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EC number: 203-473-3 | CAS number: 107-21-1
- 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
Health surveillance data
Administrative data
- Endpoint:
- health surveillance data
- Type of information:
- experimental study
- Adequacy of study:
- weight of evidence
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: basic information given
Data source
Reference
- Reference Type:
- review article or handbook
- Title:
- Ethylene glycol.
- Author:
- MAK documentation
- Year:
- 1 991
- Report date:
- 1991
Materials and methods
Test guideline
- Qualifier:
- no guideline followed
- GLP compliance:
- not specified
Test material
- Reference substance name:
- Ethane-1,2-diol
- EC Number:
- 203-473-3
- EC Name:
- Ethane-1,2-diol
- Cas Number:
- 107-21-1
- Molecular formula:
- C2H6O2
- IUPAC Name:
- ethane-1,2-diol
Constituent 1
Results and discussion
- Results:
- There are still frequent reports of acute intoxication after ingestion of ethylene glycol [2, 9, 17 - 24]. The early literature has been summarized in a review [25]. The smallest dose which resulted in death in such a case of poisoning was about 100 mL [26]. The clinical symptoms of ethylene glycol intoxication have been described in detail; it develops in four phases. In phase I (30 minutes to 12 hours after ingestion) the gastrointestinal tract and CNS are affected most. The early symptoms which have been d escribed include nausea, vomiting, agitation, stupor, generalized inhibition of reflexes, epileptiform fits and convulsions. Coma, respiratory paralysis or cardiocirculatory failure can cause death even in this early phase. Other symptoms include acute gastritis, meningoencephalitis, metabolic acidosis, leukocytosis (10000- 40000/mm3) with polymorphonuclear cells, proteinuria, haematuria, calcium oxalate, crystalluria and hypocalcaemia which is considered to be the cause of clonic muscle spasms, tetanus and functional cardiac disorders. The eyes are also affected with nystagmus, ophthalmoplegia, papilloedema and optic atrophy. In phase II (12 to 24 hours) the main symptoms involve the cardiopulmonary system: tachycardia, tachypnoea, bronchopneumonia, pulmonary oedema and congestive heart failure which can result in death within 24 to 72 hours [9, 17]. Pathological examination reveals focal haemorrhage in the pleura, lungs, heart and pericardium together with degenerative myocardial damage [9]. Occasionally, oxalate crystals are observed in the lung parenchyma [19] and brain [27]. This phase can be omitted [17] so that phase I is followed immediately by phase III (4 to 72 hours) which is characterised essentially by kidney damage. Pain can develop in the costovertebral angle and the lumbar region. The degree of kidney damage varies from slightly increased blood urea levels to anuria with acute tubular necrosis. Oliguria can develop after only 12 hours and persist for up to 50 days [9]. Histological examination reveals dilation of the tubuli, degeneration of the tubulus epithelium with intratubular and intracellular crystalline deposits. In almost all surviving patients, renal function returns to normal within 50 days at most; however, one case has been described in which tubulus atrophy was followed by chronic renal insufficiency with progressive interstitial fibrosis [20]. Phase IV (6 to 14 days) mostly involves CNS degeneration. Typical findings include facial diplegia, increased protein levels in the spinal fluid, anisocoria, blurred vision, dysphagia, hyperreflexia and ataxia [17], progressive cerebral oedema [18] and deposits of calcium oxalate crystals in the brain [24, 28]. The suspected site of damage is cranial nerve VII [17]. Liver necrosis with fatty degeneration and lymphocytic infiltration has also been reported [18].
_________________
[2]
Jacobsen, D. et al., Amer. J. Med. 84, 145 (1988)
[9]
Parry, M.F., R. Wallach: Amer. J. Med. 57, 143 (1974)
[17]
Factor, S.A., N.S. Lava: N.Y. St. I. Med. 87, 179 (1987)
[24]
Gaultier, M. et al., Europ. J. Toxicol.9, 373 (1976)
[25]
Friedmann, E. et al., Amer.J . Med. 32, 891 (1962)
[26]
Winek, C. et al.: in Winek, C. L. (Ed.): Toxicology Annual Vol. 3, p 297, Marcel Dekker Inc., New York, 1979
[27]
Patscheider, H., H. Hetzel: Arch. Toxikol. 19, 143 (1961)
[19]
Yale, J.A., B. Widdop, N.H. Bluett: Postgradm. ed. J. 52, 598 (1976)
[20]
Gutman, R.A., C.B. Hamon, G.E. Striker: Arch. intern. Med. 126, 914 (1970)
[18]
Frang, D., S. Csata, K. Szernenyei, G. Hamvasi: Z. Urol. Nephrol. 7, 465 (1967)
[28]
Pons, C.A., R.P. Custer: Amer. J. med. Sci. 211, 54 (1946)
Applicant's summary and conclusion
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.
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