WORKPLACE SAFETY AND INSURANCE APPEALS TRIBUNAL DECISION NO. 1170/96R2

Transcription

1 WORKPLACE SAFETY AND INSURANCE APPEALS TRIBUNAL DECISION NO. 1170/96R2 BEFORE: L. Gehrke: Vice-Chair HEARING: September 20, 2006 at Toronto Oral Post-Hearing activity completed October 23, 2006 DATE OF DECISION: November 28, 2006 NEUTRAL CITATION: 2006 ONWSIAT 2795 DECISION UNDER APPEAL: WSIB Hearings Officer decision dated August 8, 1994 APPEARANCES: For the worker: For the employer: Interpreter: L. Morreale, Office of the Worker Adviser not participating E. Pistarelli /NAME/LANGUAGE 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

3 Decision No. 1170/96R2 REASONS (i) Introduction [1] In Decision No. 1170/96R, I granted a reconsideration of Decision No. 1170/96. This is my decision on the merits of the appeal. The deceased worker s estate appeals the decision of the decision of the Hearings Officer dated August 8, 1994 that the worker s obstructive airways disease was not caused by his work as a labourer and bricklayer in the construction industry. For the reasons given below, I allow the appeal on the merits. (ii) Analysis [2] The deceased worker was employed as a bricklayer s helper from 1959 to 1983, when he retired on a Canada Disability Pension. His main job was mixing mortar. This entailed putting bags of dry cement in a mixer and then adding bricksand. He would shovel the bricksand into the drum and then mix it manually. He described his job as handling from 200 to 300 bags of cement and sand on average per day, breaking the bags and pouring their contents into a cement mixer. He described working in a cloud of dust. The deceased worker s family provided to me a compendium of documents detailing the worker s job description. This includes a description of the worker s appearance when he returned home from work each day as covered in dust from head to toe. [3] The report of Mr. E. McCloskey, Director of Occupational Health, Ministry of Labour, which was solicited by the Tribunal in this case, confirms that bricklayer helpers are exposed to significant respiratory silica up to the allowable limits and above recommended levels. [4] I am satisfied on a balance of probabilities based on the worker s job description and Mr. McCloskey s letter confirming exposure of bricklayer helpers to significant respiratory silica, that the worker was exposed to significant respiratory silica in the course of his employment. [5] Dr. P.Thomas, Associate Professor of Medicine University of Toronto and Consultant Respirologist, St. Michael s Hospital, the worker s treating respirologist, and Dr. J.P. McLeod, a Tribunal appointed medical assessor who assisted me in the reconsideration of this appeal, diagnosed and found that there was a causal relationship between the worker s diagnosed COPD and his work as a bricklayer s helper. Dr. W.K.C. Morgan, respirologist, who assisted the Tribunal as medical assessors in the previous adjudication of this appeal, suggested an alternate diagnosis of sarcoidosis. The autopsy report found silicosis and did not find sarcoidosis. I have found the opinions of Dr. Thomas and Dr. MacLeod to be more persuasive than that of Dr. Morgan. The reports of Dr. Thomas and Dr. MacLeod are consistent with the exposure evidence and with the autopsy results in this case. [6] In June 1980, Dr. Rodriguez, the worker s treating respirologist, concluded that pulmonary function studies showed mild COPD. A chest x ray on June 6, 1984 showed bilateral infiltrates compatible with sarcoidosis, silicosis or alveolar carcinoma. Dr. Rodriguez stated that he could not confirm a diagnosis of silicosis, and was inclined to think this was sarcoidosis. However, further investigation was required. A bronchoscopy was performed. After review of the bronchoscopy, Dr. Rodriguez ruled out cancer and apparently ruled out

4 Page: 2 Decision No. 1170/96R2 sarcoidosis, stating the most likely diagnosis is silicosis with some conglomerate features. Dr. Rodriguez then filed a doctor s first report with the Board on August 14, 1994, stating the worker s diagnosis as pulmonary silicosis, and stating the worker had had shortness of breath and chronic bronchitis since By the time the claim was filed, the worker had retired and was in receipt of a Canada Disability Pension. [7] In April 1985, Dr. Vingilis for the Advisory Committee on Occupational Chest Disease provided a diagnosis of not yet diagnosed bilateral pulmonary infiltrates. Sarcoidosis, to be considered. This is very unlikely to be silicosis because this man was never exposed to silica dust in Canada. The reason the Committee thought that the worker was never exposed to silica dust was based on a job description of doing routine manual labour as a construction worker on residential and commercial sites. The Committee concluded: He never used fire bricks or silica bricks and in reality he was never exposed to silica dust. [8] In March 1988, the Occupational Chest Disease Review Committee reviewed the worker s case and stated: The findings are those of radiological appearances consistent with silicosis but to the knowledge of the Committee, there has been no adequate history of silica exposure in Ontario. [9] In March 1989 Occupational Chest Disease Review Committee found that x- ray changes in the worker s lungs were certainly most typical for silicosis. However, there was a negative history of occupational exposure and negative tissue diagnosis. The Review Committee wrote to Dr. Thomas on March 29, 1989: To the best of our knowledge the claimant had worked all the time as a construction worker. his only exposure was to cement [10] A lung biopsy suggested by the Review Committee in July 1990 showed non-specific fibrosis. The worker s treating respirologist, Dr. Thomas, in a report dated October 25, 1990 found that a CT scan showed fibrosis and multiple enlarged lymph nodes calcified consistent with silicosis. Pulmonary function studies were in keeping with industrial exposure to silica. A CT of the thorax on April 22, 1991 showed possible silicosis. Dr. Thomas reported on July 15, 1992 lung biopsy showed fibrosis with silica crystals. [11] In a memo dated January 10, 1994, Dr. Roos, writing for the Chest Disease Review Committee concluded that there was no evidence that his exposure to cement dust caused his fibrotic lung disease. Dr. Thomas responded to Dr. Roos opinion on April 29, 1994: The evidence is very strong that this man s restrictive and obstructive lung disease was caused by his 24 year exposure to industrial dust inhalation. It would be interesting if other consultants could come up with other possible causes for this man s changes. I do not think that would be possible, therefore we must presume that his exposure is the cause of his pulmonary disease. [12] Dr. Roos found in a report dated March 28, 2003 that there were radiological findings consistent with silicosis, but that there was no adequate history of silica exposure in Ontario. [13] Thus, throughout the history of the worker s case, the Occupational Chest Disease Committees denied the worker entitlement for silicosis because they thought he had never been

5 Page: 3 Decision No. 1170/96R2 exposed to silica in Ontario. This was based upon inadequate information indicating a history of exposure to cement only. In fact, the worker was also exposed to sand, which can be in excess of 50% of the mortar mixture. Sand consists of crystalline silica, which causes significant concentrations of respirable silica in the air to which bricklayer s assistants are exposed, according to the report of Mr. E. McCloskey, Director of the Occupational Health and Safety Branch Operations Division of the Ontario Ministry of Labour. Mr. McCloskey states, in a letter dated March 19, 1997 to Tribunal Counsel Office, which was requested in this case: In reference to your letter of January 27, 1997 regarding the appeal of a deceased worker, which is currently before the Workers Compensation Appeals Tribunal, we have determined that a mortar mixture normally contains sand and cement. Sand, in large part (>90%), consists of crystalline silica, while there is no silica in the cement. A mortar mixture may contain sand in excess of 50%. As far as we know, the composition of the mortar mixture between 1959 and 1980 did not change significantly. As most of the silica related diseases are caused due to inhalation of silica, the Ministry has some limited data for the concentrations of respirable crystalline silica in air to which the bricklayer s helpers were exposed during Such concentrations were 0.9, 0.14 and 0.20 mg/m3 respectively for the three helpers monitored. Current Ontario exposure limit for respirable crystalline silica in Regulation 845/90 is set at 0.2 mg/m3 over an 8-hour work day and a 40-hour work week, but the employer is obligated to reduce exposure to the lowest practicable level with a view to achieve at least 0.1mg/m3. [14] Mr. McCloskey s evidence satisfies me on a balance of probabilities that bricklayer helpers are exposed to significant amounts of respirable crystalline silica. The worker worked as a bricklayer s helper for 24 years, mixing cement and sand together to make mortar. In this process, he was exposed to significant amounts of respirable crystalline silica. The Chest Disease Committees did not have any information that the worker was exposed to respirable crystalline silica at the time they made their decisions. In fact, they thought that the worker was not exposed to silica at all. Since their reports are based on a wrong assumption of no exposure to respirable silica, it follows that their conclusion, that the worker s diagnosed silicosis was not caused by his work because he was not exposed to respirable silica, cannot be accepted as reliable. [15] Next, I address the issue whether the worker likely suffered from silicosis or sarcoidosis. Dr. Rodriguez ruled out sarcoidosis based upon his review of the worker s bronchoscopy in The issue was revived by the Chest Disease Review Committee in the context of their inability to explain the fibrosis in the worker s lungs, absent exposure to silica (which we now know to be based on false information that the worker had not been exposed to silica). [16] The Panel that originally heard this appeal requested a report from tribunal-appointed medical assessor, Dr. W.K.C. Morgan, Professor of Medicine and Director, Chest Disease Service, University of Western Ontario. Dr. Morgan concluded: In the various records that have been forwarded to me there are a number of errors and misconceptions in regard to the presence of silica exposure and its various effect. These need to be put in perspective before considering whether [the worker], firstly has been

6 Page: 4 Decision No. 1170/96R2 exposed to significant quantities of silica, and secondly whether the disease from which he suffered is compatible with a diagnosis of silicosis. The sand that is mixed with cement is seldom airborne, and the particles are too large to travel through the airways and be deposited in the respiratory bronchioles or alveoli. Respiratory particles are not visible while the sand that is mixed with cement is clearly visible. The mixing of cement with sand is no more of a hazard as far as silica is concerned, than is living on the seashore, or in the deserts of the Okanagan Valley or Nevada. Were sand a hazard then nobody living in the Sahara or in other deserts where virtually all of what one walks on consists of pure silica. Silica is a hazard only when the subject is exposed to excessive concentrations of respirable silica. Such circumstances may be present in a number of workers. These include tunnelers, miners, rock crushers, sandblasters, those who manufacture fire bricks and ceramics, in grinders, foundry workers, all of whom under certain circumstances are exposed to respirable silica. Brick laying is not a recognized cause of silicosis, for example, although the manufacture of fire bricks can produce silicosis, there is no evidence that [the worker] ever made fire bricks. In the case of [the worker], we are not exactly sure what he did at all the listed work places, but he seems to have spent most of his life working as a bricklayer. The off the cuff remarks made by him, and other persons about him being exposed to silica are clearly inappropriate, because neither he nor anybody else around him, would know whether the ambient air contained silica or not. They would be even more ignorant of the size of any particles in the air. Moreover, virtually all of the firms and facilities in which he worked have closed down and are no longer productive. We have no way of knowing for certain whether he had any hazardous exposures, but it seems unlikely. There is a comment about him having worked as a sandblaster for a time, yet this is not substantiated elsewhere or in his work history. [The worker s] work history as it has been recorded suggests that there is very little evidence of [the worker] being exposed to much in the way of crystalline silica or any other noxious inhalable agent. The mixing of sand with cement for the production of concrete and/or mortar is usually carried out in concrete mixers and is probably associated with no more risk than is the making of sand castles by children on the beach. [17] Dr. Morgan concluded that it was highly improbable that the worker had silicosis, based on the worker s occupational exposure, the history, the physical signs, the relevant pathology and the chest radiographs. Dr. L. Hutton, of London Health Sciences Centre, reviewed guest films from St. Michael s Hospital taken 1987, 1989, 1991, 1992 and Dr. Hutton was of the opinion that radiographic appearance would be in keeping with silicosis, although in a slightly atypical distribution, and also in keeping with sarcoidosis. Dr. Morgan provided a further report on November 10, 1997, taking into account the review of the x-rays considered by Dr. Hutton. Dr. Morgan concluded that the x-rays suggested either sarcoidosis or silicosis. However, Dr. Morgan preferred a diagnosis of sarcoidosis because he was of the opinion that the worker was not exposed to silica and because little or no evidence of silicosis was found at biopsy. Dr. Morgan wrote: Little or no evidence of silicosis has been found at biopsy. One wonders whether this is because it is not there or because appropriate techniques were not used. I am willing to accept one biopsy as being falsely negative, however, the fact that he has had three or four goes much against a diagnosis of silicosis. Also against this diagnosis is the fact that [the worker] was exposed to cement not to sand. The sand that one mixes with cement is not likely, since it consists of large particles, to cause silicosis.

7 Page: 5 Decision No. 1170/96R2 The alternative diagnosis is sarcoidosis. Certainly, the appearances are compatible with this diagnosis. One would have thought, however, that had [the worker] suffered from sarcoidosis, the transbronchial biopsies would have shown granulatoma. Based on the information that is currently available to me, I think it much more likely that [the worker] had sarcoidosis than silicosis, although I cannot definitely exclude the latter. [18] New evidence submitted with the worker s reconsideration request consists of a response to Dr. Morgan by Dr. Thomas. Dr. Thomas wrote on August 31, 2004 in part: Sarcoidosis was thrown in as a diagnosis without evidence and this would be unlikely in an elderly white Caucasian male There was no clinical evidence of this disease. The patient s age, sex, race, pulmonary activity, radiology and pathology were all against that diagnosis. No non-caseating granuloma were noted which would be consistent with sarcoidosis. [The worker] was exposed to cement for almost 30 years, this exposure can result in fibrosis, there was fibrosis present. When the clinician sees the patient with diffuse pulmonary fibrosis and a history of work in a potentially risky occupation he may be tempted without detailed investigation to attribute the disease to that risk or if he overlooks a relevant occupational hazard he may wrongly relegate the disease to some other cause (WR Parkes, occupational lung disorders). What then is the case with [the worker]. He was exposed for 23 years to cement, perhaps some silica, perhaps some asbestos. He died from respiratory and heart failure caused by a mixture of chronic obstructive lung disease and pulmonary fibrosis. He had not smoked for over 35 years. New evidence is in keeping with cement causing bronchitis and pulmonary fibrosis. No other cause for this man s pulmonary disease was ever shown. The man had severe bronchitis and pulmonary fibrosis. Both diseases are compatible with the inhalation of cement. [19] I requested a further tribunal-appointed medical assessor s report by Dr. J. P. MacLeod, Consulting Respirologist and Associate Professor, University of Ottawa. Dr. MacLeod conducted a medical literature search of the relationship between exposure to cement dust or sand and interstitial pulmonary fibrosis, and also provided an analysis of the issues in this case. Dr. MacLeod s report calls into question the conclusions reached by Dr. Morgan. Dr. MacLeod concluded that a diagnosis of complicated silicosis was more probable than a diagnosis of sarcoidosis in this case, and that it was probable that the worker was exposed to respirable silicates as a bricklayer, writing: I do not believe the diagnosis of complicated silicosis can be excluded by this pathological examination, which did not include estimating the burden of silicates in the entire lungs or electron microscopy. Dr. Morgan eloquently indicates numerous examples of incorrect assumptions regarding silicate content of cement dust. This does not prove our case cannot have silicosis. Dr. Morgan concludes the radiological picture is not incompatible with silicosis. Although he states there are usually plentiful amounts of dust seen lung section, this is not always the case The scanty amount of bi-refringent silica particles seen at postmortem does not exclude the diagnosis of silicosis. Unfortunately the lung was not ashed to precisely measure the dust content. Absence of proof is not absence of truth. The diagnosis of Stage IV sarcoidosis is offered by Drs. Morgan and Mullen as more likely. There may be no difference in radiological findings and pulmonary function testing between these disorders. The tempo of this patient s lung disease is faster than any case of sarcoidosis I have encountered in a Caucasian. The absence of typical

8 Page: 6 Decision No. 1170/96R2 microscopic pathology after several biopsies in the earlier phase of his illness and after post mortem examination is as unusual for sarcoidosis as it is for silicosis. I do not believe the available information allows us to exclude either of these diagnoses. The clinical picture is more suggestive of complicated silicosis if one accepts the patient had exposure to silicates sometime during his occupation. The focus of previous reports on the ability of cement dust to have been the cause of this case s lung disease may have been too narrow. He may have been around workers cutting bricks which do contain sand. There could be abrasion of brick surface as bricks are slid off the stack, pulverizing sand particles to finer silicates which could have been inhaled. He might have been working near sandblasting on a renovation project with no respiratory protection. Bricklayers may be exposed to respirable quartz dust of 0.32 mg/m3 (Dutch limits are mg/m3). (19) Danish studies of dust at building sites similar to where this case must have worked found mg/m3 of respirable quartz dust (20). It is probable that [the deceased worker] was exposed to silicates in the workplace. The patient had smoked, possibly until the 1980s. The level of COHb of 3.2% found on admission suggests at least heavy exposure to second hand smoke. Tobacco has been implicated as an aggravating factor in occupational lung disease of cement factory workers and could have played a role here (3,13). Conclusion: I am unable to absolutely prove from the available information that the lung disease causing this patients death was caused by Stage IV sarcoidosis or complicated silicosis related to his work as a mortar mixer. I am certain that cement dust exposure does not cause his type of lung disease. I suspect he had exposure to silicates as a consequence of his occupation. For that reason I favour Silicosis with progressive massive fibrosis as the cause of his death. [20] In my view, the reports of Dr. Thomas and Dr. MacLeod report are persuasive. Dr. MacLeod s opinion is consistent with the view of the worker s treating respirologist, Dr. Thomas as well as his prior treating respirologist, Dr. Rodriguez, and with the findings on autopsy of silicosis (not sarcoidosis). Further, Dr. MacLeod s opinion also supports the view and is consistent with other evidence (Mr. McCloskey s letter) of significant respirable silica exposure in the course of the worker s occupation as a bricklayer s assistant. Dr. Morgan was of the view that cement workers are not exposed to silica. This is an important factual basis for his opinion. I have found for the reasons set out above that the worker was exposed to respirable silica. I prefer the opinions of Dr. MacLeod and of Dr. Thomas, the worker s treating respirologist, which are consistent with the evidence of the worker s exposure to respirable silica and consistent with the autopsy report, which found silicosis and did not find sarcoidosis. [21] It is a well-accepted principle at common law and in workers compensation law that the causal relationship between the work and the injury (in a compensation situation) is that of significant or material contribution. The issue to be addressed is whether the work contributed in a significant or material way to the development of the medical condition in question. A material contribution need not be the sole contribution, but must be more than a minimal contribution. Causation need not be determined with scientific precision. Medical experts ordinarily determine causation in terms of certainties, but the law requires a lesser standard. If it is the function of the trier of fact, not the medical witnesses to make a legal determination of the question of causation, using a robust and pragmatic approach, where there is medical

9 Page: 7 Decision No. 1170/96R2 uncertainty with respect to causation. Reasonable inferences may be made from the primary facts of the case. Causation is determined on a balance of probabilities, or applying the benefit of the doubt where the evidence is equally weighted. However, a finding of causation may not be made based on mere speculation or evidence of a possibility, rather than a probability. 1 [22] In this case, the evidence persuades me on a balance of probabilities that the worker suffered from silicosis consistent with his exposure to respirable silica in the course of his employment. The Worker s Compensation Act, Board policy and medical science have long recognized that silicosis results from exposure to respirable silica. The evidence does not establish any plausible alternate cause for the worker s silicosis. Therefore, I find that the worker s silicosis resulted from his employment. 1 See the judgments of the Supreme Court of Canada in Snell v. Farrell, [1990] 2 S.C.R. 311, [1990] S.C.J. No. 73; Laferriere v. Lawson [1991] 1 S.C.R. 541 per Gonthier J.

10 Page: 8 Decision No. 1170/96R2 DISPOSITION [23] The appeal of the worker s estate is allowed. The worker had entitlement to benefits under the Workers Compensation Act for silicosis resulting from his exposure to respirable silica in the course of his employment. DATED: November 28, 2006 SIGNED: L. Gehrke