Nickel Exposure Research Articles

Association between the nickel exposure and lipid profiles in general population from NHANES.

This study is to investigate the association between nickel exposure and serum lipid profiles. We analyzed the population from the National Health and Nutrition Examination Surveys (NHANES) 2017-2018. Urinary nickel exposure was measured using inductively coupled-plasma mass spectrometry. Serum lipid profiles, including triglyceride (TG), total cholesterol (TC), high-density lipoprotein-cholesterol (HDL-C), and low-density lipoprotein-cholesterol (LDL-C), were measured using the standard biochemistry assays. The association between urinary nickel and lipid profiles was examined using multivariable linear regression models and restricted cubic spine plots. There was a significant negative relationship between nickel level and TC (β, - 9.67; 95% CI, - 13.58 to - 5.76), HDL-C (β, - 1.57; 95% CI, - 2.98 to - 0.16), and LDL-C (β, - 5.88; 95% CI, - 11.04 to - 0.71) after adjusting for potential confounding factors. Furthermore, restricted cubic spines showed that only HDL-C was nonlinearly associated with nickel (p for nonlinearity 0.004). However, nickel exposure was not related to the level of triglyceride. The exposure to nickel was linearly associated with serum total cholesterol and LDL-C while nonlinearly associated with HDL-C in general population.

Assessment of Health Impact of Heavy Metals Contained in Wild Berries of Shrubs for the Population of the Murmansk Region

Background: Studies of wild berries of local shrubs carried out in the Murmansk Region showed an increased accumulation of heavy metals in them, especially near the Severonickel plant. High concentrations of industrial pollutants were measured in blueberries, lingonberries and crowberries. Objective: To assess health effects of population exposure to nickel and copper in wild berries of small shrubs in the Murmansk Region. Materials and methods: We tested metal contents in blueberries, lingonberries and crowberries gathered in August–September of 2016–2018 at ten stationary monitoring plots located along the industrial pollution gradient in the meridional (south) direction on the leeward side of the Severonickel plant. Health risk assessment was conducted in accordance with Guidelines R 2.1.10.1920-04, Health Risk Assessment from Environmental Chemicals. Results: Values of carcinogenic risk from oral exposure to nickel contained in the berries were unacceptably high (> 1.0E-03) at all monitoring plots. Estimates of chronic non-carcinogenic risk from nickel exposure were also high while those from copper exposure were unacceptable only for crowberry. Hazard index values for the unidirectional effect of copper and nickel on the digestive tract and liver were unacceptably high (> 1.0) at most monitoring plots for all the berries studied. Discussion: High risk values for the local population necessitate the development of recommendations for exposure reduction, such as limiting the annual consumption of berries to 6 kg, avoiding berry picking at a distance of up to 15 km from the Seve- ronickel plant, etc. Conclusions: The predicted levels of carcinogenic and non-carcinogenic risks associated with exposure to nickel and copper were estimated as unacceptably high, thus indicating a pronounced industrial impact on boreal ecosystems in the zone of influence of the enterprise, extending more than 15 km from its industrial site. It is critical to develop appropriate recommendations for the population consuming wild-growing blueberries, cowberries and crowberries picked in this industrially contaminated area.

Toxicity Effects of Combined Mixtures of BDE-47 and Nickel on the Microalgae Phaeodactylum tricornutum (Bacillariophyceae).

Nickel and 2,2’,4,4’-tetrabromodiphenyl ether (BDE-47) are two environmental pollutants commonly and simultaneously present in aquatic systems. Nickel and BDE-47 are individually toxic to various aquatic organisms. However, their toxicity mechanisms are species-dependent, and the toxic effects of combined mixtures of BDE-47 and nickel have not yet been investigated. The present study investigated the toxic effects of combined mixtures of BDE-47 and nickel in the diatom Phaeodactylum tricornutum. BDE-47 and nickel mixtures significantly decreased cell abundance and photosynthetic efficiency, while these cells’ reactive oxygen species (ROS) production significantly increased. The EC50-72 h for BDE-47 and mixtures of BDE-47 and nickel were 16.46 ± 0.93 and 1.35 ± 0.06 mg/L, respectively. Thus, combined mixtures of the two pollutants enhance their toxic effects. Interactions between BDE-47 and nickel were evaluated, revealing synergistic interactions that contributed to toxicity in P. tricornutum. Moreover, transcriptomic analyses revealed photosynthesis, nitrogen metabolism, the biosynthesis of amino acids, the biosynthesis of secondary metabolites, oxoacid metabolism, organic acid metabolism, carboxylic acid metabolism, and oxidation-reduction processes were considerably affected by the mixtures. This study provides evidence for the mechanisms of toxicity from combined BDE-47 and nickel exposure while also improving our understanding of the ecological risks of toxic chemicals on microalgae.

Toxicity and Metabolomic Impact of Cobalt, Chromium, and Nickel Exposure on HepaRG Hepatocytes.

Cobalt, chromium, and nickel are used in orthopedic prostheses. They can be released, accumulate in many organs, and be toxic. The aim of this study is to evaluate the cytotoxicity of these metals on human hepatocytes and to improve our knowledge of their cellular toxicity mechanisms by metabolomic analysis. HepaRG cells were incubated for 48 h with increasing concentrations of metals to determine their IC50. Then, a nontargeted metabolomic study using liquid chromatography-high-resolution mass spectrometry (LC-HRMS) was done at IC50 and at a lower concentration (100 nM), near to those found in the blood and liver of patients with prostheses. IC50 were defined at 940, 2, and 1380 μM for Co, Cr, and Ni, respectively. In vitro, Cr appears to be much more toxic than Co and Ni. Metabolomic analysis revealed the disruption of metabolic pathways from the low concentration of 100 nM, in particular tryptophan metabolism and lipid metabolism illustrated by an increase in phenylacetylglycine, a marker of phospholipidosis, for all three metals. They also appear to be responsible for oxidative stress. Dysregulation of these pathways impacts hepatocyte metabolism and may result in hepatotoxicity. Further investigations on accessible biological matrices should be conducted to correlate our in vitro results with the clinical data of prostheses-bearing patients.

Biomonitoring of Urinary Nickel Successfully Protects Employees and Introduces Effective Interventions.

Nickel is a heavy metal used in many industries. Nickel exposure can induce respiratory diseases and allergic reactions, and increase cancer risk. This study evaluated the introduction of a grinding and polishing system to prevent injuries from nickel toxicity in workers. We performed a controlled, interventional, before-and-after study from January 2018 to December 2019 at a faucet component industrial manufacturing site. Results from workplace environmental monitoring, questionnaire responses, and biomonitoring were collected before and after the intervention. Thirty-seven workers (100% men) aged 25.0 (interquartile range (IQR): 22.0–33.5) years were categorized into two groups, those with and without nickel exposure. In the exposed group, the median exposure time was 18.0 months (IQR 14.0–20.0 months). Urinary nickel concentration was lower in the exposed group than in the non-exposed group (13.8 (IQR 1.7–20.7); 23.1 (IQR 11.3–32.8) μg/g creatinine, respectively; p = 0.047). The median urinary nickel concentration was lower in the second year than in the first year (17.4 (IQR 2.2–27.4), 7.7 (IQR 4.3–18.5) μg/g creatinine, respectively; p = 0.022). Significant reductions in urinary nickel concentration were observed following the intervention and educational program. Thus, biomonitoring of urinary nickel concentration can successfully reflect the effectiveness of interventions and their relationship to nickel exposure.

Can Lemna minor mitigate the effects of cadmium and nickel exposure in a Neotropical fish?

We aimed to evaluate if Lemna minor can mitigate the observed effects of cadmium (Cd) and nickel (Ni) exposure in Prochilodus lineatus. Fish were exposed for 96 h to 20 µg L-1 of Cd, 1.5 mg L-1 of Ni, or to a mixture of these two metals. In all tests, one group was exposed to the metals with duckweed on the water surface, and other group was exposed only to the metals, without plants. After each exposure, samples of P. lineatus tissues were collected to evaluate multiple biomarkers. Duckweed prevented bioaccumulation in some fish tissues and attenuated changes in acetylcholinesterase activity, increases in erythrocytic nuclear abnormality frequency, and hyperglycemia. However, the changes in plasma ion concentrations, reduction in activity of ion transport enzymes, and histological damage were not mitigated. Therefore, we concluded that L. minor partially attenuates the effects caused by Cd and Ni exposure.

Nickel and cobalt release from beauty tools: A field study in the German cosmetics trade.

Relevant nickel and cobalt release from hairdressing tools has recently been evidenced. Comparable data are not available for tools used in beauty salons. Screening of beauty tools for nickel and cobalt release. Three hundred eight beauty tools were tested in seven beauty salons located in two North-German states. A nickel spot test and a cobalt spot test were used to test the tools for nickel release and cobalt release, respectively. One hundred forty-three of 308 beauty tools overall (46.4%; 95% confidence interval [CI]: 40.8%-52.2%) released nickel and 18 of 308 beauty tools overall (5.8%; 95%CI: 3.5%-9.1%) released cobalt. Nickel release was found in 22 of 99 metal tools (22.2%; 95%CI: 14.5%-31.7%) and 121 of 209 tools with metallic parts (57.9%; 95%CI: 50.9%-64.7%); cobalt release was detected in 3 of 99 metal tools (3.0%; 95%CI: 0.63%-8.6%) and 15 of 209 tools with metallic parts (7.2%; 95%CI: 4.1%-11.6%). Nickel and cobalt are emitted at allergologically relevant levels by a wide range of beauty tools (i.e., metal tools and tools with metallic parts) utilized in the German cosmetics trade. Beauty tools should thus be considered occupational sources of nickel and cobalt exposure.

Ni2+-Assisted Hydrolysis May Affect the Human Proteome; Filaggrin Degradation Ex Vivo as an Example of Possible Consequences.

Deficiency in a principal epidermal barrier protein, filaggrin (FLG), is associated with multiple allergic manifestations, including atopic dermatitis and contact allergy to nickel. Toxicity caused by dermal and respiratory exposures of the general population to nickel-containing objects and particles is a deleterious side effect of modern technologies. Its molecular mechanism may include the peptide bond hydrolysis in X1-S/T-c/p-H-c-X2 motifs by released Ni2+ ions. The goal of the study was to analyse the distribution of such cleavable motifs in the human proteome and examine FLG vulnerability of nickel hydrolysis. We performed a general bioinformatic study followed by biochemical and biological analysis of a single case, the FLG protein. FLG model peptides, the recombinant monomer domain human keratinocytes in vitro and human epidermis ex vivo were used. We also investigated if the products of filaggrin Ni2+-hydrolysis affect the activation profile of Langerhans cells. We found X1-S/T-c/p-H-c-X2 motifs in 40% of human proteins, with the highest abundance in those involved in the epidermal barrier function, including FLG. We confirmed the hydrolytic vulnerability and pH-dependent Ni2+-assisted cleavage of FLG-derived peptides and FLG monomer, using in vitro cell culture and ex-vivo epidermal sheets; the hydrolysis contributed to the pronounced reduction in FLG in all of the models studied. We also postulated that Ni-hydrolysis might dysregulate important immune responses. Ni2+-assisted cleavage of barrier proteins, including FLG, may contribute to clinical disease associated with nickel exposure.

Urinary Nickel Was Associated with the Prevalence of Diabetes: Results from NHANES.

The study aimed to investigate the association between nickel exposure and the presence of diabetes (DM). The participants were analyzed from the National Health and Nutrition Examination Surveys (NHANES) 2017-2018. Urinary nickel exposure was measured using inductively coupled-plasma mass spectrometry. DM was diagnosed based on the WHO standards. The association between nickel and DM or fasting glucose was examined using multivariable linear regression models and logistic regression models. A total of 1899 participants (933 men and 966 women) were included in our study, of whom 342 (18.0%) were diagnosed with DM. There was a significant positive association between nickel level and DM (OR: 1.27, 95%CI: 1.04-1.56) after adjusting for potential confounding factors. Comparing with the lowest quartile, the highest quartile independently increased a 0.66-fold higher risk of DM (OR: 1.66, 95%CI: 1.13-2.44]). In addition, nickel exposure was independently related to the level of fasting glucose. The exposure to nickel was associated with a higher risk of DM in general population.

Chlorogenic Acid-Loaded Mesoporous Silica Nanoparticles Modified with Hexa-Histidine Peptides Reduce Skin Allergies by Capturing Nickel

Nickel-induced contact dermatitis is a severe allergic reaction to objects or environments that contain nickel. Many nanomaterials have been developed to reduce skin allergies by capturing nickel, but few agents are effective and safe. In this work, mesoporous silica nanoparticles (MSN) were synthesized and decorated with hexa-histidine peptides (denoted as MSN-His6), making it a strong nickel chelator. Subsequently, a dietary polyphenol, chlorogenic acid, was loaded into the mesopores of MSN (denoted as MSN-His6@CGA), realizing the potential of its anti-inflammatory properties. In vitro and in vivo experiments revealed that the synthesized MSN-His6@CGA nanoparticles exhibited more stable and stronger chelation, better biocompatibility, and ideal allergy-relieving ability, whether for environmental metal contamination or for allergic contact dermatitis caused by prolonged nickel exposure. Thus, the application of mesoporous silica-based nanoparticles may represent an ideal approach to alleviate skin allergies by capturing nickel, which would benefit people who suffer from metal-induced contact dermatitis.

A Multi-Organ-on-Chip Approach to Investigate How Oral Exposure to Metals Can Cause Systemic Toxicity Leading to Langerhans Cell Activation in Skin.

Investigating systemic toxicity in vitro is still a huge challenge. Here, a multi-organ-on-chip approach is presented as a typical case of topical exposure of oral mucosa to metals, which are known to activate the immune system and in turn may result in skin inflammation. Reconstructed human gingiva (RHG) and reconstructed human skin containing MUTZ-3–derived Langerhans cells (MUTZ-LC) in the epidermis (RHS-LC) were incorporated into a HUMIMIC Chip3plus, connected by dynamic flow and cultured for a total period of 72 h. Three independent experiments were performed each with an intra-experiment replicate in order to assess the donor and technical variations. After an initial culture period of 24 h to achieve stable dynamic culture conditions, nickel sulfate was applied topically to RHG for 24 h, and LC activation (maturation and migration) was determined in RHS-LC after an additional 24 h incubation time. A stable dynamic culture of RHG and RHS-LC was achieved as indicated by the assessment of glucose uptake, lactate production, and lactate dehydrogenase release into the microfluidics compartment. Nickel exposure resulted in no major histological changes within RHG or RHS-LC, or cytokine release into the microfluidics compartment, but did result in an increased activation of LC as observed by the increased mRNA levels of CD1a, CD207, HLA-DR, and CD86 in the dermal compartment (hydrogel of RHS-LC (PCR)). This is the first study to describe systemic toxicity and immune cell activation in a multi-organ setting and can provide a framework for studying other organoids in the future.

Involvement of Ca2+ and ROS signals in nickel-impaired human sperm function

As one of the main environmental pollutants and occupational hazards, nickel has been reported to have mutagenic, carcinogenic, and teratogenic properties, as well as reproductive toxicity. However, how nickel affects human reproduction is still unclear. In this study, the toxicity of nickel on human sperm and the underlying mechanisms were evaluated in vitro. We found that NiCl2 (10, 50, and 250 μM) impaired sperm total motility and progressive motility in a dose- and time-dependent manner. In addition, sperm hyperactivation and the ability of human sperm to penetrate a viscous medium were found to be compromised after nickel exposure. Mechanically, NiCl2 significantly inhibited the basal intracellular Ca2+ signaling. Besides, reactive oxygen species (ROS), superoxide, and malondialdehyde levels were increased in human sperm after exposure to different concentrations of NiCl2. Consistently, eliminating excess ROS by N-acetyl-L-cysteine or tocopherol significantly alleviated nickel-impaired sperm motility. Taken together, these results revealed that nickel could compromise sperm functions by interfering with Ca2+ signaling and inducing excessive oxidative stress. These findings suggest that, in the high and occupational nickel exposure environments, the contribution of nickel toxicity to the males who wish to preserve their fertility is worthy of careful evaluation.

Nickel and cobalt: Underestimated contact allergens in hairdressers?

Introduction: Nickel and cobalt were not regarded as pertinent contact allergens in the hairdressing trade for the last decades. It was even stated that the relevance of nickel allergy in the hairdressing trade has been overestimated for several years. Recently, nickel and cobalt release from a multitude of metal tools in the German hairdressing trade was documented in two field studies. Methods: Review of two field studies. Results: In 2019, nickel release from 9.2% of 229 tested metallic hairdressing tools was evidenced, and in 2021, nickel release from 27.6% as well as cobalt release from 2.1% of 475 tested tools was detected in overall 30 North German hairdressing salons. Tweezers, sectioning clips, hair clips, and straight razors were identified as nickel as well as cobalt releasing tools. Crochet hooks and tail combs were identified as only nickel releasing tools. Discussion: A variety of metallic tools – which are used daily by hairdressers – release nickel and/or cobalt in allergologically relevant amounts. This circumstance has to be considered problematic with regard to the development of work-related allergic contact dermatitis. Thus, nickel and cobalt should possibly receive greater attention as potential contact allergens in the hairdressing trade. Conclusion: The proven nickel and cobalt release from metallic hairdressing tools might entail legal ramifications in terms of insurance law. In case of nickel and cobalt allergies within the occupational group of hairdressers, metal tools might be considered as feasible sources for nickel and cobalt exposure.

Complementary square wave voltammetry and tandem mass spectrometry analysis to identify and detect compensatory genomic changes in nematodes due to nickel (II) exposure

Nickel is a toxic heavy metal that may cause negative health outcomes including cancer upon exposure [1]. Square wave voltammetry was used to assay DNA directly extracted from nickel-exposed nematodes that had originated from either high or low Ni-containing environments in order to assess the role of evolutionary genetics in the Ni toxicity process. Extracted DNA was immobilized on pyrolytic graphite (PG) electrodes following layer by layer (LbL) protocols and then electrochemically oxidized in the presence of Ru(bpy)3+ to generate electrocatalytic oxidative currents at ∼+1.05 V vs. SCE. Both C. elegans and P. pacificus nematodes were utilized, each with a volcanic or cosmopolitan soil source strain. DNA oxidative peak currents (Ip) increased for all nematode strains upon exposure to 50 μg/L Ni2+, but those originating from volcanic soils exhibited significantly (40–50%) lower Ip upon Ni2+ exposure compared to similarly exposed nematodes from cosmopolitan soils. Further SWV analysis was performed on DNA from a series of C. elegans N2xCB4856 recombinant inbred advanced intercross line populations (RIALs). A continuum of Ip magnitude was seen as a function of Ni2+ exposure among the RIAL strains indicating Ni-tolerance is complex and affected by multiple loci. The majority of the DNA from Ni-exposed individual RIAL strain cultures produced an increase in oxidative current in comparison to DNA from analogous Ni-unexposed cultures of the same RIAL strains. Liquid chromatography tandem mass spectrometry (LC-MS/MS) analysis on acid hydrolyzed nematode DNA provided validation of the electrochemical findings. Guanine and oxidatively damaged guanine content were monitored via appropriate m/z mass transitions. Guanine content in all Ni-exposed RIAL DNA was lower, while oxidatively damaged guanine was elevated compared to unexposed nematodes in all but one analyzed RIAL. Combined, the complementary electrochemical and MS/MS data provide evidence that evolutionary genetics leads to genetic protection from environmental toxicants, suggesting a possibility that multiple genes are involved in the protection of the organism from Ni exposure.

Transcriptional repression of E-cadherin in nickel-exposed lung epithelial cells mediated by loss of Sp1 binding at the promoter.

E-cadherin plays a central role in the stability of epithelial tissues by facilitating cell-cell adhesion. Loss of E-cadherin expression is a hallmark of epithelial-mesenchymal transition (EMT), a major event in the pathogenesis of several lung diseases. Our earlier studies showed that nickel, a ubiquitous environmental toxicant, induced EMT by persistently downregulating E-cadherin expression in human lung epithelial cells and that the EMT remained irreversible postexposure. However, the molecular basis of persistent E-cadherin downregulation by nickel exposure is not understood. Here, our studies show that the binding of transcription factor Sp1 to the promoter of E-cadherin encoding gene, CDH1, is essential for its expression. Nickel exposure caused a loss of Sp1 binding at the CDH1 promoter, resulting in its downregulation and EMT induction. Loss of Sp1 binding at the CDH1 promoter was associated with an increase in the binding of ZEB1 adjacent to the Sp1 binding site. ZEB1, an EMT master regulator persistently upregulated by nickel exposure, is a negative regulator of CDH1. CRISPR-Cas9-mediated knockout of ZEB1 restored Sp1 binding at the CDH1 promoter. Furthermore, ZEB1 knockout rescued E-cadherin expression and re-established the epithelial phenotype. Since EMT is associated with a number of nickel-exposure-associated chronic inflammatory lung diseases including asthma, fibrosis and cancer and metastasis, our findings provide new insights into the mechanisms associated with nickel pathogenesis.

Dietary Heavy Metal Exposure among Finnish Adults in 2007 and in 2012.

For the non-smoking and non-occupationally exposed population in Europe, food is the main source of heavy metal exposure. The aim of the study was to estimate the dietary exposure of the Finnish adult population to cadmium, lead, inorganic arsenic, inorganic mercury and methyl mercury as well as nickel using governmental as well as industry data on heavy metal occurrence in foodstuffs and the data from two national food consumption surveys conducted in 2007 and 2012. The sources of heavy metal exposure were estimated for the working-age population (25 to 64 years) and for the elderly (65 to 74 years). Exposure differences between years and between population groups were compared statistically. The mean exposure of women aged 25 to 45 years to cadmium and lead was statistically significantly (p < 0.001) higher, and the methyl mercury exposure lower (p = 0.001) than that of women aged 46 to 64 years. For nickel and inorganic arsenic the differences were lower but still statistically significant (p < 0.05). Between genders, significant difference (p < 0.05) was only seen for lead and nickel. Mean cadmium exposure was significantly higher in 2012 than in 2007. For at least 95% of the adult population, the risk of health damage from mercury or nickel exposure is negligible, but the margin of exposure for lead and inorganic arsenic is small and shows a possible risk of cancer or neurotoxic effects.

Environmental Nickel Exposure and Diabetes in a Nationally Representative Sample of US Adults.

Laboratory studies have shown that nickel exposure may adversely affect glucose metabolism. However, studies about the effects of environmental nickel exposure on diabetes pathogenesis in humans are sparse. We aimed to evaluate the association of urinary nickel concentrations, as a biomarker of environmental nickel exposure, and diabetes in a nationally representative sample of US adults. The data from a nationally representative population (n = 1585) in the National Health and Nutrition Examination Survey 2017-18 were used. Diabetes (n = 330) was defined as self-reported physician's diagnosis, HbA1c ≥ 6.5%, fasting plasma glucose ≥ 126 mg/dL, or 2-h plasma glucose ≥ 200 mg/dL. Urinary nickel concentrations were determined by inductively coupled plasma mass spectrometry. Logistic regression with sample weights was used to estimate the odds ratios (ORs) of diabetes and 95% confidence intervals (CIs). Urinary nickel concentrations were higher in individuals with diabetes (weighted median 1.23 μg/L) than those without diabetes (1.01 μg/L). After adjustment for urinary creatinine and other risk factors for diabetes, the OR of diabetes comparing the highest with lowest quartile of urinary nickel concentrations was 2.70 (95% CI 1.39-5.24; Ptrend = 0.03). Environmental nickel exposure is positively and significantly associated with diabetes in U.S. adults.

Hydrogen-Rich Water Alleviates the Nickel-Induced Toxic Responses (Inflammatory Responses, Oxidative Stress, DNA Damage) and Ameliorates Cocoon Production in Earthworm.

In recent years, studies investigating the protective effect of hydrogen-rich water (HRW) against different diseases and the toxicity of some substances have attracted increasing attention. Here, we assessed the effects of hydrogen-rich water on different nickel-induced toxic responses (reactive oxygen species (ROS), tumor necrosis factor-alpha (TNF-α), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) of stress responses, histopathological changes) and cocoon production in earthworm model. Earthworms were randomly divided into two main groups: water (W) group including control (CW: ultrapure water), 10 (10W), 200 (200W), and 500 (500W), and hydrogen-rich ultrapure water (HRW) group including control (CHRW: hydrogen-rich ultrapure water), 10 (10HRW), 200 (200HRW), and 500 (500HRW) mg of nickel chloride kg-1 soil for 14days. We found that cocoon production was less affected by the nickel exposure of earthworms in the 500HRW group compared to the 500W group. The ROS levels in 200HRW and 500HRW groups were less than that of 200W and 500W, respectively. The epithelial degeneration, epithelial necrosis, and necrosis in muscle fibers in tissues of earthworm were less damaged in 200HRW and 500HRW groups compared to 200W and 500W, respectively. HRW groups significantly reduced the expression of 8-OHdG induced by nickel exposure and inflammatory cytokine response including TNF-α. The study showed that hydrogen-rich water could alleviate the toxic effects of nickel-induced oxidative and inflammatory damages in earthworms. The HRW treatment known for its cheap and eco-friendly propertıes without any negative effects on the ecosystem can be used as a green method for alleviating the toxification effects of heavy metals in contaminated soil and increasing cocoon production of earthworms.

Assessing reference levels of nickel and chromium in cord blood, maternal blood and placenta specimens from Ankara, Turkey

Objective:Placenta is a temporary organ that connects the developing fetus and the mother. However, it cannot protect the embryo against chromium (Cr) and nickel (Ni) exposure. Quantification of Cr and Ni in biological and ecological subjects is challenging. Thus, the first goal of this study was to provide a validated Graphite Furnace Atomic Absorption Spectrometry (GFAAS) method to determine Cr and Ni in mother-newborn specimens. The second goal was to assess the reference Ni and Cr contents in cord blood, maternal blood, and placenta samples in a population from Ankara.Material and Methods:Biological samples were collected from 100 healthy mother-newborn pairs. Metal levels were quantified by GFAAS. Method validation of this toxicological analysis was performed by the use of certified reference materials, and assessed through accuracy, precision, specificity, range, quantitation, and detection limits.Results:Mean Cr levels of maternal blood, placentas, and cord blood were 0.337±0.222 μg/L, 0.221±0.160 μg/kg, 0.121±0.096 μg/L, respectively while mean Ni concentrations were 0.128±0.093 μg/L, 0.124±0.067 μg/kg, 0.099±0.067 μg/L, respectively. The method showed linearity with excellent correlation coefficients (r2) for Cr (0.9994) and Ni (0.9999). Satisfactory recovery and coefficient of variation for Cr and Ni were 102.85% and 102.35%; 1.75% and 2.91%, respectively. Relative error did not exceed 3%, demonstrating the accuracy of the method. Control charts were drawn to assess inter-day stability. The predicted reference ranges for Cr and Ni concentrations in maternal blood, placenta and cord blood were: Cr 0.033-0.75 μg/L; 0.032-0.526 μg/kg; 0.031-0.309 μg/L and for Ni were 0.011-0.308 μg/L; 0.024-0.251 μg/kg; 0.066-0.209 μg/L, respectively.Conclusion:The reported reference values of biological specimens in this paper will provide complementary aid to health professionals in terms of assessment of environmental and occupational exposure.

Estimating nickel exposure in respirable dust from nickel in inhalable dust.

The conversion of dust components is of high importance for retrospective evaluations of exposure levels, of occupational diseases or the time trend of occupational dust exposure. For this purpose, possibilities to convert nickel concentrations from inhalable to respirable dust are discussed in this study. Therefore, 551 parallel measurements of nickel concentrations in inhalable and respirable dust fractions were extracted from the exposure database MEGA (maintained at the Institute for Occupational Safety and Health of the German Social Accident Insurance) and investigated by linear regression analysis of ln-transformed concentrations. Inhalable dust is the most important predictor variable, showing an adjusted coefficient of determination (adj. R2) of 0.767 (R2 adjusted to sample size). Since multilinear regression analysis, cannot be applied, further description of data is gained by splitting the whole dataset into working activity groups (e. g. 'high temperature processing', adj. R2=0.628,' filling/transport/storage' adj. R2=0.741, 'machining/abrasive techniques', adj. R2=0.777). From these groups, four task restrictive subgroups, so-called 'heuristic groups', can be derived by pooling similar working tasks with similar regression coefficients and enhanced quality measures (adj. R2 between 0.724 and 0.924): 'welding (grinding time fraction [GTF]<5%)', 'welding (grinding time fraction [GTF]>5%)', 'high temperature cutting' and 'grinding'. For the working activity group 'high temperature processing' and the heuristic group 'welding' the determination of the grinding time fraction and its inclusion or exclusion from a dataset has a huge impact on the description of data and whether a transformation of nickel concentrations using the natural logarithm (ln) is necessary or not. In case of GTF < 5%, the conversions functions are linear, all other conversion functions are power functions with exponents between 0.713 and 0.986. It is possible to develop conversion functions for estimating the nickel concentration in the respirable dust fraction (cR(Ni)) out of the nickel concentration in the inhalable dust fraction (cI(Ni)). For the estimation of Nickel in respirable dust other studies, it is recommend to use the conversion functions of the heuristic trial and error groups. Limitations of the possibility to use the conversion functions are discussed.