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EC number: 207-997-3 | CAS number: 504-63-2
- 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
Direct observations: clinical cases, poisoning incidents and other
Administrative data
- Endpoint:
- direct observations: clinical cases, poisoning incidents and other
- Type of information:
- experimental study
- Adequacy of study:
- supporting study
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- study well documented, meets generally accepted scientific principles, acceptable for assessment
Data source
Reference
- Reference Type:
- publication
- Title:
- Unnamed
- Year:
- 1 987
Materials and methods
- Study type:
- clinical case study
- Principles of method if other than guideline:
- Three patients who died in infancy showed an unusual urinary organic pattern with excessive excretion of 3-hydroxypropionic acid. Propan-1, 3-diol was also present in the urine of all three cases. A fourth patient, also severely ill, showed similar urinary abnormalities. Investigations were conducted to determine the cause of the abnormal urinary profile.
- GLP compliance:
- no
Test material
- Reference substance name:
- Propane-1,3-diol
- EC Number:
- 207-997-3
- EC Name:
- Propane-1,3-diol
- Cas Number:
- 504-63-2
- Molecular formula:
- C3H8O2
- IUPAC Name:
- propane-1,3-diol
- Details on test material:
- - Analytical purity: not applicable
Constituent 1
Method
- Type of population:
- general
- Subjects:
- - Sex: male and female
- Age: infant - Ethical approval:
- not applicable
Results and discussion
Any other information on results incl. tables
In all the urines examined the 3-hydroxypropionic acid peak was very prominent, in most cases the largest on the chromatogram. No other metabolites suggestive of propionyl-CoA carboxylase deficiency were present in excess nor was there any indication of other recognised metabolic disease. Examination of the lactic acid peak revealed that it also contained propan-1, 3-diol (as the bis-trimethylsilyl derivative) in a molar ratio to lactate ranging from 0.8 to 3.1.
In patient 4, the urine abnormalities were less marked with, initially, a greater excretion of 1, 3-propandiol than of 3-hydroxypropionic acid. The introduction of a medium-chain triglyceride-rich diet was accompanied by the excretion for the first time of malonic acid, as well as the expected medium-chain dicarboxylic aciduria. While still on this diet the patient was given neomycin (250 mg/kg per day). This resulted in the disappearance of all the abnormal 3-carbon metabolites.
Propan-1, 3-diol has not been reported in human urine before though it has been found in combined form in heart and lung phospholipids. Propan-1, 3-diol can be formed from glycerol by Lactobacillus spp. Its presence in the urine of all four patients is consistent with the idea that overgrowth by some specific type of gut bacterium was the cause of the characteristic urinary organic acid abnormalities. The two unusual metabolites excreted by all four patients, 3-hydroxypropionic acid and propan-1, 3-diol, may be obtained by oxidation or reduction respectively of the aldehyde group of 3-hydroxypropionaldehyde.
Applicant's summary and conclusion
- Executive summary:
Three patients who died in infancy showed an unusual urinary organic acid pattern with excessive excretion of 3-hydroxypropionic acid but none of the other metabolites normally associated with propionyl-CoA carboxylase deficiency. Propan-1, 3-diol was present in the urine in all three cases. In the two patients examined propionyl-CoA carboxylase activity was not deficient in cultured skin fibroblasts. A fourth patient, also severely ill, showed similar urinary abnormalities. Feeding a medium-chain triglyceride-rich diet to this patient increased the ratio of 3-hydroxypropionic acid to propan-1, 3-diol and resulted also in the appearance of malonic acid in the urine. These abnormal metabolites disappeared on the administration of neomycin and presumably were produced by gut bacteria.
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