Best Practices for Dust Control in Metal/Nonmetal Mining

Best Practices for Dust Control in Metal/Nonmetal Mining


By Anita Wolfe and Jay Colinet

Pneumoconioses are lung diseases caused by the inhalation and deposition of mineral dust in the lungs. Known pneumoconioses include, but are not limited to, coal workers’ pneumoconiosis and silicosis. These diseases are usually associated with working in a high-risk, mineral-related industry such as mining.

Occupational exposures to respirable crystalline silica occur in a variety of industries and occupations because of its extremely common natural occurrence. Respirable crystalline silica is defined as particles with aerodynamic diameters less than 10 microns [NIOSH 2002]. Workers with high exposure to crystalline silica include miners, sandblasters, tunnel builders, silica millers, quarry workers, foundry workers, and ceramics or glass workers. Silica refers to the chemical compound silicon dioxide (SiO2), which occurs in a crystalline or noncrystalline (amorphous) form [NIOSH 2002]. Crystalline silica may be found in more than one form: alpha quartz, beta quartz, tridymite, and cristobalite [USBM 1992a; Heaney 1994]. In nature, the alpha form of quartz is the most common [Virta 1993]. This form is so abundant that the term quartz is often used in place of the general term crystalline silica [USBM 1992b; Virta 1993].

Quartz is a common component of rocks; consequently, mine workers are potentially exposed to quartz dust when rock is cut, drilled, crushed, and transported. Occupational exposures to respirable crystalline silica are associated with the development of silicosis, lung cancer, pulmonary tuberculosis, and airways diseases. These exposures may also be related to the development of autoimmune disorders, chronic renal disease (loss of kidney function), and other adverse health effects. In 1996 and 2009, the International Agency for Research on Cancer (IARC) reviewed the published experimental and epidemiologic studies of cancer in animals and workers exposed to respirable crystalline silica and concluded that there was sufficient evidence
to classify silica as a human carcinogen [IARC 1997; Straif et al. 2009].

Silicosis is also a fibrosing disease of the lungs caused by the inhalation, retention, and pulmonary reaction to the crystalline silica. When silicosis becomes symptomatic, the primary symptom is usually dyspnea (difficult or labored breathing and/or shortness of breath), first noted with activity or exercise and later, as the functional reserve of the lung is also lost, at rest. However, in the absence of other respiratory diseases, there may be no shortness of breath and the disease may first be detected through an abnormal chest x-ray. The x-ray may at times show quite advanced disease with only minimal symptoms. The appearance or progression of dyspnea may indicate the development of complications including tuberculosis, airways obstruction, progressive massive fibrosis (PMF), or cor pulmonale (enlargement of the right side of the
heart). A productive cough is often present.

A worker may develop one of three types of silicosis, depending on the airborne concentrations of respirable crystalline silica:

  • Chronic Silicosis: Usually occurs after 10 or more years of exposure at relatively
    low concentrations. Swellings caused by the silica dust form in the lungs and lymph
    nodes of the chest. This disease may cause people to have trouble breathing and
    may be similar to chronic obstructive pulmonary disease.
    (2) Accelerated Silicosis: Develops 5 to 10 years after the first exposure. Swelling in
    the lungs and symptoms occur faster than in chronic silicosis.
    (3) Acute Silicosis: Develops after exposure to high concentrations of respirable
    crystalline silica and results in symptoms within a period of a few weeks to 5 years
    after the initial exposure [NIOSH 1986; Parker and Wagner 1998]. The lungs
    become very inflamed and can fill with fluid, causing severe shortness of breath and
    low blood oxygen levels.

PMF can occur in either simple or accelerated silicosis but is more common in the accelerated form. Figure 1-1 shows a lung that has been damaged by silicosis.

Figure 1-1. Section of the freeze-dried human lung with silicosis.

In an effort to prevent the development of silicosis in miners working in metal/nonmetal mines, MSHA regulates their exposure to respirable silica. When quartz levels in respirable dust samples are greater than 1%, a respirable dust standard (permissible exposure limit) is calculated by dividing 10 mg/m3 by the sum of the percent quartz plus 2. For example, if a sample contains 8% quartz, the respirable standard would be equal to 1 mg/m3 (i.e., 10 ÷ (8 + 2)). This regulation places the upper limit of exposure to respirable quartz at 100 µg/m3.

MSHA compliance sampling data identify those occupations in metal/nonmetal mining that are high-risk occupations for overexposure to quartz. Figure 1-2 shows the percent of samples collected by MSHA inspectors that exceeded the permissible exposure limit (PEL) for a number of high-risk occupations in metal/nonmetal mining.

Figure 1-2. Inspector samples for select occupations from 2004–2008 that exceeded the PEL.


A doctor may diagnose silicosis based on the combination of an appropriate history of exposure to silica dust, compatible changes in chest imaging or lung pathology, and the absence of plausible alternative diagnoses. A chest radiograph is often sufficient for diagnosis, but in some cases, a computed tomography (CT) scan of the chest can be helpful. Lung biopsy, a procedure where a sample of lung tissue is taken for lab examination, is not usually required if a compatible exposure history and findings on chest imaging are present. Pulmonary function tests and blood tests to measure the amounts of oxygen and carbon dioxide in the blood (arterial blood gases) can help in objectively assessing the level of impairment caused by silicosis.

Epidemiologic studies of gold miners in South Africa, granite quarry workers in Hong Kong, metal miners in Colorado, and coal miners in Scotland have shown that chronic silicosis may develop or progress even after occupational exposure to silica has been discontinued [Hessel et al. 1988; Hnizdo and Sluis-Cremer 1993; Ng et al. 1987; Kreiss and Zhen 1996; Miller et al. 1998]. Therefore, removing a worker from exposure after diagnosis does not guarantee that silicosis or silica-related disease will stop progressing or that an impaired worker’s condition will

Treatment of silicosis may include the use of bronchodilators (medications to open the airways) or supplemental oxygen. Once the disease is detected, it is important to protect the lungs against respiratory infections, therefore a doctor may recommend vaccinations to prevent influenza and pneumonia. In some cases of severe disease, a lung transplant may be recommended. Prognosis depends on the length and level of exposure to respirable quartz dust. There is no cure for this lung disease and it cannot be reversed. Consequently, control technologies must be implemented in an effort to prevent the development of the disease. As an added measure of protection, a respirator program can be implemented for workers exposed to silica dust.


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