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Cadmium [Cd, 48]
for environmental exposure (above 10 μg/L), and occupational exposure (up to
50 μg/L) (WHO 2011b).
Cadmium absorption after dietary exposure in humans is relatively low (3%–5%),
but it is efficiently retained in the kidney and liver, where it is bound to metallothioneinen (MT, a low molecular weight cysteine-rich, intracellular protein) (Pappas
et al. 2011).
Cadmium is primarily toxic to the kidney, especially to the proximal tubular
cells, where it accumulates over time, and may cause a decrease in the glomerular filtration rate, and eventually renal failure. It can also cause bone demineralization, either through direct bone damage or indirectly, as a result of renal dysfunction
(EFSA 2012a). Increased levels of Cd measured in blood or urine have been found to
be associated with various cardiovascular end-points, including myocardial infarction, stroke, heart failure, hypertension, and changes in arterial function (aortic pulse
wave velocity and carotid, brachial, and femoral pulse pressures). However, the epidemiological evidence for an association between cardiovascular diseases and Cd is
weak (WHO 2011b).
Cadmium and its compounds have been classified by the International Agency
for Research on Cancer (IARC) as carcinogenic to humans (group 1), with sufficient
evidence for lung cancer. Also, positive associations have been observed between
exposure to Cd and Cd compounds and cancers of the kidney and prostate. Most of
the evidence is derived from high Cd exposure of exposed workers through inhalation (IARC 2012a).
Cadmium in the environment has been a concern since the 1960s, when a painful
bone disease was reported to have been caused by Cd industrial pollution in an area
in Japan (mine Zn–Pb). People who consumed the polluted rice and drunk the river
water over a period of 30 years were found to have accumulated a large amount of Cd
in their bodies, which leads to a serious osteoporosis—such as bone disease, known
to the Japanese as itai-itai disease.
Toxicity of Cd is significantly enhanced for children, who are exposed to even low
levels. Adverse effect of Cd exposure on child development resulted from Cd-induced
neurotoxicity. Exposure to Cd may have a negative effect on fetal growth. Recently,
in a large, population-based, longitudinal mother–child cohort in Bangladesh
(n = 1.616) an association between maternal Cd exposure and birth size in girls (but
not in boys) was observed. Recently, based on data from the same cohort (n = 1.305),
an association between early-life Cd exposure and lower child intelligence scores is
argued (Concha et al. 2013).
Children and infants may have higher exposure to metals, because they consume
more food in relation to their body weight and absorb metals more readily than
adults. Children with higher Cd levels are three times more likely to have learning
disabilities, and participate in special education.
The Joint FAO/WHO Expert Committee on Food Additives (JECFA) noted that
the existing health-based guidance value for Cd was expressed on a weekly basis
(provisional tolerable weekly intake, or PTWI, but, owing to Cd exceptionally long
half-life, considered that a monthly value was more appropriate. The Committee,
therefore, withdrew the PTWI of 7 μg/kg bw and established a provisional tolerable
monthly intake of 25 μg/kg bw (WHO 2011b), whereas the European Food Safety