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Occupational asthma: Definitions, epidemiology, causes, and risk factors

INTRODUCTION

Occupational asthma (OA) is a form of work-related asthma characterized by variable airflow obstruction, airway hyperresponsiveness, and airway inflammation attributable to a particular exposure in the workplace and not due to stimuli encountered outside the workplace [1-3]. Two types of OA are distinguished based on their appearance after a latency period: (1) OA caused by workplace sensitizers: allergic or immunological (with a latency period); (2) OA caused by irritants: nonallergic or nonimmunologic, irritant-induced asthma including reactive airways dysfunction syndrome (RADS).

Occupational asthma accounts for approximately 10 to 25 percent of adult onset asthma [4,5]. In the case of allergic OA, a high degree of clinical suspicion is needed as the latency period for sensitization varies from a few months to several years, depending on several factors, including the intensity of exposure, the specific sensitizing agent, and individual susceptibility.

The definition, epidemiology, causes, and risk factors of OA are reviewed here. The pathophysiology, clinical assessment, diagnosis, and management of OA and reactive airways dysfunction are discussed separately. (See "Occupational asthma: Pathogenesis" and "Occupational asthma: Clinical features and diagnosis" and "Reactive airways dysfunction syndrome and irritant-induced asthma".)

DEFINITIONS

Several terms are used to define the various forms of work-related asthma [6]:

Occupational asthma (OA) begins during adulthood and is induced by exposure to immunologic or non-immunologic stimuli found in the workplace [4].

             

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Literature review current through: Sep 2014. | This topic last updated: May 5, 2014.
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References
Top
  1. Bernstein IL, Bernstein DI, Chan-Yeung M, Malo JL. Definition and classification of asthma in the workplace. In: Asthma in the workplace, 4th ed, Malo JL, Chan-Yeung M, Bernstein DI (Eds), CRC Press, Boca Raton, FL 2013. p.1-5.
  2. Tarlo SM, Balmes J, Balkissoon R, et al. Diagnosis and management of work-related asthma: American College Of Chest Physicians Consensus Statement. Chest 2008; 134:1S.
  3. Tarlo SM, Lemiere C. Occupational asthma. N Engl J Med 2014; 370:640.
  4. Dykewicz MS. Occupational asthma: current concepts in pathogenesis, diagnosis, and management. J Allergy Clin Immunol 2009; 123:519.
  5. Maestrelli P, Boschetto P, Fabbri LM, Mapp CE. Mechanisms of occupational asthma. J Allergy Clin Immunol 2009; 123:531.
  6. Tarlo SM, Malo JL, Third Jack Pepys Workshop on Asthma in the Workplace Participants. An official ATS proceedings: asthma in the workplace: the Third Jack Pepys Workshop on Asthma in the Workplace: answered and unanswered questions. Proc Am Thorac Soc 2009; 6:339.
  7. Henneberger PK, Redlich CA, Callahan DB, et al. An official american thoracic society statement: work-exacerbated asthma. Am J Respir Crit Care Med 2011; 184:368.
  8. Lemière C, Boulet LP, Chaboillez S, et al. Work-exacerbated asthma and occupational asthma: do they really differ? J Allergy Clin Immunol 2013; 131:704.
  9. Mapp CE, Boschetto P, Maestrelli P, Fabbri LM. Occupational asthma. Am J Respir Crit Care Med 2005; 172:280.
  10. Nicholson PJ, Cullinan P, Taylor AJ, et al. Evidence based guidelines for the prevention, identification, and management of occupational asthma. Occup Environ Med 2005; 62:290.
  11. Jaakkola MS, Gautrin D, Malo JL. Disease occurrence and risk factors. In: Asthma in the workplace, 4th ed, Malo JL, Chan-Yeung M, Bernstein DI. (Eds), CRC Press, Boca Raton, FL 2013. p.18-39.
  12. 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 Health 2002; 28:49.
  13. Janson C, Anto J, Burney P, et al. The European Community Respiratory Health Survey: what are the main results so far? European Community Respiratory Health Survey II. Eur Respir J 2001; 18:598.
  14. Centers for Disease Control and Prevention (CDC). Work-related asthma--38 states and District of Columbia, 2006-2009. MMWR Morb Mortal Wkly Rep 2012; 61:375.
  15. Henneberger PK, Mirabelli MC, Kogevinas M, et al. The occupational contribution to severe exacerbation of asthma. Eur Respir J 2010; 36:743.
  16. Malo JL, Chan-Yeung M. Occupational asthma. J Allergy Clin Immunol 2001; 108:317.
  17. Gautrin D, Newman-Taylor AJ, Nordman H, Malo JL. Controversies in epidemiology of occupational asthma. Eur Respir J 2003; 22:551.
  18. Torén K, Blanc PD. Asthma caused by occupational exposures is common - a systematic analysis of estimates of the population-attributable fraction. BMC Pulm Med 2009; 9:7.
  19. Gautrin D, Ghezzo H, Infante-Rivard C, Malo JL. Natural history of sensitization, symptoms and occupational diseases in apprentices exposed to laboratory animals. Eur Respir J 2001; 17:904.
  20. Gautrin D, Ghezzo H, Infante-Rivard C, et al. Long-term outcomes in a prospective cohort of apprentices exposed to high-molecular-weight agents. Am J Respir Crit Care Med 2008; 177:871.
  21. Malo JL, Chan-Yeung M. Agents causing occupational asthma. J Allergy Clin Immunol 2009; 123:545.
  22. McDonald JC, Keynes HL, Meredith SK. Reported incidence of occupational asthma in the United Kingdom, 1989-97. Occup Environ Med 2000; 57:823.
  23. Piipari R, Keskinen H. Agents causing occupational asthma in Finland in 1986-2002: cow epithelium bypassed by moulds from moisture-damaged buildings. Clin Exp Allergy 2005; 35:1632.
  24. Cullinan P, Harris JM, Newman Taylor AJ, et al. An outbreak of asthma in a modern detergent factory. Lancet 2000; 356:1899.
  25. Moscato G, Pignatti P, Yacoub MR, et al. Occupational asthma and occupational rhinitis in hairdressers. Chest 2005; 128:3590.
  26. Muñoz X, Cruz MJ, Orriols R, et al. Occupational asthma due to persulfate salts: diagnosis and follow-up. Chest 2003; 123:2124.
  27. Muñoz X, Cruz MJ, Orriols R, et al. Validation of specific inhalation challenge for the diagnosis of occupational asthma due to persulphate salts. Occup Environ Med 2004; 61:861.
  28. Weichel M, Glaser AG, Ballmer-Weber BK, et al. Wheat and maize thioredoxins: a novel cross-reactive cereal allergen family related to baker's asthma. J Allergy Clin Immunol 2006; 117:676.
  29. Palacin A, Quirce S, Armentia A, et al. Wheat lipid transfer protein is a major allergen associated with baker's asthma. J Allergy Clin Immunol 2007; 120:1132.
  30. Constantin C, Quirce S, Grote M, et al. Molecular and immunological characterization of a wheat serine proteinase inhibitor as a novel allergen in baker's asthma. J Immunol 2008; 180:7451.
  31. Gomez-Casado C, Garrido-Arandia M, Pereira C, et al. Component-resolved diagnosis of wheat flour allergy in baker's asthma. J Allergy Clin Immunol 2014.
  32. Donnelly R, Buick JB, Macmahon J. Occupational asthma after exposure to plaster casts containing methylene diphenyl diisocyanate. Occup Med (Lond) 2004; 54:432.
  33. Heederik D, Houba R. An exploratory quantitative risk assessment for high molecular weight sensitizers: wheat flour. Ann Occup Hyg 2001; 45:175.
  34. 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 Hyg 2001; 45:97.
  35. Baur X, Chen Z, Liebers V. Exposure-response relationships of occupational inhalative allergens. Clin Exp Allergy 1998; 28:537.
  36. Butcher BT, Jones RN, O'Neil CE, et al. Longitudinal study of workers employed in the manufacture of toluene-diisocyanate. Am Rev Respir Dis 1977; 116:411.
  37. Brooks SM, Malo JL, Gautrin D. Irritant-induced asthma and reactive airways dysfunction syndrome. In: Asthma in the workplace, 4th ed, Malo JL, Chan-Yeung M, Bernstein DI. (Eds), CRC Press, Boca Raton, FL 2013.
  38. Leroyer C, Perfetti L, Cartier A, Malo JL. Can reactive airways dysfunction syndrome (RADS) transform into occupational asthma due to "sensitisation" to isocyanates? Thorax 1998; 53:152.
  39. Baatjies R, Lopata AL, Sander I, et al. Determinants of asthma phenotypes in supermarket bakery workers. Eur Respir J 2009; 34:825.
  40. Gautrin D, Ghezzo H, Infante-Rivard C, Malo JL. Incidence and determinants of IgE-mediated sensitization in apprentices. A prospective study. Am J Respir Crit Care Med 2000; 162:1222.
  41. Le Moual N, Kauffmann F, Eisen EA, Kennedy SM. The healthy worker effect in asthma: work may cause asthma, but asthma may also influence work. Am J Respir Crit Care Med 2008; 177:4.
  42. Wang TN, Lin MC, Wu CC, et al. Risks of exposure to occupational asthmogens in atopic and nonatopic asthma: a case-control study in Taiwan. Am J Respir Crit Care Med 2010; 182:1369.
  43. Gautrin D, Infante-Rivard C, Dao TV, et al. Specific IgE-dependent sensitization, atopy, and bronchial hyperresponsiveness in apprentices starting exposure to protein-derived agents. Am J Respir Crit Care Med 1997; 155:1841.
  44. Slovak AJ, Hill RN. Does atopy have any predictive value for laboratory animal allergy? A comparison of different concepts of atopy. Br J Ind Med 1987; 44:129.
  45. Chan-Yeung M, Lam S, Koener S. Clinical features and natural history of occupational asthma due to western red cedar (Thuja plicata). Am J Med 1982; 72:411.
  46. Patiwael JA, Jong NW, Burdorf A, et al. Occupational allergy to bell pepper pollen in greenhouses in the Netherlands, an 8-year follow-up study. Allergy 2010; 65:1423.
  47. Nicholson PJ, Mayho GV, Roomes D, et al. Health surveillance of workers exposed to laboratory animal allergens. Occup Med (Lond) 2010; 60:591.
  48. Paggiaro PL, Loi AM, Rossi O, et al. Follow-up study of patients with respiratory disease due to toluene diisocyanate (TDI). Clin Allergy 1984; 14:463.
  49. Venables KM, Dally MB, Nunn AJ, et al. Smoking and occupational allergy in workers in a platinum refinery. BMJ 1989; 299:939.
  50. Venables KM, Topping MD, Howe W, et al. Interaction of smoking and atopy in producing specific IgE antibody against a hapten protein conjugate. Br Med J (Clin Res Ed) 1985; 290:201.
  51. Venables KM, Upton JL, Hawkins ER, et al. Smoking, atopy, and laboratory animal allergy. Br J Ind Med 1988; 45:667.
  52. Maestrelli P, Yucesoy B, Park HS, Wisnewski AV. Mechanisms, genetics, and pathophysicology. In: Asthma in the workplace, 4th ed, Malo JL, Chan-Yeung M, Bernstein DI. (Eds), CRC Press, Boca Raton, FL 2013.
  53. 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 Immunol 2002; 109:867.
  54. Gao Z, Dosman JA, Rennie DC, et al. Association of Toll-like receptor 2 gene polymorphisms with lung function in workers in swine operations. Ann Allergy Asthma Immunol 2013; 110:44.
  55. Ye YM, Kang YM, Kim SH, et al. Relationship between neurokinin 2 receptor gene polymorphisms and serum vascular endothelial growth factor levels in patients with toluene diisocyanate-induced asthma. Clin Exp Allergy 2006; 36:1153.
  56. Bernstein DI, Kissling GE, Khurana Hershey G, et al. Hexamethylene diisocyanate asthma is associated with genetic polymorphisms of CD14, IL-13, and IL-4 receptor α. J Allergy Clin Immunol 2011; 128:418.
  57. Bernstein DI. Genetics of occupational asthma. Curr Opin Allergy Clin Immunol 2011; 11:86.
  58. Piirilä P, Wikman H, Luukkonen R, et al. Glutathione S-transferase genotypes and allergic responses to diisocyanate exposure. Pharmacogenetics 2001; 11:437.