Nickel Exposure Research Articles

Heavy Metal Ion and Haptoglobin Association with Career Duration in Pharmaceutical Industries: A Potential Occupational Hazard?

Introduction: Due to the increase growth of industrialization, the problem of environmental pollution has increased worldwide.
 Aims & Objectives: A cross-sectional comparative study was designed to find out association between heavy metal ion (lead & nickel), haptoglobin and years of working in Pharmaceutical inddustries.
 Place and duration of study: Pharmaceutical industry located at Quaid-e-Azam Industrial Estate Kot Lakhpat, Lahore, Punjab. Duration of study was January 2019 to June 2019.
 Material & Methods: A total of 58 workers of a pharmaceutical industry were included in the study.35 age matched subjects with no history of any disease were taken as controls. A brief questionnaire was filled by each participant. Heavy metals present in serum sample of patients were digested by concentrated Nitric Acid. The digested samples were analyzed to estimate the level of lead and nickel using atomic absorption spectrophotometry available at the Department of IMBB University of Lahore.Data was entered and analyzed by SPSS 20, p ? 0.05 was taken as significant.
 Results: Mean age of workers was 40.64 years with BMI 23.52 kg/m2. Their work of experience or duration of work in industries was 1-5 years, 6-10 years and > 10 years. Majority had dry cough followed by running nose, breathless end of day and headache. Levels of lead, nickel and haptoglobin was significantly raised compared to controls. Association of lead and nickel exposure with years of working experience showed that with increasing working experience or duration of workers the levels of lead and haptoglobin was markedly raise (5.9 ± 2.8 mg/l) as compared to the level of nickel (2.58 ± 1.05 mg/l).
 Conclusion: Exposure of lead and nickel increases the level of haptoglobin and causes health issue in the workers of Pharmaceutical factors. Levels of these heavy metals increased in circulation of workers with the increasing of their duration of work or work experience.

Abstract 324: Nickel exposure alters extracellular vesicles biogenesis to carry NUPR1 and mediate cancer progression

Abstract Nickel (Ni), a group I human carcinogen by the International Agency for Research on Cancer (IARC) alters expression of various oncogenic molecules in cells resulting in adoption of cancer cell phenotypes, such as anchorage-independent growth, migration, and invasion. Cancer cell phenotypes are altered by internal genetic or epigenetic changes or in response to external signals mediated by soluble proteins or extracellular vesicles. However, few studies have linked extracellular vesicles (EVs) in response to environmental pollutants, such as Ni. Nuclear Protein 1 (NUPR1) is a stress response protein that is upregulated in cancer cells and it is also upregulated in cells following chronic Ni exposure. However, the role of NUPR1 in EV biogenesis or EV-mediated cancer progression is unknown. To explore the potential role of EVs in Ni-induced cancer progression, this study examined the effect of Ni-exposure on EV signature. Sizes and concentration of EVs from BEAS-2B cells, 6 weeks-Ni-treated BEAS-2B cells (Ni-6W) and Ni-transformed BEAS-2B cells (Ni-3) were identified by nanoparticle-tracking analysis (NTA) and transmission electron microscopy (TEM). In the results, showed that Ni-6W and Ni-3 released more EVs compared to the control. The transcription expression levels of EVs biogenesis markers, CD63, CD82 and Flotillin-1 (FLOT) were coincidentally increased in Ni-6W and Ni-3 compared to the BEAS-2B. We further identified that inhibition of NUPR1 by using the shRNA or NUPR1 inhibitor ZZW-130 can rescue the increased releasing of EVs induced by Ni exposure. Here we demonstrated that Ni exposure elevated EV release and that these Ni-altered EVs contributed to a pro-inflammatory environment associated with tumorigenesis and cancer progression. Moreover, we provided a new method of regulating EVs biogenesis by targeting NUPR1, this would be crucial for EV-based cancer therapy. Citation Format: Shan Liu, Angelica Ortiz, Juan Iovanna, Max Costa. Nickel exposure alters extracellular vesicles biogenesis to carry NUPR1 and mediate cancer progression [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 324.

Nickel exposure induces gut microbiome disorder and serum uric acid elevation

Serum uric acid elevation has been found in long-term nickel (Ni) exposure occupational workers, but the mechanism is unclear. In this study, the relationship between Ni exposure and uric acid elevation was explored in a cohort of 109 participants composed of a Ni-exposed workers group and a control group. The results showed that Ni concentration (5.70 ± 3.21 μg/L) and uric acid level (355.95 ± 67.87 μmol/L) in the serum were increased in the exposure group with a significant positive correlation (r = 0.413, p < 0.0001). The composition of gut microbiota and metabolome revealed that the abundance of uric acid-lowering bacteria, such as Lactobacillus, Lachnospiraceae_Unclassfied and Blautia were reduced while pathogenic bacteria including Parabacteriadies and Escherichia-Shigella were enriched in Ni group, accompanied by impaired intestinal degradation of purines and upregulated biosynthesis of primary bile acids. Consistent with human results, the mice experiments showed that Ni treatment significantly promotes uric acid elevation and systemic inflammation. Lactobacillus and Blautia in gut microbiota were reduced and inflammation-related taxa Alistipes and Mycoplasma were enriched in the Ni treatment. In addition, LC-MS/MS metabolomic analysis indicated that purine nucleosides were accumulated in mice feces, which increased purine absorption and uric acid elevation in the serum. In summary, this study provides evidence that UA elevation was correlated with heavy metals exposure and highlighted the role of gut microbiota in intestinal purine catabolism and in the pathogenesis of heavy metal-induced hyperuricemia.

Assessment of human health risks associated with airborne arsenic, nickel and lead exposure in particulate matter from vehicular sources in Sao Paulo city

ABSTRACT Air pollution is a critical public health concern. The present study assessed the risk to human health of airborne Potentially Toxic Elements (PTE) arsenic, nickel and lead exposure in particulate matter (PM10–2.5) in Sao Paulo, Brazil. Statistical analysis was performed using R Software and the risk assessment for human health was carried out according to the methods of the United States Environmental Protection Agency. The results for mean annual concentration of PTE (ng m−3) were within the limits stipulated for air-quality by international agencies (arsenic <6, nickel <20 and lead <150). Airborne arsenic and lead showed higher mean concentrations during the winter than the other seasons (p < 0.05). However, the results showed a greater health risk for the adult population and during the winter season. These findings highlight the importance of air pollution as a risk factor for population health.

Thermal modulation of mitochondrial function is affected by environmental nickel in rainbow trout (Oncorhynchus mykiss)

In this study, we investigated the combined effects of temperature and nickel (Ni) contamination on liver mitochondria electron transport system (ETS) enzymes, citrate synthase (CS), phospholipid fatty acid composition and lipid peroxidation in rainbow trout (Oncorhynchus mykiss). Juvenile trout were acclimated for two weeks to two different temperatures (5˚C and 15˚C) and exposed to nickel (Ni; 520 μg/L) for three weeks. Using ratios of ETS enzymes and CS activities, our data suggest that Ni and an elevated temperature acted synergistically to induce a higher capacity for reduction status of the ETS. The response of phospholipid fatty acid profiles to thermal variation was also altered under nickel exposure. In control conditions, the proportion of saturated fatty acids (SFA) was higher at 15˚C than at 5˚C, while the opposite was observed for monounsaturated (MUFA) and polyunsaturated fatty acids (PUFA). However, in nickel contaminated fish, the proportion of SFA was higher at 5˚C than at 15˚C, while PUFA and MUFA followed the opposite direction. A higher PUFA ratio is associated with higher vulnerability to lipid peroxidation. Thiobarbituric Acid Reactive Substances (TBARS) content was higher when the PUFA were in higher proportions, except for Ni-exposed, warm-acclimated fish, in which we reported the lowest level of TBARS but the highest proportion of PUFA. We suspect that the interaction of nickel and temperature on lipid peroxidation is due to their synergistic effects on aerobic energy metabolism, as supported by the decrease in the activity of complex IV of the ETS enzyme activity in those fish, or on antioxidant enzymes and pathways. Overall, our study demonstrates that Ni exposure in heat-challenged fish can lead to the remodelling of the mitochondrial phenotype and potentially stimulate alternative antioxidant mechanisms.

Association between urinary nickel with obesity status in adults: A cross-sectional study.

The prevalence of obesity is on the rise and is connected to numerous factors. However, the relationship between obesity and nickel has never been investigated. Our study aimed to explore the association between urinary nickel and obesity Status in adults. From the 2017-2018 National Health and Nutrition Examination Surveys (NHANES), 1,705 participants ≥18 years of age were enrolled. To explore further the relationship among urinary nickel, body mass index (BMI), and waist circumference(WC), Weighted multivariate linear regression analyses and further subgroup analyzes were conducted. Urinary nickel does not correlate with BMI level but positively correlates with WC. In the subgroup analyzed according to sex, Urinary nickel has a positive correlation with BMI and WC in males but has a negative correlation in females. Secondary stratification analysis according to sex and race, Urinary nickel positively correlates with BMI in White males. It also positively correlates with WC in both White and Black males. A correlation was found between urinary nickel levels and BMI and WC in adult males. Adult men, especially those already obese, may need to reduce nickel exposure.

Association of urinary nickel levels with diabetes and fasting blood glucose levels: A nationwide Chinese population-based study

Some epidemiological studies support a relationship between nickel exposure and diabetes in the general population. To address this, we tested the association of nickel exposure with diabetes in 10,890 adults aged ≥ 18 years old from the China National Human Biomonitoring study conducted in 2017–2018. Urinary nickel concentrations and fasting blood glucose (FBG) were measured, and lifestyle and demographic data were collected. Weighted logistic and linear regressions were used to estimate the associations of urinary nickel levels with diabetes prevalence and FBG. Restricted cubic splines (RCS) were used to test for the dose-response relationship. The odd ratio (95% confidence interval [CI]) of diabetes for the highest versus lowest quartiles of urinary nickel concentrations was 1.74 (1.28, 2.36) in the multivariate model (p trend =0.001). Each one-unit increase in log-transformed urinary nickel concentrations was associated with a 0.36 (0.17, 0.55) mmol/L elevation in FBG. The RCS curves showed a monotonically increasing dose-response relationship of urinary nickel with diabetes as well as FBG levels, and then tended to flatten after about 4.75 μg/L of nickel exposure. The nickel-diabetes association was stronger in individuals with lower than those with higher rice consumption (OR: 2.39 vs. 1.72). Our study supports a positive association between nickel exposure and diabetes prevalence in Chinese adults, especially in individuals with lower rice consumption. Further large-scale prospective studies are needed to validate our findings.

Novel nanowire self-assembled hierarchical CeO2 microspheres loaded with nickel-based catalysts for hydrogen production from steam reforming of glycerol

The nickel-based catalysts with shape-specific CeO2 nanocrystals (hierarchical and spheres) and adjustable impregnation solvents were successfully synthesized. The synthesized Ni-CeO2 catalysts were used as the model catalyst to study the structure-dependent catalytic behavior and catalytic reaction mechanism for hydrogen production from glycerol steam reforming (GSR). Ni/CeO2-HE with the hierarchical structure and ethanol impregnation solvent obtained the strongest metal-support interaction. Electron effects because of the strong interaction between nickel and cerium dioxide promoted the formation of reducible nickel species. High nickel reduction and nickel dispersion contributed to the maximum active nickel exposure surface area, thus Ni/CeO2-HE exhibited superior glycerol conversion than other catalysts. The abundant oxygen vacancies generated due to strong Ni-CeO2 interaction facilitated the dissociation of water, thereby achieving a high yield of H2 for Ni/CeO2-HE. As a comparison, Ni/CeO2 and Ni/CeO2-E showed relatively poor catalytic activity due to lower exposed specific surface area and oxygen vacancy concentration. Moreover, the strong oxygen storage-release ability (CO-OSCC) promoted the oxidation of carbon deposition on Ni/CeO2-HE. As a result, Ni/CeO2-HE obtained good catalytic stability with no inactivation within 25 h. The study of the modulation role of Ni-CeO2 interaction on catalytic behavior can provide valuable guidelines for designing efficient catalysts for GSR.

Polyadenylation of canonical histone H3.1 in carcinogenesis.

Canonical histone messenger RNAs (mRNAs) are transcribed during S phase and do not terminate with a poly(A) tail at the 3' end. Instead, the histone mRNAs display a stem-loop structure at their 3-end. Stem-loop-binding protein (SLBP) binds the stem-loop and regulates canonical histone mRNA metabolism. We previously demonstrated that exposure to arsenic, an environmental carcinogen, induces polyadenylation of canonical histone H3.1 mRNA, causing transformation of human cells in vitro. Arsenic decreased cellular levels of SLBP by inducing its proteasomal degradation and inhibiting SLBP transcription via epigenetic mechanisms. Similarly, we also reported that nickel and arsenic have similar effects on canonical histone mRNA transcription and translation. Most recently, we further demonstrated that bisphenols' exposure increased polyadenylation of canonical histone H3.1 mRNA possibly through down-regulation of SLBP expression. This facilitates the abnormal stability of at least one canonical histone isoform (H3.1), and also increases H3 protein levels. Excess expression of canonical histones have been shown to increase sensitivity to DNA damage as well as increase the frequency of missing chromosomes and induce genomic instability. Thus, polyadenylation of canonical histone mRNA following arsenic, nickel and bisphenols exposure may contribute to metal and bisphenol-induced carcinogenesis.

Assessment of impact of nickel stress on the accumulation, pigments and protein content of water hyacinth (Pontederia crassipes L.)

Pontederia crassipes L. plants were collected and exposed to different concentrations (Control, 0.01, 0.1, 1.0 and 10.0 ppm) of Ni by using NiSO4 in medium in the laboratory. The effect of Ni2+ concentrations on visible symptoms such as toxicity, pigments (Chlorophyll- a, b and total) contents were estimated. Plants exposed to high nickel (1.0 and 10.0 ppm) showed visible toxicity symptoms such as wilting, chlorosis in young leaves, browning of roots noticed after 6 days of treatment. Nickel was accumulated more in stem (651.1µg/g dry weight) than leaves (115.23 µg/g dry weight) at 6 days of treatment. Nickel exposure decreased Chlorophyll-a, b and total chlorophyll contents. Body water content decreased at high nickel (1.0 and 10.0 ppm). Increased nickel concentrations increases antioxidants such as proline content. On the other hand carotenoids and protein contents at 1.0 ppm of nickel were decreased. The low level of nickel stimulates photosynthetic pigments and antioxidative parameters.

Insight into the effect of CeO2 morphology on catalytic performance for steam reforming of glycerol

Shape-specific CeO2 nanocrystals (spheres, rods, cubes and nanoparticles) with well-defined crystal facets were successfully synthesized and used as the support to synthesize series Ni/CeO2. Ni/CeO2 was employed as the model catalysts to study the structure dependent behavior and reaction mechanism for hydrogen production from glycerol steam reforming (GSR). The metal-support interaction was finely tuned by altering the morphology of CeO2 support, which in turn affected the exposed specific surface area of nickel and oxygen vacancy concentration. The relationship between exposed surface area of active nickel as well as surface oxygen vacancies and catalytic performance was studied. Ni/CeO2-S with the mainly exposed (111) type planes obtained the strongest metal-support interaction. Electron effects due to the strong metal-support between nickel and cerium dioxide facilitated the formation of readily reducible nickel species (Niδ+). High nickel reduction and nickel dispersion contributed to the maximum active nickel exposure surface area, thus Ni/CeO2-S showed exceptional glycerol conversion. Meanwhile, the strong Ni-CeO2 interaction resulting in abundant oxygen vacancies that facilitated the dissociation of water to produce hydrogen, thus possessing a high H2 yield. Conversely, Ni/CeO2-NR and Ni/CeO2-NC have lower exposure areas and oxygen vacancy concentrations due to the different exposed crystal planes, and therefore have relatively poor catalytic activity. Moreover, the strong oxygen storage-release ability (CO-OSC-OSCC) promoted the oxidation of carbon deposition on Ni/CeO2-S. Additionally, carbon deposition was mainly the filamentous carbon growing towards the periphery, hence, Ni/CeO2-S obtained up to 25-h catalytic stability. The study of the regulatory role of Ni-CeO2 interaction on catalytic behavior can offer worthwhile direction for designing high-efficiency GSR catalysts.

Occupational disease predictors in the nickel pyrometallurgical production: a prospective cohort observation

BackgroundPyrometallurgical nickel production exposes workers to a wide range of occupational risk factors, including nickel aerosol, occupational noise and heat, but occupational (compensation) claims do not get enough attention in the literature. We, therefore, aimed to identify and analyze new occupational disease predictors in order to tailor prevention measures in the nickel pyrometallurgical production workers.MethodsIn a prospective observational study, a cohort of workers grouped in 16 occupations (N = 1424, 88% males, median age 39 (interquartile range (IQR) 31–47 years)), was fixed in 2007 at a large nickel production plant in the Russian High North. We then followed the cohort until 2021 and analyzed the association of selected predictors, including exposure to nickel and occupational group, with the risk of an occupational (compensation) claim in a Cox regression analysis.ResultsWith 18,843 person-years of observation, occupational disease claims were confirmed in 129 workers (9% of the initial cohort, N = 108 men (84%)). Top three diagnoses were chronic bronchitis (3.81 cases/1000 workers/year), sensorineural deafness (2.36 cases/1000 workers /year) and musculoskeletal disorders (1.90 cases/1000 workers/year). Smoking was significantly associated with each diagnosis (adjusted hazard ratio (HR) ranged from 2.56 (95% confidence interval (CI) 1.17–5.57) for bronchitis to 6.69 (95% CI 1.46–30.64) for chronic obstructive pulmonary disease (COPD)). High nickel exposure was associated with occupational bronchitis and occupational asthma, whereas associations of occupational groups were also identified for COPD, asthma and musculoskeletal disorders.ConclusionSmoking, high exposure to nickel and specific exposure in the occupational groups increase the risk of occupational disease claims and should be prioritized directions for targeted intervention.

Occupational exposure to nickel and hexavalent chromium and the risk of lung cancer in a pooled analysis of case-control studies (SYNERGY).

There is limited evidence regarding the exposure-effect relationship between lung-cancer risk and hexavalent chromium (Cr(VI)) or nickel. We estimated lung-cancer risks in relation to quantitative indices of occupational exposure to Cr(VI) and nickel and their interaction with smoking habits. We pooled 14 case-control studies from Europe and Canada, including 16 901 lung-cancer cases and 20 965 control subjects. A measurement-based job-exposure-matrix estimated job-year-region specific exposure levels to Cr(VI) and nickel, which were linked to the subjects' occupational histories. Odds ratios (OR) and associated 95% confidence intervals (CI) were calculated by unconditional logistic regression, adjusting for study, age group, smoking habits and exposure to other occupational lung carcinogens. Due to their high correlation, we refrained from mutually adjusting for Cr(VI) and nickel independently. In men, ORs for the highest quartile of cumulative exposure to CR(VI) were 1.32 (95% CI 1.19-1.47) and 1.29 (95% CI 1.15-1.45) in relation to nickel. Analogous results among women were: 1.04 (95% CI 0.48-2.24) and 1.29 (95% CI 0.60-2.86), respectively. In men, excess lung-cancer risks due to occupational Cr(VI) and nickel exposure were also observed in each stratum of never, former and current smokers. Joint effects of Cr(VI) and nickel with smoking were in general greater than additive, but not different from multiplicative. In summary, relatively low cumulative levels of occupational exposure to Cr(VI) and nickel were associated with increased ORs for lung cancer, particularly in men. However, we cannot rule out a combined classical measurement and Berkson-type of error structure, which may cause differential bias of risk estimates.

The Ni(II)-Binding Activity of the Intrinsically Disordered Region of Human NDRG1, a Protein Involved in Cancer Development.

Nickel exposure is associated with tumors of the respiratory tract such as lung and nasal cancers, acting through still-uncharacterized mechanisms. Understanding the molecular basis of nickel-induced carcinogenesis requires unraveling the mode and the effects of Ni(II) binding to its intracellular targets. A possible Ni(II)-binding protein and a potential focus for cancer treatment is hNDRG1, a protein induced by Ni(II) through the hypoxia response pathway, whose expression correlates with higher cancer aggressiveness and resistance to chemotherapy in lung tissue. The protein sequence contains a unique C-terminal sequence of 83 residues (hNDRG1*C), featuring a three-times-repeated decapeptide, involved in metal binding, lipid interaction and post-translational phosphorylation. In the present work, the biochemical and biophysical characterization of unmodified hNDRG1*C was performed. Bioinformatic analysis assigned it to the family of the intrinsically disordered regions and the absence of secondary and tertiary structure was experimentally proven by circular dichroism and NMR. Isothermal titration calorimetry revealed the occurrence of a Ni(II)-binding event with micromolar affinity. Detailed information on the Ni(II)-binding site and on the residues involved was obtained in an extensive NMR study, revealing an octahedral paramagnetic metal coordination that does not cause any major change of the protein backbone, which is coherent with CD analysis. hNDRG1*C was found in a monomeric form by light-scattering experiments, while the full-length hNDRG1 monomer was found in equilibrium between the dimer and tetramer, both in solution and in human cell lines. The results are the first essential step for understanding the cellular function of hNDRG1*C at the molecular level, with potential future applications to clarify its role and the role of Ni(II) in cancer development.

Associations of nickel exposure and kidney function in U.S. adults, NHANES 2017–2018

BackgroundsNickel (Ni) is a ubiquitous heavy metal, but epidemiological studies on the association between Ni and kidney function are limited and controversial. AimWe aimed to explore the relationship between urinary Ni concentrations and kidney function in U.S. adults. MethodsThis was a cross-sectional study based on the 2017–2018 National Health and Nutrition Examination Survey (NHANES) (n = 1588). Multiple linear regression models, logistic regression models, and restricted cubic spline models (RCS) were fitted to explore the associations between urinary Ni and estimated glomerular filtration rate (eGFR), urinary albumin-creatinine ratio (UACR), and the odds of impaired kidney function, which was defined as an eGFR ≤ 60 mL/min per 1.73 m2, or UACR ≥ 30.0 mg/g. Bayesian kernel machine regression (BKMR) was used to account for joint-metal effects. ResultsCompared with the lowest quartile, urinary Ni at the third quartile was associated with increased eGFR (β = 2.42, 95 % CI: 0.23–4.19); the highest quartile of urinary Ni was correlated with increased UACR (β = 0.10, 95 % CI: 0.02–0.18), as well as higher odds of impaired kidney function (OR=1.65, 95 % CI:1.08–2.54). Urinary Ni had a nonlinear inverted U-shape relationship with eGFR (Pnonlinear = 0.007), and linear J-shape associations with UACR (Pnonlinear = 0.063) and impaired kidney function (Pnonlinear= 0.215). Metal interaction of urinary Ni with cadmium (Cd) on eGFR was observed. ConclusionsOur findings provided evidence that Ni exposure linked with declined kidney function and might interact with Cd exposure. Considering the cross-sectional design of the NHANES study, further prospective studies are necessary.

Prenatal exposure to nickel and atopic dermatitis at age 3 years: a birth cohort study with cytokine profiles.

Nickel, the fifth most common element on Earth, is the leading inducer of contact allergies in humans, with potent immunological effects. Nickel-induced contact allergies predominantly affect females. Maternal exposure to nickel has been associated with several developmental abnormalities. However, how a maternal nickel exposure affects the development of atopic diathesis and immune abnormalities in children has never been addressed. We aimed to determine whether maternal nickel exposure affects the development of atopic dermatitis and immune abnormalities in their children. Using a birth cohort study, we analysed 140 mother-child pairs recruited in 2012-2015 from central Taiwan. Maternal exposure to nickel was estimated using urinary nickel levels measured by inductively coupled plasma mass spectrometry (ICP-MS). The serum levels of 65 analytes and IgE in 3-year-old children were profiled with a multiplex ELISA. The correlation between the maternal urinary nickel concentration and serum analyte levels was assessed using Spearmen's correlation. Multivariant regression analysis was performed to evaluate the association between maternal urinary nickel levels and serum analyte concentrations in their children. The geometric means of the maternal urinary nickel and the children's serum IgE levels were 2.27 μg/L and 69.71 IU/mL, respectively. The maternal nickel exposure was associated with increased serum levels of IL-1β, IL-2, TNF-α, and leukaemia inhibitory factor (LIF) but with decreased serum levels of matrix metalloproteinase-1 (MMP-1), IL-2R, and eotaxin-1 in the children. In addition, the development of childhood atopic dermatitis at 3 years old was significantly associated with the child's serum levels of IgE and IL-2R, but it was negatively associated with the maternal nickel exposure. This is the first study showing the potential immunological effects of maternal nickel exposure in their children at an early developmental stage.

Mediation Effect of Body Mass Index on the Association of Urinary Nickel Exposure with Serum Lipid Profiles.

The objective of this study was to determine the relationship of urinary nickel (U-Ni) exposure to serum lipid profiles and the mediation effect of body mass index (BMI) in a US general population. We analyzed the cross-sectional data from 3517 participants in the National Health and Nutrition Examination Survey (NHANES) (2017-March 2020). Multivariable linear regression and restricted cubic spline (RCS) regression were conducted to explore the association of U-Ni with four serum lipids and four lipids-derived indicators. Mediation analysis was performed to examine the effect of BMI on the relationship between U-Ni levels and serum lipid profiles. Compared with the lowest quartile, the β with 95% confidence intervals (CIs) in the highest quartile were − 12.83 (− 19.42, − 6.25) for total cholesterol (TC) (P for trend < 0.001), − 12.76 (− 19.78, − 5.74) for non-high-density lipoprotein cholesterol (non-HDL-C) (P for trend = 0.001) and − 0.29 (− 0.51, − 0.07) for TC/HDL-C (P for trend = 0.007) in the fully adjusted model. RCS plots showed the linear association of log2-transformed U-Ni levels with TC, non-HDL-C and TC/HDL-C (P for nonlinearity = 0.294, 0.152, and 0.087, respectively). Besides, BMI decreased monotonically in correlation with increasing U-Ni levels (P for trend < 0.001). Mediation analysis revealed that BMI significantly mediated the relationship of U-Ni to TC, non-HDL-C and TC/HDL-C with mediated proportions of 11.17%, 22.20% and 36.44%, respectively. In summary, our findings suggest that BMI mediates the negative association of U-Ni with TC, non-HDL-C, and TC/HDL-C in the US general population.Supplementary InformationThe online version contains supplementary material available at 10.1007/s12011-022-03375-4.

Plasma Nickel Levels Correlate with Low Muscular Strength and Renal Function Parameters in Patients with Prostate Cancer.

Nickel is associated with cancer in occupational exposure. However, few studies have been devoted to analyzing the effects of nickel at environmental concentrations in cancer patients. In this work, the concentration of nickel in blood samples from patients with prostate cancer (PCa) was evaluated because this metal displays androgenic and estrogenic effects that play a crucial role in prostate carcinogenesis and treatment. We, therefore, compared blood nickel concentration in patients with PCa (non-occupationally exposed) (n = 46) with those in control age-matched individuals (n = 46). We also analyzed if there was any association between sociodemographic factors, clinical variables, geriatric evaluation assessment results, blood cell counts, or biochemical, androgen and estrogen concentrations. Using inductively coupled plasma-mass spectroscopy on the plasma samples, we observed a mean nickel level of 4.97 ± 1.20 µg/L in the PCa group and 3.59 ± 0.49 µg/L in the control group, with a non-significant effect (p = 0.293) between the two groups. The nickel concentration was significantly correlated with patient age (p = 0.005) and reduced handgrip strength (p = 0.003). Regarding biochemical parameters, significant associations were found with the renal glomerular filtration rate (p = 0.024) and blood urea levels (p = 0.016). No significant correlations were observed with other blood analytical parameters or testosterone or estradiol levels. These specific renal function and muscle strength effects were observed at environmental nickel exposure levels believed to be safe or at least far from the high concentrations observed after occupational exposure. Therefore, these parameters deserve further study, given that they could help pinpoint further public health concerns regarding nickel exposure in the general population.

Nickel Toxicity with Reference to Female Reproductive Physiology, Pregnancy and Teratogenesis: A Brief Review

Nickel has been known to adversely affect the female reproductive system and pregnancy, and cause teratogenesis. This review aims to analyse these effects of nickel. The implications of maternal oxidative stress and hormonal perturbations caused due nickel exposure have been discussed. Increased placental permeability, unidirectional foetal exposure through blood and milk leading to defects during organogenesis are analysed, along with post parturition eventualities such as stillbirth and altered sex ratios. Efforts are made to understand the ameliorative effects of selenium and possible future directions of research in the broad area are enumerated.

The Effect of Nickel Exposure on Oxidative Stress of Vicia faba Plants.

Heavy metal contamination is a serious threat for terrestrial ecosystems. Thus, they could be accumulated in living organisms leading consequently to harmful consequences. In this context, the present work aims to evaluate the effects of four increasing Nickel (Ni) nominal concentrations (T: 0mg/kg, C1: 150mg/kg, C2: 250mg/kg, C3: 500mg/kg) on agronomic and biochemical parameters in bean (Vicia faba) plants. The measured exposure concentrations were in the range of 96.69%-104.18% of the nominal concentrations. Bean's responses were evaluated at biometric levels, chlorophyll content and biochemical parameters namely catalase glutation-S-transferase activities and malondialdehyde content, in booth parts of plants. Our data revealed a marked negative effect of Ni exposure on bean plant development and chlorophyll content. Biochemical biomarkers reported that plants anti-oxidative defense system has been significantly affected specially in roots at the high Ni concentration. Briefly, resistance mechanisms of Vicia faba to Ni seem to imply an activation of the antioxidant system and a limitation of the reactive oxygen species.