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Relationships between the physical properties of carbon nanotubes (CNTs) and their toxicities have been studied. However, little research has been conducted to investigate the pulmonary and pleural inflammation caused by short-fiber single-walled CNTs (SWCNTs) and multi-walled CNTs (MWCNTs). This study was performed to characterize differences in rat pulmonary and pleural inflammation caused by intratracheal instillation with doses of 0.15 or 1.5mg/kg of either short-sized SWCNTs or MWCNTs. Data from bronchoalveolar lavage fluid analysis, histopathological findings, and transcriptional profiling of rat lungs obtained over a 90-day period indicated that short SWCNTs caused persistent pulmonary inflammation. In addition, the short MWCNTs markedly impacted alveoli immediately after instillation, with the levels of pulmonary inflammation following MWCNT instillation being reduced in a time-dependent manner. MWCNT instillation induced greater levels of pleural inflammation than did short SWCNTs. SWCNTs and MWCNTs translocated in mediastinal lymph nodes were observed, suggesting that SWCNTs and MWCNTs underwent lymphatic drainage to the mediastinal lymph nodes after pleural penetration. Our results suggest that short SWCNTs and MWCNTs induced pulmonary and pleural inflammation and that they might be transported throughout the body after intratracheal instillation. The extent of changes in inflammation differed following SWCNT and MWCNT instillation in a time-dependent manner., (Copyright © 2016 The Authors. Published by Elsevier Ireland Ltd.. All rights reserved.)

Assessing in vitro cellular responses to molecular events is an effective mean to elucidate the toxicological behavior of the ultrafine nanoparticles. In this study, we utilized the DNA microarray analysis technique to determine the gene expression profiles of the human keratinocyte HaCaT cells exposed to anatase titanium dioxide (TiO(2)) particles of different (7 nm, 20 nm and 200 nm) average diameters without illumination. Cells were incubated for 24 h with TiO(2) particles, which were dispersed in the culture medium and size-fractionated such that the concentration of titanium in all the fractionated samples was nearly equivalent. According to the cluster analysis, only genes involved in the 'inflammatory response' and 'cell adhesion', but not the genes involved in 'oxidative stress' and 'apoptosis', were over-represented among the genes that were up-regulated in HaCaT cells. After 24 h exposure to ultrafine 7 nm TiO(2) particles, we observed altered expression levels of genes involved in matrix metalloproteinase activity (MMP-9 and MMP-10) and cell adhesion (fibronectin FN-1, integrin ITGB-6, and mucin MUC-4). These results suggest that the ultrafine TiO(2) particles without illumination have no significant impact on ROS-associated oxidative damage, but affect the cell-matrix adhesion in keratinocytes for extracellular matrix remodeling.

There are several conflicting reports on the genotoxicity of fullerene C(60) in the literature. To determine the genotoxic potential of C(60) nanoparticles, we prepared stable nano-sized C(60) suspensions using 0.1% carboxymethylcellulose sodium (CMC-Na) or 0.1% Tween 80 aqueous solution. We conducted a bacterial reverse mutation test with Ames Salmonella typhimurium TA98, TA100, TA1535, and TA1537 strains and Escherichia coli strain and a chromosomal aberration test with cultured Chinese hamster CHL/IU cells in the presence and absence of metabolic activation under dark conditions and visible light irradiation using a stable C(60) nanoparticle suspension with CMC-Na. In addition, we performed a bone marrow micronucleus test using a stable C(60) nanoparticle suspension with Tween 80 on ICR mice. C(60) nanoparticles did not show a positive mutagenic response up to the maximum dose of 1000 microg/plate with any tester strain in the bacterial reverse mutation test regardless of metabolic activation and irradiation, although a slight but not significant increase in the number of revertants was observed in TA100 and WP2 uvrA/pKM101. No increase in the incidence of chromosomal aberrations was observed at any C(60) nanoparticle dose regardless of metabolic activation and irradiation in the chromosomal aberration test up to the maximum doses of 100 and 200 microg/mL. In addition, the micronucleus test showed that the in vivo clastogenic ability of the C(60) nanoparticles was negative up to the maximum dose of 88 mg/kg x 2. Therefore, we concluded that the stable and well-characterized C(60) nanoparticles did not have genotoxic ability in the bacterial reverse mutation assay, in vitro chromosome aberration assay, nor in vivo micronucleus assay.