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PubMed1994

Occupational exposure to chromium and nickel in Finland--analysis of registries of hygienic measurements and biological monitoring.

Two large data bases, one with the results of analyses on total dust, nickel, total and hexavalent chromium, and the other, with concentrations of chromium and nickel in workers' urine, have been accumulated in the Finnish Institute of Occupational Health. Data were analysed to assess occupational exposure to chromium and nickel during the last decade, using the International Standard Industrial Classifications for grouping industrial activities. Number of analyses was highest in fabricated metal products manufacturing, and welders and sheet metal workers were the largest and most heavily exposed groups. Occupational exposure limits were exceeded in 15.8% of all chromium measurements (500 micrograms m-3 for total chromium and 50 micrograms m-3 for hexavalent chromium). Recommended biological action level (BAL) (1.0 mumol l.-1) was exceeded in 0.8-7.1% of the cases in different years. Altogether, 18.3% (range 7.6-28.3%) of the air nickel measurements were higher than the occupational exposure limit for nickel compounds (100 micrograms m-3), but only 0.2-3.1% of results exceeded the BAL for nickel (1.30 mumol l.-1).

Chromium↗
PubMed1991

Studies of the binding of chromium(III) complexes to phosphate groups of adenosine triphosphate.

The binding of a number of chromium complexes to ATP has been studied by 31P NMR spectroscopy. The results are consistent with the formation of outer-sphere complexes between ATP and the chromium species. The magnitude of the binding constant has been determined as approximately 500 mol-1 dm3 (pH = 7.00) for the interaction of trisethylenediamine chromium(III) with ATP. Under our experimental conditions no NMR signals are observed from complexes in which chromium(III) is bound directly to the phosphate groups of ATP. The relative stability of the inner sphere complexes of chromium(III) and glutathione or ATP is probably not a significant factor in determining the toxicity of chromium(III) complexes.

Adenosine Triphosphate↗
PubMed1996

Chromium(VI) treatment of normal human lung cells results in guanine-specific DNA polymerase arrest, DNA-DNA cross-links and S-phase blockade of cell cycle.

Previous studies have shown that in vitro treatment of a synthetic double-stranded DNA template with chromium(III), or chromium(VI) in the presence of ascorbate, resulted in guanine-specific DNA polymerase arrests that correlated strongly with DNA-DNA cross-linking. In vivo chromium(VI) undergoes a more complicated intracellular cascade of reductive metabolism than is achievable in an in vitro model. Moreover, in living cells, DNA is highly packaged in the form of chromatin which may alter the accessibility of DNA to chromium. A repetitive primer-extension assay was employed to determine whether chromium forms polymerase-arresting lesions in vivo. Normal human lung fibroblasts treated with chromium(VI) exhibited adduct levels of 0.13-0.92 mmol Cr/mol DNA-nucleotides in the total genome (0.26-1.84 Cr adducts/Kbp DNA) and DNA interstrand cross-links. Genomic DNA was isolated and alphoid sequences (1-5% of the genome) were used as a substrate for repetitive primer extension using Taq polymerase. The results showed a dose-dependent, guanine-specific, replication termination, even at low doses resulting in greater than 90% survival. The same treatment resulted in dose-dependent suppression of thymidine incorporation into DNA immediately after treatment. Thymidine incorporation increased during the first 6 h after the 2-h exposure, probably related to the repair of the single strand breaks, but then returned to high suppression levels at 24 h. The chromate treatments inhibited cell growth by specific blocking of the progression of cells through S-phase of the cell cycle. The results confirmed our studies in cell-free systems and taken together they strongly indicate that guanine-guanine DNA interstrand cross-links induced by chromate in living cells is the lesion responsible for blocking DNA replication processivity.

Base Sequence↗
PubMed1993

Chromium in human nutrition: a review.

This review summarizes the results of 15 controlled studies supplementing defined Cr(III) compounds to subjects with impaired glucose tolerance. Three of these (3-4 mumol Cr/d for > 2 mo) produced no beneficial effects: serum glucose, insulin and lipid concentrations remained unchanged. The remaining 12 interventions improved the efficiency of insulin or the blood lipid profile of subjects (ranging from malnourished children and healthy middle-aged individuals to insulin-requiring diabetics). In addition, three cases of impaired glucose tolerance after long-term total parenteral alimentation responding to Cr supplementation have been reported. Chromium potentiates the action of insulin in vitro and in vivo; maximal in vitro activity requires a special chemical form, termed Glucose Tolerance Factor and tentatively identified as a Cr-nicotinic acid complex. Its complete structural identification is a major challenge to chromium research. The development and validation of a procedure to diagnose chromium status is the second challenge. Such a test would allow the assessment of incidence and severity of deficiency in the population and the selection of deficiency in the population and the selection of chromium-responsive individuals. The third challenge is the definition of chromium's mode of action on parameters of lipid metabolism that have been reported from some studies but not others. Future research along these lines might establish whether chromium deficiency is a factor in the much discussed "Syndrome X" of insulin resistance.

Animals↗
PubMed1998

Chromium update: examining recent literature 1997-1998.

Trivalent chromium is an essential nutrient required for sugar and fat metabolism. The majority of people eating typical Western diets consume less than the upper limit of the estimated safe and adequate daily dietary intake, which is set at 50-200 micrograms per day. Insufficient chromium intake is associated with signs and symptoms similar to those seen in diabetes and cardiovascular diseases. The efficacy of chromium in the general population relates to its prevention of deficiency or a reduction in the risk of chronic diseases. It is possible that doses above the estimated safe and adequate daily dietary intake are necessary for the treatment of certain chronic disease states. In a study performed in China, the use of 1000 micrograms of chromium per day (five times above the upper limit of the estimated safe and adequate daily dietary intake) was highly effective in relieving many of the symptomatic manifestations of type 2 diabetes mellitus, including a return of the HbA1C levels into the normal range. Most recent evidence strongly supports the conclusion that there is little fear of toxic reactions from chromium consumption. In addition to type 2 diabetes mellitus, chromium supplementation may be useful to direct overall weight decrements specifically towards fat loss with the retention of lean body mass and to ameliorate many manifestations of aging.

Aging↗
PubMed1983

Studies on contact sensitivity to chromium in the guinea pig. The role of valence in the formation of the antigenic determinant.

Guinea pigs sensitized with either the trivalent chromium chloride or the hexavalent potassium dichromate are capable of reacting in vivo and in vitro to challenges with both chromium salts. This double reactivity is retained also after repeated restimulations with only 1 of these chromium compounds. From the failure to select lymphocytes directed specifically against a chromium determinant of a particular valence it is concluded that by sensitization with chromium salts of different valences a common determinant or closely related determinants are formed. It is suggested that this determinant is formed by chromium in the trivalent form.

Animals↗
PubMed1991

Lymphocyte proliferation test as a diagnostic aid in chromium contact sensitivity.

We investigated the clinical applicability of the lymphocyte proliferation test (LPT) in chromium contact sensitivity. 6 out of 8 chromium-sensitive patients were positive in the LPT, whereas none of 8 non-chromium-sensitive controls responded in vitro to tri- or hexavalent chromium compounds. LPT thus appeared to offer an additional diagnostic tool in chromium sensitivity. We also studied cellular interactions in 4 of our chromium-sensitive patients. Sensitized T-lymphocytes could be activated to proliferate only in the presence of accessory cells, of which epidermal Langerhans cells (LC) appeared more efficient than blood adherent cells.

Adult↗
PubMed1978

Comparison of radio-opaque pellets and chromium sesquioxide as inert markers in studies requiring accurate faecal collections.

Radio-opaque pellets (ROP) similar to those currently used to measure gastrointestinal transit time have been compared with chromium sesquioxide to assess their suitability for use as inert markers in the gut. Five healthy subjects took both markers with every meal for two separate three week periods while taking metabolically controlled diets. Overall recovery of both markers was satisfactory; ROP 99.7 +/- 0.3% (SD) and chromium 97.8 +/- 1.6% (SD). A comparison of the amount for each marker recovered in 69 separate faecal collection periods of various lengths showed close agreement (R = 0.99) and the tail-off in marker excretion after cessation of ROP and chromium intake was similar, although slightly more prolonged for chromium. The amount of marker retained in the gut was 13.5% greater for chromium at the end of the three week study periods. Both markers proved satisfactory for correcting variations in faecal calcium output. The ROP, however, offer clear advantages over chromium in that they are considerably easier and quicker to measure, the method of measurement using x-rays does not alter the stools and faecal handling is minimised. The precision of ROP measurement is greater and, because of the variety of ROP available, they offer more flexibility for metabolic studies. In addition, stool by stool analysis is possible enabling simultaneous measurement of mean transit time to be made in experimental subjects.

Adult↗
PubMed2005

The role of biomembranes in chromium (III)-induced toxicity in vitro.

The role of biomembranes in the chronic toxicity of environmentally occurring chromium acetate hydroxide was investigated by using primary human fibroblasts. Transport of chromium acetate hydroxide across the plasma membrane of the cell, and the effects of chromium (III) ions on the plasma membrane as well as other intracellular membranes, were determined during six weeks of continuous exposure by using atomic absorption spectrometry, observation of cell morphology, membrane integrity assays (for lactate dehydrogenase leakage and lysosomal membrane disruption), and mitochondrial assays (for mitochondrial dehydrogenase activity and mitochondrial transmembrane potential analysis). The type of cell death induced by long-term exposure was determined in terms of phosphatidylserine externalisation, caspase-3 activation, and chromatin fragmentation. Chromium acetate hydroxide, at a concentration of 100 micromol/l, accumulated in exposed cells, inflicting plasma membrane damage and suppressing mitochondrial function. Antioxidant co-enzyme Q, at a concentration of 10 micromol/l, partially prevented plasma membrane damage and mitochondrial dysfunction. Exposure to chromium acetate hydroxide produced apoptosis, necrosis and an intermediate type of cell death in primary human fibroblasts. These results show that the plasma membrane and mitochondrial membrane are important targets for chronic chromium acetate hydroxide toxicity, and that this in vitro system holds promise for studying the toxicity resulting from long-term exposure to metal ions.

Apoptosis↗
PubMed1992

Sex hormones and semen quality in welders exposed to hexavalent chromium.

Recent experimental studies in rodents document the spermatotoxic effects of water-soluble hexavalent chromium. Welders comprise, worldwide, a major occupational group with acknowledged exposure to chromium. This study examines the relationship between semen quality and chromium in the urine and blood of a population of 30 tungsten inert gas (TIG) stainless steel welders, 30 mild steel welders and 47 non-welding workers. Each subject provided two to three semen samples. The chromium concentration ranged from 0.17 to 4.74 nmol mmol1 creatinine (median 1.08) in post-shift spot urine and from 6.0 to 46.4 nmol l-1 in blood. None of several semen parameters deteriorated with increasing level of internal exposure to chromium. Low-level exposure to hexavalent chromium associated with TIG stainless steel and mild steel welding do not appear to be a major hazard for human spermatogenesis.

Adult↗
PubMedDate not supplied

Employee exposure to chromium and plasma lipid oxidation.

Exposure to chromium increases free-radical species in the body, which has an adverse biologic effect. In view of evidence that the oxidation of low-density lipoproteins is important in the pathogenesis of atherosclerosis, the authors measured plasma lipid oxidation and antioxidant levels in 11 welders chronically exposed to chromium and compared them with levels in 15 matched controls. Exposure level was determined by urinalysis. Plasma lipid peroxidation and susceptibility to oxidation were determined by measuring generated thiobarbituric acid reactive substance (TBARS) and lipid peroxides. Total plasma antioxidant status and serum paraoxonase activity were also measured. The Kruskal-Wallis test was used to test for statistical significance. There was no significant difference between the groups with regard to lipid peroxidation, plasma lipid susceptibility to oxidation, total plasma antioxidant status, or serum paraoxonase. Three workers with urinary chromium levels over the biologic exposure index limit (> 10.0 microg/g creatinine) had higher plasma lipid peroxidation and lipid susceptibility to oxidation compared with the rest of the study group. The results suggest that welders exposed to chromium have increased plasma lipid oxidation. The small numbers of subjects and those with elevated urinary chromium limit the power of this preliminary study. Further studies of the association of chromium with plasma lipid oxidation are warranted.

Antioxidants↗
PubMed2006

Effect of chromium on vertebrae, femur and calvaria of adult male rats.

Alloys of chromium have a long history of success in the surgical treatment of many orthopaedic defects. Nonetheless, prostheses loosening are commonly found around arthoplasties due to corrosion of metals. On this basis, it is hypothesized that chromium accumulation interferes with remodeling of bone. The present study aims to analyse the toxic effects of chromium on bone phosphatases in various regions of the bone in rats. Rats were treated with chromium intraperitoneally (0.5 mg/kg) in the form of potassium dichromate for 5 days. The accumulation of chromium is approximately 5.2-fold in the vertebrae, 8.9-fold in the femur and 8.7-fold in the calvaria, when compared to control. Chromium administration significantly reduced the activity of enzymes, eg, alkaline phosphatase (ALP) and tartrate-resistant acid phosphatase (TRAP). The study revealed a significant increase in the concentration of calcium, altered bone formation rate and bone morphology in the femur, vertebrae and calvaria. The interesting findings of the current study suggest altered bone turnover.

Animals↗
PubMed1991

Effects of vitamins on chromium(VI)-induced damage.

The effects of vitamin E and vitamin B2 on DNA damage and cellular reduction of chromium(VI) were investigated using Chinese hamster V-79 cells. Pretreatment with alpha-tocopherol succinate (vitamin E) resulted in a decrease of DNA single-strand breaks produced by Na2CrO4, while similar treatment with riboflavin (vitamin B2) enhanced levels of DNA breaks. In contrast, levels of DNA-protein crosslinks induced by Na2CrO4 were unaffected by these vitamins. Electron spin resonance (ESR) studies showed that incubation of cells with Na2CrO4 resulted in the formation of both chromium(V) and chromium(III) complexes, and cellular pretreatment with vitamin E reduced the level of the chromium(V) complex, whereas pretreatment with vitamin B2 enhanced the level of this intermediate. However, the levels of chromium(III) were unchanged by these vitamins. The uptake of chromate was not affected by vitamin E or vitamin B2, nor were the levels of glutathione or glutathione reductase activity, which are both capable of reducing chromate. ESR studies demonstrated that a chromium(V) species was formed by the reaction of Na2CrO4 with vitamin B2 and that vitamin B2 enhanced the formation of hydroxyl radicals during the reaction of Na2CrO4 and hydrogen peroxide. Treatment cells with Na2CrO4 resulted in a decrease of glutathione reductase activity, and pretreatment with vitamin E restored the enzyme activity suppressed by this metal. However, pretreatment with vitamin B2 enhanced the inhibition of this enzyme by Na2CrO4. Using a colony-forming assay, pretreatment with vitamin E dramatically decreased the cytotoxicity of Na2CrO4, while pretreatment with vitamin B2 was found to result in only a decrease of cell lethality of this metal.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

The chemistry of chromium and some resulting analytical problems.

Chromium, named for its many-colored compounds, exists in the oxidation states of -2 to +6 inclusively. The compounds exhibit a wide range of geometries including square planar, tetrahedral, octahedral, and various distorted geometries. Chromium is found in nature principally as the chromite ore FeCr2O4 in which chromium is in the +3 state. The existence of a particular oxidation state is dependent on many factors including pH, redox potentials, and kinetics. Thermodynamically, +3 and +2 are the most stable states, while the +3 and +6 oxidation states are the most common ones found in aqueous solution. Kinetically, chromium +3 is substitutionally inert: for water exchange k(sec-1) = 2.5 x 10(-6), due to the presence of the half-filled d(t2g)3.4A2g state. On the other hand, protonation/deprotonation is quite rapid. Polymerization is very slow but is promoted at higher pHs; acid cleavage of the protonated oligomers is also quite slow. Chromium +6 as the chromate ion is strongly oxidizing at low pHs and less so in basic solution. The chromate ion does form some polyacids and polyanions. These factors must be considered in analyzing samples for total chromium and for the amounts of each oxidation state.

Chemistry Techniques, Analytical↗
PubMed1991

Chromium-induced kidney disease.

Kidney disease is often cited as one of the adverse effects of chromium, yet chronic renal disease due to occupational or environmental exposure to chromium has not yet been reported. Occasional cases of acute tubular necrosis (ATN) following massive absorption of chromate have been described. Chromate-induced ATN has been extensively studied in experimental animals following parenteral administration of large doses of potassium chromate (hexavalent) (15 mg/kg body weight). The chromate is selectively accumulated in the convoluted proximal tubule where necrosis occurs. An adverse long-term effect of low-dose chromium exposure on the kidneys is suggested by reports of low molecular weight (LMW) proteinuria in chromium workers. Excessive urinary excretion of beta 2-microglobulin, a specific proximal tubule brush border protein, and retinol-binding protein has been reported among chrome platers and welders. However, LMW proteinuria occurs after a variety of physiologic stresses, is usually reversible, and cannot by itself be considered evidence of chronic renal disease. Chromate-induced ATN and LMW proteinuria in chromium workers, nevertheless, raise the possibility that low-level, long-term exposure may produce persistent renal injury. The absence of evidence of chromate-induced exposure may produce persistent renal injury. The absence of evidence of chromate-induced chronic renal disease cannot be interpreted as evidence of the absence of such injury. Rather, it must be recognized that no prospective cohort or case-control study of the delayed renal effects of low-level, long-term exposure to chromium has been published.

Animals↗
PubMed1994

Effects of chromium on DNA replication in vitro.

Chromium is an environmentally significant human carcinogen with complicated metabolism and an unknown mechanism of mutagenesis. Chromium(VI) is taken up by cells as the chromate anion and is reduced intracellularly via reactive intermediates to stable Cr(III) species. Chromium(III) forms tight complexes with biological ligands, such as DNA and proteins, which are slow to exchange. In vitro, CrCl3.6H2O primarily interacts with DNA to form outer shell charge complexes with the DNA phosphates. However, at micromolar concentrations, the Cr(III) binds to a low number of saturable tight binding sites on single-stranded M13 DNA. Additional chromium interacts in a nonspecific manner with the DNA and can form intermolecular DNA cross-links. Although high concentrations of Cr(III) inhibit DNA replication, micromolar concentrations of Cr(III) can substitute for Mg2+, weakly activate the Klenow fragment of E. coli DNA polymerase I (Pol I-KF), and act as an enhancer of nucleotide incorporation. Alterations in enzyme kinetics induced by Cr(III) increase DNA polymerase processivity and the rate of polymerase bypass of DNA lesions. This results in an increased rate of spontaneous mutagenesis during DNA replication both in vitro and in vivo. Our results indicate that chromium(III) may contribute to chromate-induced mutagenesis and may be a factor in the initiation of chromium carcinogenesis.

Chromium↗
PubMed2002

Chromium determinations in blood cells: clinical relevance demonstrated in patients with diabetes mellitus type 2.

As an essential nutrient involved in carbohydrate and lipid metabolism, chromium is of extraordinary importance for patients with diabetes. Plasma concentrations do not reflect the chromium supply; thus, we determined the element's content in blood cells in order to evaluate the body status. We investigated 86 blood donors (C) and 35 diabetics type 2 (Dm2). After the isolation of the blood cells by using a density centrifugation, the chromium concentrations were determined by electrothermal atomic absorption spectrometry. Compared to C, Dm2 had higher values in plasma, erythrocytes, and platelets (248%, 61%, and 91%, respectively) and lower contents in polymorphonuclear and mononuclear leukocytes (each -35%, age- and sex-matched groups with n=35, each p<0.01). The poorer the metabolic control assessed by HbA1c, the higher were the chromium concentrations in plasma (r=+0.46, n=33, p=0.007, increase 11.1% per %HbA1c) and the lower were the values in mononuclear leukocytes (r=-0.45, n=33, p=0.008, decrease 17.8% per %HbA1c). The changed amounts in plasma and in mononuclear cells in increasing hyperglycemia could be the result of an intracellular/extracellular redistribution of the element. High plasma levels might explain the renal chromium losses of diabetics, whereas the lymphocytes could reflect a decreasing chromium body state.

Adult↗
PubMed2002

Effects of dietary chromium and ascorbic acid supplementation on digestion of nutrients, serum antioxidant status, and mineral concentrations in laying hens reared at a low ambient temperature.

This experiment was conducted to evaluate the effects of chromium (chromium picolinate, CrPic) and vitamin C (L-ascorbic acid) supplementation on the digestion of nutrients and serum concentration of some antioxidant vitamins and minerals of laying hens (Hy-Line) reared at a low ambient temperature (6.8 degrees C). One hundred twenty laying hens (32 wk old) were divided into 4 groups, 30 hens per group. The laying hens were fed either a basal diet or the basal diet supplemented with either 400 microg of Cr/kg diet, 250 mg of L-ascorbic acid/kg diet, or 400 microg of Cr plus 250 mg L-ascorbic acid/kg diet. The digestibility of nutrients (DM, OM, CP, and EE) increased by the supplementation of chromium and vitamin C (p < 0.05). Supplemental chromium and vitamin C also increased serum vitamin C and E but decreased malondialdehyde concentrations (p < 0.05). Additionally, supplemental chromium and vitamin C caused an increase in the serum concentrations of Fe, Zn, Mn, and Cr (p < 0.05) but a decrease in Cu concentration. The results of the present study showed that each dietary supplement influenced most of the parameters measured in a similar way. Also, a combination of the two supplements resulted in an additive effect, and supplementing a combination of vitamin C (250 mg/kg of diet) and chromium (400 microg Cr/kg diet) may offer a potential protective management practice in preventing cold-stress-related depression in the performance of laying hens.

Animal Feed↗