[Hazards through chromium-IV-compounds--G 15].
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Chromium↗
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Percutaneous absorption of trivalent and hexavalent chromium. A comparative investigation in the guinea pig by means of 51Cr.
By means of an in vivo isotope technique, the so-called disappearance measurements, a comparison was made during a five-hour period between the percutaneous absorption in the guinea pig of a trivalent (chromic chloride) and a hexavalent (sodium chromate) chromium compound. Nine different concentrations of each substance were studied. We found that in the concentration interval 0.017-0.239 molar the relative absorption of the hexavalent compound was somewhat higher, but the differences were not statistically significant. On the other hand, in the higher concentrations (0.261-0.398 molar) more of the hexavalent compound was absorbed, and the differences were statistically significant. This difference in percutaneous absorption for various concentrations can perhaps account for the divergent results, in respect to the absorption of trivalent and hexavalent chromium compounds, which have recently been published.
Animals↗
Crystalline and water soluble Cr(4+) and Cr(5+) model compounds for chromium toxicity studies.
We discuss two complexes of Cr(4+) for their possible utility as models for Cr toxicity studies. They are Cr(dien)(O2)2(.)H2O (dien = diethylenetriamine) and Cr(NH3)3(O2)2, which have been recently characterized by x-ray diffraction and magnetic techniques. We present their optical and infrared absorption spectra as quick aids in their identification procedure. We also summarize the general properties of some well-characterized Cr(5+) compounds. All of these compounds are water soluble with the Cr(5+) samples being fairly stable in basic solutions. They can all be prepared as pure crystals with a shelf life of over 2 years when stored in a refrigerator.
Chromium Compounds↗
[The change of valence of chromium by acid treatment].
There are many kinds of chromium compounds in nature, and most of them exist as Cr6+- and Cr3+-compounds. Generally, these two kinds of compounds are stable in normal circumstances. When the chromium in biomaterial or in atmospheric substances is analyzed, the samples are usually ashed with strong acids at high temperatures to destroy the organic components, and chromium compounds are changed to water soluble salts in this ashing process. And then chromium is determined in various methods. The relation between the used acids and the behavior of chromium were investigated, and the following facts have been cleared. Though the total amount of chromium in the samples remains constant, the valence of chromium is apt to change easily in the ashing process (Cr6+ in equilibrium Cr3+). As Cr3+ is more stable than Cr6+ in acid solution, the reductive reaction proceeds mainly as (Cr6+ leads to Cr3+). But each acid has the peculiar reductive action on Cr6+. Even if the same acid is used, its reductive power changes very sensitively as the used conditions are altered. The reductive action of mixed acid differs from that of original acid remarkably. Certain acid has the oxidizing action on Cr3+. Thus, the mechanisms and reactions between strong acids and chromium are very complicated. So, for the determination of the amounts of individual Cr6+ and Cr3+, the oxidizing or reductive action of the used acid must be considered cautiously.
Cations↗
Chromium hexavalent compounds.
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Animals↗
[Toxicological and analytical lists: chromium and its compounds].
The main aspects of occupational exposure to chromium and chromium compounds are surveyed. Special attention is paid to the toxic action of this metal at the different target organs. The nutritional aspect of CrIII is examined preliminarily, and data detailing the metal contents in water and food are provided. As far the different working processes that entail occupational exposure to chromium are concerned, hygienic and environmental problems are discussed while identifying the average environment exposure to the different chemical forms of chromium (CrIII, CrIV, soluble and not soluble), as a function of the worker's tasks, and the relevant human response (total human Cr). Different hygienic and environmental standards in force in various countries and applicable to chromium compounds are compared. Additional information is given on the main aspects of chromium metabolism (absorption, distribution, excretion), and on the prevailing toxic actions, with specific reference to cancerogenesis. As far as biologic monitoring of the exposed people is concerned, the significance of Cr-U as dose-exposure indicator is discussed, also in the light of a critical review of the reference values. The report describes a series of analytical methods for the identification of chromium in aqueous and biologic matrices. The problems connected with health monitoring and fitness for work are eventually covered.
Chromium↗
Induction of apoptotic cell death by particulate lead chromate: differential effects of vitamins C and E on genotoxicity and survival.
Certain hexavalent chromium compounds are documented human carcinogens. Exposure of cells to particulate forms of chromium results in cell-enhanced dissolution of particles in the extracellular microenvironment and chronic production of chromium oxyanions, which are taken up by the cell through an anion transport system and are genotoxic and clastogenic. It was previously shown that apoptosis is the mode of cell death of nearly all of the Chinese hamster ovary cells (CHO-AA8 cell line), which die after high-dose, short-term treatments with soluble sodium chromate. In this report the mode of cell killing by particulate lead chromate and of low-dose continuous treaments of soluble sodium chromate designed to mimic conditions of ionic chromate uptake after lead chromate exposure was examined. CHO-AA8 cells were treated for 24 hr with doses of sodium chromate or lead chromate which cause a 50% decrease in survival in colony-forming effeciency assays. Longer treatments (up to 72 hr) at the same doses did not decrease survival further than the 24-hr exposure. Morphological changes indicative of apoptosis, as well as internucleosomal DNA fragmentation, were detectable by 24 hr after treatment with lead chromate or soluble sodium chromate. All of the cells killed by treatments with lead chromate particles underwent apoptosis as the mode of cell death and this was accurately modeled in cell culture by continuous treatments with low-dose soluble sodium chromate. Exposure of cells to hexavalent chromium compounds causes a spectrum of DNA damage which can be selectively altered by pretreatment of cells with antioxidant vitamins prior to chromium exposure. Here we show that ascorbate and alpha-tocopherol markedly inhibited the chromosomal aberrations induced by both particulate and soluble chromate compounds, even though chromium adduct levels were not decreased by either vitamin pretreatment. Cell survival assays showed that ascorbate, but not alpha-tocopherol, protected cells from apoptosis induced by sodium chromate. The results differentiate chromium-induced apoptosis from both chromosomal damage and adduct levels and suggest that other lesions sensitive to ascorbate but not tocopherol are the proximal inducing signal for chromium-induced apoptosis.
Animals↗
Molecular mechanisms of transformation of C3H/10T1/2 C1 8 mouse embryo cells and diploid human fibroblasts by carcinogenic metal compounds.
Carcinogenic arsenic, nickel, and chromium compounds induced morphological and neoplastic transformation but no mutation to ouabain resistance in 10T1/2 mouse embryo cells; lead chromate also did not induce mutation to ouabain or 6-thioguanine resistance in Chinese hamster ovary cells. The mechanism of metal-induced morphological transformation was likely not due to the specific base substitution mutations measured in ouabain resistance mutation assays, and for lead chromate, likely not due to this type of base substitution mutation or to frameshift mutations. Preliminary data indicate increases in steady-state levels of c-myc RNA in arsenic-, nickel-, and chromium-transformed cell lines. We also showed that carcinogenic nickel, chromium, and arsenic compounds and N-methyl-N-nitro-N-nitrosoguanidine (MNNG) induced stable anchorage independence (Al) in diploid human fibroblasts (DHF) but no focus formation or immortality. Nickel subsulfide and lead chromate induced Al but not mutation to 6-thioguanine resistance. The mechanism of induction of Al by metal salts in DHF was likely not by the type of base substitution or frameshift mutations measured in these assays. MNNG induced Al, mutation to 6-thioguanine resistance, and mutation to ouabain resistance, and might induce Al by base substitution or frameshift mutations. Dexamethasone, aspirin, and salicylic acid inhibited nickel subsulfide, MNNG, and 12-O-tetrade-canoylphorbol-13-acetate (TPA)-induced Al in DHF, suggesting that arachidonic acid metabolism and oxygen radical generation play a role in induction of Al. We propose that nickel compounds stimulate arachidonic acid metabolism, consequent oxygen radical generation, and oxygen radical attack upon DNA.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Acute toxic effect of sodium dichromate on metabolism.
The effect of sodium dichromate on cellular metabolism was investigated. Intraperitoneal injection of sodium dichromate into the rat (20 or 40 mg/kg) caused significant increases in serum lactate, pyruvate, and creatinine concentrations within 15 min after intoxication. Severe hyperglycemia occurred thereafter, as a result of increased hepatic glycogenolysis, which was seen in the first 2 h after dichromate. However, liver glycogen was resynthesized in 24 h-fasted rats after glucose refeeding. Dichromate decreased serum total amino acids, with a consequent increase in blood urea nitrogen (BUN) concentration. Unlike HgCl2 (2 mg/kg, i.p.), As2O3 (5 mg/kg, i.p.), and KCN (5 mg/kg, i.p.), dichromate showed the largest metabolic disturbance only in the early period after treatment. In addition, dichromate produced cyanosis, which appeared during the period of the accelerated glycolysis and breakdown of creatinine phosphate. Regardless of chemical species, only the hexavalent chromium compounds had an effect on the cellular metabolism. Trivalent chromium compounds had no effect at all. These results suggest that dichromate possesses a characteristic dual action on cellular metabolism, which might be related to its metabolic fate.
Amino Acids↗
Efficacy of chromium supplementation in athletes: emphasis on anabolism.
As the biologically active component of glucose tolerance factor (GTF), the essential trace mineral chromium is now being marked to athletes. GTF potentiates insulin activity and is responsible for normal insulin function. Thus, insulin's effects on carbohydrate, fat, and protein metabolism are dependent upon the maintenance of adequate chromium stores. Due to excessive chromium loss and marginal chromium intake, athletes may have an increased requirement for chromium. Therefore, in some circumstances the dietary supplementation of a chromium compound may be efficacious. The restoration and maintenance of chromium stores via supplementation would promote optimal insulin efficiency, necessary for high-level athletic performance. However, potential anabolic effects of enhanced insulin function would likely be marginal, and reports of short-term anabolic increases from the supplementation of an organic chromium compound need to be confirmed.
Animals↗
Occupational exposures and pancreatic cancer: a meta-analysis.
OBJECTIVES: Consolidation of epidemiological data on pancreatic cancer and worksite exposures. METHODS: Publications during 1969-98 were surveyed. Studies without verified exposures were excluded. Meta-analyses were conducted on data from 92 studies covering 161 populations, with results for 23 agents or groups of agents. With a standard format, five epidemiologists extracted risk estimates and variables of the structure and quality of each study. The extracted data were centrally checked. Random meta-models were applied. RESULTS: Based on 20 populations, exposure to chlorinated hydrocarbon (CHC) solvents and related compounds was associated with a meta-risk ratio (MRR) of 1.4 (95% confidence interval (95% CI) 1.0 to 1.8). Nickel and nickel compounds were considered in four populations (1.9; 1.2 to 3.2). Excesses were found also for chromium and chromium compounds (1.4; 0.9 to 2.3), polycyclic aromatic hydrocarbons (PAHs) (1.5; 0.9 to 2.5), organochlorine insecticides (1.5; 0.6 to 3.7), silica dust (1.4; 0.9 to 2.0), and aliphatic and alicyclic hydrocarbon solvents (1.3; 0.8 to 2.8). Evidence on pancreatic carcinogenicity was weak or non-positive for the following agents: acrylonitrile (1.1; 0.0 to 6.2); arsenic (1.0; 0.6 to 1.5); asbestos (1.1; 0.9 to 1.5); diesel engine exhaust (1.0; 0.9 to 1.3); electromagnetic fields (1.1; 0.8 to 1.4); formaldehyde (0. 8; 0.5 to 1.0); flour dust (1.1; 0.3 to 3.2); cadmium and cadmium compounds (0.7; 0.4 to 1.4); gasoline (1.0; 0.8 to 1.2); herbicides (1.0; 0.8 to 1.3); iron and iron compounds (1.3; 0.7 to 2.5); lead and lead compounds (1.1; 0.8 to 1.5); man-made vitreous fibres (1.0; 0.6 to 1.6); oil mist (0.9; 0.8 to 1.0); and wood dust (1.1; 0.9 to 2.5). The occupational aetiological fraction of pancreatic cancer was estimated at 12%. In a subpopulation exposed to CHC solvents and related compounds, it was 29%; to chromium and chromium compounds, 23%; to nickel and nickel compounds, 47%; to insecticides, 33%; and to PAHs, 33%. CONCLUSION: Occupational exposures may increase risk of pancreatic cancer. High quality studies are called for on interactions between occupational, environmental, and lifestyle factors as well as interactions between genes and the environment.
Air Pollutants, Occupational↗
The safety and efficacy of high-dose chromium.
The data on the standards for chromium requirements and the safety of various chromium compounds and doses are reviewed. The 350-fold difference between the acceptable daily intake and the calculated reference dose for humans of 70 mg per day seems without precedent with respect to other nutritional minerals. Previous claims of mutagenic effects of chromium are of questionable relevance. While studies have found DNA fragmentation (clastogenic effects) by chromium picolinate, anecdotal reports of high-dose chromium picolinate toxicity are few and ambiguous. The beneficial effects of chromium on serum glucose and lipids and insulin resistance occur even in the healthy. Serum glucose can be improved by chromium supplementation in both types 1 and 2 diabetes, and the effect appears dose dependent. Relative absorption of various chromium compounds is summarized and the mechanism of low molecular weight chromium binding substance (LMWCr) in up-regulating the insulin effect eight-fold is discussed. There is evidence of hormonal effects of supplemental chromium besides the effect on insulin. Chromium supplementation does result in tissue retention, especially in the kidney, although no pathogenic effect has been demonstrated despite considerable study.
Adult↗
Molecular and cellular mechanisms of transformation of C3H/10T1/2 Cl 8 and diploid human fibroblasts by unique carcinogenic, nonmutagenic metal compounds. A review.
Work from our laboratory showed that carcinogenic metal salts of arsenic, nickel, and chromium induced morphological transformation of cultured C3H/10T1/2 Cl 8 (10T1/2) mouse embryo cells, and that many of the transformants grow in soft agarose and form tumors in nude mice. Concentrations of arsenic, nickel, and chromium compounds that induced morphological transformation did not induce mutation to ouabain resistance in 10T1/2 cells. This indicated that the mechanism of metal induced morphological transformation was likely not caused by induction of base substitution mutations, and in the case of lead chromate, likely not caused by frameshift or deletion mutations. In addition, we showed that carcinogenic arsenic, nickel, and chromium compounds, and MNNG, induced anchorage independence in diploid human fibroblasts. Anchorage-independent cell strains derived from anchorage-independent colonies were stable but did not form foci and eventually senesced, therefore, arsenic and nickel compounds and lead chromate induced stable anchorage independence as an isolated phenotype. Nickel compounds and lead chromate induced anchorage independence but not mutation to ouabain resistance or to 6-thioguanine resistance. Hence, the mechanism of induction of anchorage independence by these metal salts in human fibroblasts was likely not via induction of base substitution, frameshift, or deletion mutations that would be measured in these mutation assays.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Oxochromium(V) species formed with 2,3-dehydro-2-deoxy-N-acetylneuraminic or N-acetylneuraminic (sialic) acids: an in vitro model system of oxochromium(V) species potentially stabilized in the respiratory tract upon inhalation of carcinogenic chromium(VI) compounds.
The human respiratory tract is rich in sialoglycoconjugates. These polyfunctional, oxygen-rich molecules stabilize potentially genotoxic oxoCr(V) species, which has relevance to the metabolic fate of carcinogenic Cr(VI) compounds when inhaled as dusts, mists, and fumes during occupational exposure. A series of oxoCr(V) species formed from solutions of Cr(VI) and the reductant, glutathione (GSH), in the presence of an excess of small molecule ligands that model sialoglycoconjugates, either 2,3-dehydro-2-deoxy-N-acetylneuraminic acid (I) or N-acetylneuraminic acid (II), have been characterized as a function of pH value, using electron paramagnetic resonance (EPR) spectroscopy (Cr(V) = d(1)). Where [I] or [II] is in large excess of [Cr(V)-GSH], oxoCr(V)-I or -II species form (g(iso) = 1.97-1.98) via ligand-exchange reactions in which oxygen donor atoms from the carboxylic acid (I), tert-2-hydroxycarboxylato(2-) (II), and/or diolato(2-) groups (I, II) feature in the oxoCr(V) coordination sphere. At pH approximately 7.1 (where [Cr(V)-GSH]:[II] << 1), the oxoCr(V)-II complexes remain EPR active for 24 h (with t(1/2) approximately 380 min). The parent EPR spectrum from oxoCr(V)-I or -II solutions represents the sum of spectra from individual linkage isomers; using EPR spectral simulation procedures, coupled with empirical EPR spectroscopic data for previously characterized oxoCr(V)-hydroxycarboxylato and -diolato species, a signature EPR spectrum has been predicted for each oxoCr(V)-I or -II linkage isomer, with defining g(iso) and (1)H a(iso) values and signal multiplicities. At pH values > 7.0, the major EPR signal (g(iso) approximately 1.980) is a septet, indicating the presence of oxoCr(V)-I or oxoCr(V)-II species with coordination from two O(8),O(9)-diolato(2-) chelates, with six magnetically equivalent protons ((1)H a(iso) approximately 0.7 x 10(-)(4) cm(-)(1)). At pH values < 7.0, where carboxylato binding competes with diolato binding, the species (g(iso) approximately 1.979) most likely feature mixed binding modes from one diolato(2-) and one tert-2-hydroxycarboxylato(2-) chelate (oxoCr(V)-II) or one diolato(2-) chelate, one monodentate carboxylato(1-) group, and aqua and/or hydroxo oxygen donors (oxoCr(V)-I). In I and II, the relative concentration of the oxoCr(V) linkage isomer featuring donation via the O(7),O(8) diolato group is about 1 order of magnitude smaller than the concentration of the O(8),O(9) linkage isomer. The dominance of oxoCr(V)-I or -II linkage isomers with O(8),O(9) donation correlates with the dihedral angle in these isomers (O(9)-C(9)-C(8)-O(8) approximately 65 degrees ) being more favorably disposed toward metal binding, as compared to the O(7),O(8) analogue (O(7)-C(7)-C(8)-O(8) approximately 163 degrees ). These results have important implications with respect to the nature of the oxoCr(V) species that may potentially form in the sialoglycoconjugate-rich environment of the human respiratory tract upon inhalation of carcinogenic Cr(VI) compounds.
Carcinogens, Environmental↗
Methods for determining soluble and insoluble Cr III and Cr VI compounds in welding fumes.
An analytical procedure for simultaneous determination of soluble and insoluble Cr III and Cr VI compounds in welding fumes has been proposed. In the welding fume samples collected on a membrane filter, total chromium was determined with atomic absorption spectrophotometry (AAS). Glass filters with collected samples were divided into two parts. In one part of the sample, soluble and insoluble chromium was determined by means of AAS. The separation of soluble chromium III and VI was carried out on diphenylcarbazide resin. In the second part of the sample total chromium VI was determined by means of the colorimetric method with s-diphenylcarbazide. The difference in the results of these determinations allowed the calculation of the content of total Cr III, Cr III insolub. and Cr VI insolub. The results of determining chromium compounds in welding fumes samples collected in the welder's breathing zone and in experimental chambers are also presented in this paper. The content of total chromium in the fumes determined by AAS (from a membrane filtr) and that calculated from the sum of soluble and insoluble chromium (from a glass filter) were concordant and within the limits of the admissible error for the method. Total chromium content in welding fume samples collected individually was found to range from 2.4-4.2%. The percentage of particular chromium compounds as compared to total chromium (100%) amounted: total Cr III--34%, total Cr VI--66%, soluble chromium--66% and in this Cr III--20% and Cr VI--43%, insoluble chromium--34% and in this: Cr III--14% and Cr VI--20%.
Air Pollutants, Occupational↗
[Bacteria reducing chromium in nature and in effluents of industrial plants].
Bacteria capable of hexavalent chromium (Cr6+) reduction can be found in Cr6+-containing sewage and sediments of purification tanks of industrial plants. They cannot be detected in water and soil samples containing no chromium compounds. Bacteria reducing chromium belong to the genera Aeromonas, Escherichia, Pseudomonas and Enterobacter. Their activity of Cr6+ reduction correlates with the high resistance to the elevated content of this ion in the medium. The fine cell structure of these bacteria is described.
Aeromonas↗
Chromium oxidation state imaging in mammalian cells exposed in vitro to soluble or particulate chromate compounds.
Hexavalent chromium compounds are known carcinogens for the respiratory tract in humans. The mechanism of cell transformation by hexavalent chromium compounds is not fully understood although a role for intracellular reduction is sought. The aim of this study was to determine the distribution of Cr valence states in human cells after in vitro exposure to soluble or particulate chromium compounds. A synchrotron X-ray-based microprobe was used to investigate the cellular reduction of Cr(VI) and to image chromium oxidation states in cells. It was shown that soluble Cr(VI) compounds are fully reduced to Cr(III) in cells. Cr(III) is homogeneously distributed within the cell volume and therefore present within the nucleus. In the case of low solubility particulate chromate compounds, Cr(VI) can coexist in the cell environment, as particles in the perinuclear region, together with intracellular and intranuclear Cr(III). Chemical distribution maps also suggest that intracellular Cr(III) originates from extracellular dissolution and reduction of lead chromate rather than from intracellular engulfed particles. The possible stronger carcinogenicity of low solubility chromate vs soluble chromate compounds may derive from the combinative genotoxic effects of intranuclear Cr(III) and the persistent exposure to a strong oxidant, Cr(VI).
Animals↗
Chromium.
Chromium occurs primarily in the trivalent state (III), which is the most stable form, or in the hexavalent state (VI), which is a strong oxidizing agent. Elemental chromium (0) does not occur naturally on earth. Trivalent chromium (III) is an essential trace metal necessary for the formation of glucose tolerance factor and for the metabolism of insulin. Commercial applications of chromium compounds include tanning (III), corrosion inhibition, plating, glassware-cleaning solutions, wood preservatives (VI), manufacture of safety matches, metal finishing (VI), and the production of pigments (III, VI). Hexavalent chromium (VI) contaminated local soil when chromium waste slag was part of the fill material present in residential, public, and industrial areas. In some urban areas, about two-thirds of the chromium in air results from the emission of hexavalent chromium from fossil fuel combustion and steel production. The remaining chromium in air is the trivalent form. The residence time of chromium in air is < 10 days, depending on the particle size. Trivalent compounds generally have low toxicity and the gastrointestinal tract poorly absorbs these compounds. Hexavalent chromium is a skin and mucous membrane irritant and some of these hexavalent compounds are strong corrosive agents. Hexavalent chromium compounds also produce an allergic contact dermatitis characterized by eczema. Sensitivity to trivalent compounds is much less frequent, but some workers may react to high concentrations of these compounds. Hexavalent chromium is recognized by the International Agency for Research on Cancer and by the US Toxicology Program as a pulmonary carcinogen. The increased risk of lung cancer occurs primarily in workers exposed to hexavalent chromium dust during the refining of chromite ore and the production of chromate pigments. Although individual studies suggest the possibility of an excess incidence of cancer at sites outside the lung, the results from these studies are inconsistent.
Animals↗