• silicosis
• pneumoconioses
• inorganic dusts

We read with interest the article by Hoy et al reporting silicosis in seven Australian workers fabricating artificial stone countertops,1 and the letter by Barber et al who could not identify cases in the UK.2 We describe two cases of silicosis in workers employed in a two-man company producing and installing artificial stone kitchen countertops.

The first worker made the countertops by mixing epoxy resin, gravel, sand, pigment and quartz flour (99.4% quartz; 10% of the particles <5 µm, 50% <30 µm, according to the technical data sheet). Approximately 200 kg of quartz flour were used weekly. After curing, the countertops were dry cut, ground and polished. No dust measurements were made. The worker occasionally used a dust mask. He underwent periodic occupational health examination, however, without chest X-ray. In earlier jobs, he had had no silica exposure. In 2015, at age 41, after 9.5 years of employment, he had dry cough without dyspnoea. He had never smoked. Chest auscultation and pulmonary function tests (PFTs) were normal—total lung capacity (TLC) was 6.1 L (95%pred), diffusing capacity of the lung for carbon monoxide (DLco) was 94%pred. High-resolution CT (HRCT) showed bilateral diffuse micronodules with an upper lobe and posterior predominance and enlarged hilar and mediastinal lymph nodes (figure 1). Bronchoalveolar lavage revealed 38% lymphocytes (normal <20%). Mediastinal lymph node histopathology demonstrated silicotic nodules and birefringent particles (figure 1). After silicosis was diagnosed, he quit his job. Two years later, his cough had disappeared and PFTs were unchanged.

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Figure 1

First worker: (A, B) High-resolution CT showing bilateral diffuse micronodules with an upper lobe and posterior predominance. (C) Light microscopic image of a mediastinal lymph node obtained by endobronchial ultrasound-guided fine-needle aspiration showing dense collagenous tissue containing fibroblasts, compatible with a silicotic nodule (∗), adjacent to an area of dust accumulation. No granulomas were observed (H&E; x200). (D) Polarised light microscopy demonstrating numerous birefringent particles (arrowheads) (x200).

The second worker installed the countertops at customers’ homes, which involved stone grinding. Occasionally, he helped the first worker at the workshop. In his previous job, he had made concrete statues for 15 years. In 2012, at age 46, after 9 years of employment in the countertop company, this ex-smoker (<10 pack-years) started to have exertional dyspnoea, cough and nocturnal wheezing. Chest auscultation and X-ray were considered normal. PFTs were unremarkable (TLC 6.9 L, 97%pred) except for a mildly decreased DLco (77.5%pred). Histamine bronchial challenge was positive (PD₂₀=0.25 mg). Asthma was diagnosed, and inhaled corticosteroids/long-acting beta-agonist initially improved symptoms. Because of his occupational exposure, HRCT was performed 3 years later and showed bilateral centrilobular and subpleural micronodules with an upper lobe and posterior predominance and slightly enlarged hilar and mediastinal lymph nodes, some containing punctiform calcifications—compatible with silicosis. Five years after initial presentation and continued—but reduced—exposure, PFTs remained unchanged.

Similarly to the cases described by Hoy et al, 1 the first worker developed respiratory symptoms after <10 years of making and processing high-silica content artificial stone. The second worker had silica exposure for nearly 25 years in his current and previous job, possibly both contributing to his lung disease. Outbreaks of artificial stone-associated silicosis have been described in Israel, Italy and Spain.3–6 To our knowledge, no cases have been published in Belgium nor in its surrounding countries (UK, France, Germany, The Netherlands). Considering the increasing popularity of artificial stone countertops, we expect more cases to be diagnosed. Industry-specific preventive strategies are needed, especially among small enterprises.