You are here

Article Text

Article menu

Download PDFPDF

Original article
Evidence based guidelines for the prevention, identification, and management of occupational asthma
  1. P J Nicholson1,
  2. P Cullinan2,
  3. A J Newman Taylor2,
  4. P S Burge3,
  5. C Boyle4
  1. 1Procter & Gamble, Whitehall Lane, Egham, Surrey, UK
  2. 2National Heart & Lung Institute, Manresa Road, London, UK
  3. 3Heartlands Hospital, Bordesley Green East, Birmingham, UK
  4. 4Health & Safety Executive, Magdalen Court, Bootle, UK
  1. Correspondence to:
 Dr P J Nicholson
 British Occupational Health Research Foundation, 6 St Andrews Place, Regents Park, London NW1 4LB, UK; nicholson.pjpg.com

Abstract

Background: Occupational asthma is the most frequently reported work related respiratory disease in many countries. This work was commissioned by the British Occupational Health Research Foundation to assist the Health and Safety Executive in achieving its target of reducing the incidence of occupational asthma in Great Britain by 30% by 2010.

Aim: The guidelines aim to improve the prevention, identification, and management of occupational asthma by providing evidence based recommendations on which future practice can be based.

Methods: The literature was searched systematically using Medline and Embase for articles published in all languages up to the end of June 2004. Evidence based statements and recommendations were graded according to the Royal College of General Practitioner’s star system and the revised Scottish Intercollegiate Guidelines Network grading system.

Results: A total of 474 original studies were selected for appraisal from over 2500 abstracts. The systematic review produced 52 graded evidence statements and 22 recommendations based on 223 studies.

Discussion: Evidence based guidelines have become benchmarks for practice in healthcare and the process used to prepare them is well established. This evidence review and its recommendations focus on interventions and outcomes to provide a robust approach to the prevention, identification, and management of occupational asthma, based on and using the best available medical evidence. The most important action to prevent cases of occupational asthma is to reduce exposure at source. Thereafter surveillance should be performed for the early identification of symptoms, including occupational rhinitis, with additional functional and immunological tests where appropriate. Effective management of workers suspected to have occupational asthma involves the identification and investigation of symptoms suggestive of asthma immediately they occur. Those workers who are confirmed to have occupational asthma should be advised to avoid further exposure completely and early in the course of their disease to offer the best chance of recovery.

  • BOHRF, British Occupational Health Research Foundation
  • ES, evidence statement
  • HMW, high molecular weight
  • LMW, low molecular weight
  • OA, occupational asthma
  • PEF, peak expiratory flow
  • RCT, randomised controlled trial
  • RCGP, Royal College of General Practitioners
  • RPE, respiratory protective equipment
  • SIGN, Scottish Intercollegiate Guidelines Network
  • SBPT, specific bronchial provocation testing
  • occupational asthma
  • evidence based medicine
  • prevention

https://doi.org/10.1136/oem.2004.016287

Statistics from Altmetric.com

    Request Permissions

    If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

    Work related asthma, where there is an association between symptoms and work, includes: work aggravated asthma (pre-existing or coincidental new onset asthma worsened by workplace exposure); and occupational asthma (OA; new onset asthma caused by workplace exposure). OA can be either: hypersensitivity induced OA characterised by latency between first exposure to a substance at work and the development of symptoms; or irritant induced OA that occurs shortly after a high exposure to an irritant gas, fume, or vapour at work. Almost 90% of cases of occupational asthma are of the hypersensitivity type1–6 and are the focus for this review.

    This review was commissioned and funded by the British Occupational Health Research Foundation (BOHRF) to provide a robust approach to the prevention, identification, and management of OA, based on and using the best available medical evidence.7

    METHODS

    We systematically searched Medline and Embase from 1966 and 1974 respectively to the end of June 2004. Pairs of working group members reviewed over 2500 abstracts independently to select 474 papers for further, independent critical review; single case studies and narrative reviews were excluded. Data from 223 papers were entered into evidence tables7 and contributed to the evidence statements.

    Criteria for grading evidence and recommendations were developed primarily to guide inferences about treatment; questions about disease frequency, aetiology, diagnosis, and prognosis require other hierarchies.8 There are few meta-analyses and randomised controlled trials (RCTs) related to OA, and so little Scottish Intercollegiate Guidelines Network (SIGN) grading system level 1 evidence. Therefore we graded evidence statements (ES) and recommendations using both the revised SIGN grading system 2000 for levels of evidence (table 1) and recommendations (table 2), and the modified 1995 Royal College of General Practitioners (RCGP) three star system used in the BOHRF Occupational Health Guidelines for the Management of Low Back Pain at Work (table 3).9 In accordance with current opinion, recommendations appear in behaviourally specific terms.10

    View this table:
    Table 1

     Revised SIGN grading system for levels of evidence

    View this table:
    Table 2

     Revised SIGN grading system for recommendations

    View this table:
    Table 3

     Modified RCGP three star system

    RESULTS AND DISCUSSION

    Background

    OA is the most frequently reported occupational respiratory disorder in westernised industrialised populations.5,11,12 Where mining is common, for example, South Africa and the Czech Republic, OA is the second commonest occupational respiratory disorder after pneumoconiosis.4,13

    Main messages

    • Reducing airborne exposure reduces the number of workers who develop occupational asthma.

    • Occupational rhinitis may indicate an increased risk of a worker developing occupational asthma, particularly when IgE associated and especially in the year after the onset of rhinitis.

    • Health surveillance can detect occupational asthma at an earlier stage of disease and contribute to improved clinical outcome.

    • Asking workers about symptoms that improve regularly when away from work is more sensitive than enquiring about symptoms that deteriorate when at work.

    • Outcome is better in workers who have shorter duration of symptoms prior to diagnosis, relatively normal lung function at diagnosis, and no further exposure to the causative agent after diagnosis.

    There are no complete registries of OA so the true frequency of the disease is unknown. Published frequencies come from surveillance schemes, compensation registries, or epidemiological studies of the relation between asthma and occupation. The incidence, predominant causative agents, and jobs most commonly reported to incur risk depend on the methodology of data collection, case definition, and predominant work sectors and occupations. Studies generally do not distinguish between hypersensitivity and irritant causes. One systematic review showed an attributable risk of 9%,14 while the highest scoring studies showed an attributable risk of 15%, a figure supported by another review.15

    ES1*** SIGN 2++

    Occupational factors are estimated to account for 9–15% of cases of asthma in adults of working age, including new onset or recurrent disease.14,15

    ES2*** SIGN 2++

    The annual population incidence of occupationally related asthma ranges from an estimated 12–170 cases per million workers with an estimated mean of 47 cases per million workers.6,14,16,17

    ES3* SIGN 3

    The population incidence of OA may be underestimated by as much as 50%.18

    ES4* SIGN 3

    The reported incidence of OA has not decreased in recent years.19–21

    Policy implications

    • Employers should implement programmes to prevent occupational asthma by removing or reducing exposure to its causes.

    • Employers and their health and safety personnel should provide regular health surveillance (respiratory questionnaire with functional and immunological tests, where appropriate) to workers where a risk of occupational asthma is identified.

    • Employers and their health and safety personnel should ensure that measures are taken to ensure that workers diagnosed as having of occupational asthma avoid further exposure to its cause in the workplace.

    ES5*** SIGN 2++

    The most frequently reported agents include isocyanates, flour and grain dust, colophony and fluxes, latex, animals, aldehydes, and wood dust.3,4,6,12,13,17,19,22–24

    ES6*** SIGN 2++

    The workers most commonly reported to surveillance schemes of OA include paint sprayers, bakers and pastry makers, nurses, chemical workers, animal handlers, welders, food processing workers, and timber workers.3,6,12,13,17,21–25

    ES7** SIGN 2+

    The workers reported from population studies to be at increased risk of developing asthma include bakers, food processors, forestry workers, chemical workers, plastics and rubber workers, metal workers, welders, textile workers, electrical and electronic production workers, storage workers, farm workers, waiters, cleaners, painters, plastic workers, dental workers, and laboratory technicians.26–29

    Four main risk factors have been identified for OA: the causative factor of exposure to an agent at work; the predisposing factors of atopy and genetic predisposition; and the contributing factor of cigarette smoking.

    A direct relation between OA and exposure to an agent at work occurs with acid anhydrides,30,31 cimetidine,32 colophony,33 enzymes,34–38 green coffee and castor bean,39 flour allergens,40–45 crab,46 isocyanates,47–49 laboratory animal allergens,50–52 piperazine,53 platinum salts,54 prawns,55 and western red cedar.56 Most studies also showed a positive exposure-response relation for sensitisation. Studies limited to sensitisation showed a relation with exposure to acid anhydrides,57 enzymes,37,58,59 laboratory animals,60 and platinum salts.61

    ES8*** SIGN 2++

    The risk of sensitisation and OA is increased by higher exposures to many workplace agents.30–32,34–56

    Differences in ascertaining atopy, from personal or family history of allergy to tests for specific immunoglobulin E (IgE), can cause inconsistencies between observations. Atopy is reported to increase the risk of OA in workers exposed to enzymes,38,62,63 isocyanates,47,64 laboratory and other animals,50–52,64–74 bakery allergens,44,75–79 and some reactive dyes.80 Other studies show no association between atopy and OA due to exposure to cork,81 isocyanates,48,82,83 enzymes,35 glutaraldehyde,84 salmon,85 crab,86 hexahydrophthalic anhydride,87 platinum salts,61,88 and plicatic acid.89 Atopy is associated with increased risk of sensitisation in workers exposed to enzymes,36,37,42,58,63,90–93 green coffee and castor bean,39,94 bakery allergens,42–44,75,76,95,96 laboratory animals,50 crab,86 prawn,55 and acid anhydrides.57,97

    ES9*** SIGN 2++

    Atopy increases the risk of developing OA caused by exposure to many high molecular weight (HMW) agents that induce the production of specific IgE antibodies.38,50–52,62,63,65,66,68–79

    That only some workers develop OA despite similar exposures, suggests underlying genetic susceptibility. Studies have examined genetic predisposition to OA attributed to isocyanates,98–105 complex platinum salts,106 western red cedar,107 acid anhydrides,108 and laboratory animal proteins.70,109 Studies had small sample sizes and their findings were inconsistent or unreplicated.

    ES10** SIGN 2−

    Genetic polymorphisms that code for human leucocyte antigen (HLA) class II genes or respiratory antioxidant mechanisms may predispose to OA for a number of agents.70,98,101–103,107

    Smoking increases the risk of OA in workers exposed to: isocyanates,47,64,83 platinum salts,54,88,111 salmon,85 and snow crab.86 Smoking increases the risk of sensitisation in studies with exposure to green coffee and castor bean,39,94 platinum salts,61,110,111 prawn,55 and flour.95 The role of smoking is unclear for OA due to other agents. Some studies show increased risk of laboratory animal asthma in smokers,50,74,112 whereas others show no effect.51,65,68,69,113 For acid anhydrides, studies show both negative31,87 and positive97 correlation with specific IgE. Conflicting evidence also exists for detergent enzymes.38,114 In bakery workers, one study showed an increased risk of sensitisation in smokers,95 but the risk of OA does not appear to be increased.42,44,75,95

    ES11** SIGN 2+

    Cigarette smoking can increase the risk of developing OA with some sensitising agents.47,54,64,83,85,86,88,111

    Co-morbid rhinitis or rhino-conjunctivitis is reported in 45–90% of subjects suffering from IgE associated OA attributable to acid anhydrides,115,116 laboratory animals,50,68,69 snow crab,86 and wheat flour.44

    ES12** SIGN 2+

    Occupational rhinitis and OA frequently occur as co-morbid conditions in IgE associated OA.19,44,50,68,69,86,115–117

    ES13** SIGN 2+

    Rhino-conjunctivitis is more likely to appear before the onset of IgE associated OA.19,50,68,69,115,117,118

    ES14* SIGN 2−

    The risk of developing OA is highest in the year after the onset of occupational rhinitis.19,118

    While the latent interval between first exposure and the onset of OA can extend to many years,19,119–121 risk is highest soon after first exposure to laboratory animal allergens,50,52,65,68,69,112 isocyanates,122 platinum salts,54,88,111 and azodicarbonamide.123

    ES15** SIGN 2+

    IgE sensitisation and OA are most likely to develop in the first years of exposure for workers exposed to azodicarbonamide, enzymes, complex platinum salts, isocyanates, and laboratory animal allergens.50,52,54,65,68,69,88,111,112,122,123

    Prevention

    With any study of preventive measures, it is difficult to distinguish the relative effect of one measure against another, since they are usually implemented as a composite programme. Studies show that reducing exposure leads to fewer cases of OA from acid anhydrides,31,124 detergent enzymes,34,36 isocyanates,49 laboratory animals,66,125 and latex.126–128

    ES16** SIGN 2+

    Reducing airborne exposure reduces the number of workers who become sensitised and who develop OA.31,34,36,49,66,125–128

    Respiratory protective equipment (RPE) only offers protection when worn properly, removed safely, and either replaced or maintained regularly. Studies are few and small; one observed a significant association between symptoms and even brief removal of RPE.48

    ES17* SIGN 3

    The use of RPE reduces the incidence of, but does not completely prevent, OA.48,83,129

    Pre-placement examinations should be used to establish a baseline for periodic health surveillance rather than to detect and exclude susceptible individuals from workplaces. Little is known about host susceptibility factors, except for atopy in those exposed predominantly to high molecular weight agents. The efficiency of screening out susceptible job applicants depends partly on the frequency of the trait in the general population.

    ES18* SIGN 3

    The positive predictive values of screening criteria are too poorly discriminating for screening out potentially susceptible individuals, particularly in the case of atopy where the trait is highly prevalent.67,77,111,123,130–132

    ES19* SIGN 3

    A previous history of asthma is not significantly associated with OA.67,68

    Periodic health surveillance aims to identify sensitised workers or cases of OA at early and reversible stages of disease. There are few, and no concurrent comparison studies of the efficacy of health surveillance for OA. The only study from which valid conclusions can be drawn is of isocyanate workers, in whom health surveillance was linked to a mandatory programme of control of exposure. Workers with isocyanate induced asthma were diagnosed sooner after symptoms began, had better lung function and better outcome than workers who had asthma attributable to other workplace agents133 although the results might partly be attributable to concomitant reduction in exposure. Few studies have evaluated the separate components of health surveillance, questionnaires, spirometry, and identification of specific IgE. In one, all true cases of OA were identified by questionnaire, spirometry producing many false positives due to poor inspiratory effort and no additional cases of asthma.134 In another, spirometry detected one case of OA in addition to two cases identified by questionnaire.135 Skin prick and serological tests can detect specific IgE in workers who have become sensitised to HMW agents and a few low molecular weight (LMW) agents (complex platinum salts, acid anhydrides, and some reactive dyes).

    ES20* SIGN 3

    Health surveillance can detect OA at an earlier stage of disease and outcome is improved in workers who are included in a health surveillance programme.133

    ES21* SIGN 3

    Screening questionnaires may lead to an underestimate of the prevalence of asthmatic symptoms.136,137

    ES22* SIGN 3

    Spirometry detects few cases of OA that would not otherwise be detected by respiratory questionnaire.134,135

    ES23** SIGN 2+

    Skin prick testing and blood sampling of exposed workers to conduct immunological tests is feasible in the workplace.138–140

    ES24** SIGN 2+

    Prospective surveillance for the development of specific IgE antibodies can be used as part of a broader risk management programme to reduce the incidence of OA.36,90

    Identification and evaluation of OA

    Most evidence relating to the diagnosis of OA emanates from specialist settings where the prior probability of disease and positive predictive values of tests may be high. History alone produces false positive diagnoses, requiring further validation. Serial measurement of peak expiratory flow (PEF) is the simplest initial investigation. When performed and interpreted to validated standards there are few false positive results, but about 20% false negatives. Skin prick or blood tests for specific IgE are available for most HMW agents and a few LMW agents but few standardised allergens are commercially available. OA can usually be diagnosed without specific bronchial provocation testing (SBPT).

    The symptoms of any type of asthma have high sensitivity but lower specificity, whereas the question “have you been told by a doctor that you have asthma” has a higher specificity but lower sensitivity.141 Asking about deterioration at work is an insensitive method of diagnosing OA. Questioning about symptoms that are better on days away from work has a sensitivity of 58–100% for validated OA and is enhanced by asking about symptoms improving on holiday. Work related symptoms are common in those with negative SBPT.

    ES25** SIGN 2+

    In the clinical setting questionnaires that identify symptoms of wheeze and/or shortness of breath that improve on days away from work or on holiday have a high sensitivity, but relatively low specificity for OA.138,142–147

    ES26* SIGN 3

    Free histories taken by experts have high sensitivity, but their specificity may be lower.117,142,143,145,148–150

    No good studies compare cross-shift changes with SBPT. Such testing is unlikely to be either sensitive or specific since measures of airflow obstruction show diurnal variation in most normal workers that is increased in most asthmatics. In one study a fall in FEV1 of >10% post-shift was found in 5% of asymptomatic workers and 32% of those with work related asthma symptoms.

    ES27* SIGN 3

    Pre- to post-shift changes in lung function cannot be recommended for the validation or exclusion of OA.151,152

    Serial PEF was studied in small case series of patients attending specialist clinics or workplace surveys. Over 70% of subjects in four clinical series and each of the workforce populations returned acceptable records. A single case series of 74 patients attending a specialist clinic reports the highest combination of sensitivity and specificity with PEF measured at least four times daily. Less frequent readings produced higher specificity but lower sensitivity. Six series report high levels of agreement (averaging 80%) between expert assessors. A single series, using non-expert assessors, reports much lower inter-observer agreement. Eight case series report direct and blinded comparisons of serial PEF measurement and either SBPT or an expert diagnosis based on a combination of other evidence. Sensitivities and specificities were consistently high, averaging 80% and 90% respectively. Three case series compare visual inspection of PEF records by experts with a variety of statistical indices. One computed analysis reported sensitivity of 75% and specificity of 94% when analysis was calibrated using the opinion of one expert in cases whose OA was mostly attributable to LMW agents.

    ES28** SIGN 3

    Acceptable PEF series can be obtained in around two thirds of those in whom a diagnosis of OA is being considered.139,146,147,153–158

    ES29* SIGN 3

    The diagnostic performance of serial PEF measurements falls when fewer than four readings a day are made.159

    ES30** SIGN 3

    There is high level of agreement between expert interpretations of serial PEF records.155,159–164

    ES31** SIGN 3

    The sensitivity and specificity of serial PEF measurements are high in the diagnosis of OA.146,147,155,159,162,164–166

    ES32** SIGN 3

    Statistical analysis of serial PEF measurements is of limited diagnostic value compared to expert interpretation.147,155,162

    ES33** SIGN 2+

    Computed analysis of PEF records has good diagnostic performance.160,167

    Many studies show that non-specific bronchial hyper-reactivity is normal in 5–40% of SBPT positive workers. Testing with higher concentrations of methacholine or histamine at which some non-asthmatics react reduces the number of, but still leaves some, non-reacting asthmatics. A normal test of non-specific reactivity is not sufficiently specific to exclude OA.

    ES34*** SIGN 2++

    A large number of concordant studies from different centres using different methodologies showed that increased non-specific reactivity is often found in workers with OA. There are however many reports of normal methacholine or histamine reactivity within 24 hours of exposure in workers with confirmed OA.142–145,149,150,162,166,168–177

    ES35** SIGN 2−

    Changes in non-specific reactivity at and away from work alone have only moderate sensitivity and specificity for diagnosis.146,162,177

    ES36* SIGN 3

    Paired measurements of non-specific reactivity may be achieved in the workplace.177,178

    The sensitivities and specificities of skin prick or serological tests to detect specific IgE vary between allergens and with positive cut-off levels. Serological tests may not be as sensitive as skin prick testing.179 The presence of specific IgE confirms sensitisation to an agent at work, but alone does not confirm OA, or necessarily its cause. There is a high false positive rate although, with HMW agents, few false negatives. Specific IgE is an insensitive but specific test for isocyanate induced OA,180 although this may depend on the time since last exposure. A small study reported greater sensitivity for MDI (83%) than TDI (27%).181

    ES37** SIGN2+

    Both skin prick and serological tests are highly sensitive for detecting specific IgE and OA caused by most HMW agents, but are not specific for diagnosing OA.51,182

    ES38** SIGN2+

    Both skin prick and serological tests are sensitive for detecting specific IgE and OA caused by acid anhydrides and some reactive dyes, but have a lower specificity for diagnosing OA.179,183–186

    ES39** SIGN2+

    Skin prick tests are highly sensitive but less specific for OA caused by complex platinum salts.138,174,175

    SBPT is used as the gold standard for OA diagnosis, making assessments of its diagnostic validity difficult. Standardised methods are lacking for many occupational agents. The threshold exposure increases with time since last exposure, making tests less sensitive after prolonged absence from work. Individuals can have non-specific reactions to SBPT at concentrations likely to be found in the workplace and negative SBPT with otherwise good evidence of OA when challenge concentrations are below occupational exposure standards.151,152,170,173,176

    ES40− SIGN 4

    Carefully controlled specific challenges come closest to a gold standard test for some agents causing OA.

    ES41− SIGN 4

    A negative test in a worker with otherwise good evidence of OA is not sufficient to exclude the diagnosis.

    Management of the worker with OA

    The outcome of interventions following a confirmed diagnosis of OA may depend on several factors, including the worker’s age and the causative agent. Early diagnosis and early avoidance of further exposure, either by relocation of the worker or substitution of the hazard, offer the best chance of complete recovery. If these are impossible, workers should be relocated to low or occasional exposure areas and have increased health surveillance. Studies investigating the effectiveness of RPE in those with OA are limited to small studies in provocation chambers or limited case reports. The risk of unemployment may148 or may not,187,188 be higher than in other adult asthmatics and may fall with increasing time from diagnosis.189 No studies make direct comparisons between different systems of rehabilitation. There is one small RCT of the effect of inhaled corticosteroids on recovery from OA after ceasing exposure.

    ES42*** SIGN 2+

    The symptoms and functional impairment of OA caused by various agents may persist for many years after avoidance of further exposure to the causative agent.89,122,190–209

    ES43*** SIGN 2++

    The likelihood of improvement or resolution of symptoms or of preventing deterioration is greater in workers who have no further exposure to the causative agent.89,204,205,210–216

    ES44** SIGN 2+

    The likelihood of improvement or resolution of symptoms or of preventing deterioration is greater in workers who have relatively normal lung function at the time of diagnosis.89,193,201,205,206,217,218

    ES45** SIGN 2+

    The likelihood of improvement or resolution of symptoms or of preventing deterioration is greater in workers who have shorter duration of symptoms prior to diagnosis.89,189,204–206,213,218,219

    ES46** SIGN 2+

    The likelihood of improvement or resolution of symptoms or of preventing deterioration is greater in workers who have shorter duration of symptoms prior to avoidance of exposure.189,193,205,213,218,219

    ES47* SIGN 3

    Redeployment to a low exposure area may lead to improvement or resolution of symptoms or prevent deterioration in some workers, but is not always effective.85,204,205,210,211,220,221

    ES48* SIGN 3

    Air fed helmet respirators may improve or prevent symptoms in some but not all workers who continue to be exposed to the causative agent.204,222–226

    ES49** SIGN 2−

    Approximately one third of workers with OA are unemployed up to six years after diagnosis.148,187–189,207,209,227–229

    ES50** SIGN 2−

    Workers with OA suffer financially.148,188,207,227,228,230

    ES51− SIGN 4

    Systems that incorporate retraining may be more effective than those that do not.227,231

    ES52* SIGN 1+

    Inhaled corticosteroids used after cessation of exposure may provide small clinical benefits to workers with OA.161

    Recommendations

    Recommendations appear in table 4 and are followed by references to supporting evidence statements in brackets.

    View this table:
    Table 4

     Principal recommendations

    Acknowledgments

    BOHRF Research Working Group: AJ Newman Taylor (Chair), PJ Nicholson (Vice Chair), PS Burge, C Beach, P Cullinan, C Francis, PFG Gannon, C Boyle, M Levy, R Miguel, MJ Nieuwenhuijsen, RG Rawbone, D Romano-Woodward, AJ Scott, O Tudor, EV Warbrick.

    BOHRF External Reviewers: CAC Pickering, SC Stenton. Patient representative: S Ozanne.

    REFERENCES

    1. ↵
      Milton DK, Solomon GM, Rosiello RA, et al. Risk and incidence of asthma attributable to occupational exposure among HMO members. Am J Ind Med1998;33:1–10.
      OpenUrlCrossRefPubMedWeb of Science
    2. Chatkin JM, Tarlo SM, Liss G, et al. The outcome of asthma related to irritant exposures: a comparison of irritant-induced asthma and irritant aggravation of asthma. Chest1999;116:1780–5.
      OpenUrlCrossRefPubMedWeb of Science
    3. ↵
      Meyer JD, Holt DL, Cherry N, et al. SWORD 98: surveillance of work-related and occupational respiratory disease in the UK. Occup Med (Lond)1999;49:485–9.
    4. ↵
      Hnizdo E, Esterhuizen TM, Rees D, et al. Occupational asthma as identified by the Surveillance of Work-related and Occupational Respiratory Diseases programme in South Africa. Clin Exp Allergy2001;31:32–9.
      OpenUrlCrossRefPubMedWeb of Science
    5. ↵
      Provencher S, Labreche F, De Guire. Physician based surveillance for occupational respiratory diseases: the experience of PROPULSE, Quebec, Canada. Occup Environ Med1997;54:272–6.
      OpenUrlAbstract/FREE Full Text
    6. ↵
      Ameille J, Pauli G, Calastreng-Crinquand A, et al. Reported incidence of occupational asthma in France, 1996–99. The ONAP programme. Occup Environ Med2003;60:136–41.
      OpenUrlAbstract/FREE Full Text
    7. ↵
      Newman Taylor AJ, Nicholson PJ, Cullinan P, et al.Guidelines for the prevention, identification and management of occupational asthma: evidence review and recommendations. London: British Occupational Health Research Foundation, 2004.
    8. ↵
      Glasziou P, Vandenbroucke J, Chalmers. Assessing the quality of research. BMJ2004;328:39–41.
      OpenUrlFREE Full Text
    9. ↵
      Waddell G, Burton AK. Occupational health guidelines for the management of low back pain at work—evidence review. London Faculty of Occupational Medicine 2000.
    10. ↵
      Michie S, Johnston M. Changing clinical behaviour by making guidelines specific. BMJ2004;328:343–5.
      OpenUrlFREE Full Text
    11. ↵
      Kor AC, Lee HS, Chee CB, et al. Occupational asthma in Singapore. Singapore Med J2001;42:373–7.
      OpenUrlPubMed
    12. ↵
      McDonald JC, Keynes HL, Meredith SK. Reported incidence of occupational asthma in the United Kingdom 1989–97. Occup Environ Med2000;57:823–9.
      OpenUrlAbstract/FREE Full Text
    13. ↵
      Brhel P. Occupational respiratory diseases in the Czech Republic. Ind Health2003;41:121–3.
      OpenUrlPubMedWeb of Science
    14. ↵
      Blanc PD, Toren K. How much adult asthma can be attributed to occupational factors? Am J Respir Crit Care Med1999;107:580–7.
      OpenUrl
    15. ↵
      Balmes J, Becklake M, Blanc P, et al. American Thoracic Society statement: occupational contribution to the burden of airway disease. Am J Respir Crit Care Med2003;167:787–97.
      OpenUrlCrossRefPubMedWeb of Science
    16. ↵
      Karjalainen A, Kurppa K, Virtanen S, et al. Incidence of occupational asthma by occupation and industry in Finland. Am J Ind Med2000;37:451–8.
      OpenUrlCrossRefPubMedWeb of Science
    17. ↵
      Meredith SK, Taylor VM, McDonald JC. Occupational respiratory disease in the United Kingdom 1989: a report to the British Thoracic Society and the Society of Occupational Medicine by the SWORD project group. Br J Ind Med1991;48:292–8.
      OpenUrlPubMedWeb of Science
    18. ↵
      de Bono J, Hudsmith L. Occupational asthma: a community based study. Occup Med (Lond)1999;49:217–19.
    19. ↵
      Cortona G, Pisati G, Dellabianca A, et al. Allergopatie professionali respiratorie: l’esperienza delle Unita Operative Ospedaliere di Medicina del Lavoro in Lombardia dal 1990 al 1998. [Respiratory occupational allergies: the experience of the Hospital Operative Unit of Occupational Medicine in Lombardy from 1990 to 1998], G Ital Med Lav Ergon2001;23:64–70.
      OpenUrlPubMed
    20. Reijula K, Haahtela T, Klaukka T, et al. Incidence of occupational asthma and persistent asthma in young adults has increased in Finland. Chest1996;110:58–61.
      OpenUrlCrossRefPubMedWeb of Science
    21. ↵
      Meyer JD, Holt DL, Chen Y, et al. SWORD 99: Surveillance of work-related and occupational respiratory disease in the UK. Occup Med2001;51:204–8.
      OpenUrlAbstract
    22. ↵
      Gannon PFG, Burge PS. The SHIELD scheme in the West Midlands Region, United Kingdom. Br J Ind Med1993;50:791–6.
      OpenUrlPubMedWeb of Science
    23. Sallie BA, Ross DJ, Meredith SK, et al. SWORD ’93. Surveillance of work-related and occupational respiratory disease in the UK. Occup Med (Lond)1994;44:177–82.
    24. ↵
      Toren K, Jaervholm B, Brisman J, et al. Adult-onset asthma and occupational exposures. Scand J Work Environ Health1999;25:430–5.
      OpenUrlPubMedWeb of Science
    25. ↵
      Karjalainen A, Kurppa K, Martikainen R, et al. Exploration of asthma risk by occupation—extended analysis of an incidence study of the Finnish population. Scand J Work Environ Health2002;28:49–57.
      OpenUrlCrossRefPubMedWeb of Science
    26. ↵
      Jaakkola JJK, Piipari R, Jaakkola MS. Occupation and asthma: a population-based incident case-control study. Am J Epidemiol2003;158:981–7.
      OpenUrlAbstract/FREE Full Text
    27. Johnson AR, Dimich-Ward-HD, Manfreda J, et al. Occupational asthma in adults in six Canadian communities. Am J Respir Crit Care Med2000;162:2058–62.
      OpenUrlPubMedWeb of Science
    28. Kogevinas M, Anto JM, Soriano JB, et al. The risk of asthma attributable to occupational exposures. A population-based study in Spain. Spanish Group of the European Asthma Study. Am J Respir Crit Care Med1996;154:137–43.
      OpenUrlPubMedWeb of Science
    29. ↵
      Kogevinas M, Anto JM, Sunyer J, et al. Occupational asthma in Europe and other industrialised areas: a population-based study. Lancet1999;353:1750–4.
      OpenUrlCrossRefPubMedWeb of Science
    30. ↵
      Grammer LC, Shaughnessy MA, Lowenthal M, et al. Risk factors for immunologically mediated respiratory disease from hexahydrophthalic anhydride. J Occup Med1994;36:642–6.
      OpenUrlPubMedWeb of Science
    31. ↵
      Liss GM, Bernstein D, Genesove L, et al. Assessment of risk factors for IgE-mediated sensitization to tetrachlorophthalic anhydride. J Allergy Clin Immunol1993;92:237–47.
      OpenUrlCrossRefPubMedWeb of Science
    32. ↵
      Coutts IL, Lozewicz S, Dally MB, et al. Respiratory symptoms related to work in a factory manufacturing cimetidine tablets. BMJ1984;288:1418.
    33. ↵
      Burge PS, Edge G, Hawkins R, et al. Occupational asthma in a factory making flux-cored solder containing colophony. Thorax1981;36:828–34.
      OpenUrlAbstract/FREE Full Text
    34. ↵
      Cathcart M, Nicholson P, Roberts D, et al. Enzyme exposure, smoking and lung function in employees in the detergent industry over 20 years. Medical Subcommittee of the UK Soap and Detergent Industry Association. Occup Med (Lond)1997;47:473–8.
    35. ↵
      Cullinan P, Harris JM, Newman-Taylor AJ, et al. An outbreak of asthma in a modern detergent factory. Lancet2000;356:1899–900.
      OpenUrlCrossRefPubMedWeb of Science
    36. ↵
      Juniper CP, How MJ, Goodwin BFJ, et al. Bacillus subtilis enzymes: a 7 year clinical, epidemiological and immunological study of an industrial allergen. J Soc Occup Med1977;27:3–12.
      OpenUrlPubMedWeb of Science
    37. ↵
      Vanhanen M, Tuomi T, Nordman H, et al. Sensitization to industrial enzymes in enzyme research and production. Scand J Work Environ Health1997;23:385–91.
      OpenUrlPubMedWeb of Science
    38. ↵
      Weill H, Waddell LC, Ziskind M. A study of workers exposed to detergent enzymes. JAMA1971;26:425–33.
      OpenUrl
    39. ↵
      Osterman K, Zetterstrom O, Johansson SG. Coffee workers asthma. Allergy1982;37:313–22.
      OpenUrlPubMedWeb of Science
    40. ↵
      Brisman J, Jaervholm B, Lillienberg L. Exposure-response relations for self report asthma and rhinitis in bakers. Occup Environ Med2000;57:335–40.
      OpenUrlAbstract/FREE Full Text
    41. Cullinan P, Lowson D, Nieuwenhuijsen MJ, et al. Work related symptoms, sensitisation, and estimated exposure in workers not previously exposed to flour. Occup Environ Med1994;51:579–83.
      OpenUrlAbstract/FREE Full Text
    42. ↵
      Cullinan P, Cook A, Nieuwenhuijsen MJ, et al. Allergen and dust exposure as determinants of work-related symptoms and sensitization in a cohort of flour-exposed workers; a case-control analysis. Ann Occup Hyg2001;45:97–103.
      OpenUrlAbstract/FREE Full Text
    43. Heederik D, Houba R. An exploratory quantitative risk assessment for high molecular weight sensitizers: wheat flour. Ann Occup Hyg2001;45:175–85.
      OpenUrlAbstract/FREE Full Text
    44. ↵
      Houba R, Heederik D, Doekes D. Wheat sensitization and work-related symptoms in the baking industry are preventable. An epidemiologic study. AmJ Respir Crit Care Med1998;158:1499–503.
      OpenUrlCrossRefPubMedWeb of Science
    45. ↵
      Musk AW, Venables KM, Crook B, et al. Respiratory symptoms, lung function, and sensitisation to flour in a British bakery. Br J Ind Med1989;46:636–42.
      OpenUrlPubMedWeb of Science
    46. ↵
      Ortega HG, Daroowalla F, Petsonk EL, et al. Respiratory symptoms among crab processing workers in Alaska: epidemiological and environmental assessment. Am J Ind Med2001;39:598–607.
      OpenUrlCrossRefPubMedWeb of Science
    47. ↵
      Meredith SK, Bugler J, Clark RL. Isocyanate exposure and occupational asthma: a case-referent study. Occup Environ Med2000;57:830–6.
      OpenUrlAbstract/FREE Full Text
    48. ↵
      Petsonk EL, Wang ML, Lewis DM, et al. Asthma-like symptoms in wood product plant workers exposed to methylene diphenyl diisocyanate. Chest2000;118:183–93.
      OpenUrlCrossRefPubMedWeb of Science
    49. ↵
      Tarlo SM, Liss GM, Dias C, et al. Assessment of the relationship between isocyanate exposure levels and occupational asthma. Am J Ind Med1997;32:517–21.
      OpenUrlCrossRefPubMedWeb of Science
    50. ↵
      Cullinan P, Cook A, Gordon S, et al. Allergen exposure, atopy and smoking as determinants of allergy to rats in a cohort of laboratory employees. Eur Respir J1999;13:1139–43.
      OpenUrlAbstract/FREE Full Text
    51. ↵
      Kruize H, Post W, Heederik D, et al. Respiratory allergy in laboratory animal workers: a retrospective cohort study using pre-employment screening data. Occup Environ Med1997;54:830–5.
      OpenUrlAbstract/FREE Full Text
    52. ↵
      Platts-Mills T-A, Longbottom J, Edwards J, et al. Occupational asthma and rhinitis related to laboratory rats: serum IgG and IgE antibodies to the rat urinary allergen. J Allergy Clin Immunol1987;79:505–15.
      OpenUrlCrossRefPubMedWeb of Science
    53. ↵
      Hagmar L, Bellander T, Ranstam. et al Piperazine-induced airway symptoms: exposure-response relationships and selection in an occupational setting. Am J Ind Med1984;6:347–57.
      OpenUrlPubMedWeb of Science
    54. ↵
      Calverley AE, Rees D, Dowdeswell RJ, et al. Platinum salt sensitivity in refinery workers: incidence and effects of smoking and exposure. Occup Environ Med1995;52:661–6.
      OpenUrlAbstract/FREE Full Text
    55. ↵
      McSharry C, Anderson K, McKay IC, et al. The IgE and IgG antibody responses to aerosols of Nephrops norvegicus (prawn) antigens: the association with clinical hypersensitivity and with cigarette smoking. Clin Exp Immunol1994;97:499–504.
      OpenUrlPubMedWeb of Science
    56. ↵
      Brooks SM, Edwards JJ Jr, Apol A, et al. An epidemiologic study of workers exposed to western red cedar and other wood dusts. Chest1981;80:30S–32S.
      OpenUrlCrossRef
    57. ↵
      Nielsen J, Welinder H, Jonsson B, et al. Exposure to hexahydrophthalic and methylhexahydrophthalic anhydrides—dose-response for sensitization and airway effects. Scand J Work Environ Health2001;27:327–34.
      OpenUrlPubMedWeb of Science
    58. ↵
      Houba R, Heederik DJ, Doekes G, et al. Exposure-sensitization relationship for alpha-amylase allergens in the baking industry. Am J Respir Crit Care Med1996;154:130–6.
      OpenUrlCrossRefPubMedWeb of Science
    59. ↵
      Nieuwenhuijsen MJ, Heederik D, Doekes G, et al. Exposure-response relations of alpha-amylase sensitisation in British bakeries and flour mills. Occup Environ Med1999;56:197–201.
      OpenUrlAbstract/FREE Full Text
    60. ↵
      Heederik D, Venables KM, Malmberg P, et al. Exposure-response relationships for work-related sensitization in workers exposed to rat urinary allergens: results from a pooled study. J Allergy Clin Immunol1999;103:678–84.
      OpenUrlCrossRefPubMedWeb of Science
    61. ↵
      Merget R, Kulzer R, Dierkes-Globisch A, et al. Exposure-effect relationship of platinum salt allergy in a catalyst production plant: conclusions from a 5-year prospective cohort study. J Allergy Clin Immunol2000;105:364–70.
      OpenUrlCrossRefPubMedWeb of Science
    62. ↵
      Juniper CP, Roberts DM. Enzyme asthma: fourteen years clinical experience of a recently prescribed disease. J Soc Occup Med1984;34:126–32.
      OpenUrlCrossRef
    63. ↵
      Zentner A, Jeep S, Wahl R, et al. Multiple IgE-mediated sensitizations to enzymes after occupational exposure: evaluation by skin prick test, RAST, and immunoblot. Allergy1997;52:928–34.
      OpenUrlPubMedWeb of Science
    64. ↵
      Ucgun I, Ozdemir N, Metintas M, et al. Prevalence of occupational asthma among automobile and furniture painters in the center of Sekisehir (Turkey): the effects of atopy and smoking habits on occupational asthma. Allergy1998;53:1096–100.
      OpenUrlPubMedWeb of Science
    65. ↵
      Agrup G, Belin L, Sjostedt L, et al. Allergy to laboratory animals in laboratory technicians and animal keepers. Br J Ind Med1986;43:192–8.
      OpenUrlPubMedWeb of Science
    66. ↵
      Botham PA, Davies GE, Teasdale EL. 1987 Sep. Allergy to laboratory animals: a prospective study of its incidence and of the influence of atopy on its development, Br J Ind Med1987;44:627–32.
      OpenUrlPubMedWeb of Science
    67. ↵
      Cockcroft A, Edwards J, McCarthy P, et al. Allergy in laboratory animal workers. Lancet1981;1:827–8.
      OpenUrlPubMedWeb of Science
    68. ↵
      Gautrin D, Infante-Rivard C, Ghezzo H, et al. Incidence and host determinants of probable occupational asthma in apprentices exposed to laboratory animals. Am J Respir Crit Care Med2001;163:899–904.
      OpenUrlPubMedWeb of Science
    69. ↵
      Gautrin D, Ghezzo H, Infante-Rivard C, et al. Natural history of sensitization, symptoms and occupational diseases in apprentices exposed to laboratory animals. Eur Respir J2001;17:904–8.
      OpenUrlAbstract/FREE Full Text
    70. ↵
      Jeal H, Draper A, Jones M, et al. HLA associations with occupational sensitization to rat lipocalin allergens: a model for other animal allergies? J Allergy Clin Immunol2003;111:795–9.
      OpenUrlCrossRefPubMedWeb of Science
    71. Sjostedt L, Willers S. Predisposing factors in laboratory animal allergy: a study of atopy and environmental factors. Am J Ind Med1989;16:199–208.
      OpenUrlPubMedWeb of Science
    72. Sjostedt L, Willers S, Orbaek P. A follow-up study of laboratory animal exposed workers: the influence of atopy for the development of occupational asthma. Am J Ind Med1993;24:459–69.
      OpenUrlPubMedWeb of Science
    73. Krakowiak A, Palczynski C, Walusiak J, et al. Allergy to animal fur and feathers among zoo workers. Int Arch Occup Environ Health2002;75:S113–16.
    74. ↵
      Venables KM, Tee RD, Hawkins ER, et al. Laboratory animal allergy in a pharmaceutical company. Br J Ind Med1988;45:660–6.
      OpenUrlPubMedWeb of Science
    75. ↵
      Baur X, Degens PO, Sander I. Baker’s asthma: still among the most frequent occupational respiratory disorders. J Allergy Clin Immunol1998;102:984–97.
      OpenUrlCrossRefPubMedWeb of Science
    76. ↵
      De Zotti R, Bovenzi M, Molinari S, et al. Respiratory symptoms and occupational sensitization in a group of trainee bakers: results of a 6-month follow up. Med Lav1997;88:155–65.
      OpenUrlPubMed
    77. ↵
      De Zotti R, Bovenzi M. Prospective study of work related respiratory symptoms in trainee bakers. Occup Environ Med2000;57:58–61.
      OpenUrlAbstract/FREE Full Text
    78. Droste J, Myny K, Van Sprundel M, et al. Allergic sensitization, symptoms, and lung function among bakery workers as compared with a nonexposed work population. J Occup Environ Med2003;45:648–55.
      OpenUrlCrossRefPubMedWeb of Science
    79. ↵
      Talini D, Benvenuti A, Carrara M, et al. Diagnosis of flour-induced occupational asthma in a cross-sectional study. Respir Med2002;96:236–43.
      OpenUrlCrossRefPubMedWeb of Science
    80. ↵
      Docker A, Wattie JM, Topping M, et al. Clinical and immunological investigations of respiratory disease in workers using reactive dyes. Br J Ind Med1987;44:534–41.
      OpenUrlPubMedWeb of Science
    81. ↵
      Winck JC, Delgado L, Murta R, et al. Cork workers’ occupational asthma: lack of association with allergic sensitisation to fungi of the work environment. Int Arch Occup Environ Health2004;77:296–300.
      OpenUrlCrossRefPubMedWeb of Science
    82. ↵
      Butcher BT, Jones R, O’Neil C, et al. Longitudinal study of workers employed in the manufacture of toluene diisocyanate. Am Rev Respir Dis1977;116:411–21.
      OpenUrlPubMedWeb of Science
    83. ↵
      Cullen MR, Redlich CA, Beckett WS, et al. Feasibility study of respiratory questionnaire and peak flow recordings in autobody shop workers exposed to isocyanate-containing spray paint: observations and limitations. Occup Med (Lond)1996;46:197–204.
    84. ↵
      Di Stefano F, Siriruttanapruk S, McCoach J, et al. Glutaraldehyde: an occupational hazard in the hospital setting. Allergy1999;54:1105–9.
      OpenUrlCrossRefPubMedWeb of Science
    85. ↵
      Douglas JD, McSharry C, Blaikie L, et al. Occupational asthma caused by automated salmon processing. Lancet1995;346:737–40.
      OpenUrlCrossRefPubMedWeb of Science
    86. ↵
      Cartier A, Malo JL, Forest F, et al. Occupational asthma in snow crab processing workers. J Allergy Clin Immunol1984;74:261–9.
      OpenUrlCrossRefPubMedWeb of Science
    87. ↵
      Grammer LC, Shaughnessy MA, Yarnold PR. Risk factors for immunologically mediated disease in workers with respiratory symptoms when exposed to hexahydrophthalic anhydride. J Lab Clin Med1996;127:443–7.
      OpenUrlCrossRefPubMedWeb of Science
    88. ↵
      Venables KM, Dally MB, Nunn AJ, et al. Smoking and occupational allergy in workers in a platinum refinery. BMJ1989;299:939–42.
    89. ↵
      Chan-Yeung M, Lam S, Koener S. Clinical features and natural history of occupational asthma due to western red. Cedar (Thuja plicata). Am J Med1982;72:411–15.
      OpenUrlCrossRefPubMedWeb of Science
    90. ↵
      Flood DF, Blofeld RE, Bruce CF, et al. Lung function, atopy, specific hypersensitivity, and smoking of workers in the enzyme detergent industry over 11 years. Br J Ind Med1985;42:43–50.
      OpenUrlPubMedWeb of Science
    91. Greenberg M, Milne JF, Watt A. Survey of workers exposed to dusts containing derivatives of Bacillus subtilis. BMJ1970;2:629–33.
    92. Newhouse ML, Tagg B, Pocock SJ, et al. An epidemiological study of workers producing washing powder. Lancet1970;1:689–93.
      OpenUrlCrossRefPubMedWeb of Science
    93. ↵
      Witmeur O, Wolf-Jurgensen P, Hoegh-Thomsen J, et al. Medical experience in enzyme production. Acta Allergol1973;28:250–9.
      OpenUrlPubMedWeb of Science
    94. ↵
      Romano C, Sulotto F, Piolatto G, et al. Factors related to the development of sensitization to green coffee and castor bean allergens among coffee workers. Clin Exp Allergy1995;25:643–50.
      OpenUrlCrossRefPubMedWeb of Science
    95. ↵
      De Zotti R, Larese F, Bovenzi M, et al. Allergic airway disease in Italian bakers and pastry makers. Occup Environ Med1994;51:548–52.
      OpenUrlAbstract/FREE Full Text
    96. ↵
      Prichard MG, Ryan G, Musk AW. Wheat flour sensitisation and airways disease in urban bakers. Br J Ind Med1984;41:450–4.
      OpenUrlPubMedWeb of Science
    97. ↵
      Venables KM, Topping MD, Howe W, et al. Interaction of smoking and atopy in producing specific IgE antibody against a hapten protein conjugate. BMJ1985;290:201–4.
    98. ↵
      Balboni A, Baricordi OR, Fabbri LM, et al. Association between toluene diisocyanate-induced asthma and DQB1 markers: a possible role for aspartic acid at position 57. Eur Respir J1996;9:207–10.
      OpenUrlAbstract
    99. Beghe B, Padoan M, Moss CT, et al. Mapp CE. Lack of association of HLA class I genes and TNF alpha-308 polymorphism in toluene diisocyanate-induced asthma. Allergy2004;59:61–4.
    100. Bernstein JA, Munson J, Lummus ZL, et al. T-cell receptor V beta gene segment expression in diisocyanate-induced occupational asthma. J Allergy Clin Immunol1997;99:245–50.
      OpenUrlCrossRefPubMedWeb of Science
    101. ↵
      Bignon JS, Aron Y, Ju LY, et al. HLA class II alleles in isocyanate-induced asthma. Am J Respir Crit Care Med1994;149:71–5.
      OpenUrlPubMedWeb of Science
    102. Mapp CE, Beghe B, Balboni A, et al. Association between HLA genes and susceptibility to toluene diisocyanate-induced asthma. Clin Exp Allergy2000;30:651–6.
      OpenUrlCrossRefPubMedWeb of Science
    103. ↵
      Mapp CE, Fryer AA, De-Marzo N, et al. Glutathione S-transferase GSTP1 is a susceptibility gene for occupational asthma induced by isocyanates. J Allergy Clin Immunol2002;109:867–72.
      OpenUrlCrossRefPubMedWeb of Science
    104. Piirila P, Wikman H, Luukkonen R, et al. Glutathione S-transferase genotypes and allergic responses to diisocyanate exposure. Pharmacogenetics2001;11:437–45.
      OpenUrlCrossRefPubMedWeb of Science
    105. ↵
      Rihs HP, Kroells TB, Huber H, et al. No evidence for the influence of HLA class II in alleles in isocyanate-induced asthma. Am J Ind Med1997;32:522–7.
      OpenUrlCrossRefPubMedWeb of Science
    106. ↵
      Newman Taylor AJ, Cullinan P, Lympany PA, et al. Interaction of HLA phenotype and exposure intensity in sensitisation to complex platinum salts. Am J Respir Crit Care Med1999;160:435–8.
      OpenUrlPubMedWeb of Science
    107. ↵
      Horne C, Quintana PJ, Keown PA, et al. Distribution of DRB1 and DQB1 HLA class II alleles in occupational asthma due to western red cedar. Eur Respir J2000;15:911–14.
      OpenUrlAbstract
    108. ↵
      Young RP, Barker RD, Pile KD, et al. The association of HLA-DR3 with specific IgE to inhaled acid anhydrides. Am J Respir Crit Care Med1995;151:219–21.
      OpenUrlPubMedWeb of Science
    109. ↵
      Sjostedt L, Willers S, Orbaek P. Human leukocyte antigens in occupational allergy: a possible protective effect of HLA-B16 in laboratory animal allergy. Am J Ind Med1996;30:415–20.
      OpenUrlCrossRefPubMedWeb of Science
    110. ↵
      Baker DB, Gann PH, Brooks SM, et al. Cross-sectional study of platinum salts sensitization among precious metals refinery workers. Am J Ind Med1990;18:653–64.
      OpenUrlPubMedWeb of Science
    111. ↵
      Niezborala M, Garnier R. Allergy to complex platinum salts: a historical prospective cohort study. Occup Environ Med1996;53:252–7.
      OpenUrlAbstract/FREE Full Text
    112. ↵
      Krakowiak A, Szulc B, Gorski P. Occupational respiratory diseases in laboratory animal workers; initial results. Int J Occup Med Environ Health1997;10:31–6.
      OpenUrlPubMed
    113. ↵
      Meijer E, Grobbee DE, Heederik D. Detection of workers sensitised to high molecular weight allergens: a diagnostic study in laboratory animal workers. Occup Environ Med2002;59:189–95.
      OpenUrlAbstract/FREE Full Text
    114. ↵
      Johnsen CR, Sorensen TB, Ingemann Larsen A, et al. Allergy risk in an enzyme producing plant: a retrospective follow up study. J Occup Environ Med1997;54:671–5.
      OpenUrlCrossRef
    115. ↵
      Grammer LC, Ditto AM, Tripathi A, et al. Prevalence and onset of rhinitis and conjunctivitis in subjects with occupational asthma caused by trimellitic anhydride (TMA). J Occup Environ Med2002;44:1179–81.
      OpenUrlPubMedWeb of Science
    116. ↵
      Wernfors M, Nielsen J, Schutz A, et al. Phthalic anhydride-induced occupational asthma. Int Arch Allergy Appl Immunol1986;79:77–82.
      OpenUrlPubMedWeb of Science
    117. ↵
      Malo JL, Lemiere C, Desjardins A, et al. Prevalence and intensity of rhinoconjunctivitis in subjects with occupational asthma. Eur Respir J1997;10:1513–15.
      OpenUrlAbstract
    118. ↵
      Karjalainen A, Martikainen R, Klaukka T, et al. Risk of asthma among Finnish patients with occupational rhinitis. Chest2003;123:283–8.
      OpenUrlCrossRefPubMedWeb of Science
    119. ↵
      Bar-Sela S, Teichtahl H, Lutsky I. Occupational asthma in poultry workers. J Allergy Clin Immunol1984;73:271–5.
      OpenUrlPubMedWeb of Science
    120. Kim YK, Son JW, Kim HY, et al. New occupational allergen in citrus farmers: citrus red mite (Panonychus citri). Ann Allergy Asthma Immunol1999;82:223–8.
      OpenUrlPubMedWeb of Science
    121. ↵
      Munoz X, Cruz MJ, Orriols R, et al. Occupational asthma due to persulfate salts: diagnosis and follow-up. Chest2003;123:124–9.
      OpenUrl
    122. ↵
      Venables KM, Dally MB, Burge PS, et al. Occupational asthma in a steel coating plant. Br J Ind Med1985;42:517–24.
      OpenUrlPubMedWeb of Science
    123. ↵
      Slovak AJ. Occupational asthma caused by a plastics blowing agent, azodicarbonamide. Thorax1981;36:906–9.
      OpenUrlAbstract/FREE Full Text
    124. ↵
      Drexler H, Schaller KH, Nielsen J, et al. Efficacy of measures of hygiene in workers sensitised to acid anhydrides and the influence of selection bias on the results. J Occup Environ Med1999;56:202–5.
    125. ↵
      Fisher R, Saunders WB, Murray SJ, et al. Prevention of laboratory animal allergy. J Occup Environ Med1998;40:609–13.
      OpenUrlCrossRefPubMedWeb of Science
    126. ↵
      Allmers H, Schmengler J, Skudlik C. Primary prevention of natural rubber latex allergy in the German health care system through education and intervention. J Allergy Clin Immunol2002;110:318–23.
      OpenUrlCrossRefPubMedWeb of Science
    127. Levy D, Allouache S, Chabane MH, et al. Powder-free protein-poor natural rubber latex gloves and latex sensitisation. JAMA1999;281:988.
      OpenUrlCrossRefPubMedWeb of Science
    128. ↵
      Tarlo SM, Easty A, Eubanks K, et al. Outcomes of a natural rubber latex control program in an Ontario teaching hospital. J Allergy Clin Immunol2001;108:628–33.
      OpenUrlCrossRefPubMedWeb of Science
    129. ↵
      Grammer LC, Harris KE, Yarnold PR. Effect of respiratory protective devices on development of antibody and occupational asthma to an acid anhydride. Chest2002;121:1317–22.
      OpenUrlCrossRefPubMedWeb of Science
    130. ↵
      Venables KM, Upton JL, Hawkins ER, et al. Smoking, atopy, and laboratory animal allergy. Br J Ind Med1988;45:667–71.
      OpenUrlPubMedWeb of Science
    131. Newill CA, Evans R, Khoury-MJ. Pre-employment screening for allergy to laboratory animals: epidemiologic evaluation of its potential usefulness. J Occup Med1986;28:1158–64.
      OpenUrlPubMedWeb of Science
    132. ↵
      Renstrom A, Malmberg P, Larsson K, et al. Prospective study of laboratory animal allergy: factors predisposing to sensitisation and development of allergic symptoms. Allergy1994;49:548–52.
      OpenUrlPubMedWeb of Science
    133. ↵
      Tarlo SM, Liss GM, Yeung KS. Changes in rates and severity of compensation claims for asthma due to diisocyanates: a possible effect of medical surveillance measures. Occup Environ Med2002;59:58–62.
      OpenUrlAbstract/FREE Full Text
    134. ↵
      Kraw M, Tarlo SM. Isocyanate medical surveillance: respiratory referrals from a foam manufacturing plant over a five year period. Am J Ind Med1999;35:87–91.
      OpenUrlCrossRefPubMedWeb of Science
    135. ↵
      Bernstein DI, Korbee L, Stauder T, et al. The low prevalence of occupational asthma and antibody-dependent sensitization to diphenylmethane diisocyanate in a plant engineered for minimal exposure to diisocyanates. Ann Allergy Asthma Immunol1993;92:387–96.
      OpenUrl
    136. ↵
      Gordon SB, Curran AD, Murphy J, et al. Screening questionnaires for bakers’ asthma—are they worth the effort? Occup Med1997;47:361–6.
      OpenUrlAbstract/FREE Full Text
    137. ↵
      Stenton S, Beach JR, Avery AJ, et al. The value of questionnaires and spirometry in asthma surveillance programmes in the workplace. Occup Med1993;43:203–6.
      OpenUrlAbstract/FREE Full Text
    138. ↵
      Merget R, Schultze-Werninghaus G, Muthorst T, et al. Asthma due to the complex salts of platinum: a cross-sectional survey of workers in a platinum refinery. Clin Allergy1988;18:569–80.
      OpenUrlCrossRefPubMedWeb of Science
    139. ↵
      Redlich CA, Stowe MH, Wisnewski AV, et al. Subclinical immunologic and physiologic responses in hexamethylene diisocyanate-exposed auto body shop workers. Am J Ind Med2001;39:587–97.
      OpenUrlCrossRefPubMedWeb of Science
    140. ↵
      Vedal S, Chan-Yeung M, Enarson DA, et al. Plicatic acid-specific ige and nonspecific bronchial hyperresponsiveness in western red-cedar workers. J Allergy Clin Immunol1986;78:1103–9.
      OpenUrlCrossRefPubMedWeb of Science
    141. ↵
      Schlunssen V, Schaumburg I, Heederik D, et al. Indices of asthma among atopic and non-atopic woodworkers. Occup Environ Med2004;61:504–11.
      OpenUrlAbstract/FREE Full Text
    142. ↵
      Baur X, Huber H, Degens PO, et al. Relation between occupational asthma case history, bronchial methachlorine challenge, and specific challenge test in patients with suspected occupational asthma. Am J Ind Med1998;33:114–22.
      OpenUrlCrossRefPubMedWeb of Science
    143. ↵
      Malo JL, Ghezzo H, L’Archeveque J, et al. Is the clinical history a satisfactory means of diagnosing occupational asthma? Am Rev Respir Dis1991;143:528–32.
      OpenUrlPubMedWeb of Science
    144. Vandenplas O, Delwiche JP, Evrard G, et al. Prevalence of occupational asthma due to latex among hospital personnel. Am J Respir Crit Care Med1995;151:54–60.
      OpenUrlCrossRefPubMedWeb of Science
    145. ↵
      Vandenplas O, Binard-Van-Cangh F, Brumagne A, et al. Occupational asthma in symptomatic workers exposed to natural rubber latex: evaluation of diagnostic procedures. J Allergy Clin Immunol2001;107:542–7.
      OpenUrlCrossRefPubMedWeb of Science
    146. ↵
      Cote J, Kennedy S, Chan-Yeung M. Sensitivity and specificity of PC20 and peak expiratory flow rate in cedar asthma. J Allergy Clin Immunol1990;85:592–8.
      OpenUrlCrossRefPubMedWeb of Science
    147. ↵
      Cote J, Kennedy S, Chan-Yeung M. Quantitative versus qualitative analysis of peak expiratory flow in occupational asthma. Thorax1993;48:48–51.
      OpenUrlAbstract/FREE Full Text
    148. ↵
      Axon EJ, Beach JR, Burge PS. A comparison of some of the characteristics of patients with occupational and non-occupational asthma. Occup Med1995;45:109–11.
      OpenUrlAbstract/FREE Full Text
    149. ↵
      Koskela H, Taivainen A, Tukiainen H, et al. Inhalation challenge with bovine dander allergens: who needs it? Chest2003;124:383–91.
      OpenUrlCrossRefPubMedWeb of Science
    150. ↵
      Ricciardi L, Fedele R, Saitta S, et al. Occupational asthma due to exposure to iroko wood dust. Ann Allergy Asthma Immunol2003;91:393–7.
      OpenUrlPubMedWeb of Science
    151. ↵
      Burge PS, O’Brien IM, Harries MG. Peak flow rate records in the diagnosis of occupational asthma due to colophony. Thorax1979;34:308–16.
      OpenUrlAbstract/FREE Full Text
    152. ↵
      Burge PS, O’Brien IM, Harries MG. Peak flow rate records in the diagnosis of occupational asthma due to isocyanates. Thorax1979;34:317–23.
      OpenUrlAbstract/FREE Full Text
    153. ↵
      Henneberger PK, Stanbury MJ, Trimbath LS, et al. The use of portable peak flowmeters in the surveillance of occupational asthma. Chest1991;100:1515–21.
      OpenUrlCrossRefPubMedWeb of Science
    154. Hollander A, Heederik D, Brunekreef B. Work-related changes in peak expiratory flow among laboratory animal workers. Eur Respir J1998;11:929–36.
      OpenUrlAbstract
    155. ↵
      Leroyer C, Perfetti L, Trudeau C, et al. Comparison of serial monitoring of peak expiratory flow and FEV1 in the diagnosis of occupational asthma. Am J Respir Crit Care Med1998;158:827–32.
      OpenUrlPubMedWeb of Science
    156. Malo JL, Trudeau C, Ghezzo H, et al. Do subjects investigated for occupational asthma through serial peak expiratory flow measurements falsify their results? J Allergy Clin Immunol1995;96:601–7.
      OpenUrlCrossRefPubMedWeb of Science
    157. Quirce S, Contreras G, Dybuncio A, et al. Peak expiratory flow monitoring is not a reliable method for establishing the diagnosis of occupational asthma. Am J Respir Crit Care Med1995;152:1100–2.
      OpenUrlPubMedWeb of Science
    158. ↵
      Revsbech P, Anderson G. Diurnal variation in peak expiratory flow rate among grain elevator workers. Br J Ind Med1989;46:566–9.
      OpenUrlPubMedWeb of Science
    159. ↵
      Malo JL, Cote J, Cartier A, et al. How many times per day should peak expiratory flow rates be assessed when investigating occupational asthma? Thorax1993;48:1211–17.
      OpenUrlAbstract/FREE Full Text
    160. ↵
      Baldwin DR Gannon P, Bright P, et al. Interpretation of occupational peak flow records: level agreement between expert clinicians and Oasys-2. Thorax2002;57:860–4.
      OpenUrlAbstract/FREE Full Text
    161. ↵
      Malo JL, Cartier A, Ghezzo H, et al. Compliance with peak expiratory flow readings affects the within- and between-reader reproducibility of interpretation of graphs in subjects investigated for occupational asthma. J Allergy Clin Immunol1996;98:1132–4.
      OpenUrlCrossRefPubMedWeb of Science
    162. ↵
      Perrin B, Lagier F, L’Archeveque J, et al. Occupational asthma: validity of monitoring of peak expiratory flow rates and non-allergic bronchial responsiveness as compared to specific inhalation challenge. Eur Respir J1992;5:40–8.
      OpenUrlAbstract/FREE Full Text
    163. Zock JP, Brederode D, Heederik D. Between- and within- observer agreement for expert judgment of peak flow graphs from a working population. J Occup Environ Med1998;40:969–72.
      OpenUrlCrossRefPubMedWeb of Science
    164. ↵
      Liss GM, Tarlo SM. Peak expiratory flow rates in possible occupational asthma. Chest1991;100:63–9.
      OpenUrlCrossRefPubMedWeb of Science
    165. Bright P, Newton DT, Gannon PF, et al. Improved analysis of serial peak expiratory flow in suspected occupational asthma. Monaldi Arch Chest Dis2001;56:281–8.
      OpenUrlPubMed
    166. ↵
      Burge PS. Occupational asthma in electronics workers caused by colophony fumes: follow-up of affected workers. Thorax1982;37:348–53.
      OpenUrlAbstract/FREE Full Text
    167. ↵
      Gannon PFG, Newton DT, Belcher J, et al. Development of OASYS-2: a system for the analysis of serial measurement of peak expiratory flow in workers with suspected occupational asthma. Thorax1996;51:484–9.
      OpenUrlAbstract/FREE Full Text
    168. ↵
      Anees W, Huggins V, Pavord ID, et al. Occupational asthma due to low molecular weight agents: eosinophilic and non-eosinophilic variants. Thorax2002;57:231–6.
      OpenUrlAbstract/FREE Full Text
    169. Brisman J, Lillienberg L, Belin L, et al. Sensitisation to occupational allergens in bakers’ asthma and rhinitis: a case-referent study. Int Arch Occup Environ Health2003;76:167–70.
      OpenUrlPubMedWeb of Science
    170. ↵
      Cartier A, Grammer L, Malo JL, et al. Specific serum antibodies against isocyanates: association with occupational asthma. J Allergy Clin Immunol1989;84:507–14.
      OpenUrlCrossRefPubMedWeb of Science
    171. Hargreave FE, Ramsdale EH, Pugsley SO. Occupational asthma without bronchial hyperresponsiveness. Am Rev Respir Dis1984;130:513–15.
      OpenUrlPubMedWeb of Science
    172. Lemiere C, Cartier A, Malo JL, et al. Persistent specific bronchial reactivity to occupational agents in workers with normal nonspecific bronchial reactivity. Am J Respir Crit Care Med2000;162:976–80.
      OpenUrlCrossRefPubMedWeb of Science
    173. ↵
      Lin FJ, Chen H, Chan-Yeung M. New method for an occupational dust challenge test. Occup Environ Med1995;52:54–6.
      OpenUrlAbstract/FREE Full Text
    174. ↵
      Merget R, Schultze-Werninghams G, Bode F, et al. Quantitative skin prick and bronchial provocation tests with platinum salt. Br J Ind Med1991;48:830–7.
      OpenUrlPubMedWeb of Science
    175. ↵
      Merget R, Dierkes A, Rueckmann A, et al. Absence of relationship between degree of nonspecific and specific bronchial responsiveness in occupational asthma due to platinum salts. Eur Respir J1996;9:211–16.
      OpenUrlAbstract
    176. ↵
      Moscato G, Dellabianca A, Vinci G, et al. Toluene diisocyanate-induced asthma: clinical findings and bronchial responsiveness studies in 113 exposed subjects with work-related respiratory symptoms. J Occup Med1991;33:720–5.
      OpenUrlCrossRefPubMedWeb of Science
    177. ↵
      Tarlo SM, Broder I. Outcome of assessment for occupational asthma. Chest1991;100:329–35.
      OpenUrlCrossRefPubMedWeb of Science
    178. ↵
      El-Zein M, Malo JL, Infante-Rivard C, et al. Incidence of probable occupational asthma and changes in airway calibre and responsiveness in apprentice welders. Eur Respir J2003;22:513–18.
      OpenUrlAbstract/FREE Full Text
    179. ↵
      Park JW, Kim CW, Kim KS, et al. Role of skin prick test and serological measurement of specific IgE in the diagnosis of occupational asthma resulting from exposure to vinyl sulphone reactive dyes. Occup Environ Med2001;58:411–16.
      OpenUrlAbstract/FREE Full Text
    180. ↵
      Tee RD, Cullinan P, Welch J, et al. Specific IgE to isocyanates: a useful diagnostic role in occupational asthma. J Allergy Clin Immunol1998;101:709–15.
      OpenUrlCrossRefPubMedWeb of Science
    181. ↵
      Pezzini A, Riviera A, Paggiaro P, et al. Specific IgE antibodies in twenty-eight workers with diisocyanate-induced bronchial asthma. Clin Allergy1984;14:453–61.
      OpenUrlCrossRefPubMedWeb of Science
    182. ↵
      Vandenplas O, Delwiche JP, Evrard G, et al. Prevalence of occupational asthma due to latex among hospital personnel. Am J Respir Crit Care Med1995;151:54–60.
    183. ↵
      Baur X, Czuppon A. Diagnostic validation of specific IgE antibody concentrations, skin prick testing, and challenge tests in chemical workers with symptoms of sensitivity to different anhydrides. J Allergy Clin Immunol1995;96:489–94.
      OpenUrlCrossRefPubMedWeb of Science
    184. Grammer L, Shaughnessy M, Kenamore B. Utility of antibody in identifying individuals who have or will develop anhydride-induced respiratory disease. Chest1998;114:1199–202.
      OpenUrlCrossRefPubMedWeb of Science
    185. Howe W, Venables KM, Topping MD, et al. Tetrachlorophthalic anhydride asthma: evidence for specific IgE antibody. J Allergy Clin Immunol1983;7:5–11.
    186. ↵
      Park HS, Kim YJ, Lee MK, et al. Occupational asthma and IgE antibodies to reactive dyes. Yonsei Med J1989;30:298–304.
      OpenUrlPubMed
    187. ↵
      Cannon J, Cullinan P, Newman-Taylor AJ. Consequences of occupational asthma. BMJ1995;311:602–3.
      OpenUrlFREE Full Text
    188. ↵
      Larbanois A, Jamart J, Delwiche JP, et al. Socioeconomic outcome of subjects experiencing asthma symptoms at work. Eur Respir J2002;19:1107–13.
      OpenUrlAbstract/FREE Full Text
    189. ↵
      Ross DJ, McDonald JC. Health and employment after a diagnosis of occupational asthma: a descriptive study. Occup Med (Lond)1998;48:219–25.
    190. ↵
      Allard C, Cartier A, Ghezzo H, et al. Occupational asthma due to various agents: Absence of clinical and functional improvement at an interval of four or more years after cessation of exposure. Chest1989;96:1046–9.
      OpenUrlCrossRefPubMedWeb of Science
    191. Barker RD, Harris JM, Welch JA, et al. Occupational asthma caused by tetrachlorophthalic anhydride: a 12-year follow-up. J Allergy Clin Immunol1998;101:717–19.
      OpenUrlCrossRefPubMedWeb of Science
    192. Chan-Yeung M, Maclean L, Paggiaro PL. Follow-up study of 232 patients with occupational asthma caused by western red cedar (Thuja plicata). J Allergy Clin Immunol1987;79:792–6.
      OpenUrlCrossRefPubMedWeb of Science
    193. ↵
      Hudson P, Cartier A, Pineau L, et al. Follow-up of occupational asthma caused by crab and various agents. J Allergy Clin Immunol1985;76:682–8.
      OpenUrlCrossRefPubMedWeb of Science
    194. Lemiere C, Cartier A, Dolovich J, et al. Outcome of specific bronchial responsiveness to occupational agents after removal from exposure. Am J Respir Crit Care Med1996;154:329–33.
      OpenUrlCrossRefPubMedWeb of Science
    195. Lozewicz S, Assoufi BK, Hawkins R, et al. Outcome of asthma induced by isocyanates. Br J Dis Chest1987;1:14–22.
    196. Mapp CE, Corona PC, De Marzo N, et al. Persistent asthma due to isocyanates: a follow-up study of subjects with occupational asthma due to toluene diisocyanate (TDI). Am Rev Respir Dis1988;137:1326–9.
      OpenUrlCrossRefPubMedWeb of Science
    197. Marabini A, Brugnami G, Curradi F, et al. Response to bronchoprovocation test and outcome of occupational asthma. A follow-up study of subjects with TDI asthma. Med del Lavoro1994;85:134–41.
      OpenUrl
    198. Merget R, Reineke M, Rueckmann A, et al. Nonspecific and specific bronchial responsiveness in occupational asthma caused by platinum salts after allergen avoidance. Am J Respir Crit Care Med1994;150:1146–9.
      OpenUrlCrossRefPubMedWeb of Science
    199. Moller DR, Brooks SM, Mckay RT, et al. Chronic asthma due to toluene diisocyanate. Chest1986;90:494–9.
      OpenUrlCrossRefPubMedWeb of Science
    200. O’Donnell TV, Welford B, Coleman, eds. Potroom asthma: New Zealand experience and follow-up. Am J Ind Med1989;15:43–9.
      OpenUrlPubMedWeb of Science
    201. ↵
      Padoan M, Pozzato V, Simoni M, et al. Long-term follow-up of toluene diisocyanate-induced asthma. Eur Respir J2003;21:637–40.
      OpenUrlAbstract/FREE Full Text
    202. Paggiaro PL, Loi AM, Rossi O, et al. Follow-up study of patients with respiratory disease due to toluene diisocyanate (TDI). Clin Allergy1984;14:463–9.
      OpenUrlCrossRefPubMedWeb of Science
    203. Paggiaro PL, Vagaggini B, Dente FL, et al. Bronchial hyperresponsiveness and toluene diisocyanate. Long-term change in sensitized asthmatic subjects. Chest1993;103:1123–8.
      OpenUrlCrossRefPubMedWeb of Science
    204. ↵
      Pisati G, Baruffini A, Zedda S. Toluene diisocyanate induced asthma: outcome according to persistence or cessation of exposure. Br J Ind Med1993;50:60–4.
      OpenUrlPubMedWeb of Science
    205. ↵
      Rosenberg N, Garnier R, Rousselin X, et al. Clinical and socio-professional fate of isocyanate-induced asthma. Clin Allergy1987;17:55–61.
      OpenUrlCrossRefPubMedWeb of Science
    206. ↵
      Tarlo SM, Liss G, Corey P, et al. A workers’ compensation claim population for occupational asthma. Comparison of subgroups. Chest1995;107:634–41.
      OpenUrlCrossRefPubMedWeb of Science
    207. ↵
      Vandenplas O, Jamart J, Delwiche JP, et al. Occupational asthma caused by natural rubber latex: outcome according to cessation or reduction of exposure. J Allergy Clin Immunol2002;109:125–30.
      OpenUrlCrossRefPubMedWeb of Science
    208. Venables KM, Topping MD, Nunn AJ, et al. Immunologic and functional consequences of chemical (tetrachlorophthalic anhydride)-induced asthma after four years of avoidance of exposure. J Allergy Clin Immunol1987;80:212–18.
      OpenUrlCrossRefPubMedWeb of Science
    209. ↵
      Venables KM, Davison AG, Newman-Taylor AJ. Consequences of occupational asthma. Respir Med1989;83:437–40.
      OpenUrlPubMedWeb of Science
    210. ↵
      Burge PS. Non-specific bronchial hyper-reactivity in workers exposed to toluene di-isocyanate, diphenyl methane di-isocyanate and colophony. Eur J Respir Dis1982;123:91–6.
      OpenUrl
    211. ↵
      Merget R, Schulte A, Gebler A, et al. Outcome of occupational asthma due to platinum salts after transferral to low-exposure areas. Int Arch Occup Environ Health1999;72:33–9.
      OpenUrlCrossRefPubMedWeb of Science
    212. Moscato G, Dellabianca A, Perfetti L, et al. Occupational asthma: a longitudinal study on the clinical and socioeconomic outcome after diagnosis. Chest1999;115:249–56.
      OpenUrlCrossRefPubMedWeb of Science
    213. ↵
      Tarlo SM, Banks D, Liss G, et al. Outcome determinants for isocyanate induced occupational asthma among compensation claimants. Occup Environ Med1997;54:756–61.
      OpenUrlAbstract/FREE Full Text
    214. Valentino M, Pizzichini MA, Monaco F, et al. Latex-induced asthma in four healthcare workers in a regional hospital. Clinica di Medicina del Lavoro, Universita’ di Ancona, Ospedale Regionale Torrette, Italy. Occup Med (Lond)1994;44:161–4.
    215. Valentino M, Rapisarda V. Course of isocyanate-induced asthma in relation to exposure cessation: longitudinal study of 50 subjects. G Ital Med Lav Ergon2002;24:26–31.
      OpenUrlPubMed
    216. ↵
      Vandenplas O, Delwiche JP, Depelchin S, et al. Latex gloves with a lower protein content reduce bronchial reactions in subjects with occupational asthma caused by latex. Am J Respir Crit Care Med1995;151:887–91.
      OpenUrlPubMedWeb of Science
    217. ↵
      Maghni K, Lemiere C, Ghezzo H, et al. Airway inflammation after cessation of exposure to agents causing occupational asthma. Am J Respir Crit Care Med2004;169:367–72.
      OpenUrlCrossRefPubMedWeb of Science
    218. ↵
      Park HS, Nahm DH. Prognostic factors for toluene diisocyanate-induced occupational asthma after removal from exposure. Clin Exp Allergy1997;27:1145–50.
      OpenUrlCrossRefPubMedWeb of Science
    219. ↵
      Piirila PL, Nordman H, Keskinen HM, et al. Long-term follow-up of hexamethylene diisocyanate-, diphenylmethane diisocyanate-, and toluene diisocyanate-induced asthma. Am J Respir Crit Care Med2000;162:516–22.
      OpenUrlPubMedWeb of Science
    220. ↵
      Grammer LC, Shaugnessy MA, Henderson J, et al. A clinical and immunologic study of workers with trimellitic-anhydride-induced immunologic lung disease after transfer to low exposure jobs. Am Rev Respir Dis1993;14:54–7.
    221. ↵
      Grammer LC, Shaughnessy MA, Kenamore BD. Clinical and immunologic outcome of 42 individuals with trimellitic anhydride-induced immunologic lung disease after transfer to low exposure. Allergy Asthma Proc2000;21:355–9.
      OpenUrlCrossRefPubMedWeb of Science
    222. ↵
      Laoprasert N, Swanson MC, Jones RT, et al. Inhalation challenge testing of latex-sensitive health care workers and the effectiveness of laminar flow HEPA-filtered helmets in reducing rhinoconjunctival and asthmatic reactions. J Allergy Clin Immunol1998;102:998–1004.
      OpenUrlCrossRefPubMedWeb of Science
    223. Muller-Wening D, Neuhauss M. Protective effect of respiratory devices in farmers with occupational asthma. Eur Respir J1998;12:569–72.
      OpenUrlAbstract
    224. Obase Y, Shimoda T, Mitsuta K, et al. Two patients with occupational asthma who returned to work with dust respirators. Occup Environ Med2000;57:62–4.
      OpenUrlAbstract/FREE Full Text
    225. Slovak AJM, Orr RG, Teasdale EL. Efficacy of the helmet respirator in occupational asthma due to laboratory animal allergy (LAA). Am Ind Hyg Assoc J1985;46:411–15.
      OpenUrlCrossRefPubMedWeb of Science
    226. ↵
      Taivainen AI, Tukiainen HO, Terho EO, et al. Powered dust respirator helmets in the prevention of occupational asthma among farmers. Scand J Work Environ Health1998;24:503–7.
      OpenUrlPubMedWeb of Science
    227. ↵
      Ameille J, Pairon JC, Bayeux MC, et al. Consequences of occupational asthma on employment and financial status: a follow-up study. Eur Respir J1997;10:55–8.
      OpenUrlAbstract/FREE Full Text
    228. ↵
      Gannon PFG, Weir DC, Robertson AS, et al. Health, employment and financial outcomes. Br J Ind Med1993;50:491–6.
      OpenUrlPubMedWeb of Science
    229. ↵
      Marabini A, Dimich-Ward H, Kwan SY, et al. Clinical and socioeconomic features of subjects with red cedar asthma. A follow-up study. Chest1993;104:821–4.
      OpenUrlPubMedWeb of Science
    230. ↵
      Bernstein DI, Karnani RF, Bernstein CK, et al. Clinical and occupational outcomes in health care workers with natural rubber latex. J Allergy Clin Immunol2003;90:209–13.
      OpenUrlCrossRef
    231. ↵
      Malo JL, Dewitte JD, Cartier A, et al. The Quebec system of indemnification for occupational asthma. Description, efficacy, and costs. Rev Mal Respir1993;10:313–23.
      OpenUrlPubMedWeb of Science

    Footnotes

    • Financial support: This study was supported by a grant from the British Occupational Health Research Foundation, 6 St Andrew’s Place, London NW1 4LB. Catherine Boyle was funded by the Health & Safety Executive.

    • Competing interests: none

    Linked Articles