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|Title:||Epoxy composite dusts with and without carbon nanotubes cause similar pulmonary responses, but differences in liver histology in mice following pulmonary deposition|
|Authors:||SABER Anne T; MORTENSEN Alicja; SZAREK Jozef; KOPONEN Ismo Kalevi; LEVIN Marcus; JACOBSEN Nicklas R; POZZEBON Maria Elena; MUCELLI Stefano P; RICKERBY David; KLING Kirsten; ATLURI Rambabu; MADSEN Anne Mette; JACKSON Petra; KYJOVSKA Zdenka O.; VOGEL Ulla; JENSEN Keld Astrup; WALLIN Håkan|
|Citation:||PARTICLE AND FIBRE TOXICOLOGY vol. 13 no. 1 p. 1-20|
|Publisher:||BIOMED CENTRAL LTD|
|Type:||Articles in periodicals and books|
|Abstract:||Background: The toxicity of dusts from mechanical abrasion of multi-walled carbon nanotube (CNT) epoxy nanocomposites is unknown. We compared the toxic effects of dusts generated by sanding of epoxy composites with and without CNT. The used CNT type was included for comparison. Methods: Mice received a single intratracheal instillation of 18, 54 and 162 μg of CNT or 54, 162 and 486 μg of the sanding dust from epoxy composite with and without CNT. DNA damage in lung and liver, lung inflammation and liver histology were evaluated 1, 3 and 28 days after intratracheal instillation. Furthermore, the mRNA expression of interleukin 6 and heme oxygenase 1 was measured in the lungs and serum amyloid A1 in the liver. Printex 90 carbon black was included as a reference particle. Results: Pulmonary exposure to CNT and all dusts obtained by sanding epoxy composite boards resulted in recruitment of inflammatory cells into lung lumen: On day 1 after instillation these cells were primarily neutrophils but on day 3, eosinophils contributed significantly to the cell population. There were still increased numbers of neutrophils 28 days after intratracheal instillation of the highest dose of the epoxy dusts. Both CNT and epoxy dusts induced DNA damage in lung tissue up to 3 days after intratracheal instillation but not in liver tissue. There was no additive effect of adding CNT to epoxy resins for any of the pulmonary endpoints. In livers of mice instilled with CNT and epoxy dust with CNTs inflammatory and necrotic histological changes were observed, however, not in mice instilled with epoxy dust without CNT. Conclusions: Pulmonary deposition of epoxy dusts with and without CNT induced inflammation and DNA damage in lung tissue. There was no additive effect of adding CNT to epoxies for any of the pulmonary endpoints. However, hepatic inflammatory and necrotic histopathological changes were seen in mice instilled with sanding dust from CNT-containing epoxy but not in mice instilled with reference epoxy.|
|JRC Directorate:||Health, Consumers and Reference Materials|
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