Silicosis: causes, types, symptoms, diagnosis, pathological anatomy, treatment

By Cristiano Antonino On Apr 12, 2023

Silicosis is a type of pneumoconiosis, i.e. a lung disease caused by the inhalation of dust, e.g. at work, and in fact silicosis is a typical occupational respiratory disease

Silicosis is usually caused by inhaling dust of free crystals of silicon (silicon dioxide, quartz) and is characterised by pulmonary fibrosis with distinct nodules and, in more advanced stages, by fibrosis with confluent nodules and impaired respiratory function.

Silicosis is undoubtedly the longest known occupational respiratory disease.

Causes of silicosis

Silicosis generally arises after prolonged inhalation of small particles of free crystalline silica in metal mines (lead, anthracite, copper, silver, gold), foundries, ceramic factories and sandstone and granite mining.

Free silica crystals are one form of free silica, a relatively pure form of silica not combined with silicidic acid.

It usually takes 20-30 years of exposure before the disease becomes manifest, although it develops in < 10 years when exposure to dust is very high, such as in tunnel construction, abrasive soap factories and during blasting operations.

The current limit for free silica in the air of industrial environments is 100 mg/m3, an 8-hour time-weighted average based on the percentage of silica in the dust.

The formula for ascertaining whether the limit is exceeded is mg/m3.

Who is at risk?

Workers who inhale dust containing more than 1% are most exposed, particularly high-risk occupations are:

working in mines;
stone cutting;
production of abrasives;
foundry work;
glass or ceramic production work;
work in the refractory industry;
surface cleaning or the discolouration of jeans by sandblasting.

However, the hazard depends not only on the type of work, but also on the percentage of crystalline silicon dioxide in the inhaled air and the length of time it is in the environment.

Pathological anatomy and pathophysiology of silicosis

Respirable free silica particles are phagocytosed by alveolar macrophages and enter the lymphatics and interstitial tissue.

The macrophages cause the release of cytotoxic enzymes that induce fibrosis of the lung parenchyma.

When a macrophage dies, silica particles are released and phagocytosed by other macrophages and the process may repeat.

The typical initial lesion is the formation of distinct hyaline silica nodules in both lungs.

The dying macrophages release silica into the interstitial tissue around the second generation of respiratory bronchioles, where a nodule forms.

Subsequently, fusion of the fibrotic nodules results in confluent masses, with retraction of the upper portions of the lung and emphysema and marked distortion of the lung architecture.

Ventilation and gas exchange are impaired.

The reduction of all lung volumes distinguishes the overall pathophysiological picture of confluent silicosis from that of advanced pulmonary emphysema.

In the advanced stages of confluent silicosis, severe functional impairments occur and respiratory failure, their extreme consequence, may progress along with a worsening of the rx picture for a limited time (i.e., 2-5 years) even after exposure has stopped.

When dust exposure is extremely high and silico-proteinosis develops, the alveolar spaces fill with a proteinaceous material similar to that found in alveolar proteinosis and mononuclear cells infiltrate the septa.

Symptoms and signs

Patients with simple nodular silicosis have neither symptoms nor, usually, respiratory impairment.

They may complain of coughing and expectoration, but these symptoms are due to industrial bronchitis and occur with the same frequency in subjects with normal rx.

Although uncomplicated silicosis impairs respiratory function to a small extent, patients with stage 2 or 3 disease (see diagnosis, below) occasionally have a slight reduction in lung volumes, but values rarely fall below reference limits.

Confluent nodule silicosis, on the other hand, may result in severe dyspnoea, coughing and sputum

The severity of breathlessness is related to the size of the confluent masses in the lungs.

When the masses are very large, the patient achieves severe disability.

As the masses invade and obliterate the vascular bed, pulmonary hypertension and right ventricular hypertrophy set in.

In advanced stages, objective signs of consolidation and pulmonary hypertension may be present.

Non-hypoxaemic pulmonary heart disease is ultimately a cause of death.

In confluent (complicated) silicosis, especially in the terminal stages, alterations in respiratory function are common.

These include decreased lung volumes and diffusing capacity and airway obstruction, often with pulmonary hypertension and occasionally mild hypoxaemia.

CO2 retention is rare.

In many silica patients, the serum contains anti-polon autoantibodies and antinuclear factors.

Individuals exposed to silica in the work environment and who have a positive tuberculin test have an increased risk of developing TB.

In general, the greater the amount of silica present in the lungs, the higher the risk.

Diagnosis

Diagnosis is based on characteristic x-ray changes and a history of exposure to free silica.

Simple silicosis is recognised by the presence of numerous small round or regular opacities on chest X-ray and is classified into categories 1, 2 and 3 according to their prevalence.

Confluent nodule silicosis is revealed by the presence of an opacity > 1 cm in diameter on a background of category 2 or 3 simple silicosis.

A number of other diseases that may mimic simple silicosis include milar TB, welders’ siderosis, sarcoidosis, haemosiderosis and coal miners’ pneumoconiosis.

However, the presence of ‘eggshell’ calcifications in the hilar and mediastinal lymph nodes distinguishes silicosis from other occupational respiratory diseases.

Silico-tuberculosis resembles confluent nodule silicosis on X-ray.

Differentiation can be made by culture test of sputum.