Blueprint
for General Causation Analysis
in Toxic Tort Litigation†
William O.
Dillingham
Patrick J.
Hagan
Rodrigo E.
Salas
I.
Introduction
This
article discusses some of the legal and scientific principles that are
appropriate to the step-by-step judicial determination of what type of general
causation expert testimony should be admitted in toxic tort cases. Specifically, it provides a blueprint for
analyzing general causation in the context of toxic tort litigation and
examines the extent to which Daubert I
and its progeny, when taken to their logical extensions, guide the
admissibility determination.[1]
Since
1923, when the United States Court of Appeal for the District of Columbia
Circuit decided Frye v. United
States,[2]
courts have been concerned with the introduction of “junk science” in the
courtroom. Rigorous examination of expert testimony,
(1) assur[es] that those persons most qualified
to assess the validity of the scientific technique would have the determinate
voice, (2) provid[es] a “minimal reserve of experts” to critically examine each
technique in a particular case, [and] (3) promot[es] uniformity of decision
based on finding consensus in the scientific community . . . .[3]
Additional compelling reasons exist for limiting the
encroachment of junk science into the courtroom: a “posture of judicial caution
in this area [is] supported by the considerable weight jurors tend to give to
scientific evidence presented by experts with impressive credentials,” a
“misleading aura of certainty . . . often envelops a new scientific process,
obscuring its currently experimental nature,” and “scientific proof may in some
instances assume a posture of mystic infallibility in the eyes of a jury.”[4]
Two key
legal concepts of causation have emerged as courts have attempted to keep junk
science out of the courtroom: general causation and specific causation. Courts define general causation as “the capacity of a product to cause injury,”
and specific causation as “proof that
the product in question caused the injury of which the plaintiff complains.”[5] General causation may be thought of as a
scientifically established cause-and-effect relationship. To satisfy this burden, sufficient hypotheses
and testing must be demonstrated to establish that a disease or condition can arise from exposure to a certain
substance. Specific causation, on the
other hand, involves a variety of factors including level, duration and
proximity of exposure, also known as “dose,” which tend to show that the
person’s alleged exposure, in fact, caused
his or her condition.[6]
Accordingly,
a toxic tort plaintiff’s burden is twofold: first, to show that the substance
to which he was allegedly exposed is capable of causing his injury; and second,
to show that said exposure was the actual cause of the injury.[7] Toxic tort plaintiffs must prove the
admissibility of their expert testimony in both general causation and specific
causation context by a preponderance of proof.[8] To determine whether a toxic tort plaintiff
can satisfy his or her burden of proof, courts must make “a preliminary
assessment of whether the reasoning or methodology underlying the testimony is
scientifically valid and of whether that reasoning or methodology properly can
be applied to the facts in issue.”[9] This article only addresses judicial
intervention and edification relating to general causation.[10]
The United
States Supreme Court in Daubert I,
when asked to determine what kind of expert testimony or evidence was
admissible under the Federal Rules of Evidence (“FRE”), enumerated several
factors to assist judges in performing their gate-keeping function.[11] The United States Court of Appeals in Daubert II expounded on that
gate-keeping function, holding that trial courts are to undertake a two-part
analysis: (1) whether the experts’ testimony reflects “scientific knowledge,” i.e., whether the experts’ findings are
derived by the scientific method; and (2) whether the experts’ testimony is
“relevant to the task at hand,” i.e.,
that it logically advances a material aspect of the proposing party’s case.[12] More recently, the Supreme Court clarified
that the gate-keeping responsibilities imposed by FRE 702 extend to the
testimony of all experts.[13]
The Supreme
Court has also acknowledged that, in disease causation cases, “conclusions and
methodology are not entirely distinct from one another.”[14]
The Court warned that,
[N]othing
in either Daubert or the Federal
Rules of Evidence requires a district court to admit opinion evidence that is
connected to existing data only by the ipse
dixit of the expert. A court may conclude that there is simply
too great an analytical gap between the data and the opinion proffered.[15]
A “methodology-based”
inquiry, as described herein, properly considers every aspect of the
reasoning/scientific process, from the selection of the data, to the
interpretation of that data and, finally, to the conclusions that may be
derived from the data.[16]
As discussed hereinafter, when
assessing expert medical causation testimony, a methodology-based inquiry
requires, at a minimum, consideration of the following factors:
·
Replicated human epidemiological studies to prove
causation in toxic tort cases;
·
Epidemiological studies that address the agent at
issue;
·
Epidemiological studies that address the disease at
issue;
·
Epidemiological studies that must be statistically
significant; while,
·
Opinions that rely solely on in vivo or in vitro studies
ought to be inadmissible.
The foregoing list of disease causation evidentiary
requirements demonstrates that valid epidemiological evidence is the lynchpin
of general causation and illustrates the depth to which analytical courts have
probed in evaluating general causation testimony in toxic tort cases. The following step-by-step general causation
analysis insures that there will be no bridging of the scientific method by
“leaps of faith” that might undermine the reliability of the entire scientific
reasoning process or the conclusions derived therefrom.
II.
Epidemiology: The Lynchpin Of
General Causation
Epidemiology is “the study of
distribution of disease in populations and the risk factors associated with
particular diseases.”[17] Epidemiology studies[18]
are the most useful and conclusive methodology used to validate causal
relationships in toxic tort cases.[19] “Epidemiologists use an analytical tool known
as the null hypothesis, which postulates that there is no association between a
specific exposure and a particular outcome.”[20] “The goal of an epidemiology study is to
determine whether one can reject the null hypothesis and conclude that, in
fact, there is an association between the exposure and the outcome.”[21] Accordingly, numerous courts have held that
epidemiological evidence is the prime scientific undertaking required to prove
general causation.
For
example, in Grant v. Bristol-Myers
Squibb,[22]
the court excluded the testimony of the plaintiffs’ experts due to their failure
to explain why their opinions should overcome the twenty epidemiological
studies that either found no association or no statistically significant
association between breast implants and systemic disease.[23] In fact, it has been stated that “epidemiological
studies provide ‘the primary generally accepted methodology for demonstrating a
causal relation between a chemical compound and a set of symptoms or disease.’”[24]
A.
Reference to Single Epidemiological Study Not Sufficient
Courts have
repeatedly held that the epidemiological evidence necessary to prove general
causation must be replicated,[25]
which requires that the association in an epidemiological study be observed in
other studies among different subjects and variables.[26] Replication of results is a basic requirement
of the scientific method as scientists generally cannot be assured that the
results of any individual study are not due to bias, confounding[27]
or chance.[28] The inability to replicate a study calls into
question the data therein, the analytical model utilized, the conclusions
reached and, at times, all aspects of the study. Thus, absent evidence from valid and
replicated epidemiological studies, a single study showing a cause-and-effect
relationship does not establish that relationship for purposes of general
causation.
III.
Epidemiological Studies Must Address Agent At Issue In Litigation
In order to establish general causation, the
epidemiological studies offered as a basis for expert opinion ought to address
the agents at issue in the litigation.[29]
In Siharath v. Sandoz Pharmaceuticals Corp.,[30]
two plaintiffs, each of whom suffered hemorrhagic strokes after taking a
bromocriptine drug, brought a products liability action against Sandoz
Pharmaceuticals. Both plaintiffs were
postpartum women who suffered a stroke after taking Parlodel, which was
prescribed to suppress lactation. The
issue before the court was whether the drug was capable of causing and whether
it, in fact, caused the strokes or whether the temporal association of taking
the drug and a subsequent stroke was merely coincidental.[31] The Siharath
plaintiffs argued that bromocriptine, the active ingredient in the drug
Parlodel, caused hypertension, seizures and ischemic strokes. The plaintiffs further contended that
Parlodel, through bromocriptine, could also cause hemorrhagic strokes.
On a motion to exclude the
plaintiffs’ expert testimony of causation, the determinative issue was whether
the epidemiological evidence relied upon by the plaintiffs’ experts was sufficiently
reliable and relevant to establish causation.
The Siharath court explained,
“the burden is on Plaintiffs to show that well-conducted epidemiological
studies do show a statistically significant relationship between Parlodel[ ]
and seizures and stroke. It is not
defendant’s burden to show the lack of such relationship.”[32] The Siharath
plaintiffs brought forward four epidemiological studies which investigated a
possible association between Parlodel and stroke. After examining the plaintiffs’ epidemiological
evidence, the Siharath court
concluded that each of the studies, for separate reasons, lacked the requisite
reliability to support the plaintiffs’ arguments that Parlodel could cause
seizures and hemorrhagic strokes.[33]
Since “no evidence [had]
been offered of an increase in postpartum strokes after [Parlodel] was approved
for suppression of lactation [and] no evidence [had] been offered of a decrease
of postpartum strokes after the approval for suppression of lactation was
withdrawn,” the court questioned whether “the causation opinions of plaintiffs’
experts [were] merely speculative and not
based on scientific knowledge.”[34] Thus, it was improper to simply extrapolate
from one chemical to another, or to lump chemicals together: studies where exposure
to the chemical is unverified, unquantified, unidentified, or otherwise
speculative cannot provide reliable foundational support for a causation
opinion concerning that chemical.[35]
As Siharath
demonstrated, in order for epidemiological evidence – or any other type of
reliable scientific knowledge – to be relevant, it must, at a minimum, address
the specific agent at issue. Where
experts offer general causation opinions, the scientific literature they rely
upon to formulate those opinions should include epidemiological studies that
concern the same agent at issue in the litigation; otherwise, the proffered
evidence ought to be inadmissible as it is unreliable.
IV.
Epidemiological Studies Must Address
Disease At Issue In Litigation
In order to establish
general causation, the epidemiological studies offered as a basis for expert
opinion should also address the specific diseases at issue in the litigation.[36] As the Siharath
court wrote, “the burden is on Plaintiffs to show that well-conducted
epidemiological studies do show a statistically significant relationship
between Parlodel and seizures and strokes,” and “. . . Plaintiffs’ [sic] have not pointed to a
single case report involving a postpartum woman who suffered a hemorrhagic
stroke.”[37]
The Texas Supreme Court in Havner also reiterated the requirement that, according to accepted
scientific methodology, epidemiology studies must address the disease of
concern. At issue in Havner was the cause of a birth defect
that resulted in Kelly Havner being born without fingers on her right
hand. During the course of her
pregnancy, Kelly’s mother had taken Bendectin to relieve nausea and other
symptoms associated with morning sickness.
Alleging that Bendectin had caused their daughter’s limb reduction
defect, the Havners sued Merrell Dow, the maker of Bendectin, on theories of
negligence, defective design and defective marketing. On a motion challenging the legal sufficiency
of the plaintiffs’ causation evidence, studies on Bendectin were submitted,
which demonstrated statistically significant results but that dealt with birth
defects other than limb reduction defects.
In determining the utility of these studies on the causation
relationship before it, the Havner court
wrote, “these studies cannot of course support a finding that Bendectin causes limb reduction defects.”[38]
It is improper to simply extrapolate from one disease
to another, or to lump diseases together.
Studies that analyze a different disease or a different form of a
disease do not, and cannot, provide any support for making a causal link
between the disease at issue and the agent in dispute.[39] As one court has stated, “[o]ne simply cannot
assume that just because a substance causes a particular kind of cancer, it
will cause another type.”[40] Therefore, studies that do not address the
disease at issue lack any indicia of scientific reliability and methodology.[41] For these reasons, when experts offer general
causation opinions, the scientific literature they rely upon to formulate those
opinions should include epidemiological studies that concern the same disease
at issue in the litigation. Otherwise,
the proffered evidence is unreliable and ought to be inadmissible.
V.
Epidemiological Studies Must Be Statistically Significant
In
order to disprove the null hypothesis, i.e.,
in order to establish an association between a specific exposure and a
particular outcome, epidemiologists must establish whether those individuals
exposed to the particular agent have a greater risk of developing the
particular outcome than those not so exposed.
In epidemiological terms, the difference in risk of contracting the
disease is known as the “relative risk.”[42] As the
Siharath court explained:
A relative risk of 1.0 means that the agent has no effect on the
incidence of disease. When the relative
risk reaches 2.0, the agent is responsible for an equal number of cases of
disease as all other background causes.
A relative risk of 2.0 implies a 50 percent likelihood that an exposed
individual’s disease was caused by the agent in question. . . . Thus, in
the world of epidemiology, the threshold for concluding that an agent was more
likely than not the cause of a disease is a relative risk greater than 2.0.[43]
Therefore,
to establish a causal relationship, the plaintiffs’ experts must be able to
opine a causation factor greater than 50-50 and must establish that the
purported chemical-disease association is statistically significant. Faced with the plaintiffs’ experts who could
not and would not opine a causation factor greater than 50-50, in Jones v. Ortho Pharmaceutical Corp,[44] the California Court of Appeal
declared:
If the experts cannot predict probability in these
situations, it is difficult to see how courts can expect a jury of laymen to be
able to do so. [¶] This requirement
does in some instances place extraordinary burdens of proof on claimants. But
once the theory of causation leaves the realm of lay knowledge for esoteric
scientific theories, the scientific theory must be more than a possibility to
the scientists who created it.[45]
The court further reasoned that since “[t]he testimony of plaintiff’s
experts [was] such that it was equally probable that the development of the carcinoma
in situ was due to a cause for which defendant could not be liable,” it could
only conclude “that plaintiff did not establish a prima facie case and that the motion for nonsuit was properly
granted.”[46]
Absent evidence that the
relative risk is equal to or greater than 2.0, there is a fifty percent or more
chance that the “disease was not associated with the exposure.”[47] Therefore, when the relative risk is less
than 2.0, the null hypothesis cannot be disproved.
In addition to measuring
relative risk, an epidemiological study must also measure the probability that
a particular risk is due to chance, a concept expressed in terms of a
confidence interval.[48] Under generally accepted epidemiologic
methods, a confidence interval indicates how much that observed results might
be expected to vary due to chance.
Specifically, a confidence interval shows the range of relative risk
values within which the result could be expected to fall ninety-five percent of
the time due to random variation or chance.[49] When the confidence interval is ninety-five
percent and contains a number greater
than one, chance is considered an unlikely explanation for the observed
result and the result is considered statistically significant. When the confidence interval is ninety-five
percent and contains the number one or a number less than one, the observed result is more likely than not due to
chance and, therefore, is not statistically significant. [50] Only when the confidence interval is
ninety-five percent and contains a number greater than one, may the observed
association be deemed a true association.[51] Only when chance is eliminated as a potential
cause of the observed association may the null hypothesis be disproved.
VI.
Opinions Relying Solely On In Vivo Or In Vitro Studies Should Be Inadmissible
Evidence of in vivo[52]
and in vitro [53]studies
alone is insufficient to establish causation, since there is no generally
accepted method for extrapolating from that type of evidence to reach
conclusions about similar effects in humans.[54]
Courts overwhelmingly hold that
drawing causation conclusions in humans from animal studies, in the absence of
confirming human epidemiology, is generally insufficient to satisfy
admissibility standards.[55] The main reason for these concerns is that “[e]xtrapolations
from animal studies to human beings generally are not considered reliable in
the absence of a credible scientific explanation of why such extrapolation is
warranted.”[56] The use of animal studies to prove causation
in humans has, at a minimum, two distinct disadvantages:
First,
extrapolating from animals to humans is difficult because “differences in
absorption, metabolism, and other factors may result in interspecies variation
in responses.” … Second, “the high
doses customarily used in animal studies requires consideration of the
dose-response relationship and whether a threshold no-effect dose exists.”[57]
In
addition, “laboratory animal studies . . . are generally viewed with more
suspicion than epidemiological studies, because they require making the
assumption that the chemicals behave similarly in different species.”[58]
Thus, to ensure that an expert’s
conclusions based on animal studies are reliable, “there must exist ‘a
scientifically valid link between the sources or studies consulted and the
conclusion reached.’”[59] Expert testimony concerning general causation
in humans, which is solely derived from animal studies, is unreliable and ought
to be inadmissible in a court of law.
Similarly, reliance on in vitro studies to opine general causation
in humans is insufficient to establish admissibility. Courts have consistently held that laboratory
studies on Petrie dishes or test tubes are not generally accepted as
predicative of the human experience.[60] The same concerns relating to in vivo studies are present (and are
amplified) in in vitro studies:
species specificity (differences in absorption, metabolism), route of exposure,
dose, etc. Accordingly, expert testimony
concerning general causation in humans, which is solely derived from in vitro studies, is unreliable and
ought to be inadmissible in a court of law.
VII.
Conclusion
In determining the admissibility of
expert causation testimony, trial courts should not only adhere to the judicial
process but also scrupulously analyze the proffered testimony to ensure that
the scientific process has been followed.
In performing their gatekeeping function, judges must strictly
scrutinize each step of the analytical process utilized by the expert in question
to determine the reliability of the proffered evidence or opinion testimony.
This article has outlined a few of the more prevalent scientific concepts that
courts have used to assist in determining the admissibility of expert testimony
offered on general causation.
Of note, there are additional, more
traditional concepts, which also guide the general causation
determination. These were expressly
recognized by the United States Supreme Court in Daubert I, and include: (1) whether the experts’ theories or
techniques have been tested; (2) whether the theory or technique has been
subjected to peer review and publication; (3) in the case of a particular
scientific technique, what is the known or potential rate of error; and (4)
whether the theory or technique has been generally accepted. Those concepts also have been subject of
ample commentary and judicial decisions and, therefore, have not been addressed
here. Those admissibility requirements
in conjunction with the instant “blueprint” should guide the resolution of the
first causation threshold, general causation.
Only after reliable, relevant, and
admissible evidence concerning general
causation has been put forth by a toxic tort plaintiff should the issue of specific causation be reached.
Endnotes
† Submitted by the authors on behalf of
the FDCC Toxic Tort and Environmental Law Section.
[1] Daubert v. Merrell Dow Pharms., Inc., 509
[2] 293 F. 1013 (D.C. Cir. 1923).
[3] People v. Leahy, 882 P.2d 321, 325 (
[4] Kelly, 549 P.2d at 1244-46.
[5] Siharath v. Sandoz Pharms. Corp., 131 F. Supp. 2d 1347, 1352
(N.D. Ga. 2001) (citing Wheat
v. Sofamor, S.N.C, 46 F. Supp. 2d 1351, 1357 (N.D. Ga. 1999) (product
liability action excluding testimony that failed to establish (1) that Parlodel
is capable of causing stroke
and (2) that Palodel did in fact cause
plaintiffs’ strokes)).
[6] Siharath,
131 F. Supp. 2d at 1352. See e.g.
D. T. Ralston, Toxic Tort Causation – Not
Just Chemical Exposure Plus Symptoms, Maely’s
Daubert Rep., Vol. 4, No. 5, at 15-25 (2000).
[7] See
e.g., Raynor v. Merrell Pharms.,
Inc., 104 F.3d 1371, 1376 (D.C. Cir. 1997).
[8] Daubert
I, 509
[9] Daubert
I, 509
[10] As the name implies, specific
causation inquiries are fact and case-specific.
This paper will focus solely on foundational principles dealing with
general causation and, therefore, will not explore admissibility requirements
concerning specific causation.
[11] Daubert
I, 509 U.S. at 593-95
(factors include (1) whether the experts’ theories or techniques have been
tested; (2) whether the theory or technique has been subjected to peer review
and publication; (3) in the case of a particular scientific technique, what is
the known or potential rate of error; and (4) whether the theory or technique
at issue has widespread acceptance).
[12] Daubert
v. Merrell Dow Pharms., Inc., 43 F.3d 1311, 1315 (9th Cir. 1995)
(applying
[13] Kumho
Tire Co., Ltd. v.
[14] Gen.
Elec. Co. v. Joiner, 522
[15]
[16] The scientific method calls for the formulation
of a scientific hypothesis, designing a study that can answer it, collecting
objectively verifiable evidence that will address the hypothesis, and drawing
only those conclusions supported by the evidence. See Landrigan v. Celotex
Corp., 605 A.2d 1079, 1088 (N.J. 1992) (with respect to proffered
testimony regarding the causation of plaintiff-decedent’s colon cancer, holding
that the trial court “should examine each step in [the expert’s] reasoning”); Hall v. Baxter Healthcare Corp., 947
F. Supp. 1387, 1401 (D. Or. 1996) (“This court need not and should not ignore
any step in that process, but must ensure that in each step, from initial
premise to ultimate conclusion, the expert faithfully followed valid scientific
methodology.”).
[17] Wade-Greaux
v.
[18] In
re Agent Orange Litigation, 611 F. Supp. 1223, 1231 (E.D.N.Y. 1985) (citing
Dore, A Commentary on the Use of
Epidemiological Evidence in Demonstrating Cause-in-Fact, 7 Harv. Envtl. L. Rev. 429, 431 (1983)
(“Epidemiological studies rely on ‘statistical methods to detect abnormally
high incidences of disease in a study population and to associate these
incidences with unusual exposures to suspect environmental factors.’”); see also Siharath v. Sandoz Pharms. Corp., 131 F. Supp. 2d 1347, 1356
(N.D. Ga. 2001) (“Epidemiologists employ cohort studies, case control studies,
and ecological studies to determine whether individuals exposed to an agent
have a greater risk of developing the disease in question.”).
[19] See Allen v. Pa. Eng. Co., 102 F.3d 194,
197 (5th Cir. 1996) (quoting Brock, 874 F.3d at 311 (“Undoubtedly, the most
useful and conclusive type of evidence in a [products liability] case is
epidemiological studies”); Lopez v.
Wyeth-Ayerst Labs., Inc., 1996 WL 784566 *1, *3 (N.D. Cal. 1996) (“epidemiological evidence is one
of the most valuable pieces of scientific evidence in causation”); Casey v. Ohio Med. Prods., 877 F.
Supp. 1380, 1385 (N.D. Cal. 1995) (considering lack of epidemiological study an
important factor in determining reliability).
[20] Wade-Greaux, 874 F. Supp at 1451-52.
[21]
[22] 97 F. Supp. 2d 986 (D.
[23] See
also Hall v. Baxter Healthcare
Corp., 947 F. Supp. 1387, 1403 (D. Or. 1996) (excluding plaintiff’s
expert’s testimony on causation between breast implant and systemic disease); Brock v. Merrell Dow Pharms., Inc., 874
F.2d 307, 315 (5th Cir. 1989) (affirming District Court’s exclusion of
testimony of plaintiffs’ experts finding that they did not present sufficient
proof that ingestion of Bendectin during pregnancy caused Poland’s Syndrome); In re Breast Implant Litig., 11 F.
Supp. 2d 1217, 1224 (D. Colo. 1998) (excluding testimony of plaintiffs’ experts
for failure to use valid, statistically significant epidemiological studies
showing an association between breast implants and auto-immune diseases); Allen, 102 F.3d at 194 (affirming District Court’s exclusion of
plaintiffs’ experts for their failure to present valid, statistically
significant epidemiological studies showing an association between ethylene
oxide and brain cancer); Wade-Greaux
v. Whitehall Labs., Inc., 874 F. Supp.1441, 1484 (D. V.I. 1994)
(excluding testimony of plaintiffs’ experts and granting summary judgment for
defendant where plaintiffs’ experts failed to conduct or rely on valid,
consistent epidemiological studies showing an association between over-the-counter
asthma medications and skeletal birth defects); Haggerty v. Upjohn Co., 950 F. Supp. 1160, 1168 (S.D. Fla. 1996)
(granting defendant’s motion for summary judgment while holding that plaintiff
did not show a genuine issue of material fact with respect to medical causation
of a prescription sleeping medication and its claimed psychiatric side
effects); and Lynch v. Merrell-Nat’l
Labs., Inc., 830 F.2d 1190, 1196-97 (1st Cir. 1987) (affirming summary
judgment for Bendectin manufacturer where plaintiff offered only criticism of
defendant’s epidemiological evidence with no epidemiological evidence of her
own).
[24] Siharath
v. Sandoz Pharms. Corp., 131 F. Supp. 2d 1347, 1356 (N.D. Ga. 2001)
(applying Daubert II) (citing Conde v. Velsicol Chem. Corp., 804 F.
Supp. 972 (S.D. Ohio 1992), aff’d,
24 F.3d 809 (6th Cir. 1994)).
[25] See Blum v. Merrell Dow Pharms., Inc., 705
A.2d 1314, 1323 (
[26] Havner, 953 S.W.2d at 727 (“[I]t is
important that any conclusions about causation be reached only after an
association is observed in studies among different groups and that the
association continues to hold when the effects of other variables are taken
into account.”).
[27] Wade-Greaux, 874 F. Supp. at 1452 (“A
‘confounding factor’ is an exposure to one agent that is temporally associated
with exposures to other agents, such that they appear to be having the same
effect.”) A well-conducted epidemiology
study will use statistical techniques to eliminate the possible effects of
confounding factors.
[28] See
id. (“[A]bsent a large
single study with an overwhelmingly high rate ratio, epidemiologists generally
require several individual positive
studies linking a specific exposure with a particular outcome before
they draw any conclusions as to an association.”).
[29] See Mitchell v. GenCorp, Inc., 165 F.3d
778, 782 (10th Cir. 1999) (“Without scientific data supporting their
conclusions that chemicals similar to benzene cause the same problems as
benzene, the analytical gap in the experts’ testimony is simply too wide for
the opinions to establish causation”); Lofgren v. Motorola, 1998 WL 299925,
at *17 (Ariz. Super.
[30] 131
F. Supp. 2d 1347 (N.D.