Occupational asthma
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Lakshmi Gopalakrishnan, M.B.B.S. [2]
Overview
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Asthma is defined as a respiratory disease caused by narrowing of the air passages that is synonymous with difficulty in breathing, tightness of chest, nasal irritation, coughing and wheezing.
Occupational asthma is defined as:
“A disease 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]
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
Historical Perspective
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:
Overview
Historical Perspective
- The first person to use it in reference to a medical condition was Hippocrates in 450 BC, and he believed that tailors, anglers and metalworkers were more likely to be affected by the disease. Although much research has been done since, the inflammatory component of asthma was recognized only in the 1960s.* In 1700, Bernardino Ramazzini, Doctor of Philosophy and Medicine from parma, Italy published the book De Morbis Artificum Diatriba (A Treatise on the Diseases of Workers). Although researchers like Olaus Magus had done work on diseases due to occupational causes as early as 1555, this was the first comprehensive work on work-related diseases. This volume described in detail the diseases of workers in 52 different occupations.[1] Thus, this formed the basis for the emergence of occupational medicine and even today, it is an important reference. Due to his important contribution to this field, Dr. Ramazzini is considered the father of occupational medicine.* Similarly, Dr. Jack Pepys, for his contribution to research on asthma in the workplace, is also considered as the father of occupational asthma[2]. His work on the role of aspergillus species in pulmonary diseases as an important pathogenic factor for farmer’s lung has been heavily influenced the emergence of occupational asthma as an occupational disease. And, thanks to his work on Specific Inhalation Challenge, the compensatible aspect of the disease was recognized.
References
- ↑ Major R H: A History of Medicine. CHEST, VOL. 57, NO. 4, APRIL 1970. C.C. Thomas Springfield 1954
- ↑ Occupational Asthma: The Past 50 years. Chan-Yeung M.
Classification
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:
Overview
Classification
References
Pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:
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
Causes
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:
Overview
Causes
References
Differentiating Occupational asthma from other Diseases
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:
Overview
Differentiating Occupational asthma from Other Diseases
References
Epidemiology and Demographics
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:
Overview
Epidemiology and Demographics
- Asthma affects as much as 15% of the Canadian population[1] (and this is true of other developed countries too) and has increased four fold in the last 20 years. Various reasons can be identified for this increase that includes better diagnostic facilities along with a greater awareness regarding the disease have shown to play a major role. But, one cannot deny the part of increased environmental pollution. Researchers have been working on the relation between the environment and human health since long and the air we breathe is the primary cause for lung diseases like asthma, rhinitis, COPDs, etc. that affect us today.
- Approximately, 10 to 15% of adult-onset asthma cases are affected by an aggravation of symptoms while at work and an improvement when away, which implies that they may be suffering from occupational asthma.[2][3] Thus, when an individual’s asthma is caused, not aggravated, by workplace materials, it is defined as occupational asthma (“OA”). In the USA, OA is considered the most common occupational lung disease[4].
- At present, over 400 workplace substances have been identified as having asthmagenic or allergenic properties[5]. Their existence and magnitude vary from region to region and the type of industry and can be as varied as wood dust (cedar, ebony, etc.), persulfates (Hairsprays), zinc or even seafood like prawns. For example, in France the industries most affected in order of importance are Bakeries and cake-shops, automobile industry and hairdressers[6], whereas in Canada the principle cause is wood dust, followed by isocyanates.
References
- ↑ C-Health: Asthma in Canada(2007)
- ↑ Dykewicz MS (2009) Occupational asthma: current concepts in pathogenesis, diagnosis, and management. J Allergy Clin Immunol 123 (3):519-28; quiz 529-30. DOI:10.1016/j.jaci.2009.01.061 PMID: 19281900
- ↑ 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
- ↑ http://www.lni.wa.gov/Safety/Research/files/AsthmaCme.pdf
- ↑ http://www.asmanet.com/asmapro/agents.htm
- ↑ Reported incidence of occupational asthma in France, 1996–99: the ONAP programme. J Ameille, G Pauli, A Calastreng-Crinquand, D Vervloët, Y Iwatsubo, E Popin, M C Bayeux-Dunglas and M C Kopferschmitt-Kubler2 and the corresponding members of the ONAP
Risk Factors
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:
Overview
Risk Factors
References
Screening
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:
Overview
Screening
References
Natural History, Complications, and Prognosis
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:
Overview
Natural History
Complications
Prognosis
References
Diagnosis
Diagnosis
History and Symptoms | Physical Examination | Laboratory Findings | EKG | Chest X ray | Other Diagnostic Studies
Treatment
Treatment
Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies
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