(See also Overview of Environmental Pulmonary Disease.)
Occupational asthma is development of asthma (or worsening of preexisting asthma) by occupational exposure (1). Symptoms typically develop over months to years because of sensitization to an allergen encountered in the workplace. Once sensitized, the worker invariably responds to much lower concentrations of the allergen than that which initiated the response. There two types of occupational asthma—one has an immune-mediated mechanism of action and the other a nonimmune-mediated mechanism. Occupational asthma accounts for 10% to 25% of adult-onset asthma diagnosed by medical providers (2, 3).
Numerous chemicals and other agents that may be encountered in the workplace have been identified as causing occupational asthma. A list of workplace airborne allergens that have been associated with occupational asthma can be found at the Commission des normes, de l'équité, de la santé et de la sécurité du travail.
Several other airway diseases caused by inhalational workplace exposures can be distinguished from occupational and occupationally aggravated asthma.
In reactive airways dysfunction syndrome (RADS), which is nonallergenic, people with no history of asthma develop persistent, reversible airway obstruction after acute overexposure to irritant dust, fumes, or gas. Airway inflammation persists even after removal of the acute irritant, and the syndrome is indistinguishable from asthma.
In reactive upper airways syndrome, upper airway (ie, nasal, pharyngeal) mucosal symptoms develop after acute or repeated exposure to airways irritants.
In irritant-associated vocal cord dysfunction, which mimics asthma, abnormal apposition and closure of the vocal cords, especially during inspiration, occur after acute irritant inhalation.
In industrial bronchitis (irritant-induced chronic bronchitis), bronchial inflammation causes cough after acute or chronic irritant inhalation.
In bronchiolitis obliterans, bronchiolar damage occurs after acute inhalation of gases (eg, anhydrous ammonia). The 2 major forms are proliferative and constrictive. The constrictive form is more common and may or may not be associated with other forms of diffuse lung injury. Recently, cases of bronchiolitis obliterans have been reported in workers exposed to the chemical diacetyl during the manufacture of butter-flavored microwave popcorn. So-called popcorn workers’ lung may occur in workers exposed to other flavorings and in some consumers exposed to this chemical.
Other terms sometimes used to classify forms of asthma in the workplace include work-exacerbated asthma, irritant-induced asthma, and occupational nonasthmatic eosinophilic bronchitis (4).
1. Henneberger PK, Redlich CA, Callahan DB, et al: An Official American Thoracic Society Statement: Work-exacerbated asthma. Am J Respir Crit Care Med 184(3):368–378, 2011. doi: 10.1164/rccm.812011ST
2. Dykewicz MS: Occupational asthma: current concepts in pathogenesis, diagnosis, and management. J Allergy Clin Immunol 123(3):519–528; quiz 529–530, 2009. doi: 10.1016/j.jaci.2009.01.061
3. Maestrelli P, Boschetto P, Fabbri LM, Mapp CE: Mechanisms of occupational asthma. J Allergy Clin Immunol 123(3):531–542; quiz 543–544, 2009. doi: 10.1016/j.jaci.2009.01.057
4. Tarlo SM, Malo JL, Third Jack Pepys Workshop on Asthma in the Workplace Participants: An official ATS proceedings: Asthma in the workplace: the Third Jack Pepys Workshop on Asthma in the Workplace: Answered and unanswered questions. Proc Am Thorac Soc 6 (4):339–349, 2009. doi: 10.1513/pats.200810-119ST.
Occupational asthma is caused by both immune- and non–immune-mediated mechanisms.
Immune-mediated mechanisms involve IgE- and non–IgE-mediated hypersensitivity to workplace allergens. Hundreds of occupational allergens exist, ranging from low molecular weight chemicals to large proteins. Examples include grain dust, proteolytic enzymes used in detergent manufacturing, red cedar wood, isocyanates, formalin (rarely), antibiotics (eg, ampicillin, spiramycin), epoxy resins, and tea. Occupational asthma is the most common occupational-related lung disease diagnosed in developed countries (1).
Non–immune-mediated inflammatory mechanisms involve direct irritation of the respiratory epithelium and upper airway mucosae. Common causes include exposure to chlorine gas, hydrochloric acid, and anhydrous ammonia.
US military personnel deployed to Iraq and Afghanistan have been found to be at increased risk for asthma (and also bronchiolitis obliterans). Possible causes include emissions from open-air burn pits and industrial fires, desert dust, and vehicular exhaust.
Symptoms of occupational asthma include shortness of breath, chest tightness, wheezing, and cough, often with upper respiratory symptoms such as sneezing, rhinorrhea, and tearing. Upper airway and conjunctival symptoms may precede the typical symptoms of asthma by months or years. Symptoms may develop during work hours after specific dust or vapor exposure but often do not become apparent until several hours after leaving work, thereby making the association with occupational exposure less obvious. Nocturnal wheezing may be the only symptom. Often, symptoms disappear on weekends or during vacations, although with ongoing exposure, temporal exacerbations and relief become less apparent.
Diagnosis of occupational asthma depends on recognizing the link between workplace allergens and asthma. Diagnosis is suspected on the basis of an occupational history of allergen exposure. A safety data sheet (mandatory at all work sites) can be used to identify potential allergens, and substances listed can be used to direct immunologic testing (eg, skin prick, puddle, or patch testing) of suspected antigens to demonstrate that an agent in the workplace is affecting a worker. An increase in bronchial hyperresponsiveness after exposure to the suspected antigen is also helpful in making the diagnosis.
In difficult cases, a carefully controlled inhalation challenge test done in the laboratory confirms the cause of the airway obstruction. Such procedures should be done only at centers experienced in inhalation challenge testing and capable of monitoring and treating the sometimes severe reactions that can occur.
Pulmonary function tests or peak expiratory flow measurements that show decreasing airflow during work are further evidence that occupational exposure is causative.
Methacholine challenge tests can be used to establish the degree of airway hyperreactivity. Sensitivity to methacholine may decrease after exposure to the occupational allergen has ceased.
Differentiation from idiopathic asthma is generally based on the pattern of symptoms, demonstration that allergens are present in the workplace, and the relationship between exposure to allergens and symptoms and physiologic worsening.
(See also Drug Treatment of Asthma.)
Treatment of occupational asthma is the same as that for idiopathic asthma, including inhaled bronchodilators and corticosteroids. Treatment should also include removal of the patient from ongoing exposure to the causative agent.
Dust suppression is essential. However, elimination of all instances of sensitization and clinical disease may not be possible. Once sensitized, patients with occupational asthma may react to extremely low levels of airborne allergen. Patients who return to environments in which the allergen persists generally have a poorer prognosis, with more respiratory symptoms, more abnormal lung physiology, a greater need for drugs, and more frequent and severe exacerbations. Whenever possible, a symptomatic person should be removed from a setting known to cause symptoms. If exposure continues, symptoms tend to persist. Occupational asthma can sometimes be cured if it is diagnosed early and exposure ceases.
Occupational asthma can be non–immune-mediated or develop after months or years of sensitization.
Consider reviewing workplace safety data sheets for potential allergens if workers develop new respiratory symptoms.
Consider immunologic testing and an inhalation challenge test.
Treat as for asthma and remove the patient from the environment containing the allergen.