| 词条 | Ethylene glycol poisoning |
| 释义 |
| name = Ethylene glycol poisoning | image = Ethylene glycol.svg | caption = Ethylene glycol | synonyms = Ethylene glycol toxicity | field = Emergency medicine | symptoms = Early: intoxication, vomiting, abdominal pain[1] Later: decreased level of consciousness, headache, seizures[1] | complications = Kidney failure, brain damage[1] | onset = | duration = | types = | causes = Drinking ethylene glycol[1] | risks = | diagnosis = Calcium oxalate crystals in the urine, acidosis or increased osmol gap in the blood[1] | differential = | prevention = | treatment = Antidote, hemodialysis[6] | medication = Fomepizole, ethanol[6] | prognosis = | frequency = > 5,000 cases per year (US)[8] | deaths = }}Ethylene glycol poisoning is poisoning caused by drinking ethylene glycol.[1] Early symptoms include intoxication, vomiting and abdominal pain.[1] Later symptoms may include a decreased level of consciousness, headache, and seizures.[1] Long term outcomes may include kidney failure and brain damage.[1] Toxicity and death may occur after drinking even a small amount.[1] Ethylene glycol is a colorless, odorless, sweet liquid, commonly found in antifreeze.[1] It may be drunk accidentally or intentionally in an attempt to cause death.[6] When broken down by the body it results in glycolic acid and oxalic acid which cause most of the toxicity.[1][17] The diagnosis may be suspected when calcium oxalate crystals are seen in the urine or when acidosis or an increased osmol gap is present in the blood.[1] Diagnosis may be confirmed by measuring ethylene glycol levels in the blood; however, many hospitals do not have the ability to perform this test.[1] Early treatment increases the chance of a good outcome.[6] Treatment consists of stabilizing the person, followed by the use of an antidote.[6] The preferred antidote is fomepizole with ethanol used if this is not available.[6] Hemodialysis may also be used in those where there is organ damage or a high degree of acidosis.[6] Other treatments may include sodium bicarbonate, thiamine, and magnesium.[2] More than 5000 cases of poisoning occur in the United States each year.[3] Those affected are often adults and male.[4] Deaths from ethylene glycol have been reported as early as 1930.[27] An outbreak of deaths in 1937 due to a medication mixed in a similar compound, diethylene glycol, resulted in the Food, Drug, and Cosmetic Act of 1938 in the United States which mandated evidence of safety before new medications could be sold.[5] Antifreeze products sometimes have a substance to make it bitter added to discourage drinking by children and other animals but this has not been found to be effective.[2] Signs and symptomsSigns of ethylene glycol poisoning depend upon the time after ingestion.[30] Symptoms usually follow a three-step progression, although poisoned individuals will not always develop each stage.[6][7]
SourcesThe most common source of ethylene glycol is automotive antifreeze or radiator coolant, where concentrations are high.[33] Other sources of ethylene glycol include windshield deicing agents, brake fluid, motor oil, developing solutions for hobby photographers, wood stains, solvents, and paints.[33] Some people put antifreeze into their cabin’s toilet to prevent it from freezing during the winter, resulting in toxicities when animals drink from the toilet.[33] Small amounts of ethylene glycol may be contained in holiday ornaments such as snow globes.[33] The most significant source of ethylene glycol is from aircraft de-icing and anti-icing operations, where it is released onto land and eventually to waterways near airports experiencing cold winter climates.[51] It is also used in manufacturing polyester products.[51] In 2006, approximately 1540 kilotonnes of ethylene glycol were manufactured in Canada by three companies in Alberta, with most of the production destined for export.[51] PathophysiologyThe three main systems affected by ethylene glycol poisoning are the central nervous system, metabolic processes, and the kidneys.[6] 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.[6] Seizures may occur due to a direct effect.[8] 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 by aldehyde dehydrogenase.[6] The increase in metabolites may cause encephalopathy or cerebral edema.[10] 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.[6] The kidney 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.[6] 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.[6] The rate-limiting step in this cascade is the conversion of glycolic to glyoxylic acid.[11] Accumulation of glycolic acid in the body is mainly responsible for toxicity.[12] ToxicityEthylene glycol has been shown to be toxic to humans[13] and is also toxic to domestic pets such as cats and dogs. A toxic dose requiring medical treatment varies but is considered more than 0.1 mL per kg body weight (mL/kg) of pure substance. That is roughly 16 mL of 50% ethylene glycol for an 80 kg adult and 4 mL for a 20 kg child. 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.[65] The orally lethal dose in humans has been reported as approximately 1.4 mL/kg of pure ethylene glycol.[6] That is approximately 224 mL (7.6 oz.) of 50% ethylene glycol for an 80 kg adult and 56 mL (2 oz.) for a 20 kg child. Although survival with medical treatment has occurred with doses much higher than this, death has occurred with 30 mL of the concentrate in an adult.[14][15][16] 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.[17] 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.[18] Ethylene glycol is not well absorbed through skin meaning poisoning following dermal exposure is also uncommon.[19] DiagnosisAs many of the clinical signs and symptoms of ethylene glycol poisoning are nonspecific and occur in many poisonings the diagnosis is often difficult.[20] It is most reliably diagnosed by the measurement of the blood ethylene glycol concentration. Ethylene glycol in biological fluids can be determined by gas chromatography.[21] 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.[6] 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.[76][22] 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.[23] 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.[6] 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.[6] 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.[24] 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.[25][26] PreventionAntifreeze products for automotive use containing propylene glycol in place of ethylene glycol are available, and are generally considered safer to use, as it possesses an unpleasant taste in contrast to the perceived "sweet" taste of toxic ethylene glycol-based coolants, and only produces lactic acid in an animal's body, as their muscles do when exercised.[27]{{Unreliable source?|date=October 2012}} When using antifreeze products containing ethylene glycol, recommended safety measures include:
TreatmentStabilization and decontaminationThe 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 benefit 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.[6] The usefulness of gastric lavage has, however, been questioned, and it is now no longer used routinely in poisoning situations.[28] 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.[6] It is only used in the presence of a toxic dose of another poison or drug.[29] 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.[6] Patients presenting with metabolic acidosis or seizures require treatment with sodium bicarbonate and anticonvulsives such as a benzodiazepine respectively.[6] 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.[20] Intubation and respiratory support may be required in severely intoxicated patients; patients with hypotension require treatment with intravenous fluids and possibly vasopressors.[103] AntidotesFollowing 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 and fomepizole. This antidotal treatment forms the mainstay of management of ethylene glycol poisoning. The toxicity of ethylene glycol comes from its metabolism to glycolic acid and oxalic acid. The goal of pharmacotherapy is to prevent the formation of these metabolites. Ethanol acts by competing with ethylene glycol for alcohol dehydrogenase, the first enzyme in the degradation pathway. Because ethanol has a much higher affinity for alcohol dehydrogenase, about a 100-times greater affinity, it successfully blocks the breakdown of ethylene glycol into glycolaldehyde, which prevents the further degradation. Without oxalic acid formation, the nephrotoxic effects can be avoided, but the ethylene glycol is still present in the body. It is eventually excreted in the urine, but supportive therapy for the CNS depression and metabolic acidosis will be required until the ethylene glycol concentrations fall below toxic limits. 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.[6] Fomepizole is a potent inhibitor of alcohol dehydrogenase; similar to ethanol, it acts to block the formation of the toxic metabolites.[20][30][31] Fomepizole has been shown to be highly effective as an antidote for ethylene glycol poisoning.[31][109] It is the only antidote approved by the U.S. Food and Drug Administration for the treatment of ethylene glycol poisoning.[6] Both antidotes have advantages and disadvantages. Ethanol is readily available in most hospitals, is inexpensive, and can be administered orally as well as intravenously. Its adverse effects include intoxication, hypoglycemia in children, and possible liver toxicity.[29] Patients receiving ethanol therapy also require frequent blood ethanol concentration 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{{Clarify|date=March 2012}} and the approved dosing regimen maintains therapeutic concentrations without the need to monitor blood concentrations 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.[32][33] Despite the cost, fomepizole is gradually replacing ethanol as the antidote of choice in ethylene glycol poisoning.[31][34] Adjunct agents including thiamine and pyridoxine are often given, because they may help prevent the formation of oxalic acid.[6] 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.[20] HemodialysisIn 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.[11][35] 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 patient's condition is deteriorating despite treatment.[8][20] 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.[6] If hemodialysis is not available, then peritoneal dialysis also removes ethylene glycol, although less efficiently.[36] PrognosisTreatment for antifreeze poisoning needs to be started as soon after ingestion as possible to be effective; the earlier treatment is started, the greater the chance of survival.[30][125] Cats must be treated within 3 hours of ingesting of antifreeze to be effective, while dogs must be treated within 8–12 hours of ingestion.[33] Once kidney failure develops, the prognosis is poor.[33] Generally, if the patient is treated and survives then a full recovery is expected.[128] Patients who present early to medical facilities and have prompt medical treatment typically will have a favorable outcome.[37] Alternatively, patients presenting late with signs and symptoms of coma, hyperkalemia, seizures, or severe acidosis have a poor prognosis.[65] 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.[38][39][40][41] 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.[42][136] EpidemiologyEthylene glycol poisoning is a relatively common occurrence worldwide.[43][138][44][45] Human poisoning often occurs in isolated cases, but may also occur in epidemics.[46][47][48] Many cases of poisoning are the result of using ethylene glycol as a cheap substitute for alcohol or intentional ingestions in suicide attempts.[49] Less commonly it has been used as a means of homicide.[50][51] Children or animals may be exposed by accidental ingestion; children and animals often consume large amounts due to ethylene glycol having a sweet taste.[52] In the United States there were 5816 cases reported to poison centers in 2002.[53] Additionally, ethylene glycol was the most common chemical responsible for deaths reported by US poison centers in 2003.[54] 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.[55][56] However, these numbers may underestimate actual numbers because not all cases attributable to ethylene glycol are reported to poison control centers.[57] Most deaths from ethylene glycol are intentional suicides; deaths in children due to unintentional ingestion are extremely rare.[58] 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.[59] 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.[58][60][61] 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.[58][62][63] Specifically, Mullins finds that bittering of antifreeze does not reduce reported cases of poisoning of preschoolers in the US state of Oregon.[62] Similarly, White found that adding bittering agents did not decrease the frequency or severity of antifreeze poisonings in children under the age of 5.[63] Additionally, another study by White found that suicidal persons are not deterred by the bittered taste of antifreeze in their attempts to kill themselves.[58] 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). Poisoning of a raccoon was diagnosed in 2002 in Prince Edward Island, Canada.[164] An online veterinary manual provides information on lethal doses of ethylene glycol for chicken, cattle, as well as cats and dogs, adding that younger animals may be more susceptible.[64] HistoryEthylene glycol was once thought innocuous; in 1931 it was suggested as being suitable for use as a vehicle or solvent for injectable pharmaceutical preparations.[65] Numerous cases of poisoning have been reported since then, and it has been shown to be toxic to humans.[13] Environmental effectsEthylene glycol involved in aircraft de-icing and anti-icing operations is released onto land and eventually to waterways.[51] A report prepared for the World Health Organization in 2000 stated that laboratory tests exposing aquatic organisms to stream water receiving runoff from airports have shown toxic effects and death (p. 12).[169] Field studies in the vicinity of an airport have reported toxic signs consistent with ethylene glycol poisoning, fish kills, and reduced biodiversity, although those effects could not definitively be ascribed to ethylene glycol (p. 12).[169] The process of biodegrading of glycols also increases the risk to organisms, as oxygen levels become depleted in surface waters (p. 13).[169] Another study found the toxicity to aquatic and other organisms was relatively low, but the oxygen-depletion effect of biodegradation was more serious (p. 245).[172] Further, "Anaerobic biodegradation may also release relatively toxic byproducts such as acetaldehyde, ethanol, acetate, and methane (p. 245)."[172] In Canada, Environment Canada reports that "in recent years, management practices at Canada’s major airports have improved with the installation of new ethylene glycol application and mitigation facilities or improvements to existing ones."[51] Since 1994, federal airports must comply with the Glycol Guidelines of the Canadian Environmental Protection Act, monitoring and reporting on concentrations of glycols in surface water.[66] Detailed mitigation plans include storage and handling issues (p. 27), spill response procedures, and measures taken to reduce volumes of fluid (p. 28).[176] Considering factors such as the "seasonal nature of releases, ambient temperatures, metabolic rates and duration of exposure", Environment Canada stated in 2014 that "it is proposed that ethylene glycol is not entering the environment in a quantity or concentration or under conditions that have or may have an immediate or long-term harmful effect on the environment or its biological diversity".[51] In the U.S., airports are required to obtain stormwater discharge permits and ensure that wastes from deicing operations are properly collected and treated.[178] Large new airports may be required to collect 60 percent of aircraft deicing fluid after deicing.[178] Airports that discharge the collected aircraft deicing fluid directly to waters of the U.S. must also meet numeric discharge requirements for chemical oxygen demand.[178] A report in 2000 stated that ethylene glycol was becoming less popular for aircraft deicing in the U.S., due to its reporting requirements and adverse environmental impacts (p. 213), and noted a shift to the use of propylene glycol (p. I-3).[172] Other animalsOnce kidney failure has developed in dogs and cats, the outcome is poor.[33] See also
References1. ^1 2 3 4 5 6 7 8 9 10 11 12 13 {{cite journal|last1=Kruse|first1=JA|title=Methanol and ethylene glycol intoxication.|journal=Critical Care Clinics|date=October 2012|volume=28|issue=4|pages=661–711|pmid=22998995|doi=10.1016/j.ccc.2012.07.002}} , accessed Sept. 11, 2014.[67][68][69][70][71][72][73][74][75][76]2. ^1 2 3 4 5 6 7 8 {{cite journal|last1=Beauchamp|first1=GA|last2=Valento|first2=M|title=Toxic Alcohol Ingestion: Prompt Recognition And Management In The Emergency Department.|journal=Emergency Medicine Practice|date=September 2016|volume=18|issue=9|pages=1–20|pmid=27538060}} 3. ^1 {{cite book|last1=Naidich|first1=Thomas P.|last2=Castillo|first2=Mauricio|last3=Cha|first3=Soonmee|last4=Smirniotopoulos|first4=James G.|title=Imaging of the Brain: Expert Radiology Series|date=2012|publisher=Elsevier Health Sciences|isbn=978-0323186476|page=960|url=https://books.google.com/books?id=W26K3Jxhq1kC&pg=PA960|language=en|deadurl=no|archiveurl=https://web.archive.org/web/20170908221959/https://books.google.com/books?id=W26K3Jxhq1kC&pg=PA960|archivedate=2017-09-08|df=}} 4. ^1 {{cite book|last1=Ferri|first1=Fred F.|title=Ferri's Clinical Advisor 2017: 5 Books in 1|date=2016|publisher=Elsevier Health Sciences|isbn=9780323448383|page=794|url=https://books.google.com/books?id=rRhCDAAAQBAJ&pg=PA794|language=en|deadurl=no|archiveurl=https://web.archive.org/web/20170908221935/https://books.google.com/books?id=rRhCDAAAQBAJ&pg=PA794|archivedate=2017-09-08|df=}} 5. ^1 {{cite book|last1=Shaw|first1=Leslie M.|title=The Clinical Toxicology Laboratory: Contemporary Practice of Poisoning Evaluation|date=2001|publisher=Amer. Assoc. for Clinical Chemistry|isbn=9781890883539|page=197|url=https://books.google.com/books?id=pXvFGqz44pYC&pg=PA197|language=en|deadurl=no|archiveurl=https://web.archive.org/web/20170908221959/https://books.google.com/books?id=pXvFGqz44pYC&pg=PA197|archivedate=2017-09-08|df=}} 6. ^1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 {{cite journal | author = Brent J | authorlink= Jeffrey Brent| title = Current management of ethylene glycol poisoning | journal = Drugs | volume = 61 | issue = 7 | pages = 979–88 | year = 2001 | pmid = 11434452 | doi = 10.2165/00003495-200161070-00006 | issn = 0012-6667 | url=https://pdfs.semanticscholar.org/3ab9/b4cc872e76dfd6495df02b76709952d7f17b.pdf}} 7. ^{{cite journal|last1=Hess|first1=R|last2=Bartels|first2=MJ|last3=Pottenger|first3=LH|title=Ethylene glycol: an estimate of tolerable levels of exposure based on a review of animal and human data.|journal=Archives of Toxicology|date=December 2004|volume=78|issue=12|pages=671–80|pmid=15372138|doi=10.1007/s00204-004-0594-8}} 8. ^1 2 {{cite journal |vauthors=Barceloux DG, Krenzelok EP, Olson K, Watson W | title=American Academy of Clinical Toxicology Practice Guidelines on the Treatment of Ethylene Glycol Poisoning. Ad Hoc Committee | journal=Journal of Toxicology: Clinical Toxicology | year=1999 | pages=537–60 | volume=37 | issue=5 | pmid=10497633 | doi=10.1081/CLT-100102445 | issn=0731-3810}} 9. ^{{cite journal |vauthors=Bobbitt WH, Williams RM, Freed CR |title=Severe ethylene glycol intoxication with multisystem failure |journal=Western Journal of Medicine |volume=144 |issue=2 |pages=225–8 |date=February 1986 |pmid=3953092 |pmc=1306577 |doi= |issn=0093-0415 }} 10. ^{{cite journal |author=Maier W |title=Cerebral computed tomography of ethylene glycol intoxication |journal=Neuroradiology |volume=24 |issue=3 |pages=175–7 |year=1983 |pmid=6828232 |doi= 10.1007/BF00347839 |issn=0028-3940|doi-broken-date=2019-02-18 }} 11. ^1 {{cite journal |vauthors=Gabow PA, Clay K, Sullivan JB, Lepoff R |title=Organic acids in ethylene glycol intoxication |journal=Annals of Internal Medicine |volume=105 |issue=1 |pages=16–20 |date=July 1986 |pmid=3717806 |doi= 10.7326/0003-4819-105-1-16|url= |issn=0003-4819}} 12. ^{{cite journal |vauthors=Clay KL, Murphy RC |title=On the metabolic acidosis of ethylene glycol intoxication |journal=Toxicology and Applied Pharmacology |volume=39 |issue=1 |pages=39–49 |date=January 1977 |pmid=14421 |doi= 10.1016/0041-008X(77)90175-2|url= |issn=0041-008X }} 13. ^1 {{cite journal |vauthors=Friedman EA, Greenberg JB, Merrill JP, Dammin GJ |title=Consequences of ethylene glycol poisoning. Report of four cases and review of the literature |journal=The American Journal of Medicine |volume=32 |issue= 6|pages=891–902 |date=June 1962 |pmid=13895244 |doi= 10.1016/0002-9343(62)90035-9|url= |issn=0002-9343}} 14. ^{{cite journal |vauthors=Eder AF, McGrath CM, Dowdy YG, Tomaszewski JE, Rosenberg FM, Wilson RB, Wolf BA, Shaw LM |title=Ethylene glycol poisoning: toxicokinetic and analytical factors affecting laboratory diagnosis |journal=Clinical Chemistry |volume=44 |issue=1 |pages=168–77 |date=January 1998 |pmid=9550575 |doi= |url=http://www.clinchem.org/cgi/pmidlookup?view=long&pmid=9550575 |issn=0009-9147}} 15. ^{{cite journal |author=Field DL |title=Acute ethylene glycol poisoning |journal=Critical Care Medicine |volume=13 |issue=10 |pages=872–3 |date=October 1985 |pmid=4028762 |doi= 10.1097/00003246-198510000-00024|url= |issn=0090-3493}} 16. ^{{cite journal |vauthors=Amathieu R, Merouani M, Borron SW, Lapostolle F, Smail N, Adnet F |title=Prehospital diagnosis of massive ethylene glycol poisoning and use of an early antidote |journal=Resuscitation |volume=70 |issue=2 |pages=285–6 |date=August 2006 |pmid=16808995 |doi=10.1016/j.resuscitation.2005.12.014 |url= |issn=0300-9572}} 17. ^{{cite journal |vauthors=Hodgman MJ, Wezorek C, Krenzelok E |title=Toxic inhalation of ethylene glycol: a pharmacological improbability |journal=Journal of Toxicology: Clinical Toxicology |volume=35 |issue=1 |pages=109–11 |year=1997 |pmid=9022663 |doi=10.3109/15563659709001176 |url=}} 18. ^{{cite journal |vauthors=Wills JH, Coulston F, Harris ES, McChesney EW, Russell JC, Serrone DM |title=Inhalation of aerosolized ethylene glycol by man |journal=Clinical Toxicology |volume=7 |issue=5 |pages=463–76 |year=1974 |pmid=4613525 |doi= 10.3109/15563657408988020|url= |issn=0009-9309}} 19. ^{{cite journal |vauthors=Driver J, Tardiff RG, Sedik L, Wester RC, Maibach HI |title=In vitro percutaneous absorption of [14C] ethylene glycol |journal=Journal of Exposure Analysis and Environmental Epidemiology |volume=3 |issue=3 |pages=277–84 |date=July 1993 |pmid=8260837 |doi= |issn=1053-4245 }} 20. ^1 2 3 4 {{cite journal |author=Hall TL |title=Fomepizole in the treatment of ethylene glycol poisoning |journal=Canadian Journal of Emergency Medical Care |volume=4 |issue=3 |pages=199–204 |date=May 2002 |pmid=17609006 |doi=10.1017/s1481803500006382 |url=http://www.cjem-online.ca/sites/default/files/pg199.pdf |issn=1481-8035 |deadurl=yes |archiveurl=https://www.webcitation.org/5m71phrDu?url=http://www.cjem-online.ca/sites/default/files/pg199.pdf |archivedate=2009-12-18 |df= }} 21. ^{{cite journal |vauthors=Aarstad K, Dale O, Aakervik O, Ovrebø S, Zahlsen K |title=A rapid gas chromatographic method for determination of ethylene glycol in serum and urine |journal=Journal of Analytical Toxicology |volume=17 |issue=4 |pages=218–21 |date=July 1993 |pmid=8371550 |doi= 10.1093/jat/17.4.218|issn=0146-4760 }} 22. ^{{cite journal |vauthors=Hoffman RS, Smilkstein MJ, Howland MA, Goldfrank LR |title=Osmol gaps revisited: normal values and limitations |journal=Journal of Toxicology: Clinical Toxicology |volume=31 |issue=1 |pages=81–93 |year=1993 |pmid=8433417 |doi=10.3109/15563659309000375 |url= |issn=0731-3810 }} 23. ^{{cite journal |author=Glaser DS |title=Utility of the serum osmol gap in the diagnosis of methanol or ethylene glycol ingestion |journal=Annals of Emergency Medicine |volume=27 |issue=3 |pages=343–6 |date=March 1996 |pmid=8599495 |doi= 10.1016/S0196-0644(96)70271-8|url= |issn=0196-0644}} 24. ^{{cite journal |vauthors=Jacobsen D, Akesson I, Shefter E |title=Urinary calcium oxalate monohydrate crystals in ethylene glycol poisoning |journal=Scandinavian Journal of Clinical and Laboratory Investigation |volume=42 |issue=3 |pages=231–4 |date=May 1982 |pmid=7134806 |doi= 10.3109/00365518209168078|url= |issn=0036-5513}} 25. ^{{cite journal |vauthors=Winter ML, Ellis MD, Snodgrass WR |title=Urine fluorescence using a Wood's lamp to detect the antifreeze additive sodium fluorescein: a qualitative adjunctive test in suspected ethylene glycol ingestions |journal=Annals of Emergency Medicine |volume=19 |issue=6 |pages=663–7 |date=June 1990 |pmid=2344083 |doi= 10.1016/S0196-0644(05)82472-2|url= |issn=0196-0644}} 26. ^{{cite journal |vauthors=Wallace KL, Suchard JR, Curry SC, Reagan C |title=Diagnostic use of physicians' detection of urine fluorescence in a simulated ingestion of sodium fluorescein-containing antifreeze |journal=Annals of Emergency Medicine |volume=38 |issue=1 |pages=49–54 |date=July 2001 |pmid=11423812 |doi=10.1067/mem.2001.115531 |url= |issn=0196-0644}} 27. ^{{cite web |url=http://www.resteddoginn.ca/antifreeze.php |title=Ethylene Glycol Poisoning |author=Pieter Klapwijk |date=January 27, 2010 |website= |publisher=The Rested Dog Inn |accessdate=October 11, 2012 |deadurl=no |archiveurl=https://web.archive.org/web/20130126003300/http://www.resteddoginn.ca/antifreeze.php |archivedate=January 26, 2013 |df= }} 28. ^{{cite journal |vauthors=Vale JA, Kulig K |title=Position paper: gastric lavage |journal=Journal of Toxicology: Clinical Toxicology |volume=42 |issue=7 |pages=933–43 |year=2004 |pmid=15641639 |doi=10.1081/CLT-200045006 |url= |issn=0731-3810 }} 29. ^1 2 {{cite journal |vauthors=Jacobsen D, McMartin KE |title=Antidotes for methanol and ethylene glycol poisoning |journal=Journal of Toxicology: Clinical Toxicology |volume=35 |issue=2 |pages=127–43 |year=1997 |pmid=9120880 |doi=10.3109/15563659709001182 |issn=0731-3810}} 30. ^1 {{cite journal |author=Brent J |title=Fomepizole for ethylene glycol and methanol poisoning |journal=The New England Journal of Medicine |volume=360 |issue=21 |pages=2216–23 |date=May 2009 |pmid=19458366 |doi=10.1056/NEJMct0806112 |issn=0028-4793}} 31. ^1 2 {{cite journal |vauthors=Brent J, McMartin K, Phillips S, Burkhart K, Donovan J, Wells M, Kulig K | title = Fomepizole for the treatment of ethylene glycol poisoning. Methylpyrazole for Toxic Alcohols Study Group | journal = The New England Journal of Medicine | volume = 340 | issue = 11 | pages = 832–8 |date=March 1999 | pmid = 10080845 | doi = 10.1056/NEJM199903183401102 | issn = 0028-4793}} 32. ^{{cite journal |author=Shannon M |title=Toxicology reviews: fomepizole--a new antidote |journal=Pediatric Emergency Care |volume=14 |issue=2 |pages=170–2 |date=April 1998 |pmid=9583406 |doi= 10.1097/00006565-199804000-00021|url= |issn=0749-5161}} 33. ^{{cite journal |vauthors=Scalley RD, Ferguson DR, Piccaro JC, Smart ML, Archie TE |title=Treatment of ethylene glycol poisoning |journal=American Family Physician|volume=66 |issue=5 |pages=807–12 |date=September 2002 |pmid=12322772 |doi= |url=http://www.aafp.org/link_out?pmid=12322772 |issn=0002-838X |format=Free full text}} 34. ^1 {{cite journal |vauthors=Borron SW, Mégarbane B, Baud FJ |title=Fomepizole in treatment of uncomplicated ethylene glycol poisoning |journal=The Lancet |volume=354 |issue=9181 |pages=831 |date=September 1999 |pmid=10485727 |doi=10.1016/S0140-6736(99)80015-4 |url= |issn=0140-6736}} 35. ^{{cite journal |vauthors=Moreau CL, Kerns W, Tomaszewski CA, McMartin KE, Rose SR, Ford MD, Brent J |title=Glycolate kinetics and hemodialysis clearance in ethylene glycol poisoning. META Study Group |journal=Journal of Toxicology: Clinical Toxicology |volume=36 |issue=7 |pages=659–66 |year=1998 |pmid=9865233 |doi= 10.3109/15563659809162613 |issn=0731-3810}} 36. ^{{cite journal |vauthors=Aakervik O, Svendsen J, Jacobsen D |title=[Severe ethylene glycol poisoning treated with fomepizole (4-methylpyrazole)] |language=Norwegian |journal=Tidsskrift for den Norske Lægeforening : Tidsskrift for Praktisk Medicin, NY Række |volume=122 |issue=25 |pages=2444–6 |date=October 2002 |pmid=12448112 |doi= |issn=0029-2001 }} 37. ^{{cite journal |vauthors=Velez LI, Shepherd G, Lee YC, Keyes DC |title=Ethylene glycol ingestion treated only with fomepizole |journal=Journal of Medical Toxicology |volume=3 |issue=3 |pages=125–8 |date=September 2007 |pmid=18072148 |pmc=3550067 |doi=10.1007/BF03160922 |issn=1556-9039 }}{{dead link|date=September 2017 |bot=Level C |fix-attempted=yes }} 38. ^{{cite journal |vauthors=Jacobsen D, McMartin KE |title=Methanol and ethylene glycol poisonings. Mechanism of toxicity, clinical course, diagnosis and treatment |journal=Medical Toxicology |volume=1 |issue=5 |pages=309–34 |date=September 1986 |pmid=3537623 |doi= 10.1007/bf03259846|url= |issn=0112-5966}} 39. ^{{cite journal |vauthors=Berger JR, Ayyar DR |title=Neurological complications of ethylene glycol intoxication. Report of a case |journal=Archives of Neurology |volume=38 |issue=11 |pages=724–6 |date=November 1981 |pmid=7305705 |doi= 10.1001/archneur.1981.00510110084016|url= |issn=0003-9942}} 40. ^{{cite journal |vauthors=Lewis LD, Smith BW, Mamourian AC |title=Delayed sequelae after acute overdoses or poisonings: cranial neuropathy related to ethylene glycol ingestion |journal=Clinical Pharmacology & Therapeutics |volume=61 |issue=6 |pages=692–9 |date=June 1997 |pmid=9209253 |doi=10.1016/S0009-9236(97)90105-3 |url= |issn=0009-9236}} 41. ^{{cite journal |vauthors=Spillane L, Roberts JR, Meyer AE |title=Multiple cranial nerve deficits after ethylene glycol poisoning |journal=Annals of Emergency Medicine |volume=20 |issue=2 |pages=208–10 |date=February 1991 |pmid=1996809 |doi= 10.1016/S0196-0644(05)81226-0|url= |issn=0196-0644}} 42. ^{{cite journal |vauthors=Nizze H, Schwabbauer P, Brachwitz C, Lange H |title=[Fatal chronic oxalosis after sublethal ethylene glycol poisoning] |language=German |journal=Der Pathologe |volume=18 |issue=4 |pages=328–34 |date=July 1997 |pmid=9380607 |doi=10.1007/s002920050224 |url=http://link.springer.de/link/service/journals/00292/bibs/7018004/70180328.htm |issn=0172-8113 |deadurl=yes |archiveurl=https://web.archive.org/web/20001002115301/http://link.springer.de/link/service/journals/00292/bibs/7018004/70180328.htm |archivedate=2000-10-02 |df= }} 43. ^1 {{cite journal |vauthors=Davis DP, Bramwell KJ, Hamilton RS, Williams SR |title=Ethylene glycol poisoning: case report of a record-high level and a review |journal=The Journal of Emergency Medicine|volume=15 |issue=5 |pages=653–67 |date=September 1997 |pmid=9348055 |doi=10.1016/S0736-4679(97)00145-5|url= |issn=0736-4679}} 44. ^{{cite journal |vauthors=Kotwica M, Czerczak S |title=Acute poisonings registered since 1970: trends and characteristics. Analysis of the files collected in the National Poison Information Centre, Łódź, Poland |journal=International Journal of Occupational Medicine and Environmental Health |volume=20 |issue=1 |pages=38–43 |year=2007 |pmid=17509968 |doi=10.2478/v10001-007-0010-8 |url= |issn=1232-1087}} 45. ^{{cite journal |vauthors=Krenová M, Pelclová D, Navrátil T, Merta M |title=Experiences of the Czech toxicological information centre with ethylene glycol poisoning |journal=Biomedical Papers of the Medical Faculty of the University Palacký, Olomouc, Czechoslovakia |volume=149 |issue=2 |pages=473–5 |date=December 2005 |pmid=16601813 |doi=10.5507/bp.2005.083 |url=http://publib.upol.cz/~obd/fulltext/Biomed/2005/2/473.pdf |issn=1213-8118 |deadurl=yes |archiveurl=https://web.archive.org/web/20090306082805/http://publib.upol.cz/~obd/fulltext/Biomed/2005/2/473.pdf |archivedate=2009-03-06 |df= }} 46. ^{{cite journal |title=Ethylene glycol intoxication due to contamination of water systems |journal=MMWR. Morbidity and Mortality Weekly Report |volume=36 |issue=36 |pages=611–4 |date=September 1987 |pmid=3114608 |doi= |issn= 0149-2195 |author1= Centers for Disease Control (CDC)}} 47. ^{{cite journal |vauthors=Leikin JB, Toerne T, Burda A, McAllister K, Erickson T |title=Summertime cluster of intentional ethylene glycol ingestions |journal=JAMA: The Journal of the American Medical Association |volume=278 |issue=17 |pages=1406 |date=November 1997 |pmid=9355997 |doi= 10.1001/jama.278.17.1406|url= |issn=0098-7484}} 48. ^{{cite journal |vauthors=Goldsher M, Better OS |title=Antifreeze poisoning during the October 1973 War in the Middle-East: case reports |journal=Military Medicine |volume=144 |issue=5 |pages=314–5 |date=May 1979 |pmid=113700 |doi= 10.1093/milmed/144.5.314|url= |issn=0026-4075}} 49. ^1 {{cite journal |vauthors=Leth PM, Gregersen M |title=Ethylene glycol poisoning |journal=Forensic Science International |volume=155 |issue=2–3 |pages=179–84 |date=December 2005 |pmid=16226155 |doi=10.1016/j.forsciint.2004.11.012 |url= |issn=0379-0738}} 50. ^{{cite journal |vauthors=Armstrong EJ, Engelhart DA, Jenkins AJ, Balraj EK |title=Homicidal ethylene glycol intoxication: a report of a case |journal=The American Journal of Forensic Medicine and Pathology|volume=27 |issue=2 |pages=151–5 |date=June 2006 |pmid=16738434 |doi=10.1097/01.paf.0000203221.17854.38 |url= |issn=0195-7910}} 51. ^{{cite web | last = Munro | first = Ian | title = Death by anti-freeze 'perfect murder' | website = | publisher = The Age | date = October 13, 2007 | url = http://www.theage.com.au/news/world/death-by-antifreeze-perfect-murder/2007/10/12/1191696176894.html | doi = | accessdate = 2008-10-01 | deadurl = no | archiveurl = https://web.archive.org/web/20080118153009/http://www.theage.com.au/news/world/death-by-antifreeze-perfect-murder/2007/10/12/1191696176894.html | archivedate = January 18, 2008 | df = }} 52. ^{{cite book | veditors = Goldfrank LR, Flomenbaum NE, Lewin NA, Howland MA, Hoffman RS, Nelson LS | title = Goldfrank's toxicologic emergencies | year = 2002| pages = 980–90 | publisher = McGraw-Hill | isbn = 978-0-07-136001-2 | oclc = 48177200}} 53. ^1 2 {{cite journal |vauthors=Caravati EM, Erdman AR, Christianson G, etal |title=Ethylene glycol exposure: an evidence-based consensus guideline for out-of-hospital management |journal=Clinical Toxicology |volume=43 |issue=5 |pages=327–45 |year=2005 |pmid=16235508 |doi=10.1080/07313820500184971 |url= |last12=Troutman |first12=WG |last13=American Association Of Poison Control |first13=Centers |issn=1556-3650}} 54. ^1 {{cite journal |vauthors=Watson WA, Litovitz TL, Klein-Schwartz W, ((Rodgers GC Jr)), Youniss J, Reid N, Rouse WG, Rembert RS, Borys D |title=2003 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System |journal=American Journal of Emergency Medicine |volume=22 |issue=5 |pages=335–404 |date=September 2004 |pmid=15490384 |doi= 10.1016/j.ajem.2004.06.001|url= |issn=0735-6757}} 55. ^{{cite web | title = Annual Report 2007 | publisher = Victorian Poisons Information Centre | year = 2008 | url = http://www.austin.org.au/Assets/Files/Annual%20Report%2007.pdf | accessdate = 2008-10-12 | deadurl = yes | archiveurl = https://web.archive.org/web/20110224075800/http://www.austin.org.au/Assets/Files/Annual%20Report%2007.pdf | archivedate = 2011-02-24 | df = }} 56. ^{{cite web | title =Annual Report 2007 | publisher = New South Wales Poisons Information Centre | year = 2008 | url =http://www.chw.edu.au/poisons/2007_annual_report.pdf | accessdate = 2008-10-12|archiveurl = https://web.archive.org/web/20080802094436/http://www.chw.edu.au/poisons/2007_annual_report.pdf |archivedate = August 2, 2008|deadurl=yes}} 57. ^{{cite journal |vauthors=LaKind JS, McKenna EA, Hubner RP, Tardiff RG |title=A review of the comparative mammalian toxicity of ethylene glycol and propylene glycol |journal=Critical Reviews in Toxicology |volume=29 |issue=4 |pages=331–65 |date=July 1999 |pmid=10451263 |doi= 10.1080/10408449991349230|url= |issn=1040-8444}} 58. ^1 2 3 {{cite journal |vauthors=White NC, Litovitz T, White MK, Watson WA, Benson BE, Horowitz BZ, Marr-Lyon L |title=The impact of bittering agents on suicidal ingestions of antifreeze |journal=Clinical Toxicology |volume=46 |issue=6 |pages=507–14 |date=July 2008 |pmid=18584362 |doi=10.1080/15563650802119700 |url= |issn=1556-3650 }} 59. ^{{cite journal |vauthors=Jackson MH, Payne HA |title=Bittering agents: their potential application in reducing ingestions of engine coolants and windshield wash |journal=Veterinary and Human Toxicology |volume=37 |issue=4 |pages=323–6 |date=August 1995 |pmid=8540219 |doi= |issn=0145-6296}} 60. ^{{cite journal |vauthors=Neumann CM, Giffin S, Hall R, Henderson M, Buhler DR |title=Oregon's Toxic Household Products Law |journal=Journal of Public Health Policy |volume=21 |issue=3 |pages=342–59 |date=1 January 2000|pmid=11021047 |doi= 10.2307/3343331 |issn=0197-5897 |jstor=3343331 }} 61. ^{{cite web | last = Saunders | first = Morgan | title = Law Targets Poisonings by Antifreeze | website = | publisher = groundreport.com | date = June 2, 2009 | url = http://www.groundreport.com/Arts_and_Culture/Law-Targets-Poisonings-by-Antifreeze_2 | format = | doi = | accessdate = 2009-06-18 | deadurl = yes | archiveurl = https://web.archive.org/web/20090607050230/http://www.groundreport.com/Arts_and_Culture/Law-Targets-Poisonings-by-Antifreeze_2 | archivedate = June 7, 2009 | df = }} 62. ^1 {{cite journal |vauthors=Mullins ME, Zane Horowitz B |title=Was it necessary to add Bitrex (denatonium benzoate) to automotive products? |journal=Veterinary and Human Toxicology |volume=46 |issue=3 |pages=150–2 |date=June 2004 |pmid=15171494 |doi= |issn=0145-6296 }} 63. ^1 {{cite journal |vauthors=White NC, Litovitz T, Benson BE, Horowitz BZ, Marr-Lyon L, White MK |title=The impact of bittering agents on pediatric ingestions of antifreeze |journal=Clinical Pediatrics |volume=48 |issue=9 |pages=913–21 |date=November 2009 |pmid=19571333 |doi=10.1177/0009922809339522}} 64. ^"The Merck Veterinary Manual: Overview of Ethylene Glycol Toxicity" {{webarchive|url=https://web.archive.org/web/20170118045434/http://www.merckvetmanual.com/toxicology/ethylene-glycol-toxicity/overview-of-ethylene-glycol-toxicity |date=2017-01-18 }}, accessed Sept. 11, 2014. 65. ^{{cite journal|vauthors= Hanzlik PJ, Seidenfeld MA, Johnson CC|title= General properties, irritant and toxic actions of ethylene glycol|journal= The Journal of Pharmacology and Experimental Therapeutics|volume= 41|issue= 4|pages= 387–406|year= 1931|doi= |url= http://jpet.aspetjournals.org/cgi/reprint/41/4/387|deadurl= no|archiveurl= https://web.archive.org/web/20081013202204/http://jpet.aspetjournals.org/cgi/reprint/41/4/387|archivedate= 2008-10-13|df= }} 66. ^[https://www.ec.gc.ca/lcpe-cepa/default.asp?lang=En&n=FD028E79-1 "Glycol Guidelines"] {{webarchive|url=https://web.archive.org/web/20140913080539/https://www.ec.gc.ca/lcpe-cepa/default.asp?lang=En&n=FD028E79-1 |date=2014-09-13 }}, Government of Canada, Environment Canada, Jan. 20, 1994. 67. ^1 2 3 4 5 6 J.J. Mackenzie, "Prevent Antifreeze Poisoning", in Laurie Halse Anderson, Vet Volunteers: Acting Out (2012), Puffin Books, {{ISBN|9780142416761}}, p. 125. 68. ^1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 "Antifreeze Poisoning in Dogs & Cats (Ethylene Glycol Poisoning)" {{webarchive|url=https://web.archive.org/web/20140912071909/http://www.petpoisonhelpline.com/2011/02/antifreeze-poisoning-in-dogs-cats-ethylene-glycol-poisoning/ |date=2014-09-12 }}, Pet Poison Helpline, accessed Sept. 11, 2014. 69. ^1 2 3 4 "College of Veterinary Medicine: Pet Health Topics: Antifreeze Poisoning" {{webarchive|url=https://web.archive.org/web/20150210050224/http://www.vetmed.wsu.edu/ClientED/antifreeze.aspx |date=2015-02-10 }}, Washington State University, accessed Sept. 11, 2014. 70. ^1 {{cite journal | author = Eder Anne F. | year = 1998 | title = Ethylene glycol poisoning: toxicokinetic and analytical factors affecting laboratory diagnosis | url = http://www.clinchem.org/content/44/1/168.long | journal = Clinical Chemistry | volume = 44 | issue = 1 | pages = 168–177 | display-authors = etal | deadurl = no | archiveurl = https://web.archive.org/web/20141203020327/http://www.clinchem.org/content/44/1/168.long | archivedate = 2014-12-03 | df = }} 71. ^1 {{cite journal | author = Foley Peter | year = 2002 | title = Ethylene glycol toxicosis in a free-ranging raccoon (Procyon lotor) from Prince Edward Island | journal = The Canadian Veterinary Journal | volume = 43 | issue = 4| pages = 291–292 | pmc=339239 | pmid=11963664|display-authors=etal}} 72. ^1 2 3 4 5 6 "Government of Canada: Environment Canada: Ethylene Glycol (Final Content)" {{webarchive|url=https://web.archive.org/web/20140913080206/http://www.ec.gc.ca/lcpe-cepa/default.asp?lang=En&n=4B7409ED-1&offset=1&toc=show |date=2014-09-13 }}, April 16, 2014. 73. ^1 2 3 "Concise International Chemical Assessment Document 22: Ethylene Glycol: Environmental Aspects" {{webarchive|url=https://web.archive.org/web/20131031002942/http://www.who.int/ipcs/publications/cicad/en/cicad22.pdf |date=2013-10-31 }}, World Health Organization, 2000. 74. ^1 "Glycol Mitigation Strategies: The Canadian Approach" {{webarchive|url=https://web.archive.org/web/20140913081913/http://www.sae.org/events/icing/presentations/2007s6sattar.pdf |date=2014-09-13 }}, Saleem Sattar, Transport Canada, Sept. 26, 2007. 75. ^1 2 3 "Airport Deicing Effluent Guidelines" {{webarchive|url=https://web.archive.org/web/20150221084920/http://water.epa.gov/scitech/wastetech/guide/airport/index.cfm |date=2015-02-21 }}, United States Environmental Protection Agency, accessed Sept. 12, 2014. 76. ^1 2 3 "Preliminary Data Summary: Airport Deicing Operations (Revised)" {{webarchive|url=https://web.archive.org/web/20140327062631/http://water.epa.gov/scitech/wastetech/guide/airport/upload/2005_10_07_guide_airport_airport.pdf |date=2014-03-27 }}, United States Environmental Protection Agency, August 2000. }} External links{{Medical resources| DiseasesDB = | ICD10 = {{ICD10|T|51|8|t|51|8}} | ICD9 = | ICDO = | OMIM = | MedlinePlus = | eMedicineSubj = emerg | eMedicineTopic = 177 | MeshID = }}
4 : Toxic effects of substances chiefly nonmedicinal as to source|RTT|RTTEM|Toxicology |
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