Occupational asthma classification: Difference between revisions

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{{Occupational asthma}}
{{Occupational asthma}}
{{CMG}}
==Overview==
== Pathogenesis ==
*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 the result of multiple genetic, environmental, and behavioral influences.
:*The three main types of occupational asthma are:<ref name="pmid19281901">Maestrelli P, Boschetto P, Fabbri LM, Mapp CE (2009) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=19281901 Mechanisms of occupational asthma.] ''J Allergy Clin Immunol'' 123 (3):531-42; quiz 543-4. [http://dx.doi.org/10.1016/j.jaci.2009.01.057 DOI:10.1016/j.jaci.2009.01.057] PMID: [http://pubmed.gov/19281901 19281901]</ref>
::*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.<ref name="pmid11470996">Piirilä P, Wikman H, Luukkonen R, Kääriä K, Rosenberg C, Nordman H et al. (2001) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=11470996 Glutathione S-transferase genotypes and allergic responses to diisocyanate exposure.] ''Pharmacogenetics'' 11 (5):437-45. PMID: [http://pubmed.gov/11470996 11470996]</ref><ref name="pmid11994713">Mapp CE, Fryer AA, De Marzo N, Pozzato V, Padoan M, Boschetto P et al. (2002) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=11994713 Glutathione S-transferase GSTP1 is a susceptibility gene for occupational asthma induced by isocyanates.] ''J Allergy Clin Immunol'' 109 (5):867-72. PMID: [http://pubmed.gov/11994713 11994713]</ref>
:*Skin exposure and inhalation of aero-allergens are the common modes of exposure in patients suffering from occupation asthma.<ref name="pmid18317018">Redlich CA, Herrick CA (2008) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=18317018 Lung/skin connections in occupational lung disease.] ''Curr Opin Allergy Clin Immunol'' 8 (2):115-9. [http://dx.doi.org/10.1097/ACI.0b013e3282f85a31 DOI:10.1097/ACI.0b013e3282f85a31] PMID: [http://pubmed.gov/18317018 18317018]</ref>
*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 [[Beta-adrenergic agonist#β2 agonists|β2 agonist]] or elaboration of [[substance P]] by injured sensory nerves.


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==References==
==References==
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Revision as of 14:42, 24 September 2012