Why silicosis is on the rise – and what to do about it

Australia is currently in the midst of a major outbreak of silicosis primarily due to the installation of artificial stone benchtops. This is particularly affecting young and vulnerable workers.

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There has been a worrying increase in silicosis cases in Australia recently due to workers being exposed to high concentrations of silica dust from artificial or engineered stone.

The outbreak has been fuelled by the housing boom, and the availability of imported artificial or engineered stone, which is cheaper than natural marble and which comes in many different varieties.

Artificial stone silicosis is a progressive disease characterised by a shorter latency and more rapid loss of lung function than the usual chronic silicosis.¹

This disease is entirely preventable through safe workplace practices. Strategies to reduce high intensity silica dust exposure such as dust control, strict enforcement of occupational health and safety regulations and respiratory surveillance of workers are urgently required to prevent further cases from occurring.

BACKGROUND

Silicosis is one of the earliest recognised occupational lung diseases.

Classical silicosis is a chronic pneumoconiosis (or lung fibrosis due to dust inhalation) which was recognised in the time of Pliny. Four different types of silicosis are recognised. (See table 1 below).

Until recently, cases have usually been older men in industries such as mining, tunnelling, tiling, refractory brick work and the pottery industry. Classically, slowly progressive disease occurs.²

However, recent outbreaks in modern industries, such as sandblasting in denim jean production,³ jewellery polishing^4-6 and artificial stone benchtop production and finishing have been associated with an acute accelerated variant of silicosis which is affecting  younger workers early in their careers.

Artificial stone (also known as engineered, reconstituted and manufactured stone) is a popular and new building material used primarily in the fabrication of kitchen and bathroom benchtops. The artificial stone is a composite material made of finely crushed elements including quartz as the major filler, with the addition of coloured glass and metals bound together by a polymer resin.⁷ The silica content of artificial stone is approximately 90%, far higher than natural stones (natural marble 3%, granite 30%).⁸

Due to its high silica content, very high respirable free silica is produced by mechanical cutting methods, especially if dry cut. Artificial stone has therefore become a source of hazardous silica exposure for workers employed in manufacturing, finishing and installing of artificial stone benchtops.

Since artificial stone first became commercially available, cases of artificial stone silicosis have been reported in Spain,⁹ Italy, ¹⁰ Israel¹¹ and the United States.¹²

In Australia, the index case was described in 2015, followed more recently by several cases reported in 2017 ^{1, 13, 14}; the true prevalence of silicosis is likely to be much higher than that reported in the literature to date. A recent Queensland audit published in February 2019 reported a further 98 cases of silicosis in a four month period, with 15 cases documented to be advanced end stage disease.¹⁵

To date, 151 Queensland workers have been diagnosed with silicosis, 25 of whom have progressive massive fibrosis.¹⁶ However, there is currently no centralised system for recording disease burden across Australia. Affected individuals in many of the sites of outbreaks have been subcontractors in the building and construction industry or else from a non-English speaking background; these workers seem to have little or no education about risks of  crystalline silica dust and have usually been doing dry cutting.

HISTORY, RISKS AND PATHOGENESIS

Artificial stone silicosis is characterised by a shorter latency period and more rapid loss of lung function than chronic silicosis, with the median duration of exposure to artificial stone associated dust being 7.3 years (range 4-10) in one recent Australian study.¹

This form of silicosis develops after a short duration but high intensity exposures, and is termed accelerated (or progressive) silicosis. Accelerated silicosis has been comparatively poorly described compared with classical silicosis, but seems to be the type occurring in Australia currently in artificial stone workers.¹⁷

While the minimum total lung burden of respirable crystalline silica needed to trigger silicosis is not fully established,  the cumulative dose of silica  is very important.¹⁸ Crystalline silica in artificial stone becomes respirable when disturbed by cutting and grinding.

Much research into the exposure-response relationship between mechanical cutting methods and silicosis has been conducted, but relatively little into artificial stone silicosis. The risk appears greatest when dry cutting is performed¹⁹ and at high concentrations (>2mg/m³), even if exposure is brief.²⁰

Once respirable crystalline silica particles are inhaled, they are phagocytosed by alveolar macrophages, causing oxidative stress, apoptosis and upregulation of pro-inflammatory and pro-fibrotic pathways.

This damages the pulmonary parenchyma, leading to the development of fibrosis and permanent distortion of the lung parenchyma, resulting in reduction in gas exchange and eventual chronic respiratory failure.²¹

Reducing exposure at an early stage slows but may not arrest the natural progression of disease.²²

SIGNS AND SYMPTOMS

In the early stages of silicosis, workers are usually asymptomatic. As the disease progresses, however, dyspnoea, dry cough and constitutional symptoms such as fatigue and weight loss may occur. It should be noted that symptoms are often a late manifestation, and many patients are asymptomatic until severe disease is established.

Silica exposure may lead to impaired immune function and increase the risk of other disorders, including tuberculosis, chronic obstructive pulmonary disease, lung cancer, scleroderma, rheumatoid arthritis and chronic renal disease.¹⁸ The diagnosis of tuberculosis should be considered in any patient who has come from, or who visits, a country with a high incidence of tuberculosis.

_{FIGURE 1: CXR and CT scan from the same individual stoneworker with ILO category 3 artificial stone silicosis, illustrating the increased sensitivity and improved diagnostic accuracy of high resolution CT scanning in artificial stone silicosis compared with plain chest radiography. (Reproduced with the kind permission of the patient)}

DIAGNOSIS

Diagnosis of artificial stone silicosis relies on a thorough history of exposure to silica dust and compatible radiological features, together with exclusion of other causes.¹⁸

Occupational history

A careful and complete occupational history is arguably the most important factor in making a diagnosis. This includes a complete chronological employment and exposure history including a careful account of all jobs worked, with details of the actual tasks performed and dust exposure details. A thorough respiratory and medical history is also essential to assist in excluding other causes. Potential environmental or domestic exposures should also be documented, as well as drug exposures and of course smoking history (and vaping).

Radiology

Chest X-rays have historically been used as the primary imaging modality to detect lung disease due to silica exposure. However, preliminary data from Australian centres caring for workers with engineered stone-related lung disease have found that chest X-rays are failing to reliably detect disease.

One recent study from Queensland found that 43% of workers with International Labour Organisation classified normal chest X-rays had disease visible on computed tomography.²³ For this reason, a high resolution CT of the chest is now recommended by the Australian and New Zealand College of Radiologists as the primary imaging modality to be used for screening exposed workers, but has to be performed according to the appropriate technique.²⁴

Computed tomography has higher sensitivity for detecting early disease and greater accuracy in characterising the patterns of disease (See figure 1, above).  The interstitial lung abnormalities identified on CT in engineered stone workers are heterogeneous. They can include subtle findings such as small ground glass attenuation and nodules to areas of bilateral progressive massive fibrosis.

Other characteristic findings include centri-lobular nodules, nodal enlargement with or without calcification and pleural thickening.²⁵ A multidisciplinary approach to establishing a diagnosis of interstitial lung disease due to occupational exposure is strongly recommended.²⁴

Respiratory function testing

In the early stages of the disease, spirometry may be normal, and respiratory function testing may not be sensitive enough to detect early lung injury among exposed populations.^{7, 26.} As silicosis progresses, obstruction, restriction or mixed ventilatory deficits may develop.²⁷ The rate of decline in lung function in those with artificial stone silicosis far exceeds the expected rate of decline in healthy patients.²⁸

Serial lung function testing is potentially a way of monitoring progress and predicting prognosis, but has yet to be fully evaluated.

Bronchoscopy and bronchoalveolar lavage

An increased number of lymphocytes and neutrophils characterises the inflammatory process associated with progression in classical silicosis.²⁹ Silica particles and activated macrophages can be also be detected.

Bronchoalveolar lavage in artificial stone silicosis also demonstrates lymphocytosis, with one study finding a cell differential lymphocyte percentage ranging from 31-54% .¹ However, such lavage lymphocytosis also occurs in other interstitial lung diseases and silica assessment on bronchoalveolar lavage or histopathology is not always available.  No information on the prognostic value of such investigations is available yet in artificial stone silicosis.

Lung biopsy

Thoracic lymph node biopsy can be performed using endoscopic bronchial ultrasound, but again this can be non-specific. Thoracoscopic or open lung biopsy can be used in cases where the diagnosis is uncertain, and is currently the gold standard for diagnosis.

Histology from explanted lungs in patients with artificial stone silicosis has been shown to include the presence of both chronic fibrotic/nodular silicosis and alveolar proteinosis suggestive of silicoproteinosis within the same lung.¹⁷

TREATMENT

There is no established effective treatment for silicosis other than supportive care. In recent years, however, lung transplantation has emerged as a potential intervention for end-stage disease.

Several other emerging treatment options are currently being explored including treatment with anti-fibrotic agents.

PREVENTION

Given the absence of specific and curative interventions, it is essential that prevention of unnecessary exposure to respirable crystalline silica occurs. Every effort should be made to reduce dust exposure levels for workers working with artificial stone, and all workplaces with significant exposures are required to undertake independent assessments of personal workplace respirable crystalline silica levels. 

The current Time Weighted Average Workplace Exposure Standard (TWA-WES) in Australia and New Zealand is 0.1mg/m³ of respirable crystalline silica over eight hours; however, this was derived from chronic silicosis literature.²²

The Australian Institution of Occupational Hygiene, Faculty of Occupational and Environmental Medicine (AFOEM) of the Royal Australasian College of Physicians (RACP) and the Thoracic Society of Australia and New Zealand (TSANZ) have recommended that the TWA-WES be urgently reduced, even as low as  0.05mg/m³.²¹

At an industry level, all workplaces are responsible for undertaking independent assessments of personal workplace respirable crystalline silica dust levels and implementing measures using the hierarchy of hazard controls to minimise exposure if CFA (coal fly ash) levels are potentially over the limit.³⁰

Three of these measures, in order of effectiveness include: the substitution of hazardous practices to those that are less hazardous (such as sourcing composite stone benches with a lower percentage of silica); the use of engineering controls (wet cutting and local exhaust ventilation); and personal protective equipment with fit testing.

Equipment should meet industry expectations and include work clothing that does not collect dust, and respiratory protective equipment appropriate to the measured silica level.

Generally, a minimum of a P2 efficiency half-face respirator is required  to protect against respirable crystalline silica³⁰ and disposable paper dust masks are not effective. ²² Concerningly, occupational practices reported by subjects are not in keeping with those advised by regulatory bodies, with 68% of subjects in a recent Australian study reporting a failure to abide by any hazard controls.²³

Government and Statutory bodies also have an important role.

In September 2018, the Queensland government announced a ban on dry cutting of artificial stone and the launch of a health screening program for workers³¹ as well as a mandatory notification of cases to their central registry. ³³

Queensland has also been pro-active in auditing workplaces in the manufactured stone industry, with more than 140 workplaces involved and close to 600 notices issued. ³² Unfortunately, other states have not been as vigilant and there remains no national registry for reporting disease burden. However, the federal government has recently established a National Dust Diseases Taskforce and a central registry is likely to be one of several outcomes.

The Lung Foundation and TSANZ have recently filed a joint submission recommending that similar programs to Queensland (where active case finding is undertaken) should be implemented in NSW and throughout Australia, targeting workplaces involved in manufacturing stone. Victoria and South Australia have recently implemented such programs.

A system is needed for mandatory country-wide notification of artificial stone silicosis which is shared with the regulator, requiring an audit of the workplace of the diagnosed worker and with free respiratory surveillance for the worker.³²

In the interim, the onus falls on medical practitioners to opportunistically evaluate patients by taking occupational histories and enabling early chest imaging. (See table 2 above) 

The RACP recommends a full occupational history should be taken from all building industry workers in conjunction with lung function testing (including DLCO) and a chest X-ray.²²

Suspected patients should then be referred to a respiratory physician and/or occupational and environmental physician who will then be able to address all the relevant issues including workplace assessment, and potential removal from further dust exposure.

CONCLUSION

Australia is currently in the midst of a major outbreak of silicosis primarily due to the installation of artificial stone benchtops. This is particularly affecting young and vulnerable workers and should not be occurring in the 21^st century.

Urgent identification of those exposed to hazardous levels of silica and appropriate health assessments, long term health surveillance programs and personalised management are needed.

Samantha Ennis is a respiratory registrar in the Department of Thoracic Medicine, St Vincent’s Hospital, Sydney.

Deborah Yates is a respiratory physician with qualifications also in Occupational Medicine and Conjoint Associate Professor at The University of NSW.

References

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