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Ethylene Glycol

Ethylene Glycol
30.May.2017-Expires: 7 days - Do not archive



Ethylene Glycol




Predominantly used as a deicer or antifreeze in cooling systems. Ethylene glycol is also used in hydraulic brake fluids, as a solvent, and as an industrial humectant. Large amounts are used as a chemical intermediate. It may also be used as a glycerin substitute in commercial products including paints, detergents and cosmetics.


Intervention Level


Appropriate medical management and observation in an emergency department is recommended for:
- Any ingestion more than a witnessed lick or exploratory taste (e.g. a small sip)
- Ingestions where the dose is unknown
- Symptomatic patients
- Eye exposures if more than mild, resolving symptoms
Any patient showing signs or symptoms following skin or inhalational exposure should be assessed at a medical facility.


Appropriate medical management and observation in an emergency department is recommended for:
- Ingestions of more than 10 mL of ethylene glycol
- Ingestions where the dose is unknown
- Exposures with intent to self-harm
- Symptomatic patients
- Eye exposures if symptoms are more than mild and resolving
Any patient showing signs or symptoms following skin or inhalational exposure should be assessed at a medical facility.

Observation Period

Observation at Home

If the patient does not require medical observation they can be monitored at home for 8 hours in the care of a reliable observer.
The patient should be medically assessed if any symptoms develop, including:
Slurred speech
Stumbling or difficulty in moving

Medical Observation

Patients accidentally ingesting ethylene glycol should be monitored for 4 hours and may then be discharged into the care of a reliable observer provided:[1]
They are asymptomatic
Venous bicarbonate level is greater or equal to 20 mmol/L (mEq/L)
Serum (or breath) ethanol level is zero in adults


A serum ethylene glycol is the preferred investigation, but is commonly not readily available at most institutions. An ethylene glycol ingestion may be inferred from an increased osmolal gap (in the early stages of intoxication) indicating a solute (glycol) load. However, this test cannot rule out ethylene glycol exposure in the presence of a normal osmolar gap.
Once the glycol is metabolized this level will drop and may be replaced by an increased anion gap, indicating an increased organic acid (glycol metabolite) load, with an accompanying metabolic acidosis. Investigation should therefore include:
Serum ethylene glycol level (where available in a practical time frame ie: 1 to 2 hours)
Serum ethanol level (required for osmolal gap calculation)
Osmolal gap (elevated in early stages of poisoning)
Serum electrolytes including:
Chloride (required for anion gap calculation)
Anion gap (elevated in later stages of poisoning)
Arterial pH
Serum bicarbonate
Urinalysis including:
Examination under UV light (Wood’s lamp) for fluorescence
(Fluorescein contained in many antifreeze solutions and eliminated in the urine will fluoresce when expose to UV light). A negative result does not rule out ethylene glycol exposure (fluoroscein is rapidly eliminated by the kidneys and may have already been excreted prior to presentation. Also, the ingested ethylene glycol may not contain fluoroscein). Care must be exercised when performing this test as plastic containers may exhibit some degree of fluorescence under a UV light. A glass container is preferable and previous experience with visualizing fluoroscein containing urine is useful.
Microscopic examination for crystalluria
(In the later stages of intoxication calcium oxalate crystals may form in the urine)
Presence in the urine of either fluorescein or calcium oxalate crystals indicates ethylene glycol exposure, but their absence does not exclude this poisoning.
If a serum ethylene glycol level measurement is not available a presumptive diagnosis of poisoning may be based on:
A history or suspicion of ethylene glycol ingestion plus any 2 of the following;[2]
Arterial pH < 7.3
Serum bicarbonate < 20 mmol/L (20 mEq/L)
Osmolal gap > 10 mOsm/L
Presence of urinary oxalate crystals
A history or suspicion of ethylene glycol ingestion within the last 1 hour and osmolal gap > 10 mOsm/L
NOTE: Patients, particularly children, presenting within an hour of suspected ethylene glycol ingestion may not have any abnormal surrogate markers of ingestion. In these instances, close observation and serial monitoring of acid-base and renal function status should be performed. Any development of early metabolic acidosis would be highly suggestive of recent ethylene glycol exposure.

Admission Criteria

Hospital admission is recommended:
- For any patient with abnormal biochemistry
- In all symptomatic cases
Ensure the receiving hospital is able to provide:
The specific antidotes (Ethanol or Fomepizole)
Advanced care/ICU facilities, and



Initial management includes airway protection and administration of IV fluids. Gastric decontamination may be performed within 1 to 2 hours of ingestion via nasogastric aspiration provided the airways are protected. Late presenters may exhibit severe acidosis with compensatory tachypnea, treat with: sodium bicarbonate, intubation with hyperventilation (hyperventilate as acidosis will otherwise worsen and may prove fatal), and hemodialysis. Seizures require a benzodiazepine - closely monitor breathing. Administer glucose in those with CNS depression and suspected hypoglycemia (unless rapid glucose screen indicates otherwise); concurrently administer thiamine and multivitamins if alcoholism is suspected.
Effective antidotes exist in the form of either ethanol or fomepizole. Any patient with an elevated osmolal gap and an anion gap acidosis requires aggressive treatment including the administration of an antidote. It is recommended that patients receiving ethanol therapy be monitored in an intensive care setting. Other indications for intensive care include: coma, seizures, renal failure, hypotension, or ethylene glycol level > 8.1 mmol/L (50 mg/dL). Those with significant acidosis or a high serum ethylene glycol level should be hemodialyzed to reverse acidosis and/or reduce glycol and toxic metabolite levels.
Supportive care includes management of acidosis with generous sodium bicarbonate; administration to return base excess to normal within 12 to 24 hours is recommended. Large quantities may be required, and iatrogenic hypernatremia may occur. Hemodialysis will be required in severe cases of acidosis. Calcium administration is only indicated if cardiac dysrhythmia occurs (particularly QT prolongation), or seizures prove unresponsive to management. Correct hypoglycemia, hyperkalemia and hypomagnesemia. Calcium oxalate crystals may form in any organ with resultant multiorgan dysfunction/failure. The kidneys are often afflicted, and close monitoring and support of renal function is required due to the risk of acute renal failure. Should this occur hemodialysis is required until recovery. There is also risk of ARDS, and fluid balance will require careful (possibly invasive) monitoring. Stupor or coma indicates metabolic encephalopathy or cerebral edema.[3] Cranial nerve palsies may occur some 4 to 18 days following ingestion and usually spontaneously resolve over weeks to months without specific therapy.[4][5][6] Co-factor replenishment with thiamine and pyridoxine is not necessary unless the patient is considered vitamin deficient (e.g. history of alcoholism).
For eye exposures, if more than mild, resolving symptoms are present following irrigation, a full ophthalmologic examination should be undertaken, including slit lamp examination and fluorescein staining. If there is evidence of injury an ophthalmologist should be consulted. Treatment should follow standard protocols for the management of eye irritation.
Emergency Stabilization
Enhanced Elimination
Supportive Care
Fluid and electrolytes


Ensure Adequate Cardiopulmonary Function

Emergency stabilization includes appropriate airway management, ensuring intravenous access, cardiac monitoring, and obtaining initial laboratory values.


Ensure the airway is protected (intubation may be required), and administer oxygen. Establish secure intra-venous access.


Hypotension may be significant due to GIT fluid loss, and in such cases fluid replacement should be aggressive where possible, having regard to renal function.
Immediately establish secure intravenous access.
Where the systolic blood pressure is below normal blood pressure ranges for the age group:[7]
Age (years)
Normal Systolic Blood Pressure (mm Hg)
< 1
70 to 90
1 to 2
80 to 95
2 to 5
80 to 100
5 to 12
90 to 110
> 12
100 to 120
Administer normal (0.9%) saline
10 mL/kg IV over 5 to 10 minutes
If the systolic blood pressure does not return to the normal range, give a further 10 mL/kg body weight normal saline over 5 to 10 minutes. If intravenous access cannot be obtained consider intra-osseus access.
Administer a bolus of normal saline if systolic blood pressure is less than 100 mmHg.
Normal (0.9%) saline dose:
10 mL/kg IV over 5 to 10 minutes
If the systolic blood pressure does not return to the normal range, give a further 10 mL/kg body weight normal saline over 5 to 10 minutes.


Most toxic seizures are short-lived and often do not require intervention.[8]
Administer a benzodiazepine as first-line treatment to patients with seizure activity.[8]
Blood glucose concentration should be promptly determined. If the result indicates hypoglycemia, or is unobtainable, 50% dextrose should be administered IV (preceded by thiamine in adults).
Seizures due to ethylene glycol intoxication may prove unresponsive to standard management unless hypocalcemia is corrected.


IV dextrose is indicated (even if blood glucose cannot be quickly measured) in patients with altered mental status, unusual behavior, coma or seizures. Hypoglycemic patients may present with focal neurological deficits.[9] However, these may also be due to cerebral ischemia. As administration of dextrose may exacerbate ischemic injury,[10] it is important to verify hypoglycemia with blood glucose measurement prior to use - unless this would lead to unacceptable delay in administration.
Must be administered to adult patients considered alcoholic or malnourished.

Thiamine dose
100 mg IV

Emergency Monitoring

Electrolytes including:
Chloride (for calculation of anion gap)
Anion gap (elevated later in poisoning)
Serum ethanol concentration (used in calculation of osmolal gap)
Osmolal gap (elevated early in poisoning)
Arterial blood gases including:
Arterial pH
Serum ethylene glycol concentration



Nasogastric Aspiration

Nasogastric aspiration is recommended if the quantity of liquid ingested is both systemically toxic and in sufficient volume to aspirate. As this procedure may increase the risk of vomiting and pulmonary aspiration, the airway must be protected in all patients. Accurate placement of the nasogastric tube must also be ensured in all patients.
Nasogastric aspiration is recommended if the patient has presented early (within 1 to 2 hours) following ingestion of ethylene glycol.

Single Dose Activated Charcoal

Activated charcoal is not considered an effective decontaminant for this ingestion as ethylene glycol is rapidly absorbed from the gastrointestinal tract and has poor binding affinity for activated charcoal. Unless there is concern for coingestants, there is little benefit from activated charcoal administration in ethylene glycol ingestions.


Remove contact lenses. Irrigate immediately with water or saline for at least 15 minutes. If the eye is contaminated with solid particles, the eyelid should be completely everted and any solid material removed as quickly as possible whilst continuing to irrigate. A topical anesthetic may be necessary in some patients, especially children, to enable the patient to open the lids sufficiently for effective irrigation.
If, following irrigation, any of the following are apparent:
Ocular pain (other than mild and resolving)
Erythema (other than mild and resolving)
Decreased visual acuity
Ocular discharge/crusting
The patient should receive a full ophthalmologic examination, including slit lamp examination and fluorescein staining. If there is evidence of injury an ophthalmologist should be consulted.


Remove the patient from the exposure. If respiratory symptoms such as shortness of breath are present, administer oxygen and provide additional support if necessary.


Remove any contaminated clothing or jewelery. Wash the affected area thoroughly with soap and water until all of the contaminant is removed.


Appropriate use of antidotes in glycol poisoning is essential. Ethanol has long been regarded as an effective intervention, though objective data is lacking,[11] and is cheap and available.[12] Fomepizole has proven efficacy,[13] but suffers the disadvantage of expense. Both act by inhibiting alcohol dehydrogenase, thus reducing the metabolic conversion of glycol to toxic metabolites (acids).
Thiamine and pyridoxine may be indicated as therapeutic adjuncts. Theoretically, they act as cofactors in the formation of non-toxic metabolites of ethylene glycol. No data exists to support this assumption, but they may benefit those with a history of ethanol abuse or inadequate nutrition (e.g. those vitamin deficient).



Ethanol is indicated if:[14]
- Reliable history of ingestion of a toxic quantity of ethylene glycol; or
- Plasma ethylene glycol concentration is greater than 3.2 mmol/L (20 mg/dL) or;
- Recent ingestion of greater than 0.2 mL/kg ethylene glycol and presence of osmolal gap of greater than 10 mosm/L or;
- History or clinical suspicion of ethylene glycol poisoning and at least two of the following:
Arterial pH < 7.3
Serum bicarbonate < 20 mmol/L (20 mEq/L)
Osmolal gap > 10 mosm/L
Presence of urinary oxalate crystals

Dose and Administration

Loading Dose
For acceptable efficacy, the blood ethanol concentration should be maintained between 22 and 33 mmol/L (100 to 150 mg/dL). To achieve this both a loading dose and maintenance infusion are required. Either 100% ethanol diluted for intravenous use may be infused, or liquor (e.g. vodka, gin) may be administered orally.
Prior to use of ethanol therapy a blood ethanol determination should be made to identify if the patient has an existing ethanol concentration requiring a modification of the loading dose. Monitoring in an intensive care setting is required during administration.
As ethanol may depress respiration, mechanical hyperventilation is recommended in those with reduced level of consciousness.[15]
Oral ethanol loading dose
To calculate the loading dose of oral ethanol the following equation may be applied:
Dose =  (BEC x wt x Vd) / (C x SpG)
desired blood ethanol concentration (mg/dL)
amount of beverage (mL)
patient’s weight (kg)
volume of distribution (0.6 L/kg)
concentration of alcohol (% v/v)
specific gravity (0.8) [converts % v/v to % w/v]
Note: The term "proof" describing alcohol content of beverages should be halved to obtain the proper % v/v value (e.g. 60 proof = 30% v/v ethanol).
To obtain a therapeutic blood ethanol concentration of 125 mg/dL in a 70 kg patient using whisky (80 proof and therefore 40% v/v ethanol), the loading dose will be:
Loading Dose =  (125 x 70 x 0.6)  /  (40 x 0.8)  = 164 mL whiskey
This should be administered as a 20% or less solution (e.g. diluted with water or fruit juice).
Intravenous ethanol loading dose
To prevent vascular damage when administering intra-venous ethanol the 100% alcohol must first be diluted to either a 5 or 10% solution in 5% dextrose and water (some solutions are ready made).
To reach the desired blood ethanol concentration of 22 to 33 mmol/L (100 to 150 mg/dL) administer:
- 12 to 18 mL/kg of 5% w/v ethanol, over 30 minutes, or;
- 6 to 9 mL/kg of 10% w/v ethanol, over 30 minutes.
(Alternatively, the above equation may be used, using 5 or 10% for concentration (C). Multiply by 0.8 (SpG) ONLY if formulation is % v/v not % w/v).
When diluting 100% alcohol, it’s specific gravity of 0.8 must be taken into account. Therefore, to produce a:
10% w/v solution
Dilute 100% ethanol 8 fold (e.g. one 20 mL vial of 100% alcohol to 140 mL 5% dextrose [making total volume of 160 mL]). This solution may be preferable to reduce fluid load in pediatric patients, or those suffering cerebral edema.
5% w/v solution
Dilute 100% ethanol 16 fold (e.g. one 20 mL vial of 100% alcohol to 300 mL 5% dextrose [making total volume of 320 mL]).
Maintenance Dose
The rate of maintenance infusion will vary due to individual differences in ethanol metabolism.
Different rates of metabolism:[16][17]
Non-alcoholic adult
3.3 to 4.3 mmol/L/h (15 to 20 mg/dL/h)
Alcoholic adult
6.5 to 8.7 mmol/L/h (30 to 40 mg/dL/h)
6.5 mmol/L/h (30 mg/dL/h)
The Loading Dose Equation can be used to calculate both oral and IV maintenance doses. Replace BEC with metabolism rate from the equation. Remember NOT to multiply by 0.8 (SpG) if formulation is already % w/v.
Oral ethanol maintenance dose
The Loading Dose Equation can be used to calculate both oral and IV maintenance doses. Replace BEC with metabolism rate from the equation. Remember NOT to multiply by 0.8 (SpG) if formulation is already % w/v.
E.g. In a non-alcoholic 70 kg adult patient (e.g. elimination rate estimated as 20 mg/dL/h) the maintenance dose using 40% v/v ethanol and the above equation will be:
Maintenance Dose =  (20 x 70 x 0.6) / (40 x 0.8)  =  26 mL/h whiskey
This should be administered as a 20% or less solution (e.g. diluted with water or fruit juice).
Intravenous ethanol maintenance dose
5% w/v solution:
3.6 mL/kg/h
1.8 to 2.4 mL/kg/h
3.6 to 4.8 mL/kg/h
10 % w/v solution:
1.8 mL/kg/h
0.9 to 1.2 mL/kg/h
1.8 to 2.4 mL/kg/h

Antidote Endpoint

Ethanol administration may be discontinued if ethylene glycol levels can no longer be detected or are less than 2.4 mmol/L (15 mg/dL) with a normalized arterial pH - this is likely to take 2 to 3 days given ethylene glycol's half-life of elimination of 17 hours. [14]


Hypoglycemia may occur, especially in children.[18] Once an infusion has been commenced blood glucose concentrations must be determined on a frequent basis (every 20 to 60 minutes). It may be necessary to add dextrose to intravenous solutions, or give glucose if ethanol is being administered orally.[19]


While availability is limited by purchase price, fomepizole appears preferable to ethanol. It is more particularly indicated in those with altered mental status, patients suffering hepatic disease, or those critically ill but lacking confirmation of poisoning. Its administration to pediatric patients avoids the disadvantages of ethanol (e.g. inebriation, hypoglycemia).


Fomepizole is indicated if:
- Plasma ethylene glycol concentration greater than 3.2 mmol/L (20 mg/dL) or;
- Recent ingestion of greater than 0.2 mL/kg ethylene glycol and presence of osmolal gap greater than 10 mosm/L or;
- History or clinical suspicion of ethylene glycol poisoning and at least two of the following
Arterial pH < 7.3
Serum bicarbonate < 20 mmol/L (20 mEq/L)
Osmolal gap > 10 mosm/L
Presence of urinary oxalate crystals
Particular indications:
- Altered mental status
- Hepatic disease
- Critically ill patients lacking confirmation of ethylene glycol toxicity
- Pediatric patients (avoids the inebriation and hypoglycemia that may occur with ethanol administration)

Dose and Administration

Loading dose[20]
- 15 mg/kg diluted in 100 mL of normal saline or 5% dextrose in water and administered by IV infusion over 30 minutes
Maintenance doses[20]
- 10 mg/kg should be administered every 12 hours for 4 doses, then;
- 15 mg/kg every 12 hours thereafter if indicated
Maintenance fomepizole should be administered in the same fashion as the loading dose. Dosing requirements will change if hemodialysis is required – as outlined in the enhanced elimination section.

Antidote Endpoint

Fomepizole may be discontinued when ethylene glycol plasma concentrations are either undetectable, or below 3.2 mmol/L (20 mg/dL) in an asymptomatic patient with a normal pH.[20]

Adverse Effects

Abdominal pain, skin rash, nausea, headache and pain at site of injection have been reported following fomepizole use.[20]


Pyridoxine acts as a co-factor in the conversion of glyoxylic acid to the non-toxic metabolite glycine. While the clinical benefit of pyridoxine administration for the treatment of ethylene glycol poisoning has not been demonstrated in healthy individuals, it is recommended for use in malnourished or alcoholic patients who may have vitamin deficiencies.[14]

Dose and Administration

The formulation should be diluted at least 1 to 5.
- 50 to 100 mg pyridoxine given as an IV infusion over 15 to 30 minutes every six hours
- Continue for two days[21]


Profound peripheral neuropathy may occur after very large single doses[22] or a series of doses (for example a total of > 2 g/kg pyridoxine over a three day period).[23] The sensory (if not motor) disturbances are potentially irreversible.[24]


Thiamine acts as a co-factor in the conversion of glyoxylic acid to the non-toxic metabolite alpha-hydroxy-beta-ketoadipate. While the clinical benefit of thiamine administration for the treatment of ethylene glycol poisoning has not been demonstrated in healthy individuals, it is recommended for use in malnourished or alcoholic patients who may have vitamin deficiencies.[14]

Dose and Administration

- Administer 100 mg IV or IM thiamine every six hours
- Continue for two days[21]


Symptoms following ethylene glycol ingestion can be divided into three acute stages and one sub-chronic phase.
Initial symptoms of ethylene glycol ingestion are due to the direct toxicity of ethylene glycol. CNS effects predominate and include inebriation (without the alcohol odor on the breath), gastrointestinal upset, and drowsiness. In severe cases, coma, and seizures may develop.[25]
In subsequent phases of intoxication, the various metabolites of ethylene glycol are responsible for the presenting symptoms, which in the second phase of poisoning include, metabolic acidosis and cardiopulmonary symptoms 12 to 24 hours post ingestion.[26] In significant poisonings, severe metabolic acidosis with compensatory hyperventilation can develop with multiple organ failure. Tachycardia, mild hypertension, pulmonary edema, and congestive heart failure are all believed to be due to the deposition of calcium oxalate crystals within the vascular tree, myocardium and the lung parenchyma.[27] Most deaths occur in this second phase.[21]
The renal phase of intoxication, beginning 24 to 48 hours after ingestion, is marked by the predominance of oliguria, acute tubular necrosis, renal failure, and occasionally bone marrow suppression. Hematuria and proteinuria are common. In severe poisonings, renal failure may appear early and progress to anuria.[27] Calcium oxalate crystals may be detected in the urine of some patients. Renal symptoms may last up to 45 days or more.[21] In addition, cranial nerve palsies that develop in some patients may persist for weeks to months.[6] Convulsions and coma are considered ominous signs.[28]
Following inhalation, irritation of the nose and throat can occur. Its low evaporation rate (and vapor pressure) at ambient temperatures make it unlikely to present an acute inhalation hazard in most situations; systemic effects would not typically be expected following inhalation.
Eye exposure to vapors or direct contact with the liquid may lead to eye irritation; significant eye injury would not be expected.
Skin contact is unlikely to cause harm to the skin on brief or occasional contact but prolonged or repeated exposure may lead to irritation. It is possible absorption through the skin could lead to systemic effects following large prolonged exposures.

Routes of Exposure

Symptoms predominantly occur following ingestion of ethylene glycol. However, toxicity is also possible via dermal, intravenous and intramuscular routes.

Onset/Duration of Symptoms

There are three acute stages of ethylene glycol poisoning and one sub-acute stage that may occur[29][30][31]
Stage I: Neurological Phase
0.5 to 12 hours post-ingestion
Metabolic acidosis
CNS depression
Stage II: Cardiopulmonary Phase
12 to 24 hours post-ingestion
Severe metabolic acidosis
Adult respiratory distress syndrome (ARDS)
Congestive heart failure
Stage III: Renal Phase
24 to 72 hours post-ingestion
Acute tubular necrosis
Renal failure
Subacute Stage
Onset several (5 to 20) days after ingestion
Cranial nerve neuropathies
Most deaths are reported in Stage II. The severity of these stages and their progression from one to the other often depends on the amount ingested.

Severity of Poisoning

Mild Ethylene Glycol ToxicityModerate Ethylene Glycol ToxicitySevere Ethylene Glycol Toxicity
Mild metabolic acidosis
Pulmonary edema
Congestive cardiac failure
Severe metabolic acidosis
Multiple organ failure


General Effects

Chronic exposures to ethylene glycol vapor may result in CNS abnormalities and lymphocytosis.[32]


[1] Jolliff HA, Dart RC, Bogdan GM, Daly FF. Can the diagnosis of ethylene glycol (EG) toxicity be made without serum EG and osmolality values? [abstract]. J Toxicol Clin Toxicol 2000; 38 (5): 539-40.
[2] Brent J. Current management of ethylene glycol poisoning. Drugs 2001; 61 (7): 979-88.
[3] Maier W. Cerebral computed tomography of ethylene glycol intoxication. Neuroradiology 1983; 24 (3): 175-7.
[4] Spillane L, Roberts JR, Meyer AE. Multiple cranial nerve deficits after ethylene glycol poisoning. Ann Emerg Med 1991 Feb; 20 (2): 208-10.
[5] Lewis LD, Smith BW, Mamourian AC. Delayed sequelae after acute overdoses or poisonings: cranial neuropathy related to ethylene glycol ingestion. Clin Pharmacol Ther 1997 Jun; 61 (6): 692-9.
[6] Berger JR, Ayyar DR. Neurological complications of ethylene glycol intoxication. Report of a case. Arch Neurol 1981 Nov; 38 (11): 724-6.
[7] Mackway-Jones K, Molyneux E, Phillips B, Wieteska S, editors. Advanced paediatric life support: the practical approach. 3rd ed. London: BMJ Books; 2001.
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[14] Barceloux DG, Krenzelok EP, Olson K, Watson W. American Academy of Clinical Toxicology Practice Guidelines on the Treatment of Ethylene Glycol Poisoning. Ad Hoc Committee. J Toxicol Clin Toxicol 1999; 37 (5): 537-60.
[15] Paasma R, Hovda KE, Hassanian-Moghaddam H, Brahmi N, Afshari R, Sandvik L, Jacobsen D. Risk factors related to poor outcome after methanol poisoning and the relation between outcome and antidotes--a multicenter study. Clin Toxicol (Phila) 2012 Nov; 50 (9): 823-31.
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[32] Troisi FM. Chronic intoxication by ethylene glycol vapour. Br J Ind Med 1950; 7: 65-6.

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