Occupational bronchial asthma

Occupational asthma is a reversible airway obstruction that develops after months or years of sensitization to an allergen that a person encounters in the workplace. Symptoms of occupational asthma include shortness of breath, wheezing, coughing, and sometimes allergic symptoms of the upper respiratory tract. Diagnosis is based on an occupational history, including an examination of the nature of the job, allergens in the work environment, and the temporal association between the job and the symptoms.

Skin allergy testing and inhalation challenge tests may be used in specialized centers but are not usually required. Treatment of occupational asthma involves removing the person from the environment and using asthma medications as needed.

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Causes of occupational bronchial asthma

Occupational asthma is the development of asthma in workers who have no previous history; symptoms of occupational asthma typically develop over months to years following sensitization to allergens encountered in the workplace. Once sensitized, the worker invariably responds to much lower concentrations of the allergen than that which initiated the reaction. Occupational asthma is distinguished from occupational aggravation of asthma, which is an exacerbation or worsening of asthma in workers with previously clinical or subclinical disease following single or repeated exposure to workplace pulmonary irritants such as dusts and fumes. Occupational aggravation of asthma, which is more common than occupational asthma, usually improves with reduction in exposure and adequate treatment of the asthma. It has a better prognosis and does not require a high level of clinical research on trigger allergens.

Several other respiratory diseases caused by inhalational exposures in the workplace must be distinguished from occupational asthma and occupationally related aggravation of asthma.

In nonallergen-induced reactive airways dysfunction syndrome (NADS), people without a history of asthma develop persistent, reversible airway obstruction after acute overexposure to an irritant dust, smoke, or gas. Airway inflammation persists even after the acute irritant is removed, and the syndrome is indistinguishable from asthma.

In upper airway reactivity syndrome, symptoms develop in the mucous membrane of the upper airway (i.e., nasal, pharyngeal area) after acute or repeated exposure to airway irritants.

In irritant-induced vocal cord dysfunction, a condition that resembles bronchial asthma, there is an abnormal closing and closure of the vocal cords, especially during inspiration, following acute irritant inhalation.

In industrial bronchitis (irritant-induced chronic bronchitis), bronchial inflammation leads to the development of cough after acute or chronic exposure to inhaled irritants.

In obliterative bronchiolitis, acute bronchiolar damage develops after acute inhalation exposure to gases (eg, ammonium anhydride). Two main forms are known - proliferative and constrictive. The constrictive form is more common and may or may not be associated with other forms of diffuse lung damage.

Occupational asthma is caused by both immune and non-immune mechanisms. Immune mechanisms include IgE- and non-IgE-mediated hypersensitivity to workplace allergens. There are hundreds of occupational allergens, ranging from low molecular weight chemicals to large proteins. Examples include grain dust, proteolytic enzymes used in detergent manufacture, cedar wood, isocyanates, formalin (rarely), antibiotics (e.g., ampicillin, spiramycin), epoxy resins, and tea.

"Non-immunomediated" inflammatory mechanisms responsible for occupational respiratory diseases cause direct irritation of the respiratory epithelium and mucous membrane of the upper respiratory tract.

Symptoms of occupational asthma

Symptoms of occupational asthma include shortness of breath, chest tightness, wheezing, and coughing, often with symptoms of upper airway irritation such as sneezing, rhinorrhea, and runny nose. Upper airway and conjunctival symptoms may precede typical asthma symptoms by months or years. Symptoms of occupational asthma may develop during work hours after exposure to certain dusts or vapours, but often may not be apparent for several hours after work, making the association with an occupational allergen less obvious. Nocturnal wheezing may be the only symptom. Symptoms often disappear at weekends or during vacations, although with continued exposure to allergens such temporary exacerbations and remissions become less obvious.

Diagnostics of occupational bronchial asthma

The diagnosis of occupational asthma depends on the identification of a link between workplace allergens and clinical asthma. The diagnosis is suspected based on occupational history and exposure to the allergen. The Material Safety Data Sheet can be used to list potential allergens and to confirm the diagnosis when immunological tests (e.g., skin prick, wash, or patch tests) performed with suspected antigens demonstrate that the antigen present in the workplace is causative. An increase in bronchial hyperreactivity after exposure to the suspected antigen can also be used to clarify the diagnosis.

In difficult cases, a carefully controlled inhalation test performed in a laboratory confirms the cause of the airway obstruction. Such procedures should be performed in clinical centers experienced in inhalation testing and able to monitor the sometimes severe reactions that may occur. Pulmonary function tests or peak flow measurements that show decreased airflow during work are another clue that occupational factors are 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 ceases.

Differential diagnosis of occupational asthma from idiopathic asthma is usually based on the relationship of symptoms, identification of allergens in the workplace, and the relationship between allergen exposure, symptoms, and physiological impairment.

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Treatment of occupational bronchial asthma

Treatment for occupational asthma is the same as for idiopathic asthma, including inhaled bronchodilators and glucocorticoids.

How is occupational asthma prevented?

Occupational asthma is prevented by dust control. However, eliminating all sensitizing substances is probably not possible. Once patients with occupational asthma become sensitized, they may react to extremely low levels of inhaled allergen. Those who return to an environment in which the allergen persists generally have a poorer prognosis, more respiratory symptoms, more changes in pulmonary physiology, greater need for medications, and more frequent and severe exacerbations. Whenever possible, the symptomatic person should be removed from the environment in which symptoms occur. If exposure continues, symptoms tend to persist. Occupational asthma can sometimes be cured if it is diagnosed early and exposure is stopped.