Definition and etiology
Chronic occupational bronchitis (COB) is an inflammatory bronchial disease of non-infectious origin caused by prolonged exposure to industrial dust or harmful chemical agents. Unlike bronchial asthma, the disease is not allergic in nature: the damaging agents do not have a sensitizing effect, but exert a direct irritant and cytotoxic effect.
Key etiological factors:
- irritant chemical substances (gases, vapors, aerosols);
- coarse industrial dust, including fibrogenic dust;
- duration of exposure — the pathology develops over years and decades.
Risk groups: miners, factory workers exposed to unfavorable workshop air conditions, smokers (as a contributing factor).
Stages of pathogenesis
Two principal stages are distinguished in the pathogenesis of COB:
- Non-infectious stage — the occupational bronchial lesion proper.
- Secondary infection stage — pertains to complications of the disease.
Upper respiratory tract involvement
The primary link in pathogenesis is catarrhal inflammation of the mucous membrane in response to irritants and dust. The process then progresses through stages:
- Hypertrophy of the nasopharyngeal mucosa with hypersecretion and symptoms resembling ARVI;
- Atrophic changes in chronically inflamed tissues;
- development of the clinical picture of rhinopharyngolaryngitis.
At this stage, a decline in upper respiratory tract defense functions is already noted, making the worker vulnerable to further damage to the lower airways.
Trophic disorders of the tracheobronchial tree
The key stage is damage to the tracheobronchial tree (TBT). The following processes develop:
- Destruction of the ciliated epithelium under the action of toxins — the phenomenon of "bronchial baldness." Normally, cilia provide mucociliary clearance by propelling foreign particles upward; in COB, this mechanism is lost.
- Decrease in the production of local immunity factors: α1-antitrypsin, surfactant, lysozyme, interferons; reduction in the number of T-lymphocytes and macrophages.
- Decreased bronchial moisture — incoming particles penetrate freely into the distal parts of the lungs.
The result is a sharp drop in barrier function and susceptibility to any infection.
Dyscrinia and dyskinesia syndrome
Dyscrinia is a characteristic sign indicating the development of COB. It develops due to dysfunction of goblet cells:
- Hypercrinia — in the early stages, irritated goblet cells actively produce excess sputum; clinically manifested as a severe cough with sputum, especially in the mornings;
- Hypocrinia — upon exhaustion and death of goblet cells, mucus production drops sharply.
The stage concludes with the development of dyskinesia — impaired normal outflow of secretion and foreign substances from the TBT. Elimination of damaging agents becomes impossible, creating a vicious circle.
Bronchial obstruction, fibrosis, and complications
Persistent clearance impairment and chronic inflammation lead to the development of bronchial obstruction. In the early stages, the process is reversible: bronchial patency is reduced due to edema, hypersecretion, and spasm, but morphological changes are not yet present.
With continued exposure to the harmful factor, bronchial fibrosis develops — an irreversible morphological change in the wall with collapse of small bronchi and the formation of non-functioning fibrotic structures.
Against the background of impaired clearance, secondary infection naturally occurs. Main complications:
- Pulmonary emphysema — distension of the terminal parts of the TBT during difficult expiration;
- COPD (chronic obstructive pulmonary disease) — the ultimate outcome of uncontrolled occupational bronchitis, according to the GOLD concept;
- recurrent bronchopulmonary infections.
Key points
- COB is a non-infectious and non-allergic bronchial inflammation caused by dust and chemical irritants.
- Pathogenesis includes the non-infectious stage and the secondary infection stage.
- The lesion begins with catarrhal inflammation, hypertrophy, and atrophy of the upper respiratory mucosa.
- Destruction of the ciliated epithelium ("bronchial baldness") disrupts mucociliary clearance.
- Production of α1-antitrypsin, surfactant, lysozyme, and interferons decreases, and the levels of T-lymphocytes and macrophages drop.
- Dyscrinia is phased: hypercrinia is replaced by hypocrinia upon the death of goblet cells.
- Bronchial obstruction is reversible, whereas bronchial fibrosis with collapse is irreversible.
- Natural outcomes are pulmonary emphysema and COPD.