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EC number: 618-920-1
CAS number: 93280-40-1
specific data on toxicokinetics, metabolism and distribution is
available for the registered substance Vanadate(1-),
oxo[phosphato(3-)-κO]-, hydrogen, hydrate (2:2:1).
oxo[phosphato(3-)-κO]-, hydrogen, hydrate (2:2:1) is a dark-grey powder
with a meldting point > 400°C and a water solubility of ca. 150 g/L
(determination via V: 148 g/L ± 17 g/L and determination via P: 156 g/L
± 16 g/L f or at 20°C). For
this compound the oxidation state of V(+4).
data from soluble +4-valent and +5-valent
vanadium substance were taken into account to address toxicokinetics,
metabolism and distribution of the registered substance.
comment on grouping and read across
unnecessary (animal) testing, a comprehensive grouping and read-across concept
has been developed, which is described in detail further below.
concept is based on the chemistry / composition of all substances and on
a experimental studies for (i) water solubility and (ii) in-vitro
bioaccessibility studies: assessment of the solubility and speciation of
vanadium substances in five different artificial physiological fluids.
Robust summaries for these studies are provided in each registration
conclusions of this testing programme can be summarised as follows:
Bioaccessibility – Read-across
The dissolution of metallic vanadium
and tri-, tetra and pentavalent vanadium substances was assessed in
various artificial physiological media. These were selected to simulate
relevant human-chemical interactions (as far as practical), i.e. for
contact of a test substance with skin, or for a substance entering the
human body by inhalation or by ingestion. There is no
internationally agreed guideline for these tests (e.g. OECD). However,
similar tests have been conducted for several metal substances and
alloys incl. steel in previous risk assessments or in recent preparation
for REACH, and some results have been published (e.g. Stopford et al,
2003, Herting et al, 2006; Midander et al, 2007). The composition of
these artificial test media has been discussed by Kuhn and Rae, 1988;
Moss, 1979, Stopford et al, 2004; Herting et al, 2006; Midander et al,
2007 and references therein. This test programme included the following
pH 7.4) is a standard physiological solution that mimics the ionic
strength of human blood serum. It is widely used in research and medical
health care (e.g. Hanawa, 2004; Okazaki and Gotoh, 2005) as reference
test solution for comparison with data from simulated physiological
pH 7.4) mimics interstitial fluid within the deep lung under normal
health conditions (Stopford et al, 2004)Artificial lysosomal fluid(ALF,
pH 4.5) simulates intracellular conditions in lung cells occurring in
conjunction with phagocytosis and represents relatively harsh conditions
(Stopford et al, 2004).
Artificial gastric fluid(GST,
pH 1.5) mimics the very harsh digestion milieu of high acidity in the
Artificial sweat solution(ASW,
pH 6.5) simulates an exposure scenario in contact with human skin, i.e.
the hypo-osmolar fluid, linked to hyponatraemia (loss of Na+from
blood), that is excreted from the body when sweating. This fluid is
recommended in the available standard for the testing of nickel release
from nickel containing products (EN1811, 1998).
Vanadium substances were incubated
with freshly made solutions at a solid to liquid ratio of 0.1 g/L. This
loading is similar to the loading in transformation/dissolution testing
in environmental media according to OECD Series No. 29. Two exposure
periods (2h and 24h) were used, and exposure times were strictly
controlled to enable modelling of the dissolution process as a rate over
time. The relative surface area of the test substances was determined by
BET-absorption measurements. These absorption measurements allow for an
assessment of the dissolution process in relation to sample surface area
and total sample mass.
After cessation of the incubation
period, the remaining solid material was separated from the supernatant,
pH was measured and the supernatant solutions were analysed for
dissolved vanadium concentration(s) by appropriate, validated analytical
methods (i.e. ICP-MS).Speciation analysis of V(IV) and V(V) was
performed by HPLC coupled to ICP-MS. The concentration of possible
further species (i.e. V(III)) was determined indirectly by subtracting
the amount of V(IV) and V(V) from the total amount of vanadium.
of vanadium substances in physiological relevant media
Dissolved V [%]
2-h exposure time
24-h exposure time
Tetravalent vanadium compound (i.e. VOSO4)
Phosphate-buffered saline (PBS, pH 7.4)
29 % tetravalent V
68 % pentavalent V
100 % pentavalent V
Gamble’s solution (GMB, pH 7.4)
100 % pentavalent V
Artificial lysosomal fluid (ALF, pH 4.5)
94 % tetravalent V
15 % pentavalent V
90 % tetravalent V
11 % pentavalent V
Artificial gastric fluid (GST, pH 1.5)
74 % tetravalent V
32 % pentavalent V
50 % pentavalent V
Artificial sweat solution (ASW, pH 6.5)
54 % tetravalent V
51 % pentavalent V
32 % tetravalent V
72% pentavalent V
Pentavalent vanadium compound (i.e. NaVO3)
93 % pentavalent V
65 % tetravalent V
40 % pentavalent V
100 % tetravalent V
4 % tetravalent V
90 % pentavalent V
6 % tetravalent V
5 % tetravalent V
89 % pentavalent V
99 % pentavalent V
Pentavalent vanadium compound (i.e. V2O5)
97 % pentavalent V
98 % pentavalent V
91 % tetravalent V
95 % pentavalent V
94 % pentavalent V
The results of this bioaccessibiliy
testing programme can be summarised as follows:
The readily soluble vanadium substance
such as VOSO4, NaVO3, and V2O5dissolve
practically completely in all physiological media already after only a
short period of time, rendering them to be expected of similar and
Upon dissolution, all vanadium
substances more or less finally transform to the pentavalent form in all
media except ALF; here, even the pentavalent forms are converted almost
completely to the tetravalent species already after a short period of
In bioaccessibility tests of tetra-
and pentavalent vanadium substances and metallic vanadium, tetra- and
pentavalent forms dissolved completely within 2h in various media
selected to simulate relevant human-chemical interactions (i.e. PBS
mimicking the ionic strength of blood, artificial lung, lysosomal, and
gastric fluid as well as artificial sweat). Despite differences in
solubility, the bioaccessibility data suggest the following:
All vanadium substances upon dissolution
transform predominantly into pentavalent forms in physiological media,
with the exception of ALF in which tetravalent V was the predominant
species present after 2 and 24h.
vanadiumdissolves into pentavalent forms in PBS and GMB, and
predominantly to tetravalent forms in ALF and GST
expected, pentavalent vanadium substances are released and retained as
pentavalent forms in physiological media, with the exception of ALF in
which tetravalent V dominates after 2h and is the only form present
Table: Conclusion on bioavailability
factors of different vanadium substances for risk characterisation and
The published animal data on oral
absorption of vanadium substances is summarised in the table below:
Table: Animal data on oral absorption
of vanadium substances
2.6design/reporting inadequate,sampling/analysis and mass balance incomplete,72h sampling period(bladder and intestinal content not subtracted)
Conklin et al. 1982
4.2design incomplete only 24h urinary excretion considered for result
Al-Bayati et al. 1991
17.5(based on urinary secretion), design/reporting inadequate,sampling/analysis and mass balance incomplete,120h sampling period, (bladder content not subtracted)
Wiegmann et al. 1982
16.5(based on balance of faecal excretion)admin via food (100ppm), design incomplete,
7d feeding/sampling,analysis incomplete(bladder and intestinal content not subtracted)
Adachi et al. 2000
39.7(based on balance of faecal excretion),
admin via food (0.1-25ppm), design incomplete,14d feeding/sampling, analysis incomplete(bladder and intestinal content not subtracted)
Bogden et al. 1982
2.6not assignable, (only abstract available)
Sollenberger et al. 1981
16.0highly relevantrel. bioavailability assessed based on comparison of AUC after iv vs oral admin,120h sampling period, radiotracer analysis
Azay et al. 2001
According to EFSA (2004), “the
low concentration of vanadium normally present in urine compared with
the daily intake and the faecal levels indicate, that less than 5% of
ingested vanadium is absorbed (WHO, 1996). The results of animal studies
are in general in agreement with this conclusion. Uptake of radioactive
vanadium pentoxide given orally to rats was 2.6% of the administered
dose (Conklin et al., 1982). Other studies in rats have indicated that
amounts greater than 10% can be absorbed from the gastrointestinal tract
under some conditions (Bogden et al., 1982; Wiegmann et al., 1982).“
For pentavalent vanadium, the studies
by Conklin et al. (1982), Al-Bayati et al. (1991) and Bogden et al.
(1982) are considered incomplete because of study design (administration
and analytical procedure) and sampling period. The studies by Wiegmann
et al. (1982) and Adachi (2000), despite limitations in their design,
allow a reasonable assessment of oral absorption of pentavalent V forms
and yield a consistent picture of ca. 16% oral absorption.
For tetravalent absorption, the study
by Sollenberger et al. (1991) cannot be assessed, whereas the study by
Azay et al (2001) has a very reliable study design (AUC determination
after concurrent i.v. and g.i. administration), yielding an oral
absorption of 16% for tetravalent V, in line with the value obtained for
in-vivo data are available on soluble tetra- and pentavalent vanadium
substances (V2O5, NaVO3, and VOSO4),
suggesting an oral absorption value of 16%.
According to WHO
(1988), absorption by this route is generally considered to be very low
for vanadium substances.
absence of measured data on dermal absorption, current guidance suggests
the assignment of either 10% or 100% default dermal absorption rates. In
contrast, the currently available scientific evidence on dermal
absorption of metals (predominantly based on the experience from
previous EU risk assessments) yields substantially lower figures, which
can be summarised briefly as follows:
dermal absorption values for metals or metal substances in studies
corresponding to the most recent OECD test guidelines are typically 1 %
or even less. Therefore, the use of a 10 % default absorption factor is
not scientifically supported for metals. This is corroborated by
conclusions from previous EU risk assessments (Ni, Cd, Zn), which have
derived dermal absorption rates of 2 % or far less (but with
considerable methodical deviations from existing OECD methods) from
considering that under industrial circumstances many applications
involve handling of dry powders, substances and materials, and since
dissolution is a key prerequisite for any percutaneous absorption, a
factor 10 lower default absorption factor may be assigned to such “dry”
scenarios where handling of the product does not entail use of aqueous
or other liquid media. This approach was taken in the in the EU RA on
zinc. A reasoning for this is described in detail elsewhere (Cherrie and
Robertson, 1995), based on the argument that dermal uptake is dependent
on the concentration of the material on the skin surface rather than
following default dermal absorption factors for metal ions are therefore
proposed (reflective of full-shift exposure, i.e. 8 hours):
exposure to liquid/wet media: 1.0
dry (dust) exposure: 0.1
approach is consistent with the methodology proposed in HERAG guidance
for metals (HERAG fact sheet - assessment of occupational dermal
exposure and dermal absorption for metals and inorganic metal
substances; EBRC Consulting GmbH / Hannover /Germany; August 2007).
The fate and
uptake of deposited particles depends on the clearance mechanisms
present in the different parts of the airway. In the head region, most
material will be cleared rapidly, either by expulsion or by
translocation to the gastrointestinal tract. A small fraction will be
subjected to more prolonged retention, which can result in direct local
absorption. More or less the same is true for the tracheobronchial
region, where the largest part of the deposited material will be cleared
to the pharynx (mainly by mucociliary clearance) followed by clearance
to the gastrointestinal tract, and only a small fraction will be
retained (ICRP, 1994). Once translocated to the gastrointestinal tract,
the uptake will be in accordance with oral uptake kinetics.
the material deposited in the head and tracheobronchial regions would be
translocated to the gastrointestinal tract without any relevant
dissolution, where it would be subject to gastrointestinal uptake at a
ratio of 16%(regardless
of whether the ingested material is either tetra- or pentavalent).In
contrast, the material that is
deposited in the pulmonary region may be assumed by default to be
absorbed to 100%. This absorption value is chosen in the absence of
relevant scientific data regarding alveolar absorption although knowing
that this is a conservative choice. Thus, the following predicted
inhalation absorption factors can be derived for vanadium substances.
For further information on particle size, see IUCLID section 4.5.
Head/TB (=GI) [%]
Absorption factor via inhalation [%]
Vanadium pentaoxide- Granules
Vanadium pentaoxide – Powder
A number of
vanadium dependent enzymes have been found in lower organisms, such as
bacteria and algae. In higher animals and humans, however, no specific
biochemical function has yet been identified for vanadium. Nevertheless,
the possibility has been considered that vanadium might play a role in
the regulation of some enzymes, such as the Na+/K+exchanging
ATPase, phosphoryl-transfer enzymes, adenylate cyclase and protein
kinases. Therefore, its role in hormone, glucose, lipid, bone and tooth
metabolism has also been discussed (WHO, 1996). Vanadium
substances have been shown to mimic the action of insulin in isolated
cell systems, animal models and diabetic patients. Therefore, their use
in the therapy of diabetes mellitus has been considered (Shechter, 1990;
Shamberger, 1996). Vanadium has also
been suggested as an aid in body building, but there is no evidence that
it is effective (Fawcett et al., 1996). Altogether,
vanadium has not been shown to be essential for humans and does not have
a nutritional value. Even though some signs of vanadium deficiency have
been reported in goats and rats (WHO, 1996), vanadium deficiency has not
been identified in humans.
Vanadium is an
element, and as such, is not subject to metabolisation as such. However,
vanadium transforms rather quickly to predominantly pentavalent vanadium
species upon dissolution which can be expected to represent the
under all physiological circumstances perhaps except for inhalation and
subsequent uptake by the lysosomes of macrophages.
available, vanadium is subject to changes in speciation or valence, i.e.
interconversion of the two oxidation states, the tetravalent form,
vanadyl (VO2+) and the pentavalent form vanadate (VO3-).
The anionic pentavalent form is reported to predominate in extracellular
fluids whilst the cationic tetravalent vanadyl ion appears to be the
most common intracellular form. Thus, in the oxygenated blood, it
circulates as vanadate but in tissues, it is retained mainly as vanadyl.
Depending on the availability of reducing agents, including reduced
glutathione-SH, NADPH, NADH, and oxygen, vanadium may be reduced,
reoxidised, and/or undergo redox cycling.
Chasteen et al., 1986have verified the
simultaneous presence of vanadium (IV) and (V) species in biological
media (tissues, blood, urine and faeces) after dietary supplementation
of rats with 15-25 ppm vanadyl sulfate for 180 days, as well as oral
(gavage) administration of48V (100 µg V/kg bw) either as
vanadyl sulfate or as ammonium vanadate. To avoid oxidation of vanadium
(IV) to (V), dissection was performed under a nitrogen atmosphere, and
excised tissues were frozen in liquid nitrogen. Most important is the
conclusion that ingested vanadyl (IV) is retained as such during the
gastric passage and eliminated via faeces or urine, with little
absorption in the intestine. In contrast, vanadate (V) is apparently
quantitatively reduced in the gastric milieu to (IV) vanadium. However,
circulating vanadyl in blood appears to partly oxidise to the
pentavalent state due to the oxygen tension. These conclusions appear to
be in line with EFSA (2004) and ATSDR (1992).
According to EFSA (2004), “absorbed
vanadium is transported in the serum mainly bound to transferrin.
Extracellular vanadium is present in the form of vanadate (5+)
and intracellular vanadium most likely in the vanadyl (4+)
According to ATSDR (1992),Vanadium
can reversibly bind to transferrin protein in the blood and then be
taken up into erythrocytes. These two factors may affect the biphasic
clearance of vanadium that occurs in the blood. There is a slower uptake
of vanadyl into erythrocytes compared to the vanadate form. Five minutes
after an intravenous administration of radiolabeled vanadate or vanadyl
in dogs, 30% of the vanadate dose and 12% of the vanadyl dose is found
in erythrocytes (Harris et al. 1984). It is suggested that this
difference in uptake is due to the time required for the vanadyl form to
be oxidized to vanadate.
When V+4 or V+5 is administered
intravenously, a balance is reached in which vanadium moves in and out
of the cells at a rate that is comparable to the rate of vanadium
removal from the blood (Harris et al. 1984). Initially, vanadyl leaves
the blood more rapidly than vanadate, possibly due to the slower uptake
of vanadyl into cells (Harris et al. 1984). Five hours after
administration, blood clearance is essentially identical for the two
forms. A decrease in glutathione, NADPH, and NADH occurs within an hour
after intraperitoneal injection of sodium vanadate in mice (Bruech et
al. 1984). It is believed that vanadate requires these cytochrome P-450
components for oxidation to the vanadyl form. A consequence of this
action is the diversion of electrons from the monooxygenase system
resulting in the inhibition of drug dealkylation (Bruech et al. 1984).
Vanadium in the plasma can exist in
a bound or unbound form (Bruech et al. 1984). Vanadium as vanadyl
(Patterson et al. 1986) or vanadate (Harris and Carrano 1984) reversibly
binds to human serum transferrin at two metalbinding sites on the
protein. With intravenous administration of vanadate or vanadyl, there
is a short lag time for vanadate binding to transferrin, but, at 30
hours, the association is identical for the two vanadium forms (Harris
et al. 1984). The vanadium-transferrin binding is most likely to occur
with the vanadyl form as this complex is more stable (Harris et al.
1984). The transferrin-bound vanadium is cleared from the blood at a
slower rate than unbound vanadium in rats, which explains a biphasic
clearance pattern (Sabbioni and Marafante 1978). The metabolic pathway
appears to be independent of route of exposure (Edel and Sabbioni 1988).“
Placental transfer, and transfer
via mother’s milk
„Analytical studies have shown very
low levels in human milk (Byrne and Kosta 1978). Evidence from animal
studies supports the occupational findings(ATSDR, 1992).
Acute studies with rats showed the
highest vanadium concentration to be located in the skeleton. Male rats
had approximately 0.05% of the administered 48V in bones, 0.01% in the
liver, and <0.01% in the kidney, blood, testis, or spleen after 24 hours
(Edel and Sabbioni 1988). Conklin et al. (1982) reported that after 3
days, 25% of the absorbed vanadium pentoxide was detectable in the
skeleton and blood of female rats. In female rats exposed to sodium
metavanadate in the diet for 7 days, the highest concentrations of
vanadium were found in bone, followed by the spleen and kidney (Adachi
et al. 2000b); the lowest concentration was found in the brain.In a
study byDaiet al., 1994 with non-diabetic and
streptozotocin-diabetic rats given vanadyl sulfate in their
drinking-water (0.5–1.5 mg/mL) for 1 year, vanadium concentrations were
distributed in the following order: bone > kidney > testis > liver >
pancreas > plasma > brain. Vanadium was found to be retained in these
organs 16 weeks after cessation of treatment while plasma concentrations
were below the limits of detection at this time.These findings appear to
be in line with EFSA (2004) and ATSDR (2008).
According to EFSA (2004), “after
administration by different routes to rats, the highest amounts were
found in lungs (after intratracheal installation), bone, kidneys, liver
and spleen. Studies on rats and mice showed a three-compartment model
for elimination with plasma half-times of 15 minutes, 14 hours and 8.5
days (Lagerkvist et al., 1986).”
„Oral exposure for an intermediate
duration produced the highest accumulation of vanadium in the kidney.
Adult rats exposed to 5 or 50 ppm vanadium in the drinking water for 3
months had the highest vanadium levels in the kidney, followed by bone,
liver, and muscle (Parker and Sharma 1978). The retention in bone may
have been due to phosphate displacement. All tissue levels plateaued at
the third week of exposure. A possible explanation for the initially
higher levels in the kidney during intermediate-duration exposure is the
daily excretion of vanadium in the urine. When the treatment is stopped,
levels decrease in the kidney. At the cessation of treatment, vanadium
mobilized rapidly from the liver and slowly from the bones. Other tissue
levels decreased rapidly after oral exposure was discontinued. Thus,
retention of vanadium was much longer in the bones (Edel et al. 1984;
Parker and Sharma 1978). In rats exposed to approximately 100 mg/L
vanadium in drinking water as vanadyl sulfate or ammonium metavanadate
for 12 weeks, significant increases, as compared to controls, in bone,
kidney, and liver vanadium levels were observed; no alterations in
vanadium muscle levels were found (Thompson et al. 2002). The highest
concentration of vanadium was found in the bone, followed by the kidney
and liver. Tissue vanadium concentrations were significantly higher in
rats exposed to ammonium metavanadate as compared to animals exposed to
vanadyl sulfate.“(ATSDR, 2008)
According to EFSA (2004), “studies
on rats and mice showed a three-compartment model for elimination with
plasma half-times of 15 minutes, 14 hours and 8.5 days (Lagerkvist et
studies showed that urinary vanadium levels significantly increased in
exposed workers (Gylseth et al. 1979; Kiviluoto et al. 1981b; Lewis
1959; Orris et al. 1983; Zenz et al. 1962). Male and female workers
exposed to 0.1-0.19 mg/m3 vanadium in a manufacturing company, had
significantly higher urinary levels (20.6 μg/L) than the
nonoccupationally exposed control subjects (2.7 μg/L) (Orris et al.
1983). The correlation between ambient vanadium levels and urinary
levels of vanadium is difficult to determine from these epidemiological
studies (Kiviluoto et al. 1981b). In most instances, no other excretion
routes were monitored. Analytical studies have shown very low levels in
human milk (Byrne and Kosta 1978). Evidence from animal studies supports
the occupational findings. Vanadium administered intratracheally to rats
was reported to be excreted predominantly in the urine (Oberg et al.
1978) at levels twice that found in the feces (Khoads and Sanders 1985).
Three days after exposure to vanadium pentoxide, 40% of the recovered
48V dose was cleared in the urine while 30% remained in the skeleton,
and 2%-7% was in the lungs, liver, kidneys, or blood (Conklin et al.
1982). Epidemiological studies and animal studies suggest that
elimination of vanadium following inhalation exposure is primarily in
the urine“.(ATSDR, 1992).
vanadium is poorly absorbed in the gastrointestinal tract, a large
percentage of vanadium is excreted unabsorbed in the faeces in rats
following oral exposure. More than 80% of the administered dose of
ammonium metavanadate or sodium metavanadate accumulated in the feces
after 6 or 7 days (Adachi et al. 2000b; Patterson et al. 1986). After 2
weeks of exposure, 59.1±18.8% of sodium metavanadate was found in the
feces (Bogden et al. 1982). However, the principal route of excretion of
absorbed vanadium is through the kidney in animals. Approximately 0.9%
of ingested vanadium was excreted in the urine of rats exposed to sodium
metavanadate in the diet for 7 days (Adachi et al. 2000b). An
elimination halftime of 11.7 days was estimated in rats exposed to
vanadyl sulfate in drinking water for 3 weeks (Ramanadham et al. 1991).“(ATSDR-Draft,
Hamel & Duckworth (1995) examined the
mechanisms controlling metabolism and pharmacokinetics of oral V
administration, i.e. the accumulation of V in various organs from rats
fed a liquid diet for 18 days, containing no or supplemental V at
varying concentrations given as sodium orthovanadate or vanadyl sulfate.
Organs of non-supplemented animals contained widely varying
concentrations (ng of V/g dry tissue weight) with brain < fat < blood <
heart < muscle < lung < liver < testes < spleen < kidney. All organs
accumulated V in a dose dependent manner, but not all organs were at
steady state conditions after 18 days. Additional rats were fed both V
substances, switched to control diet, and assayed at 0, 4 and 8 days to
calculate organ halftimes of V. Insulin sensitive tissue tissues,
including liver and fat, had shorter halftimes than tissues that are
relatively less insulin sensitive, including spleen, brain and testes.
Sodium orthovanadate and vanadyl sulfate fed rats showed similar
accumulation and elimination patterns.Vanadium elimination halftimes in
various tissues were 3.57–15.95 or 3.18–13.50 days following a one-week
exposure to 8.2 mg V/kg/day as sodium metavanadate or vanadyl sulfate,
Table: Vanadium elimination halftimes
in organs in rats exposed to 8.2 mg V/kg/day for 1 Week (Hamel &
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EFSA (2004) Opinion of the scientific
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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.
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