Urine chromium excretion

Morris B, MacNeil S, Fraser R, et al. 1995b. Increased urine chromium excretion in normal pregnancy. Clin Chem 41(10) 1544-1545. 

Intestinal absorption of is low, ranging from 0.4% to 2.5%, so fecal output is mainly unabsorbed dietary chromium. Absorption is increased marginally by ascorbic acid, amino adds, oxalate, and other dietary factors. After absorption, chromium binds to plasma transferrin with an affinity similar to that of iron. It then concentrates in human liver, spleen, other soft tissue, and bone. Urine chromium output is around 0.2 to 0.3 U,g/day, the amount excreted being to some extent dependent upon intake. Paradoxically, urine output appears to be relatively increased at low dietary levels. Thus 2% is lost in urine at an intake of lOpg/day, but only 0.5% at an intake of 40pg/day. Both running and resistive exercise increases urine chromium excretion. 

There appears to be a chromium pool in individuals who are not chromium deficient (136). When there is an increase in level of cHculating insulin in response to a glucose load, an increase in circulating chromium occurs over a period of 0.5—2 h. This is foUowed by a decline and excretion of chromium in urine increases. Chromium deficiency is indicated when no increase or a small increase in blood chromium level or urine chromium occurs. 

Information regarding the excretion of chromium in humans after dermal exposure to chromium or its compounds is limited. Fourteen days after application of a salve containing potassium chromate(VI), which resulted in skin necrosis and sloughing at the application site, chromium was found at 8 mg/L in the urine and 0.61 mg/100 g in the feces of one individual (Brieger 1920). A slight increase (over background levels) in urinary chromium levels was observed in four subjects submersed in a tub of chlorinated water containing 22 mg chromium(VI)/L as potassium dichromate(VI) for 3 hours (Corbett et al. 1997). For three of the four subjects, the increase in urinary chromium excretion was less than 1 pg/day over the 5-day collection period. 

A number of factors have been shown to alter the rate of excretion of chromium in humans. Intravenous injection of calcium EDTA resulted in a rapid increase in the urinary excretion of chromium in metal workers (Sata et al. 1998). Both acute and chronic exercises have been shown to increase chromium excretion in the urine, though the increased excretion did not appear to be accompanied with decreased levels of total native chromium (Rubin et al. 1998). An increased rate of chromium excretion has been reported in women in the first 26 weeks of pregnancy (Morris et al. 1995b). Chromium supplementation did not appear to alter the rate of excretion into breast milk in postpartum women (Mohamedshah et al. 

The main route of excretion of absorbed chromium is via the kidneys in urine. However, the variability in urinary chromium excretion is such that it is impossible to distinguish occupational and environmental exposures to chromium from that due to dietary supplementation (Gauglhofer and Bianchi 1991). 

Absorbed chromium is principally excreted in the urine with a small amount being eliminated in hair, sweat, and bile. Urine levels appear to be a useful indicator of chromium intake when dietary intake is >40 p.g/day however, excretion becomes constant when the intake is <40 jt,g/day. Urine chromium levels have been reported to be increased in diabetes, glucose loading, strenuous running, and physical trauma. Anderson has stated that urine chromium does not appear to be related to blood glucose, insulin, lipid, or any other studied clinical variables [11]. 

Each time that the GTF is called upon to do its work, there is a corresponding rise in the amount of chromium excreted in the urine. Apparently, the GTF is utilized less efficiently by diabetics who need injections of insulin than it is by normal, healthy people. Hence, diabetics might have above average needs for this factor. 

Urinary excretion data from 15 female and 27 male subjects given 200 pg chromium(III) as chromium trichloride indicated that gastrointestinal absorption was at least 0.4% (Anderson et al. 1983). Net absorption of chromium(III) by a group of 23 elderly subjects who received an average of 24.5 pg/day (0.00035 mg chromium(III)/kg/day) from their normal diets was calculated to be 0.6 pg chromium(III)/day, based on an excretion of 0.4 pg chromium/day in the urine and 23.9 pg chromium/ day in the feces, with a net retention of 0.2 pg/day. Thus about 2.4% was absorbed. The retention was considered adequate for their requirements (Bunker et al. 1984). 

Normal urinary levels of chromium in humans have been reported to range from 0.24—1.8 pg/L (0.00024-0.0018 mg/L) with a median level of 0.4 pg/L (0.0004 mg/L) (Iyengar and Woittiez 1988). Humans exposed to 0.05-1.7 mg chromium(III)/m3 as chromium sulfate and 0.01-0.1 mg chromium(VI)/m3 as potassium dichromate (8-hour time-weighted average) had urinary excretion levels from 0.0247 to 0.037 mg chromium(III)/L. Workers exposed mainly to chromium(VI) compounds had higher urinary chromium levels than workers exposed primarily to chromium(III) compounds. An analysis of the urine did not detect the hexavalent form of chromium, indicating that chromium(VI) was rapidly reduced before excretion (Cavalleri and Minoia 1985 Minoia and Cavalleri 1988). 

An acute, oral dose of radioactive chromium(III) as chromium chloride or chromium(VI) as sodium chromate was administered to humans after which feces and urine were collected for 24 hours and 6 days, respectively, and analyzed for chromium. The amount of chromium in the 6-day fecal collection was 99.6 and 89.4% of the dose for chromium(ni) and chromium(VI) compounds, respectively. The amount of chromium in the 24-hour urine collection was 0.5 and 2.1% of the dose for chromium(ni) and chromium(VI) compounds, respectively (Donaldson and Barreras 1966). In subjects drinking 0.001-0.1 mg chromium(VI)/kg/day as potassium chromate in water for 3 days, <2-8% of the dose was excreted in the urine (Finley et al. 1997). The percentage of the dose excreted appeared to increase with increasing dose. 

Rats given a subcutaneous injection of potassium dichromate (chromium(VI)) and chromium nitrate (chromium(III)) excreted 36% of the chromium(VI) dose in urine and 13.9% in the feces within 7 days ... 

Chromium(VI) readily enters erythrocytes, where it is reduced to chromium(III) by glutathione, and chromium(III) is essentially trapped within erythrocytes, where it binds to proteins, primarily hemoglobin. This may explain the fact that chromium shows little toxicity at sites distant from administration sites (De Flora and Wetterhahn 1989). The chromium(ni) trapped within the erythrocytes would be released upon natural destruction of the erythrocyte and excreted in the urine. 

Gregus and Klaassen carried out a comparative study of fecal and urinary excretion and tissue distribution of eighteen metals in rats after intravenous injection. Total (fecal + urinary) excretion was relatively rapid (over 50% of the dose in 4 days) for cobalt, silver and manganese between 50 and 20% for copper, thallium, bismuth, lead, cesium, gold, zinc, mercury, selenium and chromium and below 20% for arsenic, cadmium, iron, methylmercury and tin. Feces was the predominant route of excretion for silver, manganese, copper, thallium, lead, zinc, cadmium, iron and methylmercury whereas urine was the predominant route of excretion of cobalt, cesium, gold, selenium, arsenic and tin. Most of the metals reached the highest concentration in liver and kidney. However, there was no... 

Hexavalent chromium (6 ") is a recognized carcinogen, and industrial exposure to fiimes and dusts containing this metal is associated with increased incidence of lung cancer, dermatitis, and skin ulcers. Environmental health risks arise from soil contamination by Cr " waste disposal sites left by the leather tanning and dyestuff industries. Cr is more efficiently absorbed than Cr " and its toxicity and carcinogenic effects involve reduction to Cr and Cr " by cysteine, with the formation of intracellular DNA adducts. Cr species are relatively nontoxic partly because of their poor intestinal absorption and rapid excretion in urine. 

Trivalent chromium is the most stable form in the food supply. Absorption estimates for chromium(III), based on metabolic balance studies or on urinary excretion from physiological intakes, range from 0.4 to 2.5% (Doisy et al. 1971 Bunker et al. 1984 Anderson and Kozlovsky 1985 Offenbacher etal. 1986 Anderson 1987). Because of analytical problems associated with the measurement of chromium absorption, several investigators have used the urinary excretion of chromium as an indicator of absorption. When dietary chromium intake was 10 pg per day, 2% of that amount was absorbed (estimated as urinary excretion), whereas at a chromium intake of 40 pg only 0.4-0.5% of the chromium was recovered in the urine (Anderson and Kozlovsky 1985). 

The percentage of a chromium dose excreted in the urine is independent of the oxidation state of the administered chromium. About 21%-22% is excreted in the 24 h following intravenous injection of a soluble salt of either Cr(III) or Cr(VI) in rats (Cikrt and Bencko 1979). 

Not all chromium is excreted in the urine, however. Cikrt and Bencko (1979) found 0.5% of an intravenous dose of Cr Cl3 and 3.5% of an intravenous dose of Na2Cr 04 in the bile of rats during the first 24 h after administration. The chief difference in the behaviors of the two oxidation states of chromium was a more rapid excretion of Cr(VI) during the first few... 

The resorption of hexavalent chromium compounds is 3-5 times higher than resorption of trivalent chromium compounds. In blood, hexavalent chromium enters into blood cells and erythrocytes more easily than trivalent chromium and binds to haemoglobin. Trivalent chromium is resorbed in the blood plasma bound to a-globuhn and transferrin. Transferrin provides chromium transportation to the tissues. In some target tissues, chromium from transferrin binds to apochromoduhn with the formation of chromodulin. In the cells, about 50% of chromium is contained in the nucleus and about 20% in the cytoplasm. Chromium is excreted from the body mainly in the urine. Excessive intake of chromium by experimental animals or chromium intoxication also leads to excretion of chromodulin in the urine. Biosynthesis of this metaUopeptide thus participates in the detoxification of chromium. 

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