessor Ozonoff for purposes of theselawsuits is entirely outside of the scientificmainstream. Professor Ozonoff rejects bothmethods discussed, insisting instead boththat the plaintiffs' risks cannot be quantifiedand, that they are significant. Whatevermethod his is, it is not toxicology and it isnot science. The near-complete absence ofnumbers in his reports indicates his non-quantitative approach. (paragraph 13).”
Like the plaintiffs in Daubert II, the plaintiffs here attempt toshow causation circumstantially. However, they must provethat their injuries were the result of the accused cause and notsome independent factor. In most cases of the diseases at issuein this case, doctors and scientists have little knowledge aboutthe etiology of the diseases, have identified other causes ofthem, or know that all of the diseases occur in the absence ofexposure to TCE.
As noted in Daubert II, in terms of statistical proof, theplaintiff must establish not just that the ingestion of thechemical increased somewhat the likelihood of the diseaseoccurring but that it caused some specific statistical increasein the likelihood of the injury. See Daubert II at p. 1320. TheCourt considered the “background rate” of the disease at issueand noted that it is important to require a plaintiff to show thatsuch defects or diseases were the result of something otherthan the statistically probable occurrence of the disease in thepopulation. As in Daubert II, none of the plaintiffs' expertswere willing to make any type of risk assessment in this case.“Relative risk” or “odds ratios” generally refers to the risk ofdisease among the exposed group to the chemical compared tothe risk of disease among the general population or unexposedgroup. See Berry v. CSX Transportation, Inc., 704 So.2d 633,640 (App.1997, RMSE at 176).
The courts have wrestled with the concept of the applicationof “relative risk” and “confidence intervals” to risk estimationin toxic tort cases. See Daubert II at 1321. While the Daubertcourt appeared to require testimony that demonstratedthe statistical increase or probability increase of disease
was more than double other courts have not followedsuch an arbitrary requirement. Nevertheless, it appearsepidemiological studies should be required to demonstrateconsistency in findings suggesting a statistically significantincrease in the probability of the relative risk of the disease toan exposed group similar to that experienced by the plaintiffs.Here, as in Daubert II, the plaintiffs' experts' evaluation of theepidemiological studies made vague assertions that there wasstatistically significant relationships between “chlorinatedhydrocarbons”, “hydrocarbons”, “chemicals”, “halogenatedhydrocarbons”, and other chemicals and the diseases at issuewhile not stating that any of the studies showed a consistent,replicated result across the spectrum for TCE and the specificdiseases with a relative risk greater than two. Such studieswould thus not be helpful, and indeed would only serveto confuse the jury if offered to prove rather than refutecausation. The court in Daubert II noted a “relative risk ofless than two may suggest [toxicity] but it actually tends todis prove legal causation, as it shows that [the chemical oragent] does not double the likelihood of [the disease].” Id. at1321. The strongest inference that could be drawn from muchof the plaintiffs' expert testimony is that the experts believethat it is “possible” that the chemical may have caused thedisease or contributed to its manifestation. They generally didnot testify that it was more probable than not the cause ofthe disease. Furthermore, as noted in Daubert II, any tailoringof the plaintiffs' experts' conclusions at the hearing stageof the proceedings which contradicted their earlier opinionsand findings set forth in their reports, fatally underminedany attempt to show that their findings were “derived bythe scientific method,” rather than an attempt to salvage anadversarial opinion for trial.
*15 Finally, Dr. Tannenbaum testified about reliabilityof information and studies of mixed solvents for purposesof drawing scientific conclusions about the effect of TCE.He found that such data was unreliable. He found thatthe only property necessarily shared by solvents is their“solvating” action-that is, their ability to dissolve othermaterials (Affidavit, paragraph 24). His testimony that thecarcinogenicity of TCE cannot be predicted by studiesof mixed solvents “as there is no a priori toxicologicalbasis for believing their toxicities will be similar and goodreason for believing otherwise” was unchallenged by anycredible evidence by the plaintiffs (paragraph 24). As notedin the RMSE, reliable epidemiology studies must answerthe question: “Is exposure to the agent associated with
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disease?” (Id. 128). Such an observation was consistent withDr. Tannenbaum's testimony that, “if one is interested inthe biological effects of TCE, one must study TCE andnot other compounds.” Thus, the Court finds extremelycredible Dr. Tannenbaum's conclusion that it is not generallyaccepted scientific methodology to rely on data relating toother chemical or mixed compounds to arrive at conclusionsregarding the carcinogenicity of TCE. Dr. Tannenbaum'scriticism of Dr. Ozonoff's “methodology” and “scientifictechnique” was particularly harsh but valid. So too wasDr. Tannenbaum's criticism of Dr. Kilburn. With respectto areas of toxicological evidence, the Court finds that Dr.Tannenbaum's testimony regarding general acceptance in thatfield to be credible.
In McKenzie v. Westinghouse Electric Corp. 674 A.2d 1167(Pa1996), the court dealt with an issue similar to the onebefore this court. There, the plaintiffs sought recovery fromthe defendant for injuries suffered by their daughter. Theplaintiffs argued that the defendant's electrical plant producedcertain chemical substances that contaminated drinking waterused by Mrs. McKenzie during her pregnancy, leading tobirth defects in the child. The plaintiffs presented experttestimony purporting to prove that chemicals (TCE and DCE)were teratogenic, while conceding that this view was notgenerally accepted in the scientific community. Plaintiffsargued, however, that the methodology used by their expertswas generally accepted and that their testimony establishedcausation and, therefore, should have been admitted. 674A.2d at 1171. Plaintiffs argued that it was up to the jury todetermine whether their experts' testimony was believable.
The court, in rejecting the argument, held that “there mustbe a showing, not that the studies establishing the causalrelationship follow generally accepted methodologies, butthat the existence of the causal relationship is generallyaccepted by the relevant medical community.” Id. at 1172.Furthermore, like the expert's opinions as in Blum v.
Merrell Dow Pharmaceuticals, Inc., 705 A.2d 1314, 1322(Sup.Ct.1997), the underlying scientific principal of theplaintiffs' expert testimony in this case is not generallyaccepted in the relevant scientific communities.
*16 In Blum, as in McKenzie, the court concluded that“if the critical ‘underlying principal’ that must be generallyaccepted before scientific evidence is admissible is that‘bendectin causes club feet,’ the Blums' causation evidence
is not reliable and is inadmissible under Frye/Topah.” Id. at1323. Additionally, in Blum, the court addressed the issueof whether the methodology utilized by the plaintiffs' expertwitnesses was generally accepted. The court noted that thedefense experts agreed that each of the individual types ofanalyses relied upon by the plaintiffs had scientific validityand could contribute to an accurate picture of scientific fact.Id. at 1323. That is, the experts relied upon: chemical structureanalysis, in vitro studies, in vivo studies and epidemiologicalstudies. However, the defendants in Blum pointed out thatit was the way in which the studies were utilized by theplaintiffs' experts that was not generally accepted. The courtfound the argument persuasive. Id. at 1323. The courtalso found that an expert's self-serving assertion that hisconclusions were ‘derived by the scientific method’ cannotbe deemed conclusive. Id. at 1323 (citing Daubert, 43 F.3dat 1315-16).
The court in Blum, as here, noted that it was faced with the useby scientists of complicated scientific and epidemiologicalevidence. The court noted that under this analysis it didnot consider whether the expert's conclusions regarding theteratogenic effects of the chemical at issue in that case weregenerally accepted. Rather, the court determined that the“underlying principal” which must be generally accepted waswhether the methods used by the experts to arrive at theirconclusions actually gave an accurate prediction of humanteratogenicity. Id. at 1323. The court in Blum concludedthat assessing the teratogenicity of drugs is more complexthan simply collecting certain types of data. Id. The courtfound, as numerous defense scientists testified to in this case,that “replicated epidemiological studies consistently findinga strong association are necessary to establish causation.”Id. at 1323. The court also noted that animal studiescould provide evidence suggestive of causation but, again,animal studies without epidemiological studies supporting thegeneral conclusions to be drawn cannot prove causation inhumans because drugs used in animals do not necessarilyhave the same effect in humans. Id. at 1323.
The plaintiffs' experts' methodologies utilized in this casesuffer from similar defects as those analyzed by the courtin Blum . There, as here, the fact that epidemiologicalstudies are universally utilized by scientists, does notinexorably lead to the conclusion that the way theywere utilized by plaintiffs' experts in this case areappropriate. The Court finds that the selective utilization of
epidemiological studies to the exclusion of other confoundingand conflicting epidemiological studies without sufficientscientific explanation made the epidemiological methodologyone that clearly was not appropriate or generally accepted
amongst scientists. 1
*17 In the RMSE, in discussing the use of epidemiology tosupport causation findings, the manual, as did the scientistsin this case, found that seven factors should be consideredwhen a scientist seeks to determine whether an “association”between an agent and a disease is causal. These factors guidethe scientist in making a judgment about causation. They are:
1. The strength of the association;
2. The temporal relationship;
3. Consistently of the association;
4. Biologic plausibility (coherence with existingknowledge); 5. Consideration of alternative explanation;
6. Specificity of the association; and
7. Dose response relationship.
(RMSE pages 160-161). The Court finds persuasive andcredible the defense expert testimony that the most importantof these factors is probably # 1 and 3. That is, the relativerisk is one of the cornerstones for causal inferences. Relativerisk measures the strength of the association. The higher therisk, the greater the likelihood that the relationship is causal(RMSE page 161). Consistency is also extremely important.All credible scientists agree that the need to replicateresearch findings is important in most fields of science.In epidemiology, research findings often are replicated indifferent populations. As noted by the scientists in this case,as well as in the RMSE, “consistency in these findings isan extremely important factor in making a judgment aboutcausation.” (RMSE page 162).
Although specificity is a critical element of the criteria,plaintiffs' experts routinely relied on studies that did notaddress the types of diseases at issue in this case. Courts andscientists have repeatedly rejected this type of assumption.See Christopherson v. Allied-Signal Corp., 939 F.2d 1106(5th Cir.1991). In that case, the court affirmed the exclusionof the testimony of Dr. Miller (who also was presentedby the plaintiffs in this case) who attempted to testify that
exposure to nickel and cadmium caused the plaintiff's coloncancer. The court in Christopherson found that Dr. Millerbased his opinions on a speculative extrapolation from studiesrelating to lung cancer, not colon cancer. See also, Kennedy v.Collagen Corp., 991 F.Supp. 1185 (N.D.Cal.1998); Valentinev. Pioneer Chlor Alkalai, Inc., 921 F.Supp. 666, 673-674(D.Nev.1996) (precluding Dr. Kilburn, (also testifying for theplaintiffs in this case) from testifying that chlorine gas had aneffect on the human brain and central nervous system becausethey were “novel, and ... unsupported by scientific researchextraneous to this litigation.”).
Additionally, as noted above, in Dr. Tannenbaum's testimony,which the Court has found credible and generally acceptedin the relevant scientific community, extrapolation fromstudies of different chemicals does not constitute acceptedmethodology in the absence of a scientific and accepted basisfor doing so. See Schudel v. General Electric, 120 F.3d 991(9th Cir.1997).
*18 Plaintiffs' experts have also not followed properscientific technique or methodology in their reliance inmany cases on animal studies without demonstrating theappropriateness of considering them in their methodologicalapproach to their opinions. The recognized weakness inanimal studies “arises from the fact that different species ofanimals react differently to the same stimuli for reasons notentirely understood. Immune systems, nervous systems, andmetabolism (i.e. physical processing of chemical compounds)may differ greatly between species.” Turpin v. MerrellDow Pharmaceuticals, Inc., 959 F.2d 1349, 1359 (6thCir.1992); see also In re Paoli R.R. Yard PCB Litigation,35 F.3d 717, 143 (3rd Cir.1994). (“Animal studies maybe methodologically acceptable to show that chemical Xincreases the risk of cancer in animals, but they may notbe methodologically acceptable to show that chemical Xincreases the risk of cancer in humans.”) There was noacceptable methodology demonstrated by any of plaintiffs'experts to support their reliance on high doses of drugsadministered to animals in many studies and a failure toaccount for known predisposition to diseases in other studies.
Throughout these proceedings, it has also been a matterof great concern to the Court that the experts retained byplaintiffs were apparently willing to “assume” the presence ofa “significant” dose of TCE to each of the plaintiffs. It appearsuncontroverted that each of the plaintiffs' experts was willing
to give an opinion in the absence of any accurate informationabout dosage. As noted in Mancuso v. Consolidated EdisonCo., 967 F.Supp. 1437 (S.D.N.Y.1997):
“As courts have recognized, it is improperfor an expert to presume that the plaintiff“must have somehow been exposed to ahigh enough dose to exceed the threshold[necessary to cause the illness], therebyjustifying his initial diagnosis. This iscircular reasoning. See O'Connor, 807F.Supp. at 1396, Cavallo, 892 F.Supp. at764 n. 12; Claar v. Burlington N.R.R.Co., 29 F.3d 499, 502-03 (9th Cir.1994)(“Coming to a firm conclusion first and thendoing research to support it is the antithesisof [the scientific] method.” However, thisappears to be exactly what Dr. Schwartzdid. Dr. Schwartz's own testimony revealsthat he simply assumed the plaintiffs hadbeen subjected to an exposure high enoughto cause their ailments.
Mancuso, 962 F.Supp. at 1450. As stated by a number ofexperts, including Dr. Tannenbaum, a noted toxicologist,a central tenet of toxicology is that “the dose makes thepoison.” As Dr. Tannenbaum and Dr. Guzelian and othersdemonstrated to this Court, there is no general acceptance inany scientific community that any dose of TCE, no matterhow small, is capable of causing the various diseases at issuein this case. As noted in Cuevas v. E.I. DuPont DeNemoursand Co., 956 F.Supp. 1306, 1312 (S.D.Miss.1997) knowledgeof the amount and duration of exposure are “essentialelement[s] to a valid toxicological opinion determiningwhether a chemical caused certain reactions.” Scientificmethodology dictates that comparison of the known orestimated exposure to established reactive dose levels isthe cornerstone of toxicology. Reaching their opinions firstand then doing research to support them suggests that theplaintiffs' experts' opinions are “result-oriented” rather thanthe result of good scientific technique or methodology. Seealso Cartwright v. Home Depot USA, Inc., 936 F.Supp. 900,906 (M.D.Fla.1996).
*19 An appropriate technique or scientific methodologydemands that plaintiffs' experts show more than that they“believe” that a certain chemical agent “may sometimes”
cause the kind of harm that the plaintiffs allege occurredin this case. As noted in Wright v. Willamette Industries,Inc., 91 F.3d 1105, 1107 (8th Cir.1996) “at a minimum,we think that there must be evidence from which the factfinder can conclude that the plaintiff was exposed to levelsof that agent that are known to cause the kind of harm thatthe plaintiff claims to have suffered.” See also, Schudel,120 F.3d at 997 (court excluded expert testimony where“[plaintiff's] exposure was neither long enough nor intenseenough to fall within the ranges described in the studies Dr.Morton relied upon”); Sutera v. Perrier Group of America,Inc., 986 F.Supp. 655, 662 (D.Mass.1997) (excluding experttestimony where no epidemiologic studies associated benzenewith acute promyelocytic leukemia at the dose experienced bythe plaintiff). In this case, there is an absence of epidemiologicstudies and toxicological evidence that suggest an associationbetween plaintiffs' diseases at the level of TCE exposure theyexperienced in this case.
There is no credible scientific evidence in the record tosupport a conclusion by the Court that plaintiffs' expertsfollowed appropriate methodologies or generally acceptedmethodologies in arriving at conclusions that appear to besupported by nothing more than supposition, hunches, andselective reliance on studies that they urge support their, insome instances, revolutionary hypothesis about the causationof diseases in this case. Plaintiffs' experts provided no reliablejustification for extrapolating from either the epidemiologicor high-dose animal studies they urged supported theirmethodologies. Instead, they persistently avoided making anyquantification of the risk actually associated with the levelsof exposure at issue in this case preferring to make vagueassertions that the exposures were “significant.”
As noted above, consistency in the epidemiologic literatureis a critical requirement in fulfilling the Hill criteria.Consistency refers to whether studies conducted by differentpeople at different times show the same association betweena specific chemical and a specific disease. As Dr. Li noted inhis affidavit, “Having reviewed Dr. Ozonoff's list of studiesof TCE and cancer, (pps 49-51 of his report), I find markedlack of consistency among the types of cancers reported tooccur excessively.” Dr. Li Affidavit page 4, paragraph 13.Thus, Dr. Li concluded that the data relied upon by Dr.Ozonoff failed to meet the Hill criteria of consistency whichis a necessary condition precedent to a scientifically validattribution of causation which goes directly to an acceptable
methodology that is generally accepted by scientists. Thus, itappears repeatedly that plaintiffs' experts' opinions are morethe result of advocacy than good science.
*20 Additionally, the affidavit provided by Dr. Cole notedthat numerous studies not relied upon or scientificallydistinguished by Dr. Ozonoff provide substantial informationto suggest that no association between TCE and cancer exists.The issue, of course, is not which of these studies is morereliable but rather to note that good scientific technique ormethodology generally accepted by scientists does not permitscientists to selectively choose only those studies whichsupport an hypothesis and to ignore the rest in attemptingto arrive at a conclusion. It appears almost without questionbased on the testimony of the various experts that this is thetype of exercise that scientists generally do not engage in.
With the above principles in mind, the Court will undertakea review of each of the plaintiffs' proffered expert'sopinions. This discussion, of course, is not exhaustive andprobably could not detail all of the substantial evidencethat was presented in the hearing. The analysis was mademore difficult by the obfuscation of the essential questionat issue. That is: “IS TCE at low-level environmentaldoses causally connected to any of the diseases at issuein this case?” The issue was made more difficult bythe plaintiffs' lawyers constant reference to the studies,evidence, and exhibits as evidence that: “solvent exposures”,“organic solvents”, “volatile organic chemicals”, “chemicalexposures”, “chlorinated hydrocarbons”, “hydrocarbons”,“halogenated hydrocarbons” have been “associated” inepidemiological or other studies with “cancer” or otherdiseases. The Court finds that the reliable, credible scientificevidence presented in this case supports the conclusion thatthe relevant scientific community does not generally acceptmethodologies which attempt to make a causation judgmentabout a chemical's relationship to a disease that rely onmixed-chemical studies, those without dose data, or to otherdiseases. Thus, the use by plaintiffs' counsel throughoutthese proceedings of the above terms interchangeably asif they were synonymous with “TCE” was scientificallyunsupportable and did little more than confuse an alreadyextraordinarily complex inquiry.
DR. OZONOFF'S OPINION 2
As noted above, Dr. David Ozonoff was plaintiffs' “generalcausation” expert. Plaintiffs sought to have Dr. Ozonoff offeropinions that exposure to TCE, apparently at any level, maycause the array of diseases alleged to have been caused by theplaintiffs' exposure to TCE in this case. After the initial filingof Motions 2 through 10 and the arguments on them, plaintiffslater also sought to have Dr. Ozonoff testify that Dr. Olshanused an appropriate methodology and reached appropriateplaintiff-specific causation opinions.
The defendants argue that Dr. Ozonoff's testimony isinadmissible for three reasons. First, they argue that Dr.Ozonoff's general causation theory is not generally acceptedin the relevant scientific and medical communities (indeed,the defendants note that TCE is not even considered arisk factor by experts in these diseases in the fields inwhich they practice); second, Dr. Ozonoff's general causationtheory was not derived from generally accepted scientificmethodology and thus there is no scientific foundation forhis theory; and, three, Dr. Ozonoff has not based his specificcausation opinions on generally accepted scientific methods.The defendants argue that because Dr. Ozonoff's theories arenot generally accepted, are based on flawed methodology, andlacks scientific foundation, that his opinions failed to meet theFrye criteria and are not admissible.
*21 Dr. Ozonoff's methodology was criticized extensivelyby the experts testifying for the defense. However, aconsistent theme was presented which the Court findscredible and which severely undermines the reliability andacceptability of Dr. Ozonoff's methodology. See Affidavitsby Dr. Grufferman, Dr. Cole and Dr. Tannenbaum. Dr. Colefound that Dr. Ozonoff's reliance on the various studies helisted in his report to be unacceptable epidemiologic practice.See Cole Affidavit page 12, paragraphs 41-43. Importantly,Dr. Cole also noted the methodology employed by Dr.Ozonoff is inconsistent with those employed by independentresearch organizations such as IARC which writes reviewsof the scientific literature related to effects on biologicsystems by various chemical or biological agents. In Johnson,supra, it is important to note that the court found that theexistence of an “NRC report” demonstrated that importantscientific principles in that case had been demonstrated tobe generally accepted in the relevant scientific community.166 Ariz. at 331. The Johnson court also found that theadoption by the NRC of the principle at issue in that
case was strong evidence of general acceptance within therelevant scientific community. Dr. Cole noted IARC makesa determination about the carcinogenicity of various agents,including chlorinated solvents, after evaluating the scientificliterature and evaluating the strength of the evidence fromcarcinogenicity from human and experimental animal data.IARC Monograph, Vol. 63 (1995). See Cole Affidavit page22, paragraph 74. Dr. Cole noted that IARC defines aGroup 2-A agent or mixture to those substances “whenthere is limited evidence of carcinogenicity in humans andsufficient evidence in animals.” Id. Dr. Cole notes that“limited evidence of carcinogenicity” is considered to be apositive association observed between exposure to the agent,mixture or exposure circumstance and cancer for which acausal interpretation is considered “by the working group tobe credible, but chance, bias or confounding cannot be ruledout with reasonable confidence.” Id.
Of course, it is appropriate public policy for healthorganizations such as IARC and the EPA to make judgmentsconcerning the health and safety of the population based onevidence which would be less than satisfactory to support aspecific plaintiff's tort claim for damages in a court of law.The evidence at the hearing demonstrated that not one ofthe high-dose TCE-only human epidemiologic studies thatDr. Ozonoff purported to rely upon reached the conclusionthat a casual relationship existed between TCE and cancerin humans. In addition, not one “review article” nor anychapter in any authoritative textbook even suggested thatthere was sufficient evidence to establish a causal relationshipbetween TCE and any of the diseases at issue. This evidencewas important because it supports the conclusion that therelevant scientific community does not generally accept theconclusion and theories put forth by Dr. Ozonoff. Even Dr.Levy's textbook, an expert retained by the plaintiffs, didnot list TCE as an occupational carcinogen. Dr. Levy alsoadmitted that neither OSHA or NIOSH regulate TCE as aknown human carcinogen. Dr. Levy attempted to supportthe position that the plaintiffs' experts had followed anappropriate methodology. Dr. Levy noted that he thoughtit was appropriate for the plaintiffs' experts to rely onPCE studies because he stated they were similar chemicals.However, in cross-examination, in response to a questionas to whether or not there were slight differences in themetabolism in PCE and TCE in the human body, he testifiedthat he did not know. He also testified that he did not knowwhether PCE formed trichloroacetic chloride. Overall, the
court found that Dr. Levy's testimony added little weight tothe proposition that the plaintiffs' experts followed generallyaccepted methodologies in their respective fields. The Courtfinds that Dr. Levy's knowledge, experience and expertise inthe various areas applicable to the individual diseases was notsufficiently demonstrated to warrant attaching a great deal ofcredibility or weight to his testimony. This Court was alsotroubled by the fact that Dr. Levy was apparently the onlyscientist who testified who devotes a substantial amount ofhis time to litigation practice.
*22 Dr. Davis, an expert also retained by the plaintiffs,who has written a textbook on clinical occupational andenvironmental medicine did not list TCE on her list of“chemical and physical agents for which there is sufficientevidence to establish a causal relationship.” See RT, 4/20/98,128. Interestingly, Dr. Davis wrote in 1985:
“No readily discernible logic yet allowsregulatory agencies to anticipate futurerisks. The agencies continue to mount areactive response to externally generatedpressures. This often leaves them shorton science and long on speculation. Yetto delay occupational or environmentalregulation in the name of better sciencebecause no human harm has yet beendetected makes experimental subjects ofthose exposed in the meantime.”
Davis, “The ‘Shotgun Wedding’ of Science and Law: RiskAssessment and Judicial Review” Columbia Journal ofEnvironmental Law, Vol. 10. pp. 67, 100 at p. 99 (1985).For this very reason, it is clear that the plaintiffs' experts didnot follow an acceptable methodology by simply “assuming”that if the exposures exceeded the M.C.L. § limits set by theEPA that it was somehow indicative of “causation” of cancer.There was simply no credible evidence to support such aconclusion presented at any time during this hearing.
Defendants' experts who are indisputably among the world'sleading epidemiologists, toxicologists, rheumatologist,neuro-oncologists and teratologists, confirm that Dr.Ozonoff's theories in this case are not generally acceptedin the scientific and medical communities. Dr. Ruddy, aleading expert on rheumatology, who testified as an expertfor the first time at this hearing, testified that TCE is not afactor considered by rheumatologist in assessing the cause of
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systemic lupus. Dr. Mueller also testifying for the first timein her professional career. She is considered to be a leadingepidemiologist on Hodgkin and non-Hodgkin's lymphoma.She testified that TCE was not generally accepted as a riskfactor for either disease. Dr. Brent, a teratologist, testified thatit is not generally accepted that TCE is a teratogen and is notlisted in any review article as an agent which is responsible forhuman congenital malformations. Importantly, the testimonyof these experts on the question of whether TCE is generallyaccepted to be a cause of the cancers at issue, of lupus,and of congenital malformations went unchallenged anduncontradicted at the evidentiary hearing in this case. WhenDr. Ozonoff was questioned as to whether it was generallyaccepted that TCE caused any diseases, he mentioned onlytwo, neither of which are at issue in this case. (RT, 4/15/98,pp. 169-170).
It was apparent based on the testimony presentedthrough affidavits and at the hearing, that Dr. Ozonoff's“methodology” essentially set out to answer the questionas to whether any set of facts or studies were consistentwith cause and effect. That is precisely what a scientist isnot trained to do. As Drs. Cole and Grufferman testified,epidemiologists attempt to determine whether “associations”are valid rather than due to bias, chance or error. In order todifferentiate between a real statistical association and causalassociation, that is, to assess whether there is any answer otherthan cause and effect, epidemiologists utilize and employthe Hill criteria. See Dr. Grufferman, RT, 4/24/98, p. 156;Dr. Cole, 4/29/98, p. 155; Dr. Mueller, 4/27/98, p. 105.It appeared that Dr. Ozonoff's fundamental inquiry waswhether there was some explanation of the data that couldbe found to be consistent with his theory of causation. Suchan approach appears to be unsound scientifically and wasnot supported by any other testimony or literature presentedto the Court as being an acceptable methodology. As Dr.Li and Dr. Guzelian testified, it appears that Dr. Ozonoffwas able to reach his conclusions by simply ignoring ormisapplying fundamental methodology utilized universallyby epidemiologists. Because he sought, apparently, onlyexplanations consistent with his theory of causation, heappeared to ignore serious flaws that had been identified inalmost all of the studies he relied upon.
*23 All of the expert epidemiologists who testified forthe defense explained that relying on some low-dose studiesas positive while judging findings of high-dose, cohort
studies as weak, inconsistent, non-specific, and “negative”i.e those which were inconsistent with the proposition thatTCE causes cancer in humans, is not simply a differencein expert judgment; it is a serious methodological flaw anddemonstrates that Dr. Ozonoff's opinions were not based ondata or methodology generally accepted by experts in the fieldas reliable but were his own personal opinions and the “ipsedixit of the testifying expert.”
It also does not appear to be generally accepted methodologyamongst scientists to base a causation opinion about TCEon studies of other chemicals. It is apparently well-knownthat small differences in chemicals and molecular structurecan and do result in substantial differences in toxicityand carcinogenicity. Bigner, 4/27/98, p. 104; Tannenbaum,5/1/98, p. 41. Thus, it does not appear to be a generallyaccepted methodology to argue by analogy under thecircumstances of this case. See Guzelian, 4/23/98, p. 53;Bigner, 4/27/98, p. 108. Furthermore, as noted above,the testimony of Dr. Tannenbaum demonstrated that theanalogy from PCE to TCE is not empirically or scientificallysupportable. See also Guzelian, 4/23/98, p. 51. The plaintiffs'experts' positions that it is appropriate to study mixedexposures to determine the carcinogenicity of TCE does notappear to be supported by good science or the methodologiesemployed by independent agencies such as IARC and U.S.regulatory agencies that evaluate TCE. Dr. Ozonoff, 4/15/98,p. 181. While Dr. Ozonoff agreed with IARC methodology,he clearly does not follow it. Ozonoff, 4/15/98, p. 172. Dr.Ozonoff's extrapolations from studies of other “solvents” arecontrary to what appeared to be generally accepted scientificmethodologies.
It also does not appear to be generally accepted epidemiologicmethodology to presume that different diseases may bepresumed to have a common etiologic origin until such isdemonstrated. See Cole, RT, 4/29/98, p. 144. As Dr. Guzeliantestified, one of the lessons that science has apparentlylearned about known carcinogens is that “when they act, theyact at a specific site or perhaps one or two sites, but theydon't act in a disparate way.” See Guzelian, RT, 4/23/98, p.59. It does not appear that simply “aggregating” diseases, forthe purpose of establishing causation, is a generally acceptedscientific methodology.
There is simply no reliable human epidemiology thatestablishes a causal relationship between TCE and leukemia
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or Hodgkin's disease. Dr. Ozonoff's “assumption” that thediseases, Hodgkin's disease, leukemia, and NHL are the“same” or very similar diseases and that, therefore, allepidemiology studies can be relied on is simply not supportedby the evidence. Dr. Mueller, 4/27/98, p. 91. Dr. Ozonoff'slumping of the lympohematopoetic cancers derived from aserious methodological flaw-that is his use of “genotoxicity”to create a novel theory for identification of carcinogens.There is clearly no evidence in the record to suggest thatthis theory of data interpretation is generally accepted by anyscientific community.
*24 It also appears that Dr. Ozonoff's heavy relianceon experimental animal studies and the nature ofthe extrapolations he drew from them are not propermethodologies which scientists recognize as generallyacceptable. Finally, it appears that Dr. Ozonoff's attempt toapply “differential diagnoses” to determining whether TCEcaused specific plaintiff's illnesses is unequivocally rejectedby the scientific community as an inappropriate basis uponwhich to make a causation determination. Plaintiffs' expertfailed to use any generally accepted method to demonstrateor calculate any increased risk that any of the plaintiffs wereexposed to as a result of their contact with TCE. As Dr.Ozonoff admitted on cross-examination, a “meaningful” riskis something that increases the risk by 50 percent or doublesor triples it. Thus, it is clear that some risk calculation couldhave been made and it appears that appropriate scientificmethodology demands that some attempt be made to evaluatethe risk based on the exposure incurred by the individualplaintiffs. That requirement was clearly not fulfilled by theattempt to misapply the well-recognized medical use of a“differential diagnoses” in an attempt to “rule out” othercauses and by process of elimination arrive at a singularcause-TCE-for the various diseases. The reliance on thisapproach resulted in sheer speculation by the expert.
Dr. Ozonoff's and Dr. Lemen's testimony is, therefore,inadmissible for the above reasons.
DR. OLSHAN
Plaintiffs noticed Dr. Jerry Olshan, an osteopathic physician,as an expert to testify about the various causes of the plaintiffs'diseases with respect to NHL, leukemia and Hodgkin'slymphoma. Under Arizona Rules of Evidence 702, a witnesscannot testify as an expert unless he or she possesses thenecessary level of “knowledge, skill, experience, training or
education.” This Rule requires a court to decide whethera witness' training and experience qualify him to renderopinions of an expert nature. Lay v. City of Mesa, 168 Ariz.552, 554, 815 P.2d 921 (App.1991).
Dr. Olshan lacked the necessary training and experience tooffer an opinion necessary to assist the jury in this case.Dr. Olshan had no training or background in toxicology,epidemiology, occupational medicine or environmentalmedicine. He had almost no practical experience with diseasecausation, because his medical practice did not involvediagnosing the cause of diseases. Furthermore, he has neverconducted any research on the origin of Hodgkin's disease,NHL or leukemia, the three diseases for which he was goingto offer an individual causation opinion in this case. Norhas he ever conducted any research into TCE and, in fact,it appears that he no prior contact with the literature in thisarea at all prior to this litigation. Moreover, it appears thatplaintiffs' counsel were primarily responsible for “educating”Dr. Olshan in order to attempt to develop an expertisesufficient to allow him to testify at trial on the issue ofcausation.
*25 Assuming that general causation has been established, ascientist must next consider the specific individual's medicaland exposure history. The expert must inquire as to whetherthe individual has experienced a dose of sufficient magnitudeto be capable of producing the observed disease or ofso increasing the risk of disease as to demonstrate likelycausation. See, Dr. Grufferman Affidavit, p. 6, paragraph24. In order to be anything more than speculation, thisdetermination requires support in reliable epidemiologic dataor other science. In other words, a scientist or expert must beable to point to data which demonstrated a generally acceptedmethodology supporting the conclusion that the plaintiffexperienced an exposure dose in duration comparable to otherdata which supports the conclusion. Id. However, if evidencefrom high-dose setting shows no association, it is very likelythat there also will be no causal association in settings withlower environmental exposures. See Cole Affidavit, p. 12,paragraph 40. An expert must be able to account for and ruleout alternative risk factors for an individual's disease. Dr.Grufferman, p. 6 paragraph 25.
Dr. Olshan lacks the specialized training necessary to offerhelpful, expert testimony on sophisticated issues of medicalcausation relevant to this case. The fact that Dr. Olshan
is a practicing osteopathic physician does not demonstratethat he is “automatically qualified to answer any questionrelating to medicine.” See Gaston v. Hunter, 121 Ariz. 33, 51,588 P.2d 326 (App.1978). The plaintiffs' choice of approachto demonstrating causation has effectively insulated Dr.Olshan's opinion from any effective cross-examination. Dr.Olshan has no experience, special knowledge, or educationrelating to TCE, its composition or its effects and, in fact,does not consider himself to be a medical causation expert.RT, 4/16/98, p. 39. Not until after this case was commenceddid Dr. Olshan first obtain any medical treatises addressingthe issue of causes of cancer in humans. Dr. Olshan did notundertake any comprehensive review of the medical literatureaddressing causation and even admitted that much of theliterature he reviewed was specifically selected by plaintiffs'counsel. RT, 4/16/98, p. 39. Given his lack of training andbackground, it is clear that Dr. Olshan simply does not possessthe level of knowledge necessary to permit the jurors toevaluate any opinions he may have related to alleged medicalcausation of the plaintiffs' diseases for which he was tenderedas an expert.
Dr. Olshan is incapable of applying the Hill criteria to supporta causation opinion and is unable to explain, describe, orapply them as part of a scientific causation methodology. Dr.Olshan would not be able to assist the jury in deciding anyissue relevant to this case. Dr. Olshan has essentially testifiedthat his opinion is grounded upon the conclusions and reportdeveloped by Dr. Ozonoff. Dr. Olshan's testimony, if it wereto assist the jury, would require that he be able to offer reasonsfor his conclusions about the causation of the diseases in theplaintiffs. He simply does not have the education, training, orbackground to justify his conclusions.
*26 The ability to diagnose and treat a disease issubstantially different from the expertise required to assessits genesis to a reasonable degree of scientific certainty.It is undisputed that Dr. Olshan has never rendered ascientific opinion regarding whether a toxic agent causeda specific individual's disease. While Dr. Olshan claimedto have reviewed literature about TCE, his familiarity withthe chemical and its effect on humans and animals is quitelimited. His awareness of epidemiologic studies is apparentlylimited to those relied upon and discussed by Dr. Ozonoff.He was essentially unfamiliar with the studies in general andcould not discuss them at trial in a manner which wouldpermit the jury to evaluate his opinion. When unable to
explain the basis for his conclusions, Dr. Olshan inevitablyfell back upon the rationale that if Dr. Ozonoff set it forth inhis report, it was the basis for his opinion.
Dr. Ozonoff was not offered as a plaintiff-specific causationexpert (until far too late in these proceedings) and, in fact,made it quite clear during his testimony that he “did nothave the time” to review the individual plaintiff's cases tomake such a determination. Therefore, the trier of fact wouldhave to rely exclusively upon the analysis of the literatureand science by Dr. Ozonoff to determine actual causationin each specific plaintiff's case. It was apparent that Dr.Olshan was not prepared to offer such testimony to a jury. Dr.Olshan also admitted that his novel opinion that TCE causedHodgkin's disease, non-Hodgkin's lymphoma and leukemiawere not generally accepted in the scientific community.Olshan, Deposition, pp. 78-108. Dr. Olshan also testified thatthe sole basis for his conclusion that TCE could cause thosediseases was based upon Dr. Ozonoff's opinion. Id. p. 148.In fact, further supporting this Court's conclusion that Dr.Ozonoff's theories are not generally accepted in the scientificcommunity, plaintiffs' own purported expert, Dr. Olshan,indicated that he was not aware of any other scientist whobelieved that exposure to TCE could cause any of the diseasesthat Dr. Olshan was testifying about other than Dr. Ozonoffand the unidentified authors of a few studies. Dr. Olshan'sapparent exclusive reliance on Dr. Ozonoff's report, whichwas prepared in connection with litigation, to the exclusionof any independent literature or other scientific evidence isnot part of any generally accepted causation methodology. Dr.Grufferman, 4/24/98, pp. 153-154; Dr. Guzelian, 4/23/98, pp.103-104.
Not only did Dr. Olshan fail to apparently conduct anyindependent review or analysis of the literature addressingthe health effects of TCE, but he was also unable to provideany scientific or methodological basis as to how he arrivedat his ultimate conclusion in the individual cases of theseplaintiffs. Incredibly, Dr. Olshan testified that although hewould probably not be able to understand the “negative”epidemiological studies concerning TCE that they would stillnot alter his opinion even if the studies were shown to him andexplained. He testified that he would change his opinion onlyif he consulted with Dr. Ozonoff and Dr. Ozonoff concurred.Deposition at 221-222. Thus, as the defendants argue, Dr.Olshan was not prepared to testify about medicine or science,his testimony was simply dogma.
*27 Interestingly, one of the few authorities Dr. Olshanrelied upon, a textbook on cancer by Schottenfeld andFraumeni, which he acknowledged as an “authoritativetreatise on the causes of cancer in humans” and a sourceupon which he relied for his current knowledge of Hodgkin'sdisease, non-Hodgkin's lymphoma and leukemia, did not listTCE as a risk factor for any of those diseases. The textdoes not even mention TCE. However, in the chapter onHodgkin's disease, it does state that no chemical compoundshad been identified as risk factors for Hodgkin's disease andthat the data in any event was not consistent. (See Plaintiffs'Exhibit 761.) Dr. Mueller, one of the authors of the text,testified that this conclusion remains generally accepted inthe scientific community today. See Mueller, RT, 4/27/98, pp.96-97. When confronted with this passage from the textbookand questioned about its failure to support any connection ofTCE to disease causation, Dr. Olshan testified that it wouldhave no effect on his causation opinions although he wasunable to identify any methodology which allowed him todismiss the conclusions set forth in the text.
The inability to offer any basis for his opinions was pervasivein the foundation for Dr. Olshan's testimony. He was simplyunable to offer any explanations about how he arrived athis causation opinions other than to justify them by relianceupon Dr. Ozonoff's report. It is also clear that Dr. Olshan,like other plaintiffs' experts, arrived at his causation opinionslong before he knew the amount of TCE exposure to any ofthe plaintiffs. Dr. Olshan merely assumed that each plaintiffhad been exposed to a “significant” amount of TCE. Whilethis term was never precisely defined during the affidavitsor testimony during the hearing, it appears that the plaintiffs'experts agreed that the amount was over the M.C.L. § set bythe EPA of 5 ppb. However, there is no generally acceptedscientific basis for drawing conclusions about carcinogenicitybased solely on evidence that exposure might have, at times,been above 5 ppb.
It was also apparent that Dr. Olshan had no knowledge aboutthe specific levels of TCE which might be toxicologicallysignificant and, therefore, he was clearly insulated from cross-examination on this important issue. Although Dr. Olshanclaimed to have considered and “ruled out” the plaintiffs'exposure to various chemicals and other environmentalfactors known to cause cancer, he made no effort to assessthe level of those exposures or to explain how other risk
factors played no part in his causation determination. Again,it appears that his inability to do so was based upon hislack of knowledge, experience and training in the area ofmaking causation determinations about environmental factorscapable of causing cancer. Dr. Olshan's reliance on theM.C.L. § as predictive of cancer risk was clearly misplaced.The EPA's calculation of the M.C.L. § is a regulatory levelthat is designed only to protect not to predict. As Dr.Guzelian explained, the EPA's risk assessment methodologydetermines the highest theoretical number of excess cancersthat may occur in the population exposed continuously tocertain levels of TCE for 70 years. See Guzelian, RT, 4/23/98,pp. 79-92. Based on that methodology, the results are that oneexcess cancer in a population of one million may theoreticallyoccur. This does not even mean that one excess cancernecessarily will occur as the EPA qualifies that statement bynoting that “such an estimate, however, does not necessarilygive a realistic prediction of the risk. The true value of the riskis unknown and may be as low as zero.” Dr. Guzelian id.
*28 Finally, in conducting his purported medical causationanalysis, Dr. Olshan misapplied the clinical diagnostictechnique of “differential diagnosis.” As Dr. Olshanrecognized, that technique is used by clinicians to identifyparticular diseases or problems which an individual patientmay have based upon the patient's symptoms. Dr. Olshanand Dr. Ozonoff both improperly attempted to expand thiswell-recognized clinician tool to an improper techniqueof causation methodology. See Dr. Li Affidavit, p. 8,paragraph 22. Dr. Olshan was neither a properly qualifiedexpert witness, Rule 702, 703, nor did he demonstrate thathis conclusions were supported by any generally acceptedmethodology.
Dr. Olshan's testimony is, therefore, inadmissible for theabove reasons.
DR. MILLER'S OPINION REGARDING CAUSATIONOF PLAINTIFFS' RHABDOMYOSARCOMA
The defendants attack both Dr. Miller's qualifications totestify on the causation of rhabdomyosarcoma as well as themethodology in arriving at his opinion. By his own admission,Dr. Miller has never conducted any research concerningrhabdomyosarcoma nor has he ever treated a patient with thatdisease. RT, 4/21/98, pp. 55-57. In fact Dr. Miller testified thiswas the first time he has ever attempted to determine the causeof rhabdomyosarcoma (RMS) in any individual. Dr. Miller's
lack of expertise in this area was clearly evident during hisdeposition. (Deposition pp. 73-76). Dr. Miller admitted thatwhat he knows about RMS he has learned during this case.RT, 4/21/98 id. Dr. Miller's lack of expertise, experienceand knowledge about RMS is indicative of a more profoundunfamiliarity with cancer epidemiology in general. Dr. Millerwas unfamiliar with cancer epidemiology in general, has notlooked at any cancer epidemiology textbooks outside thecontext of litigation. RT, 4/21/98, p. 49. Incredibly, Dr. Millercould not articulate the Hill criteria and admitted that he didnot know what the criteria were or how to apply them. (MillerDeposition, pp. 68-69).
Dr. Miller's lack of expertise with RMS and cancerepidemiology extended to his lack of experience and trainingwith respect to TCE. Dr. Miller conceded that causes of RMSwere not an area that he specialized in.
Even assuming that Dr. Miller had the necessary training,education or experience on the subject of causation ofRMS, Dr. Miller's specific causation opinions are premisedon the general causation theory that TCE causes RMS inhumans. Dr. Miller conceded that he could not name anyother scientist who shared his belief that TCE causes RMS.RT, 4/21/98, p. 61. Dr. Grufferman confirmed that Dr.Miller's theory is not generally accepted by the scientificcommunity. Dr. Grufferman has studied RMS for over 15years. He noted that the accepted methodology for answeringthe general causation question consists of the applicationof the Hill criteria. See Grufferman, Affidavit, paragraph22. He also noted that accepted methodology for reachingcausation conclusions requires consideration of both generaland specific causation. That is, first, can the chemical at issuecause the disease generally? Second, did the chemical at issueactually cause this specific individual's disease? Grufferman,Affidavit, paragraph 21; RMSE, p. 167.
*29 Dr. Grufferman also testified that in applying the Hillcriteria to determine causation it is not appropriate to ignorethe lack of a strong, specific or consistent epidemiologicassociation and then rely principally on analogy to differentchemicals or diseases. Id . paragraph 23. Dr. Gruffermantestified that such analogies may be useful for generatingacademic hypothesis for further study, but that they do notprovide a reliable foundation for reasonably certain scientificcausation conclusions. Id. Dr. Grufferman also noted that Dr.Miller failed to follow any scientifically accepted or reliable
methodology in reaching his conclusion that TCE exposurecaused the plaintiffs' RMS. Id. paragraph 29. Dr. Gruffermanstated that Dr. Miller's opinions constitute “a speculativehunch or guess, rather than a causation conclusion groundedon reliable scientific data.” Id. paragraph 29. Dr. Gruffermantestified that Dr. Miller's general causation opinion aboutRMS had no foundation in the scientific literature, had neverbeen published or peer reviewed, and, to his knowledge wasnot shared by any body of scientists. Id. paragraph 30.
Furthermore, Dr. Grufferman noted that even in Dr. Miller'sown affidavit he admitted that he had no scientific datashowing any excess of RMS in TCE-exposed populations.He further noted that although Dr. Miller cited 10 articlesin support of his conclusions, that none of those articlesdrew any association between TCE and RMS and noneprovided any foundation for drawing a scientific conclusionabout “association, let alone causation.” Id. paragraph 33.Dr. Grufferman accurately noted that none of the articles didmore than suggest the hypothesis that workers exposed to anunspecified mixture and dose of chemicals might be at anincreased risk of cancers-but cancers other than RMS! Dr.Grufferman concluded that it was not scientifically acceptableto extrapolate from such generalized articles and studies toa completely different conclusion that TCE causes RMS. Id.paragraph 32. More specifically, Dr. Grufferman stated thatit was simply not an acceptable scientific methodology toassume that because one chemical might be associated withcancer generally that this specific chemical, TCE, causesRMS. Id.
Dr. Grufferman is perhaps the world's foremost expert onthe etiology of childhood RMS having conducted moreoriginal research on the subject than any other person in theworld. RT, 4/24/98, p. 150. Dr. Grufferman testified thatDr. Miller's general causation theory was “conjecture” and“absolute science fiction” without any support in the scientificliterature. RT, 4/24/98, p. 207. Incredibly, Dr. Miller testifiedthat his opinions were based primarily on research conductedby Dr. Grufferman! Dr. Grufferman, who holds a medicaldegree as well as a Master's Degree in Public Health, a Masterof Science in Epidemiology from Harvard University Schoolof Public Health and a Doctorate of Public Health fromHarvard, has conducted extensive original research in the areaof Hodgkin's and non-Hodgkin's lymphoma and was electeda fellow of the American Association for Advancement ofScience “for important contributions to the epidemiology
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of leukemia and the lymphomas.” Grufferman, Afidavit,paragraph 11.
*30 Dr. Grufferman's conclusion that Dr. Miller'sconclusions were based on his “own speculative, misleadingextrapolations from dissimilar studies that typically involveother cancers or other chemicals and provide no reliablescientific basis” is clearly supported by all of the evidencepresented thus far in both affidavits and during testimonyat the hearing. Dr. Miller testified there is not a singleepidemiologic study of any kind that reports an associationbetween TCE and RMS. RT, 4/21/98, p. 22. No animal studiessupported Dr. Miller's theory. He failed to explain how theetiology of other diseases that he claimed were demonstratedby animal studies could be utilized to form a conclusionabout the cause of RMS in humans. The defendants notedon several occasions that Dr. Miller's testimony has beenexcluded in other cases. See e.g. Christopherson, 939 F.2d1106 at 1108, 1115. As in Christopherson, this Court findsthat Dr. Miller's opinion was supported only by his credentialsand his persistent refusal to acknowledge the inadequacy ofhis methodology.
Dr. Miller's attempt to extrapolate his conclusion that becauseTCE is genotoxic that it is “at least plausible” that TCE mightcause cancer at different sites is also clearly an unacceptablescientific approach to a causation conclusion. No scientist hastestified in these hearings by way of affidavit or otherwisethat simply because something is “plausible” that it is anaccepted scientific basis upon which to draw a causationconclusion. Even Dr. Levy, another plaintiffs' expert, agreedthat the proper methodology for determining the cause ofplaintiffs' RMS required examination of the exposures thatthe developing fetus might have encountered as a result of themother's exposure. He also testified that it was important tolook at environmental, occupational and other exposures ofthe parents prior to conception. See Dr. Levy, RT, 4/17/98,p. 50. Yet, Dr. Miller admitted that he did not have that typeof information prior to making his causation opinions. Dr.Miller RT, 4/21/98, p. 68. Nor did Dr. Miller ever attemptto review the plaintiffs' medical records or their families'medical records even though the records would have revealedthe presence of many risk factors that Dr. Miller consideredto be relevant to the issue of causation.
Dr. Miller admitted that the history of one of the plaintiffs,consisting of two major congenital birth defects, together
with the development of RMS, precluded ruling out aninutero event as the cause of that plaintiff's RMS! RT, id.pp. 77-78. Rather than scientifically rule out that risk factor,however, Dr. Miller simply dismissed it assuming withoutexplanation that TCE still played a role in the developmentof RMS. Interestingly, Dr. Miller's affidavit opined that in-utero exposure to TCE could have caused both the plaintiff'sbirth defects and RMS! However, there was no dispute in theevidence that the plaintiff had been conceived and born inthe State of New York and there was no possibility that TCEwas possible for any in-utero events. However, Dr. Millercompletely ignored the high likelihood that the plaintiff wasexposed to radiation in-utero. Dr. Miller conceded that in-utero radiation was a risk factor for RMS.
*31 Dr. Grufferman noted that while pregnant with theplaintiff, the plaintiff's mother had at least two portable chestx-ray examinations. Dr. Grufferman noted that portable chestx-rays convey large doses of ionizing radiation and that itwas likely that the plaintiff suffered considerable radiationexposure prior to birth. RT, 4/24/98, p. 203. Finally, Dr.Miller expressly refused to offer an opinion that TCE wasa “but-for” cause for either of the plaintiff's RMS. Thus,the plaintiffs failed to create a jury question on the mostessential element of their case-even assuming that Dr. Millerhad been qualified to offer an opinion and had followedproper scientific methodology in forming it-which he did not.
Dr. Miller's testimony is, therefore, for the above reasonsinadmissible.
DR. KILBURN'S OPINION REGARDING BRAINTUMORS
Dr. Kilburn's proffered opinions concerning a cause/effectrelationship between plaintiffs' exposure to TCE and thediseases of which plaintiffs complain is without sufficientfoundation, was not derived from generally acceptedmethodology, was not based on any reasonably reliablescientific methodology and is speculative and conjectural.His methodologies utilized in this case do not appear to beaccepted by the medical or scientific community.
Dr. Kilburn was the plaintiffs' expert who opined thatexposure to TCE caused primary brain tumors in four of theplaintiffs. The defendants argue that Dr. Kilburn's hearingtestimony only confirmed that the purported methodologythat he used to reach his opinion was not generally accepted
in the relevant scientific community and was not of a typereasonably relied upon by experts in the field.
At his deposition, Dr. Kilburn had testified that he was notaware of any studies that demonstrated that TCE exposure cancause brain tumors in humans. Kilburn, Deposition at p. 14.Dr. Kilburn has testified that he has no special expertise inbrain tumors. At the evidentiary hearing, Dr. Kilburn couldnot testify as to whether his opinion that TCE caused braincancer was generally accepted in the relevant medical orscientific community. (RT, 4/22/98, p. 125).
There is clearly a scientific community that addressesthe causes of brain tumors. Dr. Bigner, who testified onbehalf of the defendants, testified about the existence ofan “international neuro-oncology community” and that itdid not consider TCE as a cause or even a potential causeof brain tumors. This testimony was unchallenged by Dr.Kilburn or any other plaintiffs' “expert”. (RT, 4/27/98,p. 114). Dr. Bigner also testified that there was not asingle published study indicating that TCE has caused braintumors in laboratory animals even at maximum tolerateddoses throughout their effective lifetimes. There appeared tobe a complete absence of any literature demonstrating anassociation between TCE and brain tumors in human beingsat low-levels of exposure.
During his testimony, Dr. Kilburn attempted to rely on severalscientific studies which he alleged supported his position.The defendants argue that he never discussed or mentionedany of these studies anywhere in his expert report whichplaintiffs were required to file in early 1997. During hisdeposition, Dr. Kilburn testified that in reaching his opinionabout causation, he had relied only upon literature cited inhis report. Dr. Kilburn's opinion also apparently changedduring his testimony at the hearing in this case regardingcausation. Dr. Kilburn had been unwilling to testify duringhis deposition that it was his opinion that “but-for” exposureto TCE plaintiffs would not have developed brain tumors. SeeKilburn Deposition, p. 83; RT, 4/22/98, p. 157. The plaintiffsapparently are taking the position that because Dr. Kilburnconducted a later survey of scientific literature to determinewhether there were any studies that might support an opinionof causation that this “methodology” should be consideredappropriate.
*32 The epidemiological evidence has apparently nevershown an association between TCE and primary brian tumors
in humans nor have any experimental animal studies shownsuch a relationship. Dr. Bigner testified that a generallyaccepted methodology, supporting a causation opinion thatTCE causes primary brain tumors in humans, would includedemonstrating that TCE is an animal neuro-carcinogen inexperimental animal studies. Furthermore, in order for ascientist to arrive at this type of conclusion, the methodologywould require that human epidemiological studies bereproduced “in time, in space and by others” to support astatistically significant association between TCE exposureand development of brian tumors in humans. Finally, thescientists would have to demonstrate a biologically plausibleexplanation for the associations. (RT, 4/27/98, p. 92; Bigner,Affidavit, paragraph 13). The methodology suggested by Dr.Bigner appears to be consistent and corroborated by thetestimony of all of the other experts testifying in this case.
Although Dr. Kilburn purports to place a great deal ofimportance on human epidemiological studies prior tothe hearing, the only study apparently upon which Dr.Kilburn relied that specifically considered whether TCE wasassociated with brain cancer in humans was a 1994 study byHeineman, et al (Plaintiffs' Ex. 493). Dr. Kilburn indicatedthat this study was the “key” study upon which he relied.See Kilburn Affidavit, paragraph 18; Kilburn Deposition,p. 49. However, this “key” study apparently found nostatistically significant association between exposure to TCEand incidents of brain tumors. Even though Dr. Kilburnattempted to suggest that his causation opinion was based onother studies at the hearing, it was clear that these studiesdid not support his conclusion. The literature relied uponeither did not mention TCE at all or evaluated it only in thecontext of mixed solvents and he ignored studies that foundno association between TCE and brain tumors. The testimonyfrom other scientists during the hearing overwhelminglydemonstrated that this is clearly not appropriate methodologyfor a scientist to follow in arriving at a causation opinion.Again, the conclusion appeared to be more litigation-driventhan science oriented.
Dr. Kilburn did not and apparently could not challengeDr. Bigner's testimony that not a single study showed thatTCE caused brain tumors in animals, let alone humans.See Bigner testimony RT, 4/27/98, p. 88-90. Nor did Dr.Kilburn ever dispute that TCE appears to have none of thespecific properties common to known animal carcinogensaccording to standard criteria used in the neuro-oncology
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community. (Bigner, RT, 4/27/98, p. 33; Bigner Report at31). Although Dr. Kilburn apparently believed that animalstudies were very important to his conclusion that TCEwas a carcinogen, he apparently considered it unimportantthat none of the studies had found TCE to have causedbrain tumors in animals. (RT, 4/22/98, p. 92). Interestingly,Dr. Kilburn suggested that a proper animal had not beenidentified to accurately determine in an experimental animalstudy whether brain cancer excesses could be detected.Dr. Bigner's testimony on this point was more credibleand contradicted Dr. Kilburn's apparently unsupported andspeculative statement. Dr. Bigner, who has apparentlyconducted numerous experiments with chemical and otheragents to cause the induction of brain tumors in animals,testified that a particular rat used by the NTP is an excellentstrain to use in detecting neuro-carcinogens and that braintumor excesses had been detected in this strain upon exposureto ethylene oxides and other chemicals. (Bigner, RT, 4/27/98,p. 91).
*33 Finally, Dr. Kilburn agreed that in making a causationdetermination that it was important to consider whethera chemical was biologically capable of causing disease.Although Dr. Kilburn appeared to agree that DNA damage isa necessary initiating event to cancer formation in the brian,he presented no evidence other than his own speculationto support his theory that TCE causes such damage inastrocytes-the type of brain cells in which cancer developedin these plaintiffs. Dr. Bigner testified that there are manymechanisms in the brain that protect and repair its cells.Thus, he stated the critical issue is not whether TCE causesDNA damage but whether it causes unrepaired DNA damagein astrocytes. Dr. Kilburn apparently completely failed toconsider this fact and it appears that it would be impropermethodology to proceed forward to a conclusion based onincomplete consideration of this issue. Moreover, Dr. Kilburndid not cite or rely on a single study, publication or anyother type of scientific evidence to support his theory thatTCE causes damage to the brain's DNA. Apparently theonly basis for his assumption was that he agreed with Dr.Ozonoff's conclusion that TCE was genotoxic. Neither of thestudies upon which Dr. Ozonoff or Dr. Kilburn indirectlyrelied discusses whether TCE causes genetic damage tohuman brain cells. It is indisputable that neither articleconsidered whether the brain's protective mechanisms repairsuch damage.
As Dr. Bigner noted in his report, the only known causeof brain cancer in humans is ionizing radiation. However,there are a number of inherited or genetic syndromes thatmay contribute to the development of brain tumors. (BignerReport at 2). Dr. Kilburn apparently did not consider anygenetic components or attempt to discuss or evaluate howthey may have caused or contributed to the plaintiffs' cancers.Dr. Kilburn's elimination from consideration of alternativerisk or confounding factors does not appear to be in stepwith mainstream scientific thought on proper methodologyfor arriving at causation opinions.
Dr. Kilburn's testimony is, therefore, for the above reasonsinadmissible.
DR. KILBURN'S OPINION REGARDING LUPUS
The defendants argue that the only evidence plaintiffspresented for their contention that TCE caused the lupusdiseases of the plaintiffs involved in this case was thetestimony of Dr. Kilburn. Initially, the defendants argue thatDr. Kilburn could not be considered a member of the “relevantscientific community” capable of offering an opinion as tothe cause of lupus in this case. They note that Dr. Kilburnis neither a rheumatologist nor an immunologist. Moreover,they note that Dr. Kilburn conceded that his theory that theTCE exposures in this case caused lupus is a theory that hasnot been generally accepted within the medical community.(Kilburn deposition at 177). In fact, the defendants arguethat Dr. Kilburn's own research in this case contradicted thethesis that exposure to TCE can cause lupus because a studyconducted in the Phoenix area by Dr. Kilburn showed noassociation between exposure and the disease.
*34 Although purporting to rely on an epidemiologicalstudy that suggested an association between TCE and anincreased incidence of symptoms associated with lupus, theCourt finds that Dr. Ruddy's testimony that the conclusionsin the Kilburn and Worshaw study are not generally acceptedwithin the rheumatologic community as being persuasiveor reliable. The study appears to have had significant andsubstantial methodological flaws and the Court finds thatthe various scientists who testified in this case testifiedconvincingly that it is not appropriate methodology inarriving at a causation conclusion to rely on flawed studiesselectively chosen to support a causation conclusion.
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Dr. Kilburn also relied on other studies, which like othersrelied upon by plaintiffs' experts, were not related solely, toTCE but exposures to numerous potential carcinogens. Healso relied on another study that never mentioned TCE and inwhich the author suggested that the results they observed intheir study might have been caused by exposure to biologicfactors.
Dr. Kilburn also asserted that his novel scientific theorythat exposure to TCE can cause lupus can be found instudies that link exposure to TCE with the development ofscleroderma. The Court finds that is not generally accepted inthe rheumatologic community. The more credible testimonydemonstrated convincingly that these are distinctive diseasesand that evidence of etiology of one is not relevant necessarilyto the etiology of the other. See Dr. Ruddy, RT, 4/24/98,p. 33. Dr. Ruddy noted that contrary to the opinions ofDrs. Kilburn and Ozonoff, SLE and systemic sclerosis(scleroderma) are separate and different medical conditions.(Affidavit paragraph 35). Although these two diseases areclassified as “rheumatic disorders” and may share clinicalfeatures such as arthritis and a positive test for ANA, they aredistinct clinical entities and have different organ pathology.Id. He also noted that the American College of Rheumatologyused two different sets of classification criteria for the twodiseases. Dr. Ruddy's testimony substantially underminedthe reliability of the methodology purportedly utilized byDr. Kilburn in coming to his conclusion about the originof the SLE in the plaintiffs in this case. The Court findsthat Dr. Ruddy's testimony persuasively illustrated that themethodology utilized by Dr. Kilburn was not one generallyaccepted by the relevant scientific community in coming tocausation opinions regarding the origin or etiology of SLE inspecific individuals. Dr. Ruddy also explained how the animalstudies utilized by the plaintiffs would not be reasonablyrelied upon in the rheumatologic community as support forthe proposition that TCE causes lupus. (RT, 4/24/98 at pp.48-49). The Court finds that Dr. Ruddy's testimony wascredible and convincing regarding the differences betweenlupus and scleroderma; that is, the mechanisms of disease, thepathologies, the clinical presentation of the known risk factorsare clearly different. Thus, the Court finds that Dr. Ruddy'sconclusion that it is not an appropriate scientific methodologyto rely on evidence relating to the causes of sclerodermain making a judgment about the causes of lupus to be the
more credible and persuasive evidence on what is generallyaccepted in the relevant scientific community.
*35 As with other plaintiffs' experts, Dr. Kilburn filedhis report about the link between TCE and lupus beforehe received any information about the dose of TCE towhich the plaintiffs were allegedly exposed. Dr. Kilburn,as other plaintiffs' experts, merely relied upon counsels'statements that a “significant” exposure to TCE had occurred.As noted earlier, Dr. Guzelian offered a credible scientificopinion that generally dose is important to consideration oftoxicity. If dose is not specified, then generally potentialtoxicity cannot be evaluated. Dr. Kilburn failed to considerany dose-response relationship when utilizing his purported“methodology.”
The Court found particularly credible the testimony ofDr. Ruddy who found that Dr. Kilburn's purported“methodology” in this case was generally not accepted bythe relevant scientific community investigating the causes oflupus. As Dr. Ruddy stated, it is not possible to simply arraya list of risk factors for lupus, tick them off one-by-one andcome down to the last one and say, “well, that's got to beit, because 99 times out of a hundred it's none of those riskfactors but it is something else.”
Dr. Ruddy was the Chair of the Immunology Departmentat the University of Virginia. He is also the editor of theleading text on Rheumatology in the field. He is a Professorof Internal Medicine, Microbiology and Immunology in theDivision of Rheumatology, Allergy and Immunology at theMedical College of Virginia. He received his medical degreewith honors from Yale University School of Medicine anddid post-graduate training in Internal Medicine at HarvardMedical School. He has also spent time with the Public HealthService as an epidemiologist at the Communicable DiseaseCenter (now the Center for Disease Control and Prevention)in Atlanta, Georgia. He is board certified in Internal Medicineand in the sub-specialty of Rheumatology (since 1972). Heholds other board certifications in fields relevant to theinquiry before this court. As noted above, he has served forthe past 18 years as the co-editor of the leading textbook in thefield of Rheumatology. He testified and stated in his affidavitthat his area of research interest involves the mechanisms ofimmunologically-mediated inflammation. Such mechanismsunderlie the pathogenesis of many rheumatic diseases,including systemic lupus erythematosus (SLE). He has
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authored over a hundred peer-reviewed scientific articles atleast half of which are related to clinical aspects of rheumaticdiseases including systemic lupus. (Affidavit paragraph 14).
Like almost all other scientists who testified at the hearing,Dr. Ruddy indicated that accepted methodology in his fieldfor research and causation conclusions required considerationof both general and specific causation. (Affidavit paragraph22). Again, like almost all other scientists testifying at thehearing, Dr. Ruddy readily identified the Hill criteria asthe applicable criteria that scientists use before reachingconclusions about causation. See also IARC Monographon the Evaluation of Carcinogenic Risks to Humans, Vol.63 (1995) p. 16(d) (“Criteria for Causality”). Dr. Ruddynoted that in applying these criteria it is not appropriatefor a scientist to ignore the lack of a strong, specific orconsistent epidemiologic association and then rely principallyon analogy to different chemicals or diseases. (Paragraph24). Dr. Ruddy noted that in reaching a conclusion regardingspecific, individual causation that a “scientist must inquire asto whether the individual has experienced a dose of sufficientmagnitude to be capable of producing the observed diseaseor if so increasing the risk of disease as to demonstrate likelycausation. In order to be anything more than speculation, thisdetermination requires support in reliable epidemiologic data.In other words, the scientists should rely on epidemiologicstudies in which the cases experienced an exposure dose induration comparable to the individual in question.” (Affidavitparagraph 25).
*36 Dr. Ruddy also criticized the plaintiffs' experts'suggestion that no scientist can definitively rule out all otherrisk factors and pinpoint to a “single” cause. Dr. Ruddysuggested that the plaintiffs' experts had entirely missed thepoint. He stated, “The goal is not to definitively rule outother risk factors but rather to determine whether there isany basis other than speculation for the conclusion that aparticular risk factor caused (i.e. played a necessary role inthe development of) the individual's disease. For instance,if a systemic lupus patient is female, a long-term smoker,has been exposed to hydrazines in the work place, and hasa family history of systemic lupus or other autoimmunediseases, it would be difficult to do more than speculatethat some other less-established risk factor was more likelythan not also responsible for the systemic lupus.”. (Affidavitparagraph 26).
Dr. Ruddy's opinion is not simply an illustration that expertsdisagree but rather illustrates a much more fundamentalflaw in the basic methodology adopted by the plaintiffs'expert in arriving at a causation opinion. Dr. Ruddy alsotestified without contradiction that all of the literature inthe field suggested that drug-induced lupus was differentthan etiologic lupus. Dr. Ruddy indicated that all of theliterature suggested that when the agent causing drug-inducedlupus was eliminated, the disease was gone. Dr. Ruddy alsorejected as not generally accepted by the relevant scientificcommunity that scleroderma and SLE “evolve” or “morph”from one disease into the other. He stated that is a very rareevent and not generally accepted. He also rejected as havingany scientific merit the claim that the diseases have the sameetiology.
He also testified that the rheumatological communitygenerally did not rely on the dry-cleaner studies to concludethat TCE can cause lupus. He stated that there simply areno sound epidemiological studies that support the conclusion.Dr. Ruddy also criticized papers relied upon by plaintiffs'experts as utilizing improper methodology noting that thepapers were so flawed that no scientist could reasonablyrely upon them. It is interesting to note that the causationanalysis utilized by the IARC in coming to conclusions aboutthe carcinogenic effect of chemical agents suggested thatIARC's analysis also required an evaluation of the “qualityof individual epidemiological studies of cancer.” (IARCMongraph, id. p. 16). Thus, it appears supported byindependent sources that the testimony from defense expertsthat part of the accepted methodology for scientists in arrivingat causation conclusions is to evaluate the “quality of theepidemiological studies” relied upon is a part of an acceptedmethodology. Dr. Ruddy testified that no one in the relevantscientific community that he was aware of accepted theKilburn study as a reliable, quality study to be relied uponin drawing conclusions about TCE. Dr. Ruddy testified thatin the rheumatologic community TCE was not consideredas even having been shown to have an “association” withSLE. Dr. Ruddy noted that each of the studies relied onby the plaintiffs were flawed, weak, and didn't support thehypothesis for which they were being utilized. Dr. Ruddyalso rejected, without contradiction by any other scientists,the notion that a lack of “negative” studies was somehowimportant. Most scientists who testified agreed that it wasvery difficult to get negative studies published so there was no
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expectation in the relevant scientific community that negativestudies would necessarily exist.
*37 Dr. Kilburn's lack of awareness of importantepidemiological studies and risk factors related to SLEfurther undermine the Court's confidence in his attention toproper methodological methods in arriving at his conclusions.Finally, even assuming that Dr. Kilburn's testimony on lupusmight have been admissible, Dr. Kilburn could not opine asto the increase in risk of contacting lupus allegedly caused byexposure to TCE. See RT, 4/22/98, pp. 7-8.
Dr. Kilburn's testimony is, therefore, for the above reasonsinadmissible.
DR. GOLDBERG'S OPINION ON CARDIAC BIRTHDEFECTS
Dr. Goldberg, who is not a teratologist, asserted in his initialreport that it was more probable than not that the plaintiff'sexposure to trichloroeythlene and its “break-down products”caused the abnormal function of the aortic valve in oneof the plaintiffs in this action. (Dr. Goldberg Report p. 5).However, during his testimony, Dr. Goldberg was unwillingto testify that TCE, alone, more probably than not can causecongenital cardiac malformations. He was only willing tooffer the opinion that “TCE and PCE more probably than notcause-well, I have to strike the word ‘cause’-are associatedwith congenital cardiac malformations.” (RT, 4/14/98, p. 77).Thus, it is clear this testimony alone would not be sufficientto demonstrate a causal relationship sufficient to warrantsubmitting Dr. Goldberg's opinion to the jury even assumingit were otherwise admissible. However, for the reasons setforth by the defendants, Dr. Goldberg's opinion does not meetthe test for admissibility under Frye.
Dr. Goldberg based his opinion that TCE caused congenitalheart disease on an unacceptable methodology. Dr. Goldbergagreed that the epidemiologic study that he relied on stated,in its conclusion, that it did not establish a cause and effectrelationship between TCE and congenital heart disease. (RT,4/14/98, p. 103). He also agreed that animal studies didnot establish a cause and effect relationship in humans.Id. p. 76. There was simply no valid, reliable scientificbasis upon which Dr. Goldberg could have opined thatthe cardiac defect at issue in this case was caused by anyexposure to TCE. As noted by numerous other scientists, itis simply unacceptable scientific methodology for a scientist
to simply ignore epidemiological studies which do notdemonstrate consistency or specificity. It is also clear that hesimply disregarded basic principles accepted in the generalteratologic community and biological plausibility argumentsthat contradicted his position.
Dr. Brent's affidavit and testimony suggested that there is agenerally accepted methodology in the teratology communityfor concluding that a chemical or other agent may be ahuman teratogen. (Brent, Affidavit, p. 4; RT, 4/29/98, p.35). The criteria are self-explanatory and Dr. Goldberg'stestimony did not demonstrate that he followed them in anysignificant way. As noted by a number of the scientists whotestified, the Hill or other criteria for developing causationgenerally require that the causal association be reproduciblein time, space and by others. See RT, 4/29/98, p. 38; Bigner,Affidavit, p. 6; RT, 4/28/98, p. 57. It is interesting to notethat such studies do exist and have been reported for all otherrecognized teratogens. (RT, 4/29/98, p. 38). However, nosuch studies have ever been produced for TCE despite therelative frequency of study and the lengthy period TCE hasbeen in use. The sole study upon which Dr. Goldberg relied,his own, was demonstrated to have serious methodologicalflaws and the Court finds the testimony that the relevantscientific community would not find this study suitable forreliance in drawing conclusions in any accepted methodologyto be persuasive.
*38 The animal models upon which Dr. Goldberg reliedused chick embryos. Although chick studies are apparentlyappropriately used in teratology for studying embryonicdevelopment and mechanisms of abnormal development,they are never relied upon by teratologists to drawconclusions regarding a chemical's potential for humanteratogenicity. (RT, 4/29/98, p. 62). And although rat studiescan be useful in proving teratogenicity, the design and resultsof the rat studies relied upon by Dr. Goldberg were not of thetype scientists would rely upon in a proper methodology fordrawing causation conclusions.
Finally, Dr. Goldberg failed to consider the biologicalplausibility of his position. Dr. Brent's testimony wasconvincing in rejecting his study as based on any appropriateconsideration of biological plausibility for his conclusion.As with the other testifying plaintiffs' experts, Dr. Goldbergreached his causation opinion without knowing the doseor exposure the plaintiff's mother allegedly received during
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her first trimester of pregnancy. He “assumed” that sheexperienced a “significant” exposure. As with almost all ofthe other testifying plaintiffs' experts, it was unclear as toexactly how each interpreted this phrase. Dr. Goldberg alsopurported to use a “differential diagnosis” method to evaluatethe plaintiff's case which other experts have demonstratedconvincingly is not the generally accepted methodology inthe scientific community for making scientific causationdeterminations.
Dr. Goldberg's testimony, therefore, is inadmissible for theabove reasons.
DR. WEDEEN'S OPINIONS REGARDING KIDNEYDISEASE
The defendants argue that Dr. Wedeen's testimony at thehearing confirmed that his methodology underlying his“novel acceleration theory” was neither reliable nor generallyaccepted in any relevant scientific community. The defenseargues that in the absence of generally accepted theorythat TCE can accelerate preexisting kidney disease, that theplaintiff cannot meet her burden of showing that a triable issueof material fact exists on the element of causation.
Again, as with other plaintiffs' experts, Dr. Wedeen purportedto use a “differential diagnosis method” in evaluating theplaintiff in coming to a conclusion regarding the causationof her kidney disease. It is clear from the overwhelmingevidence in this case that no scientist would use a “differentialdiagnosis” to eliminate some risk factors and state that adisease was “caused” by a certain chemical agent. Thatis not an appropriate application of a well-recognizedclinical technique. Again, the testimony demonstrated thatDr. Wedeen's methodology was flawed for the same reasonsas other experts tendered by the plaintiffs. He relied on
selected on epidemiological studies which identified otherrisk factors associated with kidney disease which he simplyignored. He was unable to measure any effect of alternativerisk factors or to satisfactorily demonstrate how he eliminatedthem in applying what appeared to have been his own“unique methodology”. Like other experts, he also reliedon studies involving chemicals other than TCE, ignored thedose-response relationship in the studies he did rely on andapparently did not apply the Hill criteria of specificity byextrapolating from studies that involved other diseases.
*39 None of the materials upon which Dr. Wedeen claimedto be relying actually linked TCE to the specific chemical atissue and FSGS, plaintiff's specific condition. Thus, there wasno reliable scientific technique or methodology utilized uponwhich to draw his novel “acceleration” opinion. Finally, Dr.Wedeen admitted that there was nothing about the course ofthe plaintiff's disease that indicated that anything about it wasworse than it would have been had she not been exposed toTCE.
Dr. Wedeen's testimony, therefore, is inadmissible for theabove reasons.
IT IS ORDERED granting defendants' Motion in Limine and,in the alternative, Motions for Summary Judgment for thereasons set forth above.
IT IS FURTHER ORDERED that in view of the lack ofevidence on “causation” resulting from the above ruling thateach Motion for Summary Judgment as to these plaintiffsis granted and Judgment shall be entered on behalf of thedefendants.
IT IS FURTHER ORDERED defendants shall forthwithsubmit a form of Judgment for signature by the Court.
Footnotes
1 “Novel Scientific Expert Evidence in Arizona State Courts,” Eckstein and Thumma, Arizona Attorney, June 1998, p. 16.
2 Dr. Richard Lemen was also retained by the plaintiffs. He prepared a report, an affidavit, and testified. While it is not clear why
his opinion was not separately addressed by the parties in their closing memoranda, the Court notes that he was part of the “tiered”
causation approached adopted by the plaintiffs. He, along with Dr. Ozonoff, was presented as an expert in epidemiology who reviewed
the literature and opined about TCE's relationship to diseases. Dr. Lemen offered an expert epidemiologic opinion purporting to link
studies to disease “causation” (Hodgkin's, NHL, Leukemia, Lupus, and cardiac birth defects). His opinion suffered from the same
defects as Dr. Ozonoff's and will not be addressed separately.
