Route of occupational exposure
The primary route of crystalline silica exposure is via inhalation.
The target organs and potential effects of crystalline silica exposure include:
- Silicosis – acute, accelerated, chronic, PMF
- Lung cancer
- Chronic obstructive pulmonary disease
- Renal disease
- Rheumatoid arthritis
Airborne crystalline silica can bioaccumulate in the lungs and cause disease of the respiratory system. There is no clear ‘no observable adverse effects level’ (NOAEL) demonstrated for crystalline silica. Risks to health are occurring at levels previously thought to be acceptable. Limitations in technology make it difficult to determine a NOAEL if it occurs at very low levels of exposure.
Large bioaccumulated loads of crystalline silica in the lung substance (or lung parenchyma) can cause a build-up of connective tissue, termed silicosis, a specific form of pneumoconiosis. Silicosis is an irreversible and progressive condition. Early silicosis may have no untoward effects. However, severe forms can result in poor gas exchange, difficulty in breathing and death. Evidence suggests crystalline silica interacts with other respiratory hazards, like tobacco smoke, to cause airway diseases. Smokers are more susceptible to the long term effects of silica dust exposure.
Silicosis requires prolonged exposure to substantial airborne quantities of respirable crystalline silica to develop. Four clinical patterns of diffuse lung disease may be seen with silicosis:
- simple nodular silicosis
- progressive massive fibrosis
- accelerated silicosis, and
- acute silicosis or silicoproteinosis.
Factors thought to influence the potential for respirable crystalline silica to cause silicosis include:
- polymorphic types of crystalline silica with cristobalite, tridymite and quartz appearing more reactive and cytotoxic than coesite and shishovite
- the presence of other minerals (e.g. aluminium containing materials), reduces the toxic effect of quartz; however, this may only be a temporary effect
- the total surface area of individual particles; smaller particle size fractions would be expected to cause more lung damage than larger size fractions, and
- freshly fractured versus ‘aged’ surfaces; increased cytotoxicity occurs when crystalline silica particles are cleaved into smaller fragments with reactive free radical species forming on the surface of the particles; there is an ‘aging’ process where free radical activity decays with time; this occurs slowly in air but rapidly in water.
Acute silicosis occurs after a short exposure to very high levels of silica when the alveolar spaces fill with a lipid and proteinaceous exudate. This may occur after exposure in underground work or enclosed spaces where respiratory protection is not worn. Working with composite stone containing high amounts of crystalline silica also has been linked to cause acute silicosis.
Acute silicosis causes rapidly progressive dyspnoea and death, usually within months of onset.
Workers with acute silicosis may be expected to have a largely restrictive functional abnormality with gas exchange abnormalities.
Simple silicosis is the most common pattern with a profusion of small rounded opacities less than one centimetre in diameter throughout the lung fields but predominantly in the upper lobes of the lung. Hilar lymph nodes may be prominent and calcification can be seen. Pulmonary function is usually well preserved. As silicosis progresses, the individual nodules enlarge and coalesce in a transition to progressive massive fibrosis.
Progressive massive fibrosis occurs as individual lesions conglomerate to form larger masses (more than one centimetre) and emphysema develops in lung tissue as the conglomerate shrinks through fibrosis. Substantial impairment of pulmonary function occurs.
Accelerated silicosis is rare but can develop within two to five years with intense exposure to crystalline silica dust.
Exposure to silica at levels that appear not to cause overt silicosis can cause chronic bronchitis and chronic obstructive airways disease. An increased susceptibility to tuberculosis occurs in workers with established silicosis. Epidemiological studies have revealed an excess prevalence of autoimmune disease like scleroderma, rheumatoid arthritis and systemic lupus erythematosus.
In the last 10 years several studies have linked crystalline silica with renal disease, particularly glomerulonephritis.
The respirable fraction of quartz has been classified as a category 1A carcinogen according to the Globally Harmonized System of Classification and Labelling of Chemicals (GHS) as it has been shown to cause cancer in humans.
Several work related exposure studies indicate crystalline silica is a potential human carcinogen. There is strong evidence people with many forms of pulmonary fibrosis, including silicosis, have an increased risk of developing lung cancer. A number of epidemiological studies from around the world have shown an increased risk for lung cancer among workers exposed to crystalline silica.
The following GHS classification for the respirable fraction of quartz has been taken from Safe Work Australia’s Hazardous Chemicals Information System.
- Specific target organ toxicity (repeated exposure) – category 1 (causes damage to organs through prolonged or repeated exposure)
- Carcinogenicity – category 1A