No abstract

Much concern has been raised over the health consequences of workers exposed to carbon nanotubes. In order to characterize multi-wall carbon nanotubes (MWCNT) suspended in a phosphate-buffered saline containing 0.1% Tween 80 for an intratracheal instillation study.

The dissolution rates of rare earth oxides and two types of rare earth containing functional materials into water, saline solution, and Gamble's fluid were measured in order to evaluate the biological effects of rare earth-containing functional materials. The tested materials were yttrium, lanthanum, cerium and neodymium oxides, and neodymium-boron-iron magnet alloy (NdBFe) and lanthanum-mish-metal-nickel-cobalt (LmNiCo) hydrogen-containing alloy. The dissolution rates of the rare earth oxides were very low, resulting in concentrations of rare earth elements in the test solutions of the order of ppb. In the most extreme case, Gamble's fluid dissolved 1,400 times more of the rare earth oxides than pure water. Fairly high concentration of neodymium were found in the dissolving fluids, which means that trace neodymium present as an impurity in each rare earth oxide dissolved preferentially. For yttrium oxide, the ratio of neodymium to yttrium that dissolved in the saline solution was greater than 78,000 to 1, taking into account the amount of each that was originally present in the yttrium oxide.

No abstract

This study aimed to (1) determine the deposition and clearance rates of utrafine metallic nickel (Uf-Ni) in rats after a 5 hours single inhalation exposure, and (2) to histopathologically examine the pulmonary lesions induced at dose levels comparable to the Occupational Exposure Limit recommended in Japan (OEL). The exposure concentrations of Uf-Ni for the 3 groups were 0.15 (Low), 1.14 (Medium), and 2.54 (High) mg/m3. Five rats/group were sacrificed at Oh and 1, 3, 7, 14, and 21 days post exposure. The amount of Ni in the lung accumulated dose-dependently. The halftimes for Ni in the lung were estimated as 32 days on average, and were similar to each other regardless of the initial dosage. The histopathologically observed pulmonary lesions induced by a single inhalation of Uf-Ni were, (1) a significant increase in lung weight in the High and Medium groups with time, (2) accumulation of foamy alveolar macrophages (AM), (3) degenerated AM indicating alveolar lipoproteinosis which was aggravated for up to 4 weeks in the High group and (4) acute calcification of the degenerated AM was remarkable. The present results suggest that even a single inhalation of Uf Ni induces potency of lung lesions at dose levels comparable to the OEL (1 mg/m3 as Ni), or the TWA of ACGIH (1.5 mg/m3 for elemental/metal).

Acute and subacute lung toxicity of nickel fumes was examined by single and repeated intratracheal instillation of nickel fumes and Ni203 and NiO powders in the rat. LD50 of nickel fumes was estimated as 38.2 mg/kg body weight (b.w.) according to the method of Litchfield and Wilcoxon. Body weight gain was retarded as in the order of a single dose of 13.0 mg Ni203/kg>14.3 mg nickel fumes/kg>1.4 mg Ni203/kg>13.0 mg Ni0/kg b.w. compared to controls. The histopathological changes in the lungs of the 14.3 mg nickel fumes/kg-dosed rats were milder than those induced by administration of 13.0 mg Ni203/kg but severer than those induced by administration of 1.4 mg Ni203/kg b.w. A single administration of NiO powder did not produce any histopathological effects on the lungs. The repeated administration of nickel fumes produced persistent edema and proteinosis in the alveoli. The nickel fumes, which were chemically composed of 97% of NiO and 3% of Ni203, were very fine particles about 5-10 nm in diameter, partly aggregated into larger particles and spherical particles about 0.6 ,um in diameter. Solubility in distilled water and saline was in the order of nickel fumes>Ni203 powder>>NiO powder. It was suggested that a toxic Ni203 component and very fine particles of nickel fumes are involved in the acute lung toxicity of nickel fumes. The epithelial injury induced by reactive oxygen and hydroxy radicals, which would be produced during the process of conversion of Ni(III) to Ni(II) and phagocytosis of nickel fumes by macrophages and polymorphonuclear cells, are presumed to be involved in the pathogenesis of nickel fumes-induced lung lesion.

No abstract

The dimensions of man-made mineral fiber whiskers are similar to those of some kinds of asbestos. Thus these mineral fibers raise the concern for potential health hazard for workers exposed in the occupational environments. This study was designed to define acute biological effects of intratracheally administered titanium dioxide whiskers (TO1) compared with nonfibrous titanium dioxide (TOP) and UICC amosite (Ams), and their relations to acute lung inflammation in rats. The observed geometric mean length (microm) and width (microm) and geometric standard deviation are: TO1(2.1[2.0], 0.14[1. 53]); Ams (4.3[3.3], 0.31[1.9]); and TOP (50 nm, 1-2 microm aggregates). Ten-week-old Wistar-Jcl male rats received a single tracheal injection of test materials at doses between 0.05 and 1.0 mg/rat. Control animals were injected with the same volume of saline. Lung tissue and bronchoalveolar lavage (BAL) fluid were collected from rats on days 1, 3, and 7 after administration. In the group injected with TO1, total protein, cytokine-induced neutrophil chemoattractant (CINC)/growth-regulated gene product (GRO), interleukin (IL) 1beta, and tumor necrosis factor (TNF) alpha increased on day 1. Subsequently, total elastolytic activity and fucose levels in BAL increased by day 3. All parameters, except for fucose in BAL, recovered to the normal levels. Animals in the Ams group showed increased total protein and CINC/GRO and decreased total elastolytic activity in a dose-dependent manner on day 1. The fucose level increased on day 3 in the Ams group. All parameters returned to their control levels on day 7. Animals in the TOP group did not show significant changes any of parameters during the experimental period. Gene expression of TNF-alpha and monocyte chemoattractant protein (MCP) 3 in the lung increased dose-dependently in the animals treated with the three materials. The mRNAs for eotaxin and MIP-1alpha were overexpressed in the lung of animals treated with Ams and TO1, while RANTES mRNA was overexpressed dose-dependently in the lung of animals treated with Ams on day 1. Onset of inflammatory response was more rapid in the Ams group than the TO1 group. Recovery of the fucose level in BAL was slower in the TO1 group than in the Ams group, though we observed similar histopathological changes in the lung of animals with TO1 or Ams. We conclude that whisker-induced acute biological effects in the lung may be related to the shape of the whiskers and not to their chemical composition or surface crystal structure, showing biological effects similar to those of UICC amosite.