Filed 7/9/19
                 CERTIFIED FOR PUBLICATION

 IN THE COURT OF APPEAL OF THE STATE OF CALIFORNIA

                  SECOND APPELLATE DISTRICT

                          DIVISION THREE



JOHNSON & JOHNSON                       B286283
TALCUM POWDER CASES.
                                        JCCP No. 4872


                                        (Los Angeles Super. Ct.
ELISHA ECHEVERRIA,                      No. BC628228)
as Trustee, etc.,

      Plaintiff and Appellant,

      v.

JOHNSON & JOHNSON et al.,

      Defendants and Appellants.



      APPEALS from a judgment of the Superior Court of
Los Angeles County, Maren E. Nelson, Judge. Affirmed in part,
reversed in part, and remanded.
      Robinson Calcagnie, Mark P. Robinson, Kevin F. Calcagnie;
Ferguson Case Orr Paterson, Wendy C. Lascher; Esner, Chang &
Boyer, Stuart B. Esner and Holly N. Boyer for Plaintiff and
Appellant.
      Proskauer Rose, Bart H. Williams, Manuel F. Cachán;
Munger, Tolles & Olson, Mark R. Yohalem, Michael. R. Doyen;
Tucker Ellis, Michael C. Zellers; Sidley Austin and David R.
Carpenter for Defendants and Appellants.
      Cole Pedroza, Curtis A. Cole, Cassidy C. Davenport and
Scott M. Klausner for California Medical Association, California
Dental Association, and California Hospital Association as Amici
Curiae on behalf of Defendants and Appellants.

                     _________________________


                           INTRODUCTION
       This case is one of several coordinated suits in which the
plaintiffs allege talcum powder products manufactured by Johnson
& Johnson and Johnson & Johnson Consumer Inc. (JJCI;
collectively, defendants) caused them to develop ovarian cancer. In
July and August 2017, bellwether plaintiff Eva Echeverria’s case
was tried to a jury on a single claim of negligent failure to warn.
The jury returned a verdict in Echeverria’s favor against both
defendants, awarding compensatory damages of $68 million against
Johnson & Johnson and $2 million against JJCI. The jury awarded
punitive damages of $340 million against Johnson & Johnson and
$7 million against JJCI.1 Defendants filed motions for judgment
notwithstanding the verdict (JNOV) as to liability and punitive
damages, as well as a joint motion for a new trial. The trial court
granted the motions. Both sides have appealed.



1     Echeverria died in September 2017. Her daughter, Elisha
Echeverria, acting as trustee for the 2017 Eva Elaine Echeverria
Living Trust, was substituted as plaintiff in October 2017.


                                  2
        We affirm the JNOV in favor of Johnson & Johnson, but
partially reverse as to JJCI. To establish her negligence claim,
Echeverria was required to prove each defendant had a legal duty
to warn consumers about hazards inherent in their talc-based
products; they breached that duty; and the breach caused
Echeverria’s injury. The causation element required evidence that
talc-based products not only cause ovarian cancer in general
(general causation), but also that defendants’ products caused
Echeverria’s ovarian cancer in particular (specific causation). We
conclude there was no substantial evidence to support a finding of
liability as to Johnson & Johnson, a parent company that stopped
manufacturing Johnson’s Baby Powder in 1967, several years before
there were any investigations or studies about a link between
genital talc use and ovarian cancer. The evidence also failed to
support a finding of malice as required for a punitive damages
award, and we affirm the JNOV in favor of JJCI on that ground.
We conclude there was substantial evidence to support the jury’s
other findings as to JJCI. However, we must apply a different
standard of review when evaluating the trial court order granting
JJCI’s motion for a new trial. We determine the causation evidence
was in significant conflict and would have supported a defense
verdict. We therefore reverse the JNOV in favor of JJCI as to
liability, but affirm the trial court order granting JCCI’s motion for
a new trial.
         FACTUAL AND PROCEDURAL BACKGROUND
General Background
       Plaintiff Eva Echeverria began using Johnson’s Baby Powder
as a feminine hygiene product in 1965, when she was 11 years old.
She continued using the product two to three times each day,
applying it to her genital area, underwear, and sanitary napkins,
until 2016. She also briefly used the product “Shower to Shower.”



                                  3
In 2007, Echeverria was diagnosed with invasive, serous, high-
grade ovarian cancer.
      Johnson & Johnson manufactured Johnson’s Baby Powder
from 1893 until 1967. In 1967, JJCI began manufacturing the
product. JJCI is a wholly owned subsidiary of Johnson & Johnson.

Investigations of a Link Between Talc and Ovarian Cancer
in the Scientific, Medical, and Regulatory Communities
      According to Echeverria’s evidence at trial, the first
epidemiological study to investigate a link between talc and ovarian
cancer was published in 1982. In the decades that followed,
researchers published over 30 additional epidemiological studies
exploring whether there is an association between talc use and
ovarian cancer. The parties’ experts offered competing trial
testimony about the validity, significance, and proper interpretation
of these studies.2
       Other scientific studies have hypothesized that talc causes
ovarian cancer by creating inflammation in the ovaries. Studies
have concluded talc can migrate from the vagina into the peritoneal
cavity, where the ovaries are located. Experts for both sides
testified talc causes inflammation. Studies have found chronic
inflammation plays a role in the development of some types of
cancer. Studies referenced at trial have also indicated increased
inflammation may be linked to ovarian cancer. However, no



2      The parties’ appellate briefing includes citations to documents
that were identified at trial, but not admitted, such as complete
copies of scientific publications. “It is axiomatic that in reviewing
the liability aspect of a judgment based on a jury verdict, we may
not review exhibits identified, but not admitted at trial.” (Frank v.
County of Los Angeles (2007) 149 Cal.App.4th 805, 815.)


                                  4
published studies, regulatory agencies, or scientific organizations
have concluded talc-based inflammation causes ovarian cancer.
       The World Health Organization International Agency for
Research on Cancer (IARC) evaluates the carcinogenicity of
different agents. In 2006, the IARC evaluated talc. The agency
characterized perineal use of talc as possibly carcinogenic to
humans, giving it a “2B” rating. This rating reflected a
determination that there was “limited evidence” of carcinogenicity
in humans and in experimental animals. The limited evidence
determination meant: “A possible association has been observed
between exposure to talc and ovarian cancer for which a causal
interpretation is considered by the working group to be credible, but
chance, bias, and confounding could not be ruled out with
reasonable confidence.”
       Some medical and scientific organizations have publicly
identified genital talc use to be a risk factor for ovarian cancer,
while others have not. In 2014 and 2015, the National Cancer
Institute identified perineal talc use as a risk factor for ovarian
cancer; in 2017, it indicated the weight of the evidence does not
support an association between perineal talc exposure and an
increased risk of ovarian cancer.

Defendants’ Response to Ongoing Questions Regarding a
Link Between Talc and Ovarian Cancer
      The evidence at trial included a series of documents from
defendants’ files regarding talc and Johnson’s Baby Powder.
Several of the documents lacked identified authors or other
information to distinguish whether they were generated by Johnson
& Johnson or JJCI. Other documents reflected communications
between or among employees of both companies.




                                 5
       In 1964, W.H. Ashton, a Johnson & Johnson scientist, penned
a memo to the file regarding plans for a test of a baby powder
product composed of cornstarch, rather than talc. The goal was to
“determine a preference rating” of Johnson’s Baby Powder
compared to another product. The memo suggested “Dry Flo,” “a
low substituted A1 salt of mildly treated cornstarch,” could be used
as a potential additive. Although other potential additives were
identified, Ashton wrote Dry Flo “has a very appealing tone because
it would open the door to a merchandising advantage which could
refer to an all starch product . . . .” The memo reported: “Since the
meeting, Ashton established the largest commercial uses of Dry Flo
are in Vitamin A manufacture . . . and as a condom lubricant where
it replaced talc because it was found to be absorbed safely in the
vagina whereas, of course, talc was not.”
       A 1975 letter on “Johnson & Johnson” letterhead bore the
subject line “Talc in the Ovaries.” A handwritten note on the
document suggested a Johnson & Johnson scientist’s contact with a
cancer research institute may have provided “the opening to put us
on notice re: the talc/ovary problem.”
       Documents from 1986 and 1992 acknowledged genital talc use
had been “implicated” or “linked” to ovarian cancer. The 1986
document expressed a continuing belief that talcum powder
products were safe. It referenced a Cosmetics, Toiletries, and
Fragrance Association (CTFA) sponsored animal study concluding
talc does not migrate, and also cited the company’s “extensive
experience in use.” Still, the documents recognized that cancer
concerns, risks from inhalation, and a move among health
professionals to discourage use of talc-based powders on babies, all
posed a potential obstacle to sales.
       Documents from 1993 to 1995 reflected defendants’
awareness of epidemiological studies about talc use and ovarian



                                 6
cancer, their creation of a “Worldwide Talc Steering Committee,”
their monitoring of scientific studies and regulatory action on talc,
and their strategies to respond to adverse press or media inquiries
about talc safety issues. For example, a 1994 document prepared by
a JJCI employee proposed answers to questions about a causal link
between talc and cancer, and about two specific epidemiological
studies. The proposed answers stated one study did not show a
causal relationship between talc and ovarian cancer, while the
other study found a higher incidence of ovarian cancer in women
who routinely used talc, yet ultimately concluded talc was unlikely
to be the cause of the majority of epithelial ovarian cancers. In
response to the question of whether cosmetic talc use could lead to
ovarian cancer, the document offered the answer: “Studies in
animals have shown that talc does not migrate from the vagina to
the ovaries. In conventional animal dosing studies, there is no
evidence of ovarian cancer. Based on the available scientific data,
no cause and effect relationship has been established showing that
the use of talc can cause ovarian cancer.”
       A 1995 memo on “Johnson & Johnson Consumer Products
Worldwide” letterhead, authored by “John Hopkins of Johnson &
Johnson,” addressed methods for responding to “adverse press and
media issues around talc.” The memo laid out three potential
strategies, ranging from “do nothing,” to a more “pro-active”
strategy. Hopkins reported they had been taking the first
approach: “We do not cause waves and we give no further publicity
to adverse comments.” Hopkins recommended a middle approach
that would entail “responding to articles in the press, possibly
including medical journals where we believe we can influence
future behaviors and comment.” A note from a vice president of
research and development suggested “it might be worthwhile to
have some effort” in the “proactive” strategy as well.



                                 7
       In 1997, an outside consultant wrote to a JJCI employee,
offering criticisms of CTFA responses to claims of a link between
talc and ovarian cancer. The consultant noted “several
investigators have independently reported talc particles in ovarian
tissue” and it was inaccurate to state that studies had failed to
demonstrate “any real association” between hygienic talc and
ovarian cancer. The letter pointed out that at least nine studies
published in the open literature had shown a statistically
significant association between the two. The consultant cautioned
that denying the association “risks that the talc industry will be
perceived by the public like it perceives the cigarette industry:
denying the obvious in the face of all evidence to the contrary. This
would be a particularly tragic misperception in view of the fact that
the industry does have powerful, valid arguments to support its
position.” He suggested the better arguments were that the study
results were “ambiguous, inconsistent, contradictory and therefore
inconclusive . . . .” He concluded the letter: “I realize that CTFA is
not J&J. However, I believe that a defeat or embarrassment of
CTFA also negatively affects J&J to some extent.”
       In 2002, a director of product safety at Luzenac, defendants’
talc supplier in the United States, sent a document to Ashton
reporting: “We’ve been successful thus far in fending off the
[National Toxicology Program (NTP)] classification of talc as being
a potential human carcinogen. But we must also keep an eye out
for IARC. If they decide to re-review the status of talc because of all
the ovarian epidemiology studies that have been published since
1986, IARC can surprise us all and decide to list ‘talc’ as a potential
human carcinogen. . . . Their threshold for required medical
evidence is predictably quite minimal. You might want to counsel
your management on this potential (and not to be too complacent
about the status of talc).”



                                  8
       In 2004, the same Luzenac employee forwarded Ashton a
study published earlier that year. He indicated the study “offers
some compelling evidence in support of the ‘migration’ hypothesis.
Combine this ‘evidence’ with the theory that talc deposition on the
ovarian epithelium initiates epithelium inflammation—which leads
to epithelium carcinogenesis—and you have a potential formula for
NTP classifying talc as a causative agent in ovarian cancer.” In
2006, Luzenac began including the IARC 2B classification in its talc
material data safety sheets (MSDS).
       Internal documents and e-mails from 2005 and 2006 reflected
discussions among several individuals, including JJCI employees in
the United States and Johnson & Johnson “regulatory” and
“research” employees in Europe, about NTP and IARC evaluations
of talc as a potential carcinogen. The e-mails referenced a project to
“defend talc” and efforts to prevent a classification of talc as a
carcinogen. They revealed the correspondents’ desire for certain
“helpful” scientists to participate in the evaluations. The e-mails
also discussed efforts to promote or develop studies or documents
“that scientifically support the lack of a relationship of talc and
ovarian cancer.”
       In 2016, the Food and Drug Administration (FDA) issued a
request to JJCI for information on talc. The JJCI response noted
that in 2014, the FDA reviewed the safety of talc and denied citizen
petitions filed in 1994 and 2008. The “ ‘FDA did not find that the
data submitted presented conclusive evidence of a causal
association between talc use in the perineal area and ovarian
cancer.’ ” According to the response, the FDA also reviewed “the
toxicity literature from 1980 to 2008 and did not find enough
additional support at that time for the types of warning labels
proposed” in the citizen petitions.




                                  9
      The JJCI response summarized the company’s position: “At
Johnson & Johnson Consumer Inc., our confidence in using talc is
based on more than 100 years of safe use and more than 30 years of
research by independent researchers, scientific review boards and
global regulatory authorities. Various agencies and governmental
bodies have examined whether talc is a carcinogen, and none have
concluded that it is. The scientific literature, post-market
experience, and expert opinion do not support the association of talc
and ovarian cancer.”

The Expert Testimony at Trial
       Echeverria offered the testimony of four experts:
pharmacologist and toxicologist Dr. Laura Plunkett; epidemiologist
Dr. Jack Siemiatycki; pathologist Dr. John Godleski; and
Echeverria’s treating gynecologic oncologist, Dr. Annie Yessaian.
       There was extensive pretrial litigation on the admissibility of
plaintiff’s proposed expert testimony, including a hearing pursuant
to Sargon Enterprises, Inc. v. University of Southern California
(2012) 55 Cal.4th 747. The trial court ruled only Dr. Yessaian
would be allowed to testify as to “specific causation,” i.e., offering an
opinion that talc caused Echeverria’s ovarian cancer. The other
experts whose testimony was not completely excluded were allowed
to testify only about general causation, i.e., offering an opinion that
talc in general may cause ovarian cancer. Dr. Godleski was also
allowed to provide opinions based on his personal examination of
Echeverria’s tissues.
       Defendants offered the testimony of Dr. Alan Andersen, a
biophysicist and former high-level employee at the FDA and the
Cosmetic Ingredient Review (CIR); Dr. Douglas Weed, an
epidemiologist and medical doctor; Dr. Juan Felix, a gynecologic
pathologist; and Dr. Cheryl Saenz, a gynecologic oncologist.



                                   10
General Causation: Plaintiff’s Expert Testimony
       Dr. Laura Plunkett
       Dr. Plunkett is a former assistant professor of pharmacology
and toxicology at the University of Arkansas. She is currently a
consultant in the areas of toxicology, pharmacology, and human
health risk assessment. Dr. Plunkett opined talc is toxic, it can
migrate from the vagina to the ovaries, it can cause inflammation in
human tissues, and chronic inflammation can cause ovarian cancer.
Plunkett’s opinion that talc is toxic was based on animal studies
and human and animal cell studies. Plunkett testified she cited
hundreds of studies in her expert report, a few of which she
highlighted in her testimony.
       For example, Plunkett described a 1984 study in which the
injection of a talc solution near rat ovaries caused precancerous
lesions in the rat’s tissues. Plunkett also relied on a 1993 NTP
study showing rats exposed to airborne talc for two years—a
lifetime—developed precancerous lesions and, in some cases,
tumors. She noted “dozens” of earlier studies established “talc can
cause inflammation at the site.”
       Plunkett also discussed two human cell studies. According to
Plunkett, a 2007 study found talc produced neoplastic
transformation in human ovarian cells.3 A 2009 study showed talc
had effects in human cells, “as far as the type of genes it turns on
and off,” that are similar to the effects observed with compounds
known to cause cancer. Plunkett testified these studies supported
her opinion that talc initiates an inflammatory response that leads

3      Plunkett described “neoplastic” or “neoplasm”: “That means
tumor. So transformation is a process where it takes a cell and
where the cell is changing from a preneoplastic cell—or a normal
cell to a preneoplastic cell, taking on the characteristics of a cell
that could become a cancer cell and could form a tumor.”


                                  11
to cancer. Her opinion that talc can migrate from the vagina to the
upper genital tract and to the ovaries was based on five studies
dating from the early 1960’s to the early 2000’s, each of which she
described for the jury.
       Defendants tested and challenged Plunkett’s interpretation of
these scientific studies on cross-examination. She acknowledged
weaknesses and limitations in the studies, but still felt they
provided useful information. She also admitted there were several
studies that came to different conclusions about the role of chronic
inflammation in the development of ovarian cancer and the effect of
talc on the female genital system.
       Plunkett additionally based her opinion on her review of the
epidemiological literature, including six meta-analyses showing a
statistically significant increased risk between exposure to talc in
the genital area and ovarian cancer. Plunkett explained that no
single study could conclude talc causes cancer. Instead, she
described each study as a piece of the causation puzzle.
       Having reviewed the scientific data, Plunkett opined that
regular genital use of talc sets up a chronic inflammatory condition
in the cells that causes them to change to precancerous cells. The
precancerous cells eventually lead to tumor growth, metastasizing
tumors, and “full-blown advanced stage ovarian cancer.” Plunkett
also evaluated the Bradford Hill criteria, a framework for
considering whether a substance causes a disease.4 She opined she


4     The criteria are temporal relationship, strength of the
association, dose-response relationship, replication of the finding,
biological plausibility, consideration of alternative explanations,
cessation of exposure, specificity of the association, and consistency
with other knowledge. (Green et al., Reference Guide on
Epidemiology in Reference Manual on Scientific Evidence (3d ed.
2011) 549, 600 (hereafter, Reference Guide).) Epidemiologists use


                                  12
had enough information relevant to the criteria to state, to a
reasonable degree of scientific and professional certainty, that
genital exposure to talc causes ovarian cancer.

       Dr. Jack Siemiatycki
       Dr. Siemiatycki is an epidemiologist and professor at the
University of Montreal and McGill University. He has over 200
peer-reviewed publications and numerous honors and awards for
his work in epidemiology and biostatistics.
       Siemiatycki explained several epidemiological concepts to the
jury. He informed the jury that “relative risk” is the risk of
developing a disease among people exposed to a particular chemical
agent or toxin, divided by the risk of developing the disease among
those not exposed to the same agent. He offered an example: “So if
the risk of cancer in the general population . . . is 4 percent in the
general population but among a group of people with a certain
environmental exposure it is 6 percent, the relative risk of cancer
due to that environmental exposure would be 6 percent divided by 4
percent equals 1.5.”
       Siemiatycki then elaborated: “[W]hen the risk is exactly the
same among the exposed and the unexposed, then the relative risk
will be 1. . . . The risk among the exposed is the same. . . . And that
means the agent, whatever the exposure is, has no effect on the risk
of developing the disease. . . . . If the relative risk is greater than 1,
it means exposure to that agent increases the risk of developing the
disease. If the relative risk is less than 1, so the risk among the


these factors when considering whether a statistical association
reflects a causal relationship. They “reflect criteria proposed by the
U.S. Surgeon General in 1964 in assessing the relationship between
smoking and lung cancer and expanded upon by Sir Austin
Bradford Hill in 1965 . . . .” (Ibid., fns. omitted.)


                                   13
exposed is less than the risk among the unexposed, it means that
exposure to the agent prevents the disease.”
      Siemiatycki explained the related concepts of “confidence
intervals” and “statistical significance.” Statistical significance
concerns the question, “how solid is our belief that the relative risk
that we observe in a study is really precise and accurate?”
Statistical significance depends on a number of factors, including
the size of the study. Siemiatycki provided the jury with an
example in which a study estimated a relative risk of 1.2, with a
95 percent probability that the true estimate is between 1.1 and 1.3.
“That’s a pretty tight interval, and we call that a confidence
interval. We call it a 95 percent confidence interval when we
calculate it in such a way that it covers 95 percent of the underlying
relative risks that are compatible with this estimate from this
study.” If the results of a study have a confidence interval that
includes relative risk numbers under 1—reflecting decreased risk—
they are not statistically significant. In those cases, the results
could be due to chance. However, Siemiatycki disagreed that a
study with a nonstatistically significant result must be disregarded.
Such studies still contain information that may be useful when
combined with evidence from other studies.
      Siemiatycki chaired the 2006 IARC working group on talc.
The group concluded the association between perineal talc use and
ovarian cancer could have other possible explanations. The
available evidence was not strong enough to exclude chance, bias,
and confounding—the presence of another factor that may be
causing the disease—as explanations for the association that had
been observed between talc and ovarian cancer.
      Siemiatycki’s current opinion is that it is more likely than not
genital talc use can cause ovarian cancer. His change of opinion
was based in part on a 2013 study which, he testified, showed a



                                 14
dose-response pattern—increased risk with increased exposure—
that was missing in earlier studies. Siemiatycki opined the 2013
study, as well as studies published in 2015 and 2016, led him to
conclude the statistical evidence associating genital talc use and
ovarian cancer is now much stronger than it was 10 years earlier.
       Siemiatycki also conducted a meta-analysis using existing
talc literature to develop an opinion for the litigation. His analysis
of 28 or 29 studies led him to believe there is a “very, very strong
statistical association between use of talc and ovarian cancer.” The
analysis resulted in a relative risk of 1.28, with a confidence
interval of 1.18 to 1.38, rendering the results highly statistically
significant. In other words, Siemiatycki found a 28 percent greater
risk of ovarian cancer among women who used talc compared to
women who had not used talc.
       Siemiatycki evaluated the Hill factors and concluded they
support an opinion that there is a causal relationship between
genital talc use and ovarian cancer. He testified that for as many
as half of the known carcinogens for which there is epidemiologic
data, the data show relative risk estimates less than 2.0. Like
Plunkett, Siemiatycki testified epidemiologists typically do not
write articles stating “this causes that.” He explained “that sort of
communication tends to come from authoritative agencies who have
the capacity to integrate the viewpoints of multiple experts and,
preferably, multiple experts from multiple disciplines.”

General Causation: Defendants’ Expert Testimony
      Dr. Alan Andersen
      Dr. Andersen is a former director of the CIR. He described
the CIR as an independent review group, but also admitted an
industry trade group is the CIR’s sole funder. Andersen testified
the group’s mission is to review and assess the safety of ingredients



                                 15
in an “open, unbiased, and expert manner,” and to publish the
results in peer-reviewed scientific literature. In 2011, a CIR panel
began a review of the safety of talc and concluded, in 2013, that talc
is safe.
       The CIR panel determined available data “did not reliably
demonstrate” talc could migrate from the perineal area into the
ovaries. The panel concluded the epidemiological data did not
consistently reveal statistically significant positive associations
between talc use and ovarian cancer; there were uniformly small
risk ratio estimates; and other plausible alternative explanations of
the association had not been ruled out. The panel did not see a
consistent dose-response pattern reflected in the available
literature. The panel also concluded there was no plausible
biological mechanism to explain how genital talc use could cause
ovarian cancer. It found a “lack of credible defensible evidence of
carcinogenicity from the results of epidemiological studies of
occupational exposures and animal bioassays.” The panel
determined the available cellular studies were “unremarkable,”
meaning there were no adverse cellular effects relating to talc.

       Dr. Douglas Weed
       Dr. Weed, medical doctor and epidemiologist, is a former chief
of the office of preventive oncology at the National Cancer Institute,
and currently a consultant. Based on his review of the scientific
literature and the Hill criteria, Weed opined it has not been
established that talc use causes ovarian cancer. In his evaluation of
the epidemiological literature, he concluded the published cohort
studies show no association between genital talc use and ovarian
cancer. The case-control studies establish only a “weak” association




                                  16
reflected in a relative risk estimate of 1.3.5 Weed opined the
studies do not establish a dose-response pattern.
       Weed further testified that some studies call into question the
proposed biological mechanism of migrating talc particles causing
inflammation. For example, although one would expect that women
who used genital talc but had tubal ligation or hysterectomies
would experience a reduced risk of ovarian cancer, Weed testified
studies reveal “a mix of results.” Similarly, studies show no
uniformly reduced risk of ovarian cancer in women who use
medications that reduce inflammation. Weed also indicated studies
have not established genital talc use increases the risk of other
kinds of cancer in the female genital tract.

Pathology: Plaintiff’s Expert Testimony
      Dr. John Godleski
      Dr. Godleski is a professor of pathology, recently retired from
Harvard Medical School and the Harvard School of Public Health,
where he continues to consult on research programs. He has close
to 150 peer-reviewed publications, including a case report regarding
the presence of talc particles in the lymph nodes of a woman
diagnosed with ovarian cancer who had used genital talc for over 30
years.


5     Case-control and cohort studies are two types of
epidemiological observational studies. In case control studies,
researchers take two groups of people, one with the disease and one
without, and both groups are asked about exposures they have had.
In cohort studies, researchers study two groups, one whose
participants have been exposed to the studied agent and an
unexposed group. Researchers then observe and measure the
incidence of the disease in both groups. (Reference Guide, supra, at
pp. 556-559.)


                                 17
      Godleski examined slides of Echeverria’s gynecologic tissue,
using electron microscopy and x-ray analysis to identify talc
particles. He found 11 talc particles and fibers in the examined
tissues—eight particles of talc in ovarian tissue, and three talc
particles in pelvic peritoneum and omentum tissue. Godleski
opined that finding 11 particles in a small sample indicated there
was a “substantial burden of talc” in Echeverria’s tissue. He was
“convinced” the particles were present as the result of perineal talc
use.
      Godleski admitted his expert reports submitted before trial
did not mention that he observed inflammation in Echeverria’s
tissues. However, at trial Godleski testified he observed a talc
particle, and other particles with characteristics of talc, near or
“involved with” macrophages, which are cells that are signals of an
inflammatory reaction. Godleski believed this suggested the
occurrence of a chronic inflammatory process. The talc particle
involved with a macrophage was from a slide of Echeverria’s
ovarian tissue. The other particles and cells were from a slide of
Echeverria’s pelvic peritoneum tissue. Godleski testified “to a
reasonable degree of medical certainty that the presence of talc
found in a woman’s ovarian tissue can be contributory evidence for
a causal link between the presence of talc and the development of a
woman’s ovarian cancer.”

Pathology: Defendants’ Expert Testimony
      Dr. Juan Felix
      Dr. Felix is the former director of gynecologic pathology at the
University of Southern California (USC) Keck Medical Center. He
is currently a professor and the director of anatomic pathology at
the Medical College of Wisconsin. Felix testified that 75 to
80 percent of cases of ovarian cancer have an unknown cause. He



                                 18
also testified exposure to talc “guarantees” there will be chronic
inflammation in the body, and talc in a woman’s peritoneal cavity
will produce inflammation and chronic toxicity. However, he opined
the inflammation would take the form of adhesions and
granulomas, neither of which causes ovarian cancer.
       Felix reviewed Echeverria’s tissue slides and found no
inflammation or evidence of the inflammatory reaction Godleski
described. Felix testified that macrophages do not cause or
contribute to the growth of ovarian cancer. He has seen hundreds
of cases in which inflammation caused cancer and, in those cases,
the inflammation was everywhere, not hidden or in an isolated
area. He testified the presence of a tumor would not obscure the
presence of talc-induced inflammation.

Specific Causation: Plaintiff’s Expert
      Dr. Annie Yessaian
      Dr. Yessaian is a double board-certified gynecologic oncologist
at USC. She handles over 150 surgeries each year and also teaches
and supervises medical students. Yessaian began treating
Echeverria in 2007.
      Yessaian conducted a “differential diagnosis” to form an
opinion for the litigation about the cause of Echeverria’s cancer.6

6     “Differential diagnosis, or differential etiology, is a standard
scientific technique of identifying the cause of a medical problem by
eliminating the likely causes until the most probable one is
isolated. . . . [Citation.] . . . [¶] The first step in the diagnostic
process is to compile a comprehensive list of hypotheses that might
explain the set of salient clinical findings under consideration.
[Citation.] The issue at this point in the process is which of the
competing causes are generally capable of causing the patient’s
symptoms or mortality. . . . [¶] After the expert rules in all of the
potential hypotheses that might explain a patient’s symptoms, he or


                                  19
Yessaian considered several “protective factors,” which “are very
well known and established to reduce a woman’s risk of developing
ovarian cancer.” These were parity—how many children a woman
has delivered to term, use of oral contraception, bilateral tubal
ligation, and breastfeeding. Echeverria had one child, so Yessaian
considered this “a factor.” Echeverria used oral contraception very
briefly, breastfed her daughter very briefly, and did not have tubal
ligation.
       Yessaian considered genital talcum powder. She took note
that Echeverria used talcum powder two or three times a day for
over 40 years, resulting in over 30,000 genital applications in her
lifetime. Yessaian reviewed migration studies establishing there is
a biologically plausible way for talc to go from the external
environment to the peritoneal cavity. She looked at “other
evidence” relating to a mechanism of “talc sitting in the peritoneal
cavity” and “participating in that whole cascade of process from
inflammation to malignant transformation to leading to cancer.”
Yessaian did not have specific evidence of this mechanism taking
place in Echeverria. However, she considered Godleski’s findings
that talc was present in Echeverria’s ovary, omentum, and
peritoneal cavity, all places where cancerous tumors were found.
       Yessaian also considered numerous epidemiological studies.
At trial, she discussed studies that found 20, 40 and 60 percent
increases in the risk of serous ovarian cancer in women exposed to
talc. She also indicated she relied on four studies with odds ratios



she must then engage in a process of elimination, eliminating
hypotheses on the basis of a continuing examination of the evidence
so as to reach a conclusion as to the most likely cause of the
findings in that particular case.” (Clausen v. M/V New Carissa (9th
Cir. 2003) 339 F.3d 1049, 1057-1058.)


                                 20
or relative risk estimates above 2.0.7 A 1982 study showed an odds
ratio of 3.28, while a 1992 study resulted in an odds ratio of 4.8.8 A
1999 study showed an overall odds ratio of 2.15, with a stratified
result of 1.70 for serous ovarian cancer. A 2009 study showed an
overall odds ratio of 2.08, and a 1.70 estimate for the serous
subtype. Yessaian believed the results of the 2009 study suggested
Echeverria was at an even higher risk than the overall risk
estimate reflected in the study, given the extent of her talc use. All
four studies had statistically significant results. Yessaian further
testified about four studies that provided evidence of dose response.
       Yessaian also “evaluated . . . 13 factors that could have an
implication in ovarian cancer in general.” She considered genetic
mutation as a potential cause and ruled it out. During the course of
treating Echeverria, Yessaian ordered genetic testing on multiple
occasions. The testing revealed no abnormalities in the mismatch


7      Before trial, the court ruled Yessaian’s testimony would be
allowed, provided she could opine based solely on studies showing
risk estimates greater than 2.0. As discussed in greater detail
below, the court relied on cases concluding only epidemiological
studies with relative risk estimates greater than 2.0 (“doubling the
risk”) are useful to the jury as support for a specific causation
opinion. These cases reason “a relative risk of 2.0 implies a 50%
probability that the agent at issue was responsible for a particular
individual’s disease. This means that a relative risk that is greater
than 2.0 permits the conclusion that the agent was more likely than
not responsible for a particular individual’s disease. [Citation.]”
(In re Silicone Gel Breast Impl. Prod. Liab. Lit. (C.D.Cal. 2004) 318
F.Supp.2d 879, 893.)
8     In case-control studies, the association between the exposure
to an agent and the disease is reflected as an odds ratio rather than
as a relative risk. (Reference Guide, supra, at pp. 568-569.)



                                 21
repair genes known to increase the risk of ovarian cancer and no
clinically significant gene mutations.
       Yessaian considered and ruled out fertility medications and
hormone replacement therapy as Echeverria had not used either
one. She considered endometriosis and polycystic ovarian syndrome
and ruled both out; Echeverria did not suffer from either condition.
Yessaian considered tobacco and alcohol use since Echeverria had
used both for a short time. Yessaian ruled out tobacco, indicating
the data on tobacco and ovarian cancer are “inconclusive at best,
especially if you look at for serous.” Yessaian also ruled out alcohol
use, concluding Echeverria’s alcohol consumption was not
significant enough to cause her ovarian cancer.
       Yessaian considered family history. Echeverria’s mother had
pancreatic cancer. Her aunt had colon cancer. No family members
had ovarian or breast cancer. Yessaian noted the aunt with colon
cancer was diagnosed in her 80’s and genetic testing had
established Echeverria’s cancer was not genetically related.
Yessaian thus ruled out family history of cancer.
       Yessaian considered Echeverria’s age. She believed 52 to be
an average age for ovarian cancer incidence and therefore not a
likely cause.
       She considered menarche, the age at which Echeverria had
her first menstrual period, and menopause. Yessaian explained:
“The idea is if a woman gets her periods so, so young and then gets
her menopause so, so late, she has all these long, long years of
ovulation. One of the theories is that with every ovulation the
surface of the ovary has an injury. And when the body tries to
repair that injury—cancer is kind of like a repair gone wrong. . . .
So that’s why the more ovulations you had, like early—you know,
they start their periods at nine and they are menopausal at like 55
and beyond, they’ve had so much more ovulations, more chances of



                                 22
damage to the surface, more damage or repair process that could go
off, so that’s why. And [Echeverria] was so average in her age of
menarche and also her age at menopause. She was menopausal
before I saw her.” Yessaian thus ruled out menarche and
menopause, or the number of ovulatory cycles, as a cause.
       Yessaian considered and ruled out Echeverria’s obesity. She
explained obesity is a standard risk factor for uterine cancer: “[T]he
more estrogen you have through these cells producing more
estrogen in the fatty tissue, the more likely you are to get uterine
cancer and breast cancer. The data on these two are very, very
solid.” Yessaian testified there is no similar “solid evidence”
identifying obesity as a risk factor for ovarian cancer. Yessaian had
reviewed the available literature and found no correlation between
obesity and serous ovarian cancer.
       Yessaian thus concluded “talc was more probable than not the
causing agent in Ms. Echeverria’s developing high-grade serous
ovarian cancer,” and that it is more probable than not that but for
her use of talc, she would not have developed the cancer. Yessaian
testified her opinion was not based on a single study, factor, or
element. Rather it was the “totality of all the evidence and the
factors” she considered.
       On cross-examination, Yessaian admitted she did not have
any evidence there was inflammation in Echeverria’s ovarian
tissue. If Echeverria had been over 60 years old, Yessaian would
have attributed the cancer to aging and would have concluded it
was more than 50 percent likely that advancing age and the
corresponding accumulation of “genetic hits” caused the cancer.
Since Echeverria was younger—52 when diagnosed—Yessaian
found age less likely to be the cause. Yessaian admitted no one
could completely rule out age as a contributing factor but she was
trying to figure out “which factor stands out.”



                                 23
       As to a high number of ovulatory cycles, Yessaian opined it
was not an “independent risk factor for postmenopausal ovarian
cancer.” She testified she could not rule out the number of
ovulatory cycles “as a hundred percent, but it more likely than not
was not a factor.”
       Yessaian agreed that in general terms for ovarian cancer, as
well as other cancers, it might be true that the “biggest cause” is
“unknown etiology.” She also agreed that “unknown etiology” could
be a cause of Echeverria’s ovarian cancer, but opined that was “less
probable than not.” She explained the statement “the leading cause
of cancer is an unknown etiology” applies to everyone and ovarian
cancer in general. She distinguished Echeverria’s case: “Not Ms.
Echeverria’s specific serous and with everything else included in
her history, having ruled out genetics, and we’ve been talking about
this whole talc and migration and use and et cetera. That
statement holds true as a blanket general, not for this particular—
Ms. Echeverria’s case.” She later elaborated that she had “studied
all the details in [Echeverria’s] particular case. And when you’re
putting an etiology of all cancers, that’s for everybody else, the
population of the world in general. We’re talking about how we
evaluated this patient’s case in detail and studied all other factors
involved. She’s not a generic part of the population. I’m talking
about a case that—a patient that has been studied and evaluated in
[detail].”
       Defense counsel asked if Yessaian’s differential diagnosis
started with the assumption that it was possible to find a cause of
the cancer without considering the possibility that an unknown risk
factor caused the cancer, or that it developed spontaneously.
Yessaian answered: “I objectively evaluated all risk factors to the
best of my knowledge and ability . . . . I did not have any
preconceived conclusion for which I wanted to fit my . . . workup



                                 24
. . . . I always assume unknown is part of what I do. I want to
make sure—can I find something known? Because I look for what I
know. I look for known. And if I don’t find something known, then
I say, okay, it’s unknown. I mean there’s no publication that says
let’s look at unknown—the role of unknown. We look at what we
know. And we cannot find something we know, then, okay, sorry,
we tried. It’s unknown.”
         Counsel asked for the basis for Yessaian’s testimony that it is
less than 50 percent likely that the cause of Echeverria’s cancer is
unknown. Yessaian answered: “At the risk of sounding redundant
and repetitive, all the risk factors that I included, ruling in, ruling
out the fact about her talc exposure, the epidemiologic data that
support, the total evidence that I provided in my report and my
knowledge of her . . . . Because I’ve studied Ms. Echeverria’s case
specifics. I looked at all the risk factors that applied to her. I’ve
looked at the protective factors that could apply to her, the talc
exposure, the epidemiology, . . . the migration, all of that put
together. I cannot do the same assessment for every patient out
there in the general population. So not all patients with cancer get
that dissection of possible etiology.”

Specific Causation: Defendants’ Expert
       Dr. Cheryl Saenz
       Dr. Saenz is a gynecologic oncologist and clinical professor at
the University of California, San Diego. Saenz opined perineal use
of talc does not contribute to the development of ovarian cancer.
She based her opinion on her over 20 years of clinical experience
treating thousands of women with ovarian cancer, a review of the
literature on the topic, and the absence of evidence “that talc is a
consistently credible scientific cause of ovarian cancer.” Saenz
testified several factors increased Echeverria’s risk for developing



                                   25
ovarian cancer: her family history of cancer, even though her
family members had different kinds of cancer; her morbid obesity;
the fact that she had her first child late, at 36 years old; and her
early menarche at age 11.
        Saenz disagreed with Yessaian’s opinion that vaginal talc use
was more likely than not the cause of Echeverria’s cancer. She
testified ovarian cancer is multifactorial and there is no way for her
to say exactly what causes a patient to develop the disease. Saenz
does not consider unknown etiology to be a risk factor, instead “it’s
a fact. We don’t know what causes the majority of ovarian cancers
. . . over 50 percent.” Saenz opined it is more likely than not talc
had nothing to do with Echeverria developing ovarian cancer. She
has operated on thousands of women with ovarian cancer and has
never seen inflammation in any of her ovarian cancer patients.
        Saenz critiqued Yessaian’s method of considering
epidemiological studies. She explained the epidemiological
“literature is being published to try and determine whether or not
there are certain associations, to try and determine whether or not
there are certain relationships. It’s not meant to be a mathematical
model that you can then just plug your patient into and do a
calculation of her individual risk.”
        Saenz also testified specifically about a 2016 study both she
and Yessaian had cited in their reports. Saenz testified the study
showed a relative risk estimate of 1.33 for serous invasive ovarian
cancer, for women who, like Echeverria, were postmenopausal at
the time of diagnosis and used talc more than 24 years. Yet, for
women who, also like Echeverria, were postmenopausal at the time
of diagnosis, did not use hormone replacement therapy, and used
talc more than 24 years, the study showed a relative risk of 1,




                                 26
indicating no increased risk.9 Both results had confidence intervals
rendering them not statistically significant. Saenz continued: “So
in my opinion, again, I do not think you should ever use literature
to see what happened with one individual patient. But if you’re
going to pull the numbers that apply to Ms. Echeverria, this paper
says that she is not at an increased risk of developing ovarian
cancer based on her years of talc use.”

Jury Verdict and Posttrial Motions
      The jury returned a verdict finding both defendants liable for
negligent failure to warn. The jury awarded Echeverria a total of
$70 million in compensatory damages; $68 million as to Johnson &
Johnson and $2 million as to JJCI. The jury awarded $347 million
in punitive damages; $340 million against Johnson & Johnson, and
$7 million against JJCI. Defendants filed separate motions for
JNOV and a joint motion for a new trial. The trial court granted
the three motions.
                            DISCUSSION
I.    Judgment Notwithstanding the Verdict
      A.     Standard of Review
      “ ‘ “A motion for judgment notwithstanding the verdict may be
granted only if it appears from the evidence, viewed in the light
most favorable to the party securing the verdict, that there is no
substantial evidence in support. [Citation.] [¶] . . . As in the trial
court, the standard of review [on appeal] is whether any substantial
evidence—contradicted or uncontradicted—supports the jury’s
conclusion.” ’ [Citation.]” (Webb v. Special Electric Co., Inc. (2016)
63 Cal.4th 167, 192.) We, like the trial court, may not reweigh the


9      The testimony did not indicate whether this result was
stratified for serous ovarian cancer alone.


                                 27
evidence or judge the credibility of witnesses. “ ‘ “ ‘If the evidence is
conflicting or if several reasonable inferences may be drawn, the
motion for judgment notwithstanding the verdict should be
denied. . . .’ ” ’ [¶] When an appellate court reviews an order
granting JNOV, it will ‘ “ ‘resolve any conflict in the evidence and
draw all reasonable inferences therefrom in favor of the jury’s
verdict.’ ” ’ [Citation.]” (In re Coordinated Latex Glove Litigation
(2002) 99 Cal.App.4th 594, 606.)
       The testimony of a single witness may be substantial
evidence, including the testimony of an expert. However, “when an
expert bases his or her conclusion on factors that are ‘speculative,
remote or conjectural,’ or on ‘assumptions . . . not supported by the
record,’ the expert’s opinion ‘cannot rise to the dignity of substantial
evidence’ . . . . [Citations.]” (Wise v. DLA Piper LLP (US) (2013)
220 Cal.App.4th 1180, 1191-1192; Jennings v. Palomar Pomerado
Health Systems, Inc. (2003) 114 Cal.App.4th 1108, 1117-1118.)
       B.      No Substantial Evidence Supported
       the Jury’s Verdict as to Johnson & Johnson
       Johnson & Johnson stopped producing Johnson’s Baby
Powder in 1967. The trial court concluded there was no substantial
evidence that Johnson & Johnson knew of any risk of harm from
perineal use of talc prior to 1967, there was no evidence at trial
sufficient to find the company directly liable after that time, and no
substantial evidence to find Johnson & Johnson vicariously liable
for any JJCI tort.
       On appeal, Echeverria argues the trial court misinterpreted
the law and ignored evidence supporting the jury’s findings. We
find no merit in these arguments.
               1.     Failure to warn
       A manufacturer has a duty to warn of facts which make a
product dangerous or likely to be dangerous. “[A] product ‘likely’ to



                                   28
be dangerous will ‘in all probability’ or ‘probably’ be dangerous.”
(Valentine v. Baxter Healthcare Corp. (1999) 68 Cal.App.4th 1467,
1483 (Valentine).) To establish a negligent failure to warn claim,
the plaintiff must prove “ ‘that a manufacturer or distributor did
not warn of a particular risk for reasons which fell below the
acceptable standard of care, i.e., what a reasonably prudent
manufacturer would have known and warned about.’ ” (Carlin v.
Superior Court (1996) 13 Cal.4th 1104, 1112 (Carlin).) “[A]
reasonable manufacturer [is] not charged with knowing more than
what would come to light from the prevailing scientific and medical
knowledge.” (Valentine, at pp. 1483-1484.) “The manufacturer has
no duty to warn of risks that are ‘merely speculative or conjectural,
or so remote and insignificant as to be negligible.’ [Citation.]” (T.H.
v. Novartis Pharmaceuticals Corp. (2017) 4 Cal.5th 145, 164
(Novartis).)
       Under California law, a manufacturer generally has no duty
to warn of risks from another manufacturer’s product, and is
typically liable only for harm caused by its own product. (O’Neil v.
Crane Co. (2012) 53 Cal.4th 335, 349, 365; Taylor v. Elliott
Turbomachinery Co., Inc. (2009) 171 Cal.App.4th 564, 593-596.) It
was undisputed that Johnson & Johnson ceased manufacturing
Johnson’s Baby Powder after 1967. Echeverria was required either
to establish that Johnson & Johnson breached a duty to warn
between 1965 and 1967, or to advance and prove a theory under
which the company could be liable even after it stopped
manufacturing the product.
             2.    There was no substantial evidence
             Johnson & Johnson breached a duty to warn
             prior to 1967
       Echeverria contends Johnson & Johnson knew or should have
known Johnson’s Baby Powder was unsafe by 1967 and it breached



                                  29
its corresponding duty to warn consumers. There was no
substantial evidence to support this theory. According to
Echeverria’s evidence at trial, the first epidemiological study to
investigate a link between perineal use of talc and ovarian cancer
was published in 1982, 15 years after Johnson & Johnson ceased
manufacturing the product. On appeal, Echeverria refers to a 1971
study as evidence of Johnson & Johnson’s knowledge of the
dangerousness of talc. Yet, plaintiff’s experts identified a 1982
study as the “first” epidemiological study to address the issue. The
1971 study was only obliquely mentioned when referenced in other
documents. In any event, the 1971 study does not assist
Echeverria’s argument since it was published four years after JJCI
became responsible for Johnson’s Baby Powder. There was no
evidence that Johnson & Johnson knew or should have known of
the study or its results prior to the 1971 publication date.
       The only pre-1967 evidence Echeverria offered to support her
claim was the 1964 internal memo, in which the scientist Ashton
wrote that Dry Flo had replaced talc as a condom lubricant
“ ‘because it was found to be absorbed safely in the vagina whereas,
of course, talc was not.’ ” There was no evidence providing the
context of this statement, no evidence that anyone had raised
concerns regarding a link between talc and ovarian cancer by 1964,
and no further explanation of the memo.10


10    During the cross-examination of a defense expert, the jury
was shown a 1996 article from the “Jersey Journal,” reporting that
condom makers were no longer using talc due to “women’s health
concerns.” The article stated: “ ‘Concern about talc as an ovarian
carcinogen goes back 50 years in the medical literature.’ ” The trial
court instructed the jury it was not to consider the statements in
the article for their truth. The article was not admitted into
evidence. The statements in the article cannot support Echeverria’s


                                 30
      Even if the jury could reasonably infer from the 1964 memo
that Johnson & Johnson knew talc posed some danger to consumers
because it was not safely absorbed into the vagina, this is a far cry
from knowledge that perineal talc use created a risk of ovarian
cancer. (Carlin, supra, 13 Cal.4th at pp. 1112, 1116 [manufacturer
must warn of particular risk]; see also Mitchell v. City of Warren
(6th Cir. 2015) 803 F.3d 223, 230 [jury may not speculate that a
manufacturer should have known about one risk because a
separately known risk revealed the mere possibility of the first].)
While inferences may support a judgment, “ ‘ “the inference must be
a reasonable conclusion from the evidence and cannot be based
upon suspicion, imagination, speculation, surmise, conjecture or
guesswork. [Citation.]” ’ ” (Joaquin v. City of Los Angeles (2012)
202 Cal.App.4th 1207, 1219.) The jury could not reasonably infer
from the 1964 memo that Johnson & Johnson was aware at that
time of a risk of ovarian cancer from genital talc use.
      Echeverria argues the jury could infer from later documents
that Johnson & Johnson knew or reasonably should have known in
earlier years of the risks of genital talc use. But the next document
admitted from defendants’ files, which referenced “the talc/ovary
problem,” dated from 1975, eight years after Johnson & Johnson
ceased manufacturing baby powder, and over a decade after Ashton
wrote the 1964 memo. No document admitted at trial referred to
the 1964 memo or cast any light on its interpretation. There was no
legitimate basis for the jury to conclude from later documents,
which reflected later developments in scientific knowledge about a
link between talc and ovarian cancer, that Johnson & Johnson had
similar knowledge in 1964. Indeed, Echeverria’s own expert,



claims that the 1964 Ashton memo reflected an awareness that
genital talc use created a risk of ovarian cancer.


                                 31
Dr. Plunkett, testified that the fact that “talc is dangerous and
capable of causing cancer” was likely to have been known since the
early 1990’s; over two decades after Johnson & Johnson stopped
producing Johnson’s Baby Powder.
       Echeverria further argues the trial court erred in requiring
evidence that Johnson & Johnson “knew or should have known
prior to 1967 that talc more probably than not caused ovarian
cancer.” But, in our view, the most salient portion of the trial court
ruling is the conclusion that “[t]here was no showing that as of 1967
there was any suggestion by the scientific or medical community
that talc was associated with ovarian cancer.” We agree with the
trial court that there was no evidence indicating a link between
ovarian cancer and talc was even suspected by 1967. Based on the
evidence at trial about what was known or reasonably knowable by
1967, a risk of ovarian cancer from perineal talc use would have
been entirely speculative and conjectural, and Johnson & Johnson
had no duty to warn of such risks.
             3.    There was no legal basis for the jury to find
             Johnson & Johnson liable for breaching a duty to
             warn after it ceased manufacturing the product
       Echeverria argues that even if Johnson & Johnson did not
breach a duty to warn while it was manufacturing Johnson’s Baby
Powder, a manufacturer has a continuing duty to warn after it
stops making a product, and it remains liable even after a third
party begins manufacturing the product. However, the authorities
Echeverria cites for these propositions do not support her
argument.
       For example, in Novartis, the court held a prescription drug
maker that negligently fails to warn while it is producing a drug
may be liable when the plaintiff is harmed by another
manufacturer’s generic bioequivalent. Liability may continue even



                                 32
after the original drug maker sells its rights in the brand-name
drug to a successor. (Novartis, supra, 4 Cal.5th at p. 156.) Yet, the
Novartis court’s reasoning and analysis are inextricably tied to the
“distinctive legal framework governing labeling for brand-name and
generic pharmaceuticals.” (Ibid.) Federal regulations governing
prescription drug labeling require the makers of generic
bioequivalents, and successor manufacturers, to match the original
brand-name manufacturer’s warning label as a default. (Id. at
pp. 157-158, 182-183.) As a result, the original brand-name
manufacturer’s failure to issue an adequate warning label may have
foreseeable effects on consumers using another manufacturer’s
generic bioequivalent, and on consumers who use the drug after a
successor manufacturer takes over production and sales. (Id. at pp.
174, 182-183, 192.)
       This case presents no such unique circumstances that would
take it outside of the general rule that a manufacturer has no duty
to warn of risks posed by another manufacturer’s product. (O’Neil
v. Crane Co., supra, 53 Cal.4th at pp. 364-366; Taylor v. Elliott
Turbomachinery Co., Inc., supra, 171 Cal.App.4th at pp. 593-596.)
Further, as to successor prescription drug manufacturers, the
Novartis court held “a brand-name manufacturer’s sale of the rights
to a drug does not, as a matter of law, terminate its liability for
injuries foreseeably and proximately caused by deficiencies present
in the warning label prior to sale.” (Novartis, supra, 4 Cal.5th at
p. 191, italics added.) Novartis concerned continuing liability for a
negligent failure to warn in labeling that occurred prior to a
manufacturer divesting itself of the rights to the drug. (Id. at pp.
183, 188, fn. 9 [court’s holding would not prevent the manufacturer
in a given case from arguing it did not breach its duty given the
scientific knowledge at the time].) This holding is of no assistance
to Echeverria because there was no substantial evidence that



                                 33
Johnson & Johnson negligently failed to warn prior to 1967, when it
was manufacturing Johnson’s Baby Powder. Novartis does not
support Echeverria’s argument.
       The other authorities Echeverria cites are equally inapt.
Hernandez v. Badger Construction Equipment Co. (1994) 28
Cal.App.4th 1791, and Balido v. Improved Machinery, Inc. (1972) 29
Cal.App.3d 633, concerned the manufacturers’ alleged negligence in
failing to correct a defect affecting an earlier model of a product still
in use. Neither case addressed a duty to warn after the
manufacturer has stopped making the product altogether, when the
original product is no longer in use, or when the plaintiff alleges she
was harmed by the product a different entity manufactured and
sold.
       Echeverria did not argue that Johnson & Johnson had a
separate duty to take corrective efforts as to the product it
manufactured prior to 1967. (See, e.g., CACI No. 1223 [instructions
for theory a defendant was negligent because it failed to
recall/retrofit the product].) There was no evidence that Echeverria
was using talcum powder Johnson & Johnson manufactured, i.e.,
before 1967, years later. Indeed, such an inference would be
unreasonable in light of the evidence regarding her frequency of
use. (Valentine, supra, 68 Cal.App.4th at p. 1482 [jury properly
instructed that manufacturer’s duty to warn is a continuous duty
which lasts as long as the product is in use; under the instructions
given “as more information about adverse effects develops over
time, the manufacturer must continue to provide physicians with
warnings, at least so long as it is manufacturing and distributing
the product”].) Echeverria did not present a legal theory to the jury
that allowed it to find Johnson & Johnson liable for breaching a
duty to warn that continued even after it stopped manufacturing
the product, or after the product was no longer in use.



                                   34
       In her reply brief, Echeverria cites several cases from other
jurisdictions espousing theories of products liability applicable to
nonmanufacturers, such as “apparent manufacturer” liability, or
the liability of a trademark licensor. Echeverria did not advance
any such theory at trial. She tried the case on a negligent failure to
warn theory only, not on a version of nonmanufacturer products
liability represented in the cases she now cites on appeal. The
jury’s verdict cannot be upheld based on legal or factual theories
that were not advanced below. (Rayii v. Gatica (2013) 218
Cal.App.4th 1402, 1409; Richmond v. Dart Industries, Inc. (1987)
196 Cal.App.3d 869, 874.) Nor was the jury required to make
findings that would have been necessary for such a theory, even if it
applied to Echeverria’s negligent failure to warn claim. (See Bay
Summit Community Assn. v. Shell Oil Co. (1996) 51 Cal.App.4th
762, 778 [factors necessary for strict liability of defendant outside of
vertical distribution chain but involved in the production and
marketing enterprise of a defective product]; Kasel v. Remington
Arms Co. (1972) 24 Cal.App.3d 711, 725-726; cf. Cleveland v.
Johnson (2012) 209 Cal.App.4th 1315, 1334 [verdict alternatively
affirmed on ground for which the jury made necessary findings in
association with another issue].)
              4.     There was no evidence to support a finding
              of liability arising out of Johnson & Johnson’s
              continued involvement in talc issues or based on it
              “directing” JJCI
       Echeverria contends the jury could reasonably find Johnson &
Johnson had a continuing duty to warn because it played an active
role in efforts to denigrate or conceal a link between talc and
ovarian cancer. She asserts several documents from defendants’
files that concerned talc referred to “Johnson & Johnson” only,
suggesting the parent company’s involvement. She also points to



                                  35
evidence that Johnson & Johnson was a member of the CTFA and it
agreed to support a talc task force,11 and communications about
talc included both Johnson & Johnson and JJCI employees.
Echeverria argues this evidence showed the parent company was
“directly involved” in failing to warn of the risks of Johnson’s Baby
Powder.
       We disagree. The relevant question for purposes of the
negligence claim is whether Johnson & Johnson, no longer the
manufacturer of the injury-causing product, had a duty to
Echeverria after 1967. (Ladd v. County of San Mateo (1996) 12
Cal.4th 913, 917-918.) Evidence that Johnson & Johnson took
actions to defend talc, to participate in industry trade groups, or to
avoid a NTP or IARC characterization of talc as a carcinogen, does
not in itself create a basis to hold Johnson & Johnson liable to
Echeverria for negligence. Echeverria has failed to articulate a
legal theory, supported by substantial evidence, that would have
allowed the jury to find Johnson & Johnson had and breached a
duty to Echeverria, even though JJCI was responsible for the
product she used. Indeed, Echeverria’s failure to cite any legal
authorities to support her theory—either below or on appeal—
arguably waives this argument altogether. (Ewald v. Nationstar
Mortgage, LLC (2017) 13 Cal.App.5th 947, 948.)
       Similarly, Echeverria contends the evidence showed Johnson
& Johnson was “directing” JJCI’s actions, without citing legal
authorities to specify her underlying legal theory. Nonetheless, the
trial court considered Echeverria’s arguments to reflect an agency
or alter ego theory of liability. The court concluded there was no
substantial evidence to support either theory. We agree. JJCI is a

11   There was evidence that a JJCI executive signed an
agreement committing “Johnson & Johnson” to contribute funds for
a CTFA task force.


                                  36
wholly owned subsidiary of Johnson & Johnson, but evidence of a
legal relationship between the two corporations is not, without
more, sufficient for Johnson & Johnson to be held liable for JJCI’s
actions. (Institute of Veterinary Pathology, Inc. v. California Health
Laboratories, Inc. (1981) 116 Cal.App.3d 111, 119.) Ambiguity
arising out of similar company names is also not enough to
establish liability. The record is devoid of any evidence of the
relationship between Johnson & Johnson and JJCI, beyond the fact
of the parent-subsidiary relationship and interaction of some
employees. (Santa Clarita Organization for Planning &
Environment v. Castaic Lake Water Agency (2016) 1 Cal.App.5th
1084, 1106 [having some common personnel is not enough to show
subsidiary is alter ego of parent].)
       The trial court properly rejected Echeverria’s claims that
internal documents showed Johnson & Johnson directed or
controlled JJCI. At most, the documents established Johnson &
Johnson was involved in issues related to talc, sometimes in
coordination with JJCI. The documents failed to create an
inference that any such coordination was in fact control, or that
Johnson & Johnson treated JJCI as merely a conduit or
instrumentality of itself. (Santa Clarita Organization for Planning
& Environment v. Castaic Lake Water Agency, supra, 1 Cal.App.5th
at pp. 1104-1106; Sonora Diamond Corp. v. Superior Court (2000)
83 Cal.App.4th 523, 541-542.)
       There was no substantial evidence to support a finding that
Johnson & Johnson was liable to Echeverria for negligently failing
to warn of the risks of perineal talc use. The trial court properly
granted JNOV to Johnson & Johnson.




                                  37
       C.      Substantial Evidence Supported the Jury’s
       Finding That JJCI Breached Its Duty to Warn
       In its motion seeking JNOV, JJCI argued the evidence did not
show that the prevailing scientific knowledge established talc to be
dangerous by 2007, when Echeverria was diagnosed with ovarian
cancer. The trial court rejected this theory as a ground for JNOV
because defendants had not requested an equivalent jury
instruction. On cross-appeal, defendants argue this was error and
the trial court should have granted JNOV to JJCI on this
alternative ground. Echeverria contends there was substantial
evidence that JJCI breached a duty to warn.
       We need not decide if the trial court erred in concluding
defendants’ failure to request a jury instruction on “prevailing
scientific knowledge” prevented any consideration of the argument
as a basis for JNOV. Even if this was error, substantial evidence
supported the jury’s finding that JJCI breached a duty to warn of
the risks of ovarian cancer from genital talc use, even with a 2007
cutoff date.
       “Negligence law in a failure-to-warn case requires a plaintiff
to prove that a manufacturer or distributor did not warn of a
particular risk for reasons which fell below the acceptable standard
of care, i.e., what a reasonably prudent manufacturer would have
known and warned about.” (Anderson v. Owens-Corning Fiberglas
Corp. (1991) 53 Cal.3d 987, 1002.) As explained above, there is no
duty to warn of risks that are merely speculative or conjectural. A
manufacturer is “not charged with knowing more than what would
come to light from the prevailing scientific and medical knowledge.”
(Valentine, supra, 68 Cal.App.4th at pp. 1483-1484.) But the
evidence as it applied to JJCI was sufficient to allow the jury to
conclude the known risks of genital talc use were concrete enough




                                 38
that it was unreasonable for JJCI to fail to warn consumers of
them.
       The evidence established that between 1967 and 2007, there
were several epidemiological studies finding a statistically
significant association between genital talc use and ovarian cancer,
as well as studies concluding talc can migrate to the ovaries.
Internal documents reflected JJCI’s knowledge of the studies and of
the evidence of increased risk of ovarian cancer associated with
perineal talc use. The 1997 outside consultant letter reported to
JJCI that by November 1994 “there had been about 9 studies (more
by now) published in the open literature that did show a
statistically significant association between hygienic talc use and
ovarian cancer,” and that several independent reports provided a
basis to conclude talc is capable of migrating to the ovaries. The
evidence also established JJCI knew of the possibility the NTP or
the IARC might designate talc as a carcinogen, and JJCI worked to
avoid such a designation.
       JJCI argues the scientific evidence was inconclusive and did
not establish a causal connection between talc and ovarian cancer.
The jury could reasonably conclude the risks were significant and
well-documented enough that JJCI had a duty to warn consumers.
Studies had repeatedly shown an association between perineal talc
use and ovarian cancer and there was evidence supporting a
biological mechanism. A 1992 study recommended that women not
use genital talc due to the risk of ovarian cancer. A 1999 study
suggested women should be warned of the risks of ovarian cancer
from genital talc use. In 2004, Luzenac was communicating its
concern about the different pieces of evidence that together
suggested a causal connection between perineal talc use and
ovarian cancer. In 2006, Luzenac added a warning on its MSDS
about the IARC 2B designation. That no regulatory or scientific



                                 39
organization has conclusively identified talc as causing ovarian
cancer is relevant, but not dispositive on the question of whether
JJCI acted as a reasonably prudent manufacturer in deciding not to
warn.
       Relying on Valentine, JJCI further argues there is no duty to
warn unless it is probable, rather than possible, that the
defendant’s product causes harm, and there was no evidence by
2007 that talc was a probable cause of ovarian cancer.
       In Valentine, the court considered the difference between
strict liability and negligent failure to warn claims to determine
whether a jury’s conclusion that the defendant was not liable for
strict liability failure to warn necessarily exonerated the defendant
on a negligent failure to warn theory. (Valentine, supra, 68
Cal.App.4th at pp. 1480-1481, 1482.) The court concluded the
instructions given in the case on strict liability failure to warn
subsumed the elements of a negligent failure to warn claim.
       The Valentine court reasoned: “The manufacturer’s duty, per
strict liability instructions, to warn of potential risks and side
effects envelopes a broader set of risk factors than the duty, per
negligence instructions, to warn of facts which make the product
‘likely to be dangerous’ for its intended use. A ‘potential’ risk is one
‘existing in possibility’ or ‘capable of development into actuality,’
while a product ‘likely’ to be dangerous will ‘in all probability’ or
‘probably’ be dangerous. Stated differently, if [the defendant]
adequately warned of potential risks and side effects, it of necessity
warned of facts likely to render the product dangerous to the user.
But, conversely, one could discharge the duty to warn of likely risks
without discharging the duty to warn of potential risks. In sum, the
manufacturer’s strict liability duty to warn is greater than its duty
under negligence, and thus negligence requires a greater showing




                                  40
by plaintiffs.” (Valentine, supra, 68 Cal.App.4th at p. 1483, fns.
omitted.)
       Here, there was substantial evidence that, if credited, allowed
the jury to find that by 2007, a reasonable manufacturer would
conclude there were facts showing genital talc use was likely to be
dangerous, or “probably” dangerous. As noted above, there was
evidence of repeated studies showing a statistical association
between perineal talc use and ovarian cancer, evidence of migration
of talc to the ovaries, and, according to the IARC designation, a
credible but inconclusive causal interpretation of the observed
association between talc use and increased risk of ovarian cancer.
       Moreover, as it concerned JJCI, this was not a case in which
the evidence established the alleged danger was unknown or
unknowable because of lack of scientific knowledge. Instead, the
evidence presented a question of whether what was known was
significant enough that JJCI acted unreasonably in failing to give
an appropriate warning. What was known by 2007 went beyond,
for example, “[k]nowledge of a potential side effect which is based
on a single isolated report of a possible link between a prescription
drug and an injury . . . .” (Finn v. G.D. Searle & Co. (1984) 35
Cal.3d 691, 701.) While the evidence may not have been definitive
or overwhelming, it was not so limited that we may determine the
only reasonable conclusion was the risk of ovarian cancer from
perineal talc use was unknown or unknowable in light of the
prevailing scientific and medical knowledge.
       “The question whether there has been a breach of duty is
usually a fact issue for the jury and may be resolved only as a
matter of law if the circumstances do not permit a reasonable doubt
as to whether the defendant’s conduct violates the degree of care
exacted of [it]. [Citations.] If there is room for honest difference of
opinion . . . as to whether there has been a breach of duty, the



                                  41
question becomes one of fact for the jury.” (Putensen v. Clay
Adams, Inc. (1970) 12 Cal.App.3d 1062, 1077; Carlin, supra, 13
Cal.4th at p. 1116; Finn v. G.D. Searle & Co., supra, 35 Cal.3d at
p. 700 [jury determines the reasonableness of the manufacturer’s
conduct in negligent failure to warn cases]; see also Saller v. Crown
Cork & Seal Co., Inc. (2010) 187 Cal.App.4th 1220, 1239.) There
was substantial evidence to support the jury’s finding that a
reasonably prudent manufacturer would have known about the risk
of ovarian cancer from genital talc use, and would have warned
about that risk. (Carlin, at p. 1115; Anderson v. Owens-Corning
Fiberglas Corp., supra, 53 Cal.3d at p. 1002.)
      D.     Substantial Evidence Supported the Jury’s
      Finding on Specific Causation
      The trial court ruled Yessaian’s specific causation opinion was
insufficient as a matter of law, identifying two main deficiencies in
the testimony. First, the court reasoned Yessaian relied on
epidemiological studies that did not support her opinion and she
had no other basis for her conclusions. Second, the court found
Yessaian purported to rule out other potential causes of
Echeverria’s cancer but she either failed to completely eliminate
alternative causes, or she did so based on speculation alone.
Echeverria argues these conclusions misconstrued the record and
were legal error. Keeping in mind the standard of review, we
conclude the evidence was sufficient to support the jury’s causation
finding.
      “ ‘ “Causation” is an essential element of a tort action.
Defendants are not liable unless their conduct . . . was a “legal
cause” of plaintiff’s injury. [Citations.].’ [Citation.] ‘Generally, the
burden falls on the plaintiff to establish causation. [Citation.] . . .
In the context of products liability actions, the plaintiff must prove
that the defective products supplied by the defendant were a



                                  42
substantial factor in bringing about his or her injury. [Citations.]’ ”
(Whiteley v. Philip Morris, Inc. (2004) 117 Cal.App.4th 635, 696.) A
defendant’s negligence is not a substantial factor in bringing about
harm if the plaintiff would have sustained the injury without the
defendant’s negligence. (Viner v. Sweet (2003) 30 Cal.4th 1232,
1240-1241.)
       “[I]n a personal injury action causation must be proven within
a reasonable medical probability based upon competent expert
testimony. Mere possibility alone is insufficient to establish a
prima facie case. . . . There can be many possible ‘causes,’ indeed, an
infinite number of circumstances which can produce an injury or
disease. A possible cause only becomes ‘probable’ when, in the
absence of other reasonable causal explanations, it becomes more
likely than not that the injury was a result of its action.” (Jones v.
Ortho Pharmaceutical Corp. (1985) 163 Cal.App.3d 396, 402-403;
Sparks v. Owens-Illinois, Inc. (1995) 32 Cal.App.4th 461, 476-477.)




                                  43
            1.    Yessaian’s Reliance on Epidemiological
              Studies Supported Her Opinion12
       The trial court relied in part on Daubert v. Merrell Dow
Pharmaceuticals, Inc. (9th Cir. 1995) 43 F.3d 1311 (Daubert II), in
evaluating the sufficiency of Yessaian’s opinion. In Daubert II, the
plaintiffs alleged the drug Bendectin caused their limb reduction
birth defects. However, every published study had concluded the
drug was not a teratogen. Epidemiological studies reported no
statistical association between the drug and birth defects. (Id. at


12     The trial court framed this issue as a lack of evidence to “rule
in” talc as part of the differential diagnosis. We question what
appears to be the combination of two distinct methods of proving
specific causation—the use of epidemiological studies alone and the
use of a differential etiology. The “ruling in” step of a differential
diagnosis involves creating a list of causes that are generally
capable of causing the disease. (Clausen v. M/V New Carissa,
supra, 339 F.3d at pp. 1057-1058.) In contrast, the 2.0 relative risk
threshold is typically invoked with regard to specific causation—
whether the agent caused an individual plaintiff’s disease. (In re
Silicone Gel Breast Impl. Prod. Liab. Lit., supra, 318 F.Supp.2d at
p. 893 [relative risk of 2.0 not necessary to establish general
causation]; King v. Burlington Northern Santa Fe Ry. (Neb. 2009)
762 N.W.2d 24, 46-47 [declining to set 2.0 relative risk threshold for
general causation].) In fact, the Reference Guide suggests
“[d]ifferential etiologies are most critical when the agent at issue is
relatively weak and is not responsible for a large proportion of the
disease in question.” (Reference Guide, supra, at p. 618.) The
Reference Guide also notes ruling out known causes may allow a
relative risk under 2.0 to support an inference that the agent more
likely than not caused the plaintiff’s disease. (Id. at pp. 616-618.)
However, we need not take up this issue. Whether as part of the
differential diagnosis or as a separate means of proof, we conclude
Yessaian’s reliance on epidemiological studies was a valid basis for
her ultimate opinion.


                                  44
p. 1314.) The court concluded the plaintiffs’ expert testimony on
whether the drug was capable of causing limb reduction birth
defects did not reflect findings that were derived by the scientific
method and did not amount to “good science.” (Id. at pp. 1315-1316,
1319-1320.)
       The court further held that even if the plaintiffs could show
their experts’ findings were in fact derived by the scientific method,
the plaintiffs still could not establish causation. Statistical
probabilities derived from epidemiological studies were the only
evidence the plaintiffs offered to show the drug caused their
individual injuries. (Daubert II, supra, 43 F.3d at p.1320.) The
plaintiffs had to establish that their mothers’ use of the drug more
than doubled the likelihood of birth defects because “only then can
it be said that Bendectin is more likely than not the source of their
injury.” (Ibid.) The Daubert II court thus held that “[f]or an
epidemiological study to show causation under a preponderance
standard, ‘the relative risk of limb reduction defects arising from
the epidemiological data . . . will, at a minimum, have to exceed “2”.’
[Citation.] That is, the study must show that children whose
mothers took Bendectin are more than twice as likely to develop
limb reduction birth defects as children whose mothers did not.”
(Id. at p. 1321.)
       The court noted a “statistical study showing a relative risk of
less than two could be combined with other evidence to show it is
more likely than not that the accused cause is responsible for a
particular plaintiff’s injury.” (Daubert II, supra, 43 F.3d at p. 1321,
fn. 16.) This was of no help to the Daubert II plaintiffs, however,
since their experts did not seek to differentiate the plaintiffs from
the subjects of the statistical studies they relied on. The court
concluded “[t]he studies must therefore stand or fall on their own.”
(Ibid.)



                                  45
       In Cooper v. Takeda Pharmaceuticals America, Inc. (2015)
239 Cal.App.4th 555 (Cooper), a panel of this court adopted the
Daubert II reasoning that only studies showing relative risk
estimates greater than 2.0 are useful to the jury and may properly
be used to “extrapolate from generic population-based studies to
conclusions about what caused a specific person’s disease.” (Cooper,
at p. 593.) However, the studies at issue in Cooper had relative risk
estimates greater than 2.0. (Id. at pp. 562-564.) The court had no
occasion to consider what role, if any, studies with lower relative
risk estimates may play in an expert’s opinion.13
             a.   Yessaian relied on studies with risk ratios
                  greater than 2.0
      Here, Yessaian relied on four studies which reported risk
ratios greater than 2.0. The trial court rejected Yessaian’s reliance
on the two studies that reported a 1.7 odds ratio for the serous
histologic subtype. Still, the court acknowledged that left two
studies with odds ratios greater than 2.0. These studies reported

13    Numerous commentators have criticized the use of a 2.0
relative risk threshold as a prerequisite to establishing specific
causation. (See, e.g., Egilman et al., Proving Causation: The Use
and Abuse of Medical and Scientific Evidence Inside the
Courtroom—An Epidemiologist’s Critique of the Judicial
Interpretation of the Daubert Ruling (2003) 58 Food & Drug L.J.
223; Geistfeld, Scientific Uncertainty and Causation in Tort Law
(2001) 54 Vand. L.Rev. 1011; Finley, Guarding the Gate to the
Courthouse: How Trial Judges Are Using Their Evidentiary
Screening Role to Remake Tort Causation Rules (1999) 49 DePaul
L.Rev. 335; Greenland, Relation of Probability of Causation to
Relative Risk and Doubling Dose: A Methodologic Error That Has
Become a Social Problem (1999) 89 Am.J. Public Health 1166.) The
validity of a 2.0 threshold is not before us as Echeverria argues
Yessaian in fact relied on epidemiological studies showing risk
estimates greater than 2.0.


                                 46
the risk of ovarian cancer among genital talc users to be over three
and over four times greater than the risk in the unexposed. The
trial court discounted Yessaian’s reliance on these studies because
the results were not stratified by histologic subtype. However,
there was no evidence offered at trial indicating study results were
categorically irrelevant unless they showed stratified results for the
serous subtype. Yessaian explained why she thought these
particular risk estimates were appropriate when considering
Echeverria’s case. The jury could accept her explanations.
       The lack of stratification for serous ovarian cancer in these
two studies could certainly affect the weight of the evidence.
Indeed, the trial court appeared to weigh the evidence when
concluding that, “[i]n light of the other studies presented,” including
the studies showing 1.7 odds ratios for serous ovarian cancer, and
one study in which “no increased risk was shown,” the two studies
with risk estimates greater than 2.0 were not substantial evidence
supporting Yessaian’s opinion. But we may not weigh the evidence
at this stage. We have no basis to conclude Yessaian’s reliance on
the two “greater than 2.0” studies was invalid. Yessaian had
epidemiological support for her opinion that talc was more likely
than not responsible for causing Echeverria’s ovarian cancer, based
on odds ratios greater than 2.0.
             b.    Yessaian’s reliance on studies with risk
                   estimates less than 2.0 provided additional
                   support for her opinion
       We also conclude Yessaian’s reliance on epidemiological
studies with risk estimates less than 2.0 offered additional support
for her opinion. Several courts have held, consistent with
Daubert II, that while studies reporting relative risk estimates
under 2.0 may not on their own establish specific causation, they
may be combined with other evidence to provide proof of causation,



                                  47
or to render an expert’s testimony sufficiently reliable to be
admissible. (See, e.g., Ambrosini v. Labarraque (D.C. Cir. 1996) 101
F.3d 129, 135 [exclusion of expert testimony not warranted because
it failed to “establish the causal link to a specified degree of
probability”]; In re Joint Eastern & Southern Dist. Asbestos Lit. (2d
Cir. 1995) 52 F.3d 1124, 1134 [declining to set standard mortality
ratio “floor” as a matter of law]; Landrigan v. Celotex Corp. (N.J.
1992) 605 A.2d 1079, 1087 [under some circumstances a study with
relative risk less than 2.0 could support specific causation finding;
2.0 relative risk is “not so much a password to a finding of causation
as one piece of evidence, among others” for court to determine
whether expert has used a sound methodology]; Carruth &
Goldstein, Relative Risk Greater Than Two in Proof of Causation in
Toxic Tort Litigation (Winter 2001) 41 Jurimetrics J. 195 [collecting
cases between 1982 and 1999]; see also In re Hanford Nuclear
Reservation Litigation (9th Cir. 2002) 292 F.3d 1124, 1136-1137
[district court erred in requiring threshold level of radiation
creating relative risk greater than 2.0 without regard to
individualized factors].)
        Similarly, here, Yessaian did not rely on epidemiological
studies with risk estimates under 2.0 alone to conclude talc was a
substantial factor in causing Echeverria’s ovarian cancer. As
explained above, she relied on studies with greater than 2.0 odds
ratios. Yessaian also considered the dose-response relationship
reflected in at least four studies, as well as Echeverria’s history of
using talc for over 40 years, two or three times each day. Moreover,
Yessaian did not only rely on epidemiological studies. She
considered the migration studies and evidence regarding the
general processes of inflammation and resulting carcinogenesis, in
combination with the evidence of talc particles in Echeverria’s
ovarian tissues and other areas where the cancer was found. Her



                                 48
differential diagnosis evaluated and ruled out other known causes
and risk factors. It was therefore permissible for Yessaian to also
rely in part on epidemiological studies with risk ratios less than 2.0.
             2.     Yessaian’s Opinion Was Not Invalid for
             Failure to Rule Out Other Known Causes or the
             Possibility of an Unknown Cause
       The trial court concluded Yessaian did not properly employ
the differential diagnosis methodology because her opinion ruling
out age and the number of ovulatory cycles was speculative. The
court also found Yessaian only “discounted” certain risk factors
rather than eliminating them. The court additionally concluded
Yessaian merely speculated when opining Echeverria’s cancer was
not idiopathic. Echeverria asserts these conclusions ignored the
evidence and misapplied the law. We conclude the entirety of the
evidence established Yessaian’s methodology was not fatally flawed
and her opinion was sufficiently supported.
       Cooper instructs our analysis. In Cooper, the plaintiff alleged
the defendant’s drug caused his bladder cancer. (Cooper, supra, 239
Cal.App.4th at p. 561.) Following a jury verdict in the plaintiff’s
favor, the trial court struck the specific causation expert’s testimony
as speculative and lacking foundation, and granted JNOV. (Ibid.)
The expert had conducted a differential diagnosis based on his
review of the plaintiff’s medical records, review of the relevant
literature, and his own scientific research. (Id. at pp. 566-567.) He
ruled out numerous potential causes and risk factors, eventually
concluding the defendant’s drug was the “ ‘most substantial
causative factor.’ ” (Id. at pp. 567-570, 583.)
       The reviewing court held the trial court erred when it ruled
the expert’s testimony was inadmissible because he failed to
“adequately consider and definitively rule out” potential causes of
the cancer other than the defendant’s drug. (Cooper, supra, 239



                                  49
Cal.App.4th at p. 577.) The court explained: “Under the applicable
substantial factor test, it is not necessary for a plaintiff to establish
the negligence of the defendant as the proximate cause of injury
with absolute certainty so as to exclude every other possible cause of
a plaintiff’s illness, even if the expert’s opinion was reached by a
performance of a differential diagnosis.” (Id. at p. 578, original
italics.)
       The defendant did not identify any relevant evidence about
other causes it claimed the expert overlooked. The Cooper court
reasoned the “critical point” was the defendant could not point to
any substantial evidence to indicate that the expert ignored another
cause of bladder cancer, other than the drug, such that his opinion
was unreliable. (Cooper, supra, 239 Cal.App.4th at p. 585.)
       The Cooper expert acknowledged there are many possible
causes of bladder cancer and much still unknown about the etiology
of the disease. This was not a proper basis for exclusion of the
testimony in the absence of any substantial evidence to support the
proposition that other possible causes in fact affected the plaintiff.
(Cooper, supra, 239 Cal.App.4th at pp. 585-586.) The court
reasoned: “California has rejected the notion that an expert must
‘exclude all “possibilities” ’ in reaching a specific causation opinion.
[Citation.] Bare conceivability of another possible cause does not
defeat a claim; the relevant question is whether there is ‘substantial
evidence’ of an alternative explanation for the disease.” (Ibid.)
       In this case, the trial court concluded Yessaian did not
sufficiently rule out age and number of ovulatory cycles. Our
review of the record reveals that Yessaian considered these two risk
factors and explained her decision to rule each factor out. As to age,
Yessaian explained that while half of all women who get ovarian
cancer do so between the ages of approximately 52 to 60 years old,
Echeverria was on the younger side of that range. Were Echeverria



                                   50
older at the time of diagnosis, Yessaian said she would have
identified age—and the larger number of accompanying “genetic
hits”—as a more likely cause of the cancer. But since Echeverria
was at the younger end of the spectrum, Yessaian found age to be
an unlikely cause.
       As to the number of ovulatory cycles, Yessaian explained that
Echeverria’s age at menarche and menopause were both average.
She described the risk related to ovulatory cycles as involving
abnormally long periods of ovulation that occur when a woman has
early menarche and late menopause. She did not believe
Echeverria fit into this category, later noting Echeverria was
menopausal at age 48, younger than the average age of menopause
in American women. She also testified that she relied on several
studies, included in her report, which informed her opinion that
menarche at age 11 was not young enough to conclude early
menarche was a cause of the cancer. She additionally opined that
the number of ovulatory cycles is not an independent risk factor for
postmenopausal ovarian cancer, referencing a particular study to
support that opinion.
       Yessaian considered both age and number of ovulatory cycles
and explained why she found them improbable as independent
causes of Echeverria’s ovarian cancer. This was adequate.
Yessaian was not required to conclusively exclude other potential
causes for her testimony to be sufficiently reliable to support her
opinion. (Cooper, supra, 239 Cal.App.4th at pp. 585-586; see also
Johnson v. Mead Johnson & Co., LLC (8th Cir. 2014) 754 F.3d 557,
563 [experts not required to rule out all possible causes when
performing differential etiology; such considerations go to the
weight of the evidence]; Messick v. Novartis Pharmaceuticals Corp.
(9th Cir. 2014) 747 F.3d 1193, 1198 [expert must provide reasons
for rejecting alternative hypotheses using scientific methods and



                                 51
not based on speculation or subjective beliefs; expert may rely on
clinical experience and need not identify sole cause for opinion to be
reliable]; Westberry v. Gislaved Gummi AB (4th Cir. 1999) 178 F.3d
257, 265-266 [causation opinion not inadmissible for failure to rule
out every possible alternative cause unless expert offers no
explanation for why she has concluded an alternative cause was not
the sole cause]; Heller v. Shaw Industries, Inc. (3d Cir. 1999) 167
F.3d 146, 156-157 [same].)
       Defendants argue for a restrictive reading of Yessaian’s
testimony, taking isolated portions to conclude she “discounted”
alternative causes rather than eliminating them. This approach
conflicts with the standard of review we must apply. Yessaian used
varying language to describe her process of rejecting other risk
factors as the cause of Echeverria’s cancer. Taken as a whole,
however, and drawing all inferences in favor of the verdict, the
record supports the conclusion that Yessaian did “rule out”
alternative causes, either concluding they were not independent
risk factors, or explicitly testifying that in her opinion these other
factors were not a cause. As in Cooper, defendants did not point to
any substantial evidence to indicate Yessaian ignored age or
number of ovulatory cycles, such that her opinion was unreliable or
mere conjecture. (Cooper, 239 Cal.App.4th at p. 585; see King v.
Burlington Northern Santa Fe Ry., supra, 762 N.W.2d at pp. 50-51
[expert did not fail to consider other possible hypotheses;
defendant’s alternative suggestions for cause of disease affected
weight of testimony only].) Defendants challenged Yessaian’s
explanations on cross-examination and offered competing expert
testimony. It was appropriate for the jury to determine the
credibility of Yessaian’s testimony and to weigh it against
contradictory evidence.




                                 52
       We also find the reasoning of Cooper instructive when
considering “unknown causes.” There was no substantial evidence
that unknown, yet-to-be-identified causes of ovarian cancer acted on
Echeverria and provided an alternative explanation for her disease.
As the court explained in Cooper, something more than bare
conceivability or plausibility of other causes is required before
another cause must be chosen as a matter of law as a cause in fact
over the defendant’s conduct. (Cooper, supra, 239 Cal.App.4th at
p. 581.)
       As to the largely idiopathic nature of ovarian cancer, Yessaian
testified the statement that “unknown etiology is the leading cause
of cancer” is a general statement, applicable to the population as a
whole. Her entire opinion was directed to answering the question of
whether Echeverria’s cancer had a known cause or, in other words,
that the cancer was not idiopathic. Yessaian’s testimony indicated
she did not ignore idiopathy but instead determined there was in
fact a known cause of the cancer, based on the factors she described.
The credibility of her explanation was for the jury to determine.
(See Wendell v. GlaxoSmithKline LLC (9th Cir. 2017) 858 F.3d
1227, 1237 [expert not required to eliminate all other possible
causes of a condition for the testimony to be reliable; true in
patients with multiple risk factors and in cases where there is a
high rate of idiopathy]; In re Diet Drugs (E.D.Pa. 2012) 890
F.Supp.2d 552, 562 [experts not required to exclude unknown or
idiopathic causes for differential diagnosis to be reliable basis for
their opinions].)
       The authorities defendants cite do not mandate a different
result. In each case cited, the court first concluded the plaintiff
failed to provide evidence of general causation. Stated otherwise,
the plaintiffs’ experts failed to provide any admissible evidence that
the defendants’ products were capable of causing the disease at



                                 53
issue, in anyone. Without any evidence demonstrating the alleged
toxin was even capable of causing disease, the experts could not
reliably conclude the toxin caused the plaintiff’s disease, even if
other known causes were ruled out. (Tamraz v. Lincoln Elec. Co.
(6th Cir. 2010) 620 F.3d 665, 674-675 [expert had no nonspeculative
basis to identify manganese exposure as a cause of the plaintiff’s
parkinsonism]; Henricksen v. ConocoPhillips Co. (E.D.Wa. 2009)
605 F.Supp.2d 1142, 1162-1163, 1169-1170 [expert’s opinion that
exposure to benzene in gasoline could cause AML was not supported
by reliable studies and was based on assumptions only]; Doe v.
Ortho-Clinical Diagnostics, Inc. (M.D.N.C. 2006) 440 F.Supp.2d
465, 477 [expert testimony was inadmissible to establish general
causation and differential diagnosis was therefore inappropriate].)
       Here, defendants have not argued there was no substantial
evidence of general causation. We have also concluded Yessaian’s
use of epidemiological and other scientific evidence to support her
opinion identifying talc as the cause of Echeverria’s cancer was
proper. (Compare Hall v. Conoco Inc. (10th Cir. 2018) 886 F.3d
1308, 1312-1316 [errors and inconsistencies in calculating plaintiff’s
exposure to benzene invalidated expert’s opinion ruling it in as
potential cause and differential diagnosis unreliable for largely
idiopathic disease]; Milward v. Rust-Oleum Corp. (1st Cir. 2016)
820 F.3d 469, 475-476 [expert had no scientifically valid basis to
rule in benzene and could not use differential diagnosis to rule out
idiopathic diagnosis], with Wendell v. GlaxoSmithKline LLC, supra,
858 F.3d at pp. 1234, 1237 [opinion not pure conjecture that patient
with obvious and known risk factors led to assumption that those
risk factors were the cause instead of idiopathy]; In re E.I. DuPont
de Nemours and Company (S.D.Ohio 2016) 342 F.Supp.3d 773, 783-
787 [rejecting a rule that plaintiff may not rely on differential
diagnosis when cause of disease is unknown in majority of cases;



                                 54
expert opinion that plaintiff’s disease had a known cause
sufficiently reliable to be admitted].)
       In addition, while Yessaian was the sole specific causation
expert, other evidence admitted at trial was relevant to the issue.
Godleski, for example, opined there was evidence of a chronic
inflammatory process in Echeverria’s tissues. In addition to
providing a general causation opinion, Siemiatycki proffered an
opinion that epidemiological evidence established a dose-response
pattern, thus corroborating Yessaian’s opinion related to dose-
response data.
       We consider whether there is any substantial evidence,
contradicted or uncontradicted, to support the jury’s verdict.
Yessaian’s opinion had multiple elements. One was the differential
diagnosis ruling out other known causes. Another was
epidemiological evidence in the form of studies showing risk ratio
estimates greater than 2.0. Yet another was the evidence of dose
response, evidence of Echeverria’s consistent and long years of
heavy exposure, and the evidence of talc in her ovarian and other
tissues. While a differential diagnosis alone may be insufficient as
the sole basis for an opinion on the etiology of a largely idiopathic
disease, that is not the situation before us. (See In re Diet Drugs,
supra, 890 F.Supp.2d at p. 563; Henricksen v. ConocoPhillips Co.,
supra, 605 F.Supp.2d at pp. 1162-1163 [not impossible to prove
specific causation in cases where most diagnoses are idiopathic but
“in those cases, analysis beyond a differential diagnosis is
required”].)
       Taken together, Yessaian’s specific causation opinion was
supported by the epidemiological literature, including studies
showing risk ratios greater than 2.0, her testimony regarding the
biological mechanism in general and the presence of talc in
Echeverria’s ovarian tissue and other areas where the cancer was



                                 55
present, her clinical experience and treatment, her explanations
addressing and ruling out other known risk factors and causes, and
portions of the testimony of the other experts. (In re Joint Eastern
& Southern Dist. Asbestos Lit., supra, 52 F.3d at pp. 1132-1133
[admissibility assessments concern individual pieces of evidence,
but a sufficiency inquiry asks whether the collective weight of a
litigant’s evidence is adequate to present a jury question; the issue
is whether epidemiological and clinical data already in evidence
was sufficient to justify the jury’s verdict finding causation].)
       The weaknesses in Yessaian’s testimony affected the weight
of the evidence. They did not represent fundamental
methodological flaws that rendered her testimony conjectural or
insufficient as a matter of law. We may not reweigh the evidence,
make credibility determinations, or disregard reasonable inferences
that may be drawn in favor of the verdict. Substantial evidence
supported the jury’s finding that talcum powder was a substantial
factor in causing Echeverria’s cancer.
       E.    The Trial Court Properly Granted JNOV
       in Favor of JJCI as to Punitive Damages
       Echeverria contends the trial court erred in granting JNOV
as to punitive damages. We find no error.
       Under Civil Code section 3294, a plaintiff may recover
punitive damages by proving, by clear and convincing evidence, that
the defendant acted with malice, fraud, or oppression. (Civ. Code,
§ 3294, subd. (a).) Malice “means conduct which is intended by the
defendant to cause injury to the plaintiff or despicable conduct
which is carried on by the defendant with a willful and conscious
disregard of the rights or safety of others.” (Id., subd. (c)(1).)
       When there is no evidence the defendant intended to harm
the plaintiff, there must be evidence of conduct that is both willful
and despicable. (Lackner v. North (2006) 135 Cal.App.4th 1188,



                                 56
1211, 1213.) Conscious disregard for the safety of another may be
found “ ‘where the defendant is aware of the probable dangerous
consequences of his or her conduct and he or she willfully fails to
avoid such consequences.’ ” (Pfeifer v. John Crane, Inc. (2013) 220
Cal.App.4th 1270, 1299. (John Crane).) “ ‘Despicable conduct’ is
conduct that is ‘ “so vile, base, contemptible, miserable, wretched or
loathsome that it would be looked down upon and despised by
ordinary decent people.” ’ [Citation.] Such conduct has been
described as having the character of outrage frequently associated
with crime.” (Butte Fire Cases (2018) 24 Cal.App.5th 1150, 1159;
College Hospital Inc. v. Superior Court (1994) 8 Cal.4th 704, 725.)
      “[S]ince the jury’s findings were subject to a heightened
burden of proof, we must review the record in support of these
findings in light of that burden. In other words, we must inquire
whether the record contains ‘substantial evidence to support a
determination by clear and convincing evidence . . . .’ [Citation.]”
(Shade Foods, Inc. v. Innovative Products Sales & Marketing, Inc.
(2000) 78 Cal.App.4th 847, 891 (Shade Foods).) JNOV was proper
on the issue of punitive damages if no reasonable jury could find
Echeverria’s evidence provided clear and convincing proof of malice.
(Hoch v. Allied-Signal, Inc. (1994) 24 Cal.App.4th 48, 60-61.)
      Viewed in the light most favorable to Echeverria, the evidence
established JJCI was aware of studies showing an association
between talc and ovarian cancer, studies showing talc could migrate
from the vagina to the ovaries, and the theory and corresponding
research suggesting talc caused inflammation, eventually leading to
ovarian cancer. The evidence further established that, at least
between the 1990’s and 2006, JJCI’s response to these studies was
to mount a defense against them. In attempts to influence or
persuade agencies such as the NTP and IARC, and in response to
media or governmental inquiry, JJCI’s strategy was to describe the



                                 57
flaws of these studies, point out inconclusive results, and highlight
the absence of any established causal link. The jury could
reasonably infer that, faced with the possibility that talc might be
shown to cause ovarian cancer, JJCI’s response was focused solely
on avoiding such a conclusion.
       However, it was also undisputed that there has not been
direct, conclusive evidence establishing genital talc use causes
ovarian cancer. While various entities have conducted evaluations
of the entire body of relevant evidence, these have resulted in
conclusions that fall short of a declaration that perineal use of talc
is carcinogenic. The evidence demonstrated it is not universally
accepted in the scientific or medical community that talc is even a
significant risk factor for ovarian cancer. We note that despite the
published cell, epidemiological, and animal studies, as well as the
IARC 2B designation, Yessaian, a highly experienced gynecologic
oncologist, had not warned her patients or their family members
away from genital talc use until this litigation. She neither asked
Echeverria about her talc use, nor advised her to stop using it.
       There was no evidence JJCI had any information about the
dangers or risks of perineal talc use that was unavailable to the
scientific or medical community. The company’s critiques of
available evidence were largely consistent with third party entities’
evaluations of the same studies, including nontrade groups such as
the IARC and the FDA. (Cf. Boeken v. Philip Morris (2005) 127
Cal.App.4th 1640, 1652-1655.)
       Echeverria’s epidemiological expert, Dr. Siemiatycki, testified
that in 2006, when he chaired the IARC working committee on talc,
he and the committee did not believe the available evidence was
sufficient to conclude perineal use of talc caused ovarian cancer.
Although there was evidence that JJCI attempted to “defend talc”
and to avoid a carcinogenic designation by the IARC committee,



                                  58
there was no evidence JJCI’s efforts had any impact on the
committee’s ultimate conclusion that perineal talc use was possibly
a carcinogen. Siemiatycki testified his changed opinion about
perineal talc use was driven in large part by a study published in
2013, six years after Echeverria was diagnosed with ovarian cancer,
which he believed provided dose-response data that was previously
absent.
       A defendant’s entire course of conduct may be considered for
purposes of assessing punitive damage awards, including post-
injury conduct. (Butte Fire Cases, supra, 24 Cal.App.5th at p. 1176;
Hilliard v. A.H. Robins Co. (1983) 148 Cal.App.3d 374, 399-401.)
We disagree, however, that JJCI’s actions or omissions in response
to studies published after Echeverria incurred her injuries, which
have offered new evidence or analysis, demonstrate a pattern or
course of conduct that establishes the company’s ongoing conscious
disregard of the safety of others that would apply equally to
Echeverria. Scientific evidence developed post-injury did not create
a reasonable inference that JJCI was acting with malice, pre-injury,
in failing to warn of probable dangerous consequences of the
product. Further, the post-injury conduct continued to fall short of
establishing clear and convincing evidence of malice.
       Siemiatycki testified he believed the evidence of causation
had grown stronger than it was in 2006. Yet, he also admitted the
2013 study he relied upon for evidence of dose response included
two analyses, one which showed a dose response and one which did
not. There was further undisputed evidence that epidemiological
studies published in 2016 and 2017 showed statistical associations
no greater, and in some cases weaker, than those of earlier studies.
Echeverria offered no evidence of any growing general scientific
consensus that talc causes ovarian cancer. (Cf. John Crane, supra,
220 Cal.App.4th at p. 1302 [malice shown where it was widely



                                59
accepted during relevant time period that product was carcinogenic;
causal connection at significant exposure levels not disputed].)
        Defendants point out that the FDA has not concluded there is
a causal link between talc and ovarian cancer. A defendant’s
compliance with, or actions consistent with, governmental
regulations or determinations about a product do not necessarily
eviscerate a claim for punitive damages. (John Crane, supra, 220
Cal.App.4th at pp. 1301-1302.) But, here, the evidence showed the
IARC has identified genital use of talc as possibly causing ovarian
cancer and the statistical association between talc and ovarian
cancer remains under scientific investigation. (See Satcher v.
Honda Motor Co. (5th Cir. 1995) 52 F.3d 1311, 1316-1317 [no
evidence to support punitive damages where there was a genuine
dispute in scientific community about the benefit of the proposed
safety measure, no independent organization required it, industry
as a whole rejected the safety measure, and there were no definitive
conclusions about effectiveness of the measure].) The evidence
established that JJCI has refused to draw a causal connection
between perineal talc use and ovarian cancer before experts in the
relevant fields have done so. The jury could reasonably conclude
this was unreasonable and negligent. But it is not clear and
convincing evidence of “despicable conduct,” that is, conduct
“ ‘ “[having] the character of outrage frequently associated with
crime.” [Citation.]’ ” (American Airlines, Inc. v. Sheppard, Mullin,
Richter & Hampton (2002) 96 Cal.App.4th 1017, 1050.)
        In Shade Foods, the court noted “[a] record that presents a
close case with regard to the sufficiency of the evidence of bad faith
will inevitably provide a tenuous basis for supporting an award of
punitive damages, since both the bad faith and punitive damage
findings rest on inferences to be drawn from the same evidence.”
(Shade Foods, supra, 78 Cal.App.4th at p. 893.) Similar reasoning



                                 60
applies here, since the failure to warn and punitive damages
findings both rested on inferences to be drawn from the same
evidence about the strength of the causal connection between talc
and ovarian cancer, what JJCI knew about the risks of perineal talc
use, when it obtained such knowledge, and what its legal
responsibilities were with the information available. As in Shade
Foods, while we have concluded there was sufficient evidence to
support the jury’s finding that JJCI breached its duty to warn of the
risks of perineal talc use, we do not take the further step of
upholding the jury’s finding that JJCI acted with malice. (Ibid.)
There was no substantial evidence to support a finding, by clear and
convincing evidence, of despicable conduct which JJCI carried out
with a willful and conscious disregard of the safety of others. (Civ.
Code, § 3294, subd. (c).)
II.    The Trial Court Did Not Abuse Its Discretion
       in Granting JJCI’s Motion for New Trial
       The trial court granted defendants’ motion for new trial on
the grounds of insufficiency of the evidence (Code Civ. Proc.,
§ 657(6)), errors in law (id., § 657(7)), jury misconduct (id., § 657(2)),
and excessive damages (id., § 657(5).) Echeverria contends the trial
court erred as to each ground. We find no abuse of discretion in the
trial court order granting the new trial motion on the ground of
insufficiency of the evidence.
       A.    Standard of Review
       In her appellate briefing, Echeverria largely asserts the
JNOV and new trial order must be reversed for the same reasons.
Although we have concluded the JNOV in favor of JJCI as to
liability must be reversed because there was substantial evidence to
support the jury’s verdict, we apply a different standard of review
when considering the trial court’s order granting a new trial. The
California Supreme Court explained the differing standards in Lane



                                   61
v. Hughes Aircraft Co. (2000) 22 Cal.4th 405 (Lane). In Lane, the
trial court granted JNOV and, alternatively, a motion for new trial
based on insufficiency of the evidence. The new trial order cross-
referenced findings the trial court made in granting the JNOV. (Id.
at p. 413.) The appellate court reversed the JNOV, finding
substantial evidence supported the verdict. The court then
determined it did not need to consider whether the evidentiary
record supported the new trial order since it had analyzed whether
sufficient evidence supported the verdicts with respect to the JNOV.
(Id. at p. 411.) Our high court held the appellate court erred in
applying the same standard when reviewing the JNOV and new
trial order. (Id. at pp. 415-416.)
       As the Lane court explained, “an order granting a new trial
under [Code of Civil Procedure] section 657 ‘must be sustained on
appeal unless the opposing party demonstrates that no reasonable
finder of fact could have found for the movant on [the trial court’s]
theory.’ [Citation.] Moreover, ‘[a]n abuse of discretion cannot be
found in cases in which the evidence is in conflict and a verdict for
the moving party could have been reached . . . .’ [Citation.] In other
words, ‘the presumption of correctness normally accorded on appeal
to the jury’s verdict is replaced by a presumption in favor of the
[new trial] order.’ [Citation.]” (Lane, supra, 22 Cal.4th at p. 412.)
Since the evidence in Lane could have supported a defense verdict,
the appellate court erred in reversing the new trial order.
       This case presents similar procedural circumstances. Thus,
although we have determined the JNOV in favor of JJCI as to
liability must be reversed, we separately analyze the new trial
order. “We defer to the trial court’s resolution of conflicts in the
evidence if the decision is supported by substantial evidence and
reverse only if there is no reasonable basis for the court’s decision or
the decision is based on a legal error. [Citations.] [¶] An order



                                  62
granting a new trial ‘will not be disturbed unless a manifest and
unmistakable abuse of discretion clearly appears. . . . So long as a
reasonable or even fairly debatable justification under the law is
shown for the order granting the new trial, the order will not be set
aside.’ [Citation.]” (Bell v. Bayerische Motoren Werke
Aktiengesellschaft (2010) 181 Cal.App.4th 1108, 1122.)
      B.     Discussion
      In granting the motion for new trial on the ground of
insufficient evidence, the trial court concluded that, “[s]itting as the
thirteenth juror, the Court is of the firm conclusion that the
evidence of specific causation is not sufficient to support the verdict,
for the reasons set forth above respecting the JNOV . . . and for the
additional reason that Yessaian did not consider all available
epidemiology and apply it to the facts relative to Echeverria except
when it favored Echeverria.” The court found evidence of both
specific and general causation was “lacking,” citing the “lack of
anything other than a hypothesis about causation and the nature of
the epidemiological evidence presented . . . .”
      We find no abuse of discretion. We reject Echeverria’s
argument that the court made legal errors that require reversal of
both the order granting JNOV in favor of JJCI and the order
granting a new trial. In our view, the trial court’s ruling granting
JNOV to JJCI as to liability must be reversed because the trial
court weighed the evidence and made credibility determinations
when rejecting and evaluating aspects of Yessaian’s testimony. In
ruling on the new trial motion, however, the court was permitted to
assess the credibility of witnesses, weigh the evidence, and draw
inferences from the evidence different from those the jury may have
drawn. (Licudine v. Cedars-Sinai Medical Center (2016)
3 Cal.App.5th 881, 900; Fountain Valley Chateau Blanc




                                  63
Homeowner’s Assn. v. Department of Veterans Affairs (1998) 67
Cal.App.4th 743, 751.)
       The causation evidence was in significant conflict. For every
plaintiff’s expert, there was a defense expert who offered opposing
testimony, based on his or her own significant experience and
review of the same or similar evidence and scientific literature.
With respect to specific causation, the trial court found Yessaian
“cherry picked” the studies without sufficient justification and the
weight of the epidemiological evidence undermined her opinion.
There was evidence to support this finding, namely, the testimony
of defense experts Weed and Saenz, whose evaluation of the
epidemiology conflicted with that of Yessaian. Although Yessaian
did not rely on epidemiological studies alone, they remained an
important basis of her opinion.
       The trial court also found there was no evidence of
inflammation present in Echeverria’s tissue, rejecting Godleski’s
testimony and inferences that could be drawn from it. While we
have concluded a trier of fact could credit Godleski’s opinion that he
observed a chronic inflammatory process in Echeverria’s tissues, a
reasonable trier of fact could equally have determined defense
expert Felix’s testimony was the more credible. Based on his
examination of Echeverria’s tissue slides, Felix opined he saw no
evidence of cancer-causing inflammation and, had it been present, it
would have been easy to find.
       A reasonable jury could have given more weight to the
defense interpretations of the epidemiology, rejected Yessaian’s
interpretation of the literature as overly narrow or biased,
questioned Godleski’s testimony and credited Felix’s testimony, and
concluded the evidence did not sufficiently establish talc was a
substantial factor in causing Echeverria’s cancer.




                                 64
       The evidence also supported the trial court’s reasoning on
general causation. While Plunkett offered an opinion that talc
causes ovarian cancer, a reasonable trier of fact would have been
entitled to discredit or reject her testimony, in view of the
limitations and critiques of several studies she relied upon. The
weaknesses in the studies and her opinion were highlighted in her
own testimony on cross-examination, and brought out in Andersen’s
and Weed’s testimony. Weed also testified the available
epidemiological and other scientific evidence did not support the
conclusion that talc causes ovarian cancer. He, too, applied the Hill
criteria and found the evidence did not support the factors
sufficiently to state the “weak” statistical association between talc
and ovarian cancer reflects a causal relationship.
       Despite the conclusive nature of Plunkett’s ultimate opinion,
other evidence indicated no governmental or scientific agency has
reached similar conclusions, and medical institutions have not
uniformly taken steps to identify genital talc use as even a risk
factor for ovarian cancer. Indeed, there was evidence that a 2017
National Cancer Institute physician data query concluded the
weight of the evidence did not support an association between
perineal talc use and ovarian cancer.
       The evidence at trial would have supported a verdict in JJCI’s
favor. The trial court did not abuse its discretion in granting the
motion for new trial on the ground of insufficiency of the evidence.
(McFarland v. Voorheis-Trindle Co. (1959) 52 Cal.2d 698, 707.) We
need not address the additional grounds on which the trial court
granted the motion.




                                 65
                           DISPOSITION
        The judgment and the trial court order granting Johnson &
Johnson judgment notwithstanding the verdict are affirmed. The
portions of the court’s judgment and order granting JJCI judgment
notwithstanding the verdict as to punitive damages are affirmed.
The portions of the judgment and order granting JJCI judgment
notwithstanding the verdict as to liability are reversed. The trial
court’s order granting a new trial to JJCI is affirmed. The matter is
remanded for further proceedings consistent with this opinion. The
parties shall bear their own costs on appeal.

      CERTIFIED FOR PUBLICATION.




                                                 ADAMS, J.*
We concur:




      LAVIN, Acting P.J.




      EGERTON, J.




*     Judge of the Los Angeles Superior Court, assigned by the
Chief Justice pursuant to article VI, section 6 of the California
Constitution.


                                 66
