SUMMARY DECISION NO. 718/98. Asthma.

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1 SUMMARY DECISION NO. 718/98 Asthma. The worker started working as a bricklayer in 1974 and as an industrial bricklayer in He began experiencing respiratory symptoms in He continued working until The worker appealed a decision of the Appeals Officer granting benefits for asthma on an aggravation basis only. The Panel accepted the opinion of a Tribunal medical assessor and found that there was only a small possibility that he became sensitized by agents at work. The most likely cause of the worker's ongoing symptoms was an onset of asthma that was coincidental with his employment. The Panel noted that asthma is a fairly common condition and that less than 15% of all asthmas have an occupational cause. Spontaneous onset was far more prevalent. The Panel concluded that the worker's asthma was not caused by employment. Rather, his condition was aggravated by workplace exposure, as found by the Board. The appeal was dismissed. [8 pages] DECIDED BY: McCombie; Timms; Nipshagen DATE: 13/03/2000 ACT: WCA

2 2000 ONWSIAT 608 WORKPLACE SAFETY AND INSURANCE APPEALS TRIBUNAL DECISION NO. 718/98 [1] This appeal was first heard in Burlington on May 19, 1998, by a Tribunal Panel consisting of : N. McCombie : Vice-Chair, G.M. Nipshagen: Member representative of employers, D.C. Timms : Member representative of workers. THE APPEAL PROCEEDINGS [2] The worker appeals the decision of Appeals Officer J. Tinto, dated January 28, That decision concluded that the worker s entitlement for an asthmatic condition was on an aggravation basis only. Entitlement was therefore limited and further lost time benefits were denied. [3] The worker appeared and was represented by P. Gowan, a private consultant. The accident employer was notified of the hearing but did not participate. THE EVIDENCE [4] The Panel considered the material included in the Case Record prepared by the Tribunal Counsel Office (Exhibit #1). In addition, we considered two Addenda (Exhibits #2 and 3), the Tribunal s discussion paper on asthma 1 (Exhibit #4), two post-hearing Addenda (Exhibits #5 and #6) and Ms. Gowan s written submissions (Exhibit #7). [5] The Panel also heard oral evidence from the worker. Submissions were made at time of the hearing by Ms. Gowan. In addition, as noted, she provided written submissions on the post hearing evidence. THE ISSUES [6] In a previous decision from Appeals Officer Tinto, dated October 11, 1996, it was ruled that the worker s asthmatic condition is a result of workplace exposure. Following this ruling, the Board s operating levels only allowed benefits for an acute phase and entitlement was considered complete once the worker was no longer in the employment setting. [7] This caused the file to be returned to Appeals Officer Tinto for clarification. The January 28, 1997, Appeals Officer decision currently before the Panel is that clarification and confirms that the worker s entitlement ended once he had left the work environment. 1 Susan M. Tarlo, Asthma and the Workplace, November 1996.

3 Page: 2 Decision No. 718/98 THE REASONS (i) Background [8] As noted, following the hearing, the Panel sought further information. The Panel sent the following memorandum to the Tribunal Counsel Office, on May 25, We quote it at length to provide the factual background and to indicate the Panel s concerns. The memorandum started by asking about policy: Firstly, we note that the issue is entitlement to an asthmatic condition. The Board has a policy entitled Determining Permanent Impairment Due to Asthma, Operational Policy Manual, Document # While this deals with the NEL determination, there is some discussion that is useful to the case before us. This policy document was included in the original Case Record at pp Please confirm with the Board that this is also applicable policy. [9] The Board responded to this, by letter dated October 30, 1998, by agreeing that Operational Policy Manual, Document # may be of relevance. The Panel continued: Secondly, the Board has also noted that the worker may be included in a law suit with respect to asbestos exposure. The letter to the worker, dated September 7, 1993, states that the worker suffered from a work-related asbestos disease for which Workers Compensation Board benefits were paid. The worker is unaware of any such benefits and we would like to find out what information the Board s Legal Branch was relying on and what the status of the law suit is. [10] The October 1998 letter also indicated that the worker is part of a lawsuit referred to as the Webb Class Action #3 lawsuit. No benefits have been paid and the issue is still pending. There is no indication when this will be resolved. The Panel s memorandum then concluded: Thirdly, we note that there are a number of differing medical opinions on file. The Board appears to have accepted, as do we, the following factual background: 1. The worker started work as a bricklayer in In 1980 he began working exclusively as an industrial bricklayer, involved in the repair of industrial furnaces. He also did similar work in tanks such as acid tanks, sulphur tanks, etc. This work was obtained through a union hiring hall and he worked at many different locations, mainly in the Sarnia area. 2. It is accepted that the worker worked in dusty and often confined spaces. The exact nature of his exposure is not clear, but included silica, cement, lime, asbestos, welding fumes, etc. (See the WSIB industrial hygienist s report, pp ) 3. The worker first developed respiratory symptoms in 1982 and sought medical attention in He continued to work until 1991, when he stopped after another attack. He has not worked since. 4. The worker has a smoking history, according to his evidence, of cigarettes a day between the mid 1970s and 1987, when he quit. 5. The worker claims that there is no family history of respiratory disease. 6. The worker has been diagnosed with asthma. His respiratory condition has not improved appreciably since he left employment.

4 Page: 3 Decision No. 718/98 7. The Board accepted that the worker s work environment would temporarily aggravate his asthma. However, this entitlement was limited to the aggravation period only and did not extend to the overall condition. The Board allowed this claim on a limited, aggravation basis only. The Appeals Officer first ruled that the worker s workplace exposure could cause the onset of symptoms and therefore the asthmatic condition resulted from this exposure and there should be no limitation on benefits. On a reconsideration, on his own motion, the Appeals Officer determined that there was a question of clarification between sensitizer and irritant and found that, as a definitive sensitizing agent has not been established, the prior rulings limiting entitlement were, in fact, correct. [E]ntitlement under the Workers Compensation Act ended once he left the furnace exposure. There are a number of medical opinions. Board Dr. Debow (at p. 172) was of the opinion that: 1. The worker developed an asthmatic condition during the course of his work in relationship to the presence of dust. He has continued to have problems with asthma since that period of time. As stated above, some people do develop and continue to have asthmatic reactions even in the absence of original occupational cause or aggravation. 2. It is possible that further comments can be made on receipt of Dr. Davies report. Dr. B.J. Davies, a specialist in internal medicine, provided a report dated September 9, 1993, at p That report noted that the worker s asthma, might be compatible with occupational asthma, however, his symptoms do not appear to be diminishing, despite a prolonged absence from any industrial exposure. In a further opinion from a Board doctor, this time Dr. C.R. Woolf, it is indicated, at p. 150: This is a complex problem and there is a great deal of medical material. It seems clear that the claimant has developed asthma, possibly in 1982 but quite definitely by May It is very unlikely from the exposure information that this asthma is of an occupational nature. However, exposure to various dusts can cause some irritation and flare-ups of asthma. It seems very unlikely that the original dust exposure has caused a permanent irritation of the asthma although occasional flare-ups would seem acceptable as related to dust exposure. OPINION: It is unlikely that the claimant has occupational asthma. It is unlikely that there is a permanent irritation of the non-compensable asthmatic condition. It is unlikely that the condition is related to cigarette smoking. There is no evidence for the diagnosis of silicosis. Dr. D. G. McCormack, a specialist in internal and respiratory medicine, also saw the worker. There are a number of reports from him. His June 26, 1995, report (at p. 216) gave an opinion that there were reasonable grounds to find the worker s lung condition was related to his employment. As noted, the Board accepted limited entitlement. This limitation was based on the view that it had not been established that the worker had been sensitized by workplace exposure. It was also noted that the condition persisted after removal from exposure.

5 Page: 4 Decision No. 718/98 [11] The Panel then suggested a number of questions for a Tribunal assessor. Those questions, and the answers from Dr. S. M. Tarlo, a Tribunal assessor specializing in occupational lung disease and the author of the Tribunal discussion paper, are as follows: 1. Assuming that the worker has had asthma since 1982, and continued to work in a dusty environment for a further nine years, what long term effect, if any, would the workplace exposure have on the development and severity of the worker s disease? Answer: Asthma is a relatively common condition in Canada, occurring in about 7% of the total population. Most asthma is not caused by the workplace and it has been estimated that between 2-15% of patients with asthma have an occupational cause. A uniform feature of asthma both non-occupational asthma and occupational asthma is that the airways are more reactive than normal and are more likely than normal to become narrowed transiently on exposure to airborne substances which can irritate the airways. This includes small dust particles which are not trapped in the nose and throat, fumes, sprays and smoke. In addition, cold air and exercise are very common triggers of asthma in almost all patients with asthma whether or not this is occupational. Therefore, in almost any patient with asthma, exposure to moderate levels of dust, smoke, fumes, sprays or cold air will aggravate their asthma on a transient basis. Examples of such conditions would be walking into a smoky bar, shoveling snow, or workplace exposure to moderate or high levels of dusts, smoke or fumes. Occasionally, (accounting for about 7% of occupational asthma), a very high accidental exposure to a respiratory irritant such as acid fumes or smoke from a fire, can actually cause asthma. If this occurs, it generally is as a result of a single extremely high accidental exposure and causes the new onset of asthma within 24. hours of this exposure, usually leading to an emergency visit and hospital admission at that time. This can be followed by persisting asthma for up to several years even without further exposure to the causative agent. This is termed irritant induced asthma or reactive airways dysfunction syndrome. There is controversy as to whether a non-massive exposure can also cause asthma. It has been suggested that recurrent exposure to very high levels of an irritant such as recurrent accidental exposures to chlorine gas, could cause asthma but this is also unproven, and cannot be objectively or reliably assessed in -an individual patient. As noted above, it is far more common for workplace respiratory irritant agents such as dusts and fumes to exacerbate preexisting or coincidental asthma rather than to actually cause asthma. In relation to the documentation provided on [the worker], there has been information to suggest that he did have exposure to levels of dusts in the workplace that likely would aggravate symptoms in a person with asthma on the basis of an irritant effect. Such a response produces temporary changes, worsening asthma for a period that can range from a few minutes to several days or even a week or two but would not be expected to produce any permanent worsening of asthma severity. There is no indication from the records provided, that there was a high accidental exposure within 24 hours of the onset of his asthma symptoms initially and therefore, no indication that this patient had irritant induced asthma or RADS. There is a theoretical possibility that he may have developed asthma coincidentally, possibly in 1982 or 1983 and that subsequently if he was exposed to an extremely high level of dust or fumes on 1 or more occasion, that this might have caused a more prolonged exacerbation of asthma which could have persisted for months, or even years, but there is no indication in the records that there were markedly higher exposure levels to dusts and fumes on the occasions when his asthma led to emergency visits and hospital admissions as compared with other working days. It would appear more likely that the workplace dusts and fumes caused a temporary exacerbation of asthma in this patient. 2. How significant is it that the worker s symptoms have continued unabated in the eight years since he left his occupation? Does this fact preclude an occupational cause?

6 Page: 5 Decision No. 718/98 Answer: There are 3 possibilities to account for continuing asthma for 8 years since leaving the occupation. a. If asthma started coincidentally from the workplace, then it would be likely to persist on a long term basis. As noted above, most asthma is not caused by the workplace and is of unknown cause. It can start at any age and often persists throughout life after the onset. b. If asthma was caused by "sensitization" to a particular substance in the workplace leading to asthma which was specifically exacerbated at work by this agent, and if he had continued to have exposure to this after the onset of asthma from 1983 until stopping work in 1991, for 8 years then it is possible that asthma could subsequently continue after leaving the occupation. In patients in Ontario who we have reviewed, who have had asthma related to a workplace sensitizer, 70% have improvement or clearing of their asthma after leaving the workplace but 30% do not at a 2 year follow up. A recent publication indicates that the outcome is better after 5 years away from the workplace but still there can be some patients who do not improve, particularly if they have continued to work for several years after the onset of their asthma and have continued during that time to be exposed to a specific work sensitizer. c. If asthma was initially caused by a very high level of a workplace irritant such as extremely high levels of dusts or fumes, or if such very high exposure exacerbated asthma after it's onset, then it is possible that such an exacerbation could persist for months or even up to 8 years after leaving the workplace. 3. Assuming the smoking history noted above, what role, if any, would this activity play in the development of the asthmatic condition? Answer: The smoking history in the file has been noted to be probably cigarettes a day between the mid 1970s and 1987 when he quit. Cigarette smoke is a respiratory irritant which would have similar effects on asthma as would smoke, dust, fumes or sprays in the workplace. Similarly, the effects on asthma would be expected to be transient. Therefore, cigarette smoke may have exacerbated asthma in this patient up until a few weeks after the time he quit but would not be expected to have an effect on his asthma after It is noted that in there were concerns about a heart condition. Is the finding of atrial fibrillation in 1984 significant with respect to his asthma? Answer: Atrial fibrillation can be due to a primary heart problem or can be secondary to other conditions such as thyroid disease. If a patient has a severe exacerbation of asthma, the oxygen saturation in the blood can be significantly reduced and the heart may not receive an adequate supply of oxygen. This can trigger an abnormal rhythm in the heart while these conditions last. In addition, some asthma treatment such as aminophylline or other theophylline products as were used in this patient during emergency room visits for his asthma can also increase the risk of an abnormal rhythm in the heart, especially with higher doses in a patient with severe asthma exacerbation at that time. Alternatively, atrial fibrillation can start for no apparent reason. In this patient, the report from Dr. Tamblyn, case record pages indicate that the symptoms in this patient on Nov began suddenly with weakness, faintness and lightheadedness and palpitations. There is note made that his asthma had been "acting up a bit lately but no worse than usual". This history is more suggestive of coincidental onset of atrial fibrillation rather than atrial fibrillation caused by a severe exacerbation of asthma. This appears to have been a transient episode and his rhythm appears to have reverted to normal with treatment. A later ECG in 1992 showed an increased heart rate but normal sinus rhythm. The episode of atrial fibrillation would not affect his asthma. 5. The Board has indicated that the worker was not sensitized at work. The Board s Policy Report (pp ) indicates that sensitization is a function of the immune system. Can you comment on any immune response in this case? Would the lack of an immune response rule out an occupational origin of the

7 Page: 6 Decision No. 718/98 asthmatic condition or rule out an occupational contribution to the chronicity of the condition. Answer: Sensitization is the term used to describe the response whereby an individual can develop asthma as a result of exposure to a particular substance, for example animal dander, and once sensitized, exposures to even extremely low levels of this substance will exacerbate asthma. The other feature of sensitization is that there is a latency period, this means that the person initially is exposed to this agent for a period of weeks, months or years without developing symptoms but once symptoms have resulted from this then further exposure to this agent will trigger symptoms. Usually sensitization is caused by an allergic response but in the case of some workplace agents asthma can be caused and subsequently exacerbated by a specific agent without a clear allergic mechanism being proven on the basis of skin tests or laboratory antibody tests. Examples of this would be isocyanates and red cedar. There are around 300 different substances which have been described as sensitizers in the workplace capable of causing asthma on this basis. When asthma has been caused by a workplace sensitizer, in about 90% of patient there is a clear history of worsening at work and improvement off work over weekends or holidays. In this patient, there was no identified workplace sensitizer. This does not rule out the possibility of a sensitizer being present but makes it unlikely. Except in the case of sensitizers which are derived from animals or plants, in which case skin tests or laboratory tests for antibodies can be performed, in the case of sensitizers which are chemical agents, it is usually very difficult to assess a specific immune response in individual patients. In this case, it would appear unlikely that the patient was sensitized at work based on the lack of an identified sensitizer at work and the absence of clearly identified history of improvement on weekends and holidays away from work. However, this possibility cannot be absolutely ruled out. As noted above, under question 2, there is a small possibility of an occupational contribution to the chronicity of asthma in this patient but it would appear to be unlikely and a more likely possibility would be ongoing unrelated asthma. 6. There is a suggestion that the worker has allergies (p. 256), although to what is not clear. We understand that there may be an association between allergies and asthma. Can you explain the significance of this finding? Answer. A reference to allergies was made on page 256 by Dr. Levine in his letter but no details of this were given in his letter. On review of his notes, page , it would appear that Dr. Levine has used a clinical ecology approach in his assessment of this patient and I cannot see reference to conventional allergy testing to common aeroallergens. The letter from Dr. McCormack on. page 217 and 218 dated June indicates that the patient was recently assessed by Dr. Mazza who did not feel that allergy was a significant part of his illness. Dr. Mazza practices conventional allergy and I would suggest that it would be helpful to obtain his records on this patient including allergy skin testing to further assess whether he is allergic. If he were not allergic as suggested by Dr. McCormack's letter, then asthma could still occur unrelated to the workplace and it has been estimated that at least 30% or adult asthmatics are not allergic. [12] As is indicated in her answers above, Dr. Tarlo thoroughly reviewed the material and she was of the opinion that a further medical examination was not necessary. (ii) Conclusions [13] The Panel notes that this is fundamentally a medical question. It is accepted that the worker s workplace exposure, at least temporarily exacerbated the worker s asthmatic condition. [14] Ms. Gowan argues that the worker s asthma condition is causally related to his work environment. She challenges Dr. Tarlo s findings on the grounds that Dr. Tarlo only answered the Panel s questions and did not provide a case summary which would indicate her

8 Page: 7 Decision No. 718/98 understanding of the worker s work environment. It was Ms. Gowan s view that there were a number of unidentified sensitizers. She therefore challenges Dr. Tarlo s conclusion that there was no specific workplace sensitizer identified. [15] The Panel notes that these cases do present profound evidentiary problems. We do not know, and cannot now find out with certainty, the exact nature of this worker s exposure and at what levels he was exposed. With this lack of evidence, we must rely on the medical probability. [16] In this case, we accept Dr. Tarlo s report. We do not agree with Ms. Gowan s contention that the report fails to display an adequate understanding of the work environment. It is not the responsibility of a Tribunal assessor to automatically summarize the information in the materials before the Tribunal. In this case, the Panel itself provided a summary of the worker s history. And, in reviewing Dr. Tarlo s report, it is apparent to us that she did carefully review the relevant information. [17] Dr. Tarlo concludes that the likelihood that the work environment caused that is, that he was sensitized by an agent at work the worker s asthma, is a small possibility. The much more likely scenario, according to Dr. Tarlo is that the worker s onset of asthma was coincidental with his employment. [18] It is noted that asthma is a fairly common condition and that, at most, less that 15% of all asthmas can have an occupational cause. It is apparent that the spontaneous onset of an asthmatic condition is far more prevalent. [19] Under these circumstances, we cannot accept that, on a balance of probabilities, the worker s asthma was caused by his work environment. The Board s conclusion that the work environment only aggravated the asthmatic condition is supported by the evidence before this Panel, including that obtained from Dr. Tarlo. THE DECISION [20] The appeal is denied. DATED: March 13, 2000 SIGNED: N. McCombie, G.M. Nipshagen, D.C. Timms