A Workers' Compensation Claim Population for Occupational Asthma*

A

Workers' Compensation

Claim

Population

for

Occupational Asthma*

Comparison of

Subgroups

Susan M. Tarlo, MBBS, FCCP; Gary Liss, MD; Paul Corey, PhD; andIrvin Broder, MD

Study objectives: (1) To compare patientswith claims submittedtotheOntarioWorkers'CompensationBoard

(WCB)foroccupational asthma,inrelationtotheWCB

decisions reached ofoccupational asthma (OA);

aggra-vationofasthmafromirritantexposures(AA);unrelated asthma; no asthma; and (2) to assess determinants of

outcomeofWCBaccepted claimsatpermanent

disabil-ity assessments.

Design: A retrospective reviewof609claims submitted to theWCB 1984to 1988.

Results: TheWCBdecisionreached wasOAin39% of

claims,mostlyattributedto isocyanates(57% ofthese).

A further 39% were accepted for AA. Exposure to a

known sensitizer occurred in91% with OA andto an

irritant in 67% with AA. Fortypercent with AA were

attributedtoaspilloraccidentalexposureand68%had preceding asthma. Those with AAwere more likelyto

have clearing of symptoms by the time of their main assessment(43%vs20%with OA) andweremorelikely

tohave remained inthe same work (35%vs 20%with

Claims accepted for occupational asthma (OA)

have been increasing over several years in

On-tarioandnowoutnumberclaims forpneumoconiosis.

In 1982, 17claims were accepted for OA,30for

sil-icosis, and 12 for asbestosis while in the year 1985, there were 54for OA, 33for silicosis, and20for as-bestosis. Similar increases have been reported from Quebec where claims accepted forOArosefrom6in

1977 to 97 in 1987.1

We have recently reported the results of

assess-mentsforOAinpatientsreferredtooneoccupational lung diseasecenterinOntario.2However, lessthana

quarter of all Ontario claimants were seen in that

center, and the findings could differ from those amongallcompensationclaims forOAasthmatothe

Ontario Workers' Compensation Board (Ontario

*From the Gage Research Institute, Department of Medicine,

Universityof Toronto(Drs. Tarlo, CoreyandBroder),and

On-tarioMinistry of Labour(Dr. Liss), Toronto, Ontario, Canada. Thisstudywassupported by the Ontario Workers'

Compensa-tionBoard.

ManuscriptreceivedNovember24, 1993;revisionaccepted

Au-gust16, 1994.

Reprint requests: Dr. Tarlo, Gage Research Institute, 223 College Street, Toronto, Ontario MST 1R4 Canada

OA).Of200OAacceptedclaims reviewedatameanof

1.9yearslater, clearing of asthma occurredin19% and milder asthma in 47%. Outcome was best with early

diagnosis (p<0.05), and milder impairment of pulmo-naryfunction at initial assessment (p<0.05).

Conclusions: Patientswith asthma inducedbya

work-place sensitizer demonstrate some differences from those relatedto workplace irritants. Accurate categori-zationandearlyremoval ofthose with OA offers the best

prognosis. (Chest 1995;107:634-41)

Key words: occupational asthma; compensation; asthma; outcome

WCB). In addition, the routine follow-up by the

WCB of accepted claims for disability rating could allow assessment of outcome variables.

Previousstudies ofprognosisinOAhavegenerally 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 causativeagents.8'9 With the exception of the study of Chan-Yeung et a13 of 232 redcedar workers, fol-low-upreportshaveincludedrelatively smallgroups of subjects. The present study describes diagnostic

categoriesandoutcomevariablesinarelatively large population of subjects with OAfrom manydifferent

causative agents.

MATERIAL AND METHODS

Claims submittedforOAsincemid-1984tothe OntarioWCB

havebeen givenadecisionof(1) OA, (2)aggravationofasthma

(c)unrelatedasthma,or(d)otherdecision.Thetermaggravation of asthma(AA)wasgenerally applied by the WCBtoasthma that

occurredatwork,eitherwith ahistory of preceding asthmaor,

inthose withnoknownpreviousasthma,inthe absence ofa

spe-cific sensitizer. This includedincreasedairway reactivity

appar-ently triggered by irritantfactors insubjects with no previous

knownasthma. TheWCBgenerally provided alowerrangeof

compensation for those givenadecision ofAAthantothose with OA.

AA=aggravationofasthma; FEF50=forcedexpiratoryflow

at 50% vitalcapacity; FEF75=forced expiratory flow at

75%vitalcapacity;FEV,=forcedexpiratoryvolumein1s;

OA=occupational asthma; PC20=provocation

concentra-tioncausing a20% fallinFEV1; WCB=OntarioWorkers'

The WCBdecision was initially reachedby one of three

occu-pational physicians at the WCB with a majorinterest in OA, of-tenwith the aid of an independent specialized assessment. The initial decision was subjectto appeal to the WCB and if further

rejected, could be appealed through the Workers Compensation

Appeal Tribunal, consisting of a nonmedicalpanel. Thus, the

fi-nal WCB decision could be reached at any of these stages and would not necessarily reflect the non-WCB physician diagnosis. Fileswere 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 as-sessments prior toandafter the WCBdecision (referredto

sub-sequently as the assessment of the main assessing physician). The following information was abstracted: (1) demographic details, including age, gender, smoking history, type and durationofwork exposure,and work status at the time of assessment; (2)natureand duration of upper and lower respiratory tract symptoms, im-provement ondays or weeks off work, and timing of any wors-ening at work; (3) history of anyprevious asthmasymptoms be-foreimplicated work exposure, and family history of asthma or allergic diseases; (4) medication requirements; (5) results of investigations ifperformed such as pulmonary function tests (ex-pressed as percent of age and height adjusted predicted normal

values'0),andresponse toabronchodilator; histamine or meth-acholine challenge expressed as PC20 (provocation concentration causing a 20%fallinFEVI);skin testresponses tocommon aller-gen extracts and specific workplace antigens, expressed where available from the mean wheal diameter as 1+ (1 to 2mm on prick test or .5mmon intradermaltest), 2+ (3 to 5mmonprick testor 6 to 9 mm onintradermal test), 3+ (6 to 9mmonprick testor >10 mm onintradermal test),4+(>10 mm on prick test

or .10mm with pseudopods on intradermal test); serial peak flow assessments at work and off work expressed as positive or negativeforwork-related changes as interpreted by the main as-sessingphysician;serial histamineormethacholinechallenge

re-sults within 48 h ofatypical working day and after7daysormore

off work; andspecific laboratory chamber challenge witha

sus-pected 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) fol-low-up results obtained1 to 2yearslater, including work status, symptoms, medication requirements, and pulmonary function results.

Theamountof 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, serialpeakflow measurements, spe-cific work allergen skin tests, and specificinhalation challenge.

Sincethese tests wereperformedinmanydifferentcentersunder the direction of manyphysicians, themethodology of thesetests wasnot uniform. That used in our center, where 19% of this

population had beenassessed,has been describedpreviously.2No

uniform criteria wereappliedtotheinterpretation of serialpeak flowmeasurements in thisstudy,sincetheoriginalreadingswere not always available. Therefore, the peak flow interpretation reached bythe attending physician wasaccepted as recorded. Methacholine and histamine responsivenessareexpressedasPC20 and are used in theanalysesasactual values or areseparatedinto

PC20responses greateror lessthan12mg/mL, whichistakenin

thisstudyasthecutoff foranormal response.

Follow-up assessmentswereperformedfordisability decisions

in all subjects whose claims were accepted for OAand AA if asthma was present at the initial assessment. The follow-up

assessmentfordisability rating wasgenerallyperformed 1 to2 years after theinitial WCB decision. The medicalreassessment wasperformed either byoneof the threeWCBphysiciansor a

respirologist selected by theWCB.

Statistical Analysis

Thegeneral linear models procedure(GLM of SAS) was used for analysis ofvariance, t test for Student's t tests, and FREQ for

x2analyses.Sinceinformation availableinthefileswasnot

com-plete for all patients, missing data were excluded from calcula-tions ofpercentages and from statistical analyses.

RESULTS

Total Group

Atotal 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 adecision by the WCB of AA, and a diagnosis of this by the main assessing physician

(34%).

Of thosewith a WCB decision ofAA, 68% had ahistory ofpreceding asthma. Unrelatedasthma was diagnosed in 6% of the total group by the physician

and10% were giventhis decisionby the WCB while otherdiagnoseswerereachedby the physician in 11% and otherdiagnosesordecisions by the WCB in 13%.

Insufficient informationwas theconclusion 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 diagnosisofOAand 66%withunrelatedasthma, but

only22% ofthosewith AA. A further 40%of the

to-tal number ofpatients wereassessedby other

respirol-ogists orallergists,2%by otherinternists, and 15%by

their primary carephysician or an emergency phy-sician alone.

Themostcommonexposure agents (Table1) were isocyanates(28%).Paintswereimplicatedas the most

likelycausative agent in 5.5% of claims while metal

fumes or dusts,

flour,

grain dusts, and solvents each

accounted for 4% of all claims. Recognized sensitiz-ers such as cedar dust (3%), animals (2%), and

soldering fumes (1%)were lesscommon.

Specific

ir-ritants such as acids and welding fumes were also

eachimplicatedin2% orlessof all claims.In 17% of

subjects,

nonspecified

dusts, fumes, or sprays were

implicated;60%of these weresubjects given a WCB decision of AA.

As might be expectedin apopulation 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.

Serialpeak flowrateswere

performed

atworkand off work by 25%, methacholine or histamine challenge offwork in34%,andduring a workingweek in23%

(both

off work and during aworking week in

12%).

A

specific

work allergen skin test was

performed

in

12% and

specific

laboratory

challenge

with a work

Table 1-Main Implicated Exposure Agents in WCB Decision Groups*

Unrelated

OA AA Asthma Other Total No. ofsubjects 235 234 58 82 609

Primarily sensitizing agents

Isocyanates 135 19 4 13 171 Flour 17 4 2 3 26 Metalfumes/dusts 11 6 2 6 25 Red cedar 11 0 1 0 12 Grain 9 8 0 5 22 Solderingfumes 5 2 0 0 7 Acrylicfumes 5 2 0 0 7 Woods (noncedar) 3 8 3 2 16 Amines 3 1 1 1 6 Enzymes 3 1 0 0 4 Latex 3 2 1 0 6 Animals 2 9 2 1 14

Primarilyirritantagents

Paint fumes 1 22 5 6 34 Solvents 3 11 4 5 23 Calcium oxide 1 9 2 0 12 Sulfuricacid/SO2 2 8 1 4 15 Hydrochloric acid/Cl 0 9 0 2 11 Ammonia 0 7 1 1 9 Cigarette smoke 0 7 5 2 14 Glutaraldehyde 1 6 0 1 8 Welding fumes 2 5 4 2 13

*Other agentseachimplicatedinone or twosubjectswithOAincludepsyllium, platinumsalts,insects,foods, plants,anddyes.Other agents each implicatedinfourorlesssubjects withAAinclude ozone,pesticides, fungi,cottonfibers,cold air, and oilmists.Unspecified dusts, fumes,or

sprayswere implicatedin anadditional64subjects withAA.

Table2-Investigations byWCB Decision Group Unrelated

OA AA Asthma Other Total pValue*

No. 235 234 58 82 609

Skintestspositive 77/154 94/136 27/46 43/57 241/393 <0.01

>1 commonallergen (50%) (69%) (59%) (75%) (61%)

(>2+response)

Skintestspositive 31/41 14/20 4/7 4/8 53/76 NS

toworkagent (76%) (70%) (57%) (50%) (70%) (-1+response) FEVI, % predicted 98+26t 88+28 83+35 91+29 93 ±28 0.01 No. assessed 168 83 25 41 317 FVC 105±22 99+23 87+ 21 97+ 24 101±23 <0.005 No. assessed 169 84 25 40 318 FEF50 79±38 68±40 84±45 83±48 77±40 NS No. assessed 123 63 16 24 226 FEF75 72±49 65 + 47 78 + 63 65+34 69 + 48 NS No. assessed 124 60 17 24 225 Peak flows 56/94 14/34 1/11 1/13 72/152 <0.005 supporting OA (60%) (41%) (9%) (8%) (47%) PC20off work4 10.6±15 9+14 6.8+6.8 13.5±13 10.3±14.3 NS No. assessed 132 42 11 21 206 PC20atwork 4.7+±10 4.8± 11 11.4±12.6 9.4±6.1 5.5±10.7 NS No. assessed 84 37 11 10 142

Laboratory challenge positive 33/43 4/8 0/6 0/6 38/63 0.01

(77%) (50%) (0%) (0%) (60%)

PC20prechallenge 10.9+±18 16.8±31 7.2+2 6.0 11.2+±18 NS

No. assessed 14 4 3 1 22

PC20postchallenge 5.1+9 5.0+ 7 7.5+6 6.0 5.6+6 NS

No. assessed 13 3 4 1 21

*p values relatetosubgroups excluding the total group.

fStandarddeviation.

Table3-Comparison ofPatients AccordingtoWCB Decision: Demographics

Unrelated

OA AA Asthma Other Total pValue

Value* No. 235 234 58 82 609 Mean age, yr 40+13t 41±12 42±12 44±13 41+12 NS Male, % 69 65 69 51 65 NS Neversmoked, % 32 39 43 35 29 NS Currentsmokers,% 27 25 18 23 21 NS

Meanpack-yrofsmokers 14+15 15±12 16±17 22 ±22 15 ±15 NS

History ofprevious asthma, % 8 68 46 27 35 <0.0001

Yearssince onsetof previous asthma 18.0+13 17.6±14 18.7+15 21.1±18 18.1±14 NS

Familyhistoryof asthma, % 15 29 28 31 24 <0.01

*pvalues relatetocomparisonsofsubgroupsexcluding the totalgroup. 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% ofthoseperformingthe test), 20% had no continuing symptoms. Ninety-one

per-from repeated methacholine or histamine challenge cent wereassessed 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

de-specific laboratory challenge in 6% (60% of those scribed in 91%, exposure to a presumed irritant in7%,

tested). and to unknown agents in 2%. The most commonly

OccupationalAsthma implicated exposure agentwasisocyanates (Table 1)

Occupational Asthma in

57%

of subjects. In addition to

spirometry,

meth-Among the 235 patients who were given a WCB acholine or histamine challenge was performed

decisionofOA, the mean age was 40years, and 69% within 48 h of a work day in 36% of those withOA, weremen(Table3).One third had neversmoked. All and off work in 56% (Table 2), while the challenge describedasthmasymptoms and80%with available was performed both after a work day and off work

information also hadnasal 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

symptomsduring weekendsoff work, and 88% dur- agent were performed in 18%. Table 4-Work-RelatedData inWCB Decision Groups

Unrelated p

OA AA Asthma Other Total Value*

No. 235 234 58 82 609 Yearsofsymptoms 2.8±4.2t 1.2 ±2.6 3.1± 4.3 2.5+4.8 2.2+3.8 <0.0001 atwork Yearsofsymptoms 2.8±4.3 1.3±3.0 3.6±5.3 2.7±4.9 2.3+4.0 <0.0001 before WCBsubmission Yearsofsymptoms 3.1± 4.4 1.4± 2.8 3.9±5.4 2.7±4.9 2.5+4.0 <0.0001

beforemain assessment

Exposure yearstowork 6.8+7.6 7.4±8.1 8±8.1 8.2+9.4 7.3+8 NS

agent

Improvement onweekends, % 70 65 41 48 55 <0.0001

Improvementonholidays, % 88 81 54 69 73 <0.0001

Leftwork, % 63 42 62 71 56 <0.0001

Samework,% 20 35 22 17 26 <0.0005

Outof usualexposure 15 17 9 4 17 <0.05

butatworkplace, %

Asymptomaticat 20 43 14 24 28 <0.0001

mainassessment, So

Asymptomaticand 19 24 11 17 19 <0.01

outof workarea, %

*pvalues relatetocomparisonsof subgroupsexcludingthe totalgroup.

tStandard deviation.

Aggravation of Asthma and Comparisons With

OA

Theonlydemographicfeatures(Table 3) that were significantly different between those with AA and OA were thehistory 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 withOA). Clearing ofpreviousasthmaprior to the onset of work-attributedsymptoms 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 work-related symptoms, for a mean of 5.5 years (data not shown in tables).

As might be expected, there was a high level of

concordanceamong the main assessingphysicianand WCBforthediagnosisof AA with ahistoryofasthma (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 therewas ahistory of precedingasthma (72%) (data not shown intables).

Symptoms, medication use,and physicalfindings

ofwheezingweresimilarinprevalence to those with OA, when recorded in the patient file (data not

shown). Therewas a similar prevalence of improve-mentduringweekends and holidays as in those with OA (Table 4). Althoughthe duration of exposure to theimplicated work agent was similar to those with OA, the duration ofwork-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).

Thosewith AA weresignificantlylesslikely to have

had exposure to isocyanates than those with OA (Table 1),and were more likely tohave exposure to agents other than the most commonly recognized sensitizers(Table 1). Exposure to a known respiratory irritant (most commonly paints, solvents, acids, am-monia, or calcium oxide) occurred in 67%. An

acci-dentalexposureor

spill

was

reported

in40%.Among thosewithAAandno

history

of asthma

(70 patients),

exposure agentswere

mainly

agentsconsideredtobe irritant such as acids, solvents,

welding

fumes,

and nonorganic dusts (Table 5), although 34% of these

subjects hadexposureto

potential

sensitizerssuchas

isocyanates, eggs,

flour,

andmetal dustsorfumes. All

objectivediagnostictests were

performed

inasmaller proportion of patients withAAthan OA. When these tests were performed, however, resultswere not

sig-nificantly 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

Table5-Exposure Agents inThose With a WCB Decisionof AggravationWho Had NoHistoryof

Asthma (70 Patients)* Agents No. Isocyanates 9 Solvents 7 Metaldusts/fumes 6 Acids 5 Chlorine 4

Syntheticfibers dusts 4

Weldingfumes 4

Grain dusts 4

Cutting orlubricatingoils 4

Calcium oxide dust 3

Cokeovens 3

Sawdust 3

MetabisulphiteorSo2 3

Flour 2

Spray paints (nonisocyanate) 2

Methylmethacrylate/acrylic monomer 2

Molds 2

Glues 2

Feathers 2

*Agentsinsinglecasesonly: 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 pre-viousasthma.They didnotdiffereither insymptoms or physical findings of wheezing. They did have a

longerdurationof symptoms at work (Table4),and were less likely to be asymptomatic by the time of assessment. Theywere significantly less likelyto

de-scribe improvement in symptoms on weekends(41 %) or holidays (54%) (Table 4). Exposure to the most commonOA sensitizer, isocyanates, was less common inthosewith unrelated asthma (Table 1), and these patients were more likely to have unspecified expo-sures orexposure to agentsother than themost com-mon agentsinducing OA.

As with patients classified as having AA, investi-gations were lesscommonly performedthan among those with OA;but whenperformed,as expected, the test results were more likely to be normal or not supportiveofanoccupationalcomponentthanamong patientswithOA or AA.Airflowlimitation 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 nosignificant differenceinmean values forflowrates at 50% and 75%ofvital capacity.

Follow-up Results

Follow-up assessment had been performed for the purpose ofdisability rating in 285 of the 469 accepted claims for OA and AA (69%). Only 46% of these pa-tients wereworking atfollow-up,8%doing the same

Table6-Patient Variables Relatedto Outcomeof Accepted Claimsin 200 PatientsWithOA StatusasRated byExaminingPhysicianatFollow-up

Cleared Milder Unchanged Worse pValue

No.ofsubjects 38 94 40 28 First WCB assessment FEV1, %predicted 108+24* 97 ±23 97 ±27 86±37 <0.05 No.assessed 29 65 31 19 FVC 110+21 103±22 105±23 97±25 NS No. assessed 30 65 32 19 FEF50 110± 45 79 ±34 70± 31 52+323 0.0001 No. assessed 20 49 23 15 FEF75 110±66 78±43 74+33 75±89 NS No.assessed 21 48 24 15 MeanPC20atworkt 11.2+21 4.5± 11 1.5±1.9 2.1±4 NS No. assessed 10 37 18 12 '12mg/mL 8 35 18 11 >12mg/mL 2 2 0 1 Yearsofsymptoms 1.4+ 1.7 2.5±4.8 2.8 ±4.9 4.4±3.7 NS

beforeleavingexposure

Yearsof symptoms 2.0+2.4 2.9 + 4.7 4.2 ±5.3 5.3+4.9 <0.05

beforemain assessment

Follow-upWCB assessment FEV1, %predicted 111±16 103+±17 92+22 69+26 0.0001 No. assessed 22 69 30 20 FVC 116+14 108±14 104±19 90±25 0.0001 No. assessed 22 68 29 20 FEF50 95+31 83+31 68 + 32 35+24 0.0001 No. assessed 19 66 28 17 FEF75 94+15 78 ± 40 75 ±36 31+16 NS No. assessed 12 19 11 2 Mean PC20 20.6±15 9.0±8 3.5±4.4 2.2±2.0 0.001 No. assessed 15 36 17 5 <12mg/mL 2 24 14 5 >12mg/mL 13 12 3 0 <0.005 *Standard deviation. tMethacholineorhistaminePC20, mg/mL.

up (70%)werethose whoseclaims were

accepted

for

OA. Asthma hadcleared in 19% with OA, was

clin-ically considered milder in47%,

unchanged

in 20%,

and worse in 14% in the opinion of the assessing

physician. The mean duration since the first assess-ment was 1.9±1.5years.

Pulmonary

functiontesting at follow-up (Table 6)

paralleled

the outcome

find-ings, with worse asthma associated with greater

im-pairment of function.

Twovariables were associatedwiththeoutcomeof OA.First, theduration ofsymptomspriortothemain

assessment was

directly

related to the outcome

(Ta-ble

6).

This was indicated

by

the duration ranging

fromameanof2.0±2.4yearsinthosewith

clearing,

to 5.3±4.9yearsinthose withworsening 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,anFEV1meanof 108±24%

predicted

was

initially present in those with subsequent clearing,

and 86±37% in thosewith worsening asthma.

Sim-ilarly the initial assessment mean methacholine or

histamine PC20,

although

measuredin aminorityof

subjects

while

working, ranged

from a mean of

11.2±21

mg/mL

in those who

cleared,

down to a meanof2.1±4

mg/mL

inthose who had worsening

of asthma on

follow-up.

Greater improvement was found in those with a WCBdecisionofOAthaninthose withAA

(data

not shown in

tables).

Among those with OA, 20% had

clearing

of asthma and 46% were mildervs 7% and

30%,

respectively,

with AA. Fewer with AA had a

follow-up

assessment

(85

subjects),

but

analyses

of

theseshowedatrendtosimilaroutcomeassociations. In

addition,

prognosis for those with asthma attrib-uted to isocyanates was better than for those with other causes of OA.

Clearing

of asthma occurred in 20% and improvement occurred in afurther 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,

andmay not

necessarily

reflect the true Ontario in-cidence or distribution ofcausativeagents in thetime

periodassessed,sincemany patientswithOAmaynot

be reported to the WCB or be

eligible

to submit a claim. Our categorization ofpatientsinto diagnostic groups has been on the basis of the WCB decision, stemming

largely

from themain

physician

assessment. WerecognizethattheWCBdecision mayattimes

be different from that which mightbereached

by

a

physician

specializing

in OA.However, there wasgood agreement betweendiagnoses 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 substan-tively the same. We electedto usetheWCBdecision since it was reached

by

agroup of three physicians

at the WCB and thus maybe more consistent.

Objective investigations were not

performed

in

manysubjects, possibly duetolimitationspreviously

described,2

suchas

difficulty

inarranging workplace peakflowassessmentsand

methacholine

challengein

subjects who had terminated their employment by

the time of main assessment (56% of all patients). Wherethereisinsufficient information or testsshow

borderlineresponses,thebenefitof thedoubtisgiven

by the WCB toward a diagnosis of OA or AA.

Therefore, no strict diagnostic criteria could be

appliedtobettercategorize thesesubjects,andthere

likelywere somepatients whodidnottruly belongin

the

diagnostic

category givento

them.

Therefore, this study cannotbe

directly

compared withstudies per-formed in a single center, using a standardized

approach.2-7 Nevertheless,

it is of interestthat many

ofthe

findings

inthisstudyare consistent withthese other

reports.2-7

Itis unlikely that the outcome

cate-gories were

significantly

influenced by inaccurate diagnosesinone decision group more thanother

de-cisiongroupssincethepercentage of patientsineach ofthe

follow-up

outcomecategories who had

objec-tiveconfirmation ofOA wassimilar (data notshown).

Some misclassification of claim decisions might have resulted from nonmedical decisions made

dur-ing appeals proceedings. The presence of misclassi-fication isfurther suggestedby thefinding of an

ap-parently positive

challenge

to known sensitizers in

three patients with AA, with

flour,

isocyanates, or cobalt.

Compensation for AA and acute airway irritant

effectsis not

uniformly

acceptedanddoesnotoccur,

forexample, in Quebec or in Britain under the

cat-egory of

OA.""1

Aproposed

medicolegal

definitionof OA from an author in the United

States12

also includes only specificsensitizing agents. Thesubjects includedinthediagnosticcategoryofaggravationin Ontario have beenseparately classified from OA for

the purpose of compensation. They can be divided

intothose withandwithout

preceding

known asthma and subdivided into

subjects

with exposure to

un-usually

high

levelsof

potential

irritantsubstances and

subjects exposed

to

currently

acceptable

levels. Two

thirdsof

patients

inthis

accepted

claim category of

AA had known

preceding

asthma,

which worsened

while

working

with

potential

airway irritants,suchas

acid fumes or

aerosols,

ammonia,

chlorine, paint

fumes, solvents,

orirritantdusts. Theremainingone

third had no

previous

documented

asthma,

and

de-veloped

changes

of asthma while

working

with no sensitizerexposureordidnotdemonstrate

sensitivity

toknownsensitizers. Thisincluded patientswith

ac-cidentalexposure toa

high-dose

irritantor

repeated

exposure to irritants with no

single high

concentra-tion

incident,

such as has been described

previous-ly.13"14

Therefore,

aproportionofthesepatients may

have had asthma induced

by

their work exposure

whileothersmayhave had coincidentalonsetofasthma withirritant exacerbation

by

workplace

substances.

ThosewithAAwereless

likely

thanthosewithOA

tohaveexposuretothemainrecognizedsensitizerin

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

thetimeof main assessment

(43%

vs

20%).

This greater

clearing

of symptoms in

patients

withAAmayreflecta proportionof

subjects

with transient symptoms related to

spills

or tempo-rary exposures to irritant substances. This is

sup-ported

by

the

finding

thatamongthosewith AA,35%

remainedinthesameworkenvironment

by

thetime

oftheir main assessmentbut morethanhalf(52% of

those still at the same

work)

reported a clearing of work-related symptoms. In contrast, of those with

OA,

only

20%remainedatthesamework

by

thetime oftheirmainassessment,and

only

3

(7%)

ofthosestill

at the same work

reported

clearing

of

work-attrib-uted symptoms.

The greater

prevalence

of transient symptoms in

those withAA

might

also

explain

the fact thatfewer

of those withAA were referred fortertiary

special-ist assessment, and fewer underwent detailed

inves-tigation

(Table 2)

such as

peak

flow assessments,

measurementofairwayreactivity, andskintestingor

challenge

with

workplace substances.

When these

testswere

performed, however,

resultswerenot

sig-nificantly

different from those with OA (Table

2),

suggesting thatat least a subsetmayhave had simi-lar functional

changes

to those with OA. They may

not have been classified

by

the WCB ashaving OA

due to

preceding

asthma

(150

patients classified as

AA had a

history

of asthma and 14 had a question-able

history)

or lack of a recognized workplace sen-sitizer. These observations support the concept of

providing some degree of compensation for such patients and the need for detailed investigation of these patients when feasible.

InOntario in the time period studied, isocyanates were themostcommonly identified suspect agents in allthe claims (30%) and the most commoncausative

agent in claims accepted for OA (58%) (Table 1). They werealso a significant attributed cause of irri-tant airway responses (11% of AA). This represents a

higher proportion of OA than compensated or

re-ported to the SWORD surveillance system in the United Kingdom in

1988.15

Conversely, flour and grain dustsaccounted forasimilar proportion ofOA

accepted claims in Britain and Ontario (18% and 17%,respectively), whileplatinum salts andsoldering flux accounted for higher proportions of

compen-sated cases in

Britain,11

possiblyreflectingdifferences

in occupational exposures.

Comparison ofthisstudywiththatof Yassi,'6 who reviewed earlier Ontario WCB claims from 1975 to 1981, isdifficult due to some differences in classifi-cation of accepted claims. However, our finding of

isocyanatesas the presumed causative agent in 58% of those with OA isfar greaterthan in theearlier re-view where isocyanates accounted for 27% of OA.

The proportion due to flour or grain is unchanged

(17% vs 18%). At follow-up, unemployment was

higherinthepresentstudy,54%o of those followedup ascompared with lessthan 40% in thepreviousstudy. Ofinterest, herfollow-up questionnaire, 2to 8years

after the WCB decision was reached, found 15% of subjectstobefreeof asthmasymptoms, similarto our

finding of 19%.

Theoutcome of asthmaamong all patients whose claims were accepted for OA and who were

reas-sessed was similar to previous

studies3,17-19

in that

clearing of asthma occurred inonly 19%,a meanof

1.9 years after the first assessment

(Table 6).

How-ever, anadditional47% had milder asthma. Among

subjectswithimprovement andthose withclearingof

asthma,thepositivechange occurredat a meanof0.9

years, suggesting thatitisreasonable toperformthe assessment for permanent disability around 2 years after leaving work.Inthewholegroupat

follow-up,

theprognosis

appeared

tobeworst inthose withAA

who had no prior history of asthma; 48% of the 33

seen were worseat

follow-up

as

compared

with14%

of those with OA and no prior history of asthma. Our

findings

oftheprognostic importanceof

early

diagnosisof OA andremoval from exposure,and the better prognosis in those with initial

relatively

mild pulmonary function impairment areconsistentwith

findingsof Chan-Yeung et

al3

in cedar workers and

the

findings

ofMappeta17 andPisati eta16 in

isocy-anate-induced asthma,andextendtheir

findings

to a

larger group of patients with OA from many more

causes than previously

reported.8'9

Further studies areneededtoassess whether earlyrecognitioncan be

best achieved by appropriate surveillance programs

in industries such as those using isocyanates that ac-count for mostcompensatedcases ofOA in Ontario.

ACKNOWLEDGMENT: Theauthors wish to thank Mary Har-purandJustinaGreene for data gathering and processing, and Dr. C.Smith andDr. P. Carrof the Ontario Workers'Compensation Boardfortheircooperation in this study as well as Kerrie Cheung

fortypingassistance.

REFERENCES

1 MaloJL.Compensationfor occupational asthmainQuebec.In:

Merchant JA, ed. Workshop on environmental and

occupa-tional asthma. Chest1990;98S:236S-239S

2 TarloSM, BroderI. Outcomeof assessment for occupational asthma. Chest 1991;100:329-35

3 Chan-YeungM, MacLean I,PaggiaroPL. Followupstudy of

232patients withoccupationalasthmacausedbyWesternred cedar(Thujaplicata).JAllergy Clin Immunol1987; 79:792-96 4 Paggiaro PL, Loi AM, Rossi0,etal. Follow upstudy ofpatients with respiratorydiseasedue totoluene diisocyanate(TDI). Clin Allergy1984; 14:463-69

5 LosewiczS, AssoufiBK,HawkinsR, etal.Outcomeof asthma inducedbyisocyanates. BrJDisChest 1987; 81:14-22 6 PisatiG, BaruffiniA,ZeddaS.Toluenediisocyanate induced

asthma:outcomeaccordingtopersistence orcessationof expo-sure. BrJInd Med 1993; 50:60-4

7 Mapp CE, Corona PC,DeMarzo N, et al.Persistentasthmadue toisocyanates. Am Rev Respir Dis 1988; 137:1326-29 8 VenablesKM, Davison KG,Newman-TaylorAJ.Consequences

ofoccupationalasthma. RespirMed 1989;83:437-40 9 HudsonP, Cartier A, Pineau L, etal. Follow-upof occupational

asthmacaused by crab and otheragents. JAllergyClin Immu-nol 1985; 76:682-88

10 Schoenberg JB,Beck GJ, Bouhuys A. Growth and decay of

pulmonary function in healthy blacks and whites. Respir

Physiol1978; 33:367-93

11 ReportbyIndustrialDiseaseSubcommittee ofIndustrial Inju-riesAdvisory CouncilonOccupationalAsthma.Departmentof Health and SocialSecurity. London:HMSO, 1981; 7-19 12 Smith DD. Medical-legal definition of occupationalasthma.

Chest1990; 98:1007-11

13 BrooksSM, Weiss MA, Bernstein IL. Reactive airways dys-functionsyndrome (RADS). Chest1985;88:376-84

14 Tarlo SM, Broder I. Irritant-induced occupational asthma. Chest1989; 96:297-300

15 MeredithSK,TaylorVM, McDonaldJC. Occupational respi-ratory disease in theUnited Kingdom 1989: areport to the British Thoracic Society and the Society of Occupational Medicine bythe SWORD project group. Br J IndMed 1991; 48:292-98

16 Yassi A. Health and socioeconomicconsequences of

occupa-tionalrespiratoryallergies: apilotstudyusingworkers' com-pensationdata. AmJ Ind Med 1988; 14:291-98

17 MaloJL, Cartier A,GhezzoH,etal.Patternsofimprovement

inspirometry,bronchialhyperresponsivenessandspecificIgE

antibody levels after cessation of exposure in occupational

asthmacaused by snow-crab processing. Am RevRespir Dis

1988; 136:807-12

18 RosenbergN, Garnier R,RousselinR,etal.Clinical and

socio-professionalfate of isocyanate induced asthma. ClinAllergy

1987; 17:55-61

19 Burge PS. Occupationalasthmainelectronicsworkerscaused bycolophony fumes: follow-up of affected workers. Thorax

1982;37:348-53