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PubMed1999

Synergistic induction of hydroxyl radical-induced DNA single-strand breaks by chromium(VI) compound and cigarette smoke solution.

Chromium(VI) compounds and cigarette smoke are known human carcinogens. We found that K2Cr2O7 and cigarette smoke solution synergistically induced DNA single-strand breaks (0.23+/-0.04 breaks per DNA molecule) in pUC118 plasmid DNA. K2Cr2O7 alone or cigarette smoke solution alone induced much less strand breaks (0.03+/-0.01 or 0.07+/-0.02 breaks per DNA molecule, respectively). The synergistic effect was prevented by catalase and by hydroxyl radical scavengers such as deferoxamine, dimethylsulfoxide, d-mannitol, and Tris, but not by superoxide dismutase. Ascorbic acid enhanced the synergism. Glutathione inhibited strand breakage only at high concentrations. Electron spin resonance (ESR) studies using a hydroxyl radical trap demonstrated that hydroxyl radicals were generated when DNA was incubated with K2Cr2O7 and cigarette smoke solution. Hydroxyl radical adduct decreased dose-dependently when strand breakage was prevented by catalase, deferoxamine, dimethylsulfoxide, d-mannitol or Tris, but not significantly by superoxide dismutase. We also used ESR spectroscopy to study the effects of different concentration of ascorbic acid and glutathione. The results showed that hydroxyl radical, which is proposed as a main carcinogenic mechanism for both chromium(VI) compounds and cigarette smoke solution was mainly responsible for the DNA breaks they induced.

Antioxidants↗
PubMed1989

Evaluation of issues relating to the carcinogen risk assessment of chromium.

Important issues in the carcinogenic risk assessment of chromium compounds are whether both trivalent and hexavalent chromium compounds are carcinogenic, the role of solubility in the carcinogenic response, and the carcinogenicity of ingested chromium. Hexavalent chromium compounds are carcinogenic to animals via several routes of exposure, while trivalent chromium compounds, although they demonstrate evidence of genotoxicity, have not been shown in animal studies to be carcinogenic. Workers in chromate production plants, where the risk of lung cancer is elevated, are exposed to both trivalent and hexavalent chromium compounds. A cancer unit risk estimate for Wistar rats exposed to a hexavalent chromium aerosol (sodium dichromate) is less than the risk estimate for workers in chromate production. If this difference is biologically real, a possible explanation may be that trivalent compounds also have a carcinogenic effect. For hexavalent chromium compounds, it is contended that only sparingly soluble hexavalent chromium compounds are carcinogenic. Recent evidence, however, indicates that highly soluble hexavalent chromium compounds are also carcinogenic. Animal ingestion studies have not found trivalent chromium compounds to be carcinogenic by ingestion; hexavalent compounds have not been studied. Research by EPA to address the issue of valence state and solubility with respect to carcinogenicity is currently being conducted.

Animals↗
PubMedDate not supplied

The toxicology of chromium with respect to its chemical speciation: a review.

The properties of trivalent and hexavalent chromium are reviewed with respect to acute and chronic oral toxicity, dermal toxicity, systemic toxicity, toxicokinetics, cytotoxicity, genotoxicity and carcinogenicity. The hexavalent chromium compounds appear to be 10-100 times more toxic than the trivalent chromium compounds when both are administered by the oral route. Dermal irritancy and allergy are more frequently caused by contact with soluble hexavalent chromium compounds. The cytotoxicity of soluble and insoluble hexavalent chromium compounds to fibroblasts is 100-1000 times greater than that demonstrated by trivalent chromium compounds. In short-term tests, the hexavalent chromium compounds demonstrated genotoxic effects four times more frequently than did the trivalent chromium compounds. Carcinogenicity appears to be associated with the inhalation of the less soluble/insoluble hexavalent chromium compounds. The toxicology of chromium does not reside with the elemental form. It varies greatly among a wide variety of very different chromium compounds. Oxidation state and solubility are particularly important factors in considering the toxicity of chromium with respect to its chemical speciation.

Animals↗
PubMed1996

[Squamous epithelial carcinoma of the tongue after occupational exposure to chromium VI compounds].

BACKGROUND: The major key risk factors of head and neck cancer are chronic alcohol and tobacco consumption. There ist further increasing evidence that exposure to hazardous occupational agents increases the cancer risk substantially. CASE REPORT: By means of a case report and an overview of the literature, the role of occupational exposure to hexavalent chromium compounds as a risk factor of head and neck cancer is analysed. RESULTS AND CONCLUSIONS: The mechanisms of chromium carcinogenesis are outlined. Possible interactions of life-style factors and occupational factors which may influence the cancer risk in a synergistic manner are also discussed. Critical analysis of the literature provides evidence of a possible role of occupational exposition to hexavalent chromium compounds as a risk factor for oral squamous cell cancer.

Carcinogens, Environmental↗
PubMed1999

In vitro metabolism and permeation studies in rat jejunum: organic chromium compared to inorganic chromium.

The purpose of these studies was to compare the in vitro absorption of two inorganic chromium(III) compounds: chromium chloride and chromium nitrate, with organic chromium(III)-picolinate; and to investigate if any in vitro metabolism of chromium(VI) takes place. The in vitro metabolism studies showed that chromium (VI) was reduced by artificial gastric juice. The reduction followed first order kinetics with a half-life of 23 min. The studies also showed that the chromium picolinate complex was stable in artificial gastric juice for 4 hours. By the rat everted gut sac technique, chromium chloride, chromium nitrate and chromium picolinate penetrated the rat jejunum with 165 +/- 59, 160 +/- 26 and 127 +/- 36 ng chromium per g rat jejunum, respectively, whereas the permeability coefficients (Papp) were 0.7 +/- 0.3, 1.0 +/- 0.4, and 9.6 +/- 2.2 microns/min, respectively. Absorption studies on pig intestine in Ussing chambers showed a nearly total adsorption of chromium(III) by the chambers, resulting in unreliable data.

Animals↗
PubMed1985

Chromium: a review of environmental and occupational toxicology.

The following topics are covered in this brief review on the environmental and occupational toxicology of chromium: occurrence, production and uses of chromium and chromium compounds; experimental toxicology; chromium toxicity for man; hygienic and ecologic aspects of chromium contamination of the environment. The review provides a conclusive evidence which suggests that chromium, especially its hexavalent form, is both toxic and carcinogenic, but its trivalent form is physiologically essential in the metabolism of insulin. It is also emphasized that among the major sources of environmental chromium today are the cement industry and the increasingly widespread use of chromium compounds added as an anticorrosion admixture to a variety of cooling systems, e.g. in large power plants, which may greatly contribute to the overall pollution of outdoor air at the sites.

Aging↗
PubMed1992

Mutational specificity of chromium(VI) compounds in the hprt locus of Chinese hamster ovary-K1 cells.

Chromium(VI) compounds exert their genotoxicity and mutagenicity by complex metabolic reducing pathways that generate a variety of reactive forms of chromium and free radicals. To investigate the molecular nature of chromium-induced mutations, we characterized the entire coding region of the hypoxanthine (guanine) phosphoribosyltransferase (hprt) gene of 27 independent mutants derived from chromium(VI) oxide (CrO3)-treated Chinese hamster ovary-K1 cells, by direct sequencing of PCR-amplified cDNA. Among these mutants, 10 consisted of single base substitutions, five contained two base substitutions, one had four base substitutions, six were splicing mutations, and five exhibited single base pair insertions or deletions. All of the base substitutions and most of the frameshift mutations observed were located at A/T-rich sequences. More than 90% of the base substitutions (22/24) occurred in A.T base pairs. Among them, T-->A and T-->G transversions (18/22) predominated. The mutational hotspots for single and double base substitutions were the 3' thymidine of 5'PuT and thymidines of 5'ATTT sequences respectively. This mutational specificity was also observed in CHO-K1 cells treated with two other chromium(VI) compounds, namely K2Cr2O7 and PbCrO4. Strand bias was noticed in chromium mutagenicity, since 77% of T base substitutions occurred on the non-transcribed strand. This highly sequence-specific mutation spectrum suggests that a particular form of chromium may directly interact with DNA at these hotspot sequences.

Amino Acids↗
PubMed1997

Elevated serum levels of pantropic p53 proteins in chromium workers.

OBJECTIVES: This study investigated the possibility of applying serum pantropic p53 proteins in molecular epidemiologic studies, as a biomarker of environmental carcinogenesis. The serum levels of pantropic p53 proteins were determined in workers with past exposure to hexavalent chromium compounds. METHODS: Thirty-one male workers occupationally exposed to hexavalent chromium compounds in the production of chromium compounds for 0 to 23 years served as the exposed group. The referents were 10 volunteers without work-related exposure to chemicals. In the determination of pantropic p53 proteins, commercially available kits for enzyme-linked immunosorbent assay were used which quantitatively detected both mutant and wild-type human p53 proteins. RESULTS: The serum level of pantropic p53 proteins was in the range of 116.4 to 1122.6 pg/ml for the exposed workers and of 117.4 to 305.8 pg/ml for the referents. Nineteen percent of the exposed workers had a high p53 protein level (6 out of 31) when compared with the referents. All but 1 of the 6 workers had been occupationally exposed to chromium compounds for more than 11 years. Two of the 3 workers with a past history of lung cancer also showed high levels. CONCLUSIONS: Our findings confirm that the application of p53 proteins as a biomarker of environmental carcinogenesis merits further exploration.

Adult↗
PubMed1983

Dietary chromium - forms and availabilities.

The chromium naturally occurring in plants eluted from Sephadex G-25 at approximately 2600 D. Total chromium was quantitated with flameless atomic absorption spectrophotometry. A plant ligand tagged with radioactive chromium both in vivo and in vitro migrated on Sephadex G-25 identically to the naturally occurring chromium compound. The molecular weight of the radioactively tagged chromium compound was 2600 daltons on Sephadex G-25. Similar complexes isolated from plant species were found attached to an organic ligand. The ligand appears to have 2 components, differing in composition by an amine group. This extremely stable (KD = 9 X 10(-5)anionic complex does not contain peptide or deoxyribose units. When alfalfa was exposed to either Cr(III) or Cr(VI), only Cr(III) was isolated in this organic chromium compound. The alfalfa bioreduction system can be saturated, as evidenced by Cr(VI) isolation of ionic in those plant extracts incubated with high levels of Cr(VI) in vitro. The gastrointestinal chromium physiology studies show that the radioactively labelled plant chromium compounds remained intact through the gastrointestinal tract up to the large intestine. Some degradation products were identified in the rat cecum. Approximately 30% of the plant chromium available to the rat was absorbed across the gastrointestinal tract.

Animals↗
PubMed1981

The carcinogenicity of chromium.

The carcinogenicity of chromium compounds is reviewed with specific attention to the gaps in knowledge for risk estimation and research needs. The most important problems at present are whether trivalent chromium compounds cause cancer, and whether there is a difference in cancer causing effects between the soluble and the slightly soluble hexavalent compounds in the practical exposure situation. Dose estimates for risk estimation based on epidemiological investigations are also lacking. Present evidence indicates that the trivalent chromium compounds do not cause cancer although high concentrations in some in vitro systems have shown genetic toxicity. Hexavalent chromium compounds cause cancer in humans, in experimental animals and exert genetic toxicity in bacteria and in mammalian cells in vitro. Epidemiological evidence and animal experiments indicate that the slightly soluble hexavalent salts are the most potent carcinogens, but proper identification and characterization of exposure patterns in epidemiological work are lacking. Workers also tend to have mixed exposures. Soluble and slightly soluble salts are equally potent genotoxic agents in vitro. Further work for establishing dose estimates for risk evaluation in epidemiological work is important. In vitro systems should be applied for further identification of the mechanism of the carcinogenic effects, and animal experiments are urgent for comparison of the carcinogenic potency of the different hexavalent salts. Hexavalent chromium salts must be regarded as established carcinogens, and proper action should be taken in all industries with regard to such exposure. At present the carcinogenic risk to the general population caused by chromium compounds seems to be negligible, chromium in cigarettes, however, is an uncertainty in this respect. The amount of chromium and the type of chromium compounds inhaled from cigarettes is not known.

Animals↗
PubMed1996

The influence of atmospheric chromium on selenium content and glutathione peroxidase activity in blood of tannery workers.

The concentration of selenium and thiobarbituric acid reactive substances (TBARS) and activity of glutathione peroxidase (GSH-Px) were determined in blood of 34 workers of a tannery in Gniezno, Poland, who worked in an area containing chromium compounds. Fourteen workers were exposed to chromium compounds at concentrations of 0.11 +/- 0.07 mg Cr/m3 (mean +/- SD) and 20 at concentrations 5-10 times lower i.e., 0.022 +/- 0.009 mg Cr/m3. Excretion of Se in urine was measured in all of the investigated workers. Decreased Se concentration in whole blood and blood plasma and elevated TBARS concentration in blood plasma were found in the whole group of investigated tanners as compared to controls. Tanners working in areas with high chromium concentrations had a statistically significant decrease in Se concentration in blood and plasma and decreased urinary excretion of the microelement as compared with other tanners. TBARS concentration was 2.5 times lower in workers exposed to higher chromium concentrations (p < 0.005) than in other workers. Positive linear correlations were found between the concentration of Se in blood and the amount of the element excreted in urine (r = 0.48; p < 0.005), the concentration of Se in blood plasma and in urine (r = 0.46; p < 0.01), and the concentration of Se in blood and erythrocyte GSH-Px activity (r = 0.42; p < 0.02). The observed differences between Se concentration in blood and urine of tannery workers and people who are not employed in the industry may indicate a kind of specific adaptation of the body to the working environment containing chromium compounds.

Adult↗
PubMed2003

Occupation and larynx and hypopharynx cancer: a job-exposure matrix approach in an international case-control study in France, Italy, Spain and Switzerland.

OBJECTIVE: To investigate the effect of exposure to occupational agents on the risk of hypopharyngeal/laryngeal cancer. METHODS: Case-control study conducted during 1979-1982 in six centres in South Europe. An occupational history and information on exposure to non-occupational factors were collected for 1010 male cases of hypopharyngeal/ laryngeal cancer as well as for 2176 population controls. The exposure to 10 occupational agents was assessed through a job-exposure matrix. As occupational histories had been collected since 1945 major analyses were restricted to subjects aged less than 55 years (315 cases and 819 controls). RESULTS: Significant elevated risks adjusted for non-occupational variables (smoking, alcohol consumption and diet) and other occupational exposures were consistently found for organic solvents (odds ratio (OR) for ever-exposure: 1.7, 95% confidence interval: 1.1-2.5) and asbestos (OR: 1.6, 1.0-2.5). A significant positive trend for both probability of exposure and duration was found for exposure to solvents. A positive association between exposure to formaldehyde and laryngeal cancer was also suggested. No association was found for exposure to arsenic and compounds, chromium and compounds, and polycyclic aromatic hydrocarbons. Analyses restricted to subjects aged 55 or more did not show elevated risks, with the exception of wood dust (OR: 1.8, 1.3-2.7). CONCLUSIONS: In our study occupational exposure to solvents was associated with an increased risk of hypopharyngeal/laryngeal cancer. Results also provide additional evidence of an excess of risk for exposure to asbestos.

Adult↗
PubMed1987

Analytical chemistry of chromium species in the environment, and interpretation of results.

Valence-selective species determination of chromium in environmental and biological material presents intricacies primarily due to the complex nature of the samples and the instability of the oxidation states of chromium. In particular organic matter ubiquitously present in environmental samples introduces the risk of chromium(VI) reduction during analysis which takes place preferably in acidic solution. Also chromium(III) oxidation may occur in alkaline medium. Hence analytical methods should be adequately adapted to the reliable determination of chromium(VI) in blood, natural water, effluents, sediments and soil. It can be shown that polarography is most effectually suitable to the determination of chromium(VI) compounds. Chromium(VI) is electrochemically active over the entire pH range, so that medium pH can be selected for measuring, thus protecting samples most effectively from undergoing redox reactions during the analytical procedure. Other established methods such as spectrophotometry or valence-specific extraction are more crucial, because these generally require acidic medium. In some cases sample pre-treatment can be employed to eliminate reductants prior to final measurement. Very few methods are available to selectively measure chromium(III). Indirect determination is therefore preferred. Optimum conditions for the determination of total chromium by AAS are shortly outlined.

Chromium↗
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↗
PubMed2002

Comparative histological studies on liver of mice exposed to Cr(VI) and Cr(V) compounds.

Chromium toxicity is strongly dependent on its oxidation state. Cr(VI) is carcinogenic and mutagenic, although its in vivo and in vitro toxic effects are related to its intracellular fate. Inside the cells, Cr(VI) is rapidly reduced to stable Cr(III). As Cr(V) and Cr(IV) species have been reported to be formed in the Cr(VI) reduction pathways, Cr(VI)-induced damage is thought, at least in part, to arise from these hypervalent species. The study of Cr(VI) reduction mechanisms and the characterization of the effects of each reactive intermediate constitute important steps towards a better understanding of chromium toxicity. The purpose of this work is to enlarge the scope of Cr(VI)-induced alterations in mouse to other chromium species. Our studies have led to the in situ preparation of a new Cr(V) complex, 1Cr(V)-BT](2-), a stable compound at neutral pH, which mimics Cr(VI) reduction intermediates. The effect of Cr(V) on the histology of mice liver is assessed and compared with similar Cr(VI) assays. Liver toxicity was examined after single administrations of Cr(VI) or [Cr(V)-BT](2-) to mice. Both compounds produced reversible hepatic damage in a time-dependent manner. However, Cr(V) toxic effects have proved to be more rapid than with Cr(VI), permitting the role of Cr(VI) intermediates formed during intracellular chromium reduction to be highlighted.

Animals↗
PubMed1992

Defining conditions for the efficient in vitro cross-linking of proteins to DNA by chromium(III) compounds.

The formation of cross-links between bovine serum albumin and DNA in the presence of chromium(III) chloride was found to be highly pH dependent. In vitro, such lesions were only formed at acidic values of pH, but were not detected at neutral pH. Complexes of chromium(III) and GSH/GSSG similarly failed to induce DNA-protein cross-links at physiological values of pH. Our findings indicate that the cross-links generated in vitro at acidic pH may not be directly relevant to the observed formation of such lesions in cultured cells and that a physiologically relevant in vitro model for the efficient cross-linking of proteins to DNA has yet to be devised.

Bacteriophages↗
PubMed2004

Uptake of chromium(III) and chromium(VI) compounds in the yeast cell structure.

The study presented in this article investigated the influence of different Cr(III) and Cr(VI) compounds in the cultivation medium on the uptake and localization of chromium in the cell structure of the yeast Candida intermedia. The morphology of the yeast cell surface was observed by the scanning electron microscopy. Results demonstrated that the growth inhibitory concentration of Cr(III) in the cultivation medium induced changes in the yeast cell shape and affected the budding pattern, while inhibitory concentration of Cr(VI) did not cause any visible effects on morphological properties of the yeast cells. The amount of total accumulated chromium in yeast cells and the distribution of chromium between the yeast cell walls and spheroplasts were determined by atomic absorption spectroscopy. No significant differences were found neither in total chromium accumulation nor in the distribution of chromium in yeast cell walls and spheroplasts between the two of Cr(VI) compounds. Conversely, substantial differences between Cr(III) compounds were demonstrated in the total uptake as well as the localization of chromium in yeast cells.

Candida↗