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EC number: 242-734-6 | CAS number: 18996-35-5
- 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
Acute Toxicity: other routes
Administrative data
- Endpoint:
- acute toxicity: other routes
- Type of information:
- experimental study
- Adequacy of study:
- supporting study
Data source
Reference
- Reference Type:
- publication
- Title:
- A study on the comparative toxic effects of citric acid and its sodium salts
- Author:
- Grueber & Helbeisen
- Year:
- 1 948
- Bibliographic source:
- Department of Pharmacology and the Charlotte Drake Cardeza Foundation, Jefferson Medical College, Philadelphia, Pennsylvania
- Report date:
- 1948
Materials and methods
Test guideline
- Qualifier:
- no guideline available
- Principles of method if other than guideline:
- White mice, albino rats, rabbits and dogs were used as experimental animals. Equal molecular concentrations of citric acid, monosodium citrate, disodium citrate and trisodium citrate were compared. 599 intraperitoneal injections of 0.0477 molar solutions were made in 477 mice. 384 intraperitoneal injections of 0.381 molar solutions were made into 299 rats. 361 intravenous injections of 0.0119 molar solutions were made into the tail veins of 279 mice. 158 intravenous injections of 0.477 molar solutions were made into lateral ear veins of 100 rabbits.The LD50 was determined each method of administration for each substance. 80 intravenous injections of 0.25 molar solutions were made into the tail veins of 80 mice. 20 mice were used for each compound. Under ether anesthesia lumbar cordotomies were performed on 7 dogs. As soon as the animals recovered fromt he anesthetic the left femoral artery was cannulated and connected to a mercury manometer using heparin asti anticoagulant. Four animals received trisodium citrate (2.94g/kg/100cc) and the other three were given equual molar quantities of citric acid (2.1g/kg/100cc) intravenously at a constant rate of 0.67 cc/minute until death resulted.
- GLP compliance:
- not specified
- Limit test:
- no
Test material
- Reference substance name:
- Sodium dihydrogen citrate
- EC Number:
- 242-734-6
- EC Name:
- Sodium dihydrogen citrate
- Cas Number:
- 18996-35-5
- Molecular formula:
- C6H8O7.Na
- IUPAC Name:
- dihydrogen sodium citrate
Constituent 1
Test animals
- Species:
- other: various
Results and discussion
Effect levelsopen allclose all
- Dose descriptor:
- LD50
- Effect level:
- 1.76 other: mM/kg
- Remarks on result:
- other: monosodium citrate, rabbits, i.v.
- Dose descriptor:
- LD50
- Effect level:
- 0.23 other: mM/kg
- Remarks on result:
- other: monosodium citrate, mice, i.v.
- Dose descriptor:
- LD50
- Effect level:
- 7.6 other: mM/kg
- Remarks on result:
- other: monosodium citrate, mice, i.p.
- Dose descriptor:
- LD50
- Effect level:
- 6.3 other: mM/kg
- Remarks on result:
- other: monosodium citrate, rats, i.p.
Any other information on results incl. tables
The visible responses of mice, rats, rabbits and dogs to toxic doses of citric acid, monosodium citrate, disodium citrate and trisodium citrate were similar and consisted primarily of increased general activity, hyperapnea, vasodilation of the peripheral vessels, salivation, muscle twitching, clonic and tonic convulsions, cyanosis, Cheyne-Stokes respiration and some deaths. In all of the animals receiving single injections, except those injected intraperitoneally with citric acid, if recovery occurred it was apparently complete within a few minutes. These findings are explained adequately by the fact that there is formation of double salts with calcium which do not liberate calcium ions. Citric acid and its sodium salts have the same toxicity when given slowly intravenously to rabbits. When citric acid was given intraperitoneally to rats and mice a number of animals died as long as one week after recovery from the immediate toxic effects. Gross post-mortem examinations performed upon many of these animals did not reveal the cause of death. If these compounds are injected rapidly intravenously in mice significant differences in toxicity are observed. It would appear that the acid rather than the citrate part of the molecule is the cause of this difference in toxicity. In those experiments on mice which intravenous injections of 0.25 molar solutions were made at a constant rate of six cubic centimeters per minute (1.5mM of the drug per minute) no significant differences in the averages of the individual lethal doses were noted. In the 80 experiments (20 for citric acid and 20 for each of its sodium salts) the average dose necessary to kill all of the animals witht he standard deviation was 2.08 +/-0.11, 2.01 +/-0.09, 2.21 +/-0.1 and 2.24 +/-0.51 for citric acid, monosodium citrate, disodium citrate and trisodium citrate respectively. In the experiments on dogs in which blood pressures were recorded there was a gradual fall in blood pressure during citric acid injection until near death when the pressure fell precipitously to zero. When sodium citrate was used the blood pressure remained fairly normal during the injection until just prior to death of the animal when it fell abruptly to zero.
Applicant's summary and conclusion
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