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PubMed1990

One hundred years of chromium and cancer: a review of epidemiological evidence and selected case reports.

The present review is motivated by the fact that 100 years have passed since the first cancer case in a chromium worker was reported in Scotland. Old and recent case reports and epidemiological studies among chromate workers are reviewed to elucidate the importance of valency states and water solubility of chromium compounds for carcinogenic potency. It is concluded that all chromium[VI] compounds should be considered carcinogenic among exposed populations, and that no evidence has been presented indicating that human exposure to chromium[III] is associated with increased cancer risk. Strong evidence has been presented that zinc chromate is a potent carcinogen and suggests that calcium chromate may be a potent carcinogen. Evidence also suggests that water-soluble chromates in general may be more potent carcinogens than those with low solubility. Primary and secondary prevention of chromate-related cancer and the success in preventive measures are briefly discussed, and recommendations for future research are made.

Chromates↗
PubMed2001

The trail of chromium(III) in vivo from the blood to the urine: the roles of transferrin and chromodulin.

The chromium-binding oligopeptide chromodulin (also known as low-molecular-weight chromium-binding substance) has been shown to activate the tyrosine kinase activity of the insulin receptor in response to insulin and has been proposed to be part of a novel autoamplification mechanism for insulin signaling. The model requires that Cr3+ be moved from the blood to insulin-sensitive tissues in response to insulin and subsequently be lost in the urine as chromodulin; however, the model has not been tested by in vivo studies. In vivo studies with rats have shown that the iron transport protein transferrin serves as the major chromic ion transport agent and that this transport is stimulated by insulin. The ion is transported to a variety of tissues, while liver and kidneys are the major target. In hepatocytes, chromodulin occurs in appreciable levels in the cytosol and in the nucleus. Apochromodulin levels appear to be maintained under homeostatic control, although the only detectable form of urinary chromium is probably chromodulin. Increases in urinary chromium loss in response to insulin are reflected by increases in chromodulin, establishing a direct link between carbohydrate metabolism and the oligopeptide.

Animals↗
PubMed1988

Recent advances in biological monitoring of hexavalent chromium compounds.

Intratracheal instillation of 51CrCl3 in anaesthetized rabbits resulted in partial absorption. In blood, the absorbed material was entirely confined to the plasma compartment. By contrast, after similar application of Na251CrO4 the bulk of blood radioactivity was present in red blood cells (RBC). It is suggested that Cr (VI) may enter the body not reduced via the lung and may be deposited in RBC for the cell's lifetime (approximately 110 d). Since inhalation of Cr (VI)-containing aerosols or particles is the main occupational exposure route for man, it is concluded that the chromium content of RBC could be used as a selective biological indicator for exposures to (carcinogenic) hexavalent chromium. The new theoretical concept was confirmed in a pilot study with workers of a dye pigment plant. Elevated chromium content of whole blood evoked by exposure to chromate particles correlated strongly with increased chromium values in RBC (correlation coefficient: 0.86).

Animals↗
PubMed1978

Effects of glucose and chromium(III) concentrations in the medium on the uptake of 51Cr by brewer's yeast.

The incorporation of trivalent chromium into S. carlsbergensis as function of time, the effects of chromium and glucose concentrations in the medium on the uptake of 51Cr by the yeast cells, and the effect of chromium on growth of the yeast were studied. 51Cr was taken up by yeast cells most rapidly during the logarithmic growth period in Sabouraud's liquid medium containing 5% glucose. Cells grown in a medium containing only 0.5% glucose at the beginning of cultivation incorporated very little 51Cr, and incorporation ceased when the glucose concentration was reduced to less than 0.1%. Addition of 5% glucose into this culture resulted in a very rapid increase in the 51Cr uptake. The second glucose addition did not notably increase the rate of 51Cr uptake by the yeast. Chromium, reduced yeast growth slightly, however, was not clearly toxic.

Biological Transport↗
PubMed2000

A comparison of the in vitro genotoxicity of tri- and hexavalent chromium.

Chromium can be found in the environment in two main valence states: hexavalent (Cr(VI)) and trivalent (Cr(III)). Cr(VI) salts are well known human carcinogens, but the results from in vitro studies are often conflicting. Cr(VI) primarily enters the cells and undergoes metabolic reduction; however, the ultimate product of this reduction, Cr(III) predominates within the cell. In the present work, we compared the effects of tri- and hexavalent chromium on the DNA damage and repair in human lymphocytes using the alkaline single cell gel electrophoresis (comet assay). Potassium dichromate induced DNA damage in the lymphocytes, measured as the increase in comet tail moment. The effect was dose-dependent. Treated cells were able to recover within a 120-min incubation. Cr(III) caused greater DNA migration than Cr(VI). The lymphocytes did not show measurable DNA repair. Vitamin C at 50 microM reduced the extent of DNA migration. This was either due to a decrease in DNA strand breaks and/or alkali labile sites induced by Cr(VI) or to the formation of DNA crosslinks by Cr(VI) in the presence of vitamin C. Vitamin C, however, did not modify the effects of Cr(III). Catalase, an enzyme inactivating hydrogen peroxide, decreased the extent of DNA damage induced by Cr(VI) but not the one induced by Cr(III). Lymphocytes exposed to Cr(VI) and treated with endonuclease III, which recognizes oxidized pyrimidines, displayed greater extent of DNA damage than those not treated with the enzyme. Such an effect was not observed when Cr(III) was tested. The results obtained suggest that reactive oxygen species and hydrogen peroxide may be involved in the formation of DNA lesions by hexavalent chromium. The comet assay did not indicate the involvement of oxidative mechanisms in the DNA-damaging activity of trivalent chromium and we speculate that its binding to cellular ligands may play a role in its genotoxicity.

Carcinogens, Environmental↗
PubMed1960

The use of DFP32 as a red cell tag with and without simultaneous tagging with chromium 51 in certain animals in the presence or absence of random destruction.

DFP(32), used to label erythrocytes in vitro, combines with cell constituents in two stages, the first almost immediate and involving tributyrinase inactivation, the second slower (more than 40 minutes) involving cholinesterase inactivation. Raising the DFP concentration increases the amount irreversibly bound, but increases even more the immediate post-transfusion elution, and DFP is unsuited for investigating erythrocyte viability of stored samples. In vivo tagging by intramuscular injection is satisfactory and normal survival curves are linear since the sample tagged has normal age distribution of cells in absence of random destruction. Here DFP(32) curves are easier to interpret than Cr(51) curves. In sheep, chromium elution occurs at two different rates producing a rapid initial drop followed by a slower one of about 3 per cent daily. Random destruction alters cell age distribution. New equations are derived for cases in which this is constant both with and without chromium elution; they were applied satisfactorily to dog and sheep blood. Analysis of such curves is difficult; approximate values for random destruction rates can be obtained though not potential life spans. Chromium curves can be analyzed only with the help of DFP(32) or similar curves, and yield little additional information. DFP(32) and chromium can be used simultaneously to provide controls.

Animals↗
PubMed1981

Effect of chromium chloride supplementation on glucose tolerance and serum lipids including high-density lipoprotein of adult men.

Chromium deficiency may cause insulin resistance, hyperinsulinemia, impaired glucose tolerance, and hyperlipidemia, recovered by chromium supplementation. The effect of chromium supplementation on serum lipids and glucose tolerance was tested in a double-blind 12-wk study of 23 healthy adult men aged 31 to 60 yr. Either 200 micrograms trivalent chromium in 5 ml water (Cr) or 5 ml plain water (W) was ingested daily 5 days each week. Half the subjects volunteered for glucose tolerance tests with insulin levels. At 12 wk high-density lipoprotein cholesterol increased in the Cr group from 35 to 39 mg/dl (p less than 0.05) but did not change in the water group (34 mg/dl). The largest increase in high-density lipoprotein cholesterol and decreases in insulin and glucose were found in those subjects having normal glucose levels together with elevated insulin levels at base-line. The data are thus consistent with the hypothesis that Cr supplementation raises high-density lipoprotein cholesterol and improves insulin sensitivity in those with evidence of insulin resistance but normal glucose tolerance.

Adult↗
PubMed2003

Chromium allergy: significance of both Cr(III) and Cr(VI).

Most studies investigating chromium allergy have been performed with Cr(VI). However, real exposure to chromium from leather products includes both Cr(III) and Cr(VI). We have determined and compared the minimum elicitation threshold (MET) concentration for Cr(III) and Cr(VI) in Cr(VI)-sensitive patients. In addition, reactions to combinations of Cr(III) and Cr(VI) were compared to reactions elicited by Cr(III) and Cr(VI) alone. Dilution series of Cr(III) and Cr(VI) were applied in Finn Chambers on the back of 18 patients. The patches were left for 2 days and readings were done on days 2, 3 and 7. The MET10% for Cr(III) and Cr(VI) was calculated from the dose-response curves to be 0.18 microg/cm2/48 h (6 p.p.m.) and 0.03 microg/cm2/48 h (1 p.p.m.), respectively. No significant differences in the response to combined Cr(III) and Cr(VI) solutions versus single solutions were found. Cr(III) was concluded to play an important role in chromium allergy, because Cr(III) and Cr(VI) were both capable of eliciting eczema at low concentrations. Rather than regarding chromium dermatitis as a result of Cr(VI) allergy alone, it may be more correct to consider it as a result of a combined Cr(III) and Cr(VI) allergy.

Carcinogens, Environmental↗
PubMed1984

Corrosion resistance of a passivated and non-passivated cobalt-chromium alloy.

The release of cobalt and chromium from a passivated and non-passivated cobalt-chromium alloy in artificial saliva has been measured using nuclear tracer technique. The corrosion resistance of the passivated specimens was improved by a factor of about four compared to the non-passivated specimens with regard to the initial cobalt release. The specimens were exposed to the saline solutions for periods up to about 8 wk. The cobalt release is associated mainly with electrochemical corrosion processes, since particulate matter retained on a filter was only registered to a minor extent. It is suggested that the decrease in release of cobalt and chromium after passivation is connected to the formation of Cr-O and/or Cr-OH bonds in the protective film which impede the movement of cobalt and chromium from the alloy into the saliva.

Chemical Phenomena↗
PubMed1983

Kinetics of trace element chromium(III) in the human body.

Chromium(III) has been reported to be an essential trace element involved in the control of glucose metabolism by insulin. We have studied the distribution and kinetics of intravenous [51Cr]chromium(III) in six human subjects using a whole-body scintillation scanner, a whole-body counter, and plasma counting. Principal concentrations were found in the liver, spleen, soft tissue, and bone. The data were fit to a model consisting of a plasma pool in equilibrium with fast (T1/2 = 0.5-12 h), medium (1-14 days), and slow (3-12 mo) compartments, and transfer rates were calculated for exchanges between compartments. Each of the imaged organs appeared to contain varying proportions of each compartment. Two patients with hemochromatosis, in which iron overload is postulated to exclude chromium transport, were found to have altered rate constants. The results should be useful in assessing the metabolism and nutritional requirement of chromium(III) in humans and its importance in disease processes such as diabetes.

Autoradiography↗
PubMed1993

Genetic control of delayed-type hypersensitivity to chromium chloride.

Genetic control of delayed-type hypersensitivity (DTH) to chromium chloride antigen was studied in various strains of mice. Mice with I-Ab,d,f,k,r were high magnitude responders, whereas those with I-Aq,s were low magnitude responders. Studies with recombinant strains indicate that chromium chloride DTH may be influenced by the I-A region of H-2. DTH to chromium chloride is an antigen-specific response. We further revealed that response to chromium chloride does not cross-react with response to cobalt or nickel chloride. Also, transfer experiments using lymph node cells suggest that these responses are mediated by CD4+8-, Ia-T cells.

Animals↗
PubMed1989

Induction of lipid peroxidation in mice by hexavalent chromium and its relation to the toxicity.

Comparative effects of hexavalent (K2Cr2O7:Cr(VI)) and trivalent chromium (Cr(NO3)3:Cr(III)) on the development of lipid peroxidation, and the relationship between the lipid peroxidation and damage to tissues were studied using male ddY strain mice. The animals were administered with either of two chemicals at a dose of 20 mg Cr/kg by a single intraperitoneal injection. The results obtained were as follows: (1) Lipid peroxidation in the liver, as measured by the synthesis of thiobarbituric acid reactive substances (TBARS), showed a significant increase at 24 and 48 hr after Cr(VI) injection, while in the kidney it was observed only at 48 hr. In the mice administered with Cr(III), TBARS formation in the liver went down below the control levels, while no change was observed in the kidney. (2) Chromium contents in the liver and kidney showed a maximum level at 6 hr after injection of Cr(VI) and then those declined to the half of the maximum level at 48 hr, respectively. Chromium contents in the liver and kidney of the mice injected with Cr(III) were lower than those injected with Cr(VI) during the experimental period. (3) Increases of TBARS formation in the liver, chromium content in the liver and kidney, and ornithine carbamyl transferase (OCT) activity indicative of the liver cell damage, and urea nitrogen content in the serum, indicative of the kidney damage, observed at 24 hr after injection of Cr(VI) were inhibited by simultaneous injection of 100 mg/kg of L-ascorbic acid, as antichrome agent, respectively. These observations might suggest a possible causative role of lipid peroxidation in Cr(VI) toxicity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

[Effects of chromium compounds on the respiratory system. 5. Long term inhalation of chromic acid mist in electroplating by C57BL female mice and recapitulation of our experimental studies].

Long term inhalation of CrO3 mist by C57BL mice The effects of the chromic acid mist used in electroplating on the respiratory system of C57BL mice (female; n = 43) were examined histopathologically after exposure for 12 months to the mist (1.81 mgCr/m3-120 min, twice a week). Among the 23 mice sacrificed at 12 months after the first exposure, three cases of perforation in the nasal septs, a case of proliferative change of the tracheal epithelium, nine cases of emphysema and four of adenomatous metaplasia of the lungs were observed on antopsy. Among the 20 mice which were sacrificed six months after the last exposure, the same changes as the 12-month exposure group were also observed in the nasal septum, trachea and lungs, but papillomas observed in the nasal epithelia of six mice and adenoma in the lung of a mouse were new findings not seen in the 12-month exposure group. These results suggest that, in view of the low incidence of spontaneous lung tumor in C57BL mice, inhalation of chromic acid mist in electroplating might be a risk factor of lung cancer. Additionally, the occurrence of papillomas in the nasal epithelium demonstrates the need of directing attention to the possible development of cancer of the upper respiratory tract in chromium electroplating workers. Recapitulation on our experimental studies Upon completion of our five reports on the effects of chromium compounds on the respiratory system, a recapitulation of our experimental studies was made and compared with the findings of a number of reports on chromium. It was experimentally and epidemiologically confirmed that hexavalent chromium compounds act as carcinogens and cause specific biological effects on the respiratory system. These characteristics of hexavalent compounds might be attributable to the strong oxidizing potency and/or high permeability through the cell membrane. Furthermore, hexavalent compounds might be entirely different in biological action from trivalent compounds which are chemically most stable.

Aerosols↗
PubMedDate not supplied

Chromium-51 release from human blood platelets by anti A antibody.

Platelets were obtained by differential centrifugation from Group A donors and were incubated with Na2-51Cr04. After washing to remove excess chromium, the platelets were exposed for one hour to Anti A antibody which showed agglutinating activity only. Chromium release was no greater than that of controls. Hemolytic Anti A in the presence of rabbit complement released 15 percent more chromium than controls. Anti P1A1, a platelet specific antibody, when incubated with platelets in the presence of rabbit complement released 45 percent more chromium than controls. It appears that Anti A antibody is not as destructive to platelets as a platelet specific antibody is, even when the Anti A antibody shows hemolytic activity with red cells. These observations are in agreement with previous in vivo studies of ABO incompatible platelets.

ABO Blood-Group System↗
PubMedDate not supplied

Red cell volume determination using a stable isotope of chromium.

OBJECTIVE: To validate and improve a method of red cell volume determination by use of a stable isotope of chromium. METHODS: Twelve subjects were sequentially injected with red blood cells labeled with a stable isotope of chromium (53Cr) and red blood cells labeled with radioisotopic chromium (51Cr). Measurement of 53Cr dilution was by gas chromatography/mass spectrometry. Measurement of 51Cr dilution was by gamma counter. RESULTS: Comparison of the two methods led to results that differed on average by 34.5 +/- 45.0 mL (1.8 +/- 2.2%), 0.3 to 3.2%, 95% confidence interval. CONCLUSION: Measurement of red cell volume by use of a stable isotope of chromium is accurate, with potential applications including measurement in pregnant women and children or other groups in whom exposure to radioisotopes is undesirable.

Blood Volume↗
PubMed1996

Risk of lung cancer among former chromium smelter workers.

Hexavalent chromium is a known carcinogen. Previous epidemiologic studies in the 1950s of United States workers from seven facilities producing chromium compounds from chromite ore have reported a markedly increased risk for dying from lung cancer. As part of a high risk notification project of workers from four of these facilities, a mortality study was performed. The cohort was assembled in 1990-1991 from the Social Security records of four former chromate producing facilities in northern New Jersey. The study subjects were known to have worked at these facilities some time between 1937 and 1971. Proportionate mortality and proportionate cancer mortality ratios (PCMR) were calculated. The overall risk for lung cancer was a PCMR of 1.51 (confidence limits [CL] 1.29-1.74) for white men and 1.34 (CL 1.00-1.75) for black men. These risks increased with increasing duration of employment and latency since time of first employment. The PCMR for greater than 20 years duration of work and more than 20 years since first exposure was 1.94 (CL 1.15-3.06) for white men and 3.08 (CL 1.13-6.71) for black men. The risk for lung cancer for white men remains elevated more than 20 years after exposure has ceased (PCMR, 1.29; CL 1.03-1.60). The PCMR for nasal cavity/sinus cancer was also found to be a significantly increased, 5.18 (CL 2.37-11.30). A cluster of bladder cancer was seen among black workers from one facility, (PCMR, 3.30; CL 1.42-6.51). Despite the cessation of exposure, former chromium workers remain at significantly increased risk of lung cancer. Although there have been case reports of nasal cavity/ sinus cancer in association with chromium exposure, this is the first epidemiologic study to report a significant increase in these cancers. Limitations in this study include lack of exposure data and lack of information on smoking habits. The lack of increase in other smoking-related diseases besides lung cancer indicates that the increase in lung cancer cannot be attributed to cigarette smoking. The ongoing elevated risk of lung cancer after cessation of exposure emphasizes the need for developing early detection texts for lung cancer.

Chromium↗
PubMed2000

Chromium(VI) induces p53-dependent apoptosis in diploid human lung and mouse dermal fibroblasts.

Some forms of hexavalent chromium [Cr(VI)] are known to cause damage to respiratory-tract tissue and DNA and are thought to be human lung carcinogens. In general, Cr(VI) is mutagenic and carcinogenic at doses that also evoke some cell death, and we previously showed that the predominant mode of death is apoptosis. Because p53 has been shown to initiate apoptosis after genotoxic insults, the objective of these experiments was to determine whether p53 is activated in and necessary for apoptosis of normal diploid human lung fibroblasts (HLF cells) after chromium exposure. By using annexin(V) staining and fluorescent microscopy, we found that Cr(VI) caused up to 14% of HLF cells to undergo apoptosis within 24 h after exposure. In addition, by using western blotting, we found that p53 protein levels increased fourfold to sixfold after exposure to sodium chromate. Because the major function of p53 is as a transcription factor, it must be translocated from the cytoplasm to the nucleus after chromate exposure to be active. Immunofluorescence studies using an antibody against p53 showed that, after chromate exposure, p53 was located in the nucleus of the treated HLF cells. The necessity of p53 for chromium-induced apoptosis was examined in two ways. One approach used dermal fibroblasts from p53 wild-type, heterozygous, and null mice, and the other approach used HLF cells that were transiently transfected with the human papilloma virus E6 gene, which targets p53 for degradation and creates a functional p53-null cell. These studies showed that chromium-induced apoptosis was p53 dependent. Mol. Carcinog. 28:111-118, 2000.

Animals↗
PubMed1987

Chromium content of organs of chromate workers with lung cancer.

The content of chromium was measured in organs of six chromate workers who had worked in a chromate chemical manufacturing plant, had been exposed to a considerable amount of chromium for over 10 years, and had died of lung cancer. The chromium in the lungs of workers averaged 51.5 micrograms/g (range 24.8-210 micrograms/g), while levels in the lungs of non-exposed controls were 0.07-1.01 micrograms/g. Organs other than the lungs of the workers also had more chromium than those of the controls. Moreover, it was apparent that the metal remained in the lungs long after exposure to chromate had ceased.

Adult↗