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EC number: 231-130-8
CAS number: 7440-21-3
Johnston et al. (2000) conducted
a 90-day subchronic inhalation toxicity study with amorphous and
crystalline silica. The exposure pattern followed OECD test 413 guidance
'Subchronic inhalation toxicity: 90-day study'. The GLP status was not
mentioned. Male Fischer-344 rats (200–250 g) were exposed for 6 h/day,
on 5 days/wk, for up to 13 weeks to 3 mg/m3crystalline
(cristobalite, mass median aerodynamic diameter 1.3 μm) or 50 mg/m3amorphous
silica (hydrophilic pyrogenic Aerosil® 200 Degussa, mass median
aerodynamic diameter 0.81 μm). The genotoxic effects on the lung were
characterized 13 weeks of exposure. Endpoints included mutation in thehprtgene
of isolated alveolar cells in anex vivoassay, changes in
bronchoalveolar lavage (BAL) fluid markers of cellular and biochemical
lung injury and inflammation, expression of mRNA for the chemokine
MIP-2, and detection ofapoptosis. After 13 weeks of exposure, the
percentage of lavage neutrophils, MIP-2 expression, and lactate
dehydrogenase levels as an indicator of cytotoxicity were increased in
both silicas. All parameters remained increased for crystalline silica
and decreased rapidly for amorphous silica during the 8-month recovery
period. Increasedhprtmutation frequency in alveolar epithelial
cells was detected with crystalline silica, but not with amorphous
silica. Increased TUNEL staining indicative for apoptosis was seen in
macrophages and terminal bronchiolar epithelial cells mainly after
exposure to amorphous silica. Lung burdens of silica were 819 and 882 μg
for crystalline and amorphous silica, respectively. In summary,
genotoxic effects in alveolar epithelial cells occurred only after
crystalline but not amorphous silica exposure, despite a high degree of
inflammatory response after subchronic exposure to both types of silica.
The authors suggest that the additional factors to inflammation, such as
biopersistence of particles and direct or direct cytotoxicity to target
cells, are important determinants of secondary genotoxic events.
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