WORKPLACE SAFETY AND INSURANCE APPEALS TRIBUNAL DECISION NO. 1142/05

Transcription

1 WORKPLACE SAFETY AND INSURANCE APPEALS TRIBUNAL DECISION NO. 1142/05 BEFORE: M.F. Keil: Vice-Chair HEARING: May 26, 2005 at Sudbury Oral DATE OF DECISION: July 26, 2006 NEUTRAL CITATION: 2006 ONWSIAT 1646 DECISION(S) UNDER APPEAL: WSIB ARO decision dated February 8, 2002 concluding that the worker s death from lung cancer did not result from his employment as an underground miner APPEARANCES: For the worker: K. Conley, U.S.W.A., Local 6500 For the employer: Interpreter: G. Hughes, Consultant none 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. 1142/05 REASONS (i) Background [1] The worker, born in 1930, worked for the accident employer as an underground nickel miner from 1950 until the beginning of Over the years he worked as a shoveller, a nipper, a slusherman, a motorman, a blaster and, very briefly, as a driller, switch conductor and process labourer. [2] In a medical report from 1973, Dr. Trobridge comments on the worker's recurrent pneumonia. In 1974 the same physician diagnoses the worker as having chronic bronchitis. He also comments that the worker weighs over 200 pounds and is still smoking about 15 cigarettes a day. In 1981 Dr. Trobridge notes that the worker smokes about a pack a day, has mild to moderate restrictive lung disease and probably peripherally situated bronchial carcinoma. Specialist Dr. Kivenen sees the worker in February of 1982 and notes a cigarette a day history, concluding that the worker has a malignancy right lung, as well as chronic obstructive lung disease (COLD). The cancer diagnosis is subsequently confirmed as being squamous cell carcinoma. The worker is also seen by Dr. P. Cano, who describes the worker as a heavy smoker. [3] The carcinoma was inoperable, the worker's condition deteriorated and he died on May 22, The autopsy revealed a massive empymea present in the right pleural cavity, with the left pleural cavity almost completely obliterated by dense fibrous adhesions. The right lung was almost completely obliterated by a massive firm white tumor mass. Within the left lung there was marked edema present and moderate congestion. [4] The widow filed a claim for compensation benefits in 1990 and the Board subsequently carried out an investigation. When interviewed, the widow advised the worker had been a minimal smoker, less than ½ a pack a day. She did not know how long he had smoked. Board Chest Disease Consultant Dr. Gray reviewed the worker's file. He noted that the autopsy did not comment on any fibrotic change in either lung or give any indication of asbestos being present. There were also a number of chest x-rays, none of which suggested any pleural plaque or pleural fibrosis or parenchymal infiltrative changes of the lung bases that might make one consider asbestos effects being present. Dr. Gray concluded there was no support for asbestos exposure based on changes that might have occurred in the chest x-rays and referred to the worker's smoking. The Claims Adjudicator denied the widow s claim. [5] As preparation for the hearing before Appeals Resolution Officer, Mr. Conley asked for an opinion from Occupational Health Clinics for Ontario Workers Inc. (OHCOW). Occupational Health Physician Dr. J. Anderson reviewed the file materials and interviewed the widow. In his report dated May 18, 2001, the physician accepted the widow s account of the worker smoking approximately 10 cigarettes a day. Dr. Anderson relied on an OHCOW occupational hygiene report stating: [The worker] worked from 1950 to 1973 as an underground miner at [the accident employer], resulting in approximately 23 years of underground experience. It is known that during the earlier years of mining, underground conditions were described as some of the dustiest years, when no personal protective (sic) was available.

3 Page: 2 Decision No. 1142/05 While working underground at [the accident employer], [the worker] had the potential to be exposed to several suspected carcinogens, for example diesel emissions, oil mists and blasting agents. Diesel emissions, oil mists and blasting agents all contain polycyclic aromatic hydrocarbons (PAHs), such as benzo(a)pyrene, benzo(a)anthracene and pyrene, which may be linked to an increase risk of cancer (esp. benzo(a)pyrene) of the lungs. He may also have been exposed to known carcinogens such as silica and asbestos. [6] Dr. Anderson concluded that on the balance of probabilities, occupational exposure appear(ed) to be the most predominant factor in the etiology of [the worker] cancer of the lung. [7] The ARO concluded that the worker s smoking history was the most likely cause of the worker's death and that there was no evidence of asbestos or silicosis in the worker's claim. (ii) Relevant epidemiology [8] The Board has policies for compensating miners who develop lung cancer with gold mining and/or uranium mining experience. Board Operational Policy Document No , entitled Lung Cancer in the Nickel Producing Industry states that lung cancer is an occupational disease for workers employed in the sintering, leaching or calcining processes of the nickel industry, as well as for lung cancer resulting from exposure to soluble nickels relating to nickel smelting or refining. There is no policy for general underground nickel mining and the reasons for this can be found in the following chronology. In March of 1994, the Industrial Disease Standards Panel issued its report to the Workers' Compensation Board on Lung Cancer in the Hardrock Mining Industry (IDSP Report No. 12). 1 That report concluded the following based on most of the studies it considered: the majority of miners have more than one ore experience there is generally a statistically significant excess of lung cancer among Ontario hardrock miners when gold and/or uranium are part of the exposure mix, the risk is generally higher generally, there is a dose/response relationship between mining exposure and the development of lung cancer. [9] The IDSP concluded that a probable connection existed between all hardrock mining and lung cancer. [10] As a follow-up to the IDSP report, the Board asked Dr. Ka Sing Yeung to prepare a paper on the causal relationship between underground nickel mining and lung cancer based on a review of the epidemiological literature. In her report from August of 1994, Dr. Ka Sing reviewed five publications (between 1989 and 1994), although none of them was dedicated exclusively to the subject of lung cancer in nickel miners. She noted that the table from the Kusiak report suggested that there was a modest increase in SMR (standardized mortality ratio) 2 for nickel 1 It should be noted that at the time of this report the Vice-Chair of this appeal was employed by the IDSP as a program coordinator. As such, she was involved peripherally at the end stage of the report. She did not participate in any research but did provide some editing assistance. 2 Dr. Ka Singh defined her terms as follows:

4 Page: 3 Decision No. 1142/05 miners who had also mined gold before However, those who did not mine gold and started nickel mining before 1935 still had a significant increase in lung cancer SMR. [11] Based on the reports studied, Dr. Ka Sing concluded: there is a modest increase in the overall lung cancer SMR s in [the cohort of nickel miners from one of the Ontario mines studied]; lung cancer SMR s based on duration of employment do not show a dose-response relationship between duration of nickel mining and SMR in either [of the two Ontario mining cohorts]; analyses based on year started mining showed inconsistent results among the three studies; Roberts et al. and Kusiak et al. showed a higher SMRs among those who started earlier in the 1930 s than those who started later; Shannon showed the highest SMR among those who started mining after 1960 as compared to those who started in earlier periods; there is no increase in lung cancer SMR among nickel miners who did not mine gold before 1945 except for nickel miners who started nickel mining before [12] The Board epidemiologist did suggest that it was possible that nickel mining itself did not cause lung cancer but, rather, served to amplify the lung cancer risk of other mining exposures The standardized mortality ratio (SMR) is used in occupational epidemiology to measure the relative chance of developing a disease in an occupational group. It is computed by dividing the number of deaths due to a disease in a group of workers (such as lung cancer in nickel miners) by the number of deaths due to this disease in a group of people with comparable year of birth and gender but who do not have the same occupation. (This is sometimes referred to as observed deaths (in the miners) versus expected deaths (general population)). The SMR is often expressed as a percent the ratio multiplied by 100. A true SMR of 100 or less usually indicates that there is no excess risk of developing the disease: an SMR greater than 100 usually indicates that there is an excess risk of developing the disease. If all confounding factors are accounted for, the magnitude of the SMR reflects the magnitude of the disease risk associated with the occupational exposures. However, the SMR observed is a study subject to the influence of chance. The likelihood of observing an SMR that is greater than 100 by chance when the true SMR is no more than 100 is inversely proportional to the number of workers in a study group. In studies which have adequate numbers of workers, the likelihood of observing an SMR greater than 100 when the true SMR is no more than 100 is low. Therefore, in such studies, when the observed SMR is greater than 100, the observation is called statistically significant. This means that there is a high likelihood that the true SMR is indeed greater than 100. In studies where the number of workers is small, there is a high likelihood than an SMR greater than 100 is observed by chance.. When this occurs, it is uncertain whether there is a true occupational hazard, and the finding is called statistically non-significant. In epidemiologic reports, statistical significance is indicated by either a p-value or a confidence interval (CI). A p-value of 0.05 means that the chances of observing such an SMR, when the true SMR is 100 or less, is 5%. A 95% CI gives a range of the probable value of the true SMR. When a 95% CI includes the value of 100, it is probable that the true SMR is 100 or less regardless of the observed value of the SMR

5 Page: 4 Decision No. 1142/05 (e.g. gold mining and/or uranium mining). However, she went on to say that there was little evidence of this to date. She concluded that it was possible that nickel mining [had] a weak effect on the development of lung cancer. Dr. Ka Sing suggested that an occupational hygiene assessment of each individual lung cancer case to determine work-relatedness might be a useful approach. [13] In December of 1995, Dr. J. Julian and Dr. D. Muir produced A Study of Cancer Incidence in Ontario Nickel Miners (prepared for the Occupational Diseases Panel). A final version was released in January of The study was based on 54,500 miners from one employer and 11,600 from another. The study concluded as following on lung cancer and underground miners: An excess risk 3 in underground miners with more than 25 years of exposure was found but results are not consistent when grouped by decade of first exposure. Similar results were reported by Roberts et al. (1989b) and ICNCM (1990). [14] The Board's Medical and Occupational Disease Policy Branch (MODPB) prepared a summary report on the above study paper dated February 19, It summarized the findings on lung cancer and nickel miners as follows: There was no excess of lung cancer among the overall cohort of nickel underground miners (548 cases, SIR =102). For underground miners with more than 25 years of exposure, an SIR of 146 (208 cases) was observed. The finding varied with decade of first exposure. The excess incidence was most evident among those long term miners who started mining nickel in 1930 or earlier (27 cases, SIR = 185). [15] It should be noted that, as of this date, the Board has neither accepted nor rejected the recommendations of IDSP Report #12. 3 The Julian and Muir Study explained what measures of risk their Study used in analyzing the risk of cancer in the groups of miners studied, and the tests they used to assess whether their results were statistically significant or whether the results obtained could be due to chance. One of the main measures of risk that they used was the Standardized Incidence Ratio (the SIR ). This measure compares the number of cancer cases observed in a defined population, to the number of cancer cases expected in a comparison population (in this case, Ontario males of the same age). To avoid using fractions, the ratio is multiplied by 100. In their study, Julian and Muir explained this measure of risk (the SIR ), and the use of confidence intervals to test the statistical significance of the findings as follows: The common method of expressing mortality risk is by calculating the Standardized Mortality Ratio (SMR) which is 100 times the observed number of deaths divided by the number of expected deaths based on the general population of Ontario. A similar approach is used for cases of disease and is known as the Standardized Incidence Ratio (SIR) For SIR a value of 100 indicates that the number of cases observed is the same as that expected. The 95% confidence interval (CI) is an indication of whether or not the finding is simply due to chance. If the lower limit of the CI is greater than 100, then this indicates that we have a high degree of confidence that the risk is true, and not simply the result of chance

6 Page: 5 Decision No. 1142/05 [16] There is no denying the importance of epidemiological evidence in establishing whether a casual relationship between certain exposures and certain diseases exists. The nature of epidemiological evidence has been well discussed in Tribunal Decision No. 600/97 as follows: (a) The nature of epidemiological evidence 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 4. 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 5. 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 6 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. 7 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? 8, 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?). 4 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 Rothwell v. Raes (1988), 66 O.R. (2d) 449 at page W.C.A.T.R Rothwell v. Raes (1988), 66 O.R. (2d) 449, additional reasons at (1989), 69 O.R. (2d) Proceedings of the Royal Society, Section of Occupational Medicine. Vol. 58 (1965), pages

7 Page: 6 Decision No. 1142/05 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. (b) The meaning of the term statistically significant Statistical significance has to do with the mathematical probability that a research finding is by chance (e.g. it occurred because of some sampling error). When the Julian and Muir Study reported that there was a statistically significant elevated risk for men in the single category of between 30 and 34 years of exposure, the term statistically significant did not mean there was strong evidence of causation. In this regard, Dr. Miller wrote: Statistical significance has nothing to do with the extent of risk. It has however, much to do with the size of the sample being studied. Thus a very small, even a negligible risk, can be demonstrated with high statistical significance if a large enough sample is available for study. In contrast, even a very high risk may not be statistically significant (i.e. one cannot exclude with confidence chance as an explanation for the finding) if the sample of subjects studied is very small. In practice, one establishes causality in epidemiology by applying well recognised criteria (Bradford Hill, IARC) Likewise, in his paper, Sir Bradford Hill noted that formal tests of significance cannot answer questions about whether a statistical association between exposure and disease can be interpreted as showing a cause-and-effect relationship. He wrote that formal tests of significance can, and should, remind us of the effects that the play of chance can create, and they will instruct us in the likely magnitude of those effects. Beyond that they contribute nothing to the proof of our [causation] hypothesis. It is also the case that a research finding that has been found (using the accepted mathematical tests of probability) to be statistically significant may in fact have been a chance finding. Even the standard used to decide whether a statistical association is statistically significant indicates that there is some possibility of chance (i.e. about 1 time in 20 for a 95% confidence interval). The worker s representatives based their argument that the worker s cancer was due to his employment primarily on the following statement in the Julian and Muir Study: The INCO underground production mining cohort experienced an excess of about 19 colo-rectal cancers and a statistically significant elevated risk for men in the single category of between 30 and 35 years of exposure (see Table 42).

8 Page: 7 Decision No. 1142/05 Board Scientist R. Gaertner wrote the following with respect to the possibility that a finding in a Study as large as the Julian and Muir Study can meet the standard of statistical significance but still be by chance (particularly if the finding is restricted to a subgroup): in a study of this magnitude, the many comparisons undertaken will result in significant elevations by chance alone. Therefore, even though a result for a subgroup is statistically significant, given the many times one has made comparisons (like throwing the dice), the significant finding can still be due to chance In this regard, Dr. Gaertner gave an example of a subgroup of sinter workers (with 2 to 4 years exposure) for which the Study reported a finding of statistically significant elevated risk that was found to be a spurious result (because the findings for the group as a whole showed no dose-response relationship). The above descriptions of the meaning of statistically significant indicate that, although it is important that the statistical finding (the SIR of 161) with respect to the 30 to 34 year exposure group is statistically significant (because that reduces the possibility that the finding is due to chance), there is still some possibility that the finding is by chance. And even if it is not by chance, the term does not mean the statistically significant association is a strong association, or that it establishes causation. (c) The meaning of a Standardized Incidence Ratio (SIR) A Standardized Incidence Ratio ( SIR ) as used in Table 42 of the Julian and Muir Study: Is a figure representing a statistical comparison between the number of cases of colorectal cancer among the studied group of underground miners and the number of cases of colo-rectal cancer that would be expected based on cancer rates in the comparison population of Ontario males of the same age. The SIR is a fraction with the actual number of cases of colo-rectal cancer observed in the population of miners in the numerator of the fraction and the number of colorectal cases of cancer expected in the comparison population. This is multiplied by 100. e.g. observed cases in the group of miners x 100 expected cases in the comparison population An SIR of 100 indicates that the number of cases observed in the studied population is the same as that expected (based on the incidence rates in the comparison population). Anything significantly in excess of 100 is described as excess risk. The excess risk may sometimes be expressed as a percentage. For example, an SIR of 125 means the actual number of cases observed was 25% higher than expected. An SIR of 200 (also described as a relative risk of 2) means that twice as many cases of cancer were observed in the studied population (the exposed population) than were expected based on cancer incidence rates in the comparison population (the non-exposed population). The SIR is a statistical measure of the difference between the actual number of cases observed and the expected number of cases. It does not give any direct evidence about a medical model of causation, or about levels of actual industrial exposure, or about causation in the individual case. It does not establish causation and a number of other factors (such as those described in Sir Austin Bradford Hill s paper The Environment and Disease: Association or Causation?) must be considered before any inferences about causation are drawn. [17] While Tribunal Decision No. 600/97 deals with colo-rectal cancer, its explanation of terms is still relevant and helpful in providing a context for discussion.

9 Page: 8 Decision No. 1142/05 [18] That decision went on to discuss when a significant statistical risk would result in compensation. In that case there was an SIR of 161. The Panel in Decision No. 600/97 had also been provided with an opinion by Dr. Miller and arrived at the following: 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 (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 analysing 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 years exposure. Likewise, Dr. Muir finds an SMR (standard mortality ratio) or SIR (based upon incidence rather than mortality) 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 nonoccupational 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 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). (iii) Submissions [19] Mr. Conley submitted that the worker had a number of years working as a slusherman and as a nipper (similar to the work of a slusherman). The worker would have had exposure to asbestos on the slusher machines, as well as in other occupations. The working conditions would not be the same as today, nor would the safety standards. He acknowledged that smoking would have been a factor in the worker's development of lung cancer but argued that workplace

10 Page: 9 Decision No. 1142/05 exposures would also have been a significant contributing factor. Mr. Conley also commented that the OHCOW report had been supportive, commenting on the many exposures the worker would have experienced. [20] Mr. Hughes submitted that the worker's smoking habits would more reliably be obtained from the treating physicians (as their information would have come from the worker) rather than the widow. The physicians noted that the worker smoked a pack a day and was a heavy smoker. He suggested that Dr. Anderson s report should be discounted because the physician had relied on a light smoking history and that was clearly incorrect. Mr. Hughes suggested that at best the worker would have had intermittent asbestos exposure over a ten year period. Dr. Gray, a chest disease expert, concluded there was no suggestion of asbestos present in the worker's chest x-rays or in the autopsy report. Mr. Hughes also noted that the worker had COPD and chronic bronchitis, two other conditions scientifically linked to smoking. Lastly, Mr. Hughes argued that epidemiological studies did not indicate a statistically significant risk for nickel miners with less than 25 years exposure who had not started before (iv) Conclusions [21] With respect to the worker's smoking history, I conclude on the preponderance of the evidence that the worker most likely had a pack history. I appreciate that the widow advised Dr. Anderson that the worker was a light smoker based on his habits at home, but she would not have had the opportunity to view him when he was at work. No one argued that the worker would not have smoked while in the workplace. Further, the treating specialists could only have obtained a smoking history from the worker and he would have had no reason to artificially inflate his smoking habit. Consequently, when the physicians concluded that the worker was pack a day smoker, that evidence could only have come directly from the worker. While I cannot say with certainty when the worker started smoking, he did not stop until a few months before his death in 1982 and he had smoked as long as his wife knew him. I find it reasonable - as an estimate - to conclude that he would have started in his late teens. This produces a 35 year smoking history. Even if the worker had started smoking when he was 20, it would still amount to over a 30 year smoking history. [22] Although the risks from smoking are not discussed directly in this case, I refer to Decision No. 807/01 and its general findings on the risks associated with smoking: An epidemiologist from the Board's MODPB provided an opinion dated February 26, 1996, in which it was pointed out that a 50 pack year smoking history resulted in a relative risk of developing lung cancer of at least 15 (equivalent to an SMR of 1500). The following was also noted: Squamous cell carcinomas generally have higher relative risks from smoking than all lung cancers together. One recent study of lung cancers, excluding adenocarcinoma, found a more than 30 fold risk after pack years and a 60-fold risk after 50 or more pack-years. [23] In the instant case, the worker did not have a 40 pack years but he did have In my view, this signifies that the worker would most likely have had at least a fold risk. I would also refer to the opinion of internist Dr. Ahmad, as set out in Tribunal Decision No. 600/904:

11 Page: 10 Decision No. 1142/05 The World Health Organization classified lung cancers into nine types according to the histological cell type. 1. Squamous cell 2. Small cell 3. Adenocarcinoma 4. Large cell 5. Adenosquamous 6. Carcinomas with Sarcomoid elements 7. Carcinoid tumors 8. Carcinoma of Salivary type 9. Unclassified. Only four account for 95% of the total: Adenocarcinoma, Squamous cell carcinoma, Small cell carcinoma and Large cell carcinoma. Tobacco smoking causes ninety percent of lung cancers. Only ten percent of smokers develop cancer of the lung. [24] What the above demonstrates is that smoking was probably the major reason for the worker's lung cancer. It remains for me to address whether workplace exposures might reasonably be seen to be a significant contributing factor. [25] According to the epidemiological studies (in particular the one that studied Ontario miners over a considerable period), there is no excess risk for miners with less than 25 years underground who did not start mining in the 1930 s and who did not have gold mining experience. The worker in this case had less than 25 years experience, worked solely as a nickel miner, and started employment in Accordingly, one can see he does not fall within the parameters of the higher risk group. [26] Mr. Conley has submitted there was asbestos exposure and that might have had an impact on the development of the worker's lung cancer. This is possible but, as noted by Dr. Gray, there was no evidence of silicosis or asbestosis in the worker's chest x-rays or autopsy. Any asbestos exposure was sufficiently minimal that it had left no physical trace. Further, the worker had evidence of COLD and chronic bronchitis. In this regard it is useful to consider the literature on this subject. Respirologist Dr. L. Holness and Dr. D. Muir, Director Occupational Health Program, McMaster University, prepared a discussion paper of COPD for the Tribunal. That paper summarized the results from various studies examining the specific types of dust that can cause chronic obstructive pulmonary disease, such as silica and coal dust exposure. They provided the following overview of COPD: COPD (Chronic Obstructive Lung Disease) is a narrowing of the small airway of the lung which causes the patient to have difficulty in breathing. Chronic bronchitis, strictly speaking, refers to a chronic productive cough with sputum. It may or may not be combined with COPD in the patient. The two names COPD and Chronic Bronchitis are often used interchangeably to refer to narrowing of the small airways. The condition usually deteriorates when the cause continues (generally cigarette smoking). On stopping exposure it continues unchanged the patient does not get worse but, unfortunately, does not get better, there is good evidence of this in the case of cigarette smokers. The overwhelming cause [of COPD] is cigarette smoking. Dust exposure if heavy enough and for a prolonged period of time can have the same effect The paper goes on to state that there is a dose response relationship between COPD and cigarette smoking and dust exposure. The paper identifies cigarettes as the main culprit in tobacco associated COPD. [27] In the instant case, we have evidence of three conditions COPD, chronic bronchitis and lung cancer all of which can be causally related to smoking and a worker who has a significant smoking history. While the worker was an underground miner he was not in a high risk group (according to the epidemiological studies) for lung cancer. Similarly, while there was some

12 Page: 11 Decision No. 1142/05 minimal asbestos exposure, there are no clinical indicia that the asbestos exposure had been such as to leave physical traces in the worker's lungs. [28] The occupational hygienist at OHCOW mentioned exposures to PAHs, asbestos and to diesel fumes as contributing to the worker s overall risks in developing lung cancer. From my admittedly lay perspective, this amounts to double counting. The epidemiological study of Ontario miners would have drawn its results based on the miners total experience. Let us suppose miners exposures while nickel mining including diesel fumes, PAHs and asbestos increased the risk of developing lung cancer. This would have been demonstrated in increased SIR or SMR results from the study. This was not the case. There were no higher risks associated with miners with less than 25 years underground 25 years that would have included exposure to diesel fumes, PAHs and some asbestos. One cannot count these exposures twice in order to suggest there would be an increased risk. [29] Considering the other exposures as separate entities would only be reasonable and provide persuasive evidence if it could be demonstrated, on the balance of probabilities, that a worker's specific exposures were much greater than those of the average underground miner. In this case, there has been no evidence put forward that the worker had exposure to PAHs or diesel fumes or asbestos that was qualitatively or quantitatively more significant than would be expected in general underground miner experience. [30] While epidemiological studies discern patterns over large groups, helping to draw an inference of causation, they must be considered within the context of the specific facts in any particular case. In this case I can find no specific facts that would persuade me to find that the worker's workplace exposures were a significant contributing factor. There was no employment of a significant risk such as working in the sinter plant (or other processes covered by Board Operational Policy Document No ). His chest x-rays and autopsy did not reveal the presence of asbestos or silicosis. Lastly, he had other conditions associated with smoking. [31] The preponderance of the evidence leads me to conclude that the worker's experience as an underground miner did not cause or make a significant contribution to his lung cancer.

13 Page: 12 Decision No. 1142/05 DISPOSITION [32] The appeal is denied. DATED: July 26, SIGNED: M.F. Keil.