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

Abstract and Introduction


Objectives: We provide an update of the issues surrounding health risk assessment of exposure to cadmium in food.
Data sources: We reviewed epidemiologic studies published between 2004 and 2009 concerning the bioavailability of cadmium in food, assessment of exposure, and body burden estimate, along with exposure-related effects in nonoccupationally exposed populations.
Data extraction and synthesis: Bioavailability of ingested cadmium has been confirmed in studies of persons with elevated dietary exposure, and the findings have been strengthened by the substantial amounts of cadmium accumulated in kidneys, eyes, and other tissues and organs of environmentally exposed individuals. We hypothesized that such accumulation results from the efficient absorption and systemic transport of cadmium, employing multiple transporters that are used for the body's acquisition of calcium, iron, zinc, and manganese. Adverse effects of cadmium on kidney and bone have been observed in environmentally exposed populations at frequencies higher than those predicted from models of exposure. Increasing evidence implicates cadmium in the risk of diseases that involve other tissues and organ systems at cadmium concentrations that do not produce effects on bone or renal function.
Conclusions: Population data raise concerns about the validity of the current safe intake level that uses the kidney as the sole target in assessing the health risk from ingested cadmium. The data also question the validity of incorporating the default 5% absorption rate in the threshold-type risk assessment model, known as the provisional tolerable weekly intake (PTWI), to derive a safe intake level for cadmium.


Because of its high rates of soil-to-plant transfer, cadmium is a contaminant found in most human foodstuffs, which renders diet a primary source of exposure among nonsmoking, nonoccupationally exposed populations (Clemens 2006; Franz et al. 2008; McLaughlin et al. 2006). A safe intake limit of 7 µg cadmium/week/kg body weight was set based on the critical renal cadmium concentration of between 100 and 200 µg/g wet weight that corresponds to a urinary threshold limit of 510 µg/g creatinine [World Health Organization (WHO) 1989, 1993]. However, numerous studies have revealed adverse kidney effects at urinary cadmium levels < 0.5 µg/g creatinine (Satarug and Moore 2004). Further, accumulating evidence links environmental exposure to cadmium with increased cancer incidence. For example, in prospective studies in Japan and the United States, excess cancer mortality was found to be associated with environmental exposure to cadmium (Arisawa et al. 2007b; Menke et al. 2009; Nishijo et al. 2006). Åkesson et al. (2008) observed increased endometrial cancer risk in a Swedish cohort among participants who consumed > 15 µg/day of cadmium, mainly from cereals and vegetables. These findings suggest a very large health burden associated with exposure to cadmium at levels experienced by many populations worldwide.

This review provides an update on cadmium exposure levels and the potential adverse health effects they may elicit in adult populations. We focus first on key issues underpinning health risk assessment of low-level cadmium in the diet, including bioavailability of dietary origin, the 5% default absorption rate, thresholds and safe intake levels, and the kidney as a specific target for cadmium accumulation. Second, we review epidemiologic studies from 2004 to 2009 that link exposure levels to observed effects in classic targets (kidney and bone) along with newly identified potential target organs. We also summarize evidence that links cadmium with diabetes, diabetic nephropathy, hypertension, peripheral artery disease (PAD), myocardial infarction, diminished lung function, periodontal disease, and age-related macular degeneration (AMD). Evidence from prospective studies reveal potential causal relationships of cadmium exposure with life prognosis (all-cause mortality) and excess cancer mortality and suggest that cadmium is at least a comorbidity factor if not a causative factor. Specifically, we summarize cadmium-cancer associations for the lung, pancreas, breast, endometrium, prostate, and urinary bladder.


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