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PubMed1995

Urinary excretion of chromium as an indicator of exposure to various chromium forms in MMA/SS welders.

Increased levels of Cr discharged with urine after working shift, Cr-U (arithmetic mean 15.8 mu g/g creatinine), and Cr buildup during working shift, DeltaCr-U (arithmetic mean 3.8 mu g/g creatinine), were observed in 15 MMA/SS welders exposed during the working week to welding fumes containing Cr VI (33-56%) - mainly soluble (87%) and Cr III (44-67%) - mainly insoluble (72%). The highest correlation coefficients were obtained for DeltaCr-U vs. Cr total (r = 0.58), Cr VI (r = 0.56) and soluble Cr III in the air. Increased DeltaCr-U value for exposures at MAC Cr VI (16.8 mu g/g creatinine) was demonstrated in welders employed longer than 7 years and exposed to Cr VI below MAC level, which might suggest that the duration of employment affects that value within the low range of concentration of Cr VI in the air (< 0.03 mg/m3). Nevertheless, linear relationship between DeltaCr-U for exposures to Cr VI at MAC levels and duration of employment was not confirmed for wide range of air Cr VI (0.005-0.4 mg/m3). Similar DeltaCr-U values at MAC for Cr VI (6.4 and 6.6 mu g/g creatinine) were obtained for all welders, and those employed over 7 years, respectively, which may suggest that this parameter can be misleading.

Adult↗
PubMed2001

An investigation of the chromium oxidation state of a monoanionic chromium tris(catecholate) complex by X-ray absorption and EPR spectroscopies.

The well-known monoanionic Cr tris(3,5-di-tert-butylcatecholato) complex, [Cr(DTBC)3]-, has been studied by X-ray absorption spectroscopy. The multiple-scattering fit to the XAFS gave good correlation (R = 19.8%) and good values for all of the bond lengths, angles, and Debye-Waller factors. The principal bond lengths and angles around the metal center (Cr-O, 1.96 A; O-C, 1.28 A; O-Cr-O, 81.8 degrees; Cr-O-C, 113.3 degrees) were most consistent with the XRD structure for [Cr(X4C6O2)3]- (X = Cl, Br), compared to those in other oxidation states, [Cr(DTBC)3], [Cr(Cl4C6O2)3], and [Cr(O2C6H4)3]3-. The XANES spectrum shows the main K edge at 6003.3 eV and a preedge peak at 5992.9 eV, which is approximately 8% of the intensity of the main K edge. The XANES data were compared to those for Cr-ehba complexes (ehbaH2 = 2-ethyl-2-hydroxybutanoic acid) of known oxidation states (III, IV, and V) and show, in conjunction with EPR spectroscopy and a reevaluation of XRD structures and theoretical calulations, that the complex is best described as a Cr(V) center with delocalization from the catechol ligands. The [Cr(catecholato)3]n+ (n = 1, 0) complexes have similar EPR spectroscopic and structural properties, respectively, to the 1- complex and are also best described as Cr(V) complexes. Such intermediates are important in the redox reactions of catechol(amine)s, and oxidized amino acids (e.g., DOPA), with carcinogenic Cr(VI) and may have relevance in Cr-induced cancers.

Journal Article↗
PubMed2002

Acid-base equilibrium of aqua-chromium-dioxolene complexes aimed at formation of oxo-chromium complexes.

A series of aqua-Cr(III)-dioxolene complexes, [Cr(OH(2))(3,5-Bu(2)SQ)(trpy)](ClO(4))(2) (1s), [Cr(OH(2))(3,5-Bu(2)Cat)(trpy)]ClO(4) (1c), [Cr(OH(2))(3,6-Bu(2)SQ)(trpy)](ClO(4))(2) (2), [Cr(OH(2))(Cat)(trpy)]ClO(4) (3), [Cr(OH(2))(Cl(4)Cat)(trpy)]ClO(4) (4), [Cr(OH(2))(3,5-Bu(2)SQ)(Me(3)-tacn)](ClO(4))(2) (5), [Cr(OH(2))(Cat)(Me(3)-tacn)]ClO(4) (6), and [Cr(OH(2))(Cl(4)Cat)(Me(3)-tacn)]ClO(4) (7) (Bu(2)SQ = di-tert-butyl-o-benzosemiquinonate anion, Bu(2)Cat = di-tert-butylcatecholate dianion, Cat = catecholate dianion, Cl(4)Cat = tetrachlorocatecholate dianion, trpy = 2,2':6',2' '-terpyridine, and Me(3)-tacn = 1,4,7-trimethyl-1,4,7-triazacyclononane), were prepared. On the basis of the crystal structures, redox behavior, and elemental analyses of these complexes, dioxolene in 1c, 3, 4, 6, and 7 coordinated to Cr(III) as the catechol form, and the ligand in 1s, 2, and 5 was linked to Cr(III) with the semiquinone form. All the aqua-Cr(III) complexes reversibly changed to the hydroxo-Cr(III) ones upon dissociation of the aqua proton, and the pK(a) value of the aqua-Cr(III) complexes increased in the order 6 > 3 approximately 1c > 7 > 5 approximately 4 > 1s. Hydroxo-Cr(III)-catechol complexes derived from 1c, 3, 4, 6, and 7 did not show any signs of dissociation of their hydroxy proton. On the other hand, hydroxo-Cr(III)-semiquinone complexes were reduced to hydroxo-Cr(III)-catechol in H(2)O/THF at pH 11 under illumination of visible light.

Journal Article↗
PubMed2000

Hydrogen atom and hydride transfer in the reactions of chromium(IV) and chromium(V) complexes with rhodium hydrides. Crystal structure of a superoxorhodium(III) product.

The aquachromyl ion, Cr(IV)aqO2+, reacts with the hydrides L(H2O)RhH2+ (L = L1 = [14]aneN4 and L2 = meso-Me6-[14]aneN4) in aqueous solutions in the presence of molecular oxygen to yield Cr(aq)3+ and the superoxo complexes L(H2O)RhOO2+. At 25 degrees C, the rate constants are approximately 10(4) M(-1) s(-1) (L = L1) and 1.12 x 10(3) M(-1) s(-1) (L = L2). Both reactions exhibit a moderate deuterium isotope effect, kRhH/kRhD = approximately 3 (L1) and 3.3 (L2), but no solvent isotope effect, kH2O/kD2O = 1. The proposed mechanism involves hydrogen atom abstraction followed by the capture of LRh(H2O)2+ with molecular oxygen. There is no evidence for the formation of L(H2O)Rh2+ in the reaction between L(H2O)RhH2+ and (salen)CrVO+. The proposed hydride transfer is supported by the magnitude of the rate constants (L = L1, k = 8,800 M(-1) s(-1); (NH3)4, 2,500; L2, 1,000) and isotope effects (L = L1, kie = 5.4; L2, 6.2). The superoxo complex [L1(CH3CN)RhOO](CF3SO3)2.H2O crystallizes with discrete anions, cations, and solvate water molecules in the lattice. All moieties are linked by a network of hydrogen bonds of nine different types. The complex crystallized in the triclinic space group P1 with a = 9.4257(5) A, b = 13.4119(7) A, c = 13.6140(7) A, alpha = 72.842(1)degrees, beta = 82.082(1) degrees, gamma = 75.414(1) degrees, V = 1587.69(14) A3, and Z = 2.

Journal Article↗
PubMed1998

Stabilization of a chromium-containing solid waste: immobilization of hexavalent chromium

This article describes the stabilization/solidification (S/S) of a steel industry waste, using a common type-F fly ash from a coal power station as the main binder. The waste, which contains hazardous levels of metals, may be stabilized by a conventional S/S to achieve permissible Pb, Cd, and Zn concentrations in the Toxicity Characteristic Leaching Procedure (TCLP) leachates of S/S solids. On the other hand, the stabilization of Cr(VI), also present in the waste, requires a reducing pretreatment stage with ferrous sulfate to attain TCLP leachates within limits. A bibliographic study on the stabilization of Cr(VI)-containing wastes is included in the paper, along with a discussion on the lowest Cr concentration in TCLP and aqueous (DIN) leachates.

Journal Article↗
PubMed2005

[Speciation analysis of chromium(VI) and chromium(III) in water sample using flame atomic absorption spectrometry with TOA-benzene extraction separation system].

A rapid and sensitive method for the sequential determination of Cr(VI) and Cr(III) in water samples based on flame atomic absorption spectrometry with TOA-benzene extraction separation system has been developed. In the H2SO4 medium. Cr(VI) in sample solution was extracted into the organic phase by using the TOA-Benzene and Cr(III) remained in the water phase. Cr(VI) in the organic phase and Cr(III) in the water phase were determined separately by AAS. This method is simple, fast and of microscale. The results obtained by this method agreed well with those obtained by conventional method. The recoveries are 95.0%-102% for Cr(VI) and 94.8-103% for Cr(III). The relative standard deviations were 2.9% for Cr(VI) and 2.6% for Cr(Ill). The system has enrichment effect for Cr(VI), and the detection limits are 6.6 microg x L(-1) for Cr(VI) and 0.20 mg x L(-1) for Cr(III). The maximum extracted amount of Cr(VI) by TOA was 4.6 mg x mL(-1).

English Abstract↗
PubMed2002

Cytotoxicity and oxidative mechanisms of different forms of chromium.

Chromium exists mostly in two valence states in nature: hexavalent chromium [chromium(VI)] and trivalent chromium [chromium(III)]. Chromium(VI) is commonly used in industrial chrome plating, welding, painting, metal finishes, steel manufacturing, alloy, cast iron and wood treatment, and is a proven toxin, mutagen and carcinogen. The mechanistic cytotoxicity of chromium(VI) is not completely understood, however, a large number of studies demonstrated that chromium(VI) induces oxidative stress, DNA damage, apoptotic cell death and altered gene expression. Conversely, chromium(III) is essential for proper insulin function and is required for normal protein, fat and carbohydrate metabolism, and is acknowledged as a dietary supplement. In this paper, comparative concentration- and time-dependent effects of chromium(VI) and chromium(III) were demonstrated on increased production of reactive oxygen species (ROS) and lipid peroxidation, enhanced excretion of urinary lipid metabolites, DNA fragmentation and apoptotic cell death in both in vitro and in vivo models. Chromium(VI) demonstrated significantly higher toxicity as compared with chromium(III). To evaluate the role of p53 gene, the dose-dependent effects of chromium(VI) were assessed in female C57BL/6Ntac and p53-deficient C57BL/6TSG p53 mice on enhanced production of ROS, lipid peroxidation and DNA fragmentation in hepatic and brain tissues. Chromium(VI) induced more pronounced oxidative damage in multiple target organs in p53 deficient mice. Comparative studies of chromium(III) picolinate and niacin-bound chromium(III), two popular dietary supplements, reveal that chromium(III) picolinate produces significantly more oxidative stress and DNA damage. Studies have implicated the toxicity of chromium picolinate in renal impairment, skin blisters and pustules, anemia, hemolysis, tissue edema, liver dysfunction; neuronal cell injury, impaired cognitive, perceptual and motor activity; enhanced production of hydroxyl radicals, chromosomal aberration, depletion of antioxidant enzymes, and DNA damage. Recently, chromium picolinate has been shown to be mutagenic and picolinic acid moiety appears to be responsible as studies show that picolinic acid alone is clastogenic. Niacin-bound chromium(III) has been demonstrated to be more bioavailable and efficacious and no toxicity has been reported. In summary, these studies demonstrate that a cascade of cellular events including oxidative stress, genomic DNA damage and modulation of apoptotic regulatory gene p53 are involved in chromium(VI)-induced toxicity and carcinogenesis. The safety of chromium(III) is largely dependent on the ligand, and adequate clinical studies are warranted to demonstrate the safety and efficacy of chromium(III) for human consumption.

Animals↗
PubMed1983

Differential toxicity and clearance kinetics of chromium(III) or (VI) in mice.

The acute and subacute toxicities of several chromium(III) and chromium(VI) compounds were determined in NZC and (CxO) mice injected i.p. The distal median lethal doses (more than 10 days after treatment) averaged (17.9 +/- 1.8) X 10(-6) g chromium/g body weight regardless of the oxidation state of the chromium compound injected (chromium(III) sulphate may be an exception), but acute toxicity (3 days) was much greater with chromium(VI) compounds. Acid digests of entire male mice that were administered i.p. one-sixth of the distal LD50, either once or repeatedly at weekly intervals, were analysed to determine the whole body persistence and clearance kinetics of chromium. Mice dosed once with chromium(III) retained 6.5 times more chromium at 21 days than mice treated with chromium(VI). When chromium(III) was given at weekly intervals mice accumulated 6 times more chromium by 8 weeks than chromium(VI)-treated mice, though only the latter showed symptoms of chronic toxicity. Whole body chromium concentrations continued to rise with further chromium(III) treatments, but slowly declined with chromium(VI). Analyses of fecal and urinary excretion confirmed most of the urinary chromium clearance occurred soon after injection, and that chromium excretion from chromium(VI)-treated animals was much faster in both urine and feces than from mice given chromium(III). The differential storage and clearance kinetics of chromium(III) and chromium(VI) compounds may be significant in experimental chromium carcinogenesis studies and in the toxicology of chromium in workers exposed industrially to potentially carcinogenic chromium-containing dusts or aerosols.

Animals↗
PubMed1989

Chromium cross-links glutathione and cysteine to DNA.

The formation of chromium-DNA adducts, and chromium-mediated peptide-DNA or amino acid-DNA cross-links was measured after treatment of calf thymus DNA and defined DNA polynucleotides in vitro with potassium dichromate in the presence of glutathione or cysteine. The level of chromium bound to DNA after reaction with chromium(VI) in the presence of glutathione increased with increasing glutathione concentration to a level of approximately 1.4 x 10(-2) chromium per nucleotide. Glutathione and chromium were associated with the DNA in a 1:1 ratio. Reaction of chromium(VI) with DNA in the presence of cysteine led to a maximal level of chromium binding that was 10-fold lower than that measured with glutathione, with 2-4 cysteine bound per chromium. The thiol-chromium-DNA complexes were stable to dialysis at room temperature against diethylenetriaminepentaacetic acid, orthophenanthroline and ethylenediaminetetraacetic acid. However, when the chromium-DNA complexes were dialyzed against ethylenediaminetetraacetic acid at 37 degrees C to chelate bound chromium, equivalent amounts of chromium and thiol were lost from the DNA, suggesting that thiol was associated with the DNA-bound chromium. These results suggest that chromium mediates cross-linking of cysteine and glutathione to DNA, to form glutathione-chromium-DNA and (cysteine)2-4-chromium-DNA complexes. In order to probe the DNA base and sequence specificity of glutathione-chromium-DNA adduct formation, chromium and glutathione binding to polynucleotides of defined composition was determined. Preferential binding of chromium to guanine-containing polynucleotides was observed. These results suggest that the interaction of chromium with thiol-containing amino acids and peptides may be important in chromium genotoxicity, and indicate that the thiol-activated chromium may target guanine bases in DNA.

Chromium↗
PubMed1992

In vivo formation of chromium(V) in chick embryo liver and red blood cells.

In order to understand the possible role of reactive intermediates in the formation of tissue-specific DNA damage by chromium(VI), electron paramagnetic resonance spectroscopy was used to study the in vivo formation of chromium(V) in the liver and red blood cells of 14 day chick embryos following treatment with chromium(VI). In vivo administration of sodium dichromate onto the inner shell membrane of 14 day chick embryos resulted in the formation of a persistent chromium(V) species in liver cells (g = 1.987). The intensity of the chromium(V) signal in liver cells plateaued at 70 min and persisted for 240 min after treatment with chromium(VI). The dependence of chromium(V) formation on the dose of sodium dichromate administered to the embryo was clearly different in liver versus red blood cells. Chromium(V) was detected in red blood cells only at high doses of sodium dichromate (0.50-0.60 mmol/kg), whereas chromium(V) was undetectable in red blood cells at lower doses of sodium dichromate (0.10-0.30 mmol/kg) which produced clear evidence for chromium(V) in liver. Uptake studies showed that total chromium levels in red blood cells were 10-fold greater than in liver cells, and that up to 10% of the total chromium existed as chromium(V) in liver and red blood cells in vivo. Depletion of glutathione by pretreatment of embryos with L-buthionine-S,R-sulfoximine (BSO) for 24 h prior to treatment with a high dose of sodium dichromate (0.60 mmol/kg) caused both a decrease in the levels of chromium(V) species produced and a decrease of chromium uptake into red blood cells 50 min after treatment. At this high dose of chromium(VI), BSO pre-treatment had no effect on the level of the chromium(V) or on chromium uptake into liver cells after a 70 min incubation period. Thus, the concentration of chromium(V) inside the cell correlated with the levels of chromium taken up into the cell. Chromium(V) may be the form of chromium which is responsible for induction of DNA damage following in vivo administration of sodium dichromate.

Animals↗