This article contains material excerpted from the “AIOH Position Paper: Respirable Silica and Occupational Health Issues” published by the Australian Institute of Occupational Hygienists, Inc.
About Respirable Crystalline Silica (RCS)
Silica is silicon dioxide, one of the most abundant minerals in the earth’s crust. It is present in almost all types of rock, sands, clays, shales, and gravel. It is also a major constituent of construction materials such as bricks, tiles, and concrete.
Silicon dioxide occurs in non-crystalline and in crystalline form. Crystalline silica is an aggressive, lung-damaging dust when it can penetrate deep into the lung in sufficient quantity. For the crystalline dust particles to reach the extremities of the lung where they have the potential to do damage, they must be particularly small (less than 10 microns in diameter), and this size is defined as “respirable”. Therefore, we call the toxic form of this dust “respirable crystalline silica” or RCS.
Historically, respirable crystalline silica dust has been responsible for a large burden of occupational ill health, with countless deaths from silicosis, a disease which results in the formation of scar tissue in the lung. There is no treatment and no cure for silicosis.
While there is little support for the hypothesis that occupational silica exposure is a direct acting cancer initiator, but there is compelling evidence that many forms of pulmonary fibrosis, including silicosis, constitute major risks for human lung cancer. Therefore, management’s primary aim should be to protect against silicosis.
Images below are from CDC (Center for Disease Control)
Slide Show: Lung sections from victims of pneumoconiosis
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Diseases Caused by Respirable Crystalline Silica Exposure
Silicosis is a fibrotic lung disease caused by the inhalation of RCS. It has been described as chronic silicosis, accelerated silicosis, and acute silicosis. Silicosis cannot be cured, it can only be prevented.
- Chronic silicosis (including simple and complicated silicosis), is the most common form and results in fibrotic changes to the lungs after 10 to 30 years of exposure.
- Simple silicosis, the usual form of chronic silicosis, is characterized by the presence of discrete rounded fibrous nodules in the lung. On the X-ray, these are seen as 3 – 6 mm discrete rounded opacities that appear predominantly in the upper and middle lung zones. Respiratory symptoms or lung function impairment may not be observed unless the person smokes or has a coexistent disease.
- Complicated silicosis results when the silicotic nodules increase in size and coalesce into large lesions greater than 1 cm in diameter. The conglomerate lesions may obliterate bronchi and vessels and cause marked distortion of lung structure and function. The disease results in progressive massive fibrosis (PMF). When progressive massive fibrosis occurs, the patient develops progressive respiratory symptoms from a reduction in lung volume, distortion of bronchi, and bullous emphysema. The main symptom is shortness of breath, which is progressive and ultimately disabling, potentially leading to cardiorespiratory failure.
- Accelerated silicosis results from the inhalation of very high concentrations of silica dust over a period typically in the order of 5 to 10 years. Although accelerated silicosis develops in a pattern similar to that of simple silicosis, the time from initial exposure to the onset of the disease is shorter and the progression to complicated silicosis is more rapid.
- Acute silicosis develops from the inhalation of high concentrations of RCS over a short period (7 months to 5 years). The air spaces fill with the thick proteinaceous material (fluid and cells). Symptoms of acute silicosis include a cough, weight loss, and fatigue. This may progress rapidly to respiratory failure over a period of several months. Death occurs after a few months. Acute silicosis has been reported among sand-blasters and drillers, and has historically been reported mainly among silica powder workers.
Silica particles can destroy or alter the metabolism of the pulmonary macrophage, thereby reducing its capacity for anti-bacterial defense. In addition, the presence of silica in the lungs compromises the immune system, leaving those affected at much higher risk of succumbing to pulmonary tuberculosis.
Chronic obstructive pulmonary disease (COPD)
The literature is showing an increased weight of evidence regarding exposure to RCS causing COPD, which is known by a number of names including chronic obstructive pulmonary disease (COPD), chronic obstructive airway disease (COAD), chronic airflow obstruction (CAO) and chronic airway limitation (CAL). It is also referred to as chronic bronchitis and emphysema.
Nine studies showed an excessive risk for lung cancer. These included refractory brick workers, pottery workers, diatomaceous earth workers, foundry workers, granite workers, and mine workers, (although not coal-mine workers). Increased lung cancer risk appears to be found only in those with silicosis.
Renal (Kidney) Disease
Increased risk of renal disease has been implicated with elevated exposures to crystalline silica. A recent US study found a doubling of risk of non-malignant renal disease but no increase in renal cancer.
Measuring the Risk
For RCS to present a risk to health it must be inhaled. Exposure is therefore assessed by measuring the airborne concentration.
- The AIOH supports the current ASCC (Australian Safety and Compensation Council) occupational exposure standard of 0.1 mg/m3 for respirable crystalline silica.
- The AIOH strongly recommends near full-shift sampling, that is an 8-hour sample period or 12-hour sample period for an 8 or 12-hour shift, respectively.
- The AIOH also strongly recommends the use of a NATA accredited laboratory to do RCS analysis and that the results are reported on NATA test certificates.
Controlling the Risk
The control principles that apply to RCS are similar to those that apply to all mechanically generated dust exposures.
- Position personnel so they are out of the dust either in enclosed and filtered cabins or so they are working upwind of dust emission;
- Design and operate processes and activities to minimize emission, release and spread of dust;
- Use sharp cutting tools that minimize the generation of large quantities of fine dust;
- Use wet processes to prevent dust generation;
- Use water suppression to prevent dust spread;
- Ensure ore passes are not emptied below the brow point and crusher chutes are kept full;
- Use water curtains and rubber curtains to prevent dust release, particularly at conveyor transfer points and chute draw points;
- Use ventilation, either dilution or extraction, to control dust spread and dust release;
- Ensure suppressed dust is captured by scrubbing or filtering so it cannot be re-entrained in workplace air;
- Apply good house-keeping practices to prevent dust build-up;
- Provide training in the health effects of dust and its control;
- Where adequate control of exposure cannot be achieved by other means, provide, in combination with other control measures, suitable PPE. For most exposures to RCS this will be a P1 or P2 (MERV 16) efficiency half face respirator. Ensure training is provided in the use and limitations of respiratory protective equipment (eg have a clean-shaven policy). Face fit testing is also recommended, as per AS 1715 (1994).
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- AIOH Position Paper: Respirable Silica and Occupational Health Issues from the Australian Institute of Occupational Hygenists, Inc.
- NIOSH: Silica Topic Page – Information from the USA based National Insititute of Safety and Occupational Health on all aspects of RCS.
- NIOSH Publications on Silica (By Industry)
- Construction Workers should know: Silica– It’s more than dust
University of Washington website designed to help those in the construction industry anticipate and control silica exposures.
- The European Network on Silica: there is a Good Practices Guide available in all European languages that include controls for respirable crystalline silica generation.