SUMMARY DECISION NO. 893/90. Cancer (lung) (squamous cell); Exposure (asbestos); Causation (medical evidence); Smoking.

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1 SUMMARY DECISION NO. 893/90 Cancer (lung) (squamous cell); Exposure (asbestos); Causation (medical evidence); Smoking. The worker was a rigger/boilermaker at an oil refinery. The worker's widow appealed a decision of the Hearings Officer denying entitlement for the worker's death from lung cancer. Asbestos was used as an insulating material at the refinery. The worker had intermittent exposure to asbestos over the 22 years he worked as a rigger/boilermaker. The worker was also a heavy smoker. There is no dispute that smoking is the number one cause of lung cancer. The issue was whether asbestos exposure was also a significant contributing factor in the development of the worker's lung cancer. A block of tissue from the worker's lung was analyzed by a doctor who identified 14 amosite fibres in the tissue sample. Using a standard conversion formula, the doctor translated those 14 fibres to a value of 3,100,000 fibres per gram of dry lung, which was 310 times over that of the general population. The majority of the Panel found this to be the best evidence of intensity of exposure. Even allowing for the high potential for error due to the small size of the sample, this evidence was more reliable than vague recollections of co-workers and evidence of an industrial hygienist that was based in large part on imprecise information. The majority of the Panel found that the most reliable evidence regarding asbestosis and asbestosrelated lung cancer was that of a study which suggested that asbestos-related cancer is associated with some degree of histologically demonstrable asbestosis but noted that slight and moderate asbestosis may be undetected. In this case, although there was no clinical diagnosis of asbestosis, there was some evidence of fibrosis and scarring. The majority of the Panel concluded that workplace exposure to asbestos was a significant contributing factor to development of the worker's lung cancer. The appeal was allowed. The Employer Member, dissenting, found no reliable quantitative evidence of high exposure to asbestos. The doctor's report relied upon by the majority was problematic due to the small size of the sample. The evidence of the industrial hygienist indicated exposure well below current exposure limits in Ontario. The probable cause of the worker's cancer was cigarette smoking. [37 pages] PANEL: Sandomirsky; B. Cook; Nipshagen (dissenting) DATE: 08/10/96 WCAT DECISIONS CONSIDERED: Decision No. 1188/87 (1988), 10 W.C.A.T.R. 122 consd; Decision No. 134/89 (1993), 26 W.C.A.T.R. 32 consd; Decision No. 375/92 (1993), 28

2 W.C.A.T.R. 32 refd to; Decisions No. 809/88 consd, 246/89 refd to, 1009/89 refd to, 47/91 refd to, 699/91 refd to, 266/93 consd CASES CONSIDERED: Snell v. Farrell (1990), 72 D.L.R. (4th) 289 (S.C.C.) refd to BOARD DIRECTIVES AND GUIDELINES: Operational Policy Manual, Document No APPENDICES: Review of Tribunal decisions on asbestos and lung cancer.

3 WORKERS COMPENSATION APPEALS TRIBUNAL DECISION NO. 893/90 This appeal was heard on November 26 and December 20, 1990, February 18 and 19 and October 10, 1991, June 21 and 22, 1993, and April 4 and 5, 1995, by a Tribunal Panel consisting of: J. Sandomirsky : Vice-Chair, G.M. Nipshagen : Member representative of employers, B. Cook : Member representative of workers. THE APPEAL PROCEEDINGS The worker s widow appeals the Hearings Officer decision dated December 5, That decision denied her deceased husband initial entitlement to compensation benefits for lung cancer, which he claimed was causally related to his exposure to asbestos while in the course of his employment with the accident employer. The worker s widow was represented at the hearings by N. Godbout, a lawyer with the Industrial Accident Victims Group of Ontario (I.A.V.G.O.). D. Wilkens, also a lawyer with I.A.V.G.O., presented final oral submissions. R. Fiorentino appeared for the employer with its representative C. Osborne, a lawyer with the firm Fraser & Beatty. The Panel was assisted during the course of the proceedings by D. Revington, a lawyer in the Tribunal Counsel Office. THE EVIDENCE The Panel reviewed the Case Description and approximately 33 Addenda and other documents, in addition to transcripts of the oral evidence. 1 The worker s case included the testimony from J. MacDonald, the superintendent of maintenance, P. Donnelly, an operator, and the worker s widow. The employer called I. McDonald, the superintendent of operations, L. MacKenzie, shift foreman of operations, M.Plouffe, the worker s supervisor, T. Bowles, superintendent of maintenance, Dr. W.K.C Morgan, a specialist in chest diseases and N. Murray, an industrial hygienist, as witnesses. We heard submissions from Mr. Wilkens and Ms. Osborne and received written submission from Mr. Revington. THE NATURE OF THE CASE The worker was employed by the accident employer between 1955 and 1979, first as a labourer and then, from 1959, as a rigger/boilermaker. He was diagnosed with lung cancer in December 1983 and died in 1985, at the age of 69. His widow claimed that her husband s lung cancer, and death, were causally related to his exposure to asbestos at work. The Hearings 1 A list of the exhibits is contained in the Tribunal s administration file. 1

4 Officer concluded that the worker did not have a clear and adequate history of at least ten years of occupational exposure to asbestos and, therefore, did not meet the Board s policy criteria for entitlement to benefits for asbestos related lung cancer. THE PANEL S REASONS (i) The co-worker s evidence The Panel heard extensive oral evidence regarding the nature of the work performed by a rigger/boilermaker at the oil refinery where the worker was employed, and the extent to which that employment may have exposed him to asbestos. In general terms, the rigger/boilermakers were involved in two types of work: the maintenance of the refinery towers during shut-down periods, and regular plant maintenance during the rest of the year. The refinery had four production complexes, or units, and each complex consisted of many towers. According to the evidence presented at the hearing, the units were shut down for maintenance on a staggered and cyclical basis. The Panel heard conflicting evidence from the witnesses regarding the length of time it took to do the shut-down maintenance. Mr. MacDonald recalled that each unit took from six to nine weeks to repair during a shut-down, and that the maintenance cycle for the whole facility could take up to nine months of the year. Mr. Donnelly recalled that each unit was shut down for two to three weeks. He estimated that the total shut down period was 9 to 12 weeks. Mr. McDonald testified that the catalytic cracking unit was shut down every two years for four to six weeks and other units were shut down every year for one to two weeks. Mr. Plouffe recalled that some units were shut down every year, and some every three years, and the whole cycle could last for 12 to 15 weeks. Mr. Bowles estimated that a shut-down period of a major unit might take three weeks and that there would be no more than nine weeks that a series of units were shut down in a year. He testified that 1966, 1969, 1972, 1974, 1976 and 1977 were shut-down years and that in 1967 and 1971 there were emergency shut-downs. He recalled that 1969 was the only year when everything was shut down at the same time for a six-week period. During the shut-down period, the biggest job for the rigger/boilermakers involved repairing the heat exchangers. The exchangers were units approximately 20 feet long, two to four feet in diameter, weighing up to 10 to 15 tons, that contained a bundle of rods. The rigger/boilermakers opened up the exchangers and removed and repaired the rods. To get access to the rods, the exchangers had to be detached from the pipes and the ends removed. This work necessitated the removal and re-application of the insulation that covered the pipe joints and the exchanger heads. The evidence varied on how long it took to remove the insulation in order to open the exchangers. Mr. MacDonald and Mr. Donnelly estimated that it could take up to half an hour. Mr. McDonald estimated that it took about a minute to remove the insulation from the exchanger heads, unless it was stuck on, and then it could take five minutes. Mr. Plouffe and Mr. Bowles testified that the exchanger heads were fitted with prefabricated insulated coverings, which were removed without disturbing the insulation. 2

5 The rigger/boilermakers also repaired the internal trays during the shutdown maintenance. The witnesses testified that the towers contained a series of trays that were attached to the tower by hangers and seating rings and that there was an insulating gasket between the seating ring and the tray to prevent leakage. The rigger/boilermakers removed the trays and replaced the gasket on the seating rings. Sometimes the old gasket material became adhered to the rings and tray and had to be scraped off. The Panel also heard conflicting evidence from the witnesses about which workers performed the insulation work. Mr. Plouffe and Mr. Bowles testified that it was company policy to have qualified insulators perform all the insulation work. They also testified that it was the labourers job to remove the gaskets from the seating rings. However, the other witnesses testified that, while the maintenance crew included labourers and licensed insulators, a team of rigger/boilermakers working on a piece of equipment would likely remove and re-apply the insulation as part of the operation. Furthermore, the majority of the witnesses indicated that, even if the rigger/boilermakers themselves were not working directly with the insulation, there could be up to 100 maintenance men working in the tower at the same time on different jobs and it was likely that they were all exposed to the material that was being repaired and removed, regardless of whether they were doing the work themselves. All the witnesses agreed that the old insulation was dry and crumbly and that removing it produced dust the consistency of powder. They explained that the insulation was generally removed by knocking it with a wrench until it crumbled and fell away from the metal it was covering. Mr. MacDonald described the workers as working in clouds of insulation during the shut-down maintenance periods. Mr. Donnelly testified that, with two or three crews working on the exchangers at the same time, there was always a dust problem and the workers were continually exposed to dry insulation. Mr. McDonald testified that there was some dust. Mr. Plouffe and Mr. Bowles testified that the work was not that dusty, at least not dusty enough to remove the workers from the units. None of the witnesses could state with any certainty what type of material was used for insulation. Mr. MacDonald understood that it contained asbestos. Mr. Donnelly testified that he was told by management that the insulation was made of asbestos. He also noted that Johns Mansville s name appeared on the boxes containing the insulation material. Mr. Bowles concurred that the insulation used on the pipes was made of asbestos and came from Johns Mansville, however, he stated that some time in the mid-1960s they stopped using asbestos insulation and switched to calcium silica for insulation. Nonetheless, he agreed that, as much of the refinery was built prior to this time, most of the insulation contained asbestos. Mr. MacDonald and Mr. Donnelly testified that the gasket was made of asbestos. There was little awareness until the late 1970s that asbestos was harmful and, therefore, the employer provided no special protection for the workers. When the refinery was phased out in the early 1980s, it voluntarily engaged in a multi-million dollar asbestos removal program. Mr. Mackenzie, who was in charge of the demolition and clean up starting in 1984, testified that, although it was not known what percentage of the insulation actually contained asbestos, the removal was handled as if all of it was made of asbestos. Unfortunately, there are no records or blueprints of the refinery as they were given to the demolition contractor and destroyed after the demolition was completed. When the rigger/boilermakers were not involved in shut-down maintenance, they performed general maintenance. This work included pipe repairs. There were thousands of miles of piping in the 3

6 refinery, all of which was covered with insulation. The rigger/boilermaker assisted the pipefitter to install the pipes by attaching the pipe hangers and supports. Before they could do the work on the pipes, the insulation had to be removed. The furnaces too were insulated, and repair work involved insulation removal. None of the witnesses were able to testify with any certainty about the length of time it took to perform any of these tasks. Nor could they recall the actual work schedule that the worker was on over the course of his 22-year history as a rigger/boilermaker at the refinery. (ii) Neil Murray s testimony Mr. Murray is an industrial hygienist employed by another refinery company since He provided the Panel with estimates of the levels of exposure to asbestos the worker may have had while engaged in the various jobs involving asbestos. Mr. Murray had no personal knowledge of the refinery where the worker was employed. The estimates were based on information provided by Ms. Osborne about the amount of time the worker spent on each particular task, as well as a table of dust concentrations in various construction processes set out in an article from the Journal of Environmental Hygiene 2 and his knowledge and experience in the refinery business. Mr. Murray set out the following findings in his report: 1. Removing and replacing asbestos rope when cleaning trays and towers. Time weighted average exposure over 8 hours = f/cc. 2. Repairing exchangers. Time weighted average exposure over 8 hours between = 0.2 f/cc 3. Installing pipe hangers. between = 0.1 f/cc Time weighted average exposure over 8 hours between = 0.16 f/cc 4. Combined exposure estimates. between = 0.04 f/cc Time weighted average exposure over 8 hours between = 0.06 f/cc between = 0.03 f/cc In summary, Mr. Murray concluded that the figures suggested that the worker did not have significant long term exposure to asbestos. In his opinion, the exposure was well below the current limit of 1.0 f/cc for chrysotile and 0.5 f/cc for amosite. Mr. Murray testified that, to his knowledge, amosite was generally used in the refinery business. 2 Probable Asbestos Dust Concentrations in Construction Processes 35 (October 1984). 4

7 (iii) Dr. Morgan s testimony Dr. Morgan submitted a number of medical reports on behalf of the employer in this case. He also testified at the hearing. Dr. Morgan stressed two primary points. First, it is his view that the majority of informed medical and scientific opinions supports the conclusion that exposure to low levels of asbestos does not result in any increased risk of lung cancer. Second, that the increased risk of lung cancer due to exposure to asbestos occurs only where asbestosis is already present. In other words, there is no statistically significant excess risk of abestos-exposed workers developing lung cancer if they do not already have asbestosis. According to Dr. Morgan, it follows that, as an excess risk of developing lung cancer from exposure to asbestos is linked to exposure sufficient to result in asbestosis, exposure to asbestos at levels below the current standards creates no risk of developing asbestosrelated lung cancer. Dr. Morgan described asbestosis as a fibrotic condition of the lung induced by the inhalation of asbestos. He then explained that a clinical diagnosis of asbestos can be made when the patient demonstrates a number of diagnostic criteria, including a history of exposure to asbestos, x-rays showing small irregular opacities, pulmonary function abnormalities involving deceased lung volume and reduced diffusing capacity, physical signs such as crackles in the lungs and clubbing of the finger, and, where available, post-mortem evidence of fibrosis in the lungs. In Dr. Morgan s opinion, the worker in this case did not have asbestosis. Dr. Morgan based this opinion in part on his interpretation of the evidence regarding the worker s asbestos exposure and in part on the pathology report submitted to the Board by Dr. A.C. Ritchie in January In that report Dr. Ritchie noted that: Asbestos bodies are easily found in the sections of the lung. They are not numerous, but do indicate that [the worker] was exposed more to asbestos than is the general population, though the exposure was not massive. Dr. Morgan interpreted this report to mean that the asbestos fibres in the worker s lung were relatively scanty. He accepted that the worker s lungs may have contained more asbestos than might be found in the general population, but, in his view, that did not put the worker at greater risk of developing lung cancer because he did not have enough asbestos exposure to develop asbestosis. He stated that, if the worker had asbestosis, you would see millions of fibres all over the place. Dr. Morgan then discussed the relationship between smoking and lung cancer. He stated that oat cell and squamous cell cancers are the two most common types of lung cancers associated with cigarette smoking. However, these types of cancers are also associated with asbestos-related cancer. Dr. Morgan testified that a smoker with no exposure to asbestos had the same risk of developing lung cancer as a smoker who was exposed to asbestos, but did not have asbestosis. He then referred us to a report 3 which showed that the relative risk of a smoker, who was not exposed to asbestos, dying of lung cancer was 11 times greater than a non-smoker non-exposed worker. However, the risk of a 3 The Health Consequences of Smoking - A Report of the Surgeon General, U.S. Department of Health and Human Services, Rockville, Maryland, 1985, p

8 smoker, who was exposed to asbestos, was about 52 times greater, and the risk for a heavy smoker, who was exposed to asbestos, was 87 times greater than a non-smoker non-exposed worker. Therefore, the relative risk of a smoker, who was also exposed to asbestos, dying of lung cancer was about five time greater than a smoker who was not exposed to asbestos. However, these risks values, according to Dr. Morgan, were based on workers with high exposure. He was not aware of any studies dealing with workers who had moderate exposure to asbestos. Dr. Morgan also reviewed the evidence regarding the worker s smoking history. He prefaced his remarks by noting that 60% of the patients he sees have diseases related to smoking. He also noted that it was not unusual to find inconsistencies in the reported smoking history. He explained that patients feel guilty about their smoking habit and under-report their use of tobacco. In his opinion, the evidence in this case suggests that the worker was a very heavy smoker, which meant that he smoked over two packages of cigarettes a day. Finally, Dr. Morgan addressed the issue of whether the scarring identified in the pathology reports was a factor in the development of the worker s lung cancer. Dr. F. Harris, who provided a surgical pathology report after the worker s surgery in 1983, concluded that the worker had squamous cell carcinoma which appeared to be arising from a scar in the lung. Dr. Morgan reviewed the pathology reports and concluded that the reference to an isolated scar was not evidence of asbestosis. He stated that such a scar could result from pneumonia or pulmonary embolus. Dr. Morgan was also of the view that it was rare for squamous carcinoma to arise in a scar. Nor did he think that the scar was caused by asbestos bodies as asbestosis affected all of the lung. Dr. Morgan concluded by stating that, while the worker was diagnosed with squamous bronchogenic carcinoma which, as Dr. Ritchie noted in his report, is one of the types found with increased incidence in asbestos workers, there is little evidence to suggest that asbestos played any role in the etiology of the worker s lung cancer. He based this opinion on the fact that there was little evidence of significant asbestos exposure and no evidence of asbestosis. Therefore, Dr. Morgan was firmly of the opinion that it is not necessary to invoke any cause of the worker s cancer other than smoking. (iv) Dr. R. Wong s report The worker s representative submitted a report from Dr. R. Wong, dated October 29, Dr. Wong noted that a relationship between asbestos exposure and lung cancer is dependent on findings regarding latency, tumour type and location and exposure. Dr. Wong concluded that, in this case, asbestos exposure contributed significantly to the development of the worker s lung cancer, given the latency period of 27 years, the location of the cancer in the right lower lobe and frequent exposures to asbestos over a 20-year period. In reaching his conclusions regarding the worker s exposure to asbestos, Dr. Wong relied on an outline of the worker s employment duties in a letter from Ms. Godbout, which estimated that he was required to perform tasks involving asbestos 75% of the time. 6

9 Dr. Wong also commented on the fact that the worker was a heavy smoker and that smoking may act synergistically with asbestos to increase the risk of developing lung cancer. Finally, he noted that, while lung cancer occurred more frequently in workers with asbestosis, it also appeared in excess among heavily exposed workers with no pathologic evidence of asbestosis. In other words, that asbestosis was not a prerequisite for the development of asbestos-related lung cancer. Dr. Morgan commented on Dr. Wong s report. It was his view that the Panel should not put much weight on the report because it was erroneously based on the assumption that the worker was exposed to significant amounts of asbestos. He also disagreed with the conclusion that smoking always acted synergistically with asbestos to increase the risk of lung cancer, and took issue with the comments about the relationship between asbestosis and the risk of lung cancer. (v) The worker s widow s evidence The worker s widow presented her husband s workbook, which contained information about his employment. She testified that, at the time they married in 1937, her husband was employed as a blacksmith. He entered the military in Italy in 1939 and spent a number of years as a prisoner of war. Between 1947 and 1949, he worked in Saudi Arabia as a refinery worker. He was a blacksmith again in Italy between 1949 and 1953, when he emigrated to Canada. He began working as a labourer with the accident employer in 1955 and, in 1957, became a rigger/boilermaker. (vi) Smoking evidence The worker s window testified that, as far as she knew, the worker started smoking when he came to Canada. She was not sure if he smoked one package a day or two. Mr. MacDonald testified that the workers were not allowed to smoke in the refinery, but they could smoke in the maintenance shops. The Board Investigator interviewed the worker in 1985 and, according to that conversation, the worker stated that he smoked two packages of cigarettes a day over a 20-year period. (vii) Pathology reports from Dr. B.J. Mullen and Dr. A. Churg During Dr. Morgan s testimony and in one of his reports, he suggested that it might be possible to digest the lung tissue remaining from the worker s surgery to try to determine the number of asbestos fibres present in his lungs. After some discussion with the parties, the Panel decided to follow up on this suggestion and asked Mr. Revington to write to Dr. Mullen, the staff pathologist at Mount Sinai Hospital, for his views on the value in performing additional tests on the lung tissue samples. In a letter dated July 18, 1991, Dr. Mullen explained that there is a difference between finding asbestos fibres and asbestos bodies in lung tissue. Asbestos fibres appear in an inhaled unprocessed form, whereas asbestos bodies consist of fibres coated with iron and protein bypulmonary macrophages. Only asbestos bodies are detected on examination of routine tissue sections using light microscopy, whereas asbestos fibres are detected through a detailed mineralogical analysis of tissue digest using either phase microscopy or a specialized electronic microscopic technique. Dr. Mullen noted that, while the identification of asbestos bodies in tissue sections usually indicates higher than background exposure, occasional bodies may be found in patients with only background exposure. In his view, the assessment of exposure based on identification of asbestos bodies is limited because some patients and some sizes and types of asbestos fibres appear to form bodies poorly. Therefore, 7

10 uncoated fibres can be present in large numbers even if there are few asbestos bodies. Dr. Mullen also noted that the examination of asbestos bodies provides no information about the type of asbestos fibre present. He also cautioned that the presence of asbestos bodies and uncoated fibres in lung tissue were markers of exposure only. After reviewing Dr. Mullen s report, the Panel elected to forward the tissue blocks left from the worker s 1984 segmentectomy to Dr. Churg at the University of British Columbia, who, Dr. Mullen advised, had the equipment and expertise to perform the appropriate tests. In a report dated April 14, 1992, Dr. Churg advised that he found 14 asbestos fibres in the lung tissue and that all the fibres were amosite. Dr. Churg reported that (u)sing the standard formula for converting the number of fibres identified on the grid to concentration in tissue, this translates to a value of 3,100,000 fibres of amosite asbestos/gm of dry lung. However, he cautioned that the analysis of tissue from paraffin block can be treacherous because of the small amount of tissue examined and the consequent problems arising from inhomogeneity of fibre distribution. Also, he noted that they do not have standards for background values for tissue from paraffin. Nonetheless, Dr. Churg was of the view that the following conclusions could be drawn in this case: Using wet tissue, our maximum background value for amosite in the general population is 10,000 fibres/gm dry lung. Were we using wet tissue, then a value of 3,100,000 amosite fibres/gm dry lung would indicate very high level occupational exposure, in fact a level seen in patients with asbestosis. While I do not believe that direct translation of values from wet tissue to paraffin is possible, the fact that only amosite fibres are found and that the calculated concentration is very high suggests to me that the patient probably has had substantial amosite asbestos exposure. Since patients with pure amosite exposure are rare to non-existent in North America, I presume this patient has also had substantial chrysotile exposure. Dr. Mullen forwarded the report from Dr. Churg to the Tribunal summarizing the findings as follows:... [Dr. Churg] was able to digest a small amount of lung parenchyma from the surgical resection and identified 14 asbestos fibres all of which were amosite. Based on his sampling protocol, this translates to 3.1 x 10(6) fibres of amosite asbestos/gm dry lung. Using his wet tissue amosite numbers as background, the 3.1 x 10(6) fibres of amosite asbestos/gm dry lung would represent a 310x increase over the maximum background value for amosite in the general population. This level of asbestos, were it derived from wet tissue would indicate a very high exposure. As the majority of asbestos used in North America is chrysotile, with amosite and the other amphibole types of asbestos as contaminants, the finding of pure amosite asbestos most likely indicates significant chrysotile exposure as well. Although one would expect to 8

11 find a mixture of asbestos types, the absence of chrysotile can be explained by its tendency to break and dissolve in lung tissue. Dr. Mullen also stressed, however, that the absolute fibre concentration results in this study must be interpreted with caution because of the different methodology, small sample size, type of sample used and lack of standards for background values for specimens with paraffin. Nonetheless, he was of the view that it could be safely concluded that the worker had substantial amosite exposure even though there was some question about the absolute numerical value. After receiving these reports from Dr. Churg and Dr. Mullen, the Panel sent them to the parties for review. Ms. Osborne requested that we obtain further information regarding Dr. Churg s findings. After consultation with Ms. Godbout, the Panel asked Dr. Mullen to answer a number of additional questions about Dr. Churg s results. In a report dated November 2, 1992, Dr. Mullen reported the following: The major limitation of the use of paraffin block samples is the sample size. The larger the sample, the more accurate the results are likely to be in part because of the error inherent in weighing small samples and multiplying by large numbers and in part because of the variations in fibre concentration within the lung. Quantitative assessment of asbestos bodies in wet lung tissue requires a piece of wet lung weighing between 3-5 gm which would be equivalent to a piece of dry lung of approximately 1-2 gm. In the present case, only gm of dry lung was available for analysis. To determine the number of fibres per/gm of dry lung the number of fibres identified is divided by the number of grid squares examined and the weight of the dry lung specimen. This is then multiplied by a constant which varies somewhat from lab to lab; in this case the constant is 110,000. The major limitation in using this formula in the present case is the accuracy to which one can measure a small amount of lung tissue. Only gm of dry lung was available for examination in this case. Minor errors in weighing the small amount of lung tissue would be magnified resulting in large differences in the number of fibres. For example, if there was a gm difference in the true weight from the measured weight (10%) there would be a decrease in approximately 300,000 fibres per/gm of dry lung. 9

12 The background value is determined from examination of autopsy and surgical lung specimens in the reference laboratory in patients with no known asbestos exposure. The 10,000 fibres/gm dry lung value refers to background levels in Vancouver. The mean value of fibres in the Vancouver population is 1,000 fibres/gm dry lung with a median of 0 fibres/gm dry lung. The 10,000 fibres/gm dry lung refers to the 95% confidence interval. The probability of finding chrysotile fibres is dependent on the extent of exposure and the time from exposure. The likelihood of finding other types of asbestos fibres is dependent on the type of fibres inhaled and the time from exposure as amphibole fibres are more persistent than chrysotile fibres. In answer to the question about how amosite and chrysotile compare with regard to retention and accumulation in the lung, Dr. Mullen notes that chrysotile is poorly retained and accumulated while amosite is persistent. He also notes that the reactivity of each fibre type is not well understood, but there is some evidence that amosite is more dangerous than chrysotile. Ms. Osborne also asked Dr. Morgan to comment on Dr. Churg s and Dr. Mullen s reports. Dr. Morgan highlighted a number of problems that he saw with the fibre digestion results. First, he notes that, as pure amosite exposure was rare to non-existent in North America, the identification of 14 amosite fibres is most unusual.. Therefore, assuming the worker s exposure was only to amosite, it is his view that it likely did not occur in North America. Dr. Morgan then commented on the presumption that a finding of amosite fibres indicates that the worker had substantial chrysotile exposure. He noted that the conclusion is based on the fact that amosite was most frequently mixed with chrysotile in the manufacture of asbestos cement pipes and insulation and, as chrysotile leaches out of the lungs, workers exposed to it generally have relatively few chrysotile fibres and relatively more tremolite fibres in their lungs. However, Dr. Morgan stated that one would still expect to find tremolite and some chrysotile fibres if the worker was exposed to significant concentrations of chrysotile. On this point Dr. Morgan stated that: I do not believe that it is possible to explain the pure amosite in his lungs to his job as a rigger or boiler maker in North America since chrysotile was almost invariably present as the major constituent of insulation, etc. Moreover, chrysotile fibres, although often fewer than tremolite fibres, are frequently found in the lungs of the general public. Dr. Morgan also commented on the difficulty of fibre identification and calculation errors inherent in relying on a very small volume of lung. He noted that there were inaccuracies related to the reliance on wet lung fibre counts for background figures and further difficulties in translating values from wet tissue to paraffin. In addition, the deposition of asbestos in the lungs was not uniform and tended to be greater in certain regions. Finally, Dr. Morgan questioned why there was no fibrosis found in the worker s lung if, as Dr. Churg concluded, the findings in the small piece of dry lung indicated that he had very high exposure to 10

13 asbestos. Dr. Morgan suggested that Dr. Churg s opinion regarding exposure is not as reliable as his own, given that it is based on one small area of the lung, whereas his opinion is based on a consideration of the worker s x-rays, occupational exposure and the history of the development of the lung cancer. Therefore, after considering Dr. Churg s findings, Dr. Morgan confirmed his conclusion that, in light of Dr. Ritchie s finding of few asbestos bodies, epidemiological evidence that the rigger/boilermaker trades showed no increased incidence of lung cancer and the absence of fibrosis in the worker s lungs, the worker s cancer was not caused by asbestos exposure at work. (viii) Assessor report from Dr. D.C.F. Muir The Panel also requested a medical report from Dr. Muir, a Tribunal assessor and specialist in respiratory and occupational diseases, regarding the relationship between asbestos exposure and lung cancer. In a report dated August 1, 1991, Dr. Muir addressed the question of whether there is a consensus in the scientific literature regarding a threshold level of exposure to asbestos above which there is an excess risk of developing lung cancer. He noted that: Epidemiological evidence does not provide direct evidence of a threshold level. This is because those plants where levels are low have not been in operation long enough to demonstrate an absence of risk. Pathological research suggests that there might be a threshold level and those who believe that asbestosis must precede cancer think there is a threshold because, as noted below there does seem to be a threshold level for asbestosis. There is certainly no consensus. In response to a question about whether there is a consensus on the risk of developing lung cancer from exposure to levels of asbestos lower than that which would produce asbestosis, Dr. Muir stated that: This question is the same as asking whether lung cancer caused by asbestos is always preceded by asbestosis. There is no consensus on this issue. Most writers probably take the view that asbestosis comes first but there are well known writers who disagree vigorously. It is a question of tremendous importance to industry. This is because there probably is a threshold for asbestosis. It follows that if asbestosis is prevented then asbestos related lung cancer will be prevented at the same time. Dr. Muir went on to advise that there is a general consensus that asbestosis does not occur at low levels of exposure. He also stated that these answers would not be different for smokers and nonsmokers. Dr. Muir reiterated Dr. Morgan s evidence regarding the criteria used to diagnose asbestosis. He stated that the radiograph is the most important measure, but, as other diseases cause similar radiographic changes, it is customary to inquire about the history of exposure to asbestos. In Dr. Muir s view, a pathological examination of lung tissue provides the most reliable method of diagnosing asbestos-related lung cancer. However, the reliability depended on there being sufficient lung material as a small section (a biopsy) is not adequate unless the disease is severe. 11

14 Finally, Dr. Muir stated that it is uncertain whether the degree of risk of developing asbestosrelated lung cancer depends on the type of asbestos or fibre dimension. Dr. Muir ended his report with a suggestion. He noted that the real problem in the case was in apportioning the blame between the two separate causes of the worker s cancer, smoking and asbestos exposure. He noted that the worker was a heavy smoker and, if the Panel could identify the probable level of asbestos exposure, it should be possible to calculate the proportion of risk attributable to asbestos. However, if the Panel decides that asbestosis must precede asbestos-induced lung cancer, the calculation was unnecessary. (ix) Report from Dr. J. Bernard. L. Gee Ms. Osborne also requested additional expert evidence. She obtained a report from Dr. Gee, a consultant in pulmonary disease in Connecticut. The purpose of the report, as outlined in the introduction by Dr. Gee, was to address four questions: Does a review of the literature indicate that there is a threshold for asbestos-caused cancer, and must asbestosis be present for asbestos exposure to have been a causative factor in the development of lung cancer? Is there an emerging consensus on this issue? What considerations explain any conflicting views on this issue? Is there an excess of lung cancers among oil refinery workers? In response to these questions, Dr. Gee provided an extensive report in which he first noted the following: Excess lung cancers in the classic heavily exposed insulator cohort yield SMR s in the range. By contrast, smoking effects in the general population yield a persistent risk of times that of a non-smoking general population. Thus, statistically, smoking is currently the dominant influence on lung cancer for asbestos workers. Dr. Gee then reviewed the epidemology studies of various cohort groups and stated that there is a lung cancer/asbestos threshold and that there is a statistical association between the prevalence or incidence of asbestosis and lung cancer risk in many cohorts. According to Dr. Gee, the association implies either both exhibit similar dose responses or there is some causal interrelationship. 12

15 Dr. Gee noted that the epidemiological association between lung cancer risk and asbestosis is necessarily based on a clinical, rather than a pathological, diagnoses. In this context, he referred to a study by Sluis-Cremer 4 that reported no excess of lung cancer in the absence of pathological evidence of asbestosis. Dr. Gee noted that, although mild asbestosis can be detected by a pathological examination of lung biopsy material before x-ray and lung function tests were affected, most studies involve the diagnosis of asbestosis based on clinical criteria. Dr. Gee reported that the mechanism(s) of asbestos-related carcinogenesis is largely unknown. However, he noted that certain features of inflammation and fibrogenesis are germane to carcinogenesis (cancer causation). In other words, asbestosis, along with other inflammatory scarring lung disorders are characterized by activated macrophage and neutrophil release of oxidizing products notably 02 free radicals. Dr. Gee concluded that it is the inflammatory response - asbestosis - that relates to the bronchial changes, not the asbestos exposure alone. Dr. Gee commented on the theory that smoking and asbestos exposure interact multiplicatively to cause greater excess lung cancers and suggested that there are serious grounds for discounting this view. Finally, Dr. Gee noted that commercial chrysotile causes less lung cancer than amphiboles (amosite and crocidolite). After reviewing the subject from a biological, clinical and epidemiological level, together with the literature cited by both parties, Dr. Gee provided the following opinion, which he acknowledged was not universally accepted, but, in his view, represented a majority consensus: (a) Smoking is the single most important cause of lung cancer, even in asbestos workers. (b) Asbestos does under certain circumstances cause excess lung cancer, at least in smokers. (c) The most important biologic and epidemiologic factor causing excess lung cancer is clinical asbestosis. (d) The excess lung cancers in AWCs [asbestos worker cohort] were numerically probably accounted for by the prevalence of asbestosis in the cohort. (f) There are important changes in the lung cancer rates in the last twenty years. Smoking related cancers increased in the past decades. More AWCs with little or no excess lung cancers are reported particularly but not exclusively, for asbestos workers exposed since about 1970, when OSHA and other worker exposure standards were changed, the risk from smoking either greatly exceeds or totally eclipses that from asbestos exposure. 4 G.K. Sluis-Cremer, B.N. Bezuidenhout, Relations Between Asbestosis and Bronchial Cancer in Amphibole Asbesto Miners; British Journal of Industrial Medicine 1989; 46:

16 (x) (g) Society was historically influenced by earlier valid observations of excess lung cancer deaths in heavily asbestos-exposed cohorts. The media and, sad to say, many professional persons have yet to appreciate the extent of current epidemiologic data and scientific information which continue to support Weil s suggestions that asbestosis and lung cancer are statistically and causally interrelated. Workplace standards began to control asbestosis in the 1970s. Consequently, asbestos-related as opposed to smoking-related lung cancer rates sharply declined. Report from Dr. Patrick Hessel Ms. Osborne also submitted an expert report from Dr. Hessel, the Director of the Epidemology Unit of the Alberta Asthma Centre and associate professor in the Department of Health Services Administration and Community Medicine at the University of Alberta. Ms. Osborne asked Dr. Hessel to examine the epidemiological studies on lung cancer in asbestos-exposed workers and provide an opinion on whether lung cancer can be attributed to asbestos exposure in the absence of asbestosis. Dr. Hessel began his report by commenting on the sources of errors in epidemiological studies of workers exposed to asbestos. First, he noted that it is difficult to establish cause and effect using epidemiology as it is an observational science which documents exposures and diseases in an attempt to draw conclusions regarding possible links between the two. Second, studies depend on existing records to quantify past exposures and diseases and, as the data may not have been collected for scientific study, its accuracy, representativeness and completeness may be limited. Or, in other cases, the data may not exist at all and must be extrapolated from existing data and supplemented by the recollections of long-term workers. Finally, in the case of asbestos and its relationship with lung cancer, there may be errors in assessing the presence of asbestosis. Dr. Hessel noted that, although a histiologic assessment is generally considered the most accurate method of establishing the presence of asbestosis, usually the diagnosis is made on the basis of a combination of x-ray evidence, clinical signs and a history of asbestos exposure. However, Dr. Hessel stated that x-rays are neither sensitive nor specific enough with regard to the diagnosis of asbestosis and that slight, and even moderate asbestosis, which can be diagnosed histologically, may be missed by x-rays. Dr. Hessel noted the following consequences of these facts: If asbestosis is present histologically, the result of missing it on the x-ray would be to bias the risk estimate for the association between asbestosis and lung cancer, or asbestosis and dust exposure to the null and blur threshold. The misinterpretation of smoking-induced fibrosis on x-ray as asbestosis would overstate the relationship between asbestosis and lung cancer because smokers are at increased risk of developing lung cancer. Dr. Hessel then reviewed the Sluis-Cremer study. He noted that this study set out to specifically test the relationship between asbestos exposure and lung cancer in relation to asbestosis and that the quality of the data made it the most compelling of all the studies on the issue. According to Dr. 14

17 Hessel, the strengths of the study included the histological confirmation of both lung cancer and asbestosis, the long history of extensive dust and fibre monitoring and the availability of excellent documentation of occupational, medical and smoking histories. The weakness of the study was that it was a proportional mortality study, which suffered from the fact that it compared proportions of deaths rather than rates of death. According to Dr. Hessel, the Sluis-Cremer study showed that:... among those without asbestosis, there were fewer deaths from lung cancer than would be expected. Those with slight asbestosis had a three-fold excess of lung cancer and those with moderate/pronounced asbestosis had a nearly four-fold excess of lung cancer. After reviewing other epidemiological studies, and discussing the threshold for asbestos exposure and lung cancer, Dr. Hessel concluded his report with the following: There can be little doubt that asbestos exposure in a variety of settings can result in lung cancer. In asbestos-exposed individuals these cancers occur more often in the lower lobes of the lungs; the usual site of asbestosis. Thresholds probably exist for both asbestosis and lung cancer in relation to asbestos exposure. The available data do not permit determination of whether the observed thresholds are the same for lung cancer and asbestosis. The Ontario Royal Commission (1984) estimated the threshold for asbestosis at 25 fibres/ml-yr. Browne (1986) estimated the threshold for asbetos related lung cancer at between 25 and 100 fibers/ml-yr. As noted, errors in measuring both dose and disease are common and have predictable results. In the end the best evidence can be obtained from studies with the least error. The study by Sluis-Cremer and Besuidenhout (1989) stands out as the most credible in this regard. It included measures of exposures and diseases that were the best obtainable and the analysis was designed to address the issue specifically. The study included only amphibole miners. The data from Liddell and McDonald (1980) related to chrysotile miners and millers. Though not based on autopsy data, the results are consistent with those of Sluis-Cremer and Bezuidenhout (1989). It is not possible to say on the basis of the epidemiologic data whether the occurrence of asbestotic fibrosis stimulates or facilitates the carcinogenic process, or whether asbestos is capable of inducing tumours at doses high enough to cause asbestosis, or higher. Cullen (1987), however, presents some convincing evidence that fibrosis is involved in the carcinogenic process. On the basis of this evidence it can be concluded that, in the absence of asbestosis (assessed histologically) it is unlikely that a lung cancer in as asbestos-exposed individual can be attributed to asbestos exposure. 15

18 (xi) Submissions (a) Mr. Wilkens Mr. Wilkens submitted that the general test the Panel must apply in this case was whether, on the balance of probabilities, it was more likely than not that the worker s lung cancer was caused by smoking alone or in combination with asbestos exposure. In other words, the Panel must determine whether exposure to asbestos was a significant contributing factor to the development of the worker s lung cancer. Mr. Wilkens referred us to Decision No. 134/89 5 which set out four criteria to consider when examining the relationship between asbestos exposure and lung cancer: the intensity of exposure to asbestos; evidence of fibrotic change in the lung; the location of the cancer; and the type of cancer. He argued that in this case, the worker met all the criteria. On the question of latency, Mr. Wilkens noted that the worker worked for 24 years for the accident employer starting in 1955 and was diagnosed with lung cancer in That established a 27-year latency period, which is within the expectation for the development of cancer. Regarding the type and location of the cancer, he noted that the worker was diagnosed with squamous cell cancer in the lower lobe, which is commonly an asbestos-related cancer. The more problematic criteria in this case, according to Mr. Wilkens, was the intensity of exposure and the presence of fibrotic change in the lung. He reviewed the exposure evidence noting that there was contradictory testimony from the witnesses regarding the worker s duties and the time it took to do each of the tasks. He also noted that none of the witnesses recalled what jobs the worker actually performed. Only Mr. MacDonald commented that he may have done more pipe-hanger work because he was good at it and, in later years, because of his age. Mr. Wilkens argued that the more reliable oral evidence came from the men who actually performed the jobs, not Mr. McDonald, Mr. Bowles or Mr. Plouffe, who were aware of the company policy regarding insulation, but did not do the work. The majority of witnesses, he argued, agreed that the rigger/boilermakers often removed insulation while working on exchangers or pipe hangers. Mr. Wilkens suggested that, regardless of the exact details of the work, given the amount of asbestos used in the refinery, there could be no doubt that the worker had significant exposure to it. Mr. Wilkens also asked the Panel not to rely on Mr. Murray s assumptions regarding the worker s exposure. He noted the calculations did not consider background exposure and argued that there was good reason to believe that all the workers were in the towers at the same time in order to meet the shut-down timetable. Mr. Wilkens urged us to rely on Dr. Churg s analysis of the asbestos in the worker s lung and use that information to reach a finding on exposure. Dr. Churg concluded that the worker s lungs contained 3,100,000 of asbestos per gram of dry lung. Mr. Wilkens argued that this represented a 5 (1993), 26 W.C.A.T.R 32 16

19 figure eight times greater than the expected fibre count for the average North American. 6 He submitted that, even taking into account the doubts about the accuracy of the fibre count due of the small sample size, it is safe to assume that the error is not in the magnitude of eight times. Therefore, despite the caution urged by Drs. Churg, Mullen and Morgan regarding the fibre count process, this evidence confirms that the worker had substantial exposure to asbestos. Furthermore, Mr. Wilkens argued that the absence of chrysotile asbestos is explained by the fact that it broke down in the lung while amosite fibres were retained in the lung. Mr. Wilkens rejected Dr. Morgan s suggestion that the presence of amosite fibres in the lung indicated that the exposure occurred outside North America. He argued there was nothing to suggest that, whatever exposure the worker may have had in the 18 months he was employed in a refinery in Saudi Arabia, it outweighed the 24 years of exposure while employed with the accident employer. Finally, Mr. Wilkens noted that Drs. Churg and Mullen did not have the same concern as Dr. Morgan and explained the substantial presence of amosite in the worker s lung as evidence of an equivalent amount of exposure to chrysotile. Regarding Dr. Ritchie s findings of asbestos bodies, Mr. Wilkens submitted that, although he only found few asbestos bodies in the lung, he noted that they were found easily. On this point, Mr. Wilkens referred us to Decision No. 375/92 7 where Dr. Ritchie was quoted to say that is was unusual to find one asbestos body in the lung. Mr. Wilkens also reviewed the evidence regarding fibrotic changes in the worker s lung. He argued that, although there was no report of asbestosis, there was evidence of fibrotic change and scarring. Dr. Morgan was of the view that a clinical diagnosis of asbestosis must be made before finding a relationship between asbestos exposure and cancer, Mr. Wilkens argued that that standard was too high for the adjudication of a compensation claim. He submitted that it was not necessary to make a positive medical diagnosis to conclude that the worker s lung cancer was related to asbestos exposure. Furthermore, he argued that the Sluis-Cremer study established that the failure to diagnose asbestosis by clinical standards did not rule out the presence of asbestosis. He noted that Sluis-Cremer found that the greatest increase of risk of asbestos-related lung cancer was between those workers with no histological evidence of asbestosis and those with slight asbestosis. Mr. Wilkens argued that, in light of the Sluis-Cremer findings, a histological diagnosis of asbestosis could not be ruled out and, therefore, neither could the possibility that the worker had slight asbestosis. He submitted that the failure to make a clinical diagnosis of asbestosis did not mean that the worker did not have evidence of slight asbestosis that may have been detected post-mortem. Finally, Mr. Wilkens reviewed the worker s smoking history. Although there was some contradictory evidence regarding the worker s smoking, he accepted that the worker would be classified as a heavy smoker. But, he argued that smoking, rather than being an alternative cause of the worker s lung cancer, had a synergistic relationship with asbestos exposure. 6 7 Table from W.K.C. Morgan & A. Seaton, Occupational Lung Diseases, 3rd. Ed. [to be published]. (1994), 28 W.C.A.T.R. 32 (at page 36). 17

20 (b) Ms. Osborne Ms. Osborne submitted that the worker s lung cancer was not related to his exposure to asbestos. She noted that, while there was no dispute that the worker was exposed to asbestos, there was a dispute regarding the degree of exposure. Relying on the reports from Drs. Morgan, Gee and Hessel, Ms. Osborne submitted that there now is a consensus in the scientific community that there is no evidence of an increase risk of lung cancer from levels of exposure to asbestos below the threshold level for the development of asbestosis. She argued that the evidence established that there is a strong statistical relationship between the presence of asbestosis and lung cancer, which is consistent with the biological knowledge regarding scarring and the development of cancer. Ms. Osborne also pointed out that mortality rates for lung cancer in individuals without clinical evidence of asbestosis is the same as that for cigarette smokers. In addition, she noted that Dr. Gee expressed some doubt about whether there is a synergistic relationship between asbestos exposure and smoking. Reviewing the medical evidence in this case, Ms. Osborne submitted that there is no dispute that there were insufficient findings to support a clinical diagnosis of asbestosis. She also argued that there is no clinical or biopsy evidence of fibrosis. Ms. Osborne submitted further that, the fact that the worker developed squamous cell cancer did not assist in determining the etiology as that type of cancer is associated with both asbestos exposure and smoking. Furthermore, the finding of cancer in the worker s lower lobe is also a neutral etiological factor. Although Dr. Churg discovered 14 fibres of amosite asbestos in the worker s lung, Ms. Osborne argued that, given the minute amount of lung tissue examined and the difficulty of translating the findings, the test did not provide an accurate indication of the worker s exposure to asbestos. Ms. Osborne urged us to rely on Dr. Morgan s opinion as a noted expert in the field of asbestos-related cancer. Dr. Morgan is of the view that, in the absence of clinical evidence of asbestosis, and in the presence of the worker s smoking history, there is no need to invoke any cause other than smoking for the worker s lung cancer. He argued that, without the evidence of asbestosis, the worker was at no greater risk of developing lung cancer than a non-exposed smoker. Ms. Osborne also asked us to give considerable weight to the evidence of Neil Murray. Mr. Murray identified the components of the work that involved asbestos, estimated the degree of exposure and concluded that the worker s likely exposure to asbestos was well below current regulated limits. She argued that, given the hygienist s expertise in analyzing jobs, using time components and measuring the risk of hazardous exposure, Mr. Murray s evidence was more reliable than the evidence from coworkers. This left the question of whether the cumulative effect of exposure to asbestos at low levels created a cancer risk. Again Ms. Osborne argued that the weight of authority supported the position that asbestosis is a necessary precursor to asbestos-related lung cancer and, as there was no evidence that the worker had asbestosis, the risk caused by exposure to asbestos was not a significant contributing factor to the development of his lung cancer. (xii) The relevant legislation and Board policy 18