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At least 19 recordsLinked to original sources
PubMed1991

[Exposure to chromium compounds during processing of chromium iron ore].

The work verifies data gathered by Occupational Hygiene departments of Sanitary-Epidemiological Stations about workers exposure to chromium compounds in the processing of chrome iron ore. Research showed that 7 plants were involved in the processing of chrome iron ore and that the number of workers directly employed in the process amounted to 215-230. About 150 workers were exposed to high concentrations of chromium compounds which exceeded hygienic standards. All of them were employed only in metallurgical plants. The remaining 80-100 workers subjected to the study exposed to relatively low chromium concentrations were employed in chemical plants and refractory materials plants.

Air Pollutants, Occupational↗
PubMed1983

Lymphocyte stimulation by trivalent and hexavalent chromium compounds in patients with chromium sensitivity. An aid to diagnosis.

Peripheral blood lymphocytes from 31 patients with a positive patch test to potassium dichromate (K2Cr2O7) and from 24 healthy controls were stimulated with various concentrations of chromium chloride (CrCl3) and/or chromium basic sulphate (Cr4(SO4)5(OH)2), sodium chromate (Na2CrO4) or K2Cr2O7 on various days of culture. Both trivalent and hexavalent chromium compounds could induce lymphocyte transformation, as measured by increased DNA synthesis. The response occurred in the T-enriched population and was monocyte dependent. Lymphocytes from 11 of these patients could not be stimulated with the chromium compounds in vitro, whereas the in vivo serial dilution test (SDT) was positive in 4 and negative in 7 of them. Lymphocytes from 2 patients with a negative in vivo SDT showed a positive response in vitro. The strength of the in vivo SDT results did not correlate well with the height of in vitro responses. The DNA synthesis test seems to be a reliable in vitro method to aid in the diagnosis of chromium sensitivity.

Adult↗
PubMed1986

Induction of SOS genes of Escherichia coli by chromium compounds.

The induction of several SOS genes of Escherichia coli such as recA, umuC, and sfiA by hexavalent (K2Cr2O7, K2CrO4, and CrO3) and trivalent (CrCl3, Cr(NO3)3, and (CH3COO)3Cr) compounds of chromium was studied. Induction was measured as beta-galactosidase activity, using lacZ gene fusions under the control region of different SOS genes. The hexavalent chromium forms induced the genes responsible for massive synthesis of RecA protein, error-prone repair, and inhibition of cell division. On the other hand, the trivalent chromium compounds were unable to induce any of the SOS genes tested. Individual assay of hexavalent chromium compounds showed that K2Cr2O7 was a stronger inducing agent of those three SOS genes tested than K2CrO4, which, in turn, was stronger than CrO3. All this data led to the conclusion that hexavalent chromium compounds, but not trivalent, are proficient agents of induction of the SOS system and can produce indirect mutagenesis in Escherichia coli.

Cell Division↗
PubMed1996

[Molecular effects of chromium compound activity].

Chromium(VI) compounds produce a variety of DNA damage such as DNA single strand breaks, alkali-labile sites and DNA-protein cross-links in vivo and in cultured cells. Chromium(III) compounds bound to isolated DNA and proteins. Cr(VI) readily entered cell through general anion channels. In contrast, Cr(III) did not readily cross cell membranes. Inside cells Cr(VI) is reduced through intermediates to Cr(III) by cellular reductants. Reactive intermediates formed during intracellular Cr(VI) reduction might be responsible for some chromate genotoxicity. Ascorbic acid decreases chromate induced alkali-labile sites and chromium inhibition of glutathione reductase, but it enhances DNA-protein cross-links and cytotoxicity caused by this metal.

Animals↗
PubMed1999

Thirteen-week subchronic rat inhalation toxicity study with a recovery phase of trivalent chromium compounds, chromic oxide, and basic chromium sulfate.

The toxicity of trivalent chromium compounds; chromic oxide and basic chromium sulfate, was investigated in rats in a 13-week nose-only inhalation study that included a 13-week recovery period. Nose-only exposures to insoluble chromic oxide dust at 4.4, 15, or 44 mg/m3 or soluble basic chromium sulfate dust at 17, 54, or 168 mg/m3 (trivalent chromium equivalent concentrations of 3, 10, and 30 mg/m3) were carried out for 6 h/day, 5 days/week. No compound-related mortality occurred. General toxic effects, only observed with high-exposure levels of basic chromium sulfate, included sporadic signs of labored breathing and depressed body weights. No apparent compound-related effects were noted for sperm motility or morphology, for any concentration of either test material. Bronchoalveolar lavage fluid evaluations showed test material in mononuclear cells with chromic oxide and increased neutrophils, protein, lactic dehydrogenase and cellular debris with basic chromium sulfate. The principle effects for both materials were primarily to the respiratory tract. Chromic oxide caused pathological changes in the bronchial and mediastinal lymphatic tissue and lungs, consisting of the presence of pigment-laden macrophages, lymphoid and septal hyperplasia, and interstitial inflammation similar to that observed with other inert dusts. Basic chromium sulfate produced more severe and widespread effects in the nasal cavity, larynx, lungs, and mediastinal lymph node. Effects were characterized by accumulation of foreign material, infiltration of alveolar macrophages, septal cell hyperplasia, and granulomatous and chronic inflammation. Pigment was still present in chromic oxide and, to a lesser extent, in basic chromium sulfate-treated animals after the 13-week recovery period, with partial recovery of the pathological lesions. A NOAEL was not established for either test material, but 4.4 mg/m3 was thought to be near the NOAEL level for subchronic exposure to chromic oxide. The results of this study indicate significant differences in toxicity to the respiratory tract between trivalent chromium compounds chromic oxide and basic chromium sulfate. These are likely related to differences in acidity and water solubility, rather than chromium concentration per se. This conclusion is substantiated by the lack of effect on other internal organs.

Administration, Inhalation↗
PubMed1983

[Effects of chromium compounds on the respiratory system. 2. Difference between water-soluble hexavalent and trivalent compounds].

Transference and transformation of chromium compounds, known as occupational carcinogens, in the lung of rats were studied by determining blood chromium levels after a single mist inhalation or an intravenous injection of water-soluble chromic acid (hexavalent) and chromium chloride (trivalent). Conclusion drawn from this study are as follows: Transference of chromium from the lung to the blood stream is ended quickly after the inhalation of chromic acid mist. Alveolar permeability of hexavalent chromic acid is much higher than that of trivalent chromium chloride. The greater part of the transferred chromium in the blood after the inhalation of chromic acid mist is not transformed to any other form; therefore, it seems to be present as the hexavalent form. The hexavalent chromic acid in the blood diffused to the liver, kidneys and the spleen, but the trivalent chromium chloride distributed only in the blood. The hexavalent chromic acid in the blood decreased more slowly than the trivalent chromium chloride. The biological half-time of the chromic acid in the blood was about 60 hours, whereas that of the chromium chloride was only about 2 hours. These results suggest that the water-soluble hexavalent chromium compounds may be apparently different from the trivalent chromium compounds in the transference from the lung and following distribution in the body. These differences might be caused by the high permeability through the cell membrane in hexavalent chromium compounds and the high possibility of binding with proteins in trivalent chromium compounds.

Aerosols↗
PubMed2006

[Studies on the nephrotoxicity of chromium compounds].

The toxicity of chromium in different valent are quite different. Cr (III) is a necessary trace element of human body, but excessive intake of Cr (III) may bring about health lesion. Cr (VI) is generally considered 1,000 times more toxic than Cr (III). Renal damge may happen when people contact or intake excessive chromium compounds. The renal function and the concentration of enzyme and protein may be changed. Kidney necrosis can happen in heavy cases. The metaboly of chromium compounds and its nephrotoxicity were reviewed in this paper.

Animals↗
PubMed1998

Sexual maturation and fertility of male and female mice exposed prenatally and postnatally to trivalent and hexavalent chromium compounds.

The reproductive toxicity of trivalent and hexavalent chromium compounds was investigated in male and female mice exposed to 1000 ppm chromium chloride and potassium dichromate via their mother during gestational and lactational periods. Fertility was reduced in male offspring exposed to either trivalent or hexavalent chromium compounds. Body weights and weights of testes, seminal vesicles and preputial glands were reduced in trivalent-exposed male offspring. The exposure of female mice offspring to trivalent and hexavalent chromium compounds delayed sexual maturation. Fertility was reduced in female offspring exposed to either trivalent or hexavalent chromium compounds. The exposure of female mice to hexavalent chromium compound reduced the number of implantations and viable fetuses respectively. Body weight and weights of ovaries and uteri were reduced in trivalent-exposed female offspring. The results indicate that under our experimental conditions, the exposure of male and female mice offspring to either trivalent or hexavalent chromium compounds during gestational and lactational periods impair reproductive functions and fertility in adulthood.

Animals↗
PubMed1997

Long-term exposure of male and female mice to trivalent and hexavalent chromium compounds: effect on fertility.

Sexually mature male and female mice at 50 days of age were exposed to trivalent (Chromium chloride) or hexavalent (potassium dichromate) chromium compounds in drinking water for 12 weeks. The effects of the direct chromium exposure on fertility was assessed at day 140 of age. Fertility was significantly reduced in males exposed to the trivalent chromium compound. The number of implantation sites and the number of viable fetuses was significantly reduced in females impregnated by males exposed to the hexavalent chromium compound. The number of resorptions and dead fetuses was increased in females impregnated by males exposed to trivalent and hexavalent chromium compounds. The exposure of female mice to trivalent and hexavalent chromium compounds significantly reduced the number of implantation sites and the number of viable fetuses. The number of females with resorptions was significantly increased in hexavalent chromium exposed females. The number of resorptions was increased in trivalent and hexavalent exposed females. Body, seminal vesicles and preputial gland weights were significantly reduced in males exposed to trivalent and hexavalent chromium, whereas testes weight was significantly increased in males exposed to these compounds. Furthermore, ovarian weight was significantly increased in females exposed to trivalent and hexavalent chromium, whereas uterine weight was significantly decreased in trivalent chromium exposed females. In conclusion, the ingestion of trivalent and hexavalent chromium compounds by adult male and female mice would cause adverse effects on fertility and reproduction.

Animals↗
PubMed1998

Investigations on the nephrotoxicity and hepatotoxicity of trivalent and hexavalent chromium compounds.

In contrast to trivalent chromium (Cr(III)) compounds, hexavalent chromium ((Cr(VI)) compounds are oxidizing agents capable of directly inducing tissue damage and possessing carcinogenic, mutagenic and teratogenic potency. After oral or dermal absorption of Cr(VI), the kidney is the main target organ for chromium accumulation, which might result in acute tubular necrosis in humans. In contrast, an acute toxic effect of Cr(VI) on the liver has not yet been described. Therefore, we used two established epithelial cell lines from the kidney (Opossum kidney cells) and the liver (Hep G2 cells) to design an in vitro-assay which is able to examine acute toxic effects of chromium compounds. Cells of both cell lines were treated with various concentrations of Cr(III) and Cr(VI) ranging from 0.01 micromol/l to 1 mmol/l for 24 h. Thereafter, cell morphology, organization of the intracellular cytoskeleton, number of viable cells and mean cell volume were examined. The results show that Cr(VI), but not Cr(III), has an acute cytotoxic effect and causes a dose-dependent loss in cell viability. The effective dose that caused 50% of cell death was 5 micromol/l for kidney epithelial cells and 50 micromol/l for liver epithelial cells. This means that kidney epithelial cells are 10 times more sensitive towards Cr(VI) treatment than liver epithelial cells and this might explain the known nephrotoxicity in vivo. The loss in cell viability was accompanied by a rounding and detachment of the cells and a marked reduction of intracellular F-actin-containing stress fibers. Microtubules and intermediate-sized filaments were observed to be unaffected. Only in the case of kidney epithelial cells, a dose-dependent cell volume increase was observed after Cr(VI) treatment at concentrations up to 50 micromol/l. At higher concentrations, the cell volume decreased due to the high number of cells undergoing lysis and the appearance of cellular fragments. Various chloride channel blockers with different specificities, molecular structures and inhibitory potentials were tested for their ability to prevent Cr(VI)-induced cell damage. None of the channel blockers was able to inhibit cell damage, suggesting that the uptake of Cr(VI) through the general anion transport system of the cell membrane might be only one facet of cellular uptake and toxification. The data presented here not only confirm the different organ-specific effects of Cr(III) and Cr(VI), but also provide a basis for future experiments on the understanding of acute toxicity of Cr(VI) compounds. Moreover, the results demonstrate that the designed in vitro-assay might be a useful tool to prove whether non-toxic Cr(III) can be oxidized to Cr(VI) under specific industrial conditions (for example, in the leather or chrome industry).

Animals↗
PubMed1997

Effects of different chromium compounds on blood pressure and lipid peroxidation in spontaneously hypertensive rats.

In a previous study, we found that oral chromium nicotinate overcame sucrose-induced hypertension in spontaneously hypertensive rats (SHR). Accordingly, we examined more chromium compounds to determine if others were more or less effective in regulating blood pressure (BP) of SHR. Since chromium is postulated to be an antioxidant, we also assessed the ability of different chromium compounds to alter free radical formation measured by determining thiobarbituric acid reactive substances (TBARS). The control group of SHR ingested a diet low in chromium, and 5 other groups ate the same diet with various chromium compounds added at 5 ppm-chloride, acetate, nicotinic acid-glycine-cysteine-glutamic acid (NA-AA), picolinate, and nicotinate. Following this, the rats were challenged with drinking water containing 5% and 10% w/v sucrose. Except for NA-AA, all chromium compounds inhibited the sucrose-induced elevation of systolic BP; and acetate, picolinate, and nicotinate chromium compounds lowered HbAIC below control. Only chromium acetate and nicotinate significantly lowered both hepatic and renal TBARS. Chromium picolinate lowered hepatic TBARS, and chromium chloride and NA-AA lowered neither. We conclude that chromium, rather than a specific ligand, plays a major role in ameliorating sucrose-induced BP elevations and can act as an antioxidant.

Animals↗
PubMed2006

Toxicity and carcinogenicity of chromium compounds in humans.

Chromium is a human carcinogen primarily by inhalation exposure in occupational settings. Although lung cancer has been established as a consequence of hexavalent chromium exposure in smokers and nonsmokers, some cancers of other tissues of the gastrointestinal and central nervous systems have also been noted. Except for a few reports from China, little is known about the health risks of environmental exposures to chromium. Likewise, there has been a lack of epidemiological studies of human exposure to hexavalent Cr by drinking water or ingestion, and it has been suggested that humans can perhaps tolerate hexavalent Cr at higher levels than the current drinking water standard of 50 ppb. This review highlights the most recent data on the induction of skin tumors in mice by chronic drinking-water exposure to hexavalent chromium in combination with solar ultraviolet light. This experimental system represents an important new animal model for chromate-induced cancers by ingestion of drinking water, and it suggests by extrapolation that chromate can likely be considered a human carcinogen by ingestion as well. The potential use of this animal model for future risk assessment is discussed.

Animals↗
PubMed1980

Metabolic fate of chromium compounds. I. Comparative behavior of chromium in rat administered with Na251CrO4 and 51CrCl3.

Comparative metabolic fate of labelled chromium chloride and sodium chromate and interaction of these compounds in the rat liver and blood were investigated after their oral and intravenous administration. Gastrointestinal absorption of both compounds was below 1% of the oral dose, but trivalent chromium showed higher radioactivity than the hexavalent form in rats (biological half-life: CrCl3 91.79 days, Na2CrO4 22.24 days). The higher residual activity of the trivalent chromium was also observed after intravenous administration. Both forms of chromium were excreted more in the urine via the kidney than in the intestinal tract after intravenous administration. When 51CrCl3 and Na251CrO4 were injected into rats, in the time-distribution patterns of 51Cr in the organs, a significant difference was shown between oxidation states of the two compounds, especially in subcellular fractions of the liver and blood constituents. This significant difference mainly observed in the rat blood came from the fact that trivalent chromium possessed a high binding activity for transferrin in plasma, while hexavalent chromium was permeable into red cells and bound with hemoglobin.

Animals↗
PubMed2003

Environmental evaluation of different variants of the chromium compound production model using chromic waste.

This work presents research results on the evaluation of environmental effects of utilizing chromic waste in chromium compound production processes. The comprehensive evaluation of three chromium compound production models takes into consideration the total cumulated hazard coefficients. The implementation of the new chromium compound production model into industrial practice in 1999 allows the hazard to the natural environment to decrease by 75% in relation to the hazard caused by the old production model used until 1995. The coefficient of the target chromium compound production model was 199%, much higher than 100%. This results from the negative values of the total cumulated hazard coefficients for those cases where the sodium chromate production unit could be a big "consumer" of chromic waste.

Chromium↗
PubMed1995

Physico-chemical fate of chromium compounds in the sheep lung model.

Transmission electron microscopy (TEM) equipped with energy-dispersive x-ray analysis (EDX), electron spectroscopy for chemical analysis (ESCA), secondary ion mass spectrometry (SIMS), and laser microprobe for mass analysis (LAMMA) were used to follow the fate of chromium compounds deposited in the sheep tracheal lobe. Four chromium compounds were used: two chromium(VI) compounds (lead chromate and chromium trioxide) and two chromium(III) compounds (chronic oxide and chromium sulfate). Chromium trioxide is very soluble and the other three are slightly soluble. The compositions, concentrations, and sizes of particles were determined in the bronchoalveolar lavages (BAL) at d 2, 3, 5, and 30 after instillation and on the lung samples collected at d 31. The concentrations of particles in the BAL samples separated the chromium compounds in two groups where Cr2O3 and PbCrO4 (as Pb) were higher than Cr2(SO4)3, PbCrO4 (as Cr), and CrO3. The half-life for alveolar clearance of Cr2O3 and Cr2(SO4)3 has been calculated respectively at 11 and 80 d. Prismatic PbCrO4 particles break up in the lung and sustain a high concentration of isometric particles of lead chromate and another lead-containing compound in the BAL. The CrO3 instilled particles react with endogenous compounds or are transformed to insoluble hydroxyl complexes instead of diffusing very rapidly through the alveolar-capillary barrier. The alveolar clearance as measured in the BAL is not different from the control.

Animals↗
PubMedDate not supplied

[Reparative DNA synthesis in the lymphocytes of persons coming in contact with chromium compounds in industry].

The intensity of repair DNA synthesis in the lymphocytes of persons who were in contact with chromium compounds was studied depending on the contact duration. It is discovered that the intensity of repair DNA synthesis is reduced with the increase of the contact duration with chromium compounds. It is suggested that the mutagenic effect of chromium compounds is connected with the influence on the repair DNA synthesis in human cells.

Cells, Cultured↗