Cadmium body burden

Drasch, G.A. 1983. An increase of cadmium body burden for this century an investigation on human tissues. Sci. Total Environ. 26 111-120. 

Lock K, Janssen CR. 2001. Zinc and cadmium body burdens in terrestrial oligochaetes use and significance in environmental risk assessment. Environ Toxicol Chem 20 2067-2072. 

Buchet JP, Eauwerys R, Roels El, Bernard A, Bruaux P, Claeys F, DucofFre G, De Plaen P, Staessen J, Amery A, Eijnen P, Thijs L, Rondia D, Sator F, Saint-Remy A, Nick L. Renal effects of cadmium body burden of the general population. Eancet 1990 336 699-702. Nordberg GF, Goyer RA, Nordberg M. Comparative toxicity of cadmium metallothionein and cadmium chloride on mouse kidney. Arch Pathol 1975 99 192-197. 

Lauwerys R, Hardy R, Job M, Buchet JP, Roels H, Bruaux P, Rondia D. Environmental pollution by cadmium and cadmium body burden an autopsy study.Toxicol Lett 1984 23 287-289. 

Drasch G, Kauert G and Von Meyer L (1985) Cadmium body burden of an occupationally non burdened population in southern Bavaria. Int Arch Occup Environ Health 55 141-148. 

Sartor, F., Rondia, D., Claeys, F., Buchet, J.P., Ducoffre, G.. Lauwereys, R., Staessenr, J.. and Amery, A. Factors influencing the cadmium body burden in a population study. In Nordberg, G.F., Herber. R.F.M.,and Alessio, L. (Eds.). Cadmium in the human environ-... 

Cadmium introduced into the body through inhalation or ingestion is transported by the albumin fraction of the blood plasma to the liver, where it accumulates and is stored principally as a bound form complexed with the protein metallothionein. Metallothionein-bound cadmium is the main form of cadmium subsequently transported to the kidney it is these 2 organs, the liver and kidney, in which the majority of the cadmium body burden accumu-iates. As much as one half of the total body burden of cadmium may be found in the kidneys (Nordberg and Nordberg 1988). 

Current exposure levels remain sufficiently low to prevent the accumulation of cadmium body burdens sufficient to cause disease in the future by monitoring CDB as an indicator of recent cadmium exposure ... 

CDU Is widely used as an indicator of cadmium body burdens (Nordberg and Nordberg 1988). CDU is the major route of elimination and, when CDU is measured, it is commonly expressed either as pg Cd/I urine (unadjusted), pg Cd/I urine (adjusted for specific gravity), or pg Cd/g CRTU (see Section 5.2.1). The metabolic model for CDU Is less complicated than CDB, since CDU is dependent in large part on the body (i.e., kidney) burden of cadmium. However, a small proportion of CDU still may be attributed to recent cadmium exposure, particularly if exposure to high airborne concentrations of cadmium occurred. Note that CDU Is subject to larger interindividual and day-to-day variations than CDB, so repeated measurements are recommended for CDU evaluations. 

About 0.02% of the cadmium body burden is excreted daily in urine. When the critical cadmium concentration (about 200 ppm) in the kidney is reached, or if there is sufficient cadmium-induced kidney dysfunction, dramatic increases in CDU are observed (Nordberg and Nordberg 1988). Above 200 ppm, therefore, CDU concentrations cease to be an indicator of cadmium body burden, and are instead an index of kidney failure. 

Medical monitoring mandated by the final cadmium rule includes a combination of regular medical examinations and periodic monitoring of 3 analytes CDB, CDU and B2MU. As indicated above, CDB is monitored as an indicator of current cadmium exposure, while CDU serves as an indicator of the cadmium body burden B2MU is assessed as an early marker of irreversible kidney damage and disease. 

As stated in Section 4.3, CDB concentrations are representative of ongoing levels of exposure to cadmium. Among those who have been exposed chronically to cadmium for extended periods, however, CDB may contain a component attributable to the general cadmium body burden. 

Prior to the onset of renal dysfunction, CDU concentrations provide a general indication of the exposure history (i.e., body burden) (see Section 4.3). Once renal dysfunction occurs, CDU levels appear to increase and are no longer indicative solely of cadmium body burden (Friberg and Elinder 1988). 

Travis D and Haddock A. (1980). Interpretation of the obsen/ed age-dependency of cadmium body burdens in man. Environmental Research, 22, 46-60. 

Sugita M (1978) The biological half-time of heavy metals. The existence of a third "slowest" component. Int. Arch. Occup. Environ. Health 41 25-40 Travis CC, Haddock AG (1980) Interpretation of the observed age-dependency of cadmium body burdens in man. Environ. Res. 22 46-60 Webster WS (1979) Cadmium-induced fetal growth retardation in mice and the effects of dietary supplements of zinc, copper, iron and selenium. J. Nutr. 109 1646-1651... 

E ig. 4. Schematic representation of cadmium accumulation in renal cortex as a function of duration of exposure. Corresponding levels of cadmium in kidney cortex (CdKc), liver (CdL), and urine (CdU) and of the estimated cadmium body burden (Cd-body) are indicated. The CdU levels were obtained from (a) the relationship log CdU.CdKc or (b) the relationship log CdU.-Cd-body. These relationships between the various parameters apply only to Cd workers without renal dysfunction (from Roels et al. 1981a)... 

In summary, it can be concluded that the probability of developing Cd-induced renal dysfunction in male Cd workers appears to be very low when the critical CdU level of 10 yg/g creatinine is not regularly exceeded. This CdU level corresponds to an average cadmium body burden of 160 mg. From the dose-response relationship between CdB and the prevalence of signs of renal dysfunction, at least in workers currently exposed to cadmium, a value of 1 yg Cd/100 ml whole blood is proposed as a tentative no-effect level for long-term Cd exposure (Buchet et al. 1980b). 

Cadmium in urine reflects the body burden of cadmium, especially the cadmium concentration in the main accumulation organ, the kidney (organ-specific accumulation). Therefore, it can be regarded as indicator of the cumulative long term exposure. As long as the renal function remains normal, the concentration of cadmium in urine is well correlated with the total cadmium body burden. After cadmium-induced irreversible tubular renal dysfunction with microproteinuria, the cadmium excretion in urine tends to increase, as cadmium is released from renal depots [2,3]. 

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