Occupational Asthma | Causes, Symptoms, and Managements

Introduction

Occupational asthma is asthma caused by work-related exposure to a pulmonary sensitizing agent.

Thus, OA can be classified into two types based on its pathogenesis.

Sensitizer-induced OA, also known as “immunologic OA,” and “allergic OA” or “OA with latency period”.

Causes of Occupational Asthma

Sensitizers for occupational asthma are divided into high molecular weight compounds (HMW) and low molecular weight compounds (LMW).

High-molecular-weight agents

  • Cereal.
  • Flour.
  • Wheat.
  • Rye.
  • Buckwheat.
  • Barley.

Animals

  • Rats.
  • Mice.
  • Rabbits.
  • Seafood.

Enzymes

  • Amylase.
  • Subtilisine.
  • Maxatase.
  • Pancreatin.
  • Bromelain.
  • Latex.
  • Hevea tree protein.

Low-molecular weight agents

Di-isocyanates

  • Toluene di-isocyanate.
  • Hexamethylene di-isocyanate.
  • Methylene diphenyl-di-isocyanate.

Acrylates

  • Cyanoacrylates.
  • Methacrylates.
  • Di- and tri-acrylates.

Persulphate salts

  • Hairdressing products (bleach).

Biocides

  • Formaldehyde.
  • Glutaraldehyde.
  • Quaternary ammonium compounds.

Metals

  • Chromium.
  • Nickel.
  • Cobalt.
  • Platinum.

Wood dust

  • Western red cedar.
  • Iroko.
  • Obeche.
  • Oak.

Acid anhydrides

  • Phthalic.
  • Trimellitic.
  • Maleic anhydrides.

Amines

  • Triethanolamine.
  • Ethylene diamine.
  • Isophorone diamine.

Symptoms of Occupational Asthma

After repeated exposure to a pulmonary sensitizing agent, the condition is characterized by the onset of asthma symptoms like dyspnea, coughing, and wheezing.

Depending on the specific substance and sensitivity, symptoms may appear immediately or several hours later.

The person may become more sensitive after repeated exposure and react to lower airborne concentrations of the substance.

Diagnosis of Occupational Asthma

The diagnosis depends on proving that workplace factors are causing variable and reversible airway obstruction.

Normally, occupational history and serial lung function assessments are required.

The evaluation should seek to establish the following:

  • Exposure to substances that could be allergens or irritants.
  • The presence of a temporal relationship.
  • Natural disease progressions, such as rhinitis, coughing, and wheezing.
  • Factors that are aggravating and relieving.
  • Using medications that could mask workplace effects.

Management of Occupational Asthma

The preferred treatment for OA is to remove the worker from further exposure.

Occupational asthma is treated similarly to non-OA with inhaled corticosteroids, long-acting β2-agonists, leukotriene modifying agents, xanthine oxidase inhibitors, and oral corticosteroids.

Summary

Occupational asthma (OA) is asthma caused by work-related exposure to a pulmonary sensitizing agent.

Sensitizers for occupational asthma are divided into high molecular weight compounds (HMW) and low molecular weight compounds (LMW).

After repeated exposure to a pulmonary sensitizing agent, the condition is characterized by the onset of asthma symptoms like dyspnea, coughing, and wheezing.

The diagnosis depends on proving that workplace factors are causing variable and reversible airway obstruction.

Normally, occupational history and serial lung function assessments are required.

The preferred treatment for OA is to remove the worker from further exposure.

Occupational asthma is treated similarly to non-OA with inhaled corticosteroids, long-acting β2-agonists, leukotriene modifying agents, xanthine oxidase inhibitors, and oral corticosteroids.

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References

  1. Harbison, R. D., Bourgeois, M. M., & Johnson, G. T. (2015). Hamilton & Hardy’s Industrial Toxicology. Hoboken, New Jersey John Wiley & Sons, Inc.
  2. Guidotti, T. L. (2011). Global occupational health. Oxford University Press.
  3. Tan, J., & Bernstein, J. A. (2014). Occupational Asthma: An Overview. Current Allergy and Asthma Reports, 14(5). From SpringerLink
  4. Cormier, M., & Lemière, C. (2020). Occupational asthma. The International Journal of Tuberculosis and Lung Disease, 24(1), 8–21. From PubMed

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