Complicated silicosis resulting from occupational exposure to engineered stone products

Clinical record

A 54-year-old man, formerly a smoker, presented with a 6-year history of chronic cough and exertional breathlessness without previous respiratory illnesses. Born in Vietnam, he came to Australia as a refugee at the age of 20 years. A screening chest x-ray was performed on his arrival in Australia; as the patient was not informed about any abnormality, this was assumed to be normal. He commenced work as a labourer; he denied exposure to silica-containing materials and did not participate in activities typically associated with silica exposure (such as jack-hammering) during this period. About 15 years later, the patient started a job manufacturing stone benchtops. He cut, ground, finished and installed the benchtops, using a popular brand of engineered stone comprising > 85% crystalline silica. Occasionally, he made benchtops from granite and marble. During the first 7 years of this work, the patient did not use any respiratory protective equipment, but later used a simple paper mask. Despite some dust extraction facilities in the factory, he reported that the environment was visibly dusty and that dust suppression with water was hardly ever used.

At presentation, chest examination showed scattered fine crackles and bronchial breath sounds bilaterally in the upper zones. Spirometry showed restriction (forced expiratory volume in 1 second [FEV₁]/forced vital capacity [FVC], 1.9/2.6 L [73% and 82% predicted, respectively]) and no bronchodilator reversibility; gas transfer was reduced (diffusing capacity of the lungs for carbon monoxide [Dlco], 60% predicted, carbon monoxide transfer coefficient [Kco], 92%).

Multiple sputum specimens tested negative for acid-fast bacilli. Levels of inflammatory markers were within reference levels, and the result of a screening test for autoimmunity and vasculitis was negative. A computed tomography (CT) scan of the chest (Box 1) showed confluent bilateral calcified fibrotic masses in the upper zones, with marked volume loss, distortion and perilesional bullae. Occasional small peripheral lung nodules were present, predominantly distributed in the upper zones. There was calcified mediastinal lymphadenopathy.

Bronchoscopic washings tested negative for acid-fast bacilli and malignant cells. Positron emission tomography (PET) scanning showed intense uptake in the confluent densities (maximum standardised uptake value, 10.6) and mediastinal lymphadenopathy. CT-guided fine-needle aspiration biopsy was negative for malignant cells. Transbronchial fine-needle aspiration biopsy of lymph nodes using endobronchial ultrasound was non-diagnostic. An open biopsy of the right upper lobe lesions and paratracheal lymph nodes was performed. Histological analysis of the lung sample showed numerous large sclerotic silicotic nodules surrounded by collections of histiocytes (Box 2). Analysis of lymph node sections confirmed prominent nodular silicosis.

Overall, the findings, including PET, were compatible with a diagnosis of complicated silicosis with progressive massive fibrosis. The patient continued to experience worsening breathlessness, despite treatment with bronchodilators and inhaled corticosteroids. He subsequently developed bilateral pneumothoraces, requiring temporary intercostal drain insertion, and is now listed for lung transplantation.

Lessons from practice

• Silicosis is a disabling but entirely preventable occupational lung disease caused by exposure to inhaled free crystalline silica.

• Recent outbreaks of silicosis have been associated with the manufacture of relatively new engineered stone products that are used for kitchen and bathroom benchtops.

• Medical practitioners should be aware that cutting and installing these engineered artificial stone products can be a hazardous occupational exposure.

• Appropriate dust suppression practices and the use of respiratory protective equipment should be reinforced to prevent silica-related diseases.