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Toxicological information

Health surveillance data

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health surveillance data
Type of information:
experimental study
Adequacy of study:
weight of evidence
2 (reliable with restrictions)
Rationale for reliability incl. deficiencies:
other: basic information given

Data source

Reference Type:
review article or handbook
Ethylene glycol.
MAK documentation
Report date:

Materials and methods

Test guideline
no guideline followed
GLP compliance:
not specified

Test material

Constituent 1
Chemical structure
Reference substance name:
EC Number:
EC Name:
Cas Number:
Molecular formula:
ethylene glycol

Results and discussion

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].
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Applicant's summary and conclusion