| 1.1 Substance|
| 1.2 Group|
| 1.3 Synonyms|
| 1.4 Identification numbers|
| 1.4.1 CAS|
| 1.4.2 Other numbers|
| 1.5 Brand names/Trade names|
| 1.6 Manufacturers, importers|
| 2.1 Main risks and target organs|
| 2.2 Summary of clinical effects|
| 2.3 Relevant laboratory analyses/sample collection|
| 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 Other 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 ENTRY|
| 5.1 Oral|
| 5.2 Inhalation|
| 5.3 Dermal|
| 5.4 Eye|
| 5.5 Parenteral|
| 5.6 Others|
| 6.1 Absorption by route of exposure|
| 6.2 Distribution by route of exposure|
| 6.3 Biological half-life by route of exposure|
| 6.4 Metabolism|
| 6.5 Elimination by route of exposure|
| 7.1 Mode of action|
| 7.2 Toxicity|
| 7.2.1 Human data|
| 184.108.40.206 Adults (volunteer and clinical case data)|
| 220.127.116.11 Children|
| 7.2.2 Relevant animal data|
| 7.2.3 Relevant in vitro data|
| 7.2.4 Workplace standards|
| 7.2.5 Acceptable daily intake (ADI) and other guideline levels|
| 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 Tests for active ingredient|
| 8.2.2 Tests for biological sample|
| 8.3 Other laboratory analyses|
| 8.3.1 Biochemical investigations|
| 8.3.2 Arterial blood gas analyses|
| 8.3.3 Haematological or Haemostasiological investigations|
| 8.3.4 Other relevant biomedical analyses|
| 8.4 Interpretation|
| 8.5 References (in section 13)|
|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 by:|
| 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 Systematic description of clinical effects|
| 9.4.1 Cardiovascular|
| 9.4.2 Respiratory|
| 9.4.3 Neurologic|
| 18.104.22.168 CNS|
| 22.214.171.124 Peripheral nervous system|
| 126.96.36.199 Autonomic nervous system|
| 188.8.131.52 Skeletal and smooth muscle|
| 9.4.4 Gastrointestinal|
| 9.4.5 Hepatic|
| 9.4.6 Urinary|
| 184.108.40.206 Renal|
| 220.127.116.11 Others|
| 9.4.7 Endocrine and reproductive systems|
| 9.4.8 Dermatologic|
| 9.4.9 Eye, ears, nose, throat: local effects|
| 9.4.10 Haematologic|
| 9.4.11 Immunologic|
| 9.4.12 Metabolic|
| 18.104.22.168 Acid-base disturbances|
| 22.214.171.124 Fluid and electrolyte disturbances|
| 126.96.36.199 Others|
| 9.4.13 Allergic reactions|
| 9.4.14 Other clinical effects|
| 9.4.15 Special risks: pregnancy, breastfeeding, enzyme deficiencies|
| 9.5 Others|
| 10.1 General principles|
| 10.2 Relevant laboratory analyses and other investigations|
| 10.2.1 Sample collection|
| 10.2.2 Biomedical analysis|
| 10.2.3 Toxicological analysis|
| 10.2.4 Other investigations|
| 10.3 Life-supportive procedures and symptomatic treatment|
| 10.4 Decontamination|
| 10.5 Elimination|
| 10.6 Antidote treatment|
| 10.6.1 Adults|
| 10.6.2 Children|
| 10.7 Management discussion: alternatives, controversies and research needs.|
|11. ILLUSTRATIVE CASES|
| 11.1 Case reports from the literature|
| 11.2 Internally extracted data on cases|
| 11.3 Internal cases|
|12. ADDITIONAL INFORMATION|
| 12.1 Availability of antidotes and antisera|
| 12.2 Specific preventive measures|
| 12.3 Other|
|14. AUTHOR(S), REVIEW(S), DATE, COMPLETE ADDRESSES|
1.4 Identification numbers
1.4.2 Other numbers
RTECS: MN 9275000
UN Number: 1208 (Ref: United Nations, 1989)
EC Number: 601-007-01-4
(Ref: Commission of the European Communities, 1987)
1.5 Brand names/Trade names
1.6 Manufacturers, importers
Importer: Produced by many companies and widely imported.
2.1 Main risks and target organs
The target organs are: central and peripheral nervous
system, respiratory system, heart, skin and eyes. Chemical
pneumonia usually occurs after ingestion and aspiration to
the lungs. CNS depression, convulsion, coma and death may
follow acute exposures to large concentrations.
Inhalation of hexane usually causes eye, nose, throat and
respiratory irritation, which are rapidly reversible, when
exposure is discontinued.
Symptoms are more severe if ingestion or inhalation are
associated with exposure to other hydrocarbons, which may
potentiate the effects.
Exogenous catecholamines may precipitate a fatal ventricular
arrhythmia in the sensitized myocardium.
Secondary risks: the products resulting from n-hexane
combustion (thermal decomposition) are CO and CO2.
2.2 Summary of clinical effects
Acute exposure to considerable concentrations of n-
hexane may cause: cough, wheezing, bloody frothy sputum,
headache, dizziness, tachycardia and fever.
Gastrointestinal symptoms occur on ingestion.
Exposure to high concentrations of n-hexane occurs usually by
inhalation, and causes the following symptoms:
- Respiratory system: slow and shallow respiration;
aspiration of n-hexane may cause pulmonary oedema and
- Cardiovascular system: tachycardia. Ventricular
dysrhythmia is rare.
- Central nervous systems: vertigo, giddiness, narcotic
syndrome. In heavy exposure unconsciousness,
convulsions and coma may occur.
- Peripheral nervous system: chronic exposure may produce
important peripheral neuropathy (motor-sensory) and CNS
- Gastrointestinal tract: nausea, vomiting and anorexia.
- Dermatitis and conjunctival irritation may occur.
2.3 Relevant laboratory analyses/sample collection
- n-Hexane and its metabolites may be found in urine but
only in recent exposures.
- Biomedical analysis should be requested according to the
clinical state of the patient (at least blood, urine,
ECG and chest x-ray in case of poisoning).
- A sample of the product involved should be available for
analysis if needed.
- After chronic exposure, functional and neurological
studies should also be requested:
- electrophysiological studies may show decreased motor
sensory nerve conduction with an increased distal
- electromyography may suggest neurogenic disease
- sural nerve biopsy (giant axonopathy and other
2.4 First-aid measures and management principles
In case of severe exposure by inhalation: move patient
to fresh air, support respiratory and cardiovascular
function. Endotracheal intubation, oxygen and assisted
ventilation may be necessary. Avoid use of catecholamines,
as cardiac dysrrhythmias are potential complications.
Gastric aspirations and lavage may be considered only in the
conscious patient and when ingestion has been superior to 2
to 3 mk/kg or when n-hexane is associated with a more toxic
substance. The unconscious patient should be pre-
In case of eye exposure, irrigation is required.
Skin decontamination should be done and contaminated clothes
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
n-Hexane is a straight-chain saturated hydrocarbon
obtained from certain petroleum fractions after various
thermal or catalytic cracking steps.
Commercial hexane may contain from 20 to 85% n-hexane and
varied amounts of hexane isomer (2-methylpentane, 3-
methylpentane, 2,3-dimenthylbutane), cyclopentane,
cyclohexane and small quantities of pentane and heptane
isomers, acetone, methyl ethyl ketone, dichloromethane and
trichloroethylene (ACGIH, 1989; Perbellini, et al., 1980,
1981). Trace amounts of benzene (0.05%) may be present
(Baker & Rickert, cited in IPCS draft, 1989).
3.2 Chemical structure
Molecular weight: 86.18
(C= 83.62% H= 16.38%)
3.3 Physical properties
Boiling point: 68.64 °C
Melting point: -95 °C
Flash point: -21.6 °C (closed
Autoignition temperature: 225 °C
Explosive limits(vol % in air): LEL: 1%, VEL: 7.5%
Critical temperature: 234 °C
Relative vapour density (air = 1) 2.97
Vapour pressure: 20.0 kPa at 25 °C
Evaporation rate: Rapid: specific
Refractive index n20: D 1.375
Saturation vapour concentration: 20% at 25 °C
Solubility in water: 9.5 mg/L at 25 °C;
Insoluble at °C
Solubility in other liquids: Miscible with
log Pow 25 °C = 3.6
Ionization potential: 10.18 eV
3.4 Other characteristics
Commercial hexane is a mixture of hexane isomers with
other hydrocarbons (e.g. cyclopentane, cyclohexane, pentane
Stable material: probably not sensitive to mechanical
Explosion data: vapour can be readily ignited by static
discharge. Liquid can accumulate static charge by flow or
Incompatibility: strong oxidizing agents (e.g., peroxides,
nitrates, perchlorates) can increase risk of fire and
Corrosivity to metal: not corrosive.
Hazardous decomposion product: none.
Hazardous polymerization: does not occur.
4. USES/HIGH RISK CIRCUMSTANCES OF POISONING
Main uses are as: rubber and adhesive solvent
(shoe factory); extraction of vegetable oil (soybean,
callous seed, flaxseed); pharmaceutical and cosmetic
It is also a cleaning agent for textiles, furniture
and leather products. N-hexane is also used for:
determination of refracture index of minerals, filling
for thermometers, denaturant for alcohols. May become
a substance of abuse to "sniffers".
4.2 High-risk circumstances of poisoning
Adults may be exposed in the workplace or in case of
"Glue-sniffing" or n-hexane sniffing may be a habit in
teenagers and young adults.
Accidental ingestion may occur in children.
4.3 Occupationally exposed populations
Laboratory workers which use the solvent for extraction
procedures, chemists and pharmacists may be exposed. The
factory, glues/adhesives industry workers or people involved
in printing and painting industry.
5. ROUTES OF ENTRY
Is the most frequent route of exposure.
Absorption may occur but is slow.
Absorption is minimal
No data available.
6.1 Absorption by route of exposure
The pharmacokinetics of n-hexane have been widely
investigated in the rat, but much less in known in
n-hexane is absorbed following inhalation, ingestion, or by
topical application to the skin. In human volunteers about
28% of inhaled n-hexane was taken up by the lungs (Court &
Milks, 1982). According to Mutti & Falzai (1984) alveolar
retention is about 25% of the inhaled dose of n-hexane and
the final absorption is 15% to 17% in relation to the total
The n-hexane molecule crosses easily the alveolar-capillary
membrane and enters the bloodstream.
Alveolar uptake was greater in obese individuals. Although
the alveolar uptake rate decreased during physical exercise,
the total uptake of n-hexane increased slightly as a result
of the higher lung ventilation rate. A net lung uptake of
112 mg/8 h was reported in workers exposed to 180 mg/m3 (51
ppm) n-hexane (Perbellini et al., 1985). Alveolar air
concentrations of n-hexane correlated with blood
concentrations in industrial workers exposed to commercial
hexane (Brugnone et al., 1984).
It is poorly absorbed from the gastrointestinal tract as are
other aliphatic compounds.
Dermal absorption is very slow. Although the percutaneous
absorption of n-hexane in man has not been well studied, this
route of exposure has been implicated in some case reports of
peripheral neuropathy (Nomiyana et al., 1973; Takahashi et
Peak blood levels occur in less than 1hour following
inhalation or percutaneous exposure (Graham et al.,
6.2 Distribution by route of exposure
n-hexane has great affinity for high lipid content
tissues and is rapidly metabolized to hydroxylated compounds
before being converted to 2,5-hexanedione.
The thermodynamic distribution coefficient of n-hexane
between the organism and the atmosphere was calculated to be
= 12 (Filser et al., 1987).
6.3 Biological half-life by route of exposure
Mutti et al., (1984) found that the respiratory
elimination of n-hexane in recently exposed workers was
biphasic. They reported that the median half-lives of the
fast and slow phases were 11 minutes and 99 minutes,
At the first step of the exudative metabolism by
cytochrome P-450, the carbons 1, 2 and 3 of n-hexane molecule
are hydroxylated and form hexanols in different proportions
(in all species of animals).
n-hexane is metabolized by the mixed function oxidase system
in the liver (Graham et al., 1987) forming alcohols which are
conjugated to glucuronic acid or converted to carbon monoxide
(Finkel, 1983). 1-Hexanol and 3-Hexonal are less toxic
metabolites. The former is oxidated to hexanoic acid, which
undergoes the usual lipid metabolism. 3-Hexanol, a minor
metabolite, has not been fully investigated (Boudene, 1988).
2-Hexanol is the most important metabolite.
According to experimental studies carried out in animals (Di
Vincenzo et al., 1976) and in men (Perbellini et al., 1980)
the metabolism of n-hexane and methyl-n-butyl ketone is
2-Hexanol is the main metabolite; it gives origin to 2,5-
hexanedione which is responsible for the neurological
Perbellini et al., (1980) reported that 2,5-hexanedione was
found in urine as the main n-hexane metabolite.
2-hexanol and 2,5-hexanedione were identified as n-hexane
metabolites also in animals (Di Vincenzo et al., 1976). The
last metabolite was found as a methyl-n-butylketone
metabolite in human serum (Di Vincenzo et al., 1978).
Perbellini et al., (1981) suggest that 2,5-hexanedione and,
secondly, 2-hexonal might be used as a reliable indicator for
monitoring environmental exposure to n-hexane, because these
metabolites are not detectable in urine of unexposed
Fedthe & Bolt (1987) detected 5,5-dihydroxy-2-hexanone as an
n-hexane metabolite. In relation to 2,5-hexanedions, the
amount detected was about 10 times higher in rat's urine and
4 times higher in the urine of humans. This metabolite may
be the result of a detoxification route (Fedtke & bolt,
Workers exposed to n-hexane for about 7 hours/day without
protective devices had the following metabolites in urine: 2-
hexanol, 2-methyl-2-pentanol, 3-methyl-2-pentanol,
cyclohexanol, cyclohexanone and thichloroethanol (each one:
0.1mg/L), gamma-valerolactone (0.25 mg/L) and 2,5-hexanedione
(0.4 mg/L) (Governa et al., 1987).
In humans exposed to concentrations of up to 200 ppm, steady
state blood levels were dose-dependent; accumulation occurred
in humans exposed to as little as 1 ppm.
6.5 Elimination by route of exposure
Filser et al., (1987) found that only 17% (in rat) and
20% (in man) of inhaled n-hexane was exhaled unchanged.
Mutti et al., (1984) found that approximately 10% of the
total uptake (mean: 166 mg) of unchanged n-hexane was
excreted from the lungs and about 3 mg/g creatinine of 2,5
hexanedione was detected in urine of workers exposed to 50
ppm in air, during the post-exposure period.
Although these authors and others (Iwata et al., 1983;
Perbillini et al., 1981) observed a close relation between
mean daily exposure and urinary excretion of 2,5-hexanedione,
for Mutti et al., (1984) it was not possible to measure this
metabolite at exposure levels lower than 50 mg/m3
(approximately 14 ppm) at the end of the working day.
Governa (1987) proposed that urinary concentrations of 2,5-
hexanedione can serve as a predictive measurement for early
detection of neurotoxic lesions at preclinical stages.
7.1 Mode of action
Damage to the respiratory tract and circulatory
disturbances are probably due to the same mechanism as for
The rapidity of onset and the extent of the chemical
pneumonitis is due to n-hexane's low viscosity, which allows
rapid spread over large areas of the lung. After the first
24 hours, the extent of pulmonary compromise is related to
severity: 30% or more of lung infiltration requires
approximately 2 to 4 weeks for resolution. Long-term
pulmonary effects have not been observed.
Hadjiivanova et al., (1987) reported important alterations in
the quantity and composition of pulmonary surfactant in rats
after short-term exposure (4260 ppm) of n-hexane.
The lungs of the rats exposed to hexane at different
concentrations showed a direct toxic effect on pneumocytes;
fatty degeneration, change of alveolar bodies of type II
pneumocytes and increased detachment of cells (Schnoy et al.,
The CNS and behavioural effects observed after exposures to
n-hexane are due to its lipid-containing cells. Neural
membrane modifications and reduction of the brain's oxidative
metabolism may explain the neurobehavioural changes and CNS
The peripheral neuropathy has been studied in detail and
numerous theories are postulated.
The nerve damage is basically an axonal swelling with
accumulation of neurofilaments along the nerve fibres. This
occurs initially on the proximal sides of the nodes of
Ranvier in distal parts of the fibres and progresses
proximally along the nerves and internodal regions.
The distal part of the nerve degenerates and myelin may
disintegrate around the swelling with the axon remaining
intact (producing secondary demyelination).
Another theory suggests that reduction of energy production
in the axon results in disruption of axonal transport,
alteration of protein structure, and inadequate proteolysis
of neurofilaments in the nerve terminal.
A chemical theory on the origin of damage was proposed by
Graham et al., (1985) who attributed the accumulation of
neurofilaments to protein crosslinking at the amine
7.2.1 Human data
188.8.131.52 Adults (volunteer and clinical case data)
Inhalation of 5000 ppm of n-hexane
for 10 minutes resulted in vertigo and
giddiness. Exposure to 2000 ppm for the same
length of time did not cause symptoms
(Patty, cited in IPCS draft, 1989).
Probably comparable to similar
compounds, but no particular data
7.2.2 Relevant animal data
Most of the relevant animal data refer to the
central and peripheral neurological damage, but some
other studies have been done. It is interesting to
remark that rabbits are not sensitive to n-hexane's
Male rats exposed repeatedly to high concentrations of
n-hexane in a pattern similar to human "sniffing"
(drug abuse) showed neurotoxic levels of 2,5-
hexanedione. Those levels increased after repeated
daily exposures, suggesting induction of liver
microsomal enzymes synthesizing 2,5-hexanedione from
hexane. The minimal sustained plasma levels which
induce neurotoxicity are less than 50 mg/mL in the rat
(Howd et al., 1982).
Nylen et al., (1989) observed a severe atrophy
involving the seminiferous tubules with loss of the
nerve growth factor in the immunoreactive germ cell
line of rats after 61 days of exposure to 1000 ppm of
n-hexane. Permanent testicular damage was found in
some animals which had a total loss of the germ cell
line lasting up to 14 months after the post-exposure
period. Simultaneous administration of n-hexane (1000
ppm) with toluene (1000 ppm) or xylene (1000 ppm) did
not cause germ cell line alterations or testicular
7.2.3 Relevant in vitro data
In vitro toxicity of n-hexane and 2,5-
hexanedione has been evaluated in the isolated
perfused rabbit heart (Raje, 1983). The force of
cardiac contraction was significantly reduced
following 1 hour of perfusion with 9.6 mg/L n-hexane
and with 0.35% v/v of 2,5-hexanedione.
Spinal neurone cell cultures exposed to n-hexane and
butanone (methyl-ethyl-ketone) developed the neural
swelling faster than when exposed only to n-hexane
(Veronesi et al., 1984).
7.2.4 Workplace standards
The US standard is the time-weighted average
(TWA) = 500 ppm although the ACGIH recommended not
more than 100 ppm. Industrial exposures for more than
6 months to 190 ppm have been associated with
polyneuropathy (Wang et al., 1986). Several values
OSHA/TWA (1989) 500 ppm, 1800 mg/m3
NIOSH/OSHA (1985) 100 ppm
510 ppm/15 min ceiling
ACGIH TLV (1989) 50 ppm, 180 mg/m3
other isomers 500 ppm,
ACGIH STEL (1989) other isomers 1000 ppm,
IDLH 5000 ppm
Conversion factor: 1 ppm n-hexane in air =
7.2.5 Acceptable daily intake (ADI) and other guideline
No data available.
Human data are not available. Animal tests are negative.
No data on teratological effects available, but a study
in pregnant rats showed n-hexane blood concentrations in the
fetus equal to that found in maternal blood (Court & Milks,
No data available
Simultaneous exposure with other solvents (especially
with ketones) increases n-hexane toxicity in humans and
animals. Methyl-n-butylketone is by itself responsible for
an identical neuropathy to that observed by n-hexane.
Toluene, butanone and n-hexane are common components of glue.
Butanone (methyl-ethyl-ketone = CH3-CO-C2H2) increases
n-hexane neurotoxicity both in humans and experimentally
(Veronesi et al., 1984).
Toluene seems to decrease n-hexane's neurotoxic effect, as it
may reduce the oxidative metabolism and increase the
generation of 2hexanol (Iwata et al., 1984).
2-Butanone (methyl-ethyl-ketone, MEK, CH3-CO-C2H2) increases
n-hexane neurotoxicity. Rats exposed to n-hexane (9000 ppm)
and butanone (1000 ppm) develop a more severe and early
polyneuropathy than rats exposed only to n-hexane (10 000
ppm) (Altenkirch et al., 1978). The biochemical mechanism is
not well understood.
2-Propanol (isopropanol, (CH3)2CHOH) enhances the induction
of n-hexane-metabolizing enzymes and increases the 2-hexanol
concentration in the liver and kidney (Zahlsen et al., 1984).
The effect of monoketones (ketone, a metabolite of
isopropanol or MEK) may be due to a transient decrease of the
energy generating process in the axon through a reversible
combination of the ketones with glyceraldehyde-3-phosphate
dehydrogenase or another enzyme involved in anaerobic
glycolysi (Boudene, 1988).
Methyl isobutyl ketone (MIBK, C6H120) mixed with n-hexane
significantly increased aniline hydroxylase and cytochrome P-
450 activity in the liver of exposed hens (Abou Donia et al.,
1985). The latter effect suggests that MIBK potentiates the
neurotoxic effect of n-hexane.
Carbon tetrachloride toxicity may be increased by ketone
metabolites of n-hexane (Charbonneaum et al., 1986).
The effect of sympathomimetic drugs combined with that of
acute n-hexane exposure may induce cardiac arrhythmias.
8. TOXICOLOGICAL AND OTHER ANALYSES
8.2 Toxicological Analytical Methods
8.2.1 Tests for active ingredient
8.2.2 Tests for biological sample
8.3 Other laboratory analyses
8.3.1 Biochemical investigations
8.3.2 Arterial blood gas analyses
8.3.3 Haematological or Haemostasiological investigations
8.3.4 Other relevant biomedical analyses
8.5 References (in section 13)
9. CLINICAL EFFECTS
9.1 Acute poisoning
Nausea, vomiting, and irritating of nasal and
oropharyngeal mucosa. Headache, CNS depression and
coma may develop. Severe chemical pneumonitis and
even pulmonary oedema may result from aspiration of n-
hexane into the lungs. Tachycardia and, rarely,
Brief exposure (10 minutes at 1500 ppm) can
cause upper respiratory irritation, nausea and
headache. Dizziness and drowsiness occur at 5000 ppm
and massive exposure may cause unconsciousness,
convulsions and death. Exposures below 500 ppm do not
usually induce CNS depression. Tachycardia and,
rarely, ventricular arrhythmia.
9.1.3 Skin exposure
Direct contact may cause irritation.
9.1.4 Eye contact
Eye irritation did not occur in volunteers
exposed to 500 ppm hexane vapour for 3 to 5 minutes
(Nelson, cited in IPCS draft, 1989), but vapour
exposure at higher concentrations can cause eye
irritation. Pain may occur if there is direct contact
with the liquid.
N-hexane splashed into the eye may cause corneal
opacification and lipolysis and loss of epithelial
9.1.5 Parenteral exposure
9.2 Chronic poisoning by:
No data available
Dizziness, weakness, weight loss, anaemia,
nervousness, pain in the limbs, peripheral numbness
and paraesthesia occur, preceding sensori-motor
ascending polyneuropathy. CNS symptoms including
dysarthria, motor incoordination and visual
difficulties may be masked by the
9.2.3 Skin exposure
Produces local erythema, oedema and burns.
Symptoms of systemic toxicity as for inhalation may
9.2.4 Eye contact
9.2.5 Parenteral exposure
No data available
No data available
9.3 Course, prognosis, cause of death
Course and prognosis
The main symptoms of exposure are neurological. After acute
inhalation, vertigo, drowsiness and fatigue occur immediately
and are followed by headache and CNS depression or coma if
exposure continues. Pulmonary and cardiac effects may occur
Causes of sudden death are the following:
- Anoxic death may be produced by either airway occlusion
or aspiration pneumonia "sniffers" who frequently use a
plastic bag over the head may suffocate.
- Respiratory depression caused by the solvent may involve
the cerebral respiratory centre leading to respiratory
- Cardiac arrhythmia may occur, due to the lowering of the
myocardial threshold to the arrhythmogenic effects of
catecholamines which is favoured by hypoxia.
- Sudden death may rarely occur in industrial accidents
associated with anaesthetic effects noted at high levels
of exposure in enclosed areas, but "sniffers" constitute
the main group at risk.
Peripheral neuropathy occurs after prolonged, repeated
The effects are first seen between several months to one year
after the beginning of long-term hexane exposure. Among glue
sniffers, the course may be subacute, heading to PNS
involvement within 2 months.
The first symptoms are symmetrical numbness and paesthesia in
the distal extremities, most notably in feet or hands.
Headache, anorexia and dizziness may precede or coincide with
neuropathy. Improvement of symptoms is noted after cessation
of exposure and mild cases may recover completely. The
disease may progress even for 1 to 4 months after
9.4 Systematic description of clinical effects
Tachycardia may occur. N-hexane may decrease
the myocardial threshold to the arrhythmogenic effects
of endogenous and exogenous catecholamines, causing
dysrrhythmias, predominantly ventricular arrhythmias
and, very rarely, sudden death due to ventricular
Aspiration may cause chemical pneumonia, cough,
wheezing and pulmonary irritation may progress to
pulmonary oedema with hypoxia, bloody sputum, and
fever. Slow and shallow respiration may be noted.
After exposure to high concentrations, respiratory
arrest might occur.
Acute exposure to n-hexane may cause
CNS depression, coma and convulsions. Acute
CNS effects may be due to hypoxia following
aspiration and/or directly result from
inhalation or ingestion.
Neuropsychiatric disability may follow
chronic inhalation. Axons are affected after
chronic inhalation exposure, but symptoms may
be obscured by the polyneuritis. During the
recovery phase of the polyneuritis,
dysarthria, blurred vision, ataxia and
spasticity become evident.
Cranial nerve neuropathy has been reported by
Yamamura from a Japanese survey where 33 of
93 exposed workers presented cranial nerve
paralysis (Lolin, 1989). Optic atrophy has
been reported in a few cases.
184.108.40.206 Peripheral nervous system
Sensory or sensorimotor
polyneuropathy represents the main effect
after chronic exposure and is characterized
by insidious onset. Large and long axons are
affected early (the sciatic nerve is
especially vulnerable). Pain in the limbs
weakness and muscle wasting occur, as well as
sensory loss in a "stocking and glove"
pattern. The conduction velocity is
The distribution is symmetrical and initially
involves only hands and feet. In more severe
cases, weakness and weightloss are seen. The
patient may have abdominal pain, cramps in
the legs and loss of ankle reflexes. Hand
muscular weakness may make seizing objects or
pinching difficult. Pure motor neuropathy is
unusual. Loss of pinprick and touch
sensation is limited to hands and feet. In
some cases, weakness and atrophy increase and
progress to involve the proximal muscle
Axonal regeneration may take months or years.
Residual disability can occur (Cavanagh,
1979; Schaumburg and Spencer,
220.127.116.11 Autonomic nervous system
Glue sniffers have shown autonomic
disturbances such as hyperhydrosis of the
hands and feet, which may be followed by
18.104.22.168 Skeletal and smooth muscle
Muscular atrophy may appear
subsequently to poly-neuropathy.
Nausea, vomiting, abdominal pain and diarrhoea
occur after ingestion. Symptoms resulting from
ingestion generally develop within 6 hours of
Fatty changes in the liver may occur after
Protenuria in the exposed workers in
the shoe industry (Caudarella et al., 1981)
were significantly higher when compared to
control group, but no effects on serum
creatinine levels were detected.
No data available
9.4.7 Endocrine and reproductive systems
No data available in humans.
Serious lesions, some of them causing sterility, were
reported in rats exposed to n-hexane (Nylen et al.,
1989; De Martino et al., 1987).
Irritation of skin, erythema, oedema and
9.4.9 Eye, ears, nose, throat: local effects
Eye irritation did not occur in volunteers
exposed to 1760 mg/m3 (500 ppm) of hexane vapour for
3-5 minutes (Nelson et al., 1943). Higher
concentrations would produce irritation.
Leucocytosis is observed. Aplastic anaemia
may occur in chronic exposure to n-hexane contaminated
No data available.
22.214.171.124 Acid-base disturbances
No data available.
126.96.36.199 Fluid and electrolyte disturbances
No data available
No data available
9.4.13 Allergic reactions
A skin test done in 25 subjects with undiluted
n-hexane applied (25% solution) was negative (Kligman,
cited in IPCS draft, 1989).
Prolonged occlusive skin contact for 1 to 5 hours with
liquid n-hexane caused erythema and, after 5 hours,
blistering (Oettel, cited by IPCS draft, 1989). In
another study, 0.l mL of n-hexane was rubbed into skin
daily for 18 days and neither erythema nor oedema were
observed (Wahlberg, 1984a, 1984b).
9.4.14 Other clinical effects
No data available.
9.4.15 Special risks: pregnancy, breastfeeding, enzyme
No data available
No data available.
10.1 General principles
In cases of skin and/or eye contact only
decontamination and clinical observation are needed, although
in some cases, ophthalmological advice is required.
If important amounts have been ingested and/or inhaled:
maintain open airway, provide respiratory assistance if
necessary. Oxygen is indicated. Treatment is symptomatic
and supportive. There is no antidote.
Do not induce vomiting.
Avoid the use of catecholamines.
10.2 Relevant laboratory analyses and other investigations
10.2.1 Sample collection
Collect urine or blood samples, in a tightly
closed receptacle (n-hexane is very
10.2.2 Biomedical analysis
- Arterial blood gases should be monitored in case
of respiratory symptoms.
- Complete blood count.
- ECG monitoring.
- Chest x-rays should be done on admission and
repeated according to the clinical situation.
- Measure blood glucose (Hypoglycemia has been
- Serum electrolytes determination and renal and
liver function tests may be needed.
- Electrodiagnostic after chronic exposure studies
include: electromyography, nerve conduction
velocity (NCV, which shows progressive slowing),
visual evoked potentials and electroretinograms
(may indicate axonal degeneration in the CNS
- Nerve-muscle biopsy (sural) may be useful in
10.2.3 Toxicological analysis
n-hexane measured in urine of human exposure.
Imbriani et al., (cited by Boudene, 1988) found a good
correlation between workplace air levels of n-hexane
and urinary concentration in exposed workers.
Cu = 9.0669 x Ci + 0.8396
Cu(œg/L) = urinary concentration of n-hexane
Ci(mg/m3) = workplace air level
n-hexane metabolites in urine.
10.2.4 Other investigations
Berthold CM (cited by Lolin Y, 1989) suggests
that electron-microscopic examination of sural nerve
biopsy materials should be used for detecting sub-
Neuro-behavioural studies may be of interest.
10.3 Life-supportive procedures and symptomatic treatment
Initial management depends on the severity of the
illness: the respiratory function is of main concern after n-
hexane aspiration on inhalation.
A clear airway (naso or orotracheal intubation) and
artificial respiration with oxygen should be provided in all
patients with respiratory symptoms. Arterial blood gases
should be monitored.
Respiratory tract symptoms are treated symptomatically.
Oxygen is given whenever respiratory symptoms occure and
broncholytic treatment may be useful. Arterial and other
blood gases must be repeatedly monitored. If signs of
respiratory insufficiency appear, mechanical ventilation
shall be considered at an early stage. Positive and
expiratory pressure has been claimed to be of value in these
In case of pulmonary oedema corticosteroides may be
indicated. Secondary bacterial infection is treated with
CNS-depression, coma and convulsions are treated
symptomaticly, including ensurance of clear airway, assisted
ventilation and administration of anticonvulsive agents.
Arrythmias are treated in accordance with general principles.
Any metabolic disturbances are corrected.
Endogenous catecholamines should be avoided, and if used,
they should be given in low dosage and under close
Continuous positive airway pressure (CPAP) or positive end-
expiratory pressure (PEEP) should be used when indicated.
For treatment of pulmonary oedema corticosteroids are
indicated. Preventive treatment of chemical pneumonia with
antibiotics may be controversial.
Exogenous catecholamines should be avoided, as they may
precipitate an ventricular dysrhythmia. They should only be
used in the lower dosage ranges with careful ECG monitoring
for cardiac resuscitation.
The rest of the treatment is supportive, and a close
monitoring of vital signs is required.
In case of eye contact: flush immediately with room-
temperature running water for at least 15 minutes.
Skin contact: remove clothing, wash the skin thoroughly with
mild soapy water.
Ingestion: rinse mouth copiously. No decontamination is
indicated if the n-hexane ingested does not contain relevant
concentration of other toxic compounds. If ingested n-hexane
is contaminated with significant amounts of halogenated
hydrocarbons) the substances must be removed from the
gastrointestinal tract. Gastric lavage should be done in a
comatose patient only after intubation with a cuffed only
Activated charcoal does not effectively absorb n-hexane and
its presence in the stomach may induce vomiting and increase
the risk of aspiration.
No data available
10.6 Antidote treatment
No antidote available
No antidote available.
10.7 Management discussion: alternatives, controversies and
- Induction of vomiting or gastric lavage are
contraindicated, except when ingestion of n-hexane is over
2 to 3 mL/kg or n-hexane contains another more toxic
chemical (e.g. pesticide). In this case, extreme caution
should be taken to avoid aspiration, since small amounts
of n-hexane will involve severe chemical pneumonitis
(Ellenhorn & Barceloux, 1988).
- Mild observations of hepatic aminotransferase levels have
been reported in exposed workers (Ellenhorn & Barceloux,
- Dose-response relationship of n-hexane is still unclear.
Although peripheral neuropathy has been fully documented
effects on the CNS need further studies.
- Genotoxic and teratogenic studies are still insufficient
to draw valid conclusions.
- Use of corticosteroids may in chemical pneumonia be
11. ILLUSTRATIVE CASES
11.1 Case reports from the literature
The most significant report from literature are those
describing the studies of occupationally exposed populations:
Japanese sandal workers, Italian shoe industry, Taiwan press-
proofing workers, tungsten carbide mills and extraction
A review of the n-hexane induced polyneuropathy in industrial
workers in Japan is given by Takeuchi (1993). It is suggested
that urinary levels of 2,5-hexanedione could serve as an
indicator for monitoring exposure to n-hexane (Takeuchi,
Neurological symptoms in the limbs were shown to be
significantly increased in metal can manufacturing workers
compared to unexposed workers (Bachmann et al., 1993).
In Italy twenty workers exposed over a long period to n-
Hexane were shown not to have significant neurological
anomalies. However, the amplitude of the sensory nerve action
potentials (SNAP), recorded from the sural, median and ulnar
nerves, were decreased compared to control groups (Pastore et
Chemotaxis, measured with human polymorphonuclear leukocytes,
was impaired in apparently healthy shoe workers exposed to n-
hexane (Governa et al., 1994).
Primary axonal polyneuropathy and secondary segmental
demyelination was observed in 27 Turkish males exposed
occupationally to n-hexane (Oge et al., 1994).
Fifteen workers occupationally exposed to n-hexane for 5 to
21 years were studied with evoked potentials and averaged
extraocular retinograms. Compared to a non-exposed group of
10 controls, they had changes indicating cerebral dysfunction
(Seppalainen et al., 1979).
A report on 3 women who suffered motor polyneuropathy
following occupational exposure to a glue containing 80.4% of
n-hexane describe in detail the nerve changes. Myelin
sheaths and axons of large diameter fibres showed
polymorphous changes and muscles showed degeneration atrophy
and degenerative changes, with lymphocytic infiltrates and
phagocytosis (Scelsi et al., 1980).
Sanagi (cited in IPCS draft, 1989) investigated the effect of
exposure to n-hexane in a factory producing a tungsten
carbide ally where the materials were mixed with n-hexane and
acetone by ball mills. Fourteen workers (concurrently
exposed) aged less than 50 years with an exposure duration of
1 to12 years (mean: 6.2 years) were studied and another group
consisting of 5 workers (previously exposed) aged less than
50 years with exposure durations of 1 to16 years (mean: 5.2
years). The mean 8 hour time average concentration of n-
hexane over a period of 2 years was 204 mg/m3 (58 ppm), and
the average concentration for acetone was 22 to 69 ppm.
Headaches, hyperaesthesia in the limbs, and muscle weakness
were reported more often by the exposed group. Three exposed
workers complained of paraesthesias. There was a slightly
higher prevalence of diminished bicipital and patellar deep
tendon reflexes in the exposed group. There were significant
effects on muscle strength and vibration sensation.
Electrophysiological studies showed no signs of
neuropathology in the workers, but in the concurrently
exposed workers, conducting velocities in the posterior
tibial nerve were significantly reduced.
Huang & Chu (1989) studied evoked potentials, somatosensory
brianstem auditory, and pattern-reversal visual evoked
potentials (SEP, BAEP,, and PVEP) in 5 patients with chronic
n-hexane polyneuropathy. The results obtained were: in SEPs,
the median central conducting (N13 to N20) was normal but the
tibial central conduction (N22 to P40) was delayed. The
central conducting time (I to V interval) of the BAEP was
also prolonged. However, the P100 latency of the PVEP was
normal. These data indicate that the spinal cord and
brainstem are primarily affected in chronic n-hexane
11.2 Internally extracted data on cases
11.3 Internal cases
(to be completed by PC)
12. ADDITIONAL INFORMATION
12.1 Availability of antidotes and antisera
12.2 Specific preventive measures
Limiting exposure, training and education of workers
are the most important methods to prevent n-hexne effects in
the occupational health context.
Engineering controls are required. Methods include
mechanical ventilation (dilution and local exhaust). A non-
sparking grounded ventilation system separate from exhaust
ventilation systems should be used.
Personal protective equipment and respiratory protection
should be available for emergencies, for work to be done in
poorly ventilated areas or for specific maintenance
operations. Protective gloves resist n-hexane, but mixtures
with other solvents (e.g. MEK) may allow penetration of
gloves and other protective clothing.
Disposal: burn in a chemical incinerator equipped with an
after burner and scrubber. Extra care in igniting is
necessary as this material is highly flammable.
No data available
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14. AUTHOR(S), REVIEW(S), DATE, COMPLETE ADDRESSES
Author: Hilda Triador
CIAT, Piso 7
Hospital de Clinicas
Date: February 1990
Peer reivew: Strasbourg, France, May 1990
Newcastle-upon-Tyne, United Kingdom, January
IPCS Review: November 1990.
Finalised: IPCS, April, 1997