Silica inhalation

Exposures to relatively low concentrations of silica for a prolonged period may be capable of causing hilar node fibrosis, impairing the clearance of any silica inhaled subsequently. In one case, 30 years of exposure to <0.1mg/m led to hilar node fibrosis and calcification in an exposed stonemason subsequent exposure for 5 years to about 2 mg/m led to rapid, progressive silicosis that proved fatal. Estimates of exposure tallied with postmortem measurement of lung burden, suggesting retention of all dust deposited in the lungs over his final period of work. ... 

Vuorio, E.I., Makela, J.K., Vuorio, T.K., Poole, A. and Wagner, J.C. (1989). Characterization of excessive collagen production during development of pulmonary fibrosis induced by chronic silica inhalation in rats. Br. J. Exp. Pathol. 70, 305-315. 

Influence of silica inhalation on the pulmonary clearance of Listeria monocytogenes. Pre-exposure of rats to sihca (15 mg/m ) for 59 days (6 h/day, 5 days/week) caused substantial increases in the number of lavagable neutrophils and lactate dehydrogenase activity compared with the air control, whereas sihca inhalation for both 21 and 59 days significantly enhanced the pulmonary clearance of Listeria monocytogenes compared with air controls (Antonini et d. 2000). 

Asbestos or silica inhalation studies in rats showed that the antioxidant response and, more specifically, mRNA levels of Mn superoxide dismu-tase and heme oxygenase, correlated well with the inflammatory response in broncho-alveolar lavage fluid (Janssen et al. 1992). The upregulation of ornithine decarboxylase (Marsh and Mossman 1991) and c-fosic-jun protooncogenes (Heintz et al. 1993), need further human studies. 

There is a sufficient evidence that crystalline silica inhaled from occupational sources in the form of quartz or cristobalite has carcinogenic properties in humans. There is also sufficient evidence in experimental animals for the carcinogenicity of quartz and cristobalite. Carcinogenicity may be dependent on inherent characteristics of the crystalline silica, or on external factors affecting its biological activity, or distribution of its polymorphs. ACGIH TWA is 0.05 mg/m respirable fraction for cristobalite, quartz, and tridymite forms, and 0.1 mg/m for tripoli. The maximum exposure for up to 30 min per work day should not exceed 5 times... 

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). 

Silica [14808-60-7], crystalline (inhaled in the form of quartz or cristobalite from occupational sources) (Vol. 68 1997) Solar radiation (Vol. 55 1992)... 

Fillers fibreglass, silicas, calcium carbonate, powdered metal pigments some may be absorbed potential primary irritant dust inhalation low toxicity... 

Silane, see Silicon tetrahydride Silica, Amorphous Total inhalable dust Respirable dust Precipitated... 

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). 

Silicosis Pneumoconiosis resulting from inhalation of crystalline silica (quartz). 

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). 

Brown, J.M., Pfau, J.C., and Holian, A., Immunoglobulin and lymphocyte responses following silica exposure in New Zealand mixed mice., Inhal. Toxicol., 16, 133, 2004. 

While some particulates, such as silica, produce well-recognized pathological effects, others, such as carbon dust, are more or less inert. However, there is no dust that does not produce some effect on the lungs when inhaled continually for perhaps years. Excessive concentrations of nuisance dusts in the air may cause reduction in visibility as well as uncomfortable deposits in the eyes, ears, and nasal passages, or even can cause... 

C Foundry workers Foundry sands Silica crystals Suspended dusts Inhalation... 

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. 

Evidence of the relatively benign nature of aluminum dust in measured concentrations lies in the 27-year experience of administration of freshly milled metal particles to workers exposed to silica as a suggested means of inhibiting the development of silicosis. Inhalation of aluminum powder of particle size of 1.2 p, (96%), over 10- or 20-minute periods several times weekly, resulted in no adverse health effects among thousands of workers over several years. 

It has generally been believed that the capacity of inhaled natural graphite dust to cause a disease is largely the result of its crystalline silica component. ... 

Adverse health effects have not been reported for workers exposed to magnesite containing no asbestos and <1% crystalline silica. No cases of human systemic magnesium intoxication from inhalation of magnesite have been reported. 

The 2003 ACGIH threshold limit valuetime-weighted average (TLV-TWA) for particulate matter containing no asbestos and <1% crystalline silica is 3mg/m for respirable size fraction and lOmg/m for inhalable mass fraction. Exposure to any substance in the particulate mass that has a designated TLV should be controlled to that value. 

The 2003 ACGIH proposed threshold limit value-time-weighted average (TLV-TWA) for amorphous silica, natural diatomaceous earth, is lOmg/m for the inhalable particulate and 3mg/m for respirable dust containing no asbestos and <1% quartz. 

In animal studies, significant increases in adenocarcinomas and squamous cell carcinomas of the lung have occurred in rats after inhalation or intratracheal instillation in rats, but not in hamsters. Increasing in vitro and in vivo evidence suggests that the rat lung tumor response to crystalline silica exposure is a result of marked and persistent inflammation and epithelial proliferation. However, other pathways such as a role for crystalline silica surfacegenerated oxidants or a direct genotoxic effect cannot be ruled out. 

Driscoll KE, Lindenschmidt RC, Maurer JK, et al Pulmonary response to inhaled silica or titanium dioxide. Toxicol Appl Pharmacol 111 201-210, 1991... 

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

Individuals whose jobs expose them to unusually high particulate concentrations are especially susceptible to health problems from the pollutant. For example, men and women who work with the mineral asbestos are very prone to development of a serious and usually fatal condition known as asbestosis, in which fibers of the mineral become embedded in the interstices (the empty spaces within tissue) of the lung. Similar conditions are observed among coal workers who inhale coal dust (pneumoconiosis, or black lung disease) textile workers (byssinosis, or brown lung disease) those who work with clay, brick, silica, glass, and other ceramic materials (silicosis) and workers exposed to high levels of beryllium fumes (berylliosis). 

Industrial processes, such as mUling and mining, construction work, and the burning of wood or fossil fuel, generate particulates that can be directly toxic or can serve as vectors for the transfer of bound material, such as sulfuric acid, metals, and hydrocarbons, into the lungs. Natural products such as pollen, anthrax spores, and animal dander can elicit toxic reactions on inhalation or skin contact. The inhalation of asbestos, silica, or coal dust can cause pneumoconiosis, which may develop into serious lung disease. The size of the particle, ventilatory rate, and depth of breathing will determine the extent of pulmonary deposition. 

Inhalation of certain fine dusts may constitute a health hazard. For example, exposure to silica, asbestos, and beryllium oxide dusts over a period of time results in the potential risk of lung disease. OSHA regulations specify the allowable levels of exposure to ingestible and respirable materials. Material Safety Data Sheets, OSHA form 20, available from manufacturers, provide information about hazards, precautions, and storage pertinent to specific refractory products. 

Sealant Manufacturing. Most sealants use mineral-based fillers which may contain small amounts of crystalline silica. If crystalline silica is present, dust control is important to prevent inhalation of these particles. Crystalline silica is a known cause of silicosis, a debilitating disease of the lung. Another common safety concern in sealant manufacturing is the use of flammable materials. Not all sealants use flammable ingredients, but for those that do, proper inerting and grounding are needed to prevent potential explosions. 

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