Pneumoconiosis is a group of diseases characterized by a diffuse fibrotic reaction in the lungs induced by inhalation of organic or inorganic particulate matter and chemical fumes and vapors. The pathogenesis of the fibrosis is through the release of fibrogenic chemical mediators.

Although the end-point is fibrosis, the pattern and location varies with the type.

Coal Workers' Pneumoconiosis: The pathology ranges from anthracosis (carbon deposited in lung macrophages and lymphatics) to progressive massive fibrosis. The fibrosis occurs primarily in the upper zones of the lungs.

The pathologic lesions are of 3 types



There are 3 basic pathologic patterns of response to silica

Silica is ingested by macrophages. The activated macrophages release powerful chemical mediators like interleukin-1 and tissue necrosis factor which cause fibrosis. nodular fibrosis and larger, dense scars occur primarily in the upper zones of the lung. Silica is present in the nodules.

Radiological  features of Silicosis are:

PFT features of Silicosis

Occupation/Exposure for Silicosis:


  1. The primary pathology in the lung is diffuse interstitial fibrosis which early on predominates in the lower zones of the lungs. The histologic changes vary from bronchiolocentric fibrosis to honeycomb lung. The asbestos body is a unique feature of this type of fibrosis. Asbestos bodies, which are the hallmark of exposure to asbestos, are found within the fibrosis or alveolar spaces or occasionally in foreign-body giant cells. An asbestos body consists of a central core fiber of asbestos that is coated with an iron-protein-mucopolysaccharide layer forming a golden-brown, segmented, dumb bell appearance. Iron stains, e.g., Prussian blue, can make detection easy
  2. Pleural plaques (circumscribed areas of fibrosis) are the most common manifestation of asbestosis.
  3. High incidence of mesothelioma and bronchogenic carcinoma.

Radiological features of Asbestosis

PFT features of Asbestosis:

Occupation/Exposure for Asbestosis:

Berylliosis: Beryllium induces cell-mediated immunity resulting in non-caseating granulomas scattered throughout the lungs and hilar lymph nodes. The granulomas "burn out," becoming fibrotic and forming fine nodular densities throughout the parenchyma.  Clinically and radiologically resembles Sarcoidosis. In the past