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PubMed1990

[Skin Barrier creams for protection against aqueous solutions of chromium and nickel compounds].

The purpose of the investigation was to evaluate the efficiency of two protective creams elaborated in my laboratory, devised for protection of skin exposed to aqueous solution of chromium and nickel compounds. The creams were tested by the measurement of Cr2O7(2-) and Ni2+ absorption rate through the skin in rats and excretion of these metals in urine after termination of exposure. It was found that absorption rate both ions through the skin and their excretion in urine decreased in presence of creams. However, correlation between absorption rate and excretion of these metals in urine was not found.

Animals↗
PubMed1988

Chromium in urine, serum and red blood cells in the biological monitoring of workers exposed to different chromium valency states.

Using personal air sampling exposure to hexavalent and trivalent chromium was measured in 22 workers mainly exposed to Cr(VI) and in 15 workers mainly exposed to Cr(III) as basic chromium sulphate. Determination of Cr(VI) in the urine of all the subjects using a selective technique by ETA-AAS and liquid anion exchangers failed to show detectable amounts of the hexavalent form, the detection limit of the technique being 0.05 micrograms/L. A clear relationship between exposure and postshift urinary total chromium was found in subjects exposed to Cr(VI), while urinary levels in workers exposed to chromic sulphate high concentration proved lower. Determination of total chromium in serum and red blood cells showed a significant increase of chromium levels in erythrocytes of workers exposed to Cr(VI) while in subjects mainly exposed to Cr(III) an increase of the serum fraction was observed. The results demonstrate that Cr(III) is absorbed through the respiratory tract, but its kinetics and distribution in the body are not the same as for Cr(VI), and are not adequately monitored by short-term urinary determinations. Oxidation states of chromium largely influence uptake, mechanism of absorption, transport and organ distribution as well as toxicity of chromium-containing compounds. In particular, hexavalent derivatives are known to induce adverse effects, both acute and chronic, in occupationally exposed subjects, while there is little conclusive evidence for toxic effects caused by trivalent chromium compounds. Biological monitoring of exposure to chromium(VI) has usually been performed by determining total chromium levels in urine, whereas biological monitoring data in subjects occupationally exposed to Cr(III) are still scanty.(ABSTRACT TRUNCATED AT 250 WORDS)

Chromium↗
PubMed1990

An oxygen dependence in chromium mutagenesis.

Evidence is provided that mutagenicity in Salmonella by a chromium(VI) salt and a chromium(III) compound has a differential dependence on the presence of oxygen. The mutagenic chromium(III) compound, cis-dichlorobis(2,2'-bipyridyl)chromium(III), reverted Salmonella strains, TA102 and TA2638, only under aerobic conditions. Potassium dichromate (chromium VI) required the presence of oxygen to revert the Salmonella strain TA102 but induced a moderate reversion frequency in TA2638 under anaerobic conditions. The data also support a role for oxygen radicals in chromium-mediated mutagenesis and suggests at least two pathways by which chromium compounds can induce mutations.

2,2'-Dipyridyl↗
PubMed1998

Effect of supplementation with chromium picolinate on antibody titers to 5-hydroxymethyl uracil.

Recent in vitro studies have shown that chromium (III) compounds such as chromium picolinate, a popular dietary supplement among people trying to lose weight, produce chromosome damage. We monitored levels of DNA damage in a chromium picolinate supplement trial by measuring antibodies titers to an oxidized DNA base, 5-hydroxymethyl-2'-deoxyuridine (HMdU), by enzyme-linked immunosorbent assays. Ten obese volunteer women completed a 8-week course of 400 micrograms chromium picolinate per day. In either absolute titers or percent of the baseline value, there were no changes in antibody titers at 4 or 8 weeks. The titers were very stable within individuals and those of one individual rarely crossed over others, which was reflected in an intraclass correlation coefficient of 0.99 (95% confidence interval: 0.96-1.00). There were no effects on glucose and lipid metabolism in this period. The results of this trial suggest that chromium (III) picolinate in a dose typically used for nutrient supplementation dose not increase oxidative DNA damage, as measured by anti-HMdU antibody levels.

Analysis of Variance↗
PubMed2005

Non-destructive rapid analysis discriminating between chromium(VI) and chromium(III) oxides in electrical and electronic equipment using Raman spectroscopy.

The European Union has banned chromium(VI) compounds in electrical and electronic equipment (EEE), such as chromate conversion coating films. Chromium(III) compounds are not banned. Using Raman spectroscopy without any preparation, we distinguished chromium(VI) oxide from chromium(III) oxide and chromium(III) hydroxide in chromate conversion coating films. Raman bands of chromium(VI) oxide were detected in films at around 1000 and 500 cm(-1), while chromium(III) compounds generated no bands in the region between 2000 and 200 cm(-1). The analysis took about 1 min, whereas the usual diphenylcarbazide-colorimetric method for analyzing chromium(VI) compounds takes about 10 h.

Journal Article↗
PubMed1989

Acute and chronic systemic chromium toxicity.

Although chromium and compounds containing it have been recognized as having potential severe adverse effects on health for more than 160 years, understanding of the systemic toxicology and true hazard of these compounds is still not complete. A review of the current state of knowledge is attempted in this paper, with appropriate attention given to the complications of multiple valence states and solubility. Selected chromium compounds, particularly hexavalent ones, are carcinogens, corrosives, delayed contact sensitizers, and have the kidney as their primary target organ. But chromium is also an essential element for humans. The body clearly possesses some effective detoxification mechanisms for some degree of exposure to hexavalent chrome compounds. The significant features of acute and chronic chromium toxicity are presented in view of these considerations.

Air Pollutants↗
PubMed2000

Toxicity of sodium molybdate and sodium dichromate to Daphnia magna straus evaluated in acute, chronic, and acetylcholinesterase inhibition tests.

As a result of a widespread application in numerous industrial processes, chromium is a contaminant of many environmental systems. Chromium and their compounds are toxic to both invertebrates and vertebrates and, for this reason, there has been a search for suitable and less toxic alternatives. Molybdenum compounds have been studied as alternative to chromium compounds for some industrial applications. The toxicity of chromium is well known but the effects of molybdenum and molybdenum mining on natural populations and communities of freshwater invertebrates have not often been studied. However, chromium, and molybdenum (and their compounds) are included in the same list (List II) of European Union dangerous substances. In this study, the acute and chronic effects of sodium molybdate and sodium dichromate to Daphnia magna Straus were evaluated. Furthermore, in vitro and in vivo effects of these two metals on acetylcholinesterase (AChE) activity of D. magna Straus were investigated. LC(50) values determined at 48 h were 0.29 and 2847.5 mg L(-1) for chromium (as sodium dichromate) and molybdenum (as sodium molybdate), respectively. No significant in vitro effects of both metals on AChE were found. However, both toxicants inhibited AChE in vivo at concentrations under the respective 48-h LC(50) values. Both sodium dichromate and sodium molybdate inhibited the reproduction and growth of D. magna, but the concentrations inducing significant effects were different for the two chemicals. Sodium molybdate had significant lower toxicity to D. magna Straus than sodium dichromate.

Acetylcholinesterase↗
PubMed2001

In vivo reduction of chromium (VI) and its related free radical generation.

Chromium (VI) compounds are widely recognized as human carcinogens. Extensive studies in vitro and in model systems indicate that the reactive intermediate, Cr (V), generated by cellular reduction of Cr (VI), is likely the candidate for the ultimate carcinogenic form of chromium compounds. Here we review our current understanding of the in vivo reduction of Cr (VI) and its related free radical generation. Our results demonstrate that Cr (V) is indeed generated from the reduction of Cr (VI) in vivo, and that Cr (V) thus formed can mediate the generation of free radicals. Cr (V) and its related free radicals are very likely to be involved in the mechanism of Cr (VI)-induced toxicity and carcinogenesis. These studies also illustrate that in vivo EPR spectroscopy and magnetic resonance imaging can be very useful and powerful tools for studying paramagnetic metal ions in chemical and biochemical reactions occurring in intact animals.

Animals↗
PubMed1981

Cytotoxic and clastogenic effects of soluble and insoluble compounds containing hexavalent and trivalent chromium.

Cr(III) and Cr(VI) compounds of varying solubilities have been tested in vitro for their ability to inhibit cell growth and nucleic acid and protein syntheses in BHK cells, to induce alterations in the mitotic cycle in HEp cells, and to increase the frequency of chromosomal aberrations and sister chromatid exchanges (SCE) in CHO cells. All Cr(VI) compounds, and particularly those containing soluble Cr(VI), such as potassium dichromate and zinc yellow, differentially inhibit macromolecular syntheses in BKH cells, that of DNA being always the most affected. Among Cr(III) compounds, which generally have very low cytotoxicity, chromite is particularly active, and inhibits cell growth and DNA synthesis even more than the poorly soluble Cr(VI) compounds. Preincubation in growth medium, with or without metabolizing cell cultures, solubilizes considerable amounts of Cr(VI) from zinc yellow and chromite, but significant amounts are also obtained from the most insoluble Cr(VI) pigments. When BHK cells are treated with such preincubated solutions, reduction of soluble Cr(VI) to Cr(III) by cell metabolites is seen with all Cr(VI) compounds, accompanied by decreased cytotoxicity. The same differences between Cr(VI) and Cr(III) compounds apply to the cytotoxic effects on mitosis of HEp cells and the clastogenic effects on CHO cells. The activity of chromite, the only Cr(III) pigment capable of significantly increasing the frequency of SCE, is due to contamination with soluble Cr(VI). In contrast to the very low cytotoxicity of Cr(III), much higher chromium levels are detected in the cells incubated with soluble Cr(III) than with the same concentrations of soluble Cr(VI). 50% and 75% of chromium accumulated in the cells during treatments with Cr(VI) and Cr(III) respectively remains firmly bound to the cells, even when they are incubated for up to 48 h in normal growth medium. Chromium accumulated in the cells after treatment with Cr(III) is most probably bound to the cell membrane, whereas some of the Cr(VI) is transported through the cell membrane and reduced in the cell nucleus. The results of the present investigation are in agreement with those obtained with the same Cr(VI) and Cr(III) compounds in mutagenicity assays in bacteria and carcinogenicity tests in rodents. A re-evaluation of the mechanisms of chromium carcinogenisis is proposed.

Animals↗
PubMed2004

[Occupation related thoracic tumors].

It is estimated that about 4% of cancer mortality is attributed to occupational risk factors. Due to long latency periods it is often difficult to establish causal relationships. Thoracal cancer accounts for about 88% of all compensated occupational cancers in Germany. Most important exposures and diseases are asbestos-related lung cancer, asbestos-related malignant mesothelioma and radiation induced lung cancer (by Radon and its decay products). Lung cancer caused by nickel compounds, hexavalent chromium, arsenic and its compounds, coke oven gases and polycyclic aromatic hydrocarbons are rare. Silica-dust induced lung cancer can be compensated as occupational disease if a silicosis is present. In Germany every physician is obliged to notify a suspected occupational cancer as well as other occupational diseases.

Asbestosis↗
PubMed1994

Role of paramagnetic chromium in chromium(VI)-induced damage in cultured mammalian cells.

Chromium(VI) compounds are known to be potent toxic and carcinogenic agents. Because chromium(VI) is easily taken up by cells and is subsequently reduced to chromium(III), the formation of paramagnetic chromium such as chromium(V) and chromium(III) is believed to play a role in the adverse biological effects of chromium(VI) compounds. The present report, uses electron spin resonance (ESR) spectroscopy; the importance of the role of paramagnetic chromium in chromium(VI)-induced damage in intact cultured cells is discussed, based upon our studies with antioxidants including vitamin E (alpha-tocopherol), B2 (riboflavin), C (ascorbic acid), and so on. These studies appear to confirm the participation of paramagnetic Cr such as chromium(V) and Chromium(III) in chromium(VI)-induced cellular damage.

Animals↗