121 research outputs found
Mechanistic studies of corrosion product flaking on copper and copper-based alloys in marine environments
AbstractThe mechanism of corrosion product flaking on bare copper sheet and three copper-based alloys in chloride rich environments has been explored through field and laboratory exposures. The tendency for flaking is much more pronounced on Cu and Cuâ4wt%Sn than on Cuâ15wt%Zn and Cuâ5wt%Alâ5wt%Zn. This difference is explained by the initial formation of zinc and zincâaluminum hydroxycarbonates on Cu15Zn and Cu5Al5Zn, which delays the formation of CuCl, a precursor of Cu2(OH)3Cl. As a result, the observed volume expansion during transformation of CuCl to Cu2(OH)3Cl, and concomitant corrosion product flaking, is less severe on Cu15Zn and Cu5Al5Zn than on Cu and Cu4Sn
Surfaceârain interactions: Differences in copper runoff for copper sheet of different inclination, orientation, and atmospheric exposure conditions
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Bioaccessibility, bioavailability and toxicity of commercially relevant iron- and chromium-based particles: in vitro studies with an inhalation perspective
<p>Abstract</p> <p>Background</p> <p>Production of ferrochromium alloys (FeCr), master alloys for stainless steel manufacture, involves casting and crushing processes where particles inevitably become airborne and potentially inhaled. The aim of this study was to assess potential health hazards induced by inhalation of different well-characterized iron- and chromium-based particles, i.e. ferrochromium (FeCr), ferrosiliconchromium (FeSiCr), stainless steel (316L), iron (Fe), chromium (Cr), and chromium(III)oxide (Cr<sub>2</sub>O<sub>3</sub>), in different size fractions using in vitro methods. This was done by assessing the extent and speciation of released metals in synthetic biological medium and by analyzing particle reactivity and toxicity towards cultured human lung cells (A549).</p> <p>Results</p> <p>The amount of released metals normalized to the particle surface area increased with decreasing particle size for all alloy particles, whereas the opposite situation was valid for particles of the pure metals. These effects were evident in artificial lysosomal fluid (ALF) of pH 4.5 containing complexing agents, but not in neutral or weakly alkaline biological media. Chromium, iron and nickel were released to very low extent from all alloy particles, and from particles of Cr due to the presence of a Cr(III)-rich protective surface oxide. Released elements were neither proportional to the bulk nor to the surface composition after the investigated 168 hours of exposure. Due to a surface oxide with less protective properties, significantly more iron was released from pure iron particles compared with the alloys. Cr was predominantly released as Cr(III) from all particles investigated and was strongly complexed by organic species of ALF. Cr<sub>2</sub>O<sub>3 </sub>particles showed hemolytic activity, but none of the alloy particles did. Fine-sized particles of stainless steel caused however DNA damage, measured with the comet assay after 4 h exposure. None of the particles revealed any significant cytotoxicity in terms of cell death after 24 h exposure.</p> <p>Conclusion</p> <p>It is evident that particle and alloy characteristics such as particle size and surface composition are important aspects to consider when assessing particle toxicity and metal release from alloy particles compared to pure metal particles. Generated results clearly elucidate that neither the low released concentrations of metals primarily as a result of protective and poorly soluble surface oxides, nor non-bioavailable chromium complexes, nor the particles themselves of occupational relevance induced significant acute toxic response, with exception of DNA damage from stainless steel.</p
Metal bioaccessibility in synthetic bodyfluidsâA way to considerpositive and negative alloying effects in hazard assessments
Hazard classification of metal alloys is today generally based on their bulk content, an approach that seldom reflects the extent of metal release for a given environment. Such information can instead be achieved via bioelution testing under simulated physiological conditions. The use of bioelution data instead of bulk contents would hence refine the current hazard classification of alloys and enable grouping. Bioelution data have been generated for nickel (Ni) and cobalt (Co) released from several stainless steel grades, one low-alloyed steel, and Ni and Co metals in synthetic sweat, saliva and gastric fluid, for exposure periods from 2 to 168 h. All stainless steel grades with bulk contents of 0.11â10 wt% Ni and 0.019â0.24 wt% Co released lower amounts of Ni (up to 400-fold) and Co (up to 300-fold) than did the low-alloyed steel (bulk content: 0.034% Ni, 0.015% Co). They further showed a relative bioaccessibility of Ni and Co considerably less than 1, while the opposite was the case for the low-alloyed steel. Surface oxide- and electrochemical corrosion investigations explained these findings in terms of the high passivity of the stainless steels related to the Cr(III)-rich surface oxide that readily adapted to the fluid acidity and chemistry
Cobalt nanoparticles trigger ferroptosis-like cell death (oxytosis) in neuronal cells : Potential implications for neurodegenerative disease
Abstract The neurotoxicity of hard metal-based nanoparticles (NPs) remains poorly understood. Here, we deployed the human neuroblastoma cell line SH-SY5Y differentiated or not into dopaminergic- and cholinergic-like neurons to study the impact of tungsten carbide (WC) NPs, WC NPs sintered with cobalt (Co), or Co NPs versus soluble CoCl2. Co NPs and Co salt triggered a dose-dependent cytotoxicity with an increase in cytosolic calcium, lipid peroxidation, and depletion of glutathione (GSH). Co NPs and Co salt also suppressed glutathione peroxidase 4 (GPX4) mRNA and protein expression. Co-exposed cells were rescued by N-acetylcysteine (NAC), a precursor of GSH, and partially by liproxstatin-1, an inhibitor of lipid peroxidation. Furthermore, in silico analyses predicted a significant correlation, based on similarities in gene expression profiles, between Co-containing NPs and Parkinson's disease, and changes in the expression of selected genes were validated by RT-PCR. Finally, experiments using primary human dopaminergic neurons demonstrated cytotoxicity and GSH depletion in response to Co NPs and CoCl2 with loss of axonal integrity. Overall, these data point to a marked neurotoxic potential of Co-based but not WC NPs and show that neuronal cell death may occur through a ferroptosis-like mechanism.Peer reviewe
Adsorption of bio-organic eco-corona molecules reduces the toxic response to metallic nanoparticles in <i>Daphnia magna</i>
As the use of engineered nanomaterials increases, so does the risk of them spreading to natural ecosystems. Hitherto, knowledge regarding the toxic properties of nanoparticles (NPâs) and their potential interactions with natural bio-organic molecules adsorbed to them, and thereby forming surface coronas, is limited. However, we show here that the toxic effect of NPs of tungsten carbide cobalt (WCâCo) and cobalt (Co) on the crustacean Daphnia magna is postponed in the presence of natural biological degradation products (eco-corona biomolecules). For Daphnia exposed to WCâCo NPs the survival time increased with 20â25% and for Co NPs with 30â47% after mixing the particles with a solution of eco-corona biomolecules before exposure. This suggests that an eco-corona, composed of biomolecules always present in natural ecosystems, reduces the toxic potency of both studied NPs. Further, the eco-coronas did not affect the particle uptake, suggesting that the reduction in toxicity was related to the particle-organism interaction after eco-corona formation. In a broader context, this implies that although the increasing use and production of NPs may constitute a novel, global environmental threat, the acute toxicity and long-term effects of some NPs will, at least under certain conditions, be reduced as they enter natural ecosystems
Location of cobalt impurities in the surface oxide of stainless steel 316L and metal release in synthetic biological fluids
Since 2021, cobalt (Co) is in Europe classified as carcinogen in quantities exceeding 0.1 wt-%. This affects nickel-rich stainless steels, which contain about 0.2 wt-% Co impurities. Previous findings show the bioaccessibility of Co in stainless steel to be primarily determined by the corrosion resistance. It has been unclear whether Co is distributed heterogeneously in the alloy and the outermost surface and whether a specific location would pose a risk for Co release under specific exposure conditions. This study aimed at locating Co in stainless steel 316L (0.2 wt-% Co) surfaces prior to and after exposure to different synthetic body fluids for 24 h at 37 °C. Time-of-flight secondary ion mass spectrometry (ToF-SIMS), X-ray photoelectron spectroscopy (XPS), and inductively coupled plasma mass spectrometry (ICPMS) investigated the location of Co in the surface oxide and extent of release along with other metals (iron, chromium, nickel, and manganese) into synthetic biological fluids (gastric fluid, pH 1.5; lysosomal fluid, pH 4.5; phosphate buffered saline-PBS, pH 7.4). Co was homogeneously distributed along with metallic nickel beneath the surface oxide and co-released with other metals upon surface reformation and passivation. Exposure in PBS resulted in the incorporation of both Co and phosphate in the oxide
Surface modified Ti6Al4V for enhanced bone bonding ability - effects of silver and corrosivity at simulated physiological conditions from a corrosion and metal release perspective
Abstract Different surface treatments, with and without silver (Ag), of a Ti6Al4V alloy for increased bone bonding ability were investigated and compared with non-treated surfaces. Studies were conducted at 37â°C in phosphate buffered saline (PBS, pH 7.4) of varying hydrogen peroxide (H2O2) and bovine serum albumin (BSA) concentrations. Increased levels of metal release and corrosion were observed in the presence of both H2O2 and BSA due complexation with Ti and Al in the surface oxide, respectively. Ag release was enhanced by the presence of BSA. Galvanic effects by Ag were minor, but possibly observed in the most corrosive environment
Corrosion and runoff rates of Cu and three Cu-alloys in marine environments with increasing chloride deposition rate
AbstractBare copper sheet and three commercial Cu-based alloys, Cu15Zn, Cu4Sn and Cu5Al5Zn, have been exposed to four test sites in Brest, France, with strongly varying chloride deposition rates. The corrosion rates of all four materials decrease continuously with distance from the coast, i.e. with decreasing chloride load, and in the following order: Cu4Sn>Cu sheet>Cu15Zn>Cu5Al5Zn. The patina on all materials was composed of two main layers, Cu2O as the inner layer and Cu2(OH)3Cl as the outer layer, and with a discontinuous presence of CuCl in between. Additional minor patina constituents are SnO2 (Cu4Sn), Zn5(OH)6(CO3)2 (Cu15Zn and Cu5Al5Zn) and Zn6Al2(OH)16CO3·4H2O/Zn2Al(OH)6Cl·2H2O/Zn5Cl2(OH)8·H2O and Al2O3 (Cu5Al5Zn). The observed Zn- and Zn/Al-containing corrosion products might be important factors for the lower sensitivity of Cu15Zn and Cu5Al5Zn against chloride-induced atmospheric corrosion compared with Cu sheet and Cu4Sn.Decreasing corrosion rates with exposure time were observed for all materials and chloride loads and attributed to an improved adherence with time of the outer patina to the underlying inner oxide. Flaking of the outer patina layer was mainly observed on Cu4Sn and Cu sheet and associated with the gradual transformation of CuCl to Cu2(OH)3Cl of larger volume. After three years only Cu5Al5Zn remains lustrous because of a patina compared with the other materials that appeared brownishâreddish.Significantly lower release rates of metals compared with corresponding corrosion rates were observed for all materials. Very similar release rates of copper from all four materials were observed during the fifth year of marine exposure due to an outer surface patina that with time revealed similar constituents and solubility properties
Genotoxicity and inflammatory potential of stainless steel welding fume particles: an in vitro study on standard vs Cr(VI)-reduced flux-cored wires and the role of released metals.
Welders are daily exposed to various levels of welding fumes containing several metals. This exposure can lead to an increased risk for different health effects which serves as a driving force to develop new methods that generate less toxic fumes. The aim of this study was to explore the role of released metals for welding particle-induced toxicity and to test the hypothesis that a reduction of Cr(VI) in welding fumes results in less toxicity by comparing the welding fume particles of optimized Cr(VI)-reduced flux-cored wires (FCWs) to standard FCWs. The welding particles were thoroughly characterized, and toxicity (cell viability, DNA damage and inflammation) was assessed following exposure to welding particles as well as their released metal fraction using cultured human bronchial epithelial cells (HBEC-3kt, 5-100 ”g/mL) and human monocyte-derived macrophages (THP-1, 10-50 ”g/mL). The results showed that all Cr was released as Cr(VI) for welding particles generated using standard FCWs whereas only minor levels (\u3câ3% of total Cr) were released from the newly developed FCWs. Furthermore, the new FCWs were considerably less cytotoxic and did not cause any DNA damage in the doses tested. For the standard FCWs, the Cr(VI) released in cell media seemed to explain a large part of the cytotoxicity and DNA damage. In contrast, all particles caused rather similar inflammatory effects suggesting different underlying mechanisms. Taken together, this study suggests a potential benefit of substituting standard FCWs with Cr(VI)-reduced wires to achieve less toxic welding fumes and thus reduced risks for welders
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