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Occupational
asthma is reversible airway obstruction that develops after months
to years of sensitization to an allergen encountered in the workplace.
Symptoms are dyspnea, wheezing, cough, and, occasionally, upper
respiratory allergic symptoms. Diagnosis is based on occupational
history, including assessment of job activities, allergens in the
work environment, and a temporal association between work and symptoms.
Allergen skin testing and provocative inhalational challenge may
be used in specialized centers but are usually unnecessary. Treatment
involves removing the person from the environment and using asthma
drugs as needed.
Occupational asthma is development of asthma in a worker who has no previous history of asthma. Symptoms typically develop over months to years from 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. Occupational asthma differs from occupationally aggravated asthma, which is an exacerbation or worsening of asthma in workers with previously existing asthma as a result of single or repeated workplace exposures to pulmonary irritants such as dusts and fumes. Occupationally aggravated asthma, which is more common than occupational asthma, generally subsides with reduction of exposure and appropriate asthma treatment. It has a better prognosis and does not require the same level of clinical investigation of specific triggering allergens.
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 possibly in some consumers exposed to this chemical.
Etiology
Occupational asthma is caused by both immune- and non–immune-mediated mechanisms. Immune mechanisms involve IgE- and non–IgE-mediated hypersensitivity to workplace allergens. Hundreds of occupational allergens exist, ranging from low mol wt 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.
Non–immune-mediated inflammatory mechanisms cause direct irritation of the respiratory epithelium and upper airway mucosae.
Symptoms and Signs
Symptoms 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 asthmatic symptoms 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
Diagnosis depends on recognizing the link between workplace allergens and asthma. Diagnosis is suspected on the basis of an occupational history of allergen exposure. A materials safety data sheet 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 person. 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.
Treatment
Treatment is the same as for idiopathic asthma, including inhaled bronchodilators and corticosteroids (see Asthma: Drug therapy). Treatment should also include removal of the patient from ongoing exposure to the causative agent.
Prevention
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 produce symptoms. If exposure continues, symptoms tend to persist. Occupational asthma can sometimes be cured if it is diagnosed early and exposure ceases.
Last full review/revision June 2008 by Lee S. Newman, MD
Content last modified June 2008
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