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Diss Factsheets

Administrative data

Link to relevant study record(s)

Description of key information

As no information specific on Burnt Oil Shale is available, toxicokinetic data concerns crystalline silica as the main toxicologically relevant component. Crystalline silica is not particularly soluble in body fluids and therefore not readily absorbed and distributed. Animal studies indicate that, after oral exposure, most of the silica entering the organism is expected to be excreted unmetabolized via the feces, some silica would be dissolved, absorbed and excreted as silicic acid via urine, and a smaller fraction would remain in the tissue.
Particles deposited in the respiratory bronchioles and proximal alveoli are cleared more slowly and are more likely to injure the lung. Animal studies have shown that respirable quartz particles can be deposited in the lung and translocated into epithelial cells and to the interstitium and may eventually accumulate in the lymph nodes.

Key value for chemical safety assessment

Additional information

There are no available data on basic toxicokinetics specific for Burnt Oil Shale (BOS). Therefore, the information given here regards to crystalline silica as the main toxicologically relevant component. In general, crystalline forms of silica are not particularly soluble in the lung and the gastrointestinal tract and are not absorbed and distributed as readily (US EPA, 1996).

In humans, inhalation of “respirable” particles involves exposure to the particles in a mineral dust that are able to penetrate into the alveolar regions of the lungs. It is generally considered that respirable particles have an aerodynamic diameter of < 3 - 4 µm, while most particles larger than 5 µm may be deposited in the tracheobronchial airways and thus not reach the alveolar region (IARC, 1997). Particles deposited in the respiratory bronchioles and proximal alveoli are cleared more slowly and are more likely to injure the lung. There are few data on quartz dust burdens in human lungs, and no conclusions have been drawn about the clearance kinetics of quartz particles in humans (IARC, 1997). Most of the data regarding disposition of cristobalite particles comes from animal studies. The disposition of cristobalite was monitored in alveolar fluid, free cells, lung tissue and lymph nodes over six months following eight days of exposure of rats for 7 h per day to 11-65 mg/m3 particles with a mass median aerodynamic diameter of around 1.0 µm. 24 hours were allowed to elapse for tracheobronchial clearance and thereafter rats were killed at regular time-points for assessment of the lung burden in the various compartments. The data were then applied to a number of mathematical models and the best fit determined. The model that fitted the data best used no clearance of quartz via the mucociliary escalator, which was explained by the relative toxicity of the test material to macrophages, preventing their movement (Vacek et al., 1991).

The mechanism by which air-borne particles are eliminated from the pulmonary alveoli was studied by exposing rats to the inhalation of silica clouds for brief periods, the distribution of dust being observed in animals killed immediately and at intervals up to 6 months thereafter. The recognition of particles was facilitated by the use of reflected dark-ground illumination. Deposition of dust within the acinus was extensive and irregular. With increasing survival, aggregates formed in relation to proximal respiratory air passages or less commonly in the distal extremity of the acinus (Heppleston, 1963). The clearance of cristobalite and two types of quartz following inhalation exposure in rats was investigated. There were very large differences in the clearance of the three samples, with cristobalite being cleared markedly more slowly than the two types of quartz. These differences have been a result of the greater severity of lung injury and inflammation caused by inhalation of cristobalite compared to the two quartz types (Hemenway et al.,1990). Heating of cristobalite increased its accumulation in the lungs and lymph nodes. Quartz heated to 800°C for 24 h was found in high amounts in the thymus and lymph nodes of rats exposed by inhalation; an unheated sample was biologically inactive (Hemenway et al., 1994). Rat lung clearance of cristobalite primarily occurred within two weeks after short-term inhalation exposure. Particles moved between alveolar space and lung tissues and the concentration in the alveolar space fluctuated depending on the macrophage population. During the months after exposure particles accumulated in the mediastinal lymph nodes and thymus. Kidney, spleen, liver, and blood had negligible concentrations of silica (Absher, 1992). Some studies have investigated absorption, distribution and excretion of silica after exposure via the gastrointestinal tract. Rodent ingestion studies found that 95% of silica is not absorbed and is excreted in the feces unmetabolized; 4% is excreted in urine, and 1% remains in tissues (FASEB, 1979). It is suggested that the healthy gastrointestinal barrier plays hardly any part in both silica absorption and extrapulmonary silicosis (Gonzalez Huergo and Rojo Ortega, 1991). In dogs and rabbits administered silica dust intragastrically, urinary concentrations of silica increased but blood concentrations did not vary significantly. According to the authors, quartz is "slightly" soluble in body fluids and is readily excreted in the urine as silicic acid after absorption following inhalation or ingestion (King et al., 1933). In another study, administration of 5 g quartz in 20 mL of milk by stomach tube to cats showed an average urinary excretion of 20.8 mg silicic acid within 120 hours. Non treated animals excreted an average of 8.6 mg in 120 hours. This suggests that ca. 12.2 mg (corresponding to ca. 0.24% of the administered material) had been absorbed and excreted as silicic acid via urine (King and McGeorge, 1938). In one study, rats receiving silica flour orally in large amounts were shown to have crystals of these substances in uninflammated myocardium. Entry was via the intestinal epithelium (Reimann et al., 1965).