Oil shale, thermal processing waste

Endpoint summary

Description of key information

No studies via oral or dermal exposure are available for Burnt Oil Shale (BOS), and limited or no data are available on crystalline silica for the same exposure routes. Toxicokinetic data of crystalline silica suggest minimal absorption and bioavailability upon oral exposure and virtually no absorption via the dermal route.
Lung inflammation, cellular proliferation and ultimately fibrosis are the main toxic effects most likely to occur after repeated short- and long-term exposure to respirable crystalline silica particles (MMAD < 5 µm). Animal dose-response data for crystalline silica are limited. The lowest published toxic concentration for chronic (two-year intermittent) inhalation exposure in rats was 0.74 mg/m³. However, human data indicate a significant risk of developing chronic silicosis at exposure levels as low as 0.05 mg/m³ in occupational settings. Therefore, 0.05 mg/m³ is regarded as the LOAEC for respirable crystalline silica.

Key value for chemical safety assessment

Repeated dose toxicity: via oral route - systemic effects

Endpoint conclusion

Endpoint conclusion:

no study available

Repeated dose toxicity: inhalation - systemic effects

Endpoint conclusion

Endpoint conclusion:

no study available

Repeated dose toxicity: inhalation - local effects

Endpoint conclusion

Endpoint conclusion:

adverse effect observed

Dose descriptor:

LOAEC

0.05 mg/m³

Species:

other: epidemiological human data

Repeated dose toxicity: dermal - systemic effects

Endpoint conclusion

Endpoint conclusion:

no study available

Repeated dose toxicity: dermal - local effects

Endpoint conclusion

Endpoint conclusion:

no study available

Additional information

Repeated dose toxicity: oral

There are no data available on the toxicity of Burnt Oil Shale (BOS) upon repeated oral exposure. There are limited animal data available on oral exposure to crystalline silica, the main toxicologically relevant component of BOS. Due to its physicochemical properties and based on the available data on toxicokinetics of crystalline silica (see Chapter 7.1), no relevant absorption via the gastrointestinal tract is expected. However, renal effects after subchronic oral exposure have been reported in one animal study. Male guinea pigs exposed to crashed quartz via drinking water (250 mg/L) for four months showed tubulointerstitial nephritis. Lesions were, however, more severe in animals given magnesium trisilicate (Dobbie and Smith, 1982). 

Additionally, available information on amorphous silica was also taken into account.

Rats exposed to fumed hydrophobic silica in diet for 35 days showed histopathological changes in the liver (atrophy of the epithelium, decrease of the basophilic nuclei and of the glycogen content) at 1000 mg/kg bw/day and higher. No treatment-related effects were observed in rats fed 500 mg/kg bw/day (Lewinson et al., 1994). In another study with the same type of silica, no effects were observed in rats exposed to 500 mg/kg bw/day in diet for 6 months (Lewinson et al., 1994). In other studies, higher oral NOAEL values (≥2500 mg/kg bw/day) have been reported for rats and mice after subacute exposure and rats after subchronic and chronic exposure (OECD SIDS, 2004).

 

Repeated dose toxicity: dermal

 

There are no data available on the toxicity of Burnt Oil Shale (BOS) upon repeated dermal exposure. There are no animal data available on dermal exposure to crystalline silica, the main toxicologically relevant component of BOS. Due to its physicochemical properties and based on the available data on toxicokinetics of crystalline silica (see Chapter 7.1), no relevant absorption through the epithelium of the gastrointestinal tract is expected, and hence, both crystalline silica particles and BOS are very unlikely to be absorbed by the skin.

 

Repeated dose toxicity: inhalation

 

There are no data available on the toxicity of Burnt Oil Shale (BOS) upon repeated inhalation exposure. There are animal data available on inhalation exposure to crystalline silica (quartz), the main toxicologically relevant component of BOS.

Quartz dust induces cellular inflammationin vivo. Inhalation of aerosolized quartz particles impairs alveolar macrophage clearance functions and leads to progressive lesions and pneumonitis. Long-term inhalation studies of rats and mice have shown that quartz particles produce cellular proliferation, nodule formation, suppressed immune functions, and alveolar proteinosis. Adequate dose-response data for rats or other rodents are not available because few multiple-dose studies have been performed (IPCS 2000).

Fischer-344 (F344) rats were exposed for 6 h/day, 5 days/week for 6 months to 0, 2, 10, or 20 mg Min-U-Sil 5/m³. Exposure to these silica particles (MMAD 2.4 µm) increased collagen and elastin content of lungs; caused birefringent crystals in foamy cytoplasm of macrophages that had accumulated in end airway luminal spaces; and induced Type II cell hyperplasia in alveolar compartment and intralymphatic microgranulomas around bronchioles in some animals. Quartz-dependent increases in collagen and elastin were 110%, 111%, and 116% for collagen (as hydroxyproline) and 102%, 109%, and 109% for elastin, respectively, for each exposure group relative to controls. The lowest exposure level of 2 mg/m³ is regarded as the LOAEC based on lung composition data and histopathological findings (Kutzman, 1984a).

In the same study, a satellite group of Fischer-344 (F344) rats, which had been exposed for 6 h/day, 5 days/week for 6 months to 0, 2, 10, or 20 mg Min-U-Sil 5/m3, were then maintained for further 6 months under SPF conditions prior to assessment. Exposure to these silica particles increased weight and collagen, elastin, deoxyribonucleic acid, and protein content of lungs (particularly at higher exposures of 10 and 20 mg/m³), indicating continued tissue proliferation and fibrogenesis during incubation; increased number of silica particles and inflammation at end airways, focal fibrosis and intralymphatic granulomata, and overall severity and frequency of lesions. Alveolar proteinosis observed in the 20 mg/m³ group. Quartz increases in collagen and elastin were 116%, 128%, and 136% for collagen (as hydroxyproline) and 107%, 119%, and 130% for elastin, respectively, for each exposure group relative to controls. The lowest exposure level of 2 mg/m³ is regarded as the LOAEC based on lung composition data and histopathological findings (Kutzman, 1984b).

A chronic inhalation study of crystalline silica (DQ-12, MMAD 1.4 µm) was conducted by exposure of groups of F-344 rats for 6 hr/day, 5 days/week for 24 months. Crystalline silica concentration was 1 mg/m³, and the concentration of respirable aerosol was reported to be 0.74 mg/m³. Lung inflammation and a time-dependent increase in lung-to-body weight relative to control were observed. By the end of the study, 92.3% of the treated animals showed moderate lung fibrosis. Furthermore, primary lung tumours occurred in 19% of the silica-exposed rats, while tumour incidence occurred in 3% of the control animals. Survival was not affected by the particle treatment (Muhle et al., 1991). The respirable aerosol concentration of 0.74 mg/m³ is the lowest published toxic concentration for chronic inhalation exposure in rats (NTP, 2009).

Studies carried out to compare the toxic potential of amorphous and crystalline silica both after short- and long-term inhalative exposure have clearly shown that effects induced by crystalline are generally more severe than those induced by amorphous silica. Adverse effects mainly include inflammatory responses in the lung at early stages which may lead to the development of fibrosis/silicosis at later time points (Arts et al., 2007; Johnston et al., 2000; Pratt, 1983; Reuzel et al., 1991; Schepers, 1981; Wahrheit, 1995).

Several epidemiologic studies demonstrate that workers have a significant risk of developing chronic silicosis when they are exposed to respirable crystalline silica over a working lifetime at a mean concentration of 0.05 mg/m³ (NIOSH, 2002). Therefore, this concentration is regarded as the LOAEC for chronic silicosis in humans.

Justification for selection of repeated dose toxicity inhalation - local effects endpoint:
No study was selected as the relevant information regarding the effect level was derived from epidemiological human data.

Justification for classification or non-classification

Burnt Oil Shale is mainly composed of silica. The respirable fraction of the crystalline polymorph (i.e. crystalline silica particles with a mean aerodynamic diameter (MMAD) ≤5 µm) represents the component of major toxicological concern. Therefore, classification and labelling of Burnt Oil Shale will be determined by the overall content of respirable crystalline silica.

 

Respirable crystalline silica causes damage mainly restricted to the lung after repeated exposure by inhalation.

 

Thus, by applying the generic concentration limits determining the classification of a preparation according to the Dangerous Preparations Directive (DPD), Burnt Oil Shale will be classified as follows:

 

- T, R48/23, for a respirable crystalline silica concentration ≥10% by weight.

- Xn, R48/20, for a respirable crystalline silica concentration between 1% and <10% by weight.

- No classification needed for a respirable crystalline silica concentration <1% by weight.

 

By applying the generic concentration limits of ingredients of a mixture classified as a specific target organ toxicant that trigger classification of a mixture according to CLP, Burnt Oil Shale will be classified as follows:

 

- STOT-RE Cat. 1, for a respirable crystalline silica concentration ≥10% by weight.

- STOT-RE Cat. 2, for a respirable crystalline silica concentration between 1% and <10% by weight.

- No classification needed for a respirable crystalline silica concentration <1% by weight.