The Full Wiki

Ethylene glycol poisoning: Wikis


Note: Many of our articles have direct quotes from sources you can cite, within the Wikipedia article! This article doesn't yet, but we're working on it! See more info or our list of citable articles.


From Wikipedia, the free encyclopedia

Ethylene glycol poisoning
Classification and external resources

Ethylene glycol
eMedicine emerg/177

Ethylene glycol poisoning is caused by the ingestion of ethylene glycol. Ethylene glycol is most commonly found as the primary ingredient of automobile antifreeze and hydraulic brake fluids. It is a toxic, colorless, odorless, almost nonvolatile liquid with a sweet taste. Following ingestion the symptoms of poisoning follow a three step progression starting with intoxication and vomiting, before causing metabolic acidosis, cardiovascular dysfunction, and finally acute kidney failure. The major cause of toxicity is not the ethylene glycol itself but its metabolites. The major metabolites causing toxicity are glycolic acid and oxalic acid.

Medical diagnosis of poisoning is most reliably done by measurement of ethylene glycol in the blood. However many hospitals do not have the facilities to perform this test and need to rely on abnormalities in the body’s biochemistry to diagnose poisoning. Diagnosis can also be aided by examining the urine for the presence of calcium oxalate crystals. Treatment consists of initially stabilizing the patient followed by the use of antidotes. The antidotes used are either ethanol or fomepizole (Antizol). The antidotes work by blocking the enzyme responsible for metabolizing ethylene glycol and therefore halt the progression of poisoning. Hemodialysis is also used to help remove ethylene glycol and its metabolites from the blood. As long as medical treatment is undertaken the prognosis is generally good with most patients making a full recovery. Poisoning is relatively common and due to its taste, children and animals will sometimes consume large quantities of ethylene glycol. Denatonium benzoate, a bittering agent, is added to many antifreeze products to try to prevent ingestion.



Ethylene glycol has been shown to be toxic to humans.[1] A toxic dose requiring medical treatment varies but is considered more than 0.1 mL per kg body weight (mL/kg) of pure substance. Poison control centers often use more than a lick or taste in a child or more than a mouthful in an adult as a dose requiring hospital assessment.[2] The orally lethal dose in humans has been reported as approximately 1.4 mL/kg of pure ethylene glycol.[3] Although survival with medical treatment has occurred with doses much higher than this, death has occurred with just 30 mL of the concentrate in an adult.[4][5][6] In the EU classification of dangerous substances it is 'harmful' (Xn) while more toxic substances are classified as 'toxic' (T) or 'very toxic' (T+). The U.S. Environmental Protection Agency‎ generally puts substances which are lethal at more than 30 g to adults in Toxicity Class III.

Ethylene glycol has a low vapor pressure; it does not evaporate readily at normal temperatures and therefore high concentrations in air or intoxication are unlikely to occur following inhalational exposures.[7] There may be a slight risk of poisoning where mists or fogs are generated, although this rarely leads to poisoning as ethylene glycol causes irritation and coughing when breathed in, alerting victims to its presence.[8] Ethylene glycol is not well absorbed through skin meaning poisoning following dermal exposure is also uncommon.[9]

Signs and symptoms

Symptoms of ethylene glycol poisoning usually follow a three-step progression, although poisoned individuals will not always develop each stage.[3]


Glycolic acid is the major metabolite of ethylene glycol responsible for toxicity

The three main systems affected by ethylene glycol poisoning are the central nervous system, metabolic processes, and the kidneys.[3] The central nervous system is affected early in the course of poisoning as the result of a direct action of ethylene glycol. Similar to ethanol, it causes intoxication, followed by drowsiness or coma.[3] Seizures may occur due to a direct effect.[10 ] The toxic mechanism of ethylene glycol poisoning is mainly due to the metabolites of ethylene glycol. Initially it is metabolized by alcohol dehydrogenase to glycolaldehyde, which is then oxidized to glycolic acid. The increase in metabolites may cause encephalopathy or cerebral edema.[12] The metabolic effects occur 12 to 36 hours post ingestion, causing primarily metabolic acidosis which is due mainly to accumulated glycolic acid. Additionally, as a side effect of the first two steps of metabolism, an increase in the blood concentration of lactic acid occurs contributing to lactic acidosis. The formation of acid metabolites also causes inhibition of other metabolic pathways, such as oxidative phosphorylation.[3]

The renal toxicity of ethylene glycol occurs 24 to 72 hours post ingestion and is caused by a direct cytotoxic effect of glycolic acid. The glycolic acid is then metabolized to glyoxylic acid and finally to oxalic acid. Oxalic acid binds with calcium to form calcium oxalate crystals which may deposit and cause damage to many areas of the body including the brain, heart, kidneys, and lungs.[3] The most significant effect is accumulation of calcium oxalate crystals in the kidneys which causes kidney damage leading to oliguric or anuric acute kidney failure.[3] The rate-limiting step in this cascade is the conversion of glycolic to glyoxylic acid. [13] Accumulation of glycolic acid in the body is mainly responsible for toxicity.[14]


Urine microscopy showing calcium oxalate crystals in the urine

As many of the clinical signs and symptoms of ethylene glycol poisoning are nonspecific and occur in many poisonings the diagnosis is often difficult.[15] It is most reliably diagnosed by the measurement of the blood ethylene glycol concentration. Ethylene glycol in biological fluids can be determined easily by gas chromatography.[16] Many hospital laboratories do not have the ability to perform this blood test and in the absence of this test the diagnosis must be made based on the clinical presentation of the patient.[3] In this situation a helpful test to diagnose poisoning is the measurement of the osmolal gap. The patients' serum osmolality is measured by freezing point depression and then compared with the predicted osmolality based on the patients' measured sodium, glucose, blood urea nitrogen, and any ethanol that may have been ingested. The presence of a large osmolal gap supports a diagnosis of ethylene glycol poisoning. However, a normal osmolar gap does not rule out ethylene glycol exposure because of wide individual variability.[17][18]

The increased osmolal gap is caused by the ethylene glycol itself. As the metabolism of ethylene glycol progresses there will be less ethylene glycol and this will decrease the blood ethylene glycol concentration and the osmolal gap making this test less useful.[19] Additionally, the presence of other alcohols such as ethanol, isopropanol, or methanol or conditions such as alcoholic or diabetic ketoacidosis, lactic acidosis, or kidney failure may also produce an elevated osmolal gap leading to a false diagnosis.[3]

Other laboratory abnormalities may suggest poisoning, especially the presence of a metabolic acidosis, particularly if it is characterized by a large anion gap. Large anion gap acidosis is usually present during the initial stage of poisoning. However, acidosis has a large number of differential diagnosis, including poisoning from methanol, salicylates, iron, isoniazid, paracetamol, theophylline, or from conditions such as uremia or diabetic and alcoholic ketoacidosis. The diagnosis of ethylene glycol poisoning should be considered in any patient with a severe acidosis.[3] Urine microscopy can reveal needle or envelope-shaped calcium oxalate crystals in the urine which can suggest poisoning; although these crystals may not be present until the late stages of poisoning.[20] Finally, many commercial radiator antifreeze products have fluorescein added to enable radiator leaks to be detected using a Wood's lamp. Following ingestion of antifreeze products containing ethylene glycol and fluorescein, a Wood's lamp may reveal fluorescence of a patient’s mouth area, clothing, vomitus, or urine which can help to diagnose poisoning.[21][22]



Stabilization and decontamination

The most important initial treatment for ethylene glycol poisoning is stabilizing the patient. As ethylene glycol is rapidly absorbed, gastric decontamination is unlikely to be of benfit unless it is performed within 60 minutes of ingestion. Traditionally, gastric lavage or nasogastric aspiration of gastric contents are the most common methods employed in ethylene glycol poisoning.[3] The usefulness of gastric lavage has, however, been questioned, and it is now no longer used routinely in poisoning situations.[23] Ipecac-induced vomiting is not recommended. As activated charcoal does not adsorb glycols, it is not recommended as it will not be effective at preventing absorption.[3] It is only used in the presence of a toxic dose of another poison or drug.[17] Patients with significant poisoning often present in a critical condition. In this situation stabilization of the patient including airway management with intubation should be performed in preference to gastrointestinal decontamination.[3] Patients presenting with metabolic acidosis or seizures require treatment with sodium bicarbonate and anticonvulsives such as a benzodiazepine respectively.[3] Sodium bicarbonate should be used cautiously as it can worsen hypocalcemia by increasing the plasma protein binding of calcium. If hypocalcemia occurs it can be treated with calcium replacement although calcium supplementation can increase the precipitation of calcium oxalate crystals leading to tissue damage.[15] Intubation and respiratory support may be required in severely intoxicated patients; patients with hypotension require treatment with intravenous fluids and possibly vasopressors.[24]


Following decontamination and the institution of supportive measures, the next priority is inhibition of further ethylene glycol metabolism using antidotes. The antidotes for ethylene glycol poisoning are ethanol or fomepizole. This antidotal treatment forms the mainstay of management of ethylene glycol poisoning. Ethanol is a competitive inhibitor of ADH. Ethanol acts by competing with ethylene glycol for alcohol dehydrogenase. Pharmaceutical grade ethanol is usually given intravenously as a 5 or 10% solution in 5% dextrose, but it is also sometimes given orally in the form of a strong spirit such as whisky, vodka, or gin. Alcohol dehydrogenase has about a 100 times greater affinity for ethanol than for ethylene glycol; ethanol therapy saturates the enzyme inhibiting further ethylene glycol metabolism thus limiting the formation of toxic metabolites.[3]

Fomepizole is a potent inhibitor of alcohol dehydrogenase, similar to ethanol it acts to block the formation of the toxic metabolites.[15][24][25] Fomepizole has been shown to be highly effective as an antidote for ethylene glycol poisoning.[25][26] It is the only antidote approved by the U.S. Food and Drug Administration for the treatment of ethylene glycol poisoning.[3] Both antidotes has advantages and disadvantages. Ethanol is readily available in most hospitals, inexpensive, and can be administered orally as well as intravenously. Its adverse effects include intoxication, hypoglycemia in children, and possible liver toxicity.[17] Patients receiving ethanol therapy also require frequent blood ethanol level measurements and dosage adjustments to maintain a therapeutic ethanol concentration. Patients therefore must be monitored in an intensive care unit. Alternatively, the adverse side effects of fomepizole are minimal and the approved dosing regimen maintains therapeutic concentrations without the need to monitor blood levels of the drug. The disadvantage of fomepizole is that it is expensive. Costing US$1,000 per gram; an average course used in an adult poisoning would cost approximately $3,500 to 4,000.[27][28] Despite the cost, fomepizole is gradually replacing ethanol as the antidote of choice in ethylene glycol poisoning.[25][26] Adjunct agents including thiamine and pyridoxine are often given based on the fact that they may help prevent the formation of oxalic acid.[3] The use of these agents is based on theoretical observations and there is limited evidence to support their use in treatment; they may be of particular benefit in people who could be deficient in these vitamins such as malnourished or alcoholic patients.[15]


In addition to antidotes, an important treatment for poisoning is the use of hemodialysis. Hemodialysis is used to enhance the removal of unmetabolized ethylene glycol, as well as its metabolites from the body. It has been shown to be highly effective in the removal of ethylene glycol and its metabolites from the blood. [13][29] Hemodialysis also has the added benefit of correcting other metabolic derangements or supporting deteriorating kidney function. Hemodialysis is usually indicated in patients with severe metabolic acidosis (blood pH less than 7.3), kidney failure, severe electrolyte imbalance, or if the patients condition is deteriorating despite treatment.[10 ][15] Often both antidotal treatment and hemodialysis are used together in the treatment of poisoning. Because hemodialysis will also remove the antidotes from the blood, doses of antidotes need to be increased to compensate.[3] If hemodialysis is not available, then peritoneal dialysis also removes ethylene glycol, although less efficiently.[30]


Generally if the patient is treated and survives then a full recovery is expected.[31] Patients who present early to medical facilities and have prompt medical treatment typically will have a favorable outcome.[32] Alternatively, patients presenting late with signs and symptoms of coma, hyperkalemia, seizures, or severe acidosis have a poor prognosis.[2] Patients who develop severe central nervous system manifestations or stroke who survive may have long term neurologic dysfunction; in some cases they may recover, although convalescence may be prolonged.[33][34][35][36] The most significant long-term complication is related to the kidneys. Cases of permanent kidney damage, often requiring chronic dialysis or kidney transplantation, have been reported after severe poisoning.[37][38]


Ethylene glycol poisoning is a relatively common occurrence worldwide.[38][39][40][41] Human poisoning often occurs in isolated cases, but may also occur in epidemics.[42][43][44] Many cases of poisoning are the result of using ethylene glycol as a cheap substitute for alcohol or intentional ingestions in suicide attempts.[31] Less commonly it has been used as a means of homicide.[45][46] Children or animals may be exposed by accidental ingestion; children and animals often consume large amounts due to ethylene glycol having a sweet taste.[47] In the United States there were 5816 cases reported to poison centers in 2002.[2] Additionally, ethylene glycol was the most common chemical responsible for deaths reported by US poison centers in 2003.[39] In Australia there were 17 cases reported to the Victorian poison center and 30 cases reported to the New South Wales poison center in 2007.[48][49] However, these numbers may underestimate actual numbers because not all cases attributable to ethylene glycol are reported to poison control centers.[50] Most deaths from ethylene glycol are intentional suicides; deaths in children due to unintentional ingestion are extremely rare.[51]

In an effort to prevent poisoning, often a bittering agent called denatonium benzoate, known by the trade name Bitrex, is added to ethylene glycol preparations as an adversant to prevent accidental or intentional ingestion. The bittering agent is thought to stop ingestion as part of the human defense against ingestion of harmful substances is rejection of bitter tasting substances.[52] In the United States, eight states (Oregon, California, New Mexico, Virginia, Arizona, Maine, Tennessee, Washington) have made the addition of bittering agents to antifreeze compulsory.[51][53][54] Three follow up studies targeting limited populations or suicidal persons to assess the efficacy of bittering agents in preventing toxicity or death have, however, shown limited benefit of bittering ethylene glycol preparations in these two populations.[51][55][56] Specifically, Mullins finds that bittering of antifreeze does not reduce reported cases of poisoning of preschoolers in the US state of Oregon.[55] Similarly, White found that adding bittering agents did not decrease the frequency or severity of antifreeze poisonings in children under the age of 5.[56] Additionally, another study by White found that suicidal persons are not deterred by the bittered taste of antifreeze in their attempts to kill themselves.[51] These studies did not focus on poisoning of domestic pets or livestock, for example, or inadvertent exposure to bittered antifreeze among a large population (of non-preschool age children).


Ethylene glycol was once thought innocuous; in 1931 it was suggested as being suitable for use as a vehicle or solvent for injectable pharmaceutical preparations.[57] Numerous cases of poisoning have been reported since then, and it has been shown to be toxic to humans.[58]


  1. ^ Friedman EA, Greenberg JB, Merrill JP, Dammin GJ (June 1962). "Consequences of ethylene glycol poisoning. Report of four cases and review of the literature". The American journal of medicine 32: 891–902. doi:10.1016/0002-9343(62)90035-9. ISSN 0002-9343. PMID 13895244.  
  2. ^ a b c Caravati EM, Erdman AR, Christianson G, et al. (2005). "Ethylene glycol exposure: an evidence-based consensus guideline for out-of-hospital management". Clinical toxicology (Philadelphia, Pa.) 43 (5): 327–45. doi:10.1080/07313820500184971. ISSN 1556-3650. PMID 16235508.  
  3. ^ a b c d e f g h i j k l m n o p q r s t u Brent J (2001). "Current management of ethylene glycol poisoning". Drugs 61 (7): 979–88. doi:10.2165/00003495-200161070-00006. ISSN 0012-6667. PMID 11434452.  
  4. ^ Eder AF, McGrath CM, Dowdy YG, Tomaszewski JE, Rosenberg FM, Wilson RB, Wolf BA, Shaw LM (January 1998). "Ethylene glycol poisoning: toxicokinetic and analytical factors affecting laboratory diagnosis". Clinical chemistry 44 (1): 168–77. ISSN 0009-9147. PMID 9550575.  
  5. ^ Field DL (October 1985). "Acute ethylene glycol poisoning". Critical care medicine 13 (10): 872–3. doi:10.1097/00003246-198510000-00024. ISSN 0090-3493. PMID 4028762.  
  6. ^ Amathieu R, Merouani M, Borron SW, Lapostolle F, Smail N, Adnet F (August 2006). "Prehospital diagnosis of massive ethylene glycol poisoning and use of an early antidote". Resuscitation 70 (2): 285–6. doi:10.1016/j.resuscitation.2005.12.014. ISSN 0300-9572. PMID 16808995.  
  7. ^ Hodgman MJ, Wezorek C, Krenzelok E (1997). "Toxic inhalation of ethylene glycol: a pharmacological improbability". Journal of toxicology. Clinical toxicology 35 (1): 109–11. doi:10.3109/15563659709001176. PMID 9022663.  
  8. ^ Wills JH, Coulston F, Harris ES, McChesney EW, Russell JC, Serrone DM (1974). "Inhalation of aerosolized ethylene glycol by man". Clinical toxicology 7 (5): 463–76. doi:10.3109/15563657408988020. ISSN 0009-9309. PMID 4613525.  
  9. ^ Driver J, Tardiff RG, Sedik L, Wester RC, Maibach HI (July 1993). "In vitro percutaneous absorption of [14C] ethylene glycol". Journal of exposure analysis and environmental epidemiology 3 (3): 277–84. ISSN 1053-4245. PMID 8260837.  
  10. ^ a b c Barceloux DG, Krenzelok EP, Olson K, Watson W. (1999). "American Academy of Clinical Toxicology Practice Guidelines on the Treatment of Ethylene Glycol Poisoning. Ad Hoc Committee". Journal of toxicology. Clinical toxicology 37 (5): 537–60. doi:10.1081/CLT-100102445. ISSN 0731-3810. PMID 10497633.  
  11. ^ Bobbitt WH, Williams RM, Freed CR (February 1986). "Severe ethylene glycol intoxication with multisystem failure" (Free full text). Western journal of medicine 144 (2): 225–8. ISSN 0093-0415. PMID 3953092. PMC 1306577.  
  12. ^ Maier W (1983). "Cerebral computed tomography of ethylene glycol intoxication". Neuroradiology 24 (3): 175–7. ISSN 0028-3940. PMID 6828232.  
  13. ^ a b Gabow PA, Clay K, Sullivan JB, Lepoff R (July 1986). "Organic acids in ethylene glycol intoxication". Annals of internal medicine 105 (1): 16–20. ISSN 0003-4819. PMID 3717806.  
  14. ^ Clay KL, Murphy RC (January 1977). "On the metabolic acidosis of ethylene glycol intoxication". Toxicology and applied pharmacology 39 (1): 39–49. doi:10.1016/0041-008X(77)90175-2. ISSN 0041-008X. PMID 14421.  
  15. ^ a b c d e Hall TL (May 2002). "Fomepizole in the treatment of ethylene glycol poisoning" (pdf). CJEM: Canadian Journal of Emergency Medical Care: JCUM: Journal Canadien De Soins Médicaux D'urgence 4 (3): 199–204. ISSN 1481-8035. PMID 17609006.  
  16. ^ Aarstad K, Dale O, Aakervik O, Ovrebø S, Zahlsen K (July 1993). "A rapid gas chromatographic method for determination of ethylene glycol in serum and urine". Journal of analytical toxicology 17 (4): 218–21. ISSN 0146-4760. PMID 8371550.  
  17. ^ a b c Jacobsen D, McMartin KE (1997). "Antidotes for methanol and ethylene glycol poisoning". Journal of toxicology. Clinical toxicology 35 (2): 127–43. doi:10.3109/15563659709001182. ISSN 0731-3810. PMID 9120880.  
  18. ^ Hoffman RS, Smilkstein MJ, Howland MA, Goldfrank LR (1993). "Osmol gaps revisited: normal values and limitations". Journal of toxicology. Clinical toxicology 31 (1): 81–93. doi:10.3109/15563659309000375. ISSN 0731-3810. PMID 8433417.  
  19. ^ Glaser DS (March 1996). "Utility of the serum osmol gap in the diagnosis of methanol or ethylene glycol ingestion". Annals of emergency medicine 27 (3): 343–6. doi:10.1016/S0196-0644(96)70271-8. ISSN 0196-0644. PMID 8599495.  
  20. ^ Jacobsen D, Akesson I, Shefter E (May 1982). "Urinary calcium oxalate monohydrate crystals in ethylene glycol poisoning". Scandinavian journal of clinical and laboratory investigation 42 (3): 231–4. ISSN 0036-5513. PMID 7134806.  
  21. ^ Winter ML, Ellis MD, Snodgrass WR (June 1990). "Urine fluorescence using a Wood's lamp to detect the antifreeze additive sodium fluorescein: a qualitative adjunctive test in suspected ethylene glycol ingestions". Annals of emergency medicine 19 (6): 663–7. doi:10.1016/S0196-0644(05)82472-2. ISSN 0196-0644. PMID 2344083.  
  22. ^ Wallace KL, Suchard JR, Curry SC, Reagan C (July 2001). "Diagnostic use of physicians' detection of urine fluorescence in a simulated ingestion of sodium fluorescein-containing antifreeze". Annals of emergency medicine 38 (1): 49–54. doi:10.1067/mem.2001.115531. ISSN 0196-0644. PMID 11423812.  
  23. ^ Vale JA, Kulig K (2004). "Position paper: gastric lavage". J. Toxicol. Clin. Toxicol. 42 (7): 933–43. doi:10.1081/CLT-200045006. ISSN 0731-3810. PMID 15641639.  
  24. ^ a b Brent J (May 2009). "Fomepizole for ethylene glycol and methanol poisoning". N. Engl. J. Med. 360 (21): 2216–23. doi:10.1056/NEJMct0806112. ISSN 0028-4793. PMID 19458366.  
  25. ^ a b c Brent J, McMartin K, Phillips S, Burkhart K, Donovan J, Wells M, Kulig K (March 1999). "Fomepizole for the treatment of ethylene glycol poisoning. Methylpyrazole for Toxic Alcohols Study Group". The New England journal of medicine 340 (11): 832–8. doi:10.1056/NEJM199903183401102. ISSN 0028-4793. PMID 10080845.  
  26. ^ a b Borron SW, Mégarbane B, Baud FJ (September 1999). "Fomepizole in treatment of uncomplicated ethylene glycol poisoning". Lancet 354 (9181): 831. doi:10.1016/S0140-6736(99)80015-4. ISSN 0140-6736. PMID 10485727.  
  27. ^ Shannon M (April 1998). "Toxicology reviews: fomepizole--a new antidote". Pediatric emergency care 14 (2): 170–2. ISSN 0749-5161. PMID 9583406.  
  28. ^ Scalley RD, Ferguson DR, Piccaro JC, Smart ML, Archie TE (September 2002). "Treatment of ethylene glycol poisoning" (Free full text). American family physician 66 (5): 807–12. ISSN 0002-838X. PMID 12322772.  
  29. ^ Moreau CL, Kerns W, Tomaszewski CA, McMartin KE, Rose SR, Ford MD, Brent J (1998). "Glycolate kinetics and hemodialysis clearance in ethylene glycol poisoning. META Study Group". Journal of toxicology. Clinical toxicology 36 (7): 659–66. doi:10.3109/15563659809162613. ISSN 0731-3810. PMID 9865233.  
  30. ^ Aakervik O, Svendsen J, Jacobsen D (October 2002). "[Severe ethylene glycol poisoning treated with fomepizole (4-methylpyrazole)]" (in Norwegian). Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række 122 (25): 2444–6. ISSN 0029-2001. PMID 12448112.  
  31. ^ a b Leth PM, Gregersen M (December 2005). "Ethylene glycol poisoning". Forensic science international 155 (2-3): 179–84. doi:10.1016/j.forsciint.2004.11.012. ISSN 0379-0738. PMID 16226155.  
  32. ^ Velez LI, Shepherd G, Lee YC, Keyes DC (September 2007). "Ethylene glycol ingestion treated only with fomepizole" (PDF). Journal of medical toxicology : official journal of the American College of Medical Toxicology 3 (3): 125–8. ISSN 1556-9039. PMID 18072148.  
  33. ^ Jacobsen D, McMartin KE (September 1986). "Methanol and ethylene glycol poisonings. Mechanism of toxicity, clinical course, diagnosis and treatment". Medical toxicology 1 (5): 309–34. ISSN 0112-5966. PMID 3537623.  
  34. ^ Berger JR, Ayyar DR (November 1981). "Neurological complications of ethylene glycol intoxication. Report of a case". Archives of neurology 38 (11): 724–6. ISSN 0003-9942. PMID 7305705.  
  35. ^ Lewis LD, Smith BW, Mamourian AC (June 1997). "Delayed sequelae after acute overdoses or poisonings: cranial neuropathy related to ethylene glycol ingestion". Clinical pharmacology and therapeutics 61 (6): 692–9. doi:10.1016/S0009-9236(97)90105-3. ISSN 0009-9236. PMID 9209253.  
  36. ^ Spillane L, Roberts JR, Meyer AE (February 1991). "Multiple cranial nerve deficits after ethylene glycol poisoning". Annals of emergency medicine 20 (2): 208–10. doi:10.1016/S0196-0644(05)81226-0. ISSN 0196-0644. PMID 1996809.  
  37. ^ Nizze H, Schwabbauer P, Brachwitz C, Lange H (July 1997). "[Fatal chronic oxalosis after sublethal ethylene glycol poisoning"] (in German). Pathologe 18 (4): 328–34. doi:10.1007/s002920050224. ISSN 0172-8113. PMID 9380607.  
  38. ^ a b Davis DP, Bramwell KJ, Hamilton RS, Williams SR (September 1997). "Ethylene glycol poisoning: case report of a record-high level and a review". The Journal of emergency medicine 15 (5): 653–67. doi:10.1016/S0736-4679(97)00145-5. ISSN 0736-4679. PMID 9348055.  
  39. ^ a b Watson WA, Litovitz TL, Klein-Schwartz W, Rodgers GC Jr, Youniss J, Reid N, Rouse WG, Rembert RS, Borys D (September 2004). "2003 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System". The American journal of emergency medicine 22 (5): 335–404. doi:10.1016/j.ajem.2004.06.001. ISSN 0735-6757. PMID 15490384.  
  40. ^ Kotwica M, Czerczak S (2007). "Acute poisonings registered since 1970: trends and characteristics. Analysis of the files collected in the National Poison Information Centre, Łódź, Poland". International journal of occupational medicine and environmental health 20 (1): 38–43. doi:10.2478/v10001-007-0010-8. ISSN 1232-1087. PMID 17509968.  
  41. ^ Krenová M, Pelclová D, Navrátil T, Merta M (December 2005). "Experiences of the Czech toxicological information centre with ethylene glycol poisoning" (PDF). Biomedical papers of the Medical Faculty of the University Palacký, Olomouc, Czechoslovakia 149 (2): 473–5. ISSN 1213-8118. PMID 16601813.  
  42. ^ "Ethylene glycol intoxication due to contamination of water systems". MMWR. Morbidity and mortality weekly report 36 (36): 611–4. September 1987. ISSN 0149-2195. PMID 3114608.  
  43. ^ Leikin JB, Toerne T, Burda A, McAllister K, Erickson T (November 1997). "Summertime cluster of intentional ethylene glycol ingestions". JAMA : the journal of the American Medical Association 278 (17): 1406. doi:10.1001/jama.278.17.1406. ISSN 0098-7484. PMID 9355997.  
  44. ^ Goldsher M, Better OS (May 1979). "Antifreeze poisoning during the October 1973 War in the Middle-East: case reports". Military medicine 144 (5): 314–5. ISSN 0026-4075. PMID 113700.  
  45. ^ Armstrong EJ, Engelhart DA, Jenkins AJ, Balraj EK (June 2006). "Homicidal ethylene glycol intoxication: a report of a case". The American journal of forensic medicine and pathology : official publication of the National Association of Medical Examiners 27 (2): 151–5. doi:10.1097/01.paf.0000203221.17854.38. ISSN 0195-7910. PMID 16738434.  
  46. ^ Munro, Ian (October 13, 2007). "Death by anti-freeze 'perfect murder'". The Age. Retrieved 2008-10-01.  
  47. ^ [edited by] Lewis R. Goldfrank ... [et al.] ; with 116 contributors. (2002). Goldfrank LR, Flomenbaum NE, Lewin NA, Howland MA, Hoffman RS, Nelson LS. ed. Goldfrank’s toxicologic emergencies. McGraw-Hill. pp. 980–90. ISBN 0-07-136001-8. OCLC 48177200.  
  48. ^ "Annual Report 2007" (PDF). Victorian Poisons Information Centre. 2008. Retrieved 2008-10-12.  
  49. ^ "Annual Report 2007" (PDF). New South Wales Poisons Information Centre. 2008. Retrieved 2008-10-12.  
  50. ^ LaKind JS, McKenna EA, Hubner RP, Tardiff RG (July 1999). "A review of the comparative mammalian toxicity of ethylene glycol and propylene glycol". Critical reviews in toxicology 29 (4): 331–65. doi:10.1080/10408449991349230. ISSN 1040-8444. PMID 10451263.  
  51. ^ a b c d White NC, Litovitz T, White MK, Watson WA, Benson BE, Horowitz BZ, Marr-Lyon L (July 2008). "The impact of bittering agents on suicidal ingestions of antifreeze". Clinical toxicology (Philadelphia, Pa.) 46 (6): 507–14. doi:10.1080/15563650802119700. ISSN 1556-3650. PMID 18584362.  
  52. ^ Jackson MH, Payne HA (August 1995). "Bittering agents: their potential application in reducing ingestions of engine coolants and windshield wash". Veterinary and human toxicology 37 (4): 323–6. ISSN 0145-6296. PMID 8540219.  
  53. ^ Neumann CM, Giffin S, Hall R, Henderson M, Buhler DR (1 January 2000). "Oregon's Toxic Household Products Law". Journal of public health policy 21 (3): 342–59. doi:10.2307/3343331. ISSN 01975897. PMID 11021047.  
  54. ^ Saunders, Morgan (June 2, 2009). "Law Targets Poisonings by Antifreeze". Retrieved 2009-06-18.  
  55. ^ a b Mullins ME, Zane Horowitz B (June 2004). "Was it necessary to add Bitrex (denatonium benzoate) to automotive products?". Veterinary and human toxicology 46 (3): 150–2. ISSN 0145-6296. PMID 15171494.  
  56. ^ a b White NC, Litovitz T, Benson BE, Horowitz BZ, Marr-Lyon L, White MK (November 2009). "The impact of bittering agents on pediatric ingestions of antifreeze". Clinical Pediatrics 48 (9): 913–21. doi:10.1177/0009922809339522. PMID 19571333.  
  57. ^ Hanzlik PJ, Seidenfeld MA, Johnson CC (1931). "General properties, irritant and toxic actions of ethylene glycol". The Journal of pharmacology and experimental therapeutics 41: 387–406.  
  58. ^ Friedman EA, Greenberg JB, Merrill JP, Dammin GJ (June 1962). "Consequences of ethylene glycol poisoning. Report of four cases and review of the literature". The American journal of medicine 32: 891–902. doi:10.1016/0002-9343(62)90035-9. ISSN 0002-9343. PMID 13895244.  


Got something to say? Make a comment.
Your name
Your email address