A Workers' Compensation Claim Population for Occupational Asthma*

Transcription

1 A Workers' Compensation Claim Population for Occupational Asthma* Comparison of Subgroups Susan M. Tarlo, MBBS, FCCP; Gary Liss, MD; Paul Corey, PhD; and Irvin Broder, MD Study objectives: (1) To compare patients with claims submitted to the Ontario Workers' Compensation Board (WCB) for occupational asthma, in relation to the WCB decisions reached of occupational asthma (OA); aggravation of asthma from irritant exposures (AA); unrelated asthma; no asthma; and (2) to assess determinants of outcome of WCB accepted claims at permanent disability assessments. Design: A retrospective review of 609 claims submitted to the WCB 1984 to Results: The WCB decision reached was OA in 39% of claims, mostly attributed to isocyanates (57% of these). A further 39% were accepted for AA. Exposure to a known sensitizer occurred in 91% with OA and to an irritant in 67% with AA. Forty percent with AA were attributed to a spill or accidental exposure and 68% had preceding asthma. Those with AA were more likely to have clearing of symptoms by the time of their main assessment (43% vs 20% with OA) and were more likely to have remained in the same work (35% vs 20% with OA). Of 200 OA accepted claims reviewed at a mean of 1.9 years later, clearing of asthma occurred in 19% and milder asthma in 47%. Outcome was best with early diagnosis (p<0.05), and milder impairment of pulmonary function at initial assessment (p<0.05). Conclusions: Patients with asthma induced by a workplace sensitizer demonstrate some differences from those related to workplace irritants. Accurate categorization and early removal of those with OA offers the best prognosis. (Chest 1995; 107:634-41) AA=aggravation of asthma; FEF50=forced expiratory flow at 50% vital capacity; FEF75=forced expiratory flow at 75% vital capacity; FEV,=forced expiratory volume in 1 s; OA=occupational asthma; PC20=provocation concentration causing a 20% fall in FEV1; WCB=Ontario Workers' Compensation Board Key words: occupational asthma; compensation; asthma; outcome Claims accepted for occupational asthma (OA) have been increasing over several years in Ontario and now outnumber claims for pneumoconiosis. In 1982, 17 claims were accepted for OA, 30 for silicosis, and 12 for asbestosis while in the year 1985, there were 54 for OA, 33 for silicosis, and 20 for asbestosis. Similar increases have been reported from Quebec where claims accepted for OA rose from 6 in 1977 to 97 in We have recently reported the results of assessments for OA in patients referred to one occupational lung disease center in Ontario.2 However, less than a quarter of all Ontario claimants were seen in that center, and the findings could differ from those among all compensation claims for OA asthma to the Ontario Workers' Compensation Board (Ontario *From the Gage Research Institute, Department of Medicine, University of Toronto (Drs. Tarlo, Corey and Broder), and Ontario Ministry of Labour (Dr. Liss), Toronto, Ontario, Canada. This study was supported by the Ontario Workers' Compensation Board. Manuscript received November 24, 1993; revision accepted August 16, Reprint requests: Dr. Tarlo, Gage Research Institute, 223 College Street, Toronto, Ontario MST 1R4 Canada 634 WCB). In addition, the routine follow-up by the WCB of accepted claims for disability rating could allow assessment of outcome variables. Previous studies of prognosis in OA have generally been restricted to groups with asthma caused by a single sensitizer, such as Western red cedar3 or isocyanates.4-7 Few studies have included multiple causative agents.8'9 With the exception of the study of Chan-Yeung et a13 of 232 red cedar workers, follow-up reports have included relatively small groups of subjects. The present study describes diagnostic categories and outcome variables in a relatively large population of subjects with OA from many different causative agents. MATERIAL AND METHODS Claims submitted for OA since mid-1984 to the Ontario WCB have been given a decision of (1) OA, (2) aggravation of asthma (c) unrelated asthma, or (d) other decision. The term aggravation of asthma (AA) was generally applied by the WCB to asthma that occurred at work, either with a history of preceding asthma or, in those with no known previous asthma, in the absence of a specific sensitizer. This included increased airway reactivity apparently triggered by irritant factors in subjects with no previous known asthma. The WCB generally provided a lower range of compensation for those given a decision of AA than to those with OA. Workers' Compensation Claim Population for Occupational Asthma (Tarlo et al)

2 The WCB decision was initially reached by one of three occupational physicians at the WCB with a major interest in OA, often with the aid of an independent specialized assessment. The initial decision was subject to appeal to the WCB and if further rejected, could be appealed through the Workers Compensation Appeal Tribunal, consisting of a nonmedical panel. Thus, the final WCB decision could be reached at any of these stages and would not necessarily reflect the non-wcb physician diagnosis. Files were reviewed of all claims for OA submitted to the WCB between mid-1984 and mid-1988 inclusive. From each file a standardized format was completed, from the most detailed assessments prior to and after the WCB decision (referred to subsequently as the assessment of the main assessing physician). The following information was abstracted: (1) demographic details, including age, gender, smoking history, type and duration of work exposure, and work status at the time of assessment; (2) nature and duration of upper and lower respiratory tract symptoms, improvement on days or weeks off work, and timing of any worsening at work; (3) history of any previous asthma symptoms before implicated work exposure, and family history of asthma or allergic diseases; (4) medication requirements; (5) results of investigations if performed such as pulmonary function tests (expressed as percent of age and height adjusted predicted normal values'0), and response to a bronchodilator; histamine or methacholine challenge expressed as PC20 (provocation concentration causing a 20% fall in FEVI); skin test responses to common allergen extracts and specific workplace antigens, expressed where available from the mean wheal diameter as 1+ (1 to 2 mm on prick test or.5 mm on intradermal test), 2+ (3 to 5 mm on prick test or 6 to 9 mm on intradermal test), 3+ (6 to 9 mm on prick test or >10 mm on intradermal test), 4+ (>10 mm on prick test or.10 mm with pseudopods on intradermal test); serial peak flow assessments at work and off work expressed as positive or negative for work-related changes as interpreted by the main assessing physician; serial histamine or methacholine challenge results within 48 h of a typical working day and after 7 days or more off work; and specific laboratory chamber challenge with a suspected workplace agent; (6) the clinical diagnosis made by the main assessing physician after completion of any arranged investigations, and the WCB diagnostic decision; and (7) follow-up results obtained 1 to 2 years later, including work status, symptoms, medication requirements, and pulmonary function results. The amount of objective investigation could vary widely from physical examination alone, to performance of full pulmonary function tests with assessment of airway reactivity by histamine or methacholine challenge, serial peak flow measurements, specific work allergen skin tests, and specific inhalation challenge. Since these tests were performed in many different centers under the direction of many physicians, the methodology of these tests was not uniform. That used in our center, where 19% of this population had been assessed, has been described previously.2 No uniform criteria were applied to the interpretation of serial peak flow measurements in this study, since the original readings were not always available. Therefore, the peak flow interpretation reached by the attending physician was accepted as recorded. Methacholine and histamine responsiveness are expressed as PC20 and are used in the analyses as actual values or are separated into PC20 responses greater or less than 12 mg/ml, which is taken in this study as the cutoff for a normal response. Follow-up assessments were performed for disability decisions in all subjects whose claims were accepted for OA and AA if asthma was present at the initial assessment. The follow-up assessment for disability rating was generally performed 1 to 2 years after the initial WCB decision. The medical reassessment was performed either by one of the three WCB physicians or a respirologist selected by the WCB. Statistical Analysis The general linear models procedure (GLM of SAS) was used for analysis of variance, t test for Student's t tests, and FREQ for x2 analyses. Since information available in the files was not complete for all patients, missing data were excluded from calculations of percentages and from statistical analyses. RESULTS Total Group A total of 609 files was reviewed from the 4-year period. A diagnosis/decision of OA was reached in about one third of subjects both by the physician (35%) and the WCB (39%). A similar proportion (39%) was given a decision by the WCB of AA, and a diagnosis of this by the main assessing physician (34%). Of those with a WCB decision of AA, 68% had a history of preceding asthma. Unrelated asthma was diagnosed in 6% of the total group by the physician and 10% were given this decision by the WCB while other diagnoses were reached by the physician in 11% and other diagnoses or decisions by the WCB in 13%. Insufficient information was the conclusion in 12% of claims by the assessing physician. Overall, 40% of claims were assessed by one or more of eight non-wcb physicians with a known interest in OA, including 59% of those with a final diagnosis of OA and 66% with unrelated asthma, but only 22% of those with AA. A further 40% of the total number of patients were assessed by other respirologists or allergists, 2% by other internists, and 15% by their primary care physician or an emergency physician alone. The most common exposure agents (Table 1) were isocyanates (28%). Paints were implicated as the most likely causative agent in 5.5% of claims while metal fumes or dusts, flour, grain dusts, and solvents each accounted for 4% of all claims. Recognized sensitizers such as cedar dust (3%), animals (2%), and soldering fumes (1%) were less common. Specific irritants such as acids and welding fumes were also each implicated in 2% or less of all claims. In 17% of subjects, nonspecified dusts, fumes, or sprays were implicated; 60% of these were subjects given a WCB decision of AA. As might be expected in a population assessed by many different physicians, where most workers had left the implicated environment, and many were symptom free, further investigations were limited (Table 2). Spirometric tests were performed in only 52% of all subjects and mean values were normal. Serial peak flow rates were performed at work and off work by 25%, methacholine or histamine challenge off work in 34%, and during a working week in 23% (both off work and during a working week in 12%). A specific work allergen skin test was performed in 12% and specific laboratory challenge with a work CHEST / 107 / 3 / MARCH,

3 Table 1-Main Implicated Exposure Agents in WCB Decision Groups* Unrelated OA AA Asthma Other Total No. of subjects Primarily sensitizing agents Isocyanates Flour Metal fumes/dusts Red cedar Grain Soldering fumes Acrylic fumes Woods (noncedar) Amines Enzymes Latex Animals Primarily irritant agents Paint fumes Solvents Calcium oxide Sulfuric acid/so Hydrochloric acid/cl Ammonia Cigarette smoke Glutaraldehyde Welding fumes *Other agents each implicated in one or two subjects with OA include psyllium, platinum salts, insects, foods, plants, and dyes. Other agents each implicated in four or less subjects with AA include ozone, pesticides, fungi, cotton fibers, cold air, and oil mists. Unspecified dusts, fumes, or sprays were implicated in an additional 64 subjects with AA. Table 2-Investigations by WCB Decision Group Unrelated OA AA Asthma Other Total p Value* No Skin tests positive 77/154 94/136 27/46 43/57 241/393 <0.01 >1 common allergen (50%) (69%) (59%) (75%) (61%) (>2+ response) Skin tests positive 31/41 14/20 4/7 4/8 53/76 NS to work agent (76%) (70%) (57%) (50%) (70%) (-1 + response) FEVI, % predicted t ± No. assessed FVC 105 ± ±23 <0.005 No. assessed FEF50 79±38 68±40 84±45 83±48 77±40 NS No. assessed FEF75 72 ± NS No. assessed Peak flows 56/94 14/34 1/11 1/13 72/152 <0.005 supporting OA (60%) (41%) (9%) (8%) (47%) PC20 off work4 10.6± ± ±14.3 NS No. assessed PC20 at work 4.7+±10 4.8± ± ± ±10.7 NS No. assessed Laboratory challenge positive 33/43 4/8 0/6 0/6 38/ (77%) (50%) (0%) (0%) (60%) PC20 prechallenge 10.9+± ± ±18 NS No. assessed PC20 postchallenge NS No. assessed *p values relate to subgroups excluding the total group. fstandard deviation. IPC20 of methacholine or histamine. 636 Workers' Compensation Claim Population for Occupational Asthma (Tar/oet al)

4 Table 3-Comparison of Patients According to WCB Decision: Demographics Unrelated OA AA Asthma Other Total p Value Value* No Mean age, yr 40+13t 41±12 42 ± 12 44± NS Male, % NS Never smoked, % NS Current smokers, % NS Mean pack-yr of smokers ±12 16±17 22 ±22 15 ±15 NS History of previous asthma, % < Years since onset of previous asthma ± ± ±14 NS Family history of asthma, % <0.01 *p values relate to comparisons of subgroups excluding the total group. tstandard deviation. agent in 10%. Support for a diagnosis of OA came ing holidays (Table 4). However, 63% had left work from results of peak flow studies in 12% of the total by the time of the main physician assessment, and study population (47% of those performing the test), 20% had no continuing symptoms. Ninety-one perfrom repeated methacholine or histamine challenge cent were assessed by a specialist physician (allergist, at work and off work in 5% (54% of those tested), respirologist, or occupational physician). specific skin tests in 8% (70% of those tested), and Exposure to a known sensitizing agent was despecific laboratory challenge in 6% (60% of those scribed in 91%, exposure to a presumed irritant in 7%, tested). and to unknown agents in 2%. The most commonly OccupationalAsthma implicated exposure agent was isocyanates (Table 1) Occupational in 57% of subjects. In addition to spirometry, meth- Among the 235 patients who were given a WCB acholine or histamine challenge was performed decision of OA, the mean age was 40 years, and 69% within 48 h of a work day in 36% of those with OA, were men (Table 3). One third had never smoked. All and off work in 56% (Table 2), while the challenge described asthma symptoms and 80% with available was performed both after a work day and off work information also had nasal symptoms, although 40% in 22%. Serial peak flow readings were assessed in of files did not mention their presence or absence. 40% and specific skin tests to a work agent in 17%. Seventy percent had a history of improvement in Specific challenges in the laboratory with a work symptoms during weekends off work, and 88% dur- agent were performed in 18%. Table 4-Work-Related Data in WCB Decision Groups Unrelated p OA AA Asthma Other Total Value* No Years of symptoms 2.8 ± 4.2t 1.2 ± ± < at work Years of symptoms 2.8 ± ± ± ± < before WCB submission Years of symptoms 3.1± ± ± ± < before main assessment Exposure years to work ±8.1 8± NS agent Improvement on weekends, % < Improvement on holidays, % < Left work, % < Same work, % < Out of usual exposure <0.05 but at workplace, % Asymptomatic at < main assessment, So Asymptomatic and <0.01 out area, % of work *p values relate to comparisons of subgroups excluding the total group. tstandard deviation. CHEST / 107 / 3 / MARCH,

5 Aggravation of Asthma and Comparisons With OA The only demographic features (Table 3) that were significantly different between those with AA and OA were the history of previous asthma (68% of those with AA vs 8% of those with OA), and the family history of asthma (29% of those with AA vs 15% of those with OA). Clearing of previous asthma prior to the onset of work-attributed symptoms was reported in only 19 of the 150 (12%) with AA and preceding asthma, while among the 18 with previous asthma whose claims were accepted as OA, 12 (67%) had clearing of their asthma prior to the onset of workrelated symptoms, for a mean of 5.5 years (data not shown in tables). As might be expected, there was a high level of concordance among the main assessing physician and WCB for the diagnosis of AA with a history of asthma (91%) and OA without previous asthma (87%). The concordance was less for a diagnosis of AA, when there was no history of asthma (71%) and for OA when there was a history of preceding asthma (72%) (data not shown in tables). Symptoms, medication use, and physical findings of wheezing were similar in prevalence to those with OA, when recorded in the patient file (data not shown). There was a similar prevalence of improvement during weekends and holidays as in those with OA (Table 4). Although the duration of exposure to the implicated work agent was similar to those with OA, the duration of work-attributed symptoms was less in those with AA than in those with OA (at the time of main assessment, 1.4 years vs 3.1 years). Those with AA were significantly less likely to have had exposure to isocyanates than those with OA (Table 1), and were more likely to have exposure to agents other than the most commonly recognized sensitizers (Table 1). Exposure to a known respiratory irritant (most commonly paints, solvents, acids, ammonia, or calcium oxide) occurred in 67%. An accidental exposure or spill was reported in 40%. Among those with AA and no history of asthma (70 patients), exposure agents were mainly agents considered to be irritant such as acids, solvents, welding fumes, and nonorganic dusts (Table 5), although 34% of these subjects had exposure to potential sensitizers such as isocyanates, eggs, flour, and metal dusts or fumes. All objective diagnostic tests were performed in a smaller proportion of patients with AA than OA. When these tests were performed, however, results were not significantly different from those with OA. Unrelated Asthma, and Comparisons With OA and AA The 58 patients who were classified by the WCB as having unrelated asthma were not significantly 638 Table 5-Exposure Agents in Those With a WCB Decision of Aggravation Who Had No History of Asthma (70 Patients)* Agents Isocyanates 9 Solvents 7 Metal dusts/fumes 6 Acids 5 Chlorine 4 Synthetic fibers dusts 4 Welding fumes 4 Grain dusts 4 Cutting or lubricating oils 4 Calcium oxide dust 3 Coke ovens 3 Sawdust 3 Metabisulphite or So2 3 Flour 2 Spray paints (nonisocyanate) 2 Methylmethacrylate/acrylic monomer 2 Molds 2 Glues 2 Feathers 2 *Agents in single cases only: ammonia, fur, leather, dusts, printing fumes, cinaminic alcohol, fiberglass, eggs, tobacco smoke, urea formaldehyde insulation, epoxy resins. different in demographic findings from those with OA or AA (Table 3) except for their history of previous asthma. They did not differ either in symptoms or physical findings of wheezing. They did have a longer duration of symptoms at work (Table 4), and were less likely to be asymptomatic by the time of assessment. They were significantly less likely to describe improvement in symptoms on weekends (41 %) or holidays (54%) (Table 4). Exposure to the most common OA sensitizer, isocyanates, was less common in those with unrelated asthma (Table 1), and these patients were more likely to have unspecified exposures or exposure to agents other than the most common agents inducing OA. As with patients classified as having AA, investigations were less commonly performed than among those with OA; but when performed, as expected, the test results were more likely to be normal or not supportive of an occupational component than among patients with OA or AA. Airflow limitation as assessed by spirometry showed more marked reduction in forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) among those with unrelated asthma. There was no significant difference in mean values for flow rates at 50% and 75% of vital capacity. Follow-up Results Follow-up assessment had been performed for the purpose of disability rating in 285 of the 469 accepted claims for OA and AA (69%). Only 46% of these patients were working at follow-up, 8% doing the same job as at the time of diagnosis. Most of those followed Workers' Compensation Claim Population for Occupational Asthma (Tarlo et al) No.

6 Table 6-Patient Variables Related to Outcome of Accepted Claims in 200 Patients With OA Status as Rated by Examining Physician at Follow-up Cleared Milder Unchanged Worse p Value No. of subjects First WCB assessment FEV1, % predicted * 97 ±23 97 ±27 86 ± 37 <0.05 No. assessed FVC ±22 105±23 97±25 NS No. assessed FEF50 110± ±34 70± No. assessed FEF75 110±66 78± ±89 NS No. assessed Mean PC20 at workt ± ± ±4 NS No. assessed '12 mg/ml >12 mg/ml Years of symptoms ± ± ± 3.7 NS before leaving exposure Years of symptoms ± <0.05 before main assessment Follow-up WCB assessment FEV1, % predicted 111± ± No. assessed FVC ±14 104±19 90± No. assessed FEF No. assessed FEF ± ± No. assessed NS Mean PC ±15 9.0±8 3.5± ± No. assessed <12 mg/ml >12 mg/ml <0.005 *Standard deviation. tmethacholine or histamine PC20, mg/ml. up (70%) were those whose claims were accepted for OA. Asthma had cleared in 19% with OA, was clinically considered milder in 47%, unchanged in 20%, and worse in 14% in the opinion of the assessing physician. The mean duration since the first assessment was 1.9 ± 1.5 years. Pulmonary function testing at follow-up (Table 6) paralleled the outcome findings, with worse asthma associated with greater impairment of function. Two variables were associated with the outcome of OA. First, the duration of symptoms prior to the main assessment was directly related to the outcome (Table 6). This was indicated by the duration ranging from a mean of 2.0 ± 2.4 years in those with clearing, to 5.3 ± 4.9 years in those with worsening of asthma. Second, the pulmonary function status at the initial assessment showed a similar direct association with the status of the worker's asthma at follow-up. For example, an FEV1 mean of 108 ± 24% predicted was initially present in those with subsequent clearing, and 86 ± 37% in those with worsening asthma. Similarly the initial assessment mean methacholine or histamine PC20, although measured in a minority of subjects while working, ranged from a mean of 11.2±21 mg/ml in those who cleared, down to a mean of 2.1 ± 4 mg/ml in those who had worsening of asthma on follow-up. Greater improvement was found in those with a WCB decision of OA than in those with AA (data not shown in tables). Among those with OA, 20% had clearing of asthma and 46% were milder vs 7% and 30%, respectively, with AA. Fewer with AA had a follow-up assessment (85 subjects), but analyses of these showed a trend to similar outcome associations. In addition, prognosis for those with asthma attributed to isocyanates was better than for those with other causes of OA. Clearing of asthma occurred in 20% and improvement occurred in a further 52% of those with isocyanate OA, as compared with 16% and 32%, respectively, in those with other causes (p<0.05). This may reflect an earlier diagnosis of a well-recognized sensitizer. DISCUSSION This survey reflects the claims received by the Ontario WCB for suspected work-related asthma, CHEST / 107 / 3/ MARCH,

7 and may not necessarily reflect the true Ontario incidence or distribution of causative agents in the time period assessed, since many patients with OA may not be reported to the WCB or be eligible to submit a claim. Our categorization of patients into diagnostic groups has been on the basis of the WCB decision, stemming largely from the main physician assessment. We recognize that the WCB decision may at times be different from that which might be reached by a physician specializing in OA. However, there was good agreement between diagnoses reached by the WCB and the main assessing physician, and when results were analyzed using the physician diagnosis instead of the WCB diagnosis, the findings were substantively the same. We elected to use the WCB decision since it was reached by a group of three physicians at the WCB and thus may be more consistent. Objective investigations were not performed in many subjects, possibly due to limitations previously described,2 such as difficulty in arranging workplace peak flow assessments and methacholine challenge in subjects who had terminated their employment by the time of main assessment (56% of all patients). Where there is insufficient information or tests show borderline responses, the benefit of the doubt is given by the WCB toward a diagnosis of OA or AA. Therefore, no strict diagnostic criteria could be applied to better categorize these subjects, and there likely were some patients who did not truly belong in the diagnostic category given to them. Therefore, this study cannot be directly compared with studies performed in a single center, using a standardized approach.2-7 Nevertheless, it is of interest that many of the findings in this study are consistent with these other reports.2-7 It is unlikely that the outcome categories were significantly influenced by inaccurate diagnoses in one decision group more than other decision groups since the percentage of patients in each of the follow-up outcome categories who had objective confirmation of OA was similar (data not shown). Some misclassification of claim decisions might have resulted from nonmedical decisions made during appeals proceedings. The presence of misclassification is further suggested by the finding of an apparently positive challenge to known sensitizers in three patients with AA, with flour, isocyanates, or cobalt. Compensation for AA and acute airway irritant effects is not uniformly accepted and does not occur, for example, in Quebec or in Britain under the category of OA.""1 A proposed medicolegal definition of OA from an author in the United States12 also includes only specific sensitizing agents. The subjects included in the diagnostic category of aggravation in Ontario have been separately classified from OA for the purpose of compensation. They can be divided 640 into those with and without preceding known asthma and subdivided into subjects with exposure to unusually high levels of potential irritant substances and subjects exposed to currently acceptable levels. Two thirds of patients in this accepted claim category of AA had known preceding asthma, which worsened while working with potential airway irritants, such as acid fumes or aerosols, ammonia, chlorine, paint fumes, solvents, or irritant dusts. The remaining one third had no previous documented asthma, and developed changes of asthma while working with no sensitizer exposure or did not demonstrate sensitivity to known sensitizers. This included patients with accidental exposure to a high-dose irritant or repeated exposure to irritants with no single high concentration incident, such as has been described previously.13"14 Therefore, a proportion of these patients may have had asthma induced by their work exposure while others may have had coincidental onset of asthma with irritant exacerbation by workplace substances. Those with AA were less likely than those with OA to have exposure to the main recognized sensitizer in Ontario, isocyanates (1l1% vs 58%) (Table 1), had a shorter mean duration of symptoms before WCB submission and main assessment (1.2 years vs 2.8 years) (Table 4), and they were more likely to be asymptomatic by the time of main assessment (43% vs 20%). This greater clearing of symptoms in patients with AA may reflect a proportion of subjects with transient symptoms related to spills or temporary exposures to irritant substances. This is supported by the finding that among those with AA, 35% remained in the same work environment by the time of their main assessment but more than half (52% of those still at the same work) reported a clearing of work-related symptoms. In contrast, of those with OA, only 20% remained at the same work by the time of their main assessment, and only 3 (7%) of those still at the same work reported clearing of work-attributed symptoms. The greater prevalence of transient symptoms in those with AA might also explain the fact that fewer of those with AA were referred for tertiary specialist assessment, and fewer underwent detailed investigation (Table 2) such as peak flow assessments, measurement of airway reactivity, and skin testing or challenge with workplace substances. When these tests were performed, however, results were not significantly different from those with OA (Table 2), suggesting that at least a subset may have had similar functional changes to those with OA. They may not have been classified by the WCB as having OA due to preceding asthma (150 patients classified as AA had a history of asthma and 14 had a questionable history) or lack of a recognized workplace sensitizer. These observations support the concept of Workers' Compensation Claim Population for Occupational Asthma (Tarlo et al)

8 providing some degree of compensation for such patients and the need for detailed investigation of these patients when feasible. In Ontario in the time period studied, isocyanates were the most commonly identified suspect agents in all the claims (30%) and the most common causative agent in claims accepted for OA (58%) (Table 1). They were also a significant attributed cause of irritant airway responses (11% of AA). This represents a higher proportion of OA than compensated or reported to the SWORD surveillance system in the United Kingdom in Conversely, flour and grain dusts accounted for a similar proportion of OA accepted claims in Britain and Ontario (18% and 17%, respectively), while platinum salts and soldering flux accounted for higher proportions of compensated cases in Britain,11 possibly reflecting differences in occupational exposures. Comparison of this study with that of Yassi,'6 who reviewed earlier Ontario WCB claims from 1975 to 1981, is difficult due to some differences in classification of accepted claims. However, our finding of isocyanates as the presumed causative agent in 58% of those with OA is far greater than in the earlier review where isocyanates accounted for 27% of OA. The proportion due to flour or grain is unchanged (17% vs 18%). At follow-up, unemployment was higher in the present study, 54%o of those followed up as compared with less than 40% in the previous study. Of interest, her follow-up questionnaire, 2 to 8 years after the WCB decision was reached, found 15% of subjects to be free of asthma symptoms, similar to our finding of 19%. The outcome of asthma among all patients whose claims were accepted for OA and who were reassessed was similar to previous studies3,17-19 in that clearing of asthma occurred in only 19%, a mean of 1.9 years after the first assessment (Table 6). However, an additional 47% had milder asthma. Among subjects with improvement and those with clearing of asthma, the positive change occurred at a mean of 0.9 years, suggesting that it is reasonable to perform the assessment for permanent disability around 2 years after leaving work. In the whole group at follow-up, the prognosis appeared to be worst in those with AA who had no prior history of asthma; 48% of the 33 seen were worse at follow-up as compared with 14% of those with OA and no prior history of asthma. Our findings of the prognostic importance of early diagnosis of OA and removal from exposure, and the better prognosis in those with initial relatively mild pulmonary function impairment are consistent with findings of Chan-Yeung et al3 in cedar workers and the findings of Mapp et a17 and Pisati et a16 in isocyanate-induced asthma, and extend their findings to a larger group of patients with OA from many more causes than previously reported.8'9 Further studies are needed to assess whether early recognition can be best achieved by appropriate surveillance programs in industries such as those using isocyanates that account for most compensated cases of OA in Ontario. ACKNOWLEDGMENT: The authors wish to thank Mary Harpur and Justina Greene for data gathering and processing, and Dr. C. Smith and Dr. P. Carr of the Ontario Workers' Compensation Board for their cooperation in this study as well as Kerrie Cheung for typing assistance. REFERENCES 1 Malo JL. 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