Nickel Concentrations In Urine Research Articles

Urinary cadmium concentration is associated with the severity and clinical outcomes of COVID-19: a bicenter observational cohort study

BackgroundCadmium and nickel exposure can cause oxidative stress, induce inflammation, inhibit immune function, and therefore has significant impacts on the pathogenesis and severity of many diseases. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can also provoke oxidative stress and the dysregulation of inflammatory and immune responses. This study aimed to assess the potential associations of cadmium and nickel exposure with the severity and clinical outcomes of patients with coronavirus disease 2019 (COVID-19).MethodsWe performed a retrospective, observational, bicenter cohort analysis of patients with SARS-CoV-2 infection in Taiwan between June 2022 and July 2023. Cadmium and nickel concentrations in blood and urine were measured within 3 days of the diagnosis of acute SARS-CoV-2 infection, and the severity and clinical outcomes of patients with COVID-19 were analyzed.ResultsA total of 574 patients were analyzed and divided into a severe COVID-19 group (hospitalized patients) (n = 252; 43.9%), and non-severe COVID-19 group (n = 322; 56.1%). The overall in-hospital mortality rate was 11.8% (n = 68). The severe COVID-19 patients were older, had significantly more comorbidities, and significantly higher neutrophil/lymphocyte ratio, C-reactive protein, and interleukin-6 than the non-severe COVID-19 patients (all p < 0.05). Blood and urine cadmium and urine nickel concentrations were significantly higher in the severe COVID-19 patients than in the non-severe COVID-19 patients. Among the severe COVID-19 patients, those in higher urine cadmium/creatinine quartiles had a significantly higher risk of organ failure (i.e., higher APACHE II and SOFA scores), higher neutrophil/lymphocyte ratio, lower PaO2/FiO2 requiring higher invasive mechanical ventilation support, higher risk of acute respiratory distress syndrome, and higher 60-, 90-day, and all-cause hospital mortality (all p < 0.05). Multivariable logistic regression models revealed that urine cadmium/creatinine was independently associated with severe COVID-19 (adjusted OR 1.643 [95% CI 1.060–2.547], p = 0.026), and that a urine cadmium/creatinine value > 2.05 μg/g had the highest predictive value (adjusted OR 5.349, [95% CI 1.118–25.580], p = 0.036).ConclusionsUrine cadmium concentration in the early course of COVID-19 could predict the severity and clinical outcomes of patients and was independently associated with the risk of severe COVID-19.

An ICP-MS Study for Quantitation of Nickel and Other Inorganic Elements in Urine Samples: Correlation of Patch Test Results with Lifestyle Habits.

Nickel (Ni) is a frequently used metal in the production of many products, and Ni exposure occurs in humans through food, inhalation, and skin. Studies reported Ni as the most common allergen diagnosed in the serial patch test. The main purpose of our study was to determine the concentration of Ni and other elements in the urine samples of individuals with Ni-sensitivity and to determine the effect of lifestyle habits on these variables. This study was conducted with 388 participants; additionally, both Ni patch test and inorganic analysis (for 24 elements)method in urine with inductively coupled plasma-mass spectrometry (ICP-MS)were applied to all participants. Ninety-two (23.7%) of the participants were found to have nickel sensitivity with a mean urine concentration of 4.475 μg/g creatinine (median=4.260; SD=2.527). The urine nickel concentration was significantly different between female and male participants (p =0.001). We found a significant correlation between Ni and other metals alongside various element pairs. The mean urine Ni concentration of the individuals with a positive Ni sensitivity test result was not different from that of the participants without Ni sensitivity (4.475 vs 4.256 μg/g creatinine, respectively; p = 0.068). The high accuracy, recovery, and repeatability data obtained from the analyses indicate that this study is efficient and appropriate for the quantitative determination of nickel and other elements in urine samples. Ni-containing objects and Ni-rich foods should be of concern for individuals with hypersensitivity reactions to the element.

Determination of nickel in urine by ultrasonic-assisted ionic liquid microextraction-graphite furnace atomic absorption spectrometry

Objective: To set up a new method to determine the nickel of urine in urine using dispersive liquid-liquid microextraction (DLLME) coupled with graphite furnace atomic absorption spectrometry (GFAAS) . Methods: From September 2018 to September 2019, the methanol, pyrrolidine dithiocarbamate and ionic liquid 1-hexyl-3-methyl-imidazolium hexafluorophosphate were used as dispersive solvent, the chelating agent and extraction solvent for the preconcentration of nickel, respectively. After adding into buffer solution of pH 9, ultrasonic dissolving for 10 minutes, centrifugal separation and then discarding the supernatant, the precipitate was saved. Dissolving the precipitate by methanol, mixing thoroughly on a vortex mixer, the 15 μl of the mixed solution was used for determination by graphite furnace atomic absorption spectrometry. Results: The linear correlation coefficient of urine nickel concentration in the range of 2.0-10.0 μg/L, r=0.999, with the detection limitation of 0.43 μg/L. The recovery rate and the relative standard deviations were 95.6%-103.7% and 2.53%-4.82%, respectively. Conclusion: The method, which has low detection limit, high recovery rate and good precision, is suitable for the determination of nickel in urine for the occupational populations exposure to nickel and non-occupational exposure.

Behavioral interventions to reduce nickel exposure in a nickel processing plant

ABSTRACTNickel is a widely-used material in many industries. Although there is enough evidence that occupational exposure to nickel may cause respiratory illnesses, allergies, and even cancer, it is not possible to stop the use of nickel in occupational settings. Nickel exposure, however, can be controlled and reduced significantly in workplaces.The main objective of this study was to assess if educational intervention of hygiene behavior could reduce nickel exposure among Indonesian nickel smelter workers. Participants were randomly assigned to three intervention groups (n = 99). Group one (n = 35) received only an educational booklet about nickel, related potential health effects and preventive measures, group two (n = 35) attended a presentation in addition to the booklet, and group three (n = 29) received personal feedback on their biomarker results in addition to the booklet and presentations. Pre- and post-intervention air sampling was conducted to measure concentrations of dust and nickel in air along with worker's blood and urine nickel concentrations. The study did not measure significant differences in particles and nickel concentrations in the air between pre- and post-interventions. However, we achieved significant reductions in the post intervention urine and blood nickel concentrations which can be attributed to changes in personal hygiene behavior. The median urinary nickel concentration in the pre-intervention period for group one was 52.3 µg/L, for group two 57.4 µg/L, and group three 43.2 µg/L which were significantly higher (p< = 0.010) than those measured in the post-intervention period for each of the groups with 8.5 µg/L, 9.6 µg/L, and 8.2 µg/L, respectively. A similar pattern was recorded for serum nickel with significantly (p < 0.05) higher median concentrations measured in the pre-intervention period for group one 1.7 µg/L, and 2.0 µg/L for group 2 and group 3 compared with the post intervention median serum nickel levels of 0.1 µg/L for all groups.The study showed that educational interventions can significantly reduce personal exposure levels to nickel among Indonesian nickel smelter workers.

Acute pneumonitis associated with nickel carbonyl exposure in the workplace

Background: We describe the clinical course of one industrial technician occupationally exposed to nickel carbonyl (NiC).Case report: A 50-year-old male industrial technician presented with complaints of nausea, myalgia, and cough to a local clinic after suspected occupational exposure to nickel carbonyl. He has no history of lung disease or smoking. His initial urine nickel concentration was 692 ug/L. He had infiltrates on the initial chest X-ray (CXR) and an oxygen saturation (O2) of 97% on room air. The patient was started on disulfiram 1 g by mouth (PO), 500 mg six hours after the first dose, then 250 mg twice daily for five days with prednisone 60 mg by mouth for five days. He presented 48 hours later with worsening respiratory symptoms. His O2 saturation decreased to 85% despite two days of oral steroids, and he was admitted to a hospital. He received prednisone 60 mg/day PO, 4 L nasal O2, and disulfiram 500 mg twice daily. He was discharged on day 7 post-exposure with disulfiram and prednisone.Case discussions: NiC is a severe respiratory irritant. Disulfiram was used off-label and was based on an established company protocol.Conclusions: Inhalation exposure to NiC resulted in a delayed respiratory dysfunction which responded to disulfiram treatment.

Acute inhalational metallic nickel poisoning

Objective To investigate the clinical characteristics of acute inhalational metallic nickel poisoning and its treatment effect. Methods Data including epidemiology, clinical features, laboratory tests, imaging examinations, therapy protocol as well as prognosis were collected and analyzed. Results Thoracic CT scan of all patients demonstrated as bilateral diffuse infiltration. Nickel concentration in both blood and urine were high in all patients and the concentration was positively associated with poisoning severity. All 4 patients received glucocorticoid treatment, 2 of whom with acute respiratory distress syndrome were admitted to ICU to initiate mechanical ventilation and were given sodium dimercaptopropanesulfonate. All patients survived to hospital discharge. Conclusions Acute inhalational metallic nickel poisoning is uncommon and early symptoms are inconclusive. The blood and urine nickel concentration is helpful to judge the severity of the disease. Pulmonary diffuse infiltration is the main clinical feature. Glucocorticoid, chelation therapy as well as symptomatic treatment are effective therapies to relief disease severity. Key words: Acute; Metallic nickel; Inhalational; Poisoning; Nickel concentration; Acute respiratory distress syndrome; Mechanical ventilation; Glucocorticoid; Chelation therapy

Commentary: Environmental chemicals and diabetes: which ones are we missing?

Commentary: Environmental chemicals and diabetes: which ones are we missing?

Influence of dietary factors, age and nickel contact dermatitis on nickel excretion

Nickel is a frequently detected cause of allergic contact dermatitis. Ingestion of nickel may lead to flares of nickel contact dermatitis. We examined nickel excretion in the urine of 164 female patients with and without nickel contact dermatitis. The associations between age, atopic dermatitis, nickel contact dermatitis and nickel exposure through nutrition (e.g. dietary supplements) and by patch tests were investigated prospectively. Nickel was measured with atomic absorption spectrometry with two different standardized methods. A nickel detection limit of 0.2 µg/l was exceeded by all samples. The 95th percentiles of urine nickel concentration were 3.77 µg/l (age 18-30 years) and 3.98 µg/l (age 31-46 years). Bivariate analyses pointed to significantly increased nickel excretion with increasing age, ingestion of dietary supplements, drinking of stagnant tap water, and consumption of nickel-rich food. In the multivariate analysis, age and dietary supplements remained significant predictors of high nickel excretion. A non-significant increase in the median concentration of nickel was observed after the administration of conventional nickel patch tests. Patients with atopic eczema showed urine nickel concentrations similar to those in non-atopic controls. The 95th percentile of nickel excretion in our study population markedly exceeded the actual reference value of 3 µg/l. Age and consumption of dietary supplements are the most important predictors. The use of stagnant tap water and consumption of nickel-rich food contribute to the total load. These factors should be explicitly mentioned when allergic patients on a low-nickel diet are counselled. In contrast, existing nickel contact sensitization was not more frequent in subjects with higher nickel excretion. Nickel patch testing may cause transient minor systemic nickel exposure. The findings of this study extend our understanding and management of factors associated with nickel allergy.

Relationship between Nickel Exposure and the Level of Carcinoembryonic Antigen among Welders in an Automotive Plant

Background: Study on the effect of nickel exposure in the occupational setting and its association to carcinoembryonic antigen (CEA) had been studied before. Questions were raised whether the result from previous study would also show the same pattern of the urinary nickel concentration in this study. Objective: A cross-sectional study was conducted to determine the association between urine nickel concentration and CEA level among welders in automotive part workers in Malaysia. Methodology: There were 56 welders and 44 administrative workers were recruited in this study. Urine and blood samples were collected at the end of shift towards the end of workweek. CEA was assayed in serum using TECO Diagnostic ELISA Kit. Urinary nickel was determined by Graphite Furnace Atomic Absorption Spectrophotometer. Results: The mean carcinoembryonic antigen concentrations of the exposed group (4.07±2.60 ng mL-1) was significantly higher (p<0.001) than the control group (1.99±0.97 ng mL-1). Twenty seven percent of the exposed group showed values above the reference range. The mean urinary nickel level was also significantly higher (p<0.001) in the exposed group (1.99±0.91 mg L-1) than the control group. Result showed correlation between serum carcinoembryonic antigen concentration and urinary nickel concentration (r = 0.206). Conclusion: The significant elevation of urinary nickel levels in the welders compared with controls suggests that the welders were exposed to nickel fumes during welding. It is suggested that elevation of serum carcinoembryonic antigen was due to exposure to nickel during welding processes after controlling other confounding factors.

Urinary elimination of nickel and cobalt in relation to airborne nickel and cobalt exposures in a battery plant

To estimate the relationship between Ni concentrations in the ambient air and in the urine, at a battery plant using nickel hydroxide. Workers occupationally exposed to a mixture of nickel hydroxide, metallic cobalt and cobalt oxyhydroxide dust were studied during two consecutive workdays. Air levels of Ni and Co in total dust were determined by personal sampling in the breathing zone. Both metals in air were sampled by Teflon binder filters and analyzed by inductively coupled plasma absorption emission spectrophotometry. Urine was collected from 16 workers immediately before and after the work shift. Urinary Ni and Co concentrations were measured by electrothermal atomic absorption spectrometry. A poor correlation was seen between Co in the air and in post-shift urine (r = 0.491; P < 0.01), and no correlation was found between Ni in the air and in post-shift urine (r = 0.272; P = 0.15), probably due to the use of respiratory protection. The subjects were exposed to higher levels of Ni than Co (Ni (mg/m(3)) = -0.02 + 7.41 Co (mg/m(3)), r = 0.979, P < 0.0001). Thus, exposure to Co at 0.1 mg/m(3) should produce a Ni level of 0.7 mg/m(3). According to section XIII of the German list of MAK and BAT Values, a relationship between exposure to Co and urinary Co excretion, Co (microg/l) = 600 Co (mg/m(3)), has been established and the relationship between soluble or insoluble Ni salts in the air and Ni in urine was as follows: Ni (microg/l) = 10 + 600 Ni (mg/m(3)) or Ni (microg/l) = 7.5 + 75 Ni (mg/m(3)). Assuming nickel hydroxide to be soluble and to be insoluble, the Ni concentrations corresponding to Ni exposure at 0.7 mg/m(3) were calculated as 430 and 60 microg Ni/l, respectively. Similarly, exposure to Co at 0.1 mg/m(3) should result in Co urinary concentrations of 60 microg Co/l. On the other hand, a good correlation was found between Co and Ni in post-shift urine (Ni (microg/l) = 9.9 + 0.343 Co (microg/l), r = 0.833, P < 0.0001). On the basis of this relationship, the corresponding value found in our study was 0.343 x 60 microg Co/l + 9.9 = 30.5 microg Ni/l. This value was close to that calculated by the equation for a group of insoluble compounds, but about 14 times lower than that calculated by the equation for a group of soluble compounds. Our results suggest that exposure to nickel hydroxide yields lower urine nickel concentrations than the very soluble nickel salts, and that the grouping of nickel hydroxide might be reevaluated. Therefore, to evaluate conclusively the relationship between nickel hydroxide dust in the air and Ni in post-shift urine, further studies are necessary.

Urinary nickel: measurement of exposure by inductively coupled plasma argon emission spectrometry

Nickel is a rare earth metal and is widely used in modern industry. Its overexposure in human beings can provoke significant effects including lung, cardiovascular and kidney diseases. As an index of occupational exposure, urine is widely used for the monitoring of nickel concentration because it is a minimally invasive method. Recent studies have used atomic absorption spectrometry to measure nickel concentration. In this study, we introduced novel inductively coupled plasma argon emission spectrometry (ICPAES) which enables us to measure multiple elements simultaneously with smaller volume and with lower detection limits compared to conventional atomic absorption emission spectrometry, and we established the new measuring method by determining the appropriate wavelengths for nickel concentration. Furthermore, using the established new measuring method, we investigated the correlation between a single oral administration of nickel and urine elimination in rats. As a result, different concentrations of nickel standard solutions were measured by ICPAES, and among five specific wavelengths of nickel, 221.647 and 231.604 nm were chosen because they had the highest inclines of both signal to background ratio and emission intensity in simple linear regression analysis. Next, by using healthy human urine samples that had not been exposed to nickel, 231.604 nm was determined to be the most appropriate wavelength because it did not present abnormal intensity due to obstacle wavelength. Male Wistar rats received an oral administration of nickel ranging from 0.025 to 250 mg/kg, which is equivalent to 0.0015 - 15% of LD50, and during the following 24 h, urine samples were collected and the nickel concentration was measured by ICPAES. With a single oral administration of nickel, there was an increase in urine nickel concentration in a dose-dependent manner and the appropriate equation was developed. Acute renal failure was not observed in this dosage of oral nickel administration by analysing NAG, beta2-microglobulin, urine albumin and urine protein. It was concluded that the obtained nickel reference values using ICPAES would be useful for the early diagnosis of nickel intoxication and in the assessment of the exposure to nickel.

Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds

OBJECTIVESTo assess the exposure to tungsten, cobalt, and nickel in a plant producing hard metals. The main components of hard metals are tungsten carbide and cobalt metal. According to recent...

Relationship between atmospheric and urinary nickel in workers manufacturing electrical resistances using nickel oxide: role of the bioavailability of nickel.

The daily concentrations of nickel in total (ie inhalable) and respirable airborne dust (personal sampling) and in post-shift and pre-shift urine samples were monitored during five consecutive work days in 20 workers exposed to NiO in a workshop manufacturing electrical resistances. The individual daily atmospheric nickel concentrations ranged from 0.5 to 9586 micrograms Ni/m3 (geometric mean 22.9) for total dust and from 0.2 to 332 micrograms Ni/m3 (geometric mean 3.5) for respirable dust. The results of the urinary excretion of nickel suggested that the occupationally-related systemic absorption of nickel strongly differed in one subject (worker E) compared to the other 19 workers. In the latter group the nickel concentration in urine never exceeded 5 micrograms Ni/g creatinine, it did not differ between post-shift and pre-shift samples (geometric means: 1.1 versus 1.2 micrograms Ni/g creatinine), and it was only slightly higher than that measured in a group of 17 non-exposed subjects (mean 0.5 micrograms Ni/g creatinine; range 0.1-1.7); furthermore their nickel elimination in urine did not change during the days off or after two weeks of holiday. In worker E, the nickel concentration ranged from 21 to 101 micrograms Ni/g creatinine in post-shift urine, the next morning (after 16 h) it had dropped on average by 50 per cent, it decreased further during the days off, and amounted still to 4.4 micrograms Ni/g creatinine after two weeks of holiday. These divergent patterns of elimination of nickel in urine are most likely related to differences in the nature of exposure to airborne nickel involving both particle size and bioavailability of nickel. Worker E was exposed to NiO powder of 1-8 microns particle size resulting in nickel levels of the respirable fraction on average about 50 times that measured for the 19 other workers (3 micrograms Ni/m3). Transformation of the initial NiO powder into particles of 150 to 600 microns size and associated changes in physicochemical properties of NiO in the particles of the respirable fraction may explain why the urinary excretion of nickel in the 19 workers is hardly influenced by their occupational exposure to this metal. The pattern of urinary nickel elimination in worker E, however, most likely reflects very recent exposure to NiO, suggesting that the degree of bioavailability of nickel from this particular physicochemical form of NiO powder is much higher than that usually accepted for poorly soluble nickel compounds.

Occupational chronic exposure to metals

Stainless steel welders (n = 103) were examined. To estimate external exposure, personal air sampling was used. Internal exposure was quantified by the determination of nickel levels in erythrocytes, plasma and urine. Men and women (n = 123) were examined for control purposes. In the plasma and erythrocytes of the controls the nickel concentration was below the level of detection (less than 1.8 micrograms/l). The element concentrations in urine were between less than 0.1 and 13.3 micrograms/l. Of the controls 95% showed nickel levels in urine below 2.2 micrograms/l (reference value). The average concentration of nickel in the air was 93 +/- 81 micrograms/m3. The average concentration of nickel in the plasma samples was 4.9 +/- 4.0 micrograms/l (95th percentile 12.8 micrograms/l). In erythrocytes nickel could not be detected. The nickel concentrations in the urine of the welders were 18.5 +/- 28.5 micrograms/l on average (95th percentile 52.5 micrograms/l). Only a weak correlation between the nickel levels of plasma and urine could be detected (Curine = 2.07 + 8.45 Cplasma; r = 0.294; p less than 0.01). Based on our results and on the reported literature a future limit value for the nickel concentration in urine should lay between 30 and 50 micrograms/l. This value corresponds to an external exposure of 500 micrograms nickel per cubic metre.

Biological monitoring of nickel.

Measurements of nickel in body fluids, excreta, and tissues from humans with occupational, environmental, and iatrogenic exposures to nickel compounds are comprehensively reviewed. Correlations between levels of human exposures to various classes of nickel compounds via inhalation, oral, or parenteral routes and the corresponding concentrations of nickel in biological samples are critically evaluated. The major conclusions include the following points: Measurements of nickel concentrations in body fluids, especially urine and serum, provide meaningful insights into the extent of nickel exposures, provided these data are interpreted with knowledge of the exposure routes, sources, and durations, the chemical identities and physical-chemical properties of the nickel compounds, and relevant clinical and physiological information, such as renal function. Nickel concentrations in body fluids should not, at present, be viewed as indicators of specific health risks, except in persons exposed to nickel carbonyl, for whom urine nickel concentrations provide prognostic guidance on the severity of the poisoning. In persons exposed to soluble nickel compounds (e.g., NiCl2, NiSO4), nickel concentrations in body fluids are generally proportional to exposure levels; absence of increased values usually indicates non-significant exposure; presence of increased values should be a signal to reduce the exposure. In persons exposed to less soluble nickel compounds (e.g., Ni3S2,NiO), increased concentrations of nickel in body fluids are indicative of significant nickel absorption and should be a signal to reduce the exposures to the lowest levels attainable with available technology; absence of increased values does not necessarily indicate freedom from the health risks (e.g., cancers of lung and nasal cavities) associated with exposures to certain relatively insoluble nickel compounds.

Factors influencing nickel dermatitis. II.

The nickel concentrations in urine and other data of a very hypersensitive female patient have been followed during two periods exceeding 30 days each. Only a limited degree of correlation was found between the course of the nickel concentration in urine and the clinical activity of the dermatitis. In order to better evaluate the measure of the correlation and the influence of some other factors upon the activity of the dermatitis, a pathway analysis scheme has been constructed. Consideration of this scheme reveals the need for more extensive data regarding the nickel ion climate in the body.

Factors influencing nickel dermatitis. I.

The nickel concentrations in urine and blood plasma of a very hypersensitive female patient have been followed during two periods of 34 and 42 days each. A limited degree of correlation was found between the course of the nickel concentration in plasma, the nickel concentration in urine and the clinical activity of the dermatitis. Evidently other factors also influence the activity of the dermatitis; among these menstruation and stress might be expected to play a role.

Interlaboratory comparisons of nickel analyses in urine by atomic absorption spectrometry.

Two interlaboratory surveys of urine nickel analyses were performed in which eight or nine urine samples were distributed to laboratories in seven nations for measurements of nickel concentrations by atomic absorption spectrometry. In both surveys, wide discrepancies were observed in the values for urine nickel concentrations that were obtained in different laboratories by various analytical methods. This finding documents a serious need for improvement in the proficiency of nickel analyses. Nonetheless, excellent interlaboratory concordance was found in the rankings of urine samples in order of increasing nickel concentrations. Analytical techniques that involved preliminary wet or dry ashing and extration steps before flameless atomic absorption spectrometry were generally superior to techniques for direct analysis of urine by flameless atomic absorption spectrometry in respect to (a) analytical sensitivity, (b) recovery of added nickel, (c) interlaboratory precision, and (d) interlaboratory concordance of ranking of urine samples in order of increasing nickel concentrations.