Tamraz v. Lincoln Electric Co.

RECOMMENDED FOR FULL-TEXT PUBLICATION
Pursuant to Sixth Circuit Rule 206
File Name: 10a0293p.06

UNITED STATES COURT OF APPEALS
FOR THE SIXTH CIRCUIT
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Plaintiffs-Appellees, -
JEFF TAMRAZ; TERRY TAMRAZ,
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Nos. 08-4015/4016
v.
,
>
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LINCOLN ELECTRIC COMPANY; HOBART
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BROTHERS COMPANY; ESAB GROUP, INC.
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(08-4015); TDY INDUSTRIES, INC. (08-4016),
Defendants-Appellants. -
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Appeal from the United States District Court
for the Northern District of Ohio at Cleveland.
No. 04-18948—Kathleen McDonald O’Malley, District Judge.
Argued: November 18, 2009
Decided and Filed: September 8, 2010
Before: MARTIN and SUTTON, Circuit Judges; REEVES, District Judge.*

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COUNSEL
ARGUED: Stephen J. Harburg, SKADDEN, ARPS, SLATE, MEAGHER & FLOM
LLP, Washington, D.C., for Appellants. Paul Michael De Marco, WAITE,
SCHNEIDER, BAYLESS & CHESLEY CO., L.P.A., Cincinnati, Ohio, for Appellees.
ON BRIEF: Stephen J. Harburg, John H. Beisner, Jessica D. Miller, SKADDEN,
ARPS, SLATE, MEAGHER & FLOM LLP, Washington, D.C., Jonathan D. Hacker,
O’MELVENY & MYERS LLP, Washington, D.C., Irene C. Keyse-Walker, Joseph J.
Morford, TUCKER ELLIS & WEST LLP, Cleveland, Ohio, for Appellants. John R.
Climaco, John A. Peca, Jr., Dawn M. Chmielewski, Patricia M. Ritzert, CLIMACO,
WILCOX, PECA, TARANTINO & GAROFOLI CO., LPA, Cleveland, Ohio, Eric C.
Wiedemer, KELLEY & FERRARO LLP, Cleveland, Ohio, Elizabeth J. Cabraser, Robert
Nelson, LIEFF CABRASER HEIMANN & BERNSTEIN, LLP, San Francisco,
California, for Appellees.

*
The Honorable Danny C. Reeves, United States District Judge for the Eastern District of
Kentucky, sitting by designation.

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SUTTON, J., delivered the opinion of the court, in which REEVES, D. J., joined.
MARTIN, J. (pp. 21–31), delivered a separate dissenting opinion.
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OPINION
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SUTTON, Circuit Judge. At issue in this case is the often-elusive line between
admissible opinion and inadmissible speculation under Rule 702 of the Federal Rules of
Evidence and Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579 (1993).
Several manufacturers of welding supplies appeal a $20.5 million jury verdict based on
a doctor’s testimony that their products triggered “manganese-induced parkinsonism”
in a welder who used them. Because the district court exceeded its discretion in
allowing this testimony, we reverse and remand for a new trial.

I.

From roughly 1979 to 2004, Jeff Tamraz worked as an independent-contracting
welder in California. Beginning in about 2001, he began to suffer symptoms of
Parkinsonism: tremors, drooling, a “masked face” and impaired coordination on his
right side. JA 800–03.

In September 2004, Tamraz and his wife Terry sued several manufacturers of
welding supplies, alleging that the fumes from their products had caused his condition
and that labels on the products had failed to warn of the danger. The case was
consolidated with ongoing multidistrict litigation in the Northern District of Ohio. In
re: Welding Fume Prods. Liab. Litig., No. 03-cv-17000, MDL No. 1535. The district
court selected Tamraz’s case for one of several bellwether trials to guide the resolution
of the other cases. No. 03-cv-17000, R.2043 (June 6, 2007).

After summary judgment thinned the claims and defendants, Tamraz’s case went
to trial on three theories of relief (strict-liability failure to warn, negligent failure to warn
and fraud by concealment) against five defendants (The Lincoln Electric Company,
Hobart Brothers Company, The ESAB Group, Inc., BOC Group, Inc. and TDY
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Industries, Inc.). The jury found for Tamraz and against all five defendants on the
claims of strict liability and negligent failure to warn, but rejected his claim of fraud by
concealment. It awarded Jeff Tamraz $17.5 million in compensatory damages and Terry
Tamraz $3 million for loss of consortium. The defendants all filed motions to overturn
the verdict under Rule 50 of the Federal Rules of Civil Procedure. The district court
denied the challenges of every defendant save BOC Group, against whom the court
found insufficient evidence to sustain the verdict. Lincoln Electric, the ESAB Group,
Hobart Brothers and TDY Industries appealed.

II.

The manufacturers argue that the district court should not have admitted Dr.
Walter Carlini’s opinion that the manufacturers’ products triggered “manganese-induced
parkinsonism” in Tamraz, claiming it did not satisfy the requirements of Rule 702 of the
Federal Rules of Evidence. We agree.

A.

The relevant law. Rule 702 says:

If scientific, technical, or other specialized knowledge will assist the trier
of fact to . . . determine a fact in issue, a witness qualified as an expert by
knowledge, skill, experience, training, or education, may testify thereto
in the form of an opinion or otherwise, if (1) the testimony is based upon
sufficient facts or data, (2) the testimony is the product of reliable
principles and methods, and (3) the witness has applied the principles and
methods reliably to the facts of the case.
Fed. R. Evid. 702. The rule gives district courts a “gatekeeping role” in screening the
reliability of expert testimony, Daubert, 509 U.S. at 597, and we review their decisions
for abuse of discretion, Kumho Tire Co. v. Carmichael, 526 U.S. 137, 152 (1999).

The relevant science. Doctors now recognize that what James Parkinson
described nearly two centuries ago as “the shaking palsy” makes up a family of
movement disorders encompassing Parkinson’s Disease along with an assortment of
other disorders. James Parkinson, An Essay on the Shaking Palsy (1817), reprinted in
14 J. Neuropsychiatry & Clin. Neurosci. 223 (2002); see JA 130–31. The disorders have
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different causes, and they have different but overlapping symptoms, including tremors,
instability and slowness and rigidity of movement. JA 130. Diagnosing one type of
parkinsonism over another is no easy task. JA 140, 553–56.

Two forms of parkinsonism—Parkinson’s Disease and manganism—matter here.
Parkinson’s Disease is the most common type, afflicting more than a million people in
the United States alone. JA 131, 607. The typical individual with Parkinson’s Disease
suffers from a gradual loss of motor function and a tremor when at rest, both usually
developing on one side of the body, caused by deterioration of neurons in a part of the
brain called (bear with us) the substantia nigra pars compacta. JA 132, 135–36. The
causes of Parkinson’s Disease range from the obscure to the unknown. As a result,
doctors and scientists often define Parkinson’s Disease by its undetermined
cause—“idiopathic Parkinson’s Disease”—“idiopathic” being another way of saying the
medical community does not know why a given individual has the disease. In other
cases, they use a name other than Parkinson’s Disease—such as postencephalitic
parkinsonism, drug-induced parkinsonism, or toxin-induced parkinsonism—when they
know the cause. JA 131, 150. Over time, as scientists have discovered more genetic and
other causes for Parkinson’s Disease, the medical profession has defined more sub-
classifications of the disease and has had to rely less frequently on “idiopathic”
designations. JA 130–32.

Manganism is a form of parkinsonism defined by its cause: overexposure to
manganese, a hard and brittle element that resembles iron but is not magnetic. The
symptoms of manganism overlap with Parkinson’s Disease but include an action tremor
instead of a rest tremor, symmetry of symptoms and a distinct gait (“cock walk”). JA
584, 871, 1002–05. The typical manganism patient suffers neuron deterioration in a
different part of the brain from the typical Parkinson’s Disease patient—medically
speaking, the globus pallidus and the substantia nigra pars reticulata, not the substantia
nigra pars compacta—and therapies used to treat Parkinson’s Disease often do not work
with manganism. JA 134–36, 564–67.
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The diagnosis of Jeff Tamraz. Every doctor to examine Jeff Tamraz has reached
a different conclusion about where his case fits into this puzzle. No one disputes that he
suffers from parkinsonism; the question is what kind and from what cause. The first
neurologist to see Tamraz, Dr. Michael Siegel, initially diagnosed Tamraz with “an
unusual form of Parkinson’s disease due to manganese poisoning,” JA 805, but then
became less sure about the role of manganese after he consulted medical literature on the
subject, JA 808–09. He eventually concluded that Tamraz’s condition is closer to
Parkinson’s Disease than to manganism: Tamraz had a rest tremor, asymmetry of
symptoms and no “cock walk.” JA 809–11, 816–19. Although he could not rule out
manganese as the cause of the illness, JA 812, Dr. Siegel believed Tamraz’s
parkinsonism likely resulted from “factors other than exposure to manganese,” JA 817.

Tamraz’s second neurologist, Dr. Carlini, the witness at issue here, concluded
that Tamraz suffers from “manganese-induced parkinsonism,” JA 615, but not in the
sense of a manifestation of manganism, as that phrase is sometimes used, see JA 600–01.
He believed that manganese exposure caused something akin to Parkinson’s Disease in
Tamraz. JA 600. He found many of the same symptoms that led Dr. Siegel to suspect
Parkinson’s Disease rather than manganism, JA 616, 619–21, but he noted that scientists
recently had discovered genetic or environmental causes for many forms of Parkinson’s
Disease formerly considered idiopathic, JA 599, 619, and discussed literature raising the
possibility that genetics and environmental factors may cause a large fraction of
Parkinson’s Disease cases. JA 599, 601–02. Dr. Carlini hypothesized that Tamraz
might have a genetic predisposition to Parkinson’s Disease, and that manganese in lower
levels than necessary to cause manganism might nevertheless “trigger” the symptoms
of Parkinson’s Disease, like “the straw that broke the camel’s back.” JA 598–99. He
did not believe Tamraz has Parkinson’s Disease in the strict sense—that manganese in
his view caused the disease meant by definition it could not be “idiopathic” Parkinson’s
Disease—but believed it to be otherwise identical to Parkinson’s Disease. JA 599–600.

In addition to Tamraz’s treating physicians, the plaintiffs and defendants each
hired a doctor to examine Tamraz. Dr. Anthony Lang, the defendants’ doctor, testified
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that “Parkinson’s disease and manganism . . . are quite distinct and different,” JA 1300,
and concluded, based on his examination of Tamraz, that Tamraz has Parkinson’s
Disease, not manganism, see JA 467. Dr. Paul Nausieda, the plaintiffs’ doctor, testified
that Tamraz does not have Parkinson’s Disease but “a manganese-induced movement
disorder,” essentially manganism. JA 867–68. He relied on the absence of other
explanations for Tamraz’s parkinsonism and its early onset and, in contrast to the other
doctors, found that Tamraz has some symptoms more indicative of manganism than of
Parkinson’s Disease. See JA 866–73.

B.

The manufacturers do not question one aspect of Dr. Carlini’s testimony—that
Tamraz suffers from a form of parkinsonism. They dispute his conclusion that
manganese exposure caused the illness. L.E.C. Br. at 24. To put the distinction in
medical terms, they challenge Dr. Carlini’s etiology (what caused the disorder
diagnosed?), not his diagnosis (what disorder caused the set of symptoms observed?).

The problem here is that, when Dr. Carlini testified that manganese exposure
caused Tamraz’s condition, he went beyond the boundaries of allowable testimony under
Rule 702. In the video-taped deposition played at trial, Dr. Carlini opined that Tamraz
has “manganese-induced parkinsonism” “with a reasonable degree of medical certainty.”
JA 615. But the etiological component of this conclusion—the “manganese-induced”
part—was at most a working hypothesis, not admissible scientific “knowledge.” Fed.
R. Evid. 702. Because the “knowledge” requirement of Rule 702 requires “more than
subjective belief or unsupported speculation,” Daubert, 509 U.S. at 590, the testimony
should have been excluded.

The rest of Dr. Carlini’s testimony confirms the speculative nature of this
opinion. Under questioning by Tamraz’s counsel, Dr. Carlini focused on his diagnosis
of parkinsonism and barely explained why he thought manganese caused the disease.
He stated only that he diagnosed him with “manganese-induced parkinsonism” because
“that seemed the most likely explanation for his early onset parkinsonism,” based on his
“clinical examination,” “Mr. Tamraz’s history” “[a]nd just general experience and
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knowledge about movement disorders.” JA 615. Questioning by the manufacturers’
counsel brought to the surface his line of reasoning: (1) Tamraz was exposed to welding
fumes presumably containing manganese, JA 613; (2) he developed the symptoms of
Parkinson’s Disease (though not those of manganism), JA 604, 613–14, 616;
(3) scientists have identified genetic factors that cause some forms of otherwise
“idiopathic” Parkinson’s Disease, JA 599; (4) some literature has hypothesized that
toxins combined with genetics may cause other cases of Parkinson’s Disease, JA 599,
601; (5) manganese is known to cause manganism, so it would be a possible candidate
for triggering Parkinson’s Disease as well, JA 601; (6) Tamraz may have the genes for
Parkinson’s Disease, JA 621; and (7) manganese may have triggered these genes and
given Tamraz parkinsonism, JA 615.

That is a plausible hypothesis. It may even be right. But it is no more than a
hypothesis, and it thus is not “knowledge,” nor is it “based upon sufficient facts or data”
or the “product of reliable principles and methods . . . applied . . . reliably to the facts of
the case.” Fed. R. Evid. 702.

Dr. Carlini acknowledged the speculative jumps involved in steps 4, 5 and 6 of
this chain of causation—the steps necessary to his theory that manganese exposure may
cause Parkinson’s Disease in general. At step 4, he described the literature
hypothesizing a link between environmental toxins and latent genetic Parkinson’s
Disease as “all theoretical.” JA 599; see also JA 621 (“theoretical writing”). At step
5, he conceded he knew of no studies finding a link between manganese and Parkinson’s
Disease and that “studies that have looked at that . . . have not found a very strong
correlation.” JA 602; see JA 597, 599, 605, 621; see also JA 623 (“Epidemiological
studies have failed to find a correlation between manganese and Parkinson’s disease.”).
At step 6, he conceded that “speculation” led him to guess that Tamraz had “an
underlying predisposition to Parkinson’s disease,” JA 621, even though Tamraz has no
family history of Parkinson’s Disease, JA 613. A negative answer at any one of these
steps would defeat his overall theory of causation. The reality that all of them were
speculative makes the theory speculative three times over. Cf. Siharath v. Sandoz
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Pharm. Corp., 131 F. Supp. 2d 1347, 1371 (N.D. Ga. 2001) (“Three scientifically
unwarranted ‘leaps of faith’ exist in this causal chain.”), aff’d, 295 F.3d 1194 (11th Cir.
2002).

The final step required a leap of faith as well, even ignoring the jumps required
to get there. That manganese could cause Parkinson’s Disease in someone like Tamraz
does not show that manganese did cause Tamraz’s Parkinson’s Disease. Parkinson’s
Disease occurs commonly in the general population and usually without any known
cause. Any given case of Parkinson’s Disease thus might have occurred regardless of
the manganese exposure, making it hard to attribute one case to manganese over all of
the other possible causes. See Bland v. Verizon Wireless, (VAW) L.L.C., 538 F.3d 893,
897 (8th Cir. 2008); In re Breast Implant Litig., 11 F. Supp. 2d 1217, 1228–39 (D. Colo.
1998). This attribution is harder still if, as Dr. Carlini hypothesized, Tamraz already had
a genetic predisposition toward it, and even more so if, as Dr. Carlini also
acknowledged, the base probability of getting parkinsonism from such a predisposition
is unknown. See JA 601 (acknowledging that he did not know whether someone with
a genetic predisposition toward Parkinson’s Disease, as he suspected Tamraz had, would
have a 90% chance or a 10% chance of manifesting symptoms).

Dr. Carlini never explained how he made this leap—how this case stemmed from
manganese exposure. When asked how to “tell the difference between a welder with
idiopathic Parkinson’s disease and a welder . . . tipped into the Parkinson’s disease by
welding,” he answered with tests he might do, not tests he had done. JA 602. Asked
similar questions twice more, he responded twice more by listing tests he could do, not
tests he had done. See JA 603 (“[Y]ou would suspect . . . subtle differences . . . which
I bet would be possible to tease out if we had . . . some of these more advanced imaging
techniques.”); JA 622 (“[W]e haven’t tried yet. . . . Suppose—let’s just take a
hypothetical. . . .”). The closest he came to explaining why he suspected that manganese
exposure caused Tamraz’s parkinsonism is when he noted its “early onset.” JA 604,
615. But he also said that roughly ten percent of people with Parkinson’s develop
symptoms before age 50, JA 607, which, considering the high prevalence of Parkinson’s
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Disease, does not create an inference that something particularly unusual must have
caused it in Tamraz, who was 41 to 44 years old at the onset of his symptoms, JA 467.
(Other witnesses suggested that the frequency of early onset is less than ten percent, see,
e.g., JA 573, but that has no relevance to Dr. Carlini’s methodology.) Dr. Carlini’s
testimony thus suffers from a lack of foundation both for why manganese could cause
Parkinson’s Disease and why manganism caused this case of Parkinson’s Disease.

Under these circumstances, it makes no difference that Dr. Carlini purported to
find “manganese-induced parkinsonism” in Tamraz “with a reasonable degree of medical
certainty.” JA 615. Whatever Dr. Carlini understood by “with a reasonable degree of
medical certainty,” the phrase—the conclusion by itself—does not make a causation
opinion admissible. The “ipse dixit of the expert” alone is not sufficient to permit the
admission of an opinion. Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997). Minus that
one phrase, nothing in his testimony suggests the sort of “knowledge” on this point that
the Rules require—only speculation, which is generally inadmissible. “[N]o matter how
good” experts’ “credentials” may be, they are “not permitted to speculate.” Goebel v.
Denver & Rio Grande W. R.R. Co., 215 F.3d 1083, 1088 (10th Cir. 2000). Dr. Carlini
may be a “distinguished” doctor, and “his conjecture” about causation may be “worthy
of careful attention . . . . But the courtroom is not the place for scientific guesswork,
even of the inspired sort.” Rosen v. Ciba-Geigy Corp., 78 F.3d 316, 319 (7th Cir. 1996).

Rule 702, we recognize, does not require anything approaching absolute
certainty. See Daubert, 509 U.S. at 590. And where one person sees speculation, we
acknowledge, another may see knowledge, which is why the district court enjoys broad
discretion over where to draw the line. See Joiner, 522 U.S. at 139. Yet, so long as
there is a line, some forms of testimony may cross it, and that happened here. Dr.
Carlini’s opinion contains not just one speculation but a string of them: A suggests by
analogy the possibility of B, which might also apply to C, which, if we speculate about
D, could eventually trigger E, so perhaps that happened here. At some point, the train
becomes too long to pull and the couplings too weak to hold the cars together.
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C.

Tamraz resists this conclusion on a number of grounds, all unconvincing. He
first turns to Dr. Carlini’s use of the phrase “manganese-induced parkinsonism” to
describe Tamraz’s condition, JA 615, suggesting that Dr. Carlini equates the phrase with
manganism, Tamraz Br. at 33 & n.7. If manganism, as its name implies, is caused by
manganese, and if Dr. Carlini diagnosed Tamraz with manganism, the thinking goes, the
required link between manganese exposure and the disease caused by it has been solved.

The problem is that this argument mischaracterizes Dr. Carlini’s testimony.
Although some people use “manganese-induced parkinsonism” to refer to manganism,
see, e.g., JA 862, Dr. Carlini did not. He used the phrase to mean Parkinson’s Disease
that happens to have manganese exposure as its cause:

Q So you use the term manganese-induced parkinsonism to mean
the same disease as Parkinson’s disease?
A It’s the same disease, yes. It’s just triggered by manganese. . . .
It’s a very specific form of the same disease in the sense that I’m
implying that it’s triggered by a certain environmental toxin as opposed
to another.
Q But it’s pathologically and clinically Parkinson’s disease?
A It’s different, yes, than manganism. Exactly. Pathologically it
might look exactly the same as sporadic idiopathic Parkinson’s disease,
yes.

JA 600. “[E]very aspect” of Tamraz’s condition, he added, “is consistent with a
diagnosis of Parkinson’s disease.” JA 607. He used a different name for the disease
because idiopathic Parkinson’s Disease by definition has no cause, so once he assigned
a cause to the disease Dr. Carlini also had to assign a name to that “specific form of the
same disease”: “manganese-induced parkinsonism.” JA 600. But the naming did not
change the underlying diagnosis. He repeatedly emphasized that he saw none of the
symptoms of manganism in Tamraz and that his diagnosis was identical to Parkinson’s
Disease save for surmise about its cause. See JA 599–600, 616; see also JA 601 (“He
looks like [idiopathic Parkinson’s Disease] clinically.”); JA 618 (“Tamraz does not have
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manganism.”). Tamraz’s expert, Dr. Nausieda, who used “manganese-induced
parkinsonism” nearly synonymously with manganism, acknowledged that Dr. Carlini did
not mean the same thing. JA 862.

In denying the manufacturers’ motion to exclude Dr. Carlini’s causation
testimony, the district court noted that the manufacturers “ask[ed] the Court to draw
bright lines regarding diagnoses of movement disorders [i.e., between Parkinson’s
Disease and manganism] that I have already declined to draw.” JA 170–71. But it was
not just the manufacturers drawing these lines; Dr. Carlini himself called manganism and
Parkinson’s Disease “very distinctive” diseases and found Tamraz’s symptoms lined up
with Parkinson’s Disease, not manganism. JA 607. Dr. Carlini’s opinion cannot escape
its own logic.

In conflating “manganese-induced parkinsonism” with manganism, Tamraz
conflates diagnosis with etiology, eliding the distinction between Tamraz’s disease and
what caused it. Diagnosis and etiology, however, both were in play in this case.
Because Dr. Carlini diagnosed Tamraz with something akin to Parkinson’s Disease, not
manganism, and because Parkinson’s Disease unlike manganism has no standard
etiology, Dr. Carlini’s etiology must rise or fall on its own.

To use an analogy, chronic shortness of breath may be caused by diseases
ranging from emphysema to lung fibrosis to bronchitis to heart disease—which would
be the diagnosis. Heart disease, to pick one of these diagnoses, may be caused by diet,
smoking, genetics or some combination of the three—which would be the etiology. One
could not defend a verdict without linking the etiology to the diagnosis. Cf. Kelley v.
Am. Heyer-Schulte Corp., 957 F. Supp. 873, 882 (W.D. Tex. 1997) (“Essentially, this
is a bit like saying that if a person has a scratchy throat, runny nose, and a nasty cough,
that person has a cold; if, on the other hand, that person has a scratchy throat, runny
nose, nasty cough, and wears a watch, they have a watch-induced cold.”).

Tamraz likewise conflates a doctor’s expertise in diagnosis with a doctor’s
expertise in etiology, arguing for the reliability of Dr. Carlini’s causation testimony
because of his “extensive . . . experience” with diagnosing parkinsonism. Appellees’
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Response to Rule 28(j) Letter (Nov. 9, 2009). But most treating physicians have more
training in and experience with diagnosis than etiology. See David L. Faigman, Judges
as “Amateur Scientists”, 86 B.U. L. Rev. 1207, 1221–22 (2006); Edward J.
Imwinkelried, The Admissibility and Legal Sufficiency of Testimony About Differential
Diagnosis (Etiology), 56 Baylor L. Rev. 391, 405 (2004); Mary Sue Henefin et al.,
Reference Guide on Medical Testimony, in Reference Manual on Scientific Evidence
439, 471–72 (2d ed. 2000). When physicians think about etiology in a clinical setting,
moreover, they may think about it in a different way from the way judges and juries
think about it in a courtroom. See Siharath, 131 F. Supp. 2d at 1371–73. Getting the
diagnosis right matters greatly to a treating physician, as a bungled diagnosis can lead
to unnecessary procedures at best and death at worst. See Bowers v. Norfolk S. Corp.,
537 F. Supp. 2d 1343, 1361 (M.D. Ga. 2007). But with etiology, the same physician
may often follow a precautionary principle: If a particular factor might cause a disease,
and the factor is readily avoidable, why not advise the patient to avoid it? Such
advice—telling a welder, say, to use a respirator—can do little harm, and might do a lot
of good. See Joe G. Hollingsworth & Eric G. Lasker, The Case Against Differential
Diagnosis: Daubert, Medical Causation Testimony, and the Scientific Method, 37 J.
Health L. 85, 98 (2004). This low threshold for making a decision serves well in the
clinic but not in the courtroom, where decision requires not just an educated hunch but
at least a preponderance of the evidence.

None of this means that physicians may not testify to etiology—we have reversed
courts for not allowing such testimony, see, e.g., Hardyman v. Norfolk & W. Ry. Co., 243
F.3d 255, 260–67 (6th Cir. 2001)—only that courts must apply the Daubert principles
carefully in considering it. “The ability to diagnose medical conditions is not remotely
the same . . . as the ability to deduce . . . in a scientifically reliable manner, the causes
of those medical conditions.” Gass v. Marriott Hotel Servs., Inc., 501 F. Supp. 2d 1011,
1019 (W.D. Mich. 2007), rev’d on other grounds, 558 F.3d 419 (6th Cir. 2009). Doctors
thus may testify to both, but the reliability of one does not guarantee the reliability of the
other.
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Nor can Dr. Carlini’s testimony be defended as a permissibly admissible
“differential diagnosis.” A differential diagnosis seeks to identify the disease causing
a patient’s symptoms by ruling in all possible diseases and ruling out alternative diseases
until (if all goes well) one arrives at the most likely cause. See Hardyman, 243 F.3d at
260–61. We have accepted this kind of testimony before. See Glaser v. Thompson Med.
Co., 32 F.3d 969, 977 (6th Cir. 1994).

The manufacturers, however, do not challenge Dr. Carlini’s differential
diagnosis, which concluded that Tamraz suffers from parkinsonism similar to classical
Parkinson’s Disease; they challenge his etiology that manganese caused it. Many courts,
including our own, allow experts to employ a rule-in/rule-out reasoning process for
etiology as well as diagnosis—essentially, a “differential etiology,” though the term
seems to be a legal one rather than a medical one. See McClain v. Metabolife Int’l, Inc.,
401 F.3d 1233, 1252 (11th Cir. 2005); Henefin et al., supra, at 444, 481. This court’s
opinions have used “differential diagnosis” broadly to include what might better be
called “differential etiology,” but they have not had to distinguish the two concepts
because most cases involve just one of them. See, e.g., Hardyman, 243 F.3d at 259 n.2
(parties did not dispute the nature of the disease, only what caused it).

Whether we describe Dr. Carlini’s causation methodology as “differential
etiology” or “differential diagnosis,” that does not make it reliable. “[S]imply claiming
that an expert used the ‘differential diagnosis’ method is not some incantation that opens
the Daubert gate.” Bowers, 537 F. Supp. 2d at 1360. Calling something a “differential
diagnosis” or “differential etiology” does not by itself answer the reliability question but
prompts three more: (1) Did the expert make an accurate diagnosis of the nature of the
disease? (2) Did the expert reliably rule in the possible causes of it? (3) Did the expert
reliably rule out the rejected causes? If the court answers “no” to any of these questions,
the court must exclude the ultimate conclusion reached. See Best v. Lowe’s Home Ctrs.,
Inc., 563 F.3d 171, 179 (6th Cir. 2009). Dr. Carlini’s opinion fails the last two prongs
because, for the reasons already given, his efforts to “rule in” manganese exposure as a
Nos. 08-4015/4016 Tamraz et al. v. Lincoln Elec. Co. et al. Page 14

possible cause or to “rule out” other possible causes turned on speculation, not a valid
methodology. No matter the label, the testimony does not satisfy Rule 702.

All of this suffices to distinguish the cases on which Tamraz relies to admit
“differential diagnosis” testimony. In Hardyman, the trial court excluded a doctor’s
opinion that a railroad brakeman’s job activities caused his carpal tunnel syndrome
(CTS), finding the testimony unreliable because, although the doctor showed that tasks
like those the brakeman performed are known to cause CTS, he cited no studies
performed on brakemen and could not quantify how much movement and pressure
would lead to how much CTS. 243 F.3d at 261–65. We reversed, holding that the
district court demanded too much specificity and too much quantification from the
expert. Id. at 262, 265. But here the problem is not that Dr. Carlini failed to cite studies
about manganese causing Parkinson’s Disease in welders or could not quantify how
much manganese would lead to how much Parkinson’s Disease; the problem is that he
failed to cite any non-speculative evidence for his conclusion that manganese causes
Parkinson’s Disease.

Likewise, in Best, we reversed the district court for excluding a doctor’s
testimony that a chemical spill on Best’s face caused him to lose his sense of smell. 563
F.3d at 183–84. In that case, Best suffered burns on his skin and irritation to his nasal
passages immediately after the incident, and eventually lost his ability to smell
altogether. Id. at 174. We approved the doctor’s method of ruling in the chemical in
question by making a careful comparison with similar chemicals he had known to have
the same effect. Id. at 181. In this case, by contrast, Dr. Carlini analogized only to the
“theoretical” possibility of other toxins causing Parkinson’s Disease, JA 599, and did not
point to any similar elements known to cause Parkinson’s Disease. (He did mention one
chemical known to cause parkinsonism—the designer drug MPTP—but never attempted
to compare it with manganism and did not factor it into his etiology, JA 619.) In Best,
the doctor also reliably ruled out most alternative causes; the defendant argued that the
doctor also should have ruled out another possible factor but did not provide any
evidence that this factor could cause the disease. 563 F.3d at 181. Here, though, the
Nos. 08-4015/4016 Tamraz et al. v. Lincoln Elec. Co. et al. Page 15

other possibility—unknown (idiopathic) causation—currently accounts for the vast
majority of Parkinson’s Disease cases, making it impossible to ignore and difficult to
rule out. See Bland, 538 F.3d at 897. Forecasting today’s decision, Best cautioned that
“[n]ot every opinion that is reached via a differential-diagnosis method will meet the
standard of reliability required by Daubert.” 563 F.3d at 179.

Tamraz invokes the testimony of Dr. Nausieda, who also testified that manganese
exposure caused Tamraz’s sickness with no objection from the manufacturers. If Dr.
Nausieda’s testimony passes muster, Tamraz claims, so too should Dr. Carlini’s.
Tamraz Br. at 35. But we are aware of no authority, and Tamraz points to none, holding
that preserving an objection to one witness requires objecting to every similar witness.
Although Dr. Nausieda’s testimony in some ways overlapped with Dr. Carlini’s,
moreover, he reached opposite conclusions on the relevant points: He believed that
Tamraz suffers from something akin to manganism, not Parkinson’s Disease, JA 866–73,
and he believed manganese exposure could not cause Parkinson’s Disease. JA 951.
Perhaps most importantly, even to the extent that Dr. Nausieda’s testimony was
consistent with parts of Dr. Carlini’s, that would not make Dr. Carlini’s testimony
admissible. The important thing is not that experts reach the right conclusion, but that
they reach it via a sound methodology. See Daubert, 509 U.S. at 595. Comparisons
between methodologies no doubt may be instructive, and an expert may in some
circumstances rely on other experts’ testimony, see Fed. R. Evid. 703—something Dr.
Carlini did not do here. But testimony still must be judged by its methodology, not its
conclusion.

Dr. Carlini’s speculation that Tamraz might have damage to the globus pallidus
in his brain—noteworthy because globus pallidus damage characterizes manganism, not
Parkinson’s Disease, Tamraz Br. at 33 & n.7—is beside the point. Dr. Carlini primarily
expected to see cell deterioration in the substantia nigra pars compacta, which
Parkinson’s Disease characteristically damages. JA 601. That Dr. Carlini guessed
Tamraz also might have damage in the globus pallidus—and it was nothing more than
a guess, see JA 601 (“this is all highly speculative obviously”)—neither undermines his
Nos. 08-4015/4016 Tamraz et al. v. Lincoln Elec. Co. et al. Page 16

diagnosis nor supports his etiology. Globus pallidus damage would be relevant only if
Dr. Carlini had actually detected globus pallidus damage. That, however, was not the
case. There is “too great an analytical gap between the data and the opinion proffered”
for the court to admit Dr. Carlini’s opinion as testimony. Joiner, 522 U.S. at 146.

D.

Having concluded that Dr. Carlini’s causation testimony exceeded the
permissible boundaries of Rule 702, we must reverse unless we can “say, with fair
assurance, . . . that the judgment was not substantially swayed by the error.” Mike’s
Train House, Inc. v. Lionel, L.L.C., 472 F.3d 398, 409–10 (6th Cir. 2006). The error was
not harmless.

The emphasis Tamraz put on Dr. Carlini’s testimony confirmed its importance.
His counsel argued to the jury that “Dr. Carlini alone proves by a preponderance of the
evidence that this man has managnese-induced parkinsonism.” JA 1407. In their
opening argument, their closing argument and again in their rebuttal to the
manufacturers’ closing argument, counsel for Tamraz played the portion of the video
deposition in which Dr. Carlini stated that Tamraz has “[m]anganese-induced
parkinsonism” and stated that he held that belief “with a reasonable degree of medical
certainty.” JA 1317, 1374, 1395. Tamraz’s attorney emphasized this supposed
certainty: “They are going to tell you he is talking about speculation and conjecture. He
is talking about a reasonable degree of medical certainty. . . . That is the standard, and
he believes in it.” JA 1374–75.

Counsel for Tamraz also leaned heavily on Dr. Carlini’s apparent neutrality,
calling him a man who “doesn’t have a dog in this hunt,” JA 1397, and repeatedly
mentioning that Dr. Carlini received no payment for his testimony, unlike the
manufacturers’ only expert, see JA 1317, 1374–75, 1399–1400, 1411. They also
emphasized Dr. Carlini’s treating role: “regardless of what is decided in this case, Jeff
Tamraz is going to fly back home, and next month he is going to walk into Dr. Carlini’s
office for his December scheduled appointment, and they are going to sit down and talk
Nos. 08-4015/4016 Tamraz et al. v. Lincoln Elec. Co. et al. Page 17

about how to handle his manganese-induced Parkinsonism. That’s the diagnosis.” JA
1400–01.

Tamraz argues that Dr. Carlini’s testimony could not be harmful because Dr.
Nausieda also testified that Tamraz had “manganese-induced parkinsonism,” so the jury
would have heard the same conclusion even without Dr. Carlini’s testimony. But, as
shown, Dr. Nausieda and Dr. Carlini meant different things by the phrase “manganese-
induced parkinsonism.” Compare JA 600, with JA 862. Dr. Carlini was the only expert
who testified that Tamraz had the equivalent of Parkinson’s Disease caused by
manganese. Without Dr. Carlini, Tamraz would have had to convince the jury that
Tamraz suffered from manganism, not Parkinson’s Disease. With Dr. Carlini’s
testimony, however, the jury faced three choices, two of which helped Tamraz: Tamraz
won if he had manganism (as Dr. Nausieda testified) or Parkinson’s Disease caused by
manganese (as Dr. Carlini testified); the manufacturers won only if Tamraz had
Parkinson’s Disease not caused by manganese. Dr. Carlini’s testimony thus shifted the
primary question from what disease Tamraz had to whether manganese caused it.

The plaintiffs’ closing argument accordingly played down the differences
between manganism and Parkinson’s Disease and played up the causation issue, noting
that three out of four neurologists who had examined Tamraz opined one way or another
that manganese had caused Tamraz’s illness, which “could be a textbook example in law
school of preponderance of the evidence. There is more evidence in front of you that his
disease was caused by manganese in welding fumes than [that it wasn’t]. That is our
burden.” JA 1407–08; see also JA 1375 (“The only neurologist of the four that is telling
you that 20-plus years of inhaling manganese . . . has nothing to do with his condition
is the one they hired and the one that they paid.”). Given the importance of Dr. Carlini’s
testimony, we cannot say “with fair assurance” that the result would have been the same
without it.

Our ruling, however, is a narrow one. The manufacturers here do not challenge
the district court’s primary Daubert ruling on Parkinson’s Disease testimony, In re
Welding Fume Prods. Liab. Litig., No. 03-cv-17000, 2005 WL 1868046, at *22–37
Nos. 08-4015/4016 Tamraz et al. v. Lincoln Elec. Co. et al. Page 18

(N.D. Ohio Aug. 8, 2005), and so we do not decide whether other experts may testify
that manganese exposure causes Parkinson’s Disease. We simply hold that the causation
analysis in Dr. Carlini’s deposition fell short of what Daubert requires.

We leave it to the able district court judge on remand presiding over this difficult
case to decide whether to (1) present Dr. Carlini’s deposition minus his attribution of
Tamraz’s illness to manganese (as the manufacturers requested below, JA 366);
(2) exclude Dr. Carlini’s depositions altogether if the court determines it cannot or
should not sever his purely diagnostic conclusions from his etiological hypothesis (as
Tamraz suggested, in the alternative, below, JA 461); (3) allow the parties to redepose
Dr. Carlini; or (4) opt for any other amenable solution. All we conclude is that his
testimony should not have been admitted as it was.

* * * * *

No one should construe this opinion as criticism of Dr. Carlini, whom the
deposition shows to be intelligent and knowledgeable about the subject
matter—immeasurably more so than we are. But not everything a knowledgeable person
says is “knowledge” under Rule 702, no more than everything a scientist says is
“scientific.” “[A] district court judge asked to admit scientific evidence must determine
whether the evidence is genuinely scientific, as distinct from being . . . speculation
offered by a genuine scientist.” Rosen, 78 F.3d at 318. This causation opinion fell into
the latter category and therefore should have been excluded.

The sort of hypothesis Dr. Carlini presented can play a valuable role both in
medicine, where, if the costs of action are low, doctors may want to act on hypotheses
without further support, and in science generally, where all discoveries start as untested
hypotheses. From this perspective, criticizing Dr. Carlini’s hypothesis for being
speculative would be like criticizing a sapling for being short. Some hypotheses become
scientific theories and others do not.

But that is not the issue. The issue is the reliability of his opinion from a legal
perspective. And what science treats as a useful but untested hypothesis the law should
Nos. 08-4015/4016 Tamraz et al. v. Lincoln Elec. Co. et al. Page 19

generally treat as inadmissible speculation. As the Supreme Court has explained, “[t]he
scientific project is advanced by broad and wide-ranging considerations of a multitude
of hypotheses, for those that are incorrect will eventually be shown to be so . . . .
Conjectures . . . are of little use, however, in the project of reaching a quick, final, and
binding legal judgment—often of great consequence—about a particular set of events
in the past.” Daubert, 509 U.S at 597. “Law lags science; it does not lead it.” Rosen,
78 F.3d at 319.

This is an imperfect system, to be sure. Both sides agree that Mr. Tamraz is a
good man who suffers from a terrible disease; we now force him to take the chance of
prevailing at trial a second time, with less evidence than before. If he does not, yet it
turns out ten years from now that manganese causes his disease, that result will seem
unfair. But the alternative route—allowing the law to get ahead of science—would be
just as unfair. Such an approach would destroy jobs and stifle innovation unnecessarily.
See Joiner, 522 U.S. at 148–49 (Breyer, J., concurring); see also, e.g., Gina Kolata,
Panel Confirms No Major Illness Tied to Implants, N.Y. Times, June 21, 1999, at A1
(describing how scientists concluded, after years of litigation, billions in settlements and
the bankruptcy of a major manufacturer, that no evidence tied breast implants to health
problems). Rule 702 at all events has drawn the line for us, and we must enforce it. See
Daubert, 509 U.S. at 597. Because this testimony crossed that line, we reverse.

III.

In view of our decision to vacate the jury verdict, we need not reach the other
arguments raised on appeal. We note, however, that the contours of the parties’s dispute
about the propriety of a “sophisticated user” jury instruction have changed in view of
intervening law. After trial, the California Supreme Court endorsed and clarified the
defense, see Johnson v. Am. Standard, Inc., 179 P.3d 905 (Cal. 2008), and as a result the
district court may wish to consider this new authority in determining the propriety of
such an instruction at a new trial.
Nos. 08-4015/4016 Tamraz et al. v. Lincoln Elec. Co. et al. Page 20

IV.

For these reasons, we reverse and remand for a new trial.
Nos. 08-4015/4016 Tamraz et al. v. Lincoln Elec. Co. et al. Page 21

_________________

DISSENT
_________________

BOYCE F. MARTIN, JR., Circuit Judge, dissenting. The majority finds that the
district court abused its discretion in admitting Dr. Walter Carlini’s testimony because
it “went beyond the boundaries of allowable testimony under rule 702” (ante at 6),
because it was “speculative” (ante at 6), and because his deductions required “leaps of
faith.” (Ante at 8.) Because the majority reached this conclusion by acting as sitting
judges rather than under the proper standard of review, I respectfully dissent.

I.

Jeff Tamraz’s case is part of a larger multi-district litigation regarding inhalation
of manganese fumes by welders. In re Welding Rod Prods. Liab. Litig., 269 F. Supp. 2d
1365 (J.P.M.L. 2003). In April, May, and June 2005, the multi-district litigation court
conducted three weeks of Daubert hearings to test the methodologies of expert
witnesses. As part of the hearing, experts in the neurological community testified
regarding the connection between manganese exposure and various forms of
parkinsonism. The court also heard argument on the defendants’ motion to preclude
evidence that manganese exposure causes Parkinson’s Disease. The trial court
concluded that the evidence proffered was “sufficiently reliable to support the assertion
that exposure to welding fumes can cause, contribute to, or acclerate a parkinsonian
syndrome that some doctors can diagnose as [Parkinson’s Disease] . . . at least in the
abstract, as the question is presented here.” (Corrected J.A. at 166, Order, Aug. 6, 2005).

Jeff Tamraz worked as a welder from 1979 to 2004. Around 2000-2001, he
began experiencing severe neurological symptoms, which eventually became so severe
that he could not care for himself. In July 2007, Tamraz brought suit in the United States
District Court for the Northern District of Ohio against the five defendants who provided
the welding materials that Tamraz used during his welding career. He claimed that his
neurological injuries, which manifested symptoms consistent with Parkinson’s Disease,
were caused by manganese exposure.
Nos. 08-4015/4016 Tamraz et al. v. Lincoln Elec. Co. et al. Page 22

Before trial, the defendants moved to exclude parts of the testimony to be
presented by one expert, Dr. Carlini. On November 1, 2007, the court ruled on the
motion, stating:

I have read all of the briefs. I have read . . . the two depositions that were
taken of Dr. Carlini. I have gone back and reread the Court’s Daubert
opinion, which was on the main MDL docket . . . and I have decided that
I am going to deny the defendants’ motion.
To a large extent, the defendants’ motion asks the Court to draw bright
lines regarding diagnoses of movement disorders that I have already
declined to draw, and I have already decided that the current state of the
science does not require to be drawn. . . . I see nothing about [Dr.
Carlini’s] methodology that is either flawed or inconsistent with the very
diagnostic methods that other experts in this case, both the plaintiffs and
the defendants’ experts alike, have used and have described as
appropriate diagnostic methods. . . . It is clear that the defendants have
fair grounds to attack the somewhat unusual diagnosis that Dr. Carlini
renders in this case . . . but that to me goes to the weight and not the
admissibility of his testimony.

(Corrected J.A. at 170-173, Tr. of Proceedings, Nov. 1, 2007).

At trial, four experts testified regarding the cause of Tamraz’s injury. Tamraz’s
primary medical expert, Dr. Paul Nausieda, testified that Tamraz suffered from
manganese-induced parkinsonism. The defendants’ lead medical expert, Dr. Anthony
Lang, while testifying that manganese exposure can cause parkinsonism, stated that he
did not believe that Tamraz’s parkinsonism was caused by manganese exposure.
Tamraz’s former treating neurologist, Dr. Michael Siegel, first diagnosed Tamraz with
an unusual form of Parkinson’s Disease due to manganese poisoning. He later revised
his opinion to state that, while he could not rule out the possibility than manganese
exposure caused Tamraz’s injury, Tamraz likely suffered from parkinsonism resulting
from factors other than manganese exposure. Finally, Dr. Carlini testified that Tamraz
likely had a genetic predisposition to Parkinson’s Disease and that exposure to
manganese triggered his Parkinson’s to develop. The jury found defendants liable and
awarded Tamraz a total of $20.3 million in compensatory damages.
Nos. 08-4015/4016 Tamraz et al. v. Lincoln Elec. Co. et al. Page 23

Defendants appealed, claiming that the district court erred in admitting Dr.
Carlini’s testimony because it was speculative and not based upon published literature
or scientific studies. The majority agrees and reverses the district court’s decision. For
the reasons that I will discuss below, I respectfully disagree with the majority’s
reasoning and conclusions.

II.

As the majority correctly notes, “[t]his court reviews a district court’s decision
concerning expert testimony for abuse of discretion.” Popovich v. Sony Music
Entertainment, 508 F.3d 348, 359 (2007) (quoting Kumho Tire Co., Ltd. v. Carmichael,
526 U.S. 137, 152-53 (1999)). Unfortunately, while paying lip service to the correct
standard, the majority actually applies a de novo standard of review. As we have held,
“A district court abuses its discretion if it bases its ruling on an erroneous view of the
law or a clearly erroneous assessment of the evidence.” Ky. Speedway, LLC v. Nat’l
Assoc. of Stock Car Auto Racing, Inc., 588 F.3d 908, 915 (6th Cir. 2009) (quoting Brown
v. Raymond Corp., 432 F.3d 640, 647 (6th Cir.2005)) (internal quotation marks omitted).
“Thus, we will not substitute our own judgment for that of the district court and will
reverse an evidentiary decision ‘only where we are left with a definite and firm
conviction that [the district court] committed a clear error of judgment.’” In re Scrap
Metal Litigation, 527 F.3d 517, 528 (6th Cir. 2008) (quoting Conwood Co., L.P. v. U.S.
Tobacco Co., 290 F.3d 768, 781 (6th Cir. 2002)); see also Nolan v. Memphis City
Schools, 589 F.3d 257, 265 (6th Cir. 2009) (holding that “[b]road discretion is given to
district courts in determinations of admissibility . . . and those decisions will not be
lightly overturned.”).

“[Abuse of discretion review] requires a reviewing court to be highly deferential
when assessing not just a trial court’s analysis of each [Daubert] factor, but also the trial
court’s initial selection of which factors are relevant to the case at hand.” Johnson v.
Manitowoc Boom Trucks, Inc. 484 F.3d 426, 430 (6th Cir. 2007). It is within the district
court’s discretion to determine whether the testimony provided is inadmissible “junk
science” or testimony falling within the “range where experts might reasonably differ.”
Nos. 08-4015/4016 Tamraz et al. v. Lincoln Elec. Co. et al. Page 24

Kumho, 526 U.S. at 153. Thus, we must conduct our review of that decision with great
deference.

Here, because the district court found that Dr. Carlini’s “methodology . . . [was
neither] flawed or inconsistent with the very diagnostic methods that other experts in this
case, both the plaintiffs and the defendants’ experts alike, have used and have described
as appropriate diagnostic methods”, (corrected J.A. at 170-173, Tr. of Proceedings,
Nov. 1, 2007), it is far from apparent that the district court should have found Dr.
Carlini’s testimony to be unreliable. While the district court acknowledged that Dr.
Carlini’s diagnosis was “unusual”, nothing in Daubert and its progeny indicates that an
unusual diagnosis alone renders a district court’s decision to admit an expert’s testimony
an abuse of discretion. Here, the district court reasonably evaluated Dr. Carlini’s
testimony in light of a broad range of expert opinions and found that it was sufficiently
reliable to be admissible. As it was not a clearly erroneous decision so as to constitute
an abuse of discretion, the district court’s judgment should be affirmed.

Expert testimony is inherently difficult to evaluate. It is all the more so outside
the context of a trial. This is why the application of Daubert is flexible. It is why the
district court, which is able to hear and evaluate experts first-hand, is given such broad
latitude in determining whether testimony is admissible. That same reasoning counsels
that this Court interfere only in cases where it is absolutely clear that the testimony is
nothing more than “junk science” that the jury cannot be trusted to evaluate. That is not
the case here.

In reversing the district court’s decision, the majority substitutes their opinion
for that of the district court and exercises a standard of review closer to de novo than
abuse of discretion. The upshot of the majority’s opinion is that they would have found
Dr. Carlini’s testimony inadmissible had they been the trial judge, which would be
acceptable if we reviewed this case de novo. However, the majority does little to explain
why the district court’s decision to admit Dr. Carlini’s testimony was “arbitrary,
unjustifiable, or clearly unreasonable”, Plain Dealer Pub. Co. v. City of Lakewood, 794
F.2d 1139, 1148 (6th Cir. 1986), as they must do if they wish to reverse the district
Nos. 08-4015/4016 Tamraz et al. v. Lincoln Elec. Co. et al. Page 25

court’s evidentiary conclusions under the abuse of discretion standard. Although they
go to great lengths to explain why they are dissatisfied with Dr. Carlini’s “thrice-
speculative” testimony, they have not shown why admitting expert testimony, which
relies on “the very diagnostic methods that other experts in this case, both the plaintiffs
and the defendants’ experts alike, have used” is an abuse of discretion. (Corrected J.A.
at 170-173, Tr. of Proceedings, Nov. 1, 2007). In my view, the majority has, with long
arms and short sight, reached much further than our standard of review permits. For
these reasons, I cannot join the majority’s opinion.

III.

The majority offers several reasons for reversing the district court’s opinion,
none of which I find persuasive. They criticize Dr. Carlini’s testimony for being
“speculative” (ante at 6) and for its “leaps of faith.” (Ante at 8.) They also claim that
Dr. Carlini confused etiology with diagnosis. (Ante at 11.) They further take issue with
the idea of admitting his testimony under a “differential diagnosis” analysis because
many incidents of Parkinson’s Disease are idiopathic,1 a cause which, by its very
definition, cannot be “ruled out.” (See ante at 14-15.) I believe that refocusing the
question on the underlying issue that Daubert and its progeny intended to address—the
exclusion of “junk science”—and reviewing the district court’s evidentiary decisions
through the appropriate abuse of discretion lens, leaves us no choice but to affirm the
district court’s evidentiary conclusions.

A. Dr. Carlini’s Testimony is Admissible under Daubert

The path charting the judiciary’s standards for admitting or excluding expert
testimony—from the early Frye standard to Kumho’s clarification of Daubert—has been
a movement towards granting district judges greater discretion in making expert
testimony determinations. See Kumho, 526 U.S. at 137; Daubert v. Merrell Dow

1
Idiopathic disease are those for which there is no known cause—although Dr. Gregory House
may provide the better definition: “Idiopathic, from the Latin meaning we’re idiots ‘cause we can’t figure
out what’s causing it.” House: Role Model (Fox television broadcast Apr. 12, 2005).
Nos. 08-4015/4016 Tamraz et al. v. Lincoln Elec. Co. et al. Page 26

Pharm., Inc., 509 U.S. 578 (1993); Frye v. United States, 293 F. 1013 (D.C. Cir. 1923).
Today, that discretion is flexible and very broad. Kumho, 526 U.S. at 153.

Daubert’s role of ‘ensur[ing] that the courtroom door remains closed to
junk science,’ Amorgianos v. Nat’l R.R. Passenger Corp., 303 F.3d 256,
267 (2d Cir. 2002), is not served by excluding [medical expert] testimony
. . . that is supported by extensive relevant experience. Such exclusion
is rarely justified in cases involving medical experts as opposed to
supposed experts in the area of product liability. See generally Daniel
W. Shuman, Expertise in Law, Medicine, and Health Care, 26 J. Health
Pol. Pol’y & L. 267 (2001) (characterizing the effect of the Daubert and
Kumho Tire cases on claims of medical expertise as ‘[m]uch ado about
little,’ while noting that these cases have had a significant effect on toxic
tort and products liability litigation).

Dickenson v. Cardiac and Thoracic Surgery of E. Tenn., 388 F.3d 976, 982 (6th Cir.
2004). “As ‘gatekeeper,’ the trial judge is imbued with discretion in determining
whether or not a proposed expert’s testimony is admissible, based on whether it is both
relevant and reliable.” Johnson, 484 F.3d at 429 (quoting Kumho, 526 U.S. at 147). It
is for the district court to determine whether expert testimony is essentially “junk
science” rather than testimony falling within the “range where experts might reasonably
differ.” Kumho, 526 U.S. at 153.

One way in which a court may make this determination is by examining the
expert’s testimony in relation to the factors laid out by the Supreme Court.

These factors include: (1) whether a theory or technique . . . can be (and
has been) tested; (2) whether the theory has been subjected to peer
review and publication; (3) whether, with respect to a particular
technique, there is a high known or potential rate of error and whether
there are standards controlling the technique’s operation; and (4) whether
the theory or technique enjoys general acceptance within a relevant
scientific community.”

Johnson, 484 F.3d at 430 (internal quotations omitted). Six years after issuing Daubert,
the Supreme Court clarified that “the factors listed [in Daubert] do not constitute a
‘definitive checklist or test.’” Id. at 429-30 (quoting Kumho, 526 U.S. at 150). Our
Court has“recognized that the Daubert factors ‘are not dispositive in every case’ and
Nos. 08-4015/4016 Tamraz et al. v. Lincoln Elec. Co. et al. Page 27

should be applied only ‘where they are reasonable measures of the reliability of expert
testimony.’” In re Scrap Metal, 527 F.3d at 529 (quoting Gross v. Comm’r, 272 F.3d
333, 339 (6th Cir. 2001)). “Rather, the gatekeeping inquiry must be tied to the facts of
a particular case, depending on the nature of the issue, the expert’s particular expertise,
and the subject of his testimony.” Id.

While Dr. Carlini testified that he was not able to point to a specific study
showing that manganese exposure caused Parkinson’s Disease, his testimony was
supported by his own general experience and knowledge (corrected J.A. at 615, Tr.
Testimony of Walter Carlini, Sept. 13, 2007), and theoretical medical writing that
explored the connection between manganese exposure and Parkinson’s Disease.2 (Id.
at 599, Tr. Testimony of Walter Carlini, Sept. 11, 2007). When asked what publications
substantiated his claim, Dr. Carlini clarified that “[t]here is a lot of literature out there
about the potential—and it’s all theoretical—about the potential causes for sporadic
parkinsonism. And a lot of literature discusses the combination of environmental factors
together with genetic predispositions.” (Id.) He further stated that “there is a large
likelihood that what we now know as sporadic Parkinson’s disease, which is not
understood very well, is due to a combination of environmental factors together with an
underlying genetic predisposition. That’s the way the field is moving.” (Id.) He
additionally testified that, “there is [sic] a lot of studies or a lot of thinking out there . . .
which conceptualizes sporadic Parkinson’s disease as being . . . a combination of
environmental factors and genetic predisposition which is how I conceive of manganese-
triggered parkinsonism that falls under that rubric.” (Id. at 600.) He further stated that
“there is quite a bit of writing about patients—theoretical writing about patients
developing Parkinson’s disease due to a combination of genetic and environmental
factors.” (Id. at 621, Tr. Testimony of Walter Carlini, Sept. 13, 2007).

2
We must evaluate Dr. Carlini’s testimony in light of the science available to him at the time.
Any findings—positive or negative—regarding the causal connection between manganese and Parkinson’s
disease made since that time are irrelevant for this analysis. It is clear that he was referring to a then-
ongoing debate regarding the causal connection between manganese exposure and Parkinson’s Disease.
See Murry M. Finkelstein, Michael Jerett, A Study of the Relationships between Parkinson’s Disease and
Markers of Traffic-Derived and Environmental Manganese Air Pollution in Two Canadian Cities, 104
ENVTL. RES. 420-432 (2007); Link Found Between Parkinson’s Disease Genes and Manganese Poisoning,
SCI. DAILY (Feb. 2, 2009), available at http://www.sciencedaily.com/releases/2009/02/090201141559.htm
(last accessed Aug. 17, 2010).
Nos. 08-4015/4016 Tamraz et al. v. Lincoln Elec. Co. et al. Page 28

Thus, the connection between manganese and Parkinson’s disease, though not
agreed upon by every member of the scientific community, was certainly the subject of
valid scientific debate and publication at the time of Dr. Carlini’s testimony.3 The
district court succinctly explained its decision not to exclude Dr. Carlini’s evidence,
focusing on his methodology: “I see nothing about [Dr. Carlini’s] methodology that is
either flawed or inconsistent with the very diagnostic methods that other experts in this
case . . . have used and have described as appropriate diagnostic methods.” (Id. at 170-
173, Tr. of Proceedings, Nov. 1, 2007).

While Dr. Carlini’s testimony may not have satisfied every Daubert factor, it is
not necessary that it do so. Johnson, 484 F.3d at 429-30 (holding that the factors do not
constitute a definitive checklist or test); see also In re Scrap Metal, 527 F.3d at 529
(holding that the Daubert factors “are not dispositive in every case and should be applied
only where they are reasonable measures of the reliability of expert testimony.” (internal
quotations omitted)). Dr. Carlini’s testimony easily satisfied at least one Daubert factor
because the manganese-Parkinson’s Disease theory was the subject of peer review and
publication at the time of Dr. Carlini’s testimony. See infra, n.2.

Furthermore, to the extent that the connection between manganese and
Parkinson’s Disease could be tested at the time, the then-ongoing studies of individuals
exposed to manganese, who later developed Parkinson’s Disease, constitutes testing
sufficient to satisfy Daubert. Therefore, Dr. Carlini’s testimony appears to meet one, if
not several, Daubert requirements. Thus, the district court did not abuse its discretion
in admitting it, and the majority errs in so holding.

B. Speculation and Gaps in the Testimony

The majority finds that Dr. Carlini’s testimony was speculative, stating without
support that the testimony was “no more than a hypothesis, [and is] thus not
‘knowledge,’ nor is it ‘based upon sufficient facts or data’ or the ‘product of reliable
principles and methods . . . applied . . . reliably to the facts of the case.” (Ante at 7.) I
3
A quick internet search of scientific studies published in 2007 shows that a considerable number
of studies existed at the time, attempting to establish, with varying degrees of success, that manganese
exposure among welders could cause Parkinson’s Disease.
Nos. 08-4015/4016 Tamraz et al. v. Lincoln Elec. Co. et al. Page 29

disagree that Dr. Carlini’s testimony was speculative. Based on the record, it seems
clear that Dr. Carlini was relying upon scientific studies which tested the causal
connection between manganese exposure and Parkinson’s Disease. Furthermore, the
district court was exercising its broad discretion when it found that Dr. Carlini’s
methodology was reliable and consistent with the diagnostic methods used by other
experts in the case. It seems incredible that the majority—exercising a standard of
review that seems closer to de novo than abuse of discretion, and without the benefit of
having sat through the hearings and seen the experts—finds Dr. Carlini’s testimony to
be speculative.

The majority also cites gaps in Dr. Carlini’s testimony as a reason to reverse the
district court. (Ante at 8.) However, the majority’s newly-minted requirement that
scientific testimony must be without flaws or gaps and have no unprovable inferences
or assumptions runs counter to any reasonable understanding of how scientific “truth”
is reached. “Scientists disprove things. In the process they filter error from theories and
methodology, but they do not prove that the surviving methodologies—those that are left
standing or those that are changed to correct errors—are valid.” Jan Beyea & Daniel
Berger, Scientific Misconceptions among Daubert Gatekeepers: The Need for Reform
of Expert Review Procedures, 64 LAW & CONTEMP. PROBS. 327, 337 (2001).
Furthermore, the “theories that survive testing still have components that have never
been tested, contain subjective elements, and require that reasonable inferences be made
if they are to be used in real world examples.” Id. At least one other Circuit court has
found that “to the extent that [the defendant] asserts there were gaps or inconsistencies
in the reasoning . . . such arguments go to the weight of the evidence, not its
admissibility.” Campbell v. Metro. Prop. and Cas. Ins. Co. 239 F.3d 179, 186 (2d Cir.
2001) (the trial court did not abuse its discretion in admitting expert testimony that
plaintiffs were suffering from lead poisoning).

Indeed, the most cherished of scientific “truths” are the subject of constant
refinement and are frequently overturned by subsequent science. For instance, the 42-
year consensus that DNA alone determines heredity was later “dethroned as a universal
Nos. 08-4015/4016 Tamraz et al. v. Lincoln Elec. Co. et al. Page 30

principle, albeit after the 1994 article by Black et al. was published.” Id. at 335. In fact,
simultaneously accepted scientific principles are sometimes incompatible, and thus,
might fare badly under a strict Daubert application.

Imagine Euclid testifying in a modern day Daubert proceeding:
‘Professor Euclid, I understand that one of your postulates is that parallel
lines do not meet at infinity. Can you prove this to be true? Have you
ever tested this? Isn’t it also true that Professor Einstein has proven that
your geometry doesn’t work in the presence of gravity?’

Id. at 335 n. 42.

While the district court must necessarily draw lines, we must use caution in
demanding the type of finality from science that we have come to expect in law. This
is especially true when considering cases of newer scientific studies. It seems to me an
overly harsh test at the admissibility level to insist upon testimony with no “gaps”, when
the science itself may be incapable of absolute proof. Do malfeasing defendants get a
free pass on the first few victims because there is not yet a sufficient sample set to create
scientific studies with no discernable gaps? Do we tell the early victims, “I’m sorry, you
had the misfortune of getting sick too soon”, and send them home?

The fact that scientists have not reached consensus regarding medical causation
does not render reliance on a scientist’s theory improper expert testimony, particularly
when, as in this case, the expert is relying on studies that appear to have been conducted
using standard methodology. Rather, those differences should go to the weight that a
jury should give an expert’s testimony. See Best v. Lowe’s Home Centers, Inc., 563 F.3d
171, 182 (6th Cir. 2009) (finding that “admissibility under 702 does not require perfect
methodology. . . . Any weakness in [a “competent, intellectually rigorous physician’s”]
methodology [“in identifying the most likely cause of the plaintiff’s injury”] will affect
the weight that his opinion is given at trial, but not its threshold admissibility.”). In
cases where the state of scientific consensus is difficult to determine, we must defer to
the district court. The district court has the distinct advantage of having heard all the
experts testify and can weigh the reliability of a given expert’s testimony against others
Nos. 08-4015/4016 Tamraz et al. v. Lincoln Elec. Co. et al. Page 31

more easily than we can. Our valuations of complicated medical expert issues such as
these are made out of context and are therefore more likely to suffer flaws.

Because Dr. Carlini relied on scientific methodology used by other experts in his
field, see infra at 28, I do not believe that the district court abused its discretion in
admitting his testimony. The district court’s determination that Dr. Carlini’s
methodology was sufficiently reliable was certainly not clearly erroneous, so the
testimony was admissible. What weight to grant his testimony was a question for the
jury, not an appellate court sitting far removed from the trial. Because the majority has
not demonstrated that the district court abused its discretion, it errs in reversing the
district court’s decision.

IV.

For the reasons above, I respectfully dissent.