Occupational asthma

It is caused by the inhalation of harmful nox in the workplace and like all occupational diseases had to appear during work, not before. The proportion of occupational asthma in all asthma diseases ranges from 2% to 15% in different countries. However, it is estimated that this number is underestimated about 5 to 10 times.

Triggering factors:


 * high molecular weight substances (plant and animal proteins, microbial sources);
 * low molecular weight compounds (isocyanates, acid anhydrides, platinum salts);
 * irritant and pharmacological substances (smoke, smoke, fumes - Cl, NH3, insecticides);
 * synthetic organic and inorganic chemicals;
 * disinfectants,

High risk activities: grain handling, woodwork, paramedics, smoke inhalation.

Etiopathogenesis
Asthma is a chronic inflammatory disease of the airways of the lungs. The main cells involved in this process are eosinophils and mast cells, less neutrophils and basophils. Inflammation increases bronchial reactivity, this induces bronchospasm and manifestations of bronchial obstruction. If reversible obstruction or bronchial reactivity or both is caused by occupational exposure, it is occupational bronchial asthma (OA).

Two main types of OA:


 * 1) immunological asthma (sensitization induced);
 * 2) irritant asthma (caused by irritants).

1. Immunological OA

 * It occurs only in a small number of exposed.
 * It occurs after the initial asymptomatic period.
 * The asthmatic response is triggered by substances that the worker has previously tolerated well.
 * Specific immunological response to etiological agents.

High molecular weight substances induce an IgE-mediated response - the detection of specific IgE antibodies. The process of inducing asthma with low molecular weight substances is not yet known. Types of '''immunological responses: I., III. or IV'''.

2. Irritant OA
The whole process is not yet fully known, but neurogenic mechanisms and the release of neurotransmitters probably also play a role. It occurs without a previous period of sensitization and has no specific response to etiological agents. It is formed after exposure to highly irritating substances (dust, aerosol, etc.).

Asthma caused by short-term but high-intensity exposure is called RADS (Reactive Airways Dysfunction Syndrome).

Pathological changes
The disease leads to remodeling of the DC wall (thickening of the bronchial wall due to smooth muscle hypertrophy), the bronchial mucosa is heavily infiltrated by eosinophils and lymphocytes. Goblet cell hyperplasia occurs.

Clinical manifestation
Typical symptoms (shortness of breath, wheezing with a maximum in the expiration, cough, chest tightness) appear at work or at some time in connection with work. Quite often patients report a concomitant occurrence of eye symptoms, rhinitis, a feeling of nasal blockage. They recede during the weekend, holidays or when the work environment changes. When symptoms become chronic, they can completely lose their connection to the work environment.

Diagnosis

 * Spirometric examination - obstructive ventilation disorder;
 * histamine non-specific bronchoprovocation test - decrease in FEV1 by at least 20%; MEF25-75 by at least 30%; 100% increase in resistance;
 * a specific inhalation bronchoprovocation test using available probable workplace allergens;
 * bronchodilation test - evaluation of reversibility of bronchospasm in patients with permanent obstruction;
 * peak expiratory rate (PEF) series - peak-flow meter;
 * elimination and re-exposure test.

Related articles

 * Astma