In This Article Expand or collapse the "in this article" section Work-Related Asthma

  • Introduction
  • General Overview
  • Genetics/Mechanism
  • Epidemiology of Work-Related Asthma
  • Clinical Guidelines for Diagnosis of Work-Related Asthma
  • Hazard Control and Disease Prevention
  • Treatment

Public Health Work-Related Asthma
  • LAST MODIFIED: 21 April 2021
  • DOI: 10.1093/obo/9780199756797-0201

Introduction

Work-related asthma encompasses both new-onset asthma and aggravation of pre-existing asthma from work exposures/conditions. New-onset asthma can be caused by exposure to an irritant or a substance that causes sensitization. Approximately 350 substances have been identified by which exposure at work can lead to sensitization and asthma. When the term occupational asthma is used, it generally does not include work-aggravated asthma. Some authors limit the use of occupational asthma to new-onset asthma from sensitization to a substance at work, while others also include new-onset asthma from exposure to an irritant at work under this category. New-onset asthma from an acute single exposure is called reactive airways dysfunction Syndrome (RADS) (note this is not the same as reactive airways disease). New-onset asthma from repeated chronic exposure to an irritant at work as a cause of asthma has also been described, but it is not as well accepted as an entity as RADS. Aggravation of pre-existing asthma by work can occur from any exposure as well as stress, physical activity, and temperature/humidity. Unlike the work-related lung diseases such as the pneumoconioses, which cause irreversible fibrosis, work-related asthma is potentially completely reversible if diagnosed soon after onset of symptoms and the patient’s exposure to the etiologic agent ceases. Beginning in the early 1900s, asthma from exposure at work to plant material and metals first began to be reported in the medical literature. In the 1970s, Dr. Jack Pepys from England markedly advanced the identification of etiological agents by developing a practical way to perform specific inhalation challenge testing. The field has continued to advance with the recognition of an increased number of etiological agents, an understanding of the pathophysiology, an understanding of the prognosis and factors associated with a better prognosis, and the initiation of work on the interaction with genetic variability. At least in more developed countries, such as in European countries and the United States, which have implemented controls or banned the use of the mineral dusts (i.e., asbestos, silica) that have caused the most common pneumoconioses, work-related asthma has become a more important cause of new-onset work-related lung disease than the more traditional pneumoconioses.

General Overview

Multiple overviews have been written on work-related asthma, including Dao and Bernstein 2018 from the perspective of an allergist, Tarlo and Lemiere 2014 and Lau and Tarlo 2019 from the perspective of a pulmonologist, and Malo, et al. 2013 in a comprehensive book. Ayres, et al. 2011 describes the economic costs of the disease. Substances that cause work-related asthma have been grouped into high and low molecular weight antigens—animals and plants, and chemicals, respectively. Typically, individuals who become sensitized to a substance at work do so in the first two years of their exposure, but for some it may be many years after first exposure. Some individuals who become sensitized to a substance first develop nasal symptoms (allergic rhinitis) and then progress to occupational asthma. This is more likely with high molecular substances (e.g., grain dust) than a low molecular substance (e.g., toluene diisocyanate). The chance of becoming sensitized to a substance is dose-related but also has a genetic component, since typically only a minority of the workforce will become sensitized. Historically, the highest percentage of individuals affected has been among individuals in research facilities working with mice or rats (as high as 30 percent), and lower percentages in facilities using chemicals such as isocyanates (5–10 percent). Individuals who have become sensitized to a substance at work and then are exposed to the substance may have asthma symptoms at varied points after the exposure: (1) within minutes—an acute onset reaction; (2) 4–8 hours—a late onset reaction; and (3) both within minutes and also hours later—a dual onset reaction. Substances causing work-related asthma are not necessarily unique to the workplace. For example, veterinarians can become allergic to both their own pets and their animal patients, or individuals can be exposed to cleaning agents in both their home and their workplace. Brooks, et al. 1985 describes asthma after an acute exposure to an irritant (RADS), such as the mixture of cleaning products, one containing ammonia and the other bleach, which generates chlorine, or one containing an acid and the other bleach, which generates chloramine. Dumas and Le Moual 2016 reviews the literature of work-related asthma after repeated exposure to lower levels of irritants. Asthma caused by a work exposure, including RADS, has the same symptoms, physiology, and response to asthma medication and pathology as non-work-related asthma. The recognition of work-related asthma requires the health-care provider to ask about the history of onset and situation(s) that aggravate symptoms. Given the general tendency of health-care providers not to ask about work exposures, it is not surprising that the results of epidemiological studies show that work-related asthma is markedly under-diagnosed. The under-diagnosis of work-related asthma is to the detriment of patients, since removal from exposure is a key component of the treatment of work-related asthma.

  • Ayres, J. G., R. Boyd, H. Cowie, and J. F. Hurley. 2011. Costs of occupational asthma in the UK. Thorax 66:128–133.

    Describes the large direct and indirect costs of occupational asthma in the United Kingdom, and how 49 percent of the costs are borne by the individual, 48 percent by government, and only 3 percent by the employer.

  • Brooks, S. M., M. A. Weiss, and I. L. Bernstein. 1985. Reactive airways dysfunction syndrome (RADS). Persistent asthma syndrome after high level irritant exposures. Chest 88:376–384.

    The original description of cases of work-related asthma from an acute exposure to a high level of an irritant.

  • Dao, A., and D. I. Bernstein. 2018. Occupational exposure and asthma. Annals of Allergy Asthma & Immunology 120:468–475.

    A recent review article on work-related asthma written from the perspective of the allergist.

  • Dumas, O., and N. Le Moual. 2016. Do chronic workplace irritant exposures cause asthma? Current Opinion in Allergy and Clinical Immunology 16:75–85.

    A review of the literature on repeated low-level irritant exposure and the type of research needed to confirm the association.

  • Lau, A., and S. M. Tarlo. 2019. Update on the management of occupational asthma and work-exacerbated asthma. Allergy Asthma & Immunology Research 11:188–200.

    A recent review article written from the perspective of the pulmonologist. This review covers all work-related asthma including work-aggravated asthma. Tarlo and Lemiere 2014 provides a review.

  • Malo, J. L., M. Chan-Yeung, and D. I. Bernstein. 2013. Asthma in the Workplace. 4th ed. Boca Raton, FL: CRC Press.

    This is the 4th edition of the most comprehensive single source of material about work-related asthma. Includes basic pathophysiology and genetics, assessment and management, and discussion of specific causal agents. Fifth edition planned for release in 2021.

  • Tarlo, S. M., and C. Lemiere. 2014. Occupational asthma. New England Journal of Medicine 370:640–649.

    An excellent succinct review of new-onset work-related asthma from the perspective of a pulmonologist.

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