JAMIE L. ROSLING, as Personal Representative of the Estate of David Lee McMillan Petitioner
ASSOCIATED LOGGERS EXCHANGE Respondent/Insurer.
Submitted: August 2, 2017
FINDINGS OF FACT, CONCLUSIONS OF LAW, AND
M. SANDLER, JUDGE
The decedent was exposed to Libby asbestos for most of his
life and diagnosed with asbestos-related disease almost seven
years before working for Respondent's insured. However,
his condition was stable and he continued to work as a
logger. After beginning to work for Respondent's insured,
where he suffered a significant exposure to Libby asbestos,
decedent's ARD significantly and rapidly worsened and he
ultimately had to quit his job because he could no longer
physically perform it. Prior to his death, he filed an OD
claim, contending that his ARD was an OD and that he was last
injuriously exposed to the hazard of his OD while employed at
Respondent's insured. Respondent asserts that Petitioner
did not timely file his claim. In the alternative, Respondent
asserts that Petitioner's employment for its insured did
not cause his OD.
The decedent timely filed his claim. The decedent's ARD
was an OD because his exposure to Libby asbestos during his
lifetime of employment was the major contributing cause of
his ARD and because his exposure while working for
Respondent's insured was the major contributing cause of
the rapid acceleration of his ARD, which resulted in his
inability to work. Respondent is liable for Petitioner's
OD because it was the insurer at risk at the time decedent
was last injuriously exposed to Libby asbestos. Thus,
Respondent is liable for OD benefits.
1 The trial in this matter began on November 23, 2015, in
Kalispell. On December 17, 2015, counsel delivered closing
arguments. On August 2, 2017, Respondent Associated Loggers
Exchange (ALE) filed a post-trial supplemental brief by leave
of Court and this Court deemed the matter submitted for
decision. Laurie Wallace, Ethan Welder, Dustin Leftridge, and
Jon L. Heberling represented Petitioner
(McMillan).Larry W. Jones represented ALE.
2 Exhibits: This Court admitted Exhibits 2, 16, and
17 without objection. This Court admitted Exhibits 1 and 3
through 13 over the parties' respective relevancy
objections. ALE withdrew Exhibits 14 and 15.
3 Witnesses and Depositions: This Court admitted the
depositions of McMillan, Brad Black, MD, Dale and Suzanne
Riggles, and Gregory Michael Loewen, MD. McMillan, Kerri
Wilson, and Terry Spear, PhD, were sworn and testified at
4 Issues Presented: Based upon the parties'
statement of "Issues to be Determined by Court" and
their contentions in the Pretrial Order, and their arguments
at trial, this Court considers the following issues:
Issue One: Did McMillan timely file his occupational disease
Issue Two: Did McMillan sustain an occupational disease?
Issue Three: If McMillan sustained an occupational disease,
is Associated Loggers Exchange liable for it?
Issue Four: If Associated Loggers Exchange is liable for
McMillan's occupational disease, is McMillan entitled to
medical benefits and an impairment award?
Issue Five: If Associated Loggers Exchange is liable for
McMillan's occupational disease, is McMillan entitled to
permanent total disability benefits pursuant to §
Issue Six: Is McMillan entitled to costs, attorney fees
and/or a penalty?
5 The following facts are established by a preponderance of
of Asbestos in the Libby Area
6 From the 1920s to 1990, Zonolite Company and then W.R.
Grace operated a vermiculite mine, which was seven miles
northeast of Libby. The vermiculite contained a unique,
amphibole-type asbestos, called "Libby amphibole"
or "Libby asbestos."
7 The open pit mining, and the processing and transportation
of the vermiculite, released dust containing many tons of
Libby asbestos into the atmosphere each day. Libby asbestos
fibers are microscopic and remain airborne for hours once
introduced into the air.
8 The dust contaminated the air in Libby and the town had a
hazardous "background" level of asbestos when the
mine operated. The residents of Libby suffered a
"community exposure" to asbestos.
9 The dust drifted and was blown, oftentimes for miles, until
it settled and contaminated whatever it landed upon,
including the forest, duff, and soil in the area surrounding
the mine. Studies conducted from 2005 through 2013 showed
that the areas closer to the W.R. Grace mine had the highest
concentrations of Libby asbestos contamination, but that
Libby asbestos was detected in forest duff as far as 16.9
miles from the mine.
10 In the time between 2009 and 2014, researchers discovered
that logging activities, such as falling trees, hooking,
skidding, and processing, that disturb the contaminated tree
bark, duff, or soil released Libby asbestos into the air and
exposed those in the area.
11 All types of asbestos are hazardous, but Libby asbestos is
more toxic than other types, i.e., it takes a much lower
quantity of Libby asbestos to cause asbestos-related disease
(ARD) or "asbestosis," umbrella terms that describe
several conditions in which lung tissue is damaged and
scarred, including pleural thickening, pleural plaques, and
interstitial fibrosis. The scar tissue is inelastic, which
causes decreased respiratory function that worsens over time.
Exposures to Asbestos, Employment History, and Diagnosis of
12 McMillan grew up in Libby and lived most of his life in
Libby. McMillan's family has been particularly hard hit
by ARD, as McMillan's father, who worked for a time at
the W.R. Grace mine and had direct contact with vermiculite,
died of ARD. In addition, his three brothers and his sister
died from ARD. McMillan was exposed to Libby asbestos at his
home and to the Libby background asbestos while residing in
13 In 1973, when he was 17 years old, McMillan worked for
Bothman Logging, which logged in the Kootenai National
Forest. He was exposed to Libby asbestos during this work.
14 From 1974 to 1976, McMillan served in the Army. He was not
exposed to asbestos during his service.
15 In 1976, McMillan returned to Libby, and returned to
logging, primarily in the Kootenai National Forest, in areas
contaminated with Libby asbestos. He was exposed to Libby
asbestos during this work.
16 From 1980 to 1983, he worked in the oil business. He was
not exposed to asbestos during this work.
17 McMillan returned to Libby in 1983 and, for the next 28
years, worked in the logging industry for several employers.
He worked as a skidder operator, a sawyer, and worked the
landings. McMillan also helped build logging roads, including
18 During this time, McMillan primarily worked in the areas
within 10 miles of the former W.R. Grace mine. When he worked
for Owens Ventures, he worked near the vermiculite loading
facility. McMillan and his coworkers had to push piles of
vermiculite left by dump trucks out of the way to access logs
used to make a landing. He consistently worked in the dust
created by this work, which was contaminated with Libby
19 On September 24, 2001, McMillan underwent an asbestos
screening at the Center for Asbestos Related Disease (CARD)
Clinic in Libby. As part of the screening process, McMillan
filled out a questionnaire which asked him questions about
past employments, residences, and recreational activities -
including questions about logging.
20 Brad Black, MD, the medical director of the CARD clinic,
found pleural changes in McMillan's lungs. A follow-up CT
scan revealed findings consistent with ARD, and Dr. Black
recommended more diagnostic testing.
21 On December 3, 2001, Alan C. Whitehouse, MD, a physician
at the CARD clinic with significant experience treating
patients with ARD caused by Libby asbestos, reviewed a chest
x-ray, which showed "some minimal pleural
thickening," and a CT scan, which showed "one small
area of irregular, what appears to be pleural plaque."
Dr. Whitehouse stated, "These do appear to be consistent
with asbestos related disease."
22 Dr. Black testified that to diagnose ARD, one factor is
the "latency period," which is the time that passes
between an exposure of Libby asbestos and objective medical
findings of ARD, such as a chest x-ray or a CT scan. Dr.
Black testified that the latency period for ARD from Libby
asbestos is 10-20 years, although he explained that with
technological advances in scanning, the latency period is
23 On May 17, 2006, Dr. Black saw McMillan for a follow-up
visit. Dr. Black noted, "David has been short of breath
but continues to work in the woods." Dr. Black noted
that McMillan had not smoked for a year and had had less
shortness of breath since then. He also noted that
McMillan's ARD was relatively stable. Dr. Black noted
that McMillan's pulmonary function tests (PFTs), which
are objective medical findings, were "virtually
identical" to his 2005 tests and in the normal range.
Dr. Black also noted, "I reviewed his 2005 CT scan and
he has very obvious findings of sub-pleural interstitial
fibrosis along with pleural thickening scattered throughout
much of his chest."
24 On July 25, 2007, a physician at the CARD clinic examined
McMillan and found him radiographically and functionally
unchanged but noted concern that his PFTs had declined. The
physician noted that McMillan continued to work in the woods
as a sawyer and that he was able to keep up "[f]or the
most part," with some episodic shortness of breath with
25 McMillan started working for P&S Contracting (P&S)
on August 1, 2008. McMillan built and maintained logging
roads and worked as a logger. He operated heavy machinery,
including a skidder. For much of this time, he worked in
areas within 10 miles of the vermiculite mine. This work was
extremely dusty; at times, McMillan had to wear a mask.
26 McMillan was exposed to Libby asbestos in amounts far
greater than the Libby background level during this work.
However, McMillan did not know he was being exposed to Libby
27 At P&S, McMillan worked with Dale Riggles, who started
at P&S in 2009 and quit shortly after he was diagnosed
with ARD on November 9, 2010. Riggles and his wife testified
together at a deposition. Riggles remembered that McMillan
had a difficult time breathing and frequently coughed and
McMillan saying that he had ARD. Riggles knew they were
working in specific areas known to be contaminated with Libby
asbestos, but he did not discuss this with McMillan. However,
Riggles testified that, while they worked at P&S,
McMillan stated that he was generally aware that the forest
around Libby was contaminated.
28 A February 11, 2009, x-ray revealed that McMillan's
ARD continued to be stable, and primarily unchanged since
2007. However, on February 25, 2009, Dr. Black noted that
McMillan's ARD was advancing, as exhibited by a decline
in his pulmonary function tests, including 30% decline in his
diffusion capacity for carbon monoxide (DLCO) - a test which
measures the lungs' ability to transfer oxygen into the
bloodstream - since 2001.
29 On February 24, 2010, Dr. Black noted, "Dave has
noticed a significant drop in his breathing over this last
year. He cannot get up the hills readably [sic] as he has in
the past." Dr. Black noted a decline in McMillan's
PFTs. In his assessment, Dr. Black wrote: "Asbestos
related disease - he has experienced significant volume loss
and his chest x-ray suggest possibly [sic] of some increased
scarring that could be parenchymal, in addition to his
30 On March 12, 2010, a CT scan revealed a "marked
change" in McMillan's lungs. In his record dated
March 15, 2010, Dr. Black noted that the CT scan showed
"diffuse pleural changes, along with subpleural fibrosis
in both lungs starting high in the chest and going all the
way down to the diaphragm level." Dr. Black noted that
the radiographic progression "certainly explains his
problems with increasing dyspnea on exertion." McMillan
was due to return to work later that spring, but was
concerned because he became short of breath within minutes
while getting firewood and noted that walking uphill was
31 ALE started insuring P&S on July 1, 2010.
32 Dr. Black testified that after a person is diagnosed with
ARD, any ongoing, significant exposures to asbestos
contribute to the worsening of the disease. During his
deposition, Dr. Black was asked about the effects of ongoing
exposure to Libby asbestos for those already diagnosed with
ARD. Dr. Black testified:
Well, if there's ongoing exposure and it's
significant enough, it would - it would contribute to
worsening of the disease over time. But, once again, from
that exposure there's a time frame before that would
become evident because of the new entry of particles. And,
you know, you assume there's going to be a delay before
there's the sequence of molecular responses to the
fibers, there's going to be a latency from the new
exposures, but then you would anticipate that they would
further increase the disease severity over time.
33 Dr. Black did not tell McMillan which exposure pathway
caused his ARD because, in the clinical setting, Dr. Black
"couldn't tell source wise how much came [from]
here, how much came [from] there."
34 On December 17, 2011, McMillan stopped working for P&S
because he could no longer do the work as a result of his
ARD. ALE was still P&S's insurer.
35 McMillan did not obtain other employment after leaving
36 On January 23, 2012, McMillan was seen for follow-up at
the CARD clinic. His chest x-ray revealed prominent
interstitial fibrosis in both lungs and pleural thickening.
His PFTs demonstrated a decline in function over the last two
37 On February 17, 2012, Dr. Black wrote a letter in which he
opined that McMillan's ARD had progressed to a point that
impacted his ability to work and to carry on activities of
daily living. During his deposition, Dr. Black explained
that, because of his decreased lung function, McMillan
suffered from severe physical and mental fatigue. Dr. Black
estimated that the farthest McMillan could walk on a level
surface was 100 feet and that McMillan could not do any
repeated lifting. Dr. Black opined that it was remarkable
that McMillan had remained in his job as long as he had, and
Dr. Black had encouraged McMillan to leave his job sooner
because of exhaustion due to living with ARD. When asked if
McMillan had the ability to engage in gainful employment, Dr.
David's [sic] is significantly impaired with his lung
disease. As a matter of fact, he's - he ended up working
way past what I would have considered - you know, what I
would have expected based on the severity of his lung
And so he finally, you know, decided that he couldn't
keep up with what he was doing, and those are always hard for
these guys working, I mean they have a horrible time giving
up their work, and he finally made that - realized he
couldn't do it. I encouraged him earlier, because I could
see how exhausted he was.
So I would - I don't see him as employable. I don't
know who would employ him with the severity of his problems
with his lungs.
38 This Court finds that McMillan was unable to physically
perform regular employment as of the day he quit working for
39 In late 2012, Cheryl Wolleats, a former coworker at
P&S, told McMillan that several former P&S employees
were having trouble breathing and were filing occupational
disease (OD) claims against P&S. Wolleats told McMillan
that he "could have" been exposed to Libby asbestos
while working for P&S. McMillan testified that this was
the first time he heard that "asbestos was in the
logging industry." Wolleats told McMillan that he should
file a claim to "cover" himself.
40 When asked where he thought he had been exposed before
this conversation, McMillan testified, "Here in town, at
our old log house, I mean I was raised around it." This
Court finds this testimony credible.
41 On June 1, 2013, McMillan filed a First Report of Injury
or Occupational Disease for exposure to asbestos while
working for P&S. At that time, McMillan did not
"officially" know he had been exposed to Libby
asbestos while working for P&S but filed his claim so as
to "cover all the bases."
42 ALE initially denied liability because McMillan's
first report stated that the date of injury was in 2012,
after McMillan quit working for P&S. On July 14, 2014,
ALE denied liability, asserting it was "unable to
determine liability regarding the relationship, if any, of
this claim to employment at P&S Contracting." After
receiving a demand letter from one of McMillan's
attorneys, ALE obtained McMillan's medical records in
early 2015. ALE determined that the medical records did not
support McMillan's claim that his exposure to Libby
asbestos while working for P&S caused his ARD. Kerri
Wilson, ALE's claims adjuster, testified that she noted
that McMillan was diagnosed with ARD before he started
working for P&S. Wilson also testified that ALE continued
to deny liability for McMillan's claim based upon Dr.
Black's testimony that ARD had a ten-year latency period.
From this testimony, Wilson concluded that McMillan could not
have developed ARD as a result of working for P&S.
43 McMillan's lungs continued to worsen and by early
2015, he required supplemental oxygen full-time.
44 McMillan died as a result of his ARD on December 3, 2015.
45 Terry Spear, PhD, testified as an expert for McMillan. Dr.
Spear has a PhD in industrial hygiene and is a professor
emeritus at Montana Tech.
46 Dr. Spear began researching asbestos contamination in the
Libby area in 1996. Dr. Spear has co-authored at least seven
peer-reviewed articles pertaining to Libby asbestos,
including several showing that tree bark, duff, and soil in
the forest around Libby was contaminated with Libby asbestos.
The first such article was published in 2006. Dr. Spear was
also part of studies in which the researchers simulated
collecting firewood and building fire lines in the forest
around the mine to determine if these activities released
asbestos into the air. The studies showed that activities
such as cutting trees with a chainsaw and digging trenches
released asbestos fibers into the air.
47 Dr. Spear issued his expert report in this case on October
48 Dr. Spear determined that McMillan had suffered
non-occupational and occupational exposures to Libby
49 Non-occupationally, Dr. Spear determined that McMillan was
exposed to Libby asbestos just by living in Libby. Dr. Spear
also noted McMillan grew up in Libby in a log house with
vermiculite attic insulation, which leaked into the living
space. He played on the ball fields, which were contaminated,
and in vermiculite piles by the ball fields. McMillan played
inside the railroad cars by the lumber mill, which was
contaminated. McMillan also hunted and fished in the Rainy
Creek drainage, an area that was heavily contaminated.
50 Occupationally, Dr. Spear opined that McMillan suffered a
"severe exposure to asbestos fibers" while working
as a logger for 30-plus years because of the large volume of
asbestos contained within the tree bark, duff, and soil in
the areas where he worked - asbestos that became airborne
when disturbed. Dr. Spear noted McMillan worked in many areas
close to the mine site, areas that were contaminated with
Libby asbestos. McMillan's work area was dusty, and he
was exposed to contaminated dust from log-processing
activities, dusty logging roads, and soil-disturbing
activities. During his employment with Owens-Hurst Logging,
McMillan worked in an area where W.R. Grace dumped piles of
vermiculite, which McMillan and his coworkers pushed out of
the way to access logs. McMillan told Dr. Spear that they
were "knee deep in vermiculite." Additionally,
McMillan's operation of heavy equipment caused
significant soil disturbance and caused asbestos in
contaminated soil to become airborne.
51 Dr. Spear explained, "[McMillan] was in areas that he
was working in and around materials that were contaminated
with amphibole asbestos, and that the activities that he
performed disturbed these materials, releasing fibers into
his breathing zone. And so he was at risk to [sic] an
52 Dr. Spear also explained that McMillan had a
"take-home exposure" to Libby asbestos, i.e.,
asbestos contaminated his work clothes which, in turn,
contaminated his home. Dr. Spear considered McMillan's
"take-home exposure" to be an occupational exposure
and opined that during the entirety of his logging career, it
contributed to his exposure.
53 Dr. Spear also opined that McMillan's work as a logger
exposed him to levels of airborne Libby asbestos fibers well
above the background level in Libby. Thus, Dr. Spear opined
that McMillan's occupational exposure "was
significantly above the background exposure that would occur
in the town of Libby" and "greatly exceeded"
his community exposure.
54 Dr. Spear opined that McMillan's work as a logger
exposed him to a sufficient amount of Libby asbestos to cause
55 As for McMillan's work for P&S, Dr. Spear opined
that McMillan had a "severe exposure to asbestos while
working . . . for P&S," which was the same type and
kind of exposure to Libby asbestos he had had with his
previous employers in the logging industry. Dr. Spear noted
that McMillan worked a total of 2, 473.25 hours for P&S,
with many of those hours spent in the drainages near the
former W.R. Grace mine. Dr. Spear explained:
Mr. McMillan worked as an equipment operator, a sawyer, and
doing road construction. His job duties put him around many
dust generating activities in areas contaminated with
asbestos. During his employment, he was exposed to a dusty
environment from numerous sources, including: dust emanating
from the log processing activities at the logging sites, dust
emanating from the logging roads, and other activities that
disturbed asbestos fibers.
Many of the areas in which Mr. McMillan performed logging
activities and road and culvert construction were within 17
miles of the former Vermiculite mine. Every step of the
harvesting, transportation, and road building process was
dusty; from the time the logs were cut, stacked, and loaded
on trucks the asbestos dust on the bark was entrained into
the air and breathed in by workers. Mr. McMillan was exposed
to this dusty environment during his time harvesting these
contaminated logs in areas known to be contaminated with
asbestos. The most important factor influencing the extent of
airborne exposure to LA [in] Libby is the disturbance of
contaminated source materials by human activity. Through his
work as a sawyer, equipment operator and road builder, Mr.
McMillan was constantly surrounded by disturbances of
contaminated soil and dust, bark, and vermiculite dust.
56 When asked at trial how McMillan was exposed at P&S,
Dr. Spear testified:
Well, again, through his work in the forest, being out in
areas that were contaminated with Libby Amphibole, disturbing
contaminated materials, whether it be duff, soil, trees,
driving on dusty logging roads, wearing the same clothes to
and from work, basically putting asbestos fibers from where
he was working into his vehicle, and then being in that
vehicle and then going home with the same clothes and
bringing asbestos fibers into his home, and adding to
whatever fibers could have already been there.
57 Dr. Spear opined that McMillan's work at P&S
"exposed him to a level of asbestos fibers which would
have contributed to his fiber burden"and was sufficient
to either cause, contribute to, or significantly aggravate
Michael Loewen, MD
58 McMillan retained Gregory Michael Loewen, MD, to
investigate his case and offer opinions regarding his claim.
Dr. Loewen is board certified in internal medicine, pulmonary
disease, and critical care. He has published numerous
peer-reviewed papers, including more than ten related to
asbestos exposure. He has worked at the CARD clinic since
2012, where his main duties are evaluating patients for the
presence of ARD and, for the patients who have ARD, providing
treatment. Dr. Loewen did not treat McMillan.
59 Dr. Loewen issued his expert report on September 1, 2015.
60 Dr. Loewen explained that lodged asbestos fibers cause an
inflammatory response in the lungs, which results in a
scarring process, which, in turn, causes difficulty
breathing. In his report, Dr. Loewen explains the mechanism
of injury from Libby asbestos as follows:
10. In relative terms of their length to width (aspect
ratio), Libby asbestos fibers are often long and sharp, like
needles. The fibers breathed in are microscopic, as are the
alveoli (tiny air sacs) in the lungs. When breathed in, the
fibers lodge in the structure around the alveoli, and are too
small to be expelled. Asbestos fibers irritate and inflame
the lung tissue structure around the air sacs (the
interstitia). Scarring in the interstitia is interstitial
disease. When the interstitia are significantly scarred, they
can no long[er] expand or contract fully, and breathing is
11. The amphibole fibers also migrate to the outside portion
of the lung, where they scar and inflame the pleura (the lung
lining) and cause pleural disease. . . . Pleural disease
seems particularly pronounced with Libby asbestos fibers.
12. The normal pleura is actually thinner than a blown up
balloon. It is a very thin membrane, and it can expand like a
balloon. Asbestos fiber scarring causes the pleura to look
much like the orange portion of an orange rind, and can be
just as thick. . . . When the lung lining becomes as thick as
an orange rind, it can no longer expand freely and breathing
is severely restricted. Asbestos disease is generally a
restrictive lung disease.
61 Dr. Loewen explained that ARD has a "latency
period," meaning that there is a time between the
exposure to Libby asbestos, which causes immediate harm, and
the time ARD is detectable with a chest x-ray or a CT scan.
In his report, Dr. Loewen explains:
There is a latency period between exposure and the first
appearance of asbestos disease on chest x-ray or CT. During
the latency period, microscopic asbestos fibers are working
at a microscopic level, until scarring becomes detectible on
chest x-ray or CT. ATS (2004),  p.695, suggests a minimum latency
period of 15 years, based largely on chrysotile studies.
Based on clinical observation, asbestos pleural disease from
exposure to Libby asbestos has appeared radiographically in
as little as three years. With Libby asbestos, the range
generally appears to be about 3 to 50 years to diagnosis.
62 Dr. Loewen explained that ARD is a progressive disease,
though the rate of progression is variable. Dr. Loewen agreed
that once a person has ARD, he will not get any better. Dr.
Loewen also explained that ARD is "cumulative,"
meaning that the asbestos fibers that lodge in the lung are
there for life and that with additional exposure, more
asbestos fibers accumulate in the lungs, which further
damages the lungs. Dr. ...