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PubMedDate not supplied

Genotoxicity of chromium in human gastric mucosa cells and peripheral blood lymphocytes evaluated by the single cell gel electrophoresis (comet assay).

Hexavalent chromium compounds are well-recognized carcinogens. They easily penetrate the cell membrane and are reduced inside the cell to their trivalent form, which is supposed to react directly with DNA. Chromium is present in some workplaces as well as in water resources and food chain, so it can interact with the mucosa of the gastrointestinal tract. In order to elucidate the genotoxic potency of chromium in human gastric mucosa (GM) cells, the DNA-damaging effect of potassium dichromate (K2Cr2O7) was investigated using alkaline single cell gel electrophoresis (comet assay). Biopsy samples were obtained during gastroscopy from macroscopically healthy tissue of the stomach. Parallel test with human peripheral blood lymphocytes was also performed. Both types of cells were incubated at 37 degrees C with 1.6 mM of K2Cr2O7 for 1 h and after washing, were placed in a chromium-free medium to examine DNA repair. Alkaline single cell gel electrophoresis (comet assay) was used to assess DNA damage and repair. Chromium introduced a damage to DNA both in the GM cells and lymphocytes. The effect induced by K2Cr2O7 in GM cells was comparable with that caused in the lymphocytes. Treated cells were able to recover within a 60-min incubation in a chromium-free medium at 37 degrees C. The results obtained indicate that hexavalent chromium compounds, which may be found in the diet, can interact directly with DNA of the mucosa of the stomach.

Comet Assay↗
PubMed2003

[Chromium (III)-ion enhances the utilization of glucose in type-2 diabetes mellitus].

INTRODUCTION: The prevalence of the type 2 diabetes mellitus is still growing. Although the occurrence of insulin resistance is quite frequent in the whole population, diabetes not always develops because for a time the compensating mechanism avoids it. In a frequent variation of type-2 diabetes the disease is not the result of an alteration in the insulin receptor or the glucose transporter, but a genetically determined defect of the postreceptorial intracellular signaling mechanism plays a role in its occurrence. There have been investigations for decades to find out more about the role of chromium (III) ions in glucose metabolism and in the prevention of type-2 diabetes. It has also been investigated if chromium substitution can prevent or treat those forms of diabetes where chromium deficiency is suspected to be in the background of the disorder. AIM: The aim of our present investigation is to test the role of chromium (III) compounds in glucose metabolism that are known from literature. The authors examined the effect of oral chromium supplementation on antidiabetic treatment. Chromium supplementation was applied for 6 months. METHODS: Before, through and after the investigation changes in the patient's carbohydrate and lipid metabolism were followed by laboratory tests. RESULTS: At the end of our examination the cholesterin level significantly, the HbA1c level close to the significant value decreased. Due to their results the authors presume that chromium (III) compounds may be effective in the treatment of patients' with decreased glucose tolerance or type-2 diabetes mellitus as a supplement to their therapy.

Adult↗
PubMed1997

Environmental monitoring of chromium in air, soil, and water.

Historical uses of chromium have resulted in its widespread release into the environment. In recent years, a significant amount of research has evaluated the impact of chromium on human health and the environment. Additionally, numerous analytical methods have been developed to identify and quantitate chromium in environmental media in response to various state and federal mandates such as CERCLA, RCRA, CWA, CAA, and SWDA. Due to the significant toxicity differences between trivalent [Cr(III)] and hexavalent [Cr(VI)] chromium, it is essential that chromium be quantified in these two distinct valence states to assess the potential risks to exposure to each in environmental media. Speciation is equally important because of their marked differences in environmental behavior. As the knowledge of risks associated with each valence state has grown and regulatory requirements have evolved, methods to accurately quantitate these species at ever-decreasing concentrations within environmental media have also evolved. This paper addresses the challenges of chromium species quantitation and some of the most relevant current methods used for environmental monitoring, including ASTM Method D5281 for air, SW-846 Methods 3060A, 7196A and 7199 for soils, sediments, and waste, and U.S. EPA Method 218.6 for water.

Air Pollutants↗
PubMed1983

Influence of detergent washing powders on minimal eliciting patch test concentrations of nickel and chromium.

Minimum eliciting levels of nickel have been estimated in 25 nickel-sensitive subjects, and of chromium in 14 chromium-sensitive subjects by patch tests with aqueous solutions of the respective metals. The minimum level of each metal required to provoke a patch test reaction was considerably greater than that found in fabric washing powder solutions and was in the majority of patients tested of the order of 112 ppm nickel (0.05% nickel sulphate) or 885 ppm hexavalent chromium (0.25% potassium dichromate). One nickel-sensitive subject and one chromium-sensitive subject reacted to 1 ppm of the respective metal. Fabric washing powder did not significantly alter the patch test reaction to nickel sulphate or provoke reactions in nickel- or chromium-sensitive subjects. EDTA significantly reduced the number and severity of patch test reactions to nickel sulphate but not those to potassium dichromate or trivalent chromium.

Chlorides↗
PubMed1991

Chromium and disease: review of epidemiologic studies with particular reference to etiologic information provided by measures of exposure.

Dozens of epidemiologic studies have been conducted since the late 1940s in an attempt to elucidate the relationship between exposure to chromium compounds and increased rates of certain cancers observed in several industries. The relationship between employment in industries producing chromium compounds from chromite ore and lung cancer has been well established in numerous studies. The relationship between exposure to certain chromium-based pigments and chromic acid and lung cancer, although not as strong, is fairly well accepted. The data concerning emissions from stainless-steel manufacturing and disease are contradictory. Although individual studies have indicated excesses of gastrointestinal and occasionally other cancers in these industries, results are not consistent and not universally accepted. There is general agreement that chromite ore does not have an associated risk of cancer. Although the chromium compound (or compounds) responsible for disease have yet to be identified, there is general agreement that hexavalent species are responsible for these diseases and that the trivalent species are not. Hypotheses about the carcinogenicity of specific chromium compounds generally relate to their solubility in body fluids. These hypotheses, however, have generally been produced as a result of toxicologic, not epidemiologic, investigation. Well-designed epidemiologic studies incorporating detailed assessments of worker exposures have the potential to help elucidate causality, identify specific carcinogenic compounds, and quantify risk in humans, eliminating the need to extrapolate from animal data. Although the need for exposure data crucial to this effort was identified in the earliest epidemiologic studies of chromium, such studies have not been conducted. As a result, little more is known today about the relationship between this chemical and disease in humans than was known 40 years ago.

Chromates↗
PubMed1980

Galvanic cells including cobalt-chromium alloys.

Galvanic cells may be created when dentures made of cobalt-chromium alloys are placed on teeth with metallic restorations. The power of such cells was evaluated in an in vitro galvanic using amalgams, gold alloy, and nickel-chromium alloys. The amalgams and one of the nickel-chromium alloys revealed high corrosion currents when placed in contact with cobalt-chromium alloy, the conventional amalgam showing the highest values. The gold alloy and another nickel-chromium alloy exhibited low corrosion currents and they were noble with respect to cobalt-chromium.

Chromium↗
PubMed1977

[Effects of several compounds on the chromium uptake from surrounding medium by HeLa cells (author's transl)].

Radiochromium uptake from surrounding by HeLa cells was examined, the results were as follows: 1) The chromium uptake by the cells after a certain period of incubation in Ca-Mg free phosphate buffered solution (PBS) with radiosodiumchromate (Na251CrO4) was higher than that in serum free Eagle's minimum essential medium with the same concentration of the radiochromate. 2) When the various amount of L-ascorbic acid was added to the above rabiochromate containing PBS, the chromium uptake by the cells decreased with dependence on the concentration of the acid in the surrounding medium. However, when sodiumthiosulfate was added to the medium, no remarkable effect was found. 3) When cells were incubated in the radiochromic chloride(51CrCl3)containing medium with 6.5 microgram/ml of sodium oxalate, sodium acetate or sodium nitrate, the chromium uptake by the cells increased in comparison with the control. Above results suggested that the chromium uptake by the HeLa cells from surrounding medium was affected by several chemicals and the uptake or binding capacity of chromium was closely related to the reported cytotoxicity of the chromium compounds.

Ascorbic Acid↗
PubMed1997

Chromium as an industrial carcinogen: Part I.

Successive cohorts by year of hire at the same chromate plant (1931-1932, 1933-1934, 1935-1937) and the combined cohort (1931-1937) of 332 employees were followed through 1993. A total of 283 deaths (85%) of the total cohort were identified. In the combined cohort (1931-1937), 66 lung cancers were found, constituting 23.3% of all deaths and 64.7% of all cancers. The lung cancer mortality rates are shown over a span of decades, from 15 years to over 55 years, with progressive rise. Observations of lung cancer identified, employees not found, and cancer risk by age at hire are cited. Lung cancer death rates increased by gradient level of exposure to insoluble (trivalent) chromium and to soluble (hexavalent) chromium, with a pattern of increase by total chromium. Age-specific death rates for lung cancer according to the same gradient exposure range for total, insoluble, and soluble chromium are presented. The potential cancer risk extends to all forms of chromium and to total chromium.

Adult↗
PubMed1999

Mutational specificity in a shuttle vector replicating in chromium(VI)-treated mammalian cells.

An SV40-based shuttle vector, pZ189, was used to characterize the mutation specificity and to explore the mechanism of chromium mutagenesis in mammalian cells. We showed previously that mutagenic DNA damage is induced by the treatment of plasmid with chromium(VI) plus glutathione in vitro. The induced mutation pattern suggested that chromium mutagenesis can be induced by the generation of reactive oxygen intermediates. To further investigate the mechanism of chromium mutagenesis, we treated cultured mammalian cells containing normal pZ189 vector with chromium(VI). Mutations were induced by Cr(VI) in a dose-dependent manner. The majority of base substitution mutations were widely distributed across the supF mutation target gene and occurred mainly at GC basepairs. Overall, the mutation spectra were not significantly different from each other except for a mutation hot spot at position 43, observed only in plasmids from Cr(VI)-treated cells. The characteristics of Cr(VI)-induced mutations were similar to those observed in the mutation spectra induced by H2O2 treatment of the pZ189 plasmid or plasmid-containing cells. These results are consistent with the hypothesis that induction of mutations by chromium in cultured cells occurs through the generation of oxidative DNA damage.

Animals↗
PubMed1999

Genotoxic activity of different chromium compounds in larval cells of Drosophila melanogaster, as measured in the wing spot test.

Two chromium(VI) compounds (potassium chromate and potassium dichromate) and one chromium(III) compound, chromium chloride, were evaluated for genotoxic effects in the wing spot test of Drosophila melanogaster following standard procedures. This assay detects both somatic recombination and mutational events. The genotoxic effects were determined from the appearance of wing spots in flies transheterozygous for the third chromosome recessive markers multiple wing hairs (mwh) and flare-3 (flr(3)), as well as in flies heterozygous formwh and the multiply inverted TM3 balancer chromosome. Genetic changes induced in somatic cells of the wing's imaginal discs lead to the formation of mutant clones on the wingblade. Single spots are due to different genotoxic mechanisms: point mutation, deletion, chromosome breakage, and mitotic recombination; while twin spots are produced only by mitotic recombination. From our results it appears that both chromium(VI) compounds clearly increase the incidence of mutant clones by inducing high increases in the frequency of all types of clones recorded. On the contrary, chromium(III) did not increase the frequency of mutant clones. A high proportion of the total spot induction was due to mitotic recombination, confirming previously reported data on the strong recombinogenic activity of chromium(VI) compounds.

Animals↗
PubMed1999

DNA damage and repair in human lymphocytes and gastric mucosa cells exposed to chromium and curcumin.

Human population can be considered as a subject of combined exposure to chemicals. Hexavalent chromium is a well-known mutagen and carcinogen. Curcumin, a popular spice and pigment, is reported to have antineoplastic properties. The single cell gel electrophoresis (Comet assay) is a sensitive technique that allows detecting double- and single-strand DNA breaks caused by a broad spectrum of mutagens. In the present work the ability of curcumin to reduce DNA damage induced by chromium in human lymphocytes and gastric mucosa (GM) cells was investigated by using the comet assay. Chromium at 500 microM evoked DNA damage measured as significant (P < 0.001), about a two-fold increase in comet tail moment of both lymphocytes and GM cells. Curcumin at 10, 25, and 50 microM also damaged DNA of both types of cells in a dose-dependent manner: the increase in the tail moment reached about twenty times of the control value (P < 0.001). The combined action of chromium at 500 microM and curcumin at 50 microM resulted in the significant (P < 0.001) increase in the comet tail moment of both types of cells. In each case, treated cells were able to recover within 60 min. Our study clearly demonstrates that curcumin does not inhibit DNA damaging action of hexavalent chromium in human lymphocytes and GM cells. Moreover, curcumin itself can damage DNA of these cells and the total effect of chromium and curcumin is additive. Further studies are needed to establish the role of interaction of curcumin with DNA in carcinogenesis.

Cells, Cultured↗
PubMed1989

High concentrations of chromium in lung tissue from lung cancer patients.

The pulmonary chromium content was determined by plasma atomic emission spectrometer (DCP-AES) from 53 lung cancer and 43 control patients, and compared with smoking habits, severity of emphysema and occupational history. The chromium content from the lung cancer patients was higher than that from the smoking (P less than 0.025) or nonsmoking control patients (6.4 +/- 4.3, 4.0 +/- 4.0, and 2.2 +/- 0.6 microgram/g dry weight, respectively). A positive correlation between the pulmonary chromium and smoking time (P less than 0.025) and the severity of emphysema (P less than 0.001) was found in the control but not in the cancer patients. The difference in the pulmonary chromium content was greatest between those lung cancer and control patients who were light smokers or had mild emphysema. This group of lung cancer patients included subjects with occupational exposure to chromium. The possibility of occupational cancer should be considered especially with light smokers. The grade of emphysema and metals such as chromium accumulating from tobacco could serve as objective indicators of smoking.

Aged↗
PubMedDate not supplied

Bioavailability, bioaccumulation and tolerance of chromium: consequences in the food chain of freshwater ecosystems.

Many abiotic and biotic factors can influence the partitioning equilibrium of heavy metals, thus influencing metal impact on aquatic environments. Unicellular algal species release soluble organic substances able to complex metals. In our laboratory a Cr-tolerant strain was selected and isolated from a wild type strain of Scenedesmus acutus. The exudates released by the two strains counteracted the growth inhibition caused by Cr(VI) and the exudates of the Cr-tolerant strain were more effective. On the contrary, the exudates did not reduce chromium toxicity to the cladoceran Daphnia magna. The reduction of chromium effect on algae seems the consequence of an algae-specific interaction among Cr(VI), exudates and algal cells. Chromium uptake resulted to be energy-dependent since bioaccumulation rate in subdued light condition was lower than at high light intensity. The effect of Cr(VI) on algae changed depending on metabolism of the cells and in particular it seemed to be related to the bioaccumulation rate. Tolerance in the selected strain could not be ascribed to a lower uptake of chromium. The difference in sensitivity to chromium between the two strains was exploited to evaluate if tolerance acquired by algae could have consequences for Daphnia. After treatment with Cr(VI), the two strains of S. acutus were used as food source for D. magna. The results indicate that chromium is accumulated by algae in a form not available for daphnids and that Cr tolerance acquired by the algae can be of some advantage to the consumer organism.

Animals↗
PubMed2002

Selective induction of gene expression in rat lung by hexavalent chromium.

Multigene-expression analysis provides a formidable tool for evaluating cellular functions, under either physiological or pathological conditions, and for assessing their modulation by exogenous agents. We investigated multigene expression in the liver and lung of rats receiving intratracheal instillations of sodium dichromate for 3 consecutive days. Nylon membrane cDNA arrays were hybridized with standardized amounts of (32)P-labeled probes, and the results were normalized by making reference to housekeeping genes. The basal expression of 52 of 216 tested genes was 2.1-11.1 times higher in the liver than in the lung of control rats. No alteration of gene expression occurred in the liver of chromium(VI)-treated rats, consistent with the fact that this metal species, being reduced upstream, can exert effects only locally but not at a distance from the respiratory tract. In contrast, the expression of 56 genes was increased 2.1 to 3.0 times in the lung as an early response to chromium(VI) administration. The altered genes are involved in the metabolic reduction of chromium(VI) and in a variety of interconnected functions, such as multidrug resistance and stress response, protein and DNA repair mechanisms, signal transduction pathways, apoptosis, and cell-cycle modulation. Thus, short-term treatment with chromium(VI) by intratracheal administration triggered a variety of defense processes in the lung. Although the use of selected genes does not provide an exhaustive picture of overall gene expression, these findings contribute to our understanding of chromium toxicology and provide a further mechanistic support to the involvement of thresholds in chromium(VI) carcinogenesis.

Animals↗
PubMed1985

An analysis of lung cancer risk from exposure to hexavalent chromium.

Lung cancer risk in relation to airborne levels of hexavalent chromium was analyzed for chromium chemical production workers studied by Hayes, Lilienfeld, and Snell. Hayes et al [18] had observed statistically significant increases in lung cancer mortality among chromium chemical production workers hired during 1945-1959 and followed to mid-1977. A dose-response was observed by Hayes et al. in that long-term workers had a higher lung cancer risk than short-term workers. Concurrent exposure data for the study plant were abstracted from the records of a local health department. The usual air concentration of hexavalent chromium was estimated as 413 micrograms per cubic meter (micrograms/m3) during 1945-1949. Cumulative exposure estimates for individual workers could not be developed with available information. Instead, cumulative exposures in terms of micrograms/m3-years were estimated for groups of short-term workers and long-term workers (cumulative exposure = usual exposure level in micrograms/m3 X average length of exposure). For workers hired during 1945-1949, cumulative exposures were estimated as 670 and 3,647 micrograms/m3-years for short-term and long-term workers, respectively. Like most estimates based on historical data, these exposure estimates are subject to uncertainty. Nevertheless, these results suggest a potential excess risk of death from lung cancer among U.S. workers exposed to the current permissible exposure limit (PEL) for hexavalent chromium of 52 micrograms/m3 because such workers could accumulate exposures (micrograms/m3-years) similar to those associated with excess risk in Hayes et al's cohort. Moreover, many current workers are estimated to be exposed to levels above the PEL. Further exploration of the dose-response relationship for chromium carcinogenesis is indicated.

Air Pollutants, Occupational↗
PubMed1979

The effect of the time of administration of chromium trioxide on the embryotoxic response in hamsters.

Prior work has demonstrated that chromium trioxide is embryotoxic in hamsters if administered to pregnant animals early on the eighth gestation day. The major manifestations are cleft palate and an increased frequency of resorptions. In the present study a single iv dose (8 mg/kg) of chromium trioxide was injected into pregnant hamsters at 8 A.M. on either day 7, 8, 9, 10 or 11 of gestation in order to determine the effect of altering the time of treatment on embryotoxicity. Fetuses from females treated with chromium or demineralized-distilled water were collected on day 15 of gestation and were examined for the types and frequency of external and internal malformations. The number of resorption sites was recorded. Cleft palate, the major malformation detected, was produced only when chromium was administered on days 7, 8, or 9 of gestation. Since the frequency of resorptions and the incidence of cleft palate varied with the time of treatment it is concluded that the time at which chromium trioxide is injected into the pregnant hamster does influence embryotoxicity. The results suggest that an interference with embryonic growth may be an important factor in chromium-induced cleft palate in hamsters.

Abnormalities, Drug-Induced↗
PubMed1996

Absorption and elimination of trivalent and hexavalent chromium in humans following ingestion of a bolus dose in drinking water.

These studies investigate the magnitude and valence state of chromium absorbed following plausible drinking water exposures to chromium(VI). Four adult male volunteers ingested a single dose of 5 mg Cr (in 0.5 liters deionized water) in three choromium mixtures: (1) Cr(III) chloride (CrCl3), (2) potassium dichromate reduced with orange juice (cr(III)-OJ); and (3) potassium dichromate [Cr(VI)]. Blood and urine chromium levels were followed for 1-3 days prior to and up to 12 days after ingestion. The three mixtures showed quite different pharmacokinetic patterns. CrCl3 was poorly absorbed (estimated 0.13% bioavailability) and rapidly eliminated in urine (excretion half-life, approximately 10 hr), whereas Cr(III)-OJ was absorbed more efficiently (0.60% bioavailability) but more slowly (half-life, approximately 17 hr), and Cr(VI) had the highest bioavailability (6.9%) and the longest half-life (approximately 39 hr). All three chromium mixtures caused temporary elevations in red blood cell (RBC) and plasma chromium concentrations, but the magnitude and duration of elevation showed a clear trend (Cr(VI) > Cr(III)-OJ > CrCl3). The data suggest that nearly all the ingested Cr(VI) was reduced to Cr(III) before entering the bloodstream based on comparison to RBC and plasma chromium patterns in animals exposed to high doses of Cr(VI). These findings support our prior work which suggests that water-soluble organic complexes of Cr(III) formed during the reduction of Cr(VI) in vivo explain the patterns of blood uptake and urinary excretion in humans at drinking water concentrations of 10 mg/liter or less.

Administration, Oral↗
PubMed1987

Occupational chronic exposure to metals. I. Chromium exposure of stainless steel welders--biological monitoring.

External and internal chromate exposure of 103 stainless steel welders who were using manual metal are welding (MMA), metal inert gas welding (MIG) and both methods, were measured by ambient and biological monitoring. At the working places the maximum chromium trioxide concentrations were 80 micrograms/m3. The median values were 4 micrograms/m3 (MMA) and 10 micrograms/m3 (MIG). The median chromium concentrations in erythrocytes, plasma and urine of all welders were less than 0.60, 9.00 and 32.50 micrograms/l. For biological monitoring purposes, chromium levels in erythrocytes and simultaneously in plasma seem to be suitable parameters. According to our results, chromium levels in plasma and urine in the order of 10 and 40 micrograms/l seem to correspond to an external exposure of 100 micrograms chromium trioxide per cubic metre, the technical guiding concentration (TRK-value). Chromium concentrations in erythrocytes greater than 0.60 micrograms/l indicate an external chromate exposure greater than the TRK-value.

Adult↗