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PubMedDate not supplied

Cancer mortality in a pigment plant utilizing lead and zinc chromates.

Several studies of workers exposed to various forms of chromium compounds have suggested an increased incidence of respiratory cancers. Lead and zinc chromates were among the chromium compounds implicated. The Department of Preventive Medicine and Community Health of the New Jersey Medical School undertook a detailed mortality study of a pigment plant in Newark which utilized both of these compounds. We compared observed deaths from each cause among 1296 white and 650 non-white males who were employed at the plant between January 1, 1940 and December 31, 1969, with expected deaths, as computed from cause-, age-, and time-specific standard death rates for the United States. A statistically significant relative risk of 1.6 for lung cancer among white male employees was found, as well as among the cohorts of white males employed 10 yr or more. A relative risk of 1.9 was noted for individuals employed at least 2 yr who were at least moderately exposed to chromates. An increased incidence of lung cancer among non-white males and stomach and pancreatic cancer among the total cohort was also evident. These data support the validity of the association between chromate pigment exposure and lung cancer, suggesting that pigment workers and other exposed to chromates be observed carefully in regard to possible risk or pancreatic and stomach cancers.

Black People↗
PubMedDate not supplied

[Chromosome aberrations in a lymphocyte culture from persons in contact with chromium].

A detailed analysis was carried out of chromosome aberrations induced by chromium compounds in a lymphocyte culture of persons which were in contact with the compounds. It is shown that the frequency of cells with chromosome aberrations depends on the age and duration of contact with chromium and does not depend on the sex. It was marked that hexavalent chromium compounds have a higher cytogenetic activity. Mechanisms of mutagenic action of heavy metal ions are discussed (taking chromium as an example).

Adult↗
PubMed2002

Intermolecular interactions in (arene)chromium carbonyl compounds: prediction of chiral crystal packing from racemate structure.

Six X-ray crystal structures are reported, all containing substituted triphenylmethanol derivative 4 either alone or as its mono or bis(chromium tricarbonyl) complexes. All four chromium complexes studied crystallize with two independent molecules in the crystallographic asymmetric unit. It is demonstrated that from the X-ray crystal structure of the acentric racemic (+/-)-(1pR,1' 'R)(1pS,1' 'S)-[Cr(CO)(3)(eta(6)-t-BuC(6)H(3)(CMeOMe)CPh(2)OH)], (+/-)-3, it is possible to deduce the 4-fold helical structure of the chiral (-)-(1pR,1' 'R) isomer, (-)-3. The bimetallic derivatives demonstrate the ability to control intermolecular interactions by the positioning of relative stereochemistry.

Journal Article↗
PubMed1979

The cytotoxic, mutagenic and clastogenic effects of chromium-containing compounds on mammalian cells in culture.

Examples of chromic and chromate salts have been examined for their effects on a cultured Chinese hamster cell line. The responses studied were cytotoxicity, mutagenesis and clastogenesis. Chromate (hexavalent chromium) salts of both high and medium water solubility were active in producing all three classes of response, whereas an insoluble chromate salt and a soluble chromic (trivalent chromium) salt were inactive. In addition to illustrating the value of using mammalian cells in culture for screening chemicals for biological activity, the results of this study reinforce current views regarding the genotoxic properties of chromates.

Animals↗
PubMed1977

Toxicity and mutagenicity of hexavalent chromium on Salmonella typhimurium.

Four hexavalent and two trivalent chromium compounds were tested for toxicity and mutagenicity by means of the Salmonella typhimurium/mammalian-microsome test. All hexavalent compounds yielded a complete inhibition of bacterial growth at doses of 400 to 800 mug/plate, a significant increase of his(+) revertant colonies at doses ranging from 10 to 200 mug, and no effect at doses of less than 10 mug. The distinctive sensitivity of the four Salmonella strains tested (TA1535, TA1537, TA98, and TA100) suggested that hexavalent chromium directly interacts with bacterial deoxyribonucleic acid by causing both frameshift mutations and basepair substitutions. The latter mutations, which are prevalent, are amplified by an error-prone recombinational repair of the damaged deoxyribonucleic acid. On the average, 1 mumol of hexavalent chromium yielded approximately 500 revertants of the TA100 strain, irrespective of the compound tested (sodium dichromate, calcium chromate, potassium chromate, or chromic acid). The mutagenic potency of the hexavalent metal was not enhanced by adding the microsomal fraction of rat hepatocytes, induced either with sodium barbital or with Aroclor 1254. The two trivalent compounds (chromium potassium sulfate and chromic chloride), with or without the microsomal fraction, were neither toxic nor mutagenic for the bacterial tester strains.

Chromates↗
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↗
PubMed2007

Magnetic face-to-face interaction and electrocommunication in chromium sandwich compounds.

The reaction of [{(C5Me5)CrCl2}2] with [2.2](1,4)cyclophane gave [(C5Me5)Cr{[2.2](1,4)cyclophane}] (1) and [(C5Me5)Cr{[2.2](1,4)cyclophane}Cr(C5Me5)] (2), depending on the reaction conditions. X-ray structure analysis showed 2 to be a ministack which in turn is stacked in the lattice. The chromium atoms are 6.035 A apart, and the distortion of the benzene rings to boat-shaped moieties is less pronounced than in parent [2.2](1,4)cyclophane. The NMR and EPR spectra were consistent with a S=1/2 ground state for 1 and with two interacting S=1/2 centers in 2. Spin density was found in the ligand pi systems, where its sign was negative when the pi system was adjacent to chromium, while on the nonbonded benzene moiety of 1 it was positive. Cyclic voltammograms showed reductions to 1- and 2(2-), as well as oxidations to 1+, 2+, and 2(2+) which were quasireversible, whereas oxidations to 1(2+) and 2(3+) were irreversible. Interaction between the metal ions was revealed by a 260 mV separation of the redox waves belonging to 2+, and 2(2+). Both cations were isolated as [B(C6H5)4]- salts, which in solution decomposed to [2.2](1,4)cyclophane and [(C5Me5)Cr{(eta6-C6H5)B(C6H5)3}] (3). The 1H and 13C NMR spectra of 3 were in accordance with an S=1 ground state. Solid-state magnetic measurements of the dimetallic compounds showed antiferromagnetic interaction with J=-122 cm-1 for 2, J=-31 cm-1 for 2+ (ground state S=1/2), and J=-23.5 cm-1 for 2(2+) (with H=-JS1S2). The decrease of J in the series 2, 2+, and 2(2+) was traced to the number of unpaired electrons and, for the mixed-valent cation 2+, to additional double exchange.

Journal Article↗
PubMed2005

Effect of potassium dichromate on renal brush border membrane enzymes and phosphate transport in rats.

Chromium is widely used in industry but exposure to chromium compounds in the workplace can result in nephrotoxicity. Various nephrotoxicants affect the brush border membrane (BBM) lining the epithelial cells of the proximal tubule, but there have been no studies regarding the effect of potassium dichromate (K2Cr2O7), a hexavalent chromium compound, on renal BBM. In the present work, the effect of administering a single intraperitoneal dose (15 mg/kg body weight) of K2Cr2O7 on rat renal BBM enzymes and inorganic phosphate (Pi) transport was studied. The animals were administered normal saline (control) or K2Cr2O7 and sacrificed 1, 2, 4 and 8 days after treatment. K2Cr2O7 induced reversible damage to the rat kidney function as indicated by serum creatinine (Scr) and urea nitrogen levels. The activities of BBM marker enzymes were significantly decreased in isolated BBM vesicles (BBMV) and homogenates of cortex and medulla on 1, 2 and 4 days after administration of K2Cr2O7 with complete recovery to control values after 8 days. The decrease in the activities of the enzymes was mainly due to changes in maximum velocity (V(max)) values, while the Michaelis constant (Km) remained unchanged. The sodium dependent Pi transport across BBMV was reduced by 50% after treatment with K2Cr2O7. Thus, the administration of a single dose of K2Cr2O7 leads to impairment in the functions of renal BBM. These results suggest that the nephrotoxicity of K2Cr2O7 may be mediated, at least in part, by its effect on renal BBM.

Animals↗
PubMed1988

Chromium carcinogenicity; a review of experimental animal data.

Since 1932 exposure to various hexavalent chromium compounds has been known to constitute a cancer hazard to industrial workers. A number of animal studies have been performed and chromates have been administered by inhalation, intratracheally, by intravenous and subcutaneous injection, intraperitoneally and orally. The human epidemiological studies have provided convincing evidence that zinc chromate is a potent carcinogen and there is some evidence that calcium chromate and chromium trioxide also constitute a cancer hazard in humans. The human studies have not selectively confirmed carcinogenic potency for other chromium compounds. The animal studies confirm the carcinogenic potency of calcium chromate and zinc potassium chromate and present strong evidence that chromates of lead and strontium are carcinogenic in animals. The significance of the water solubility for the carcinogenic potency of the chromates has not been clarified by animal studies.

Animals↗
PubMed1987

Alveolar macrophage abnormalities in rabbits exposed to low concentrations of trivalent chromium.

Rabbits were exposed by inhalation to a trivalent chromium compound (Cr(NO3)3) at a mean chromium concentration of 0.6 or 2.3 mg/m3 for about 4 months, 5 days/week and 6 hr/day. Light microscopic examination of the lungs revealed that both chromium levels induced a nodular intraalveolar accumulation of enlarged macrophages with granular, eosinophilic cytoplasm. Some macrophages were multinucleated and some showed advanced degenerative changes with disruption of cellular borders and nuclear pyknosis. The changes were most prominent in rabbits exposed to the high concentration and were in some areas associated with a mild interstitial infiltration of lymphocytes, neutrophils, and eosinophils. Electron microscopic examination of macrophages lavaged from the lungs revealed numerous enlarged lysosomes with membranous structures, distinct rounded inclusions, which by X-ray microanalysis were found to contain high amounts of chromium, and increased numbers of laminated inclusions probably representing ingested surfactant. The number of macrophages with a smooth surface was significantly increased. The macrophages in the lung tissue showed the same changes and in addition nodules of multinucleated "giant" cells were found. Morphometric estimation of the volume density of the type II cells did not reveal any significant differences between controls and rabbits exposed to the high concentration of chromium. In spite of the elevated number of laminated structures in the macrophages the amounts of phosphatidylcholine and 1,2-dipalmitoylphosphatidylcholine were not significantly increased in the lung. This indicates a reduced catabolism of surfactant by the alveolar macrophages.

Animals↗
PubMed1978

Cytotoxic effects of hexavalent and trivalent chromium on mammalian cells in vitro.

The cytotoxic effects of hexavalent (k(2)Cr(2)O(7)) and trivalent (CrCl(3)) chromium compounds have been studied in cultured hamster fibroblasts (BHK line) and human epithelial-like cells (HEp line).K(2)Cr(2)O(7) stimulates the uptake of labelled thymidine into the soluble intracellular pool (the stimulation of nucleoside uptake represents a specific effect of Cr(6+)) while Cr(3+) always exerts an inhibitory action. DNA Synthesis is inhibited by treatment with both chromium compounds, but especially by K(2)Cr(2)O(7). Moreover, the effective CrCl(3) concentrations reduce the sensitivity of DNA and RNA to hydrolysis with perchloric acid. Treatments with k(2)Cr(2)O(7) in balanced salt solution, where Cr(6+) reduction is less marked, induce more pronounced cytotoxic effects than treatments in complete growth medium.HEp cells turned out to be more sensitive to K(2)Cr(2)O(7) than BHK fibroblasts: in the former line TdR uptake is less stimulated, DNA synthesis and cell survival are more affected. Survival of BHK cells to K(2)Cr(2)O(7) indicates a multi-hit mechanism of cell inactivation, the extrapolation number being about 10.On the basis of quantitative Cr determinations in the treatment solutions and in the treated cells, the cytotoxic effects of Cr are attributed to the action of Cr(6+) at the plasma membrane level on the mechanisms involved in nucleoside uptake, and to the interaction of Cr(3+) at the intracellular level with nucleophilic targets on the DNA molecule.

Cell Survival↗
PubMed1977

Chromosomal aberrations and morphological transformation in hamster embryonic cells treated with potassium dichromate in vitro.

The addition of K2Cr2O7, at concentrations ranging from 0.1 to 0.5 microng/ml, to hamster total embryonic cells for 24 h, resulted in consistent and drastic chromosomal aberrations including gaps, breaks and exchanges. The above effect, however, was reduced successfully by the addition of a reducing agent, Na2SO3. Among other chromium compounds examined, divalent and trivalent chromium salts were ineffective on chromosome morphology even at a concentration of 3.5 microng/ml as chromium, whereas a hexavalent compound, CrO3, was highly effective. K2Cr2O7 also enhanced the morphological transformation rate in a short-term colony assay, in whicy hamster embryonic cells (1x10(4) cells/60-mm dish) were treated and the morphology was observed 8 to 10 days after the treatment.

Animals↗
PubMedDate not supplied

Effects of pyridinium chlorochromate adulterant (urine luck) on testing for drugs of abuse and a method for quantitative detection of chromium (VI) in urine.

Pyridinium chlorochromate (PCC) as an adulterant is popular for concealing drug-positive results. When 11-nor-delta9-THC-9-carboxylic acid (THC-acid) in urine was treated with 2 mmol/L of PCC (Cr6+ 104 microg/mL), 58-100% of the THC-acid was lost. The loss increased with decreasing pH and increasing reaction time (0-3 days). Free codeine and free morphine remained unaffected by PCC at pH within the physiological range of the urine (pH 5-7). At lower pH, the loss of free morphine varied from 0 to 100%. Amphetamine, methamphetamine, benzoylecgonine, and PCP remained unaffected by PCC when exposed to the oxidant for three days in urine pH of 3-7. Chromium (VI) from PCC in a urine solution was detected by a color reaction with 1,5-diphenylcarbazide (DPC). When the reagent was added to the urine, an immediate red-violet color appeared. The chromium-DPC complex showed a characteristic absorption peak at wavelength 544 nm with a shoulder at wavelength 575 nm. The ratio of absorption was used to identify the chromium compound. The concentration of chromium (VI) was determined by measuring absorption at wavelength 544 nm and was linear over 0.5-20 microg/mL. The limit of detection of the procedure was 0.37 microg/mL.

Anti-Infective Agents↗
PubMed1980

Cancer mortality among workers exposed to zinc chromate paints.

To evaluate the carcinogenicity of chromium compounds among user industries, the proportionate mortality experience of spray painters exposed to zinc chromate primer paints and electroplaters exposed to chromic acid in the aircraft maintenance industry was examined. Compared to the mortality patterns of U.S. white males, no excess of cancer was found in the 48 deaths among electroplaters. Analysis of the 202 deaths among spray painters revealed a significant excess of cancer, primarily of the respiratory tract. The relative increase of respiratory cancer showed a positive gradient with the length of estimated exposure time, and was confined to painters whose interval from first employment to death was at least 20 years. The findings consistent with occupational exposure to chromium compounds, previously shown to be carcinogenic in manufacturing processes, but the effect of other paint constituents, tobacco smoking, or methodologic limitations could not be discounted.

Adult↗
PubMed1995

Insulin-like action of chromate on glucose transport in isolated rat adipocytes.

The effects of chromium compounds on 3-O-methylglucose (3-O-MG) transport were studied in isolated rat adipocytes. Sodium chromate significantly stimulated 3-O-MG uptake into adipocytes in a dose-dependent manner without altering the equilibrium space of 3-O-MG in adipocytes. The stimulatory effect reached the maximum at 300 microM, and the effect was 60-70% of the maximal insulin effect that was obtained with 20 nM insulin. The chromate concentration achieving a half-maximal effect was estimated at 50 microM. The effect of the combination of 1 mM chromate and 20 nM insulin was equipotent to that of 20 nM insulin alone, which showed that these two effects were not additive. The stimulatory effects of 1 mM chromate and 20 nM insulin were entirely abolished in adipocytes deprived of ATP, which indicated that these effects were completely ATP-dependent. Judging from experiments using various chromium compounds, CrO4(2-) was responsible for the insulinomimetic action. These results indicate that the action of CrO4(2-) is exerted through a mechanism analogous to that of insulin action, and that CrO4(2-) is a novel and useful tool for studying issues involved in insulin actions.

3-O-Methylglucose↗
PubMed1984

Toxicity of hexavalent chromium to the alveolar macrophage in vivo and in vitro.

In vivo and in vitro systems were used to evaluate hexavalent chromium toxicity to alveolar macrophages. Rat alveolar macrophages were exposed to 2 micrograms calcium chromate (CaCrO4, insoluble) or 2 micrograms chromium trioxide (CrO3, soluble) in live animals, in vivo, and in tissue culture, in vitro, collected by lavage from the lung. Chemiluminescence and oxygen consumption were measured as indicators of toxicity. Trypan blue dye exclusion was used to determine macrophage viability. In vivo exposure of the macrophage to either chromium compound showed no toxic effects at a 2-micrograms dose. Macrophages exposed in tissue culture, however, had values significantly different from controls. The untreated controls for both exposure methods were compared to evaluate differences resulting from methods alone.

Animals↗
PubMed1994

Chromium-induced early changes in renal function among ferrochromium-producing workers.

Urinary biochemical indicators of renal injury were examined in 84 male and 38 female ferrochromium-producing workers exposed to water-soluble chromium compounds [Cr(VI)]. The indicators examined included urinary chromium (U-Cr), alkaline phosphatase (ALP), gamma-glutamyl transferase (gamma-GT), glutamic-oxalacetic and glutamic-pyruvic transaminases (GOT & GPT), lactate dehydrogenase (LDH), N-acetyl-beta-D-glucosaminidase (NAG), total protein (TPr) and beta 2-microglobulin (beta 2-MG). The U-Cr levels in the exposed group were approximately 1.8 times that of the control group. Compared to controls, the activities of gamma-GT, NAG, ALP, GOT and LDH in the urine of workers were significantly increased whenever U-Cr concentration exceeded 45 microgram/g creatinine. The activities of gamma-GT, GOT and NAG were elevated in workers employed for longer than ten years. However, no clear dose-response relationships nor time-effect relationships were found. The present results suggest that long-term exposure to water-soluble chromium [Cr(VI)] produces chronic renal injury. The site of the injury appears to mainly involve the proximal tubule. U-Cr concentrations of > 15 microgram/g creatinine can be proposed as a threshold dosage for nephrotoxicity, and gamma-GT, NAG and ALP are early sensitive indicators of the most valuable for evaluating the renal injury.

Acetylglucosaminidase↗