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PubMed1982

The casting accuracy of nickel--chromium alloys for fixed prostheses.

The casting accuracy of four nickel--chromium alloys (Ultratek, Omega, Microbond N/P2, and Nobil-Ceram) was compared to that of a precious alloy, Jelenko "O". The experiment consisted of fabricating and fitting cast copings to a cobalt--chromium test preparation of a maxillary central incisor and measuring the marginal discrepancy in eight selected points. The experiment indicated that Jelenko "O" had the greatest casting accuracy, followed successively by Ultratek, Nobil-Ceram, Microbond N/P2, and Omega. Statistical analysis of the data revealed no significant difference between Jelenko "O" and Ultratek alloys in fit of five of eight test points, but Jelenko "O" was significantly better in fit than Nobil-Ceram, Microbond N/P2, and Omega alloys. The following conclusions may be drawn from this experiment: 1. The nickel--chromium alloys tested did not cast as consistently or as accurately as precious alloy Jelenko "O". 2. The casting accuracy may be related to the amount of casting shrinkage that occurs in each alloy type, and further research is necessary to determine if expansion compensation of the selected phosphate-bonded investment recommended by the alloy manufacturers is adequate for the casting shrinkage of the test alloys. 3. Alloy composition and technique parameters may also influence the accuracy of the casting, but further research is necessary to determine their singular effects.

Chemical Phenomena↗
PubMed1990

Properties of cobalt-chromium metal ceramic alloys after heat treatment.

A comparison of mechanical properties of seven metal ceramic alloys in as-cast and heat-treated conditions resulted in significant differences. The alloys that were tested included seven cobalt-chromium metal ceramic alloys. Mechanical properties include strength, elongation, modulus of elasticity, and microhardness. Twenty-four tensile bars were cast for each alloy. Twelve of the 24 bars for each alloy were randomly selected for heat treatment with the Ceramco technique. Results indicated that the tested alloys had similar mechanical property values as a group in both the as-cast and the heat-treated conditions. The heat treatment had little effect on the cobalt-chromium alloys, although several did become significantly harder. In either condition, the cobalt-chromium alloys showed a high value of strength, a low percent of elongation, a high modulus of elasticity, and a high value of hardness. The high value of hardness and the low percent of elongation would make these alloys difficult to handle clinically.

Analysis of Variance↗
PubMed1987

Evidence for synergism between chromium and nicotinic acid in the control of glucose tolerance in elderly humans.

Impaired glucose tolerance results from Cr restriction in animals, and Cr supplementation improves glucose tolerance in diabetic animals. These effects are presumably due to the role of Cr in glucose tolerance factor (GTF), a complex of Cr and nicotinic acid believed to facilitate insulin binding. Humans, however, do not uniformly respond to Cr supplementation. The present study was designed to evaluate the possibility that the failure results from inadequate levels of dietary nicotinic acid to serve as substrate for GTF synthesis. Sixteen healthy elderly volunteers were divided into three groups and given either 200 micrograms Cr, 100 mg nicotinic acid, or 200 micrograms Cr + 100 mg nicotinic acid daily for 28 days and evaluated on days 0 and 28. Fasting glucose and glucose tolerance were unaffected by either chromium or nicotinic acid alone. In contrast, the combined chromium-nicotinic acid supplement caused a 15% decrease in a glucose area integrated total (p less than .025) and a 7% decrease in fasting glucose. None of the treatments exerted any effect on fasting or one-hour insulin levels. Thus, these data suggest that the inability to respond to chromium supplementation may result from suboptimal levels of dietary nicotinic acid.

Aged↗
PubMed1984

Chromium, cobalt and lanthanum in lung, liver and kidney tissue from deceased smelter workers.

Lung, liver and kidney tissue concentrations of chromium, cobalt and lanthanum from 66 deceased copper smelter workers have been compared with 14 controls. Samples were taken in connection with ordinary autopsies at the local hospital. Neutron activation analysis was used. The mean exposure time for the smelter workers was 30 y, the mean time to date of death after termination of exposure was 7.4 y. A four-fold increase of chromium (p = 0.001) and a two-fold increase of cobalt (p less than 0.001) and lanthanum (p = 0.013) in lung tissue was found for smelter workers compared to controls. Of the smelters nearly one third died from malignancies (approximately 10% from respiratory cancer) and approximately 45% from cardiovascular disease. In the control group nearly 80% died from cardiovascular diseases and no malignancies were found. In lung tissues the concentration of chromium, cobalt and lanthanum did not decline with time after exposure had ended, indicating a long biological half-time. The causes of death could not be related to a single factor. The findings indicate a multifactorial genesis.

Aged↗
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↗
PubMed1988

Selected toxicological aspects of chromium(VI) compounds.

Chromium(III) is thought to be an essential element in mammals, its toxicity being very low. On the contrary, chromium (VI) is highly toxic to man, even if its effects are generally local, involving the respiratory tract and the skin. Once absorbed, chromium(VI) is quickly reduced to the trivalent form which accounts for all of this element present in the blood stream or taken up by tissues. As a result, any differences in systemic toxicity can only be attributed to differential solubilities and absorption rates. The kidney should be regarded as the critical organ, although tubular damage following occupational exposure is mostly due to acute absorption and transient in nature. Sensitive immunochemical techniques for the measurement of specific proteins in the urine have been used for the early detection of kidney damage, a possible threshold having been indicated at exposure levels yielding 15 micrograms/g creatinine in urine. Such a threshold has been confirmed by using monoclonal antibodies to reveal antigens from the brush-border of proximal tubules. Two main features of kidney damage were, however, apparent. The first one is the lack of dose-effect/response relationships, i.e. the lack of any progression toward more severe impairments when the exposure intensity increases. The second one is that the recent absorption rate more than the cumulated dose is responsible for the observed nephrotoxic effects.

Albuminuria↗
PubMed1988

Seasonal variation of thallium, lead, and chromium concentrations in airborne particulate matter collected in an urban area.

In November 1985 a research program started, with the aim to evaluate seasonal variations in the concentrations of organic and inorganic pollutants in the atmosphere of Genoa. The program provided for the collection of samples of airborne particulate in five different areas with distinct urban characteristics. First results for chromium, lead, and thallium concentrations in an industrial and in an urban area are reported. Lead showed the highest concentration at both locations (geometric mean: 1.037 and 0.476 microgram/m3, respectively) and appeared to be little affected by seasonal variation. Private traffic was confirmed as the main source of this pollutant. Chromium and thallium geometric mean concentrations were 0.006 and 0.014 microgram/m3 in site A and 0.017 and 0.015 microgram/m3 in site B, respectively. In the urban location a good negative linear correlation was found between chromium and thallium concentration and mean ambient temperature; the domestic heating plants were suspected as important emission sources of these two compounds.

Air Pollutants↗
PubMed1989

Role of epidemiologic studies in evaluating the carcinogenicity of chromium compounds.

Epidemiologic and animal studies have identified intermediately-soluble chromates as human carcinogens. Epidemiologic studies also provide moderately strong evidence to conclude that chromates do not cause cancer at sites other than the respiratory tract. This information, combined with the evidence from animal studies and in vitro experiments, has led to the conclusion that chromates do not present a carcinogenic risk from ingestion. Unfortunately, epidemiologic studies have not provided definitive answers to other questions: (i) does trivalent chromium present a cancer risk?; (ii) is there a threshold for carcinogenic effects?; and (iii) what is the appropriate model for predicting cancer risk? Mechanistic research with supporting evidence from animal studies has provided the most useful information to answer these questions. Working hypotheses are: (i) trivalent chromium is not a carcinogen; (ii) there are probably substantial differences in carcinogenic potency between chromates, with the water-soluble compounds having lower potency than intermediately-soluble compounds; (iii) only respiratory tract cancers are caused by exposure to chromates, and ingestion and chromates does not constitute a carcinogenic risk; (iv) there is probably a threshold for carcinogenic effects from chromium due to detoxification mechanisms and lack of bioavailability of low doses; and (v) currently used models for quantitative risk assessment (e.g. the low dose linearized multi-stage model) are inappropriate to predict low dose cancer risks from exposure to chromates.

Carcinogens↗
PubMed1992

Atmospheric deposition of trace elements around point sources and human health risk assessment. II. Uptake of arsenic and chromium by vegetables grown near a wood preservation factory.

Kale, lettuce, carrots and potatoes were grown in 20 experimental plots surrounding a wood preservation factory, to investigate the amount and pathways for plant uptake of arsenic and chromium. Arsenate used in the wood preservation process is converted to the more toxic arsenite by incineration of waste wood and is emitted into the atmosphere. Elevated concentrations of inorganic arsenic and chromium were found both in the test plants and in the soil around the factory. Multivariate statistical analysis of the results indicated that the dominating pathway of arsenic and chromium from the factory to the leafy vegetables grown nearby was by direct atmospheric deposition, while arsenic in the root crops originated from both the soil and the atmosphere. Consumption of vegetables grown near the source would result in an increased intake of inorganic arsenic, but the intake via the total diet was estimated to be below the provisional tolerable daily intake for inorganic arsenic established by FAO/WHO.

Air Pollutants↗
PubMed1995

Growth and behavioral effects of early postnatal chromium and manganese exposure in herring gull (Larus argentatus) chicks.

Organisms in marine environments are exposed to chromium and manganese, yet little is known of the effects of these metals on physiology and behavior. In this article we examine the effects of chromium and manganese on early neurobehavioral development in herring gulls, Larus argentatus. Each of 36 2-day-old herring gull chicks was randomly assigned to one of three treatment groups to receive either chromium nitrate (25 mg/kg), manganese acetate (50 mg/kg), or a control dose of sterile saline solution. The trios were not siblings, but were matched by age and weight. Behavioral tests examined food-begging, balance, locomotion, righting response, recognition, thermoregulation, and perception. There were significant differences in begging behavior by 5 days postinjection, and there were significant differences in weight gain throughout development until 50 days of age, when the experiment was terminated. Behavioral tests, administered from 18-48 days postinjection, indicated significant differences between control and the exposed groups for time to right themselves; thermoregulation behavior; and performance on a balance beam, inclined plane, actual cliff, and visual cliff (although not all components varied significantly). Of the 14 behavioral measures with significant differences, control birds performed best on 12.

Analysis of Variance↗
PubMed1983

Asthma and IgE antibodies induced by chromium and nickel salts.

Metal plating with chromium and nickel has secured an occupational relation with asthma for which an allergic basis has been postulated but not confirmed. A worker who developed de novo asthma after plating with nickel and chromium but not other metals was subjected to inhalational challenge and immunoserologic tests to evaluate this association. He developed acute asthma to chromium sulfate and a biphasic asthma-like response to nickel sulfate. Radioimmunoassays incorporating the challenge materials revealed specific IgE antibodies to the provocative agents but not to another metal, gold, which he could tolerate. The findings support the postulates that bronchial reactivity can be specifically induced by fumes of metallic salts, even in a previously nonallergic individual, and that an IgE type I immunopathogenic mechanism is involved.

Adult↗
PubMed1983

Separation of biologically active chromium-containing complexes from yeast extracts and other sources of glucose tolerance factor (GTF) activity.

A procedure has been developed, based on ion-exchange chromatography, that readily allows the separation of eleven apparently homogeneous chromium-containing fractions from a brewer's yeast extract. Four of the fractions are amphoteric and show no glucose tolerance factor (GTF) activity, three are classified as negative (two of which are biologically inactive, while the third one shows a slight degree of GTF activity), whereas the four cationic chromium-containing fractions all show varying degrees of GTF activity. Application of the separation procedure to other biological sources of GTF activity resulted in a spectrum of cationic fractions, over the pH range 1.75 to 12, which suggests that GTF cannot be a single species. The cationic chromium-containing fraction from pork kidney powder and fraction P-3 from yeast appear to contain the most GTF-active material and P-3 shows saturation kinetics as expected for a biologically significant substance.

Amino Acids↗
PubMed1978

Comparative studies of chromosomal aberration and mutagenicity of the trivalent and hexavalent chromium.

The comparative cytogenetic and mutagenic effects between trivalent and hexavalent chromium were investigated. Five chromium compounds, K2Cr2O7 and K2CrO4 containing Cr6+, and Cr(CH3COO)3, Cr(NO3)3 and CrCl3 containing Cr3+, were examined for their ability to induce chromosomal damage in cultures of human leukocytes, for their reactivity with DNA by a rec-assay system and for mutagenicity in the E. coli Hs30R test system. Chromosome-breaking activity was significantly higher for the compounds with hexavalent than trivalent chromium, the efficiency being in the decreasing order K2Cr2OM greater than K2CrO4 greater than Cr(CHCOO)3 greater than Cr(NO3)3, CrCl3. In the rec-assay and mutation assay, hexavalent (K2Cr2O7 and K2CrO4) and trivalent Cr(CH3COO)3) compounds gave positive results, their mutagenic potential being higher in the same order of clastogenic magnitude.

Cells, Cultured↗
PubMed1981

Mutagenicity of a series of hexacoordinate chromium (III) compounds.

17 chromium(III) compounds have been tested for DNA-damaging capabilities using an E. coli differential repair assay and for mutagenicity in strains of Salmonella typhimurium. 4 of these compounds were active in both assays. Another 4 compounds were positive only in the repair assay and 9 were devoid of activity in both assays. Most of the doubly active complexes contain aromatic amine ligands like 2,2'-bipyridine and 1,10-phenanthroline. Closely related complexes of ligands derived from saturated amines are much less active. It appears that chromium(III) in the proper ligand environment can have considerable genetic toxicity and could represent one of the several possible ultimate species in a mechanism for chromium mutagenesis and carcinogenesis.

Chromium↗
PubMedDate not supplied

Genetic effects of chromium compounds.

Seven different test systems were utilized to investigate the genetic activity of chromium compounds: infidelity of DNA replication in vitro by DNA pol alpha from calf thymus, damage of DNA detected by alkaline elution in treated mammalian cells or in DNA purified and treated in vitro, DNA repair synthesis in mammalian cells in vitro detected by autoradiography or scintillation counting after labelling with [3H]dThd, gene mutations in the Salmonella typhimurium Ames test, gene mutations (6TG resistance) in cultured hamster cells, sister-chromatid exchanges in different rodent cell cultures, and transformation to anchorage-independent growth of hamster cells in vitro (soft-agar assay). Potassium dichromate and chromium chloride were used as water-soluble Cr(VI) and Cr(III) salts. Several reference mutagens (EMS, MMS, MMC, 4NQO) were included in the single tests as positive controls. Cr(VI) was active in all the tested systems, except in the induction of DNA damage and DNA repair synthesis in cultured cells. Cr(III), on the other hand, was absolutely inactive unless a direct interaction with purified DNA was permitted by the test conditions. The relevance of data from the various tests to the understanding of the mechanisms of the genotoxic activity of chromium is discussed. Effects other than the direct interaction of Cr(III) with DNA are inferred, which can cause infidelity of the DNA polymerase functions.

Animals↗
PubMed1985

Effects of nitrilotriacetic acid on the induction of gene mutations and sister-chromatid exchanges by insoluble chromium compounds.

The influence of nitrilotriacetic acid trisodium salt (NTA) on the mutagenic and clastogenic activity of several water-insoluble or poorly soluble chromium compounds was determined by means of the Salmonella/microsome assay (plate test on TA100 strain) and the sister-chromatid exchange (SCE) test in mammalian cell cultures (CHO line). NTA in itself did not induce gene mutations nor did it increase the frequency of SCE. Cr(VI) compounds (Pb, Ba, Zn, Sr and Ca chromates) and an industrial Cr(VI) pigment, chromium orange (containing PbCrO4 PbO), were inactive or scarcely active mutagens in the Salmonella/microsome test when dissolved in water, but they were increasingly mutagenic when solubilized by 0.5 N NaOH or NTA (10 or 100 mg/ml). Also, the mutagenic activity of Cr(VI), contaminating an industrial Cr(III) pigment (chromite), was slightly enhanced by NTA. Mutagenicity of chromates was correlated with the amounts of Cr(VI) solubilized by NTA or alkali, as determined by the colorimetric reaction with diphenylcarbazide and atomic absorption spectrophotometry, and was decreased by incubation with microsomes, due to reduction of Cr(VI) to the genetically inactive Cr(III) form. In the SCE assay, the insoluble or poorly soluble Ba, Zn, Sr and Ca chromates and the insoluble Cr(VI) pigments zinc yellow (containing ZnCrO4 Zn(OH2], chromium yellow and molybdenum orange (both containing PbCrO4) were directly clastogenic due to cellular endocytosis taking place in prolonged treatments, and NTA significantly increased their chromosome-damaging activity.

Acetates↗
PubMed1993

Increased sister chromatid exchanges and tumor markers in workers exposed to elemental chromium-, cobalt- and nickel-containing dusts.

Sister-chromatid exchange (SCE) in blood lymphocytes, serum tumors markers, carcinoembryonic antigen (CEA) and tissue polypeptide antigen (TPA), and urinary excretion of chromium, cobalt and nickel were determined in 26 male workers occupationally exposed to chromium, cobalt and nickel dust and in 25 controls matched for age and smoking habits. The differences in the urinary excretion of metals between exposed persons and controls were statistically significant. An analysis of variance on the SCE rank values revealed that both exposure status (exposed persons vs. controls) and smoking habits (smokers and former smokers vs. never smokers) had a statistically significant effect. For the tumor markers, the analysis of variance did not reveal a statistically significant difference between exposed persons and controls. However, CEA serum levels were significantly correlated not only with smoking habits but also with duration of exposure. As cobalt is only weakly mutagenic, these results suggest that the small amount of absorbed chromium and nickel may have been sufficient to induce SCE. The hypothesis that tumor markers may be increased in groups of subjects exposed to genotoxic substances deserves further study.

Adult↗
PubMed1987

Circadian reduction of chromium in the gastric environment.

Samples of gastric juice from variously treated subjects efficiently reduced hexavalent chromium and decreased its mutagenicity. Chromium reduction was due to thermostable components of gastric secretions and was favoured by the acidity of the intragastric environment. The circadian monitoring of pH and of chromium reduction, as assessed by colorimetric analysis at hourly intervals, showed a basal activity (less than 10 micrograms/ml gastric juice) during the night and interdigestive periods, and peaks (tens of micrograms/ml) during the 3-4-h periods after each meal. Assays in the Ames reversion test confirmed that the decrease in mutagenicity of sodium dichromate produced by gastric juice was significantly enhanced after meals. This physiological mechanism is expected to provide an important protective barrier against the oral toxicity of this metal, and may explain its lack of oral carcinogenicity.

Chromium↗