medicine occupational asthma - postgraduate medical journal · asthma might have an occupational...

Postgrad Med J (1991) 67, 271 - 277 i) The Fellowship of Postgraduate Medicine, 1991

Occupational Medicine

Occupational asthma

S.C. Stenton and D.J. Hendrick

Chest Unit, Newcastle General Hospital, University of Newcastle upon Tyne, NE4 6BE, UK

Introduction

Occupational asthma may be defined as asthmainduced by exposure to an inhaled agent (or agents)in the workplace. Its presentation is sometimesdramatic. Occupational exposure to platinum salts,for example, has been known to induce asthma inover 50% of an exposed workforce. For thoseaffected, the consequences are often devastating,while the economic effects for an industry may beno less profound. Although occupational asthmawas barely recognized 30 years ago, its study inrecent years has led to much insight into theaetiology and the mechanisms ofasthma in general.A number of comprehensive reviews are avail-able.'`3

It is important to distinguish the induction ofasthma from the mere provocation of symptoms inthose who are already asthmatic. Any asthmaticworker whose occupation involves moderate exer-tion might wheeze at work but exercise alone willnever induce asthma in the way that chemicals andother occupational agents sometimes do. The con-cept of airway hyperresponsiveness is useful inunderstanding this distinction. It refers to theexaggerated responses of the airways to stimulisuch as exercise or cold air which are a universalfeature of active asthma. If an asthmatic state(airway hyperresponsiveness) has been induced,whether occupationally or not, exposure to thesenon-specific stimuli gives rise to bronchoconstric-tion and the symptoms of wheeze, breathlessnessand cough. In the case of occupational asthma,there is an additional specific sensitivity to thecausative agent in the same way that some, but notall, asthmatics wheeze when exposed to the housedust mite. The quantification of airway respon-siveness can be useful in assessing asthmaticactivity and in following changes associated withoccupational exposures.The overall prevalence ofoccupational asthma is

not known with any certainty. Some 3-6% of theadult population in Britain have symptoms ofasthma, and of these approximately a third deny

being affected in childhood. The prevalence ofasthma beginning in adult (working) life is there-fore likely to be 1-2% in any workforce but mostof these cases will arise coincidentally rather thanthrough a direct effect of occupation. In Japan, ithas been estimated that up to 15% of adult onsetasthma might have an occupational aetiology,though, for Britain, the figure is considered to be ofthe order of 2-5%.More accurate information about the epide-

miology of occupational asthma in Britain willshortly become available as data from two on-going investigations are analysed. Under theSWORD (Surveillance of Work-related and Occu-pational Respiratory Disease) project respiratoryand occupational physicians report each month onall new cases of presumed occupational lungdisease. In 1989, the first year in which the schemewas operational, asthma proved to be by far thesingle most commonly reported occupational lungdisease. The overall national incidence was of theorder of 20 per million employed per year but withvery much higher incidences in certain occupa-tions. The second reporting scheme is centred onthe West Midlands region and suggests that thelocal incidence of occupational asthma is appre-ciably higher.

Agents causing occupational asthma

Individual agents capable of causing occupationalasthma can be found in a wide variety of occupa-tional settings and range in type from smallmolecules such as formaldehyde (HCHO) to com-plex animal proteins. Over 200 agents are recog-nized and new cases are identified almost monthly.Some are potent and have caused asthma in almostepidemic proportions when exposures were notcontrolled. Others have caused asthma in only oneor two workers. A complete list of these agents isbeyond the scope of this article but some of themore important agents are listed in Table I wherethey are classified into five major categories:animal, vegetable, microbial, pharmaceutical andchemical. However, occupational exposures are

Correspondence: S.C. Stenton, B.Sc., M.R.C.P.Accepted: 13 September 1990

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272 S.C. STENTON & D.J. HENDRICK

Table I Some agents causing occupational asthma

1. Animal arachnids (storage mites)laboratory animals*seafood (crabs, prawns)

2. Vegetable beans (castor*, coffee, soy)colophony fumes*flour/grain*papainwoods*

3. Microbial Bacillus subtilis enzymes*mixed (humidifiers, oil mists)

4. Pharmaceutical cimetidine*cephalosporins*ipecacuanha*methyl dopapancreatic extractspenicillins*psyllium*

5. Chemical acid anhydrides*aluminium smeltingazodicarbonamide*diisocyanates*formaldehydenickelpersulphates (hairdressers)platinum salts*reactive dyesvanadium

*Prescribed agents for which state compensation can beobtained in Britain.

frequently multiple and in some cases it is clear thatoccupational asthma is present without a singleaetiological agent being identifiable. For example,asthma occurs in the aluminium smelting industrywhere workers are exposed to aluminium salts,fluorides, sulphur dioxide, carbon monoxide andseveral other gases and chemicals.4 The agent orcombination of agents responsible has not yet beenidentified.

Non-occupational exposures to domesticatedanimals are extremely common and are sometimesassociated with exacerbations of asthma. Yet theirpotency does not appear high, and occupationalasthma in their handlers is unusual. Small mam-mals are more frequently implicated, particularlyrodents whose urine may contain large amounts ofhighly allergenic protein. Asthma among exposedlaboratory workers has been reported with aprevalence ofthe order of 10%. To some extent thisis likely to reflect higher exposure levels in theconfined environment of a laboratory animalhouse as well as different asthmagenic potencies.Insects such as locusts, and mites such as the grainstorage mite (Glycophagus destructor) can alsoinduce occupational asthma. The latter contam-inates farm produce and can render farm workers,

grain handlers, dock workers, road hauliers, bakersand others at risk.Asthma among bakers is more commonly due to

flour itself or enzyme additives than any conta-minating storage mites. In some studies, up to 20%of bakers have been reported to be affected.Asthma due to flour or dust from soybean illus-trates the potential overlap between occupationaland other environmental causes of asthma. Soy-bean dust is a recognized cause of occupationalasthma and its release into the atmosphere ofBarcelona (which followed its unloading fromships in the harbour) resulted in a number ofepidemic outbreaks of asthma in that city in theearly 1980s. A total of 687 people were affected in26 outbreaks and 1155 emergency hospital admis-sions were recorded.5Wood and wood products may cause asthma.

Western Red Cedar (Thuja plicata) is the mostfrequently implicated because it is rapidly growingand widely used, but several other species (prin-cipally hardwoods) pose significant risks. In thecase ofWestern Red Cedar, plicatic acid in the sapappears to be the agent directly responsible. Colo-phony (rosin) obtained from pine tree resin iswidely used in the electronics industry as a solder-ing flux. Fumes from the soldering process containcolophony pyrolysis products and are asthma-genic. Asthma was found in 21% of workers in ahigh exposure group in one electronics factory.Enzymes obtained from Bacillus subtilis have

been used extensively by manufacturers of 'bio-logical' detergents. These enzymes are potent sen-sitizing agents and in the early days of their use,prevalences of up to 50% of occupational asthmaand rhinitis were observed. Hygiene improvementsin the manufacturing process, coupled with anencapsulation process which increased the particlesize beyond the respirable range have greatlyreduced the risk to current workers. Little evidencehas emerged of asthma attributable to these agentsin consumers, though the use of pancreatic enzy-mes for the treatment of cystic fibrosis has resultedin asthma in some families.

Occupational asthma due to other therapeuticagents is not confined to those directly involvedwith manufacture. Asthma induced by occupa-tional exposure to antibiotics and laxatives hasoccurred among nurses. Aerosolized antibiotics areincreasingly being used therapeutically, andadministration by this means may carry some riskof sensitization to patients and to staff if nebulisersare not used with extraction devices. Occupationalasthma caused by a therapeutic agent carries anadditional risk. Systemic hypersensitivity mayoccur and this provides the potential for multi-organ reactions should a worker be treated thera-peutically with an agent to which he has beensensitized occupationally.



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OCCUPATIONAL ASTHMA 273

A wide variety of low molecular weight chemi-cals are capable of causing clinical effects in theairways, which are identical to those caused bycommon aeroallergens. These agents tend to bereactive rather than inert but share no othercommon structural or chemical property. Thecommonest reported cause of occupational asthmain Britain is exposure to isocyanates such as toluenediisocyanate (TDI). These are employed in theproduction ofpolyurethanes which are widely usedin the manufacture of plastics, surface coatings andfoams. Asthma prevalences ofup to 10% have beenreported among exposed workers. Once sensitized,workers may develop symptoms following expo-sure to extremely low levels (0.001 ppm). TDI isnotorious for causing asthma in environmentswhich appear well removed from its manufactureor transport. Any process involving heating orburning polyurethane may liberate isocyanate.TDI has also been reported as a contaminant ofanoffice environment because the air conditioningintake was too close to the exhaust vent of aneighbouring building where polyurethane wasbeing made.

Mechanisms ofoccupational asthma

The mechanisms leading to asthma, whether occu-pational or non-occupational, are poorly under-stood. A type I (IgE-mediated) hypersensitivity islikely to be involved in childhood asthma but this isless obviously the case among adult asthmatics inwhom the association between allergies and asthmais not so close. Airway hyperresponsiveness, andpossibly asthma, can sometimes be induced byaccidental exposure to smoke from domestic fires,or exposure to ozone and viral upper respiratoryinfections, adding support to the view that othermechanisms can sometimes be involved.6

In some circumstances, for example amonglaboratory animal handlers, detergent workersexposed to enzymes, and platinum workers, occu-pational asthma is associated with positive skinprick tests and elevated specific IgE levels typical ofa type I hypersensitivity reaction. However, for themajority ofinducers ofoccupational asthma, speci-fic IgE antibodies have been identified in only aminority of affected workers or not at all. In thecase oflow molecular weight chemical agents, theirmolecular size is too small to allow the chemical toact as an allergen unless coupled as a hapten withbody proteins. Thus problems in identifying aspecific antibody do not necessarily imply theirabsence but may simply reflect the difficulties inpreparing a relevant hapten or in handling a highlyreactive chemical.The frequent failure to identify immunological

mechanisms has led to suggestions that 'pharma-

cological' reactions might sometimes be important.A non-occupational example of such a mechanismmight be seen with aspirin-induced bronchocon-striction which occurs in up to 10% of asthmaticpatients, probably because of alterations in prosta-glandin or leukotriene levels.7 Similarly, TDI can intheory facilitate bronchoconstriction by inhibitingbeta-adrenergic responses, and organophosphoruspesticides can cause cholinergic-mediated bron-choconstriction by inhibiting cholinesterase. How-ever, neither ofthese mechanisms seems likely to beimportant in the induction of occupational asthmain general.

Occasionally asthma arises after a single acciden-tal exposure to high levels of irritating fumes,aerosols or gases (e.g. chlorine or sulphur dioxide).This is not typical of occupational asthma and theterm 'reactive airways dysfunction syndrome' hasbeen coined.8 Symptoms begin at the time ofexposure and typical asthma persists thereafter.Asthma is frequently not exacerbated by re-expo-sure to low levels of the same chemical. An acuteinflammatory insult to the airways appears to becausative, the rapidity of the onset of symptomsmaking it unlikely that any hypersensitivitymechanism could be involved.

In the majority of cases, whether or not specificantibodies can be identified, occupational asthmabears all the hallmarks of an acquired hypersen-sitivity reaction. Only a small proportion (usuallyfewer than 10%) of exposed workers are affected.There is a latent period of weeks to years beforesymptoms develop but once developed, symptomsare provoked by exposures which were previouslytolerated and which continue to be tolerated byother workers. There is therefore no convincingevidence to suggest that occupational asthmausually arises through a unique or uncommonmechanism not relevant to asthma in general.Indeed, improving understanding of the mechan-isms leading to occupational asthma is likely tolead to a greater understanding of asthma in thepopulation at large.

Predisposing factors

Asthma has arisen with very high prevalences (over50%) in some working populations suggesting thatunder appropriate conditions everyone may besusceptible. The level of exposure is of majorimportance but, as asthma typically arises in only aminority of those exposed, there are likely to behost factors, such as pre-existing asthma, cigarettesmoking and atopy, which render some workersmore susceptible than others.A number of studies have shown an increased

prevalence among workers who have experiencedasthmatic symptoms previously, often in child-



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hood. However, as the majority ofcases of occupa-tional asthma arise in subjects without anyprevious asthmatic symptoms, this risk factorexerts only a minor effect overall. Current asthmaought to be at least as relevant but this has been lesseasy to identify. Such an effect might be masked bya number of biases such as the tendency ofemployers to discriminate against asthmatic jobapplicants and of asthmatic workers to avoidknown industrial inducers. Whether low (i.e.asymptomatic) levels of airway hyperrespon-siveness can predict or predispose to the subse-quent development of occupational asthma is asyet unknown. It does, however, appear that airwayresponsiveness is not closely associated with atopyin adults.9 This implies that if it does predispose tothe development of occupational asthma it exertsthis influence independently of atopy.

Atopy, which is the propensity to develop highlevels of IgE antibodies to common aero-allergens,is present in up to 20% of the population. As atopyposes an increased risk of occupational asthma insome occupations (e.g. detergent workers exposedto enzymes), tests for atopy have been widely usedto screen potential employees. However, atopy isnot necessarily a good predictor of the ability tomount specific IgE responses. Allergy to bee stingvenom is no more common among atopic thannon-atopic bee keepers, and for many occupationalagents (e.g. TDI and epoxy resins) atopy does notappear to confer any increased risk for the develop-ment of occupational asthma. Even when there isan association (e.g. with laboratory animalasthma), the predictive value of screening tests foratopy is poor.'0

Cigarette smoking has a variety of effects on theimmune system." It increases circulating total IgElevels but does not increase the symptoms ofallergyor the frequency of positive skin prick tests tocommon allergens. In contrast, it has a suppressiveeffect on IgG-mediated reactions, extrinsic allergicalveolitis being less common among smokers thannon-smokers. Smoking has been shown to increasethe risk of developing specific antibodies to plati-num salts in exposed workers by a factor offive andto increase their risk of developing occupationalasthma. Smoking has been found to increase therisk of asthma in other occupational settings also,for example workers exposed to epoxy resin curingagents such as tetrachlorophthalic anhydride. Onthe other hand, smoking appears to protect sawmillworkers exposed to plicatic acid against Cedarasthma. Among 185 cases of occupational asthma,70% were in lifelong non-smokers and only 5%were in current smokers. Such diverse effects ofsmoking on the risk of developing occupationalasthma might offer some clues to the mechanismsinvolved.

Diagnosis

The recognition that asthma in an affected workeris related to the occupation is often not easy. At anearly stage in the illness, symptoms may compriselittle more than an intermittent cough, occasionalbreathlessness or wheezing. A smoker may regardthese symptoms as normal and antibiotics may beprescribed for repeated 'chest infections'. Once anoccupational link is suspected, the history may beconfounded by the expectation ofcompensation orthe fear of unemployment.

Occupational asthma usually begins within 1-2years of initial exposure to the inducing agent, andnot uncommonly within a few months. Rarely, thesensitizing period is only a matter of days or weeksor symptoms may begin with an accidental heavyexposure. Once sensitized, symptoms may startwithin seconds of entering the workplace ifimmed-iate asthmatic reactions are provoked, but may bedelayed for several hours or may begin after work iflate reactions only are occurring. Under the lattercircumstances, recognition of the occupationalaetiology might be delayed.

In the early stages, airway responsiveness andasthmatic symptoms tend to increase followingexposure, and decrease when this ceases tempor-arily. Thus there may be an improvement insymptoms at weekends and especially on holidays,when away from work. As the severity of theasthma increases, these features may become lessapparent and airflow obstruction may become lessreadily reversible, making the occupational aetio-logy and the distinction from smoking related fixedairflow obstruction difficult.

Rhinitis, conjunctivitis or skin rashes may alsobe present or may affect other workers. Theknowledge that fellow workers are affected streng-thens any suspicion of occupational asthma as doesthe presence of a known asthma inducer in theworking environment. Even in the apparentabsence of both, the possibility of an occupationalcause should always be considered when asthmaarises or appreciably worsens in adult life.

If there is known exposure to a recognizedasthma-inducing agent in the workplace, the his-tory alone might suffice for a diagnosis of occupa-tional asthma to be made once asthma itself isestablished, particularly if the agent is of highpotency and other members of the workforce areaffected. Objective evidence for the presence ofasthma should be sought from tests of lung func-tion or by quantifying airway responsiveness. If thesubject has been away from work for some time, theasthma may have substantially improved or disap-peared and all tests might be normal.

Serial measurements of ventilatory function maybe useful both to confirm active asthma and to



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demonstrate work-related decrements (or improve-ments when away from work). This is most con-veniently achieved by the subject using a WrightMini-Peak Flow meter. Figure 1 illustrates suchmeasurements for a foundry worker who wasexposed to isocyanates and formaldehyde fromresins in sand moulds when they were vaporized bymolten steel. His symptoms were suggestive ofoccupational asthma and a substantial improve-ment in ventilatory function could be seen during ashort period away from work. However, the physi-cian should be aware of a number of potentialpitfalls when interpreting unsupervised measure-ments such as these. Aside from the possibility ofpoor compliance, failure to make measurements atidentical times on work and non-work days has ledto spurious results when the subject wakened lateron non-work days, thus missing the early morningdip in peak flow rate.'2

Skin prick tests or radioallergosorbent tests forspecific IgE antibodies may be useful, particularlywhen an organic agent is the suspected cause ofoccupational asthma. Skin prick tests to flour andwheat have a reported sensitivity of 96% forbakers' asthma. However, the specificity of thesetests is generally lower (of the order of 50% fordetergent enzymes), the antibodies merely reflect-ing exposure to the relevant antigen or the presenceof another allergic disease (rhinitis, eczema) ratherthan asthma. For the majority of low molecularweight chemicals there are no specific immuno-logical tests for the reasons discussed above thoughskin tests have been useful in diagnosing allergy toplatinum salts and acid anhydrides.

Further information might be sought from

measurements of ventilatory function during eithera supervised exposure in the workplace or alaboratory based series ofinhalation challenge testswith the suspected agent. Such tests are timeconsuming and not without risk. They demandsupervision by an experienced investigator andshould only be performed in centres where theappropriate expertise exists. They are not routinelyrequired to diagnose occupational asthma or tojustify a claim for compensation. Nonetheless, theyare useful in evaluating potential new causes ofoccupational asthma and in clarifying difficultcases.

Three patterns of response are recognized;'3 anisolated immediate reaction beginning within min-utes of exposure and subsiding over 1-2 hours, anisolated late asthmatic reaction beginning after 2 to8 hours (occasionally later), and a dual reaction, animmediate followed by a late reaction. The chall-enge agent and dose together with the degrees ofairway responsiveness and specific hypersensitivityare all likely to be important in determining thenature of the response. Figure 2 illustrates a lateasthmatic reaction following inhalation of theantibiotic ceftazidime in a sensitized worker. Whenthe same dose was administered a few days later ata time when airway responsiveness (and, probably,specific antibody levels) had been increased by thefirst challenge, a dual reaction occurred.

Late asthmatic reactions following inhalationchallenge tests are associated with temporary in-creases in airway responsiveness. These may bereflected in increased asthmatic symptoms andmore marked circadian rhythms in ventilatoryfunction. They may persist for several days follow-

At work Off work

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Figure 2 Two inhalation challenges with ceftazidime3.2 mg ( ) were performed about a week apart. On thefirst occasion there was an isolated late asthmatic reactionwhilst a dual reaction was seen following the secondchallenge. The results ofcontrol challenges with saline arealso shown (---).



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ing a single challenge exposure. Circadian rhythmsin asthma may, of course, confound the identifica-tion of late asthmatic reactions and it may be usefulto quantify the magnitude of such changes oncontrol days prior to any challenge. This may bedone using a summary measurement such as themean change in ventilatory function over a givenperiod (e.g. 2-12 or 2-24 hours from the time atwhich a challenge dose might be given). Changesfollowing a challenge which are significantly inexcess of normal circadian rhythms can thus berecognized.Airway responsiveness may also be quantified

directly. A commonly used method'4 involves theadministration of doubling doses of the broncho-constricting agent methacholine at 5 minute inter-vals. Forced expiratory volume in one second(FEV,) is measured following each dose and fur-ther doses are given until there has been a 20% fallin FEVY or the maximum dose has been given. Theprovoking dose (PD20) of methacholine causingexactly a 20% fall in FEV, is calculated byinterpolation from the dose-response plot. In asubject with stable asthma, repeated measurementswithin one half to twice the original value canusually be made. Figure 3 illustrates such stabilityof airway responsiveness (PD20) and the changeswhich occurred following two inhalationchallenges with a detergent ingredient, SINOS.There was an increase in airway responsiveness(decrease in PD20) which took approximately 3weeks to return to baseline. In fact the PD20eventually improved above the pre-challengebaseline, probably because the subject's occupa-tional exposures ceased at the time of the challengetests. Measurements of airway responsiveness maybe equally useful in following changes in asthmaticactivity associated with exposures at work.

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Management and outcome

Once established, occupational asthma behaves asany other form of asthma apart from the associa-tion of symptoms with specific workplace expo-sures. There is likely to be an improvement insymptoms on commencing treatment with inhaledbeta-agonists and inhaled or oral corticosteroids.However, initial management should be aimed atreducing exposure to the offending agent and,ideally, an affected worker will cease being exposedaltogether. This is likely to require a change in job,often with a loss of earnings and a risk of unem-ployment and is rarely ideal from the patient'sviewpoint. A change in the working practice whichresults in a substantial reduction in the level ofexposure may sometimes be a suitable alternative.Such an approach should only be adopted wherethere are facilities for careful supervision andregular measurement of pulmonary function andairway responsiveness. Once a worker is sensitized,symptoms and airway hyperresponsiveness may bemaintained by exposure to minute amounts of theagent and the above approach may not be success-ful.On stopping exposure to the inducing agent,

occupational asthma may improve or disappearaltogether. However, in approximately 50% ofworkers, asthma will persist and may be severe anddisabling. The most important factor in determin-ing the outcome appears to be the length of timebetween the onset ofsymptoms and the cessation ofexposure.'5 The longer the period of symptomaticexposure, the greater the risk ofpermanent asthma.The early recognition of occupational asthma isthus vital if such an outcome is to be avoided.A diagnosis of occupational asthma and identifi-

cation of the responsible agent may be equallycrucial to an industry particularly if more than asingle worker is affected. The reductions in expo-sure levels necessary to eliminate the risks to otherworkers may require costly changes to a plant orchanges in the manufacturing process, and econo-mic viability may be imperilled.

Legislative aspects

Asthma arising as a consequence of an identifiableI industrial accident has been compensatable in2 mg Britain for many years under the state administered100 120 Industrial Injuries Act. It was not, however, until

1982 that more conventional varieties of occupa-ieness (PD20 tional asthma due to certain agents became com-.llenges with pensatable and the list ofprescribed compensatableway respon- agents was extended in 1986 (see Table I). Occupa-ing the chal- tional asthma is presumed and compensationout 3 weeks, awarded ifa worker who is occupationally exposedlevels. to one of the prescribed agents develops asthma

)r

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after a preliminary 'sensitizing' period.16 A furthermethod by which compensation might be obtainedis through a civil suit against an employer. Here, ajudgement will rest entirely on the balance ofprobabilities in the individual case without refer-ence to any prescribed list. Proof of negligence onthe part of the employer will also be required andsuccess is much more difficult. On the other hand,the level of compensation is likely to be muchhigher.

Conclusions

The study of occupational asthma has provideduseful insights into the mechanisms of asthma and,

in turn, has raised numerous questions. Why doesasthma frequently continue once exposure to theinducing agent has ceased? Is there any interactionbetween occupational exposures and other envir-onmental agents, e.g. the antigenic house dust miteor mucosa-damaging viruses? What contributionare increasingly complex occupational exposuresmaking to the apparently increasing prevalenceand morbidity of asthma?From a practical viewpoint, occupational asth-

ma continues to be underdiagnosed. When asthmabegins or substantially worsens in adult life, thequestion 'is it occupational?' is too important to beignored.

References

1. Parkes, W.R. Occupational Lung Disorders, 2nd edition.Butterworths, London, 1982.

2. Chan-Yeung, M. & Lam, S. Occupational asthma. Am RevResp Dis 1986, 133: 686-703.

3. Hendrick, D.J., Walters, E.H. & Bird, A.G. Occupationalasthma. In: Raffle, P.A.B., Lee, W.R., McCallum, R.I. &Murray, R. (eds) Hunter's Diseases of Occupations. Hodderand Stoughton, London, 1987.

4. Abramson, M.J., Wlodarcazyk, J.H., Saunders, N.A. &Hensley, M.J. Does aluminium smelting cause lung disease?Am Rev Resp Dis 1989, 139: 1042-1057.

5. Hendrick, D.J. Asthma: epidemics and epidemiology. Thorax1989, 44: 609-613.

6. Busse, W.W. Respiratory infections and asthma: clues to thepathogenesis of airway hyperreactivity. In: Barnes, P.J.,Rodger, I.W. & Thomson, N.C (eds) 'Asthma: Basic Mechan-isms and Clinical Management'. Academic Press, London,1988.

7. Barnes, P.J. & Thomson, N.C. Drug induced asthma. In:Barnes, P.J., Rodger, I.W. & Thomson, N.C. (eds) Asthma:Basic Mechanisms and Clinical Management. AcademicPress, London, 1988.

8. Brooks, S.M., Weiss, M.A. & Bernstein, I.H. Reactiveairways dysfunction syndrome (RADS); persistent asthmasyndrome after high level irritant exposures. Chest 1985, 88:376-384.

9. Grainger, D.N., Stenton, S.C., Avery, A.J., Duddridge, M.,Walters, E.H. & Hendrick, D.J. The relationship betweenatopy and non-specific bronchial responsiveness. Clin ExpAllergy 1990, 20: 181-187.

10. Slovak, AJ.M. & Hill, R.N. Does atopy have any predictivevalue for laboratory animal allergy? A comparison ofdifferent concepts of atopy. Br J Indust Med 1987, 44:129-132.

11. Gerrard, J.W., Heiner, D.C., Ko, C.G., Mink, L., Meyers, A.& Dosman, J.A. Immunoglobulin levels in smokers andnon-smokers. Ann Allergy 1980, 44: 261-262.

12. Venables, K.M., Davison, A.G.C., Browne, K. & Newman-Taylor, A.J. Pseudo-occupational asthma. Thorax 1989, 44:760-761.

13. Pepys, J. & Hutchinson, B.J. Bronchial provocation tests inetiologic diagnosis and analysis of asthma. Am Rev Resp Dis1975, 112: 829-859.

14. Connolly, M.J., Avery, A.J., Walters, E.H. & Hendrick, D.J.The relationship between bronchial responsiveness tomethacholine and bronchial responsiveness to histamine inasthmatic subjects. Pulmonary Pharmacol 1988, 1: 53-58.

15. Chan-Yeung, M., Lam, S. & Koner, S. Clinical features andnatural history of occupational asthma due to Western RedCedar (Thuja plicata). Am J Med 1982, 72: 411-415.

16. Occupational asthma. Report of the Industrial InjuriesAdvisory Council. (Cmnd 8121). HMSO, London, 1981.



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