Use of this information is subject to copyright laws and may require the permission of the owner of the information, as described in the ECHA Legal Notice.
EC number: 215-149-9
CAS number: 1306-25-8
Evaluation of Cadmium and Tellurium Levels in Control Samples
The urine, faeces, kidney and liver concentrations of cadmium and
tellurium in the vehicle dosed (control) animals were all below the
lower limit of quantification.
Evaluation of Cadmium and Tellurium Levels in Samples from the
Treatment Groups (750 and 1500 ppm Cadmium telluride)
When cadmium telluride was given via the diet for 14 days at 750 and
1500 ppm, the average cadmium concentrations in faeces were 629500 and
1118333 ng/g respectively. The average concentrations of tellurium in
faeces were 697500 and 1240000 ng/g and below the lower limit of
quantification and 52 ng/mL in urine at 750 and 1500 ppm respectively.
The kidney and liver concentrations of cadmium and tellurium and urine
concentrations of cadmium were all below the lower limit of
Evaluation of Cadmium and Tellurium Levels in Samples from the
Reference Groups (30 ppm Cadmium chloride)
When cadmium chloride was given via the diet for 14 days at 30 ppm, the
average cadmium concentrations in faeces, kidney and liver were 30633,
773 and 659 ng/g respectively. The average tellurium concentration in
faeces was 947 ng/g, however, the source of the tellurium
in 2 of the animals in the reference group is unknown. The kidney, liver
and urine concentrations of tellurium and urine concentrations of
cadmium were all below the lower limit of quantification.
Remark: In the 30 ppm cadmium chloride group (Reference Group), some
measurable concentrations of tellurium were detected in faeces of two
animals (No. 11 and 12), leading to above mentioned average tellurium
concentration of 947 ng/g, even though these animals were not
exposed to tellurium via their diet. It is unclear how tellurium could
be present in the faecesof unexposed animals. The tellurium values
ranged from 1200 to 1640 ng/g wet weight. Animals were group housed,
therefore it is unlikely that these two animals (No. 11 and 12) were
exposed to cadmium telluride while animal No. 10 was not. Moreover,
samples from animal Nos. 10, 11 and 12 were measured subsequently,
therefore, the possibility of contamination from ICP equipment with
previous measured samples was not the source of tellurium
contamination/measurements. Moreover, the samples of the reference group
were measured after the samples of Group 1 followed by a blank sample,
eliminating the possibility of contamination of the equipment.
Therefore, the source of tellurium measured in the faeces of animal No’s
11 and 12 dosed with cadmium chloride is unknown.
The objectives of this 14-day pilot study (Dose Range Finding study) was
to determine whether cadmium telluride up to 100 mg/kg bw/day (1500 ppm)
was well tolerated, when given via diet for 14 days to Wistar Han rats
and to provide data for the selection of the dose levels for a
subsequent sub-chronic (90-day) oral toxicokinetic study. In addition,
the cadmium and tellurium concentrations in the liver, kidney, faeces
and urine were compared to the reference group (cadmium chloride).
The following parameters and endpoints were evaluated in this study:
clinical signs, body weights, food consumption, test article intake,
cadmium and tellurium concentrations in liver, kidney, urine and faeces,
macroscopic findings and kidney and liver weights. No test item-related
findings were noted for clinical signs, body weight, food consumption,
macroscopic findings and organ weights.
-The urine, faeces, kidney and liver concentrations of cadmium and
tellurium in the vehicle dosed (control) animals were all below the
lower limit of quantification (LLOQ).
-At 750 and 1500 ppm cadmium telluride, respectively:
• In faeces: the average cadmium concentrations were 629500 and 1118333
ng/g, and the average tellurium concentrations were 697500 and 1240000
• In urine, the average cadmium concentrations were below the lower
limit of quantification, and the average tellurium concentrations were
respectively below the
lower limit of quantification and 52 ng/mL.
• The kidney and liver concentrations of cadmium and tellurium were all
below the lower limit of quantification.
-In the 30 ppm cadmium chloride group (Reference Group), the average
cadmium concentration in faeces, kidney and liver were 30633, 773 and
695 ng/g respectively. The average tellurium concentration in faeces was
947 ng/g. The kidney, liver and urine concentrations of tellurium and
urine concentrations of cadmium were all below the lower limit of
In the 30 ppm cadmium chloride group (Reference Group), some measurable
concentrations of tellurium were detected in faeces of two animals (No.
11 and 12), leading to above mentioned average tellurium concentration
of 947 ng/g, even though these animals were not exposed to tellurium via
their diet. It is unclear how tellurium could be present in the faeces
of unexposed animals. The tellurium values ranged from 1200 to 1640 ng/g
wet weight. Animals were group housed, therefore it is unlikely that
these two animals (No. 11 and 12) were exposed to cadmium telluride
while animal No. 10 was not. Moreover, samples from animal Nos. 10, 11
and 12 were measured subsequently, therefore, the possibility of
contamination from ICP equipment with previous measured samples was not
the source of tellurium contamination/measurements. Moreover, the
samples of the reference group were measured after the samples of Group
1 followed by a blank sample, eliminating the
possibility of contamination of the equipment. Therefore, the source of
tellurium measured in the faeces of animal No’s 11 and 12 dosed with
cadmium chloride is unknown.
Based on the results of the 14-day Dose Range Finder study,
administration of cadmium telluride in diet was well tolerated in rats
at levels up to 1500 ppm (corresponding to an actual
test article intake of 161 mg/kg bw/day).
Currently in-life results collected until Week 10. No test item-related
clinical signs were observed in any of the test item groups. The
absolute body weights and body weight gain was comparable with controls.
Food consumption is still comparable with controls for all test item
of In-life is foreseen 23 Dec 2019 (last date of necropsy).
results is foreseen to be available 24 January 2020 , with Bioanalytical
Draft Report and Toxicokinetic Draft Report foreseen for 7 February and
14 February respectively
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).
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
For cadmium and
its various compounds, systemic toxicity is attributed to the cadmium
ion and differences in toxicity are principally linked to
bioavailability. Although several factors influence bioavailablity, the
main physico-chemical property of importance is solubility in water or
biological fluids. Substances with higher solubility are expected to
penetrate more easily into the organism and therefore generally show
a sparingly soluble Cd-compound. This is known from water solubility
data (cfr IUCLID section 4.8) and demonstrated by in vitro methods
‘bio-elution assays’ in which the amount of ion ‘available for
absorption’ is measured. The dissolution (e.g. elution or extraction) of
Cd++ion from surrogate (synthetic) tissue fluid is measured.
The resultant value is termed bioaccessibility and is defined as the
amount of a substance (e.g Cd++) available for absorption
(Stopford et al 2003). The bio-elution data (for details cfr IUCLID) are
summarized below .
Table- Bio-elution data on CdTe measured in different physiological
2 hours as % Cd released of total Cd content
24- 168 hours as % Cd released of total Cd Content
LysosomalBioaccesibility24- 168 hours as % Cd released of total Cd Content
SweatBioaccesibility24- 168 hours as % Cd released of total Cd Content
35.35 ± 8.69 (ref ECTX 2013)*
1.5 (ref ECTX 2018)
0.10 - 0.08
* ECTX 2013, 2 hours Bio-elution Study on
Cadmium telluride at a 0.2 g/L loading in a simulated gastric fluid was
repeated in ECTX 2018 with CdTe sample as smallest put on the market (75-250 µm)
Reason for performing
ECTX 2018 was because of variable results between repeated experiments
in ECTX 2013 and to perform the test in a series of tests in comparison
with other Cadmium CMR compounds.
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
(Sasser and Jarboe, 1977; Weigel et al.,1984; ECB, 2007).
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 al.,1980).
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;
absorption, the deposition 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
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 1μg/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 2μg/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.
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 Clark, 1988).
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.
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 > 3μg/g
creatinine), 30 years exposure to 50μg/m³
of cadmium would lead to a Cd-U of 3μg/g
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.Reproduction or further distribution of this information may be subject to copyright protection. Use of the information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner.
Welcome to the ECHA website. This site is not fully supported in Internet Explorer 7 (and earlier versions). Please upgrade your Internet Explorer to a newer version.
Do not show this message again