ReviewCurrent status of cadmium as an environmental health problem
Introduction
Cadmium has been recognised as an occupational health hazard for many decades. The risks to environmentally exposed populations were emphasized later, when it was concluded that the infamous Itai-itai disease was caused by intake of cadmium-polluted rice (Hagino and Kono, 1955). Since then, numerous studies have reported health effects of cadmium exposure in the general population also in the absence of specific industrial exposure, the main sources of exposure being food and tobacco smoke. During the last decade an increasing number of studies have found adverse health effects at much lower levels than in the earlier studies.
Section snippets
Exposure
The diet is the main source of environmental cadmium exposure in non-smokers in most parts of the world. Atmospheric deposition of airborne cadmium, mining activities and the application of cadmium-containing fertilizers and sewage sludge on farm land may lead to the contamination of soils and increased cadmium uptake by crops and vegetables grown for human consumption.
Cadmium is present in virtually all foods, but the concentrations vary to a great extent, depending on type of food and level
Renal effects
An increasing number of studies have shown early adverse health effects at much lower levels of cadmium exposure than previously anticipated. Research has focused on kidney and bone effects, but recent studies have also reported excess cancer risks at low-level environmental exposure. Although there is still a consensus that the kidney is the critical organ, effects on bone have increasingly been shown at similar low levels of exposure as for the early kidney effects.
For chronic dietary
Conclusions
Several epidemiological studies using a variety of early markers of kidney damage have identified points of departure for early effects (NOEL and BMDL) between 0.5 and 3 μg Cd/g creatinine. Recent studies suggest that decreased GFR and creatinine clearance may occur at similar cadmium dose levels, approximately at Cd-U of 1 μg Cd/g creatinine. Adverse effects on bone have been detected at U-Cd levels from 0.5 μg Cd/g creatinine. In addition, recent studies have indicated increased risk of
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