Cadmium, Environmental Exposure, and Health Outcomes

Soisungwan Satarug; Scott H. Garrett; Mary Ann Sens; Donald A. Sens


Environ Health Perspect. 2010;118(2):182-90. 

In This Article

Conclusions and Perspectives

Recent epidemiologic studies involving an exposureeffect assessment have linked low-level cadmium exposure of current populations with some adverse effects that are not restricted to kidney and bone, but include almost every organ and tissue where cadmium accumulates, including eye tissues. These data argue strongly for public health measures aimed at reducing exposure. In the past, the wide variation in cadmium body burden among people has been attributed to cigarette smoking and the high pulmonary absorption rates of cadmium in cigarette smoke. However, as revealed in the present review, the difference in body burden of cadmium between smokers and nonsmokers is less than 3-fold. We suggest that the signs of early renal injury and mild tubular impairment observed in chronic low-dose exposure situations viewed previously as benign could indeed be an early warning sign of subclinical or clinical morbidity and mortality. This assertion is substantiated by the dose response observed between cadmium body burden and all-cause mortality and cancer mortality in the Belgian and the U.S. cohorts. We also believe that cadmium is secreted in breast milk and that calcium and zinc supplements could be considered to lower the cadmium content in breast milk to minimize potential effects of early-life exposure to cadmium.

Many issues require further research. A precise risk estimate is needed to quantify the carcinogenic risk because the high prevalence of cadmium exposure means that even a small increase in risk could yield a large number of preventable cancer cases. To be valid, the threshold-based PTWI model, although appearing to be a reasonable method for deriving a safe exposure level, will require appropriate input from current scientific knowledge. Thus, revising the current safe intake level for cadmium is much needed. A strong consideration should be given to a safety factor issue, which is necessary to protect subpopulations with increased susceptibility, such as those with diabetes. Animal studies have shown that the symptoms of diabetic nephropathy and cadmium renal toxicity are enhanced when both the metal and the disease are present. The enhanced cadmium absorption noted for young age groups indicates that new intake guidelines may need to be established for pediatric populations. The application of the BMD method should be expanded and applied to other toxicity end points to identify the organs, other than the kidney, that should be considered as critical for deriving safe exposure levels. The potential genetically determined rates of cadmium absorption, uptake, accumulation, and toxicity remain largely unexplored and should be subjects of future research. With the looming cancer and chronic disease epidemics worldwide, we encourage research in the following areas: cadmium exposure assessment, identification of potential exposure sources, and the determination of cadmium body burden in future epidemiologic investigations. Such research would provide an estimate of total disease burden (cost) of population exposure. In addition, therapeutically effective chelating agents to enhance excretion of cadmium are lacking, and this factor makes prevention of cadmium accumulation pivotal. The persistence of cadmium in the environment requires a long-term approach to minimize human exposure through environmental management and maintenance of lower cadmium levels wherever possible.


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