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The aim of this study was to evaluate the effects of organic chromium (Cr) on physico-biochemical and oxidative stability of turkey meat. Ninety-six (16th weeks) male turkeys were distributed into 16 groups (4 diet × 4 replicates × 6 birds each). Four dietary treatments (T 1 , T 2 , T 3 and T 4 ) were formulated with supplementation of 0.0, 250, 500 and 750 µg Cr/kg diets, respectively. Cholesterol and fat contents in meat reduced ( p  < 0.05) in T 4 (750 µg Cr/kg) but no difference was observed in pH and drip loss. No significant effect was recorded on water holding capacity (WHC) and extract release volume (ERV) of fresh meat but the effect ( p  < 0.05) was observed on WHC and ERV in refrigerated meat. No significant difference was observed in DPPH (1, 1-diphenyl-2-picrylhydrazy) and ABTS (2, 2-azinobis-3-ethylbenzothiazoline-6-sulfonic acid) of fresh breast and thigh meat but effect ( p  < 0.05) was noticed in refrigerated meat of turkey fed T 4. Lipid oxidation (free fatty acids and Thio-barbituric acid reactive substances-TBARS) were improved in fresh as well as refrigerated meat from birds fed diet supplemented with 750 µg Cr/kg (T 4 ). Whereas, peroxide value was improved ( p  < 0.05) only in refrigerated meat. Thus, it may be concluded that inclusion of Cr at 750 µg/kg diet with basal diet improved in desirable physio-biochemical properties, antioxidant and oxidative stability of male turkey meat under cold chain.

The objectives of this study were to investigate the effects of chromium (Cr) supplementation on feed intake and meal pattern, weight gain and skeletal growth, and health and metabolic criteria of environmentally heat-loaded dairy calves during the pre-weaning period. Forty-eight newborn female calves were allotted randomly to a control group (no Cr supplement; Cr-) or a Cr group (Cr+) receiving 0.05 mg Cr (as Cr-methionine)/kg BW 0.75 . Cr was provided in the liquid feed (colostrum and milk) during the pre-weaning period. The average maximum temperature-humidity index was 83.7 U, indicating severe environmental heat load. Despite reduced meal frequency and increased in inter-meal interval, Cr supplementation tended to increase starter feed intake and total dry matter intake as a result of increased meal size and duration. Respiration rate was lower in Cr+ calves. Calf growth, rectal temperature, faecal score and incidence of diarrhoea or pneumonia were not affected by Cr supplementation, but number of days with diarrhoea and treatment duration decreased during the pre-weaning period. Cr supplementation tended to increase resting time and decreased time devoted to non-nutritive oral behaviours. At weaning, serum concentration of glucose was lower but total protein and globulin concentrations were higher in Cr+ calves. In Cr+ calves, the activity of glutathione peroxidase was higher and lower on d 49 and 63 of the study, respectively, compared to the control calves. Activity of catalase was increased on d 21 and tended to decrease on d 35 in Cr+ calves. In general, Cr supplementation to environmentally heat-loaded dairy calves decreased non-nutritive oral behaviours, improved feed intake and decreased days with diarrhoea and treatment duration, but had minimal effects on weight gain, metabolism and indicators of oxidative stress or insulin function.

Background: Previous research has demonstrated the permissive effect of insulin on muscle protein kinetics, and the enhanced insulin sensitizing effect of chromium. In the presence of adequate whole protein and/or essential amino acids (EAA), insulin has a stimulatory effect on muscle protein synthesis, whereas in conditions of lower blood EAA concentrations, insulin has an inhibitory effect on protein breakdown. In this study, we determined the effect of an amylopectin/chromium (ACr) complex on changes in plasma concentrations of EAA, insulin, glucose, and the fractional rate of muscle protein synthesis (FSR)., Methods: Using a double-blind, cross-over design, ten subjects (six men, four women) consumed 6 g whey protein + 2 g of the amylopectin-chromium complex (WPACr) or 6 g whey protein (WP) after an overnight fast. FSR was measured using a primed, continuous infusion of ring-d 5 -phenylalanine with serial muscle biopsies performed at 2, 4, and 8 h. Plasma EAA and insulin were assayed by ion-exchange chromatography and ELISA, respectively. After the biopsy at 4 h, subjects ingested their respective supplement, completed eight sets of bilateral isotonic leg extensions at 80% of their estimated 1-RM, and a final biopsy was obtained 4 h later., Results: Both trials increased EAA similarly, with peak levels noted 30 min after ingestion. Insulin tended ( p  = 0.09) to be higher in the WPACr trial. Paired samples t-tests using baseline and 4-h post-ingestion FSR data separately for each group revealed significant increases in the WPACr group (+0.0197%/h, p  = 0.0004) and no difference in the WP group (+0.01215%/hr, p  = 0.23). Independent t-tests confirmed significant ( p  = 0.045) differences in post-treatment FSR between trials., Conclusions: These data indicate that the addition of ACr to a 6 g dose of whey protein (WPACr) increases the FSR response beyond what is seen with a suboptimal dose of whey protein alone.

Background: Meat consumption is increasingly becoming a larger part of diets worldwide. However, the bioaccumulation of toxic metals from anthropogenic pollution is a potential health risk to human health., Objective: To measure the daily intake of zinc, chromium, and nickel from cow meat consumption and assess the possible health risks in an urban population in Nigeria., Methods: Dried meat samples were digested with 3 : 2HNO3 : HClO4 v/v. Zinc, chromium, and nickel concentrations were determined with atomic absorption spectrophotometer. Daily intakes of meat were obtained using a food frequency questionnaire (FFQ)., Results: The estimated daily intakes (EDI) (μg/person/day) ranges were: zinc (10 496-13 459), chromium (310·90-393·73), and nickel (26·72-34·87). Estimated daily intake for zinc was 15-30% of provisional maximum tolerable daily intake (PMTDI) and for nickel it was 8-15% of tolerable daily intake (TDI)., Conclusion: Chromium intakes were above recommended daily intake (RDI). Target hazard quotient (THQ) for nickel and zinc were within WHO/FAO limit. There was no evidence of possible health risk to consumers with regard to zinc and nickel. However, chromium intake should be of utmost concern, while disposal of tanning waste should be checked.

1. The study was conducted to ascertain the effects of supplemental organic acids and chromium (Cr) on production and carcase traits of broiler chickens. 2. A total of 120 1-d-old broiler chicks were divided into 4 treatment groups in a 2 x 2 factorial design (each treatment group contained 6 replicates with 5 birds per replicate). 3. The diets were supplemented with an organic acid blend containing ortho-phosphoric, formic and propionic acid and calcium propionate (1 g/kg diet) and inorganic trivalent chromium (Cr(3+)) as chromic chloride hexahydrate (0.5 mg/kg diet) either independently or together as a combination for 35 d. 4. Individual supplementation of organic acids and Cr(3+) and their combination significantly improved the food conversion ratio, hot and dressed carcase weight and weight of the wholesale cuts compared to the control group of birds. 5. Organic acids, either independently or along with Cr(3+), increased total accretion of ash in carcase. Protein accretion was improved by dietary Cr(3+) and organic acid supplementation compared to the control group and a further improvement in this regard was observed when Cr(3+) and organic acid were supplemented together. Across the treatment groups meat fat content and fat accretion were lower in birds receiving dietary Cr(3+) supplementation. 6. Circulatory Cr(3+) and meat Cr(3+) concentration increased compared to the other treatment groups when Cr(3+) was supplemented to the birds. 7. It was concluded that, instead of individual supplementation, a combination of Cr(3+) and organic acids may improve the production and carcase traits of broilers more effectively presumably because of an additive effect.

Chromium is well documented as an essential element for humans. Trivalent chromium, the main chemical form found in foods, is essential for maintaining normal glucose metabolism. Owing to analytical difficulties, several literature reports of chromium content of foods, especially for the lower levels, show large variability and should be interpreted with caution. Zeeman background correction, transversely heated graphite furnace atomic absorption spectrometry was used to determine the chromium content of 104 different infant formulae (cow's milk and soy protein based) marketed in Spain following an acid-digestion sample preparation procedure in a closed, pressurized and microwave digestion unit. The mean and range of chromium values, regarding types and main protein-based infant formulae are presented. Additionally, the influence of the type of container used, the impact of industrial process from different manufacturers and the physical state (powder and liquid formulae) on chromium levels is also discussed. In general, the infant formulae contain a higher chromium concentration than that found in human milk (reference range: 0.20-8.18 microg l-1), particularly in the case of hypoallergenic (18.16 +/- 7.89 microg l-1), lactose-free (11.37 +/- 3.07 microg l-1), pre-term (11.48 +/- 3.15 microg l-1) and soya (10.43 +/- 4.05 microg l-1) formulae. The maximum theoretical estimated intake of infants fed on the studied formulae was lower than the upper limit safety for trivalent chromium of 1 mg kg-1 (14 microg kg-1 b.w. day-1) recommended by the experts of Council for Responsible Nutrition (Hathcock 2004; available at: http://crnusa.org/safety.html), amounting to about 10, 15-18 and 26% of the standard (adapted and follow-up) and toddler, soya, lactose-free and pre-term, and hypoallergenic formulae, respectively. Therefore, manufacturers are called upon to make continued efforts to routinely monitor chromium levels, particularly for specialised and pre-term formulae, and at the same time, might consider the inclusion of labelling the levels of chromium at least in these complex formulations.

Hexavalent chromium [Cr(VI)] has been detected in groundwater across the United States due to industrial and military operations, including plating, painting, cooling-tower water, and chromate production. Because inhalation of Cr(VI) can cause lung cancer in some persons exposed to a sufficient airborne concentration, questions have been raised about the possible hazards associated with exposure to Cr(VI) in tap water via ingestion, inhalation, and dermal contact. Although ingested Cr(VI) is generally known to be converted to Cr(III) in the stomach following ingestion, prior to the mid-1980s a quantitative analysis of the reduction capacity of the human stomach had not been conducted. Thus, risk assessments of the human health hazard posed by contaminated drinking water contained some degree of uncertainty. This article presents the results of nine studies, including seven dose reconstruction or simulation studies involving human volunteers, that quantitatively characterize the absorbed dose of Cr(VI) following contact with tap water via all routes of exposure. The methodology used here illustrates an approach that permits one to understand, within a very narrow range, the possible intake of Cr(VI) and the associated health risks for situations where little is known about historical concentrations of Cr(VI). Using red blood cell uptake and sequestration of chromium as an in vivo metric of Cr(VI) absorption, the primary conclusions of these studies were that: (1) oral exposure to concentrations of Cr(VI) in water up to 10 mg/L (ppm) does not overwhelm the reductive capacity of the stomach and blood, (2) the inhaled dose of Cr(VI) associated with showering at concentrations up to 10 mg/L is so small as to pose a de minimis cancer hazard, and (3) dermal exposures to Cr(VI) in water at concentrations as high as 22 mg/L do not overwhelm the reductive capacity of the skin or blood. Because Cr(VI) in water appears yellow at approximately 1-2 mg/L, the studies represent conditions beyond the worst-case scenario for voluntary human exposure. Based on a physiologically based pharmacokinetic model for chromium derived from published studies, coupled with the dose reconstruction studies presented in this article, the available information clearly indicates that (1) Cr(VI) ingested in tap water at concentrations below 2 mg/L is rapidly reduced to Cr(III), and (2) even trace amounts of Cr(VI) are not systemically circulated. This assessment indicates that exposure to Cr(VI) in tap water via all plausible routes of exposure, at concentrations well in excess of the current U.S. Environmental Protection Agency (EPA) maximum contaminant level of 100 microg/L (ppb), and perhaps those as high as several parts per million, should not pose an acute or chronic health hazard to humans. These conclusions are consistent with those recently reached by a panel of experts convened by the State of California.

Chromium-based catalysts are used for the synthesis of polyethylene, but little is known about the hazard and biomonitoring possibilities of this type of chromium for workers who may be occupationally exposed to such compounds. Therefore, the bioavailability and toxicokinetics of chromium were studied in male Wistar rats after a single intratracheal instillation (2 ml/kg body weight) of various doses (1, 5, or 25 mg/kg body weight) of the catalyst (approximately 1% chromium bound to an amorphous silica matrix), either before (CAT-Cr[III]) or after (CAT-Cr[VI]) heat treatment. The results were compared with those of equivalent amounts of two chromium salts (CrCl(3) and K(2) Cr(2) O (7). Each dose group was composed of three rats. The concentration of chromium was determined by atomic absorption spectrometry in urine (collected daily for 7 d) and in plasma, erythrocytes, lung, and liver tissue obtained 2 d (only highest concentration) and 7 d after dosing. On d 2, a significant increase in lung weight was found in the animals treated with the highest dose of the hexavalent Cr products. On d 7, on the basis of body weights, lung weights, and lung histology, there was no overt toxicity, except after the highest dose of CAT-Cr(VI). The elimination of all forms of chromium was apparently monoexponential, with calculated half-life elimination times in urine of 4-11 h for Cr(III) (CAT-Cr[III] and CrCl3 ) and 8-21 h for Cr(VI) (CAT-Cr[VI] and K(2) Cr(2) O(7). On d 2, the erythro-cytes Cr concentrations were significantly higher for the hexavalent Cr products than for the trivalent Cr products. After 7 d, the erythrocytes Cr concentrations were significantly increased above control values (3 microg/L) only in rats treated with the 2 highest doses of Cr( VI) compounds (12 and 64 microg/L for K(2) Cr(2) O(7), and 14 and 79 microg/L for CAT-Cr[VI]). The present study shows that intratracheally instilled Cr(VI) and Cr(III) have different toxicokinetic profiles and that the Cr(VI) catalyst has the same bioavailability and excretion kinetics as a water-soluble Cr(VI) salt. Exposure to chromium compounds could be monitored by measuring Cr concen-trations in urine (shortly after exposure) and in erythrocytes (also at later time points after high Cr[VI] exposure).

Hexavalent chromium [Cr(VI)] is recognized as a human carcinogen via inhalation, based on elevated rates of lung cancer among occupationally exposed workers in certain industries. Cr(VI) is also genotoxic in bacterial and mammalian cell lines. In contrast, scientific panels in the United States and abroad have reviewed the weight of evidence (WOE) and decided that the available data are insufficient to conclude that Cr(VI) is an oral carcinogen. A criterion of 0.2 ppb was established by a California agency for Cr(VI) in drinking water to prevent cancer, however, this criterion was withdrawn in November, 2001. This criterion was remarkably lower than the promulgated California and federal drinking-water standards for total chromium of 50 ppb and 100 ppb, respectively. Both of the promulgated standards are designed to be protective of humans who ingest Cr(VI). This article describes a WOE analysis to examine the likelihood that Cr(VI) in drinking water poses a cancer hazard at the current U.S. drinking-water standard. The results indicate that: (1) From the historical epidemiological studies, there are a few reports of increased rates of digestive system cancer among Cr(VI)-exposed workers, although most are not statistically significant; (2) the preponderance of evidence from recent epidemiological studies of Cr(VI)-exposed workers does not support an increased risk of cancer outside of the respiratory system; (3) studies of four environmentally exposed populations are negative; (4) there is only one lifetime animal feeding study, and the findings from that study are considered to be flawed and inconclusive; and (5) recent kinetics and in vivo genotoxicity data demonstrate that Cr(VI) is reduced to nontoxic Cr(III) in saliva, in the acidic conditions of the stomach, and in blood. In short, at concentrations at least as high as the current U.S. maximum contaminant level (100 ppb), and probably at least an order of magnitude higher, Cr(VI) is reduced to Cr(III) prior to or upon systemic absorption. The weight of scientific evidence supports that Cr(VI) is not carcinogenic in humans via the oral route of exposure at permissible drinking-water concentrations.

1. The objective of this trial was to study the effects of chromium nicotinate (Cr) supplementation on the performance, carcase characteristics and blood constituents of 9 to 22 week-old male turkeys. 2. Fifty-four 8-week-old male turkeys weighing 2.9 +/- 0.28 kg were allocated at random into 9 groups with 3 dietary treatments and 3 replicates. The dietary treatment was different dietary concentrations of chromium in the basal diet, to provide 0 (control), 1 or 3 mg/kg. The feeding trial lasted for 14 weeks. 3. Results showed that 1 mg/kg chromium supplementation significantly improved weight gain and food intake at 9 to 18 weeks of age but did not significantly influence performance at 19 to 22 week of age. The breast and thigh muscle were significantly increased in birds receiving 1 mg/kg chromium supplementation but were decreased by 3 mg/kg of supplementation. 4. Dietary chromium supplementation did not significantly influence other serum constituents, including insulin, HDL, VLDL+LDL, HDL-C, VLDL-C+LDL-C, total protein, albumin, and gamma-globulin at 18 and 22 weeks of age. 5. The serum triacylglycerol (TG) and uric acid contents were significantly increased, while glycerol and alpha-globulin were significantly reduced by 3 mg/kg chromium supplementation. However, 1 mg/kg chromium supplementation significantly reduced serum cholesterol and glycerol at 18-weeks old. At 22 weeks of age, 1 mg/kg chromium supplementation significantly increased serum glucose and decreased the uric acid concentration whereas 3 mg/kg chromium supplementation significantly increased the creatinine concentration and decreased beta-globulin concentration.

This study examines the magnitude of hexavalent chromium [Cr(VI)] absorption, distribution, and excretion following oral exposure to 5 and 10 mg Cr(VI)/L in drinking water administered as a single bolus dose (0.5 L swallowed in 2 min) or for 3 d at a dosage of 1 L/d (3 doses of 0.33 L each day, at 6-h intervals). Adult male volunteers ingested deionized water containing various concentrations of potassium chromate, and samples of urine, plasma, and red blood cells (RBCs) were collected and analyzed for total chromium throughout the studies. In the bolus dose studies, a fairly consistent pattern of urinary chromium excretion was observed, with an average half life of about 39 h. However, 4-d total urinary chromium excretion and peak concentrations in urine and blood varied considerably among the 5 volunteers. Studies of repeated exposure to smaller volumes ingested at a more gradual rate (i.e., 0.33 L over 5-15 min) showed similar urinary chromium excretion patterns but generally lower chromium uptake/excretion. Given that sustained elevations in RBC chromium levels provide a specific indication of chromium absorption in the hexavalent state, these data suggest that virtually all (> 99.7%) of the ingested Cr(VI) at 5 and 10 mg Cr(VI)/L was reduced to Cr(III) before entering the blood-stream. The interindividual differences in total chromium uptake and excretion are plausibly explained by ingestion of appreciable doses on an empty stomach, which likely results in the formation of well-absorbed Cr(III) organic complexes in gastrointestinal tissues and possibly the blood. The lack of any clinical indications of toxicity in the volunteers and the patterns of blood uptake and urinary excretion of chromium are consistent with a predominant uptake of Cr(III) organic complexes [derived from Cr(VI)] that are excreted more slowly than inorganic forms of Cr(III). Therefore, it appears that the endogenous reducing agents within the upper gastrointestinal tract and the blood provide sufficient reducing potential to prevent any substantial systemic uptake of Cr(VI) following drinking-water exposures at 5-10 mg Cr(VI)/L. Based on these data, the chemical environment in the gastrointestinal tract and the blood is effective even under relative fasting conditions in reducing Cr(VI) to one or more forms of Cr(III).

The uptake and elimination of Cr(VI) in a male volunteer who ingested 2 L/d of water containing 2 mg/L for 17 consecutive days was measured. Total chromium was measured in urine, plasma, and red blood cells (RBCs) for 4 d prior to and 2 wk after dosing (34 d total). The estimated bioavailability (2%) and the plasma elimination half-life (36 h) were consistent with our previous studies of Cr(VI) ingestion in humans. Steady-state chromium concentrations in urine and blood were achieved after 7 d of Cr(VI) ingestion. Both plasma and red blood cell (RBC) chromium concentrations returned rapidly to background levels within a few days after cessation of dosing. Since the concentration of chromium in the RBC should not decrease quickly if the chromium had entered the RBC as Cr(VI), these data support our prior work suggesting that concentrations of 10 mg Cr(VI)/L or less in drinking water of exposed humans appears to be completely reduced to Cr(III) prior to systemic distribution. Clinical chemistry data indicate that no toxicity occurred.

In this study, we evaluate the significance of increased urinary chromium concentrations as a marker of chromium exposure and potential health risk. Six human volunteers ingested trivalent chromium [Cr(III)] and hexavalent chromium [Cr(VI)] at doses that are known to be safe but are much higher than typical dietary levels. The following dosing regimen was used: d 1-7, 200 micrograms/d chromium picolinate (a dietary supplement); d 8-10, Cr(VI) ingestion at the U.S. Environmental Protection Agency (EPA) reference dose (RfD) of 0.005 mg/kg/d; d 11-13, no dose; d 14-16, Cr(III) ingestion at the U.S. EPA RfD of 1.0 mg/ kg/d; and d 17-18, postdose. Urine voids were collected throughout the dosing periods and analyzed for chromium. Our findings are as follows: (1) ingestion of 200 micrograms/d of chromium picolinate yielded significantly elevated urine concentrations such that each participant routinely exceeded background, (2) ingestion of the Cr(VI) RfD (0.005 mg/kg/d) yielded individual mean urinary chromium levels (1.2-23 micrograms/L) and a pooled mean urinary chromium level (2.4 micrograms/L) that significantly exceeded background, and (3) ingestion of the Cr(III) RfD yielded no significant increase in urinary chromium concentrations, indicating that little, if any, absorption occurred. Our work identified three critical issues that need to be accounted for in any future studies that will use urinary chromium as a marker of exposure. First, a minimum urinary chromium concentration of approximately 2 micrograms/L should be used as a screening level to critically identify individuals who may have experienced elevated exposures to chromium. Second, if Cr(III) levels in soils are known to be less than 80,000 ppm and the Cr(III) is insoluble, urinary chromium concentrations are not an appropriate marker of exposure. Third, newer forms of chromium supplements that contain organic forms of Cr(III) must be considered potential confounders and their contribution to residential chromium uptake must be carefully evaluated.