Stainless Steel Corrosion Products Research Articles

Chromium accumulation and ultrastructural changes in the mouse liver caused by stainless steel corrosion products

Stainless steel (SS) corrosion products were obtained by electrochemical dissolution of SS type AISI 316L. Mice were injected subcutaneously with 0.5 ml of SS solution (containing 283 μg Fe, 69.3 μg Cr and 57 μg Ni) each 72 h, for 10 days or 14 days. After the treatment time, livers were removed and were analysed for: (a) liver wet weight; (b) contents in Fe, Cr and Ni; (c) histological and ultrastructural alterations. Results showed that the percentage of liver weight per animal body weight was significantly higher (p < 0.05) in SS-injected animals than in the control animals. The atomic absorption spectrometry analysis of dry livers showed that chromium, but not iron or nickel, had a significant increase (p < 0.05) in SS-treated mice compared to the control animals. No histopathological differences between 10 and 14 days of SS-injection could be detected, however, massive hepatic degeneration was observed in both groups when compared to the control. These histological changes in SS-treated mice were confirmed at the ultrastructural level, as hepatocytes exhibited an augmentation of vacuoles in their cytoplasm. These actual liver morphological alterations suggest that the hepatocyte function may be hampered, which constitutes a matter of some concern since liver is a blood filtering organ.

Studies on the permeability of the blood-testis barrier in stainless steel-administered mice

Previous trials performed in our laboratory have demonstrated that stainless steel corrosion products induced morphological changes in mice seminiferous cells. In this study the functional nature of the blood-testis barrier was investigated, in view of the extesive use of this metallic alloy in orthopaedic surgery. The uptake of horseradish peroxidase by the seminiferous tubules was used as a tracer method being exposed in vitro for different periods of time and observed at the ultrastructural level. Both boundary cells as well as Sertoli cells of experimental group absorbed the tracer, as manifested by vesicles and vacuoles filled with the reaction product, evidencing its role within the testis. Germ cells were also able in the uptake of this macromolecule. However, the tracer did not spread into the junctional complexes between neighboring Sertoli cells, at any interval of time used in this study, demonstrating the functional integrity of this barrier.

Stainless steel corrosion products cause alterations on mouse spleen cellular populations

Stainless steel is a metallic biomaterial commonly used in orthopaedic surgery. In this study we looked at the effects of stainless steel corrosion products on spleen, in order to evaluate their potential immunotoxicological effects. For this purpose stainless steel, type AISI 316L, was electrochemicallydissolved in a physiological salt solution. The final solution, containing 490 μg/ml Fe, 224 μg/ml Cr and 150 μg/ml Ni, was injected subcutaneously in mice. After several periods of time (4, 10 and 14 days) spleens were removed and analysed for: (a) their contents in Fe, Cr and Ni, (b) histological alterations, (c) enumeration of cellular populations. Results showed that stainless steel corrosion products accumulated in spleen, caused histological alterations, and induced changes in cellular populations. When compared to chromium and nickel, iron was the metal ion preferentially accumulated in spleen. The increase of the multinucleated giant cell population was accompanied by depletion of lymphocyte populations. This study indicates that stainless steel corrosion products can spread systemically and accumulate in spleen inducing histological and cellular alterations which may give rise to immunotoxicological consequences.

Mouse inflammatory response to stainless steel corrosion products

Corrosion occurs regularly following long-term implantation of stainless steel. Little is known about the inflammatory and immunological potential of stainless steel corrosion products. AISI 316L stainless steel was anodically dissolved in a physiologically solution, HBSS, through a chronoamperometric process by imposing an external constant current of 0.5 mA. The solution, containing 245 μg of Fe, 112 μg of Cr, 75 μg of Ni and 13 μg of Mo, was injected in the peritoneal cavity of male C57BL/6 mice. Five animals were used per survival period of time: 4, 16, 24, and 48 h, 1, 2, 4, 8 and 16 weeks. Three control mice per survival period of time were injected with HBSS. For each assay, peritoneal samples were analysed not only for the total number of cells but also for the percentages of macrophages, lymphocytes and polymorphonuclear (PMN) cells, which were estimated by differential counting on Wright-stained cytocentrifuge preparations. Our follow-up study showed that stainless steel corrosion products induced an acute inflammatory response for a period of one week as demonstrated by the influx of PMN cells and macrophages. In contrast neither a chronic inflammation nor an immune response was observed indicating that the stainless steel solution caused a minor tissue response.

Leaching of Am-241 from a Radioactive Waste Glass Corroded in the Presence of Stainless Steel Corrosion Products and/or Bentonite

AbstractThe release of Am-241 during corrosion of the radioactive waste glass, JSS-A, has been studied in the presence of corrosion products and/or uncom-pacted bentonite. The corrosion behaviour of Am-241 has been analyzed using gamma spectrometry. Adsorption of Am-241 on bentonite is observed in all cases. The contents of Am-241 in centrifuged leachates are in most cases less than 1/100 of total values. The normalized elemental mass loss of Am increases initially with corrosion time, and the values in the presence of bentonite and corrosion products are larger than those in the presence of bentonite alone. This tendency is in agreement with results previously found for other elements. The release of Am is low, only about 10–20 % of the corresponding total mass loss.

Static Leaching of Fully Radioactive Waste Glass at 90°C in the Presence of Bentonite, Granite, and Stainless Steel Corrosion Products

AbstractThe results from the JSS phase II static glass leaching experiments are presented. The experiments have been performed in the presence of bentonite, granite and stainless steel corrosion products at 90°C for 28 days. The leaching behaviour of Cs has been analysed using gamma-spectrometry. The surface of the leached glass samples has been analysed by infrared reflection spectrometry.The presence of uncompacted bentonite seems to have a very small, increasing, effect on the leach rate of the glass compared to when no bentonite is present. In the presence of compacted bentonite, a lower leach rate has beep founy than in the prgsencelof uncompacted bentonite. (For Cs 0.3 g × m−2 × d−1 and 0.7 g × m−2 × d−1 respectively.) The addition of stainless steel corrosion products seems to have a slightly increasing effect on the leach rate in the presence of compacted bentonite. The beneficial effect of granite on the leach rate seems to be overshadowed by the presence of uncompacted bentonite.

The binding of metal salts and corrosion products to cells and proteins in vitro.

The binding of metal ions from salts and from corrosion products of 316 LVM stainless steel and MP-35 to blood cells and serum proteins was studied in vitro. In the first series of experiments, metal salts were added to whole blood and then the blood separated into red cells, white cells, and serum. Nickel from nickel chloride or corrosion products of stainless steel bound in very small quantities to blood cells. Cobalt from cobalt chloride bound to both red cells and white cells. Chromium from chromic chloride (Cr3+) bound to cells in very small quantities whereas chromium from potassium dichromate (Cr6+) and corrosion products showed very high to binding to red cells and some binding to white cells. In a second series of experiments the blood was separated into its components and then the metal salts were added and the binding pattern was identical. In a third series of experiments serum which had interacted with the metal salts or corrosion products was separated into its components by isoelectric focusing on polyacrylamide gels. Almost all of the metal, whatever the source, was detected in the albumin region of the gels indicating strong binding to albumin. These studies on the cell and protein binding of the metals help to explain the dissemination of corrosion products from the site of the implant and subsequent systemic responses by some individuals.

Determination of Radiomanganese in Fission Product-Corrosion Product Mixtures.

A procedure is given for the determination of radiomanganese applicable to samples containing fission products and activated stainless steel corrosion products. The method is based on a double precipitation of manganese dioxide, ferric hydroxide scavenging, oxidation to permanganate with silver(II, and precipitation of tetraphenylarsonium permanganate. The stoichiometry and thermal stability of the final precipitate were established. The standard deviation of the method is 1.4%. (auth)