Occupational bronchial asthma

Occupational bronchial asthma is reversible airway obstruction, which develops after months and years of sensitization to an allergen that a person encounters in the workplace. Symptoms of occupational bronchial asthma are shortness of breath, wheezing, coughing and, sometimes, allergic symptoms of the upper respiratory tract. The diagnosis is based on a professional history, including research on the nature of work, allergens in the work environment and the temporary association between work and symptoms.

Skin allergic tests and provocative inhalation tests can be used in specialized centers, but are usually not required. Treatment of occupational bronchial asthma involves the removal of a person from the environment and the use of anti-asthmatic drugs as needed.

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The causes of occupational bronchial asthma

Occupational bronchial asthma is the development of bronchial asthma in workers who do not have any previous history; the symptoms of occupational bronchial asthma typically develop within months and years due to sensitization to allergens that the patient encounters in the workplace. Once sensitized, the worker invariably responds to much lower concentrations of the allergen than the one that started the reaction. Occupational bronchial asthma is different from the professionally conditioned deterioration of bronchial asthma, which is an exacerbation or worsening of bronchial asthma in workers who previously had a clinical or subclinical disease, as a result of a single or multiple exposure to pulmonary irritants, such as dust and vapors. The professionally conditioned deterioration of bronchial asthma, which occurs more often than occupational bronchial asthma, decreases usually with reduced exposure and adequate asthma treatment. It has the best prognosis and does not require a high level of clinical trials of trigger allergens.

Several other respiratory diseases caused by inhalation effects in the workplace should differ from occupational bronchial asthma and professionally conditioned deterioration of bronchial asthma.

In the syndrome of reactive airway dysfunction (RDDP), which is not due to the effect of an allergen, in people without an anamnesis of bronchial asthma, constant, reversible airway obstruction develops after acute excessive exposure to irritating dust, smoke or gas. Inflammation of the respiratory tract remains even after the removal of an acute irritant, and the syndrome is indistinguishable from bronchial asthma.

In the syndrome of reactivity of the upper respiratory tract in the mucosa of the upper respiratory tract (i.e., the nasal, pharyngeal region), symptoms develop after acute or repeated exposure to respiratory tract irritants.

When the dysfunction of the vocal cords, a condition that is similar to bronchial asthma, is caused by the irritant, pathological closure and closure of the vocal cords occurs, especially during inspiration, after acute irritating inhalation.

With industrial bronchitis (caused by an irritant chronic bronchitis) bronchial inflammation leads to the development of cough after acute or chronic effects of inhalation stimuli.

With obliterating bronchiolitis, after acute inhalation exposure to gases (eg, ammonium anhydride), acute bronchiolar damage develops. Two main forms are known: proliferative and constrictive. The constrictive form occurs more often and may or may not be associated with other forms of diffuse pulmonary involvement.

Professional bronchial asthma is caused by both immune and non-immune mechanisms. Immune mechanisms include IgE and non-1gE mediator hypersensitivity to allergens in the workplace. There are hundreds of professional allergens, in the range of chemicals of low molecular weight to large proteins. An example is grains dust, proteolytic enzymes used in the production of detergents, cedarwood, isocyanates, formalin (rarely), antibiotics (eg, ampicillin, spiramycin), epoxy resins and tea.

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

Symptoms of professional bronchial asthma

Symptoms of occupational bronchial asthma include shortness of breath, chest tightness, wheezing and coughing, often with symptoms of irritation of the upper respiratory tract such as sneezing, rhinorrhea and runny nose. Symptoms of upper respiratory tract and conjunctival can precede typical asthmatic symptoms for months and years. Symptoms of occupational bronchial asthma may develop during working hours after exposure to a specific dust or release of steam, but often may not be apparent for several hours after the end of the work, thus making association with a professional allergen less obvious. The only symptom may be night rales. Often the symptoms disappear on weekends or during the holidays, although with continued contact with allergens such temporary exacerbations and remissions become less obvious.

Diagnosis of occupational bronchial asthma

The diagnosis of "occupational bronchial asthma" depends on the identification of the link between allergens in the workplace and clinical bronchial asthma. The diagnosis is suspected on the basis of a professional history and exposure to an allergen. The Material Safety Data Sheet can be used to list potential allergens and confirm the diagnosis when immunological tests (for example, skin injections, irrigation or application tests) performed with suspected antigens demonstrate that the antigen present in the workplace causes the disease. An increase in bronchial hyperreactivity after exposure to a suspected antigen can also be taken into account in making the diagnosis more precise.

In difficult cases, a carefully controlled inhalation test performed in the laboratory confirms the cause of airway obstruction. Such procedures should be administered at clinical centers with experience in performing inhalation tests and capable of tracking sometimes severe reactions that may occur. Lung function tests or peak flowmetry that show a decrease in airflow during work is another sign that occupational factors are causal. Provocative tests with methacholine may be used to establish the degree of increased reactivity of the airways. The sensitivity to methacholine may decrease after exposure to a professional allergen.

Differential diagnosis of occupational bronchial asthma with idiopathic bronchial asthma is usually based on the correlation of symptoms, the detection of allergens in the workplace and the relationship between allergen exposure, symptoms and physiological deterioration.

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Treatment of occupational bronchial asthma

Treatment of occupational bronchial asthma is the same as with idiopathic bronchial asthma, including inhaled bronchodilators and glucocorticoids.

How is professional bronchial asthma prevented?

Prevented occupational bronchial asthma with the help of dust removal. However, the removal of all sensitizing substances is probably not possible. After patients with occupational bronchial asthma become sensitized, they can respond to extremely low levels of an inhaled allergen. Those who return to the environment in which the allergen persists, generally have a poorer prognosis, more respiratory symptoms, more pronounced changes in pulmonary physiology, greater need for drugs and more frequent and severe exacerbations. If possible, a person who has symptoms should be removed from the environment where he has symptoms. If the effect continues, the symptoms tend to persist. Occupational bronchial asthma can sometimes be cured if it is diagnosed early and the effect of the factor stops.