10. Occupational asthma

https://doi.org/10.1016/j.jaci.2007.08.005Get rights and content

A diversity of airborne dusts, gases, fumes, and vapors can induce dose-related respiratory symptoms in individuals exposed in the workplace. These agents can cause annoyance reactions, irritational effects, sensitization, or the induction of corrosive changes in the respiratory tract, depending on their composition, concentration, and duration of exposure. The prevalence of occupational asthma (OA) ranges from 9% to 15% of the asthmatic population. Factors that might influence the development of OA include the work environment, climatic conditions, genetic proclivities, tobacco and recreational drug use, respiratory infection, bronchial hyperresponsiveness, and endotoxin exposure. Pathogenetically, new-onset OA can be allergic or nonallergic in origin. The allergic variants are usually caused by high-molecular-weight allergens, such as grain dust and animal or fish protein. Selected low-molecular-weight agents are also capable of inducing allergic OA. Symptoms ensue after a latent period of months to years. Nonallergic OA can be precipitated by a brief high-level exposure to a potent irritant. Symptoms occur immediately or within a few hours of the exposure. Once the diagnosis of allergic OA is established, the worker should be removed from further exposure in the workplace. In nonallergic OA the worker can return to work if the exposure was clearly a nonrecurring event. If the diagnosis is made in a timely fashion, most workers experience improvement. Prevention is the best therapeutic intervention.

Section snippets

Prevalence

With few notable exceptions, there are no long-term prospective longitudinal studies of OA. There are a number of retrospective observational studies dealing with specific industries. Nearly all epidemiologic studies have relied on subjective data in identifying asthma. Case definition has been variable in different parts of the world, making it difficult to ascertain whether minimally symptomatic, undiagnosed non-OA was present before the incriminated work-related trigger. Equally problematic

Genetic and other factors

Atopy, asthma, and BHR are determined by multiple interacting genetic and environmental influences.5 Atopic individuals are more likely to become sensitized and have OA when exposed to high-molecular-weight (HMW) allergens. The data are less clear with low-molecular-weight (LMW) agents. The incidence of OA associated with exposure to diisocyanates, western red cedar, or the acid anhydrides do not appear to be influenced by the worker's atopic state. An increased incidence of OA in those with

Pathogenesis of OA

There are 2 basic variants of OA based on pathogenesis: allergic and nonallergic variants. The allergic variant can be further divided into classic IgE-mediated and polyimmunologic forms. The nonallergic variant can be divided into reactive airways dysfunction syndrome (RADS), pharmacologic bronchoconstriction, and reflex bronchospasm.1

The development of new-onset allergic OA requires a latent period during which sensitization develops (ie, months or years). Exposure usually involves inhalation

Diagnosis and treatment

The medical history is a key element in the initial evaluation of OA. The history should elicit the features of a work-related airway disease and provide clues to the linkage to 1 or more suspect work exposures. As expected, the history has a high degree of sensitivity (87%) but a low specificity (22%) for the diagnosis of OA.24 Patient recall of past symptoms, illnesses, and medical care is often unreliable and inconsistent. The physical examination should be carried out to accurately record

Prevention, management, and diagnosis

Adoption and enforcement of optimum industrial hygiene measures in the workplace is the only effective means to reduce or completely eliminate ambient levels of known allergens or respiratory irritants. Employers must mandate that employees use properly fit-tested and approved respirators where appropriate (spray painters using catalyzed paints) and install effective exhaust systems or develop enclosed, automated robotic processes. Management of OA is identical to that of non-OA, with the

References (28)

  • R. Piipari et al.

    Agents causing occupational asthma in Finland in 1986-2002: cow epithelium bypassed by moulds from moisture-damaged buildings

    Clin Exp Allergy

    (2005)
  • F.D. Martinez

    Gene-environment interactions in asthma

    Proc Am Thorac Soc

    (2007)
  • C.E. Mapp

    Genetics and the occupational environment

    Curr Opin Allergy Clin Immunol

    (2005)
  • P.A.B. Wark et al.

    Asthma exacerbations. 3: pathogenesis

    Thorax

    (2006)

    • Cited by (49)

    • Cluster analysis of phenotypes, job exposure, and inflammatory patterns in elderly and nonelderly asthma patients

      2024, Allergology International

    • Chemicals inhaled from spray cleaning and disinfection products and their respiratory effects. A comprehensive review

      2020, International Journal of Hygiene and Environmental Health
      Citation Excerpt :

      Irritative chemicals can be divided into corrosive or reactive irritants, which may damage tissue on the cellular level, and sensory irritants that gives the feeling of irritation through activation of the trigeminus nerve but do not damage the tissue (Nielsen and Wolkoff, 2017). Inhalation of corrosive or reactive chemicals may induce asthma (Bardana, 2008; Le Moual et al., 2018). In Tables 2 and 3, corrosive or reactive chemical irritants include the strong bases sodium and potassium hydroxide, the base ammonia, the corrosive chlorine releaser sodium hypochlorite, the strong acids sulfuric acid and methanesulfonic acid, and the oxidizing chemical hydrogen peroxide.

    • Hypersensitivity Reactions in the Respiratory Tract

      2018, Comprehensive Toxicology: Third Edition

    • Pathogenesis and Disease Mechanisms of Occupational Asthma

      2011, Immunology and Allergy Clinics of North America
      Citation Excerpt :

      Changes reflecting airway remodeling include loss of ciliated epithelial cells, increased mucous secretion by goblet cells, basement membrane thickening due to subepithelial fibrosis with fibroblast and myelofibroblast activation, and hypertrophy of airway smooth muscle cells.6 Compendia of more than 250 specific causative agents can be found in other publications or on special Web sites,9–12 and these agents can be generally subdivided based on size as HMW (>10,000 Da) or LMW (<1000 Da). HMW allergens are macromolecules capable of inducing a specific IgE antibody response and are usually associated with workplace sensitization to animals, plants, and/or microorganisms.

    • Definitions and Classification of Work-Related Asthma

      2011, Immunology and Allergy Clinics of North America
      Citation Excerpt :

      On the other hand, it is not possible to demonstrate or rule out that workplace exposure to common allergens has contributed to the initiation of immunologic OA in subjects without preexisting asthma or atopic status. It is now widely accepted that exposure to very high levels of an irritant gas, fume, aerosol, or vapor at work can induce the development of asthma.4,10,12,64–69 Recent guidelines4,64,65 and review articles12,66–69 have acknowledged that the most definitive form of asthma induced by respiratory irritants is RADS, which refers to the acute onset of asthma after a single high-level irritant exposure.38

    • Respiratory sensitization: Advances in assessing the risk of respiratory inflammation and irritation

      2011, Toxicology in Vitro
    View all citing articles on Scopus

    Disclosure of potential conflict of interest: E. J. Bardana has served as an expert witness in civil litigation and worker's compensation independent medical examinations for the states of Alaska, Washington, Idaho, and Montana.

    View full text
    Copyright © 2008 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.