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PubMed1998

Chromium and zinc contamination of parenteral nutrient solution components commonly used in infants and children.

Chromium and zinc contamination of components of parenteral nutrient (PN) solutions used in infants and children was studied. Solutions of amino acids, L-cysteine hydrochloride, dextrose, electrolytes, minerals, vitamins, multiple trace elements, and individual trace elements were obtained. A variety of manufacturers, lots, and expiration dates were represented when possible. The solutions were analyzed for chromium and zinc by flame atomic absorption spectrophotometry. In all amino acid products, chromium concentration was below the limit of detection and zinc concentration ranged from 0.06 to 4.97 mg/L. In the L-cysteine hydrochloride products, chromium was measurable in only two lots (0.11 and 0.23 mg/L); zinc was measurable in all lots (32-86 mg/L). Sodium and potassium salts of chloride and acetate had chromium concentrations of 0.02-0.23 mg/L and zinc concentrations of 0.35-0.56 mg/L. Phosphate salts contained chromium 0.39-0.44 mg/L and zinc 0.91-2.33 mg/L. In calcium gluconate, zinc concentration was 0.28-2.38 mg/L. In four lots of multiple trace elements, chromium was 92-104% and zinc was 100-113.5% of the labeled amount. A PN solution for a < 10-kg infant compounded from the components assayed would provide up to an additional 0.7 microgram of chromium per kilogram and 200 micrograms of zinc per kilogram. Zinc and chromium contaminants were detected in many of the products that are common components of PN solutions for infants and children; the contamination may be sufficient to result in the administration of zinc and chromium in amounts exceeding current recommendations.

Child↗
PubMed1997

Estimates of the chromium(VI) reducing capacity in human body compartments as a mechanism for attenuating its potential toxicity and carcinogenicity.

Estimates of the overall reducing capacity of hexavalent chromium(VI) in some human body compartments were made by relating the specific reducing activity of body fluids, cell populations or organs to their average volume, number, or weight. Although these data do not have absolute precision or universal applicability, they provide a rationale for predicting and interpreting the health effects of chromium(VI). The available evidence strongly indicates that chromium(VI) reduction in body fluids and long-lived non-target cells is expected to greatly attenuate its potential toxicity and genotoxicity, to imprint a threshold character to the carcinogenesis process, and to restrict the possible targets of its activity. For example, the chromium(VI) sequestering capacity of whole blood (187-234 mg per individual) and the reducing capacity of red blood cells (at least 93-128 mg) explain why this metal is not a systemic toxicant, except at very high doses, and also explain its lack of carcinogenicity at a distance from the portal of entry into the organism. Reduction by fluids in the digestive tract, e.g. by saliva (0.7-2.1 mg/day) and gastric juice (at least 84-88 mg/day), and sequestration by intestinal bacteria (11-24 mg eliminated daily with feces) account for the poor intestinal absorption of chromium(VI). The chromium(VI) escaping reduction in the digestive tract will be detoxified in the blood of the portal vein system and then in the liver, having an overall reducing capacity of 3300 mg. These processes give reasons for the poor oral toxicity of chromium(VI) and its lack of carcinogenicity when introduced by the oral route or swallowed following reflux from the respiratory tract. In terminal airways chromium(VI) is reduced in the epithelial lining fluid (0.9-1.8 mg) and in pulmonary alveolar macrophages (136 mg). The peripheral lung parenchyma has an overall reducing capacity of 260 mg chromium(VI), with a slightly higher specific activity as compared to the bronchial tree. Therefore, even in the respiratory tract, which is the only consistent target of chromium(VI) carcinogenicity in humans (lung and sinonasal cavities), there are barriers hampering its carcinogenicity. These hurdles could be only overwhelmed under conditions of massive exposure by inhalation, as it occurred in certain work environments prior to the implementation of suitable industrial hygiene measures.

Biological Availability↗
PubMed1986

Abnormal deposits of chromium in the pathological human brain.

Three patients presented with encephalopathies: an undiagnosed degenerative disease of the brain, a degenerative cerebral disease in a patient with a myeloma but without a myelomatous deposit in the CNS and a malignant astrocytoma. Perivascular pallidal deposits (vascular siderosis) containing chromium, phosphorus and calcium plus sometimes traces of other elements were present in the three cases. Such deposits were present in the pallidal parenchyma and around vessels in the cerebellum in one case. Calcium and phosphorus are always present in any CNS calcification but the presence of chromium has not been reported. Chromium and its compounds (ingested, injected or inhaled) are toxic to humans and animals in trace doses. Approximately 900 cases of chromium intoxication have been reported and usually have had dermatological or pulmonary lesions (including cancer) but there is no report of involvement of the CNS. Sublethal doses of chromium nitrate injected intraperitoneally in rats and rabbits results in the presence of chromium in the brain. A thorough investigation was made to find the source of the chromium in these patients. Chromium was found to be present in trace amounts in the radiological contrast agents administered to these patients and in the KCl replacement solution and in mylanta, an antacid, given to one case. The evidence that chromium induced pathological changes in these three brains is circumstantial but shows that chromium can penetrate the human brain. This study indicates that vascular siderosis found in the brains of the majority of middle-aged and elderly humans is not simply an anecdotal pathological curiosity, but that it can serve as a route of entry for toxic products into the brain.

Aged↗
PubMed2001

The effects of dietary chromium supplementation on some blood parameters in sheep.

The effects of dietary inorganic chromium on some biochemical parameters were determined in lambs fed either a control diet or a 200-ppb or 400-ppb chromium-supplemented diet. The live weight of the animals were measured and jugular blood samples were collected prior to supplementation (d 0) and on d 20, 40, and 55. On d 55, three animals from each group were slaughtered to measure subcutaneous fat. Sera were analyzed for glucose, triglyceride, total cholesterol, high-density lipoprotein (HDL) and low-density lipoprotein (LDL) cholesterol, total protein, albumin, ALT, AST, and GGT levels. Chromium supplementation had no significant effect on live weight, but subcutaneous fat was reduced significantly in both chromium groups. There was a slight decrease in glucose concentrations in the 200-ppb chromium group, although only the differences on d 55 were significant. Triglyceride levels in both chromium groups were lower than the control group with marked differences in the 400-ppb chromium group. HDL cholesterol levels increased in both treatment groups compare to control, although the differences in the 400-ppb chromium group on d 40 were significant. Serum Cr concentrations slightly but not significantly increased in both chromium groups. No significant differences were found in total and LDL cholesterol, total protein, albumin, ALT, AST, and GGT levels. In conclusion, chromium supplementation may affect carbohydrate and lipid metabolisms and lipid deposition in lambs.

Alanine Transaminase↗
PubMedDate not supplied

Removal of chromium from synthetic plating waste by zero-valent iron and sulfate-reducing bacteria.

Experiments were conducted to evaluate the potential of zero-valent iron and sulfate-reducing bacteria (SRB) for reduction and removal of chromium from synthetic electroplating waste. The zero-valent iron shows promising results as a reductant of hexavalent chromium (Cr+6) to trivalent chromium (Cr+3), capable of 100% reduction. The required iron concentration was a function of chromium concentration in the waste stream. Removal of Cr+3 by adsorption or precipitation on iron leads to complete removal of chromium from the waste and was a slower process than the reduction of Cr+6. Presence SRB in a completely mixed batch reactor inhibited the reduction of Cr+6. In a fixed-bed column reactor, SRB enhanced chromium removal and showed promising results for the treatment of wastes with low chromium concentrations. It is proposed that, for waste with high chromium concentration, zero-valent iron is an efficient reductant and can be used for reduction of Cr+6. For low chromium concentrations, a SRB augmented zero-valent iron and sand column is capable of removing chromium completely.

Adsorption↗
PubMed2000

Effect of cultivation mode on a bioprocess for chromium yeast biomass enrichment.

Defined cultivation media for yeast growth which contained 278.8 mM of glucose and 0.1 mM of chromium(III) added as K2Cr(SO4)2 x 12 H2O was used in batch and combined batch/fed-batch cultivation mode. In fed batch cultivation mode the rate of substrate addition remained constant during growth of yeast and corresponded to a growth rate of 0.25 h(-1). In both cases the growth and yeast activity was followed by on line measurement of optical density, pH and pO2 at 30 degrees C. At the end of the bioprocess the concentration of protein in yeast biomass was determined off line by the biuret reaction. Total and organically bound chromium was detected by ETA-AAS. Different cultivation modes affected the total cell protein concentration of yeast grown in media supplemented with chromium. In batch process the protein content represented 25.7% of dry yeast biomass, in contrast in the mixed bioprocess this value was 16.9% one the same period of time. The influence of cultivation mode on chromium uptake was seen in total chromium accumulation which reached 8.68 +/- 0.16 micromol g(-1) d.wt. in batch and 1.92 +/- 0.04 micromol of chromium g(-1) of dry yeast biomass in combined batch/fed-batch cultivation mode. The opposite was observed for organically bound chromium. The 60% of total accumulated chromium was organically bound during yeast growth in combined batch/fed-batch mode. When yeast was grown in batch mode this value attained 13.5%. Results suggested that a combined batch/fed-batch mode of cultivation was more effective over a batch system in chromium biotransformation to organically bound chromium, regardless of the lower protein ratio determined in the yeast biomass.

Biomass↗
PubMed2004

[Chromium and insulin resistance].

Since as early as the 50s of the last century, it has been known that chromium is essential for normal glucose metabolism. Too little chromium in the diet may lead to insulin resistance. However, there is still no standard against which chromium deficiency can be established. Nevertheless, chromium supplements are becoming increasingly popular. Various systematic reviews have been unable to demonstrate any effects of chromium on glycaemic regulation (possibly due partly to the low dosages used), but there is a slight reduction in body weight averaging 1 kg. In a double-blind randomised placebo-controlled trial in a Chinese population with type-2 diabetes mellitus, supplementation with 1000 micrograms of chromium led to a fall in the glycosylated haemoglobin level (HbA1c) by 2%. Toxic effects of chromium are seldom seen; recently, however, the safety of one of the dosage forms of chromium, chromium picolinate, has been questioned. One should be aware that individual patients with type-2 diabetes mellitus may have an increased risk of hypoglycaemic episodes when taking chromium supplements as self-medication.

Blood Glucose↗
PubMed1988

Characterization of chromium effects on a rat liver epithelial cell line and their relevance to in vitro transformation.

Chronic exposure to low concentrations or brief exposures to high concentrations of hexavalent chromium (K2CrO4) transformed a rat liver epithelial cell line as assessed by anchorage-independent growth. A clone of the transformed cells produced tumors in syngeneic animals, all of which were determined to be high grade carcinomas. The effects of various doses of chromium on cytotoxicity and cell cycle were established and related to ultimate numbers of transformants in the population. Prior to the onset of cytotoxicity, linear rates of uptake were observed at different external concentrations of chromium and the total intracellular level increased with increasing concentration. This may be due to competition for transport. A plateau in level of chromium accumulation after prolonged exposure to a low concentration (10 microM) of chromium observed with the eventual return to normal growth provided evidence for the induction of a protective mechanism. In addition, cells surviving prolonged treatment with low concentrations of chromium became resistant to the cytotoxic effects of high concentrations of the metal, further suggesting that the cells become adapted to the presence of chromium. An increase in the amount of protein associated with extracted nucleic acids was detected at the optimal transforming dose and this did not correlate with cytotoxic effects. The effectiveness of chromium in transforming the adult rat liver epithelial cell line may depend on the intracellular level of accumulation, the rate of chromium uptake, and the ability of the cell to activate a protective mechanism. The initiation of stable nucleic acid-protein complexes observed under the optimal conditions for transformation may be associated with an inability of the cell to activate a protective mechanism rapidly enough to prevent effects on the nucleus at a high concentration (1 mM) of chromium.

Animals↗
PubMed1998

Arrest of replication by mammalian DNA polymerases alpha and beta caused by chromium-DNA lesions.

We have previously shown that trivalent chromium, and hexavalent chromium in the presence of one of its primary in vivo reductants, ascorbate, can bind to DNA and form interstrand crosslinks capable of obstructing replication. This effect was demonstrated in vitro by using Sequenase Version 2.0 T7 DNA polymerase; its parent enzyme, the unmodified T7 DNA polymerase; and Escherichia coli polymerase I large (Klenow) fragment; and it was demonstrated ex vivo by using Taq polymerase and DNA from chromium-treated human lung cells as template. This study was performed to determine whether DNA-bound chromium affects mammalian DNA polymerases in the same manner. Two mammalian enzymes, DNA polymerase alpha and DNA polymerase beta, were used. DNA polymerase alpha is a processive enzyme believed to be the primary lagging-stand synthetase, whereas DNA polymerase beta is a non-processive enzyme believed to function in DNA repair by filling single stranded gaps one base at a time. DNA polymerase arrest assays were performed with each of these enzymes to replicate DNA with toxicologically relevant levels of chromium adducts produced by either trivalent chromium or hexavalent chromium and ascorbate. Both enzymes responded to chromium-DNA damage by arresting replication, and the arrests increased in a dose-dependent manner. Furthermore, the guanine-specific pattern of arrests produced when an exonuclease-free preparation of DNA polymerase beta was used corresponded exactly to the arrest patterns produced in vitro by the exonuclease-free enzyme Sequenase and ex vivo by Taq polymerase. These results suggest that replication arrest may be a common response of polymerases to DNA-chromium lesions and provide a plausible mechanism for the inhibition of DNA synthesis and S-phase cell-cycle delay that occurs in mammalian cells treated with genotoxic chromium compounds.

Ascorbic Acid↗
PubMed2002

Role of chromium supplementation in Indians with type 2 diabetes mellitus.

Type 2 diabetes mellitus is a complex metabolic disorder with adverse cardiovascular risk. The role of micronutrients has not yet been well clarified in this condition, especially in India.THE OBJECTIVES OF THIS STUDY WERE TO: (1) evaluate chromium status in Indian subjects with type 2 diabetes mellitus, (2) assess the effect of chromium picolinate (200 &mgr;g trivalent chromium twice daily) administration on glycaemic control and lipid profile in these subjects and (3) comment on the possible mechanism of any beneficial effect noted above.Fifty subjects were studied in a double blind, placebo-controlled, crossover fashion, with each treatment arm (chromium/placebo) lasting 12 weeks and 4 weeks' wash-off period in between. 50 healthy age- and sex-matched volunteers served as controls. Serum chromium level appeared to be higher in the general population in our country compared to western countries (36.5-59.5 nmol/L as compared to 2.3-40.3 nmol/L) However, the local diabetics were found to have a lower serum chromium level than the healthy controls (32.3 nmol/L against 44.7 nmol/L; p < 0.0001) and a mean increase of 3.5 nmol/L was noted after 12 weeks of chromium supplementation that was, expectedly, not seen in the placebo phase (p < 0.0001).Significant improvement in glycaemic control was noted in the chromium-treated group (DeltaFasting serum glucose = 0.44 mmol/L, p < 0.001; DeltaPost-prandial serum glucose = 1.97 mmol/L, p < 0.001; Deltaglycated hemoglobin = 0.01; p = 0.04, in comparison to placebo) This was accompanied by a significant greater fall in fasting serum insulin in the chromium-treated group, p < 0.05.The change in lipid parameters (total serum cholesterol, high density lipoprotein cholesterol, low density lipoprotein cholesterol and triglycerides) did not show significant difference between the chromium and placebo groups.Clinically significant hematological, renal or hepatic toxicity were excluded by routine hemogram, serum urea, creatinine, alanine amino transferase (ALT) and alkaline phosphatase estimations.In conclusion, chromium supplementation seems to improve glycaemic control in type 2 diabetic patients, which appears to be due to an increase in insulin action rather than stimulation of insulin secretion.

Journal Article↗
PubMed1999

Performance, serum characteristics, carcase traits and lipid metabolism of broilers as affected by supplement of chromium picolinate.

1. This study investigated the effects of dietary supplementation with chromium picolinate on the performance, serum and carcase traits and lipid metabolism of broilers. In trial 1, 120 1-day-old broilers with an equal number of males and females were assigned at random to 4 groups with 3 replicates. Four treatments with dietary supplements of 0 (control), 800, 1600 and 3200 microg/kg of chromium picolinate were used. In trial 2, 6-week-old broilers (20) were used to determine how supplements of 0, 200, 400 and 800 microg/kg chromium in an incubation medium influence their hepatocyte lipogenic capacity and adipocyte lipolysis, in vitro. 2. Dietary supplements of 1600 and 3200 microg/kg chromium in broiler diets significantly increased food consumption (P<0.05); 1600 microg/kg markedly improved weight gain (P<0.05); 1600 and 3200 microg/kg groups showed increased liver lipid content (P<0.05). However, the abdominal fat content tended to decrease in these 2 groups. 3. Dietary supplements of 1600 and 3200 microg/kg of chromium decreased serum glucose and nonesterified fatty acids (NEFA) concentrations while increasing serum phospholipid content (P<0.05). Insulin concentration decreased only in birds receiving 3200 ppb chromium (P<0.05). Serum triacylglycerol (TG) clearance rate in chromium-supplemented groups was markedly enhanced (P<0.05). 4. In addition, chromium supplemented groups had increased serum HDL contents and also reduced serum VLDL and LDL contents (P<0.05). 5. Trial 2 indicated that lipogenesis from [U-14C]glucose by isolated hepatocytes was significantly enhanced by 400 ppb chromium (P<0.05). 6. The results from this study demonstrate that a supplement of 1600 microg/kg of chromium picolinate in the ration influences the growth, carcase, serum traits and lipid metabolism of broilers.

Adipocytes↗
PubMed1993

Dietary chromium supplementation with or without somatotropin treatment alters serum hormones and metabolites in growing pigs without affecting growth performance.

Twenty-four castrated male pigs were used in a 2 x 2 treatment array to determine the main effects of and interactions between dietary chromium supplementation and pituitary porcine somatotropin (ppST) administration on growth performance and serum hormone and metabolite concentrations. The treatments were 1) control (basal diet); 2) chromium (basal diet+300 micrograms/kg diet added trivalent chromium as chromium picolinate); 3) ppST (100 micrograms/(kg body wt.d); and 4) chromium+ppST. Treatments were administered when pigs weighed between 30 and 60 kg. Blood was collected when pigs weighted 45 and 60 kg. All pigs treated with ppST exhibited improvements in growth performance (P < 0.05). Pigs given chromium showed no improvements in growth rate, feed efficiency or composition of gain. Measurements at 60 kg body weight revealed that ppST increased the cholesterol:HDL cholesterol ratio (P < 0.05). Chromium lowered serum insulin and glucose concentrations relative to controls (P < 0.05) and normalized the increase in glucose and insulin resulting from ppST treatment. No ppST x chromium interactions were noted, suggesting these changes in glucose and insulin metabolism are exerted through different mechanisms. These results indicate that chromium does not affect growth performance of young growing pigs. Chromium does normalize altered hormone and metabolite concentrations resulting from ppST treatment.

Analysis of Variance↗
PubMed1986

Chromium deficiency after long-term total parenteral nutrition.

A 63-year-old female developed unexplained hyperglycemia and glycosuria during administration of a total parenteral nutrition regimen on which she had been stable for several months. Because the patient had no history of diabetes or evidence of an infection, chromium deficiency was considered. Plasma chromium level was 0.1 microgram/dl (laboratory reference interval: 1.8-3.8 micrograms/dl). Fourteen days of supplemental intravenous chromium chloride (200 micrograms/day) allowed complete withdrawal of exogenous insulin with no further hyperglycemia or glycosuria. Correction of unexplained glucose intolerance following vigorous chromium supplementation indicates that the patient had chromium deficiency. Subsequent plasma chromium levels remained unchanged, possibly reflecting the sensitivity limits of the assay that was used, the uncertainty that exists regarding appropriate reference intervals for this element, and the fact that plasma levels do not always correlate with total body stores. The patient did not manifest peripheral neuropathy, which was present in one of the two previously reported cases, nor encephalopathy, which was reported in the other. We conclude that this patient developed chromium deficiency as a result of inadequate administration of chromium in the parenteral formula (6 micrograms/day) plus excessive enteric losses, and she presented with glucose intolerance as the only clinical manifestation of the deficiency. Caution should be exercised when interpreting plasma chromium in patients with suspected deficiency.

Blood Glucose↗
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↗
PubMed1990

Oral induction of immunological tolerance to chromium in the guinea pig.

Metal alloys used in dentistry may elicit adverse side-effects. Contact allergic reactions to metals released from such alloys are among the most frequently encountered problems. In an earlier study, we observed that oral contacts with nickel or chromium salts did not sensitize, but rather decreased the risk of subsequent sensitization to these metals. In the present study, we focused on chromium allergy and extended our earlier observations by further dose-response studies. In addition, we compared different chromium valencies as to their potential oral tolerogenic effects. Development of immunological tolerance in chromium-fed guinea pigs was demonstrated by their inability to develop chromium hypersensitivity after a subsequent immunization attempt. For these studies, the techniques of immunization and skin testing were first improved. One feeding with a high dose of K2Cr2O7 (containing hexavalent chromium) was effective in full tolerance induction. In contrast, trivalent chromium (CrCl3) induced a distinctly lower degree of tolerance, whereas metallic chromium powder was not detectably tolerogenic after a limited number of feedings. Dose-frequency-response studies with K2Cr2O7 showed that full tolerance could also be induced by an increase in the number of feedings with sub-optimal tolerogenic doses. The present results therefore support our hypothesis that long-lasting oral contact with chromium-releasing metal alloys may ultimately result in strong immune tolerance to this metal in subjects without previous skin contact with it. This view is further supported by recent insights into the unique tolerogenicity of oral, as compared with gastro-intestinal, allergenic contacts.

Administration, Oral↗
PubMed2004

Effect of lead and chromium on reproductive success of Japanese quail.

An experimental model based on application of Japanese quail (Coturnix coturnix japonica) lines with high (H) and low (L) concentrations of plasma lactate was designed in order to investigate the effects of lead and chromium on embryonic development and reproductive success of experimental groups representing different genotypes. During the first stage of the trial, mature males from quail lines H and L (marked as generation T) were fed subchronically for 12 weeks with lead as Pb(NO(3))(2) and chromium as K(2)Cr(2)O(7) (dosage 0.8 and 0.142 g/kg, respectively, in the feed). In addition, a binary mixture of both lead and chromium was administered to the third group of males. The control group consisted of untreated birds. After mating with untreated females (8 female x 5 male in each group), progeny with four genotypes were obtained. The chicks were marked as generation F1 and used in the second stage of the trial. The data obtained show that heavy metals decreased the hatchability of sexually mature quail males: chromium (14%), lead (19%), and binary lead-chromium mixture (28%). Early embryonic mortality increased as much as 2-3 times. Single lead and binary lead-chromium additions decreased fertility after treating Japanese quail during the development of sexual maturity: lead increased the number of unfertile eggs up to 30% (twofold), binary lead and chromium, up to 50% (more than threefold) relative to untreated controls. There was no effect of chromium alone on fertility. In general, hatchability, fertility, embryonic mortality and reproductive success of Japanese quail were dependent on age, sex, genotypes, and on single or binary treatment with the inorganic salts of lead and chromium.

Adaptation, Biological↗
PubMed1997

Community exposure and medical screening near chromium waste sites in New Jersey.

Chromium waste slag containing potentially hazardous levels of hexavalent chromium was used as fill material at more than 160 residential, industrial, and recreational sites. Persons living or working in the vicinity of the sites may have been exposed through inhalation, ingestion, or skin contact with contaminated soils and dusts. In 1992-1993, the New Jersey Department of Health and Senior Services (NJDHSS) and the Environmental and Occupational Health Sciences Institute (EOHSI) conducted a screening project to assess exposure to chromium and to provide medical evaluations to people living in 14 residential areas or working in 78 workplaces near chromium waste sites. The screening included a physical examination for irritant or allergic effects and a urine chromium test for recent exposure. Participants were referred for follow-up medical evaluation if specific criteria were met. Of 800 residents and 938 workers receiving the screening physical examination, 32 adults were referred for follow-up evaluation. Of 806 residents and 934 workers submitting a urine specimen for chromium analysis, 158 adults and children had levels exceeding specified criteria and were referred for follow-up evaluation. The proportion of persons referred on the basis of the urine chromium test varied among screened groups. Multiple linear regression models showed that average urine chromium differences between residents and a comparison group, adjusting for potential confounders, were highest in children under 6 years of age. Most of the persons undergoing the follow-up medical examinations revealed no apparent clinical effects attributable to chromium exposure. The screening results indicated the need for expanded environmental evaluation in specific residential areas and workplaces.

Adolescent↗
PubMedDate not supplied

Dietary chromium intake. Freely chosen diets, institutional diet, and individual foods.

Chromium content of 22 daily diets, designed by nutritionists to be well-balanced, ranged from 8.4 to 23.7 micrograms/1000 cal with a mean +/- SEM chromium content of 13.4 +/- 1.1 micrograms/1000 cal. Most diary products are low in chromium and provide less than 0.6 micrograms/serving. Meats, poultry, and fish are also low in chromium, providing 2 micrograms of chromium or less per serving. Chromium contents of grain products, fruits, and vegetables vary widely, with some foods providing greater than 20 micrograms/serving. In summary, chromium content of individual foods varies, and is dependent upon chromium introduced in the growing, transport, processing, and fortification of the food. Even well-balanced diets may contain suboptimal levels of dietary chromium.

Adult↗