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American Journal of Respiratory and Critical Care Medicine Vol 172. pp. 406-407, (2005)
© 2005 American Thoracic Society
doi: 10.1164/rccm.2506006


Editorial

Asthma May Be More Severe If It Is Work-related

Jean-Luc Malo, M.D.

Sacré-Coeur Hospital, Montreal, QC, Canada

Approximately 10% of all subjects with adult-onset asthma report that their asthma is worse at work (1). The possibility that these subjects suffer from occupational asthma—that is, asthma caused by agents in the workplace—should be examined by objective means (2). Asthma does improve in workers with occupational asthma once they are no longer being exposed to the causal agent, although the majority are left with permanent symptoms, bronchial hyperresponsiveness, and inflammation, as originally described by Chan-Yeung (3) and confirmed in numerous follow-up studies (4, 5). Conversely, subjects with occupational asthma who continue to be exposed show a deterioration of the asthmatic situation (6, 7), which may even lead to death (8). The earlier the diagnosis and removal from exposure, the more likely workers may be cured, which is a favorable outcome for patients and their physicians, as well as for its impact on public health. Even if practice guidelines for investigation and diagnosis of occupational asthma have been proposed (9, 10), delays in addressing this condition often occur and may be attributed to various causes. For example, questionnaires administered by physicians are sensitive, but not specific means of diagnosing occupational asthma (11). Moreover, simple questions like "What do you do in life?" and "What are you exposed to at work?" are often omitted during a health-related interview. Although skin-prick tests are widely used to identify allergies to ubiquitous environmental factors, such as cats and dogs, they are generally impractical and not available for detection of most occupational agents. Serial peak flow rate assessments are tedious, and specific inhalation challenges are limited to specialized centers (2). Finally, the decision to leave a job, even if it does cause asthma, is a most difficult one given the implicit socioeconomic repercussions in most countries.

Several population-based studies have identified deleterious associations between the prevalence of asthma and certain workplaces (12). The study by Le Moual and coworkers (13) in this issue of the Journal (pp. 440–445) goes one step further by showing that specific work environments are associated with increased risks of more severe asthma. In the Epidemiological Study on the Genetics and Environment of Asthma, the authors used a case-control design in which patients are recruited from asthma clinics and control subjects from electoral rolls, a department of surgery, and one check-up center. The strengths of this study are that the authors assessed the severity and control of asthma using a scale and assessed exposure with a job-exposure matrix in which a job code is coupled with information on exposure to occupational "asthmogens." Although the number of cases with either mild or severe asthma was nominal, and consequently resulted in wide confidence intervals, the authors showed that the risk of being affected with severe asthma increased in the adult-onset, but not in the childhood-onset categories, a confirmatory finding because occupational asthma begins in adult life. Moreover, the odd ratios for the association with severe asthma increased significantly for all occupational asthmogens and also increased, albeit not significantly so, for the association with mild asthma.

As acknowledged by the authors, this study can be criticized for its use of a case-control study design. This includes selection of more severe cases because these were recruited in chest clinics, and more subjects with possible work-related asthma because such patients are likely to be referred to these clinics. Subjects seen in specialized clinics do not in fact represent the whole spectrum of subjects with asthma.

The risk of occupational asthma is generally higher in the case of low-molecular-weight agents (e.g., isocyanates, metals, various chemicals) compared with high-molecular-weight agents (including latex, laboratory animals, or proteinaceous agents, such as flour). In general, surveys performed in high-risk workplaces with stringent identification of cases have shown prevalence figures of 5 to 10% and less than 5% for low- and high-molecular-weight agents, respectively. Interestingly, in the study by Le Moual and coworkers (13), the risk of developing severe asthma was also generally higher for low-molecular-weight agents. Workplaces with exposure to industrial cleaning agents are associated with increased risk of work-related asthmatic symptoms (14, 15) and more severe asthma, as shown by Le Moual and colleagues, although the nature of potential sensitizers in this type of workplace is unidentified. The greatly increased risk of severe asthma in the study by Le Moual and coworkers in textile production is unexplained.

It is relevant to test the validity of frequencies, risks, and various associations derived from epidemiologic studies by objective means. Le Moual and coworkers (13) confirmed the existence of asthma in their cases, but did not demonstrate that exposure at work was the cause of asthma. In population-based studies, it would therefore be appropriate to suggest using an approach in which a subsample identified in the epidemiologic study is investigated by objective means to verify the potential gap between frequency figures derived from epidemiologic and objective approaches. Prospective studies performed by Gautrin and coworkers (16) in apprentices at risk of occupational sensitization and asthma to high- and low-molecular-weight agents have shown that an approach that combines questionnaires with objective means (skin-prick tests, methacholine challenges) are likely to yield objective data on the true frequency of disease.

As outlined by the authors (13), their contribution to our understanding of work-related asthma also has public health and clinical implications. Occupational asthma should be excluded in every subject with recent onset of adult asthma. There is indeed a possibility of curing asthma in this instance. Furthermore, if adult asthma is or becomes more severe, objective investigation for the possibility of occupational asthma becomes most important because its risk is then higher.

FOOTNOTES

Conflict of Interest Statement: J.-L.M. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript.

REFERENCES

  1. Blanc PD, Toren K. How much asthma can be attributed to occupational factors? Am J Med 1999;107:580–587.[CrossRef][Medline]
  2. Bernstein IL, Chan-Yeung M, Malo JL, Berstein D. Asthma in the workplace, 2nd ed. New York: Marcel Dekker; 1999.
  3. Chan-Yeung M. Fate of occupational asthma: a follow-up study of patients with occupational asthma due to western red cedar (thuja plicata). Am Rev Respir Dis 1977;116:1023–1029.[Medline]
  4. Chan-Yeung M, Malo JL. Natural history of occupational asthma. In: Bernstein IL, Chan-Yeung M, Malo JL, Bernstein DI, editors. Asthma in the workplace. New York: Marcel Dekker; 1999. pp. 129–143.
  5. Maghni K, Lemière C, Ghezzo H, Yuquan W, Malo JL. Airway inflammation after cessation of exposure to agents causing occupational asthma. Am J Respir Crit Care Med 2004;169:367–372.[Abstract/Free Full Text]
  6. Côté J, Kennedy S, Chan-Yeung M. Outcome of patients with cedar asthma with continuous exposure. Am Rev Respir Dis 1990;141:373–376.[Medline]
  7. Moscato G, Dellabianca A, Perfetti L, Brame B, Galdi E, Niniano R, Paggiaro P. Occupational asthma: a longitudinal study on the clinical and socioeconomic outcome after diagnosis. Chest 1999;115:249–256.[Abstract/Free Full Text]
  8. Ortega HG, Kreiss K, Schill DP, Weissman DN. Fatal asthma from powdering shark cartilage and review of fatal occupational asthma literature. Am J Ind Med 2002;42:50–54.[CrossRef][Medline]
  9. Tarlo SM, Boulet LP, Cartier A, Cockcroft D, Côté J, Hargreave FE, Holness L, Liss G, Malo JL, Chan-Yeung M. Canadian Thoracic Society guidelines for occupational asthma. Can Respir J 1998;5:289–300.[Medline]
  10. Nicholson PJ, Cullinan P, Taylor AJ. Newman, Burge PS, Boyle C. Evidence based guidelines for the prevention, identification, and management of occupational asthma. Occup Environ Med 2005;62:290–299.[Abstract/Free Full Text]
  11. Malo JL, Ghezzo H, L'Archevêque J, Lagier F, Perrin B, Cartier A. Is the clinical history a satisfactory means of diagnosing occupational asthma? Am Rev Respir Dis 1991;143:528–532.[Medline]
  12. Becklake MR, Malo JL, Chan-Yeung M. Epidemiological approaches in occupational asthma. In: Bernstein IL, Chan-Yeung M, Malo JL, Bernstein DI, editors. Asthma in the workplace. New York: Marcel Dekker; 1999. pp. 27–65.
  13. Le Moual N, Siroux V, Pin I, Kauffman F, Kennedy SM. Asthma severity and exposure to occupational asthmogens. Am J Respir Crit Care Med 2005;172:440–445.[Abstract/Free Full Text]
  14. Karjalainen A, Martikainen R, Karjalainen J, Klaukka T, Kurppa K. Excess incidence of asthma among Finnish cleaners employed in different industries. Eur Respir J 2002;19:90–95.[Abstract/Free Full Text]
  15. Zock JP, Kogevinas M, Sunyer J, Jarvis D, Anto JM, Toren K. Asthma characteristics in cleaning workers, workers in other risk jobs and office workers. Eur Respir J 2002;20:679–685.[Abstract/Free Full Text]
  16. Gautrin D, Newman-Taylor AJ, Nordman H, Malo JL. Controversies in epidemiology of occupational asthma. Eur Respir J 2003;22:551–559.[Abstract/Free Full Text]



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