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Abstract
Cadmium is a toxic metal occurring in the environment naturally and as a pollutant
emanating from industrial and agricultural sources. Food is the main source of cadmium
intake in the non-smoking population. The bioavailability, retention and toxicity
are affected by several factors including nutritional status such as low iron status.
Cadmium is efficiently retained in the kidney (half-time 10-30 years) and the concentration
is proportional to that in urine (U-Cd). Cadmium is nephrotoxic, initially causing
kidney tubular damage. Cadmium can also cause bone damage, either via a direct effect
on bone tissue or indirectly as a result of renal dysfunction. After prolonged and/or
high exposure the tubular injury may progress to glomerular damage with decreased
glomerular filtration rate, and eventually to renal failure. Furthermore, recent data
also suggest increased cancer risks and increased mortality in environmentally exposed
populations. Dose-response assessment using a variety of early markers of kidney damage
has identified U-Cd points of departure for early kidney effects between 0.5 and 3
microg Cd/g creatinine, similar to the points of departure for effects on bone. It
can be anticipated that a considerable proportion of the non-smoking adult population
has urinary cadmium concentrations of 0.5 microg/g creatinine or higher in non-exposed
areas. For smokers this proportion is considerably higher. This implies no margin
of safety between the point of departure and the exposure levels in the general population.
Therefore, measures should be put in place to reduce exposure to a minimum, and the
tolerably daily intake should be set in accordance with recent findings.