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PubMed1988

Acute nickel toxicity in electroplating workers who accidently ingested a solution of nickel sulfate and nickel chloride.

Thirty-two workers in an electroplating plant accidently drank water contaminated with nickel sulfate and chloride (1.63 g Ni/liter). Twenty workers promptly developed symptoms (e.g., nausea, vomiting, abdominal discomfort, diarrhea, giddiness, lassitude, headache, cough, shortness of breath) that typically lasted a few hours but persisted 1-2 days in 7 cases. The Ni doses in workers with symptoms were estimated to range from 0.5 to 2.5 g. In 15 exposed workers who were tested on day 1 postexposure, serum Ni concentrations ranged from 13 to 1,340 micrograms/liter and urine Ni concentrations ranged from 0.15 to 12 mg/g creatinine. Ten subjects (with initial urine Ni concentrations greater than 0.8 mg/g creatinine) were hospitalized and treated for 3 days with intravenous fluids to induce diuresis, resulting in a mean elimination half-time (T1/2) for serum Ni of 27 hours (SD +/- 7 hour), which was significantly shorter (p less than .001) than the mean T1/2 of 60 hours (SD +/- 11 hours) in 11 subjects who did not receive intravenous fluids. Laboratory tests showed transiently elevated levels of blood reticulocytes (N = 7), urine albumin (N = 3), and serum bilirubin (N = 2). All subjects recovered rapidly, without evident sequellae, and returned to work by the eighth day after exposure.

Accidents, Occupational↗
PubMed2004

Mononuclear nickel(III) and nickel(II) thiolate complexes with intramolecular S-H proton interacting with both sulfur and nickel: relevance to the [NiFe]/[NiFeSe] hydrogenases.

Mononuclear, distorted square planar [Ni(II)(ER)(P(o-C(6)H(4)S)(2)(o-C(6)H(4)SH))](-) (ER = SePh (1), 2-S-C(4)H(3)S (2)) with a S-H proton directly interacting with both nickel and sulfur atoms were prepared by reaction of [Ni(CO)(SePh)(3)](-)/[Ni(CO)(2-S-C(4)H(3)S)(3)](-) and P(o-C(6)H(4)SH)(3), individually. The presence of combinations of intramolecular [Ni-S...H-SR]/[Ni...H-SR] interactions was verified in the solid state by the observation of an IR nu(SH) stretching band (2273 and 2283 cm(-)(1) (KBr) for complexes 1 and 2, individually) and (1)H NMR spectra (delta 8.079 (d) (CD(2)Cl(2)) and 8.39 (d) (C(4)D(8)O) ppm (-SH) for complexes 1 and 2, respectively) and subsequently confirmed by X-ray diffraction study. The exo-thiol proton (o-C(6)H(4)SH) in complexes 1 and 2 was identified as a D(2)O exchangeable proton from NMR and IR studies and was quantitatively removed by Lewis base Et(3)N to yield Ni(II) dimer [Ni(II)(P(o-C(6)H(4)S)(3))](2)(2)(-) (5). Instead of the ligand-based oxidation to form dinuclear Ni(II) complexes and dichalcogenide, oxidation of THF-CH(3)CN solution of complexes 1 and 2 by O(2) resulted in the formation of the mononuclear, distorted trigonal bipyramidal [Ni(III)(ER)(P(o-C(6)H(4)S)(3))](-) (ER = SePh (3), 2-S-C(4)H(3)S (4)) accompanied by byproduct H(2)O identified by (1)H NMR, respectively. The 4.2 K EPR spectra of complexes 3 and 4 exhibiting high rhombicities with three principal g values of 2.304, 2.091, and 2.0 are consonant with Ni(III) with the odd electron in the d(z)(2) orbital. Complex 3 undergoes a reversible Ni(III/II) process at E(1/2) = -0.67 V vs Ag/AgCl in MeCN.

Crystallography, X-Ray↗
PubMed1996

Nickel chloride/chlorides of divalent metal interactions in nickel-sensitive subjects.

To verify if the counter-ion Cl- permits the same interactions between nickel and divalent metals with physicochemical similarities as the counter-ion SO4- does, 50 sensitive subjects to nickel sulfate 5% pet. who previously gave positive patch test reactions either to 8 mu 1 of aq. nickel sulfate 0.1 M or to 8 mu 1 of aq. nickel chloride 0.1 M, or to both, were patch retested simultaneously to 8 mu 1 of, respectively, aq. nickel sulfate 0.1 M and aq. nickel chloride 0.1 M, and to 8 mu 1 of aq. mixed solutions containing, respectively, nickel chloride 0.1 M+magnesium chloride 0.3 M, nickel chloride 0.1 M+zinc chloride 0.3 M, nickel chloride 0.1 M+zinc chloride 0.5 M, nickel chloride 0.1 M+manganese chloride 0.3 M, and nickel chloride 0.1 M+manganese chloride O.5 M. Whilst 4 subjects gave a positive patch test response to only nickel sulphate, 8 gave a positive response to nickel chloride alone and the remaining 38 gave a concomitant positive response to both. In all subjects who gave positive responses to nickel chloride, the chlorides of divalent metals were not able to inhibit or reduce the positive reaction. 25 healthy subjects patch tested to both single salts and mixed solutions, and all gave negative responses. 9 of the 50 subjects, 4 who previously gave positive reactions to only nickel chloride 0.1 M, and 5 with concomitant reactions of equal intensity to both nickel chloride and nickel sulfate 0.1 M, were patch retested simultaneously to 8 mu 1 of, respectively, aq. nickel sulfate 0.1 M, aq. nickel chloride 0.1 M and aq. mixed solutions containing nickel sulfate (0.1 M) mixed with sulfates (0.3 M) and nickel chloride (0.1 M) mixed with chlorides of Mg, Zn, Mn (0.3 M). Whilst the mixed sulfate solutions were able to reduce nickel sulfate, 0.1 M patch test positive reactions, those containing chlorides, at all concentrations tested, did not inhibit the nickel chloride reactions in any of the subjects. The results of the tests to chlorides, compared to those reached on testing to sulfates of the same metals, lead us to hypothesize that the anion probably affects the uptake and local tissue distribution of the metal, modulating in this way, together with the individual cutaneous ligands, its effects.

Adult↗
PubMed1998

Nickel deficiency alters nickel flux in rat everted intestinal sacs.

This study was conducted to determine nickel absorption in nickel-deficient rats. Jejunal segments obtained from dietary nickel-depleted (13 microg nickel/kg diet) and nickel-control (1 mg nickel/kg diet) adult rats from the first generation, and suckling pups from the second offspring were used. The nickel transfer across the intestinal epithelium and nickel uptake into the intestine were measured by use of everted jejunal sacs using a wide range of nickel concentrations administered on the luminal side (1.1 x 10(-8) M til 1.0 x 10(-4) M). Both the intestinal nickel transfer and nickel uptake were influenced by the dietary nickel supply in rat offspring, but not in the adult rats from the first generation. However, in nickel-deficient offspring, the nickel transfer across the small intestine was higher than in nickel-control offspring. This difference was greater using low intraluminal nickel concentrations than high nickel concentrations, and was significant at 1.1 x 10(-8) M, 6.1 x 10(-8) M, 5.1 x 10(-7) M, 1.0 x 10(-6) M, and 5.0 x 10(-6) M. Also, nickel uptake into the intestine was somewhat greater in nickel-deficient rat pups than in nickel-control pups, and significant using 1.1 x 10(-7) M and 1.0 x 10(-6) M nickel. A definite saturation type kinetic for the intestinal nickel absorption in relation to the intraluminal nickel concentration could not be observed.

Animals↗
PubMed2003

Provocative use test of nickel coins in nickel-sensitized subjects and controls.

BACKGROUND: Consensus exists on levels of nickel release that are well tolerated in exposure to nickel-containing items in direct and continuous contact with skin (e.g. watches). The clinical relevance of nickel-containing coins eliciting nickel dermatitis associated with extensive occupational exposure (e.g. coins handled by cashiers) has not been determined. OBJECTIVES: To examine whether nickel-containing coins might be an elicitor of allergic contact dermatitis (ACD) in occupational settings with extensive exposure to coins (i.e. cashiers). METHODS: Eighteen subjects (10 nickel sensitized and eight non-nickel sensitized) completed this study after screening of history, physical examination and diagnostic patch testing (5% nickel sulphate). Each volunteer handled 10 coins (nickel-containing coins or non-nickel-containing coins) in a cross-over design at 5-min intervals (5 min handling followed by 5 min rest) for 8 h per day, for a total of 12 days excluding the weekend. One hand was gloved while the other was not during coin handling. Visual scoring and bioengineering measurements were recorded at each of four predetermined sites at baseline (day 1), end of day 5 and day 12 (last day of exposure). RESULTS: There were no statistical differences for either visual or bioengineering data comparing: (i) nickel-sensitized vs. non-nickel-sensitized subjects handling nickel-containing coins at day 1, day 5 and day 12; (ii) day 12 vs. day 1 (baseline) for nickel-sensitized subjects handling nickel-containing coins; (iii) handling of nickel-containing coins vs. non-nickel-containing coins by nickel-sensitized subjects at day 5 and day 12; (iv) gloved hand vs. ungloved hand of nickel-sensitized subjects handling nickel-containing coins at day 12. Limitations of the method and clinical extrapolation are detailed. CONCLUSIONS: Individuals handling these nickel-containing coins daily did not develop ACD, as judged by visual signs or bioengineering parameters.

Adult↗
PubMedDate not supplied

Nickel concentrations in nasal mucosa, plasma, and urine in active and retired nickel workers.

The objective of the present investigation was to study the influence of the occupational nickel exposure on the concentration of nickel in nasal mucosa, plasma and urine. Plasma, urine and biopsy specimens of nasal mucosa from 318 nickel workers, 15 retired nickel workers and 57 non-exposed controls were analyzed for nickel by atomic absorption spectrometry. The results showed that nickel exposure led significantly to raised nickel concentration in nasal mucosa, plasma and urine both in active and retired nickel workers. The average nickel concentration in the nasal mucosa was highest in workers exposed to the highest atmospheric nickel concentration, inhaled as nickel subsulphide and oxide dust. Workers exposed to aerosols of nickel chloride and sulphate at a lower atmospheric nickel concentration had, on the other hand, the highest mean nickel concentration in plasma and urine. The mucosal, plasma and urine nickel concentration were significantly correlated to duration of nickel exposure. The accumulated nickel in the nasal mucosa was retained for years after termination of the nickel exposure, and slowly released with an estimated half-life of 3.5 years.

Adult↗
PubMed1982

Bioavailability of nickel in man: effects of foods and chemically-defined dietary constituents on the absorption of inorganic nickel.

By serial determination of the change in plasma nickel concentration following a standard dose of 22.4 mg of nickel sulfate hexahydrate containing 5 mg of elemental nickel, the bioavailability of nickel was estimated in human subjects. Plasma nickel concentration was stable in the fasting state and after an unlabeled test meal, but after the standard dose of nickel in water was elevated 48.8, 73.0, 80.0, and 53.3 microgram/1, respectively, at hours 1, 2, 3, and 4. Plasma nickel did not rise above fasting levels when 5 mg of nickel was added to two standard meals: a typical Guatemalan meal and a North American breakfast. When 5 mg of nickel was added to five beverages-whole cow milk, coffee, tea, orange juice, and Coca Cola-the rise in plasma nickel was significantly suppressed with all but Coca Cola. Response to nickel also was suppressed in the presence of 1 g of ascorbic acid. Phytic acid in a 2:1 molar ratio with nickel, however, did not affect the rise in plasma nickel. The chelate of iron and ethylenediaminetetraacetate, NaFeEDTA, an iron-fortifying agent suggested for application in Central America, slightly but not significantly depressed plasma nickel rise at 2 hours, whereas disodium EDTA depressed plasma nickel levels significantly below the fasting nickel curve at 3 and 4 hours postdose. These studies suggest that the differential responses of inorganic nickel to distinct foods, beverages, and chemically-defined dietary constituents could be important to human nutrition.

Absorption↗
PubMed1999

Absorption and retention of nickel from drinking water in relation to food intake and nickel sensitivity.

Two studies were performed to examine the influence of fasting and food intake on the absorption and retention of nickel added to drinking water and to determine if nickel sensitization played any role in this regard. First, eight nonallergic male volunteers fasted overnight before being given nickel in drinking water (12 micrograms Ni/kg) and, at different time intervals, standardized 1400-kJ portions of scrambled eggs. When nickel was ingested in water 30 min or 1 h prior to the meal, peak nickel concentrations in serum occurred 1 h after the water intake, and the peak was 13-fold higher than the one seen 1 h after simultaneous intake of nickel-containing water and scrambled eggs. In the latter case, a smaller, delayed peak occurred 3 h after the meal. Median urinary nickel excretion half-times varied between 19.9 and 26.7 h. Within 3 days, the amount of nickel excreted corresponded to 2.5% of the nickel ingested when it was mixed into the scrambled eggs. Increasing amounts were excreted as the interval between the water and the meal increased, with 25.8% of the administered dose being excreted when the eggs were served 4 h prior to the nickel-containing drinking water. In the second experiment, a stable nickel isotope, 61Ni, was given in drinking water to 20 nickel-sensitized women and 20 age-matched controls, both groups having vesicular hand eczema of the pompholyx type. Nine of 20 nickel allergic eczema patients experienced aggravation of hand eczema after nickel administration, and three also developed a maculopapular exanthema. No exacerbation was seen in the control group. The course of nickel absorption and excretion in the allergic groups did not differ and was similar to the pattern seen in the first study, although the absorption in the women was less. A sex-related difference in gastric emptying rates may play a role. Thus, food intake and gastric emptying are of substantial significance for the bioavailability of nickel from aqueous solutions.

Absorption↗
PubMed1986

Effects of dietary nickel and protein on growth, nitrogen metabolism and tissue concentrations of nickel, iron, zinc, manganese and copper in calves.

Thirty male calves were used in a 2 X 3 factorial arrangement of treatments to determine the effects of dietary nickel and protein on performance, urease activity and tissue concentrations of nickel, iron, zinc, copper and manganese. Protein levels evaluated were 10.0, 12.25 and 14.5%, and nickel was supplemented at a level of 0 or 5 mg/kg of diet. Nickel did not affect growth during the 140-d study but tended to increase efficiency of gain in calves fed 14.5% protein. Rumen fluid urease activity was increased by nickel only in animals receiving the low protein diet. Urease activity in rumen fluid was higher in calves fed 10.0% than in animals fed 12.25% or 14.5% protein. Neither nickel nor protein affected urease activity in rumen epithelium. Increasing dietary protein resulted in increased urease in cecal digesta. Lung, liver, kidney and serum nickel concentrations were increased by supplemental nickel. A nickel X protein interaction was noted for kidney nickel. Nickel supplementation increased kidney nickel to a greater degree in calves fed 10.0% protein than in calves fed higher protein levels. Nickel supplementation reduced iron concentrations in lung, liver and muscle and manganese concentrations in muscle. Increased dietary protein decreased iron in liver and spleen but increased manganese concentrations in heart. These findings indicate that dietary protein influences responses of ruminants to nickel supplementation and relatively small increases in dietary nickel and protein can influence metabolism of other trace elements.

Animal Nutritional Physiological Phenomena↗
PubMed2006

Nickel represses the synthesis of the nickel permease NixA of Helicobacter pylori.

Nickel acquisition is necessary for urease activity, a major virulence factor of the human gastric pathogen Helicobacter pylori. NixA was identified as a specific nickel uptake system in this organism. Addition of small amounts of nickel to media strongly stimulates urea hydrolysis. On the other hand, high nickel concentrations are deleterious to cell growth. As a possible protective reaction, nickel uptake seems to be reduced in H. pylori grown in nickel-rich media. These observations led to investigations of regulation of the expression of the nickel permease NixA. We found that increasing the nickel concentration in media reduced the amount of NixA. In order to address the question of whether this phenomenon was subject to transcriptional or translational regulation, we quantified nixA mRNA from H. pylori by real-time PCR. The amount of nixA mRNA was gradually reduced five- to sevenfold in a time- and concentration-dependent manner. Repression could be measured as soon as 5 min after nickel addition, and the maximum repression occurred after 20 to 30 min. The maximum repression was obtained with an external nickel concentration of 100 microM. The observed nickel repression of NixA was dependent on nikR encoding the nickel-responsive regulatory protein NikR. In conclusion, we demonstrated that synthesis of the NixA nickel permease of H. pylori shows nickel-responsive regulation mediated by NikR to maintain the balance between effective nickel acquisition and a toxic overload.

Bacterial Proteins↗
PubMed1987

[Peroral nickel provocation in nondyshidrosiform and dyshidrosiform nickel eczema].

The flare-up of pompholyx-type nickel eczema induced by oral nickel challenge has been dealt with in several publications. To compare the reactivity of non-pompholyx and pompholyx-type nickel eczema, we challenged three groups of female volunteers (7 with non-pompholyx-type and 12 with pompholyx-type nickel eczema plus 10 control subjects without nickel allergy) with an oral dose of 2.5 mg nickel. By patch testing we additionally determined the degree of cutaneous nickel sensitivity using a series of nickel sulfate dilutions (5.0-0.00001%) and an possible cobalt allergy using 1% cobalt chloride. In 8 of the 19 patients with nickel allergy, the oral nickel challenge was positive (rash, flare-up at sites of healed eczema and former nickel patch tests, and worsening of preexisting eczema; acute pompholyx lesions only in patients with pompholyx-type eczema). The positive results showed the same frequency in non-pompholyx eczema (43%) as in the pompholyx type (42%). Moreover, no substantial difference was found in the degree of cutaneous nickel sensitivity between the two groups of eczema, and there was no correlation between these results and the outcome of the oral nickel challenge. An additional cobalt allergy was recorded significantly more often in pompholyx-type eczema (P = 0.048), yet there was no influence on the oral nickel challenge. The laboratory parameters examined (differential white cell count and total IgE) did not differ in either of the two eczema groups and did not change substantially during nickel challenge reactions.

Administration, Oral↗
PubMed1989

Determination of nickel in lung specimens of thirty-nine autopsied nickel workers.

Lung specimens from 39 nickel refinery workers autopsied during the period from 1978 to 1984 were analyzed for nickel. Fifteen of the workers were employed in the Roasting and Smelting Department, where exposure to nickel was predominantly in the form of nickel-copper oxides, Ni3S2 and metallic dust. The remaining 24 men worked in the Electrolysis Department. Exposure in this group was considered to be mostly to the water-soluble compounds, NiSO4 and NiCl2, but also to a lesser degree to water-insoluble nickel compounds such as nickel-copper oxides and sulphides. The arithmetic mean +/- SD for nickel concentration in lung tissues expressed in micrograms g-1 dry wt for the 39 workers was 150 +/- 280. In the workers employed in the Roasting and Smelting Department, the average nickel concentration was 330 +/- 380; for those who worked in the Electrolysis Department it was 34 +/- 48. Lung tissue from 16 autopsied persons not connected with the refinery had an average nickel concentration of 0.76 +/- 0.39. Statistical analysis based on log-normal distributions of the measured nickel concentrations allowed three major conclusions to be formulated: (1) nickel refinery workers exhibit elevated nickel levels in lung tissues at autopsy; (2) workers of the Electrolysis Department and the Roasting Smelting Department constitute distinct groups with respect to the accumulation of nickel in lung tissue; (3) workers who were diagnosed to have lung cancer had the same lung nickel concentrations at autopsy as those who died of other causes.

Aged↗
PubMed1998

Distribution of nickel in lungs from former nickel workers.

OBJECTIVE: The purpose of this work was to study the distribution of nickel within lung tissue obtained from nickel-exposed people and to evaluate the use of only one single sample for determination of the nickel burden of the lung. METHODS AND MATERIALS: The material used was lung tissue obtained from 15 former nickel refinery workers who had been exposed to a variety of nickel compounds such as Ni3S2, NiO, Ni0, NiSO4, and NiCl2. Ten samples taken from different locations of the lung as well as from the right and left bronchus and from the right lower lobe (total 13 samples per individual) were analyzed for nickel by electrothermal atomic absorption spectrometry. Samples obtained from ten people not connected to the refinery served as a reference group. RESULTS: The arithmetic mean value +/-SD for nickel concentration was 50+/-150 microg g(-1) dry wt. Biopsies collected on the center of the lower right lobe had an average nickel concentration of 82+/-252 microg g(-1). The average nickel concentration detected in the right and left bronchus was 5.9+/-11.6 and 3.8+/-6.0 microg g(-l), respectively. Lung tissue obtained from ten people not connected to the refinery had an average nickel concentration of 0.74+/-0.44 microg g(-1). CONCLUSIONS: The significant findings based on log-normal distribution of the nickel concentration were as follows: (1) samples obtained from the right lung showed no significant difference from samples taken from the left lung-a comparison of the nickel concentration detected in all the lung lobes showed that no single lobe differed from another; (2) the concentration of nickel found in the main bronchus of the refinery workers, although elevated, was significantly lower than the concentration detected in the remaining tissue; and (3) one single biopsy did not reflect the nickel burden of the lung.

Aged↗
PubMed2004

Impaired responses of peripheral blood mononuclear cells to nickel in patients with nickel-allergic contact dermatitis and concomitant atopic dermatitis.

BACKGROUND: Allergic contact dermatitis (ACD) is pathogenetically dependent on cell-mediated immune responses mediated by type 1 T lymphocytes. Atopic dermatitis (AD), in contrast, occurs as a result of sustained activation of type 2 subsets of T cells. Although atopic patients may become sensitized to various contact allergens, little is known about the influence of atopy on delayed-type hypersensitivity. OBJECTIVES: To investigate the in vitro responses of peripheral blood mononuclear cells (PBMC) to nickel stimulation in groups of atopic and nonatopic patients with patch test-verified nickel ACD. METHODS: Ten nonatopic patients with nickel ACD, 10 patients with nickel ACD and concomitant AD, 10 patients with AD but with no contact allergy, and 10 healthy persons participated in the study. PBMC were cultured in the presence or absence of nickel sulphate, phytohaemagglutinin (PHA) or tetanus toxoid (TT). [(3)H]thymidine incorporation was used to measure the rate of antigen-induced DNA synthesis and enzyme-linked immunosorbent assay was used to measure the production of interleukin (IL)-2 (type 1 cytokine) and IL-5 (type 2 cytokine). RESULTS: Nickel-stimulated PBMC of nickel-allergic patients with AD proliferated significantly less and secreted significantly lower amounts of IL-2 than cells of nonatopic nickel-allergic patients. IL-5 production was also lower in the former group, although the difference was nonsignificant. Moreover, neither the nickel-specific DNA synthesis nor the cytokine production by PBMC of atopic nickel-allergic patients differed significantly from those of healthy control persons and AD patients without contact allergy. Proliferative and secretory responses of PBMC to PHA or TT stimulation differed nonsignificantly between the groups. Nickel-induced IL-2 production correlated well with IL-5 production in nickel-allergic patients regardless of their atopic status. CONCLUSIONS: Our results indicate that PBMC of nickel-allergic patients with concomitant AD are characterized by impaired in vitro proliferative and secretory responses to the contact allergen nickel but not to the mitogen PHA or the recall antigen TT. The type 2 cytokine IL-5 may play a role in the development of ACD.

Adolescent↗
PubMed2004

Characterization of lymphocyte subpopulations and cytokine profiles in peripheral blood of nickel-sensitive individuals with systemic contact dermatitis after oral nickel exposure.

Several studies have shown that oral nickel exposure can elicit systemic contact dermatitis (SCD) in nickel-sensitive individuals. The current study describes some of the immunological mechanisms underlying such nickel-allergic reactions elicited by oral exposure to nickel. Following oral exposure to graded concentrations of nickel or placebo, blood samples were taken from nickel-sensitive individuals and from non-nickel-sensitive controls. T-cell subtypes (CD3+, CD4+, CD8+ and CD45RO+), expression of skin-homing receptor, cutaneous lymphocyte-associated antigen (CLA) and cytokine profiles [interleukin (IL)-2, IL-4, IL-5, IL-6, IL-10, interferon-gamma and tumour necrosis factor-alpha] were investigated. A definite dose-response reaction pattern to oral nickel exposure was observed among nickel-sensitive individuals. Nickel-sensitive individuals whose dermatitis flared after oral challenge with nickel showed significant decreases in fractions of CD3+ CD45RO+ CLA+ and CD8+ CD45RO+ CLA+ blood lymphocytes, suggesting migration of CD8+ 'memory' CLA+ T lymphocytes from the blood to peripheral tissues. Only those nickel-sensitive individuals who clinically reacted to oral challenge with nickel (4 mg) had elevated levels of IL-5 in the serum, indicating an activation of type 2 T lymphocytes in the peripheral blood. In conclusion, the study indicates that CD8+ CD45RO+ CLA+ T lymphocytes and T lymphocytes with a type 2 cytokine profile are involved in SCD elicited by nickel.

Administration, Oral↗
PubMed2005

Nickel on the Swedish market. Follow-up after implementation of the Nickel Directive.

The Nickel Directive aims at the prevention of sensitization and elicitation of nickel dermatitis. It limits nickel release from, and nickel content in, certain items. The Directive came into full force by July 2001. The aim of this study was to investigate the frequency on the market of items that release nickel and of nickel content in piercing posts, 2 years after coming into force of the Directive. Of special interest was to study changes compared to the situation in 1999, when a baseline study had been carried out. Nickel release from 786 items covered by the Nickel Directive was tested with the dimethylglyoxime (DMG) test, and nickel content in 18 piercing posts was analysed. Nickel release was shown from 8% of items intended for direct and prolonged contact with the skin, and 17% of the piercing posts contained too much nickel, a decrease compared to 1999. There has been significant adaptation to the requirements of the Nickel Directive. The DMG test is useful for screening for nickel release and for monitoring the market. Provided there is further adaptation to the requirements, the risk of sensitization and elicitation of nickel dermatitis will be significantly reduced.

Adolescent↗
PubMed2003

Induced sensitization to nickel in guinea pigs immunized with mycobacteria by injection of purified protein derivative with nickel.

Nickel has been reported to be one of the most common causes of allergic contact dermatitis. Despite the fact that nickel is a frequent sensitizer in humans, establishing animal models for nickel allergy has met with considerable difficulties. In clinical cases, allergic contact hypersensitivity to nickel develops much more readily in inflamed skin than normal skin. In this study, we tried to induce nickel sensitization when inflammation has been evoked in guinea pigs immunized with mycobacteria followed by co-administration of a mycobacterial component with nickel. We first examined the delayed-type hypersensitivity (DTH) reaction of mycobacterial components such as the cell wall, cell membrane, 70S ribosomal fraction, cytoplasm, tuberculin purified protein derivative (PPD), RNA and DNA from Mycobacterium bovis BCG in guinea pigs immunized with live M. bovis BCG or heat killed M. tuberculosis. When PPD was used, the hypersensitivity reaction was strongest. Next, we tested whether PPD with nickel could induce nickel sensitivity in guinea pigs immunized with mycobacteria. Strong sensitization to nickel was achieved by injecting PPD with nickel. However, if too large an amount of PPD or nickel salts was used, sensitization to nickel decreased. In this way, sensitization of nickel developed much more easily in guinea pigs immunized with mycobacteria by injection of an appropriate amount of nickel at the inflammation site induced by a suitable amount of PPD.

Animals↗
PubMedDate not supplied

Urine nickel concentrations in nickel-exposed workers.

Electrothermal atomic absorption spectrometry was employed for analyses of nickel concentrations in urine samples from nickel-exposed workers in 10 occupational groups and from non-exposed workers in two control groups. Mean concentrations of nickel in urine were greatest in workers who were exposed to inhalation of aerosols of soluble nickel salts (e.g., workers in nickel plating operations and in an electrolytic nickel refinery). Less marked increases in urine nickel concentrations were found in groups of metal sprayers, nickel battery workers, bench mechanics and are welders. No significant increases in mean concentrations of nickel were found in urine samples from workers who performed grinding, buffing and polishing of nickel-containing alloys or workers in a coal gasification plant who employed Raney nickel as a hydrogenation catalyst. Measurements of nickel concentrations in urine are more sensitive and practical than measurements of serum nickel concentrations for evaluation of nickel exposures in industrial workers.

Adult↗