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Pulmonary Pathology Online

Pathology of Pneumoconiosis

 Dr Sampurna Roy MD    

 

The pneumoconioses are diseases caused by the inhalation of inorganic dusts and represent a subset of occupational lung disease, which also includes disorders caused by the inhalation of gases, vapors, and organic material.

The many forms of pneumoconiosis have specific names, depending on the substance inhaled (Example: Silicosis, asbestosis, talcosis).

In certain instances the offending agent is uncertain and often the occupation is simply mentioned (Example: "arc welder’s lung" ).

Historically, occupations were recognized as predisposing to lung disease before an etiologic agent was recognized.  

Pneumoconiosis may be classified as either fibrotic or nonfibrotic, according to the presence or absence of fibrosis.  

Silicosis, coal worker pneumoconiosis, asbestosis, berylliosis, and talcosis are examples of fibrotic pneumoconiosis.

Siderosis, stannosis,and baritosis are nonfibrotic forms of pneumoconiosis that result from inhalation of iron oxide, tin oxide, and barium sulfate particles, respectively.

Two major issues complicate the etiology of pneumoconioses:

1) First is the variety of dusts to which the sufferer may have been exposed.

Often workers exposed to inorganic dusts work in several occupations. It is not unusual for a gold miner, for example, to become a coal miner.

In addition, mining of a particular material may generate other dusts.

The best single example of this is gold mining, where miners’ lesions are due to inhalation not of gold but of quartz (silica) from the rock in which the gold is embedded.

2) Second is the difficulty in judging the relative contributions of smoking and occupational dusts to respiratory impairment, since many workers smoke cigarettes.

The most important pathogenetic feature of inhaled dusts, that is their ability to produce fibrosis, is variable.

Thus small amounts of silica or asbestos may produce extensive fibrosis, but coal and iron are weakly fibrogenic.

In general, lung lesions reflect the dose and size of the particle delivered to the lung.

The dose is a function of the amount of dust in the ambient air and the time spent working in the environment.

It is often difficult to calculate the dose because it is unusual for persons to work in precisely the same environmental conditions throughout their working lives.

Since particles are often irregular, it is important to express size as aerodynamic particle diameter, a parameter that describes the way the particle moves in air.

The aerodynamic particle diameter determines where the inhaled dusts deposit in the lung, the most dangerous being those that reach the peripheral part of the lung, the smallest bronchioles and the acini.

The great majority of large particles (more than 10 micrometer), are filtered by the nasopharynx and never reach the lower respiratory tract.

Most particles 2 micrometer to 10 micrometer in diameter deposit on the bronchi and bronchioles and are removed by the mucociliary apparatus.

Whereas the smaller particles terminate in the acinus, the minute ones behave as a gas and are exhaled.

The alveolar macrophages, which ingest the inhaled particles, constitute the primary defense mechanism of the alveolar space.

Most of these particles ascend to the mucociliary area and are expectorated or swallowed.

Others migrate into the interstitium of the lung and then into the lymphatics.

A significant number accumulate in and about the respiratory bronchioles and terminal bronchioles.

Other particles are not phagocytosed but enter epithelial cells and migrate through them, presumably passively, into the interstitium.

An important concept in the understanding of pneumoconiosis is that of individual susceptibility, which reflects differences in airway anatomy and function, particle clearance, defense mechanisms, and immunologic activity.

Visit: Aetiology and Pathogenesis of Mesothelioma

Visit: Silicosis ; Asbestosis ; Coal Pneumoconiosis ; Talcosis.

Other Pneumoconiosis:

More than 40 inhaled minerals cause lung lesions and x-ray abnormalities.

Most, such as tin, barium, and iron, are relatively innocuous and accumulate in the lung in the same way as coal, but do not produce morphologic or functional abnormalities.

Others are uncommon and may or may not cause disability.

Two conditions are worth brief mention - Talcosis and Berylliosis.

Beryllium is used in the steel industry and was utilized in fluorescent lamps.

It differs from other pneumoconiosis in that the amount and duration of exposure may be small and the lesion may be in part a hypersensitivity phenomenon.

The lung lesions are granulomatous & identical to those seen in sarcoidosis

 

Further reading:

Genetic susceptibility in pneumoconiosis.

Expression level and significance of TGF-beta1, PDGF, CTGF in serum of patients with pneumoconiosis.

Respiratory symptoms and functional status in workers exposed to silica, asbestos, and coal mine dusts.

Recent advances in the pathogenesis and clinical assessment of mineral dust pneumoconioses: asbestosis, silicosis and coal pneumoconiosis.

Mixed pneumoconiosis: silicosis, asbestosis, talcosis, and berylliosis.

Relationship between autoimmune diseases and pneumoconiosis.

Long-term outcome after resection of non-small cell lung carcinoma complicated by pneumoconiosis.

The inorganic dust pneumoconioses.

Immunopathogenesis of asbestosis, silicosis, and coal workers' pneumoconiosis.

 

 

Dr Sampurna Roy  MD

Consultant  Histopathologist (Kolkata - India)

 

 


 

 

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