Document MGkMrB1GV3xbEDvp17ZOrrOyk

Silica exposure and its effect on the physiology of workers Contents Introduction Who are at risk to develop silicosis? Distribution and characteristics of crystalline silica Factors that influence toxicity and potential to induce fibrosis by crystalline silica Pathology associated with crystalline silica exposure Theories related to the pathogenesis of silicosis Diagnosis of silicosis Conclusion References Page 1 1 1 2 3 5 7 8 9 These veins deposited in rock fissures form the matrix for precious metals i.e., gold. Gold is therefore mainly found in quartz veins. It can therefore be expected that mining of gold will lead towards significant release of quartz. In South African mines the rock generally contains 60 - 90% SiO2 in the crystalline form of quartz (Ref.2). Alpha (low) quartz is the type of silica that is most often released during mining, blasting and construction activities. Cristobalite is associated with ceramic, refractory and diatomaceous earth industries. Cristobalite can also be formed due to processing of crude materials that involve heating to high temperatures. It is therefore important to note that silica quartz can be transformed during industrial processes, especially if heated, and this can change the crystalline structure (Figure 2). Figure 2: Influence of heating and cooling on the crystalline structure of quartz Tridymite Cristobalite The transformed crystalline structure is more pathogenic or toxic than the original alpha quartz crystalline structure. If the heating process does not exceed 578C, beta (high) quartz are formed. It will, however, revert to its original structural and physical property if cooled. If the heating process exceeds 578C but are lower than 1 470C, tridymite will form. Temperatures beyond 1 470C will result in the formation of cristabolite. Neither of the last two transformed structures can revert to alpha quarts. The melting point of transformed quartz is about 1 710C. This is the primary reason why sand is used as moulds because its melting point is higher than most of the metals that are usually used for casting processes (Ref.7). Factors that influence toxicity and potential to induce fibrosis by crystalline silica Quartz, cristobalite and tridymate have the highest potential to introduce fibrosis in the lungs. The biological reactivity of the three types of crystalline silica is not similar. Quartz potential to induce fibrosis is higher than tridymite and tridymite's potential to induce fibrosis is higher than cristobalite (Ref.8). Freshly fractured quartz proved also to have an increased potential to induce a fibrotic reaction in lung tissue compared to that of "aged" quartz. The presence of radicals on the fracture surface is the primary determinant in terms of toxicity. SiOH groups on the surface of crystalline silica are capable to form hydrogen bonds with membrane components. The hydrogen bond formation leads to membrane damage and therefore disruption of cellular integrity (Ref.9). Due to death occurs after a few months, 5-10 years and more than 10 years respectively. Table 1 summarises different occupations that are known to be associated with acute, accelerated and chronic silicosis. Table 1: Difference types of silicosis associated with different occupations (Ref.8) Type of silicosis Acute Accelerated Chronic Occupation Sandblasting, surface drilling, tunneling, silica flour milling, ceramic making, grinding Silica flour mill operations, sandblasting and other mechanically and crushing operations Inhalation of crystalline silica over prolonged periods, + 10 years of exposure to dust containing 18-30% crystalline silica Workers with silicosis are furthermore prone to develop other lung diseases due to the fibrotic effect crystalline silica have on lung tissue. Other lung diseases associated with crystalline silica exposure are increased mycobacterium infections i.e., tuberculosis, bronchogenic carcinoma and immune-mediated diseases i.e., scleroderma. A lifetime exposure to the current Occupational Safety and Health Association (OSHA) standard of 0.1 mg.m3 increase the likelihood to develop lung cancer by 30%. Recently there are indications that nephrotoxicity in workers who are exposed to silica are linked with quartz exposure. There exist numerous case reports linking acute glomerulonephritis with accelerated silicosis (Ref.11). Hotz et al. (Ref.16) mentioned that sub-clinical effects on kidney function may occur in workers who are exposed to silica for short periods. Of the mentioned diseases only silicosis, tuberculosis and bronchogenic carcinoma are compensatable diseases. A primary feature that develops in lungs of silica quartz exposed workers is nodule formation in the upper zones of the lung (Ref.17). Nodule formation is usually the result of many years of exposure to relatively low levels of dust that contain silica quartz (Ref.18). Figure 4: A microscopic photo of a typical silicotic nodule containing collagen fibres in a whorled pattern (Ref.27) The nodules are connective tissue arranged in a whorled pattern, similar to that seen if an onion interaction between crystalline silica and hydrogen ions in membranes of cells. The peroxidation of the phospholipids and unsaturated fatty acids in the membranes of the cellular and intracellular structures, results in damage of the membranes and the generation of oxygen-free radicals (Ref.11) which cause damage to intracellular structures. A result of this is that the membrane structures of the cells become more leaky (permeable) and ions move more freely over the cellular membranes. This renders the cells more vulnerable to chemical and physical stressors. Due to the damage to the intracellular structures, proteolitic enzymes are released into the cytoplasm that results in the death of the macrophage. The destruction of the alveolar macrophages leads to increased proteolitic enzyme release in the lung tissue. The outcome of this is the initiation of fibrotic reactions in the lung. Continued silica exposure and therefore frequent damage to alveolar macrophages leads to an alteration in macrophage function. This leads to activation of humoral and cellular immunity mechanisms and the release of certain inflammatory cytokines e.g., IL-1, free radicals and growth factors (Ref.19); (Ref.20). This stimulates collagen synthesis and production of antibodies against collagen. The anti-collagen antibody stimulates the fibroblasts to produce more collagen formation that eventually leads to nodule formation. Due to the alteration in macrophage function, it is now accepted that quartz exert a genotoxic effect on human cells. Quartz exposure can have a direct, primary genotoxic effect, or an indirect or secondary genotoxic effect because of the inflammation process. Figure 6 summarise all the factors, as already been discussed in the preceding text, that constitute the primary and secondary genotoxic effects quartz may have in the lungs of exposed workers. Figure 6: Primary and secondary genotoxic effects of crystalline silica on lung tissue (Ref.28) Antioxidants and DNA repair mechanisms can restore or reduce the genotoxic effect of particles due to the release of Reactive Oxygen Species (ROS) because of primary and secondary genotoxic mechanisms. If the antioxidant and DNA repair mechanisms are ineffective, the genotoxic effect may lead to apoptosis and necrosis. The increase in apoptosis is dose-dependent and it is described by Lim et al. (Ref.21) to play a role in the silica induced inflammatory process and chronic fibrosis. Apoptotic cells, cells that are programmed to die, and necrotic cells, cannot be repaired. Figure 7 illustrates the relationship between total dust load and classical silicosis. A low total dust exposure results in a much higher incidence of classical silicosis in gold miners and foundry workers compared to coal and haematite, a principal ore of iron, consisting mainly of iron (III) oxide, Fe2O3. A possible explanation for this is that the absorption of other dusts or their constituents onto the silica surface lead to a decrease in silica toxicity and therefore the pathologic response (Ref.11). This confirms the already discussed phenomenon that the surfaces of the crystalline structure play a significant role in the pathogenic potential of the structure.