Silica dust

Inhalation of crystalline or fused vitreous silica dust, usually overlong periods, causes a disabling, progressive pulmonary disease known as silicosis (84). Amorphous siUcas have not been linked to siUcosis (85), but can cause respiratory irritation. The history and poHtics of siUcosis have been reviewed (86). Standards have been set or recommended for occupational exposures (87,88) and review articles on the health effects of siUca are available (83,89). 

HS(G)72 Control of respirable silica dust in heavy clay and refractory processes... 

Total frequencies of environmental illness are difficult to measure. When causes can be identified, however, scientists observe that frequencies of occurrence of a particular illness vary directly with the severity and extent of exposure. Particularly frequent in the workplace are skin lesions from many different causes and pulmonary diseases related to the inhalation of various dusts, such as coal dust (black lung), cotton dust (brown lung), asbestos fibers (asbestosis), and silica dust (silicosis). Environmental agents can also cause biological effects without overt clinical illness (for example, chromosome damage from irradiation). 

The basis on which the TLVs are set may differ from substance to substance. For some, such as levels for silica dust, a guiding factor is protection against impairment of health. For others, it is the comfort level of the individual, such as freedom from irritation, nuisance, or other forms of stress for example, the TLV for sulfur dioxide is based on irritation and not on toxicity per se. The TLV list is reviewed annually resulting in some revisions in values and some additions to the list. 

An exception may be made when there is good reason to believe that the chief effects of the different harmful substances are not in fact additive, but independent, such as a combined exposure to silica dust and lead dust. In the determination of whether or not the additive effects are excessive, the following formula should be used ... 

As a consequence of the inhalation of mineral dusts, infiltration into the lung of inflammatory phagocytic cells, namely PMN and macrophages, occurs (Rola-Pleszczynski et al., 1984). Analysis of the cell populations of the rat pleural cavities after injection with asbestos and silica dust also showed both degranulation and reduction of the mast cell population (Edwards etal., 1984), and it is of interest to note that histamine augments the particle-stimulated generation of macrophage superoxide production (Diaz et al., 1979). 

Crystalline silica, or quartz, is an abundant mineral found in sand, rock, and soil. Respirable silica dust (particles <5pm) is a known occupational hazard of the dusty trades (e.g., pottery or china manufacturing, work involving sandblasting or abrasive grinding, some construction trades). High level exposure to respirable silica can result in the chronic, progressive lung disease silicosis, characterized by inflammation and fibrosis. 

Occupational exposure to silica dust has been identified as a risk factor for several systemic autoimmune diseases. This literature dates back almost 100 years, to the description by Bramwell of diffuse scleroderma in stone masons.26 Rheumatoid arthritis and scleroderma in miners were described in the 1950s, and more formal cohort studies of miners and of granite workers were conducted in the 1980s. Other studies focusing on silicosis patients, and several case-control studies of these diseases and of Wegner... 

Shawbury, Rapra Technology Ltd., 2002, paper 9, p.65-72, 29 cm, 012 SILICA DUSTS Bonal Y... 

The dust of silicon oxide (silicate) can burn or explode and is very harmful if inhaled. Continued exposure to silica dust causes silicosis, a form of pneumonia. 

Vitums VG, Edwards MJ, Niles NR, Borman JO Pulmonary fibrosis from amorphous silica dust. A product of silica vapor. Arch Environ Health 32 62-68, 1977... 

The progression of symptoms may continue after dust exposure ceases. Although there may be a factor of individual susceptibility to a given exposure to silica dust, the risk of onset and the rate of progression of the pulmonary lesion are clearly related to the character of the exposure (dust concentration and duration). The disease tends to occur after an exposure measured in years rather than in months. It is generally accepted that silicosis predisposes to active tuberculosis and that the combined disease tends to be more rapidly progressive than uncomplicated silicosis. 

Inhalation of silica dusts or sdicate mineral dusts can cause silicosis and other lung diseases. 

Aerosol exposures were at 6, 20, and 60 mg/rn for 5 min on days 6-13 of pregnancy in rats and days 6-18 of pregnancy in rabbits. Control aerosols consisted of water or suspensions of Neosil (silica dust), and the experiments were conducted with 12-24 animals. The adults were killed a day before parturition rat fetuses were examined for 18 abnormalities and rabbit fetuses for eight abnormalities. In addition, rats were studied for teratogenic effects after exposure to CS by intraperitoneal injection at 20 mg/kg on day 6, 8, 10, 12, or 14 of pregnancy. 

Silicosis occurs in industries in which the air is polluted by silica dust, e g., pottery, metal grinding, sandblasting and mining in rock. The inhaled silica gives rise to the production of diffuse fibrosis in the lungs moreover it facilitates the growth of the tubercle bacillus so that tuberculosis is a possible complication. A special form of silicosis, called anthracosis (black lung), occurs in coal miners who are exposed to a mixed dust, mainly of coal, with a small proportion of silica. 

The conformation of adsorbed protein was studied by means of FTIR spectroscopy. A BSA solution (12.5 mL of 500mg/L) was incubated with 125 mg of silica dusts for 5 min at 298 K. The powder was then separated from the supernatant by centrifugation (4000g for 10 min). The protein not adsorbed was removed from the dusts by washing four times in PBS. The dusts were then resuspended in 100 pi of PBS 0.01M prepared in D20 medium and incubated for 1 h at room temperature to exchange the H20 adsorbed on the sample with D20. The exchange was repeated three times. 

Qzm and A50 have different affinities for BSA. Since the experiment was done at constant pH and ionic strength, the observed differences in the amount of BSA adsorbed, and the different conformation of BSA on the two silica dusts, is ascribed to the intrinsic properties of the two silica forms such as size and morphology (down to a micro- and nano level), surface hydrophilicity, impurities at the surface, and surface charge. Qzm and A50 particles are, in fact, very different entities they differ in particle dimensions (Qzm mean diameter 1600 nm, A50 40 nm) and bulk structure, which involves different surface features such as silanol population, (quartz exhibits around 5 SiOH/nm2, A50 2-3 SiOH/nm2), hydrophilicity, micromorphology (quartz particles exhibit steps and edges due to the grinding processes, fumed silica is made up by roundish particles) and the presence of metal ion impurities. 

EFFECT OF THE SURFACE FEATURES ON IN VIVO AND/OR IN VITRO TOXICITY OF THE SILICA DUSTS... 

The reaction of the inhaled particles with endogenous molecules present in the pulmonary surfactant e.g. surfactant, antioxidant molecules and proteins may determine the fate of the particles in the early steps of the pathological process. Although the silica samples considered in the present work are very pure, with the SiC>2 content great then 98%, they strongly differ in surface properties. The observed different interaction of BSA with the dusts considered is a consequence of such variability. Since the response of macrophages to silica particles may be different depending on the amount of protein adsorbed, the in vivo and/or in vitro toxicity of the silica dusts may be affected by the different affinities for pulmonary surfactant proteins. 

Silica dust can be present in industrial atmospheres in three forms,ok quartz, cristobalite and tridymite, depending upon the process temperatures. When cristobalite or tridymite are present, one-half the value of the threshold limit formula is used. The validity of the results depends on the cyclone and pump system... 

It is this unpredictable and puzzling chemical reactivity which makes freshly formed silica dust a chemical poison that causes silicosis when it is inhaled. In many processes which deal with mineral products—e.g., the setting of cements, the milling of enamels and of pigments, the slaking of lime, etc.—solids with freshly formed surfaces are brought into contact with water. For understanding these phenomena the kinetics of hydration of incompletely screened surfaces has to be considered. 

---