Vanni v. Honeywell Internat. CA2/8 ( 2021 )

Filed 9/13/21 Vanni v. Honeywell Internat. CA2/8
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IN THE COURT OF APPEAL OF THE STATE OF CALIFORNIA
SECOND APPELLATE DISTRICT
DIVISION EIGHT
BARBARA VANNI et al., B299594
Plaintiffs and Respondents, (Los Angeles County
Super. Ct. No. BC544355)
v.
HONEYWELL INTERNATIONAL,
INC.,
Defendant and Appellant.
APPEAL from a judgment of the Superior Court of Los
Angeles County, Michele E. Flurer, Judge. Affirmed.
Horvitz & Levy, Lisa Perrochet, Curt Cutting; McDermott
Will & Emery and Alice Wong for Defendant and Appellant.
Waters Kraus & Paul, Michael B. Gurien and Michael P.
Connett for Plaintiffs and Respondents.
_________________________
INTRODUCTION
Honeywell International, Inc. (Honeywell) asks us to
reverse the jury verdict and judgment entered in favor of
respondents Barbara Vanni and her two sons, Mark and Michael
(the Vannis), in the amount of $ 1,970,716. Respondents are the
wife and sons of Donald Vanni. Donald Vanni owned and
operated a bowling alley for 30 years with his brother Fred. The
jury was asked to decide whether Donald Vanni’s death by
pericardial mesothelioma was caused by his exposure to asbestos
from drilling bowling balls that contained asbestos filler
manufactured and supplied by Honeywell’s predecessor, the
Bendix Corporation (Bendix).
The two issues on appeal are whether the verdict rests on
unfounded speculation that Bendix exposed Vanni to asbestos
and whether the verdict rests on unfounded expert opinions
about causation. In other words, did respondents prove that
Bendix exposed Donald Vanni to asbestos and, if so, was his
pericardial mesothelioma caused by that exposure to asbestos?
We conclude the evidence is sufficient to support the jury’s
verdict on both issues and affirm.
PROCEDURAL BACKGROUND
A. Evidence Code Section 402 Hearing
In 2012, Donald was diagnosed with pericardial
mesothelioma. He died in June 2013 at age 78. In 2014,
respondents filed a complaint alleging two causes of action for
negligence and strict product liability against Honeywell and
others. After motions for summary judgment were denied,
Honeywell filed motions in limine challenging the foundation for
and admissibility of the testimony of the Vannis’ expert on
2
causation.1 Honeywell moved to exclude the Vannis’ theory of
general causation (that inhalation of chrysotile asbestos can
cause pericardial mesothelioma) on the ground that no reliable
science supported Dr. Barry Horn’s expert opinion. Honeywell
also moved to exclude the Vannis’ theory of specific causation
(that HD-100, Bendix’s asbestos product, caused Donald’s
pericardial mesothelioma) on the ground that the Vannis’ expert,
Dr. Carl Brodkin, relied on unfounded assumptions about how
much asbestos would be released from drilling bowling balls
containing HD-100. The court scheduled a hearing on Dr. Horn’s
proposed opinion testimony. The motion in limine as to Dr.
Brodkin’s opinion was denied without a hearing.
On April 8, 2019, the trial court conducted a hearing
pursuant to Evidence Code2 section 402. The purpose of the
hearing was to determine whether Dr. Horn should be permitted
to testify at trial to his expert opinion that exposure to chrysotile
asbestos causes pericardial mesothelioma.
At the hearing Dr. Horn testified he is a critical care
specialist and pulmonologist. He testified mesothelioma is a
cancer which develops in serosal tissues. Serosal tissues are the
membranes which surround the lung, heart, intestines, and
scrotum. These membranes are all exactly the same cells, despite
the different locations. Dr. Horn testified he has seen “a lot” of
instances where individuals exposed to asbestos, usually by
1
For clarity, we refer to respondents Barbara, Michael, and
Mark Vanni as the Vannis. We refer to Donald Vanni as Donald.
2 Undesignated statutory references are to the Evidence
Code.
3
occupational exposure, developed pericardial plaques (scarring)
right on the heart. He concluded it was inconceivable that an
individual would develop a localized plaque without asbestos
actually getting to that site. This must mean that asbestos get to
the pericardium, the tissue surrounding the heart, although how
it does so is not entirely clear. He was aware of other diseases,
like lung and liver cancer, for which science has determined the
causes (tobacco and vinyl chloride, respectively), but not the
precise mechanisms.
The literature Dr. Horn reviewed reports that individuals
exposed to asbestos may develop non-malignant disease of the
pericardium as well as malignant disease of the pericardium,
which is pericardial mesothelioma, Donald’s diagnosis. He
reviewed case reports published in the literature by clinicians
who presented their observations of and experiences with how
patients present with symptoms, and how the disease naturally
progresses. These case reports differed from epidemiological
studies where large groups of individuals are compared and
contrasted with control groups. A small portion of the case
reports noted the patients had occupational exposure to asbestos.
Where there was a history of asbestos exposure, the clinicians
attributed pericardial mesothelioma to asbestos exposure. Dr.
Horn testified there are also case reports where exposure to
asbestos is unknown. He testified that this variant can be
explained. One explanation is that, in fact, the patient was not
exposed to asbestos. A second explanation is that the patient had
already died and investigators had very limited information on
whether there was exposure. The third explanation is the
authors of the case reports were not sufficiently knowledgeable
about how to inquire whether in fact there was exposure, or the
4
patient himself had no knowledge that he had been previously
exposed. About a third of the case reports he reviewed reported
asbestos exposure.
In addition to case reports about individual patients, there
are national registries where investigators try to identify all the
cases of mesothelioma in the country. There are tumor registries
in Italy, Japan, and Germany. There is nothing equivalent in the
United States. A registry reviews the pathology to be sure the
diagnosis is correct. It also keeps records. It interviews patients
with the disease or patient relatives to determine whether the
diagnosed individuals were exposed to asbestos. There are four
particular studies he reviewed dated 2010, 2013, 2012, and 1982.
In these registry studies, approximately 60 percent of the
patients had prior exposure to asbestos, which is not the
percentage of exposure in the general population. Dr. Horn relied
on the case reports and registry studies in forming his opinion
that Donald’s pericardial mesothelioma was caused by exposure
to asbestos.
Dr. Horn was also familiar with the Helsinki Criteria for
Attribution of Diseases to Asbestos Exposure. Several dozen
investigators from around the world who were experts in
asbestos-related disease reviewed the literature and came up
with consensus statements about asbestos and asbestosis,
asbestos and mesothelioma, and asbestos and lung cancer. They
concluded asbestos inhalation affects all serosal membrane
surfaces in the body. They concluded that an occupational
history of asbestos exposure combined with a diagnosis of
mesothelioma is enough to attribute the mesothelioma to
asbestos exposure.
5
At the section 402 hearing, Dr. Horn also testified it is not
surprising that epidemiological studies do not find pericardial
mesothelioma per se even in the most heavily exposed cohorts to
asbestos. The largest epidemiological study involved 17,800
asbestos insulation workers in North America. Nine percent died
of mesothelioma. This is an enormous number. None had
pericardial mesothelioma. They had pleural (lung) mesothelioma
and peritoneal (intestinal) mesothelioma. The World Health
Organization (WHO) accumulated 92,000 cases of mesothelioma
from various countries around the world and pericardial
mesothelioma represented 0.3 percent of the group. That means
it would occur in three of 1000 people. So if a researcher studied
just 400 people with mesothelioma, it would be completely
random whether even one person with pericardial mesothelioma
would be encountered. If a researcher did not find one person,
that would not mean asbestos does not cause pericardial
mesothelioma. One would need a study of multiple times 400
cases of mesothelioma in order to make that determination. That
kind of study has never been done. The subject groups are just
not big enough to answer the question by using epidemiological
studies.
Dr. Horn acknowledged science has not yet discovered why
some people get mesothelioma and some do not. In addition
people get non-malignant disease in the pericardium more
frequently than malignant disease. But malignant disease does
occur. He cannot explain the randomness of the disease.
On cross-examination, Dr. Horn stated exposure to
asbestos is the only thing he has seen that explains the
pericardial plaque or scarring, which looks exactly like pleural
plaque. He generally relies on epidemiological studies to
6
determine the etiology of cancer. Although he has done
epidemiological studies himself and has been a coauthor, he does
not consider himself an epidemiologist. He is unaware of any
epidemiologic studies linking Honeywell’s asbestos, HD-100, with
pericardial mesothelioma or any studies showing that drilling
holes in bowling balls increases the risk of pericardial
mesothelioma. And all studies but one on auto mechanics
exposed to brake dust with asbestos do not conclude there is an
increased risk of pericardial mesothelioma from exposure to
brake dust with asbestos.
There are no epidemiological studies or cohort studies
focused on the specific disease of pericardial mesothelioma.
There are only registry studies and case reports. The national
registry studies do not compare an identical control group with a
population. The national studies just look at the total number of
cases in the country. In the case reports it has been stated
multiple times that a potential association between pericardial
mesothelioma and exposure to chrysotile asbestos specifically (as
opposed to exposure to asbestos generally) has not been
established.
There are insufficient data to believe another type of
asbestos, amphiboles fibers, are more potent than chrysotile
fibers as a cause of pericardial mesothelioma. There are no data
showing different types of fibers have the same potency for
causing pericardial mesothelioma. But the serosal tissues
throughout the body are the same, so Dr. Horn concludes the
tissue, no matter its location, responds in the same manner to
asbestos. There is a dose-dependent relationship between
development of asbestos-related malignancies. There is a general
dose-dependent relationship with all fiber types. Specific data as
7
to pericardial mesothelioma are not published because there are
not enough cases.
Of the 48 registry studies for pericardial mesotheliomas
where an effort was made to gather a work history, 30 found
asbestos exposure. The type of asbestos was not recorded.
Because the tissue is the same, Dr. Horn did not agree that the
type of asbestos is significant in determining the cause of
pericardial mesothelioma. If asbestos affects the serosal tissue in
the lungs, it would affect the same tissue elsewhere in the body.
The 30 cases of exposure did not state the intensity, duration, or
frequency of exposure.
To Dr. Horn, exposure to asbestos in 30 out of 48 patients
established a cause and effect relationship, that is, exposure to
asbestos causes pericardial mesothelioma.
Dr. Horn testified no one in the State of California has seen
and diagnosed more people with asbestos exposure and asbestos-
related disease than he. The registry studies are reliable because
they are done by “really good investigators who understand what
we’re talking about here. That is, they’re looking at rare disease
and looking to determine whether there’s a relationship with
asbestos exposure. We’re talking about people who have
published multiple papers in the world’s literature, particularly,
the group from Italy which represents the bulk of these cases
that have been published. These are careful. These are
knowledgeable investigators.” He has been reading literature for
50 years since 1956 and is perfectly competent to interpret it.
According to multiple studies he has reviewed, chrysotile
asbestos causes mesothelioma.
Pericardial mesothelioma is this rare: In the United States
there are about 2,500 cases per year of mesothelioma. The data
8
from WHO shows 0.3 percent of mesotheliomas are pericardial
mesothelioma. This amounts to eight cases in the United States
per year. Dr. Horn could not give the likelihood of someone in the
general population just developing pericardial mesothelioma
without exposure to asbestos. He estimates it would be some
fraction of the eight.
After listening to the testimony at the section 402 hearing,
the court summarized the evidence: “So, because – I’m
summarizing. Because chrysotile causes meso, we don’t know the
exact mechanism of pericardial meso. All those workers were
exposed to asbestos. They had pericardial mesothelioma and on
that basis you believe this causal connection exists.” Dr. Horn
answered, “I do, and so do much of the people who addressed this
issue around the world do as well, as evidenced by the Helsinki
criteria published about 20 years ago.”
The trial court noted that “[i]f the opinion is based on
materials in which the expert may reasonably rely in forming the
opinion and flows in a reasoned chain of logic from those
materials rather than speculation or conjecture, the opinion may
pass even though the experts disagree with its conclusions or the
methods and materials used to reach that opinion.” The court
acknowledged that defense experts had contrary opinions. “I
think it will definitely go [to the] issue of weight versus
admissibility. [¶] The court concludes that the matters upon
which Dr. Horn relies to support his opinion on whether or not
exposure was a substantial factor in causing the plaintiff is
reasonably of the type that may be relied on in forming such
opinions. In other words, it provides a reasonable basis for the
particular opinion offered, and it is not based on mere speculation
9
or conjecture. Therefore, the court denies the motion of
Honeywell to exclude the testimony of Dr. Horn.”
B. Trial and Verdict
The trial was essentially a battle of the experts. Drs.
Steven Compton, Carl Brodkin, and Barry Horn testified on
behalf of the Vannis. Dr. James Crapo, Dr. Suresh Moolgavkar,
Sheldon Rabinovitz, and Renee Kalme testified on behalf of
Honeywell. The jury found in favor of the Vannis on their
negligence and product liability causes of action and found
Bendix was a substantial factor in contributing to Donald’s risk
of mesothelioma. It awarded $397,716 in economic damages and
$4 million in noneconomic damages. There were other
defendants. The jury assigned 40 percent fault to Honeywell,
37 percent fault to Ebonite, and 23 percent fault to Ebonite’s
other asbestos suppliers. It found that Honeywell did not act
with malice, oppression, or fraud.
The trial court entered judgment against Honeywell in the
amount of $1,970,716, reflecting the jury’s allocation of fault and
offsets for the Vannis’ settlements with other defendants. The
court awarded an additional $101,500 in costs.
EVIDENCE AT TRIAL
A. The Drilling
In 1957, 22-year-old Donald and his brother Fred Vanni
opened the Arcata Bowl bowling alley, which they operated until
October 1986. They shared bartending, bookkeeping, cooking,
oiling the lanes and repairing the pin-setting machines. They
started the bowling alley with 60 rubber bowling balls with pre-
drilled finger holes. Plastic bowling balls became popular in the
10
mid-1960’s and were the predominant bowling balls by the late
1960’s. In 1962, Donald and Fred purchased a ball-drilling
machine. Only Donald began drilling finger holes in plastic balls
in a four by eight foot unventilated “ball-drilling room.” At a
minimum it took Donald about 30 minutes to drill the holes and
he routinely drilled five to 10 balls a week, for a total weekly
drilling time of two and one-half to five hours. He also used a
hand file and sandpaper to file, sand, and smooth out the rough
edges of the drilled holes. Donald did not wear a mask or
breathing protection when he drilled and he breathed dust from
the balls because he was “right over the top of” them when he
was drilling. Donald would remove the dust from the bowling
ball by turning the ball over and blowing it off the top. After he
was done drilling, Donald would sweep and clean up the dust and
inner-ball material, causing the air to become dusty.
There were three “equally popular” brands of bowling balls
that Donald drilled: Ebonite, AMF and Brunswick. Ebonite
became the “premier brand” by the late 1960’s.
B. The Asbestos in the Bowling Balls
The use of asbestos in Ebonite’s bowling balls was not
established with precision. Ebonite had destroyed its records.
According to one former Ebonite employee, at least from 1967 on,
Ebonite used a combination of various materials in the core of
plastic bowling balls, including resin, peroxide, barytes, styrene
and asbestos. Not all the materials went into every ball. The
evidence at trial did not definitively establish that asbestos was
included in all balls.
However, Bendix, Honeywell’s predecessor, did have
records. Bendix made automotive friction products, including
brakes. Its friction products had an average asbestos content of
11
50 percent by weight. Bendix used chrysotile asbestos, which is
the least toxic of the several types of asbestos. The dust was
called HD-100. Between 1967 and 1972 Bendix supplied at least
232,000 pounds of its HD-100 to Ebonite at its bowling ball
manufacturing facility in Hopkinsville, Kentucky. Ebonite used
the HD-100 as filler in its plastic bowling balls.
C. Donald’s Level of Exposure to Asbestos
Dr. Steven Compton is a physicist and materials scientist
with asbestos-testing expertise. He was asked to find out how
much asbestos was in a product so that another scientist who
specializes in the effects of asbestos in the body could assess the
safety of the product.
Dr. Compton explained that chrysotile is a mineral that
forms in the earth. Fibers protruding from the surface are
asbestos fibers that can be mined, processed, and incorporated
into a product. Chrysotile is the predominate form of asbestos
used in commercial products. Historically, over 90 percent of
commercial products use chrysotile asbestos.
Asbestos is a mineral that is heat resistant and durable.
On the other hand, it forms long thin fibers which can be woven
into cloth in ways not possible with most other minerals. Each
asbestos fiber is a micrometer, that is, a millimeter broken up
into a thousand equal parts. When asbestos fibers are released
into the air, they can remain suspended in the air for a number of
hours, depending on conditions. Eventually they will settle onto
various surfaces, like a lunch box or an individual’s clothing,
hair, or skin. They can be resuspended into the air if something
causes them to become airborne again, like sweeping the floor or
shaking clothing. They can stay in the air for hours. Asbestos
12
does not degrade so it can be suspended and resuspended without
limit.
Honeywell obtained 26 Ebonite bowling balls manufactured
in the 1970’s before 1979. Dr. Compton tested nine of those
bowling balls to determine asbestos content and the level of fiber
release. Six of the balls were from before 1979 and three were
manufactured after that date. The balls manufactured after 1979
contained no asbestos. A bowling ball had two layers – an inside
core and an outside veneer or cover. For plastic balls, the veneer
is made from plastic.
Dr. Compton collected a sample of the inside materials by
drilling and then analyzing the material using microscopes. A
certified industrial hygienist drilled the balls. After he collected
the inner material, he prepared it to be placed onto a glass
microscope. They got rid of the non-asbestos materials that
might be present by exposing the material to heat and acid. That
isolated the material that might be asbestos. Then he analyzed
the isolated material. Dr. Compton found that all six Ebonite
bowling balls made before 1979 contained chrysotile asbestos
ranging from 6 percent to 9 percent by weight.
Dr. Compton also filed the edge of the cover to make sure it
did not have a sharp edge. He sanded the interior of the finger
hole to smooth out the surface. Dust was created by the sanding
activity. The last phase was sweeping the dust and debris off the
floor.
Dr. Compton also tested the asbestos fiber release by
drilling the balls. He opined that drilling finger holes released
breathable asbestos fibers from 0.06 to 0.17 fibers per cubic
centimeter of air, 10,000 times greater than the background level
of asbestos fibers present in the ambient air everywhere. He
13
testified that additional filing, sanding, and sweeping also
resulted in asbestos in the air well above background levels.
Dr. Compton concluded and opined that the balls
manufactured before 1979 all contained chrysotile asbestos in
quantifiable and visual amounts. He also concluded that the
activities of drilling, filing, sanding, and sweeping released fibers
that exceed ambient background air levels. He concluded that
someone drilling Ebonite balls from the 1970’s would generate
asbestos dust into the breathing space, no matter how much time
the actual drilling took.
Dr. Compton was critical of Honeywell’s testing. He noted
Honeywell’s experts never drilled an asbestos-containing ball in a
way that was represented by the facts of the case. When they
vacuumed, they filtered the dust. They did not use a
sophisticated microscope to precisely capture all the asbestos in
the samples. And they did not get rid of the non-asbestos
material before they tried to quantify the amount of asbestos in
the samples.
D. Causation of Mesothelioma
Dr. Carl Brodkin is an occupational and environmental
medical doctor with more than 30 years of experience in
diagnosis, causation, and treatment of asbestos-related diseases.
Occupational medicine deals with the diagnosis or identification
of disease and the management and treatment of disease, but it
also deals with exposure-related illness, i.e., did an exposure
cause an illness. To diagnose an asbestos-related disease that
may develop many years after exposure requires a systematic
review of a patient’s work history or else the researcher may not
appreciate that it is an asbestos-related disease.
14
In 2015, Dr. Brodkin was asked to do a medical evaluation
of Donald, who had died in 2013. He had to construct an
occupational history without Donald’s participation. He reviewed
pathology reports and Donald’s medical history and estimated
Donald’s exposure to asbestos. Once he received Dr. Compton’s
actual testing and assessment, he reviewed it to reevaluate his
initial opinion about what exposures Donald likely experienced.
Dr. Compton’s testing was more specific and gave “greater
resolution” and a more accurate basis for his own exposure
calculations. Dr. Compton’s numbers did not change his overall
opinion. Dr. Brodkin also reviewed literature that dealt with
similar activities, like drilling and sanding plastic resin materials
similar to bowling balls.
Dr. Brodkin testified that asbestos is the preeminent cause
of mesothelioma and that the more a person is exposed, the
greater the risk of developing the disease. Asbestos has a
tendency to break from larger bundles into smaller and smaller
fibers. A fiber is typically five times longer than it is wide. If you
put a thumb and forefinger as close as you can and see some air,
that space is a millimeter. A fiber is one-thousandth of a
millimeter. It is not visible to the naked eye. The fibers gain
access to the lung. Chrysotile fiber is the most common type used
in North America and Europe. It is about 95 percent of the
asbestos that are used. He testified all types of asbestos fibers
cause mesothelioma, including chrysotile, the type in the Ebonite
bowling balls. Exposure to low levels of asbestos increases the
risk of mesothelioma and no threshold has been found below
which mesothelioma cannot occur from asbestos exposure.
15
Dr. Brodkin explained that mesothelial tissue (or serosal
membrane) is found in the lung and heart and it is the same
tissue wherever it is located in the body. Once asbestos enters
the body, it migrates via the lymphatic system to all mesothelial
tissues in the body. The movement of asbestos, called kinetics,
allows the fibers to move throughout the body. The mesothelial
tissue is like cellophane and an asbestos fiber is like a splinter
which, if not removed, will scar over. Asbestos fibers cause
scarring or plaques and cause inflammation and fluid to
accumulate. Plaques develop randomly and unpredictably. In
about 70 percent of cases of mesothelioma overall, there is no
evidence of plaques.
Dr. Brodkin noted asbestos is considered a known human
carcinogen because it damages DNA or genetic material which
can affect cell growth and it causes inflammation which over
times causes cells to behave in an abnormal way. The cancer
cells replicate and divide quickly. The agencies that study
asbestos and mesothelioma do not make a distinction between
different fiber types because all fiber types cause all the asbestos
diseases. When he takes an occupational history, he is not
interested in whether someone was exposed to chrysotile or
amosite or crocidolite asbestos. He is just looking for exposure to
asbestos. All types of asbestos can travel to all the different sites
where mesothelioma can occur. Only research labs, not clinical
labs, are specialized enough to discover mesothelioma in locations
other than the lung. Dr. Brodkin testified he is unaware of any
agency in the world that has concluded that not all asbestos
fibers cause mesothelioma.
16
With Donald’s case, Dr. Brodkin had to find a well-
characterized source of asbestos and then a well-characterized
activity that disrupted the source. Asbestos has to be disturbed
so that the fibers become airborne at a concentration that is
sufficient to be breathed into the body. He also looked for direct
as opposed to indirect exposure. This is the difference between
the worker actually disturbing the asbestos through a task being
done and someone infected by contaminated clothing brought
home or by breathing in air someone else’s activity has
contaminated. He reiterated that no government or health
agencies have identified a “safe level” of asbestos because a
threshold has not been identified to date.
Dr. Brodkin noted there were four large national
epidemiological studies in Lombardy, Italy, Japan, and Germany
that investigated occupational history and pericardial
mesothelioma and they all consistently showed a strong
association between asbestos exposure and pericardial
mesothelioma. He testified that pericardial mesothelioma
represents less than 1 percent of mesotheliomas. Because of its
extreme rarity, “you need a large national study with thousands
of cases of mesothelioma” to find pericardial mesothelioma. As a
result, he did not think it was significant that some studies
reported no pericardial mesothelioma among the subject groups
because the studies were not large enough to capture the small
percentage of cases.
Dr. Brodkin also noted that case reports documenting a
history of occupational exposure to asbestos attribute pericardial
mesothelioma to that exposure. Case reports lacking information
about a known history of asbestos exposure cannot make that
connection. Getting a known history of asbestos exposure is
17
difficult because often the diagnosed patient has already died, or
the patient and his family is unaware whether the patient was
exposed. However, the large registry studies which were “well
designed to take an occupational history” showed a strong
association between pericardial mesothelioma and asbestos
exposure. He also noted that the Helsinki Criteria concluded
that asbestos caused mesothelioma disease in any mesothelial or
serosal tissue, whether it be in the lungs, heart, intestine, or
testicles. The location was irrelevant.
Relying on Dr. Compton’s testing and Bendix’s own supply
paperwork, Dr. Brodkin concluded Donald had sufficient
exposure to asbestos from drilling the Ebonite bowling balls. His
occupational history suggested no other possible source of
asbestos. Donald had a well-characterized source of asbestos (the
bowling balls) and participated in an activity (drilling, sweeping,
filing and sanding) that sufficiently disturbed the fibers so that
they became airborne in a concentration sufficient to be breathed
into the body. He opined that the Bendix asbestos filler in the
Ebonite balls was a substantial contributing factor to Donald’s
development of mesothelioma to a reasonable degree of medical
certainty.
Donald was exposed to asbestos over an 11-year period
between 1968 and 1978 when he was drilling bowling balls. The
Ebonite brand of balls contained asbestos between 1968 and 1972
when it used Bendix brake dust as filler for the balls. Using the
estimate of five drilled balls per week, Dr. Brodkin estimated
that Donald drilled 100 to 200 bowling balls between 1968 and
1972. He opined that the drilling exposed Donald to asbestos.
18
Donald drilled two inches deep which is one and one-half
inches into the asbestos-containing core. That generated a route
of exposure because his face was about one foot from the drilling
site. The second activity was sanding and filing. The third
activity was cleanup, which was a dusty operation. Dust settled
on the ground and Donald swept it up with a vacuum and
dumped the contents of the vacuum. Dr. Brodkin found a source
of exposure and activity that generated significant airborne
exposures during the 1968 through 1972 timeframe and beyond
to 1978. Sweeping resuspended the particles in the air, which
increased the duration of the exposure. Donald did not use any
mitigation measures like a mask, a respirator, an isolated
separate space, or wetting of the material, all of which have been
recommended in the United States since 1935.
Dr. Brodkin explained that based on Dr. Compton’s testing,
Donald generated .06 to .17 fiber per cubic centimeter (cc). A cc
is the size of a sugar cube of air. He opined that the
concentration of asbestos in ambient air is so low that one would
have to breathe in 500,000 sugar cubes of air to inhale a first
asbestos fibers. We take in 500 sugar cubes of air with each
breath. It would then take 1000 breaths to get the first fiber of
asbestos, which is very low and has not been associated with any
disease. With the air generated by the bowling ball drilling, one
would inhale the first asbestos fiber after only 16 sugar cubes,
instead of 500,000. At the upper end, one would only need to
inhale five sugar cubes of air to get to the first fiber. Dr. Brodkin
calculated that the magnitude of difference was 30,000 to 85,000
times the ambient level. He concluded this high concentration
increased the risk for asbestos-related disease like mesothelioma.
Dr. Brodkin found that Donald was generating and breathing
19
these fibers for four years for Bendix asbestos and another six
years beyond that for other asbestos suppliers. His opinion was
this high intensity and long duration of exposure increased
Donald’s risk of mesothelioma.
Finally, Dr. Brodkin testified that he relies on the Helsinki
Criteria in his practice to diagnose an asbestos-related
mesothelioma. The Criteria applies to any mesothelial or serosal
membrane in any location and does not distinguish between
types of asbestos. All the fiber types are potent so no distinction
is made by clinicians, the Environmental Protection Agency,
Occupational Safety and Health Administration, Centers for
Disease Control, National Institute for Occupational Safety &
Health, or the American Thoracic Society. The Helsinki Criteria
also sets out a median latency period of 30 to 57 years and a
minimum mesothelioma-free period of 10 years after exposure.
In Dr. Brodkin’s opinion, Donald fit the Criteria in that he had
exposure, a diagnosis, an appropriate latency period of 44 years
from 1968 to 2012, and no known differential risk factor other
than exposure to asbestos. He agreed with Dr. Horn that large
epidemiological studies are still not large enough to capture this
rare disease, so he also relies on case reports and national
registry studies. He is unaware of any case of pericardial
mesothelioma with a known history of asbestos exposure where
the clinician did not attribute the cause to asbestos. As for
chrysotile asbestos, Dr. Brodkin testified that in those parts of
the world where chrysotile is made into products (brakes and
textiles), there is a 400 to 3,000 percent increased rate of
mesothelioma, which demonstrates a strong association between
chrysotile and increased risk of mesothelioma. Animal studies
20
show a 25 to 75 percent rate of mesothelioma in animals injected
with chrysotile.
The third Vanni expert was Dr. Barry Horn who also gave
an opinion on the cause of Donald’s pericardial mesothelioma.
He acknowledged that the disease is always fatal and extremely
rare. The only known cause of mesothelioma in men in the
United States is prior exposure to asbestos, including chrysotile
asbestos which causes all forms of mesothelioma. He concurred
with Dr. Brodkin that there is no established minimum exposure
threshold below which mesothelioma cannot occur and that it
takes very little exposure to asbestos to cause the disease. He
also concurred with Dr. Brodkin that the disease is the same in
all mesothelial or serosal tissue, regardless of the location of the
tissue in the body.
Dr. Horn has seen patients with plaques or localized
scarring on the mesothelial tissue in the pericardium from prior
exposure to asbestos. He opined that asbestos can reach the
pericardium and flatly disagreed with anyone who did not hold
the same opinion. He had reviewed the four large national
registry studies which showed that approximately 60 percent of
those with pericardial mesothelioma had known prior asbestos
exposure. He basically repeated the testimony he gave at the
Evidence Code section 402 hearing, including his testimony that
the case reports which noted an occupational exposure to
asbestos all attribute pericardial mesothelioma to the asbestos
exposure. He went on to note that if a case report did not note
exposure, it was probably written by a doctor who was not an
expert in taking occupational exposure histories for the purpose
of identifying asbestos exposure. That was why the registry
studies were very significant, in his opinion, because they were
21
compiled by people who were experienced and knowledgeable in
taking occupational exposure histories.
Based on Dr. Compton’s testing, Donald’s history of drilling
the Ebonite bowling balls, and Donald’s medical records, Dr.
Horn opined that Donald was exposed to asbestos from drilling
bowling balls that had asbestos at the core and that he developed
pericardial mesothelioma due to that occupational exposure.
The defense presented four expert witnesses to counter the
Vanni expert testimony. First up was Renee Kalmes, a certified
industrial hygienist. Her employer, Exponent, had searched
Craigslist and eBay for Ebonite bowling balls made between 1967
and 1990. They acquired over 20, all of which were
manufactured in 1973 or later. None of the rubber Ebonite balls
contained asbestos. The six plastic Ebonite balls made between
1973 and 1978 contained some amounts of asbestos. In eight
other plastic Ebonite balls she tested, she found no asbestos.
Next was Sheldon Rabinovitz, a certified industrial
hygienist and toxicologist. He calculated the total dose of
asbestos that Donald could have experienced from Ebonite
bowling balls containing HD-100. He calculated Donald would
have been exposed to only .004 fibers per cubic centimeter per
day and over the course of four years he would have had
.016 “fiber years” of exposure. By comparison the average person
experiences .002 fiber years of exposure in very rural areas to
.1 fiber years of exposure in very industrialized areas.
Dr. James Crapo, a medical doctor specializing in
pulmonary medicine, testified on both general and specific
causation. Most cancers occur spontaneously, not as a result of
exposure to any substance. He opined both that pericardial
mesothelioma results only from spontaneous malignancy without
22
any identified external cause and that asbestos causes all types of
mesothelioma. He qualified his opinion by adding that
pericardial mesothelioma is associated with amphibole and not
with chrysotile asbestos because chrysotile does not have the
durability to reach the pericardium. Then he opined there is
insufficient evidence that inhalation of any type of asbestos fibers
causes pericardial mesothelioma and that researchers did not
find any cases of pericardial mesothelioma when studying groups
of workers who were highly exposed to asbestos. He also testified
that there is no reasonable pathway for inhaled asbestos fibers to
reach the pericardium and no evidence that such migration
actually occurs. No one studying pericardial mesothelioma has
ever found an asbestos fiber there. He also stated that
pericardial plaques are not evidence of asbestos exposure because
they develop whenever there is an infection or trauma to the
area.
As for Donald’s pericardial mesothelioma, Dr. Crapo opined
it was not caused by exposure to chrysotile asbestos; it was a
spontaneous malignancy without any external known or
identified cause, other than bad luck. He based his opinion on
the dearth of sufficient evidence in the medical literature
demonstrating an actual cause of this type of mesothelioma.
As to specific causation, Dr. Crapo opined that Donald’s
cumulative exposure to Bendix’s HD-100 would be less than his
lifetime exposure to background levels of asbestos and would not
be sufficient to cause the disease. He also expressed his opinion
that case reports cannot support an inference of causation
because they do not include control groups. They simply report
incidences of disease and exposure to toxic substances.
23
Finally, Dr. Suresh Moolgavkar, a medical doctor and Ph.D.
who conducts research on disease causation, testified. He also
opined that most cases of cancer arise due to random cell
mutation, not carcinogens in the environment. He acknowledged,
however, that pleural mesothelioma is strongly associated with
asbestos exposure in that 80 percent of all cases of pleural
mesothelioma in men are attributable to high doses of amphibole
asbestos.
Dr. Moolgavkar dismissed case reports because they are
just one physician’s observations of one patient’s disease.
Similarly, registry studies report on a number of cases of a
specific disease but are useless with respect to causation without
a proper epidemiological study. Dr. Moolgavkar published a
study in which he reviewed 237 papers on mesothelioma in the
pericardium and scrotum and concluded there was absolutely no
evidence that inhalation increased the risk of the disease. He
testified that in one study of over 30,000 heavily exposed asbestos
workers, one would expect to see between eight and 16 cases of
pericardial mesothelioma, but in fact no cases were reported.
DISCUSSION
A. Applicable Law
Honeywell challenges the sufficiency of the evidence to
support the verdict. We review the sufficiency of the evidence
under the substantial evidence standard of review. (Izell v.
Union Carbide Corp. (2014) 231 Cal.App.4th 962, 969.) Under
that standard, we consider all the evidence in the light most
favorable to the prevailing party, giving it the benefit of every
reasonable inference and resolving conflicts in support of the
24
judgment. (Howard v. Owens Corning (1999) 72 Cal.App.4th
621, 630).
In an asbestos-related injury case, causation involves two
elements: exposure and substantial factor causation. A plaintiff
“may prove causation . . . by demonstrating that the plaintiff’s
exposure to defendant’s asbestos-containing product in
reasonable medical probability was a substantial factor in
contributing to the aggregate dose of asbestos the plaintiff or
decedent inhaled or ingested, and hence to the risk of developing
asbestos-related cancer.” (Rutherford v. Owens-Illinois, Inc.
(1997) 16 Cal.4th 953, 976–977, fn. omitted (Rutherford).) The
contribution of the individual cause need only be “more than
negligible or theoretical.” (Id. at p. 978.) “Undue emphasis
should not be placed on the term ‘substantial.’ ” (Id. at p. 969.)
Expert testimony that is based on factors that are
speculative or conjectural does not constitute substantial
evidence. (Sargon Enterprises, Inc. v. University of Southern
California (2012) 55 Cal.4th 747, 771–772; Lockheed Martin Corp
v. Superior Court (2003) 29 Cal.4th 1096, 1110.) Because it is not
the trial court’s role to resolve scientific controversies, the jury
must resolve conflicts between competing expert opinions.
(Sargon, at p. 772; Rutherford, supra, 16 Cal.4th at p. 984.)
B. Substantial Evidence Supports the Jury’s Verdict that
Donald was Exposed to Asbestos
Honeywell argues the evidence was insufficient to establish
that Donald was exposed to the Bendix HD-100 asbestos. It
accurately cites Collin v. CalPortland Co. (2014) 228 Cal.App.4th
582, 589 and LAOSD Asbestos Cases (2020) 44 Cal.App.5th 475,
488 for the proposition that if a plaintiff fails to prove exposure,
there is no causation and no liability as a matter of law.
25
Honeywell argues that the Vannis failed to carry their burden
because at most they raised a “mere possibility” of exposure to
asbestos.
We disagree. The evidence was irrefutable that Bendix
supplied its asbestos dust, HD-100, to Ebonite over at least a
four-year period from 1968 to 1972 and that Ebonite used the
HD-100 as an ingredient to fill its plastic bowling balls. Bendix’s
own paperwork established the supply chain. The testing
experts, Dr. Compton for the Vannis and Renee Kalme for
Honeywell, agreed that the tested Ebonite balls from the 1970’s
contained varying levels of asbestos dust. While Ebonite’s former
employee William Duncan testified that Ebonite had different
formulas for its bowling ball filler, he confirmed that asbestos
was one of the ingredients in the filler from the late 1960’s to
1978 or 1979.
The evidence was also undisputed that Donald drilled the
bowling balls in a small unventilated space for two and one-half
to five hours per week with no mask or other breathing protection
and that he did so while standing directly in front of and very
close to the ball itself.
As set out above, the bowling ball testing by Dr. Compton
established that Donald inhaled 10,000 times the background
ambient air asbestos level through the drilling, sanding, and
filing during this period. In addition, he inhaled more fibers
through the sweeping and cleanup process. We conclude this is
more than negligible or theoretical exposure to asbestos.
That the Vannis could not present actual balls drilled by
Donald at his bowling alley to prove exposure is not dispositive.
The jury was allowed to infer that the Ebonite bowling balls from
Donald’s relevant occupational time period, randomly collected by
26
Honeywell, tested by both experts and found to contain asbestos,
were similar to the Ebonite bowling balls Donald actually drilled
which exposed him to asbestos fibers. This inference is further
supported by the Bendix documents in 1970 touting that its HD-
100 made “excellent filler in molding the inner core of bowling
balls.”
In sum, we find the evidence at trial supports a finding that
Ebonite plastic bowling balls were manufactured with some level
of asbestos from the mid-to-late 1960’s to 1978; Ebonite used the
Bendix HD-100 asbestos product to fill its balls from 1968 to
1972; and Donald’s drilling of the balls exposed him to asbestos
fibers. This was not a case of negligible or theoretical exposure.
Honeywell relies on Berg v. Colgate-Palmolive Co. (2019)
42 Cal.App.5th 630 as support for its argument that the evidence
of exposure is insufficient. In Berg, plaintiff alleged he was
exposed to asbestos from 1959 to 1962 when he used defendant’s
talc product, which was allegedly contaminated by asbestos. The
trial court granted summary judgment on the ground that
plaintiff could not prove exposure because the products he
actually tested were not proven to be from the relevant time
period, a particularly important fact because the asbestos were a
contaminant, not an intended ingredient. (Id. at pp. 632–633,
636–637.) Berg is inapplicable where, as here, the asbestos in
Ebonite’s bowling balls was an intended ingredient and the
tested balls were manufactured in the relevant time period. The
Vannis proved at trial that asbestos was among the ingredients
of the filler material in Ebonite’s plastic bowling balls from the
mid-to-late 1960’s to 1978; Bendix supplied more than 232,000
pounds of HD-100 to Ebonite from 1967 to 1972; Ebonite used the
HD-100 filler in the core of its bowling balls; and Bendix was
27
Ebonite’s exclusive supplier of asbestos filler for its bowling balls
from 1968-1972. This is more than negligible evidence that the
balls Donald drilled contained asbestos to which he was exposed
by the drilling process.
C. Substantial Evidence Supports the Jury’s Verdict that
Donald’s Exposure to Asbestos Was a Substantial Factor in
Increasing His Risk for Mesothelioma.
Honeywell next argues that the Vannis’ expert opinions on
causation are insufficient evidence because they rest on
unfounded speculation. Specifically, Honeywell argues 1) many
of the articles Dr. Horn and Dr. Brodkin relied upon expressly
contradicted their opinions; 2) neither expert relied on
epidemiological studies and instead relied on registry studies or
case reports or the Helsinki Criteria; 3) studies of the most
heavily exposed asbestos workers report no cases of pericardial
mesothelioma; 4) there is no data indicating that pericardial
mesothelioma increased in proportion to the use of asbestos.
We reject Honeywell’s arguments. First, under the
substantial evidence standard of review, we look at the evidence
in the light most favorable to the prevailing party, even if there is
contradictory evidence in the record. (Shirvanyan v. Los Angeles
Community College Dist. (2020) 59 Cal.App.5th 82, 89, fn. 2.)
That there may be articles or passages in articles that arguably
contradict the Vannis’ expert opinions is not dispositive of the
appeal in favor of Honeywell. Dr. Brodkin, for instance, edited a
textbook on occupational medicine which included opinions that
contradicted his own opinions, observations, and experience of
30 years. He explained reasonably that he edited the textbook so
that there would be a full and complete discussion of the medical
issues presented in the book. He believed each chapter author
28
presented a fair and even discussion of the issues, whether he, as
editor agreed with their opinions. Both experts backed up their
opinions with relevant literature in the field.
This brings us to Honeywell’s second objection that neither
Dr. Horn nor Dr. Brodkin relied on epidemiological studies, but
relied instead on case reports, national registry studies, and the
Helsinki Criteria. The Helsinki Criteria suffice to support the
result here. The Helsinki Criteria for Diagnosis and Attribution
is a compendium of information on mesothelioma and its
causation compiled by the world’s 20 most prominent scientists
and doctors in the field. This consensus report, updated in 2015,
reported that asbestos causes all different forms of mesothelioma.
This expert report is substantial evidence that Donald’s
pericardial mesothelioma was caused by Honeywell’s asbestos.
Honeywell also points out that many large studies of
heavily exposed workers do not show that pericardial
mesothelioma is caused by asbestos and, in particular, chrysotile
asbestos. In that same vein, Honeywell argues that the absence
of studies showing that the risk of pericardial mesothelioma
increases as the exposure to asbestos increases is dispositive in
its favor. This, again, ignores the standard of review which
requires us to view the evidence in the light most favorable to the
Vannis, notwithstanding evidence contradicting the verdict. We
find that the Helsinki Criteria, upon which the experts relied and
whose significance they explained at length to the jury, constitute
substantial evidence that exposure to asbestos increases the risk
of developing this rare type of mesothelioma.
29
DISPOSITION
The judgment is affirmed. Respondents are awarded costs
on appeal.
NOT TO BE PUBLISHED IN THE OFFICIAL REPORTS
STRATTON, Acting P. J.
We concur:
WILEY, J
OHTA, J.*
* Judge of the Los Angeles Superior Court, assigned by the
Chief Justice pursuant to article VI, section 6 of the California
Constitution.
30