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EC number: 212-783-8 | CAS number: 868-85-9
- 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
Toxicological Summary
- Administrative data
- Workers - Hazard via inhalation route
- Workers - Hazard via dermal route
- Workers - Hazard for the eyes
- Additional information - workers
- General Population - Hazard via inhalation route
- General Population - Hazard via dermal route
- General Population - Hazard via oral route
- General Population - Hazard for the eyes
- Additional information - General Population
Administrative data
Workers - Hazard via inhalation route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- DMEL (Derived Minimum Effect Level)
- Value:
- 0.03 mg/m³
- Most sensitive endpoint:
- carcinogenicity
DNEL related information
- Overall assessment factor (AF):
- 25 000
- Modified dose descriptor starting point:
- T25
Acute/short term exposure
DNEL related information
Local effects
Acute/short term exposure
DNEL related information
Workers - Hazard via dermal route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- DMEL (Derived Minimum Effect Level)
- Value:
- 0.004 mg/kg bw/day
- Most sensitive endpoint:
- carcinogenicity
DNEL related information
- Modified dose descriptor starting point:
- T25
Acute/short term exposure
DNEL related information
Workers - Hazard for the eyes
Additional information - workers
In vitro data indicate that dimethyl phosphonate has mutagenic and clastogenic potential. The available in vivo data are limited to the bone marrow and the results are conflicting with one study indicating clastogenicity. Dimethyl phosphonate should be regarded as having genotoxic potential in vivo. Dimethyl phosphonate is suspected to be a human carcinogen as well. In fact, it was tested for carcinogenicity in a 103 weeks gavage cancer study on rats and mice in doses of 100 and 200 mg/kg bw/day in male F344 rats and 50 and 100 mg/kg bw/d in female F344 rats respectively (NTP, 1985). A clear evidence of carcinogenicity was found for male rats and an equivocal evidence for female rats. In gross pathology and histopathology statistically significant squamous cell carcinoma in lung and alveolar/bronchial cell adenoma or carcinoma in male rats were found to be treatment related. In males in the highest dose the incidence of alveolar/bronchiolar adenoma is 5/50 and the incidence of the alveolar/bronchiolar carcinoma is 20/50. This incidence was well above the incidence of lung tumours in the concurrent control group (0%; 0 of 50) and the historical incidence. Alveolar-bronchiolar carcinomas were seen in 3 of 50 high dose female rats. The high dose in the female rats was 100 mg/kg, one-half of the doses given to high dose male rats. Interestingly the incidence of all lung lesions in female rats receiving 100 mg/kg bw/day was similar to that of the males receiving 100 mg/kg bw/day, suggesting that the both sexes may be equally susceptible to the pulmonary changes. Lung tumours are a leading cause of both morbidity and mortality in humans.
Regarding the forestomach carcinogenicity, statistically squamous cell carcinoma or adenoma (6/50) were observed in male rats in the highest dose group. A particular controversial aspect of interspecies extrapolation is application of rodent forestomach tumour data for predicting cancer risk in humans, given that a human counterpart for the rodent forestomach does not exist. However, genotoxic chemicals and those that cause tumours at multiple sites, at doses at or below the maximum tolerated dose, and in absence of forestomach irritation, are more likely to be relevant human carcinogens (Proctor et. al 2007).
Statistically significant mononuclear cell leukemia was observed with higher incidences in male rats of the low dose group (100 mg/kg bw/d) (vehicle control, 9/50; low dose, 15/50; high dose, 13/50). The effects observed in the mononuclear cell leukemia in rats were not dose-dependent. However, this tumour type is unique to the rat and is only common in the F344 strain and no histologically comparable tumour is found in humans. Therefore, its significance for human cancer risk is unclear.
B6C3F1 mice were treated with 100 and 200 mg/kg bw/day in the same way as described above. Statistically significant increased number of hepatocellular adenomas, were observed in the 100 mg/kg bw/day female group only. However, no evidence of carcinogenicity was concluded for B6C3F1 mice.
Taking in consideration the above mentioned data, DMEL(s) was derived on the basis of the most relevant dose descriptor. The dose descriptor T25 (the dose giving a 25% incidence of cancer in an appropriately designed animal experiment) was calculated on the basis of the above mentioned 103 weeks gavage cancer study on rats and mice (NTP, 1985) by means of the software BenchMark Dose Software Version 1.4.1b (U. S. EPA).
Several dose descriptors T25 were calculated on the basis of the incidence of the different tumours in rats. For the derivation of the DMEL the lowest dose descriptor T25, which was derived on the basis of the highest incidence of tumours in male rats (lung carcinoma, 20/50) and human relevance, was chosen.
The derivation of the DMEL is based on the dose descriptor T25 (154.327 mg/kg/day), which was modified as described in RIP-Guidance document R.8. (ECHA (2008)).
The inhalation DMEL is calculated according to the general formula: corrected T25/ 1*25000, where 25000 represent the high to low dose extrapolation, and 1 the interspecies extrapolation.
Using the T25=154.327 mg/kg/day, the corrected starting point for the inhalation route is calculated according to the following formula for workers: = T25*1/0.384*6.7/10*2.8, where 6.7/10 mg/m³ represents the human light activity, 0.38 m³/kg is the standard breathing volume for the rats for 8 hours exposure for workers, and 2.8 represent the difference between occupation al and lifetime exposure conditions (7/5 x 52/48 x 75/40). The corrected T25 is 753.951 mg/m³.
Regarding the dermal DMEL, the modification of relevant dose descriptor was performed by multiplying T25* 2.8, where the value 2.8 (7/5 x 52/48 x 75/40) represents the difference between occupational and lifetime exposure conditions. The corrected dose descriptor is 432.1156 mg/kg bw/ day.
The dermal DMEL is derived from the oral DMEL, taking in consideration the absorption difference (=1), being the dermal absorption (calculated from Danish QSAR Database on the basis of the molecular weight, the water solubility and the log Kow) of dimethyl phophonate high (0.05600 mg/cm², absorption potential 100%).
The oral DMEL is derived according to the following formula: corrected T25/25000*4, where 25000 represents the high to low dose extrapolation, and 4 the interspecies extrapolation.
The derived DNELs for inhalation and dermal exposure are 4.701 mg/m³ and 0.667 mg/kg bw/day respectively. The DNELs are higher then than the DMELs derived. However, here it is described a worse case approach, since in principle any level of exposure carries a risk and thus no dose without effect can be established. Therefore, for the effects above described DMELs have been derived on the basis of the most relevant dose descriptor.
General Population - Hazard via inhalation route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- DMEL (Derived Minimum Effect Level)
- Value:
- 0.005 mg/m³
- Most sensitive endpoint:
- carcinogenicity
DNEL related information
- Overall assessment factor (AF):
- 25 000
- Modified dose descriptor starting point:
- T25
Acute/short term exposure
DNEL related information
Local effects
Acute/short term exposure
DNEL related information
General Population - Hazard via dermal route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- DMEL (Derived Minimum Effect Level)
- Value:
- 0.002 mg/kg bw/day
- Most sensitive endpoint:
- carcinogenicity
DNEL related information
- Modified dose descriptor starting point:
- T25
Acute/short term exposure
DNEL related information
General Population - Hazard via oral route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- DMEL (Derived Minimum Effect Level)
- Value:
- 0.002 mg/kg bw/day
- Most sensitive endpoint:
- carcinogenicity
DNEL related information
- Modified dose descriptor starting point:
- T25
Acute/short term exposure
DNEL related information
General Population - Hazard for the eyes
Additional information - General Population
DMELs were derived on the basis of the most relevant dose descriptor. The dose descriptor T25 (the dose giving a 25% incidence of cancer in an appropriately designed animal experiment) was calculated on the basis of 103 weeks gavage cancer study on rats and mice (NTP, 1985) by means of the software BenchMark Dose Software Version 1.4.1b (U. S. EPA). Several dose descriptors T25 were calculated on the basis of the incidence of the different tumours in rats. For the derivation of the DMEL the lowest dose descriptors T25, which was derived on the basis of the highest incidence of tumours in male rats (lung carcinoma, 20/50) and human relevance, was chosen.
The derivation of the DMEL is based on the dose descriptor T25 (154.327 mg/kg/day), which was modified as described in RIP-Guidance document R.8. (ECHA (2008)).
The inhalation DMEL is calculated according to the general formula: corrected T25/ 1*25000, where 25000 represent the high to low dose extrapolation, and 1 the interspecies extrapolation.
Using the T25=154.327 mg/kg/day, the corrected starting point for the inhalation route is calculated according to the following formula for workers: = T25*1/1.15, where 1.15 m³/kg is the standard breathing volume for rat for 24 hours exposure of general public.
The corrected T25 is 134.197 mg/m³.
The dermal DMEL is derived from the oral DMEL, taking in consideration the absorption difference (=1), being the dermal absorption (calculated from Danish QSAR Database on the basis of the molecular weight, the water solubility and the log KOW) of dimethyl phophonate high (0.05600 mg/cm², absorption potential 100%).
The oral DMEL is derived according to the following formula: corrected T25/25000*4, where 25000 represents the high to low dose extrapolation, and 4 the interspecies extrapolation.
The DNELs for inhalation and dermal exposure are 1.159 mg/m³ and 0.333 mg/kg bw/day respectively. The derived DNELs are higher then than the DMELs derived. However, here it is described a worse case approach, since in principle any level of exposure carries a risk and thus no dose without effect can be established. Therefore, for the effects above described DMELs have been derived on the basis of the most relevant dose descriptor.
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