Court Opinion

ID: 9915191
Source: CourtListenerOpinion
Date Created: 2024-01-04 20:02:22.996299+00
Date Added: 2024-06-11T13:18:20.878896
License: Public Domain

Filed 1/4/24
                        CERTIFIED FOR PUBLICATION

               COURT OF APPEAL, FOURTH APPELLATE DISTRICT

                                    DIVISION ONE

                            STATE OF CALIFORNIA

 GARY GARNER, as Personal                    D082229
 Representative, etc.,

         Plaintiff and Appellant,
                                             (Super. Ct. No. CIVDS1720288)
         v.

 BNSF RAILWAY COMPANY,

         Defendant and Respondent.

       APPEAL from orders and judgment of the Superior Court of San
Bernardino County, Lynn M. Poncin and John Nguyen, Judges. Reversed
and remanded.
       The Yarnall Firm and Delores A. Yarnall, for Plaintiff and Appellant.
       Pacific Employment Law, Joseph P. Mascovich; Lewis Brisbois
Bisgaard & Smith, Anthony E. Sonnett, V. Alan Arshansky; Sims Law Firm
and Selim Mounedji, for Defendant and Respondent.
       Plaintiff Gary Garner appeals from a judgment entered against him
after the trial court granted BNSF Railway Company’s (BNSF) motions in
limine to exclude his causation experts, which resulted in the dismissal of his
wrongful death lawsuit before trial. Gary1 alleged that during the more than
four decades his father Melvin Garner spent working for BNSF, Melvin was
continuously exposed to toxic levels of diesel exhaust and its chemical
constituents. According to Gary, this exposure was a cause of Melvin’s non-
Hodgkin’s lymphoma, which Melvin developed after retiring from BNSF and
which led to his death in 2014. Gary retained several experts to perform a
cancer risk assessment and opine on whether diesel exhaust and its
constituents are capable of causing cancer, including non-Hodgkin’s
lymphoma, and whether Melvin’s workplace exposure to diesel exhaust in
this case was in fact a cause of his cancer. At the outset of trial, however, the
trial court granted BNSF’s motions in limine to exclude Gary’s three
causation experts from trial, finding that the science the experts relied on
was inadequate and there was too great an analytical gap between the data
and their opinions. The trial court then entered judgment in favor of BNSF
and dismissed the case.
      Because the court’s in limine rulings resulted in the equivalent of a
nonsuit, we conduct an independent review of the record to determine
whether BNSF’s motions were properly granted. We conclude that the trial
court erred in excluding Gary’s experts and therefore reverse the orders and
judgment with instructions to the trial court to enter new orders denying
BNSF’s motions in limine.
              FACTUAL AND PROCEDURAL BACKGROUND
A. Decedent’s Background
      Decedent Melvin Garner worked for BNSF as a trainman, a general
term that covers several positions, from approximately 1957 to 1999. Melvin

1     We refer to Gary and his father Melvin Garner by their first names to
avoid confusion.
                                        2
worked as a fireman from 1957 to 1964, an engineer for four months in 1964,
again as a fireman from 1965 to 1972, and again as an engineer from 1972
until his retirement in 1999. As a trainman, Melvin operated locomotives in
and outside of BNSF railyards in New Mexico, Arizona, and California.
      In October 2014, Melvin was diagnosed with non-Hodgkin’s lymphoma,
a type of blood cancer. He died on October 18, 2014.
B. Complaint
      In October 2017, Melvin’s son, Gary Garner, filed this survival and
wrongful death action against BNSF, alleging violation of the Federal
Employers’ Liability Act (45 U.S.C. § 51, et seq.) (FELA). Gary alleged that
Melvin’s non-Hodgkin’s lymphoma was caused by his occupational exposure
to various toxic substances and carcinogens, including diesel exhaust,
benzene, rock dust from railroad track ballast, asbestos fibers, and creosote.
BNSF answered the complaint, generally denying Gary’s allegations and
asserting several affirmative defenses.
C. BNSF’s Motion for Summary Judgment
      In December 2019, BNSF moved for summary judgment on two
grounds: (1) the FELA’s three-year statute of limitations barred Gary’s
action; and (2) Melvin’s alleged exposure to various substances did not cause
his non-Hodgkin’s lymphoma. On the latter ground, BNSF relied on a
declaration by their expert Dr. Peter Shields, who summarized his review of
all the available medical literature relevant to the causation allegations and
opined that none of the substances identified in Gary’s complaint have been
causally linked to the development of non-Hodgkin’s lymphoma.
      Gary opposed. He submitted declarations from three expert witnesses,
Dr. Andrew Salmon, Dr. Joseph Landolph and Dr. Robert Gale, whose
depositions had not yet been taken in support of his causation argument.

                                       3
Collectively, these experts opined that the substances listed in the complaint
can cause non-Hodgkin’s lymphoma and more probably than not were a cause
of Melvin’s non-Hodgkin’s lymphoma.
      At the summary judgment hearing, the trial court indicated that it
would tentatively deny BNSF’s motion, finding that the question of whether
“exposures to the kinds of chemicals and other substances that [Melvin] was
subjected to” can and did cause his non-Hodgkin’s lymphoma was an issue for
the jury. The parties presented additional argument regarding the issue of
causation, and the trial court then stated that it would follow its tentative
ruling, explaining: “I think these are triable issues of fact. And the
arguments that Defendant has made essentially can be made to the jury
going to the weight of the expert testimony.” In August 2020, the trial court
denied BNSF’s motion.
D. Motions in Limine
      After the court’s denial of BNSF’s summary judgment motion, the
parties engaged in expert discovery in February and March 2021. The
parties also began filing and opposing motions in limine in March 2021 in
accord with the then-scheduled trial date.
      In March 2021, both parties filed several motions in limine in
anticipation of trial. In May 2021, the case was sent to another department
for trial purposes, and trial was ultimately continued to September 2021.
The trial court heard argument on the parties’ in limine motions on
September 7 and 8, 2021.
      1. Motion in Limine No. 4 to Exclude Expert Opinion of Dr. Rosenfeld
      BNSF’s motion in limine number four moved to exclude Dr. Rosenfeld’s
opinions that (1) while working for BNSF, Melvin was exposed to significant
levels of diesel exhaust and its constituents that substantially increased his

                                       4
risk of developing non-Hodgkin’s lymphoma, and (2) BNSF failed to provide
Melvin with a reasonably safe place to work. On appeal, Gary states that the
trial court, by minute order and “without explanation,” granted this motion
along with the others excluding his causation experts, and he asks us to
reverse the trial court’s decision. However, BNSF claims the court did not
decide the issue.
        Although Gary correctly points out that the court’s September 7, 2021
minute order states that motion in limine number four was granted, this
appears to be a mistake. The minute order also states that defense counsel

requested an Evidence Code section 4022 hearing to determine preliminary
facts regarding admissibility, which the court granted, and the reporter’s
transcript shows that the court stated as follows: “The tentative is still to
deny the motion in limine [number four] and allow Dr. Rosenfeld to testify
based on the Los Altos case the Court cited, but I will grant the request for a
402 hearing for Dr. Rosenfeld.” The court never actually held the 402
hearing, however, and never issued a final ruling on motion in limine number
four.
        Where a conflict exists between the court’s statements in the reporter’s
transcript and the minute order, “we presume the reporter’s transcript is the
more accurate.” (In re A.C. (2011) 197 Cal.App.4th 796, 800–801; see also
Arlena M. v. Superior Court (2004) 121 Cal.App.4th 566, 569–570 [where the
minute order reflects something not contained in the reporter’s transcript,
“the reporter’s transcript generally prevails as the official record of
proceedings”].) We thus agree with BNSF that the trial court did not grant
its motion in limine to exclude Dr. Rosenfeld, and we do not address Gary’s
arguments as to his opinions.

2       All undesignated statutory references are to the Evidence Code.
                                        5
      2. Motion in Limine No. 7 to Exclude Expert Opinion of Dr. Salmon
      BNSF’s motion in limine number seven moved to exclude Dr. Salmon’s
opinions that: (1) Melvin’s exposure to diesel exhaust during his work at
BNSF substantially increased his risk of developing non-Hodgkin’s
lymphoma; and (2) Melvin’s exposure to diesel exhaust during his work at
BNSF was more likely than not a cause of his non-Hodgkin’s lymphoma.
BNSF argued that Dr. Salmon had no evidence linking exposure to diesel
exhaust with non-Hodgkin’s lymphoma, and that he improperly relied on
evidence suggesting a link between diesel exhaust and lung cancer to
extrapolate and form his opinion that exposure to diesel exhaust must
therefore also be linked to other kinds of cancer, including non-Hodgkin’s
lymphoma. In support of its motion, BNSF attached as exhibits Dr. Salmon’s
expert report and a handful of excerpts from his deposition. BNSF did not
submit any declarations, deposition testimony, or documentation from
Dr. Shields, on whom it had relied when seeking summary judgment, or any
other experts, nor did it include any scientific studies or journal articles with
the motion.
      Dr. Salmon’s report explained that his prediction for Melvin’s
“additional risk of cancer which he experienced as a result of these
exposures” to diesel exhaust—which was “substantial” at between 2864 and
3875 excess cancers per million people—was for “overall cancer incidence, not
confined to any particular site of tumor formation.” At deposition,
Dr. Salmon described his methodology by stating that “the risk estimate is
designed to provide an estimate as the overall risk of cancer and it doesn’t
specify that that risk be confined exclusively to the lung cancer site or other
specific sites that have been measured and considered in the risk
assessment.” According to BNSF, because Dr. Salmon could not limit the

                                        6
excess cancer risk to non-Hodgkin’s lymphoma, his opinions are not specific
to Melvin and are thus pure speculation.
      BNSF asserted that because Dr. Salmon conceded he did not rely on
any study finding that diesel exhaust causes non-Hodgkin’s lymphoma, his
opinions were irrelevant and speculative, as they were unconnected to the
data on which he purported to rely.
      Gary opposed the motion, arguing that BNSF failed to cite any
literature requiring a methodology focused solely on the cancer site at issue.
Gary argued that Dr. Salmon had explained in his report and at deposition
why an excess cancer risk calculation can properly be based on a method
looking at any organ site rather than focusing on the organ site at issue.
Dr. Salmon testified that “for chemicals that induce tumors at multiple sites,
the single-site approach may underestimate the true carcinogenic potential,”
so “a statistical procedure may be used to estimate an overall potency”—a
methodology taken directly from the Office of Environmental Health Hazard
Assessment (OEHHA) of the California Environmental Protection Agency
(EPA). Gary also argued that Dr. Salmon’s opinions were supported by the
opinions of expert Dr. Joseph Landolph, whose report explained that because
of the way diesel exhaust and many of its chemical constituents directly act
on DNA and cause genetic mutations, the effects of diesel exhaust are not
just limited to one organ in the body.
      Gary further argued that Dr. Salmon relied on credible literature
providing a reasonable basis for his specific causation opinion, and that he
was not required to point to a study conclusively finding that non-Hodgkin’s
lymphoma is caused by diesel exhaust. According to Gary, epidemiological
literature only establishes statistical associations between agents and various
diseases—it does not provide conclusions regarding whether a particular

                                         7
agent causes a particular disease. Gary stated that epidemiology involves
observational data and associations expressed as a statistic, rather than
proving causation, which is expressed as a judgment based on the weight of
the evidence.
      3. Motion in Limine No. 8 to Exclude Expert Opinion of Dr. Gale
      BNSF’s motion in limine number eight moved to exclude Dr. Gale’s
opinions that: (1) diesel exhaust and its particulates benzene, dioxin, and
formaldehyde are a cause of non-Hodgkin’s lymphoma in humans; and (2) it
is more likely than not, to a reasonable degree of medical probability, that
Melvin’s exposure to benzene, dioxin and formaldehyde via his exposure to
diesel exhaust was a cause of his non-Hodgkin’s lymphoma. BNSF argued
that although Dr. Gale acknowledged that a “dose” is necessary to calculate
an excess cancer rate, he did not and could not give an opinion regarding the
dose necessary to cause non-Hodgkin’s lymphoma. According to BNSF, this
rendered Dr. Gale’s opinions speculative. In support of its motion, BNSF
attached Dr. Gale’s expert report, 29 pages of testimony from his deposition,
and the opinion from a District of Nebraska case. BNSF again did not submit
any declarations, deposition testimony, or documentation from its own
experts, nor did it attach any scientific studies or journal articles to the
motion.
      Gary argued in opposition that BNSF’s demand for a specific number
reflecting the minimum dose necessary to causally connect diesel exhaust
exposure with non-Hodgkin’s lymphoma was neither scientifically sound nor
legally required. According to Gary, the linear no-threshold dose response
model, which Dr. Gale used, is well-established and a widely accepted method
for modeling cancer risk.

                                        8
      Gary claimed that BNSF was confusing the issue, as the relevant
question is not what dose is necessary to cause cancer, but rather whether
there is evidence of exposure to a dose that sufficiently increases the risk of
cancer such that the exposure was, more likely than not, a cause of the
cancer. Gary also argued that his experts presented a specific dose (“between
2864 and 3875 excess cancers per million persons exposed to that dose”) that
is more than trivial through the excess cancer risk calculation performed by
Dr. Salmon, which Dr. Gale relied on to support his causation opinion.
      4. Motion in Limine No. 9 to Exclude Expert Opinion of Dr. Landolph
      BNSF’s motion in limine number nine asked the court to exclude

Dr. Landolph’s general causation3 opinion that exposure to diesel exhaust
and its constituents can cause non-Hodgkin’s lymphoma. BNSF argued that
because Dr. Landolph did not rely on any study that finds that diesel exhaust
exposure causes non-Hodgkin’s lymphoma, has not published any literature
related to non-Hodgkin’s lymphoma, and has no personal knowledge of how
often Melvin would have been exposed to diesel exhaust and/or its
constituents, his opinion was speculative and must be excluded. In support
of its motion, BNSF attached Dr. Landolph’s expert report, 40 pages of
testimony from his deposition, and the same case it attached to its motion
seeking to exclude Dr. Gale. BNSF again did not submit any declarations,
deposition testimony, or documentation from its own experts, nor did it
attach any scientific studies or journal articles.

3     “General causation” refers to whether a substance is capable of causing
a particular injury or condition in the general population. “Specific
causation” refers to whether the substance caused a particular individual’s
injury or condition. (Knight v. Kirby Inland Marine Inc. (5th Cir. 2007) 482
F.3d 347, 351.)
                                        9
      BNSF also argued that Dr. Landolph’s opinion was speculative
because, like Dr. Gale, he could not pinpoint the dose necessary to cause non-
Hodgkin’s lymphoma. Dr. Landolph conceded that the general population is
exposed to diesel exhaust and its constituents in the background, but not
every individual in the general population develops non-Hodgkin’s lymphoma
as a result of that exposure. Therefore, BNSF argued, his failure to provide a
specific dose of diesel exhaust needed to cause non-Hodgkin’s lymphoma
rendered his opinion speculative.
      Gary responded that BNSF had ignored a key aspect of Dr. Landolph’s
analysis, which explained that diesel exhaust and its constituents are
mutagenic, multi-organ carcinogens, meaning that analysis of cancer at one

organ site is relevant to analysis of cancers at other sites.4 Gary also pointed
to the fact that Dr. Landolph relied on numerous publications showing that
diesel exhaust and its constituents are known human carcinogens and can
induce non-Hodgkin’s lymphoma to support his causation opinion.
      Gary further argued that, like Dr. Gale, Dr. Landolph was not required
to determine the specific dose of Melvin’s toxic exposure to diesel exhaust to
support his causation opinion. According to Gary, it is sufficient that
Dr. Landolph relied on a specific, non-trivial, calculated dose of exposure to
diesel exhaust described by Dr. Salmon as “substantial,” which was at least
3,000 times higher than de minimis. Dr. Landolph then used that dose and

4      According to Merriam-Webster Online Dictionary, “mutagenic” is
defined as “inducing or capable of inducing genetic mutation.” (Merriam-
Webster Online Dictionary (2023) <https://www.merriam-
webster.com/medical/mutagenic> [as of Dec. 26, 2023], archived at
<https://perma.cc/D657-VQ5V>.) In his expert report, Dr. Landolph describes
a “mutagenic” constituent as one that “act[s] directly on DNA, causing
mutations.” Dr. Salmon defines the term in his expert report as meaning
“affecting DNA.”
                                       10
excess cancer risk to conclude that diesel exhaust and its constituents,
particularly benzene, dioxin, and formaldehyde, are capable of causing many
different types of tumors in humans exposed to it, including non-Hodgkin’s
lymphoma. Gary argued that because there is no requirement that a plaintiff
must show that a specific dose is required before exposure to a substance is
harmful or causes the injury alleged, and Gary’s experts demonstrated in any
event that Melvin’s exposure was non-trivial, Dr. Landolph’s opinions could
not be excluded on that basis.
      5. Trial Court Ruling on BNSF’s Motions in Limine
      The trial court held two days of argument on the parties’ motions in
limine. On the first day, the court stated that its tentative ruling was to deny
each of BNSF’s motions that sought to exclude two of Gary’s experts,
Dr. Rosenfeld and Dr. Salmon. The court did, however, grant BNSF’s request
to hold a section 402 hearing for Dr. Rosenfeld, though it reiterated that its
tentative ruling was to allow Dr. Rosenfeld to testify at trial. The parties
argued the issue of causation extensively, focusing in particular on
Dr. Salmon’s causation opinions, but also discussing Dr. Gale and
Dr. Landolph.
      The following day, the trial court announced that it intended to reverse
its tentative ruling on the motion to exclude Dr. Salmon’s opinions, stating:
“[T]his Court is finding that the science relied upon by Dr. Salmon is
inadequate. There is no data, no study, and no testing linking non-Hodgkin’s
lymphoma and exposure to diesel exhaust. The Court is further finding that,
as stated in Sargon, there is simply too great an analytical gap between the
data and the opinion proffered by Dr. Salmon. Therefore, the Court reverses
the tentative and grants the defendant’s motion in limine Number 7 to
exclude the opinions of Dr. Salmon on liability and causation.”

                                       11
      The trial court also stated that its tentative rulings as to the motions
seeking to exclude Dr. Gale and Dr. Landolph would follow its ruling on
Dr. Salmon’s opinions, finding that “[t]here is a gap in the analytical data to
support the conclusions that diesel exhaust exposure is a causal link or a
causal connection to non-Hodgkin’s lymphoma.” The parties then presented
additional argument on those motions. After argument concluded, the court
granted BNSF’s motions, stating: “[I]n looking at the documents presented,
it does not seem that there is enough data for the experts to draw their
conclusion much less the Court’s [sic] -- with Dr. Salmon, there is an
analytical gap that causes the Court to grant the motions in limine to
preclude the . . . opinion of Dr. Gale on liability and causation as set forth in
the defense motion in limine Number 8 as well as the defense motion in
limine Number 9 which the Court will grant . . . excluding certain opinions of
Dr. Landol[ph] on causation.”
      The court then stated that it would sign the proposed orders from
BNSF and set a control date for dismissal to be submitted by the defense.
The appellate record contains signed orders granting BNSF’s motions in
limine numbers three, five, six, seven, eight, nine, ten, and eleven.
E. Judgment and Dismissal
      After the trial court granted BNSF’s motions in limine numbers seven,
eight, and nine, Gary had no expert witness who could establish a causal
connection between BNSF’s conduct and Melvin’s injury. On November 5,
2021, Gary filed a notice of appeal from the orders, explaining that they
operated as a nonsuit but did not expressly dismiss the case and
acknowledging the appeal may be premature because no judgment had yet
been entered.

                                        12
      On November 10, 2021, the trial court executed and filed judgment in
favor of BNSF and dismissed the case. We exercise our discretion to construe
Gary’s November 5 notice of appeal as being taken from the November 10
judgment. (See Cal. Rules of Court, rule 8.104(d).)
                                 DISCUSSION
A. Standard of Review
      The parties dispute which standard of review applies to the trial court’s
orders granting BNSF’s motions in limine to exclude Gary’s experts from
trial. BNSF argues that, under Sargon Enterprises v. University of Southern
California (2012) 55 Cal.4th 747 (Sargon), the abuse of discretion standard of
review applies to any evidentiary ruling regarding admissibility of an expert
opinion. BNSF emphasizes the Court’s language stating that, “[e]xcept to the
extent the trial court bases its ruling on a conclusion of law (which we review
de novo), we review its ruling excluding or admitting expert testimony for
abuse of discretion.” (Sargon, at p. 773.)
      Gary, on the other hand, contends that because the trial court’s in
limine rulings acted as a nonsuit or summary judgment motion, de novo
review applies. He agrees that rulings on expert testimony and motions in
limine are generally reviewed for abuse of discretion, but he points to Court
of Appeal decisions concluding that this standard does not apply where
granting the motion in limine results in dismissal of the cause of action (or
entire case) before trial. (See, e.g., McMillin Companies, LLC v. American
Safety Indemnity Co. (2015) 233 Cal.App.4th 518, 529 [abuse of discretion
“standard does not apply where (as here) the grant of the motion becomes a
substitute for a summary adjudication or nonsuit motion”].)
      We agree with Gary. California courts regularly conclude that “if the
trial court’s ruling on a motion in limine precludes an entire cause of action,

                                       13
the ruling is subject to independent review on appeal as though the court had
granted a motion for nonsuit.” (Kinda v. Carpenter (2016) 247 Cal.App.4th
1268, 1279–1280; see also Legendary Investors Group No. 1, LLC v. Niemann
(2014) 224 Cal.App.4th 1407, 1411 [“When a motion in limine ‘results in the
entire elimination of a cause of action or a defense, we treat it as a demurrer
to the evidence and review the motion de novo. . . .’ ”]; City of Livermore v.
Baca (2012) 205 Cal.App.4th 1460, 1465 (Baca) [“When, as in the present
case, the court’s order excludes all evidence on a particular claim and, as a
result, operates as a motion for nonsuit, we review the court’s order de
novo . . . .”]; Dillingham–Ray Wilson v. City of Los Angeles (2010) 182
Cal.App.4th 1396, 1402 [“When all evidence on a particular claim is excluded
based on a motion in limine, the ruling is subject to independent review as
though the trial court had granted a motion for judgment on the pleadings or,
if evidence was offered, a motion for nonsuit.”]; Fergus v. Songer (2007) 150
Cal.App.4th 552, 569–570 (Fergus) [“Where, as here, the granting of a motion
in limine disposes of one or more causes of action, it is the functional
equivalent of the granting of a nonsuit as to those causes of action.”].)
      Here, the trial court’s grant of BNSF’s motions in limine at the outset
of trial acted as the “functional equivalent” of an order granting nonsuit,
which is subject to de novo review. (See Fergus, supra, 150 Cal.App.4th at
p. 569; Edwards v. Centex Real Estate Corp. (1997) 53 Cal.App.4th 15, 27.)
The rulings deprived Gary of essential evidence on causation, resulting in a
judgment of dismissal before trial. And unlike in Sargon, where the trial
court had conducted an eight-day evidentiary hearing on the motion to
exclude the expert witness (Sargon, supra, 55 Cal.4th at p. 755), the trial
court here decided the issue solely on the papers. Though not dispositive,
this also weighs in favor of de novo review because the trial court did not

                                       14
observe any witnesses testify in court, and we are in the “ ‘same position’ ” as
the trial court “when reviewing a cold record.” (People v. Vivar (2021) 11

Cal.5th 510, 528 [adopting independent review standard].)5
      Where the trial court’s ruling operates as a nonsuit and we review the
order de novo, “ ‘all inferences and conflicts in the evidence must be viewed
most favorably to the nonmoving party.’ ” (Baca, supra, 205 Cal.App.4th at
p. 1465.) In such circumstances, we resolve all presumptions, inferences, and
doubts in the appellant’s favor, “and uphold the judgment for
respondent . . . only if it was required as a matter of law.” (Fergus, supra,
150 Cal.App.4th at pp. 569–570.)
B. Legal Principles
      1. The Trial Court’s Gatekeeping Role
      Under California law, the trial court has the duty to act as a
“gatekeeper” in determining whether to exclude expert testimony from trial.
(Sargon, supra, 55 Cal.4th at pp. 753, 770.) In carrying out its gatekeeping
function, the court is governed by sections 801 and 802.
      Section 801 provides: “If a witness is testifying as an expert, his
testimony in the form of an opinion is limited to such an opinion as is: [¶]
(a) Related to a subject that is sufficiently beyond common experience that
the opinion of an expert would assist the trier of fact; and [¶] (b) Based on
matter . . . that is of a type that reasonably may be relied upon by an expert
in forming an opinion upon the subject to which his testimony relates, unless
an expert is precluded by law from using such matter as a basis for his

5      As we will explain, the trial court’s ruling was also based on a
misunderstanding of the law under Sargon. We would thus find reversible
error even applying the abuse of discretion standard. (Hernandez v. Amcord,
Inc. (2013) 215 Cal.App.4th 659, 678 [“evidentiary rulings which are based on
a misunderstanding of the law are an abuse of discretion”].)
                                       15
opinion.” Under section 801, therefore, the trial court must exclude
speculative or irrelevant expert opinion. (Sargon, supra, 55 Cal.4th at
p. 770.)
      Section 802, which also governs the trial court’s gatekeeping role,
provides: “A witness testifying in the form of an opinion may state . . . the
reasons for his opinion and the matter . . . upon which it is based, unless he is
precluded by law from using such reasons or matter as a basis for his opinion.
The court in its discretion may require that a witness before testifying in the
form of an opinion be first examined concerning the matter upon which his
opinion is based.” This section thus permits the court to inquire as to the
reasons for an expert’s opinion and whether the material upon which the
expert relies actually supports the expert’s reasoning. (Sargon, supra,
55 Cal.4th at p. 771.) “ ‘A court may conclude that there is simply too great
an analytical gap between the data and the opinion proffered.’ ” (Ibid., citing
GE v. Joiner (1997) 522 U.S. 136, 146 (Joiner).)
      In short, “section 801 governs judicial review of the type of matter”
relied on by the expert, while “section 802 governs judicial review of the
reasons for the opinion.” (Sargon, supra, 55 Cal.4th at p. 771; see §§ 801,
subd. (b), 802.) The Supreme Court has therefore explained that, under these
sections, “the trial court acts as a gatekeeper to exclude expert opinion
testimony that is (1) based on matter of a type on which an expert may not
reasonably rely, (2) based on reasons unsupported by the material on which
the expert relies, or (3) speculative.” (Sargon, at pp. 771–772; see §§ 801,
subd. (b), 802.)
      The Court has warned, however, that trial courts must “be cautious in
excluding expert testimony. The trial court’s gatekeeping role does not
involve choosing between competing expert opinions.” (Sargon, supra, 55

                                       16
Cal.4th at p. 772.) “[T]he gatekeeper’s focus ‘must be solely on principles and
methodology, not on the conclusions that they generate.’ ” (Ibid.) Nor should
the court determine the persuasiveness of an expert’s opinion, weigh the
opinion’s probative value, substitute its own opinion for the expert’s opinion,
or resolve scientific controversies. (Ibid.) Rather, the goal “is simply to
exclude ‘clearly invalid and unreliable’ expert opinion.” (Ibid.)
      2. Liability Under FELA
      In FELA actions, railroad employees (or their representatives) seeking
to recover for on-the-job injuries have the right to sue their employer for any
injury “ ‘resulting in whole or in part from the negligence’ of the railroad or
its employees.” (Fair v. BNSF Railway Co. (2015) 238 Cal.App.4th 269, 275
(Fair), quoting Woods v. Union Pacific Railroad Co. (2008) 162 Cal.App.4th
571, 577.) “The standard under FELA is a relaxed one,” and it is well
established that the “evidence required to establish liability in an FELA case
is much less than in an ordinary negligence action.” (Fair, at p. 275.) The
employer is liable where its negligence “played any part, however small, in
the injury or death” at issue. (Rogers v. Missouri Pac. R.R. Co. (1957) 352
U.S. 500, 507–508 (Rogers).) In interpreting FELA, the United States
Supreme Court “has insisted that plaintiffs have a broad primary right to go
to the jury on factual issues” and made clear that a plaintiff should “reach the
jury on the issue of liability when there is any evidence, ‘even the slightest,’ ”
to support his case. (Jehl v. Southern Pacific Co. (1967) 66 Cal.2d 821, 834,
quoting Rogers, at p. 506.)
      We now consider whether the trial court properly discharged its
gatekeeping responsibility here by excluding Gary’s causation experts from
trial and dismissing his FELA action.

                                        17
C. Analysis
      The trial court here found that there was “simply too great an
analytical gap between the data and the opinion[s] proffered by Dr. Salmon,”
Dr. Gale, and Dr. Landolph on liability and causation. The court identified
no other flaw in the methodology used by any of the experts. We address
each expert separately, though much of the underlying data and substance of
the experts’ opinions are overlapping.
      1. Dr. Salmon’s General Causation Opinion
      Dr. Salmon has 50 years of experience analyzing the carcinogenic effect
of toxic exposure in humans, including 31 years working for what is now the
OEHHA within the California EPA. He was retained in this case to provide
an estimate of the excess cancer risk Melvin experienced due to his
occupational exposure to diesel exhaust and its constituents, or diesel
particulate matter (DPM), and whether this excess risk is more likely than
not to have been a cause of his non-Hodgkin’s lymphoma. Dr. Salmon
calculated that someone with Melvin’s DPM exposure from their employment
with BNSF would have an estimated excess cancer risk between 2864 and
3875 excess cancers per million persons. He also opined that it was more
likely than not that Melvin’s diesel exhaust exposure was a cause of his
lymphoma.
      In calculating Melvin’s excess cancer risk, Dr. Salmon relied on
Melvin’s specific exposure information, air sampling data, air modeling
studies involving railway workers, and the DPM inhalation cancer potency
factor developed by OEHHA and the California Air Resources Board to
estimate Melvin’s dose of diesel exhaust over the course of the relevant
timeframe. In doing so, Dr. Salmon used standard methodology that does not
appear to be the subject of dispute here.

                                         18
      What is in dispute is whether it was appropriate for Dr. Salmon to
conclude that Melvin’s exposure was more likely than not a cause of his non-
Hodgkin’s lymphoma, despite being unable to point to any specific study
stating that exposure to diesel exhaust causes non-Hodgkin’s lymphoma. The
trial court concluded that it was not, finding that the science Dr. Salmon
relied on in reaching his opinion was “inadequate” because “[t]here is no data,
no study, and no testing linking non-Hodgkin’s lymphoma and exposure to
diesel exhaust.” The court further found that there was “too great an
analytical gap between the data” on which Dr. Salmon did rely and the
opinion he proffered. The trial court seems to have agreed with BNSF’s
argument below that Gary’s experts, including Dr. Salmon, were not
permitted to opine at trial that diesel exhaust and its constituents, more
likely than not, are a cause of non-Hodgkin’s lymphoma, because there are no
epidemiological or other scientific studies that have already stated that
conclusion.
      This ruling reflects a misunderstanding of the law. As Gary argues,
there is no requirement that a causation expert rely on a specific study or
other scientific publication expressing precisely the same conclusion at which
the expert has arrived. (Kennedy v. Collagen Corp. (9th Cir. 1998) 161 F.3d
1226, 1229 (Kennedy) [“it is scientifically permissible to reach a conclusion on
causation without [epidemiological or animal] studies” showing a causal
link]; Wendell v. GlaxoSmithKline LLC (9th Cir. 2017) 858 F.3d 1227, 1237
(Wendell) [“Perhaps in some cases there will be a plethora of peer reviewed
evidence that specifically shows causation. However, such literature is not
required in each and every case.”]; Turner v. Iowa Fire Equipment Co. (8th
Cir. 2000) 229 F.3d 1202, 1208–1209 [“ ‘we do not believe that a medical

                                       19
expert must always cite published studies on general causation in order to

reliably conclude that a particular object caused a particular illness’ ”].)6
      This makes sense for several reasons. First, “[p]ublication . . . is not
the sine qua non of admissibility; it does not necessarily correlate with
reliability [citation], and in some instances well-grounded but innovative
theories will not have been published. [Citation.] Some propositions,
moreover, are too particular, too new, or of too limited interest to be
published.” (Daubert v. Merrell Dow Pharms., Inc. (1993) 509 U.S. 579, 593
(Daubert); see also Primiano v. Cook (9th Cir. 2010) 598 F.3d 558, 565 [“Peer
reviewed scientific literature may be unavailable because the issue may be
too particular, new, or of insufficiently broad interest, to be in the
literature.”].) As Dr. Salmon explained, this is such a case because few
studies of the potential link between diesel exhaust and non-Hodgkin’s
lymphoma have been conducted. “ ‘The first several victims of a new toxic
tort should not be barred from having their day in court simply because the
medical literature, which will eventually show the connection between the
victims’ condition and the toxic substance, has not yet been completed.’ ”
(Wendell, supra, 858 F.3d at p. 1237.)
      Second, although “[e]pidemiology focuses on the question of general
causation,” it “cannot prove causation; rather, causation is a judgment for
epidemiologists and others interpreting the epidemiologic data.” (Green et
al., Reference Guide on Epidemiology, in Reference Manual on Scientific
Evidence (3d ed. 2011) 549, 552, 598.) Epidemiological studies merely
identify associations, which do not equate to causation. (See id. at pp. 551–

6     Because Sargon took its “analytical gap” language from the United
States Supreme Court’s decision in Joiner (Sargon, supra, 55 Cal.4th at
p. 771), we may consider post-Joiner federal authorities on the issue for their
persuasive value.
                                         20
553.) It is up to the expert to “bridge the gap between association and
causation” and make that informed judgment. (Kaye and Freedman,
Reference Guide on Statistics, in Reference Manual on Scientific Evidence
(3d ed. 2011) 211, 217–218 (Statistics); accord Amador v. 3M Co. (In re Bair
Hugger Forced Air Warming Devices Prods. Liab. Litig.) (8th Cir. 2021)
9 F.4th 768, 778–780 [concluding it was not unreliable for an expert to rely on
a study to draw an inference of causation even though the study found that
the association did not establish causation, “[s]o long as the expert does the
work ‘to bridge the gap between association and causation’ ”].)
      “Whether an inference of causation based on an association is
appropriate is a matter of informed judgment, not scientific
methodology . . . .” (Rest.3d Torts, § 28 (2010) (Restatement), com. (c),
subd. (3), p. 406; see also id. at subd. (1), p. 403 [“[A]n evaluation of data and
scientific evidence to determine whether an inference of causation is
appropriate requires judgment and interpretation.”]; Milward v. Acuity
Specialty Prods. Group, Inc. (1st Cir. 2011) 639 F.3d 11, 18–19 (Milward)
[same]; Statistics, supra, at p. 222 [“In the end, deciding whether associations
are causal typically is not a matter of statistics alone, but also rests on
scientific judgment.”].) And “scientific inference typically requires
consideration of numerous findings, which, when considered alone, may not
individually prove the contention. . . . In applying the scientific method,
scientists do not review each scientific study individually for whether by itself
it reliably supports the causal claim being advocated or opposed. Rather, as
the Institute of Medicine and National Research Council noted, ‘summing, or
synthesizing, data addressing different linkages [between kinds of data]
forms a more complete causal evidence model and can provide the biological
plausibility needed to establish the association’ being advocated or opposed.”

                                        21
(Berger, The Admissibility of Expert Testimony, in Reference Manual on
Scientific Evidence (3d ed. 2011) 11, 19–20; see also Milward, at pp. 17–19
[discussing use of scientific judgment applying “weight of the evidence”
approach for determining general causation].) It was therefore appropriate
for Gary’s experts to use their experience and judgment to interpret the
available epidemiological and other data they reviewed in reaching their
causation opinions.
      Finally, in many cases where the available scientific evidence is limited
or inconclusive, there will inevitably be some analytical gap between the
underlying data and the expert’s ultimate causation opinion. But Sargon
should not be construed so broadly that the gatekeeper effectively supplants
both the expert’s reasonable scientific judgment and the jury’s role. That
would be at odds with Sargon’s emphasis on the limited role of the
evidentiary gatekeeper. (Sargon, supra, 55 Cal.4th at p. 772.) In keeping the
gate, it is not the trial court’s proper function to second-guess the judgment of
a qualified expert who has provided a reasonable scientific explanation for his
conclusions and used a scientifically accepted methodology for reaching them
based on the available data, even if the data itself is inconclusive. “So long as
an expert’s testimony rests upon ‘good grounds, based on what is known’
[citation], it should be tested by the adversarial process, rather than excluded
for fear that jurors will not be able to handle the scientific complexities.”
(Milward, supra, 639 F.3d at p. 15, internal quotation marks omitted.)
      In reaching the opposite conclusion, the trial court took issue with
Dr. Salmon’s reliance on the overall excess cancer risk and his opinion that
such risk is relevant to determining the risk of non-Hodgkin’s lymphoma:
“The Court notes in this paragraph in Dr. Salmon’s conclusion that he uses
the word ‘cancer,’ not non-Hodgkin’s lymphoma. . . . [¶] . . . [¶] In this case,

                                        22
the decedent’s injury was non-Hodgkin’s lymphoma. Therefore, this Court is
finding that the science relied upon by Dr. Salmon is inadequate.”
      But Dr. Salmon explained that his overall cancer risk assessment was
appropriate because it necessarily included an analysis of the risk of
developing non-Hodgkin’s lymphoma—particularly given that “bone marrow
(the cellular origin of Mr. Garner’s Diffuse Large B Cell Lymphoma) is a
known human target site for both cancer and non-cancer effects of the of [sic]
several components of diesel exhaust, including (but not limited to) benzene,
dioxins, formaldehyde, butadiene and the polycyclic hydrocarbons, which are
suspected significant contributors to DPM’s carcinogenic effect.” (Cf.
Milward, supra, 639 F.3d at pp. 19–20 [expert relied on studies showing that
benzene can cause “significant chromosomal damage at the stem cell level in
the bone marrow”].) Dr. Salmon also testified at deposition that “for
chemicals that induce tumors at multiple sites, the single-site approach may
underestimate the true carcinogenic potential,” so “a statistical procedure
may be used to estimate an overall potency”—a methodology taken directly
from OEHHA. Dr. Salmon noted that diesel engine exhaust is classified as a
known human carcinogen by the State of California and the International
Agency for Research on Cancer (IARC). He further explained that the IARC
has described “several studies in which elevated risks of leukemias,
lymphomas and myelomas were found in workers exposed to diesel exhaust.”
Dr. Salmon cited several scientific publications in support of his opinions.
      Dr. Landolph agreed with Dr. Salmon, explaining in his report: “It is
well-established in science that diesel exhaust and many of its chemical
constituents act directly on DNA, causing mutations. Thus, diesel exhaust
can be referred to as a mutagenic, multi-organ carcinogen, which consists of
many mutagenic multi-organ carcinogens.” According to Dr. Landolph,

                                       23
“much epidemiological literature exists to show associations between diesel
exhaust and its chemical constituents (such as PAHs like benzo(a)pyrene,
and benzene, dioxin, and formaldehyde) and the development of cancer in
multiple organ sites. Further, because diesel exhaust has been shown to be a
mixture of mutagenic carcinogens, as just explained, occurrence of tumors in
one site are relevant to development of tumors in other sites.” In support,
Dr. Landolph cited multiple epidemiological and animal studies and
explained that “strict concordance of target organs . . . in human
epidemiological studies is not necessary in order to extrapolate the results of
animal carcinogenicity studies to predict the carcinogenicity of chemicals to
humans,” and that it “has become [a] common and accepted practice in [his]
field of expertise to utilize the results of animal carcinogenicity studies to
estimate the increase in cancer risk above background in humans that each
dose of chemical carcinogen causes,” citing five sources for his opinion.
      BNSF presented no evidence calling into question the scientific validity
or reliability of any of this reasoning or methodology. It submitted no expert
declarations or reports or scientific publications contradicting plaintiffs’
experts’ opinions or suggesting that Dr. Salmon’s use of the overall cancer

risk assessment was improper or unreliable.7 Indeed, it failed to submit any
legal or scientific authority in support of its argument—including any of the
scientific materials on which Dr. Salmon relied and which the trial court,
despite not having reviewed, found to be inadequate. Although BNSF

7      We note, however, that even if BNSF had submitted studies or expert
testimony conflicting with Dr. Salmon’s opinion, that alone would not
necessarily justify its exclusion. Rather, it would more likely demonstrate
that the use of the overall cancer risk and reliance on certain studies to show
an increased risk of non-Hodgkin’s lymphoma is subject to debate. It is not
the trial court’s role to resolve such scientific controversies. (Sargon, supra,
55 Cal.4th at pp. 772–773.)
                                        24
complains in its briefing that excess cancer risk is a concept used by
regulatory agencies, there is no categorical bar to a causation expert’s
reliance on data of the type used by regulatory agencies. (Davis v. Honeywell
Internat. Inc. (2016) 245 Cal.App.4th 477, 488–489.) In these circumstances,
the trial court overstepped its limited role as an evidentiary gatekeeper by
excluding Dr. Salmon’s expert opinions.
      The error here is similar to the one committed by the district court in
Kennedy. There, the plaintiff’s causation expert gave an opinion that her
atypical systemic lupus erythematosus (SLE) was caused by Zyderm
injections for facial wrinkles. (Kennedy, supra, 161 F.3d at pp. 1228–1229.)
The expert “relied upon a wide variety of objective, verifiable evidence in
forming his opinion that Zyderm causes autoimmune disorders such as
atypical SLE . . . .” (Id. at p. 1228, italics added.) But the district court
excluded his opinions because “no epidemiological or animal studies link[ed]
Zyderm to SLE or atypical SLE.” (Id. at p. 1229, italics added.) In ruling
that the district court “abused its discretion” by finding “too great an
analytical gap . . . between the existing data and the expert’s conclusion,” the
Ninth Circuit stated: “The fact that a cause-effect relationship between
Zyderm and lupus in particular has not been conclusively established does
not render [the expert]’s testimony inadmissible.” (Id. at p. 1230, italics
added.) The expert “set forth the steps he took in arriving at his conclusion”
and his “analogical reasoning was based on objective, verifiable evidence and
scientific methodology of the kind traditionally used by rheumatologists.”
(Ibid.) And the defendant had “not introduced any evidence that [the
expert]’s reasoning [was] not scientifically valid.” (Ibid.) Accordingly, the
Ninth Circuit concluded that the analytical “gap was of the district court’s

                                        25
making.” (Ibid.; see also Milward, supra, 639 F.3d at pp. 22–23 [similarly
holding that “ ‘the gap was of the district court’s making’ ”].)
      The same is true here. Dr. Salmon gave a reasonable scientific
explanation for his causation opinions, including his reliance on the overall
cancer risk, and he cited objective, verifiable evidence supporting his
opinions. BNSF submitted no evidence that his reasoning or methodology
was scientifically invalid. The trial court also found no fault with his
methodology. The mere fact that a cause-effect relationship between
exposure to diesel exhaust and non-Hodgkin’s lymphoma “in particular” has
not been conclusively established in the scientific literature does not render
Dr. Salmon’s opinions inadmissible. (Kennedy, supra, 161 F.3d at p. 1230;
see also Milward, supra, 639 F.3d at pp. 16, 19–20 [causation expert properly
relied on scientific evidence that benzene can cause acute myeloid leukemia
(AML) “as a class” as support for his opinion that workplace exposure to
benzene caused plaintiff’s specific rare type of AML].)
      On this record, leaving adequate space for the exercise of reasonable
scientific judgment based on the available data, we conclude that the
analytical gap was not “too great” for Dr. Salmon to bridge using his own
scientific training and expertise. (Sargon, supra, 55 Cal.4th at p. 771.) The
trial court strayed beyond its gatekeeping role by weighing the probative
value of Dr. Salmon’s opinion, and the studies on which he relied, rather than
merely excluding a clearly invalid and unreliable expert opinion. (See id. at
p. 772; Cooper v. Takeda Pharmaceuticals America, Inc. (2015) 239
Cal.App.4th 555, 592 (Cooper).)
      BNSF contends on appeal that IARC must have considered all the
same data Dr. Salmon relies on to opine that diesel exhaust can be a cause of
non-Hodgkin’s lymphoma, but IARC Monograph 105 does not include non-

                                        26
Hodgkin’s lymphoma among the types of cancer that diesel exhaust has been
demonstrated to cause. According to BNSF, Gary’s experts ignore this
“critical” conclusion, and their opinions must therefore be unreliable.
      We disagree. First, although trial counsel for BNSF read to the trial
court a quote purporting to be from IARC Monograph 105, stating that for
“lymphoma, the overall evidence did not support an effect of exposure to
diesel exhaust and/or gasoline engine exhaust,” BNSF decided for strategic

reasons not to submit the publication in support of its motion in limine.8 It
also chose not to submit a respondent’s appendix on appeal or otherwise seek
to include the publication in the appellate record. We find it difficult to see
how we could conclude that IARC Monograph 105 requires exclusion of
Gary’s experts given that the record contains only a one-page excerpt of the
publication, and that excerpt does not include the statement on which BNSF
relies. We cannot decide the appeal based on evidence not included in either
the trial court or appellate record.
      In any event, we are not persuaded by BNSF’s argument. Even if we
assume that IARC Monograph 105 disclaims a link between diesel exhaust
and lymphoma, we do not agree that it is inherently unreliable for an expert
to infer causation from epidemiological studies simply because IARC or

another agency has not yet done so.9 As we have explained, “[w]hether an
inference of causation based on an association is appropriate is a matter of

8    Counsel for BNSF stated that she had “wanted to save it for cross-
examination” of Gary’s experts at trial.

9     We also note that Dr. Gale cited IARC Monograph 105 on diesel
exhaust in his report as specifically acknowledging that “[i]dentification of a
specific organ or tissue does not preclude the possibility that this agent may
cause cancer at other sites.”
                                       27
informed judgment, not scientific methodology, as is a judgment whether a
study that finds no association is exonerative or inconclusive.” (Restatement,
§ 28, com. (c), subd. (3), p. 406, italics added.) “[I]n some cases, reasonable
scientists can come to differing conclusions on whether a body of
epidemiologic data justifies an inference of causation. Similarly, reasonable
scientists may, in some instances, disagree on whether the absence of an
association is exonerative of the agent or is merely inconclusive.” (Ibid.)
Dr. Salmon was entitled to reach a different conclusion than that of IARC so
long as it is not “ ‘clearly invalid and unreliable.’ ” (Sargon, supra, 55 Cal.4th
at p. 772.)
      Further, Dr. Salmon explained in his report that the “comment that
epidemiology studies have not identified diesel exhaust as a risk factor for
non-Hodgkin’s lymphomas is, like all such claims based on negative
epidemiological evidence, unconvincing since few such studies have been
undertaken, and those that were have relatively low power to detect such an
effect. The great majority of substantial epidemiological work on diesel
exhaust effects has concentrated on lung cancer, the most widely understood
risk, and these studies excluded consideration of any other endpoint.”
Dr. Salmon also relied on epidemiological literature, including other IARC
volumes, showing associations between diesel exhaust’s chemical
constituents and cancer development in multiple organ sites, which as we
have explained, he is permitted to do.
      BNSF relies primarily on Sargon and Lockheed Litigation Cases (2004)
115 Cal.App.4th 558 (Lockheed) to argue that the trial court properly
excluded Dr. Salmon’s testimony as speculative. We find these cases
factually distinguishable.

                                         28
      In Sargon, the manufacturer of a newly patented dental implant sued a
university for breach of the parties’ contract for the university to perform
clinical testing of the implant. (Sargon, supra, 55 Cal.4th at p. 753.) In
support of its claim, the small company—whose annual net profits peaked at
$101,000—presented expert testimony opining that it would have become a
worldwide leader in the dental implant industry and earned profits ranging
from $200 million to over $1 billion had the university not breached its
contract. (Id. at pp. 753, 757.) The trial court excluded the expert’s opinion
as speculative, and the Supreme Court affirmed that ruling. (Id. at p. 753.)
      The excluded expert in Sargon was an accountant who based his lost
profits calculation on a market share approach, by which he compared
Sargon to six large, multinational dental implant companies (the “Big Six”)
that were the dominant market leaders in the industry. (Sargon, supra, 55
Cal.4th at p. 756.) Unlike the other companies, however, Sargon “had no
meaningful marketing or research and development organization and no
parent company to assist it.” (Id. at p. 757.) In fact, the expert “admitted
that by no objective business metric, such as sales or number of employees,
was Sargon in fact comparable to the ‘Big Six’. Instead, he based his
comparison solely on his belief that Sargon, like the ‘Big Six’, and unlike the
rest, was innovative, and that innovation was the prime market driver.”
(Id. at p. 777.) The expert also acknowledged that he had no expertise
regarding how innovative Sargon’s dental implant was, and the trial court
found he had no expertise in the dental implant industry at all. (Id. at
pp. 759, 766.) The trial court therefore found, and the Supreme Court
agreed, that the expert’s opinion was devoid of factual or logical basis and
rested solely on “speculation and unreasonable assumptions.” (Id. at
pp. 766–767, 781.)

                                       29
      Paraphrasing from the opinion of another appellate court, “[t]he nature
and reliability of Dr. [Salmon]’s testimony in this case bears no resemblance
to the expert testimony in Sargon. In Sargon, the expert had no reasonable
basis for his opinion on lost profits, and reached his conclusions only by
speculating and making readily discernible leaps of logic. The same cannot
be said about Dr. [Salmon]’s testimony.” (Cooper, supra, 239 Cal.App.4th at
p. 593.) Unlike the expert in Sargon, Dr. Salmon has over 50 years of
experience in the precise subject matter about which he opined—the
carcinogenic effect of toxic exposure in humans—and he reached his
conclusions after using a well-established methodology and relying on various
epidemiological studies. He and his colleagues at OEHHA formulated the
same excess cancer risk methodology he used in this case, and he explained
in detail why reliance on an all-cancer risk assessment is appropriate where,
as here, the carcinogens are mutagenic, causing cancer throughout the body.
Scientists utilizing this methodology take the available data from studies
that have been conducted, which tend to focus on “the larger risk sites,” such
as the lungs, and use it “to proximate the overall risk of cancer” to somebody
exposed to the particular carcinogen. Dr. Salmon explained that the
methodology is designed to “provide an estimate as the overall risk of cancer
and it doesn’t specify that that risk be confined exclusively to the lung cancer
site or other specific sites that have been measured and considered in the risk
assessment.” It is therefore appropriate to rely, as Dr. Salmon did, on the
epidemiological literature demonstrating associations between diesel exhaust
and its chemical constituents and cancer development in multiple organ sites.
      In Lockheed, another case on which BNSF relies, the plaintiffs’ expert
opined that their exposure to five particular chemicals supplied by
defendants was a substantial factor resulting in an increased risk of cancer.

                                       30
(Lockheed, supra, 115 Cal.App.4th at p. 564.) He based his opinion solely on
a study finding that painters who were potentially exposed to more than 130
chemicals and other substances—including known carcinogens—contracted
cancer at a higher rate than the general population. (Id. at pp. 564–565.)
The trial court found that the expert’s opinion was “based on conjecture and
speculation as to which of the many substances to which the study subjects
were exposed contributed to the greater incidence of cancer,” and the Court of
Appeal agreed. (Id. at p. 565.) Here, by contrast, Dr. Salmon relied on
various studies showing associations between exposure to diesel exhaust and
its chemical constituents and the development of cancer in multiple organ
sites.
         BNSF also submitted a notice of supplemental authority pointing to the
recent opinion in Onglyza Product Cases (2023) 90 Cal.App.5th 776
(Onglyza), where the appellate court affirmed the trial court’s exclusion of the
plaintiffs’ general causation expert, but we find that case distinguishable as
well. There, as in Lockheed, the expert relied on a single study, and the trial
court found that, as in Sargon, the expert’s opinions “went beyond [his]
expertise and were not supported by a reliable methodology.” (Onglyza, at
p. 782.) The court explained in detail why the expert’s application of the
methodology he used was unreliable and concluded that his opinion contained
“shifting results-based methodology that fails to logically and consistently
weigh all relevant evidence.” (Ibid.) The trial court here made no such
findings, and BNSF does not challenge Dr. Salmon’s methodology or

                                       31
expertise. We therefore conclude that the trial court erred in finding

Dr. Salmon’s testimony inadmissible.10
      2. Dr. Landolph’s General Causation Opinion
      Dr. Landolph is a molecular chemical carcinogenesis biologist professor
with 50 years of experience in research, teaching, and scientific advisory and
consultative activities involving the disciplines of chemistry, biochemistry,
cell biology, cell and molecular toxicology, molecular biology, and molecular
carcinogenesis, particularly as these disciplines relate to the study of
chemical carcinogenesis and chemically induced morphological and neoplastic
cell transformation. He was retained in this case to render a general
causation opinion as to whether diesel exhaust and diesel exhaust
constituents are carcinogenic in animals and/or humans, and whether these
substances and chemicals can cause various types of tumors, including non-
Hodgkin’s lymphoma. Dr. Landolph concluded that diesel exhaust and its
constituents, particularly benzene, dioxin, and formaldehyde, “are capable of
causing and/or contributing to the development [of] many different types of
tumors in humans exposed to diesel exhaust and its components, including
lung cancer and many other cancers, in particular Non-Hodgkin’s Lymphoma
(NHL) and at least one of the NHLs, DBCL [diffuse large B cell lymphoma].”

10     BNSF also moved to exclude Dr. Salmon’s specific causation opinion,
but on appeal, it does not challenge any specific aspect of this opinion.
Instead, BNSF argues only that once the trial court excluded the general
causation opinions offered by Dr. Salmon and Dr. Landolph, its exclusion of
all specific causation opinions followed as a matter of course. The trial court
did not specifically address or reject Dr. Salmon’s specific causation opinion.
For those reasons, and because we have concluded that Dr. Salmon’s general
causation opinion is admissible, we also reverse the trial court’s ruling as to
Dr. Salmon’s specific causation opinion.
                                       32
      The trial court granted BNSF’s motion to exclude Dr. Landolph’s
opinion for “the same” reason it excluded Dr. Salmon’s opinions, finding that
“[t]here is a gap in the analytical data to support the conclusions that diesel
exhaust exposure is a causal link or a causal connection to non-Hodgkin’s
lymphoma.” The court stated: “[I]n looking at the documents presented, it
does not seem that there is enough data for the experts to draw their
conclusion . . . . [T]here is an analytical gap that causes the Court to
grant . . . the defense motion in limine Number 9 . . . excluding certain
opinions of Dr. Landol[ph] on causation.”
      BNSF contends that the trial court properly excluded Dr. Landolph’s
testimony for two main reasons: (1) he, like Dr. Salmon, failed to cite a study
concluding that diesel exhaust exposure causes non-Hodgkin’s lymphoma;
and (2) he could not state with specificity what dose of diesel exhaust is
required to cause non-Hodgkin’s lymphoma.
      We disagree with BNSF’s first argument for the same reasons we have
already explained in connection with Dr. Salmon’s opinions. Dr. Landolph
was not required to identify a study conclusively stating that non-Hodgkin’s
lymphoma is caused by diesel exhaust. Instead, it was appropriate for him to
use his scientific judgment and expertise to evaluate the available data and
determine whether to draw an inference of causation. (Restatement, § 28,
com. (c), subd. (1).) In reaching his conclusions in this case, Dr. Landolph
relied on decades of education and research, scientific data, numerous human
epidemiological and animal studies showing positive associations, including
specifically to non-Hodgkin’s lymphoma, other peer-reviewed relevant
publications, and the conclusions of multiple agencies that diesel exhaust and
its constituents are multi-system mutagenic carcinogens. He examined the
data indicating a link between diesel exhaust and lung cancer and also

                                       33
analyzed studies showing associations with at least a dozen other sites,
including two diesel exhaust studies finding elevated risks for leukemias and
non-Hodgkin’s lymphoma. Dr. Landolph also relied on scientific literature
containing similar data for the chemical constituents of diesel exhaust,
including benzene, which he stated “is well known to induce many different
types of leukemias and lymphomas,” including non-Hodgkin’s lymphoma. He
explained that, “[t]aken together, the sum of the weight of all of the evidence”
supports his conclusion to a reasonable degree of scientific probability that
“diesel exhaust and its constituents . . . are capable of causing and/or
contributing to the development many different types of tumors in humans
exposed to diesel exhaust and its components, including . . . in particular
Non-Hodgkin’s Lymphoma[.]” Absent any challenge to Dr. Landolph’s
methodology, we conclude that he provided sufficient support for his scientific
judgment on causation.
      We further conclude that Gary’s experts, including Dr. Landolph, were
not required to identify the exact dose of diesel exhaust at which point the
exposure becomes toxic. The notion that there even exists such “a threshold
dose before an effect can occur is a controversial concept for which current
scientific thinking resists any universal answers and instead examines what
is known about the pathological mechanisms of the disease.” (Restatement,
§ 28, reporter’s notes, com. (c), subd. (2), p. 437, citing Proposed Guidelines
for Carcinogen Risk Assessment, 61 Fed. Reg. 17960, 17993 (Apr. 23, 1996).)
Dr. Landolph echoed this thought at his deposition, testifying that although
some people insist there must be a threshold dose to be able to causally
connect exposure to a particular chemical to increased risk of cancer, the
existence of such a threshold has never been substantiated, and it “is still a
current area of controversy today.” It is outside the scope of the trial court’s

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gatekeeping duty to resolve such scientific controversies. (Sargon, supra, 55
Cal.4th at pp. 772–773.) “The courts’ evidentiary gatekeeping function
is . . . not a warrant for judicial intervention in genuine scientific debates
over substantive principles.” (People v. Superior Court (Vidal) (2007) 40
Cal.4th 999, 1014.)
      Dr. Landolph further testified that he agreed with the EPA that such
dose-response curves are linear, meaning that there is no threshold dose of
diesel exhaust necessary to cause non-Hodgkin’s lymphoma. Instead,
Dr. Landolph explained, on a linear no-threshold dose response model,
“basically any amount confers a risk,” and the “larger the amount, the larger
the risk. So we don’t worry about trivial amounts.” (See also Johnson &
Johnson Talcum Powder Cases (2019) 37 Cal.App.5th 292, 305 (Talcum
Powder Cases) [a “dose-response pattern” means there is “increased risk with
increased exposure”].)
      BNSF presented no contrary evidence establishing that the existence of
a threshold dose is required. “[W]hile precise information concerning the
exposure necessary to cause specific harm to humans and exact details
pertaining to the plaintiff’s exposure are beneficial, such evidence is not
always available, or necessary, to demonstrate that a substance is toxic to
humans given substantial exposure and need not invariably provide the basis
for an expert’s opinion on causation.” (Westberry v. Gislaved Gummi AB (4th
Cir. 1999) 178 F.3d 257, 264; accord Sarkees v. E.I. Dupont De Nemours &
Co. (2d Cir. 2021) 15 F.4th 584, 593; Clausen v. M/V New Carissa (9th Cir.
2003) 339 F.3d 1049, 1059–1060; Hardyman v. Norfolk & W. Ry. Co. (6th Cir.
2001) 243 F.3d 255, 265–266.)
      We find it sufficient here that Dr. Salmon calculated Melvin’s dose
according to a well-established methodology, explaining that the additional

                                        35
risk of cancer Melvin experienced as a result of his exposures was
“substantial (between 2864 and 3875 per million).” This number was “well in
excess of what would be considered a level requiring remedial action. 1 in a
million is regarded as the de minimis level of cancer risk, whereas even more
permissive programs considering cost-effectiveness as well as health effects
generally regard 100 in a million as a level at which immediate remedial
action would be required.” Dr. Landolph relied on these calculations and his
opinion, based on the linear no-threshold dose response model, that the risk
of developing cancer increases with any dose increase, to conclude that
Melvin’s substantial exposure to diesel exhaust while working for BNSF—
which was “at least 3,000 times higher than deminimus [sic]”—was more
than trivial and led to a nontrivial elevation in his cancer risk.
      Although other experts (and the jury) may disagree regarding whether
there exists a threshold dose necessary to demonstrate a link between diesel
exhaust and non-Hodgkin’s lymphoma, and whether Dr. Landolph has
sufficiently shown that such a causal link even exists, BNSF’s arguments go
to the weight and not the admissibility of those opinions. “Vigorous cross-
examination, presentation of contrary evidence, and careful instruction on
the burden of proof are the traditional and appropriate means of attacking
shaky but admissible evidence.” (Daubert, supra, 509 U.S. at p. 596.) We
conclude that Dr. Landolph provided a reasonable basis for his opinions such
that he should have been permitted to present them to the jury.
      3. Dr. Gale’s General and Specific Causation Opinions
      Dr. Gale is a physician specializing in hematology and oncology with
substantial experience in statistics and epidemiology, and he has published
over 1,200 scientific articles and more than 20 books, mostly on leukemia,
transplantation, cancer biology, and immunology and radiation biology. He

                                       36
was retained in this case to opine whether occupational exposures to diesel
engine exhaust and its constituents, including but not limited to benzene,
dioxin, and formaldehyde were, to a reasonable degree of medical probability,
a cause of Melvin’s non-Hodgkin’s lymphoma. Using the weight-of-the-
evidence methodology, Dr. Gale concluded that diesel exhaust and its
particulates cause cancer in humans, that they are a cause of non-Hodgkin’s
lymphoma in humans, and that it is more likely than not, to a reasonable
degree of medical probability, that Melvin’s occupational exposure to
benzene, dioxin, and formaldehyde via his exposure to diesel exhaust was a
cause of his non-Hodgkin’s lymphoma.
      As with Dr. Landolph, the trial court declined to provide detailed
reasoning for its decision to exclude Dr. Gale, stating that “in looking at the
documents presented, it does not seem that there is enough data for the
experts to draw their conclusion much less the Court’s [sic] . . . there is an
analytical gap that causes the Court to grant the motions in limine to
preclude . . . the opinion of Dr. Gale on liability and causation[.]” BNSF
contends on appeal that Dr. Gale’s specific causation opinion was properly
excluded both because there was no admissible general causation opinion on
which to base his opinion and because, like Dr. Landolph, he could not
identify a specific dose of diesel exhaust that causes non-Hodgkin’s
lymphoma.
      We are not persuaded by BNSF’s arguments for the reasons we have
already explained. Because we have concluded that the experts’ general
causation opinions are admissible, Dr. Gale may properly base his specific
causation on those opinions. Dr. Gale also explained that “[d]etermination of
whether a substance or chemical causes cancer in humans is not tissue or
organ specific.” In other words, he agreed with Dr. Salmon and Dr. Landolph

                                       37
that analysis of cancer at one organ site is relevant to analysis of cancers at
other sites. There is nothing in the record that would allow us to reject this
as a scientifically invalid or unreasonable opinion.
      Dr. Gale further explained that “[s]everal studies report an association
between exposure to diesel engine exhaust and particulates and lymphomas.”
Further, “[c]onsiderable data in experimental animals indicate exposure to
diesel engine exhaust and particulates cause lymphomas,” and two IARC
Monographs “based on considerable additional epidemiological data” found
that “[m]ost studies show a positive association between benzene exposure
and NHL [non-Hodgkin’s lymphoma].” Dr. Gale similarly analyzed the data
on dioxin and formaldehyde, which both showed positive associations with
non-Hodgkin’s lymphoma. Based on his extensive review of the data,
Dr. Gale opined that “diesel engine exhaust and particulates, benzene, dioxin
and formaldehyde are a cause of non-Hodgkin lymphoma in humans
including diffuse large B-cell lymphoma.”
      Dr. Gale also testified at deposition that there is no “magical dose” at
which point it becomes possible for diesel exhaust to cause non-Hodgkin’s
lymphoma. Rather, he explained that for him “to opine that it is more likely
than not, to a reasonable degree of medical probability, that an exposure to
[diesel] exhaust and particulates was a substantial contributing factor or a
cause of [Melvin] developing Non-Hodgkin’s lymphoma, it’s a dose at which
the calculated likelihood of developing cancer is more than trivial.” Here,
Dr. Gale explained, Melvin’s exposure was sufficiently high to result in a
nontrivial and indeed substantial excess cancer risk. He performed a
differential diagnosis—a widely accepted method explained in the Reference
Manual on Scientific Evidence from the Federal Judicial Center that
considers other exposures and variables in determining specific causation—

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and properly used his expertise and scientific judgment to opine that it is
more likely than not, to a reasonable degree of medical probability, that
Melvin’s diesel exhaust exposure was a cause of his non-Hodgkin’s
lymphoma. (See Talcum Powder Cases, supra, 37 Cal.App.5th at pp. 327–332
[trial court erred by rejecting expert’s differential diagnosis for specific
causation opinion].) Yet again, BNSF does not challenge Dr. Gale’s
methodology in formulating his general and specific causation opinions.
      While BNSF may argue there are weaknesses in the data relied upon
by Gary’s experts or their reasoning, their opinions were not clearly invalid or
unreliable. We therefore reverse the trial court’s orders excluding the
causation opinions of Dr. Salmon, Dr. Landolph, and Dr. Gale. We
emphasize, however, that our decision is a narrow one—we draw no
conclusions regarding the probative value or persuasiveness of their
testimony. It will be up to the jury to decide whether to accept their opinions
that it is more likely than not that exposure to diesel exhaust can and did
cause Melvin’s non-Hodgkin’s lymphoma.
                                 DISPOSITION
      The judgment is reversed. The matter is remanded with directions to
the trial court to vacate its orders granting BNSF’s motions in limine to
exclude the expert opinions of Dr. Salmon, Dr. Landolph, and Dr. Gale, issue

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new orders denying those motions, and conduct further proceedings
consistent with this opinion. Gary is entitled to his costs on appeal.

                                                               BUCHANAN, J.

WE CONCUR:

McCONNELL, P. J.

DO, J.

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