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Occupational asthma: Management, prognosis, and prevention

Catherine Lemière, MD
David I Bernstein, MD
Section Editor
Peter J Barnes, DM, DSc, FRCP, FRS
Deputy Editor
Helen Hollingsworth, MD


Occupational asthma (OA) is a form of work-related asthma that is characterized by variable airflow obstruction, airway hyperresponsiveness, and airway inflammation induced by exposures in the work environment rather than exposures encountered outside the workplace [1]. Work-exacerbated asthma (also known as work-aggravated asthma) is defined as preexisting or concurrent asthma that worsens in the workplace, but is not induced by it.

The agents that cause OA include both immunologic and nonimmunologic stimuli [2]. Immunologic OA is the classic form of OA in which the worker's immune system is sensitized to an occupational agent through IgE-mediated or other immune recognition. Similar to asthma in general, immunologic OA appears to be heterogeneous and includes several phenotypes [3]. The term nonimmunologic OA is used to refer to irritant-induced asthma that results from single or multiple exposures to irritant substances at a high level of intensity. Reactive airways dysfunction syndrome (RADS), is a form of irritant-induced asthma, acutely induced by accidental high level irritant exposures in the workplace (eg, sulfur dioxide, chlorine, smoke inhalation).

The diagnosis of immunologic OA is based on the occurrence of new adult-onset asthma or worsening of previously quiescent asthma following an initial occupational exposure to a causative agent, evidence of reversible airflow obstruction and/or airway hyperresponsiveness (based on pulmonary function testing), and demonstration of respiratory sensitization to a potential causative agent [4]. Demonstration of allergic sensitization (particularly to protein allergens encountered at work) by skin prick testing or serum specific IgE supports the diagnosis of immunologic OA. The diagnosis of irritant induced asthma (eg, RADS) is made retrospectively based on the onset of cough and/or asthma symptoms following high-intensity irritant exposure(s) and demonstration of a positive methacholine challenge test.    

The management, prognosis, and prevention of OA will be reviewed here. The definition, epidemiology, causes, risk factors, pathogenesis, clinical features, evaluation, and diagnosis of OA, and the diagnosis and management of RADS and irritant–induced asthma are discussed separately. (See "Occupational asthma: Definitions, epidemiology, causes, and risk factors" and "Occupational asthma: Pathogenesis" and "Occupational asthma: Clinical features and diagnosis" and "Reactive airways dysfunction syndrome and irritant-induced asthma".)


The key element is to make the diagnosis and remove the subject from exposure as quickly as possible after the onset of symptoms. Occupational asthma (OA) may be cured if this is done rapidly and efficiently. The management of OA requires a combination of avoidance of further exposure to sensitizing agents, reduction in exposure to irritant agents (eg, environmental tobacco smoke, strong fumes and fragrances, extremes of temperature and humidity) and pharmacotherapy based on the severity of asthma. The management of occupational rhinitis, which may accompany OA, is discussed separately. (See "Occupational rhinitis".)

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Literature review current through: Nov 2017. | This topic last updated: Jun 27, 2017.
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  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. Dykewicz MS. Occupational asthma: current concepts in pathogenesis, diagnosis, and management. J Allergy Clin Immunol 2009; 123:519.
  3. Mason P, Scarpa MC, Liviero F, et al. Distinct Clinical Phenotypes of Occupational Asthma due to Diisocyanates. J Occup Environ Med 2017; 59:539.
  4. Tarlo SM, Lemiere C. Occupational asthma. N Engl J Med 2014; 370:640.
  5. Mapp CE, Boschetto P, Maestrelli P, Fabbri LM. Occupational asthma. Am J Respir Crit Care Med 2005; 172:280.
  6. Fishwick D, Barber CM, Bradshaw LM, et al. Standards of care for occupational asthma: an update. Thorax 2012; 67:278.
  7. Baur X, Sigsgaard T, Aasen TB, et al. Guidelines for the management of work-related asthma. Eur Respir J 2012; 39:529.
  8. Kim M-H, Jung J-W, Kang H-R. The Usefulness of Job Relocation and Serum Eosinophil Cationic Protein in Baker's Asthma. Int Arch Allergy Immunol 2013; 161:252.
  9. Cote J, Kennedy S, Chan-Yeung M. Outcome of patients with cedar asthma with continuous exposure. Am Rev Respir Dis 1990; 141:373.
  10. Moscato G, Dellabianca A, Perfetti L, et al. Occupational asthma: a longitudinal study on the clinical and socioeconomic outcome after diagnosis. Chest 1999; 115:249.
  11. Pisati G, Baruffini A, Zedda S. Toluene diisocyanate induced asthma: outcome according to persistence or cessation of exposure. Br J Ind Med 1993; 50:60.
  12. 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.
  13. de Groene GJ, Pal TM, Beach J, et al. Workplace interventions for treatment of occupational asthma. Cochrane Database Syst Rev 2011; :CD006308.
  14. Vandenplas O, Dressel H, Nowak D, et al. What is the optimal management option for occupational asthma? Eur Respir Rev 2012; 21:97.
  15. 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.
  16. Dumas O, Le Moual N. Do chronic workplace irritant exposures cause asthma? Curr Opin Allergy Clin Immunol 2016; 16:75.
  17. Vandenplas O, Dressel H, Wilken D, et al. Management of occupational asthma: cessation or reduction of exposure? A systematic review of available evidence. Eur Respir J 2011; 38:804.
  18. 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.
  19. Obase Y, Shimoda T, Mitsuta K, et al. Two patients with occupational asthma who returned to work with dust respirators. Occup Environ Med 2000; 57:62.
  20. Müller-Wening D, Neuhauss M. Protective effect of respiratory devices in farmers with occupational asthma. Eur Respir J 1998; 12:569.
  21. Taivainen AI, Tukiainen HO, Terho EO, Husman KR. Powered dust respirator helmets in the prevention of occupational asthma among farmers. Scand J Work Environ Health 1998; 24:503.
  22. Slovak AJ, Orr RG, Teasdale EL. Efficacy of the helmet respirator in occupational asthma due to laboratory animal allergy (LAA). Am Ind Hyg Assoc J 1985; 46:411.
  23. 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 Immunol 1998; 102:998.
  24. National Asthma Education and Prevention Program: Expert panel report III: Guidelines for the diagnosis and management of asthma. Bethesda, MD: National Heart, Lung, and Blood Institute, 2007. (NIH publication no. 08-4051). Full text available online: www.nhlbi.nih.gov/guidelines/asthma/asthgdln.htm (Accessed on June 27, 2017).
  25. Global Initiative for Asthma (GINA). 2017 GINA Report, Global Strategy for Asthma Management and Prevention. Full text available online at: http://www.ginasthma.org (Accessed on June 27, 2017).
  26. Malo JL, Cartier A, Côté J, et al. Influence of inhaled steroids on recovery from occupational asthma after cessation of exposure: an 18-month double-blind crossover study. Am J Respir Crit Care Med 1996; 153:953.
  27. Maestrelli P, De Marzo N, Saetta M, et al. Effects of inhaled beclomethasone on airway responsiveness in occupational asthma. Placebo-controlled study of subjects sensitized to toluene diisocyanate. Am Rev Respir Dis 1993; 148:407.
  28. De Marzo N, Fabbri LM, Crescioli S, et al. Dose-dependent inhibitory effect of inhaled beclomethasone on late asthmatic reactions and increased responsiveness to methacholine induced by toluene diisocyanate in sensitised subjects. Pulm Pharmacol 1988; 1:15.
  29. Varney VA, Edwards J, Tabbah K, et al. Clinical efficacy of specific immunotherapy to cat dander: a double-blind placebo-controlled trial. Clin Exp Allergy 1997; 27:860.
  30. Sundin B, Lilja G, Graff-Lonnevig V, et al. Immunotherapy with partially purified and standardized animal dander extracts. I. Clinical results from a double-blind study on patients with animal dander asthma. J Allergy Clin Immunol 1986; 77:478.
  31. Lent AM, Harbeck R, Strand M, et al. Immunologic response to administration of standardized dog allergen extract at differing doses. J Allergy Clin Immunol 2006; 118:1249.
  32. Nelson HS. Advances in upper airway diseases and allergen immunotherapy. J Allergy Clin Immunol 2007; 119:872.
  33. Leynadier F, Herman D, Vervloet D, Andre C. Specific immunotherapy with a standardized latex extract versus placebo in allergic healthcare workers. J Allergy Clin Immunol 2000; 106:585.
  34. Sastre J, Fernández-Nieto M, Rico P, et al. Specific immunotherapy with a standardized latex extract in allergic workers: a double-blind, placebo-controlled study. J Allergy Clin Immunol 2003; 111:985.
  35. Pereira C, Rico P, Lourenço M, et al. Specific immunotherapy for occupational latex allergy. Allergy 1999; 54:291.
  36. Pereira C, Pedro E, Tavares B, et al. Specific immunotherapy for severe latex allergy. Eur Ann Allergy Clin Immunol 2003; 35:217.
  37. Armentia A, Martin-Santos JM, Quintero A, et al. Bakers' asthma: prevalence and evaluation of immunotherapy with a wheat flour extract. Ann Allergy 1990; 65:265.
  38. Armentia A, Arranz M, Martin JM, et al. Evaluation of immune complexes after immunotherapy with wheat flour in bakers' asthma. Ann Allergy 1992; 69:441.
  39. Leynadier F, Doudou O, Gaouar H, et al. Effect of omalizumab in health care workers with occupational latex allergy. J Allergy Clin Immunol 2004; 113:360.
  40. Pérez Pimiento A, Bueso Fernández A, García Loria J, et al. Effect of omalizumab treatment in a baker with occupational asthma. J Investig Allergol Clin Immunol 2008; 18:490.
  41. Olivieri M, Biscardo CA, Turri S, Perbellini L. Omalizumab in persistent severe bakers' asthma. Allergy 2008; 63:790.
  42. Lavaud F, Bonniaud P, Dalphin JC, et al. Usefulness of omalizumab in ten patients with severe occupational asthma. Allergy 2013; 68:813.
  43. Ollé-Monge M, Cruz MJ, Gomez-Ollés S, et al. Effect of anti-IgE in occupational asthma caused by exposure to low molecular weight agents. Allergy 2017; 72:1720.
  44. Malo JL, Cartier A, Ghezzo H, et al. Patterns of improvement in spirometry, bronchial hyperresponsiveness, and specific IgE antibody levels after cessation of exposure in occupational asthma caused by snow-crab processing. Am Rev Respir Dis 1988; 138:807.
  45. Perfetti L, Cartier A, Ghezzo H, et al. Follow-up of occupational asthma after removal from or diminution of exposure to the responsible agent: relevance of the length of the interval from cessation of exposure. Chest 1998; 114:398.
  46. Malo JL, Ghezzo H. Recovery of methacholine responsiveness after end of exposure in occupational asthma. Am J Respir Crit Care Med 2004; 169:1304.
  47. Maghni K, Lemière C, Ghezzo H, et al. Airway inflammation after cessation of exposure to agents causing occupational asthma. Am J Respir Crit Care Med 2004; 169:367.
  48. 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.
  49. Rachiotis G, Savani R, Brant A, et al. Outcome of occupational asthma after cessation of exposure: a systematic review. Thorax 2007; 62:147.
  50. Miedinger D, Malo JL, Ghezzo H, et al. Factors influencing duration of exposure with symptoms and costs of occupational asthma. Eur Respir J 2010; 36:728.
  51. Yacoub MR, Lavoie K, Lacoste G, et al. Assessment of impairment/disability due to occupational asthma through a multidimensional approach. Eur Respir J 2007; 29:889.
  52. Malo JL, Boulet LP, Dewitte JD, et al. Quality of life of subjects with occupational asthma. J Allergy Clin Immunol 1993; 91:1121.
  53. Cullinan P, Tarlo S, Nemery B. The prevention of occupational asthma. Eur Respir J 2003; 22:853.
  54. Liss GM, Bernstein D, Genesove L, et al. Assessment of risk factors for IgE-mediated sensitization to tetrachlorophthalic anhydride. J Allergy Clin Immunol 1993; 92:237.
  55. 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.
  56. 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. Occup Environ Med 1999; 56:202.
  57. Fisher R, Saunders WB, Murray SJ, Stave GM. Prevention of laboratory animal allergy. J Occup Environ Med 1998; 40:609.
  58. 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 Immunol 2002; 110:318.
  59. Tarlo SM, Easty A, Eubanks K, et al. Outcomes of a natural rubber latex control program in an Ontario teaching hospital. J Allergy Clin Immunol 2001; 108:628.
  60. Malo JL, Chan-Yeung M. Agents causing occupational asthma. J Allergy Clin Immunol 2009; 123:545.
  61. McDonald JC, Keynes HL, Meredith SK. Reported incidence of occupational asthma in the United Kingdom, 1989-97. Occup Environ Med 2000; 57:823.
  62. 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 Med 2002; 59:58.
  63. Petsonk EL, Wang ML, Lewis DM, et al. Asthma-like symptoms in wood product plant workers exposed to methylene diphenyl diisocyanate. Chest 2000; 118:1183.
  64. Grammer LC, Harris KE, Yarnold PR. Effect of respiratory protective devices on development of antibody and occupational asthma to an acid anhydride. Chest 2002; 121:1317.
  65. Fishwick D, Barber CM, Bradshaw LM, et al. Standards of care for occupational asthma. Thorax 2008; 63:240.
  66. Tarlo SM, Liss GM. Prevention of occupational asthma. Curr Allergy Asthma Rep 2010; 10:278.
  67. Wild DM, Redlich CA, Paltiel AD. Surveillance for isocyanate asthma: a model based cost effectiveness analysis. Occup Environ Med 2005; 62:743.
  68. Jonaid BS, Rooyackers J, Stigter E, et al. Predicting occupational asthma and rhinitis in bakery workers referred for clinical evaluation. Occup Environ Med 2017; 74:564.
  69. Siracusa A, Marabini A, Folletti I, Moscato G. Smoking and occupational asthma. Clin Exp Allergy 2006; 36:577.
  70. Graham C, Rosenkranz HS, Karol MH. Structure-activity model of chemicals that cause human respiratory sensitization. Regul Toxicol Pharmacol 1997; 26:296.
  71. Jarvis J, Seed MJ, Elton R, et al. Relationship between chemical structure and the occupational asthma hazard of low molecular weight organic compounds. Occup Environ Med 2005; 62:243.