5. Coal worker’s pneumoconiosis – etiology, pathogenesis, clinical manifestations, diagnosis, differential diagnosis, treatment, medical expertise.

Introduction

Coal worker's pneumoconiosis (CWP) is a chronic fibrosing and nodular lung disease caused by long-term inhalation of coal dust, mainly in underground mining. Its course ranges from asymptomatic radiographic changes to progressive massive fibrosis and respiratory failure. This note covers the causes, mechanism, clinical picture, diagnosis, differential diagnosis, treatment and expert assessment of the disease.

Etiology and pathogenesis

The disease follows prolonged, cumulative exposure to respirable coal dust, usually over many years, and the risk rises with the total dust dose. Coal dust is mainly carbon, often with a variable free silica (quartz) content, and the silica fraction increases its fibrogenic potential. Smoking adds to airway damage and worsens the clinical course.

1. Particles of about 2\text{–}5\,\mu\text{m} reach the terminal and respiratory bronchioles and the alveoli.
2. Alveolar macrophages engulf the particles. Dust is cleared by the muco-ciliary escalator (larger particles) or transported by lymphatics to hilar and mediastinal lymph nodes, where it accumulates.
3. Dust-laden macrophages die or release cytokines (such as IL-1 and TNF-α) and fibroblast growth factors. This stimulates fibroblast proliferation and collagen deposition.
4. Dust macules form around respiratory bronchioles, with focal emphysema (dust-related peribronchiolar damage) next to them.
5. Fibrosis compresses the small pulmonary arterioles (arteriolar strangulation). This raises pulmonary vascular resistance and, in advanced disease, leads to pulmonary hypertension and cor pulmonale.
6. In some workers the nodules coalesce into conglomerate masses, called progressive massive fibrosis (PMF). The mechanism is not fully understood. PMF is related to ongoing dust exposure and can progress even after exposure stops.