Current Reviews of Allergy and Clinical Immunology
Occupational asthma,☆☆

https://doi.org/10.1067/mai.2001.116432Get rights and content

Abstract

The workplace can be responsible for approximately one in 10 cases of adult-onset asthma. Two types of occupational asthma (OA) are distinguished by whether they arise after a latency period that is necessary for acquiring sensitization or as a result of acute exposure to irritant materials (irritant-induced asthma). The pathophysiology of OA with a latency period is similar to that of nonoccupational asthma, whereas the mechanism of irritant-induced asthma is still uncertain. HLA haplotypes and other genetic polymorphisms have been found to be associated with OA. According to various sources of data, the overall frequency of OA has remained stable in the last 10 years, although the frequency of causal agents vary. Registers of causal occupations and agents have been issued on Web sites (eg, www.asmanet.com ). Improved sampling methods have shown that the degree of exposure plays a key role in the onset of the disease, whereas prospective data collected in high-risk workplaces have also identified personal risk factors (eg, atopy, smoking, and rhinoconjunctivitis). A diagnosis of OA should no longer be based on a compatible history only but should be confirmed by means of objective testing. Once the diagnosis is confirmed, the worker should be removed from exposure, and satisfactory compensation programs should be offered, the most important being retraining programs with financial compensations because affected workers are generally young. The cost-effectiveness of prevention programs in high-risk workforces should be assessed. (J Allergy Clin Immunol 2001;108:317-28.)

Section snippets

Historical aspects and definition

Although the influence of the working environment on the onset of asthma was recognized long ago, especially by Ramazzini in the early 18th century, the ongoing interest in the condition arose from the work, enthusiasm, and insight of the late Jack Pepys. Between 1960 and 1980, Pepys described numerous causes of occupational asthma (OA) and rightly suggested an experimental reproduction of the asthmatic reaction in a hospital laboratory (Fig 1), renewing interest in the late asthmatic reaction

Physiopathology

Although some agents induce asthma through type I hypersensitivity reaction with the production of specific IgE antibodies, the immunologic mechanism or mechanisms responsible for other agents, such as plicatic acid, the agent responsible for Western red cedar asthma, have not yet been clearly identified. For other agents, such as diisocyanates, both immunologic and nonimmunologic mechanisms are involved.

Frequency

The role of epidemiology and methodological issues of this discipline, as well as outcome measurements in the specific field of OA, have been thoroughly reviewed in other contributions.26, 27 In recent years, several large population-based studies of asthma, including some information on the occupation, have been carried out; a major impetus came from the European Community Respiratory Health Survey.28 Such community-based surveys have yielded estimates of the attributable risk, causative

Clinical aspects

It is important to confirm OA by means of objective testing. An open questionnaire administered during a medical consultation has a reasonable sensitivity but lacks specificity.61 Diagnosing OA on the ground of a compatible history only is unacceptable. This is especially important because the diagnosis of OA carries significant social and financial consequences. Unlike pneumoconiosis, subjects with OA tend to be young. Liss et al62 showed that subjects with OA have higher rates of

Compensation

Medicolegal agencies should require objective testing before accepting a claim for OA. Once this essential step has been taken, proper rehabilitation programs should be offered. The cost-effectiveness of the Quebec system of compensation has been reported previously.78 This scheme provides workers with a full salary generally for up to 2 years (ie, the time required for proper retraining into a new occupation for workers who can no longer stay with the same employer). In a survey of 134 workers

Conclusion

In the past 2 decades, there have been considerable advances in the field of OA through the identification of new agents, methods of diagnosis, knowledge of pathophysiology, and natural history of disease. However, a great deal of work has to be done, especially in the primary prevention of the disease. Although the reduction of exposure in high-risk industries remains the single most important tool of primary prevention, we look forward to exciting possibilities in the coming decade. Advances

Acknowledgements

We thank Denyse Gautrin for providing useful data and criticism and Lori Schubert for reviewing the manuscript.

References (91)

  • SM Tarlo et al.

    Irritant-induced occupational asthma

    Chest

    (1989)
  • SM Tarlo et al.

    Asthmatic subjects symptomatically worse at work: prevalence and characterization among a general asthma clinic population

    Chest

    (2000)
  • PD Blanc et al.

    How much asthma can be attributed to occupational factors?

    Am J Med

    (1999)
  • JL Malo

    How much asthma can be attributed to occupational factors (revisited)?

    Chest

    (2000)
  • G Moscato et al.

    Occupational asthma. A longitudinal study on the clinical and socio-economic outcome after diagnosis

    Chest

    (1999)
  • RG Hamilton et al.

    Diagnosis of natural rubber latex allergy: Multicenter latex skin testing efficacy study

    J Allergy Clin Immunol

    (1998)
  • JA Bernstein et al.

    A cross-sectional survey of sensitization to Aspergillus orizae-derived lactase in pharmaceutical workers

    J Allergy Clin Immunol

    (1999)
  • JL Malo et al.

    Quality of life of subjects with occupational asthma

    J Allergy Clin Immunol

    (1993)
  • L Perfetti et al.

    Follow-up of occupational asthma after removal from or diminution of exposure to the responsible agent

    Chest

    (1998)
  • C Graham et al.

    Structure-activity model of chemicals that cause human respiratory sensitization

    Regul Toxicol Pharmacol

    (1997)
  • H Herxheimer

    The late bronchial reaction in induced asthma

    Int Arch Allergy Appl Immunol

    (1952)
  • J Pepys et al.

    Historical aspects of occupational asthma

  • IL Bernstein et al.

    Asthma in the workplace

    (1999)
  • KS Tse et al.

    Specific IgE antibodies in workers with occupational asthma due to western red cedar

    Clin Allergy

    (1982)
  • MH Karol et al.

    Antigens which detect IgE antibodies in workers sensitive to toluene diisocyanate

    Clin Allergy

    (1980)
  • AJ Frew et al.

    Bronchial inflammation in occupational asthma due to Western red cedar

    Am J Respir Crit Care Med

    (1995)
  • AJ Frew et al.

    Specificity of antigen-induced T-cell proliferation in Western red cedar asthma (WRCA) [abstract]

    J Allergy Clin Immunol

    (1993)
  • T Shirakawa et al.

    Hard metal asthma: cross immunological and respiratory reactivity between cobalt and nickel

    Thorax

    (1990)
  • S Finotto et al.

    Increase in numbers of CD8 positive lymphocytes and eosinophils in peripheral blood of subjects with late asthmatic reactions induced by toluene diisocyanate

    Br J Ind Med

    (1991)
  • P Maestrelli et al.

    Activated CD8 T lymphocytes producing interferon-gamma (IFN-gamma) and interleukin-5 (IL-5) in bronchial mucosa of subjects sensitized to toluene diisocyanate (TDI) [abstract]

    J Allergy Clin Immunol

    (1993)
  • D Gautrin et al.

    Reactive airways dysfunction syndrome, or irritant-induced asthma

  • LP Boulet et al.

    Airway inflammation after removal from the causal agent in occupational asthma due to high and low molecular weight agents

    Eur Respir J

    (1994)
  • M Saetta et al.

    Effect of cessation of exposure to toluene diisocyanate (TDI) on bronchial mucosa of subjects with TDI-induced asthma

    Am Rev Respir Dis

    (1992)
  • LM Fabbri et al.

    Fatal asthma in a subject sensitized to toluene diisocyanate

    Am Rev Respir Dis

    (1988)
  • C Lemière et al.

    Reactive airways dysfunction syndrome due to chlorine: sequential bronchial biopsies and functional assessment

    Eur Respir J

    (1997)
  • JC McDonald

    Methodology. Study design

  • MR Becklake et al.

    Epidemiological approaches in occupational asthma

  • PGJ Burney et al.

    The European Community Respiratory Health Survey

    Eur Respir J

    (1994)
  • M Kogevinas et al.

    The risk of asthma attributable to occupational exposures

    Am J Respir Crit Care Med

    (1996)
  • D Fishwick et al.

    Occupational asthma in New Zealanders: a population based study

    Occup Environ Med

    (1997)
  • AR Johnson et al.

    Occupational asthma in adults in six Canadian communities

    Am J Respir Crit Care Med

    (2000)
  • S Meredith et al.

    Occupational asthma: measures of frequency from four countries

    Thorax

    (1996)
  • A Karjalainen et al.

    Incidence of occupational asthma by occupation and industry in Finland

    Am J Ind Med

    (2000)
  • JC McDonald et al.

    Reported incidence of occupational asthma in the United Kingdom, 1989-97

    Occup Environ Med

    (2000)
  • RA Jajosky et al.

    Surveillance of work-related asthma in selected U.S. states using surveillance guidelines for state health departments—California, Massachusetts, Michigan and New Jersey

    MMWR Morb Mortal Wkly Rep

    (1999)
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      Citation Excerpt :

      OA may result either from immunologically-mediated sensitization to occupational agents (i.e. ‘hypersensitivity induced OA’ or ‘allergic’ occupational asthma) or from exposure(s) to high concentrations of irritant compounds (i.e., ‘acute irritant-induced asthma’), best typified by the ‘reactive airways dysfunction syndrome’.2,4,5 Much of what is currently known about the incidence and etiological agents of immunological OA is based upon voluntary notification programs6–14 and medico-legal statistics or occupational disease registers.15–18 However, there is not much information available on the changes over time in the pattern of OA.

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    Supported by a grant from Glaxo Wellcome Inc., Research Triangle Park, NC

    ☆☆

    Reprint requests: Jean-Luc Malo, MD, Department of Respiratory Medicine, Sacré-Coeur Hospital, 5400 West Gouin Blvd, Montreal, Canada H4J 1C5.

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