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ALCOHOLS 
Dr. D. K. Brahma 
Department of Pharmacology 
NEIGRIHMS, SHILLONG
Why and What to Learn on 
Alcohol ? 
 The pharmacodynamics of alcohol actions in the body and 
brain, that is the pharmacological effects that produce the 
biological actions of the drug. (e.g. intoxication, organ 
damage etc.) 
 The pharmacokinetics of alcohol, that is the timing of alcohol 
distribution and metabolism within the body and brain, as well 
as the pathways involved in metabolism of ethanol and its 
major metabolites.
What are they ? 
 Ethyl Alcohol 
(Ethanol) 
Methyl Alcohol 
(Methanol)
How Manufactured ? 
• Fermentation – Sugar to Alcohol and Carbon 
dioxide 
C6H12O6→ 2(CH3-CH2-OH) + 2CO2 
(Yeasts +sugar + water = CO2 + ethanol) 
• Yeasts are living micro-organisms which die in 
concentrations of alcohol greater than 10 to 15% 
Starch Convertase 
Maltose 
• Commercially - obtained from Mollases
Alcoholic Beverages 
 Malted Liquors: Fermentation of germinating cereals (malts) – 
mostly Barley – Beers (3-6%) 
 Wines: fermentation of Natural Sugars – grapes, apples and 
other fruits 
 No distillation, <15% 
 Fortified (port) – up to 22% 
 Champagne – 12-16% (effervescent wine) 
 Spirits – Rum, Whisky, Brandy and Gin 
 40 - 55% v/v 
 Standard 42.8% v/v or 37% w/w 
 Sources: 
 Whiskey - distilled grain 
 Rum - distilled molasses 
 Gin – any sugar source 
 Brandy – Distilled wine (Grapes) 
 Vodka – fermentation of any of grain, rye, wheat, potatoes, grapes, sugar beet or mollases
Alcohol – Percentage Calculations 
 Alcohol content of beverages: 
 specific gravity of alcohol is 79 
 Therefore, 1 litre alcohol weighs 790g 
 Percent may be by weight or by volume 
 By volume: 
 1 litre alcohol add 1 litre water = 50% (vol) 
 By weight: 
 1 litre alcohol (790g), add 790g water = 50% 
(weight) 
40% alcohol by weight = 50% by volume
1litre water 
+ = 
1litre alcohol 
2 litres 50% (volume) 
1 kilo water 1 kilo alcohol 
2 kilos 50% (weight) 
+ = 
40% alcohol by weight = 50% by volume
Pharmacological actions of 
alcohol - Local 
1. Rubefacient and counterirritant to skin 
2. Irritant – soft skin and mucus 
membrane 
3. Pain, inflammation and necrosis – 
injection 
4. Astringent: Antiseptic (20 – 90%) 
 100% is dehydrating 
1. No action on spores
Effects of alcohol consumption - 
Acute 
 CNS: 
 depressant – dose dependent manner 
Plasma concentration Expected effects 
30 – 100 mg/dl Anxiolytic, euphoria and excitation 
Hesitation, restraint, caution are lost 
Impaired coordination – mood and feelings are 
altered 
100 -150 mg/dl Mental clouding, ataxia, disorganization of thought 
and impairment of memory and drowsiness 
150 – 200 mg/dl Sloppy, ataxia and drunkenness 
- Slurring of speech, loss of judgment and inhibition 
200 – 300 mg/dl Stupor and unconsciousness
Effects of alcohol consumption 
(acute) - contd. 
 Impaired performance, slowing of reflexes and 
fine discrimination impaired 
 Induces sleep – but not ideal hypnotic 
 Analgesic – but no ideal analgesic 
 Anticonvulsant action – but not ideal 
anticonvulsant 
 Mechanism: 
 GABAA receptor mediated synaptic inhibition by 
chloride channel opening 
 Inhibition of NMDA excitatory amino acid receptor 
 Stimulates 5-HT3 receptors
Effects of alcohol consumption 
(acute) - contd. 
 CVS: 
 Small doses – cutaneous vasodilatation, flushing 
 Medium dose – tachycardia and mild rise in BP 
 Large dose - Vasodilatation due to direct vascular 
smooth muscle dilatation and vasomotor centre 
depression (clinical implication) 
 Respiration: 
 Stimulation of Respiration – by irritation of 
pharyngeal and buccal mucosa 
 Central action – depression 
 Blood: 
 Moderate drinking increases HDL-cholesterol 
level 
 Decrease in LDL oxidation
Effects of alcohol consumption 
(acute) - contd. 
 GIT: 
 Dilute alcohol at low 
doses - stimulate GI 
secretion – flavour, 
aroma or direct 
action on gastrin 
secretion 
 Higher doses inhibit 
GI secretion 
 Acute consumption 
– pylorospasm, 
gastritis, vomiting, 
reflux etc 
 Mallory-Weiss lesion
Effects of alcohol consumption – 
(acute) - contd. 
 Kidney: Diuresis – increased water 
ingestion and inhibition of ADH 
 Uterus: Relaxation of uterine muscles 
 Endocrine: 
 Low dose – Adrenaline release and 
hyperglycemia 
High dose – Hypoglycemia 
 Sex - Aphrodisiac
Absorption 
 Rapidly absorbed from small intestine, 
and colon but slowly from stomach 
 First pass metabolism in stomach and 
liver 
 Maximal blood concentration within 30 to 
90 minutes 
 Can be absorbed through the lungs 
 Can be absorbed through skin
Distribution 
 Uniformly distributed throughout tissues and body 
fluids 
 Readily crosses placenta, to exposure fetus 
 Crosses BBB readily 
Elimination 
Urinary Excretion 
Exhalation 
Metabolism
Metabolism I 
H 
H 
H C OH 
H 
C 
H 
Ethanol 
H 
H C 
H 
= 
C O 
H 
Acetaldehyde 
ADH 
(ADH – Alcohol Dehydrogenase)
Metabolism II 
H 
H C 
H 
= 
C O 
H 
ALDH 
H 
H C 
H 
= 
C O 
OH 
Acetaldehyde 
Acetate 
(ALDH – Acetaldehyde Dehydrogenase)
Metabolism III 
 80-90% Metabolized 
 Also metabolized in small amounts by hepatic 
microsomal enzyme 
 Rate is constant (not increased by 
concentrations in the blood) – zero order (8-12 
ml/H of absolute alcohol) 
 About 30 ml (1 oz) in 3 hours 
 Concentration in exhaled air is 0.05% of blood 
concentration – used in medico legal purposes
Adverse Effects of Alcohol 
 Acute Effects 
 Nausea, Vomiting, hangover and traffic accidents 
 CNS Depressant 
 Depression of inhibitory control 
 Vasodilatation, warm, flushed, reddish skin 
 Emotional outbursts 
 Decreased memory & concentration 
 Poor judgment 
 Decreased reflexes 
 Decreased sexual response
Adverse Effects of Alcohol – 
contd. 
 Acute Alcohol Intoxication: 
 Estimated ED50: 150 mg/100 ml and LD50 = 500 
mg/100ml 
 Therapeutic index about 3.5 
 Hypotension, hypoglycemia, respiratory depression 
coma and death 
 Death due to respiratory depression or inhaled vomit 
 Treatment: 
 Gastric lavage 
 Endotracheal intubations 
 Fluid and electrolyte balance 
 Glucose infusion 
 Thiamine injection 100 mg in 500 ml of glucose IV 
 Haemodialysis
Consequences of acute 
Alcohol intoxication - images 
Vomiting Driving accidents Loss of inhibitions 
Hangover
Toxic Effects - Chronic 
Alcoholism 
 GIT: 
 Gastritis and damage to the mucosa – 
anaemia 
 Intestinal damage: Lack of absorption - 
Deficiency of water soluble vitamins and 
amino acids (protein deficiency) 
 Less or no food intake (enough calorie) - 
Vitamin and Protein deficiency 
(Q. Is Alcohol a total food ? Answer: No - 
Lacking in total food value)
Chronic Alcoholism – contd. 
 Liver cirrhosis – scarring of 
liver 
 Usually fatal if drinking 
is not stopped 
 Fatty infiltration 
(excess in NADH) 
 Oxidative stress and 
cellular necrosis 
 Damage to 
hepatocytes and 
inflammation – 
aldehyde 
 Glutathione 
depletion 
 Microsomal enzyme 
induction
Chronic Alcoholism – contd. 
 Neurological: Polyneuritis, pellagra, 
tremors, seizures, loss of brain mass, 
Korsakoff`s psychosis and Warnicke`s 
encephalopathy 
 CVS: Hypertension, cardiomyopathy, 
CHF arrhythmias and stroke 
 Hormonal: Impotence, gynaecomastia 
and infertility 
 Acute pancreatitis
Chronic Alcoholism – contd. 
 Reproduction 
 Alcohol is a teratogen, it causes birth 
defects. 
 Fetal Alcohol Syndrome (FAS) or Fetal 
Alcohol Effects (FAE), or Alcohol-Related 
Birth Defects (ARBD) 
 Symptoms include retardation, poor 
coordination, loss of muscle tone, low birth 
weight, slow growth, malformation of internal 
organs and peculiar facial characteristics
Fetal Alcohol Syndrome (FAS) 
Characteristics 
Growth retardation 
Facial malformations 
Small head 
Greatly reduce 
intelligence
Chronic Alcoholism - features 
• Craving: A strong need, or compulsion, to drink 
• Loss of control: The inability to limit one’s drinking on any given 
occasion 
• Tolerance: The need to drink greater amounts of alcohol in order to 
“get high” – pharmacokinetic or cellular tolerance 
• Physical dependence: Withdrawal symptoms, such as nausea, 
sweating, shakiness, sleep impairment, hallucinations, delirium 
tremens and anxiety, occur when alcohol use is stopped after a 
period of heavy drinking 
• Withdrawal syndromes: long acting BZDs like chlordizepoxide 
and diazepam 
• Naltrexone (50 mg)
Ethanol – Usefulness: 
1. Local: 
 antiseptic, rubefacient and counterirritant in sparins 
and to prevent bedsores 
 antiperspirant and aftershave 
 Alcohol sponges – to reduce body temperature 
1. Appetite stimulant and carminative: 30 – 60 ml of 7- 
10% 
2. Neuralgias: severe cancer pain – injection round the 
nerve 
3. Protection from cold 
4. Alcohol may have a protective effect from heart attack 
and stroke - frugivores 
5. Methanol Poisoning
Disulfiram (Antabuse) 
 Internationally marketed as antabuse 
 ALDH enzyme inhibitor 
 Alcohol + disulfiram rise in concentration of aldehyde in 
blood and tissue distressing aldehyde syndrome 
 Symptoms: flushing, burning sensation, throbbing headache, 
perspiration, dizziness, vomiting, visual disturbance, mental 
confusion, fainting and circulatory collapse 
 Uses: aversion technique in chronic alcoholics: only to 
motivated persons 
 Technique: abstain alcohol overnight and start with 1 gm on 
day 1 followed by 0.75 gm next day and 0.50 gm next day and 
so on. Effects start within few hrs of 1st dose and lasts for 2 
weeks 
 Mechanism: irreversible inhibition of ALDH and synthesis of 
new enzyme takes time and thus person resolves not to drink 
for distressing symptoms 
 Available as 250 mg tablets
Ethanol as Antidote 
 Methanol, Ethylene glycol, Diethylene glycol 
 Methanol poisoning – toxicological importance – 
unscrupulous mixing with alcoholic beverages 
 Formic acid is toxic: above 50 mg/dl, lethal dose 75 – 100 
ml, even 15 ml can cause blindness 
ADH ALDH 
Methanol formaldehyde Formic acid 
 Methanol poisoning: vomiting, epigastric pain dyspnoea, 
bradycardia, acidosis – permanent retinal damage and 
Death 
 Mechanism: Ethanol saturates alcohol dehydrogenase 
enzyme - no metabolism of Methanol to form Formic acid
Methanol Poisoning 
treatment 
 Patient in dark room, Ventilation and BP supportive measures 
 Gastric lavage with sodibicarb if brought immediately 
 IV sodibicarb to combat acidosis – large quantity may be 
required 
 Ethanol 10% in water – nasogastric tube with loading dose of 
0.7 ml/kg followed by 15 ml/kg/hr by infusion – continue 
treatment for several days (methanol is oxidized slowly) 
 Potassium chloride if hypokalemia occurs 
 Folinic acid or Calcium leucovorin ijection 50 mg IV every 6 Hrly 
– to enhance oxidation of formic acid 
 4-methylpyrazole – specific inhibitor of ALD – 15 mg/kg IV and 
10 mg/kg 12 Hrly. till methanol level is <20 mg/dl 
 Haemodialysis
Summary 
 Alcohol is a neuronal depressant 
 Long term exposure to alcohol brings about 
adaptive changes in the neuronal system 
 Chronic alcoholism causes toxic effects on all 
the organs especially liver 
 Withdrawal syndrome in alcoholics are treated 
by BZDs and Naltrexone 
 Antbuse/disulfiram is the drug is use as 
aversion technique in chronic alcoholics 
 Ethanol is used as antidote in Methanol 
Poisoning
Thank You

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Pharmacology of Alcohol

  • 1. ALCOHOLS Dr. D. K. Brahma Department of Pharmacology NEIGRIHMS, SHILLONG
  • 2. Why and What to Learn on Alcohol ?  The pharmacodynamics of alcohol actions in the body and brain, that is the pharmacological effects that produce the biological actions of the drug. (e.g. intoxication, organ damage etc.)  The pharmacokinetics of alcohol, that is the timing of alcohol distribution and metabolism within the body and brain, as well as the pathways involved in metabolism of ethanol and its major metabolites.
  • 3. What are they ?  Ethyl Alcohol (Ethanol) Methyl Alcohol (Methanol)
  • 4. How Manufactured ? • Fermentation – Sugar to Alcohol and Carbon dioxide C6H12O6→ 2(CH3-CH2-OH) + 2CO2 (Yeasts +sugar + water = CO2 + ethanol) • Yeasts are living micro-organisms which die in concentrations of alcohol greater than 10 to 15% Starch Convertase Maltose • Commercially - obtained from Mollases
  • 5. Alcoholic Beverages  Malted Liquors: Fermentation of germinating cereals (malts) – mostly Barley – Beers (3-6%)  Wines: fermentation of Natural Sugars – grapes, apples and other fruits  No distillation, <15%  Fortified (port) – up to 22%  Champagne – 12-16% (effervescent wine)  Spirits – Rum, Whisky, Brandy and Gin  40 - 55% v/v  Standard 42.8% v/v or 37% w/w  Sources:  Whiskey - distilled grain  Rum - distilled molasses  Gin – any sugar source  Brandy – Distilled wine (Grapes)  Vodka – fermentation of any of grain, rye, wheat, potatoes, grapes, sugar beet or mollases
  • 6. Alcohol – Percentage Calculations  Alcohol content of beverages:  specific gravity of alcohol is 79  Therefore, 1 litre alcohol weighs 790g  Percent may be by weight or by volume  By volume:  1 litre alcohol add 1 litre water = 50% (vol)  By weight:  1 litre alcohol (790g), add 790g water = 50% (weight) 40% alcohol by weight = 50% by volume
  • 7. 1litre water + = 1litre alcohol 2 litres 50% (volume) 1 kilo water 1 kilo alcohol 2 kilos 50% (weight) + = 40% alcohol by weight = 50% by volume
  • 8. Pharmacological actions of alcohol - Local 1. Rubefacient and counterirritant to skin 2. Irritant – soft skin and mucus membrane 3. Pain, inflammation and necrosis – injection 4. Astringent: Antiseptic (20 – 90%)  100% is dehydrating 1. No action on spores
  • 9. Effects of alcohol consumption - Acute  CNS:  depressant – dose dependent manner Plasma concentration Expected effects 30 – 100 mg/dl Anxiolytic, euphoria and excitation Hesitation, restraint, caution are lost Impaired coordination – mood and feelings are altered 100 -150 mg/dl Mental clouding, ataxia, disorganization of thought and impairment of memory and drowsiness 150 – 200 mg/dl Sloppy, ataxia and drunkenness - Slurring of speech, loss of judgment and inhibition 200 – 300 mg/dl Stupor and unconsciousness
  • 10. Effects of alcohol consumption (acute) - contd.  Impaired performance, slowing of reflexes and fine discrimination impaired  Induces sleep – but not ideal hypnotic  Analgesic – but no ideal analgesic  Anticonvulsant action – but not ideal anticonvulsant  Mechanism:  GABAA receptor mediated synaptic inhibition by chloride channel opening  Inhibition of NMDA excitatory amino acid receptor  Stimulates 5-HT3 receptors
  • 11. Effects of alcohol consumption (acute) - contd.  CVS:  Small doses – cutaneous vasodilatation, flushing  Medium dose – tachycardia and mild rise in BP  Large dose - Vasodilatation due to direct vascular smooth muscle dilatation and vasomotor centre depression (clinical implication)  Respiration:  Stimulation of Respiration – by irritation of pharyngeal and buccal mucosa  Central action – depression  Blood:  Moderate drinking increases HDL-cholesterol level  Decrease in LDL oxidation
  • 12. Effects of alcohol consumption (acute) - contd.  GIT:  Dilute alcohol at low doses - stimulate GI secretion – flavour, aroma or direct action on gastrin secretion  Higher doses inhibit GI secretion  Acute consumption – pylorospasm, gastritis, vomiting, reflux etc  Mallory-Weiss lesion
  • 13. Effects of alcohol consumption – (acute) - contd.  Kidney: Diuresis – increased water ingestion and inhibition of ADH  Uterus: Relaxation of uterine muscles  Endocrine:  Low dose – Adrenaline release and hyperglycemia High dose – Hypoglycemia  Sex - Aphrodisiac
  • 14. Absorption  Rapidly absorbed from small intestine, and colon but slowly from stomach  First pass metabolism in stomach and liver  Maximal blood concentration within 30 to 90 minutes  Can be absorbed through the lungs  Can be absorbed through skin
  • 15. Distribution  Uniformly distributed throughout tissues and body fluids  Readily crosses placenta, to exposure fetus  Crosses BBB readily Elimination Urinary Excretion Exhalation Metabolism
  • 16. Metabolism I H H H C OH H C H Ethanol H H C H = C O H Acetaldehyde ADH (ADH – Alcohol Dehydrogenase)
  • 17. Metabolism II H H C H = C O H ALDH H H C H = C O OH Acetaldehyde Acetate (ALDH – Acetaldehyde Dehydrogenase)
  • 18. Metabolism III  80-90% Metabolized  Also metabolized in small amounts by hepatic microsomal enzyme  Rate is constant (not increased by concentrations in the blood) – zero order (8-12 ml/H of absolute alcohol)  About 30 ml (1 oz) in 3 hours  Concentration in exhaled air is 0.05% of blood concentration – used in medico legal purposes
  • 19. Adverse Effects of Alcohol  Acute Effects  Nausea, Vomiting, hangover and traffic accidents  CNS Depressant  Depression of inhibitory control  Vasodilatation, warm, flushed, reddish skin  Emotional outbursts  Decreased memory & concentration  Poor judgment  Decreased reflexes  Decreased sexual response
  • 20. Adverse Effects of Alcohol – contd.  Acute Alcohol Intoxication:  Estimated ED50: 150 mg/100 ml and LD50 = 500 mg/100ml  Therapeutic index about 3.5  Hypotension, hypoglycemia, respiratory depression coma and death  Death due to respiratory depression or inhaled vomit  Treatment:  Gastric lavage  Endotracheal intubations  Fluid and electrolyte balance  Glucose infusion  Thiamine injection 100 mg in 500 ml of glucose IV  Haemodialysis
  • 21. Consequences of acute Alcohol intoxication - images Vomiting Driving accidents Loss of inhibitions Hangover
  • 22. Toxic Effects - Chronic Alcoholism  GIT:  Gastritis and damage to the mucosa – anaemia  Intestinal damage: Lack of absorption - Deficiency of water soluble vitamins and amino acids (protein deficiency)  Less or no food intake (enough calorie) - Vitamin and Protein deficiency (Q. Is Alcohol a total food ? Answer: No - Lacking in total food value)
  • 23. Chronic Alcoholism – contd.  Liver cirrhosis – scarring of liver  Usually fatal if drinking is not stopped  Fatty infiltration (excess in NADH)  Oxidative stress and cellular necrosis  Damage to hepatocytes and inflammation – aldehyde  Glutathione depletion  Microsomal enzyme induction
  • 24. Chronic Alcoholism – contd.  Neurological: Polyneuritis, pellagra, tremors, seizures, loss of brain mass, Korsakoff`s psychosis and Warnicke`s encephalopathy  CVS: Hypertension, cardiomyopathy, CHF arrhythmias and stroke  Hormonal: Impotence, gynaecomastia and infertility  Acute pancreatitis
  • 25. Chronic Alcoholism – contd.  Reproduction  Alcohol is a teratogen, it causes birth defects.  Fetal Alcohol Syndrome (FAS) or Fetal Alcohol Effects (FAE), or Alcohol-Related Birth Defects (ARBD)  Symptoms include retardation, poor coordination, loss of muscle tone, low birth weight, slow growth, malformation of internal organs and peculiar facial characteristics
  • 26. Fetal Alcohol Syndrome (FAS) Characteristics Growth retardation Facial malformations Small head Greatly reduce intelligence
  • 27. Chronic Alcoholism - features • Craving: A strong need, or compulsion, to drink • Loss of control: The inability to limit one’s drinking on any given occasion • Tolerance: The need to drink greater amounts of alcohol in order to “get high” – pharmacokinetic or cellular tolerance • Physical dependence: Withdrawal symptoms, such as nausea, sweating, shakiness, sleep impairment, hallucinations, delirium tremens and anxiety, occur when alcohol use is stopped after a period of heavy drinking • Withdrawal syndromes: long acting BZDs like chlordizepoxide and diazepam • Naltrexone (50 mg)
  • 28. Ethanol – Usefulness: 1. Local:  antiseptic, rubefacient and counterirritant in sparins and to prevent bedsores  antiperspirant and aftershave  Alcohol sponges – to reduce body temperature 1. Appetite stimulant and carminative: 30 – 60 ml of 7- 10% 2. Neuralgias: severe cancer pain – injection round the nerve 3. Protection from cold 4. Alcohol may have a protective effect from heart attack and stroke - frugivores 5. Methanol Poisoning
  • 29. Disulfiram (Antabuse)  Internationally marketed as antabuse  ALDH enzyme inhibitor  Alcohol + disulfiram rise in concentration of aldehyde in blood and tissue distressing aldehyde syndrome  Symptoms: flushing, burning sensation, throbbing headache, perspiration, dizziness, vomiting, visual disturbance, mental confusion, fainting and circulatory collapse  Uses: aversion technique in chronic alcoholics: only to motivated persons  Technique: abstain alcohol overnight and start with 1 gm on day 1 followed by 0.75 gm next day and 0.50 gm next day and so on. Effects start within few hrs of 1st dose and lasts for 2 weeks  Mechanism: irreversible inhibition of ALDH and synthesis of new enzyme takes time and thus person resolves not to drink for distressing symptoms  Available as 250 mg tablets
  • 30. Ethanol as Antidote  Methanol, Ethylene glycol, Diethylene glycol  Methanol poisoning – toxicological importance – unscrupulous mixing with alcoholic beverages  Formic acid is toxic: above 50 mg/dl, lethal dose 75 – 100 ml, even 15 ml can cause blindness ADH ALDH Methanol formaldehyde Formic acid  Methanol poisoning: vomiting, epigastric pain dyspnoea, bradycardia, acidosis – permanent retinal damage and Death  Mechanism: Ethanol saturates alcohol dehydrogenase enzyme - no metabolism of Methanol to form Formic acid
  • 31. Methanol Poisoning treatment  Patient in dark room, Ventilation and BP supportive measures  Gastric lavage with sodibicarb if brought immediately  IV sodibicarb to combat acidosis – large quantity may be required  Ethanol 10% in water – nasogastric tube with loading dose of 0.7 ml/kg followed by 15 ml/kg/hr by infusion – continue treatment for several days (methanol is oxidized slowly)  Potassium chloride if hypokalemia occurs  Folinic acid or Calcium leucovorin ijection 50 mg IV every 6 Hrly – to enhance oxidation of formic acid  4-methylpyrazole – specific inhibitor of ALD – 15 mg/kg IV and 10 mg/kg 12 Hrly. till methanol level is <20 mg/dl  Haemodialysis
  • 32. Summary  Alcohol is a neuronal depressant  Long term exposure to alcohol brings about adaptive changes in the neuronal system  Chronic alcoholism causes toxic effects on all the organs especially liver  Withdrawal syndrome in alcoholics are treated by BZDs and Naltrexone  Antbuse/disulfiram is the drug is use as aversion technique in chronic alcoholics  Ethanol is used as antidote in Methanol Poisoning

Editor's Notes

  1. The drunkometer collected a motorist&amp;apos;s breath sample directly into a balloon inside the machine. The breath sample was then pumped through an acidified potassium permanganate solution. If there was alcohol in the breath sample, the solution changed colour. The greater the colour change, the more alcohol there was present in the breath.