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Report to the Workers' Compensation Board on Respiratory Complications among Workers Receiving Compensation for Non-malignarit Respiratory Disease March 1993 Industrial Disease Standards Panel IDSP Report No. 11 Toronto, Ontario C60776 0004 In 1985 the Ontario legislature established the^ Industrial;Diseaise ' Standards Panel (IDSR) to investigate and idenofy' diseases related to work. The Panel is independent ofboth the .Ministry ofLabour and the Workers' Cornpensation Board. At the end of each fiscal year the WCB reimburses the Ministry for tiKe Panel's expenditures f.- The Panel's authority flows from secaon956fthe Workers ' Cam- ' 1- ' (8) (a) to investigate posable industrial dise^es;;, . T* (b) to make findings as to whether a probableconnection occupation in Ontario; .'t, ; t'.. or (c) to create, develop and revise criteria'for the aquation!6f .;claims respecting industrial diseases';;ahd^;>y.tf;.v (d) to advise on eligibility rules regarding compensation for claims. j,*;, ' Once the Panel makes a finding, the WCB is required to publish `bt !)-' To assistwith its work the Panelhasasmall staffdfresearchers, analysts and support people. In addition to ics own rafl^; the Panel > relies heav^yqntheadvicepfoutadeexpertsinsdence.thedicine Main entry tinder tide: cations amongworkersreceivingoompensation fornon-rrulignant ' respiratory disease (IDSPrqjort, ISSN 08^-7274; no. 11) -v'/:/ Includesbibliographical references;'; ISBN 0-7778-1004-2 =; V * \; J 1 '!?' '* s ' fA;' , A^A A 1. Respiratory organs--Diseases. 1. Ontario.1 Industrial Disease,?'; ' Standards Panel. H. Series. RC73I.R46 1992 616.2 093-092530^2 Additional copies of this publication are available.in writing: v ` Industrial Disease Standards Panel -h, ,y- ?v ''i ,n:j,, ' 69YongeStreet,Suite 1004 "AyTA'.; TtM-onto, Ontario M5E IK3 (416)327-4156 r i? AdA'vA.A'A' Report to the WCB on Respiratory Complications among Workers NMRD Panel Membership Panel Member5 Ms. Nicolctte Carlan (Chair) Dr. Carol Buck Mr. James Brophy Mr. William Elliott Ms. Nicole Godbout Mr. John Macnamara Mr. Homer Seguin Dr. Michael Wills Appointment May 16, 1991 to May 15, 1994 June 1, 1991 to June 16, 1994 January 23, 1992 to January 22,1995 November 7, 1991 to November 6, 1994 December 16, 1992 to December 15, 1995 November 7, 1991 to November 6, 1994 May 28, 1992 to May 27, 1995 November 7, 1991 to November 6, 1994 March 1993 C60776 0006 iV * V Report to the WCB'on Respiratory Complications among Workers NMRD Panel Staff - l ' H. ' '' -1' . Carolyn Archer: y;?; ; : r; Senior Research Officer RobertChase1? -? Medical Consultant : - ; Chris Leafloor : . . ..; ' .' / Counsel Peter Loewenthal {.? " Data Entry Clerk ;, Francis Macri yy:';-!? 1 s, i - ?-y Cara Melbye ? ?, ; Policy Analyst Policy Analyst Susan Meurer "/ ;i. PolicyAnalyst John Risk ?. ?/"y, , Researcher Dennis Shannon ? ; i . Researcher Safiriu Starey T ; , ; Administrative Officer Tracy Soyka ' ' Secretary . 'y - Jason Tung Industrial Hygenist . ( ;,- . *" r;-f ' M3rdi 1993 (L: : ''S' . h? St' .. -.-1' C-6Q7.7Q 0007 Report to the WCB on Respiratory Complications among Workers NMRD Table of Contents > Letter of Transmittal 2. Report to the Workers' Compensation Board on Respiratory Complications among Workers Receiving Compensation for Non-malignant Respiratory Disease / 3. The Nature of the Issue / 4. How the Panel Proceeded 2 5. Additional Analyses on Ontario Workers Receiving Compensation for Silicosis or Asbestosis 6 6. Panel Conclusions 8 7. Panel Recommendations 9 8. References 11 9. Appendix A--Lung Function 14 March 1993 C60776 0008 O <S) Ontario Mmistdre Ministry of du Travail Labour de I'Ontario industrial iscase tandards Panel Comite des normes en rnatiere de maladies protessionneiles 69 Yong# Slrr-t lOin Pioo Toronto Gnia^o M5E 1K3 Tijnon 4 16/02 7 --* 1S6 Fjcs*n-*iJ* 416/327--4166 69 ru VoVj^ 10* etag Toronto (Ontar.oi M5S 1KJ Tl*orion: *16/327-4 iS6 Facsimile *16/327-4 166 March 25, 1993 Mr. Odoardo Di Santo Chair Workers' Compensation Board 2 Bloor Street East, 20th Floor Toronto, Ontario M4W 3C3 Dear Mr. Di Santo: Enclosed is a copy of the Panel's "Report to the Workers' Compensation Board on Respiratory Complications among Workers Receiving Compensation for Non-malignant Respiratory Disease". I would be pleased to discuss the Report with you. Please let me know when it would be convenient to do so. Sincerely, Nicolette Carlan Chair Enclosure C60776 0009 Report to the WCB on Respiratory Complications among Workers NMRD The Nature of the Issue It is well known that the re corded cause of death, especially in complex, multifactorial cases, is frequently arbitrary or misdiag nosed. Adjudicatory problems surrounding the recorded cause of death can result in failure to recognize the compensable respi ratory disease as a significant contributing factor in the death of the worker with resultant non payment ofsurvivor's benefits to dependents. The widespread effects on die body as a result of disease mav be more complicated than the effects of a single traumatic injury. Other health problems experienced by workers who have contracted a work-related disease arc often exacerbated by the disease. These health problems however, arc not a direct conse quence of work. The Industrial Disease Standards Panel has dealt with one such issue in its Report No. 10, The Report to the Workers' Com pensation Board on Cor Pulmonale (1). In that report, the Panel found a probable connection between a compensable respiratory disease and the development of cor pulmonale, or right heart failure. This condition, though not directly caused by work, nev ertheless may develop as a secondary condition. The Board has in place a policy (Document No. 03-04-02) dealing with secondary conditions resulting from a work-related disability. The policy reads: "Workers sustaining secondary conditions that are caus ally linked to the work-related injury will derive benefits to compensate for the further aggravation of the workrelated disability or for new injuries" (2). Concern has arisen however, that workers receiving com pensation for a non-malignant respiratory disease [NMRD] sometimes fail to have secondary conditions causing deteriorat ing lung function recognized and compensated accordingly dur ing life. Furthermore, it is well known that the recorded cause of death, especially in complex, multifactorial cases, is frequently arbitrary or misdiagnosed Adjudicatory problems surrounding the recorded cause of death can result in failure to recognize the compensable respiratory disease as a significant contributing fac tor in the death of the worker with resultant non-payment of survivor's benefits to dependents. In developing this report, the Panel has attempted to address three issues: 1) Do workers commonly experience other respiratory prob lems secondary to compensable non-malignant respiratory diseases [NMRD]1? 1 Non-tmlignanc rcspirarary disease, for the purpose of this report, includes both re strictive and obstructive diseases. Restrictive disease refers to the restriction ofthe volume of air in the lung. Restrictive disease can involve the alveoli or air sacs and supporting tissue. Examples of compensable restrictive lung diseases would be asbestosis or other pneumoconioses. Obstructive disease indicates an obstruction to the flow of air through the cubes in the lung. Potentially compensable examples fh" struedve disease are emphysema, chronic bronchitis and asthma. Some diseases show both patterns. (For a discussion of the normal lung function and how various diseases impinge on that fanedoning see Appendix A.) March 1993 C60776 0010 1) It the answer to issue one is yes, are these additional respira tory problems likely to result in increased disability and mor tality? 3) What is the likely effect of a compensable respiratory disease when the worker suffers from other concurrent nonoccupational respiratory disease? The Panel is well aware that these are difficult questions, be cause although some occupational lung diseases are distinct enti ties, "most work-related respiratory morbidity and mortality is the result of an increase in bronchitis, emphysema, lung cancer and tuberculosis, in which non-occupational factors also play an important part" (3). Indeed, according to the former Advisory Committee on Occupational Chest Diseases, "concurrent nonoccupational respiratory disease is the biggest assessment confounder for the ACOCD" (4). How the Panel Proceeded If underlying respiratory disease has damaged this system, then clearance of inhaled infectious agents or of materials produced during the response to infection may be impaired, making it easier to acquire an infection and more difficult to get rid of it Background Information To assist the Panel in developing the rationale for this report, the Panel asked Dr. Linn Holness of the Department of Occu pational and Environmental Health, St. Michael's Hospital, to provide, in lay terms, an explanation of normal lung function [Appendix A] and an explanation of the impact of lung disease on lung function (5). The latter text on adverse outcomes, with modifications, follows. The respiratory tract has a number of ways by which it pro tects itself against infections. In the airways, these defense mechanisms include coughing and mucociliary clearance. The mucociliary clearance mechanism consists of die appropriate type of mucus to cany inhaled agents out of the lung and the abated cells (cells with hair-like projections which beat in sequence)to move the mucus up the respiratory tract to be ex pelled by coughing or swallowing. If underlying respiratory disease has damaged this system, then clearance ofinhaled infec tious agents or of materials produced during the response to in fection may be impaired, making it easier to acquire an infection and more difficult to get rid of it Chronic bronchitis and asthma may affect these airway defence mechanisms. If coughing is de pressed or ineffective this may decrease the removal of potential infectious agents and also make the clearance of mucus more dif ficult once die infection has occurred. In the lower respiratory tract, the air sac (alveolar) and lung tissue (parenchymal) region has several methods of defence. Al veolar macrophages (cells which consume inhaled materials) help to dear the air sacs. Inflammatory and immune responses are also important in defending this area. The impairment ofcell mediated immunity is particularly important for tuberculosis. Diseases which affect this region, such as silicosis and asbestosis, may result in impairment of these defence mechanisms and make it more difficult to fight infection. March 1993 2 C60776 0011 Report to the WCB on Respiratory Cornplications among Workers NMRD In chronic lung diseases some ot the above mechanisms mav be impaired, making it more likely that the affected individual will develop an infection and also making it more difficult to fight the infection. Further, the impairment resulting from the lung infection, added to the impairment from the underlying lung disease may be enough to reduce severely the individual's ability to transfer oxygen and carbon dioxide adequately. In general, individuals with occupational lung disease with significant impairment may still be able to manage if they have no other lung problems. For example, they may have a moderate reduction in their lung function which reduces the amount of oxygen in their blood, but even though it is reduced there is still enough for them to function. However, other additional respira tory problems, either acute problems like pneumonia, or chronic, such as chronic obstructive lung disease, which cause additional impairment in lung function, may reduce their lung function to a critical level. This results in respiratory failure which is charac terized by an insufficient level of oxygen in the blood. Medical Opinions As part of its investigation, the Panel wrote to three respirologists and posed several questions concerning compensable respi ratory illness. In one of those questions, the respirologists were asked to address the following issue: Does a compensable respiratory illness affect the worker's ability to deal with other non-work related respiratory illnesses such as pneumonia or bronchitis? [N.B. The classes of respiratory impairment referred to be low are those outlined in the American Medical Association Guides to the Evaluation of Permanent Impairment (6).] (1) "Yes, it is well established that many of the occupational lung diseases such as asbestosis, silicosis, asthma, byssinosis are associated with excessively frequent lung infections. It is therefore appropriate that any such acute condition be com pensated and if causing additional loss of function, compen sation should be applicable as occupationally related. Death under such circumstances should be accepted as work re lated. Again, I believe that this opinion would reach general agreement for cases in die Classes 3 & 4, but would have to be considered individually for cases in the Class 2" (7). Any chronic lung condition makes an episode of pneumonia or acute bronchitis more danger ous, and may lead to a further decline in lung function. (2) "The answer to this is an unequivocal "yes." For example, acute silicosis, as found in sandblasters, predisposes to acute pneumococcal pneumonia. Any chronic lung condition makes an episode of pneumonia or acute bronchitis more dangerous, and may lead to a further decline in lung function" (8). March 1993 C60776 0012 Report to the WCB on Respiratory Complications among Workers NMRD (3) "Were a subject with severe impairment of lung function due to asbestosLs, complicated silicosis, complicated coal workers' pneumoconiosis, or hard metal disease to develop pneumonia, it would certainly jeopardize to some extent his chance of recovery. There is litde doubt that this is true. In regard to bronchitis, this is not so in that diis condition pro duces little or no effect on lung function. I would stress that even were pneumonia to occur, it would only be those sub jects who have occupational disease that is fair advanced and associated with fairly severe respiratory impairment that there would be a significant effect either on prognosis or the duration of morbidity" (9). In summary, there was general agreement that many nonmalignant respiratory diseases are associated with excessively frequent lung infections. Opinion differed as to the likely conse quences of a bout of acute bronchitis. There was also general agreement that the compensable respiratory condition would have to be fairly severe (AMA Class 3 or 4] before there would be a significant effect on prognosis. One physician felt that work ers whose impairment was rated as a Qass 2 would have to be evaluated on a case by case basis if death resulted from a compli cating lung infection. The Literature According to Board statistics, the majority of awarded claims for NMRD are for asbestosis, silicosis and occupational asthma. These diseases will therefore be the focus of our review. There is no question that victims ofasbestosis frequently suffer from a shortened life-span. Likewise, compensatedsilicotics showed reduced life expectancy due largely to deaths from tuber culosis and non-malignant respi ratory disease. Deaths among Asbestotics and Silicotics: There is no question that victims of asbestosis frequendy suffer from a shortened life-span. The five-year survival of workers re ceiving compensation for asbestosis was only 69% of that of agematched Ontario males. The ten-year survival of these workers was only 53% of that of the age-matched Ontario males (10). Likewise, compensated silicotics showed reduced life expectancy due largely to deaths from tuberculosis and non-malignant respi ratory disease (11). Brown et al. studied "the Homestake cohort" of 3,328 white gold miners who worked full-time underground for at least a year between 1940 and 1965 (12). Exposure to silica as measured by total dust was strongly associated with mortality due to respi ratory tuberculosis [SMR 364] and NMRD [SMR - 279], The researchers also looked at a subcohort of workers first employed after 1951, when dust levels were thought to have been substan tially reduced. Although limited by small numbers (only 109 deaths] the authors report "it appears that the pattern of mortal ity by latency and length of underground employment for nonmalignant respiratory disease is similar to that seen in the entire March 1993 4 C60776 0013 Report to the WCB on Respiratory Complications among Workers NMRD March 1993 cohort". The risk tor NWIRD was high with an SMR of 286 (based on 4 deaths observed vs. 1.4 expected). Based on padiology reports, at least two-thirds of die individuals in the large cohort who died from NTMRD had a confirmed diagnosis of sili cosis. In the post-1951 group, of die four deaths from NMRD, none had silicosis recorded on their death certificates. Finkelstein et al., studied the mortality of 1190 Ontario min ers with compensable silicosis and found an SMR of 180 for all causes (11). For NMRD, the overall SMR was 737, and the sub group with the longest standing disability, and hence the most complete mortality profile, showed an enormous SMR of 1,140. Schuler and Runner studied selected causes of death among 2,399 certified or compensated silicones (13). Forty percent of the deaths were from NMRD including bronchitis and emphy sema while the corresponding figure for the general population was reported as at most 10-15%. In Italy, Zambon et al. also investigated 1,234 compensated silicotics with 697 deaths (14). There was a large excess of deaths due to infectious disease (8th/ICD: 001-136),SMR of 1,960 in cluding tuberculosis and silico-tuberculosis. There was also an exoess due to respiratory diseases including silicosis (ICD codes 460-519), with an SMR of 741. The authors state that tuberculo sis, silico-tuberculosis and silicosis account for almost all of the excess mortality in the silicotics. Cookson, Musk, et al. studied the mortality experience of 354 claimants for compensation for asbestosis who had worked in the Wittenoom croddolite mine and mill in Western Aus tralia (15). All-cause mortality in the cohort had an SMR of 265, and the authors state that "pneumoconiosis, malignant pleural mesothelioma, respiratory cancer, bronchitis and emphysema, and tuberculosis all contributed to excess mortality." They speculate that the increase due to bronchitis and emphysema could be "due to unrecognized pneumoconiosis and misclassification of the cause of death, or to a high proportion of cigarette smokers in the population". However symptoms of bronchitis have been reported among non-smoking asbestotics (16) and air flow limitation may be caused by peribronchial fibrosis resulting from asbestos itself (17-20). Number of radiographic opacities, age at claiming compensation, work in the mill, and degree of disability awarded by the Pneumoconiosis Board were predictors of survival but estimated total exposure to asbestos was not. The mortality of 1072 workers from the register of compen sated silicotics in Quebec who first received compensation be tween 1938 and 1985 was investigated by Infante-Rivard, Armstrong et al.(21). Only 27.7% of those compensated were miners, with 44.9% from foundries, 13.2% granite workers, 4.8% pottery, and the rest miscellaneous or unknown. The all cause SMR was 216 with a 3-fold risk of death from lung cancer, SMR = 347. Other elevated SMRs included infectious diseases at 2974, and non-malignant respiratory disease at 975. Causes of 5 C60776 0014 Report to the WCB on Respiratory Complications among Workers NMRD death in the cohort were malignancies (22.6%), pneumoconiosis (18.6%), tuberculosis (13.9%), myocardial infarction (10.6%) and chronic lung disease (7.1 %). Other causes accounted for 23.5% of deaths. In one of the few studies that provides a detailed breakdown of deaths from NMRD, Ng, Chan and Lee assessed mortality among 1419 subjects in the Hong Kong Silicosis Register from 1980-1986 (22). The following are the relevant results obtained: Cause ofDeath (ICD9) All cause Infectious Diseases Pulmonary Tuberculosis Respiratory Diseases Pneumonia Chronic bronchitis Emphysema and Asthma Chronic airway obstr. Pneumoconiosis Others SMR 302 252 383 1269 295 745 770 60994 236 Additional Analyses on Ontario Workers Receiving Compensation for Silicosis or Asbestosis At the request of Panel Staff, Dr. Murray Finkelstein of the Ministry of Labour Health Studies Branch reviewed his data on compensated asbestodcs and silicodes to ascertain if the excess mortality in these two cohorts were attributed to the compen sated respiratory disease alone (23). For the asbestodcs, the res piratory causes of death were all coded to pneumoconiosis, except for bronchopneumonia and tuberculosis. The SMRS for all non-silicosis respiratory diseases were as follows: SMRsJbr Non -Malignant Respiratory Disease ! Cohort Obs [Total] Exp SMR 1940-49 1950-59 1960-69 1970-78 21 [118] 13 [78] 20 [54] 5 [14] 10.9 11.3 9.3 2.8 193 115 215 179 Total 59 34.3 172 Thus out of a total of 264 deaths attributed to non-malignant i respiratory disease in this cohort, 59 or 22% were attributed to respiratory disease other than silicosis. March 1993 C60776 0015 Report to the WCB on Respiratory Complications among Workers NMRD Occupational Asthma The inherent difficulty in assessment of impairment/disabilicy in patients with occupational asthma is widely recognized. The American Medical Association guidelines (Guides) for evaluation of impairment are widely used by Compensation Boards but have come under criticism as inappropriate for patients with asthma who have variable air-flow obstruction (24). Morbidity and mortality from asthma have been increasing and there has been speculation that one of die contributing factors to the deaths has been a failure on the part of physicians to recognize the true severity of the condition in an individual patient (25). Older adults with asthma show increased mortality in die winter months which may be due to the frequent association with chronic obstructive lung disease (26). Respiratory infections con tribute to mortality among asthmatics (27). From 1979 through 1988, the annual asthma mortality rate in Prince Edward Island exceeded the national rate for all years except 1980. This prompted Sweet et al. (28) to undertake a study, one of the aims of which was to validate the diagnosis for all asthma deaths in P.E.I. between 1984 and 1988. The re searchers obtained information from autopsy reports, death cer tificates and hospital records. A total of 34 deaths were reported to have been caused by asthma. Although the number of cases was small, the study is relevant in that it showed that the re corded deaths of patients who die at age 50 or less are more likely to be valid than the records of older patients, who typically have other co-morbid conditions such as chronic obstructive lung disease and cardiovascular disease. The authors conclude that the recorded cause of death on the certificate which was used and is the standard form for all of Canada was frequendy invalid due to physician error and misdassification of the causes of death resulting from the correct use of international coding rules which give precedence to certain causes of death regardless of the way they are recorded on the death certificate. Once again, the impossibility of relying on death certificate data alone to determine the true cause of death is highlighted. Many patients diagnosed with chronic obstructive pulmo nary disease have a combination ofchronic bronchitis, asthma, and emphysema (29). Complicating upper respiratory infections are frequent (30). Although smoking is the most prominent etiologic agent, other contributing factors identified indude air pollution, respiratory infections and occupational exposures (31). Furthermore, it is estimated that only one-half of all patients dy ing of chronic airways obstruction are correctly designated on death certificates (31). March 1993 C60776 0016 Pane! Conclusions For compensation purposes', the issue remains, did the compen sable non-malignant respiratory' disease lead to complications during life resulting in more severe lung impairment, and did the NMRD make a significant contribution to the worker's death? The Panel is in agreement widt the statement that the boundary between occupationally caused, work-aggravated and non-work-related lung diseases is "indistinct, reflecting the multi factorial nature of the diseases" (27). Nevertheless, in our It is clear that workers suffering view, it is dear that workers suffering compromised lung func compromised lung function due tion due to occupational respiratory disease are more likely to to occupational respiratory dis suffer from more frequent and more severe respiratory infections ease are more likely to suffer such as pneumonia than the general population. This is sup from more frequent and more ported by the medical opinions we soliated and by the medical severe respiratory infections such literature. as pneumonia than the general In addition, the consistendy elevated SMRs in the literature population. for all manner of respiratory complications among workers with compensable respiratory disease strongly supports the position that such workers are much more likely to the from such compli cations than the general population. Even when studies among workers compensated for a respiratory disease indicate a defiat of deaths from a particular type of NMRD such as emphysema or bronchitis, one cannot condude that this is in fact the case. It is possible that such deaths are actually subsumed among other groups, such as deaths attributed to silicosis, for example, reflect ing the frequendy multifactorial nature of the deaths. Finally, it would seem only common sense chat an individu al's lung function reflects the cumulative impact of the insults it has received. As our consultant has stated: "individuals with oc I cupational lung disease with significant impairment may still be able to manage if they have no other lung problems. However, if they have additional impairment, [induding non-work related I impairment], their lung (unction may be reduced to a critical level". The Panel is convinced that fair public policy demands compensating those individuals whose ability to survive their cu mulative lung damage is seriously compromised by the existence of a compensable respiratory impairment. i March 1993 C60776 0017 Report to the WCB on Respiratory Complications among Workers NMRD Panel Recommendations The Panel has already considered die occurrence of Cor Pul monale among those with recognized claims for non-malignant respiratory disease. In some ways, cases of Cor Pulmonale can be viewed as a subset of what would appear to be die larger problem of correct determination of those complications of compensable NMRD that lead to increased disability or death among work ers. The Panel is aware that certain respiratory diseases can and do arise quite independendy of any workplace exposure. The Panel has already discussed many of these issues in its deliberations surrounding Cor Pulmonale. The logic requiring a thorough investigation into the cause of death to identify Cor Pulmonale among workers in receipt of benefits for non-malig nant respiratory disease is equally applicable to the larger group. The Panel is aware of the Board Policy (Document No. 03-04-02) which deals with secondary conditions resulting from a work-related disability. The policy reads: "Workers sustaining secondary conditions that are caus ally linked to the work-related injury will derive benefits to compensate for the further aggravation of the workrelated disability or for new injuries". However, the Panel is of the opinion that this policy and its im plications for additional compensation are not well-known to ei ther workers or their physicians. As a result of these deliberations the Panel was able to make findings and recommendations aimed at assisting the Board in the adjudication of these difficult claims. The Panel finds that workers who suffer from compensable nonmalignant respiratory diseases for which WCB benefits for im pairment have been paid, are likely to suffer from additional respiratory problems. Specifically for those workers the Panel finds: 1. A probable connection between the occurrence of non-malignant respiratory disease and the occur rence of respiratory infections. 2. A probable connection between the increased incidence of infection and an increased impairment during life. Furthermore, among these workers there is a greater probability of death resulting from respiratory infections. 3. An increase in mortality from concurrent noncompensable non-malignant respiratory disease as a result of the cumulative impact on lung function. March 1993 C60776 0018 Report to the WCB on Respiratory Complications among Workers NMRD In accordance with these findings the Panel recommends: 1. The Board should notify workers in receipt of a WCB award for an impairment due to non-malig nant respiratory disease and their physicians of foe existence of Policy Document No. 03-04-02. This will ensure that eligible workers are aware that ad ditional enddement may be payable for secondary respiratory conditions. 2a. The Board should investigate foe cause of death for all workers who during their lifetimes were in re ceipt of benefits for a non-malignant respiratory disease. 2b. Notwithstanding foe recorded cause of death, if foe compensable non-malignant respiratory disease is judged to have significantly contributed to foe death of foe worker, foe appropriate dependency benefits should be paid. I i March 1993 10 C60776 0019 Report to the WCB on Respiratory Complications among Workers NMRD References * Report CO the Workers' Compensation Board on Cor Pulmonale. (1DSP Report no. 10). Toronto -. Industrial Disease Standards Panel, 1992. 2. Workers' Compensation Board. Operational Policy Manual. Toronto: Worker's Compensation Board, 1991. 3. Elmes.P.C. Occupational respiratory disease. In: HowardJ.K.;Tyrer,F.H.,eds. Textbook of Occupational Medi cine. London: Longman Group, 1987. p.341. 4. RoosJ.O. Evaluation of respiratory impairment in On tario pneumoconioses procedures. Occupational Health in On tario. Vol.7,no.2(Spring 1986). p.78-91. 5. Holness,L.D. Re: Other respiratory complications - com pensated lung disease. [Letter to C. Archer], November 16, 1992. 6. American Medical Association. Guides to the Evaluation of Permanent Impairment. 3rd. ed. Chicago: American Medical Association, 1990. p. 125. 7. Begin,R. [Letter to C.Archer on the effects of compensable respiratory illness].March 13, 1992. 8. Bates,D.V. [Letter to C. Archer on the effects of compensable respiratory illness]. January 23, 1992. 9. Morgan,W.K.C.[Letter to GArcher on die effects of compensable respiratory illness]. February 12, 1992. 10. Ftnkelstein^L; Kusiak,R.; Suranyi,G. Mortality among workers receiving compensation for asbestosis in Ontario. Cana dian Medical Association Journal. Vol.l25(Aug.l,1981). p25962. 11. Finkelstein,M.; Liss,GJM.;et al. Mortality among workers receiving compensation awards for silicosis in Ontario 19401985. British journal of Industrial Medicine. Vol.44{1987). p.588-94. 12. Brown,D.P.;Kaplan,S.D.;et al. Retrospective cohort mor tality study of underground gold mine workers. In: Goldsmith, D.F.;Winn,DM.;Shy,CJVL,eds. Silica, Silicosis, and Cancer. (Cancer Research monographs, vol.2). New York: Praeger, 1986. p.335-350. March 1993 11 C60776 0020 March 1993 i 13. Schuler,G.;RuttnerJ.R. Silicosis and lung cancer in Swit zerland. In: GoldsTnith,D.F.;Wlnn,D-M.;Shy,CJVI.,eds. Silica, Silicosis, and Cancer. (Cancer Research monographs, vol.2). New Yorlc Praeger, 1986. p.357-366. 14. Zambon,P.;Simonato,L.;et al. A mortality study of work ers compensated for silicosis during 1959 to 1963 in die Veneto Region ofltaly. In: Goldsmith,D.F.;Winn,DJVL;Shy,CJVl.,eds. Silica, Silicosis, and Cancer. (Cancer Research monographs, vol.2). New York: Praeger, 1986. p.367-374. 15. Cookson,W.O.;MuskA-W.;et al. Compensation, radio graphic changes, and survival in applicants for asbestosis com pensation. British Journal of Industrial Medicine. Vol.42(l985). p.461-468. 16. Husskonen,M.S. Clinical features, mortality and survival of patients with asbestosis. Scandinavian journal of work, envi ronment and health. Vol.4(l978). p.265-74. 17. Muldoon,B.C.;Tumer-WarwickjVl Lung function stud ies in asbestos workers. British Journal of Diseases of the Chest. Vol.66(1972). p.121-32. 18. Foumier-Massey,G.;Becklake,M.R. Pulmonary function profiles in Quebec asbestos workers. Bulletin de PhysioPathologie Respiratoire (Nancy). Vol.l 1(1975). p.429-45. 19. Jodoin,G.;Gibbs,G.W.;et al. Early effects of asbestos on lung function. American review of respiratory diseases. Vol. 104(1971). p.525-35. 20. Heitt,DJVL Experimental asbestosis: an investigation of functional and pathological disturbances. British Journal of In dustrial Medicine. VoL3 5(1978). p. 135-45. 21. Infinte-Rivard,C.Armstrong, B.;et al. Lung cancer mor tality and silicosis in Quebec, 1938-85. The Lancet. (Dec.23/ 30,1989). p.1504-07. 22. Ng,T.P.;Chan,S.L.;LeeJ. Mortality of a cohort of men in a silicosis register further evidence of an association with lung cancer. American Journal of Industrial Medicine. Vol. 17(1990). p.163-71. 23. FmkeisteinJVLM. [Letter to CArcher, IDSP Staff). June 1, 1992. 12 C60776 0021 Report to the WCB on Respiratory Complications among Workers NMRD 24. Chan-Yeung,M. Evaluation ot Impairment/ Disability in Patients with Occupational Asthma. American Review of Respi ratory Diseases. Vol. 13 5(1987). p.9S0-51. 25. Nicklas.RA Perspective on asthma mortality. Annals of Allergy. Vol.63 (6 Pt 2)<Dec 1989). p.578-84. 26. Anderson,H.R. Epidemiology of asthma. British Journal of Hospital Medicine. Vol.47,no.2(Jan.23-Feb.4,1992). p.99-104. 27. Abrams,HiC. Aggravation of lung disease. Scandinavian Journal of Work, Environment and Health. Vol. 10, Spec.no .6 (Dec 1984). p.487-93. 28. SweecL-; FanJ.; O'Neill J. A validation study of asthma, Prince Edward Island, 1984-1988: l.Cause of death. Chronic Diseases in Canada. Vol.l3,no.l(Jan.-Feb.l992). p. 1-3. 29. GrossNJ. Chronic obstructive pulmonary disease. Cur rent concepts and therapeutic approaches. Chest. Vol.97(Suppl. 2) (Feb. 1990). p.l9s-23s. 30. Mahler,DA; Barlow,P.B.; Matthav.RA Chronic obstruc tive pulmonary disease. Clinics in Geriatric Medicine. Voi.2, no.2(May 1986). p.285-312. 31. Enarson,D A; Newman,S.C.; et al. Chronic airways ob struction leading to chronic hypoxemic respiratory failure, an estimate of the size and trend of the problem in Canada. Bulletin IncUnion Tuberc Lung Dis. Vol.66,no.2-3(Jun.-Sept. 1991). p. 113-23. March 1993 13 C60776 0022 Report to the WCB on Respiratory Complications among Workers NMRD 1 Appendix A-- Uoig Function j il 1 The tissues of the body require oxygen io hincnbn;'Ehc carbon dioxide they produce must also be removed. HThe transfer of oxv- : gen and carbon dioxide between thetissucs and the external en vironment is accomplished by the coordinated actiori'of the lungs and cardiovascular systernunderthe control ofthe nervous system. The main function of uie lungs is the transfer ofoxygen arid;. : carbon dioxide betweeiythe blood and the air. Air which con tains oxygen is inhaled intp the lungs.and transferred to the blood ,and red blood cells in the small blood vessels in thelung." Simi-. larly, the carbon dioxide produced in the body, istransported through the blood vessels to the liing where it,is transferred to " the air which we exhale. ; : ' J %V'`- The air moves into and out of the lungs through a branching structure of tubes or ainvaysJAsIthe airwaysbranchthe indi- ; vidual airways become progressively smaller in diameter. The large central airway is oiled die trachea which divides into bron- ;. y/- chi and the small airways are bronchioles:The air moves; '}; . through the airways by the bdlows-like action of the chest. The ; airways end in many tiny air sacs called alveoli which have thin walls and a rich supply ofsmall blood vessels called capillariia. Because of the large number of alveoli diereiis a large surfaoe area'for the transfer of the oxygen and carbdn dioxide. There are three components involved iri the normal func tioning ofthe lungs. *>?".: 1. Ventilation--the movement of the air in and out of the lungS . ' ' V; 2. Diffusion--die transfer of gases between the alveolus and[, / thecapillary t ; .. /'; 3. Perfusion--the flow of blood through the jungs \ ."T; j Ventilation depends on three^factors; 'T ;V ' l i die size or volume of die lungsi' , , { j ' !' ; * 2. die expansibility of elasticity ofthe lungs, ;and 3; die ability to move the air through the airways which is fe-. , lated to the resistance to flow in the airways. t ,, : .<' r ^ The fictors may be assessed by various lung function tests. A ^ number ofdifferent volume measurements can be made; Some ofthe common lung volumes assessed indude: Static Lung Volumes- - . ; : ,, 1. Total lung capacity (TLCh-die total amount of air in die lungs at the end Ofa fiill; inspiration , March 1993 1 : ...- -rj': \ ^ j'; ; C60776 0023 Report to the WCB on Respiratory Complications among Workers NMRD 2. Vital Capacity (VC)--the amount of air that can be expelled after a full inspiration 3. Residual Volume (RV)--the amount of air left in the lungs at the end of a full expiration 4. Tidal Volume (VT)--the amount of air expired in a normal breath 5. Functional Residual Capacity (FRC)--the amount air left in the lungs at the end of a normal expiration Dynamic Lung Volumes (volumes measured with a forced, rapid expiration) 1. Forced Vital Capacity (FVC)--the amount of air that can be forcibly and rapidly exhaled after a foil inspiration 2. Forced Expiratory Volume in 1 Second (FEV,)--the amount of air expelled in the first second of expiration The expansibility or elasticity of the lungs can be measured as the compliance of the lung. This test is more difficult to do (the individual has to swallow a balloon) and is not done on rou tine lung function testing. The ability to move air through the airways can be assessed in several ways. A simple measure is the ratio of FEV, to FVC which compares the amount exhaled in the first second with the total amount of air exhaled during a forced, rapid expiration. The flow of air can also be measured at various lung volumes. Common flow rates measured include: 1. Forced Expiratory Flow between 25% and 75% of the FVC 2. Forced Expiratory Flow at 50% of the FVC (FEF50) 3. Forced Expiratory Flow at75%ofthe FVC (FEF7S) The FEF,, represents flow in the smaller airways. Airway resistance can also be measured. Most of the resistance to airflow occurs in the larger airways. Therefore, airway resistance will not necessarily detea abnormalities in small airways unless the ab normality is large. Diffusion or the transfer of gas between the air in the alveo lus and the red blood cells in the capillaries depends on four factors: 1. the difference in the pressure of oxygen between the alveolus and the capillary March 1993 15 C60776 0024 2. the size of the barriers that the gases have to pass through which include the fluids and cells lining the alveolar space, the alveolar membrane, the capillary membrane, the fluid or plasma in the capillary, the membrane of the red blood cell and the fluid inside the red blood cell, 3. the surface area available for the transfer to take place, 4. characteristics of the blood (e.g., the number of blood cells available). The diffusing capacity for carbon monoxide (D, CO) pro vides a measure of the overall diffusion of gas from the inhaled air to the red blood cell. Perfusion depends upon the flow of blood through the blood vessels in the lung. Diseases which affect the blood vessels in the lungs such as blood dots (pulmonary emboli) may impair perfrision. Another simple test which is performed which provides an overall assessment of the function of the lung is the measure ment of the amount of oxygen and carbon dioxide in arterial blood expressed as the partial pressure oxygen and carbon diox ide (Pa02 and PaC02). There are many different types of lung disease which may adversely affect lung function. Two main types of abnormalities which are often described are obstructive and restrictive defects. An obstructive defect results in the decrease in the FEV,/ FVC ratio and flow rates and an increase in resistance. These abnormalities would be found in chronic bronchitis with assodated airway obstruction, asthma and emphysema. A restrictive defect results in a decrease in lung volumes. The FEV/FVC ratio is maintained even though die actual vol umes are decreased Typical restrictive lung diseases are intersti tial disease such as idiopathic pulmonary fibrosis, asbestosis, and hypersensitivity pneumonitis. Defects in diffusing capacity may be found in some obstruc tive disease (emphysema) and restrictive disease (idiopathic pul monary fibrosis, asbestosis, and hypersensitivity pneumonitis). March 1993 16 C60776 0025