Occupational asthma pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
== | == Pathophysiology == | ||
*Occupational asthma is characterized by variable airflow limitation and/or [[bronchial hyperresponsiveness|airway hyper-responsiveness]] due to causes and conditions attributable to a particular occupational environment and not [[Asthma pathophysiology#Stimuli or Triggering Factors|stimuli]] encountered outside the workplace.<ref name="AJRCCM">[http://ajrccm.atsjournals.org/cgi/content/full/167/3/450/ American Journal of Respiratory and Critical Care Medicine.] Vol 167. pp. 450-471, (2003). Proceedings of the First Jack Pepys Occupational Asthma Symposium.</ref><ref name="pmid18779187">Tarlo SM, Balmes J, Balkissoon R, Beach J, Beckett W, Bernstein D et al. (2008) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=18779187 Diagnosis and management of work-related asthma: American College Of Chest Physicians Consensus Statement.] ''Chest'' 134 (3 Suppl):1S-41S. [http://dx.doi.org/10.1378/chest.08-0201 DOI:10.1378/chest.08-0201] PMID: [http://pubmed.gov/18779187 18779187]</ref> | *Occupational asthma is characterized by variable airflow limitation and/or [[bronchial hyperresponsiveness|airway hyper-responsiveness]] due to causes and conditions attributable to a particular occupational environment and not [[Asthma pathophysiology#Stimuli or Triggering Factors|stimuli]] encountered outside the workplace.<ref name="AJRCCM">[http://ajrccm.atsjournals.org/cgi/content/full/167/3/450/ American Journal of Respiratory and Critical Care Medicine.] Vol 167. pp. 450-471, (2003). Proceedings of the First Jack Pepys Occupational Asthma Symposium.</ref><ref name="pmid18779187">Tarlo SM, Balmes J, Balkissoon R, Beach J, Beckett W, Bernstein D et al. (2008) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=18779187 Diagnosis and management of work-related asthma: American College Of Chest Physicians Consensus Statement.] ''Chest'' 134 (3 Suppl):1S-41S. [http://dx.doi.org/10.1378/chest.08-0201 DOI:10.1378/chest.08-0201] PMID: [http://pubmed.gov/18779187 18779187]</ref> | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
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 β2 agonist or elaboration of substance P by injured sensory nerves.
References
- ↑ American Journal of Respiratory and Critical Care Medicine. Vol 167. pp. 450-471, (2003). Proceedings of the First Jack Pepys Occupational Asthma Symposium.
- ↑ 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
- ↑ 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
- ↑ Piirilä P, Wikman H, Luukkonen R, Kääriä 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
- ↑ 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
- ↑ 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