WORKPLACE SAFETY AND INSURANCE APPEALS TRIBUNAL DECISION NO. 2127/06

Transcription

1 WORKPLACE SAFETY AND INSURANCE APPEALS TRIBUNAL DECISION NO. 2127/06 BEFORE: M. Kenny : Vice-Chair C. J. Robb : Member Representative of Employers J. A. Crocker : Member Representative of Workers HEARING: October 19, 2006 at Kitchener Oral Post-hearing activity completed on October 31, 2007 DATE OF DECISION: February 26, 2008 NEUTRAL CITATION: 2008 ONWSIAT 588 DECISION(S) UNDER APPEAL: WSIB ARO decision dated September 14, 2004 APPEARANCES: For the worker: For the employer: Interpreter: D. Covelli, Consultant Did not participate None 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. 2127/06 REASONS (i) Introduction [1] The worker is 69 years old. When he was a teenager, he was exposed to asbestos when he worked in a foundry for one or two summers. It was his job to take asbestos pipes from a rack and feed them into an automatic saw that cut the pipes both horizontally and lengthwise. There was a considerable amount of dust generated as the saw cut the asbestos pipes. [2] In 1996, the worker had surgery to examine his left lung. Among other findings, the surgeon reported that the worker had pleural plaques. [3] The Board has accepted that the worker has pleural plaques that resulted from the exposure the worker had to asbestos when he worked in the foundry for three to six months in the mid-1950s. [4] The Board found, however, that the worker does not suffer from asbestosis. [5] The Board also found that the worker s work-related pleural plaques do not interfere with the worker s pulmonary function or cause any impairment, so the worker is not entitled to be paid benefits for a permanent respiratory impairment. [6] The worker appealed the Board s decision. (ii) The issues [7] The issues to be decided in this appeal are: 1. Does the worker suffer from asbestosis? 2. If not, does the worker have a permanent impairment as a result of pleural plaques (that the Board has found to be work-related)? Does he have a permanent impairment from any other condition that results from his workplace asbestos exposure? ISSUE 1: Does the worker suffer from asbestosis? (i) The Act and Board policy [8] Since May 1992, asbestosis has been a Schedule 4 occupational disease. 1 Thus, if a worker contracts asbestosis, and the worker was employed in a process described in Schedule 4, there is an irrebuttable presumption that the asbestosis was due to the nature of the worker s employment. 2 1 Ontario Regulation 175/98 made under the Workplace Safety and Insurance Act, 1997 (the WSIA ). Formerly R.R.O. 1990, Reg Section 15(4) of the WSIA; section 134(10) of the pre-1997 Act.

3 Page: 2 Decision No. 2127/06 [9] Board Operational Policy Manual ( OPM ) Document No (now Document No ) describes when the Board allows claims for asbestosis. These OPM documents will be referred to in this decision as the Board s Asbestosis policies. [10] Claims for asbestosis are allowed when it is established that the worker has a diagnosis of asbestosis, and the worker has worked in a process described in Schedule 4. The Board s Asbestosis policies state that legislative requirements (i.e., sections 134(12) and 134(16) of the pre-1997 Act and sections 15(5) and 15(6) of the WSIAT) for 2 years of asbestos dust exposure in Ontario apply to the Asbestosis policies. [11] The Board s Asbestosis policies state the following with respect to establishing the diagnosis of asbestosis: Diagnosis: To establish asbestosis, the Board recognizes histopathological evidence of lung fibrosis due to asbestos and the current diagnostic criteria established by the American Thoracic Society (ATS) 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: (ii) 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. Medical evidence about the diagnosis of asbestosis [12] After the Tribunal hearing of the worker s appeal, the Hearing Panel prepared a Summary of Issues and Evidence, and it asked for a medical Assessor s opinion about a number of questions. The Tribunal Counsel Office referred the Panel s questions to Dr. Dildar Ahmad. [13] Dr. Ahmad is a specialist in internal medicine with a subspecialty in respirology. He has held a number of academic and hospital positions, including positions as a Professor of Medicine at the University of Western Ontario, and positions at the University Hospital as the Director of the Pulmonary Function Laboratory, the Medical Director of the Heart-Lung Transplant Program, Director of the Respiratory Observation Unit, and Physician in the Chest Unit. He has published extensively in the field of respirology. [14] The Hearing Panel asked Dr. Ahmad questions about the diagnosis of asbestosis. The Panel s questions and Dr. Ahmad s response are more fully set out in Appendix 1 of this

4 Page: 3 Decision No. 2127/06 decision. We note, however, that Dr. Ahmad s opinion distinguishes pleural plaques from asbestosis, and it includes essential criteria for a diagnosis of asbestosis. It states: The presence of pleural plaques and a history of asbestos exposure alone are not sufficient to diagnose asbestosis. Pleural plaques are strongly associated with a history of asbestos exposure, both occupational and non-occupational. They are the most common asbestos induced condition and occur after a much lower dose of asbestos exposure than is necessary to cause asbestosis Asbestosis is fibrosis of lung parenchyma caused by the inhalation of asbestos fibers Asbestosis specifically refers to interstitial pulmonary fibrosis caused by deposition of the asbestos fibers in the lung parenchyma. It does not refer to the visceral pleural fibrosis, parietal pleural lesions plaques subpleural extension of fibrosis or of the membranous bronchioles [15] Dr. Ahmad described four essential criteria for a diagnosis of asbestosis. These include a suitable history of exposure to asbestos (i.e., exposure of a suitable duration, intensity, and time interval between exposure and detectable disease), certain radiographic changes, a characteristic pattern of lung impairment, and the presence of certain clinical features (i.e.,late inspiratory crackles). (iii) Medical opinions about whether this worker has asbestosis [16] In this case, a physiatrist who was treating the worker for chronic pain and a family doctor reported that the worker suffered from asbestosis. Also, a radiologist who reported on findings of a 1998 CT scan reported that there was one area of parenchymal density that was of questionable significance but he felt it could represent the very earliest, mild changes in asbestosis. [17] On the other hand, specialists in respirology have expressed the opinion that the worker does not have asbestosis. [18] In 2003, Board Respirology Consultant Dr. David Muir reviewed x-rays from 1997 as well as a 1999 CT scan. He wrote: The chest x-rays [from 4 dates in 1997] are of good quality. They show normal lung fields and pleural plaques cannot be seen on the films. There is no evidence of asbestosis of the lung itself. The CT scan of 08/07/99 shows small bilateral pleural plaques, and confirms that there is no evidence of pulmonary asbestosis [19] Likewise, a specialist in respirology whom the worker consulted in and after 2003 (Dr. T. Carlton) wrote: [the worker] does not have evidence of interstitial lung disease i.e. asbestosis [20] In his report, Dr. Ahmad addressed the question of whether the worker has asbestosis as follows: In reviewing the medical history documented in the case record, and examination of the recent HRCT scan (2006) of this worker, I am of the opinion that [the worker] does not have asbestosis. He does not meet the diagnostic criteria of the board, nor does he meet the current clinical diagnostic criteria established by the American Thoracic Society for Asbestosis.

5 Page: 4 Decision No. 2127/06 [21] Thus, the doctors who have a specialty in respirology who have reviewed the radiological and other evidence have concluded that the worker does not have asbestosis. (iv) The submissions [22] The worker referred to opinions from a researcher in the field of asbestos-related diseases as well as a hospital publication that indicated it is very difficult to detect asbestos based mesothelioma or lung cancers in the early stages. He noted that Dr. Ahmad based his opinion that there was a lack of evidence of asbestosis on evidence presented in x-ray and CT scans, and on current diagnostic criteria. He argued, however, that given the difficulty of detecting asbestos based mesothelioma and lung cancers in the early stages, it is not possible to exclude the possibility that he has asbestosis. (v) The findings [23] We find that the worker does not suffer from asbestosis. [24] The opinions of the specialists in respirology (as well as the Board s Asbestosis policy) indicate that asbestosis is a medical diagnosis that cannot be established on the basis of asbestos exposure and a description of pulmonary symptoms alone. As indicated by Dr. Ahmad, asbestosis is fibrosis of lung parenchyma caused by the inhalation of asbestos. There are specific criteria that must be met before a diagnosis of asbestosis can be established. These criteria require not only a suitable history of exposure to asbestos, but also certain radiographic changes, a characteristic pattern of lung impairment and certain findings on examination. [25] The respirologists who examined the evidence in this case, including radiographic evidence (and the 1998 CT scan) found no evidence of asbestosis. They concluded that the diagnostic criteria for establishing asbestosis were not met. [26] We accept the opinions of Drs. Muir, Carlton, and Ahmad that the worker does not have asbestosis. In our view, these doctors are well qualified to give opinions on what is required to establish a diagnosis of asbestosis, as well as to give opinions about whether those criteria are met in a particular case. The respirologists all concluded that the worker does not have asbestosis. There is no differing opinion from a doctor with comparable qualifications in respirology. [27] We accept their opinion and find that the worker does not suffer from asbestosis. ISSUE 2: Does the worker have a permanent impairment from pleural plaques or any other asbestos-related condition? (i) The Act and Board policy [28] In 1996, the worker was found to have pleural plaques. It is not in dispute that the pleural plaques, diagnosed in 1996, were caused by workplace exposure. Thus, the pre-1997 Act applies

6 Page: 5 Decision No. 2127/06 in deciding his appeal, except to the extent that the pre-1997 Act was amended by the Workplace Safety and Insurance Act, 1997 (the WSIA ). 3 [29] In this appeal, the Board found that the worker s pleural plaques were caused by the workplace but they did not result in a permanent impairment. Thus, the Board decided the worker was not entitled to benefits for a permanent impairment of his ventilatory capacity. [30] Section 1(1) of the pre-1997 Act defines impairment and permanent impairment as follows: 1. (1) In this Act, impairment, in relation to an injured worker, means any physical or functional abnormality or loss including disfigurement which results from an injury and any psychological damage arising from the abnormality or loss; permanent impairment, in relation to an injured worker, means impairment that continues to exist after maximum medical rehabilitation of the worker has been achieved; [31] While impairment has a very broad definition, permanent impairment includes the requirement of an impairment continuing after maximum medical rehabilitation has been achieved. The degree of permanent impairment is rated in accordance with the American Medical Association ( AMA ) Guides to the Evaluation of Permanent Impairment (3 rd edition revised). 4 [32] Chapter 5 of the AMA Guides describes how the evaluation of impairment due to respiratory disease will be conducted. The AMA Guides do not provide a rating for respiratory impairment simply because pleural plaques are present. Instead, the Guides assess impairment. The Guides rate impairment from respiratory disease by evaluating the history and severity of symptoms (such as shortness of breath, cough and sputum production, wheezing), physical examination (breathing pattern, cyanosis and clubbing, and lung sounds), and physiologic tests of pulmonary function. [33] Because the pre-1997 Act and the WSIA compensate for the permanent impairment a worker suffers as a result of an injury, it is necessary to decide whether the worker suffered a permanent impairment from the pleural plaques (or any other respiratory condition that resulted from his asbestos exposure). Any respiratory impairment that is not the result of his compensable injury is not compensable. (ii) The worker s evidence about impairment [34] The worker described what he believes to be the result of his asbestos exposure. He testified that he feels that the shortness of breath and the weakness he experiences, as well as deficiencies shown in his pulmonary function tests, result from the asbestos exposure. He also 3 Section 102 of the WSIA. 4 Section 18 of Ontario Regulation 175/98; Section 15 of the R.R.O. 1990, Reg. 1102

7 Page: 6 Decision No. 2127/06 noted that he has had chest pain when walking (a burning sensation that travels to his arms and then up to his teeth) and he wonders whether this results from a lack of oxygen in his lungs (due to the effects of asbestos exposure). (iii) The worker s medical history [35] The worker tried smoking cigarettes when he was young, but it was not until he was in his late teens that he smoked heavily. He smoked about 1 to 1½ packs per day for about four years. He stopped smoking when he was about 20 years old (i.e., in about 1958). [36] There was evidence that the worker, even in high school, had positive skin tests for TB (but any follow-up x-rays were negative), and that he was treated in the 1980s for cough and chest problems that appear to have been attributed to a viral infection at that time. There was also evidence about conditions that the worker developed when he worked in Africa in the 1970s, but the worker testified that he did not have ongoing symptoms from these conditions. [37] By the end of the 1980s, the worker had developed what he described as asthma problems and he may have had pleurisy in [38] The worker described the problems he associated with asthma. He testified that in the winter, when he would go from a heated situation into the cold, his lungs seemed to fill up, so his doctor suggested that he use puffers. The worker recalled first trying an inhaler in about 1991 but he testified that he only used puffers for a few years. [39] The worker testified that he does not really feel that he has a problem with asthma. He testified that he did not continue to use puffers and he felt that they really did not do much good. [40] There is, however, evidence from 1997 and 1998 that the worker was describing problems with asthma, and his doctors diagnosed and prescribed medication for asthma at that time. However, the 2006 report from Dr. Carlton suggests that the worker was not experiencing problems with asthma when Dr. Carlton saw the worker in (iv) The worker s 1996 surgery (a) The worker s condition before the surgery [41] When he was first interviewed by the Board, the worker said that his lung disability developed when he was working in a northern community (from about 1991 to1996). [42] In a letter he wrote to the Board, the worker described problems he developed before his 1996 surgery as follows: Beginning December 1993 I began to experience a greater sensitivity to lung problems, which evidenced itself in frequent colds, flu which became very resistant to treatment, etc proved to be worse, and in December 1995 I became very sick with flu like symptoms. This carried on in 1996 until around the middle of April. At that time I had been treated for pneumonia from January through April. I lost considerable work time as a result. I was referred to a specialist in Winnipeg, Manitoba. His name was Dr. Horan As a result of his findings, I underwent exploratory surgery on May 16, 1996.

8 Page: 7 Decision No. 2127/06 [43] The worker s description of his pre-surgery problems is supported by a report from a family doctor (Dr. Kelly) who saw the worker in The doctor reported that he saw the worker in June 1994 with a three-week history of malaise, rigors and chills. At that time, this was felt to be a viral illness. The same doctor reported that he saw the worker for chest pain that seemed to be either activity or anxiety related. The doctor referred the worker to a cardiologist. The worker had a normal cardiac stress test. Dr. Kelly reported that, after this, the worker was found to have a right sided infiltrate and that he was seen again in 1995 and 1996 for symptoms that were both respiratory and general fatigue. [44] The worker testified that he was very sick in December 1995 that he had a high fever and saw a doctor in Ottawa who said he had a bad cold/flu and sent him home. The worker testified that the fever cleared up somewhat, but his pneumonia would not go away. He also recalled being very tired. [45] In April 1996, family doctor, Dr. Kelly, referred the worker to Dr. Taraska (a specialist in pulmonary disease in Winnipeg). Dr. Taraska asked Dr. Horan (a thoracic surgeon in Winnipeg) to see the worker. (b) May 1996 surgery [46] In 1996, thoracic surgeon Dr. Horan recommended that the worker have a video assisted thoracoscopic biopsy of lung and or pleura because the worker had persistent [pleural] effusion and opacification. His pre-operative diagnosis was pleural effusion, left lung, not yet diagnosed. [47] The worker described his understanding of the May 1996 surgery. He testified that he understood that his left lung was fused to his body that the cavity was covered with a white sticky substance and that, at the time of the 1996 surgery, the surgeon had to hack away at the lung quite a bit to free it. He also understood that the surgeon removed a bite sized tumour on the underside of the lung and that this was benign but it resulted from asbestos exposure. [48] The pathology report about the biopsies provided the following diagnosis: Diagnosis: Biopsy, left pleura - adhesions - pleural plaques. [49] After performing the exploratory procedure, Dr. Horan concluded: The only significant lesions were those of pleural plaques which appeared benign. The etiology of his fibrinous adhesions and pleural peel are uncertain. [50] Dr. Ahmed reviewed the various reports on file, including Dr. Horan s operative report. Dr. Ahmed described the reason for the procedure, the nature of the procedure, and the findings at the time of surgery as follows: In April of 1996, the worker was referred to a respirologist in Winnipeg by his family physician. The worker had recurrent episodes of pneumonia. His chest x-ray was abnormal and failed to resolve after the last episode. It appears that [the worker] had what is known as unresolved pneumonia with a left pleural effusion.

9 Page: 8 Decision No. 2127/06 As the diagnosis in this case was uncertain, he was referred to Dr. Horan, a thoracic surgeon for an opinion. Dr. Horan recommended that the worker undergo a thoracoscopic examination with a lung biopsy of the lesion to obtain the diagnosis, usually a standard practice in unresolved cases of pneumonia. The procedure was carried out using a thorascope; three small incisions were made in the chest wall. Trocars were inserted through these incisions, to introduce a scope for visualization and the other two were used to introduce working instruments. Under direct vision, Dr. Horan carried out decortication of the left lower lobe, mobilized the lung by removing adhesions on the upper lobe. He removed a pleural peel and noticed pleural plaques. He took multiple biopsies for diagnosis The biopsies showed pleural plaques and pleural adhesions on pathology. The worker refers to a white sticky substance that Dr. Horan saw at surgery. This more than likely was a pleural plaque and or pleural adhesions. The procedure according to the case record was performed for the diagnosis and management of the chest x-ray abnormality that had failed to clear following a respiratory tract infection. The abnormality was not caused by pleural plaques, but was as a result of an inflammatory process. [51] Thus, according to the surgeon and Dr. Ahmad, the exploratory surgery done in 1996 was performed after the worker had recurrent episodes of pneumonia/respiratory tract infections. It was performed to help diagnose and manage the worker s condition after his last episode of pneumonia because he had a chest x-ray abnormality (from a left pleural effusion) that failed to resolve. According to Dr. Ahmad, that chest x-ray abnormality was not caused by pleural plaques. Instead, it was the result of an inflammatory process. According to Dr. Muir, a postpneumonia effusion of this type is common. [52] At surgery, a surgeon removed adhesions to mobilize the lung and he also removed a pleural peel. The surgeon concluded that the cause of the adhesions and peel were uncertain. However, in his report, Dr. Ahmad described how para-pneumonic effusions are complications of pneumonia that are characterized by organized adherent fibrotic peel encapsulating the lung and Dr. Ahmad noted that the surgeon found a peel at surgery. When the surgeon removed the pleural peel, he noticed pleural plaques. (c) After the surgery [53] The worker testified that his health deteriorated after the surgery. He has not worked since He testified that, since the surgery, he has had bouts of pneumonia (at least one of which was very serious). He has also experienced shortness of breath, general weakness, and lack of energy. [54] In addition to consulting a number of doctors about his condition, the worker had pulmonary function tests ( PFTs ). [55] After the surgery in 1996, respirologist Dr. Lundy reported that he could see no pleural plaques on chest x-ray and the worker s spirometry was suggestive of a mild non-obstructive (restrictive) ventilatory defect. Dr. Lundy wrote: [The worker] had a prolonged respiratory tract infection or a series of them this past winter and early spring. How these related to his pleural disease is uncertain. What appears clear is that multiple pleural biopsies show no evidence of mesothelioma and showed no granulomas to suggest an active tuberculous pleuritis

10 Page: 9 Decision No. 2127/06 He has mild restrictive lung disease which may be related to some restriction of his left lung from his chronic pleural disease [56] Thus, although Dr. Lundy reported that the worker s mild restrictive lung disease may relate to the worker s chronic pleural disease, his report does not describe the nature of that pleural disease. It does not directly relate it to pleural plaques or any other asbestosrelated disease, and it specifically states that there is no evidence of mesothelioma. [57] In 1998, Dr. Ted Haines (a doctor with the Occupational Health Clinics for Ontario Workers Inc. ( OHCOW )) reviewed the worker s history including PFTs and the worker s statement that the worker had concern about asthma that bothered him to a mild degree in the winter only, and that responded moderately well to bronchodilator. Dr. Haines referred the worker to Dr. David Muir, a doctor whom Dr. Haines described as a respirologist with a special interest and experience in asbestos related disease. [58] Dr. Muir examined the worker in He noted that the worker s lungs were clear on auscultation. The breath sounds were normal In particular there were no basal crepitations of the type associated with asbestos exposure. After reviewing 1997 chest x-rays and concluding that these show minimal pleural plaques but with no evidence of significant pulmonary fibrosis as well as spirometry results, Dr. Muir concluded: I am able to reassure [the worker] that he has no evidence of lung fibrosis or of associated incapacity. These small areas of pleural thickening will not be associated with symptoms His spirometry is below the predicted normal and this cannot be accounted for by any of the asbestos related scarring. Although I did not have the opportunity to measure lung function after a bronchodilator it may be that he has ongoing mild asthma [59] Thus, Dr. Muir concluded that there was evidence of minimal pleural plaques but that these would not account for the below normal PFT test results. [60] In January 2003, Dr. Muir was a Respirology Consultant for the Board. He provided the Board with the following opinion about the worker s condition: The chest x-rays [from four dates in 1997] are of good quality. They show normal lung fields and pleural plaques cannot be seen on the films The CT scan of 08/07/99 shows small bilateral pleural plaques Plaques of this size do not interfere with pulmonary function and do not cause any impairment. The claimant has had asthma which is not of occupational origin. This is the cause of his impaired ventilatory capacity on January 8, 1999 It is not related to the pleural plaques which, themselves, are the result of previous asbestos exposure. The pleural effusion on the left side of the chest in April 1996 appears to have followed an episode of pneumonia in December 1995, and between January 1996 and April A post-pneumonia effusion of this type is common. Assessment: Pleural plaques only. No associated P.I. [permanent impairment]. [61] Thus, Dr. Muir concluded that the size of the worker s pleural plaques was such that they did not interfere with pulmonary function and did not cause any impairment. In his opinion, the worker s impaired ventilatory capacity resulted from (non-occupational) asthma.

11 Page: 10 Decision No. 2127/06 [62] In May 2003, OHCOW Dr. Reinhartz wrote the worker a letter in which he stated that he felt it could be argued that the worker s pleural disease was most likely secondary to asbestos, but Dr. Reinhartz thought it would be of benefit for the worker to have a full PFT at a local hospital. The worker subsequently had a PFT as well as a CT scan at a hospital. The PFT report mild-moderate airway hyperresponsiveness. Baseline mild non-obstructive defect on spiro[metry]. In asthma range. One test report also suggested that the worker s reduced vital capacity may be due to previous resection. The 2003 CT scan had reported small emphysematous bullae, early plaque like pleural based irregularities, and some prominent lymph nodes, but no obvious interstitial disease. After this testing was done, Dr. Reinhartz wrote: I had a look at your most recent CT scan which confirms the presence of pleural plaque bilaterally. There is no evidence of asbestos. You also have abnormal breathing, which may be due to your diffuse pleural disease a well. [63] Dr. Reinhartz filed a report with the Board for asbestos related pleural disease with impairment. [64] However, with respect to the findings on the worker s CT scans (including 2005 and 2006 CT scans), Dr. Ahmad found no evidence of asbestos-related pleural fibrosis. He wrote: [The worker] does not have diffuse pleural thickening on the current HRCT scans, and on previous CT scan reports there is no mention of diffuse pleural thickening or pleural fibrosis. If any of these abnormalities were present, the radiologist would have reported this finding since it is an important finding when pleural plaques are noted on CT scans. The current CT scan of the chest does not show any evidence of asbestos-related pleural fibrosis that could lead to pulmonary disability [65] In 2006, respirologist Dr. Carlton provided a report about the worker s history and tests performed in Dr. Carlton noted that the worker had a history of a restrictive pulmonary impairment and that he had, in the past, demonstrated airway hyperreactivity consistent with asthma. However, Dr. Carlton reported that the 2006 test for asthma was now negative. Dr. Carlton also noted that the worker was a former smoker but the amount of smoking that he has would not be consistent with the development of significant pulmonary disease. Dr. Carlton noted that a stage I exercise test demonstrated that the worker did have evidence of mild reduction in exercise capacity. After reviewing the worker s history and 2006 tests, Dr. Carlton wrote: This man does not have any other medical conditions i.e. significant muscle weakness, interstitial lung disease or morbid obesity to explain the reduction in his vital capacity. It is, therefore, likely due to his pleural disease. It is therefore likely that his pleural plaques are the cause of his mild restrictive pulmonary process [66] However, when Dr. Ahmad re-analyzed the results of the 2006 tests to which Dr. Carlton referred, Dr. Ahmad concluded that they did not show mild excess ventilation (as was reported) and that there were non-respiratory explanations for findings such as the mild reduction in the worker s exercise testing (i.e., deconditioning and coronary artery disease).

12 Page: 11 Decision No. 2127/06 [67] Dr. Carlton s opinion, and the tests to which he referred, were provided to Dr. Ahmad (along with all the previously-filed written evidence, as well as a description of the worker s testimony provided in the Hearing Panel s Summary of Issues and Evidence). (v) Dr. Ahmad s opinion [68] The Hearing Panel s questions to Dr. Ahmad, and his response to those questions, included the following: Question: Is it likely that the worker s asbestos-related pleural plaques contributed to the condition for which the 1996 surgery was required? Why/why not? Would the surgery itself result in permanent impairment? If so, what? Dr. Ahmad s response: The surgery was performed for diagnostic purposes, the worker had an infiltrate left lung and a left pleural effusion noted on the chest x-ray that did not resolve and the diagnosis was unclear. Asbestos related pleural effusions are a relatively early manifestation of asbestos-related pleural disease and can occur within 10 years of exposure. They are typically unilateral, can be bilateral, small and may be asymptomatic or associated with pain, mild fever, and shortness of breath. They usually resolve totally spontaneously or there may be blunting of costophrenic angle on a standard chest x-ray. The pleural plaques in this worker are not responsible for pleural effusion and lung infiltrate on the chest x-ray of The pleural effusion occurred 40 years following exposure in this case; hence it was not due to asbestos exposure. The surgery was not a formal thoractomy, but a minimally invasive thorascopic surgery. It in itself should not cause permanent impairment as it did not produce pleural fibrosis nor was there any resection of lung tissue. With this type of surgery, one is disabled for a few weeks rather than years. Upon reviewing the case records, it appears that the worker had a para-pneumonic effusion; para-pneumonic effusions are complications of pneumonia. According to various sources, they occur in 20-57% of cases of pneumonia. They are characterized by organized adherent fibrotic peel encapsulating the lung. Dr. Horan found a peel at surgery and he freed the left lower lobe. The surgeon in the discharge summary mentioned that this worker could have had tuberculous pleuritis in the past, which may have caused the problem. This lesion was not due to tuberculous pleuritis since no granulomata were seen in the pleural adhesions by the pathologist, which is a hallmark of tuberculous pleuritis. The current CT scan of the chest does not show any evidence of asbestos-related pleural fibrosis that could lead to pulmonary disability Question: Would the pleural plaques that the worker has cause any respiratory impairment? Dr. Ahmad s answer: Pleural plaques are distinctive, smooth, white raised irregular lesions found on the parietal pleura (the pleura that lines the chest wall) and rarely on the visceral pleura (lung surface). Pleural plaques are the most frequent and often the only manifestation of asbestos exposure. They have been labelled as the visiting card of asbestos exposure. They typically develop years after exposure and have no impact on lung function at rest or exertion. Usually, pleural plaques are an incidental finding on a chest x-ray, whether this is performed for routine employment health screening or some other purpose. In an unusual case where the plaques are very extensive and fuse to form a cuirass like structure or where there are extensive adhesions, they may cause shortness of breath on exertion. Large cohort studies have shown lung function reduction with pleural plaques can occur averaging about 5-10% in Forced Vital Capacity (FVC) and other static lung volume TLC, FRC and RV are not affected nor is the diffusing capacity (DLCO). This decrease in FVC is in the absence of radiologically interstitial fibrosis. Dr. Muir reviewed the

13 Page: 12 Decision No. 2127/06 chest x-rays from January 1997 to October 1997 and these films showed pleural plaques. The CT scan in July 1998 showed no evidence of fibrosis; very thin plaques were reported on this examination. [69] In answer to the Hearing Panel s question about whether the worker has any other pulmonary disease, Dr. Ahmad reviewed the worker s history from the time asthma was diagnosed in 1991 until 2003 when the worker had a positive methacholine challenge test. He concluded that the evidence was consistent with the worker having mild asthma. Dr. Ahmad noted that the repeat methacholine challenge test performed by Dr. Carlton in 2006 was negative, and he explained why a normal test does not rule out asthma. [70] Dr. Ahmad also observed that both the 2003 and the 2006 CT scans reported findings of emphysematous lesions, and he noted that the worker is a reformed smoker. Dr. Ahmad concluded that, other than pleural plaques, there was no evidence that the worker has any other asbestos induced lung disease. He noted that the worker had suggested that his symptoms could be due to pleural fibrosis, but Dr. Ahmad concluded that there is no evidence of this, or of asbestosis on his current HRCT [high resolution CT scan]. [71] After reviewing the worker s history and tests results in detail, Dr. Ahmad summarized his opinion as follows: This worker has asbestos induced pleural plaques. There is no evidence of any other asbestos induced lung disease. He has a history of mild asthma that is not occupationally induced nor are the emphysematous lesions seen on the HRCT scans of 2005 and 2006 (vi) The submissions [72] At the Tribunal hearing, the worker s representative argued that the evidence establishes the worker has a functional abnormality and there is sufficient evidence to find that it resulted from the worker s exposure to asbestos. After receiving Dr. Ahmad s opinion, the worker s representative argued that Dr. Ahmad did confirm that the worker has a respiratory impairment, and his opinion did not exclude the possibility that the worker s pleural plaques contributed to that respiratory impairment. [73] The worker also provided extensive submissions after he received Dr. Ahmad s opinion. He noted Dr. Ahmed s opinion about the exposure history required for the diagnosis of asbestosis, and he argued that this was inconsistent with opinions expressed by other professors about how even minimal levels of exposure to asbestos can lead to disease (i.e., to mesothelioma). He also reviewed the information about asthma and heart disease and argued that neither of these conditions are the source of his problem (and he offered to provide newly acquired medical information about his cardiac condition). With respect to the 1996 surgery, the worker argued that it is more likely that the asbestos caused his infection/pneumonia. He also noted the contrast between Dr. Ahmad s statement that a pleural effusion from asbestos exposure would not occur 40 years after the exposure, whereas the latency period for asbestosis is often 20 years or more after exposure. The worker argued that, given opinions from Drs. Lundy, Reinhartz, and Carleton, as well as the general difficulty of detecting certain lung diseases in the early stages, his claim should be given the benefit of doubt and granted by the Tribunal.

14 Page: 13 Decision No. 2127/06 (vii) The findings [74] The worker sincerely believes that his current symptoms result from workplace exposure to asbestos, and he asks the Hearing Panel to consider the possibility of such a relationship in view of general information about the harmfulness of asbestos and the difficulty of detecting some asbestos-related diseases (such as mesothelioma and lung cancer) in the early stages, as well as the absence of alternative explanations for his condition. However, although the presence of pleural plaques does indicate that he has had exposure to asbestos, the worker does not have asbestosis, or mesothelioma or lung cancer. And there was no evidence to suggest that pleural plaques cause these other diseases. [75] We find that the worker does not have a permanent impairment as a result of pleural plaques or any other condition related to his workplace exposure to asbestos. [76] In coming to this conclusion, we accept Dr. Ahmad s opinion that the condition that led to the 1996 exploratory surgery was not caused by pleural plaques. That condition was a left pleural effusion that likely resulted from an inflammatory process. A number of the medical reports as well as the worker s description of pre-surgery problems recount a history of recurrent episodes of pneumonia or respiratory tract infections before the 1996 surgery. Both Dr. Ahmad and Dr. Muir described how such effusions are common complications of pneumonia (Dr. Ahmad estimated they occur in 20 to 57% of cases of pneumonia), and Dr. Ahmad described how the findings at the time of the 1996 surgery were consistent with a pleural effusion caused by a para-pneumonic effusion (a complication of pneumonia). [77] We also accept the opinions of Drs. Ahmad and Muir that the nature and the size of the worker s pleural plaques are such that they would not impact on his lung function or otherwise cause impairment. Dr. Ahmad described how pleural plaques typically have no impact on lung function that it is only in an unusual case where the plaques are very extensive that some studies have shown some impact on lung function. In such cases, there may be a permanent impairment which should be rated under the AMA Guides. However, Dr. Ahmad noted that the worker s 1998 CT reported very thin plaques and Dr. Muir described findings of small bilateral pleural plaques plaques of a size that do not interfere with pulmonary function and do not cause any impairment. [78] We do note that respirologist Dr. Carlton expressed the opinion that it was likely that the worker s pleural plaques are the cause of the worker s mild restrictive pulmonary process. In coming to that opinion, Dr. Carlton relied on the fact that the worker s 2006 test for asthma was negative, and he found no other medical condition that would explain the worker s mild restrictive pulmonary process. His report did not, however, describe the nature and size of the pleural plaques differently than did the reports of Drs. Muir and Ahmad, and he did not refer to the studies or other medical sources linking pleural plaques of the type found in the worker s case to the PFT results or other findings on record. [79] In our view, Drs. Muir and Ahmad are not only very well-qualified to give a medical opinion on this issue, but Dr. Ahmad had the advantage of being able to review all past medical records about the worker s condition including records from the time of the 1996 exploratory surgery as well as more current test results and a summary of the worker s testimony.

15 Page: 14 Decision No. 2127/06 Dr. Ahmad provided a detailed review of the medical reports and fully explained the basis for his conclusions. In addition to explaining how pleural plaques typically have no impact on lung function (as well as describing the nature and findings associated with the unusual cases when they may), Dr. Ahmad concluded that there was no evidence that the worker has any other asbestos induced lung disease. We accept his opinion. [80] We also note that Dr. Ahmad suggested possible alternative non-occupational conditions that might account for some respiratory impairment. He noted the worker s history of mild asthma and explained that the negative 2006 test to which Dr. Carlton referred did not rule out asthma. Dr. Muir concluded the worker s asthma was the cause of the worker s impaired ventilatory capacity. Dr. Ahmad also noted evidence of emphysematous lesions (with a remote smoking history) as well as other possible explanations for a submaximal exercise test. Although it is helpful for us to know that there may be other possible explanations for any respiratory impairment the worker suffers, it is not necessary for us to decide whether any of these non-occupational possibilities are, in fact, the cause of the worker s symptoms. [81] We are satisfied that the evidence has established, on the balance of probabilities, that the worker does not have a permanent respiratory impairment that results from the condition that the Board has found to be compensable (i.e., pleural plaques). As set out above, he does not require treatment for the pleural plaques and they are not affecting his lung function or causing any other impairment. He has no impairment from the pleural plaques that would be ratable under the AMA Guides. It is also unlikely that he has any other asbestos induced lung disease. He is therefore not entitled to benefits for a permanent impairment.

16 Page: 15 Decision No. 2127/06 DISPOSITION [82] The worker s appeal is denied. [83] We find that the worker does not suffer from asbestosis. [84] We also find that the worker does not have a permanent impairment from the condition that the Board has found to be compensable (i.e., pleural plaques). He has no other condition related to his workplace exposure to asbestos. He is therefore not entitled to benefits for a permanent impairment from any condition related to asbestos exposure. DATED: February 26, 2008 SIGNED: M. Kenny, C. J. Robb, J. A. Crocker

17 Decision No. 2127/06 APPENDIX 1 The Medical Assessor s Opinion Regarding Asbestosis The Panel s question: What is asbestosis, and how is it diagnosed? Is the presence of pleural plaques and a history of exposure to asbestos alone sufficient to diagnose asbestosis? Dr. Ahmad s Response: Asbestosis is fibrosis of lung parenchyma caused by the inhalation of asbestos fibers. After asbestos exposure, asbestosis becomes evident only after an appreciable latent period. The duration and the intensity of exposure influence the radiologically evident of lung fibrosis. The development of asbestosis is commonly 20 years or longer following the exposure. There is a threshold dose for the development of clinical asbestosis, which is around 25 fibres/ml/year. Asbestosis specifically refers to interstitial pulmonary fibrosis caused by deposition of the asbestos fibers in the lung parenchyma. It does not refer to the visceral pleural fibrosis, parietal pleural lesions plaques subpleural extension of fibrosis or of the membranous bronchioles (small airways less than 2mm in diameter). To diagnose this disorder, one must establish that an exposure of sufficient duration and intensity has occurred. Asbestosis becomes evident only after an appreciable latency period, often 20 years following the exposure. The presenting symptoms of clinical asbestosis are dry cough and shortness of breath. The onset of such symptoms is insidious and the affected worker usually does not seek medical help until the condition is well established. The earliest physical signs of asbestosis are presence of persistent crackles over both lung bases. As the disease progresses, the crackles become more perfuse and extend from the bases to the middle and upper zones of the lung. At the time, the subjects become more breathless at rest; there are changes in the lung function. The pulmonary function abnormalities are due to increased stiffness in the lungs and impaired gas exchange. As the lungs become stiffer, all lung volumes decrease, except in those subjects who have emphysema from smoking. The Total Lung Capacity (TLC), Vital Capacity (VC) and Diffusing Capacity (DLCO) are all reduced to below 80% of predicted. The most common chest x-ray features of asbestosis are scattered small opacities, usually irregular and small, between 2 and 4mm in diameter. The lower lung zones are first affected, but as the disease progresses, the middle zones are involved. Small irregular opacities are divided into s, t, and u types according to size using the International Labour Office (ILO) system. When the radiographic and lung function abnormalities are indeterminate, high resolution computerized scan of the lung, (HRCT) is useful in revealing the characteristic parenchymal changes. Pleural plaques or thickening can be detected by HRCT in more than 80% of the cases. The diagnosis of asbestosis usually has to be made without histological examination of the lung tissue, since open lung biopsy is rarely justified. The diagnosis of asbestosis must be based on a careful consideration of all the relevant history and clinical findings, but ultimately depends on clinical judgment.

18 Decision No. 2127/06 (a) (b) (c) (d) The essential criteria for a diagnosis of asbestosis are as fellows: A suitable history of exposure to asbestos. In this context, duration and intensity of exposure, there has to be a suitable interval between the exposure and when the disease becomes detectable. Radiographic changes, the presence of small irregular opacities in the lower lung zones according to the ILO system. A characteristic pattern of lung impairment, with reduction of Forced Vital Capacity (FVC) below lower limits of normal, with a concomitant and comparable reduction in Forced Expiratory Volume 1 second (FEV1). A reduction of Total Lung Capacity (TLC) below normal limit must be present. An isolated reduction in FVC in the absence of other criteria should not be relied upon. Abnormal gas exchange, as exemplified by a reduction of Diffusing Capacity for Carbon Monoxide (DLCO), is common in the early stages of the disease, but is non specific. Presence of late inspiratory crackles at the bases. Crackles usually manifest by themselves, first in the posterior basal regions of the lungs. In the majority of cases, diagnosis of asbestosis is reasonably secure on the basis of a history of exposure, clinical features and chest x-ray findings. If there is a doubt, additional information may be obtained from HCRT scanning. In an unusual case where doubt still remains, a lung biopsy may be indicated mainly to exclude the possibility of other more easily treatable conditions. If interstitial fibrosis is confirmed on a biopsy specimen, and asbestos bodies are not visible, a fiber count by electron microscope is helpful. The presence of pleural plaques and a history of asbestos exposure alone are not sufficient to diagnose asbestosis. Pleural plaques are strongly associated with a history of asbestos exposure, both occupational and non-occupational. They are the most common asbestos induced condition and occur after a much lower dose of asbestos exposure than is necessary to cause asbestosis.