Friday, July 31, 2009


Description of Silicosis

When workers inhale crystalline silica, the lung tissue reacts by developing fibrotic nodules and scarring around the trapped silica particles [Silicosis and Silicate Disease Committee 1988]. This fibrotic condition of the lung is called silicosis. If the nodules grow too large, breathing becomes difficult and death may result. Silicosis victims are also at high risk of developing active tuberculosis [Myers et al. 1973; Sherson and Lander 1990; Bailey et al. 1974].
A worker's lungs may react more severely to silica sand that has been freshly fractured (sawed, hammered, or treated in a way that produces airborne dust) [Vallyathan et al. 1988]. This factor may contribute to the development of acute and accelerated forms of silicosis.

Types of Silicosis

A worker may develop any of three types of silicosis, depending on the airborne concentration of crystalline silica:

  • Chronic silicosis, which usually occurs after 10 or more years of exposure to crystalline silica at relatively low concentrations
  • Accelerated silicosis, which results from exposure to high concentrations of crystalline silica and develops 5 to 10 years after the initial exposure
  • Acute silicosis, which occurs where exposure concentrations are the highest and can cause symptoms to develop within a few weeks to 4 or 5 years after the initial exposure [Peters 1986; Ziskind et al. 1976]

Initially, workers with silicosis may have no symptoms. As silicosis progresses, there may be difficulty in breathing and other chest symptoms such as cough. Infectious complications may cause fever, weight loss, and night sweats. Severe mycobacterial or fungal infections can complicate silicosis and may be fatal [Ziskind et al. 1976; Owens et al. 1988; Bailey et al. 1974]. Fungal or mycobacterial infections are believed to result when the lung cells (macrophages) that fight these infections are overwhelmed with silica dust and are unable to kill mycobacteria and other organisms [Allison and Hart 1968; Ng and Chan 1991]. About half of the mycobacterial infections are caused by Mycobacterium tuberculosis (TB), with the other half caused by M. kansasii and M. avium-intracellulare [Owens et al. 1988]. Nocardia and Cryptococcus may also cause infections in silicosis victims [Ziskind et al. 1976].

Medical evaluations of silicosis victims usually show the lungs to be filled with silica crystals and a protein material [Owens et al. 1988; Buechner and Ansari 1969]. Pulmonary fibrosis (fibrous tissue in the lung) may or may not develop in acute cases of silicosis, depending on the time between exposure and onset of symptoms.

Furthermore, evidence indicates that crystalline silica is a potential occupational carcinogen [NIOSH 1988; IARC 1987; DHHS 1991], and NIOSH is reviewing the data on carcinogenicity.


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