Ethane-1,2-diol

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:

1991

Report date:

1991

Materials and methods

Test guideline

Qualifier:

no guideline followed

GLP compliance:

not specified

Test material

Test material information

Constituent 1

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

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].
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[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)