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EC number: 244-168-5
CAS number: 21041-95-2
Uptake of cadmium can occur in humans
via the inhalation of polluted air, the ingestion of contaminated food
or drinking water and, to a minor extent, through exposure of the skin
to dusts or liquids contaminated by the element (ECB, 2008; SCOEL, 2010).
In occupational settings, mainly
inhalation exposure occurs although the dermal route may also play a
role when metal, powder or dust is handled or during maintenance of
machinery. Additional uptake is possible through food and tobacco (for
example in workers who eat or smoke at the workplace).
For the general population, uptake of
cadmium occurs principally via the ingestion of food or, to a lesser
extent, of contaminated drinking water. In industrial sites polluted by
cadmium, inhalation of air and/or ingestion of soil or dusts may
contribute to significant exposure. Tobacco is an important additional
source of cadmium uptake in smokers. Finally, the consumer could be
exposed (skin, inhalation or oral) through the use of consumption
Gastrointestinal absorption of cadmium
is usually less than 5% but varies with the form of cadmium present, the
composition of the diet, age and the individual iron status. High
gastrointestinal absorption rates (up to 20%) have been observed for
example in women with lowered iron stores (serum ferritin <20 μg/L)
(Sasser and Jarboe, 1977; Weigel et al., 1984; ECB, 2007).
Cadmium is absorbed by the respiratory
route at rates varying between 2 and 50% depending on the cadmium
compound involved (water soluble or insoluble), the size of the
particles (dusts or fumes), the deposition pattern in the respiratory
tract and the ventilation rate. Values of 10 to 30% for dusts and 25-50%
for fumes are cited in the EU Summary Risk Assessment Report (RAR) (ECB,
2007) and various publications (Boisset et al., 1978; Glaser et
al., 1986; Oberdörster et al., 1979; Oberdörster and
Cox, 1989; Oberdörster, 1992; Dill et al., 1994; Hadley et
The results from studies in mouse,
rat, rabbit and in vitro human skin models suggest that, although
cadmium may penetrate through skin, absorption of soluble and less
soluble compounds is generally lower than 1% (Kimura and Otaki, 1972;
Lansdown and Sampson, 1996; Wester et al., 1992; ECB, 2008).
Following absorption, the
biodisposition of cadmium (Cd2+) is assumed to be independent
of the chemical form to which exposure occured (ECB, 2007). Cadmium is a
cumulative toxicant. It is transported from its absorption site (lungs
or gut) to the liver, where it induces the synthesis of metallothionein
which sequestrates cadmium. The cadmium-metallothionein complex is then
slowly released from the liver and transported in the blood to the
kidneys, filtrated through the glomerulus and reabsorbed in the proximal
tubule where it may dissociate intracellularly (Chan and Cherian, 1993).
There, free cadmium again induces the synthesis of metallothionein,
which protects against cellular toxicity until saturation.
In non-occupationally exposed
individuals, cadmium concentrations in kidney is generally between 10
and 50 mg/kg wet weight, with smokers showing 2 to 5-fold higher values
than non-smokers (Nilsson et al., 1995). After long-term low
level exposure, approximately half the cadmium body burden is stored in
the liver and kidneys, one third being in the kidney where the major
part is located in the cortex (Kjellström et al., 1979). The
kidney:liver concentration ratio decreases with the intensity of
exposure and is, for instance, lower in occupationally exposed workers
(7 to 8-fold ratio) (Ellis et al., 1981; Roels et al.,
1981) than in the general population (10 to 30-fold ratio) (Elinder et
al., 1985). The distribution of cadmium in the kidney is important
as this organ is one of the critical targets after long-term exposure.
In blood, most cadmium is localised in
erythrocytes (90%) and values measured in adult subjects with no
occupational exposure are generally lower than 1 μg/L in non-smokers.
Blood cadmium (Cd-B) values are 2 to 5-fold higher in smokers than in
non-smokers (Staessen et al., 1990; Järup et al.,
1998; Ollson, 2002). In the absence of occupational exposure, the mean
urinary cadmium concentration (Cd-U) is generally below 1 to 2 μg/g
creatinine in adults. While Cd-B is influenced by both recent exposure
and cadmium body burden, Cd-U is mainly related to the body burden
(Lauwerys and Hoet, 2001). Smokers excrete more cadmium than non-smokers
and their Cd-U is on average 1.5-fold higher than for non-smokers.
The placenta provides a relative
barrier, protecting the foetus against cadmium exposure. Cadmium can
cross the placenta but at a low rate (Trottier et al.,2002;
Lauwerys et al.,1978; Lagerkvist et al.,1992).
Cadmium is not known to undergo any
direct metabolic conversion such as oxidation, reduction or alkylation.
The cadmium (Cd2+) ion does bind to anionic groups
(especially sulfhydryl groups) in proteins and other molecules (Nordberg et
al., 1985). Plasma cadmium circulates primarily bound to
metallothionein and albumin (Foulkes and Blanck, 1990; Roberts and
Absorbed cadmium is excreted very
slowly, with urinary and fecal pathways being approximately equal in
quantity (< 0.02% of the total body burden per day) (Kjellström et
al., 1985). It accumulates over many years, mainly in the renal
cortex and to a smaller extent in the liver and lung. The biologic
half-life of cadmium has been estimated to be between 10 to 30 years in
kidney and 4.7 to 9.7 years in liver (Ellis et al., 1985). The
half-life in both organs is markedly reduced with the onset of renal
toxicity when tubule loss of cadmium is accelerated. The total cadmium
body burden reaches about 30 mg by the age of 30.
Biomonitoring methods for either Cd-B
or Cd-U are often used rather than airborne measurements because they
integrate all possible sources of occupational and environmental
exposures (e.g. digestive exposure at the workplace, tobacco smoking and
diet). In addition, since cadmium is a cumulative toxicant, a measure of
the body burden (i.e. Cd-U) is the most appropriate exposure parameter
for conducting risk assessments. In workers with substantial cadmium
exposure (i.e. Cd-U > 3 μg/g creatinine), 30 years exposure to 50 μg/m³
of cadmium would lead to a Cd-U of 3 μg/g creatinine(SCOEL,
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