Styrene
STYRENE
International Programme on Chemical Safety
Poisons Information Monograph 509
Chemical
1. NAME
1.1 Substance
Styrene
1.2 Group
Aromatic hydrocarbons
1.3 Synonyms
Ethenylbenzene; styrol;
styrolene; cinnamene;
cinnamenol; cinnamol;
phenylethylene; vinylbenzene;
monomeric styrene; styrene monomer;
styron; styropor;
1.4 Identification numbers
1.4.1 CAS number
100-42-5
1.4.2 Other numbers
79637-11-9 (Other CAS)
2055 (PIN-UN Number)
WL3675000 (RTECS Number)
2. SUMMARY
2.1 Main risks and target organs
The principal acute hazards from human exposure to
styrene are central nervous system depression and irritation
of the skin, eyes, and upper respiratory tract. The compound
is volatile and is readily absorbed following inhalation or
dermal contact.
Chronic exposure may produce skin, eye changes, and liver
dysfunction. As birth defects have been noted, expectant
mothers and women with ovulation and menstrual disorders
should not work in conditions exposing them to styrene.
Neurobehavioral abnormalities have been related to chronic
exposure to styrene.
Target organs are: central nervous system; skin; respiratory
tract; eyes; liver.
2.2 Summary of clinical effects
Irritation of skin and mucous membranes: eye and nasal
irritation occurred after exposure to 300 ppm of styrene.
Skin contact resulted in acute and chronic dermatitis. After
inhalation of large doses patients experienced chest burning,
wheezing, dyspnea, increased nasal secretion, metallic taste,
and vertigo. Headache, nausea, incoordination, muscular
weakness, anorexia, depression, feeling of drunkeness result
from CNS action. The clinical picture is also called "styrene
sickness".
2.3 Diagnosis
Clinical features: Irritation of skin and mucous
membranes. Nasal an eye irritation. Corneal burns after
direct contact. Headache, fatigue, weakness, depression,
feeling of drunkeness. Chest burning, wheezing, dyspnea.
The exposure to styrene may be detected by determining the
urinary styrene etabolites.
2.4 First-aid measures and management principles
Remove the victim from the area of exposure. Discard
contaminated clothing. Irrigate exposed eyes with copious
amounts of water or saline. Wash skin with soap and copious
amounts of water.
Maintain a clear airway.
Support ventilation.
If breathing has stopped begin artificial respiration.
Administer oxygen for inhalation. In case of ingestion do
not induce vomiting.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
Isolated from storax, a balsam obtained from the trunk
of Liquidambar orientalis Mill., or L. styraciflua L..
Synthesized from benzene and ethylene.
3.2 Chemical structure
Chemical name: Styrene
Molecular weight: 104.14
Molecular formula: C8-H8
Structural formula: C6H5- C=CH2
Relative molecular mass: C 92,26%; H 7,74%
3.3 Physical properties
3.3.1 Colour
Clear, colourless to yellowish liquid.
3.3.2 State/form
Volatile liquid.
3.3.3 Description
Styrene is flammable, very refractive, with a
strong pungent but tolerable and quickly disappearing
odour at ambient air levels of 100 ppm. The odour
detection limit is around 5 ppm.
Boiling point: 145.2°C
Melting point: -30.6°C
Flash point: 31°C (87 F)
Autoignition temperature: 490°C
Relative density: 0.9059 at 25°C
Vapour pressure: 10 mm at 35°C
Saturation vapour concentration: 6600 ppm at 20°C
Solubility:
practically insoluble in water;
soluble in alcohol, ether, methanol, acetone and
carbon disulfide.
Explosive limits in air: 1.1 to 6.1% by volume in air.
3.4 Hazardous characteristics
The technical material is usually 99.6% pure, and
normally contains a very small amount (12 to 15 ppm) of
tertiary butyl catechol as a polymerisation inhibitor. When
heated to 200°C it is converted into the polymer,
polystyrene. Styrene can react violently with oxidizing
agents such as peroxides, strong acids, and chlorates. Fires
involving styrene may release dangerous by-products specially
carbon dioxiode and carbon monoxide. Fires must be
extinguished with carbon dioxide or dry chemical (Budavari,
1989; Heiselman and Cannon, 1990).
4. USES
4.1 Uses
4.1.1 Uses
4.1.2 Description
Several millions of tons of styrene are used
world-wide in the production of polystyrene,
styrene-butadiene co-polymer for synthetic rubber,
styrene-acrylonitrile polymer,
acrylonitrile-butadiene-styrene copolymer, polyester
resins for reinforced fiberglass products, paints,
coatings, in the manufacture of reinforced plastics,
and as insulators (O'Donoghue, 1985; Budavari,
1989).
4.2 High risk circumstance of poisoning
The most likely circumstance of poisoning consists of
the inhalation of vapours of styrene, although skin exposure
may occur. Pungent odour usually gives adequate warning but
the odour disappears rapidly.
4.3 Occupationally exposed populations
Occupational exposure to styrene occurs during monomer
manufacture, transportation, and polymerization. Styrene is
absorbed through the skin and the respiratory tract.
Ingestion is not a significant occupational hazard.
"Styrene sickness" in industry describes a clinical picture
after heavy exposure to styrene and other solvents
(O'Donoghue, 1985).
In occupational settings, exposure to styrene varies
considerably, depending on the operations concerned. In some
processes, styrene concentrations are less than 21 mg/m3,
although occasional values of 210 mg/m3 (1 ppm=4.26 _g/m3) or
more have been reported. During styrene-butadiene rubber
production, styrene concentrations have been re-ported to
range from 42 to 840 mg/m3. In all industrial applications
high levels of exposure may occur during clean-up and
maintenance procedures (IPCS, 1983).
5. ROUTES OF ENTRY
5.1 Oral
Liquid styrene is absorbed through the digestive system,
but human cases have not been described.
5.2 Inhalation
Inhalation of vapours of styrene is a major route of
entry. Inhalation is responsible for the majority of
poisoning cases.
5.3 Dermal
Both liquid an vapour forms are absorbed through the skin.
5.4 Eye
Styrene may produce eye irritation.
5.5 Parenteral
Not relevant
5.6 Others
Not relevant
6. KINETICS
6.1 Absorption by route of exposure
Oral absorption: human information is not available, but
animal toxicity data indicate that effects after ingestion
may be similar to those described for inhalation.
Percutaneous absorption of styrene vapours is very small
(only about 2%). Absorption of liquid styrene through skin is
9 to 15 mg/cm2/h. Styrene vapours are absorbed through the
lungs. (Proctor et al, 1988). It has been shown that 59 to
88% of the dose is absorbed following inhalation of styrene
at atmospheric concentrations in the range 20 to 200 ppm but
it is greater at increased ventilations during exercise
(Fielder and Lowing, 1981).
6.2 Distribution by route of exposure
Absorbed styrene is rapidly and extensively distributed
throughout the body tissues (Fielder and Lowing, 1981).
Experimentally, styrene tissue distribution after oral acute
doses presented highest concentrations in fat, brain,kidney,
liver, and pancreas. On repeated exposure styrene gradually
accumulated in the adipose tissue but not in other tissues
(IARC, 1979).
6.3 Biological half-life by route of exposure
It was reported that the biological half-life of
styrene, as measured by the appearance of metabolites in
urine (phenylglyoxylic acid and mandelic acid), was between
eight and nine hours in humans (Bond, 1989). The styrene
concentration in blood is found to decay in a biexponential
fashion typical of a two compartment kinetics model. Blood is
proposed as the first component and tissues including adipose
tissue as the second "slow" compartment. The half-life for
styrene in blood in the initial phase is 0.58 hours and in
the terminal phase 13 hours (Guillemin and Bauer, 1979;
Harkonen et al, 1978; Ramsey and Anderson, 1984; IPCS,
1983).Studies of styrene in inspired air of volunteer
subjects estimated the half-life of concentration in adipose
tissue is two to four days (Engstrom et al, 1978).
6.4 Metabolism
The majority of the absorbed material (about 90%) in man
is metabolised in the liver by oxidation of the vinyl side
group to styrene oxide. Styrene oxide is the active
metabolite (Baselt and Cravey, 1990). The resulting major
metabolites which are excreted are mandelic acid (60-80%) and
phenylglyoxylic acid (about 30%). Only very small quantities
of hippuric acid are produced (Fielder and Lowing,
1981).
6.5 Elimination by route of exposure
The main metabolites, mandelic acid and phenylglyoxylic
acid, are excreted in the urine. Hippuric acid and
4-vinylphenol are minor metabolites of styrene. About 1 to 2%
of a dose is exhaled unchanged (Baselt and Cravey,1990).
Breath styrene concentrations represent about 25% of the
corresponding air styrene concentration during constant
exposure (Stewart and al, 1968).
7. TOXICOLOGY
7.1 Mode of Action
The exact mechanism of action is unknown.
In acute exposures styrene, as other aromatic hydrocarbons,
induces local irritation and central nervous system
depression. These effects may be transient or persistent ones
in the CNS - transient effects appear to be mediated directly
by the action within the CNS and these transient changes in
function are proportional to the measured concentrations
within the brain in animal experiments. Persistent
neurological effects have been associated with
histopathological changes in neural tissue (Baker et al,
1985).
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
Humans exposed at 376 ppm
experienced rapid onset of eye and nasal
irritation. The level defined as immediately
dangerous to life or health is 5000 ppm
(Heiselman and Cannon, 1990). Inhalation
Lowest Lethal Concentration= 10000 ppm/30
min. Inhalation Lowest Toxic Concentration =
600 ppm (Sax & Lewis, 1989).
7.2.1.2 Children
No data available.
7.2.2 Relevant animal data
Oral, rat LD50:5000 mg/kg Inhalation, rat
LC50:24 mg/m3/4 h Intraperitoneal, rat LD50:1220 mg/kg
Oral, mouse LD50: 316 mg/kg Inhalation, mouse
LC50:2160 mg/m3/2h Intraperitoneal mouse LD50:660
mg/kg (Sax and Lewis, 1989)
7.2.3 Relevant in-vitro data
Mutagenic test in-vitro present contradictory
conclusions, due to metabolic partial activation of
the compound to styrene 7,8-oxide, that is an
alkylating agent and mutagenic in many in-vitro test
systems (IPCS, 1983). Styrene vapour in hepatocyte
monolayers is not acutely toxic to the cells, even at
low oxygen tensions (Costa and Trudell, 1990). In an
in-vitro study on cytoskeletal apparatus, styrene
induced changes in the cytoskeletal elements (Malorni
et al, 1988). Styrene is mutagenic in animal and human
cells tests in vitro (IARC,1987).
7.2.4 Workplace standards
Skin:
-TLV-TWA (Threshold Limit Values - Time Weighted
Average): 50 ppm (213 mg/m3)
-TLV - STEL (Threshold Limit Values - Short-Term
Exposure Limit): 100 pmm (426 mg/m3) (ACGIH,
1992)
7.2.5 Acceptable daily intake (ADI)
Adopted biological exposure determinants:
Monitoring mandelic acid and phenylglyoxylic acid in
urine. Postshift urine samples of mandelic acid should
not exceed 800 mg per gram of creatinine. Prior to
next shift accepted value is 300 mg of mandelic acid
per gram of creatinine. Phenylglyoxylic acid in urine
in end of shift is 240 mg per gram of creatinine and
prior to next shift is 100 mg per gram of creatinine.
Accepted level of styrene in venous blood at the end
of shift is 0.55 mg/L and prior to next shift is 0.02
mg/L (ACGIH, 1992).
Evaluation of EEG in exposed individuals (Heiselmann &
Cannon, 1990; Gosselin et al, 1984).
7.3 Carcinogenicity
Studies on styrene exposure in man are inconclusive.
Some evidence suggests that occurrence of leukemia and
lymphoid tumors may be linked to styrene. IARC evaluation of
carcinogenicity of styrene to humans is: inadequate evidence.
Overall IARC evaluation of carcinogenic risk: Group 2B
(possibly carcinogenic to humans (IARC,1987).
7.4 Teratogenicity
Styrene was not proven to be teratogenic in animals. Two
cases of children with central nervous system defects were
reported but the significance is not clear due to exposure of
the women during the pregnancy to other chemicals (Holmberg,
1977).
7.5 Mutagenicity
DNA damage was observed in blood cells of workers
exposed to styrene. Styrene is mutagenic in animal tests (in
vivo) and animal and human cells test in vitro
(IARC,1987).
7.6 Interactions
There is a synergistic action between styrene and other
volatile solvents (O'Donoghue,1985).
8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
8.1 Material sampling plan
8.1.1 Sampling and specimen collection
8.1.1.1 Toxicological analyses
8.1.1.2 Biomedical analyses
8.1.1.3 Arterial blood gas analysis
8.1.1.4 Haematological analyses
8.1.1.5 Other (unspecified) analyses
8.1.2 Storage of laboratory samples and specimens
8.1.2.1 Toxicological analyses
8.1.2.2 Biomedical analyses
8.1.2.3 Arterial blood gas analysis
8.1.2.4 Haematological analyses
8.1.2.5 Other (unspecified) analyses
8.1.3 Transport of laboratory samples and specimens
8.1.3.1 Toxicological analyses
8.1.3.2 Biomedical analyses
8.1.3.3 Arterial blood gas analysis
8.1.3.4 Haematological analyses
8.1.3.5 Other (unspecified) analyses
8.2 Toxicological Analyses and Their Interpretation
8.2.1 Tests on toxic ingredient(s) of material
8.2.1.1 Simple Qualitative Test(s)
8.2.1.2 Advanced Qualitative Confirmation Test(s)
8.2.1.3 Simple Quantitative Method(s)
8.2.1.4 Advanced Quantitative Method(s)
8.2.2 Tests for biological specimens
8.2.2.1 Simple Qualitative Test(s)
8.2.2.2 Advanced Qualitative Confirmation Test(s)
8.2.2.3 Simple Quantitative Method(s)
8.2.2.4 Advanced Quantitative Method(s)
8.2.2.5 Other Dedicated Method(s)
8.2.3 Interpretation of toxicological analyses
8.3 Biomedical investigations and their interpretation
8.3.1 Biochemical analysis
8.3.1.1 Blood, plasma or serum
8.3.1.2 Urine
8.3.1.3 Other fluids
8.3.2 Arterial blood gas analyses
8.3.3 Haematological analyses
8.3.4 Interpretation of biomedical investigations
8.4 Other biomedical (diagnostic) investigations and their
interpretation
8.5 Overall Interpretation of all toxicological analyses and
toxicological investigations
Sample collection
Complete blood count. Liver function tests.Urinalysis.
Determination of mandelic and phenylglyoxylic acid in urine.
Serial measurements of potassium, calcium, magnesium, and
phosphate should be performed. Liver and kidney function
tests. Chest roentgenogram.
Toxicological analysis
Other investigations
8.6 References
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
Acute poisoning after ingestion has not been
described in humans. On the basis of the animals
studies nausea, vomitos and diarrhoea might be
expected.
9.1.2 Inhalation
Inhalation is one of the most important routes
of styrene poisoning. Described symptoms are:
conjunctivitis, throat irritation, increased nasal
secretion, metallic taste, drowsines, vertigo, ataxia,
nystagmus, loss of coordination and memory (Ellenhorn
and Barceloux, 1988).
9.1.3 Skin exposure
Skin contact may produce skin irritation,
burns, and acute dermatitis. One single prolonged
exposure may not result in absorption of harmful
amounts (Baselt,1990).
9.1.4 Eye contact
Conjunctival irritation was found in 22% of a
group of 345 workers and correlated with intensity of
exposure to styrene. Splash contact has resulted in
moderate hyperaemia of the conjunctiva and slight
injury of the corneal epithelium (Grant,
1986).
9.1.5 Parenteral exposure
Not described.
9.1.6 Other
Not relevant.
9.2 Chronic poisoning
9.2.1 Ingestion
Chronic poisoning by ingestion has not been
described.
9.2.2 Inhalation
Some workers exposed to styrene showed symptoms
of CNS depression (decreased coordination and
concentration) and abnormal EEG patterns (O'Donoghue
1985). As to the respiratory system studies are not
conclusive. Forced expiration volume in one second
(FEV1) was significantly decreased in 20% of a group
of workers exposed to styrene (Stewart et al, 1968).
"Styrene sickness" in industry describes a clinical
picture after heavy exposure to styrene and other
solvents (O'Donoghue, 1985).
9.2.3 Skin exposure
Skin contact may produce persisting itching and
erythematous papular dermatitis (Browning, 1965;
Heiselman & Cannon, 1990)
9.2.4 Eye contact
Chronic exposure was not related to significant
eye disease. (Grant, 1986). Toxic retrobulbar
neuritis was suspected after chronic exposure to
styrene (Pratt Johnson, 1964)
9.2.5 Parenteral exposure
No data available.
9.2.6 Other
No data available.
9.3 Course, prognosis, cause of death
Acute exposure to high concentrations may produce signs
of upper respiratory irritation, followed by asphyxia,
muscular weakness, coma and death from respiratory paralysis
(ILO,1983). Effects of short term styrene inhalation on
volunteers are according the vapor concentrations: around 350
to 375 ppm for 0.5 to one hour reduction of manual dexterity
and coordination and impairment of reaction time. Increasing
concentrations (>800 ppm) cause central nervous system
depression. The reversibility of these effects has not been
studied but since reports of clinically evident impairment
are rare, reversibility is likely (O'Donoghue, 1985).
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
Acute: Cardiac arrhytmias. styrene being an
aromatic hydrocarbon may increase the risk of
sensitivity of the heart to exogenic
catecholamines.
9.4.2 Respiratory
Acute and chronic: Upper respiratory
irritation. Burning sensation in the chest, wheezing,
dyspnea. Forced expiratory volume in one second (FEV1)
was changed in a group of workers. Chemical
pneumonitis may follow ingestion.
9.4.3 Neurological
9.4.3.1 Central Nervous System (CNS)
Headache, general weakness.
Increased tiredness, lightheadedness,
dizziness, loss of coordination and balance,
vertigo and ataxia. Extreme exposures may
cause unconsciousness. Minor EEG
abnormalities in chronic exposure. Slight
effects on psychomotor performance.
Persistent and premature dementia was
suspected to be caused in some workers, after
long-term exposures.
9.4.3.2 Peripheral nervous system
Peripheral neuropathy was seen only
in chronic exposure (Behari et al, 1986)
characterized by hypoesthesias and decreased
peroneal nerve conduction velocity.
9.4.3.3 Autonomic nervous system
No data available.
9.4.3.4 Skeletal and smooth muscle
Skeletal muscles may exhibit
weakness and tremors.
9.4.4 Gastrointestinal
Loss of appetite, nausea, vomiting.
9.4.5 Hepatic
Chronic: possible alterations in liver enzymes
and liver function tests.
9.4.6 Urinary
9.4.6.1 Renal
No data available.
9.4.6.2 Others
No data available.
9.4.7 Endocrine and reproductive systems
Congenital defects and increase in spontaneous
abortions have been described but the relationship to
styrene was not proven.
9.4.8 Dermatological
Mild to moderate irritation. Repeated or
prolonged contact may cause dermatitis (itching,
drying, redness).
9.4.9 Eye, ears, nose, throat: local effects
Eye irritation and conjunctivitis.
Irritation of nose and throat mean that increased
incidence of laryngeal carcinoma was suspected but not
proven.
9.4.10 Hematological
No data available.
9.4.11 Immunological
No data available.
9.4.12 Metabolic
9.4.12.1 Acid-base disturbances
No data available.
9.4.12.2 Fluid and electrolyte disturbances
No data available.
9.4.12.3 Others
Alterations in glucose metabolism
have been noted (Guillemin and Bauer,
1979).
9.4.13 Allergic reactions
No data available.
9.4.14 Other clinical effects
9.4.15 Special risks
Expectant mothers and women with ovular or
menstrual disorders shoud not work in conditions
exposing them to styrene.
9.5 Others
No data available.
10. MANAGEMENT
10.1 General principles
Rapid, effective decontamination is essential in the
management of styrene exposure. The evaluation of vital
functions and life-supporting measures are the main
principles in poisoning management. Maintain airway and
respiration. Start artificial respiration at the first sign
of respiratory failure. Administer oxygen if necessary. The
removal from the work place of individuals with elevated
values of styrene metabolites, found on repeated
measurements, should be considered.
10.2 Life supportive procedures and symptomatic treatment
Make a proper assessment of airway, breathing,
circulation and neurological status of the patient. Maintain
a clear airway. Administer oxygen if necessary. Start
artificial respiration for respiratory failure. Open and
maintain at least one intravenous route.
10.3 Decontamination
Eye exposure: irrigate with water or isotonic saline
immediately and continuously for 15 minutes. If pain or
irritation persistsconsult an ophtalmologist. Skin exposure:
Remove all contaminated clothing and shoes. Immediately flush
skin thoroughly with plenty of water for at least 15 minutes.
Water and non-abrasive soap can help remove styrene. Even in
the absence of symptoms the patient must be evaluated
medically. Inhalation: Move victim to fresh air. Begin
artificial respiration if required.
Ingestion: Do not induce vomiting. Gastric lavage may be
considered in massive and recent ingestion.The use of
activated charcoal is discussed. Do not allow the victim to
ingest any fat, oils, etc which probably may increase
absorption.
10.4 Elimination
A good urinary output is mandatory. No data available
on the value of forced diuresis or dialysis. The use of
cathartics is questionable.
10.5 Antidote treatment
10.5.1 Adults
There are no antidotes available.
10.5.2 Children
There are no antidotes available.
10.6 Management discussion
Acute exposure: styrene is an irritant to the
respiratory system and will cause CNS depression. These are
the most important points in the management of acute
episodes. Current management involves the classical
decontamination and symptomatic treatment, after careful
clinical evaluation.
Chronic exposure: monitoring the work environment and urinary
metabolites are the mandatory features concerning chronic
poisoning. Personal protection to eyes and skin as suitable
respiratory protection should be used when vapour
concentration is unknown or exceeds exposure limits.
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
Moscato et al (1987) report two cases of occupational
asthma due to styrene. Contact with styrene resulted in
coughing, breathlessness and symptoms of asthma in the two
subjects. The respiratory reaction in subject 1 was followed
by a late cutaneous rash. When the subjects were not at work
then the symptoms disappeared. In both subjects inhalation
challenge with styrene resulted in an immediate
bronchospastic reaction which was followed by the late
cutaneous rash in subject 1. Prior administration of disodium
cromoglycate (40 mg from a spinhaler) prevented the
respiratory reactions completely, but failed to prevent the
late skin response in subject 1. The complete disappearance
of the symptoms followed the removal of the subjects from the
source of the styrene. It was concluded that styrene can be a
primary cause of occupational asthma.
12. ADDITIONAL INFORMATION
12.1 Specific preventive measures
Inhalation: wear suitable respiratory protection if
vapour concentration is unknown or exceeds exposure
limits.
Skin: wear gloves, pants, overalls, jacket, boots, as needed.
Have a safety shower/eyewash fountain readily available in
the immediate work area.
Eyes: wear chemical-splash goggles or a face shield. Store
styrene in properly grounded containers, in a cool area with
adequate ventilation, away from sources of heat or sparks. In
case of spills absorb on clay or sand. Extinguish fires with
carbon dioxide or dry chemical (ILO, 1983).
12.2 Other
No data available.
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14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
ADDRESS(ES)
Author: Alberto Furtado Rahde
Rua Riachuelo 677 ap 201
90010-270 Porto Alegre
BRAZIL
Tel: 55-51-2275419
Fax: 55-51-2246563/2299067/3391564
Date: November 1992
Reviewer: Dr J. Benitez
Toxicology Treatment Program
NE-583 Montefiore University Hospital
200 Lothrop Street
Pittsburgh, PA 15213-2582
USA
Tel: 1-412-6486800
Fax: 1-412-6922815
Date: February 1995
Peer review: Cardiff, United Kingdom
Date: March 1995
Finalised: IPCS, September 1996