Isopropyl alcohol
| 1. NAME |
| 1.1 Substance |
| 1.2 Group |
| 1.3 Synonyms |
| 1.4 Identification numbers |
| 1.4.1 CAS number |
| 1.4.2 Other numbers |
| 1.5 Main brand names/main trade names |
| 1.6 Manufacturers, importers |
| 2. SUMMARY |
| 2.1 Main risks and target organs |
| 2.2 Summary of clinical effects |
| 2.3 Diagnosis |
| 2.4 First-aid measures and management principles |
| 3. PHYSICO-CHEMICAL PROPERTIES |
| 3.1 Origin of the substance |
| 3.2 Chemical structure |
| 3.3 Physical properties |
| 3.3.1 Colour |
| 3.3.2 State/form |
| 3.3.3 Description |
| 3.4 Hazardous characteristics |
| 4. USES/HIGH RISK CIRCUMSTANCES OF POISONING |
| 4.1 Uses |
| 4.1.1 Uses |
| 4.1.2 Description |
| 4.2 High risk circumstances of poisoning |
| 4.3 Occupationally exposed populations |
| 5. ROUTES OF EXPOSURE |
| 5.1 Oral |
| 5.2 Inhalation |
| 5.3 Dermal |
| 5.4 Eye |
| 5.5 Parenteral |
| 5.6 Others |
| 6. KINETICS |
| 6.1 Absorption by route of exposure |
| 6.1.1 Oral |
| 6.1.2 Inhalation |
| 6.1.3 Dermal contact |
| 6.2 Distribution by route of exposure |
| 6.3 Biological half-life by route of exposure |
| 6.4 Metabolism |
| 6.5 Elimination and excretion by route of exposure |
| 7. TOXICOLOGY |
| 7.1 Mode of action |
| 7.2 Toxicity |
| 7.2.1 Human data |
| 7.2.1.1 Adults |
| 7.2.1.2 Children |
| 7.2.2 Animal data |
| 7.2.3 In-vitro data |
| 7.2.4 Workplace standards |
| 7.2.5 Acceptable daily intake (ADI) |
| 7.3 Carcinogenicity |
| 7.4 Teratogenicity |
| 7.5 Mutagenicity |
| 7.6 Interactions |
| 8. TOXICOLOGICAL AND OTHER ANALYSES |
| 8.1 Sample |
| 8.1.1 Collection |
| 8.1.2 Storage |
| 8.1.3 Transport |
| 8.2 Toxicological analytical methods |
| 8.2.1 Test for active ingredient |
| 8.2.2 Test for biological sample |
| 8.3 Other laboratory analyses |
| 8.3.1 Haematological investigations |
| 8.3.1.1 Blood |
| 8.3.1.2 Urine |
| 8.3.2 Biochemical investigations |
| 8.3.2.1 Blood |
| 8.3.2.2 Urine |
| 8.3.2.3 Other |
| 8.3.3 Arterial blood gas analysis |
| 8.3.4 Other relevant biochemical analyses |
| 8.4 Other biomedical (diagnostic) investigations and their interpretation |
| 8.5 Overall interpretation of all toxicological analyses and toxicological investigations |
| 8.6 References |
| 9. CLINICAL EFFECTS |
| 9.1 Acute poisoning |
| 9.1.1 Ingestion |
| 9.1.2 Inhalation |
| 9.1.3 Skin exposure |
| 9.1.4 Eye contact |
| 9.1.5 Parenteral exposure |
| 9.1.6 Other |
| 9.2 Chronic poisoning |
| 9.2.1 Ingestion |
| 9.2.2 Inhalation |
| 9.2.3 Skin exposure |
| 9.2.4 Eye contact |
| 9.2.5 Parenteral exposure |
| 9.2.6 Other |
| 9.3 Course, prognosis, cause of death |
| 9.4 Description of clinical effects by system |
| 9.4.1 Cardiovascular |
| 9.4.2 Respiratory |
| 9.4.3 Neurologic |
| 9.4.3.1 Central Nervous system (CNS) |
| 9.4.3.2 Peripheral nervous system |
| 9.4.3.3 Autonomic nervous system |
| 9.4.3.4 Skeletal and smooth muscle |
| 9.4.4 Gastrointestinal |
| 9.4.5 Hepatic |
| 9.4.6 Urinary |
| 9.4.6.1 Renal |
| 9.4.6.2 Others |
| 9.4.7 Endocrine and reproductive systems |
| 9.4.8 Dermatologic |
| 9.4.9 Eye, ear, nose, throat: local effects |
| 9.4.10 Haematological |
| 9.4.11 Immunologic |
| 9.4.12 Metabolic |
| 9.4.12.1 Acid-base disturbances |
| 9.4.12.2 Fluid and electrolyte disturbances |
| 9.4.12.3 Others |
| 9.4.13 Allergic reactions |
| 9.4.14 Other clinical effects |
| 9.4.15 Special risks: pregnancy, breast feeding, enzyme deficiencies. |
| 9.5 Others |
| 9.6 Summary |
| 10. MANAGEMENT |
| 10.1 General principles |
| 10.2 Life supportive procedures and symptomatic treatment |
| 10.3 Decontamination |
| 10.4 Enhanced Elimination |
| 10.5 Antidote treatment |
| 10.5.1 Adults |
| 10.5.2 Children |
| 10.6 Management discussion |
| 11. ILLUSTRATIVE CASES |
| 11.1 Case reports from the literature |
| 12.ADDITIONAL INFORMATION |
| 12.1 Specific preventive measures |
| 12.2 Other |
| 13. REFERENCES |
| 14. AUTHOR(S), REVIEWER(S), DATE(S), COMPLETE ADDRESS(ES) |
ISOPROPYL ALCOHOL
International Programme on Chemical Safety
Poisons Information Monograph 290
Chemical
1. NAME
1.1 Substance
Isopropyl alcohol
1.2 Group
Aliphatic alcohol hydrocarbon
1.3 Synonyms
Pseudo propyl alcohol; 2-propanol;
dimethyl carbinol; isopropanol;
sec-propyl alcohol; persprit;
secondary propyl alcohol; IPA;
propan-2-ol; alcohol isopropylicus;
petrohol
1.4 Identification numbers
1.4.1 CAS number
67-63-0
1.4.2 Other numbers
UN/NA (PIN): 1219
EC Number: 603-003-00-0
RTECS: NT 8050000
(Budavari, 1996)
1.5 Main brand names/main trade names
Avantine (UK)
IPS.1 and IPS/C (Shell)
Sterets (Schering-Prebbles UK)
Sterile Pack Fluid (Ethicon)
1.6 Manufacturers, importers
Manufactured by: Shell Chemicals
British Petroleum
Mobil Oil
2. SUMMARY
2.1 Main risks and target organs
Coma, central bnervous system (CNS) depression, liver,
kidney, cardiovascular depression and brain damage.
2.2 Summary of clinical effects
Drowsiness, ataxia and stupor.
Coma and respiratory depression.
Irritation of mucous membranes and eyes.
Gastritis, gastric haemorrhage, vomiting and pancreatitis.
Cold and clammy skin, hypothermia, miosis pupils,
tachycardia, respiration slow and noisy.
Hypotension
Cardiodepression
Brain, liver and kidney damage at a later stage.
2.3 Diagnosis
Blood and urine for biomedical analysis should be collected.
Fluid balance.
Electrolytes and blood gases.
Blood glucose.
Urinalysis
Hepatic and renal function tests.
Blood pressure, temperature and vital signs.
Blood levels of isopropyl alcohol and acetone are clinically
useful.
2.4 First-aid measures and management principles
Seek medical attention immediately and transfer patient
to hospital.
Inhalation: Remove source of contamination or move patient
into fresh air. Begin artificial respiration immediately if
victim is not breathing and administer supplemental oxygen if
available. Obtain medical attention.
Eye contact: Flood affected eye(s) with copious amounts of
lukewarm, gently running water for at least 15 minutes.
During this time the upper and lower eyelids should be held
apart.
Skin contact: Rinse the affected area(s) with copious
amounts of lukewarm, gently running water for at least 15
minutes. Remove contaminated clothing and shoes.
Wash/thoroughly clean all clothing before re-using or
discard. If skin irritation exists, seek medical
attention.
Ingestion: Induce emesis at an early stage if not
contraindicated. Empty stomach by gastric aspiration and
lavage, care being taken not to induce pulmonary aspiration
of the return flow. Keep the patient warm. If respiration
is depressed or absent, endotracheal intubation and assisted
respiration may be required. Obtain medical assistance
immediately.
In severe poisonings:
maintain respiration;
maintain fluid balance;
initiate haemodialysis or peritoneal dialysis;
treat convulsions with intravenous (IV) benzodiazepines.
First aid summary:
Provide the patient with general supportive measures (warmth,
comfort and rest). Obtain medical advice and/or assistance
for all cases of ingestion or eye contact, and all but
trivial cases of inhalation or skin contact.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
Synthetic: Prepared from propylene, which is obtained
in the cracking of petroleum or by the reduction of acetone
(Budavari, 1996).
3.2 Chemical structure
Chemical name: Isopropyl alcohol
Molecular weight: 60.09
Structural formula: CH3-CH(OH)-CH3
3.3 Physical properties
3.3.1 Colour
Colourless
3.3.2 State/form
Liquid-other
3.3.3 Description
Boiling point: 82.5°C
Melting point: 89.5°C
Flash point: 11.7°C (closed cup)
17°C (open cup)
Autoignition temperature: 455.6°C
Relative density: 0.785 (Water = 1)
Vapour pressure: 4399.62 Pa at 20°C
7879.33 Pa at 30°C
Solubility: In water in all proportions at 20°C
In alcohol in all proportions at 20°C
In ether in all proportions at 20°C
Also soluble in acetone, benzene and chloroform,
insoluble in salt solutions.
Relative molecular mass: 60.09
(C: 59.96%; H: 13.42%; O: 26.62%)
pH: N/A
Viscosity: 0.00243 Poises (2.43 cP) at 20°C
Odour: Slight odour resembling a mixture of ethanol
and acetone.
Taste: Slightly bitter taste
3.4 Hazardous characteristics
Explosive limits:
Lower explosive limit: 2.5% (in air)
Upper explosive limit: 12% (in air)
Dangers associated with the vapour:
Dispersion: inflammable mixture with air.
Possible ignition: flammable liquid; may autoignite. Vapour
is heavier than air and will travel along the ground, into
work pits, etc.
Possible chemical reaction in air: none.
Possible chemical reactions with other chemicals:
Strong oxidizing agents (nitrates, perchlorates, peroxides).
Phosgene - forms isopropyl chloroformate and
hydrogenchloride.
Iron salts - explosive thermal decomposition may occur.
Hydrogen-palladium-mixture can ignite in air.
Potassium t-Butoxide
Trinitromethane (Nitroform) (Cheminfo, 1989).
Electrical and thermal conductivity with possible
consequences: no data available.
Products of combustion: carbon dioxide and carbon monoxide.
Environmental risks:
Safe disposal - dispose in a designated landfill site, or
burn in an approved solvent burner. If small amounts are
disposed of into a sink or sewer, rinse with copious amounts
of water to prevent accumulation of flammable vapours.
Notify environmental agencies (local health and wildlife
officials) in the event of any significant release of this
material into the environment.
Isopropanol is dangerous to aquatic life in high
concentrations, so prevent entry into water intakes and
waterways.
Clean up spills - stop the flow if it can be done safely.
Contain the spill. Recover liquid for recycling or disposal
if feasible. Otherwise absorb the liquid on clay, sand,
sawdust or other absorbent material.
Food chain concentration potential: None.
(EPS Canada, 1984).
4. USES/HIGH RISK CIRCUMSTANCES OF POISONING
4.1 Uses
4.1.1 Uses
Antifreeze;
vehicle;
industrial Solvent;
industrial
Miscellaneous industrial function
4.1.2 Description
In antifreeze products; solvent for gums,
shellac, essential oils, in quick drying oils,
creosote and resins: extraction of alkaloids; in quick
drying inks; in denaturing ethyl alcohol; in body
rubs, hand lotions, after-shave lotions, cosmetics and
pharmaceuticals; in manufacture of acetone, glycerol,
isopropyl acetate; antiseptic; rubefacient
pharmaceutic aid (solvent) (in concentrations up to
70%) (Ellenhorn, 1988).
4.2 High risk circumstances of poisoning
Accidental ingestion of rubbing alcohols/toiletries by
children.
Dermal/inhalation exposure in children during isopropyl
alcohol sponging for control of fever.
Intentional ingestion for alcoholic effect, or in suicide
attempts.
Occupational or accidental exposure to liquid or its vapour.
4.3 Occupationally exposed populations
Process workers in the pharmaceutical industry.
Process workers in the cosmetic industry.
Process workers in the chemical industry.
Process workers in the petroleum industry.
Analytical and other laboratory workers.
Printers.
Painters.
Carpenters and cabinet makers.
5. ROUTES OF EXPOSURE
5.1 Oral
Oral ingestion of rubbing alcohols and toilet
preparations, constitute the most common route of
exposure.
Doses of above 20 mL may produce toxic effects.
5.2 Inhalation
Inhalation of vapour from preparations.
Inhalation may occur in children being sponged with isopropyl
alcohol to control fever.
Short-term exposure limit is 500 ppm. At levels above this,
respirator or self-contained breathing apparatus is
necessary. A level of 12,000 ppm is immediately dangerous to
health and life.
5.3 Dermal
Dermal exposure to the liquid and vapour.
There is little absorption through intact skin, but
significant delayed absorption over 4 hours postulated
(Martinez, 1986).
Note risk of inhalation after prolonged skin exposure
(sponging, etc.).
5.4 Eye
Eye exposure to liquid and vapour.
Both the liquid and solvent are severely irritant.
5.5 Parenteral
No data available.
5.6 Others
No data available.
6. KINETICS
6.1 Absorption by route of exposure
6.1.1 Oral
80% of an oral dose is absorbed within 30
minutes. Absorption is complete within 2 hours
although this may be delayed in a large overdose
(Ellenhorn, 1988).
6.1.2 Inhalation
Alveolar concentration is correlated to the
environmental concentration at any given time, and the
mean alveolar clearance has been calculated at 8 L/min
(Ellenhorn, 1988).
6.1.3 Dermal contact
Absorbed through intact skin on prolonged
exposure (Martinez, 1986).
6.2 Distribution by route of exposure
Isopropyl alcohol distributes in body water with an
apparent volume of distribution of 0.6 to 0.7 L/kg. Two hours
are required for complete tissue distribution (Ellenhorn,
1986).
6.3 Biological half-life by route of exposure
Isopropyl alcohol most closely follows first order
kinetics, with a half-life of 2.5 to 3.2 hours (Daniel,
1981). The elimination half-life of the active metabolite,
acetone, is significantly prolonged to about 5 hours in rats
(Teramoto, 1987) and 22.4 hours in man (Natowicz et al.,
1985).
6.4 Metabolism
20 to 50% of an absorbed dose is excreted unchanged.
Most isopropyl alcohol is oxidized in the liver by alcohol
dehydrogenase to acetone, which is probably further
metabolized to acetate, formate, and finally carbon dioxide.
Acetone may contribute to the CNS depression seen in
isopropanol poisoning.
6.5 Elimination and excretion by route of exposure
20 to 50% of an absorbed dose is excreted unchanged (2%
of dose excreted in exhaled air).
Acetone is slowly eliminated by the lung (40%) or kidney.
Clinically insignificant excretion occurs into the stomach
and saliva (Teramoto, 1987).
Related ketoacids are not produced in sufficient quantities
to cause a severe metabolic acidosis.
7. TOXICOLOGY
7.1 Mode of action
Isopropyl alcohol is an irritant to mucous membranes and
eyes.
Isopropyl alcohol is a potent central nervous system (CNS)
depressant, and in large doses causes cardiovascular
depression. Acetone, its main metabolite, can potentiate and
lengthen the duration of the CNS symptoms. Mild acidosis may
develop from the conversion of acetone to acetic acid and
formic acid. The alcohol dehydrogenase-induced shift in
NAD/NADH may cause decreased gluconeogenesis and
hypoglycaemia (Addison, 1962).
Inebriation, peripheral vasodilation and hypothermia may also
occur.
In children, hypoglycaemia is particularly severe when
poisoning follows fasting, exercise or chronic
malnutrition.
Lactic acidosis may occur in patients with severe liver
disease, pancreatitis or receiving biguanide therapy, or as a
result of the hypovolaemia which frequently accompanies
severe intoxication.
In rat hepatocytes (Hormann et al., 1989), the following
sequence has been observed:
marked depletion of glutathione
increased malondialdehyde production
decreased protein sulphydryls content
leakage of lactic dehydrogenase with loss of membrane
integrity.
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
Adults: 1 mL/kg of a 70% solution,
but as little as 0.5 mL/kg may cause
symptoms.
The lethal dose may be as low as 240 mL (2 to
4 mL/kg). Death has been reported at a blood
level of 150 mg/dL (25 mmol/L); however,
survival after dialysis has been reported at
levels as high as 560 mg/dL.
Maximal air concentration allowable to
prevent irritation of eyes, nose and throat
is:
440 ppm (USA)
400 ppm long-term (UK)
500 ppm short-term (UK)
200 ppm (Japan).
7.2.1.2 Children
6 mL/kg (9 mL/kg of 70%) has
produced coma with a blood level of 380
mg/dL. The lethal dose is approximately 100
mL
Pediatric patients have survived serum levels
from 128 to 520 mg/dL with supportive
care.
(Ellenhorn, 1988; Martinez, 1986).
7.2.2 Animal data
LD50 (rat, oral): 4.42 to 5.84 g/kg
LD50 (mouse, oral): 4.8 g/kg
LD50 (rabbit, oral): 7.9 g/kg
(Lehman, 1944: 6.4 mL/kg)
LD50 (rabbit, dermal): 13 g/kg
Irritant dose (rabbit, skin): 500 mg/24 h (mild)
Irritant dose (rabbit, eye): 0.1 mL 70% solution
(severe eye irritant)
Common signs of acute isopropyl alcohol intoxication
of animals are hind leg paralysis, unsteadiness, lack
of muscular coordination, respiratory depression and
stupor (Cheminfo, 1989).
7.2.3 In-vitro data
No data available.
7.2.4 Workplace standards
Threshold Limit Values (TLVs)/American
Conference of Governmental Industrial Hygienists 1987
to 1988 are:
Time weighted average:
TLV-TWA 400 ppm (980 mg/m3)
Short-term exposure limit:
TLV-STEL 500 ppm (1225 mg/m3)
IDLH Value 20,000 ppm
(NIOSH, 1985; ACGIH, 1988)
OSHA PEL Final Rule Limits (OSHA, 1989):
PEL-TWA Final Rule Limit:400 ppm (>>980 mg/m3)
PEL/STEL Final Rule Limit:500 ppm (>>1225 mg/m3)
no ceiling limit
Odour threshold: 90 mg/m3 (Chris, 1985).
NIOSH REL: 400 ppm (TWA)
800 ppm (ceiling for 15 min) (CDC, 1988).
7.2.5 Acceptable daily intake (ADI)
400 ppm (TWA OSHA).
Other guideline levels:
Respiratory Protection Guidelines (NIOSH):
up to 1,000 ppm: Use a powered air purifying
respirator with organic vapour cartridge, or full
facepiece chemical cartridge.
up to 10,000 ppm: (CCROVF) respirator with organic
vapour cartridge; use a supplied air respirator
operating in continuous flow mode (GMOVc).
up to 12 000 ppm: use a gas mask with organic vapour
canister; or full facepiece self-contained breathing
apparatus; or, full facepiece supplied air respirator,
(GMOVfb/SAF/SCBAF).
Escape Respirator: GMOV/SCBA.
7.3 Carcinogenicity
Not carcinogenic by animal controls (Cheminfo, 1989).
A waste product, isopropyl oil, has been suspected to cause
respiratory tract neoplasms after occupational exposure (Weil
et al., 1952).
7.4 Teratogenicity
Decreased fetal weights and increased skeletal
malformations were noted when pregnant rats were exposed by
inhalation to concentrations that also caused maternal
toxicity (Nelson et al., 1988).
7.5 Mutagenicity
Not mutagenic in animal models (RTECS, 1989).
7.6 Interactions
Isopropyl alcohol potentiates the hepatic and renal
toxicity produced by halokenes (e.g., carbon tetrachloride)
(Ellenhorn, 1981).
8. TOXICOLOGICAL AND OTHER ANALYSES
8.1 Sample
8.1.1 Collection
Whole blood, urine, stomach contents. Collect
and store in tightly closed containers and store in a
cool place. Samples should be processed quickly to be
of use clinically. Sample size at least 5 mL. Glass
containers are preferable to plastic.
Urine samples should be collected hourly. If the air
is to be sampled for vapour concentrations, at least
50 mL is required, and this needs to be stored in a
tightly closed container.
For active material, use a sampling pump with
appropriate collecting medium: NIOSH Method S 65
(NIOSH, 1985).
8.1.2 Storage
Store in a cool place, sample could be
inflammable.
8.1.3 Transport
Transport to nearest laboratory as quickly as
possible in cool containers. Material may be
inflammable.
8.2 Toxicological analytical methods
8.2.1 Test for active ingredient
Simple qualitative:
Acetest tablets can be used in the presumptive
diagnosis of isopropyl alcohol ingestion. These will
detect the presence of acetone in the urine, which
appears approximately 3 hours after ingestion. As the
level of isopropyl alcohol drops, the level of acetone
will initially rise and then decline.
Recommended quantitative:
Gas-liquid chromatography or other specific methods
(Parker et al., 1962) similar to those used for
ethanol detection constitute the methods of
choice.
The GLC should be equipped with flame ionization
detection. Ideally the apparatus should have a
capsule sampler and recorder and the results should be
processed with calculating integrator.
Acetone can be assayed using the same apparatus. The
blood sample, 9.5 mL, is placed in an aluminium
capsule (3 mm diam. x 6 mm length), and cold welded
using a crimping tool. The sealed capsule is inserted
into the injection port of the gas chromatograph. The
injector is flushed with carrier gas (e.g., helium 30
mL/min), to remove any atmosphere introduced with the
probe. The capsule is held in the heated zone for 60
seconds to allow for vapourization of the solvents
within the capsule. The capsule is then pierced and
carrier gas takes the volatiles into the hollow needle
and then on to the chromatographic columns. A
suitable column is 6' x 1/8" S.S., with 20% Carbowax
20 M on Chromosrob W, AW-DCMS, 60/80 mesh.
The retention times are: isopropanol 2.17 minutes, and
acetone: 1.22 minutes.
Suitable temperatures are: injector: 200°C; column:
70°C; and detector: 200°C.
Typical flow rates are: carrier gas He = 30 mL/min;
hydrogen = 35 mL/min; air = 450 mL/min.
Calibration curves may be determined using
concentrations of 0.005 to 1.5 mg/mL of isopropanol
injected into fresh blood samples.
The concentration of each standard solution can be
calculated on a mg/mL basis, using the specific
gravity of blood and isopropyl alcohol and acetone. A
calibration graph is plotted by plotting peak height
(cm) against isopropyl alcohol and acetone
concentrations (mg/mL). The limit detection is 0.001
mg/mL for both solvents (Laham et al., 1979, 1980).
8.2.2 Test for biological sample
No data available.
8.3 Other laboratory analyses
8.3.1 Haematological investigations
8.3.1.1 Blood
Full blood count
Blood film.
Haematocrit.
8.3.1.2 Urine
Myoglobinuria (secondary to coma-induced
rhabdomyolysis)
Red and white blood cells
8.3.2 Biochemical investigations
8.3.2.1 Blood
Osmolal Gap:
Used to estimate blood isopropanol
concentration using the following
equation:
Osmolal gap x 6 = predicted isopropyl alcohol
level mg/dL
Osmolal gap = measured osmolality -
calculated osmolality
Anion gap
Serum electrolytes
Blood urea nitrogen
Creatinine
Glucose
Serum acetone
Hepatic transferases
8.3.2.2 Urine
Glucose
Ketone bodies (acetone)
8.3.2.3 Other
No data available.
8.3.3 Arterial blood gas analysis
Arterial pO2 and pCO2 concentrations.
Acid-base balance.
8.3.4 Other relevant biochemical analyses
No data available.
8.4 Other biomedical (diagnostic) investigations and their
interpretation
Isopropyl alcohol values do not correlate with severity
of poisoning as the metabolite acetone also interferes with
symptomatology.
High serum ketones with minimal acidosis are common in
isopropyl alcohol ingestion.
Osmolal Gap: A rise in blood isopropyl alcohol of 2 mg/dL
produces a change of 0.17 mosm/kg H2O in the osmolal gap.
A 50 mg/dL toxic blood level produces an 8 to 9 mosm increase
in the osmolal gap, and seriously toxic levels of 200 mg/dL
produce a 34 mosm change in osmolal gap. Acetone levels must
also be considered as they produce similar changes.
8.5 Overall interpretation of all toxicological analyses and
toxicological investigations
Sample collection
Isopropanol serum levels are clinically useful and
significant. Collect in glass where possible, keep cool and
tightly closed, until analysed. During treatment,
measurement of isoprpyl alcohol in hourly urine samples is
clinically useful.
Retention of samples of gastric lavage if performed, and
obtaining samples of product ingested, may be useful if
diagnostic confirmation is desired.
Biomedical analysis
Routine blood and urine analysis should be performed, with
special emphasis on:
Blood glucose (for hypoglycaemia).
Osmolal gap by freezing point depression (for predicted
isopropanol levels).
Arterial blood gas analysis (for assessment metabolic
acidosis).
Serum acetone (serum ketone bodies).
Urinary acetone (for presumptive diagnosis with Acetest
tablets).
Monitoring of fluids and electrolytes. (Acid-base balance
for normoglycaemic ketoacidosis).
Hepatic function tests (for hepatic aminotransferases).
Toxicological analysis
Plasma levels of isopropanol are indicative of the level of
poisoning. The time of ingestion is critical in determining
treatment options.
Other investigations
Respiratory function tests to gauge the degree of respiratory
depression may be useful in selected, severe poisonings.
Blood pressure (for hypotension).
Temperature (for hypothermia).
8.6 References
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
This is the common route of poisoning.
Absorption (80%) occurs within 30 minutes, and is
complete within 2 hours. Symptoms are drowsiness,
gastrointestinal pain, cramps, nausea, vomiting and
diarrhoea, with unconsciousness and death following
massive exposure. In children, more than three
swallows of 70% isopropyl alcohol results in symptoms
requiring medical observation.
Isopropyl alcohol intoxication has a rapid onset of
action (30 to 60 minutess) with peak effects occurring
within several hours. Severe poisoning presents early
with stupor leading to deep coma, respiratory
depression and hypotension. Other symptoms are
dizziness, poor coordination, headache, confusion,
gastric irritation, abdominal pain, vomiting,
haematemesis, hypotension, tachycardia, (and
cardiodepression) and loss of deep tendon
reflexes.
9.1.2 Inhalation
Common route of poisoning. Mild irritation of
the respiratory tract occurs at 400 ppm. High
concentrations can cause nausea, headache,
lightheadedness, drowsiness, ataxia and deep
narcosis.
9.1.3 Skin exposure
Brief exposures are not irritating, but
prolonged contact (4 hours) has led to toxicity with
central nervous system (CNS) effects (Martinez, 1986).
Sponging children with isopropyl alcohol for fever
control may result in significant absorption.
9.1.4 Eye contact
Vapour is mildly irritating at 400 ppm. Direct
eye contact with the liquid can cause severe
irritation (Cheminfo, 1989) and even corneal abrasion
(Osborn and Rosales, 1981).
9.1.5 Parenteral exposure
No data available.
9.1.6 Other
No data available.
9.2 Chronic poisoning
9.2.1 Ingestion
No significant changes were found in the
chemical or cellular composition of the blood or urine
after humans ingestion of 6.4 mg/kg of isopropyl alcohol
on a daily basis for 6 weeks (Cheminfo, 1989).
No long-term health effects have been reported in
humans. Rapid metabolism in the body precludes
accumulation.
9.2.2 Inhalation
An excess of sinus cancers and laryngeal
cancers has been found among workers producing
isopropyl alcohol. This could be due to the by
product, isopropyl oil.
9.2.3 Skin exposure
Chronic toxic exposure may lead to coma and
death (Broughton, 1944).
Drying, cracking and eczema may result from repeated
or prolonged skin contact.
9.2.4 Eye contact
Oxygen uptake of corneal epithelium is reduced
in the rabbit (Roseman, 1987).
9.2.5 Parenteral exposure
No data available.
9.2.6 Other
No data available.
9.3 Course, prognosis, cause of death
Central nervous system depression often lasts for 24
hours. The development of hypotension is a poor prognostic
feature. Haemodialysis should be used in severely poisoned
patients to remove the isopropyl alcohol, and to shorten the
duration of coma, together with other supportive
measures.
Death results from central nervous system (CNS) and
respiratory depression during coma.
9.4 Description of clinical effects by system
9.4.1 Cardiovascular
Hypotension from peripheral dilatation
Tachycardia
Serious arrhythmias have not been reported.
(Ellenhorn, 1988).
9.4.2 Respiratory
Respiratory depression and death.
Acetone can be detected on the breath.
(Teramoto, 1987; Buckley, 1986).
9.4.3 Neurologic
9.4.3.1 Central Nervous system (CNS)
Dizziness, poor coordination,
headache, confusion, progressing to stupor,
coma and loss of deep tendon reflexes.
Serious nervous system depression often lasts
for 24 hours. Elation does not
occur.
9.4.3.2 Peripheral nervous system
No data available.
9.4.3.3 Autonomic nervous system
Pupils are often miotic, and
nystagmus is normally present.
9.4.3.4 Skeletal and smooth muscle
Deep tendon reflexes are not present
during coma.
9.4.4 Gastrointestinal
Gastric irritation appears early, abdominal
pain and vomiting are prominent, and haematemesis may
occur (Buckley, 1986).
9.4.5 Hepatic
Hepatic dysfunction has been reported (Kulig,
1984).
9.4.6 Urinary
9.4.6.1 Renal
Acute tubular necrosis and
myoglobinuria have been reported (Buckley,
1986).
9.4.6.2 Others
No data available.
9.4.7 Endocrine and reproductive systems
No data available.
9.4.8 Dermatologic
Dryness, irritation, allergic eczema, with
repeated or chronic direct contact.
9.4.9 Eye, ear, nose, throat: local effects
Eye: vapour causes irritation, liquid may cause
intense irritation including corneal abrasion.
9.4.10 Haematological
Myoglobinuria and haemolytic anaemia have been
reported.
9.4.11 Immunologic
No data available.
9.4.12 Metabolic
9.4.12.1 Acid-base disturbances
Mild metabolic acidosis may develop
from the conversion of acetone to acetic and
formic acid.
9.4.12.2 Fluid and electrolyte disturbances
Abnormalities of serum in
electrolytes, blood urea nitrogen,
creatinine, may be noted.
9.4.12.3 Others
Hypoglycaemia, and hypothermia from
peripheral vasodilation.
Osmolal gap may be clinically significant in
suspecting the diagnosis.
Elevations of hepatic aminotransferases may
occur.
9.4.13 Allergic reactions
Allergic eczema has been reported.
9.4.14 Other clinical effects
No data available.
9.4.15 Special risks: pregnancy, breast feeding, enzyme
deficiencies.
No data available.
9.5 Others
No data available.
9.6 Summary
10. MANAGEMENT
10.1 General principles
If a small quantity of isopropyl alcohol has been
recently ingested, i.e., within 30 minutes, then emesis with
syrup of ipecac may be used. It should not be used with
ingestion of large quantities, or in the presence of central
nervous system (CNS) depression.
Gastric lavage is the treatment of choice for the removal of
large volumes of isopropyl alcohol from the stomach. In the
case of skin contamination, wash the skin thoroughly with
soap and water. If irritation and pain persist seek medical
advice.
Exposed eyes should be irrigated with copious amounts of room
temperature water for at least 15 minutes. If irritation,
pain, swelling, lachrymation persist after 15 minutes of
irrigation, seek ophthalmological advice.
10.2 Life supportive procedures and symptomatic treatment
Support respiratory function.
Support cardiovascular function.
Treat hypotension with intravenous (IV) fluids and place in
the Trendelburg position. If the patient is unresponsive,
correct dehydration and acidosis with fluids and electrolytes
and administer dopamine.
Add 200 to 400 mg dopamine to 250 mL sodium chloride 0.9%
(normal saline, NS) or glucose 5% injection, (Dextrose, D5W),
to produce 800 or 1600 mg/mL. Alternatively, add 400 mg to
500 mL of NS or D5W to produce 800 mg/mL. Begin infusion at
2 to 5 mg/kg/min, progressing in 5 to 10 mg/kg/min increments
as needed. If ventricular arrhythmias occur decrease the
rate of administration.
Support neurological function.
10.3 Decontamination
Measures to eliminate isopropanol from the
gastrointestinal tract must usually be initiated within 2
hours of ingestion and, preferably within 30 min, due to its
rapid absorption.
Due to the onset of CNS depression (which usually occurs
within 30 minutes of ingestion), ipecac-induced emesis is not
recommended.
Gastric lavage may be indicated if performed soon after
ingestion. If coma or convulsions occur, protect the airway
by cuffed endotracheal intubation. Use a large bore
orogastric tube:
Adult: 36 to 42 French
Child: 24 to 28 French.
Repeat as necessary. Lavage should return approximately the
same volume of fluid as has been given.
Lukewarm tap water or normal saline is recommended, at a rate
of 150 to 200 mL per wash (in children over 5 and adults) and
50 to 100 mL per wash in young children.
Continue until the lavage return is clear.
Activated charcoal
Administer charcoal as a slurry in water at a dilution of
30 g charcoal to 240 mL aqueous diluent. The diluent may also
be a saline cathartic or sorbitol. Usual doses are 30 to
100 g of charcoal in adults (15 to 30 g in children, and 1 to
2 g/kg in infants).
Note: Activated charcoal has limited absorptive properties
for isopropanol (1 g absorbs approximately 500 mg of
isopropanol), and the optimum dose of charcoal has not been
established.
Cathartics
Administer one dose of a saline cathartic or sorbitol mixed
with the charcoal or preferably administered separately.
Note: The safety of more than one dose of a cathartic has
not been established.
Hypermagnesaemia has been reported after repeated
administration of magnesium-containing cathartics in patients
with normal renal function. Repeated cathartic dosing should
be done with extreme caution if at all; admiistration of
cathartics should be stopped when a charcoal-coloured stool
appears.
Cathartics should not be used in patients with ileus and
saline cathartics should not be used in patients with
impaired renal function. Magnesium sulphate or sodium
sulphate are suitable cathartics and the usual dose is 20 to
30 g in adults and 250 mg/kg in children over 2 years.
Magnesium citrate oral solution USP may also be used in a
dose for both adults and children of 4 mL/kg/dose up to 200
to 300 mL/dose.
Catharsis may be effective 12 to 24 h after ingestion.
Sorbitol:
Adult: The usual dose for sorbitol will vary but is in the
order of 1 to 2 g/kg/dose to a maximum of 150 g.
Children: Over 1 year old, 1 to 1.5 g/kg/dose to a maximum of
150 g/dose. It is administered under direct medical
supervision monitoring fluid and electrolyte status. It
should be given as a 35% aqueous solution.
Skin decontamination: Wash the skin thoroughly with soap and
water. Seek medical advice if pain or irritation
persist.
Eyes: Irrigate with copious amounts of tepid water
(preferably isotone saline solution) for at least 15 minutes.
Seek specialist medical advice if pain, irritation, swelling,
lachrymation or photophobia persist.
10.4 Enhanced Elimination
Forced diuresis is not effective and should not be
used.
Haemodialysis:
Haemodialysis is useful in patients with severe life-
threatening symptoms unresponsive to standard treatment
therapy.
Note: Using haemodialysis, the metabolism of isopropanol to
acetone is rapid and should be monitored carefully.
Peritoneal dialysis:
This appears to be only minimally effective, and should only
be used in selected severe cases of poisoning where
haemodialysis is not possible.
10.5 Antidote treatment
10.5.1 Adults
There is no specific antidote.
10.5.2 Children
There is no specific antidote.
10.6 Management discussion
Haemodialysis is used on the basis that it removes
isopropanol and shortens the duration of coma. Removal of
isopropanol alcohol is 52 times, and of acetone 40 times,
more efficient through haemodialysis than through urinary
excretion (Rosansky, 1982).
Peritoneal dialysis is considerably less effective. No
advantage is to be gained by infusing ethanol to block
alcohol dehydrogenase, as the toxicity of isopropanol is
principally due to the parent compound.
Isopropanol is oxidized in the liver to acetone and treatment
options are limited to the symptomatic and supportive
measures.
11. ILLUSTRATIVE CASES
11.1 Case reports from the literature
A 2-year-old boy weighing 21 kg reportedly ingested a
small amount of 70% isopropyl alcohol rubbing alcohol. There
were no symptoms and emesis with dilute dishwashing liquid
was tried. The child refused this and was referred to the
nearest hospital. On arrival, 30 minutes after ingestion,
the child was in an unresponsive condition with laboured
respiration. No emesis had occurred. The child was started
on intravenous (IV) fluids, intubated, lavaged, and then
transferred to a children's hospital. It was found that the
child had been sponged with isopropanol for several hours in
an attempt to reduce fever. Three-and-a-half hours after
ingestion, the child was still unconscious and was
transferred to the intensive care unit (ICU) with artificial
ventilation and haemodialysis. Approximately 16 hours after
ingestion and following treatment the child was alert and
responsive. Intravenous (IV) fluids were discontinued and
the child made an uneventful recovery (Martinez, 1986).
A 38-year-old woman with Type I diabetes mellitus complained
of discomfort after applanation tonometry of the right eye.
The tonometer tip had been swabbed with a 70% isopropyl
alcohol wipe immediately before use. On examination of the
right eye, a circular area of corneal epithelial
opacification corresponding to the size of the tonometer tip
was noted. This area stained faintly with fluorescein but
stained strongly with Rose Bengal. A patch was placed on the
eye for 2 h and then removed, the patient seemed comfortable.
But 2 to 3 h later she noted significant discomfort that
persisted for 16 hours. The discomfort resolved by the next
day. A second patient showed lesser symptoms that resolved
after 24 hours (Soukiasian, 1988).
An 18-month-old child was wrapped in towels soaked with
rubbing alcohol, by her mother, in an attempt to control a
40°C fever due to otitis media. The towels were wrapped
about the child's waist for periods up to 4 hours. The child
became progressively lethargic and unresponsive to verbal and
tactile stimulation. She was admitted to the ICU unit
unconscious and unresponsive to pain, with midline fixed
miotic pupils, a temperature of 35.8°C, a pulse of 153
beats/min, and blood pressure of 100/50 mm Hg. Nasogastric
aspiration yielded strongly haem-positive "coffee-ground"
material. Laboratory studies were performed, including
arterial blood gases, electrolytes, CSF and urinalysis. Her
osmolal gap was calculated at 70 mOsm/kg (70 mmol/kg). She
was diagnosed as having mild metabolic acidosis and this
coupled with an anion gap of 20 mmol/L (20 mEq/L) and a
significant elevation in the osmolality gap, suggested the
possibility of acute intoxication with an osmotically active
substance of low molecular weight.
Toxicological studies performed 8 to 10 hours after ingestion
showed a serum level of isopropanol of 162 mg/dl (27 mmol/L),
(measured by gas chromatography). The serum acetone level was
180 mg/dL (31 mmol/L). The child received supportive care,
including airway management and intravenous hydration. She
improved over the next 12 to 24 h and was extubated and
discharged to a paediatric ward 36 hours after admission to
the ICU. She was discharged home on the 7th day with no
evidence of neurologic or other sequelae. The child
continued to do well 3 months after the event (Arditi,
1987).
A similar case was reported by Webster et al. (1985) of a
9-month-old girl. Osmolality and anion gap was seen as being
diagnostic of isopropanol poisoning. Treatment consisted of
mechanical ventilation and parenteral fluids. She was
discharged from hospital 3 days after admission, with no
evidence of neurologic or other sequelae.
A 55-year-old woman was found unconscious and unresponsive in
her home. There was no palpable pulse, HR 140 beats/min, RR
6 breaths/min. She was intubated, ventilated, but no venous
access could be obtained. The patient had been bathed with
approximately 1 litre of 70% isopropanol by her daughter.
Four hours after admission, an isopropanol level of 98 mg/dL
(165 mmol/L) and an acetone level of 43 mg/dL (7 mmol/L) were
obtained. The patient had massive skin lesions and it was
believed that absorption through the skin had occurred
(McGrath, 1989).
A 61-year-old patient was found unconscious and unresponsive
after ingesting 1480 mL of 70% isopropyl alcohol. He was
admitted to ICU 4 hours later and was immediately intubated
and started on fluid replacement with a dopamine drip for
hypotension. On examination, the patient was completely
unresponsive; pulse was 60; BP was 80/60, and pinpoint
pupils, acetone odour on breath, bradycardia and no response
to painful stimuli were noted. The following laboratory
tests were performed: blood gases; electrolytes; BUN; serum
creatinine; ketone bodies and glucose. Haemodialysis with
minimal ultrafiltration was instituted 9 hours after
ingestion, and within 1 hour the patient had spontaneous
movements and started assisting ventilation. By 2 hours, the
patient responded to verbal commands. The paper concludes
that haemodialysis is a life-saving procedure in this case,
removing approximately 27 g/hour of alcohol (50 times greater
than the amount eliminated by urinary excretion) (Rosansky,
1982).
A 4-year-old mentally retarded girl was found unconscious in
her bed by her mother, 27 hours after she had been
intentionally scalded. The mother subsequently applied gauze
soaked with isopropanol to the scald burns. The child was
then left alone in her room without food or water until she
was discovered dead. The paper suggests that a contributory
cause of death was isopropanol intoxication, resulting from
application of this chemical to burns (Russo, 1986).
A review of acute isopropyl alcohol poisoning (Lacouture et
al., 1983), provides an overview of acute poisoning with
special emphasis on clinical management. Two case reports
were presented.
A 42-year-old woman was admitted to hospital in an
unresponsive and unconscious condition. Initial treatment
consisted of endotracheal intubation, respiratory support,
administration of intravenous (IV) fluids, and gastric
lavage. There was no response to naloxone or glucose. She
was given 4 litres of lactated Ringers solution prior to her
transfer to ICU. Her depth of coma decreased and 12 hours
after admission she was alert and awake and able to breathe
on her own.
A 32-year-old man was admitted to hospital unconscious (Grade
III to IV coma). He was areflexic and unresponsive to deep
pain. There was no response to naloxone, thiamine or
glucose. Laboratory tests included isopropyl alcohol levels,
serum electrolytes, BUN, and blood gases. During intubation,
the patient suffered a cardiac arrest. He was resuscitated.
However, an arryhthmia refractory to standard therapy
necessitated insertion of a transvenous pacemaker. He was
also started on a dopamine drip and was prepared for
haemodialysis. Twenty-four hours after admission he awoke
and was orientated and co-operative.
The authors suggest that haemodialysis should be considered
in patients with hypotension and those with serum isopropyl
alcohol concentrations exceeding 400 to 500 mg/dL (66 to 83
mmol/L). They also conclude that the management of acute
isopropanol intoxication may involve supportive care only, or
may include haemodialysis.
A 23-month-old boy was admitted to hospital comatose and
unresponsive to deep stimuli. He was intubated. His pulse
became unperceptible, and cardiac compression was initiated,
together with controlled ventilation with 100% oxygen and 20
mmol of sodium bicarbonate by slow intravenous (IV) infusion
through a scalp vein. Nonadrenaline was required to correct
and maintain the BP within normal limits. It was
subsequently discovered that he had ingested approximately
200 mL of isopropanol. He was comatose for 2 days and then
slowly recovered (Light, 1969).
A further case reported by Visudhiphan (1971), concerned a
2-year-old boy suffering from isopropanol intoxication., His
blood pressure was maintained with metaraminol tartrate and
levaterenol bitartrate. His respiration was assisted with a
positive pressure respirator. He gradually improved over 2
days and made an uneventful recovery.
A comatose 46-year-old woman was admitted to hospital with
isopropanol and acetone levels of 2,000 mg/L and 120 mg/L
respectively. Pharmacokinetic analysis showed that both
isopropanol and acetone obeyed apparent first order kinetics
with half-lives of 6.4 and 22.4 hours respectively, with
similar values in cerebrospinal fluid. Two days after
admission the patient was alert and responsive. She was
subsequently discharged.
A 59-year-old man was admitted in a coma to hospital after
ingesting 1 litre of isopropyl alcohol. Laboratory data were
normal except for proteinuria and ketonuria. His condition
deteriorated rapidly, with development of hypotension and
respiratory depression. Pupils were miotic and all deep
reflexes were absent. Extra corporeal haemodialysis was
instituted; within 1 hour he was responding weakly to
painful stimuli. After 3 hour of dialysis the patient was
very active, and so the procedure was terminated (Freireich,
1967).
An 850 g girl of 25 weeks gestation was intubated at birth
and placed in a ventilator. During surgical preparation for
umbilical artery catheterization, isopropyl alcohol was
poured over the umbilical stump. After the procedure was
completed it was noted that there were two areas of erythema
bilaterally on the flank, each approximately 2 x 5 cm. These
progressed to areas of second- and third-degree burns. The
burns were treated with an antibiotic ointment and a steroid
cream, and continued to heal over a period of 3 months
(Schick, 1981; Martindale, 1989).
Similar cases were reported by Weintraub (1982), giving
details of skin burns in premature infants. The isopropyl
alcohol had been used either for conduction on ECG or for
arterial catheterization. The 4 premature infants reported
were all less than 26 weeks gestational age and their birth
weight was less than 750 g; they had suffered severe
perinatal asphyxia, hypothermia and acidosis, and they all
developed severe respiratory distress insufficiency and died
within 48 hours despite mechanical ventilation and other
supportive measures. It is recommended that the skin be
dried after application of isopropyl alcohol.
A 45-year-old white man was comatose on admission to hospital
after apparently falling from a stepladder. He was intubated
and placed on a respirator. He was found to have an osmolal
gap of 304 mOsm/kg. Serum ethanol concentration was
determined by enzymatic alcohol dehydrogenase giving a
concentration of 1.86 g/L. The osmolal gap indicated that
there was another alcohol present, and that the enzymatic
alcohol determination was in error because of its lack of
specificity. A gas chromatographic analysis showed the
presence of ethanol, acetone and isopropanol. The authors
warn of the danger of using an enzymatic procedure for
ethanol, because the method is not specific for ethanol. The
patient recovered and was discharged 2 days later.
A 28-year-old man ingested 1 litre of rubbing alcohol over a
10 minute period, and was admitted to hospital 45 minutes
later. He was comatose and unresponsive. A tracheostomy was
performed and therapy with intravenous fluids was initiated.
He made little progress and so, 16 hours after admission,
haemodialysis was started. After 2 hours he was agitated,
alert and responsible, and haemodialysis was discontinued
(King, 1970).
Junco (1969), reported a case of a 35-year-old man who had
ingested 1 pint of rubbing alcohol. The patient was
inebriated confused and tremulous. His right arm was
swollen, erythematous, tender and painful on motion. This
swelling progressed, and by the 3rd day the entire limb was
swollen. A phlebogram demonstrated blockage of the axillary
vein. He received therapy over the next 25 days, being
treated for renal failure and thrombosis. The patient was
given phenytoin, supportive fluids, electrolytes, vitamins
and whole blood. The outcome is unknown.
12.ADDITIONAL INFORMATION
12.1 Specific preventive measures
Respiratory protection:
Use self-contained breathing apparatus (in fire).
Respirator selection: see 7.2.5.1
Gloves: rubber or plastic.
Protective clothing: suitable to prevent repeated or
prolonged skin contact, e.g., coveralls, etc.
Eyes: wear suitable eye protection.
Boots: rubber.
Note: remove clothing immediately if wet or contaminated to
avoid flammability hazard.
12.2 Other
No data available.
13. REFERENCES
ACGIH (1988). Threshold limit values and biological exposure
indices for 1988-89. American Government Conference of Industrial
Hygiene, Cincinnati, Ohio
Adelson L (1962). Fatal intoxication with isopropyl alcohol
(rubbing alcohol). Am J Clin Pathol 38: 144-151
Alexander CB, McBay AJ, Hudson RP (1982). Isopropanol and
isopropanol deaths - 10 years experience. J Forensic Sci
27: 541-548
Antonova VI, Salmina ZA (1978). The maximum permissable
concentration of isopropyl alcohol in water bodied with due regard
for its action on the gonads and the progeny. Gibiena i
Sanitariya (USSR) 1: 8-11
Arditi M et al (1987). Coma following the use of rubbing alcohol
for fever control. AJDC The Pediatric Forum 141 (March): 237-238
Buckley BM, Vale JA. Poisoning by alcohols and ethylene glycol.
Prescribers Journal 26(4): 110-115
Budavari S ed. (1996) The Merck Index: An Encyclopedia of
Chemicals, Drugs, and Biologicals. 12th ed. Merck & Co., Inc,
Whitehouse Station, NJ.
CDC (1988). Recommendations for occupational safety and health
standards. MMWR 37 (Suppl S-7): 1-29
Cahaplin MA (1949). Isopropyl alcohol poisoning with acute renal
insufficiency. J Maine Med Assoc 40: 288-290
CHEMINFO (1989). Canadian Centre for Occupational Health, 1989 -
05 - 5.
Chris (1985). Hazardous chemical data US Department of
Transportation, US Coast Guard, Washington
Coppock RW, Mostrom MS, Lillie LE (1988). The toxicology of
detergents, bleaches, antiseptics and disinfectants in small
animals. Vet Hum Toxicol 30: 463-473
Corbett J, Meier G (1968). Suicide attempted by rectal
administration of drug. J Am Med Assoc 206: 2320-2321
Daniel DR, Mcanalley BH, Garriott JC (1981). Isopropyl alcohol
metabolism after acute intoxication in humans. J Anal Toxicol 5:
110-112
Dua SL (1974). Peritoneal dialysis for isopropyl alcohol
poisoning. J Am Med Assoc 1974: 230-235
Ellenhorn MJ, Barceloux DG (1988). Medical toxicology - diagnosis
and treatment of human poisoning. London, Elsevier Science
Publishing
EPS (March 1984). Manual for spills of hazardous materials
Canada, Technical Services Branch, Environmental Protection
Service
Freirich AW, Cinque TW, Xanthaky G et al (1967). Haemodialysis for
isopropanol poisoning. New Engl J Med 277: 699-700
Gadsen RH, Mellette RR, Miller JC (1958). Scrap iron
intoxication. J Am Med Assoc 1958: 1168-1220
Garrison RF (1953). Acute poisoning from the use of isopropyl
alcohol in tepid sponging. J Am Med Assoc 1953: 317-318
Grant WM (1986). Toxicology of the eye. Springfield, Illinois,
Charles C Thomas
Hurst MR (1987). Airborne levels of isopropyl alcohol
disinfectant in a laminar-airflow hood. Am J Hosp Pharm
44: 2293-2295
IARC (1979). IARC monographs on the evaluation of the
carcinogenic risk of chemicals to humans. Lyon, France,
Supplement I, IARC, 36
ILO (1983). Encyclopaedia of Occupational Health and Safety,
p 109
Jatlow PI, Bailey DN (1980). Analytical toxicology In: Sonnewirt
AC, Jarett L Ed Gradwohls' Clinical Laboratory Methods and
Diagnosis, St Louis, The CV Mosby Company, pp 407-410
Juncos L, Taguchi JT (1968). Isopropyl alcohol poisoning. J Am
Med Assoc 204: 732-734
Kelner M, Bailey DN (1983). Isopropanol ingestion: interpretation
of blood concentrations and clinical findings. J Toxicol Clin
Toxicol 20(5): 497-507
King LH et al (1970). Haemodialysis for isopropyl alcohol
poisoning. J Am Med Assoc 211: 1855
Lacouture PG, Heldreth DD et al (1989). The generation of
acetonaemia/acetonuria following ingestion of a sub-toxic dose of
isopropyl alcohol. Am J Emerg Med 7: 38-40
Lacouture PG, Wason S, Abrams L et al (1983). Acute isopropyl
alcohol intoxication. Am J Med 75: 680-686
Laham S, Protvin M et al (1981). Studies on inhalation toxicity
of 2-propanol. Drug and Chemical Toxicology 3(4): 343-360
Lehman AJ, Chase HF (1944). The acute toxicity of isopropyl
alcohol. J Lab Clin Med 29: 561-567
Light FB, Marx GF (1969). The value of gastric aspiration in a
comatose child. Anesthesiology 31: 478-480
Mackison FW, Stricoff RS, Partridge LJ, eds (1981). Occupational
health guidelines for isopropyl alcohol. In: Occupational Health
Guidelines for Chemical Hazards (DHHS (NIOSH) Publication
No 81-123) Washingtron, DC, NIOSH/OSHA (1981)
Martinez TT et al (1986). A comparison of the absorption and
metabolism of isopropyl alcohol by oral, dermal and inhalation
routes. Vet Hum Toxicol 28(3): 233-236
Mccord WM, Switzer PK, Brill HH (1948). Isopropyl alcohol
intoxication. South Med J 41: 639-642
McFadden SW, Haddow JE (1969). Coma produced by tropical
application of isopropanol. Pediatrics 43: 622-623
McGrath RB (1989). Absorption of topical isopropyl alcohol in an
adult. Critical Care Medicine 1(11): 1233
Mecilaski MB, Depner TA (1982). Peritoneal dialysis for
isopropanol poisoning. West J Med 137: 322-325
Mendelson J, Wexler D et al (1957). A study of addiction to
nonethyl alcohols and other poisonous compounds. Q J Stud Alcohol
18: 561-580
Natowicz M, Donahue J et al (1985). Pharmacokinetic analysis of a
case of isopropanol intoxication. Clin Chem 31: 326-328
Nelson BK, Brightwell DS (1988). Teratogenicity of n-propanol and
isopropanol; administered at high concentration to rats. Fd Chem
Toxic, 26: 247-254
NIOSH (1985). Pocket guide to chemical hazards Cincinnati, Ohio,
National Institute for Occupational Health and Safety
NIOSH (1976). Criteria for a recommended standard: Occupational
exposure to isopropyl alcohol, Cincinnati, Ohio, National
Institute for Occupational Health and Safety, Document number:
76-142
Osborn LM, Rosales TO (1981). Corneal abrasion during alcohol
sponging. Clin Pediatr 20: 782
OSHA (1989). 29 CFR Part 1910: Air contaminants final rule
Occupational Safety and Health Administration Federal Register
1989; 54(12): 2332-2893
Parker KD, Fontan CR, Yee JL et al (1962). Gas chromatographic
determination of ethyl alcohol in blood for mediolegal purposes.
Anal Chem, 34: 1234
Parmeggiani L Ed (1983). International Labour Organisation:
Encyclopaedia of occupational health and safety, 34th ed, Vol I.
Geneva, IL Office, p 109
Poisindex Information System. Rumach BH, ed. Micromedex, Denver,
1990
Reynolds JEF, ed (1989). Martindale, The Extra Pharmacopoeia: 29th
edition London, The Pharmaceutical Press
Rosansky SJ (1982). Isopropyl alcohol poisoning treated with
haemodialysis: Kinetics of isopropyl alcohol and acetone removal.
J Toxicol Clin Toxicol 19(3): 265-271
Roseman MJ, Hill RM (1987). Aerobic responses of the cornea to
isopropyl alcohol, measured in vivo. Acta Opthalmologica
65: 306-312
Rowe VKI, McCollister CB (1982). Alcohols. In: Clayton GD,
Clayton FE, Eds. Patty's industrial hygiene and toxicology, 3rd
revised edition Vol 2C. Toxicology New York: Toronto, Ontario:
Wiley-Interscience, pp 4527-4708
RTECS (1989). 50359 Isopropyl alcohol, RTECS #NT805000 Registry
of toxic effects of chemical substances Washington, US Department
of Health and Human Sciences
Russo S et al (1986). Scald burns complicated by isopropyl
alcohol intoxication: A case of fatal child abuse. Am J For Med
Pathology, 7(1): 81-83
Sax NI (1982), ed. Dangerous properties of industrial materials
report, 2. New York, Van Nostrand Reinhold Co No 2, 50-52
Schick JB, Milstein JM (1981). Burn hazard of isopropyl alcohol
in the neonate. Pediatrics 68: 587-588
Scrimgeour EM (1980). Outbreak of methanol and isopropanol
poisoning in New Britain, Papua New Guinea. Med J Austr 7 July:
36-38
Senz EH, Goldfarb DL (1958). Coma in a child following use of
isopropyl alcohol in sponging. J Pediatr 53: 322-323
Shepard TH (2986). Catalog of teratogenic agents, 5th ed.
Baltimore and London, The John Hopkins University Press, p 329
Sittig, Marshall (1985). Handbook of toxic and hazardous
chemicals and carcinogens, 2nd edn Park Ridge, NJ, USA, Noyes
Publications, pp 532-534
Soukiasian SH et al (1988). A complication from alcohol-swabbed
tonometer tips. Am J Ophthalmology 105(4): 424-425
Teramoto K, Horiguchi S et al (1987). 2-propanol and acetone
elimination via exhaled air after 2-propanol administration to
rats. Osaka City Med J 33(2): 153-160
US Environmental Protection Agency (1979). Chemical Hazard
Information Profile: Isopropyl alcohol. Washington, DC (December
29, 1977), also revised edition (1979)
Vasiliades J et al (1978). Pitfalls of alcohol dehydrogenase
procedure for the emergency assay of alcohol. A case study of
isopropyl overdose. Clin Chem 24: 383-385
Visudhiphan P, Kaufman H (1971). Increased cerebrospinal fluid
protein following isopropyl alcohol intoxications. NY State J Med
71: 887-888
Wallgren H (1960). Relative intoxicating effects in rats of
ethyl, propyl, and butyl alcohols. Acta Pharmacol Toxicol
16: 217-222
Weil CS, Smyth HF, Nale TW (1952). Quest for industrial
carcinogen. Arch Ind Hyg Occup Med 5: 535-547
Webster HC et al (1985). Diagnostic clinical osmometry in the
unconscious infant. Critical Care Medicine 13(12): 1076-1077
Weintraub Z, Iancu TC (1982). Isopropyl alcohol burns (letter).
Pediatrics 69(4): 506
Wimer WW, Russel JA, Kaplan HL (1983). Alcohols toxicology, Park
Ridge, NJ: Noyes Data Corporation, pp 46-55
Wise IR (1969) Alcohol sponge baths (letter) New Engl J Med
280: 840.
14. AUTHOR(S), REVIEWER(S), DATE(S), COMPLETE ADDRESS(ES)
Authors: Dr Peter Hayes
Lecturer in Pharmaceutical
Technology/Manager Production Services
Department of Pharmacy
Faculty of Medicine
University of Otago
PO Box 913
Dunedin
New Zealand
Tel: 64-3-797272/740999 Ext 8347
Fax: 64-3-797618
Trudi P Martin, MPS
Senior Pharmacist
Pharmacy Production Unit
Dunedin Hospital
Private Bag
201 Gt King Street
Dunedin
New Zealand
Tel: 64-3-740999 Ext 8347
Fax: 64-3-797618
Date: February 1990
Reviewer: Dr Per Kulling
Swedish Poison Information Centre
Karolinska Hospital
Box 60500
10401 Stockholm
Sweden
Tel: 46-8-338765
Fax: 46-8-327584
Date: March 1990
Peer Review: Strasbourg, France, April 1990
Editor: Dr M. Ruse (October, 1997)