WORKPLACE SAFETY AND INSURANCE APPEALS TRIBUNAL

Transcription

1 2005 ONWSIAT 1454 WORKPLACE SAFETY AND INSURANCE APPEALS TRIBUNAL DECISION NO. 1308/04 [1] This appeal was heard in Sault Ste Marie on August 5, 2004 by a Tribunal Panel consisting of: S. Ryan : Vice-Chair, G.V. Stewart : Member representative of employers, J.A. Crocker : Member representative of workers. THE APPEAL PROCEEDINGS [2] The deceased worker s estate appeals the decision of R. Sheridan, Appeals Resolution Officer, dated February 22, This decision denied the worker a Non-Economic Loss (NEL) award for silicosis. The decision also denied the worker initial entitlement for asbestosis. [3] The worker s daughter, LJ, appeared on behalf of the estate and was represented by R. Aubut, a consultant. The accident employer is no longer in business. THE RECORD [4] The following documents were marked as exhibits in this appeal: Exhibit #1: Case Record prepared by the Tribunal on August 24, 2000 containing a Board claim file as well Board Policy Package Nos. 19 and 30 and Operational Policy Manual Document # , Non-Economic Loss (NEL) Assessing Permanent Impairment ; Exhibit #2: Case Record Addendum No. 1 prepared by the Tribunal on September 2, 2003 containing Tribunal correspondence, medical reporting from Dr. J. Anderson, an occupational health physician with the Occupational Health Clinics for Ontario Workers Inc. (OHCOW), a report from N. Keller, occupational hygienist with OHCOW, medical reporting from Dr. G. Berg, an article on interstitial lung disease from UpToDate.com, a clinical information service, and Board Policy Packages 16, 19, 35 and 300; Exhibit #3: Correspondence from the Tribunal dated September 2, 2003; Exhibit #4: Case Record Addendum No. 2 prepared by the Tribunal on July 12, 2004 containing Tribunal correspondence, estate documentation, an article entitled Short-term Asbestos work exposure and Long-Term Observation, from the American Cancer Society and Mount Sinai School of Medicine in New York, and an article entitled Mortality Experience of Amosite Asbestos Factory Workers: Dose-Response Relationships 5 to 40 years After Onset of Short- Term Work Exposure published in 1986 in the American Journal of Industrial Medicine;

2 Page: 2 Decision No. 1308/04 Exhibit #5: Post-hearing Addendum No. 1 prepared by the Tribunal on January 6, 2005 containing additional medical evidence; and Exhibit #6: Post-hearing Addendum No. 2 prepared by the Tribunal on February 14, 2005 containing Tribunal correspondence and submissions from Mr. Aubut dated February 4, [5] The Panel heard oral evidence from the worker s daughter. Mr. Aubut offered oral and written submissions. THE ISSUES [6] The worker s estate seeks entitlement to a NEL award for his lung disease diagnosed as silicosis. The estate also seeks initial entitlement for asbestosis. THE REASONS (i) Background [7] The worker was employed as an underground miner in Ontario, Manitoba and the Yukon between the years 1946 and He remained in the mining industry until his retirement in On January 11, 1996, at age 72, the worker was diagnosed with silicosis. [8] The Board accepted entitlement for the disease, but denied the worker entitlement to a NEL award on the basis that there was no evidence of progressive massive fibrosis which would account for abnormal lung function typically associated with silicosis. [9] In his decision of February 22, 2000, the Appeals Resolution Officer confirmed the denial of a NEL award for silicosis and also denied the worker entitlement for asbestosis on the basis that the worker s exposure to asbestos was less than the two-year exposure duration required in Board policy. (ii) The documentary evidence including evidence collected after the hearing [10] A claim file was set up to investigate the worker s entitlement for lung disease when his family doctor, Dr. L. Defoa, filed a report dated July 7, In that report he advised that the worker suffered from silicosis. Dr. Defoa also advised that the worker suffered from hypertension, ischemic heart disease and dyspepsia. [11] The Case Record contains multiple chest x-ray and pulmonary function reports. These were interpreted by Dr. J.W. Robertson, an internal medicine specialist, in a report dated May 15, Dr. Robertson advised that he investigated the worker because of breathlessness and CXR [(chest x-ray)] abnormality. Dr. Robertson noted the worker s complaints of exertional dyspnea and daily coughs which were usually dry. At that time, the worker could walk one mile at a slow pace and tended to his garden. On occasion, the worker s cough produced a scanty volume of clear to yellowish sputum. He noted that the worker was exposed to gold, base metals and asbestos. He offered the following assessment: I agree that [the worker s] breathlessness and CXR abnormality result from occupational lung disease.

3 Page: 3 Decision No. 1308/04 In his forty-six years underground, patient was exposed to silica dust on a daily basis. Silicosis could account for the problem. Patient also has features of asbestosis. He had a four month asbestos exposure during the 1950 s. The CXR findings and marked depression of diffusion capacity could be explained on the basis of asbestosis, as well.... The x-ray abnormality is long standing dating back to at least I would not advise biopsy or invasive investigation. [12] On August 20, 1998, the worker was interviewed by K. Weeks, a Nurse Case Manager at the Board. The Nurse Case Manager recorded the following description of symptoms from the worker in a memorandum of that date: He is short of breath all the time reports no chest pain. He coughs frequently with yellow to green sputum production at times. He tells me he wakes during the night feeling as if he is suffocating. He wakes early just because he can sleep no longer but reports getting 6-8 [hours] sleep a night. His [family doctor] reports [on examination] crackles at bases of lungs [left greater than right] with no wheeze. He was initially thought to have CHF or angina. Dr. Roberts has done a stress test which [the worker] reports as normal. On the Form #8, [family doctor] records he may need oxygen in the future. He tells me otherwise he has no past health problems. Medications currently taken include 2 ASA daily, nitroclycerin nightly to help him sleep (??) and a stomach pill for acid. He quit smoking 7 years ago, prior to that he smoked 1[package per] day x 40 [years]. He lives with his wife and keeps busy doing the odd delivery. [13] On December 16, 1998, Dr. J. Roos, Board respirologist, reviewed the chest x-rays conducted in 1987, 1988, 1996 and 1998 as well as pulmonary function tests and functional volume capacity tests. He noted that the worker was found to have a diffusing capacity of 10.1 or 42 percent of the predicted level. He advised: The chest x-ray pattern is mixed: there is a minor nodular pattern ( small rounded opacities by the ILO classification) that is consistent with silicosis, and a major reticular pattern ( small irregular opacities ) which is consistent with diffuse parenchymal fibrosis of the fibrosing alveolitis type. I did not see any pleural disease on the plain films. The diffuse interstitial pattern is uniformly spread through the upper, middle and lower lung fields, with a definitely peripheral preponderance. This appearance is most commonly seen in cryptogenic fibrosing alveolitis, and is dissimilar from the usual presentation of silicosis. Although the sparse pattern is seen in the right and left upper and right middle zones and this part is consistent with more typical silicosis. Although the hila are prominent, they are not as prominent as they commonly are in sarcoidosis. There is a very gradual progression of both nodular and the diffuse interstitial markings throughout the period of observation and a Ministry of Labour code from 1984 mentions code 4, generalized arborisation, which would indicate that the known earliest signs of pulmonary abnormality were present in at least They seem consistent with what followed. The absence of a restrictive pattern on the [pulmonary function tests], apart from the low diffusing capacity, is more consistent with silicosis than with cryptogenic fibrosing alveolitis, which after 14 years would be expected to lead to mark restriction in most presentations. The low diffusing capacity is consistent with interstitial fibrosis and now with silicosis.

4 Page: 4 Decision No. 1308/04 Dr. Roos opined: Silicosis in severe exposures may present with a more dominant small irregular opacities pattern than with a nodular pattern, although it is not a common finding in this context. Given the difficult differential diagnosis in this claim, I would conclude that this worker has some silicosis, which does not result in a [permanent impairment] (since abnormal lung functions starts appearing only with advancing progressive massive fibrosis, and we have no evidence of that being present here). Also, there is a diffuse interstitial fibrosis which has resulted in the low diffusing capacity. Since the appearance is not suggestive in its distribution pattern of asbestosis, nor are there any pleural markers of asbestos exposure, then the most probable explanation for the second, diffuse interstitial, pattern is a mild form of cryptogenic fibrosing alveolitis, a non-occupational lung disease. I would class the latest 1998 chest x-ray appearance as category 3/2 T/Q, covering all 6 lung zones without pleural thickening. Because of the atypical appearance, I would feel that sarcoidosis has not been completely excluded but it could not be done without a biopsy, which is contraindicated here. [14] In a report dated November 8, 1999, Dr. G.W. Kivinen, respirologist, reviewed in detail the worker s employment history in the mining industry. He also noted that the worker had a 50 to 60 pack/year history of smoking, but quit about seven years prior to his report. Dr. Kivinen was asked to comment on the Board doctor s medical opinion, presumably the opinion of Dr. Roos. Dr. Kivinen opined: This patient has generalized interstitial disease with bibasilar crackles and a markedly reduced diffusing capacity. The lung volumes are still relatively well preserved. He does have mild hypoxia at rest which is somewhat accentuated on exercise. I must say I would have to agree with the consultant for the WSIB that this patient probably does have underlying idiopathic pulmonary fibrosis (or cryptogenic fibrosing alveolitis). Certainly, silicosis generally does not cause the crackles, the markedly reduced diffusing capacity and silicosis tends to be more of an upper lobe disease. The only entity that one could confuse with interstitial pulmonary fibrosis would be asbestosis and almost invariably asbestos related lung disease has a significant pleural component (which this patient does not show). Indeed his history of exposure to asbestos is fairly minimal. [15] On January 4, 2001, the worker underwent a chest x-ray and the ensuing report offered the following conclusion: Unchanged from 23/10/00. Diffuse chronic interstitial lung disease which is consistent with a history of pneumoconiosis probably silicosis. No evidence of massive pulmonary fibrosis. [16] The available documentation in the Case Record of medical investigations into the worker s lung disease resumes in The worker was admitted to hospital in February 2002 because of difficulty breathing. He was treated for his lung condition as well as pneumonia 1. The worker attended the OHCOW clinic in Sudbury where he was interviewed by N. Keller, an occupational hygienist. In a report dated April 22, 2002, she documented the worker s history of underground mining for approximately 18 years and 11 months. She noted his employment in asbestos mining for approximately three months. She noted that the worker was employed in copper, zinc, nickel and silver mining for about 26 years for a total of 45 years of experience in 1 Report from Dr. J.E. Anderson, occupational health physician at OHCOW, dated June 5, 2002 (Exhibit 2)

5 Page: 5 Decision No. 1308/04 underground mining. The occupational hygienist noted that several studies reported increased risks for idiopathic pulmonary fibrosis with a consistent set of occupational and environmental dust exposures. 2 She concluded: pulmonary fibrosis may be caused by inhalation of asbestos, silica and alpha particles from radon progeny. With silicosis, lesions are usually nodular and are likely to be more prominent in the upper lobes, while with asbestosis there is a lower lung zone prominence. Several studies have reported increased risks for idiopathic pulmonary fibrosis with a consistent set of occupational and environmental dust exposures. There is increasing evidence that exposures to dust and fumes are associated with chronic lung injury, which may promote interstitial pulmonary fibrotic diseases, such as idiopathic pulmonary fibrosis. Several reports have documented associations between exposure to metals and the development of pulmonary fibrosis. Some of the metals include metallic and oxidized aluminium, cobalt, cadmium and chromium. There is also ongoing controversy over the contribution of non-fibrogenic dusts to the development of airway disease. Therefore, it is reasonable to suggest that environmental exposures may cause idiopathic pulmonary fibrosis. [17] On April 23, 2002, the worker underwent another chest x-ray which was interpreted by Dr. J. K.K. Tjong, radiologist, as being consistent with interstitial pulmonary fibrosis. [18] Also on April 23, 2002, the worker was admitted into a Sault Ste. Marie hospital. He was examined by Dr. G. Berg, respirologist, for hypoxemia (diminished concentration of oxygen in the blood). Dr. Berg noted that a few months prior to his report, the worker was placed on oxygen and subsequently developed increasing hypoxemia, cough, shortness of breath, low grade fever and productive sputum. The worker was being treated with Prednisone. Dr. Berg opined: This 78 year old gentleman most likely has progressive idiopathic pulmonary fibrosis based on his clinical symptomatology over the past few years. Unfortunately, there may be little we can offer him at this time. He does not appear to be frankly septic or have a septic illness. He is quite hypoxemic even at rest and may require high flow oxygen as with the 5 to 6 litres he still appears to be hypoxemic. Of note, 08/05-00 at the Sudbury Regional Hospital the patient had quit smoking after 40 pack years 9 years prior to the test. He had some early airflow obstruction without significant bronchodilator improvement but interestingly his gas transfer was only 34 to 40% predicted. His TLC [total lung capacity] was 91% predicted. This would be in keeping with early interstitial disease at that time and indeed clinically and radiographically and by exercise he had disease consistent with early idiopathic pulmonary fibrosis. [19] On April 24, 2002, the worker underwent a CT scan of his chest without contrast. Dr. Tjong opined that the findings were consistent with pulmonary interstitial fibrosis. [20] In an addendum to a discharge report dated April 26, 2002, Dr. Berg advised: This gentleman was unable to have complete pulmonary function testing done, however, his base line spirometry [(measurement of air flow and lung volumes)] once again reveals fairly preserved lung volumes and flow rates. 2 The occupational hygienist cites: Baumgartner KV Occupational and environmental risk factors for idiopathic pulmonary fibrosis: a multicentre case-control study. Collaborating Centers. Am J. Epidemiol. Vol. 152, No. 4.

6 Page: 6 Decision No. 1308/04 In addition he does have emphysematous changes within his lung, on his CT scan related to his chronic smoking, this was not reported on the CT scan by the radiologist, but on further review is noted. Despite his normal spirometry, obviously he has mixed obstructive restrictive disease and severe impairment in his gas transfer related to his fibrotic changes. [21] In a report presented on June 5, 2002, Dr. J.E. Anderson, occupational health physician at OHCOW, provides a comprehensive review of the worker s history and medical reporting. However, in this report, he was not aware of the April 26, 2002 report from Dr. Berg. As of June 2002, according to Dr. Anderson, the worker was capable of very little activity before his oxygen saturation dropped. The worker slept with two pillows on a chair at night. Dr. Anderson noted that the worker suffered from chronic cough with frequent sputum, constant wheezing, constant shortness of breath, bronchitis and persistent hoarseness, difficulty swallowing, frequent indigestion and rectal bleeding or dark stools. Dr. Anderson noted that the worker smoked 20 to 25 cigarettes per day, but stopped in The worker s family members smoked in the home when he was a child. Dr. Anderson summarised the opinions and findings of Drs. Robertson, Defoa, Kivinen, Barton, Stenning, Belanger, Garces, Tjong and Roos. Dr. Anderson cites an article entitled, Idiopathic Pulmonary Fibrosis Challenges for the Future which reportedly suggested that a confident diagnosis of idiopathic pulmonary fibrosis cannot be reliably made on chest radiograph alone. High resolution CT scanning allows early identification of diffuse parenchymal lung disease. Dr. Anderson queried whether the worker s lung condition was correctly diagnosed. He advised that there were challenges to the current medical thinking that idiopathic pulmonary fibrosis is a chronic inflammatory disorder. The challenges suggest that the disease is rather an epithelial (basal cell carcinoma)/fibroblastic (development of connective tissue) disease. He felt that pathogenic mechanisms and sequence of events of aberrant lung parenchymal remodelling required clarification. Dr. Anderson acknowledged CT scan evidence of pulmonary interstitial fibrosis, but emphasised the importance of high resolution CT scanning in order to absolutely confirm the diagnosis. [22] On November 12, 2002, the worker was assessed through a telemedicine conference by Dr. Berg. The worker had requested a lung biopsy. Dr. Berg reported that the worker had developed weakness and difficulty walking 15 to 20 feet. He had developed some peripheral edema (excessive fluids in body tissue) which had been controlled by a diuretic (an agent that increases urine production). At the time of the telemedicine conference the worker remained on continuous oxygen. Dr. Berg advised: This gentleman has progressive functional decline. He is oxygen dependent. He has severe pulmonary fibrosis based on his last pulmonary function testing. Although he has not been restricted, there has been a decline in his FEVs [forced expiratory volume] still his flow rates remain remarkably adequate, but his gas transfer has dropped to 25%. I do not believe confirmation with biopsy is indicated at this time. A transbronchial biopsy is of no yield in diagnosing silicosis. A vat is probably contraindicated given the severity of his disease. [23] In a report dated December 13, 2002, Dr. Berg advised that since his last report, the worker was clinically stable from a pulmonary standpoint, but had been hospitalised a few weeks prior to his report. The worker had developed an underlying high grade transitional cell carcinoma of the bladder which had was found on a urine specimen. He also had intermittent hematuria. A CT scan conducted in November showed extensive bilateral fibrosis, honeycombing and also

7 Page: 7 Decision No. 1308/04 some small mediastinal adenopathy. Dr. Berg felt that this finding was of borderline significance. [24] The November 12, 2002 report from Dr. Berg was sent to Dr. Anderson by the worker s former representative for comment. In an addendum to his June 5, 2002 report, Dr. Anderson advised on March 3, 2003 that the recent information persuaded him that the most probable diagnosis in this case was idiopathic pulmonary fibrosis. He also agreed with Dr. Berg that the CT scan finding of emphysematous changes were probably related to chronic smoking. Dr. Anderson agreed that the worker suffered from a mixed obstructive and restrictive disease and has severe impairment in his gas transfer related to interstitial fibrotic changes. Dr. Anderson offered a new opinion: [The worker] has lung disease of varied etiology, including smoking and industrial exposures. The endpoint clinically has been emphysema, and interstitial pulmonary fibrosis. His industrial exposures, as outlined, in the occupational hygiene report estimates a 46 year history of exposure to the dusty underground mining environment. It is known that pulmonary fibrosis can be caused by inhalation of asbestos, silica, and alpha particles from radon progeny. Research has demonstrated that, it is reasonable to suggest that environmental exposures may contribute to the cause of idiopathic pulmonary fibrosis. It is probable therefore that [the worker s] industrial exposures, have played an inestimable role in the development of his idiopathic pulmonary fibrosis. [25] In 2003, the worker s health progressively declined leading him to several hospital admissions. In November 2003, the worker was admitted into Pine Falls Health Centre for pneumonia, congestive cardiac failure and which was later confirmed to be bladder cancer. [26] On December 15, 2003, the worker died. He was 79 years old. A certificate of death issued by the province of Manitoba listed the cause of death as pneumonia with lung fibrosis (end stage) and bladder cancer as conditions which each played a role in the worker s death. 3 (iii) Testimony of the deceased worker s daughter, LJ [27] LJ testified that she is presently 51 years old and the third oldest of seven siblings. She stated that her father was survived by an 86 year old brother, 83 year old sister and 79 year old twin sister. The worker s mother lived to 92 and had an aunt who lived to 89 despite smoking all of her life. [28] She recalled that since she was a child her father worked in numerous mines in Ontario, Manitoba and the Yukon. She did not recall any lengthy periods of unemployment. It was LJ s recollection that her father stopped working underground in approximately 1985 or 1986 due to health problems. She testified that her father completed the last few years of his employment in the mining industry above ground. After his retirement, her father worked in various jobs because he loved to work. 3 Exhibit #5, page 54.

8 Page: 8 Decision No. 1308/04 [29] LJ remembered that her father developed shortness of breath and a cough when she was about 19 or 20 years old. She stated that she could hear her father approaching because of his cough. She stated that he did not have a smoker s cough. LJ confirmed information in the Case Record that her father s breathing problems progressed over the years and increasingly impaired his physical abilities. Her mother died in 1984 after contracting cancer of the larynx. Her father remarried in His second wife died in August 2003 only a few months before her father passed away. LJ confirmed that no biopsy or autopsy was ever performed on her father. [30] LJ testified that, mentally, her father was well oriented right up to the time of his death. He meticulously kept track of weather conditions and demonstrated an acute memory. [31] With respect to the issue of smoking, LJ testified that her father smoked filtered cigarettes from as early as she could remember, but stopped in 1991 or He smoked in the house and at work. She estimated that he smoked about a half pack to one full pack of cigarettes per day. (iv) The submissions [32] Mr. Aubut submitted that the worker was a pack-sack miner frequently moving from one mine to another in pursuit of better paying opportunities. He submitted that as a miner the worker was exposed to a number of hazardous materials in an era when ventilation systems were notoriously poor. [33] With respect to the issue of a NEL award for silicosis, Mr. Aubut argued that silocosis is silicosis. He submitted that there was no such thing as mild silicosis and that workers diagnosed with this disease should automatically qualify for a NEL award. [34] With respect to the issue of asbestosis, the estate s representative cited an article entitled Mortality Experience of Amosite Asbestos Factory Workers: Dose-Response Relationships 5 to 40 years After Onset of Short-Term Work Exposure published in 1986 in the American Journal of Industrial Medicine. This article described a study of 820 amosite asbestos factory workers whose employment began between 1941 and The worker s were observed from 5 to 40 years after they started their employment and most of the cohort worked in the factory for only days, weeks or months. Using white males of New Jersey as the population control, Standardized Moratlity Ratios (SMRs) of 500 were reported for the cohort for lung cancer and non-infectious pulmonary diseases (including asbestosis). Mr. Aubut noted that the study concluded that the risk of cancer for brief periods of direct exposure increased only after a latent period of 25 years. At page 482 of the report, the authors write: For the men who worked various lengths of time from less than one month to 2-14 years (when the factory was closed), [the findings] show cumulative mortality results at fiveyear intervals to 40 years since the onset of work, respectively, for all causes of death. The study concluded at page 499: using the length of time worked in an amosite asbestos factory as a measure of the direct dosage of asbestos, we found that, in general, the lower the dose, the longer it took for adverse mortality experience to become evident and also the smaller the magnitude of that adverse mortality....

9 Page: 9 Decision No. 1308/04 This has very important implications for the control of cancer. If it is not possible to completely avoid exposure to asbestos (or other carcinogenic agents), at least reducing the exposure might both delay the occurrence of adverse effects and lower the frequency of their occurrence. [35] The estate s representative emphasised the evidence from OHCOW and in particular the occupational hygienist s opinion at page 10 of her April 22, 2002 report that environmental exposures may cause idiopathic pulmonary fibrosis. [36] In post-hearing written submissions under cover letter dated February 4, 2005, Mr. Aubut emphasised the worker s employment history in the mining industry during a period when there was a lack of ventilation in virtually all the mines. The estate s representative argued that the worker s exposure to toxins in the mines was a dominant factor in the development of the worker s subsequent illnesses. Mr. Aubut noted the chest x-ray dated January 4, 2001 which concluded, Diffuse chronic interstitial lung disease which is consistent with a history of pneumoconiosis probably silicosis. He wrote: (v) It has been established by the WSIB that [the worker] had silicosis but not to the extent of being a permanent impairment. How can this be. Once you contact [sic] silicosis, it is incurable and is a permanent disease. Therefore the Tribunal is bound to allow permanent impairment benefits regarding this claim. Findings and conclusions [37] We have carefully considered all of the available evidence before us, testimony of the worker s daughter and submissions of Mr. Aubut. (a) Did the worker have entitlement to a NEL assessment for silicosis? [38] In this case, there is no dispute that the worker s employment history in the mines for approximately 40 years caused the development of silicosis. The Board granted him entitlement for the disease, but denied him entitlement to a NEL assessment for that condition. [39] Section 42 of the WCA governs entitlement for a NEL award. It reads, in part: 42. (1) A worker who suffers permanent impairment as a result of an injury is entitled to receive compensation for non-economic loss in addition to any other benefit receivable under this Act.... (21) A worker may apply to the Board for a redetermination of the degree of the worker s impairment, (a) if the Board has determined that the worker has a permanent impairment; and (b) if the worker has suffered a significant deterioration of condition that was not anticipated at the time of the most recent medical assessment under this section. [40] The Board identified Operational Policy Manual Document # , Non-Economic Loss (NEL) Assessing Permanent Impairment as an applicable policy in this case. It states at page 1 of 4:

10 Page: 10 Decision No. 1308/04 Permanent Impairment Permanent impairment means any permanent physical or functional abnormality or loss (including disfigurement) which results from an injury, and any psychological damage arising from the abnormality or loss. A worker s degree of permanent impairment is expressed as a percentage of total permanent impairment of the whole person. [41] Section 42 of the WCA states that a worker who suffers permanent impairment as a result of an injury is entitled to receive compensation for non-economic loss. Board policy defines permanent impairment as any permanent physical or functional abnormality or loss (our emphasis). A worker may have a permanent physical abnormality or loss without a functional abnormality or loss. The absence of a functional abnormality or loss does not preclude entitlement to a NEL assessment under Board policy. [42] The worker was diagnosed with silicosis in 1996 at age 72. Silicosis is defined in Taber s Cyclopedic Medical Dictionary, 19 th edition, as: A form of pneumonoconiosis resulting from inhalation of silica (quartz) dust, characterised by the formation of small discrete nodules. In advanced cases, a dense fibrosis and emphysema with impairment of respiratory function may develop. [43] Silicosis is a permanent condition. The worker met the legislative and policy requirements for entitlement to a NEL assessment. However, the preponderance of evidence does not support a finding that the worker s silicosis had developed into a dense fibrosis resulting in a measurable impairment of his respiratory function. We note the opinion of Dr. Roos which was that the worker had silicosis, but no advanced progressive massive fibrosis. Dr. Kivinen advised that he agreed with Dr. Roos and noted that the worker had generalized interstitial disease with bibasilar crackles and a markedly reduced diffusing capacity. However, lung volumes were still relatively well preserved. He advised that silicosis generally does not cause crackles, the markedly reduced diffusing capacity, and tends to be more of an upper lobe disease. We note the January 4, 2001 chest x-ray which found no evidence of massive pulmonary fibrosis. [44] We acknowledge Dr. Anderson s opinion that it was probable that the worker s industrial exposures have played an inestimable role in the development of his idiopathic pulmonary fibrosis. We find it more likely, however, that the worker s history of smoking played a significant role in the development of his idiopathic pulmonary fibrosis. [45] Thus, while the worker met the criteria for a NEL assessment for silicosis, the evidence does not indicate that the silicosis produced any measurable impairment that would result in an award. The worker s entitlement to a NEL award is zero percent. (b) Did the worker have entitlement for asbestosis? [46] In his decision of February 22, 2000, the Appeals Resolution Officer denied the worker entitlement for asbestosis because [a]ccording to policy there must be evidence of two years of exposure to asbestos dust in order for the condition to be considered work-related. With respect, this interpretation of the legislation and Board policy is incorrect. Under section 134(9) of the WCA and Operational Policy Manual Document No , Industrial

11 Page: 11 Decision No. 1308/04 Diseases Asbestosis, there is a presumption that a worker s asbestosis is work-related when 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 fibers for at least two years prior to the date of diagnosis of asbestosis. The presumption does not apply to a worker who was employed in any of the above-listed industries involving the generation of airborne asbestos fibers for less than two years prior to the date of diagnosis of asbestosis. Cases that do not meet the presumption requirements are adjudicated on their merits. [47] The uncontested evidence in this case is that the worker had approximately four months exposure to asbestos in the 1950s. Therefore, the presumption clause in subsection 134(9) and Board policy does not apply. Accordingly, we will consider the real merits and justice of this worker s case. [48] The preponderance of evidence does not support the conclusion that the worker suffered from asbestosis. Dr. Robertson noted that the worker demonstrated features of asbestosis (depressed diffusion capacity). However, Dr. Roos felt that the worker s diffuse interstitial fibrosis resulted in the low diffusing capacity. He advised that since the appearance was not suggestive in its distribution pattern of asbestosis and since there were no pleural markers of asbestos exposure, the most probable explanation for the second, diffuse interstitial pattern was a mild form of cryptogenic fibrosing alveolitis, a non-occupational lung disease. Dr. Kivinen agreed. He advised that the only entity that one could confuse with interstitial pulmonary fibrosis would be asbestosis. However, he noted that almost invariably asbestos related lung disease has a significant pleural component which this worker did not demonstrate. [49] Mr. Aubut emphasised an article entitled, Mortality Experience of Amosite Asbestos Factory Workers: Dose-Response Relationships 5 to 40 years After Onset of Short-Term Work Exposure published in 1986 in the American Journal of Industrial Medicine. The authors found that the lower the dose of asbestos, the longer it took for adverse mortality experience to become evident and also the smaller the magnitude of that adverse mortality. The evidence in this case, however, is that the worker was not diagnosed with asbestosis. Therefore, he does not have entitlement for that condition. THE DECISION [50] The deceased worker s estate s appeal is allowed, in part. The worker s estate is entitled to a NEL assessment for the worker s silicosis. However, there was no pulmonary impairment due to his silicosis. The NEL award is zero percent. The worker did not have entitlement for asbestosis. DATED: June 27, 2005 SIGNED: S. Ryan, G.V. Stewart, J.A. Crocker