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EC number: 232-219-4 | CAS number: 7790-75-2
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
Endpoint summary
Administrative data
Description of key information
Key value for chemical safety assessment
Additional information
Read-across - calcium wolframate:
Calcium wolframate is the salt of wolframic acid. It is composed of calcium cations and wolframate anions so that calcium wolframate is electrically neutral (i.e. without a net charge). Any dissolution ofcalcium wolframatewill release the wolframate anion that is pH-dependent in equilibrium with undissociated wolframic acid (as based on the pKa of wolframic acid).
Thus, wolframate and wolframic acid, coexist in aqueous solution in adynamic pH-dependant equilibrium. Under neutral and basic conditions, the wolframate ion predominates whereas under more acidic conditions, the hydrogen wolframate anion and finally (below a pH of ca. 5) wolframic acid is more prevalent.
H2WO4 HWO4-+ H+ WO42-+ 2H+
The pKa values for wolframic acid is estimated to be 3.50 and 4.60 based on handbook data (Hollemann Wiberg, Lehrbuch der Anorganischen Chemie, 101.Auflage). The mean pKa value for calcium cations is estimated to be 12.6 based on handbook data (Lide, D.R., 2008).A Hägg-graph representing the equilibrium ofwolframic acid/ wolframateis provided below.
Due to its electronegativity E0(Ca/Ca2+) = -2,84V calcium is present in the environment only in the divalent cationic form. At high solution pH, i.e. above 12, calcium hydroxide complexes are formed.
Other calcium species, potentially relevant for the environmental of human health hazard assessment, are not present at environmentally or physiologically relevant redox conditions and solution pH.
According to the Hägg-graph and the Pourbaix- diagram wolframate is the dominant species under ENV conditions (Seiler et al., 2005). Anthropogenic use of W utilizes W metal or WC, which are thermodynamically unstable and when introduced into environmental systems begins to alter to a more stable form (WO42-) (Andersson and Bergstrom 2000).
Wolfram metal is (due to its negative potential (-0.09 to -1.074, pH0 - pH14)) transformed to wolframate which represents the most stable oxidation state of Wolfram(see Pourbaix Diagram below).
W + H2O/1.5 O2 --> 2 H++ WO42-
Hence, under physiological conditions wolframic acid, hydrogen wolframate and wolframate co-exist in a pH-dependent manner, irrespective of their origin.
Acute oral toxicity - wolfram metal:
Tungsten metal isnot acutely toxic via the oral routebased on an acute oral toxicity study according to OECD guideline 401 with a LD50 vaue >2,000 mg/kg bw and does not require classification according to Regulation (EC) No 1272/2008 and subsequent amendments and corrections.
Recalculating the LD50 value to CaWO4 - considering that W is the toxicological relevant species and that the solubility of CaWO4 is lower than the solubility of W metal - affords a LD50 value for CaWO4 of >3,100 mg/kg bw.
Acute oral toxicity - calcium ion:
The normal adult diet contains about 25 mmol of calcium per day. Only about 5 mmol of this is absorbed into the body per day across the intestinal epithelial cells brush border membrane and immediately bound to calbindin, which is a vitamin D-dependent calcium-binding protein. Calbindin transfers the calcium directly through the basal membrane on the opposite side of the cell, where it is actively transported into the body by TRPV6 and calcium pumps (PMCA1) (Balesaria et al., 2009). The plasma total calcium concentration is in the range of 2.2-2.6 mmol/l, whereas the normal ionized calcium is 1.3-1.5 mmol/L. Depending on the plasma albumin concentration, the main carrier of protein-bound calcium in the blood, the total calcium concentration in the blood varies. That is the reason why the biological effect of calcium is determined by the amount of ionized calcium in the blood. The plasma ionized calcium level is tightly regulated to remain within very narrow limits by a set of negative feedback systems. The chief cells in the parathyroid glands sense the calcium level by specialized calcium receptors. In response to a fall in plasma ionized calcium concentration they secrete parathyroid hormone (PTH), while calcitonin is secreted in response to a rise in plasma ionized calcium level. The main effector organs are the skeleton and the kidney.
Beside this negative regulation system of ionized calcium in the plasma, the absorption of calcium in the intestine after oral ingestion is also regulated. Calbindin, the vitamin D-dependent calcium-binding protein, is rate-limiting and down regulated when exposed to high concentrations of calcium (Bronner, 2003). “Fractional calcium absorption is inversely related to the concentration of calcium present in the gut lumen (Ireland and Fordtran, 1973) and dietary load (Heaney et al., 1990). For example, absorption from a meal containing 15 or 500 mg of calcium was 64 and 28 %, respectively (Heaney et al., 1990). In women adapted to a high (2000 mg/day) calcium diet, whole-body retention of calcium increased from 27 to 37 % when they were given a low (300 mg/day) calcium diet for two weeks (Dawson-Hughes et al., 1993)” (EFSA Scientific Opinion on Dietary Reference Values for calcium, 2015).
Calcium absorption is also affected by vitamin D status. The active metabolite of vitamin D-1,25 dihydroxyvitamin D, enhances the intestinal absorption of calcium. Inadequate vitamin D levels lead to a reduction in gastrointestinal calcium absorption of up to 50 %, resulting in only 10 % to 15 % of dietary intestinal calcium being absorbed (Holick, 2007)” (Fong & Khan, 2012).
Therefore, the dietary calcium absorption is strongly regulated by different pathways. Excess calcium intake from foods alone is difficult if not impossible to achieve. Rather, excess intakes are more likely to be associated with the use of calcium or vitamin D supplements. The abuse of these supplements can cause hypercalcemia, which is defined as a high calcium level (>2.6 mmol/L) in the blood serum. The symptoms of a single, acute overdose from accidentally or intentionally taking too many calcium or vitamin D supplements or calcium-containing antacids at one time include stomachache, constipation or diarrhea, headache, nausea and vomiting.
An example for an accidental vitamin D supplement overdose, which increases the calcium absorption, was published by Barrueto et al. (2005). A 2-year-old boy suffered from hypercalcemia and hypertension with colic and constipation resulting from an unintentional overdose with an imported vitamin D supplement (Raquiferol). The patient received a total of 2 400 000 IU of vitamin D over 4 days (estimated average requirements: 400 IU). The patient´s hypercalcemia persisted for 14 days and was complicated by persistent hypertension. However, the boy made a complete clinical recovery, which demonstrates that acute hypercalcemia, induced by vitamin D supplements, has no adverse long-term effects on human health.
One of the main undesirable side-effects of acute excessive calcium supplementation is constipation. “In fact approximately 1 of every 10 participants in the WHI calcium–vitamin D supplementation trial (Jackson et al., 2006) reported moderate to severe constipation. Usually the constipation is alleviated by increasing intakes of water or fiber-rich foods, or by trying another form of supplement (calcium citrate may be less constipating than calcium carbonate, for example)” (Ross et al. 2011).
Justification for classification or non-classification
Acute oral toxicity:
Based on the given read-across information the substance calcium wolframate does not require classification according to
Regulation (EC) No 1272/2008 and subsequentadaptations.
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