WORKPLACE SAFETY AND INSURANCE APPEALS TRIBUNAL DECISION NO. 1815/16

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WORKPLACE SAFETY AND INSURANCE APPEALS TRIBUNAL DECISION NO. 1815/16 BEFORE: S. Ryan : Vice-Chair M. Christie : Member Representative of Employers D. Besner : Member Representative of Workers HEARING: July 5, 2016 at Ottawa Oral DATE OF DECISION: August 5, 2016 NEUTRAL CITATION: 2016 ONWSIAT 2102 DECISION UNDER APPEAL: WSIB Appeals Resolution Officer (ARO) L. Diaz decision dated June 27, 2012 APPEARANCES: For the worker: For the employer: Interpreter: K. Burkimsher, Paralegal Did not participate N/A Workplace Safety and Insurance Appeals Tribunal Tribunal d appel de la sécurité professionnelle et de l assurance contre les accidents du travail 505 University Avenue 7 th Floor 505, avenue University, 7 e étage Toronto ON M5G 2P2 Toronto ON M5G 2P2

Decision No. 1815/16 REASONS (i) Introduction [1] The worker s estate appeals the ARO decision dated June 27, 2012, which denied the worker entitlement for lung cancer (small cell lung carcinoma) which was diagnosed in early 2008. The worker passed away in July 2011. (ii) Issue [2] The Tribunal must decide whether the worker s lung cancer was causally related to his employment as a mastic roofer. (iii) Background [3] In 1987, the worker was hired by the employer, a commercial roofing company. He was employed as a mastic roofer (also known as a flat roof worker or hot tar roofer) and typically worked nine months per year removing and/or installing roofs. He was exposed to coal tar pitch and asphalt fumes (containing bitumen). He was also exposed to asbestos. [4] In February 2008, the worker underwent a CT scan which indicated a small left upper lobe nodule and probable left hilar lymphadenopathy. He stopped working at that time and was ultimately diagnosed with lung cancer (small cell). [5] The worker was also a 20-to-30 pack year smoker with a family history of lung cancer. [6] Unfortunately, the worker passed away on July 13, 2011 at age 57. (iv) Analysis and conclusion [7] Since the worker claimed to be injured in 2008, the Workplace Safety and Insurance Act, 1997 (the WSIA) is applicable to this appeal. An accident is defined in section 2(1) to include: (a) a wilful and intentional act, not being the act of the worker, (b) a chance event occasioned by a physical or natural cause, and (c) disablement arising out of and in the course of employment; [8] General entitlement to benefits is governed by section 13: 13(1) A worker who sustains a personal injury by accident arising out of and in the course of his or her employment is entitled to benefits under the insurance plan. (2) If the accident arises out of the worker s employment, it is presumed to have occurred in the course of the employment unless the contrary is shown. If it occurs in the course of the worker s employment, it is presumed to have arisen out of the employment unless the contrary is shown. [9] The statutory presumption set out in section 13(2) does not apply to an injury by disablement. See, for example, Decisions No. 268 and 42/89. [10] Tribunal jurisprudence applies the test of significant contribution to questions of causation. A significant contributing factor is one of considerable effect or importance. It need not be the sole contributing factor. See, for example, Decision No. 280.

Page: 2 Decision No. 1815/16 [11] The standard of proof in workers compensation proceedings is the balance of probabilities. Pursuant to subsection 124(2) of the WSIA, the benefit of the doubt is resolved in favour of the claimant where it is impracticable to decide an issue because the evidence for and against the issue is approximately equal in weight. [12] We have carefully considered all of the available evidence in the Case Record, testimony of BM (former mastic roofer) and submissions of Mr. Burkimsher. [13] We find that the preponderance of evidence supports, on a balance of probabilities, that the worker s employment exposures as a mastic roofer did not significantly contribute to the development of his small cell lung cancer. We find that the evidence for and against entitlement is not approximately equal, thus the statutory benefit of doubt provision does not apply. [14] In reaching our conclusion, we acknowledge the report dated September 17, 2010, from Dr. P. Jugnundan, physician at Occupational Health Clinics for Ontario Workers (OHCOW), who opined: [The worker] was exposed for more than 30 years to asphalt fumes; therefore he was at an increased risk to developing carcinoma of the lungs. Twenty-one of these years were in Ontario. [15] We acknowledge Dr. Jugnundan s final report dated September 9, 2011, in which he opined, [the] worker s lung cancer, in the absence of other possible causative agents, was most likely related to his workplace exposures. Dr. Jugnundan did not comment on the relative contribution of the worker s smoking to his lung cancer. [16] We agree with Mr. Burkimsher that current epidemiology indicates that mastic roofers have an increased risk for the development of lung cancer than the general population. However, the increased risk falls short of the probable risk that the Tribunal generally requires for granting entitlement. We find that there are no extraordinary circumstances in this case that would warrant granting entitlement. (a) The epidemiology on coal tar pitch and asphalt fume exposure among mastic roofers [17] As pointed out by Mr. Burkimsher, the World Health Organization (WHO) International Agency for Research on Cancer (IARC) has evaluated medical and scientific evidence for coal tar pitch volatiles, oxidized bitumens and straight run bitumens all agents found in the mastic roofing industry. IARC rates the carcinogenicity of these agents into five groups: Group 1 carcinogenic to humans Group 2A probably carcinogenic to humans Group 2B possibly carcinogenic to humans Group 3 not classifiable as to its carcinogenicity to humans Group 4 probably not carcinogenic to humans [18] It is not disputed that coal tar pitch fumes are carcinogenic to humans. This fact has been well established in epidemiology dating back decades.

Page: 3 Decision No. 1815/16 [19] In a report addressed to Mr. Burkimsher dated May 27, 2016, D. Fulton, occupational hygienist (OH) at OHCOW, noted that IARC re-evaluated bitumen exposures and concluded in a published paper dated October 18, 2011, that: Occupational exposure to oxidized bitumens and their emissions during roofing are probably carcinogenic to humans [20] We agree with Mr. Burkimsher that this finding was not acknowledged by the Board s OH whose last report is dated June 23, 2008. In that report, the Board OH advised that asphalt fumes have not been classified in respect to carcinogenicity. [21] In the absence of any statutory presumptions, where the evidence is relatively equally balanced so that it is not practicable to decide, the benefit of doubt provision applies. Tribunal decisions generally grant entitlement for lung cancer when the epidemiology indicates a 50% or greater probability that the lung cancer was caused by employment exposures. However, as indicated in the OHCOW OH report of May 27, 2016, studies which reported increased incidence of lung cancer among roofers showed a relative risk ratio of 1.7 1.8 and an increased lung cancer standardized mortality ratio (SMR) of 1.05 1.33. These ratios fall short of the 50% probability (i.e., SMR of 2.0 1 ) generally required in Tribunal jurisprudence. [22] We note that estimates of the relative risk for lung cancer in long-term smokers compared to non-smokers range from 10 to 30 fold. 2 [23] Decision No. 600/97 is a leading case on the nature of epidemiological evidence. The Panel noted: Epidemiology is the discipline...concerned with the patterns of events affecting the health of human populations and the factors influencing these patterns....epidemiologic studies may demonstrate a statistical association between a disease and an exposure or risk factors 3. The Julian and Muir Study is an epidemiological study. It compared the number of cases of cancer in a population of Ontario nickel workers with the number of cases of cancer in a comparison population (a population of Ontario males of the same age). Epidemiological studies can identify statistical associations between particular exposures and an increased incidence of a disease but a statistical association does not in itself prove that there is a causal relationship between the studied exposure and the disease. However, an epidemiological study may justify an inference that a statistical association reflects a causal link 4. Even so, since epidemiology studies populations, not individuals, it cannot prove that a particular worker s cancer was caused by the studied exposure. With respect to the use of epidemiological evidence when deciding a particular worker s appeal, Decision No. 257/89 5 stated:...epidemiological studies analyze statistical associations between populations...rather than cause of disease in an individual case. Thus, they do not prove causality in the individual case. Nonetheless, they 1 2 3 4 5 Sometimes expressed as 200 D.M. Mannino, MD, Cigarette Smoking and Other Risk Factors for Lung Cancer in www.uptodate.com 2015 (Exhibit #5, pages 19 to 28 H.M. Ginzburg, Use and Misuse of Epidemiologic Data in the Courtroom: Defining the Limits of Inferential and Particularistic Evidence in Mass Tort Litigation (1986) 12 Am. J.L. & Medicine 425. Rothwell v. Raes (1988), 66 O.R. (2d) 449 at page 466. 14 W.C.A.T.R. 87

Page: 4 Decision No. 1815/16 can be given weight and they can be used in helping to judge whether an individual worker s disability is likely work-related. 6 In order to assess the likelihood that the statistical association indicates a cause-and-effect relationship between exposure and disease, a number of other factors will be considered. In his well-known paper entitled The Environment and Disease: Association or Causation? 7, Sir Austin Bradford Hill described the following aspects of the statistical association that should be considered before deciding that the most likely interpretation of the association is causation: 1. Strength of the association (the less strong the association, the more likely it is that factors other than the studied variable account for the association). 2. Consistency of the observed association (has the observed association been repeatedly observed by different persons in different circumstances?). 3. Specificity of the association (is the association limited to specific workers and particular sites and types of disease?). 4. Temporal relationship of the association (which is the cart and which is the horse does the association exist because the environment promotes disease or because a population with the disease is more likely to be in that environment?). 5. Biological gradient (is there a dose-response curve?). 6. Plausibility (is causation biologically plausible?). 7. Coherence (would causation be coherent with the generally known facts of the natural history and biology of the disease?). 8. Experiment (is there experimental evidence that supports the causation hypothesis - such as a reduction in incidence when an exposure is reduced?) 9. Analogy (is the association similar to that found for other known diseases that may be analogous?). Although an epidemiological study cannot prove causation, the factors described by Sir Bradford Hill are important considerations when deciding whether an inference can be made that there is a causal link. But even if it can be inferred that there likely is a causal link between the incidence of a disease and the exposure of a studied population of workers, that does not prove that the disease suffered by a particular worker in the studied population was caused by the exposure. It may, however, be sufficient to make inferences about how probable it is that a worker s disease would (or would not) have occurred without the studied exposure, and that can be considered along with other available evidence in deciding whether the exposure caused or contributed to a particular worker s disease. [24] In Decision No. 600/97, there was a SIR of 161 and the Panel noted the opinion of Dr. Miller, Tribunal Assessor, on the question of when a significant statistical risk should result in compensation. They noted: In his review of the Julian and Muir Study, Dr. Miller expressed his opinion as to how epidemiological measures of risk should be used in making decisions about compensation. He suggested that considerations of statistical significance (excluding chance) should precede considerations of compensation. And, where there are measures of risk which are statistically significant (i.e. not by chance) and which show excess risk 6 7 Rothwell v. Raes (1988), 66 O.R. (2d) 449, additional reasons at (1989), 69 O.R. (2d) 62. Proceedings of the Royal Society, Section of Occupational Medicine. Vol. 58 (1965), pages 295-300.

Page: 5 Decision No. 1815/16 (i.e. an SIR in excess of 100), he argues that the excess in risk in the exposed population should be double that in the unexposed population before compensation should be considered for the exposed group because anything less than double the risk would mean that the disease was less likely to be due to the work exposure than to other causes. In this regard, he states: Anything significantly in excess of [100 for the SIR] is the excess risk A [SIR of 200] means a doubling of risk in the exposed relative to the unexposed This means that if an SIR of greater than 200 can be validly assigned to an individual being considered for compensation, there is a greater than 50% chance that the disease was due to the exposure, i.e. a probability of causation from the exposure of greater than 50%, and the benefit of doubt criterion applies. An SIR of less than 200, therefore, implies that the disease was less likely to be due to the exposure than to other causes, and the benefit of doubt criterion should not apply In my view, only if the SIR is greater than 200 should compensation be considered for a group. If there is a dose-response relationship (usually required for causality anyway), the cut off point should be considered after carefully analyzing the data, and should take into consideration what is known about disease causation If Dr. Miller s opinion is accepted, compensation for colo-rectal cancer would not be considered for any individual in the group of underground miners with 30-34 years exposure. Likewise, Dr. Muir finds an SMR or SIR of 200 or more to be important, because he interprets this as a finding that implies that the occupational causation is [equal to or] greater than the non-occupational component. In his view, it makes a logical and widely accepted division. He stated that it was also a legitimate point of division where there is insufficient information to determine a dose/response relationship. An SMR (or SIR) which is statistically significant and which is above 200 is unlikely to be due to confounders and, in itself, is evidence of a workplace causative factor. Dr. Muir notes that findings such as those for the 30-34 year exposure group of underground miners are compatible with some contribution from workplace exposure. He suggests that, from a policy perspective, there may be other choices that can be made for compensation purposes (such as accepting a somewhat lower SMR or SIR, or providing compensation proportional to the occupational contribution to a disease). [25] In this case, the current epidemiology does not support the granting of entitlement for lung cancer. (b) The worker s employment exposure history [26] It is not disputed that the worker was employed as a mastic roofer in Ontario between 1987 and 2008. The evidence indicates that prior to this period, he also worked as a mastic roofer in Poland for a period of about 17 years. While it is reasonable to assume that the additional 17 years of exposure (not considered by the Board) would increase the worker s risk for the development of lung cancer, it does not follow, given current epidemiology, that the additional 17 years of exposure would increase his risk to a level that is probable. [27] We find that, overall, the worker s employment exposures were not materially different from the exposures that were generally present for all mastic roofers. In our view, there are no extraordinary circumstances respecting the worker s particular employment exposures that would significantly alter his probability of developing lung cancer beyond that which is expected for mastic workers generally.

Page: 6 Decision No. 1815/16 [28] The worker s first detailed statement was recorded by a Board Claims Investigator (CI) on April 25, 2008 at the worker s union hall. The worker advised that he believed he was exposed to asbestos when removing old roofs with shovels, saws and axes. The worker advised that he believed there was asbestos exposure on almost every removal job. However, he advised differently when interviewed later by a Board OH (discussed below). The worker advised that crew members rarely wore personal protective equipment (PPE). [29] In a report dated June 23, 2008, the Board OH advised that he reviewed the file and conducted telephone conversations with the worker and employer. He also reviewed epidemiological reports on the roofing industry. The Board OH summarized the worker s duties which included running the kettle, cleaning up debris, tearing off roofs, installing roofing membranes and insulation, mopping and spreading asphalt and spreading ballast. [30] With respect to asbestos exposure, the Board OH advised that asphalt was used in roofing products well into the 1980s and likely into the early 1990s which may have contained asbestos felts. However, the Board OH noted: According to both the worker and employer, asbestos was rarely used... At most, asbestos may have been encountered 3-5 days per year when it would be removed. According to both worker and employer, roof removal or tear-off probably took 2-2.5 days per week on average. [31] With respect to coal tar pitch and asphalt, the Board OH advised: Coal tar pitch (pitch) was commonly used on flat roofs in the 1950s and 1960s. However, through the 1970s and 1980s pitch was usually replaced with asphalt (petroleum based bitumen) for hot roofing work. Pitch removal and asphalt replacement is more common today. Pitch is still sometimes found in roofing mastics or patching compounds. Cold pitch products would be removed during the tear off stage and asphalt during the installation stage. According to the employer, pitch jobs occurred roughly 3-5 days per year. According to the worker, pitch related work was approximately three weeks per year. Asphalt would have been used weekly. [32] The Board OH concluded: The worker [was] likely exposed to coal tar pitch during cold roof removal no more than 10% of the time. On those occasions he may have been exposed to benzene soluble levels or CTPV as high as 0.2 mg/m3 but was not likely overexposed. Although mainly a cold process, the particles and dust from this process may have contained PAHs. The worker was probably exposed to asphalt fumes up to 50% of the time when he was working. During activities involving asphalt, he may have been over exposed to asphalt fume at times (relative to the Ontario occupational exposure limit). However, this is not regard as carcinogenic During ballasting operations, a daily occurrence for some of the work shift, the worker may have been exposed to silica containing dust, but respirable dust levels and consequently respirable silica levels were probably well below the Ontario occupational exposure limits. [33] The Board OH opined: The worker may have been rarely exposed to asbestos dust but exposures were probably low and well below the Ontario exposure limits. He may have been rarely exposed to coal tar pitch dust (cold) which may have contained PAHs but exposures were probably low and well below the Ontario exposure limits. The worker was regularly exposed to asphalt fumes, which are not considered carcinogenic, sometimes at levels exceeding the Ontario occupational exposure limits. The worker was probably exposed to some silica

Page: 7 Decision No. 1815/16 containing dusts on a regular basis, but exposures were probably low and well below the Ontario exposure limits. The worker was rarely exposed to diesel exhaust fumes. [34] We heard evidence from BM, who worked as a roofer from 1981 to 2012. BM did not know the worker or work with him. Although BM could not provide specific evidence about the worker s actual exposures, he provided general evidence about mastic roofer duties and potential exposures. [35] BM testified that about 50% of all roofing jobs required the removal of an old roof. He stated that old roofs were removed with gas-powered saws and handheld axes. Debris was thrown down a chute and removed. He estimated that an average roof would take two-to-four hours to remove. BM testified that there was always a lot of dust when removing a roof. He estimated that about 15%-to-20% of older roofs were coal tar pitch roofs and that mastic workers did not wear respiratory masks. BM testified that he could easily identify a coal tar pitch roof because of its pungent smell and bluish glow. He stated that it was not possible to remove all the coal tar pitch from a roof because of its adhesiveness. BM stated that as a result, fumes from the remaining coal tar pitch would be re-activated when applying a new layer of liquid asphalt. [36] BM testified that the use of coal tar pitch for roofing did not end in the 1960s as suggested by the Board OH. He stated that it continued to be used into the 1980s and that currently some job specifications require coal tar pitch. [37] BM testified that, typically, roofers alternated duties (mopping/spreading liquid asphalt, installing membranes, insulation and ballast and melting asphalt kegs). He explained that the kettle man arrived at the worksite before other workers and was responsible for heating asphalt (tar). He stated that the kettleman heated the liquid asphalt up to its flash point (i.e., just below the point of combustion) to temperatures up to 520 degrees Fahrenheit. Hot liquid asphalt from the kettle was pumped through a pipe into a holding tank on the roof. The kettleman replenished the kettle with kegs of asphalt and monitored the temperature of asphalt inside the kettle throughout the day. This meant that the kettleman was frequently in close proximity to the kettle and fumes from the hot liquid asphalt. The kettleman wore protective wear such as a visor, heavy clothing, long sleeves and welding gloves. [38] Typically two workers mopped the liquid asphalt over the entire surface area of the roof multiple times in between insulation, four layers of paper membranes and ballast (gravel) which were laid down by other workers. BM testified that workers on the roof were constantly exposed to asphalt fumes. [39] Overall, BM s testimony about the duties of mastic roofers was generally consistent with other descriptions in the Case Record. While there were discrepancies between his evidence and the evidence in the Case Record (i.e., the temperature of the asphalt in the kettle, percentage of the work day that a mastic roofer would be exposed to asphalt fumes, the point at which coal tar pitch was no longer used and the percentage of old coal tar pitch roofs removed), these discrepancies do not, in our view, significantly alter the probability that the worker s lung cancer was caused by his employment. In our view, there is no basis to conclude that the exposures described by BM was materially different from the exposures that were typical for mastic roofers generally and, as noted above, the epidemiology indicates only an increased risk for lung cancer, not a probable association.

Page: 8 Decision No. 1815/16 [40] Similarly, we are not persuaded by the evidence emphasized by Mr. Burkimsher that indicates that poly cyclic aromatic hydrocarbons (PAHs) were not just present in coal tar pitch, but also in bitumen particularly during spraying with elevated temperatures. Exposure to PAHs from bitumen would apply to all mastic roofers. [41] We note that apart from that of Dr. Jugnundan, who did not comment on the relative contribution of the worker s 20-to-30 pack year smoking history, there is no other medical opinion in the available evidence that suggests a causal relationship between the worker s employment exposures and his lung cancer. In a memorandum dated February 25, 2011, Dr. J. Roos, Board Medical Consultant and specialist in respirology, opined that the worker s lung cancer was not work-related. [42] For the above-stated reasons, we find that the worker s employment as a mastic roofer did not, on a balance of probabilities, significantly contribute to the development of his lung cancer.

Page: 9 Decision No. 1815/16 DISPOSITION [43] The appeal is denied. DATED: August 5, 2016 SIGNED: S. Ryan, M. Christie, D. Besner