WORKPLACE SAFETY AND INSURANCE APPEALS TRIBUNAL DECISION NO. 829/14

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1 WORKPLACE SAFETY AND INSURANCE APPEALS TRIBUNAL DECISION NO. 829/14 BEFORE: E.J. Smith : Vice-Chair M.P. Trudeau : Member Representative of Employers R.W. Briggs : Member Representative of Workers HEARING: April 15, 2014, at Sault Sainte Marie Oral DATE OF DECISION: July 4, 2014 NEUTRAL CITATION: 2014 ONWSIAT 1450 DECISION(S) UNDER APPEAL: WSIB ARO decision dated March 8, 2010 APPEARANCES: For the worker: Mr. A. LaDouceur, U.S.W.A. Local 2251 For the employer: Interpreter: Not participating Not applicable 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

2 Decision No. 829/14 REASONS (i) The issue; the outcome [1] The worker s estate appeals for initial entitlement for bladder cancer and prostate cancer. The worker was diagnosed with prostate cancer in 1999 at age 58 and with bladder cancer in 2003 at age 63. He attributed the onset of his cancers to his exposures at work. [2] The ARO considered the exposures of total suspended particulate, iron oxide, calcium oxide, carbon monoxide, sulphur dioxide, crystalline silica, coke oven emissions, coal dust, coal tar pitch volatiles, and possibly asbestos in the worker s jobs of labour, slab loader, and concast straightener. [3] We have denied the appeal for the reasons set out below. (ii) The exposure evidence [4] The worker worked from 1965 until 1996 at the employer. His exposures have been considered by the Occupational Health Clinics for Ontario Workers (OHCOW), by an industrial hygienist employed by the employer, and by an industrial hygienist employed by the Board. (a) The OHCOW report [5] The Appendix to the OHCOW report outlines the worker s exposures and, according to the worker s daughter, is based on a statement given to OHCOW by the worker that was not provided to the Board but which was provided to us in Addendum #4 at the Tribunal hearing. The worker s daughter testified that the worker dictated this statement to her before his death and she typed it for him. It states that the worker spent the first three months of his employment at the foundry, the next three months at the masonry blast furnace yard, and then 16 years at the mills. He was then in the continuous casting area from 1984 until his retirement in [6] Based on this information, the summary of exposures in the Appendix to the OHCOW report describes 16 years of exposure as a stocker, labourer, and foreman in the mills. The exposures are described as coke oven emissions, blast furnace gases, flue dust, and benzene emissions from the by-product plants as follows: Worked next 16 years 25 and 45 mill soaking pits in bloom mill yard. On slow production would be sent to other sights. Working on Coke Oven Belts, Blast Furnace Yard, Cold Mill and Plate Mill. Areas had coke oven gas-blast gas and benzene emission from the By Products Plant and in Bloom Billet Mills. Emissions from Scarfing Burning. The Soaking Pits had Blast furnace gas and coke oven gas as well as heavy concentrations of flue dust in most working areas. [7] We note that the dates are approximate because the years from 1965 until 1984 cover an elapsed time period of 19 years and not the 16 and a half years described. [8] Other than with respect to the first six months, the statement by the worker, and the OHCOW exposure summary, do not distinguish between the worker s exposures in his different assignments in his time in the mills. In particular, the Appendix refers to 16 years of exposure to scarfing fumes, which is not consistent with the other evidence. [9] Dr. Reinhartz s report dated December 16, 2008 attaches the Appendix and states:

3 Page: 2 Decision No. 829/14 [The worker] worked at the [employer] from July 1965 until August His first three months were in the foundry where he was exposed to silica mostly. The next three months were in the mason blast furnace yard which was adjacent to the coke oven batteries and the by-products plant. He was exposed to fine dust from the blast furnace gas and the coke oven emissions. As a labourer, he was then in continuous casting and handled aluminum and coke to add to the ladles and also worked in the blast furnace yards and the masonry department again to work on coke making belts in the coke oven battery and repairing pipes. (b) The information from the employer [10] The employer provided a letter dated March 7, 2005, from its industrial hygienist, which includes a more precise break down of the worker s job assignments over time and identifies the hygienist s view of the relevant emissions in each job assignment. From 1965 to 1971 the worker was a labourer, plant wide. The exposures listed by the employer s hygienist were to coke oven emissions, coke dust, coal tar pitch volatiles and possibly asbestos. From 1971 to 1985 the worker is described as a slab loader in the bloom and billet area. There is no reference to coke oven emissions in the exposures identified in this assignment. The exposures listed were to suspended particulate, iron oxide and sulphur dioxide. From 1985 until 1986, the worker was a labourer at the #1 BOSP. The exposures listed were to suspended particulate, iron oxide, calcium oxide, manganese and crystalline silica. He then worked in the concast working area from 1986 until In that area, the exposures listed were to total suspended particulate, iron oxide, chromium (total chrome) aluminum and manganese. Again, there is no reference to coke oven emissions in the exposures identified. [11] With respect to the time period after 1984 the industrial hygienist was also able to provide air sampling results which showed that the time weighted average exposure values were not exceeded for the exposures that were identified, although those test results were not available for the earlier years. (c) The review of the exposure information by the Board s industrial hygienist [12] The worker s exposures were reviewed by the Board s industrial hygienist, Mr. Lou Riklik, in a report dated May 10, Mr. Riklik has included exposure assessments for each of the time periods and each of the jobs identified by the employer. He describes that, in the six years from 1965 to 1971, the worker worked as a labourer plant wide, in the years from 1971 to 1985 that the worker worked as a slab loader in the bloom and billet area, in the years from 1985 to 1986 he worked as a labourer in steelmaking and at the No. 1 BOSP, and from 1986 to 1996 in the concast area. His exposure assessment is as follows: Exposure Assessment Scarfing involves cutting surface defects from the steel using a gas torch. The smoke from this would include both mineral oils and some polyaromatic hydrocarbons such as benzo(a)pyrene. While working as a stocker he would be adjacent to the scarfers measuring the steel that the scarfers worked on. [The worker] indicated that during the period from 1965 to 1971 he worked as a stocker measuring the steel that the scarfers were working on. For a period of six years [the worker] worked throughout the plant, including the coke ovens so he would have had occasional exposure to coke oven emissions. From 1971 to 1996 there do not appear to be any major exposures to a known bladder carcinogen beyond the background levels that would occur in a steel plant.

4 Page: 3 Decision No. 829/14 Summary Based on the available information [the worker] would have had approximately six years of occasional exposure to coke oven emissions and polyaromatic hydrocarbons as combustion products from oils. [13] The worker s exposures were also discussed in a telephone call between the worker and the Board claims adjudicator dated January 10, The memo of the claims adjudicator states: He explained that he had been at [the employer] from 1965 until For the first 15 years he worked in the rolling mills (45 and 25 ) Mills. He held the position of stocker for the first while. As a stocker he worked hand in hand with the scarfers. He would measure the steel that the scarfers worked on. There was a lot of smoke created from the scarfing. He also worked as a loader/slab loader. In this position he counted and kept track of steel for other areas. He also was in a supervisor position in total for 4 years. From 1984 to his retirement he then worked in the Concast Mill. [14] We find this description consistent with the information provided by the employer and to the Board s industrial hygienist that the worker worked in the stocker job in the first while of his employment, before he moved to the slab loader job. Therefore this evidence indicates that his exposure to the scarfing fumes was in this six year time period and not for the 16 years described by OHCOW. The employer s information was that the worker was in the labourer job between 1965 and 1971 and then in the slab loader job from 1971 to 1984, which the worker described as the job of counting and keeping track of the steel. He was later in a labourer job again from 1984 to 1986 but he is not described as having worked in proximity to the scarfers in those years. (d) Smoking history; family history [15] The worker informed the Board and OHCOW that he had smoked for approximately 10 years at four to five cigarettes a day, stopping in about This would have represented about a 2.5 pack-year smoking history. [16] From the file, his father had also had prostate cancer and so there was a history of prostate cancer in a first-degree relative. (iii) The expert evidence about the relationship between the worker s exposures and bladder and prostate cancer [17] The file also contains opinion evidence about the significance of the above exposures. [18] In his report dated December 16, 2008, Dr. Reinhartz stated: Both cancer of the bladder and of the prostate are related to PAH exposure [19] He refers to a study of coke oven workers by Costantino which showed an increase of an SMR for cancer of the prostate in a follow up of 1600 workers over 30 years. There was a relative risk of 1.67 for workers with less than five years of exposure to coke ovens. However, he does not describe whether the finding was statistically significant or whether there was a dose response effect identified at the higher years of exposure. It is also not clear what jobs these workers were doing. The worker in this appeal was a general labourer and not a coke oven worker, as such, and he was described by the Board s industrial hygienist as having had only occasional and incidental exposure to coke oven emissions, as a general labourer, even from 1965 to 1971.

5 Page: 4 Decision No. 829/14 [20] With respect to PAH exposure, Dr. Reinhartz refers to a study by Aaronson which found a statistically significant odds ratio of 1.6 for workers with 1 to 10 years of exposure to PAHs from coal. However, this worker was not working with coal and, again, his exposure to the coke oven emissions as a labourer would have been occasional. [21] Dr. Reinhartz also refers to a study by Bosetti which found a statistically significant excess risk of 1.4 for bladder cancer based on exposure to PAHs. [22] Dr. Reinhartz also expresses the opinion that the worker s young age at diagnosis for prostate cancer (of under 60) and his light smoking history support entitlement. He does not refer to the fact that the worker s father had prostate cancer. He notes that some persons have a genetic predisposition to prostate cancer. However, there is no evidence of whether this worker had the predisposition described. [23] The Board s Manager of the Occupational Disease Policy and Research Branch (ODPRB), Mr. Reimar Gaetner, provided a review of the epidemiology related to prostate cancer in steel, foundry and coke oven workers. He expressed the opinion that the emissions to which they were exposed included benzo(a)pyrene and PAHs. He identified six cohort studies as the most reliable studies. They identified a small elevated risk of 1.12 that was not statistically significant. He described the studies as inconclusive. With respect to foundry workers and steelworkers, the evidence of increased risk was also inconclusive. [24] Mr. Gaetner provided a further assessment of bladder cancer risk in coke oven workers dated April 24, He found that cohort studies showed an elevated risk of bladder cancer in coke oven workers of 1.22 which was borderline statistically significant and did not exclude confounders. He found the weakness of the association surprising given that these operations feature substantial PAH exposures, many of which are known to be carcinogenic. In his view, biological plausibility is met. He concluded that the available evidence is suggestive of an association between coke oven work and bladder cancer. However, the association was weak. The overall evidence was limited. If a causal association existed in his view it would be expected to be substantial only after long durations of work at the coke ovens, on the order of 20 to 30 years. [25] The ARO relied on the ODPRB reviews to deny entitlement both for prostate cancer and for bladder cancer. The ARO accepted the opinion of the Board industrial hygienist that the worker had only six years of relevant exposure to a significant level of carcinogens. (iv) Submissions; law and Board policy [26] We have considered Mr. LaDouceur s detailed submissions about the exposure evidence and the epidemiology in the context of our analysis and conclusions, below. [27] Generally, Mr. LaDouceur submits that the evidence supports entitlement for both the prostate cancer and the bladder cancer. He relies on the opinion of Dr. Reinhartz. He refers us to the fact that the worker was a very light smoker. He was only 58 when he was diagnosed with prostate cancer. While his father also had prostate cancer, his father had worked at the same employer as the worker. However, no details about the father s work history have been provided and there is no evidence that there was a claim to the Board for the father s prostate cancer, or that the exposure was evaluated, or that entitlement was allowed.

6 Page: 5 Decision No. 829/14 [28] With respect to the relevant legal tests, Mr. LaDouceur submits that the ARO and the ODPRB erred in how they applied the law to the entitlement question. [29] He submits that the correct legal test is the balance of probabilities. If the evidence is approximately equal in weight, the worker is entitled to the benefit of the doubt. Scientific certainty is not required. It is also not required that the workplace exposures be the only cause of the injury. It is only necessary that they be found to be a significant contributing factor in the causation of the disease. He refers us to Decision No. 809/88 to support these submissions. [30] In our view, these principles are not in dispute. However, Tribunal decisions have been consistent in noting that it is not sufficient that there be a possibility of work relatedness for the evidence for and against an issue to be equal in weight. The question that we must address is how we can determine, from the scientific evidence, when a possibility is sufficient to be accepted as a probability, or when the evidence is equal in weight. [31] We also note Decision No. 600/97, which is a leading Tribunal case addressing how epidemiological evidence may be weighed to establish whether the balance of probabilities, or the principle of the benefit of the doubt, apply to support entitlement in claims for occupational exposures. The law in this area is difficult because in industrial disease cases there is no direct evidence of whether a workplace exposure has contributed to a worker s cancer. The analysis must be based on scientific studies that address the relationship between the exposure and the disease. There may be animal studies that address whether the substance under review is carcinogenic generally. However, the extent of the exposures used in the animal studies may be much greater than the exposures encountered in the workplace. To address the significance of the workplace exposures, it is common practice to rely on epidemiological studies. Those studies examine whether the incidence of cancer (or the degree of mortality from cancer) in a particular group studied, which has been subject to a certain exposure, is greater than that of a comparable group which did not have that exposure. We understand that this is why both the Board experts and Dr. Reinhartz have relied on epidemiological studies to form the basis for their opinions. [32] However, we agree with the representative that neither the Board experts nor the ARO addressed in any detail how the epidemiological evidence is properly weighed to determine at what point it is sufficient to establish that the evidence is approximately equal in weight and that the benefit of the doubt applies. This question is directly addressed in Decision No. 600/97 and the analysis of that decision has been followed in many subsequent Tribunal Decisions. The Panel in Decision No. 600/97 considered how epidemiological analysis can be interpreted in understanding whether a risk results in possible or probable causation, as follows: 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 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 Even so, since epidemiology studies populations, not individuals, it cannot prove that a particular worker s cancer was caused by the studied exposure.

7 Page: 6 Decision No. 829/14 With respect to the use of epidemiological evidence when deciding a particular worker s appeal, Decision No. 257/89 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 can be given weight and they can be used in helping to judge whether an individual worker s disability is likely work-related 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?, 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. [33] The Panel in Decision No. 600/97 discussed how to address the issue of causation in the context of an SIR of 161 (or, if the reference point is to 1 rather than to 100, 1.6) in the context of a workers compensation claim. The Panel states: But, in a case such as this where there is one indivisible injury (cancer) and the Act provides that full compensation is paid if this injury/disease arose out of or was due to employment, we must decide whether this worker s cancer did, or did not, arise out of employment.

8 Page: 7 Decision No. 829/14 In doing so, it is important to ask whether this worker s cancer would likely have developed even in the absence of work exposure, and the SIR provides some evidence about that question. From this perspective (and assuming that a causal link can be inferred from the statistical association represented by the SIR of 161), the SIR of 161 suggests that, regardless of whether there was some additional occupational risk for miners in the year group, 100 of the 161 cases of cancer among the mining group would have been expected to occur at the age they did occur even in the absence of occupational exposure. Arguably, for those 100 cases, even if there was some occupational risk, employment was not a significant contributing factor to the development of the cancer because the cancer would have developed when it did even in the absence of occupational exposure. Using this analysis, it would only be the excess risk group (i.e. the 61 cases in the 161) for which employment was a significant contributing factor in the development of the cancer because it is this group that would not have developed the cancer but for the industrial exposure. If this type of analysis is used, the concept of benefit of doubt or balance of probabilities applies not to the extent of occupational exposure, but rather to the probability that an individual worker would be one (of the 61 excess cases) whose cancer would not have developed but for the occupational exposure. Using this analysis, the question becomes: what is the probability that an individual worker is one of those who would not have developed cancer but for the occupational exposure (i.e. what is the probability that an individual worker is one of the 61 excess risk cases)? Using the SIR of 161, that probability would be 61/161 x 100 = 38%. Thus, there would be only a 38% probability that any individual miner in this population of underground miners with 30 to 34 years experience would be one of the miners who would not have developed the cancer but for the occupational exposure (i.e. one of those in the group of 61). There would be a 62% probability that he would be one of the miners who would have developed the cancer at that age even in the absence of work exposure. Using this interpretation of the SIR, it would not be until there was an SIR of about 200 that it would be as probable as not that any worker in the group was one of the workers who would not have developed their cancer but for occupational exposure. We recognize that it is impossible to determine with certainty whether a particular worker is one who would have developed cancer even in the absence of work exposure, or whether he was one who would not have developed cancer but for the work exposure. From a medical perspective, Dr. Muir suggests that the assumption has to be made that all causative factors are uniformly spread across the whole group so the central problem lies in determining what proportion of causality is required to accept a claim. But the whole group of miners with this work exposure did not develop cancer. And the SIR of 161 suggests that the majority of the workers who did develop cancer would have developed it when they did even in the absence of work exposure. [34] Therefore the Panel concluded that, when assessing a case based on inferences drawn from epidemiological studies, it was necessary for the risks identified by the epidemiology to be equivalent to an SIR of 200 (or 2) in order to provide a basis for finding that it was as probable as not that a worker s cancer was work-related. [35] However, the Panel noted that individual workers may have risk factors that are greater or less than the factors applicable to the group studied in the epidemiology, and that those individual factors must also be taken into account.

9 Page: 8 Decision No. 829/14 [36] We agree with the above analysis. [37] We agree first that it is not sufficient that an association be established between an exposure and a cancer to establish causation. For example, it might be said that an association exists between malaria and wearing sandals, if there were a higher incidence of malaria in persons who wear sandals than in those who wear shoes. That does not mean that wearing sandals is a cause of malaria. The Bradford Hill criterion offers a useful approach to determining whether an association found in the epidemiology is sufficient to suggest causation. [38] We also agree with the ODPRB that the consistency in the study findings is an important factor to be considered in this respect. The Board found the studies that addressed prostate cancer too inconsistent to support a finding of causation. Mr. LaDouceur submits that if two scientific studies are inconsistent then the benefit of the doubt should apply. However, in the field of epidemiology, we do not accept that submission as correct. One study may be stronger or more reliable than the other. Also, the fact that two epidemiological studies find inconsistent results puts into question whether the association identified in the positive study is reliable evidence of causation. The association may result from confounders or from difficulties in the design of the study or from other factors. If an exposure is causative of a cancer, then the results that are relied upon to establish that causation should be reproducible. As already noted, causation is not directly addressed in epidemiological studies and opinions about causation must be based on inferences drawn from the studies. Inconsistent studies undermine the reliability of the evidence from which those inferences can be drawn. The benefit of the doubt applies when the evidence before and against an issue is equal in weight. It does not apply when the evidence is unreliable or when the inferences to be drawn from the evidence remain speculative or uncertain. [39] Of course, when studies are inconsistent, or otherwise fail to meet the Bradford Hill criteria, the inconsistencies or weaknesses may also be the result of design flaws or confounders in the studies that did not support an association. However, that cannot be known until there have been further, better designed, studies, or until there has been clearer identification of the confounding factors. Until the inconsistencies or weaknesses are addressed in some manner that explains why they have occurred, the studies may be insufficient to establish more than a possibility of causation. That is not sufficient for entitlement. [40] The questions of interpretation are complex and in our view are helpfully addressed by expert evidence. [41] Even when there is sufficient evidence to establish that an exposure has resulted in an excess risk, a finding of excess risk is not sufficient in and of itself to establish that it is likely, or equally as likely as not, that an exposure has caused a particular cancer. Epidemiological studies are based on mathematical data. They compare the number of cases identified in the group that incurred the exposure to the number of cases expected. We agree with Decision No. 600/97 that the proper inference from the statistical data is that there must be a doubling of risk before it can be determined that all the workers with exposures that are comparable to the exposures identified in the study are entitled to benefits on the balance of probabilities. For it to be equally as likely as not for the workplace exposures to have been a contributing factor in all of the identified cancers in a workplace, the SIR or SMR must be at or above 200 (sometimes expressed as 2 ). [42] We note also, however, that when there is an excess risk between 100 and 200, it is likely that the exposures have been a significant contributing factor in the cancers of some workers in

10 Page: 9 Decision No. 829/14 the cohort but not others. In that case the task for adjudication is to identify which workers in the cohort have been exposed at a sufficiently high level to be found to be in that group. [43] Therefore, based on the analysis of Decision No. 600/97, in cases in which there is an excess risk from the exposure at a level below 200 (or 2 ), the question for adjudication is how to identify the cases for which the exposure has been sufficient to make it likely that the worker is one of the persons whose cancer is the result of that exposure. If there are special factors to suggest that the worker had exposures at a higher level than the group studied, that may be relevant. We have considered these principles further below. [44] Mr. LaDouceur also refers us to Decision No. 1507/11 to support the case that PAHs may be a contributing factor in prostate cancer. Although the worker in that appeal had no family history of cancer, he submits that this worker s father, who had prostate cancer, had worked at the same employer as the worker. However, we note that we have no evidence of the nature or extent of the father s exposures. There is no evidence that a claim was made to the Board or investigated or allowed. We note also that Decision No. 1507/11 turns largely on that worker s cadmium exposure. There is no expert opinion that this worker had cadmium exposure that was comparable to the exposures of that worker. Decision No. 1507/11 specifically noted that given the current state of the epidemiology, the decision was made based on the specific facts of that case. We consider the facts of Decision No. 1507/11 distinguishable. (v) Analysis and conclusions (a) Based on the epidemiology and the expert evidence provided, the worker s exposure levels were below the level of exposure required for entitlement [45] We do not find the evidence sufficient to support entitlement. We accept the opinion of the Board s industrial hygienist that the worker s significant exposures to coke oven emissions, to PAHs, and to the scarfers, occurred in the years from 1965 to 1971, a period of six years. We accept the evidence of the Board s industrial hygienist that after 1971 there were no known bladder carcinogens beyond background levels for a steel plant, and that the worker would have had only approximately six years of relevant exposure to coke oven emissions and polyaromatic hydrocarbons. Given his work as a labourer, his exposures to the coke ovens would have been occasional and intermittent. He was not a coke oven worker. [46] The OHCOW report appears to have been based on a misunderstanding that the worker had these exposures for 16 years, not six. It does not specifically address what exposures the worker had when he worked as a slab loader. We prefer the report of the Board industrial hygienist because it more closely reflects what the worker told the Board about his exposures and the work history provided by the employer. [47] We have considered the representative s submissions that the worker had higher exposures in the slab loader job and in the concast department than was recognized by the Board further below, and we have explained our reasons below for not accepting those submissions. [48] Based on the six years of exposure that we have accepted, the extent of the worker s exposure is considerably below the level of exposure which the ODPRB paper suggests is sufficient to establish a likely relationship to bladder cancer, of 20 to 30 years. The Board has not accepted that any level of exposure is sufficient to establish a causal association to prostate cancer given the inconclusive epidemiology.

11 Page: 10 Decision No. 829/14 [49] We prefer the Board s assessment of the epidemiology to that of Dr. Reinhartz because it is considerably more extensive. Mr. LaDouceur referred us to the fact that Dr. Reinhartz included eight papers in his bibliography for his report, which addresses both cancers. However, Dr. Reinhartz does not address all of those studies in his discussion. It is not clear whether they all support a relationship to bladder or prostate cancer or not. In his discussion of prostate cancer, he refers to only one paper, Costantino, to support his position that there is an association between coke oven exposure and prostate cancer. He also refers to one paper, Aaronson, to support his position that there is a relationship between PAHs and prostate cancer. With respect to bladder cancer, Dr. Reinhartz again refers to one paper, by Bosetti, with respect to PAHs and coke production. He does not refer to any of the papers that provide weak or negative results as discussed in the ODPRB reviews, and which led to the conclusion in those reviews that the epidemiology is inclusive with respect to prostate cancer and weak in the case of bladder cancer. Therefore we prefer the ODPRB review with respect to these exposures and cancers because it provides a fuller overview of the scientific literature. [50] We note also that the epidemiology referred to even by Dr. Reinhartz refers to excess risks of less than 200 or 2. In the one study that he refers to that addresses prostate cancer and coke oven workers, he describes an SIR of 1.6 for all workers and less than that for white (as distinct from black) workers. A relative risk of 1.67 was identified for an individual coke oven worker with less than five years exposure. However, this appears to be a reference to a single worker, which would generally not be sufficient to form the basis for a statistically significant finding. The worker in this appeal was not a coke oven worker and his exposures to coke oven emissions, as a labourer, would have been more occasional and at a greater distance than those of the workers working directly at the coke ovens. With respect to prostate cancer and PAHs, the Aaronson paper found an odds ratio of 1.6 from coal. The Bosetti study to which Dr. Reinhartz refers, with respect to bladder cancer, found an excess risk of only 1.4. All these findings are below the level of an SIR or SMR of 200 which, as noted, has been accepted by a strong line of Tribunal decisions as the level at which work-relatedness is likely, or as likely as not, unless there are special circumstances that suggest that the worker has been subject to risks which have been greater than the cohort studied. [51] The ODPRB paper includes an extensive review of the epidemiology. It finds the studies too inconsistent to support a relationship between coke oven emissions, foundry work, or steel production and prostate cancer. The evidence is inconclusive with respect to whether a causative role exists. With respect to bladder cancer, the ODPRB paper describes that there is limited evidence to support causation. Given that there is some evidence, it addresses the question of what degree of exposure might be sufficient to support a causal relationship in an individual case. The ODPRB suggests that the scientific findings may be sufficient to support a relationship to bladder cancer in the case of 20 to 30 years of exposure. This worker had only six years of exposure to levels of coke oven emissions, PAHS, or emissions from scarfing that were sufficient to be considered of importance by the Board industrial hygienist. [52] Dr. Reinhartz points out that the worker was only 58 when diagnosed with prostate cancer, and had a smoking history of only 2.5 pack-years. He submits that these findings are relevant to the diagnosis of prostate cancer and support entitlement. However, the worker also had a family history of prostate cancer, which in our view offsets these factors. [53] In any event, the review of the overall literature by the ODPRB indicates that the evidence for an association between prostate cancer and exposures to coke oven emissions,

12 Page: 11 Decision No. 829/14 foundry workers or steelworkers is inconclusive. The definition of inconclusive evidence is that a causal association can neither be identified nor ruled out. In our view, evidence of that type is not sufficient to establish more than a possibility of a causal association. Even given the worker s comparatively young age and light smoking history, causation is not sufficiently established for entitlement to be granted for his prostate cancer. [54] With respect to the worker s bladder cancer, Dr. Reinhartz also refers to levels of excess risk that were below 200. He refers to a study that found an excess risk of 1.4. The worker s exposures are also below the level that the ODRSP has suggested would be sufficient for entitlement. We note that the ODRSP had not approached the issue based on the same mathematical analysis of probabilities that was addressed in Decision No. 600/07. However, we find its approach substantially consistent with that analysis. When the epidemiological evidence suggests that there is some weak evidence of a causal relationship, at a level between an SIR of 100 and 200 (which is what the studies reviewed suggest) then the question is whether a worker s exposures were likely comparable to the higher-exposed of the cohort studied or to the average or lower exposed in the cohort. The ODPRB suggests an exposure of 20 to 30 years might meet the standard of a sufficient exposure to support entitlement. Given that this is the only expert evidence that addresses the extent of the exposure necessary to find that the exposure has likely been causative, based on a full review of the epidemiology, we accept that opinion. Dr. Reinhartz wrongly understood that the worker had all the exposures that were described for the full 16 years. We have not accepted that description of the factual evidence. [55] Based on the expert opinion before us, the worker s exposures were not sufficient to make it likely, or as likely as not, that his exposures were a significant contributing factor in either cancer. (b) Our findings about the other submissions made by the representative [56] We have also considered how a number of other submissions made by the representative affect this finding. 1. The submissions about additional exposures which were not addressed by OHCOW or the Board (aa) The submissions about the exposures in the bloom and billet area [57] Mr. LaDouceur submits that the worker had exposures that have not been recognized by OHCOW or the Board s industrial hygienist and which have been understated by the employer s industrial hygienist. We have addressed first the submissions about exposures in the bloom and billet area, where the worker worked from 1971 until [58] Mr. LaDouceur refers us to the case of another worker, whose exposures were addressed by the Board s Dr. Patel. He has provided anonymized evidence from that file. That worker worked in the plate and strip complex. Dr. Patel describes that that other worker had exposure to pyrolysis/combustion products from lubricating oils and greases on a routine basis for approximately 25 years when working as an observer in the plate and strip complex. These products may have included PAHs. Mr. LaDouceur submits that these exposures would have been from the roller lines. He referred us to company materials which he has filed which describe the fact that there were also roller lines in the bloom and billet area. He asks us to conclude that this worker would have had similar exposures to the worker whose case was

13 Page: 12 Decision No. 829/14 addressed by Dr. Patel. He submits that the worker spent 28 years in areas where there would have been roller lines. [59] He submits that this worker would have been in close proximity to the roller lines as well as to scarfing emissions while working in the blooming mill. However, he has not provided any specific evidence to support that assertion, other than the general company materials that indicate that there were rolling mills in the bloom and billet area, referred to above. [60] We do not accept that the evidence is sufficient to support this submission. The worker worked as a slab loader when in the blooming mill and did not do a job on the rolling lines. There is no evidence that establishes what proximity he had to the rolling lines or to scarfing during this work. There is no opinion of an industrial hygienist in this case that the worker s exposures were comparable to the exposures of the other worker who worked in a different job assignment in a different area of the plant, the plate and strip mill. In his discussion with the Board adjudicator, the worker described his exposure to the scarfers as having occurred early in his employment, and we understand that reference to have been to the years 1965 to He did not describe this as an exposure in bloom and billet. The worker described his job in the bloom and billet area as to count and keep track of steel. [61] The other worker s case is also distinguishable in other respects. The file material provided indicates that that worker had five years of work as a coke oven and blast furnace worker in addition to the exposure in the plate and strip department. He also had asbestos exposure at the plate and strip complex that could have been above the 2011 TLV/TWA levels. Lead air sampling in some areas was also above the 2011 TLV/TWA. That worker had also never been a cigarette smoker. In that case, Dr. Patel described the epidemiology as uncertain but he supported entitlement for bladder cancer in particular given the 25-year history of possible exposure to PAHs, the fact that that worker was a non-smoker, the fact that his exposure began when he was only 18, and the fact that his bladder cancer was diagnosed at age 53. [62] Quite aside from the fact that the workers did different jobs in different areas of the plant, the facts of that case are quite different from this case in these respects. This worker was diagnosed with bladder cancer at about age 63 and not at age 53. He was a light smoker but he had smoked for 10 years and was not a non-smoker. He started work for the employer in these exposures in 1965, when he would have been about 24, rather than 18. [63] I note that the cancer in issue in the case reviewed by Dr. Patel was bladder cancer, and that the ODPRB recognized in its review that entitlement for bladder cancer might be appropriate for workers with 20 to 30 years of relevant exposure. This worker s claim was denied because the Board only accepted that he had six years of exposure that was of a sufficient degree to make it significant for bladder cancer. We have accepted that evidence as the best evidence available. [64] We consider the facts of this case sufficiently different that we do not find the conclusions of Dr. Patel inconsistent with the opinion expressed by the ODPRB, which is that 20 to 30 years of relevant exposure would be required for entitlement. The cases are distinguishable on their facts. (bb) The exposures in the concast area [65] Mr. LaDouceur also submits that the worker had exposures beyond those that have been recognized in the concast department for the 12 years from 1984 to He refers us to a website to establish the basis for his views about the tasks done in this area.

14 Page: 13 Decision No. 829/14 [66] However, no evidence from that website has been provided to us. Pursuant to the Tribunal s Practice Direction: Disclosure, Witnesses and the Three Week Rule, a representative is required to provide his evidence to the Tribunal three weeks prior to a hearing. It is not sufficient to provide a website reference on the date of the hearing and to expect the Panel members to conduct research after the hearing. In particular, this is because this approach precludes the Panel from the opportunity to review the scientific literature prior to the hearing, or to ask questions about it, and it precludes the representative from having the opportunity to make submissions about the materials that the Panel might identify in its research efforts after the hearing. This approach might also mean that the parties and representatives might not even know what evidence the Panel had considered in reaching its decision. [67] The Board s industrial hygienist reviewed this worker s work history but did not identify his work in the concast department as involving a significant level of exposure. The employer s hygienist provided air testing results that indicated that identified exposures were below regulatory levels, although air testing results were not available for the earlier years. [68] The evidence before us indicates that any exposures in the concast department were insufficient on a balance of probability to affect our determination. (cc) Asbestos [69] Mr. LaDouceur also refers us to several references to possible asbestos exposure which are found on file. [70] In particular, Mr. LaDouceur provided us with a job description for a straight and cut operator in the concast department that refers to the use of asbestos rope. However, the job description is dated in The worker did not work in that area until There is no evidence that asbestos rope was still being used in [71] We note that neither Dr. Reinhartz nor the Board s industrial hygienist have suggested that the worker s asbestos exposure was at a level that was significant for the worker s prostate or bladder cancer. Mr. LaDouceur has also not provided any epidemiology or expert opinion to suggest that the types of intermittent and occasional exposure to asbestos referred to in the worker s work history are relevant for his prostate or bladder cancer. [72] The evidence is insufficient for us to find that the worker had a sufficient exposure to asbestos to be relevant to his cancers, or that the epidemiology would support that that was the case. Based on the evidence before us, there is no basis for us to find that the worker s exposure to asbestos was sufficient to affect the worker s risk for these cancers. (dd) Exposure to fumes from torch-cut operations [73] The worker representative suggests that while working in the concast area the worker would have had exposure to fumes from torch-cut operations. However, again, the worker worked in the concast area after The employer provided air testing results that indicated that the exposures identified for this area in those years had been tested and were below regulatory levels. The Board s industrial hygienists did not identify this as a significant exposure for the worker s prostate or bladder cancer. Mr. LaDouceur has provided a job description indicating that torch-cut operations were carried out in the concast area but the job description is dated in 1969 and we have no way to know whether it remained accurate in 1984 when the worker worked in that area. In any event, the air testing from the relevant time period does not show results that were above regulatory levels.

15 Page: 14 Decision No. 829/14 [74] This evidence is insufficient to affect our determinations. (ee) Exposure to arsenic [75] Mr. LaDouceur submits that the worker also had exposure to arsenic, which he submits is a known cause of bladder cancer. [76] We will comment on this evidence only briefly because arsenic exposure was not raised with the Board and in our view we do not have jurisdiction to consider it. There is no final decision of the Board that addresses an injuring process (an accident ) involving arsenic. [77] Mr. LaDouceur has provided a statement from a person whom he describes as a retired metallurgist who worked at the division of the employer which he submits was the main supplier of ore to the employer during the time that the worker was employed. The statement describes that the ore contained arsenic and that: we had a lot of scale sticking to steel when we reheated it. We traced some of the problem to the arsenic level, which was tracked in each batch of ore. When we sintered at [the employer divisions] the arsenic was probably there. [78] This co-worker states in his statement that eventually this ore was phased out and other ore with less arsenic was purchased. The statement provides no information about when this phase out occurred. [79] Mr. LaDouceur submits that based on this statement exposure to arsenic would be an issue in this claim. [80] However, this statement is insufficient to establish that the worker was doing tasks that would have exposed him to levels of arsenic that were relevant to his prostate or bladder cancer. There is no information about what years would have been relevant. The worker did not describe being involved in heating ore or in sintering. Neither the Board industrial hygienist, nor the employer s occupational hygienist, nor OHCOW, have identified this as a relevant exposure for this worker. We have not been provided with any expert opinion or epidemiology to address the extent of the likely exposure, if it existed, or the degree of association between any exposure that the worker might have had and his cancers. We have not been provided with any epidemiology on this aspect of the issue. It is also unclear how the worker s exposures in this respect would have differed from the workers whose exposures in the steel industry, coke oven work and foundry work were addressed in the epidemiology discussed in the ODPRB review. [81] This submission is insufficient to affect our determinations. (ff) Exposure to chemicals from water [82] Again, we will comment on this submission only briefly. It was not raised with the Board and in our view we do not have jurisdiction to address it. [83] Mr. LaDouceur submits that the worker also had exposure to PAHs from contaminated water. The worker s daughter testified that it was her understanding that her father showered at work. Mr. LaDouceur provided a statement from another worker that the water in the pipes would sometimes be brown because of ships in the employer s slip. He provided evidence that the city moved the water intake source in June He submits that testing had identified that the water had the highest concentration level of PAHS of any Ontario city tested in 1980 and that this was why the city moved the water source. We note that he has not provided any evidence,