In general, high concentrations of dust may cause coughing and mild, temporary irritation following a short-term exposure. There is no human or animal information available specifically for quartz. Quartz can have potentially serious respiratory effects following long-term inhalation (one year or more). Refer to "Effects of Long-Term (Chronic) Exposure" below.
In general, quartz dust is not expected to be irritating to the skin. However, foreign-body reactions (granulomas) have been observed after crystalline silica accidentally got under the skin as a result of an injury. Often the effects are delayed for periods ranging from weeks up to more than 50 years.
In general, the dust is not expected to be irritating except as a "foreign object". Some tearing, blinking and mild temporary pain may occur as the solid material is rinsed from the eye by tears. One unconfirmed case is described in which foundry workers with silicosis experienced a deterioration in eyesight due to corneal opacities and there was evidence of an abnormally high silicon content in the cornea. There is no animal information available.
Quartz is probably not toxic following short-term ingestion. There is no human or animal information available. Ingestion is not a typical route of occupational exposure.
INHALATION: Prolonged or repeated exposure to fine airborne crystalline silica dust may cause severe scarring of the lungs, a disease called silicosis. The risk of developing and the severity of silicosis depends on the airborne concentration of respirable-size silica dust to which an employee is exposed and duration of exposure. Silicosis usually develops gradually over 20 years or more of exposure. Particles with diameters less than 1 micrometre and freshly cleaved particles (for example, those produced by sandblasting) are considered most hazardous. Several reliable studies have found silicosis in employees with exposure to considerably less than 1 mg/m3 respirable quartz.
The early symptoms of silicosis (cough, mucous production and shortness of breath upon exertion) are nonspecific, so the development of silicosis may not be detected until advanced stages of the disease. Silicosis may continue to develop even after exposure to crystalline silica has stopped. Evidence of silicosis can normally be seen on an X- ray.
Silicosis can vary in severity from minimal to severe. In cases of mild silicosis, there is typically no significant respiratory impairment, although there is X-ray evidence of lung injury. In severe cases, significant and increasingly severe respiratory impairment develops. There is no proven effective treatment for the disease. Life expectancy may be reduced, depending on the severity of the case. Death is not usually a direct result of silicosis, but cardiac failure (cor pulmonale) may occur as the heart has increasing difficulty pumping blood through the scar tissue in the lungs. Silicosis may be complicated by the development of bacterial infections, including tuberculosis.
"Accelerated" silicosis results from exposure to high concentrations of crystalline silica over a period of 5 to 10 years. The disease continues to develop even after exposure stops and is often associated with autoimmune diseases, for example, scleroderma (a skin disease involving thickening of the skin).
"Acute" silicosis (also referred to as "silicotic alveolar proteinosis") is rare in humans, but can develop if very high concentrations of crystalline silica dust are inhaled over a relatively short period (1-2 years) and has occurred in occupations such as sandblasting or tunnelling where exposure controls were minimal. Acute silicosis may result in death within a few years, often with tuberculosis as a complication.
Inhalation of quartz has also been associated with a number of other, less well characterized, harmful effects including effects on the kidney (glomerulonephritis), the liver, the spleen and immune system disorders (progressive systemic sclerosis, scleroderma or rheumatoid arthritis).
The International Agency for Research on Cancer (IARC) has concluded that crystalline silica in the form of quartz or cristobalite from occupational sources should be classified as carcinogenic to humans (Group 1), upgraded from its previous classification as probably carcinogenic to humans (Group 2A). This conclusion was drawn on the basis of a relatively large number of human population studies that together provide sufficient evidence in humans for the carcinogenicity of inhaled crystalline silica. In many (although not all) of these studies, lung cancer risks were elevated and could not be explained by other factors. Recent reviews have tended to conclude that if exposures are controlled to prevent silicosis, they will probably also prevent cancer. The risk of developing silicosis depends on the airborne concentration of crystalline silica, the particle size and the duration of exposure.
The US National Toxicology Program (NTP) identifies crystalline silica (respirable size) as a substance which may reasonably be anticipated to be a carcinogen. The American Conference of Governmental Industrial Hygienists (ACGIH) has not assigned a carcinogenicity designation for crystalline silica.
There is no human or animal information available.
There is no human or animal information available.
There is disagreement about whether tobacco smoke increases the severity of the effect of silica dust on respiratory impairment. Simultaneous exposure to known carcinogens, for example, benzo(a)pyrene, can increase the carcinogenicity of crystalline silica. A synergistic effect between smoking and crystalline silica and/or silicosis on risk of lung cancer, is also likely.
Quartz dust can accumulate in the lungs. Inhaled particles are deposited at various locations within the respiratory tract, depending on their shape, mass, aerodynamic characteristics and other physical properties. Most, but not all, silica is cleared from the lungs after inhalation and deposition. The elimination of quartz particles continues for many years after the last exposure. Silica is slightly absorbed into the body. Absorbed silica is deposited mainly in the liver, spleen and regional lymph nodes. Silicic acid absorbed into the blood stream is excreted through the kidneys.
Document last updated on December 22, 1997
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