Silicosis is an occupational lung disease caused by inhalation of crystalline silica. People working in occupations like sandblasting, surface drilling, tunneling, silica flour milling, ceramic making, and so forth are predisposed to develop silicosis. Crystalline forms of silica are more fibrogenic than the amorphous forms, highlighting the importance of the physical form in pathogenesis. Lung biopsy is rarely performed for the diagnosis of silicosis as it can easily be detected by occupational history and radiological features. Patients with silicosis can develop complications like tuberculosis, lung cancer, progressive massive fibrosis, cor pulmonale, broncholithiasis, or tracheobronchial compression by lymph nodes. Pleural involvement in silicosis is rare. Spontaneous pneumothorax is a pleural complication that can develop in such patients. Usually in silicosis pneumothorax is unilateral. We hereby report the lung biopsy findings and discuss the mechanism of pneumothorax development in a case of chronic silicosis who, later on died during the course of the disease.
Silicosis also known as “potters rot” is a form of pneumoconiosis caused by inhalation of crystalline silica. Crystalline silica is classified as a group 1 substance by the International Agency for Research on Cancer [
A 33-year-old male presented with progressive breathlessness and dry cough since the last 5 months and right sided pleuritic chest pain for 10 days. Patient was diagnosed elsewhere as miliary tuberculosis and was under antitubercular treatment (ATT) for four months. He was not a smoker. He worked as a bore-well driller for the past 10 years.
Blood hemogram and renal and liver functions were normal. Admission chest radiograph showed bilateral, diffuse, well-defined large rounded nodular opacities with right secondary spontaneous pneumothorax (Figure
Chest X-ray: bilateral diffuse nodular opacities with bilateral pneumothorax.
Patient was managed with tube thoracostomy, supplemental oxygen, and analgesics. After three days patient complained of acute onset chest pain on left hemithorax and dyspnoea.
Chest radiograph revealed a new pneumothorax on left side for which immediate chest tube was placed. Subsequently, patient had symptomatic relief. Fibre optic bronchoscopy revealed normal airway. Bronchoalveolar lavage cytology showed only benign bronchial epithelial cells and smear and culture for
Limited autopsy was done. Postmortem biopsy of bilateral lungs and liver was done. H and E sections of bilateral lungs revealed multiple collagenous nodules, some of which coalesced to form larger nodules (Figures
(a) Lung parenchyma showed collagenous nodules (arrow) (H&E ×100), (b) silicotic nodule: central zone of whorls of hyalinised fibrous tissue, midzone of concentrically arranged collagen fibres, and outer zone of randomly orientated collagen fibres and inflammatory cells (H&E ×200), (c) periphery of the nodules with dust laden macrophages and lymphoid cells (H&E ×200), inset: dust laden macrophages (H&E ×400), and (d) polarized light microscopy, white spots which represent silica crystals (white arrow).
Workers most prone to develop silicosis are those involved in mining, tunneling, stonework, foundry work, sand blasting, and manufacture of ceramics. On the basis of dose and lag period since onset of exposure, silicotic lesions are classified as acute, accelerated, and chronic silicosis. Acute silicosis follows heavy exposure to very large amounts of silica and is characterized by rapid onset of severe dyspnoea cough, weakness, and weight loss, often leading to death. Accelerated silicosis occurs on short term exposure to large amounts of silica. Simple chronic silicosis follows long term exposure to low amounts of silica dust. Radiographically, small (<10 mm in diameter) opacities, typically rounded, can be seen in upper lung zones.
Inhaled silica is engulfed by alveolar macrophages that cannot digest it. Instead silica damages the alveolar lysosomal membranes leading to release of proteolytic enzymes into the cytoplasm and eventual death of the macrophage. Continued silica exposure leads to an alteration in macrophage function. There is release of inflammatory cytokines, for example, IL-1, free radicals, and growth factors [
Unilateral secondary spontaneous pneumothorax is the only described pleural complication in silicosis. Spontaneous pneumothorax is usually associated with chronic silicosis with progressive massive fibrosis. The involvement is unilateral in most cases. There are only very rare cases of bilateral involvement [
Uncomplicated silicosis does not usually decrease life expectancy. Lung transplant has been performed in patients with end stage silicosis [
The authors declare that there is no conflict of interests regarding the publication of this paper.
The authors acknowledge Dr. Renu G’Boy Varghese, Professor and Head of the Department of Pathology, Pondicherry Institute of Medical Sciences, Pondicherry, who helped them with the polarizing microscopy.