Urine cadmium

Another occupational study compared 53 lead-exposed male workers (2 nonwhite, 51 white) (mean PbB, 47.4 pg/dL range, 44-51 pg/dL) from a plant processing lead and cadmium compounds with a control group of 52 workers (8 nonwhite, 44 white) (mean PbB, 8.1 pg/dL, with none exceeding 20 pg/dL) from a nonlead industry (de Kort et al. 1987). Blood pressure levels were positively correlated with PbB and urine cadmium levels, but not with blood cadmium levels. The correlation for systolic blood pressure and PbB level remained significant after controlling for confounding variables. 

Total phenol in urine Benzene in exhaled air mixed-exhaled end-exhaled Cadmium Cadmium in urine Cadmium in blood Carbon disulphide 2-Thiothiazolidine-4-carboxylic acid (= TTCA) in urine... 

Mueller PW, Smith SJ, Steimberg KK,Thun MJ.Chronic renal tubular effects in relation to urine cadmium levels. Nephron 1989 52 45-54. 

In diagnosis, indicators of renal damage. in particular microglobulin in urine, can be u.sed to monitor the effects. Blood and urine cadmium estimates (Table I) will give an objective index of the degree of exposure, and, in some cases, the cadmium content of renal biopsy tissue may be useful. 

Table 7—Urine cadmium concentrations in the U.S. adult population, cumulative frequency distribution of urinary cadmium (n=982) [in percentage]...

Table 8—Urine cadmium concentrations in workers exposed to cadmium in the workplace...

CADMIUM AND INORGANIC COMPOUND Cadmium in urine Not critical 5 pg/g creatinine B... 

Cadmium is effectively accumulated in the kidneys. When the cadmium concentration exceeds 200 gg/g in the kidney cortex, tubular damage will occur in 10% of the population, and proteins begin to leak into urine (proteinuria). When the concentration of cadmium in the kidney cortex exceeds 300 pg/g, the effect is seen in 50% of the exposed population. Typically, excretion of low-molecular weight proteins, such as beta-microglobulin, is increased, due to dysfunction of proximal tubular cells of the kidney. The existence of albumin or other high-molecular weight proteins in the urine indicates that a glomerular injury has also taken place. The excretion of protein-bound cadmium will also be increased. 

A negative correlation was found between PbB and systolic pressure in Belgian men in the Cadmibel study (a cross-sectional population study of the health effects of environmental exposure to cadmium) (Staessen et al. 1991). In this study, blood pressure and urinary cation (positive ions found in the urine, such as sodium, potassium, and calcium) concentration data were obtained from 963 men and 1,019 women multiple stepwise regression analyses were conducted adjusting for age, body mass index, pulse... 

Drasch G, Wanghofer E, Roider G. 1997. Are blood, urine, hair, and muscle valid biomonitors for the internal burden of men with the heavy metals mercury, lead and cadmium Trace Elements and Electrolytes 14(3) 116-123. 

Khera AK, Wibberiev DG, Edwards KW, et al. 1980b. Cadmium and lead levels in blood and urine in a series of cardiovascular and normotensive patients. International Journal of Environmental Studies 14 309-312. 

Biological half times of cadmium in humans is lengthy. Based on body burden and excretion data, cadmium may remain in the human body for 13 to 47 years. Although cadmium is excreted primarily in urine and feces, it tends to increase in concentration with the age of the organism and eventually acts as a cumulative poison (Hammons et al. 1978). These phenomena have not been documented adequately in wildlife species. 

In mammals, cadmium inhibits copper absorption across the intestinal mucosa (Aaseth and Norseth 1986). Intercorrelations of copper with cadmium and zinc in livers of polar bears (Ursus maritimus) are probably mediated by metallothioneins, which may contain all three metals (Braune etal. 1991). In rats, copper protects against nephrotoxicity induced by cadmium, provided that copper is administered 24 h prior to cadmium insult. Specifically, rats given 12.5 mg Cu/kg BW by way of subcutaneous injection 24 h before receiving 0.4 mg Cd/kg BW — when compared to a group receiving Cd alone — did not have excessive calcium in urine and renal cortex or excessive protein in urine. Thus, 2.8 mg Cu/kg BW protects against 0.25 mg Cd/kg BW (Liu et al. 1992). 

A number of workers have described methods for the determination of mercury in which the mercury is first reduced to the element or collected as the sulfide on a cadmium sulfide pad. It is then volatilized into a chamber for measurement. These techniques are extremely sensitive. Thillez108) recently described a procedure for urinary mercury in which the mercury is collected on platinum and then volatilized into an air stream. Rathje109) treated 2 ml of urine with 5 ml of nitric acid for 3 min, diluted to 50 ml, and added stannuous chloride to reduce the mercury to the element. A drop of Antifoam 60 was added and nitrogen was blown through the solution to carry the mercury vapor into a quartz end cell where it is measured. Six nanograms of mercury can be detected. Willis 93) employed more conventional methods to determine 0.04 ppm of mercury in urine by extracting it with APDC into methyl-n-amyl ketone. Berman n°) extracted mercury with APDC into MIBK to determine 0.01 ppm. 

Lehnert et al. 127>128) determined physiological levels of cadmium in serum and urine using atomic absorption spectroscopy. Ten milliliters of serum or 50 ml... 

Berman u°) could determine as little as 0.005 ppm cadmium in serum and 0.002 ppm in urine by extracting the cadmium from the digest with lead in sodium diethyldithiocarbamate into MIBK. Torres 112) isolated cadmium from urine by ion exchange chromatography. 

The first fractionation of urinary ampholytes in this way was carried out by Boulanger et al. (BIO) in 1952 with the use of ion-exchange resins. They had designed this procedure previously for the fractionation of ampholytes in blood serum (B8). According to this method, deproteinized urine was subjected to a double initial procedure aiming at the separation of low-molecular weight substances from macro-molecular ones. One of the methods consisted of the fractionation of urinary constituents by means of dialysis, the second was based on the selective precipitation of urinary ampholytes with cadmium hydroxide, which, as had previously been demonstrated, permits separation of the bulk of amino acids from polypeptides precipitated under these circumstances. Three fractions, i.e., the undialyzable part of urine, the dialyzed fraction, and the so-called cadmium precipitate were analyzed subsequently. 

Severe illness and death can occur from exposure to many cadmium compounds. It is absorbed in the gastrointestinal tract. However, it can be eliminated in the urine and feces in young, healthy people. 

R., Normal Levels of Cadmium in Diet, Urine, Blood, and Tissues of Inhabitants of the United States, J. 

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