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Dear Editor, We read with great interest the letter from Pelclova and Lach [[1]] on the efficacy of unithiol (2,3-dimercaptopropanesulfonate) and acetylcysteine in a patient with arthroplastic cobalt toxicity. Acetylcysteine increases cobalt urinary excretion and consistently maintains the serum cobalt concentration less than the threshold of 10 g/L, which we believe to be the goal in patients with metal-on-metal implants in order to minimise cobalt toxicity from the existing prosthesis [[3]]. The authors stated that chelation therapy, either with unithiol or acetylcysteine, is often clinically inefficient in patients with very elevated cobalt concentrations (greater than 100 g/L) as long as the damaged prosthesis remains I in situ i . [Extracted from the article]

We conclude that treatment with either unithiol or acetylcysteine is inefficient in patients with very elevated serum cobalt concentrations, especially greater than 100 µg/L, as long as the damaged prosthesis remains I in situ i . Dear Editor, Previously [[1]] we reported a 56-year-old man with severe cobalt poisoning from a damaged metal-on-ceramic hip prosthesis. However, her serum cobalt concentration reached 221 µg/L in February 2022 on the day of the surgery, which subsequently decreased to 51 µg/L 11 days after surgery, 10 µg/L 2.5 months after surgery, and 3 µg/L 6 months after surgery, all without further treatment. [Extracted from the article]

Context:Post-arthroplasty metallosis, which refers to metallic corrosion and deposition of metallic debris in the periprosthetic soft tissues of the body, is an uncommon complication. Systemic cobalt toxicity post-arthroplasty is extremely rare. The few known fatal cases of cobalt toxicity appear to be a result of replacing shattered ceramic heads with metal-on-metal or metal-on-polyethylene implants. Friction between residual shards of ceramic and cobalt–chromium implants allows release of cobalt into the synovial fluid and bloodstream, resulting in elevated whole blood cobalt levels and potential toxicity. Case details:This is a single patient chart review of a 60-year-old woman with prior ceramic-on-ceramic right total hip arthroplasty complicated by fractured ceramic components and metallosis of the joint. She underwent synovectomy and revision to a metal-on-polyethylene articulation. Ten months post-revision, she presented to the emergency department (ED) with right hip pain, dyspnea, worsening hearing loss, metallic dysgeusia, and weight loss. Chest CTA revealed bilateral pulmonary emboli (PE), and echocardiogram revealed new cardiomyopathy with global left ventricular hypokinesis with an ejection fraction (EF) of 35–40% inconsistent with heart strain from PE. Whole blood cobalt level obtained two days into her admission was 424.3 mcg/L and 24-h urine cobalt level was 4830.5 mcg/L. Although the patient initially clinically improved with regard to her PE and was discharged to home on hospital day 5, she returned 10 days later with a right hip dislocation and underwent closed reduction of the hip. The patient subsequently decompensated, developing cardiogenic shock, and respiratory failure. She went into pulseless electrical activity (PEA) and expired. Autopsy revealed an extensive metallic effusion surrounding the right hip prosthesis that tested positive for cobalt (41,000 mcg/L). There was also cobalt in the heart muscle tissue (2.5 mcg/g). A whole blood cobalt level obtained two days before she expired was 641.6 mcg/L. Discussion:This is a case of fatal cobalt-induced cardiomyopathy in a patient whose ceramic components of a total hip arthroplasty fractured causing metallosis with worsening cobalt toxicity. We recommend that when a fractured device is revised with a prosthesis with cobalt–chromium components, whole blood and urine cobalt measurements should be obtained and periodically monitored to evaluate for rising concentrations. Providers should be aware of clinical signs and symptoms of cobalt toxicity in patients who have prostheses with cobalt–chromium components. If suspected, toxicology and orthopedics should be involved for possible chelation and removal of the prosthesis. [ABSTRACT FROM PUBLISHER]

Cobalt is a widely used in the industrial production of hard metals. Cobalt ingestion has been reported to cause widespread systemic toxicity, but its effects on vision have been sparsely reported. The authors report the case of a patient who ingested cattle magnets, which remained in his stomach for an unknown duration of time. These magnets largely consist of cobalt that gradually leached into his blood stream, resulting in protean systemic manifestations, which included optic atrophy. [ABSTRACT FROM AUTHOR]

This experiment was undertaken to study the toxic effects of cobalt chloride in rats. Sixty-five rats weighing 207 ± 7 g were used. Cobalt chloride was administrated orally in low and high doses for 90 d. The aim of study was to evaluate the effects of cobalt on blood (RBC, WBC, Hb, PLT and HCT) and to investigate the abilities of deferasirox (DFX) and desferrioxamine (DFO) as chelators in removing cobalt from the blood. Cobalt and iron concentrations were determined by flame atomic absorption spectrometer (FAAS). Results show that both of chelators are able to remove cobalt but DFX was more effective, whereas the combined therapy is more efficient. [ABSTRACT FROM AUTHOR]

Recent, unexpected high failure rates of metal-on-metal hip implants have reintroduced the issue of cobalt toxicity. An adverse reaction to cobalt ions and cobalt-induced lung injury occurs during environmental exposure and is now strictly controlled. Currently adverse reaction occurs to cobalt nanoparticles during wear and tear of metal-on-metal hip implants of which the underlying mechanism is not fully understood. The putative role of the hypoxia-inducible factor (HIF) pathway in the mechanism of cobalt nanoparticle (Co-NPs) toxicity was examined using the U937 cell line, human alveolar macrophages and monocyte-derived macrophages. Co-NPs (5–20 μg/ml)-induced cytotoxicity (viability ranged from 75% to <20% of control, respectively) and reactive oxygen species (ROS), whereas a comparable concentration of cobalt ions (Co(II); up to 350 μM) did not. Co-NPs induced HIF-1α stabilization. Addition of ascorbic acid (100 µM) and glutathione (1 mM) both prevented the increased ROS. However, only treatment with ascorbic acid reduced HIF-1α levels and prevented cell death, indicating that a ROS-independent pathway is involved in Co-NPs-induced cytotoxicity. Replenishing intracellular ascorbate, which is crucial in preventing HIF pathway activation, modified Co-induced HIF target gene expression and the inflammatory response, by decreasing interleukin-1 beta (IL-1β) mRNA and protein expression. Addition of glutathione had no effect on Co-NPs-induced HIF target gene expression or inflammatory response. Thus, Co-NPs induce the HIF pathway by depleting intracellular ascorbate, leading to HIF stabilization and pathway activation. This suggests a strong, ROS-independent role for HIF activation in Co-NPs-induced cytotoxicity and a possible role for HIF in metal-on-metal hip implant pathology. [ABSTRACT FROM PUBLISHER]

Introduction. There has been some recent concern regarding possible systemic health effects resulting from elevated blood cobalt concentrations in patients with cobalt containing hip implants. To date there are no blood cobalt criteria to help guide physicians when evaluating an individual hip implant patient's risk of developing systemic health effects because historically there was little or no concern about systemic cobalt toxicity in implant patients. Objective. Our purpose is to describe recently completed research regarding the relationship between blood cobalt concentrations and clinical health effects. We discuss the possibility of systemic health effects in patients with metal containing implants and propose various blood cobalt concentrations that are not associated with an increased risk of developing certain adverse effects. Methodology. The primary literature search was conducted using PubMed and Web of Science using the following search terms: cobalt AND (toxicity OR health effects OR cardiotoxicity OR hematological OR endocrine OR immunological OR reproductive OR testicular effects OR neurological OR case report OR cohort OR Roncovite). The searches identified 6786 papers of which 122 were considered relevant. The Agency for Toxic Substances and Disease Registry toxicological profile for cobalt and the U.S. Environmental Protection Agency Office of Research and Development's National Center for Environmental Assessment's documentation on the provisional peer-reviewed toxicity value for cobalt were also utilized to identify secondary literature sources. Results. Our review of the toxicology and medical literature indicates that highly elevated blood cobalt concentrations can result in certain endocrine, hematological, cardiovascular, and neurological effects in animals and/or humans. These studies, in addition to historical clinical findings involving the therapeutic use of cobalt, indicate that significant systemic effects of cobalt will not occur below blood cobalt concentrations of 300 μg/L in most persons. Some individuals with specific risk factors for increased susceptibility (e.g., severe and sustained hypoalbuminemia) may exhibit systemic effects at lower cobalt blood concentrations. This review also describes several cobalt dosing studies performed with human volunteers that consumed cobalt for 15, 30, or 90 days. Overall, the results of these dosing studies indicate that sustained blood cobalt concentrations averaging 10-70 μg/L for up to 90 days cause no significant clinical effects (maximum concentrations approached 120 μg/L). Some proposed blood criteria for assessing implant wear and local tissue damage have been suggested by several medical groups. For example, the UK Medicines and Healthcare Products Regulatory Agency has proposed a blood cobalt guidance value of 7 μg/L, and the Mayo Clinic has suggested serum cobalt concentrations greater than 10 μg/L, but both of these values are primarily intended to address implant wear and to alert physicians to the possibility of an increased incidence of local effects. There is a clear lack of consensus regarding how to identify a specific numerical blood concentration of concern and whether whole blood or serum is a better matrix to assess total cobalt concentration. Conclusions. Based on currently available data, only under very unusual circumstances should a clinician expect that biologically important systemic adverse effects might occur in implant patients with blood cobalt concentrations less than 300 μg/L. Patients with metal-containing hip implants who exhibit signs or symptoms potentially related to polycythemia, hypothyroidism, neurological, or cardiac dysfunction should be clinically evaluated for these conditions. Polycythemia appears to be the most sensitive endpoint. [ABSTRACT FROM AUTHOR]

Despite the wide use of nanoscale materials in several industrial applications as well as in biology and medicine, very little research has been carried out on the potential toxicity of nanoparticles. We had previously obtained 10 differentially expressed mRNAs in BALB3T3 fibroblasts exposed to different forms of cobalt, i.e., microparticles, nanoparticles, and ions. Those genes represented candidate biomarkers for indicating specific cellular effects after cobalt nanoparticle exposure. In the present paper, we have further evaluated the expression of those genes by real-time RT-PCR after exposure to different forms of cobalt. Moreover, we also tested some genes associated with cobalt toxicity, such as VEGF, HIF-1α, and Bnip3. We identified biomarkers that are sensitive to cobalt ions that we think to be the reactive form. Our data, in fact, are consistent with the possibility that Co-nano, due to their large surface area, once inside the cell dissolve and act as ions. [ABSTRACT FROM AUTHOR]

Tomato ( Lycopersicon esculentum L.) cv. Alivikas was grown in refined sand at two levels of phosphorus (P): 1.5 mM (adequate) and 3.0 mM (high); 0.5 mM cobalt (Co) was supplied at each P level after 35 days of growth. Visible symptoms of Co toxicity appeared as interveinal chlorosis of young leaves after 8 days of metal supply. Biomass was depressed at both P levels with excess Co, although less at the high P level. Discontinuation of high P or Co or additional iron (Fe) supply also increased the biomass. The fresh weight of fruits was decreased, but dry weight was increased in high P supply. Quality of fruits was poor with Co‐treated plants as Co depressed the fruit fresh weight and dry weight, volume and size of fruits, concentrations of chlorophyll a, b and carotene, ascorbic acid, lycopene, reducing sugars, and starch, and increased acidity and phenols. These effects were greater with adequate vs. high P. High P (without Co) improved fruit quality by increasing fruit dry weight, volume, and size of fruits, ascorbic acid content, and reducing sugars and by decreasing acidity. Accumulation of cobalt in leaves and fruits was greater, and these plant parts developed visible Co toxicity symptoms. Fruits developed black patches with prolonged Co supply. New fruits developed after the discontinuation of the Co supply appeared green and normal, but were few in number compared with increased vegetative growth of plants (cobalt supplied with the normal level of phosphorus). Earlier flowering, fruiting, and ripening were observed in plants with high phosphorus rather than adequate P. Brown spots in fruits developed after 18–20 days of Co supply, and in the most severe case, young emerging fruits were totally brown. Amelioration of cobalt toxicity was better with discontinuation of Co than withdrawal of high P with additional Fe. [ABSTRACT FROM AUTHOR]

Purpose The persistent and alarming rates of increase in cardiovascular and renal diseases caused by chemicals such as cobalt chloride (CoCl2) in mammalian tissues have led to the use of various drugs for the treatment of these diseases. This study aims at evaluating the nephron-protective action of Naringin (NAR), a metal-chelating antioxidant against CoCl2-induced hypertension and nephrotoxicity. Methods Forty-two male Wistar rats were randomly distributed to seven rats of six groups and classified into Group A (Control), Group B (300 part per million; ppm CoCl2), Group C (300 ppm CoCl2 + 80 mg/kg NAR), Group D (300 ppm CoCl2 + 160 mg/kg NAR), Group E (80 mg/kg NAR), and Group F (160 mg/kg NAR). NAR and CoCl2 were administered via oral gavage for seven days. Biomarkers of renal damage, oxidative stress, antioxidant status, blood pressure parameters, immunohistochemistry of renal angiotensin-converting enzyme and podocin were determined. Results Cobalt chloride intoxication precipitated hypertension, renal damage, and oxidative stress. Immunohistochemistry revealed higher expression of angiotensin-converting enzyme (ACE) and podocin in rats administered only CoCl2. Conclusion Taken together, the antioxidant and metal-chelating action of Naringin administration against cobalt chloride-induced renal damage and hypertension could be through abrogation of angiotensin-converting enzyme and podocin signalling pathway. [ABSTRACT FROM AUTHOR]

In light of potential negative health effects of cobalt exposure, a characterization of inflammatory mechanisms in exposed individuals is warranted. The current study investigated cobalt exposure in the Swedish hard metal industry and its relationship to inflammatory markers, including NLRP3 inflammasome activation and white blood cell (WBC) counts. Inhalable cobalt and dust exposures, and systemic cobalt levels, were determined for 72 workers in the hard metal industry and linear regression models were applied to correlate exposure to markers of inflammasome activation and WBC counts. Mean exposures to inhalable dust (0.11 mg/m3) and cobalt (0.0034 mg/m3) were below the Swedish occupational exposure limits, and these low exposures did not correlate with any investigated outcomes. Instead, cobalt blood levels significantly correlated with a ca 10% decrease in IL-18 plasma levels per 10 nM cobalt increase. Furthermore, pre-shift cobalt blood and/or urine levels significantly correlated with some WBC measures, including decreased neutrophil-to-lymphocyte ratio, increased lymphocyte-to-monocyte ratio, and lymphocyte counts. The low inhalable particle exposures had no impact on WBC counts and inflammasome activation. Instead, systemic cobalt levels, which also include skin exposure, demonstrated possible suppressive effects on inflammatory responses in cobalt-exposed individuals in the hard metal industry. [ABSTRACT FROM AUTHOR]

A dispersive liquid-liquid microextraction procedure (DLLME) was developed and validated for the determination of cobalt and copper in environmental samples by flame atomic absorption spectrometry. The optimisation parameters of DLLME procedure including amount of chelating reagent (0.05 mg dithizone), pH (6), extraction type and volume (250 µL chloroform) and dispersive solvent (1000 µL acetone), matrix effect was investigated. Several validation variables, such as limit of detection and quantification, linearity, recovery, precision and trueness were also tested. The quantification limits of Co and Cu were found to be 9.01 and 6.14 µg L−1, respectively. The enrichment factor was 20. The trueness of the method was tested by analysis of certificated reference material (BCR-715) for Cu and calculated less than −1.11% with the relative error. The presented green microextraction method was profitably applied to real samples and the spiked recoveries calculated were more than 95% with the relative standard deviation less than 8.4%. [ABSTRACT FROM AUTHOR]

This study aimed to systematically investigate the ototoxic potential of cobalt in patients with a metal-on-metal (MoM) hip implant, using objective auditory and vestibular assessments and a questionnaire. The results of the objective evaluation were published previously, whereas the current study focused on the questionnaire outcome and its relationship to the blood cobalt level. Design and study sample: Twenty patients (33–65 years) with a primary MoM hip implant and 20 non-implanted control subjects, matched for age, gender, and noise exposure, received a questionnaire to evaluate the presence of several hearing and balance symptoms (part 1) and general neurological issues (part 2). Concerning part 1, the proportion of auditory-related symptoms in general (p = 0.022) and tinnitus (p = 0.047) was significantly higher in the MoM patient group, whereas no group difference was found for hyperacusis, increased listening effort, and decreased speech understanding. Concerning part 2, no significant group differences were detected. Within the MoM patient group, the questionnaire outcome was not significantly different between the low-exposure and high-exposure subgroups according to the blood Co level. In line with our previous study, these results potentially imply Co-induced impairment to the auditory system, despite the lack of a clear dose–response relationship. [ABSTRACT FROM AUTHOR]

This study describes experiments in which MIL-100(Fe) was used to remove Co2+ ions from the waste water. The synthesised adsorbent was characterised by Fourier-transform infrared spectroscopy (FTIR), X-ray diffraction, Brunauer–Emmett–Teller (BET) and scanning electron microscope. Statistical analysis was used to investigate the effects of different parameters. From the obtained results, the removal efficiency was enhanced with increasing contact time and pH but decreased with increasing cobalt initial concentration. The maximum removal efficiency of Co+2 was 93.4% under optimum conditions. The equilibrium adsorption data were best fitted to linearly transformed Freundlich isotherm. Adsorption kinetic data followed the pseudo second-order kinetic model. The maximum adsorption capacity of Co+2 on to the MIL-100(Fe) was found to be 119 mg g−1. The results showed that ∆G of adsorption was negative, while ∆H was positive which showed that the adsorption process was spontaneous and endothermic. The positive value of ∆S showed that disordering and randomness increased at the solid–solution interface of cobalt ions with MIL-100(Fe) particles. [ABSTRACT FROM AUTHOR]

Hip implants have improved the mobility and quality of life in millions of individuals. This review presents the evolution of scientific knowledge regarding the history and understanding of systemic and local metal toxicological concerns of hip implants designs utilizing metal-on-metal (MoM) bearing surfaces used in hip resurfacing arthroplasty (HRA) and total hip arthroplasty (THA). This analysis addresses: (1) the history of the development of MoM hip implants; (2) the clinical and toxicological rationale for introducing second-generation MoM implants in the early 2000s as an alternative to metal-on-polyethylene bearings; (3) the subsequent history regarding success and failure of second-generation MoM devices; (4) a detailed review of the history of MoM toxicology, including carcinogenic potential, metal blood levels, hypersensitivity, and release of wear particles; and (5) a review of local tissue effects and MoM patient management. We have included an analysis of MoM THA and HRA survivorship trends aggregated from over 200 studies. By around 2008, HRA continued to be a challenging procedure with variable success rates, and concurrently, some THA devices began to experience higher than expected revision rates based on annual registry reports. The unexpected THA outcomes and continued challenges with HRA devices prompted many surgeons to question the role of toxicological effects in device performance. Regarding hypersensitivity, while conversion to metal sensitized status in some MoM patients occurs based on the skin patch or lymphocyte transformation testing, there is no evidence of a causal relationship between positive test results and device failure. The weight of evidence indicates that nanoparticles released from MoM implants are cleared from the local synovial space under normal wear conditions. The available data indicate that there are no discernible increases in local or systemic tumors following CoCr alloy implantation. Systemic health effects are rarely reported in MoM implant patients and are unlikely when blood concentrations are below 300 µg/L except when patients have specific risk factors. Over time, patient management evolved to include assays aimed at predicting implant function (blood monitoring) and soft tissue reactions (MRI and ultrasound imaging). Validation of these biomarkers as a diagnostic tool for implant function, patient pain, and, ultimately, implant survival, remains lacking. After the introduction of these biomarkers, differences in implant revision decisions emerged based on imaging abnormalities, increased serum metal ion levels, and overall clinical presentation. Discrepancies in patient management algorithms and the lack of consensus in local biological effects terminology have contributed to variability in reporting incidence, etiology, and dose effects on local tissue responses in MoM implants. This variability has contributed to a debate regarding the benefit or risk of revising asymptomatic patients. Therefore, while toxicological assessments of normal functioning MoM implants indicate that MoM implants are relatively safe because of low wear and clearance of metal, more analysis of revision data is needed in order to best inform patient management decisions, particularly for asymptomatic patients, as well as patients with minor symptoms under consideration for conservative pain management treatments. [ABSTRACT FROM AUTHOR]

This article summarizes recent experimental and epidemiological data on the genotoxic and carcinogenic activities of cobalt compounds. Emphasis is on the respiratory system, but endogenous exposure from Co-containing alloys used in endoprostheses, and limited data on nanomaterials and oral exposures are also considered. Two groups of cobalt compounds are differentiated on the basis of their mechanisms of toxicity: (1) those essentially involving the solubilization of Co(II) ions, and (2) metallic materials for which both surface corrosion and release of Co(II) ions act in concert. For both groups, identified genotoxic and carcinogenic mechanisms are non-stochastic and thus expected to exhibit a threshold. Cobalt compounds should, therefore, be considered as genotoxic carcinogens with a practical threshold. Accumulating evidence indicates that chronic inhalation of cobalt compounds can induce respiratory tumors locally. No evidence of systemic carcinogenicity upon inhalation, oral or endogenous exposure is available. The scarce data available for Co-based nanosized materials does not allow deriving a specific mode of action or assessment for these species. [ABSTRACT FROM AUTHOR]

Introduction:Dicobalt edetate is one of a number of cobalt compounds that have been studied in the treatment of cyanide poisoning, their efficacy being based upon the fact that cyanide combines with cobalt to form relatively non-toxic complexes. Inorganic cobalt salts are quite toxic (cyanide and cobalt antagonise one another's toxicity) and complexes such as dicobalt edetate were studied with the aim of identifying compounds that were less acutely toxic, but which retained the antidotal properties of cobalt salts. The proprietary preparation, Kelocyanor™, contains free cobalt and glucose as well as dicobalt edetate. Objective:The aim of this study was to evaluate the published evidence for the efficacy and adverse effects of dicobalt edetate. Methods:A Pubmed search was undertaken for the period 1961–September 2015. The search terms were “dicobalt edetate”, “cobalt edetate” and “Kelocyanor”, which produced 24 relevant citations. A review of the references in four relevant books (L'intoxication cyanhydrique et son traitement,Clinical and Experimental Toxicology of Cyanides,Antidotes for Poisoning by CyanideandAntidotes) produced three further relevant papers, making a total of 27 papers. Efficacy of dicobalt edetate:There is evidence from animal pharmacodynamic studies that dicobalt edetate is an effective cyanide antidote in experimental animals. Some 39 cases of human poisoning treated with dicobalt edetate have been reported, but in only nine cases were blood cyanide concentrations measured, although administration of dicobalt edetate procured survival in four of the seven patients with concentrations in the lethal range (>3.0 mg/L). It is unlikely that death in any of the adequately documented fatal cases was attributable to treatment failure with dicobalt edetate, as it is probable that they all had suffered anoxic brain damage before treatment could be initiated. Furthermore, in one case, acute gold toxicity contributed substantially to death. Adverse effects of dicobalt edetate:Adverse effects reported have included hypertension, tachycardia, nausea, retrosternal pain, sweating, palpebral, facial and laryngeal oedema, vomiting, urticaria and/or a feeling of impending doom. Such effects appear to be more prevalent where the antidote has been administered without evidence of substantial systemic poisoning or where other antidotes have been used which might have been expected also to combine with cyanide. Although the adverse effects observed were doubtless unpleasant, and some were severe, no fatal reactions were found. Conclusions:Dicobalt edetate is an effective cyanide antidote when given to patients with systemic cyanide poisoning, but it has the potential to give rise to adverse reactions, particularly when administered in the absence of intoxication. [ABSTRACT FROM AUTHOR]

The objective of this experimental study was to demonstrate the impact of trace metal supplementation, namely nickel (Ni), cobalt (Co) and molybdenum (Mo), on the methane yields obtained from batch mesophilic anaerobic digestion of maize silage as mono-substrate. The maize silage used in this experimental work initially lacked Ni and Co. Trace metal concentration selected was 0.1 and 0.5 mg/L for Ni and Co, respectively, while it was 0.05 and 0.25 mg/L for Mo. The supplementation by Ni, Co and Mo, individually or in combination at different doses, seemed to improve the methane yields for mono-digestion of maize silage and particularly, the highest methane yield of 0.429 L CH4/g VSaddedwas obtained, when Ni, Co and Mo were supplemented together at concentrations of 0.5, 0.5 and 0.25 mg/L, respectively. [ABSTRACT FROM AUTHOR]

Cobalt (Co) can stimulate erythropoietin production in individuals at doses exceeding 25 mg CoCl2/day. Co has also been shown to exert effects on the thyroid gland, heart and nervous system at sufficient doses. The biological activity of Co is dictated by the concentration of free (unbound) ionic Co2+. Blood concentrations, as well as, urinary excretion rates of Co are reliable biomarkers for systemic Co exposure. A recent series of human volunteer Co-supplement studies simultaneously measured Co blood and urine concentrations, as well as, Co speciation in serum, and a number of biochemical and clinical parameters. It was found in these studies that peak Co whole blood concentration as high as 117 μg/L were not associated with changes in hematological parameters such as increased red blood cell (RBC) count, hemoglobin (Hgb) or hematocrit (Hct) levels, nor with changes in cardiac, neurological or, thyroid function. Using a Co biokinetic model, the estimated Co systemic tissue concentrations (e.g., liver, kidney, and heart) following 90-days of Co-dietary supplementation with ∼1 mg Co/day were found to be similar to estimated tissue concentrations in implant patients after 10 years of exposure at continuous steady state Co blood concentration of ∼10 μg/L. This study is the first to present modeled Co tissue concentrations at various doses following sub-chronic and chronic exposure. The modeled steady state tissue Co concentrations in combination with the data on adverse health effects in humans should help in the characterization of potential hazards associated with increased blood Co concentrations due to exposure to dietary supplements or cobalt-chromium (Co-Cr) containing implants. [ABSTRACT FROM AUTHOR]

The aim of the study was to implicate induction of oxidative stress and antioxidative responses with the effects of cobalt excess on sugarcane plants. Sugarcane (Saccharum officinariumL.) cv. ‘CoS 99225’ grown in refined sand at excess cobalt i.e. 100, 200, 300, 400, and 500 μM. The effect of excess cobalt (>300 μM) was observed on sugarcane as interveinal chlorosis and necrotic spots in middle leaves. Later, affected leaves turned necrotic, dry, and withered. The toxicity of cobalt was also discernible on root weight, cane yield, reduced concentration of sucrose in cane juice, carotenoides, Hill reaction activity, chlorophylls, iron (Fe), relative water content, decreased activity of catalase in leaves, and increase in concentration of lipid peroxidation, phenols, sugars, starch, proline and higher activity of peroxidase, ascorbate peroxidase and superoxide didmutase and accumulation of cobalt in sugarcane leaves. [ABSTRACT FROM PUBLISHER]

Background: Minerals, metals, clays and rocks were widely used by physicians in the past. However, it was and it is well known that some inorganic elements at high dosage may have curative effects but also serious toxicity. The effects at low or ultra-low concentrations, on the contrary, are less documented, but the idea that low dosage supplementation might be beneficial to human health is widespread even in the present period. Methods: The main information about aluminium, bismuth, cobalt, gold, lithium, nickel and silver was selected and evaluated from a vast body of medical literature. Results: In modern times, most elements are proposed for human use at levels comparable with normal dietary intake, probably for precautionary considerations. Conclusion: Some inorganic trace compounds might have unexpected effects at extremely low dosages, but scientific demonstrations of beneficial effects of supplementation are mostly not available in the medical literature. [ABSTRACT FROM AUTHOR]

The hypothesis that three known chelators deferasirox, desferrioxamine and deferiprone might be more efficient as combined treatment than as single therapies in removing cobalt from the body, was evaluated. Animals were randomly divided into a control ( n = 5) and toxic groups ( n = 90). Cobalt chloride was administrated orally. Chelators were given orally (DFX and deferiprone) or intraperitonealy (DFO) 2 weeks. Cobalt concentration was determined by FAAS. The chelation therapy results show that all three chelators are able to remove cobalt from tissues but DFX was more effective than DFO and deferiprone, whereas the combined therapy is more efficient in compare to single therapy. [ABSTRACT FROM AUTHOR]

Hip replacement with large metal-on-metal (MoM) coupling has recently been under attention for its metal ions release, inducing several disorders. Since the blood level toxicity threshold for cobalt is known, the aim of this work is to determine whether Co serum and blood levels correlate with the synovial fluid level. Beside this, the synovial fluid Co from patients without prosthesis has also been measured. Co has been determined in 54 samples (32 unilateral MoM and 22 controls) with inductively coupled plasma mass spectrometry in the three matrices. In the prosthesized group, cobalt was significantly higher compared with controls and in the synovial fluid it strongly correlated with whole blood Co ( p = 0.847) and serum ( p = 0.855). Moreover, the Co levels into whole blood and serum were significantly different. In conclusion, haematic Co concentration correctly reflects Co local level. [ABSTRACT FROM AUTHOR]

Context. With regard to biological effects, the increasing number of early failure of metal-on-metal (MoM) hip arthroplasties and possible parenteral exposure to orthopedic metal alloys have caused concern for patients and providers alike. Objective. We sought to characterize our outpatient clinical experience of patients with MoM and other forms of hip implants and associated serum/blood chromium and cobalt levels, with a focus on possible systemic sequelae. Methods. This was an observational and retrospective chart review of consecutive patients presenting to two outpatient medical toxicology clinics from January 1, 2010-June 1, 2012 with history of hip implants. Presenting signs, symptoms, and interventions were reviewed. Available cobalt and chromium levels were summarized as median concentration with interquartile range. Results. A total of 39 patients were analyzed; of the 39 patients, 26 had MoM hip implants while 13 did not. Twelve patients exhibited no symptoms and nine sought evaluation for fatigue while two other patients had been previously diagnosed with fibromyalgia. Tinnitus/hearing loss was also a frequent complaint noted in 12 patients (one presenting complaint), however there was no difference between the incidence of this symptom between the MoM and non-MoM groups. Three patients were provisionally diagnosed with demyelinating neuropathy with one patient demonstrating marked (subjective and objective) improvement after revision. Patients with MoM arthroplasties generally exhibit an approximately tenfold increase in metal ion levels than traditional arthroplasties. Finally, 20 (51.2%) patients had replacement or revision of their hip implant with subsequent decreases in metal ion levels. Discussion. A majority of our patients had minor symptoms (fatigue and muscle aches) or no symptoms (n = 23 or 59%). Documented peripheral neurotoxicity is uncommon. The decision for hip revision solely for toxicologic reasons is rare and usually involves a multidisciplinary approach. Conclusion. Most patients seeking toxicologic referral may be minimally symptomatic and seek guidance regarding elevated blood or serum metal ions; however, solely toxicologic-based interventions are unusual. Revision was associated with a decrease in metal ion levels; however, subjective complaints did not correlate with metal ion levels. [ABSTRACT FROM AUTHOR]

Cobalt (Co) is an essential element with ubiquitous dietary exposure and possible incremental exposure due to dietary supplements, occupation and medical devices. Adverse health effects, such as cardiomyopathy and vision or hearing impairment, were reported at peak blood Co concentrations typically over 700 µg/L (8-40 weeks), while reversible hypothyroidism and polycythemia were reported in humans at ∼300 µg/L and higher (≥2 weeks). Lung cancer risks associated with certain inhalation exposures have not been observed following Co ingestion and Co alloy implants. The mode of action for systemic toxicity relates directly to free Co(II) ion interactions with various receptors, ion channels and biomolecules resulting in generally reversible effects. Certain dose-response anomalies for Co toxicity likely relate to rare disease states known to reduce systemic Co(II)-ion binding to blood proteins. Based on the available information, most people with clearly elevated serum Co, like supplement users and hip implant patients, have >90% of Co as albumin-bound, with considerable excess binding capacity to sequester Co(II) ions. This paper reviews the scientific literature regarding the chemistry, pharmacokinetics and systemic toxicology of Co, and the likely role of free Co(II) ions to explain dose-response relationships. Based on currently available data, it might be useful to monitor implant patients for signs of hypothyroidism and polycythemia starting at blood or serum Co concentrations above 100 µg/L. This concentration is derived by applying an uncertainty factor of 3 to the 300 µg/L point of departure and this should adequately account for the fact that persons in the various studies were exposed for less than one year. A higher uncertainty factor could be warranted but Co has a relatively fast elimination, and many of the populations studied were of children and those with kidney problems. Closer follow-up of patients who also exhibit chronic disease states leading to clinically important hypoalbuminemia and/or severe ischemia modified albumin (IMA) elevations should be considered. [ABSTRACT FROM AUTHOR]

Co2+ exchange isotherms and Kielland plots were determined for highly-charged sodium swelling mica (Na-2-mica) and sodium Engelhard Titano-Silicate-4 (Na-ETS-4). The results showed that both Na-2-mica and Na-ETS-4 were highly selective for Co2+ at (equivalent fraction) of < 0.3. X-ray diffraction (XRD) patterns after 2Na+ → Co2+ exchange process were examined to check for change in d001-spacing of Na-2-mica. As the uptake of Co ions increased, strong ∼14 Å phase (two-layer hydrate) of Na-2-mica increased, while the ∼12 Å phase (one-layer hydrate) decreased. These synthetic ion exchangers have a great potential for decontamination of radioactive or stable cobalt from waste water and soils. [ABSTRACT FROM PUBLISHER]

Context. Cobalt intoxication has become more frequent due to the wide use of metal hip implants. Case details. A 56-year-old male patient underwent total hip prosthesis, with a ceramics-on-ceramics implant. Almost 3 years later, it was replaced by metal implant containing cobalt, chromium, and titanium. He developed weight loss, heart, thyroid, and neurological toxicity, with severe hearing loss. He was treated with 2,3-dimercaptopropane-1-sulfonate (DMPS), and cobalt excretion increased. Clinical symptoms apart from deafness gradually resolved. Conclusion. We report significant cobalt poisoning from a damaged hip replacement with cobalt containing implant and a slow abrasion of the metal by residual ceramic particles. Chelation therapy resulted in apparent benefit. [ABSTRACT FROM AUTHOR]

An optical sensor has been designed for the determination of cobalt by spectrophotometry. The sensing membrane is made by immobilizing methyltrioctylammonium chloride on a triacetylcellulose membrane. In the presence of Co(II) and thiocyanate ions, the colorless membrane changes to blue. The response time of the optode was about 7 min. The sensor can readily be regenerated with 0.02 mol L-1 sodium oxalate solution. This optode is stable and can be stored under water for more than a month without reagent leaching. The calibration curve was linear in the range of 8.5×10-6-1.3×10-4 mol L-1 of Co(II) ion with a limit of detection 5.9×10-6 mol L-1. The relative standard deviations for seven replicate measurements of 3.4×10-5 and 1×10-4 mol L-1 of Co(II) were 1.58 and 1.10%, respectively. The sensor was successfully applied to the determination of cobalt in food samples and vitamin B12 ampoule. [ABSTRACT FROM AUTHOR]

French bean (Phaseolus vulgaris L.) cv. 'Anupama' was grown in refined sand at variable levels of cobalt (Co), i.e., 0.0001 (control), 0.05, 0.10, 0.20, 0.40, and 0.50 mM, supplied as cobalt sulfate. The symptoms of excess Co (0.50 mM) appeared at day 35. In addition to growth depression, the young leaves developed chlorosis from the apex leading toward the base; the chlorosis intensified, changed to necrosis, and the infected leaves dried and withered. Under excess Co (>0.0001 mM), the flowers produced were fewer in number, smaller, and many failed to mature, leading to lower seed yield. Excess Co (>0.0001 mM) decreased the biomass, seed yield (number and weight), concentration of chlorophyll, Hill reaction activity, and activity of catalase, and deteriorated the quality of produce (sugars, starch, and protein nitrogen (N)), but it increased the concentration of phenols and activity of certain enzymes, i.e., peroxidase, ribonuclease, and acid phosphatase. The concentration of Co in various parts of French bean increased with an increase in Co supply and that of iron (Fe) decreased concomitantly. The values of threshold of toxicity and toxicity of Co were 26 and 72 μg g-1 in young leaves of French bean, respectively. [ABSTRACT FROM AUTHOR]

Reports on the rare magnetic element cobalt. History; List of physical and chemical properties; Exposure; Information on the industrial uses of cobalt compounds; Mechanism of toxicity.