Abstract
Occupational asthma (OA) accounts for up to 20 % of all new cases of asthma diagnosed annually. The definition of OA has expanded to include work-related and work-exacerbated asthma. Hundreds of potential causes have been identified in the workplace, and every year new inciting agents are being reported. High molecular weight agents (molecular weight >1000 kd) are associated with IgE-mediated type I hypersensitivity immune responses. Low molecular weight agents (molecular weight <1000 kd) include a spectrum of chemicals, some of which can react with endogenous proteins to form a new allergen capable of inducing an IgE-mediated response, but frequently these agents induce irritant-induced asthma also known as reactive airways dysfunction syndrome. Successful management of OA requires a comprehensive medical history including details about the worker’s job process and workplace exposures as well as establishing an objective diagnosis of asthma. It is also important to assess potential risk factors such as atopy. In vitro serologic testing and in vivo skin testing may be helpful in supporting a diagnosis of OA but are not diagnostic. The gold standard for diagnosis is specific provocation which may not always be possible or feasible but when performed should be conducted in a controlled medical environment under the supervision of someone with medical expertise in this area. Management of OA requires removing the worker from further exposure and treatment with medications similar to non-OA. Immunosurveillance programs have been established in some industries which have been very successful in monitoring workers exposed to potentially sensitizing agents to prevent sensitization and the subsequent development of OA.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Bibliography
Bernstein DI, et al. Diisocyanate antigen-stimulated monocyte chemoattractant protein-1 synthesis has greater test efficiency than specific antibodies for identification of diisocyanate asthma. Am J Respir Crit Care Med. 2002;166(4):445–50.
Bernstein DI, et al. Hexamethylene diisocyanate asthma is associated with genetic polymorphisms of CD14, IL-13, and IL-4 receptor alpha. J Allergy Clin Immunol. 2011;128(2):418–20.
Bernstein DI. Genetics of occupational asthma. Curr Opin Allergy Clin Immunol. 2011;11(2):86–9.
Bernstein DI, et al. CTNNA3 (alpha-catenin) gene variants are associated with diisocyanate asthma: a replication study in a Caucasian worker population. Toxicol Sci. 2013;131(1):242–6.
Bernstein JA. Material safety data sheets: are they reliable in identifying human hazards? J Allergy Clin Immunol. 2002;110(1):35–8.
Bernstein JA. Occupational asthma. In: Massoud M, editor. Allergy and asthma: practical diagnosis and management. New York: McGraw-Hill Professional; 2007. p. 145–55.
Bernstein JA, et al. Is trimellitic anhydride skin testing a sufficient screening tool for selectively identifying TMA-exposed workers with TMA-specific serum IgE antibodies? J Occup Environ Med. 2011;53(10):1122–7.
Bernstein JA, Sarlo K, Rodriguez C, Houba R. Enzymes. In: Malo JL, Chan-Yeung M, Bernstein DI, editors. Asthma in the workplace. 4th ed. New York: Taylor and Francis; 2013. p. 209–21.
Brooks SM, Weiss MA, Bernstein IL. Reactive airways dysfunction syndrome (RADS). Persistent asthma syndrome after high level irritant exposures. Chest. 1985;88(3):376–84.
Cartier A. New causes of immunologic occupational asthma, 2012–2014. Curr Opin Allergy Clin Immunol. 2015;15(2):117–23.
Chan-Yeung M, Kinsella M, Ostrow DN. Specific bronchoprovocation testing. Clin Rev Allergy. 1990;8(2–3):147–57.
Dudek W, et al. The prevalence of asthma work relatedness: preliminary data. Int J Occup Med Environ Health. 2015;28(6):1025–9.
Killorn KR, et al. The development and test re-test reliability of a work-related asthma screening questionnaire. J Asthma. 2015;52(3):279–88.
Killorn KR, et al. The use of a work-related asthma screening questionnaire in a primary care asthma program: an intervention trial. J Asthma. 2015;52(4):398–406.
Grammer LC, 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 Dis. 1993;148(1):54–7.
Grammer LC, et al. A clinical and immunologic study to assess risk of TMA-induced lung disease as related to exposure. J Occup Environ Med. 1999;41(12):1048–51.
Grammer LC, et al. Prevalence and onset of rhinitis and conjunctivitis in subjects with occupational asthma caused by trimellitic anhydride (TMA). J Occup Environ Med. 2002;44(12):1179–81.
Lummus ZL, Wisnewski AV, Bernstein DI. Pathogenesis and disease mechanisms of occupational asthma. Immunol Allergy Clin N Am. 2011;31(4):699–716, vi. Malo JL, Vandenplas O, Definitions and classification of work-related asthma. Immunol Allergy Clin N Am. 2011;31(4):645–62.
Tan J, Bernstein JA. Occupational asthma: an overview. Curr Allergy Asthma Rep. 2014;14(5):431.
Author information
Authors and Affiliations
Corresponding author
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2016 Springer International Publishing Switzerland
About this chapter
Cite this chapter
Bernstein, J.A. (2016). Occupational Asthma. In: Mahmoudi, M. (eds) Allergy and Asthma. Springer, Cham. https://doi.org/10.1007/978-3-319-30835-7_17
Download citation
DOI: https://doi.org/10.1007/978-3-319-30835-7_17
Published:
Publisher Name: Springer, Cham
Print ISBN: 978-3-319-30833-3
Online ISBN: 978-3-319-30835-7
eBook Packages: MedicineMedicine (R0)