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Hinson v. Continental Tire Americas

Court of Appeals of North Carolina

September 3, 2019

GAIL CANUP HINSON, Executrix of the ESTATE OF WALTER DUNBAR HINSON, Deceased-Employee, Plaintiff-Appellant,

          Heard in the Court of Appeals 12 March 2019.

          Appeal by Plaintiff from opinion and award entered 25 January 2018 by the North Carolina Industrial Commission. I.C. No. 240941.

          Wallace and Graham, PA, by Edward L. Pauley, for Plaintiff-Appellant.

          Fox Rothschild LLP, by Jeri L. Whitfield and Lisa K. Shortt, for Defendant-Appellee.

          McGee, Chief Judge.

         This appeal is companion to four additional appeals, COA18-766, COA18-767, COA18-768, and COA18-769 (all five together, the "bellwether cases"), consolidated for hearing by order of this Court entered 8 June 2018. The four companion appeals will be decided by opinions filed concurrently with this opinion.

         I. Procedural History

         Decedent Walter Dunbar Hinson ("Plaintiff Hinson") worked for Continental Tire the Americas ("Defendant") at Defendant's tire factory (the "factory") in Charlotte from 1967 until 1999.[1] This case and the other bellwether cases involve workers' compensation claims based on allegations that Plaintiff Hinson, along with the additional four plaintiffs[2] in the bellwether cases ("Bellwether Plaintiffs"), were exposed to levels of harmful airborne asbestos sufficient to cause asbestos-related diseases, including asbestosis.[3] The bellwether cases constitute a small percentage of a much larger number of related claims that were consolidated by the Industrial Commission (the "consolidated cases").[4] Determination of the bellwether cases will impact not only the Bellwether Plaintiffs, but also the remaining plaintiffs from the consolidated cases (together with the Bellwether Plaintiffs, "Plaintiffs" or "Consolidated Plaintiffs"). The Full Commission (the "Commission") explained the unique procedure that was adopted to handle the large volume of consolidated cases in five opinions and awards, entered on 25 January 2018, that decided the bellwether cases:

This case is part of a large group of cases (currently numbering 144) alleging occupational exposure to asbestos at [the] factory. The large group of [P]laintiffs contends that they developed asbestos-related disease, primarily asbestosis, caused by exposure to asbestos at the . . . factory[.] Defendant denied that the diagnoses of asbestosis were valid, and also denied that any employee could develop an asbestos-related disease as a result of employment with [Defendant because there was insufficient exposure to asbestos in [the] factory.
[The consolidated cases] were postured so that there would be an "initial six" cases to be tried as bellwether cases. Although the 144 cases had many issues and facts in common, it was an impossibly large number to try individually, and too difficult to manage in one joint hearing. Therefore, [Plaintiffs' counsel selected a group of six representative bellwether cases to be tried together in a consolidated manner. The evidence presented in this consolidated hearing regarding the factory, [asbestos] exposures to employees, the criteria for the diagnosis of asbestosis, the scientific evidence regarding asbestos exposure, and the potential for disease causation would be common to, and thus universally applicable to, all 144 claims. The parties agreed that evidence on the general issues was to be part of the record for all [consolidated cases], to the extent the evidence was applicable to each [P]laintiff s issues. The [B]ellwether [Plaintiffs' individual medical and employment histories would be addressed, as would scientific evidence applicable to all 144 claims regarding asbestos-related-disease-causing capabilities, including the exposure and medical causation testimony. In addressing the bellwether cases first and presenting evidence applicable to all extant claims, the assumption was that after the six cases proceeded through trial, decision and appeal, the parties would be in a better position to evaluate the remaining claims. The remaining [consolidated cases] could then be potentially resolved, or they could proceed to abbreviated hearings for the introduction of evidence regarding their individual medical and employment information.
One of these "initial six" [Bellwether P]laintiffs, Kirkland . . ., filed a Notice of Voluntary Dismissal with Prejudice on 13 November 2012. This left five Bellwether Plaintiffs to proceed through trial, decision, and appeal.[5] While under the jurisdiction of former Deputy Commissioner George Glenn, these matters were set on a course unlike that of most workers' compensation cases, in that each side was given the opportunity to have a "full trial on the science"- with freedom to prosecute the cases according to the civil procedure used in superior court. The parties were permitted to take as many pre-hearing depositions as they wished and could call as many hearing witnesses as they determined to be necessary. The [B]ellwether [Plaintiffs' cases were heard together in a consolidated posture by former Deputy Commissioner Gheen on a special-set basis in various locations over the course of thirty-eight hearing days beginning 14 February 2011 and concluding 18 February 2013. Former Deputy Commissioner Gheen's hearing of these claims also involved substantial pre-trial proceedings. [6] Much of the evidence presented was "common" evidence applicable to all 144 extant claims.
. . . . The Full Commission has reviewed and considered all hearing and deposition transcripts, along with all evidentiary exhibits, arguments, and briefs in reaching a decision in this claim.

         After hearings had already commenced, the deputy commissioner entered a 27 July 2012 order requiring that "Plaintiffs who die during the pendency of these claims shall have at least 30 blocks of lung tissue preserved for autopsy and examination by an expert of Defendant's choice." The deputy commissioner based this order on the following findings and reasoning:

[Defendant] denies that any of its employees, including claimants, would have had sufficient exposure to asbestos from working at its facility to either cause or contribute to an asbestos related disease. It has presented the testimony of multiple credible expert witnesses in support of this defense.
[] Plaintiffs' claims against [Defendant] are based, in part, on a "B-read" of an x-ray provided by Plaintiffs' expert. [7] As testified by the medical experts, radiological studies are only effective at identifying abnormal features on the x-ray that may be consistent with the disease of asbestosis, but also may be consistent with multiple other lung diseases. In order to make a diagnosis of asbestosis, a physician is called upon to rule out other possible conditions.
[] The medical experts representing both parties have repeatedly testified that the only way to positively identify whether or not a lung condition or other cancer is caused by asbestos exposure is to take a sample of and examine the actual lung tissue. However, due to the risks involved, this procedure is not done while the patient is alive; it is commonly performed at autopsy.

         Therefore, the deputy commissioner ordered that Plaintiffs save lung tissue of any Plaintiffs who died so that their lung tissue could be examined. Plaintiffs did not fully comply with this order.

         The deputy commissioner reasoned in a 30 April 2013 order: "The diagnoses [of asbestosis], or lack thereof, by the experts is based on the reading of the same radiology. Both sides argue the veracity of their own experts." "Given the opposing medical findings, . . . the undersigned Deputy Commissioner suggested to the parties" that they "jointly agree to independent medical experts or to experts chosen by the Industrial Commission to review the radiology and any other relevant medical evidence, which experts' opinion both parties would accept as final." "Alternatively the parties debated whether the Plaintiffs should be compelled to submit to a high resolution computed tomography (hereinafter 'HRCT') scan to be interpreted by a physician selected by the Commission in order to determine the presence or absence of asbestosis." Defendant agreed to the suggestion, and agreed to pay for the HRCT scans and associated costs, but Plaintiffs did not agree.

         During the hearings, "[m]uch of the evidence presented was 'common' evidence applicable to all 144 extant claims." Due to the resignation of the deputy commissioner who had presided over the hearings, the consolidated cases were assigned to a different deputy commissioner on 15 April 2015. Plaintiffs and Defendant completed submission of evidence to the deputy commissioner, and made their closing oral arguments on 26 and 27 January 2016. The deputy commissioner filed his opinions and awards in the bellwether cases on 19 December 2016, denying the claims of all five Bellwether Plaintiffs. Plaintiffs appealed to the Full Commission on 21 December 2016. The Commission heard the matters on 29 June 2017, and also denied Plaintiffs' claims by five opinions and awards entered 25 January 2018. The five 25 January 2018 opinions and awards filed in the consolidated cases each contain findings of fact common to all claims, which also include the ultimate findings and conclusions of law common to all claims. Following the common findings and conclusions, each of the five opinions and awards before us contain findings of fact and conclusions of law sections that are specific to each individual Bellwether Plaintiff, as well as the Commission's rulings denying each of the Bellwether Plaintiffs' claims.

         Bellwether Plaintiffs appealed, and Plaintiffs and Defendant filed a motion with this Court on 30 May 2018 requesting consolidation of the bellwether cases for appeal.[8] This Court ordered that a single record be submitted for all five bellwether cases, and that: "The parties shall each submit one general brief addressing common issues and five specific briefs addressing individual [P]laintiff issues." Plaintiffs and Defendant each filed a single "general brief"-ostensibly the "general brief addressing common issues" ordered by this Court. Plaintiffs' general brief is in reality the statement of facts for Plaintiffs' individual briefs. In addition, each of the five Bellwether Plaintiffs filed "specific" individual appellant briefs that are nearly identical, and almost exclusively argue common issues. Defendant responded to the Bellwether Plaintiffs' individual briefs by filing five separate appellee briefs addressing the issues specific to each of the five Bellwether Plaintiffs. Although Plaintiffs' individual briefs do not address the "common issues" separately from the "individual issues," we address all Plaintiffs' arguments concerning the "common issues" that were decided in the Commission's 25 January 2018 opinions and awards in this opinion-COA18-770. Our holdings for the "common issues" will be incorporated by reference in our opinions for the remaining four bellwether cases- COA18-766, COA18-767, COA18-768, and COA18-769. The "individual issues" will be addressed separately in each opinion.

         II. General Factual History

         Plaintiffs all allege they were exposed to asbestos while working at the factory, and further allege they developed compensable asbestos-related diseases as a result. As explained in a Fact Sheet published by the National Cancer Institute ("NCI")- which was entered into evidence:[9]

Asbestos is the name given to a group of minerals that occur naturally in the environment as bundles of fibers that can be separated into thin, durable threads. These fibers are resistant to heat, fire, and chemicals and do not conduct electricity. For these reasons, asbestos has been used widely in many industries.
Asbestos minerals are divided into two major groups: Serpentine asbestos and amphibole asbestos. Serpentine asbestos includes the mineral chrysotile, which has long, curly fibers that can be woven. Chrysotile asbestos is the form that has been used most widely in commercial applications. Amphibole asbestos has straight, needle-like fibers that are more brittle than those of serpentine asbestos and are more limited in their ability to be fabricated.

         National Cancer Institute, U.S. Department of Health and Human Services, Fact Sheet: Asbestos Exposure and Cancer Risk 1 (1 May 2009) ("NCI Fact Sheet") (citations omitted). According to the NCI Fact Sheet:

People may be exposed to asbestos in their workplace, their communities, or their homes. If products containing asbestos are disturbed, tiny asbestos fibers are released into the air. When asbestos fibers are breathed in, they may get trapped in the lungs and remain there for a long time. Over time, these fibers can accumulate and cause scarring and inflammation, which can affect breathing and lead to serious health problems.
. . . . According to [the International Agency for Research on Cancer], there is sufficient evidence that asbestos causes mesothelioma (a relatively rare cancer of the thin membranes that line the chest and abdomen), and cancers of the lung, larynx, and ovary. Although rare, mesothelioma is the most common form of cancer associated with asbestos exposure. There is limited evidence that asbestos exposure is linked to increased risks of cancers of the stomach, pharynx, and colorectum.
Asbestos exposure may also increase the risk of asbestosis (an inflammatory condition affecting the lungs that can cause shortness of breath, coughing, and permanent lung damage) and other nonmalignant lung and pleural disorders, including pleural plaques (changes in the membranes surrounding the lung), pleural thickening, and benign pleural effusions (abnormal collections of fluid between the thin layers of tissue lining the lungs and the wall of the chest cavity).
Everyone is exposed to asbestos at some time during their life. Low levels of asbestos are present in the air, water, and soil. However, most people do not become ill from their exposure. People who become ill from asbestos are usually those who are exposed to it on a regular basis, most often in a job where they work directly with the material or through substantial environmental contact.
Although it is clear that the health risks from asbestos exposure increase with heavier exposure and longer exposure time, investigators have found asbestos-related diseases in individuals with only brief exposures. Generally, those who develop asbestos-related diseases show no signs of illness for a long time after exposure. It can take from 10 to 40 years or more for symptoms of an asbestos-related condition to appear.

         Several factors can help to determine how asbestos exposure affects an individual, including:

• Dose (how much asbestos an individual was exposed to).
• Duration (how long an individual was exposed).
• Size, shape, and chemical makeup of the asbestos fibers.
• Source of the exposure.
• Individual risk factors, such as smoking and preexisting lung disease.
Although all forms of asbestos are considered hazardous, different types of asbestos fibers may be associated with different health risks. For example, the results of several studies suggest that amphibole forms of asbestos may be more harmful than chrysotile, particularly for mesothelioma risk, because they tend to stay in the lungs for a longer period of time.

Id. at 2-3 (citations omitted). The NCI Fact Sheet also states that initial examination for someone who suspects they may have an asbestos-related disease would generally include "[a] thorough physical examination, including a chest x-ray and lung function tests[.] . . . . Although chest x-rays cannot detect asbestos fibers in the lungs, they can help identify any early signs of lung disease resulting from asbestos exposure." Id. at 4 (citations omitted). However, the NCI further stated: "A lung biopsy, which detects microscopic asbestos fibers in pieces of lung tissue removed by surgery, is the most reliable test to confirm exposure to asbestos." Id.

         Plaintiffs worked in different sections of the factory, but all allege they were exposed to airborne asbestos in quantities and of a type sufficient to cause asbestos-related diseases-primarily asbestosis. The Commission made the following relevant findings of fact related to the "common issues" raised by Plaintiffs' claims:

1. Asbestos is a generic term for a group of six naturally-occurring, fibrous silicate minerals that are ubiquitous in ambient air. The general public is exposed to asbestos from natural and artificial sources through food, water, and in other ways. The background level of asbestos to which the general public is exposed varies based on several factors including geography and proximity to urban centers. Low levels of asbestos can be found in the lungs of virtually 100% of the general population. [ N.C. G.S.] § 97-62 defines asbestosis as "a characteristic fibrotic condition of the lungs caused by the inhalation of asbestos dust."
2. Plaintiffs allege that they contracted asbestosis caused by exposure to airborne asbestos during employment with [Defendant at the . . . factory[.] Additionally, some Plaintiffs allege that they also contracted diseases other than asbestosis caused by exposure to airborne asbestos during employment at [the] factory. Asbestos is not a tire component. The [P]laintiffs allege workplace exposure in the factory from one or more of four main sources: 1) airborne asbestos originating from damaged or deteriorated asbestos-containing pipe insulation; 2) powdered talc allegedly contaminated with asbestos used as a non-stick agent in certain areas of the factory; 3) asbestos-containing dust released into the air by sawing and/or otherwise working with asbestos-containing gaskets; and 4) airborne asbestos-containing brake dust that allegedly emanated from forklifts and other factory vehicles during maintenance and use. Plaintiffs allege that they were exposed to asbestos through one or more of these methods in such form and quantity and with such frequency that it caused asbestosis.
3. The . . . factory was constructed in the late 1960s and began manufacturing tires by 1969..... The factory ceased tire production on 4 July 2006.....
4. The tire-making process began in the Banbury/mixing department, a three-story area open to the rest of the factory. On the top floor of the Banbury/mixing area, chemicals and rubber were received, weighed, and mixed. On the second floor of this area, these raw materials were put into heated mixing machines. From these mixers the material was dropped down chutes to the mills on the main floor. The mills pressed the chunks of rubber material into sheets. The sheets of rubber were then hung on a line and dried using fans. Once dry, the sheets were put on pallets and sent to the "calendaring and extruding" area.
5. In the calendaring and extruding area, the rubber material was compressed into different thicknesses, shapes, and sizes for eventual use as the different components of a tire..... The compressed rubber was then transferred to the "stock prep" area, where it was cut to the correct dimensions for tire building.
6. In the "tire building" area, all of the tire pieces were layered together and pressed in a tire-building machine. . . . . The "green tires" were then transported to the curing department.
7. There were 147 clam-shell-shaped curing presses/ovens in the curing department..... The curing process, during which the "green tires" were placed in a mold and vulcanized under heat and pressure, was very hot and was operated by steam. For this reason, the curing area had more condensate and steam piping than any other area in the factory. Much of this piping was located in trenches that ran to the curing presses/ovens.
8. After curing, the tires went to the "final finish" area where they were trimmed, cleaned, and inspected. The tires that passed inspection were put on pallets and transported to the warehouse[.]
9. Steam and condensate pipes ran throughout the factory. . . . . There were at least 26, 180 linear feet of insulated steam and condensate piping in the factory. The insulation was comprised of one to two inches of an asbestos-containing cement, Thermobestos, encapsulating the steam and condensate pipes. The pipes had protective canvas and glue surrounding the Thermobestos. Asbestos insulation was removed from the market in the early 1970s and, as such, expansions at the . . . factory after a certain date would not have included the installation of asbestos-encapsulated piping. Most of the insulated steam and condensate piping was at ceiling level, 20-30 feet above the factory floor, or below floor level in the trenches that ran between and into the curing presses. The floor-level and trench-level pipe insulation was susceptible to damage by foot traffic. Forklifts could damage floor-level pipe insulation and also could damage pipe insulation at higher levels. For example, while stacking tires high in the warehouse, it was possible for the forklift payloads to strike the insulated piping.
10. Plaintiffs allege exposure to airborne asbestos originating from deteriorated pipe insulation. Plaintiffs allege that it was damaged through external molestation by workers walking on pipes, climbing on pipes, and striking the pipes with forklifts and forklift payloads. Plaintiffs also argue that internal pipe damage from ruptures forced steam to leak out of the pipes with sufficient force to cause insulation damage and cause asbestos to become airborne. Plaintiffs further allege that workers used compressed air near the damaged insulation, causing asbestos to become airborne. There is conflicting evidence regarding the amount of pipe insulation damage present at [the] factory.
11. The highest concentration of insulated piping in the factory existed in the curing department, with much of the piping at or below floor level. Plaintiffs allege that workers used a band saw to cut large asbestos-containing gaskets in the curing department. If [Plaintiffs' allegations are correct, it would be logical to expect high levels of airborne particulates in the curing department originating from damaged pipe insulation and gasket-sawing. However, the greater weight of the evidence does not support this conclusion.
12. In 1979, the . . . factory took part in an air contaminant assessment study in conjunction with The National Institute for Occupational Safety and Health (hereinafter "NIOSH"). At the time, NIOSH was studying the best methods and technologies to control air quality in the tire industry. The report reflects that [the] factory was selected for the study because it had "among the better controls for air contaminants in the industry." NIOSH performed area and personal air monitoring in each area of the plant that it expected to find measurable dust or emissions. Specifically, NIOSH measured for dust-both airborne and respirable, as well as petroleum distillates, rubber solvent, Benzene, and Toulene. The dust measurements would have measured any particulates in the air-whether the particulates were asbestos, talc, or something else. The 1979 NIOSH dust measurements found that the measured dust levels in the curing department were 1/100th of the permissible level. This was possibly due to the curing department's powerful exhaust system, which drew air up and out of the area. Except for an outlier measurement created by an employee jumping up and down in a dusty trash bin, the 1979 dust measurements at [the] factory were five to ten times less than the permissible exposure level (hereinafter "PEL") in place in 2013. NIOSH concluded that the particulate and vapor concentrations at [the factory] were well below the PEL established by the Occupational Safety and Health Administration (hereinafter OSHA), NIOSH, and the American Conference of Governmental Industrial Hygienists. NIOSH also concluded that the environmental controls (exhaust and ventilation systems) were effective.
13. There was also environmental air sampling for asbestos at [the] factory in 1985 when asbestos-containing insulation was removed from a furnace on the third floor of the mixing area. This sampling was done with background air monitoring as well as with personal air monitors on the personnel conducting the removal. In 1985, there were no regulations regarding wetting down insulation as it was removed. Therefore, the air measurements taken during this removal process record a scenario very favorable for the creation of airborne dust. However, the 1985 background air monitoring that took place showed results well below the then-current OSHA PEL. The highest recorded personal air monitoring result during the removal was also below the then-existing OSHA PEL.
14. As a result of the 1986 federal asbestos regulations, large-scale asbestos abatement procedures were undertaken at [the] factory. This process required pre-abatement area air quality monitoring to measure pre-removal levels. For this reason, there were background air samples collected for abatement projects in 1989 (curing), 1995 (calendar and extruding), and 2003 (powerhouse). In all of these areas, these measurements show that at no time was the potential exposure above the OSHA PEL. Background monitoring reflected levels to which the public at large is exposed.
15. In areas with ceiling-level piping, such as the warehouse, the evidence demonstrates that any small amount of asbestos potentially disturbed and released at ceiling level due to pipe insulation damage would have dissipated before reaching workers and would not have created any meaningful exposure.
17. Plaintiffs also allege exposure to asbestos through the inhalation of powdered talc which they allege contained asbestos. Talc is used ubiquitously by the general population in things such as makeup and baby powder. It is the most common non-asbestos mineral found in general population lung tissue. Talc was used in [the] factory as a non-stick agent. However, the amount of talc used in the . . . factory is a contested factual issue. Defendant avers that routinely, workers mistook other powdery materials used in great quantities at the factory for talc. Specifically, [Defendant contends that clay [kaolin], calcium carbonate, and zinc oxide were commonly used in vastly larger quantities and were routinely incorrectly referred to by the workers as "talc." . . . .
18. While talc from certain mines is known to be contaminated by asbestos, there was disagreement among the experts regarding the likelihood of asbestos being a contaminant in the talc used at [the] plant. Furthermore, in 1995, air monitoring was done in the calendaring area while calendaring work continued. Plaintiffs allege significant talc usage in this area. If [Plaintiffs' allegations are correct, it would be logical to expect high levels of airborne particulates in calendaring. However, the 1995 measurements, performed as calendaring work continued, found airborne particulate levels well below the then-existing OSHA PEL, and EPA clearance levels.
20..... There was contradicting testimony on the issue of cutting gaskets-with some witnesses testifying that gaskets came from the manufacturer already made to fit and did not require any sawing and other testimony that any such sawing, if it took place, would have been done in the maintenance shop, not in curing.
24. In 1986, federal government regulations mandated new procedures to identify, encapsulate, and abate workplace asbestos. As part of these new regulations, in 1987, certain employees at [the] factory were trained for the possibility that small asbestos removals would have to be performed by [Defendant's] employees..... All removal and abatement procedures were performed by outside contractors. Subsequent to the 1986 regulations, the new asbestos management policies were made known to all employees, masks were provided, and safety protocols, such as the prohibition of using compressed air on damaged insulation, were enacted. Furthermore, known asbestos-containing materials were labeled, encapsulated, and removed.
25. An asbestosis B-read is a test in which NIOSH-certified physicians view a patient's chest x-ray and score it from 0/0 (for normal lungs) through 3/3 (for lungs with severe disease). B-readers become certified (and re-certified every 4 years) based on their tested proficiency in scoring a set of standard x-rays. The first number in a B-read score reflects that reader's first impression of the film, with the second number reflecting a different number if the reader has a "second thought" or if the reader thinks another B-reader could arrive at a different conclusion. For example, a 1/0 score reflects a B-reader's conclusion that the film is mildly abnormal, but that another B-reader could read the film as normal.
26. The 1986 American Thoracic Society criteria required a B-read to be 1/1 or greater before the result was considered consistent with asbestosis. The 1986 criteria also stated: "the benefit of the doubt should be given whenever the clinical features and occupational exposure data are compatible with the diagnosis." The 2004 American Thoracic Society criteria liberalized the standard to define a 1/0 read or greater as consistent with asbestosis, but removed the "benefit of the doubt" language. Many common non-asbestos-related conditions are consistent with a 1/0 B-read. For example, cigarette smoking can cause opacities consistent with a 1/0 B-read.
27. The [P]laintiffs in these cases took part in a mass screening of chest x-rays of [Defendant's] former . . . factory workers. This mass screening was organized by [Plaintiffs' attorneys. These x-rays were reviewed by B-readers selected by [Plaintiffs' attorneys. Over 80% of [P]laintiffs in these cases were evaluated by [P]laintiffs B-readers to have "1/0" B-reads. Plaintiffs were subsequently referred by [Plaintiffs' attorneys for mass diagnostic examinations at a hotel in Charlotte performed by pulmonologists selected by [Plaintiffs' attorneys.
28. Defendant's B-readers evaluated the [Plaintiffs' x-rays as 0/0. This consistent disparity of B-reads, which, by definition, are meant to be read to a consistent standard, raises the issue of possible B-reading bias by one or both sides.
29. Asbestos-related diseases follow a dose-response relationship-the higher the cumulative [asbestos] exposure dose, the greater the risk of disease, with asbestosis generally requiring the highest dose. Pleural plaques, pleural thickening, and mesothelioma are asbestos-related conditions that generally form at a lower dose.
30. In the general population, approximately 80% of people diagnosed with asbestosis will also have bilateral pleural plaques. However, experts in these cases only identified about 10% of the [P]laintiffs diagnosed with asbestosis as also having bilateral pleural plaques. This outcome is statistically improbable. Because pleural plaques require less exposure, it is not logical that such a large group diagnosed with asbestosis would have so few with pleural plaques.
31. Pursuant to an order issued by former Deputy Commissioner Gheen, [Defendant has been entitled to autopsies and lung tissue examinations of deceased [P]laintiffs to allow pathological examinations. Although 18 [P]laintiffs have died to date, [Defendant has only been able to obtain autopsy results and tissue examinations of five deceased [P]laintiffs-Walter Hinson, Johnnie Jones, Charles Gibson, Homer Hunt, and Lloyd Cox. Walter Hinson is the only [Bellwether P]laintiff who had post-mortem pathology[.]
32. Pathological examination of lung tissue is a definitive method of determining whether an individual has an asbestos-related disease. x-rays are inherently limited in that they can only identify markings that are consistent with a pneumoconiosis such as asbestosis. These markings, as seen on radiological scans, can also be consistent with a number of unrelated conditions and diseases.
33. The accepted scientific method to diagnose asbestosis pathologically requires diffuse interstitial fibrosis AND either two or more asbestos bodies per centimeter squared OR a count of uncoated asbestos fibers that falls within that lab's range for asbestosis (accounting for the background levels found in that lab's reference population/control group). Labs also may have different methodologies to digest and identify fibers, making cross-lab comparisons problematic. Asbestos bodies are fibers that have been coated by the body as a defense mechanism. Diffuse interstitial fibrosis or scarring can be caused by numerous things other than asbestosis. Many non-asbestos-related diseases and conditions can result in a 1/0 B-read.
34. Of the five deceased [P]laintiffs who had post-mortem pathological study of their lung tissue, (Walter Hinson, Johnnie Jones, Charles Gibson, Homer Hunt, and Lloyd Cox), none had pathological evidence of asbestosis. Pathology is the most reliable method to diagnose asbestosis.
35. Pursuant to the Helsinki, OSHA, and NIOSH standards, fibers shorter than 5 micrometers [or microns] are not counted pathologically for purposes of asbestosis diagnosis or risk assessment. Fibers shorter than 5 micrometers, due to their length, are cleared quickly by the lungs and are not believed to contribute to the disease. Only fibers longer than 5 micrometers become lodged into the lung tissue, as they are too big to navigate through the lymphatic channels to be cleared by a human lung's defense mechanisms.
36. Samples of the pipe insulation at the . . . factory show the presence of two types of asbestos-amosite and chrysotile. Amosite is an amphibole. Chrysotile is a type of [serpentine] asbestos, often shorter than five micrometers, that is particularly susceptible to being broken down quickly in acidic environments, such as a human lung. Due to its length and fragility in the human lung, the clearance half-life of chrysotile asbestos in humans has been estimated to be a few weeks to a few months. Plaintiffs argue that the tissue fiber analyses in these cases under-assessed the number of fibers by not counting the chrysotile fibers because they are quickly cleared from the human lung. Many experts believe that chrysotile asbestos does not cause or contribute to asbestosis or asbestos-related disease due to its short clearance half-life and that fact that persistence of a fiber within the lung is a crucial determinant of its pathogenicity. By contrast, amphibole asbestos fibers are not susceptible to being dissolved by lung tissue and have a clearance half-life in the human body measured in decades. Because the pipe insulation at the . . . factory had both chrysotile and amphibole asbestos, the [P]laintiffs' lung pathology would show occupational exposure, if it existed, in the form of amphibole fibers.
37. [Plaintiff] Hinson . . . worked for 32 years, mainly in the curing department. The curing department had the highest concentration of insulated piping in the factory, with much of it at floor level or in exposed trenches. According to [Plaintiff] Hinson, he was also exposed to significant asbestos dust from using a band saw to cut large asbestos gaskets. If [P]laintiffs' arguments are correct, [Plaintiff] Hinson would have been exposed to a significant amount of airborne asbestos. [Plaintiff] Hinson was given a 1/0 B-read by Dr. James Johnson[.] Dr. Craig Hart at York pathology performed [P]laintiff Hinson's lung autopsy. Dr. Hart found no evidence of asbestos bodies or fibrosis, but did see evidence of smoking. The tissue was sent to Dr. Oury, who examined the sample and confirmed Dr. Hart's conclusions. Although it was not required for diagnostic purposes due to the lack of fibrosis, a fiber count analysis was done by Dr. Oury upon [Defendant's request. The fiber count analysis found 5 asbestos bodies per gram, which is a level well below that seen in individuals with asbestosis and in the range of control individuals with no history of [occupational] asbestos exposure.
38. Decedent Johnnie Jones . . . worked for 25 years in the calendar area. If [Plaintiffs' arguments are correct, he would have been subjected to significant airborne asbestos-contaminated talc exposure in his workplace environment. Decedent Johnnie Jones had a 1/0 B read from Dr. Crim. However, when Dr. Roggli performed a pathological examination of Jones' lung tissue, he found no histologic evidence of asbestosis or elevated asbestos content. Based on decedent Jones' employment history at [the factory] and his pathology results, Dr. Roggli testified that there was not sufficient exposure to asbestos at the factory . . . to contribute to or to cause an asbestos-related disease for Mr. Jones or anyone in his position.
39. Decedent Charles Gibson . . . worked at the . . . factory . . . for 31 years-holding jobs in the tire-building and warehouse departments. If [Plaintiffs' arguments are correct, Gibson would have been subjected to significant airborne asbestos exposure in his workplace environment. Decedent Gibson was found to have a 1/0 B-read according to Dr. Crim. Decedent Gibson's lung tissue was collected by York Pathology Associates after his death. Dr. Jenkins with York Pathology performed a gross tissue examination. Dr. Jenkins found no pleural plaques. Dr. Oury also examined the tissue and found no evidence of pulmonary fibrosis, no asbestos bodies, and no fibers. Talc and vermiculite were found, but the source of these materials was impossible to discern.
40. Decedent Homer Hunt . . . was employed at the . . . factory for 17 years as a mechanic-working in all areas of the factory. Among many other tasks, decedent Hunt replaced forklift brakes. If [Plaintiffs' arguments are correct, decedent Hunt would have been subjected to significant amounts of airborne asbestos-containing brake dust in his workplace environment. Decedent Hunt was a 45-year smoker who died of lung cancer in 2012. His lung tissue was collected by York pathology pursuant to the Autopsy Order. Dr. Richard Johnson and Dr. Oury examined decedent Hunt's lung tissue. No fibrosis was found in areas of the lung not impacted by the unrelated carcinoma tumor. Furthermore, there were no asbestos bodies or fibers found.
41. Decedent Lloyd Cox . . . worked at [the] factory for 31 years in the stock and bead prep area. Decedent Cox died in 2014 of viral pneumonitis complicated by other factors. Although decedent Cox had "end stage asbestosis" written on his death certificate by the Lancaster County coroner, this diagnosis is of dubious reliability in that it apparently has little or no scientific basis. The coroner does not have a college degree and did not consult with the county pathologist before writing that conclusion on the death certificate. Decedent Cox's lung tissue was collected and examined by York Pathology Associates. Surgical pathologist Dr. Sporn performed a "transbronchial biopsy." Dr. Sporn did not find any asbestos bodies and no condition was found on the biopsy that would have been caused by or contributed to by asbestos exposure. Dr. Sporn articulated that viral pneumonia was the likely cause of death. Dr. Hart performed the pathology exam, microscopically and grossly, and found that there was no interstitial fibrosis, no asbestos bodies, no pleural plaques, no asbestos fibers, and no evidence of exposure to asbestos above the general population.
42. Despite [Plaintiffs' theories of exposure, pathology results from the lung tissue of five long-term employees from a variety of departments and factory locations uniformly show a lack of fibrosis, a lack of asbestos bodies, and a lack of fibers.
44. Drs. Ghio, Barrett, Goodman, and Alexander concluded that [P]laintiffs did not have findings consistent with diagnoses of asbestosis. Given the preponderance of the evidence in view of the entire record, their opinions are given greater weight than those of Drs. Crim, Ohar, Schwartz, and Frank [Plaintiffs' experts].

         Plaintiffs argue that some of these findings are erroneous, incomplete, or misstate the facts. We will address Plaintiffs' arguments concerning the findings of fact below. Based upon these common findings of fact, the Commission determined that Plaintiffs had not meet their burden of proving they were exposed to levels of hazardous airborne asbestos capable of causing-or significantly contributing to-their alleged asbestos-related diseases. Additional facts will be discussed below.

         III. Relevant Workers' Compensation Law

         A. Standard of Review

         The issues before us are controlled by Article 1, Chapter 97 of the General Statutes-the "Workers' Compensation Act" (the "Act"). "The employee seeking workers' compensation benefits bears the burden of proving every element of compensability. The degree of proof required of a claimant under the Act is the 'greater weight' or 'preponderance' of the evidence." Hardin v. Motor Panels, Inc., 136 N.C.App. 351, 354, 524 S.E.2d 368, 371 (2000) (citations omitted). This Court's standard of review is well established:

"Appellate review of an award from the Industrial Commission is generally limited to two issues: (i) whether the findings of fact are supported by competent evidence, and (ii) whether the conclusions of law are justified by the findings of fact." Unchallenged findings of fact are presumed to be supported by competent evidence[.] The Commission's conclusions of law are reviewed de novo.

Penegar v. United Parcel Serv., __ N.C. App.__, __, 815 S.E.2d 391, 394 (2018) (citations omitted). "Whether an injury arose out of and in the course of employment is a mixed question of law and fact, and the Industrial Commission's findings in this regard are conclusive on appeal if supported by competent evidence." Culpepper v. Fairfield Sapphire Valley, 93 N.C.App. 242, 247, 377 S.E.2d 777, 780 (1989) (citation omitted).[10] The Commission's findings, including its ultimate findings, are binding "when they are supported by direct evidence or by reasonable inferences drawn from the record." Kennedy v. Duke Univ. Med. Center, 101 N.C.App. 24, 30, 398 S.E.2d 677, 680 (1990) (citations omitted). "[T]he Commission is required to evaluate the credibility of the evidence and reject any evidence it finds as not convincing." Phillips v. U.S. Air, Inc., 120 N.C.App. 538, 542, 463 S.E.2d 259, 262 (1995) (citation omitted).

[T]he Commission has sole authority to make findings of fact. This Court does not weigh the evidence. We determine only whether there is any evidence of substance in the record to support the Commission's findings; if there is, we are bound by the findings, even though the record may contain evidence supporting findings contra. There must be a complete lack of competent supporting evidence to justify disregarding the Commission's findings of fact. Where medical testimony is conflicting, the Commission decides which testimony to give the greater weight.

Carroll v. Burlington Industries, 81 N.C.App. 384, 387-88, 344 S.E.2d 287, 289-90 (1986) (citations omitted).

         B. Workers' Compensation; Occupational Diseases

         Most, if not all, Consolidated Plaintiffs allege they developed asbestosis as a result of their work at the factory.[11] See N.C. G.S. § 97-53(24) (2017). Two Bellwether Plaintiffs, Wilson and Epps, alleged they have occupational diseases as defined by N.C. G.S. § 97-53(13); colon cancer and tonsil cancer, respectively-caused by asbestos exposure at the factory. Normally, the Commission would first determine whether a plaintiff had proven an occupational disease, and only after determining that the plaintiff had met that burden would the Commission consider evidence related to compensability, or whether the occupational disease had any causal connection to the plaintiffs employment. However, for these cases we are asked to review the Commission's determinations that conditions at the factory could not have exposed Consolidated Plaintiffs to airborne asbestos of a type and in sufficient amounts to cause asbestosis, or other asbestos-related diseases-before the Commission determines whether any Consolidated Plaintiffs actually have asbestos-related diseases.[12] In light of the unusual procedure employed, a review of workers' compensation law and procedure applicable to cases of alleged compensable asbestos-related diseases is appropriate.

         "The underlying purpose of [the 1929 adoption of the] Act . . . [wa]s to provide compensation for workmen who suffer disability by accident arising out of and in the course of their employment." Henry v. Leather Co., 234 N.C. 126, 127, 66 S.E.2d 693, 694 (1951). Initially, the Act only allowed compensation for "injury by accident." See id. at 127, 66 S.E.2d at 694. However, the Act was amended in 1935 to include benefits for employees who developed compensable occupational diseases. Id. at 128, 66 S.E.2d at 694-95; N.C. G.S. § 97-52 (2017). The amendment enumerated specific diseases-like asbestosis-that were designated as "'occupational diseases within the meaning of [Article 1].'" Henry, 234 N.C. at 128, 66 S.E.2d at 694 (citation omitted); N.C. G.S. § 97-53. Later, the Act was amended to allow employees to prove that a disease not specifically enumerated in N.C. G.S. § 97-53 was a "compensable occupational disease" based upon the specific facts of the plaintiffs claim. N.C. G.S. § 97-53(13). N.C. G.S. § 97-53(13) states in relevant part: "Any disease . . . which is proven to be due to causes and conditions which are characteristic of and peculiar to a particular trade, occupation or employment, but excluding all ordinary diseases of life to which the general public is equally exposed outside of the employment" "shall be deemed to be [an] occupational disease[] within the meaning of the Act. N.C. G.S. § 97-53(13).

         "[T]he addition of G.S. 97-53 to the Act 'in nowise relaxed the fundamental principle which requires proof of causal relation between injury and employment.'" Booker v. Medical Center, 297 N.C. 458, 475, 256 S.E.2d 189, 200 (1979) (citations omitted). "It is overwhelmingly apparent that . . . disablement resulting from an occupational disease . . . must arise out of and in the course of the employment, i.e., there must be some causal relation between the injury and the employment[.]" Morrison v. Burlington Industries, 304 N.C. 1, 12, 282 S.E.2d 458, 466 (1981).

         Now, all provisions of the Act that had formerly applied only to injuries by accident also apply to compensable occupational diseases-so long as they do not conflict with more specific provisions in the Act specifically pertaining to occupational diseases. N.C. G.S. § 97-52. "[A]n employee becoming disabled by asbestosis [or other occupational disease] . . . within the terms of the specific definition embodied in G.S. [§] 97-54 should be entitled to ordinary compensation measured by the general provisions of the . . . Act. G.S. [§] 97-64." Young v. Whitehall Co., 229 N.C. 360, 366, 49 S.E.2d 797, 801 (1948).

         Therefore, the Act now provides that the terms "injury," "personal injury," or "injury by accident" also encompass "[disablement or death of an employee resulting from an occupational disease described in G.S. 97-53[.]" N.C. G.S. § 97-52; N.C. G.S. § 97-2(6) (2017) (emphasis added) ("Injury.-'Injury and personal injury' shall mean only injury by accident arising out of and in the course of the employment[.]"); see also Henry, 234 N.C. at 128, 66 S.E.2d at 694 (citation omitted) (The amendment also "broadened or extended the meaning of the word 'accident' as used in the original Act so as to include a disablement or death resulting from an occupational disease described in G.S. § 97-53[.]"). "Nothing is said in [ N.C. G.S. § 97-52] or cases construing it which could be interpreted as allowing compensation for injury from occupational ...

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