Health Dictionary
Reliable, easy-to-read patient information on common medical conditions β written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.
Occupational asthma pathophysiology
Introduction
Overview
Overview
Pathophysiology
Pathophysiology
- Occupational asthma is characterized by variable airflow limitation and/or airway hyper-responsiveness due to causes and conditions attributable to a particular occupational environment and not stimuli encountered outside the workplace.[1][2]
- Occupational asthma is the result of multiple genetic, environmental, and behavioral influences.
- The three main types of occupational asthma are:[3]
- Immunologically mediated with the involvement of specific IgE,
- Immunologically mediated without the evidence of IgE involvement, and
- Non-immunologic, irritant mediated such as in reactive airways dysfunction syndrome
- Glutathione S-transferase (GSTP1 and GSTM1) and N-acetyltransferase (NAT1) genes that are involved in airway remodeling, have shown to play are role in the pathogenesis of occupational asthma.[4][5]
- Skin exposure and inhalation of aero-allergens are the common modes of exposure in patients suffering from occupation asthma.[6]
- Certain high and low molecular weight occupational allergens such as animal proteins and platinum salts respectively, act as antigens and induce a antigen-specific IgE response that contributes to the immunologic pathogenesis.
- Non-immunologic mechanisms that play a role in the pathogenesis include the direct inhibition of Ξ²2 agonist or elaboration of substance P by injured sensory nerves.
References
References
- β American Journal of Respiratory and Critical Care Medicine. Vol 167. pp. 450-471, (2003). Proceedings of the First Jack Pepys Occupational Asthma Symposium.
- β Tarlo SM, Balmes J, Balkissoon R, Beach J, Beckett W, Bernstein D et al. (2008) Diagnosis and management of work-related asthma: American College Of Chest Physicians Consensus Statement. Chest 134 (3 Suppl):1S-41S. DOI:10.1378/chest.08-0201 PMID: 18779187
- β Maestrelli P, Boschetto P, Fabbri LM, Mapp CE (2009) Mechanisms of occupational asthma. J Allergy Clin Immunol 123 (3):531-42; quiz 543-4. DOI:10.1016/j.jaci.2009.01.057 PMID: 19281901
- β PiirilΓ€ P, Wikman H, Luukkonen R, KÀÀriΓ€ K, Rosenberg C, Nordman H et al. (2001) Glutathione S-transferase genotypes and allergic responses to diisocyanate exposure. Pharmacogenetics 11 (5):437-45. PMID: 11470996
- β Mapp CE, Fryer AA, De Marzo N, Pozzato V, Padoan M, Boschetto P et al. (2002) Glutathione S-transferase GSTP1 is a susceptibility gene for occupational asthma induced by isocyanates. J Allergy Clin Immunol 109 (5):867-72. PMID: 11994713
- β Redlich CA, Herrick CA (2008) Lung/skin connections in occupational lung disease. Curr Opin Allergy Clin Immunol 8 (2):115-9. DOI:10.1097/ACI.0b013e3282f85a31 PMID: 18317018
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: