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Pathology · Lung Diseases

Anthracosis

Anthracosis

Anthracosis is a type of pneumoconiosis caused by the prolonged inhalation of coal dust. The disease is characterized by the deposition of pigment in the respiratory system and the gradual proliferation of connective tissue.

Lung colorGray-black or slate-gray discoloration of the lung tissue
Primary processPulmonary sclerosis induced by carbon pigment
Complication"Black phthisis" with cavity formation and hemoptysis
HeartRight ventricular hypertrophy (cor pulmonale)
3 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Etiology and pathogenesis

The disease is based on the accumulation of coal dust and the development of sclerosis. The severity of fibrosis directly depends on the type of inhaled coal:

  • Anthracite dust induces the most severe sclerosis.
  • Bituminous coal dust leads to less pronounced changes.
  • Charcoal practically does not cause sclerotic processes.

There is ongoing scientific debate regarding the role of silicon dioxide ($SiO_2$). Some researchers believe that fibrosis is caused exclusively by quartz impurities in coal seams. Domestic specialists note that coal dust possesses its own sclerotic property, although it is noticeably weaker than that of pure silica dust.

Macroscopic changes and morphology

Initial manifestations of the disease are observed predominantly in the lower lung zones, but as it progresses, the pigment distributes evenly across all lobes, giving the organ a characteristic gray-black color.

With pronounced diffuse tissue proliferation, the lungs lose their air content and become dense. In pathological anatomy, this condition is referred to as slate induration (or anthracotic induration). Under the microscope, dust particles are found both freely and inside numerous macrophages. Connective tissue proliferates in the interalveolar septa, as well as around blood vessels and the bronchial tree, forming small anthracotic foci and large nodules.

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Clinical course and severe forms: "Black phthisis"

Pure anthracosis has a much longer and more benign course than silicosis because macrophages effectively eliminate coal particles via the bronchi and the lymphatic system. However, if the dust contains a high amount of silicon dioxide, mixed forms develop—anthracosilicosis (or silicoanthracosis) with massive sclerosis.

Advanced manifestations of the disease are historically referred to as "black phthisis". This form is characterized by the following signs:

  • formation of rounded or irregular cavities in the lungs with crumbly black walls;
  • accumulation of black masses in the disintegrating areas;
  • clinical symptoms accompanied by hemoptysis, resembling tuberculosis;
  • fusion of altered lymph nodes with the trachea and bronchi, carrying a risk of coal content rupture into the respiratory tract.

Associated complications

Massive involvement of the lung tissue inevitably leads to a number of severe consequences:

  • Pronounced pulmonary emphysema.
  • Chronic bronchitis and recurrent focal pneumonia.
  • Necrosis and tissue softening due to circulatory disorders and dust accumulation.
  • Rupture of lymph node contents into the bronchial lumen, which can lead to aspiration, abscess, or gangrene.
  • Development of cor pulmonale (right ventricular hypertrophy) secondary to severe pneumosclerosis.

Briefly: answers to topical questions

What macroscopic and microscopic changes occur in the regional lymph nodes of the lung in anthracosis?

In anthracosis, pronounced macroscopic changes occur in the regional lymph nodes, leading to their adhesion to surrounding tissues.

  • Macroscopic appearance — in severe anthracosis, lymph nodes fuse with the wall of the trachea or bronchi.

A possible complication is the rupture of coal masses from the lymph nodes into the lumen of the bronchial tree, which leads to the aspiration of masses into the lungs and the development of pneumonia, abscess, or gangrene. Microscopic changes in the lymph nodes in anthracosis are not described in the sources.

What is the exact pathogenesis of cor pulmonale development in anthracosis?

In anthracosis, against the background of significant pneumosclerosis and emphysema, right ventricular hypertrophy develops—cor pulmonale. The general outcome of pneumoconiotic processes sequentially involves pneumosclerosis, secondary pulmonary hypertension, and right ventricular hypertrophy; cardiopulmonary failure is possible.

How does the microscopic structure of an anthracotic nodule differ from a silicotic nodule?

An anthracotic nodule is an area of newly formed connective tissue with macrophages; large anthracotic nodes arise from the fusion of smaller foci. A silicotic nodule consists of bundles of connective tissue: in typical nodules, they are arranged concentrically or in a whorled pattern and are hyalinized. All types of silicotic nodules contain many dust particles—freely or inside coniophages.

How to memorize

Anthracosis means Anthracite (black color, slate induration, and black phthisis). Milder than silicosis, but with a risk to the right heart.

Class and exam questions

Why is pure anthracosis milder than silicosis?

Coal dust in pure anthracosis is more efficiently cleared by macrophages through the bronchial tree and lymphatic drainage, which is why the disease progresses more slowly and has a more benign course.

What is slate induration of the lungs?

This is a pathological condition in diffuse anthracotic sclerosis, where the lungs become dense, airless, and acquire a characteristic gray-black (slate) color.

What complications can arise from the rupture of lymph nodes?

Coal masses can rupture into the lumen of the bronchial tree. Their aspiration into the lungs leads to the development of pneumonia, lung abscess, or gangrene.

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What else to study on this topic

  • Differences between anthracite and bituminous coals in experiment
  • Mechanisms of anthracotic nodule formation
  • Differential diagnosis of anthracosis and pulmonary tuberculosis
  • Pathogenesis of cor pulmonale formation in pneumoconioses
  • The role of the macrophage system in coal pigment elimination

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