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Rosling v. Associated Loggers Exchange

Court of Workers Compensation of Montana

March 21, 2019

JAMIE L. ROSLING, as Personal Representative of the Estate of David Lee McMillan Petitioner
v.
ASSOCIATED LOGGERS EXCHANGE Respondent/Insurer.

          Submitted: August 2, 2017

          FINDINGS OF FACT, CONCLUSIONS OF LAW, AND JUDGMENT

          DAVID M. SANDLER, JUDGE

         Summary: 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.

         Held: 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).[1]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 trial.

         ¶ 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 claim?
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 § 39-71-702, MCA?
Issue Six: Is McMillan entitled to costs, attorney fees and/or a penalty?

         FINDINGS OF FACT

         ¶ 5 The following facts are established by a preponderance of the evidence.

         History 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.

         McMillan's Exposures to Asbestos, Employment History, and Diagnosis of ARD

         ¶ 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 Libby.

         ¶ 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 installing culverts.

         ¶ 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 asbestos.

         ¶ 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 getting shorter.

         ¶ 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 exertion.

         ¶ 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 asbestos.

         ¶ 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 pleural disease."

         ¶ 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 particularly difficult.

         ¶ 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 P&S.

         ¶ 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 years.

         ¶ 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. Black testified:

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 disease.
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 P&S.

         McMillan's Claim

         ¶ 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.

         McMillan's Death

         ¶ 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.

         Terry Spear, PhD

         ¶ 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 8, 2015.

         ¶ 48 Dr. Spear determined that McMillan had suffered non-occupational and occupational exposures to Libby asbestos.

         ¶ 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 asbestos-related disease."

         ¶ 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 an ARD.

         ¶ 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 his ARD.

         Gregory 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 restricted.
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), [2] 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. ...


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