Cobalt Exposure Research Articles

Respiratory Health and Inflammatory Markers-Exposure to Cobalt in the Swedish Hard Metal Industry.

To study the relationship between inhalable dust and cobalt, and respiratory symptoms, lung function, exhaled nitric oxide in expired air, and CC16 in the Swedish hard metal industry. Personal sampling of inhalable dust and cobalt, and medical examination including blood sampling was performed for 72 workers. Exposure-response relationships were determined using logistic, linear, and mixed-model analysis. The average inhalable dust and cobalt concentrations were 0.079 and 0.0017 mg/m, respectively. Statistically significant increased serum levels of CC16 were determined when the high and low cumulative exposures for cobalt were compared. Nonsignificant exposure-response relationships were observed between cross-shift inhalable dust or cobalt exposures and asthma, nose dripping, and bronchitis. Our findings suggest an exposure-response relationship between inhalable cumulative cobalt exposure and CC16 levels in blood, which may reflect an injury or a reparation process in the lungs.

Cobalt accumulation and iron-regulatory protein profile expression in immature mouse brain after perinatal exposure to cobalt chloride

Developing brain is very sensitive to the influence of environmental factors during gestation and the neonatal period. The aim of the study is to assess cobalt and iron accumulation in the brain as well as changes in the expression of iron-regulatory proteins transferrin receptor 1, hepcidin, and ferroportin in suckling mice. Perinatal exposure to cobalt chloride increased significantly cobalt content in brain tissue homogenates of 18-day-old (d18) and 25-day-old (d25) mice inducing alterations in brain iron homeostasis. Higher degree of transferrin receptor 1 expression was demonstrated in cobalt chloride-exposed mice with no substantial changes between d18 and d25 mice. A weak ferroportin expression was found in 18-day-old control and cobalt-treated mouse brain. Cobalt exposure of d25 mice resulted in increased ferroportin expression in brain compared to the untreated age-matched control group. Hepcidin level in cobalt-exposed groups was decreased in d18 mice and slightly increased in d25 mice. The obtained data contribute for the better understanding of metal toxicity impact on iron homeostasis in the developing brain with further possible implications in neurodegeneration.

Cobalt exposure via skin alters lung immune cells and enhances pulmonary responses to cobalt in mice.

Cobalt has been associated with allergic contact dermatitis and occupational asthma. However, the link between skin exposure and lung responses to cobalt is currently unknown. We investigated the effect of prior dermal sensitization to cobalt on pulmonary physiological and immunological responses after subsequent challenge with cobalt via the airways. BALB/c mice received epicutaneous applications (25 μL/ear) with 5% CoCl2*6H2O (Co) or the vehicle (Veh) dimethyl sulfoxide (DMSO) twice; they then received oropharyngeal challenges with 0.05% CoCl2*6H2O or saline five times, thereby obtaining four groups: Veh/Veh, Co/Veh, Veh/Co, and Co/Co. To detect early respiratory responses noninvasively, we performed sequential in vivo microcomputed tomography (µCT). One day after the last challenge, we assessed airway hyperreactivity (AHR) to methacholine, inflammation in bronchoalveolar lavage (BAL), innate lymphoid cells (ILCs) and dendritic cells (DCs) in the lungs, and serum IgE. Compared with the Veh/Veh group, the Co/Co group showed increased µCT-derived lung response, increased AHR to methacholine, mixed neutrophilic and eosinophilic inflammation, elevated monocyte chemoattractant protein-1 (MCP-1), and elevated keratinocyte chemoattractant (KC) in BAL. Flow cytometry in the Co/Co group demonstrated increased DC, type 1 and type 2 conventional DC (cDC1/cDC2), monocyte-derived DC, increased ILC group 2, and natural cytotoxicity receptor-ILC group 3. The Veh/Co group showed only increased AHR to methacholine and elevated MCP-1 in BAL, whereas the Co/Veh group showed increased cDC1 and ILC2 in lung. We conclude that dermal sensitization to cobalt may increase the susceptibility of the lungs to inhaling cobalt. Mechanistically, this enhanced susceptibility involves changes in pulmonary DCs and ILCs.

Drp-1-Dependent Mitochondrial Fragmentation Contributes to Cobalt Chloride-Induced Toxicity in Caenorhabditis elegans.

Excess cobalt may lead to metallosis, characterized by sensorineural hearing loss, visual, and cognitive impairment, and peripheral neuropathy. In the present study, we sought to address the molecular mechanisms of cobalt-induced neurotoxicity, using Caenorhabditis elegans as an experimental model. Exposure to cobalt chloride for 2 h significantly decreased the survival rate and lifespan in nematodes. Cobalt chloride exposure led to increased oxidative stress and upregulation of glutathione S-transferase 4. Consistently, its upstream regulator skn-1, a mammalian homolog of the nuclear factor erythroid 2-related factor 2, was activated. Among the mRNAs examined by quantitative real-time polymerase chain reactions, apoptotic activator egl-1, proapoptotic gene ced-9, autophagic (bec-1 and lgg-1), and mitochondrial fission regulator drp-1 were significantly upregulated upon cobalt exposure, concomitant with mitochondrial fragmentation, as determined by confocal microscopy. Moreover, drp-1 inhibition suppressed the cobalt chloride-induced reactive oxygen species generation, growth defects, and reduced mitochondrial fragmentation. Our novel findings suggest that the acute toxicity of cobalt is mediated by mitochondrial fragmentation and drp-1 upregulation.

Work-related asthma in cobalt-exposed workers

Objective Workers exposed to cobalt may develop two lung conditions, asthma or lung fibrosis. There is a relative lack of awareness of the risk of lung disease from cobalt exposure. Methods The state of Michigan requires physicians, and hospitals to report work-related asthma (WRA). A standardized telephone interview of each reported case was conducted. An industrial hygienist evaluated the reported cases’s workplace, and a physician reviewed the results to confirm the diagnosis. This is a population-based case series of all workers in whom the exposure to cobalt was confirmed as likely responsible for WRA from 1988 to 2017. We also included an illustrative case report and data on the workplace evaluations. Results Of the 35 cases identified, 77% were males, 97.1% were white, and 62.9% had a history of smoking cigarettes. Fifteen (44%) cases were involved in manufacturing cutting tools and machine tool accessories. Symptoms improved in 28 cases (80%) when away from work. Fourteen cases (40%) had emergency department visits, while 10 (28.6%) had been hospitalized for breathing problems. Spirometry had been performed for 33 (94.3%) cases. Only 13 (37.1%) reported they were informed by a doctor that their asthma was work-related. Twenty-six inspections were conducted at 21 different workplaces, where 498 coworkers were interviewed, 55 (11%) of which had respiratory symptoms at work. Six workplaces were cited for cobalt air level higher than permissible limits. These inspections resulted in $29,380 in penalties. Conclusions WRA secondary to cobalt is associated with significant morbidity. Most of the cases were unaware of their medical diagnosis.

Assessment of cobalt accumulation effect on growth and antioxidant responses in aquatic macrophyte Hydrilla verticillata (L.f.) Royle

Cobalt is an essential trace metal and plays a pivotal role in the growth of all living organisms. The exposure of cobalt in the aquatic environment is ubiquitous via both natural and anthropogenic activities. The present study was carried out to investigate the accumulation response of macrophyte Hydrilla verticillata (L.f.) Royle towards the cobalt exposure at different concentrations (1, 25, 50, 75 and 100 µM) for seven days. The results showed that the cobalt accumulation increased in treated H. verticillata (L.f.) Royle with increase in concentration. The Bioconcentration factor (BCF) values were high in plants exposed to higher concentration of cobalt. Increase in growth (shoot length) and pigments (chlorophyll a, b and total chlorophyll) were detected at 25 µM cobalt concentration, whereas the growth and pigments were declined in 50, 75 and 100 µM. There was no significant difference in the carotenoid content between control and treated plant. Antioxidant enzymes (superoxide dismutase, catalase, and peroxidase) were increased at higher concentrations of cobalt. The results indicated that the decline in growth and pigments, and an increase in antioxidant enzyme activities, were triggered by the accumulation of cobalt in the plant. These observations suggest that H. verticillata (L.f.) Royle is well equipped to accumulate low concentration of cobalt in tissues to increase its growth and detoxify ROS generation. The BCF results indicate the efficiency of using H. verticillata (L.f.) Royle as a phytostabilizer.

Toxicity of nickel and cobalt in Japanese flounder

Nickel and cobalt are essential elements that become toxic at high concentrations. Little is known about nickel and cobalt toxicity in aquatic animals. This study aimed to investigate acute and chronic toxicity of nickel and cobalt in Japanese flounder (Paralichthys olivaceous), with emphasis on oxidative stress reactions, histopathological changes, and differences in gene expression. The lethal concentration for 50% mortality (LC50) in 3 and 8 cm Japanese flounder exposed to nickel for 96 h was found to be 86.2 ± 0.018 and 151.3 ± 0.039 mg/L; for cobalt exposure, LC50 was 47.5 ± 0.015 and 180.4 ± 0.034 mg/L, respectively. Chronic nickel and cobalt exposure caused different degrees of oxidative enzyme activity changes in gill, liver, and muscle tissues. Erythrocyte deformations were detected after acute or chronic exposure to nickel and cobalt. the nickel and cobalt exposure also caused pathological changes such as spherical swelling over other gill patches, rod-like proliferations in the gill patch epithelial cell layer, and disorder in hepatocyte arrangement, cell swelling, and cytoplasm loosening. RNA-Seq indicated that there were 184 upregulated and 185 downregulated genes in the liver of Japanese flounder exposed to 15 mg/L nickel for 28 d. For cobalt, 920 upregulated and 457 downregulated genes were detected. Among these differentially expressed genes, 162 were shared by both nickel and cobalt exposure. In both nickel and cobalt, pathways including fatty acid elongation, steroid biosynthesis, unsaturated fatty acid biosynthesis, fatty acid metabolism, PPAR signaling, and ferroptosis were significantly enriched. Taken together, these results aided our understanding of the toxicity of nickel and cobalt in aquatic animals.

F-18 FDG PET brain imaging in symptomatic arthroprosthetic cobaltism

PurposeImaging studies of cobalt toxicity from cobalt-chromium alloy arthroprosthetics have focused on the local intra-articular and peri-articular presentation from failing joint replacements. Most studies investigating neurological findings have been small case series focused on the clinical findings of memory loss, diminished executive function, tremor, hearing and vision loss, depression, and emotional lability. This study utilizes software-based quantitative analysis of brain metabolism to assess the degree of hypometabolism and areas of susceptibility, determine if a pattern of involvement exists, and measure reversibility of findings after prosthetic revision to cobalt-free appliances.MethodsOver 48 months, 247 consecutive patients presenting to an orthopedic clinic with an arthroprosthetic joint containing any cobalt-chromium part were screened with whole blood and urine cobalt levels. A clinically validated inventory of 10 symptoms was obtained. Symptomatic patients with a blood cobalt level above 0.4 mcg/L or urine cobalt greater than 1 mcg/L underwent F-18 FDG PET brain imaging. Analysis was performed with FDA-approved quantitative brain analysis software with the pons as the reference region. Control group was the normal brain atlas within the software.ResultsOf the 247 consecutively screened patients, 123 had blood and urine cobalt levels above the threshold. The 69 scanned patients had statistically significant regional hypometabolism and higher symptoms inventory. Fifty-seven patients were retained in the study. Distribution of hypometabolism was in descending order: temporal, frontal, Broca’s areas, anterior cingulate, parietal, posterior cingulate, visual, sensorimotor, thalamic, and lastly caudate. Metal-on-metal (MoM) and metal-on-plastic (MoP) joint replacements produced similar patterns of hypometabolism. Of 15 patients with necessary revision surgery, 8 demonstrated improved metabolism when later re-scanned.ConclusionAll scanned patients had regions of significant hypometabolism. Neurological toxicity from elevated systemic cobalt levels following arthroprosthetic joint replacement has a pattern of regional susceptibility similar to heavy metals and solvents, differing from classical dementias and may occur at blood and urine cobalt levels as low as 0.4 mcg/L and 1 mcg/L, respectively. Presently accepted thresholds for cobalt exposure and monitoring may need revision. Quantitative F-18 FDG PET brain imaging may aid in the decision process for treatment options and timing of possible medical versus surgical intervention.

Effects of occupational cobalt exposure on the heart in the production of cobalt and cobalt compounds: a 6-year follow-up

ObjectiveIt has been suspected that cobalt is toxic to the heart. It can cause cardiotoxicity in heavily exposed humans and in experimental systems. The issue of interest for this study is whether cobalt also affects the myocardium at occupational exposure levels.MethodsTo study the effect of occupational cobalt exposure on the heart, we conducted a follow-up of workers at a cobalt production plant. The workers’ hearts had been examined by echocardiography in 1999–2000. Altogether 93 exposed and 49 non-exposed workers examined in 1999–2000 were re-examined in 2006. Occupational history and health data were collected with a questionnaire. Blood pressure was measured, and electrocardiography (ECG), laboratory tests, Holter registration, and echocardiography were conducted for all participants. Analysis of covariance (ANCOVA) was used to analyse the data.ResultsNo differences were found between the exposed and unexposed groups for any of the echocardiographic parameters in 2006. There were no differences in the laboratory values, the ECG parameters, or the results of the Holter registration of the exposed and unexposed workers.ConclusionsAlthough the previous results in 2000 suggested an association between cumulative exposure to cobalt and echocardiographic findings, the results of this new cross-sectional study with a tissue Doppler 6 years later did not confirm the association in the present cohort. If cobalt exposure affects heart muscle functions at this exposure level, the effects are smaller than those caused by physiological changes due to ageing, medication, and traditional cardiovascular risk factors, such as elevated blood pressure.

Cobalt-Induced Hypercontraction is Mediated by Generationof Reactive Oxygen Species and Influx of Calcium in Isolated RatAorta

To investigate the mechanism of cobalt-mediated phenylephrine (PE)-induced contraction in endothelium-intact isolated Wistar rat aortic rings. Effect of dose-dependent concentrations of cobalt on PE-induced contraction was investigated in isolated Wistar rat aortic rings using an organ bath system. Aortic rings were pre-incubated with verapamil (1μM and 20μM), gadolinium, apocynin, indomethacin or N-G-nitro-L-arginine methyl ester (L-NAME) separately before incubation with cobalt. Endothelium-intact aortic rings were incubated with 800nM, 1μM, 10μM, 50μM cobalt; we observed 20%, 22%, 32% and 27% increased contractions respectively, while no effect was seen in tension recording on cobalt exposure. Incubation of endothelium-intact aortic rings with 100μM apocynin and 100μM L-NAME suggested the role of NADPH oxidase in generation of reactive oxygen species (ROS) and decrease in bioavailability of nitric oxide (NO) from eNOS on exposure to cobalt. Aortic rings pre-incubated with 1μM and 20μM verapamil suggested role of both L-type and T-type calcium channels in influx of extracellular calcium in smooth muscle cells. We observed no role of store-operated calcium channels (SOCC) in calcium influx due to cobalt exposure and cyclooxygenase in generation of prostanoids in isolated aortic rings. Cobalt caused rise of PE-induced contractions as a result of the endothelial generation of ROS, by decreasing bioavailability of NO. Generation of ROS may be responsible for causing the influx of extracellular calcium through L-type and T-type Ca2+ channels in smooth muscle cells.

Cobalt accumulation in horses following repeated administration of cobalt chloride.

To monitor cobalt concentrations in urine, red blood cells and plasma after chronic parenteral administration of cobalt chloride evaluate these results against the current International Federation of Horseracing Authorities thresholds for detecting cobalt misuse. Eight mares were randomly assigned to four treatment groups, with two mares in each group: Group 1 - control group, Group 2 - 25 milligrams cobalt intravenously as CoCl2 weekly, Group 3 - 50 milligrams cobalt intravenously as CoCl2 weekly, and Group 4 - 25 milligrams cobalt intravenously mid-week and at the end of the week. Urine and blood samples were collected before each weekly administration so that trough levels were assessed. In the group receiving two doses per week, urine and blood were collected prior to the dose given at the end of each week. Samples were initially collected at time zero then weekly for 10 weeks. Three further collections of urine and blood were made at days 81, 106 and 127. Urine creatinine measurements to assess horse hydration status were performed by the Jaffe reaction method. Cobalt determinations in plasma, blood and urine were by inductively coupled plasma-mass spectrometry. Haematocrit concentrations, used to calculate red cell cobalt levels, were performed using a microhematocrit centrifuge. Statistical analyses were conducted in Genstat (v17, VSNi). Marked cobalt accumulation was evident with increasing cobalt concentrations for all sample matrices in specimens collected immediately prior to cobalt administration. Correlation between the sample matrices improved when urine cobalt concentration was adjusted for creatinine level. Red cell cobalt levels remained elevated for at least 12 weeks after cessation of administration, consistent with the lifespan of the red cell. There was no significant change in haematocrit concentrations for the duration of the study. The current urine cobalt threshold was only effective at detecting acute cobalt exposure while the plasma cobalt threshold was able to consistently identify chronic high-level cobalt exposure and potential cobalt misuse. The threshold values legislated for urine cobalt do not correlate with those set for plasma. The acute nature of urinary cobalt excretion provides a relatively small window through which cobalt administration is detected. Plasma and red cell cobalt concentrations can provide a clearer picture of potential cobalt misuse.

Biomonitoring of Metal Exposure During Additive Manufacturing (3DPrinting).

BackgroundAdditive manufacturing (AM) is a rapidly expanding new technology involving challenges to occupational health. Here, metal exposure in an AM facility with large-scale metallic component production was investigated during two consecutive years with preventive actions in between.MethodsGravimetric analyzes measured airborne particle concentrations, and filters were analyzed for metal content. In addition, concentrations of airborne particles <300 nm were investigated. Particles from recycled powder were characterized. Biomonitoring of urine and dermal contamination among AM operators, office personnel, and welders was performed.ResultsTotal and inhalable dust levels were almost all below occupational exposure limits, but inductively coupled plasma mass spectrometry showed that AM operators had a significant increase in cobalt exposure compared with welders. Airborne particle concentrations (<300 nm) showed transient peaks in the AM facility but were lower than those of the welding facility. Particle characterization of recycled powder showed fragmentation and condensates enriched in volatile metals. Biomonitoring showed a nonsignificant increase in the level of metals in urine in AM operators. Dermal cobalt and a trend for increasing urine metals during Workweek Year 1, but not in Year 2, indicated reduced exposure after preventive actions.ConclusionGravimetric analyses showed low total and inhalable dust exposure in AM operators. However, transient emission of smaller particles constitutes exposure risks. Preventive actions implemented by the company reduced the workers' metal exposure despite unchanged emissions of particles, indicating a need for careful design and regulation of the AM environments. It also emphasizes the need for relevant exposure markers and biomonitoring of health risks.

Causative exposures and temporal development of cobalt allergy in Denmark between 2002 and 2017.

Cobalt contact allergy is common, but clinical relevance is often difficult to determine. To examine the aetiology, prevalence and clinical characteristics of cobalt-allergic patients who were patch tested between 2002 and 2017 at the Department of Dermatology and Allergy, Herlev-Gentofte Hospital. Patch test data, along with patient characteristics and causative exposures, from all adult dermatitis patients seen and tested between 2002 and 2017 were analysed. Associations were tested with the χ 2 test and logistic regression. A total of 13 475 adults aged 18 to 99 years were patch tested. The overall prevalence of cobalt allergy and the prevalence of isolated cobalt allergy were 3.3% and 1.5%, respectively. The prevalence of isolated cobalt allergy decreased from 2.4% in 2006 to 2009 to 1.1% in 2014 to 2017 (Ptrend = 0.00003). Leather exposure as a relevant cause of allergic cobalt dermatitis increased from 3.7% in 2002 to 2009 to 8.3% in 2010 to 2017 (P = 0.04). The current clinical relevance of positive patch test reactions, that is, a positive reaction to cobalt combined with a history of current skin exposure to a source of cobalt, was 20.1%. We conclude that cobalt allergy is relatively common, but causative exposures are largely unknown, and the proportion of positive patch test reactions with clinical relevance is low. It is therefore currently unclear how we can better protect consumers and workers from cobalt exposure.

A Review on Arthroprosthetic Cobaltism: Manufacturer’s Product liability for causing Iatrogenic Cobalt toxicity

Cobalt toxicity is a well-documented complication of total hip arthroplasty (THA) when cobalt-chrome implants are utilized. A recent area of attention is “cobaltism, ” which results from cobalt exposure from cobalt-containing orthopedic implants, chemistry kits, weather indicators, antiquated anemia therapies, cement, fly ash, dyes, mineral wool, asbestos, molds for ceramic tiles, mining, porcelain paint, orthopedic implants, and dental hardware. Like other transition metals, cobalt is a multiorgan toxin. Organ systems affected by acute cobalt poisoning include endocrine, gastrointestinal, central and peripheral nervous system, hematologic, cardiovascular, and metabolic. Chronic inhalational exposures affect the pulmonary system and dermatologic system.

Unprecedentedly High Dust Ingestion Estimates for the General Population in a Mining District of DR Congo.

The mining of metals in low income countries is often associated with high exposure to dust that contributes to metal exposure. Here, dust ingestion estimates were made from fecal excretion of inert tracers with corrections for dietary contribution. The study took place in the cobalt mining area of Lubumbashi (DR Congo) and involved 120 nonoccupationally exposed participants in the dry season, with 51 of these being repeated in the rainy season. For each participant, duplicate meals (0-96 h), feces (24-120 h), and indoor/outdoor dust (<250 μm) were collected. The dust ingestion estimates (g day-1) were derived from Nb, Ti, and V as best tracers and were 0.28 (geometric mean), 3.3 (mean), and 13 (P95); these values are almost a factor 10 above currently accepted estimates for the general population in high income countries. Mean dust ingestion in the dry season was twice that of the rainy season, and the P95s were significantly higher in children (3-15 years) than in male adults and toddlers; geophagy (>40 g day-1) was suspected in three individuals. These data explain the previously reported extreme cobalt exposures in children and support the need to manage dust in the metal mining operations.

ВЛИЯНИЕ ПЕРИНАТАЛЬНОГО ВОЗДЕЙСТВИЯ КОБАЛЬТА НА ОБМЕН ЖЕЛЕЗА, МЕДИ, МАРГАНЦА И ЦИНКА В ОРГАНИЗМЕ НЕЗРЕЛЫХ ICR МЫШЕЙ

ВЛИЯНИЕ ПЕРИНАТАЛЬНОГО ВОЗДЕЙСТВИЯ КОБАЛЬТА НА ОБМЕН ЖЕЛЕЗА, МЕДИ, МАРГАНЦА И ЦИНКА В ОРГАНИЗМЕ НЕЗРЕЛЫХ ICR МЫШЕЙ

In vitro cobalt-stimulated hypoxia-inducible factor-1 overexpression does not correlate with cancer risk from cobalt exposure in humans

Chemical-induced pulmonary carcinogenesis in humans is usually a multi-decade process. The average age at diagnosis of lung cancer in cigarette smokers, and mesothelioma in asbestos workers, is app...

NFIL-3 regulates dendritic cells functions following nickel and cobalt exposure

NFIL-3 regulates dendritic cells functions following nickel and cobalt exposure

Prevalence of subclinical cardiac abnormalities in patients with metal-on-metal hip replacements

BackgroundMetal-on-metal (MOM) hip prostheses have a higher failure rate than conventional prostheses and leaching of cobalt and chromium has been linked to cardiomyopathy. We screened MOM subjects to evaluate if cobalt and chromium are related to subclinical cardiac dysfunction. MethodsA single centre, non-randomised, observational study using echocardiography in 95 patients who had undergone MOM hip prostheses, and 15 age matched controls with non-MOM hip replacement. Serial plasma cobalt and chromium levels were recorded, and data compared by tertiles of cobalt exposure. ResultsIndexed left ventricular (LV) end-diastolic and end-systolic volumes (EDVi and ESVi) increased with tertile of cobalt (omnibus p = 0.003 for EDVi and ESVi), as did indexed left atrial (LA) volumes (p = 0.003). MOM subjects had 25% larger EDVi than controls, 32% larger ESVi (40 ml vs. 32 ml, and 15 ml vs. 11 ml, p = 0.003 for both) and 28% larger indexed LA (23 ml vs. 18 ml, p = 0.002). There were no differences in LV systolic or diastolic function, including ejection fraction, tissue velocity and mitral E/e′. Estimated glomerular filtration rate was 18% lower in the highest tertile compared with the lowest (p = 0.01) and correlated inversely with LA volume (r = −0.36, p < 0.001) and LV EDV (r = −0.24, p = 0.02). ConclusionsNo correlations between sensitive measures of systolic or diastolic cardiac function or serum cobalt/chromium levels were observed in this study. However, there was a relationship between increasing left ventricular and left atrial volumes and declining renal function with high cobalt levels which requires further evaluation in MOM patients.

Adsorption, Bioaccumulation and Kinetics Parameters of the Phytoremediation of Cobalt from Wastewater Using Elodea canadensis.

Present paper investigates the phytoremediation of cobalt from wastewaters using Elodea canadensis. Bioaccumulation tests were conducted at various concentrations of cobalt ranging from 1 to 15mg/L. Final concentrations of cobalt in wastewaters, after phytoremediation, were less than 1mg/L. E. canadensis' hyperaccumulator character with regard to cobalt is emphasised by the amount of cobalt retained: 0.39% ± 0.02% of dry mass at an initial concentration in wastewater of 15mg/L. After 14 days of exposure to contaminant, the biomass as well as the relative growth rate has increased with the amount of cobalt in wastewaters, the plant manifesting an excellent tolerance to cobalt exposure. Adsorption of cobalt ions by E. canadensis can be well described by the Langmuir adsorption isotherm and the pseudo-second-order model equation.