Abstracts: ISEE 21st Annual Conference, Dublin, Ireland, August 25–29, 2009: Poster Presentations
Cadmium is a toxic metal, commonly used in various industrial products, such as rechargeable batteries. It is also a common pollutant in fertilizers. 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, low iron status in particular. Cadmium is efficiently retained in the kidney (half-life 10–30 years), the concentration being proportional to that in urine (U-Cd). Cadmium is nephrotoxic, initially causing renal tubular damage and 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 and eventually to renal failure. Recent data also suggest increased cancer risks and increased mortality in environmentally exposed populations. Early effects on kidneys and bone have been detected at U-Cd levels between 0.5 and 3 μg Cd/g creatinine. A large proportion of the non-smoking adult population has urinary cadmium concentrations of 0.5 μg/g creatinine or higher in areas with no specific source of cadmium exposure. For smokers this proportion is considerably higher.
There is thus no margin of safety at current exposure/dose levels in the general population. Therefore, measures should be put in place to reduce exposure to a minimum. This is reflected in the recent lowering of the tolerable weekly intake by the European Food Safety Agency to 2.5 micrograms per kilogram of body weight, based on a urinary excretion of 1.0 μg/g creatinine.