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EC number: 252-156-6 | CAS number: 34690-00-1
- 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
Link to relevant study record(s)
Description of key information
Key value for chemical safety assessment
Additional information
Based on the available data, no major differences appear to exist between animals and humans with regard to the absorption, distribution and elimination of phosphonic acid compounds in vivo. There are no actual toxicokinetics data for BHMT-H, therefore toxicokinetics data are read across from studies of related phosphonic acids and salts.
Absorption
Oral
The physicochemical properties of phosphonic acid compounds, notably their high polarity, charge and complexing power, suggests that they will not be readily absorbed from the gastrointestinal tract. This is supported by experimental data on DTPMP-H and ATMP-H which confirm that absorption after oral exposure is low, averaging 2-7% in animals and 2-10% in humans. In a study by Procter and Gamble (1978) approximately 2% of a dose of sodium hydroxyde-neutralised DTPMP-H was absorbed from a gavage dose, and 98% of the dose was excreted in faeces within 72 hours of dosing. In a well conducted and reported toxicokinetics study, approximately 2.2 % of ATMP was absorbed and 84% was rapidly eliminated in faeces after single oral administration in rats (Monsanto, 1995).
Gastrointestinal pH is a major determinant influencing uptake following oral exposure of phosphonates. It is extremely acidic in the stomach (range: pH 1-4) and alkaline in the small intestine (pH 4-7). The number of ionisations of the phosphonic acid moiety increases with increasing pH, rising from 1-2 at low pH (i.e. stomach) to 4-6 at more neutral pH (reflective of conditions in the small intestine). The negative charge on each molecule also increases with each ionisation, further reducing the already low potential for uptake. Stability constants for the interaction of phosphonic acids with divalent metal ions are high, and indicate strong binding, especially at lower pH. Complexation of a metal with a phosphonic acid would produce an ion pair of charge close to neutral which might favour absorption; however, the overall polarity of the complex would remain high thereby counteracting this potential. Overall, these considerations indicate that ingested phosphonic acid compounds will be retained within the gut lumen.
Dermal
BMHT-H is too hydrophilic to be absorbed through the skin. Using read across data from a dermal absorption study with sodium salt of DTPMP (Procter and Gamble, 1978, Reliability 2), 89% of the applied radioactivity (0.6 mg/kg bw) was recovered from the test site 72 hrours after application to rat skin, with negligible amounts in faeces (< 0.01%) and minor amounts in urine (< 2% ) and carcass (<1.5%).
Inhalation
The vapour pressure of BHMT-H is extremely low (2.7E-09 Pa). Consequently, inhalation of BHMT-H vapour is not possible. It is possible that aerosol (from aqueous solution) of BHMT-H could be inhaled; however the very high water solubility of this substance suggests that any absorption would be low.
Distribution
Based on studies on other phosphonic acids, ATMP, bone appears to be a specific site for deposition of phosphonic acids in vivo. Blood/tissue ratios demonstrate an approximate 80 to 200 fold increase in the concentration of phosphonic acids in rat sternum, tibia and femur after gavage exposure compared to that present in blood (Monsanto, 1995), with whole body radiography indicating preferential deposition in the epiphyseal plate of the long bones (Monsanto, 1995). A dose-dependent increase in radiolabel was observed in tibia and mandible in rats following gavage administration of 0.5 to 1000 mg/kg bw phosphonic acid.
Metabolism
There are no data on the metabolism of BHMT-H. However read across data from ATMP indicates that metabolism of ATMP in vivo is limited. Of the proportion of an oral dose excreted in urine, 25% is present as parent substance, approx. 50% as N-methyl derivative and the remainder as an unidentified product (Monsanto, 1995). Conversion of orally administered PACs to carbon dioxide by the rat has been variously reported as 0% (Monsanto, 1995), 0.2% (Michael et al., 1972) or 10% (Henkel, 1983), with 0.4% conversion described in humans (Procter and Gamble, 1978).
Excretion
There are no data on the excretion of BHMT-H. However information is available on the elimination of 14C-DTPMP (neutralised sodium salt) following oral or dermal administration to Sprague Dawley rats. Following gavage administration (10 mg/kg bw, 7 μCi/kg bw), faecal excretion over 72 hr accounted for 98% of the dose (94% eliminated during the first 24 hr). Trace amounts of radioactivity were detected in urine (1.3% of dose), with negligible quantities present as exhaled carbon dioxide (0.4%). The total recovery for this study was 101% (Procter and Gamble, 1978).
In addition, a dermal absorption study, 89% of a dose of14C-DTPMP (0.6 mg/kg bw; 2.3 μCi/kg bw) was recovered from the application site, with < 0.01% present in faeces, 0.02 - 2% eliminated via urine and 0.0 - 1.5% retained in the carcass after 72 hr (Procter and Gamble, 1978). No total recovery is reported for this study (but would appear to be >90%).
Reference
Michael, WR, King, WR and Wakim, JM (1972) Metabolism of disodium ethane-1-hydroxy-1,1-diphosphonate (disodium etidronate) in the rat, rabbit, dog and monkey. Toxicol Appl Pharmacol, 21, 503 - 515.
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