Court Opinion

ID: 4025730
Source: CourtListenerOpinion
Date Created: 2016-08-17 11:06:26.867068+00
Date Added: 2024-06-11T14:01:41.216172
License: Public Domain

STATE OF MICHIGAN

                            COURT OF APPEALS

TERI WALTERS and KIM WALTERS,                                          UNPUBLISHED
                                                                       August 16, 2016
               Plaintiffs-Appellants,

v                                                                      No. 319016
                                                                       Eaton Circuit Court
DONALD S. FALIK, D.D.S., d/b/a FALIK                                   LC No. 12-000658-NH
FAMILY DENTISTRY, ROBERT C. FALIK,
D.D.S., and JANE DOE,

               Defendants-Appellees.

                                           ON REMAND

Before: MURPHY, P.J., and METER and SERVITTO, JJ.

PER CURIAM.

        This case returns to us from the Michigan Supreme Court, which, in lieu of granting
leave to appeal, vacated our earlier opinion and remanded the case to this panel for
reconsideration in light of Elher v Misra, 499 Mich. 11; 878 NW2d 790 (2016). Walters v Falik,
499 Mich. 904 (2016). In the original opinion, we had reversed the trial court’s ruling that
plaintiffs’ expert’s opinion on causation was inadmissible under MRE 702 and MCL
600.2955(1). After reviewing and considering Elher, which is distinguishable, we again reverse
and remand for further proceedings.
       Given that our previous opinion was vacated in its entirety, and for purposes of providing
the necessary background information and the manner in which we had earlier analyzed the case,
we shall quote our prior opinion at length and then discuss Elher and its application to the instant
case.
                                   I. OUR EARLIER OPINION
               Plaintiff Teri Walters (hereafter “Walters”) suffered an unintended
       exposure to phosphoric acid contained in a dental etching solution supplied by
       defendants. Plaintiffs proceeded to file a negligence action against defendants.
       The trial court granted summary disposition in favor of plaintiffs on the question
       of liability, and liability is not at issue in this appeal. Subsequently, the trial court
       granted defendants’ motion in limine, precluding the testimony of plaintiffs’
       proposed expert witness, Dr. M. Eric Gershwin, on the issue of causation and
       damages. Plaintiffs claimed that the exposure to the phosphoric acid in the
                                                 -1-
etching solution triggered or caused Wegener’s granulomatosis (WG), an
autoimmune disease that Walters was diagnosed with after the exposure. As
reflected in his deposition testimony, Dr. Gershwin was prepared to testify in
support of a causal connection between the exposure to phosphoric acid and WG.
The trial court, exercising its role as gatekeeper, concluded that Dr. Gershwin’s
opinion on causation was not supported by sufficient data and reliable scientific
principles, MRE 702. We reverse and remand for further proceedings.
        On October 20, 2010, Walters went to defendants’ dental office to have a
permanent crown seated, and following the procedure, she was provided with
what she believed was a whitening solution for her teeth. Instead, a receptionist
mistakenly gave Walters an etching solution, which was never intended to be
dispensed to patients. An etching solution is used to “etch” the surfaces of teeth
in preparation for the application of dental restoratives, and it contains phosphoric
acid, which is a caustic acid and absolutely not meant to be used for teeth
whitening. Etching solution, when used properly, should only remain on a
particular tooth for about 20 seconds. A product safety data sheet regarding the
etching solution indicated that it is corrosive, can cause chemical burns to the
skin, eyes, mouth, and throat, may cause permanent tissue damage, is harmful if
swallowed, can irritate the respiratory system, and may cause swallowing
difficulties, vomiting, diarrhea, and possible shock. Etching solution should not
be exposed to moist air or water. Walters refrigerated the etching solution for a
few months without using it, but on February 11, 2011, she spread the etching
solution in her dental tray and left the tray in her mouth overnight in an attempt to
whiten her teeth. When she awoke, Walters had a burning sensation inside of her
mouth, including the sides of her tongue and along the gumline.

       Walters went to her doctor on February 24, 2011, and according to the
associated medical record, she complained of burns in her mouth as caused by the
etching solution; she was diagnosed as having a “chemical burn.” On April 5,
2011, Walters again visited her doctor, complaining of sinus trouble that had been
bothersome for a month, along with fullness in one ear. The medical record
documenting the visit indicated that the examination revealed raw and swollen
“[n]asal mucosa, septum, [and] turbinates.”1 Walters was diagnosed with sinusitis
and prescribed an antibiotic. She saw her doctor again on April 14, 2011,
complaining of sinus congestion and a very full feeling in her ears, which was at
times painful. The medical record documenting the visit indicated that Walters
had been previously prescribed two different antibiotics for the sinus problems,
which were ineffective, that she was “[p]ositive for ear pain, congestion, . . . and
sinus pressure,” and that her examination revealed “[m]ucosal edema and
rhinorrhea.” Walters was diagnosed with acute sinusitis. On May 4, 2011,
Walters saw an ear, nose, and throat doctor (ENT) to be evaluated for chronic

1
 A “turbinate” is “a small curved bone that extends horizontally along the lateral
wall of the nasal passage.” Webster’s New College Dictionary (2005).

                                        -2-
sinusitis. The associated ENT record indicated that Walters reported a sinus
infection that had been present for approximately 45 days, continual plugging and
fullness in her left ear, and ongoing sinus pain and pressure. The physical
examination revealed “dryness and crusting on the anterior septum on the left
side” and “fairly significant swelling in the ethmoid area bilaterally with
drainage.” Following numerous procedures and evaluations at a hospital, Walters
was diagnosed in June 2011 with WG, which has been explained and described as
follows:
        “[WG] is a primary vasculitis of the small blood vessels [inflammation of
the blood vessels] in which a characteristic feature is production of antineutrophil
cytoplasmic antibodies (ANCAs), usually targeted to proteinase 3 (PR 3). The
symptoms, histology, and pathogenesis go through two phases. In the first phase,
the disease is confined to the airways, causing sinusitis, otitis media, tracheal
stenosis and/or pulmonary nodules. Histology usually shows granulomatous
lesions. The second phase starts when the disease extends to other organs . . . .

       The pathogenesis of WG and other vasculitides associated with ANCAs
remains unclear, but probably involves an interaction between a genetic
susceptibility and environmental factors.” [Hamidou, Audrain, Ninin, Robillard,
Muller, and Bonneville, Staphylococcus aureus, T-cell repertoire, and Wegener’s
granulomatosis, 68 Joint Bone Spine (June 2001), p 373.2]

       Before we examine Dr. Gershwin’s deposition testimony, we will review
the medical and scientific articles and literature relating to WG in order to provide
context for Dr. Gershwin’s testimony.

       In Mahr, Neogi, and Merkel, Epidemiology of Wegener’s granulomatosis:
Lessons from descriptive studies and analyses of genetic and environmental risk
determinants, 24 Clinical and Experimental Rheumatology (Supp 41, 2006), pp S-
82, S-85 to S-87, the authors stated:

       “The etiology of WG remains unknown. Based on a growing number of
epidemiologic investigations carried out during the last 15 years, current
understanding is that of a complex disease resulting from the interplay among
multiple genetic and environmental risk factors.
                                       ***
        Analytic epidemiology aims to identify the determination of disease
occurrence with putative risk factors commonly falling into 2 major categories:
genetics and environment. In that context, the term “environment” is generally
used to designate all non-genetic variables . . . .

2
  All medical and scientific articles and literature cited in this opinion were
submitted to and filed in the trial court for purposes of the motion in limine.

                                        -3-
                                       ***
        Genetic predisposition to WG is suggested by ethnic variation . . . and by
reports of familial aggregation . . . .
                                       ***
        [S]tudies are consistent in finding positive associations between crystalline
silica exposure and risk of WG . . . and exposure to silica. . . . Exposure to
industrial pollutants such as mercury, lead, and cadmium had been found among
patients with WG but these associations were weak or statistically non-significant.
Another study revealed exposure to pesticides, particulate matter, or fumes as
potential risk factors for WG.”

         ANCA-associated vasculitides comprise WG and “environmental factors
have been considered important in the development of ANCA, including: silica
exposure, bacterial infection [and] in particular Staphylococcus aureus, viral
infection . . ., and exposure to drugs such as propylthiouracil.” Chen and
Kallenberg, The environment, geoepidemiology and ANCA-associated
vasculitides, 9 Autoimmunity Reviews (2010), pp A293-A294; see also
Staphylococcus aureus, T-cell repertoire, and Wegener’s granulomatosis, 68
Joint Bone Spine at 373 (“The many environmental factors capable of inducing
the production of ANCAs or triggering true vasculitis include toxic substances
(silica), drugs . . . , and others.”). “A case-control study carried out at the
National Institutes of Health (NIH) revealed an association with exposure to
fumes or particulates and pesticides in patients with WG compared with healthy
or rheumatic disease controls” and “exposure to metal and welding fumes has
been reported to increase the risk of . . . WG . . . .” Lane, Watts, Bentham, Innes,
and Scott, Are Environmental Factors Important in Primary Systemic Vasculitis?,
48 Arthritis & Rheumatism #3 (March 2003), pp 814-815. “A history of high
solvent exposure at any time was associated with . . . WG.” Id. at 818. In Duna,
Cotch, Galperin, Hoffman, and Hoffman, Wegener’s granulomatosis: role of
environmental exposures, 16 Clinical and Experimental Rheumatology
(November-December 1998), p 669, the authors stated that while the etiology of
WG remained unknown, “[t]he predominant involvement of the airways and the
presence of neutrophilic alveolitis at disease onset have led us to postulate that an
inhaled agent may trigger the onset of WG.” In their study, the authors found
that, as between WG and certain control groups, “[s]tatistically significant
differences occurred [greater in the WG group] in regard to . . . vocational
exposure to fumes or particulate materials . . ., residential exposure to particulate
materials from construction . . ., and occupational exposure to pesticides[.]” Id.
The authors also noted that one of several indicators reflecting the onset of WG is
sinusitis of more than two months’ duration. Id. at 670.

        With respect to the apparent link between pesticides and WG, plaintiffs
submitted scientific articles and literature regarding phosphorous and pesticides,
showing that various forms of phosphorous are common components of
pesticides. Centers for Disease Control and Prevention, Organophosphorus
Insecticides: Dialkyl Phosphate Metabolites, Biomonitoring Summary, National
                                         -4-
Biomonitoring Program (July 2013), p 1 (“Organophosphorus insecticides . . .
have accounted for a large share of all insecticides used in the United States.”);
GoodGuide, Organophosphate Pesticides: Dialkyl Phosphate Metabolites,
Scorecard (2011), p 1 (“Organophosphate pesticides account for about half of the
insecticides used in the United States.”); Betteridge, Thompson, Baker, and
Kemp, Photoelectron Spectra of Phosphorus Halides, Alkyl Phosphites and
Phosphates, Organo-Phosphorus Pesticides, and Related Compounds, 44
Analytical Chemistry #12 (October 1972), p 2005.

        We now turn to Dr. Gershwin’s deposition testimony. He testified that
“we know that autoimmunity, including [WG], occurs from a combination of
genetic susceptibility and environmental factors.” When Dr. Gershwin was asked
about environmental factors or chemicals in relation to autoimmunity, he
observed that “[i]f we’re referring to [WG], for example, we know that materials
that alter the mucosal airway, whether it’s superantigens, whether it’s silica
exposure, whether it’s chemicals and certain hydrocarbons and solvents and
pesticides[,] have been shown to be associated with patients who develop [WG].”
Dr. Gershwin conceded that there was no literature that specifically indicated that
phosphoric acid causes or contributes to WG. But he noted that one must look to
“mechanisms of action” and “depend by analogy on the science which has already
been done and peer reviewed on environmental agents, including the
epidemiological data on solvents, hydrocarbons, agricultural products, [and] silica
in ANCA-positive patients.”3 He also stated a few times that there would be no
studies in which a person was experimentally exposed to phosphoric acid, as to
conduct such testing would be unethical.

       Dr. Gershwin testified that many solvents and pesticides contain
phosphorus or phosphates, and he accurately noted a couple of times that silicon
and phosphorus are next to each other on periodic table of elements (numbers 14
and 15 respectively), although he did not elaborate on the relevancy of this fact,
simply implying a similarity in properties.4 Dr. Gershwin then testified:

       “Well, many of the hydrocarbons contain phosphates as well. I already
explained to you what the periodic table is. And incidentally, it’s not really the

3
  The literature indicated that not all patients with active WG have ANCAs
present. Wegener’s granulomatosis: role of environmental exposures, 16 Clinical
and Experimental Rheumatology at 673. However, with respect to Walters, Dr.
Gershwin testified that she “had a very high-titer ANCA.”
4
  Dr. Gershwin did indicate that “they have a number of interesting properties,
including isoelectric focusing and so forth.” We appreciate that the particular
arrangement of the elements on the periodic table is based on various properties
of the elements.

                                        -5-
phosphates that are the basis of my opinion. It’s the phosphoric acid and what
happens when it goes in solution, and I think that’s what’s critical. . . . Mrs.
Walters presented with an acute onset, . . . with a very high-titer ANCA . . . . We
had an advantage on her in understanding etiology that we won’t have in people
that have a more chronic exposure. Because, in fact, the silica exposure data
shows it’s not necessarily the duration of exposure as it is the intensity of an
exposure. And of course, in the eight hours she had a very intense exposure.

                                        ***

         So Mrs. Walters was exposed [o]n . . . February 11th, thereabouts. Her
first sort of signs are about three or four weeks later. Even though temporal
association by itself should not be the only criteria in this case, it is the perfect
criteria for a primary immune response. Meaning if I were to immunize you with
an antigen and ask how long it would take you to make a primary IGG
[immunoglobulin] response, the time period in which she manifested the sinus
symptoms is absolutely out of a textbook of immunology.

        And because her disease began with her sinus symptoms and then became
this incredible immunological storm that crescendoed into her upper airway
issues, her failures, her respiratory distress . . . .

                                        ***

       So you then go back to the primary immune response, you have
phosphoric acid, an[] intense exposure, incredible electrophilic agent that is not
supposed to be exposed to water. She puts it in her mouth, and she leaves it there.
And now you present when she finally is evaluated with a very high-titer ANCA.
You don’t usually have that scenario.

                                        ***
         [W]hen I look at the potency and the chemistry of the phosphoric acid in
the etching solution, it’s just above and beyond anything that I can even compare
it to. I mean, this was an incredible inflammatory insult. . . . [When] we look at
Mrs. Walters and we look at the chemistry of what she was exposed to, the time
period of her clinical presentation, the safety data sheets [for the etching solution],
the data that’s already available on environmental factors, this is a very important
case for the medical literature.

                                        ***
       [We] really have a plausible scientifically acceptable mechanism of action.

                                        ***
       So I think what happened is phosphoric acid hits water, disassociates,
produces an incredible inflammatory response, including neutrophil. That’s why
she had the symptoms she had. The neutrophils enter the area, they marginate

                                         -6-
acutely as they are supposed to, they degrade, the myeloperoxidase neutrophilic
antigens get released, she mounts an immune response, she boosts it, and that’s
why she has . . . WG.”

        Dr. Gershwin further testified that sinusitis does not cause WG; rather,
sinusitis is a manifestation, sign, and symptom of WG. He opined that Walters
“would not have got [WG] had it not been for the etching solution.” Dr.
Gershwin clarified that he could not state that she would not have suffered WG in
the future, given her predisposition to WG and the possibility of another type of
environmental exposure; however, he emphasized that Walters would not have
suffered WG when she did but for the exposure to the etching solution. Dr.
Gershwin opined that WG would reduce Walters’ life span by ten 10 years.

         Defendants filed a motion in limine to preclude Dr. Gershwin’s testimony.
They argued that there was no scientific support for his conclusion that the
etching solution is an environmental catalyst that, along with Walters’ alleged
predisposition to WG, caused the onset of her WG. Defendants additionally
contended that Dr. Gershwin’s testimony regarding a causal connection between
the etching solution / phosphoric acid and WG failed to meet the test for
reliability under MCL 600.2955. The trial court granted the motion, ruling that
Dr. Gershwin’s testimony was not reliable under MRE 702 and not supported by
the scientific and medical data. The trial court noted a few times that the articles
and literature expressed that the etiology or cause of WG remained unclear and
unknown. The trial court also concluded that the scientific and medical data
relied on by plaintiffs failed to show a connection between phosphorus,
phosphates, or phosphoric acid and the chemicals and environmental factors that
had been identified in literature as being associated with WG; and even that
association was tenuous. Plaintiffs appeal by leave granted.

        In Chapin v A & L Parts, Inc, 274 Mich. App. 122, 126-127; 732 NW2d
578 (2007), this Court set forth the applicable standard of review and the general
principles that are implicated when examining the admissibility of expert
testimony:

        “This Court reviews for an abuse of discretion a trial court's determination
of the qualifications of a proposed expert witness. This Court likewise reviews for
an abuse of discretion a trial court's decision whether to admit evidence, although
admission of legally inadmissible evidence is necessarily an abuse of
discretion. The interpretation of an evidentiary rule is reviewed de novo in the
same manner as the examination of the meaning of a court rule or a statute. Rules
of evidence are construed in the same way as statutes.

                                        -7-
       Before a trial court may admit any expert testimony, the trial court is
required by MRE 702[5] to ensure that each aspect of an expert witness's
proffered testimony—including the data underlying the expert's theories and the
methodology by which the expert draws conclusions from that date—is reliable.
While the exercise of this gatekeeper role is within a court's discretion, a trial
judge may neither abandon this obligation nor perform the function inadequately.
The plain language of MCL 600.2955(1)[6] establishes the Legislature's intent to

5
    MRE 702 provides:
        If the court determines that scientific, technical, or other specialized
knowledge will assist the trier of fact to understand the evidence or 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 on 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.
6
    MCL 600.2955(1) provides:
        In an action for the death of a person or for injury to a person or property,
a scientific opinion rendered by an otherwise qualified expert is not admissible
unless the court determines that the opinion is reliable and will assist the trier of
fact. In making that determination, the court shall examine the opinion and the
basis for the opinion, which basis includes the facts, technique, methodology, and
reasoning relied on by the expert, and shall consider all of the following factors:
        (a) Whether the opinion and its basis have been subjected to scientific
testing and replication.
       (b) Whether the opinion and its basis have been subjected to peer review
publication.
       (c) The existence and maintenance of generally accepted standards
governing the application and interpretation of a methodology or technique and
whether the opinion and its basis are consistent with those standards.
         (d) The known or potential error rate of the opinion and its basis.
       (e) The degree to which the opinion and its basis are generally accepted
within the relevant expert community. As used in this subdivision, “relevant
expert community” means individuals who are knowledgeable in the field of
study and are gainfully employed applying that knowledge on the free market.

        (f) Whether the basis for the opinion is reliable and whether experts in
that field would rely on the same basis to reach the type of opinion being
proffered.
        (g) Whether the opinion or methodology is relied upon by experts outside
of the context of litigation.

                                          -8-
assign the trial court the role of determining . . . whether proposed scientific
opinion is sufficiently reliable for jury consideration. The United States
Supreme Court emphasized that the inquiry is flexible and focused solely on
principles and methodology rather than ultimate conclusions, and its overarching
subject is the scientific validity—and thus the evidentiary relevance and
reliability—of the principles that underlie a proposed submission.” [Citations,
quotation marks, and alteration brackets omitted.]
        In Chapin, this Court recognized the “Sir Bradford Hill” (SBH)
methodology for examining causation, which methodology goes beyond just
using epidemiological data and is primarily intended to determine cause and
effect. Id. at 133. The SBH methodology contains nine criteria: strength of
association; temporality (cause must precede effect); biologic or response gradient
(basic toxicological knowledge); consistency; specificity, biological plausibility;
coherence; experimental evidence; and analogy. Id. at 133-134.

        Here, Dr. Gershwin’s opinion that Walters’ exposure to the phosphoric
acid in the etching solution caused her WG was predicated on: (1) the caustic
nature of phosphoric acid; (2) phosphoric acid being a WG-triggering
environmental factor or chemical; (3) the intensity and duration of the phosphoric
acid exposure (overnight while Walters slept); (4) the area of exposure (inside the
mouth where moisture exists); (5) the textbook timing of the presentation of an
immune response in relationship to the date of exposure and the overall
chronology of events; (6) the incredible extent of the immune response (a very
high-titer ANCA); (7) the manifestation and duration of a classic WG symptom,
sinusitis; (8) Walters’ predisposition to WG; and (9) the medical and scientific
literature, directly or by analogy. Dr. Gershwin’s analysis employed many of the
criteria associated with the SBH methodology; it was a cause and effect
methodology.

        With respect to the caustic nature of phosphoric acid, this was established
by the product safety data sheet regarding the etching solution, which indicated
that it is corrosive, can cause chemical burns, permanent tissue damage,
swallowing difficulties, vomiting, diarrhea, and possible shock, is harmful if
swallowed, can irritate the respiratory system, and that it should not be exposed to
moist air or water. Given that Walters slept overnight with a dental tray in her
mouth that was filled with the etching solution, there is no dispute regarding the
intensity, duration, and location of the exposure. There also does not appear to be
any dispute concerning the claimed textbook timing or chronology of the
presentation of an immune response in relationship to the date of exposure, nor as
to Walters’ very high-titer ANCA. Next, the medical and scientific literature
cited above supports the proposition that sinusitis can be a manifestation of the
onset of WG, especially where it is of long duration, as was the case with Walters.

        On the issue of the role of environmental factors and genetic influences
relative to causation, as reflected above, the medical and scientific literature did
indeed indicate that the etiology of WG remains unclear and unknown. However,
when read in context, this proposition was clearly meant to indicate that a
                                        -9-
“definitive” or “absolutely certain” etiology is unclear and unknown. In
Staphylococcus aureus, T-cell repertoire, and Wegener’s granulomatosis, 68
Joint Bone Spine at 373, the authors stated that “[t]he pathogenesis of WG and
other vasculitides associated with ANCAs . . . probably involves an interaction
between a genetic susceptibility and environmental factors.” (Emphasis added.)
In Epidemiology of Wegener’s granulomatosis: Lessons from descriptive studies
and analyses of genetic and environmental risk determinants, 24 Clinical and
Experimental Rheumatology at S-82, S-85 to S-87, the authors, while
acknowledging that the “etiology of WG remains unknown,” nonetheless stated
that “[b]ased on a growing number of epidemiologic investigations carried out
during the last 15 years, current understanding is that of a complex disease
resulting from the interplay among multiple genetic and environmental risk
factors.” (Emphasis added.) Those authors also indicated that “studies are
consistent in finding positive associations between crystalline silica exposure and
risk of WG.” (Emphasis added.) In The environment, geoepidemiology and
ANCA-associated vasculitides, 9 Autoimmunity Reviews at A293-A294, the
authors stated that “environmental factors have been considered important in the
development of ANCA.” (Emphasis added.) And in Wegener’s granulomatosis:
role of environmental exposures, 16 Clinical and Experimental Rheumatology at
669, the authors noted that while the etiology of WG remained unknown, “[t]he
predominant involvement of the airways and the presence of neutrophilic
alveolitis at disease onset have led us to postulate that an inhaled agent may
trigger the onset of WG.”
        Accordingly, while not definitive, there is medical and scientific literature
indicating that the probable or likely cause of WG is a combination of
environmental and genetic factors. We observe that plaintiffs, in order to
succeed, are not required to definitively establish a causal link between the
exposure and WG.7 Moreover, the inquiry regarding whether proposed scientific

7
   “To establish a prima facie case of negligence, a plaintiff must prove four
elements: (1) a duty owed by the defendant to the plaintiff, (2) a breach of that
duty, (3) causation, and (4) damages.” Case v Consumers Power Co, 463 Mich. 1,
6; 615 NW2d 17 (2000). The causation element encompasses both cause in fact
and proximate or legal cause. Id. at n 6. “The cause in fact element generally
requires showing that ‘but for’ the defendant’s actions, the plaintiff’s injury would
not have occurred.” Skinner v Square D Co, 445 Mich. 153, 163; 516 NW2d 475
(1994). It is not sufficient to proffer “a causation theory that, while factually
supported, is, at best, just as possible as another theory.” Id. at 164. A “plaintiff
must present substantial evidence from which a jury may conclude that more
likely than not, but for the defendant's conduct, the plaintiff's injuries would not
have occurred.” Id. at 164-165 (emphasis added). But “litigants do not have any
right to submit an evidentiary record to the jury that would allow the jury to do
nothing more than guess.” Id. at 174. The Skinner Court further observed that
“‘[t]he evidence need not negate all other possible causes’” and absolute certainty

                                        -10-
opinion is sufficiently reliable for a jury to consider “is flexible and focused
solely on principles and methodology rather than ultimate conclusions[.]”
Chapin, 274 Mich. App. at 126-127 (emphasis added). The trial court here made
an error of law in analyzing the question of the admissibility of Dr. Gershwin’s
testimony by effectively requiring plaintiffs to establish causation and their case
prior to trial and to do so definitively. And the trial court further erred by failing
to take into consideration Dr. Gershwin’s legitimate reliance on the nature,
duration, intensity, and location of the exposure, the temporal proximity of the
immune response to the date of exposure, and the duration and nature of an
expected manifestation of WG, i.e., a lengthy battle with sinusitis, which all
played a role in Dr. Gershwin’s overall analysis.
         With respect to the lack of medical or scientific literature specifically
connecting an exposure to phosphoric acid with WG, there was literature, cited
above, reflecting the prevalence of phosphates in pesticides and showing a
statistically significant association between pesticides and the development of
WG.         Organophosphorus Insecticides: Dialkyl Phosphate Metabolites,
Biomonitoring Summary, National Biomonitoring Program, at 1; Are
Environmental Factors Important in Primary Systemic Vasculitis?, 48 Arthritis &
Rheumatism at 814-815; Wegener’s granulomatosis: role of environmental
exposures, 16 Clinical and Experimental Rheumatology at 669. Also, while not
expressly stated, it appears that Dr. Gershwin’s view was that phosphoric acid is
comparable to silica, which has been linked to WG, in the context of
environmental factors that cause WG. Regardless, the lack of a specific study
looking at direct exposures to phosphoric acid is understandable considering the
ethical dilemma posed by conducting such a study. And we find our situation
analogous to that in Chapin, where “a number of epidemiological studies had
analyzed mesothelioma among automobile brake mechanics and failed to show an
association between asbestos-based automobile brake products and
mesothelioma.” Chapin, 274 Mich. App. at 135. This Court, nonetheless, allowed
the plaintiffs’ expert to testify about a causal link between exposure to asbestos-
based automobile brake products and mesothelioma, considering all of the SBH
criteria supporting causation. Id. at 140. The Chapin panel ruled:

         “This case does not present a situation involving questionable or absent
epidemiological evidence coupled with questionable or absent other evidence, or
coupled with an “expert” who actually lacks the requisite qualifications.[8] Rather,
this is a case involving strong and undisputed support for . . . [plaintiffs’ expert’s]
position, coupled with fairly consistent yet potentially questionable contradictory
evidence, depending on which expert is to be believed. Although clearly not
on causation is not required. Id. at 166, quoting 57A Am Jur 2d, Negligence,
§ 461, p 442.
8
  There is no dispute that, as found by the trial court, Dr. Gershwin is highly
qualified to give an opinion in this area of medicine; his CV is extremely
impressive.

                                         -11-
       universally accepted, and although unsupported by epidemiological studies that
       may or may not be flawed, . . . [his] opinion is certainly objective, rational, and
       based on sound and trustworthy scientific literature.” [Id.]

               As indicated, in Chapin, there were studies that actually showed no
       correlation between exposure to asbestos-based automobile brake products and
       mesothelioma, yet the expert was allowed to testify, and here there is no
       indication that there exist any studies showing that phosphoric acid does not cause
       WG. Furthermore, as in Chapin, there was other unquestionable cause-and-effect
       evidence showing a link between the exposure and WG; plus, there are
       epidemiological studies generally supporting Dr. Gershwin’s opinion. We also
       note that defendants do not counter Dr. Gershwin’s assertion that when
       phosphoric acid comes into contact with moisture, such as it did inside Walters’
       mouth, it produces an incredible inflammatory response. Again, the product
       safety data sheet regarding the etching solution provided that it should not be
       exposed to moist air or water, is harmful if swallowed, and can cause respiratory
       distress. We are not prepared to preclude Dr. Gershwin’s testimony simply
       because there is not a specific study showing that exposure to phosphoric acid
       causes WG.

               In sum, Dr. Gershwin’s testimony was based on sufficient facts or data, it
       was the product of reliable principles and methods, and Dr. Gershwin applied the
       principles and methods reliably to the facts of the case, MRE 702. The trial court
       erred in granting defendants’ motion in limine. The trier of fact will ultimately be
       free to weigh Dr. Gershwin’s opinion on causation and accept or reject it. See
       Chapin, 274 Mich. App. at 140 (“[D]eciding this case at an evidentiary hearing,
       depriving the jury of the opportunity to fulfill its proper role as fact-finder, would
       be inappropriate.”).

              Reversed and remanded for further proceedings consistent with this
       opinion. . . . .

                     II. THE ELHER OPINION AND ITS APPLICATION

        In Elher, the plaintiff underwent a laparoscopic cholecystectomy (removal of
gallbladder), and the defendant doctor clipped the common bile duct leading from the plaintiff’s
liver, which necessitated emergency surgery to repair the duct. Elher, 499 Mich. at 14-15. The
plaintiff’s expert, Dr. Paul Priebe, opined that “it is virtually always malpractice to injure the
common bile duct during a laparoscopic cholecystectomy, absent extensive inflammation or
scarring.” Id. at 15. Priebe asserted that the plaintiff’s injury reflected a breach of the standard
of care, as there was no indication of scarring or inflammation. Id. at 15, 24. The circuit court
determined that Priebe’s testimony was unreliable and inadmissible under MRE 702 and MCL
600.2955(1) because he could not cite any supporting authority for his opinion, and the court
granted summary disposition in favor of the defendants relative to the plaintiff’s malpractice
action. Id. at 17-18. This Court reversed the circuit court’s ruling in a split opinion. Id. at 18,
citing Elher v Misra, 308 Mich. App. 276; 870 NW2d 335 (2014). Our Supreme Court, reversing
this Court, held “that, under the facts of this case, in which Priebe admitted that his opinion was

                                               -12-
based on his own personal beliefs, there was no evidence that his opinion was generally accepted
within the relevant expert community, there was no peer-reviewed medical literature supporting
his opinion, plaintiff failed to provide any other support for Priebe's opinion, and defendant
submitted contradictory, peer-reviewed medical literature, the circuit court did not abuse its
discretion by excluding Priebe's testimony.” Elher, 499 Mich. at 14.

        In the Supreme Court’s analysis, it first reviewed the elements of a medical malpractice
action, the language in MRE 702, and the requirements of MCL 600.2955(1). Elher, 499 Mich.
at 21-24. In our prior opinion, we also reviewed MRE 702 and MCL 600.2955(1), and we
certainly agree with the Elher Court on the elements of a medical malpractice action, including,
as relevant here, the causation requirement. The Supreme Court next “reject[ed] plaintiff’s
contention that this [is] a case in which the breach of the standard of care is so obvious to a
layperson that no expert testimony is required.” Elher, 499 Mich. at 24. Here, our original
opinion did not place any reliance on a view that expert testimony was unnecessary to establish a
causal connection between Walters’ exposure to the phosphoric acid in the etching solution and
WG. The Elher Court next ruled:

               We conclude that the circuit court did not abuse its discretion by relying
       on two of the factors listed in MCL 600.2955 and by concluding that Priebe's
       opinion was not reliable. First, the Court of Appeals erred by concluding that the
       issue debated by the experts was not studied in peer-reviewed articles and,
       therefore, that the circuit court abused its discretion when it relied on this factor.
       The majority conceded that the article authored by [Dr. Lawrence] Way was peer-
       reviewed. Way concluded, after analyzing 252 operations, that 97% of injuries
       occur because of misperception and that such misperception errors do not
       constitute negligence. Thus, the issue being debated has been studied. Plaintiff,
       however, failed to submit any peer-reviewed medical literature in support of
       Priebe's opinion, and Priebe admitted that he knew of none. [Id. at 25.]

        In the instant case, no evidence was presented of any studies or peer-reviewed articles
specifically showing a link between WG and exposure to phosphoric acid, but then there were no
studies or articles debunking or refuting a causal connection. That said, literature was submitted
indicating a connection between WG and environmental exposure to toxic substances, including
pesticides, which, according to articles presented by plaintiffs, are often comprised of
phosphates, and a phosphate is “a salt or ester of a phosphoric acid,” Merriam-Webster’s
Collegiate Dictionary (11th ed). Moreover, there was literature submitted concerning the
general symptomology and progression of WG, which correlated to Walters’ medical history and
her exposure to the phosphoric acid, and which correlation was relied upon by Dr. Gershwin in
developing his causation opinion. And there is no dispute with respect to the caustic nature of
phosphoric acid, the general dangers presented by it, and the type and extent of the exposure (in
mouth and overnight), all of which also figured into Dr. Gershwin’s causation opinion.

       The Elher Court additionally ruled:

              The circuit court also did not abuse its discretion by relying on the lack of
       evidence regarding the degree to which Priebe's opinion was generally
       accepted. The Court of Appeals majority misinterpreted this factor. The majority

                                               -13-
       concluded that there was no widespread acceptance of any standard-of-care
       statement. But this factor requires the court to consider “[t]he degree to which the
       opinion and its basis are generally accepted within the relevant expert
       community.” Priebe admitted that he knew of no one that shared his opinion.
       While the articles submitted by defendants may have suggested that “purists” in
       the field agreed with Priebe, there was still no indication regarding the degree of
       acceptance of his opinion. The majority conceded that there was no evidence
       regarding whether Priebe's view had general acceptance within the relevant expert
       community. This was a relevant factor for the circuit court to consider. [Elher,
499 Mich. at 25-26.]

        With respect to the subject matter in this passage, we acknowledge that the record does
not show that Dr. Gershwin’s causation opinion regarding phosphoric acid and WG has been
generally accepted by the pertinent expert community, but this is due to a lack of exploration on
the topic as opposed to actual rejection of Dr. Gershwin’s view. Furthermore, Dr. Gershwin’s
comments regarding the general symptomology and progression of WG, which, again, played a
significant role in developing his causation opinion, are well-accepted in the pertinent expert
community, as reflected in the studies and literature submitted by plaintiffs.

       Our Supreme Court in Elher next observed:

               We do, however, agree with the Court of Appeals majority that all the
       factors in MCL 600.2955 may not be relevant in every case. Indeed, we agree
       with the majority that the scientific testing and replication factor does not fit the
       type of opinion at issue in this case. Therefore, the circuit court abused its
       discretion by relying on this factor. But this does not render the circuit court's
       ultimate decision an abuse of discretion. Plaintiff merely pointed to Priebe's
       background and experience in regard to the remaining factors, which is generally
       not sufficient to argue that an expert's opinion is reliable. Priebe admitted that his
       opinion was based on his own beliefs, there was no medical literature supporting
       his opinion, and plaintiff failed to provide any other support for Priebe's opinion.
       [Elher, 499 Mich. at 26.]
        Here, Dr. Gershwin’s causation opinion was not based simply on his own beliefs; rather,
it was tied to studies and literature examining the causes of WG, with Dr. Gershwin employing
scientific analogies to explain that phosphoric acid would cause a physiological response similar
to a response caused by other items discussed in the studies and literature, such as silica and
pesticides. Furthermore, as we explained in our prior opinion, Dr. Gershwin’s causation theory
was based on numerous additional factors, which included:
               (1) the caustic nature of phosphoric acid; . . .; (3) the intensity and
       duration of the phosphoric acid exposure (overnight while Walters slept); (4) the
       area of exposure (inside the mouth where moisture exists); (5) the textbook timing
       of the presentation of an immune response in relationship to the date of exposure
       and the overall chronology of events; (6) the incredible extent of the immune
       response (a very high-titer ANCA); (7) the manifestation and duration of a classic
       WG symptom, sinusitis; [and] (8) Walters’ predisposition to WG[.] [Walters v

                                               -14-
       Falik, unpublished opinion per curiam of the Court of Appeals, issued January 29,
       2015 (Docket No. 319016); unpub op at 8-9.]
       In Elher, 499 Mich. at 27, the Michigan Supreme Court concluded the analysis in its
opinion as follows:
               The circuit court also did not abuse its discretion by concluding that
       Priebe's testimony was deficient because it did not conform to MRE 702. We find
       this Court's decision in Edry v Adelman[, 486 Mich. 634; 786 NW2d 567
       (2010),] to be instructive. In Edry, this Court concluded that an expert failed to
       meet the requirements of MRE 702 because his opinion “was not based on
       reliable principles or methods;” his opinion was contradicted by the opinion of the
       defendant's expert and published literature on the subject that was admitted into
       evidence, which even he acknowledged as authoritative; and there was no
       literature supporting the testimony of plaintiff's expert admitted into evidence. As
       in Edry, Priebe's opinion “was not based on reliable principles or methods,” his
       opinion was contradicted by the opinion of defendant's expert and published
       literature on the subject that was admitted into evidence, and there was no
       literature supporting the testimony of plaintiff's expert admitted into
       evidence. Plaintiff failed to provide any support for Priebe's opinion that would
       demonstrate that it had some basis in fact and that it was the result of reliable
       principles or methods. While peer-reviewed, published literature is not always
       necessary or sufficient to meet the requirements of MRE 702, the lack of
       supporting literature, combined with the lack of any other form of support,
       rendered Priebe's opinion unreliable and inadmissible under MRE 702. [Citations
       omitted.]
        Again, Dr. Gershwin’s opinion has not been expressly contradicted, there are studies and
literature regarding WG generally and the causes of WG that lend support for his causation
opinion, and Dr. Gershwin’s opinion was supported by myriad variables or factors, as opposed to
the circumstances in Elher, where the expert’s opinion concerning the standard of care was
apparently premised solely on his own personal beliefs.

                                      III. CONCLUSION

        Having carefully scrutinized, applied, and distinguished Elher, we continue to stand by
our original holding to reverse and remand for further proceedings. Ultimately, MRE 702 and
MCL 600.2955(1) support the admission of Dr. Gershwin’s expert testimony, and the trial court
abused its discretion in ruling otherwise. Any shortcomings or deficiencies with respect to Dr.
Gershwin’s causation opinion go to the weight of his opinion that must be resolved by the trier of
fact, not its admissibility.

        Reversed and remanded for further proceedings consistent with this opinion. We do not
retain jurisdiction. Having fully prevailed on appeal, plaintiffs are awarded taxable costs under
MCR 7.219.

                                                            /s/ William B. Murphy
                                                            /s/ Deborah A. Servitto
                                              -15-