WORKPLACE SAFETY AND INSURANCE APPEALS TRIBUNAL DECISION NO. 1234/09

Transcription

1 WORKPLACE SAFETY AND INSURANCE APPEALS TRIBUNAL DECISION NO. 1234/09 BEFORE: M. Crystal : Vice-Chair B. Wheeler : Member Representative of Employers F. Jackson : Member Representative of Workers HEARING: June 16, 2009 at Kitchener Oral hearing Post-hearing activity completed on November 30, 2009 DATE OF DECISION: April 16, 2010 NEUTRAL CITATION: 2010 ONWSIAT 916 DECISION UNDER APPEAL: WSIB Appeals Resolution Officer (ARO) decision dated August 8, 2008 APPEARANCES: For the worker: For the employer: Mr. M. S. Grossman, Lawyer Ms. P. Welsh, Representative 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. 1234/09 REASONS (i) Introduction [1] This appeal was heard, in Kitchener, on June 16, The worker appeals the decision of Appeals Resolution Officer (ARO), S. Bennett, dated August 8, That decision determined that the worker was not entitled to benefits for a lung condition as a result of his employment. [2] The worker appeared and was represented by Mr. Mark S. Grossman, legal counsel. The employer also appeared and was represented by Ms. Patricia Welsh, representative. The worker testified at the appeal hearing. Submissions on the factual basis of the appeal were provided at the hearing by Mr. Grossman and Ms. Welsh. As noted below, the Panel determined that it wished to put certain questions to a Tribunal Medical assessor before rendering its final decision in this appeal. After the assessor s report was received by the Tribunal, final written submissions were provided to the Panel. The submissions provided by Ms. Welsh were dated November 3, The submissions provided by Mr. Grossman were dated November 17, (ii) The issues on appeal [3] The issue to be determined in this appeal is whether the worker is entitled to benefits for his pulmonary disease, as a result of occupational exposure to asbestos. (iii) Findings of fact made in Decision No. 1234/09I [4] At the hearing of this appeal, the Panel determined that it wished to put certain questions to a Tribunal Medical assessor before rendering its final decision in this appeal. So that the assessor would have a factual basis upon which he could answer the questions posed, the Panel made certain findings of fact concerning the worker s occupational exposure to asbestos, as well as his history of tobacco smoking. Further details concerning the circumstances of the appeal are set out in Decision No. 1234/09I, however, at the conclusion of the decision, the Panel provided the following summary of its findings of fact: 1. The worker was exposed to asbestos insulation at the accident employer s Guelph plant between 1987 and During that time, the worker s exposure was greatest while he was performing maintenance work on a boiler at that location. This work was performed twice per year, on each occasion for a period between about three to seven days. 2. The worker was exposed to asbestos insulation at the accident employer s Woodstock plant between about 1992 and During that time, the worker s exposure was greatest while he was replacing pipes at that location. This work was performed by the worker about three to five time per year, for about three or four days on each occasion. 3. The worker was exposed to asbestos at the accident employer s Burlington plant between about 1992 and During that time, the worker s exposure was greatest while he was cutting siding which included chrysotile asbestos as part of the composition of the siding material. The worker was cutting the siding on about three or four occasions during this period. The worker may also have had some exposure while drilling through the siding on other occasions, although the exposure would have been less significant on those occasions, as compared to when he was cutting the siding material. 4. The worker may also have had some incidental exposure to airborne asbestos at other times during the period of his employment with the accident employer, although it is difficult to quantify this exposure.

3 Page: 2 Decision No. 1234/09 5. The worker smoked about one pack of cigarettes per day from about the time he was 18 years old, until about the time of his heart attack in (iv) Medical information prepared by the worker s physicians [5] At the hearing, the worker testified that he had a heart attack in or about He stated that, subsequently, he was referred by his family physician to Dr. N. Kaplan, specialist in internal medicine, in order to investigate respiratory difficulties he was experiencing. Dr. Kaplan prepared a report, dated June 26, 2006, which indicated that the worker had presented at hospital in June 2006 complaining of right-sided facial numbness and severe fatigue. It stated that a subsequent CT scan of the chest demonstrated extensive bilateral fibrosis with bronchiolectasis predominantly subpleural in distribution. The report, which was addressed to Dr. Christine Macie, the respirologist to whom Dr. Kaplan was referring the worker, stated in part: [The worker] has been working with cement and welding fumes that he considers possibly toxic for almost two decades. I have no evidence that changes in his lungs are related to these environmental factors but I cannot rule it out. He is booked for full PFTs [pulmonary function tests] with the report to be forwarded to you for interpretation. [6] Dr. Macie saw the worker on July 10, 2006, and prepared a report which stated in part: Issues and plan: Pulmonary fibrosis (PF) with honeycombing and traction bronchiectasis. This is end stage of lung disease. There is no reversibility. I have ordered vasculitic and connective tissue testing to rule out other causes. There is no concomitant evidence of asbestos exposure or silica nodules so it is unlikely these are responsible. He has a history of GERD [gastroesophageal reflux disease] which is known to cause PF. His current symptoms would not be due to PF as his VC is 84% predicted and oxygen saturations 94%. There is no treatment for the disease unless reversibility is evident. The usual course of this disease is exercise desaturation, oxygen dependency and referral for single lung transplant. The median survival after diagnosis by a respirologist is 2-3 years. I suspect his PFTs will show mild restriction with reduced gas transfer and will follow the disease every 6 months for trending. All this was communicated to [the worker] and his wife. They are concerned about the effect of welding fumes and dusts at work on his breathing. Unfortunately, he does not have severe enough lung disease that these can be a significant trigger/exacerbating factor. He did not wear respiratory protection that was provided and he was a smoker. He may need to take early retirement if he feels that he is unable to work but I cannot endorse removal from the workplace due to these exposures. PF is a chronic disease and his is compatible with idiopathic PF. Obstructive airways disease. There is subtle evidence of this on PFTs with scooping pattern. He may do well with inhaled bronchodilator and steroid especially if his breathing is worsened with exposures. I have given his 8 sample of SYMBICORT BID to trial. Cardiac component. His exertional dyspnea is most likely due to cardiac compromise with added obstructive and fibrotic lung disease worsening his function. [7] Dr. Kaplan prepared a further report, dated July 18, 2006, addressed to Respirologist, Finestone Institute, St. Joseph s Hospital, in order to refer the worker for a further medical opinion about his condition. The report stated that the worker had been recently seen by Dr. Macie, and although Dr. Kaplan was sure that Dr. C. Macie did address all the issues related to [the worker s] condition the worker requested the second opinion as he feels that he needs more information about possible relationship with environmental factors and further prognosis.

4 Page: 3 Decision No. 1234/09 [8] The worker was seen by Dr. P. Gerald Cox, respirologist at the Finestone Institute, for a further opinion. Following further testing, the worker was referred for a lung biopsy. The report on the biopsy, prepared by Dr. L. Vincic, pathologist, stated in part: MICROSCOPIC There is patchy interstitial fibrosis which tends to be centrilobular and at the periphery of the lung lobules. This is associated with fibroblastic foci, a few foci of organizing pneumonia and only mild chronic inflammation. There are focal honeycomb lung changes. There is smoker's respiratory bronchiolitis. There are pleural adhesions and secondary vascular changes. There are five asbestos bodies in eight sections stained by the Perls' method. The findings are sufficient for asbestosis (Churg, Pathology of Occupational Lung Disease, 2nd edition). Helsinki criteria tend to be more strict. I am not familiar with WSIB criteria. DIAGNOSIS Interstitial fibrosis and asbestos bodies, see report above wedge resection left upper lobe lung. [9] The case materials included a report, dated March 23, 2007, prepared by Dr. J.E.M. Young, general surgeon, which indicated that the worker had a lung biopsy performed at the request of Dr. Cox, which showed interstitial fibrosis with asbestos bodies and that Dr. Young therefore concluded that the worker had a compensatible [sic] disease. A further appointment was booked with Dr. Cox for re-evaluation and ongoing treatment. [10] Dr. Cox saw the worker on April 16, His report of that date stated, in part: The last issue we dealt with today was whether or not his condition deserves compensation from WSIB. There is no doubt that he has asbestos related pulmonary fibrosis and this is responsible for impairing his lung function. Like others I find it difficult to be any more precise in attributing the source of his impairment and disability precisely. Given that he no longer smokes and that his cardiac situation has been stable since 2004, then I think it is likely that any recent or future progression could be attributed to his pulmonary fibrosis due to asbestos exposure. I have arranged for repeat pulmonary function testing to be done in the summer and I have recommended that we continue this surveillance at six monthly intervals for at least two years so that we understand whether his condition is stable or progressive. [11] The worker was referred to Occupational Health Clinics for Ontario Workers Inc. (OHCOW), where he was seen, on April 7, 2008, by Dr. Michael Pysklywec, specialist in family medicine. His report of that date concluded with the following summary: Summary: In summary, I would conclude that [the worker] developed asbestosis as a result of his work-related exposures. I come to this conclusion based on the following points: 1. he has fibrosis of the lungs as confirmed by 2 treating respirologists. 2. his lung biopsy results indicate the presence of numerous asbestos bodies. Pathologic criteria suggest that the presence of an asbestosis body in a section is consistent with significant asbestos exposure; there were asbestos bodies present in the majority of his sections. 3. Dr. Cox, his treating respirologist at the Finestone Clinic, states unequivocally that [the worker] has asbestosis.

5 Page: 4 Decision No. 1234/09 4. a Ministry of Labour investigation has confirmed asbestos exposure in 3 of the 4 work sites that they investigated. Based on a very conservative estimate, this would result in a minimum of 4 years of asbestos exposure which exceeds the WSIB policy requirements of 2 years of asbestos exposure. 5. there were no work practices in place to warn or protect [the worker] against asbestos related health effects during his employment. 6. there is no other reasonable explanation for his lung fibrosis. In light of this it would be very difficult to ignore the contribution of his asbestos exposures. The evidence seems to clearly favour the probability that his workplace asbestos exposures significantly contributed to his fibrotic lung disease. (v) Medical information prepared by the Workplace Safety and Insurance Board s (the Board s) staff and medical consultants [12] In an internal Board memorandum, dated February 27, 2007, the Board s Claims Adjudicator (CA) requested a medical opinion from Dr. David C.F. Muir, specialist in internal medicine and the Board s Chest Consultant. In a memo, dated March 27, 2007, Dr. Muir noted that the worker s CT scan in June 2006 had shown cystic subpleural fibrosis in the lower lung fields but that the rest of the lung was normal and the division between the affected zone and the rest of the lung is well defined. Further, there was no evidence of pleural thickening. It stated that these changes were characteristic of idiopathic pulmonary fibrosis, which is also know as idiopathic fibrosing alveolitis. After reviewing some of the medical literature related this condition, the memo confirmed that the worker s diagnosis was idiopathic PF which was not of occupational origin. [13] In a further memo, dated June 5, 2007, the CA indicated that, on May 31, 2007, he had spoken to Dr. Kabir, the Board s Occupational Hygienist, who had reviewed the information on file in relation to the worker s asbestos exposure. The memo stated that Dr. Kabir had advised that the worker s possible asbestos exposure would take him back to 1987 when he was first hired by the accident employer, but that since 1986 asbestos was strictly regulated in the province of Ontario at the workplaces. The memo stated that Dr. Kabir had concluded that this worker had possible short-term low level asbestos exposure levels during the work period 1987 to In a further memo, dated June 5, 2007, the CA asked Dr. Muir whether, given the hygienist opinion, Dr. Muir believed that the worker s impairment was occupationally related. In response, Dr. Muir provided a memo, dated June 5, 2007, which stated: The finding of asbestos bodies in the transbronchial biopsy is difficult to interpret because it is not quantitative. Asbestos bodies are present to a certain extent in the lungs of any resident of a large industrial city. For this reason considerable weight must be given to the exposure estimate obtained by Dr. H. Kabir. He estimates exposure to asbestos to have been minimal. In these circumstances a diagnosis of asbestosis is not appropriate and the diagnosis is of idiopathic pulmonary fibrosis; not of occupational origin. [14] In a further memo, dated February 28, 2008, the CA requested a further medical opinion from Dr. Taraschuk, another of the Board s medical consultants. The memo stated in part: This worker has appealed my decision, and contacted the Ministry of Labour to perform an assessment of the work sites with the accident employer. Their concluding report is dated [December 19, 2007]. They've provided an asbestos survey report dated [May 17, 2007] for the site where this worker previously worked.

6 Page: 5 Decision No. 1234/09 Review It appears from the [Ministry of Labour] inspection reports, as well the asbestos survey report, there is a confirmation of the presence of asbestos at 3 out 4 plants where this worker has worked in the past for the accident employer. The inspection notes this is in the piping system and the boilers. We can't determine to what extent this worker may have disturbed the asbestos in the course of his work duties. The worker himself did say that he occasionally would disturb this. It is obvious in this situation that we would not have the data to determine the level of his exposures throughout the years. Recommendation From a claim perspective, I will accept the possibility of exposure asbestos for the 2 year period as required by the asbestosis policy. If the medical information supports a diagnosis of asbestosis or occupationally related pleural plaque, I will then accept the claim. Can you please confirm the diagnosis. [15] In a further memo, dated March 5, 2008, Dr. Taraschuk referred the CA s memo on to Dr. Muir, noting that Dr. Muir had previously indicated that the worker had a diagnosis of idiopathic PF, and that the CA had additional questions. Dr. Muir responded and in a further memo, dated March 25, 2008, he stated: This is a difficult issue to resolve. The biopsy report of 27 Feb by Dr. Vincic noted five asbestos bodies in eight sections. One author (Dr. Churg) accepts this as sufficient to accept a diagnosis of asbestosis. The International Panel (Helsinki Criteria) requires two fibers or more for a section. The origin of this dispute is based on the fact that minimal asbestos exposure is common in an industrial society and a few asbestos bodies can be identified in many members of the population. Distinguishing asbestosis from fibrosing alveolitis is also difficult. The radiographs, in my opinion, are characteristic of fibrosing alveolitis and unlike those of asbestosis. I identify the reasons for this in [Dr. Muir s earlier memo]. I am well aware that some authors suggest that such a distinction is unreliable but, in my opinion, it depends on the severity of the disease and their reservations take no account of this. The final decision must be based on the reliability of significant asbestos exposure. I note the memo by [the CA], which identifies only the possibility of asbestos exposure. Based on the radiological appearances, the number of asbestos bodies being less then the Helsinki Criteria (although acceptable to Dr. Churg) and the uncertainty of the history of significant asbestos exposure, it is my opinion that the diagnosis is fibrosing alveolitis. (vi) Medical opinions from the Tribunal Medical assessor, Dr. Robert N. Rivington, respirologist [16] Subsequent to the release of Decision No. 1234/09I on June 26, 2009, the Tribunal s Medical Liaison Office (MLO), identified and retained Dr. Robert N. Rivington, respirologist, to be the medical assessor for the purposes of this appeal. The curriculum vitae provided by Dr. Rivington indicated that he had been the acting senior medical officer, at Canadian Medical Protective Association since January [17] Dr. Rivington prepared a report, dated September 22, 2009, in response to the questions that the Panel posed to him. The questions are set out in italics immediately above Dr. Rivington s responses. The report stated, in part:

7 Page: 6 Decision No. 1234/09 1. Does the worker have pulmonary fibrosis? Please explain. [The worker] has at least mild to moderate pulmonary fibrosis based on analysis of the clinical history, the physical examination findings, the lung function testing, the radiological imaging studies, and the open lung biopsy. Over the course of observation this pulmonary fibrosis seems to be stable. 2.a Does the presence of asbestos bodies, as described in the medical reports on file, establish the diagnosis of asbestosis? Please explain. The presence of asbestos bodies substantially favours the diagnosis of asbestosis rather than other causes of pulmonary fibrosis. The lengthy smoking history and the agreed upon asbestos exposure would make retention of asbestos in the lung more likely and lead to the development of these asbestos bodies. The establishment of the diagnosis is a clinical pathological correlation. Pathologists would be better able to respond reliably to this question. Clinicians rely upon pathologists to separate different triggers in the causation of pulmonary fibrosis. It certainly seems that Dr. Churg, a noted Canadian pathologist, suggests that the presence of asbestos bodies could confirm this diagnosis. b. Is the radiological appearance more characteristic of asbestosis than idiopathic pulmonary fibrosis? Please explain. In the American Thoracic Society International Consensus Statement Article (l), it was stated that the high resolution CT scanning appearance of connective tissue diseases (especially scleroderma and rheumatoid arthritis and asbestosis) are commonly similar in CT appearance to idiopathic pulmonary fibrosis, except for the presence of parenchymal bands of fibrosis and pleural plaques in patients with asbestosis. As there are no noted pleural plaques in this case, that factor is of no value. The honeycombing noted is the prime feature of this case and the majority of the parenchyma seems to be spared. This is unusual for progressive idiopathic pulmonary fibrosis that tends to involve more of the parenchyma. 3. Is the information obtained from the worker s open lung biopsy more characteristic of asbestosis than idiopathic pulmonary fibrosis? Please explain. The response to this question is difficult as the description from the report is relatively short. There is only mild inflammation favouring the asbestosis versus idiopathic pulmonary fibrosis. The fibroblastic foci are frequently described in both conditions, but especially asbestosis. The presence of asbestos bodies is more helpful in favouring asbestosis as their absence would generally exclude asbestosis in the differential diagnosis. 4. The medical information on file apparently indicates different standards to be applied in determining a diagnosis of asbestosis. We note that in his report dated April 7, Dr. Pysklywec of OHCOW, indicates that work by Dr. Andrew Churg supports the view that the finding of 1-2 bodies in a whole slide in the presence of the proper pattern of fibrosis was generally diagnostic of asbestosis. Information provided by Dr. C.F. Muir, in his memo dated March , appears to be inconsistent with this view. Is the standard advanced by Dr. Churg a reliable basis upon which to make the diagnosis of asbestos? 5. Dr. Muir's memo dated March 25, 2008 refers to the Helsinki Criteria in relation to the standard to be applied for a diagnosis of asbestosis. Is this a more reliable standard than that advanced by Dr. Churg? Is it necessary to satisfy the "Helsinki Criteria" in order to conclude that the diagnosis of asbestosis is probable? In this worker's case, is the diagnosis of asbestosis consistent with the Helsinki Criteria? The response to questions 4 and 5 are more within the realm of lung pathologists to comment upon. The standard of care is determined by the consensus of practitioners in a particular field of practice. Clinicians rely upon pathologists to interpret

8 Page: 7 Decision No. 1234/09 specimens based upon the current standards. Where a more specialized interpretation is required often pathologists will consult others with special expertise or interest to offer insight in difficult cases. The Helsinki Criteria are more stringent and much more recent. It is likely that the WSIB criteria for the diagnosis of asbestosis were created well before the recent Helsinki criteria were published. Dr Churg's comments would suggest that a heavy load of asbestos bodies would have to be present in a lung to have asbestos bodies viewed in small sections of lung biopsy specimens. 6. The worker in this case had an open lung biopsy. The memo from Dr. Muir, dated June 5, 2007 appears to indicate that Dr. Muir mistakenly believed that the worker had a transbronchial biopsy. Would the fact that Dr. Muir was apparently mistaken in this respect affect the reliability of his views relating to the worker's diagnosis? I believe this error in stating a transbronchial biopsy versus open lung biopsy is likely not the cause of the statements from Dr. Muir. A transbronchial biopsy specimen would be much smaller than the open lung biopsy and any asbestos bodies would likely be very significant on such a small piece of tissue. In the open lung biopsy only one asbestos body was noted in the majority of fields analyzed. I believe Dr. Muir felt that the asbestos bodies were a marker of exposure to an industrial environment rather than confirmatory of a causative component to the pulmonary fibrosis. 9. Do you believe that the worker's level of exposure to asbestosis [sic], as described in the Panel s internal [sic] decision, contributed to his lung disease? I do believe that the exposure, on the balance of probability, did contribute to the development of limited fibrosis. Whether the extent of fibrosis noted in this worker causes his current symptoms is another question. 8 Can you provide any other medical information, which you feel would be helpful to the Vice-Chair or Panel and parties in this appeal? It is important to note that there has been no progression of pulmonary function abnormalities between the observations 06/07/06 and 02/07/07. Such stability of lung function is somewhat unusual in typical idiopathic pulmonary fibrosis. Idiopathic pulmonary fibrosis [sic is characterized by?] progressive decline in lung function. IPF usually features a poor prognosis with survival post diagnosis of 3.2 to 5 years. The median survival is 28.2 months, according to literature. In contrast, pulmonary function in patients with asbestosis is often stable. The mean vital capacity may fall 18% over the ensuing ten years, suggesting a different natural history of the condition as well. A more rapid progression with a visible year-to-year increase in symptoms and progression of radiological fibrosis, a deterioration in pulmonary function testing and other difficulties certainly would favour idiopathic pulmonary fibrosis over asbestosis. Options in this case could include a consultation with additional pathologists with a special expertise in pulmonary fibrosis and asbestosis. Additionally, observation of the natural history of [the worker s] condition would be helpful to determine the rate of progression. It certainly would seem that the natural history is much more in keeping with asbestosis than idiopathic pulmonary fibrosis. I believe this condition will likely be stable. The intercurrent pulmonary difficulties may be causing some of the symptoms of dyspnea on effort. The document number [i.e., Operational Policy Manual Document No on the subject of Asbestosis ] could be revised and updated to include the more recent ATS reference concerning asbestosis. It may also wish to be updated to determine their preferred standard regarding the required number of asbestos bodies based on the review of the clinical standard of proof required.

9 Page: 8 Decision No. 1234/09 References: 1. Idiopathic Pulmonary Fibrosis: Diagnosis and Treatment. International Consensus Statement Am. J. Respir Crit Care Med 161; Diagnosis and Management of non-malignant Diseases related to Asbestos. Am. J. Respir Crit Care Med 170: 2004; (vii) Applicable law and policy [18] Board Operational Policy Manual Document No on the subject of Determining the Date of Injury provides that in the case of industrial disease, where the injury is alleged to have occurred on a cumulative basis, the date of accident is established as the date when the illness or disease first becomes apparent. In this case, the worker s pulmonary fibrosis became apparent at the time of his CT scan in June Accordingly, the worker s entitlement to benefits in this appeal is governed by the Workplace Safety and Insurance Act, [19] The issue in this appeal is whether the worker is entitled to benefits for pulmonary disease as a result of occupational exposure to asbestos. OPM Document No , on the subject of Asbestosis, applies in the circumstances of this appeal. That policy document states in part: Policy Asbestosis in workers exposed to asbestos dust in Ontario employment is an occupational disease as peculiar to and characteristic of a process, trade or occupation involving exposure to asbestos. If the worker was employed in Ontario in any mining, milling, manufacturing, assembling, construction, repair, alteration, maintenance or demolition process involving the generation of airborne asbestos fibres for at least 2 years before the date of diagnosis of asbestosis, the asbestosis is conclusively deemed to have been due to the nature of the employment. Guidelines Entitlement Claims for asbestosis are allowed when it is established that the worker has a diagnosis of asbestosis, and worked in any mining, milling, manufacturing, assembling, construction, repair, alteration, maintenance or demolition process involving the generation of airborne asbestos fibres. The legislative requirements of sections 15(5) and 15(6) of the Workplace Safety and Insurance Act for 2 years of asbestos dust exposure in Ontario apply to this policy. Diagnosis To diagnose asbestosis, the WSIB recognizes histopathological evidence of lung fibrosis due to asbestos and the current diagnostic criteria established by the American Thoracic Society (ATS)*. * American Thoracic Society: The diagnosis of non-malignant diseases related to asbestos. Am. Rev. Respir. Dis. 134: , Current ATS criteria In the absence of pathologic examination of lung tissue, the diagnosis of asbestosis is made based on a careful consideration of all relevant clinical findings. It is necessary that there is

10 Page: 9 Decision No. 1234/09 a reliable history of asbestos exposure an appropriate time interval between exposure and detection. The ATS regards the following clinical criteria to be of recognized value chest roentgenographic evidence of type "s", "t", and "u", small irregular opacifications of a profusion of 1/1 or greater a restrictive pattern of lung impairment with a forced vital capacity below the lower limit of normal a diffusing capacity below the lower limit of normal bilateral late or pan inspiratory crackles at the posterior lung bases not cleared by cough. When available, positive results from a computerized axial tomography (CAT) scan are also considered for diagnosis of asbestosis. (viii) Analysis Whether the worker s level of exposure meets the requirements of the policy [20] We have summarized our findings that were included in Decision No. 1234/09I, above. We note that in her submissions, the employer s representative made further detailed submissions relating to the extent of the worker s exposure to asbestos. She sought to determine the actual number of days during the worker s employment that he was exposed to asbestos. The fact that the worker had some measure of exposure to asbestos in his employment does not appear to be contentious. [21] According to the calculations provided by the employer s representative, the employer s representative concluded that the worker was probably exposed to asbestos during 584 days spread throughout the period of his employment. We have taken into account, however, our finding that the worker was also probably exposed to some measure of airborne asbestos at other times during his employment, but that data was not available to allow us to quantify this exposure. [22] We have also taken into account the fact that, in 2007, the Ministry of Labour undertook an investigation of the employer s worksites, and concluded that the presence of asbestos was positively identified in 3 of the 4 locations visited by the Ministry of Labour Inspectors and Industrial Hygiene consultants. We have indicated the nature of the worker s exposure in Decision No. 1234/09I. [23] The policy document indicates that the required level of exposure to asbestos will be met if the worker was employed in Ontario in any mining, milling, manufacturing, assembling, construction, repair, alteration, maintenance or demolition process involving the generation of airborne asbestos fibres for at least 2 years before the date of diagnosis of asbestosis We do not interpret the policy document to mean that a time in/time out approach to the calculation of periods of exposure, such as that proposed by the employer, should be applied. Taking the approach advanced by the employer s representative, however, we note that the worker s exposure was a few months less than two years. [24] We note that the employer s calculations excluded weekend days and vacation time, and we do not interpret the Board s policy to mean that, the period of employment during which there was exposure to asbestos should be calculated so that time, such as weekends, should be excluded. In any event, we have found that there was additional exposure to airborne asbestos which would be difficult to quantify, but which should nevertheless be given some consideration.

11 Page: 10 Decision No. 1234/09 [25] We also note that the Board s CA concluded, in his memo dated February 28, 2008 that he accepted that the 2 year period as required by the asbestosis policy had been satisfied from a claims perspective. Given our interpretation of the policy document that the two years reflects the period of the worker s employment when he was exposed to asbestos, and noting that, in addition to the period when the worker was clearly exposed to asbestos, he was likely exposed to airborne asbestos during further periods of time, we are satisfied that the two year period set out in the policy is met in the worker s case. Whether the worker has a diagnosis of asbestosis [26] We note that, in addition to the consideration of the length of time during which the worker was exposed to asbestos, the policy document also requires that, in order to be entitled to benefits, a diagnosis of asbestosis is required. The policy document states that certain factors should be considered in determining whether there is a valid diagnosis of asbestosis in the absence of pathologic examination of lung tissue. In this case, however, there was pathologic examination of lung tissue in that an open lung biopsy of the worker s lung tissue was performed on the worker. We interpret the policy to mean that the biopsy should be the basis of the diagnosis. [27] The problem in this case, however, is that there is a difference of opinion among the experts who have considered the results of the biopsy. Dr. Vincic, the pathologist who provided the report on the biopsy, indicated that there are five asbestos bodies in eight sections stained by the Perls method. He concluded that this evidence was sufficient for asbestosis under the standards provided in Pathology of Occupational Lung Disease, 2 nd edition, by Dr. Andrew Churg, but noted that the Helsinki Criteria tend to be more strict. [28] These different standards were discussed by Dr. Muir in his final memo on the subject, dated March 25, In that memo, Dr. Muir indicated that this is a difficult issue to resolve and noted that the origin of this dispute [i.e., the differing approaches taken, respectively, by the Helsinki Criteria and by Dr. Churg] is based on the fact that minimal asbestos exposure is common in an industrial society and a few asbestos bodies can be identified in many members of the population. He concluded that, based on the worker s history of exposure to asbestos, as between the diagnoses of asbestosis, or idiopathic PF, it was more probable that the worker s correct diagnosis was idiopathic PF. [29] We note however that a different view was expressed by: Dr. Vincic, the pathologist, who noted the different standards provided by Dr. Churg and the Helsinki Criteria, but concluded nevertheless that a diagnosis of asbestosis was appropriate; Dr. Young, who stated in his report, dated March 23, 2007, that he concluded that the worker had a compensable condition; Dr. Cox, who indicated that there was no doubt that [the worker] has asbestos related pulmonary fibrosis ; and Dr. Pysklysec, the physician who saw the worker at OHCOW, and who provided detailed reasons, excerpted above, for his view that asbestosis was an appropriate diagnosis. [30] We have taken into account Dr. Muir s impressive qualifications and experience as a respirologist. Nevertheless, prior to seeking advice from Dr. Rivington, the medical assessor that

12 Page: 11 Decision No. 1234/09 we retained for the purposes of this appeal, we conclude that the preponderance of evidence favoured a diagnosis of asbestosis. [31] Having considered Dr. Rivington s evidence, we conclude that, on a balance of probabilities, asbestosis is the appropriate diagnosis. In this regard we have taken into account Dr. Rivington s conclusions that: the presence of asbestos bodies substantially favours the diagnosis of asbestosis rather than other causes of pulmonary fibrosis; honeycombing was the prime feature of this case and the majority of the parenchyma seem[ed] to be spared. Dr. Rivington considered this to be unusual for progressive idiopathic pulmonary fibrosis which was the competing differential diagnosis; the fact that the worker s disease had been relatively stable, rather than progressive, tended to support the diagnosis of asbestosis, rather than idiopathic PF; Dr. Rivington stated that he believed that the worker s exposure to asbestos, on the balance of probability, did contribute to the development of limited fibrosis. [32] We have taken into account the fact that Dr. Rivington indicated, in a few places in his report, that it might be useful to obtain a further view from a pathologist to comment on the significance of asbestos exposure to the worker s fibrosis. We note that one of the opinions favouring the diagnosis of asbestosis was provided by Dr. Vincic, who is a pathologist. It appears to us that the preponderance of evidence before us favours the diagnosis of asbestosis, and that a further view from another pathologist would be unlikely to resolve the scientific dispute which is apparent in this case. [33] Alternatively, we have taken into account section 119(2) of the Act which provides that: 119 (2) If, in connection with a claim for benefits under the insurance plan, it is not practicable to decide an issue because the evidence for or against it is approximately equal in weight, the issue shall be resolved in favour of the person claiming benefits. [34] We note that there is significant evidence for and against the proposition that the worker s exposure to asbestos contributed significantly to his respiratory disease. Our primary finding is that the preponderance of evidence supports entitlement in this case. In the alternative, we conclude that the evidence for and against entitlement in this case is approximately equal in weight, and that, in keeping with the provision of the Act noted above, the issue of entitlement should be resolved in favour of the worker.

13 Page: 12 Decision No. 1234/09 DISPOSITION [35] The appeal is allowed. 1. The worker is entitled to benefits for his pulmonary disease, as a result of occupational exposure to asbestos. 2. The Board is directed to determine the nature and extent of the worker s entitlement to benefits. DATED: April 16, 2010 SIGNED: M. Crystal, B. Wheeler, F. Jackson