SUMMARY

DECISION NO. 1110/96

Exposure (silica dust); Chronic obstructive lung disease; Pneumonia. The worker worked as a miner from 1939 to 1974. He received a 30% pension for silicosis. The worker died in 1994 of pneumonia, secondary to chronic obstructive pulmonary disease. The worker's widow appealed a decision of the Appeals Officer denying entitlement to dependency benefits. The worker suffered from a significant silicotic condition during the last 20 years of his life. Although the medical evidence was not as extensive as the Panel would have liked, the Panel concluded that the silicosis was a significant contributing factor to the conditions which caused the worker's death. The appeal was allowed. [6 pages]

PANEL: Strachan; Crocker; Apsey DATE: 04/12/96

WORKERS’ COMPENSATION APPEALS TRIBUNAL DECISION NO. 1110/96 This appeal was heard in the City of Sudbury on November 18, 1996, by a Tribunal Panel consisting of: I.J. Strachan: Vice-Chair, R.H. Apsey : Member representative of employers, J.A. Crocker: Member representative of workers. THE APPEAL PROCEEDINGS The worker’s widow appealed a December 7, 1995, Appeals Officer decision. The decision denied her entitlement to dependency benefits. The worker’s widow claimed that his death was causally related to his compensable silicotic condition. C. Chenier, United Steelworkers of America, Local 5417, represented the worker’s widow. The employer received notice of the hearing but elected not to attend. THE EVIDENCE The Panel reviewed the Case Description containing the Board file materials together with two Addenda containing additional medical materials. The Panel also heard submissions from Ms. Chenier. THE NATURE OF THE CASE The Panel must determine whether the worker’s widow is entitled to dependency benefits on the basis that the worker’s compensable silicotic condition was a significant contributing factor to his death on March 14, 1994. THE PANEL’S REASONS (i)

Background

The worker worked for various mining employers for most of the years between 1939 through 1974. He began work with the accident employer in 1957. He left his employment as a mill operator with the employer in October 1974 and filed a WCB claim based on silicosis. He did not work after 1974. An April 1975 medical assessment indicated that the worker had silica dust effects, but recommended no award. A September 1976 re-assessment resulted in a 20% permanent disability award. The award was increased to 30% in 1978 and was reconfirmed from time to time on subsequent examinations. The worker underwent surgery for a collapsed left lung in 1982. The worker was admitted to hospital on September 31, 1993, and subsequently in February and March 1994. He died of respiratory failure on March 14, 1994. The final diagnosis was pneumonia, secondary to chronic obstructive pulmonary disease (“COPD”)

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Decision No. 1110/96 associated with atrial fibrillation. As the worker’s representative pointed out, the medical note on the worker’s health initially suggested the primary cause was COPD; subsequently the numbering was changed to indicate that the most responsible diagnosis was firstly pneumonia, secondly COPD, thirdly bronchitis and fourthly atrial fibrillation. (ii)

Worker’s submissions

Ms. Chenier noted the change in numbering in the medical report and suggested that pneumonia was the culmination of the worker’s silicotic/COPD conditions which were significant contributing factors to his death. She noted that the medical reports indicated that the worker had stopped smoking in 1965. She submitted that any smoking history should be viewed as a “thin skull” situation and referred the Panel to page 6 of the 1990 discussion paper prepared by Dr. D.L. Holness entitled “Chronic Obstructive Lung Disease” (COPD): In summary, these studies examining the effect of silica dust exposure on lung function have suggested that chronic obstructive lung disease and emphysema can develop in silica-exposed workers, particularly in smokers. The question of individual susceptibility has been raised, namely that a small group of exposed workers appear to be particularly susceptible to this effect. When large population-based studies are carried out, the group of susceptibles with a significant effect are diluted by those who do not develop problems, and therefore an overall adverse effect may not [be] detected. The relationship appears to have dose-response characteristics and those with higher exposures appear to be at greater risk. Because of the differences in dust-sampling technique it is difficult to directly compare the results or provide a definite answer regarding the magnitude of effect at any specific level of exposure. The widow’s representative also submitted that the worker’s compromised lung function related to his silicosis made him more susceptible to severe respiratory infections such as pneumonia. She referred to the following page 8 excerpt from the Industrial Disease Standards Panel (“IDSP”) March 1993 Report to the Workers’ Compensation Board on Respiratory Complications among Workers Receiving Compensation for Non-malignant Respiratory Disease: ... The Panel is in agreement with the statement that the boundary between occupationally caused, work-aggravated and non-workrelated lung diseases is “indistinct, reflecting the multifactorial nature of the diseases”(27). Nevertheless, in our view, it is clear that workers suffering compromised lung function due to occupational respiratory disease are more likely to suffer from more frequent and more severe respiratory infections such as pneumonia than the general population. This is supported by the medical opinions we solicited and by the medical literature.

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Decision No. 1110/96 In addition, the consistently elevated SMRs in the literature for all manner of respiratory disease strongly supports the position that such workers are much more likely to die from such complications than the general population. Even when studies among workers compensated for a respiratory disease indicate a deficit of deaths from a particular type of NMRD such as emphysema or bronchitis, one cannot conclude that this is in fact the case. It is possible that such deaths are actually subsumed among other groups, such as deaths attributed to silicosis, for example, reflecting the frequently multifactorial nature of the deaths. Finally, it would seem only common sense that an individual’s lung function reflects the cumulative impact of the insults it has received. As our consultant has stated: “individuals with occupational lung disease with significant impairment may still be able to manage if they have no other lung problems. However, if they have additional impairment, [including non-work related impairment], their lung function may be reduced to a critical level”. The Panel is confinced that fair public policy demands compensating those individuals whose ability to survive their cumulative lung damage is seriously compromised by the existence of a compensable respiratory impairment. In the representative’s submission, the compensable silicotic condition and COPD produced a strain on the worker’s system which ultimately led to his death. In her submission, the evidence for and against the issue of a “significant contributing factor” was at least approximately equal and therefore the worker was entitled to the benefit of doubt on the causation issue as required by the Act. (iii)

Conclusions

The medical evidence establishes that the worker suffered from a significant silicotic condition during the last 20 years of his life. Although Dr. McMillan indicated in an October 24, 1974, report that “... there was no question that [the worker] does have quite marked limitation of respiratory function with limitation of chest expansion and with quite marked cysnosis at rest ...” and that “... in view of the fact that he does have silica dust inhalation effects, a claim should be initiated for him”, the WCB Advisory Committee report dated April 9, 1975, indicated “dust effects. No radiological evidence of silicosis”. However, the September 1, 1976, report to Dr. Stewart at the WCB from Dr. J. Roos of the Advisory Committee on Occupational Chest Diseases, Ministry of Health, indicated the worker had silicosis and rated his disability at 20%. The same report recommended a re-examination in two years time. The October 5, 1978, report on the worker’s silicosis rated the disability at 30%. Periodic reviews continued the disability rating at 30%.

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Decision No. 1110/96 The worker did not work after 1974. He had surgery for a collapsed left lung in 1982. By 1993, he was using oxygen from an oxygen compressor. The November 1, 1993, radiological report read in part: There is no interval change from a previous examination of Jan. 15-93. There are severe chronic changes in the left lung with both fibrosis and emphysematous changes. I suspect these changes are due to scarring from tuberculosis. The worker died of respiratory failure on March 14, 1994. As indicated earlier in the decision, the final diagnosis was pneumonia, secondary to COPD associated with atrial fibrillation. The Appeals Officer concluded that the emphysema referred to in the medical reports arose from the worker’s smoking history. He concluded there was no entitlement in the worker’s claim for COPD which he appeared to attribute to the worker’s smoking history. He also concluded that no medical opinion had been submitted suggesting the worker’s death was a direct result of the compensable silicotic condition. The Appeals Tribunal, in its case law, does not require that the compensable condition be the direct cause of a worker’s death when considering survivor benefits. The Appeals Tribunal, in considering such entitlement, awards dependency benefits where the compensable condition was a “significant contributing factor” in the worker’s death. In the case before us, obviously pneumonia and COPD were considered to be conditions “most responsible” for the worker’s death. In our opinion, attributing all COPD to non-compensable factors and eliminating silicosis as an element of the worker’s COPD creates an artificial distinction in this case. In our view, both the worker’s silicosis and COPD contributed to obstruction of the lung airways and decreased oxygen uptake which in turn caused the worker to work harder at breathing and to tire easily. The medical reports indicate that he had pulmonary fibrosis in his left lung and that he was admitted to hospital from time to time because of difficulty in breathing and increased loss of volume in his left lung. The February 17, 1994, radiological report from Dr. Doubilet read: Comparison was made with the previous examination of Nov. 1st, 1993. As on the previous examination, there are severe chronic changes in the left lung and left-sided pleura with an s-shaped scoliosis. There is considerable loss of volume in the left lung. On the previous examination, the right lung was clear. On this examination, there is an increase in interstitial markings diffusely through the right lung with thickening of the minor fissure. This suggests congestive heart failure supra-imposed on chronic disease. A diffuse pneumonia could not be excluded and further follow-up is suggested.

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Decision No. 1110/96 Although the medical evidence in this appeal is not as extensive as we might desire, we agree with the submission of the widow’s representative that the evidence for and against the issue of causation is “approximately equal”. We conclude that the worker’s widow is entitled to the benefit of doubt on the issue of whether the worker’s compensable lung condition was a significant contributing factor to his death. We conclude that the widow is entitled to survivor benefits. THE DECISION The appeal is allowed. The worker’s widow is entitled to dependency benefits.

DATED: December 4, 1996

SIGNED: I.J. Strachan, R.H. Apsey, J.A. Crocker J.A. Crocker

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