UNITED NATIONS ENVIRONMENT PROGRAMME
INTERNATIONAL LABOUR ORGANISATION
WORLD HEALTH ORGANIZATION
INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY
ENVIRONMENTAL HEALTH CRITERIA 186
This report contains the collective views of an international group of
experts and does not necessarily represent the decisions or the stated
policy of the United Nations Environment Programme, the International
Labour Organisation, or the World Health Organization.
First draft prepared by Dr P. Lundberg (National Institute of
Occupational Health, Sweden), Dr M. Crookes (Building Research
Establishment, United Kingdom), and Dr S. Dobson and Mr P. Howe
(Institute of Terrestrial Ecology, Monks Wood, United Kingdom)
Published under the joint sponsorship of the United Nations
Environment Programme, the International Labour Organisation, and the
World Health Organization, and produced within the framework of the
Inter-Organization Programme for the Sound Management of Chemicals.
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sound management of chemicals in relation to human health and the
WHO Library Cataloguing in Publication Data
(Environmental health criteria ; 186)
1.Ethylbenzene - toxicity 2.Benzene derivatives
3.Environmental exposure I.Series
ISBN 92 4 157186 1 (NLM Classification: QV 633)
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ENVIRONMENTAL HEALTH CRITERIA FOR ETHYLBENZENE
2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL
2.2. Physical and chemical properties
2.3. Conversion factors
2.4. Analytical methods
2.4.1. Ethylbenzene in air
2.4.2. Ethylbenzene in water
2.4.3. Ethylbenzene in biological material
2.4.4. Metabolites of ethylbenzene in urine
3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE
3.1. Natural occurrence
3.2. Anthropogenic sources
3.2.1. Production processes
3.2.2. Production levels
4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION AND TRANSFORMATION
4.1. Transport and distribution between media
220.127.116.11 Aerobic degradation
18.104.22.168 Anaerobic degradation
4.2.2. Abiotic degradation
5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE
5.1. Environmental levels
5.1.2. Surface water and sediment
5.1.4. Urban run-off, effluent and landfill leachate
5.2. General population exposure
5.2.1. Environmental sources
5.3. Occupational exposure during manufacture,
formulation or use
5.3.1. Biological monitoring
6. KINETICS AND METABOLISM IN LABORATORY ANIMALS AND HUMANS
6.1.1. Skin absorption
6.1.2. Absorption via inhalation
6.1.3. Absorption after oral intake
6.3. Metabolic transformation
6.4. Elimination and excretion
7. EFFECTS ON LABORATORY MAMMALS AND IN VITRO TEST SYSTEMS
7.1. Single exposure
7.2. Short-term exposure
7.3. Long-term exposure
7.3.1. Oral exposure
7.3.2. Inhalation exposure
7.4. Skin and eye irritation, sensitization
7.5. Reproductive toxicity, embryotoxicity
7.6. Mutagenicity and related end-points
7.8. Other special studies
7.9. Factors modifying toxicity
8. EFFECTS ON HUMANS
8.1. Volunteer studies
8.2. Occupational exposure
9. EFFECTS ON OTHER ORGANISMS IN THE LABORATORY AND FIELD
9.2. Aquatic organisms
9.3. Terrestrial organisms
10. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE ENVIRONMENT
10.1. Evaluation of human health risks
10.2. Evaluation of effects on the environment
12. FURTHER RESEARCH
13. PREVIOUS EVALUATION BY INTERNATIONAL BODIES
NOTE TO READERS OF THE CRITERIA MONOGRAPHS
Every effort has been made to present information in the criteria
monographs as accurately as possible without unduly delaying their
publication. In the interest of all users of the Environmental Health
Criteria monographs, readers are requested to communicate any errors
that may have occurred to the Director of the International Programme
on Chemical Safety, World Health Organization, Geneva, Switzerland, in
order that they may be included in corrigenda.
* * *
A detailed data profile and a legal file can be obtained from the
International Register of Potentially Toxic Chemicals, Case postale
356, 1219 Châtelaine, Geneva, Switzerland (Telephone No. 9799111).
* * *
This publication was made possible by grant number 5 U01
ES02617-15 from the National Institute of Environmental Health
Sciences, National Institutes of Health, USA, and by financial support
from the European Commission.
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WHO TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR ETHYLBENZENE
Dr D. Anderson, BIBRA Toxicology International, Carshalton, Surrey,
Dr A. Bobra, Environment Canada, Orleans, Ontario, Canada
Dr K. Hatfield, Division of Standards Development and Technology
Transfer, National Institute for Occupational Safety and Health,
Cincinnati, Ohio, USA
Mr L. Heiskanen, Environmental Health Assessment and Criteria Section,
Chemical Safety Unit, Department of Human Services and Health,
Mr P. Howe, Institute of Terrestrial Ecology, Monks Wood, Abbots
Ripton, Huntingdon, Cambridgeshire, United Kingdom
Dr You-xin Liang, Department of Occupational Health, Shanghai Medical
University, Shanghai, China
Professor M. Lotti, Institute of Occupational Medicine, University of
Padua, Padua, Italy (Chairman)
Dr P. Lundberg, Department of Toxicology, National Institute of
Occupational Health, Solna, Sweden (Co-rapporteur)
Dr Vesa Riihimaki, Institute of Occupational Health, Helsinki, Finland
Dr Leif Simonsen, National Institute of Occupational Health,
Representatives of other Organizations
Dr P. Montuschi, Institute of Pharmacology, Faculty of Medicine and
Surgery, Catholic University of the Sacred Heart, Rome, Italy
(representing the International Union of Pharmacology)
Dr B.H. Chen, International Programme on Chemical Safety, World Health
Organization, Geneva, Switzerland (Secretary)
IPCS TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR ETHYLBENZENE
A WHO Task Group on Environmental Health Criteria for
Ethylbenzene met at the British Industrial Biological Research
Association (BIBRA) Toxicology International, Carshalton, Surrey,
United Kingdom, from 27 February to 2 March 1995. Dr D. Anderson
opened the meeting and welcomed the participants on behalf of the host
institute. Dr B.H. Chen, IPCS, welcomed the participants on behalf of
the Director, IPCS, and the three IPCS cooperating organizations
(UNEP/ILO/WHO). The Task Group reviewed and revised the draft
criteria monograph and made an evaluation of the risks for human
health and the environment from exposure to ethylbenzene.
Dr P. Lundberg, National Institute of Occupational Health,
Sweden, Dr M. Crookes, Building Research Establishment, United Kingdom
and Dr S. Dobson and Mr P. Howe, Institute of Terrestrial Ecology,
Monks Wood, United Kingdom, prepared the first draft of this
monograph. The second draft was prepared by Dr Lundberg and Mr Howe,
incorporating comments received following the circulation of the first
draft to the IPCS Contact Points for Environmental Health Criteria
monographs. Dr S. Soliman, College of Agriculture & Veterinary
Medicine, Saudi Arabia, contributed to the final text of the document.
Dr B.H. Chen and Dr P.G. Jenkins, both members of the IPCS
Central Unit, were responsible for the overall scientific content and
technical editing, respectively.
The efforts of all who helped in the preparation and finalization
of the document are gratefully acknowledged.
* * *
Financial support for this Task Group was provided by the United
Kingdom Department of Health as part of its contributions to the IPCS.
FID flame ionization detection
GC gas chromatography
MS mass spectrometry
PID photoionization detection
VOC volatile organic compound
Ethylbenzene is an aromatic hydrocarbon manufactured by
alkylation from benzene and ethylene. The estimated yearly production
in the USA is about 5 million tonnes, and in 1983 it was approximately
3 million tonnes in western Europe. Ethylbenzene is a colourless
liquid with a sweet gasoline-like odour. It is mainly used for the
production of styrene. It is also used in technical xylene as a
solvent in paints and lacquers and in the rubber and chemical
manufacturing industries. It is found in crude oils, refined
petroleum products and combustion products.
Ethylbenzene is a non-persistent chemical, being degraded
primarily by photo-oxidation and biodegradation. Volatilization to
the atmosphere is rapid. The photo-oxidation reaction of ethylbenzene
in the atmosphere may contribute to photochemical smog formation.
The log octanol-water partition coefficient is 3.13, indicating a
potential for bioaccumulation. However, the limited evidence
available shows that ethylbenzene bioconcentration factors are low for
fish and molluscs. Elimination from aquatic organisms appears to be
Ethylbenzene levels in air at rural sites are generally less than
2 µg/m3. Mean levels of ethylbenzene ranging from 0.74 to 100 µg/m3
have been measured at urban sites. The levels of ethylbenzene found
in surface waters are generally less than 0.1 µg/litre in
non-industrial areas. In industrial and urban areas ethylbenzene
concentrations of up to 15 µg/litre have been reported. Ethylbenzene
levels in sediments are generally less than 0.5 µg/kg, although levels
between 1 and 5 µg/kg have been found in sediments from heavily
industrialized areas. Concentrations in uncontaminated groundwater are
generally less than 0.1 µg/litre, but are much higher in contaminated
The acute toxicity of ethylbenzene to algae, aquatic
invertebrates and fish is moderate. The lowest acute toxicity values
are 4.6 mg/litre for the alga Selenastrum capricornutum (72-h EC50
based on growth inhibition), 1.8 mg/litre for Daphnia magna (48-h
LC50) and 4.2 mg/litre for rainbow trout (96-h LC50). No information
is available regarding chronic exposure of aquatic organisms to
There is limited information regarding the toxicity of
ethylbenzene to bacteria and earthworms. There are no data for
terrestrial plants, birds or wild mammals.
Human exposure to ethylbenzene occurs mainly by inhalation;
40-60% of inhaled ethylbenzene is retained in the lung. Ethylbenzene is
extensively metabolized, mainly to mandelic and phenylglyoxylic acids.
These urinary metabolites can be used to monitor human exposures.
Ethylbenzene has low acute and chronic toxicity for both animals
and humans. It is toxic to the central nervous system and is an
irritant of mucous membranes and the eyes. The threshold for these
effects in humans after short single exposures was estimated to be
about 430-860 mg/m3 (100-200 ppm).
Inhalation of ethylbenzene for 13 weeks by rats and mice at
concentrations up to 4300 mg/m3 (1000 ppm) did not lead to
histopathological lesions. The no-observed-effect level, based on
increased liver weight in rats, was 2150 mg/m3 (500 ppm).
Ethylbenzene is an inducer of liver microsomal enzymes. It is
not mutagenic or teratogenic in rats and rabbits. No information is
available on reproductive toxicity or carcinogenicity of ethylbenzene.
A guidance value of 22 mg/m3 (5 ppm) has been calculated from
animal studies. The estimated exposure of the general population
(even in the worst case situation) is below this guidance value.
Long-term occupational exposure to ethylbenzene concentrations
estimated to be of this order of magnitude did not cause adverse
health effects in workers.
2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL METHODS
Empirical formula: C8H10
Chemical name: Ethylbenzene
Synonyms: Phenylethane, EB, Ethylbenzol
Relative molecular mass: 106.16
CAS registry number: 100-41-4
RTECS registry number: DA 07000000
EEC number: 601-023-00-4
2.2 Physical and chemical properties
Some physical and chemical properties of ethylbenzene are given
in Table 1.
The solubility of ethylbenzene in water is 152 mg/litre at 20°C
and 101.3 kPa (DEC, 1992) and 138 mg/litre at 15°C (Heilbron et al.,
1946). Ethylbenzene is soluble in ethanol, diethylether and most
other organic solvents (ECETOC, 1986; DEC, 1992). At room temperature
ethylbenzene is a colourless liquid with a sweet, gasoline-like odour
The odour threshold concentration in air is about 2 mg/m3 and in
water about 0.1 mg/litre (temperature not stated) (Anon, 1987; DEC,
1992). Ethylbenzene floats on water and, because of its significant
vapour pressure and low water solubility, it will disperse in the
atmosphere (ECETOC, 1986).
Table 1. Some physical and chemical properties of ethylbenzenea
Physical state (20°C; 101.3 kPa) liquid
Boiling point (°C) (101.3 kPa) 136.2
Melting point (°C) -94.95
Density (25°C; g/cm3) 0.866
Vapour pressure (kPa at 20°C) 1.24
Flash point (°C) 12.8
Refractive index (15°C, D line) 1.49857
Saturation % in air (20°C; 101.3 kPa) 1.2
Explosion limits (20°C; 101.3 kPa) 1-7.8
Log octanol/water partition coefficient (Log Kow) 3.13
Henry's Law Constant (Pa m3/mol) 887
Log Sorption Partition Coefficient (Log Koc) 1.98-3.04
Water Solubility (20°C; 101.3 kPa; mg/L) 152
a From: Heilbron et al. (1946); Sax (1979); Verschueren (1983);
Ullman (1983); Anon (1987); Weast (1988); ATSDR (1990);
Cavender (1993); DEC (1992); Mackay et al. (1992)
2.3 Conversion factors
1 ppm = 4.3 mg/m3 at 20°C and 101.3 kPa
1 mg/m3 = 0.23 ppm at 20°C and 101.3 kPa
2.4 Analytical methods
2.4.1 Ethylbenzene in air
Ethylbenzene in air can be analysed according to NIOSH (1984).
The air is sampled on a solid sorbent (coconut shell charcoal) and
desorbed with carbon disulfide. Aliquots are analysed by gas
chromatography (GC) with flame ionization detection (FID). With a
desorption volume of 0.5 ml, 2.17-8.62 mg can be measured. The
detection limit is about 0.1 mg/m3 for a 10-litre sample. Other
volatile organic solvents are possible interferences (NIOSH, 1984).
To avoid the use of carbon disulfide, sampling on montmorillonite
clays (minerals consisting of a three-layer aluminosilicate lattice)
and thermal desorption have been used (Harper & Purnell, 1990). This
method has not, however, yet been fully evaluated under actual
sampling conditions in the field.
A method using photoionization detection (PID) for GC, instead of
FID, has been described. PID is one to two orders of magnitude more
sensitive to most aromatics than is FID (Hester & Meyer, 1979). In an
evaluation of sampling and analytical methods for monitoring several
volatile organic compounds in air, sampling in a stainless steel
canister was shown to be the best. Using cryogenic pre-concentration
followed by gas-liquid chromatography (GLC) equipped with a selective
detector, ethylbenzene could be analysed at the ppb level (Jayanty,
The sensitivity of the GC/FID method for analysing ethylbenzene
and other volatile organic compounds can be improved by using wide
bore capillary columns (0.4-0.75 mm internal diameter). By this
means, ethylbenzene can be separated from the C8 isomers even in
complex mixtures (Frank et al., 1990). Several kinds of Bentones with
structures similar to that of Bentone 34 have been tested and compared
for the purpose of improving the resolution of ethylbenzene and xylene
isomers by GC. Bentone SD-3 was found to have higher selectivity
toward these close-boiling compounds than the well-known stationary
phase Bentone 34 (Zlatkis & Jiao, 1991).
Ultraviolet-spectrometry has also been used for analysis
(Yamamoto & Cook, 1968). Commercial detection tubes are available
with a detection range of 132.3-1764.0 mg/m3 (DEC, 1992) and of
4.41-220 µg (Gentry & Walsh, 1987).
2.4.2 Ethylbenzene in water
Determination of ethylbenzene in water has been performed by
using the "head-space" technique coupled to GLC, in combination with
mass spectrometry (MS) or infrared detection (Rosen et al., 1963;
Burnham et al., 1972; Kleopfer & Fairless, 1972; Grob, 1973). A
purge-and-trap method has been developed for determination of four
pollutants, including ethylbenzene, in aqueous samples. Water samples
are purged at 50°C with helium and the analytes are trapped on Tenax
GC. The trap is thermally desorbed directly into a gas chromatograph
equipped with FID. The method is laboratory validated for the range
of 20-500 ppb using a 5 g aqueous sample (Warner & Beasley, 1984).
Zhang & Pawliszyn (1993) developed a headspace solid phase
microextraction technique to determine ethylbenzene and other volatile
organic compounds (VOC) in water. The detection limit was found to be
at the ng/litre level.
2.4.3 Ethylbenzene in biological material
The head-space technique can also be used for measurements of
ethylbenzene in blood. The detection limit has been reported to be
0.01 mg/litre (Radzikowska-Kintzi & Jakubowski, 1981). The head-space
methodology must, however, be optimized specifically for blood rather
than using parameters derived from head-space experiments with aqueous
media (Dills et al., 1991).
An analytical method has been developed that enables the
determination of ethylbenzene and other volatile organic compounds in
10 ml of blood samples at the ng/litre level. The method depends on
purge-and-trap GC/MS and shows excellent reproducibility and recovery
even at ultra-trace levels (Ashley et al., 1992).
A method for analysing ethylbenzene in subcutaneous fat was
described by Wolff et al. (1977). Fat biopsies are obtained by using
a 30 cm3 silanized glass syringe and a size 16 G needle. The fat
globules are washed from the syringe and needle by saline. The fat-
saline suspension is frozen and thawed to 0°C prior to analysis. Fat
globules are weighed and aliquots of CS2 are added. The solution is
analysed by GC with dual flame ionization detectors.
A method for the determination of ethylbenzene and other
alkylbenzenes in plant foliage was developed by Keymeulen et al.
(1991). Using a gas chromatograph-quadrupole mass spectrometer in
the selected-ion monitoring mode, calibration graphs and detection
limits for these hydrocarbons were determined. Extraction was
performed with dichloromethane and the optimum extraction time was
found to be 6 h.
Murray & Lockhart (1981) prepared fish muscle for analysis by
extraction with dichloromethane and clean up on a florisil column.
Samples were analysed using GC with a FID. A detection limit of
5 µg/g was achieved with 98-102% recovery. A procedure to identify and
quantify ethylbenzene in fish samples by GC/MS using a fused-silica
capillary column (FSCC) and vacuum extraction has been developed
(Hiatt 1981, 1983; Dreisch & Munson 1983). Improved resolution and
detection limits at the ng/g level have been achieved with this
2.4.4 Metabolites of ethylbenzene in urine
One of the biomarkers of human exposure to ethylbenzene is the
urinary concentration of mandelic acid. Mandelic acid is also a
metabolite of styrene. Methods to monitor mandelic acid in urine were
initially developed in order to evaluate exposure to styrene.
In the GC method, mandelic acid is determined after extraction
from urine by diethyl ether (Engström & Rantanen, 1974; Gromiec &
Piotrowski, 1984). The detection limit for mandelic acid by this
method was 1.0 mg/litre. Gas chromato-graphic methods require
derivatization of the acid with diazomethane or silyl reagent before
analysis. This is not necessary for the HPLC or the ITP methods
(Sollenberg, 1991). Urinary samples extracted by diethyl ether can
also be determined by isotachophoresis (ITP) with a detection limit of
0.04 mmol/litre (Sollenberg, 1991). This method is comparable to a
high-performance liquid chromatographic (HPLC) method first described
in 1977, with a detection limit of 0.01 mmol/litre (Ogata et al.,
1977; Sollenberg, 1991).
Determination of another major metabolite of ethylbenzene,
phenylglyoxylic acid, in the urine of occupationally exposed people
has been carried out by HPLC methods. The limit of determination is
0.1 mg/litre (Inoue et al., 1995).
HPLC and ITP techniques can also be used for the simultaneous
determination of mandelic and phenylglyoxylic acids in the urine of
rats (Sollenberg et al., 1985).
GC methods have been developed for analysis of other metabolic
products of ethylbenzene. Simultaneous determination of several
minor metabolites in urine from man and rats (e.g., acetophenone,
1-phenylethanol, omega-hydroxyacetophenone, 4-ethylphenol,
2,4-dimethylphenol and 3-methylbenzylalcohol) can be achieved with one
method (Engström, 1984a).
3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE
3.1 Natural occurrence
Ethylbenzene is present in crude oil (Wiesenburg et al., 1981).
3.2 Anthropogenic sources
Ethylbenzene is present in refined products (Korte & Boedefeld,
1978). It is produced by incomplete combustion of natural materials,
making it a component of forest fires and cigarette smoke.
3.2.1 Production processes
About 90% of all ethylbenzene used in the chemical industry is
produced via the classic Friedel-Crafts alkylation of benzene with
ethylene using soluble aluminium chloride catalyst. These
liquid-phase processes generally involve ethyl chloride or
occasionally hydrogen chloride as a catalyst promoter. In a variation
on this method, dry benzene plus ethylene, catalyst and promoter are
fed continuously to the alkylation reactor (Lewis et al., 1983;
Other procedures which have been employed to a much lesser extent
for the preparation of ethylbenzene include fractionation of petroleum
and ultra-fractionation from a mixed xylene stream (Seader, 1982;
Fishbein, 1985). It is not, however, economical to isolate
ethylbenzene from the catalytic raffinate (Fishbein, 1985; ECETOC,
An interesting approach for the preparation of ethylbenzene has
been developed by Levesque & Dao (1989). In this method the
alkylation of benzene to produce ethylbenzene was performed
successfully using an aqueous solution of ethanol of concentration
similar to a fermentation broth.
3.2.2 Production levels
In the USA, the production of ethylbenzene in 1982 and 1983 was
3.0 and 3.6 million tonnes, respectively (Webber, 1984). According to
Fishbein (1985), the annual capacity for the production of
ethylbenzene was estimated to be about 4.6 million tonnes in the USA
in 1983. In 1986, production in the USA was reported to be
approximately 4.1 million tonnes (US ITC, 1987). The estimated annual
production for ethylbenzene was 5.3 and 5.1 million tonnes for 1993
and 1992, respectively, in the USA. Ethylbenzene was the 19th in 1993
and the 18th in 1992 chemical out of the top 50 chemicals in the USA
(US Chemical Industry, 1994). In 1983 the production of ethylbenzene
in western Europe was around 3 million tonnes (ECETOC, 1986).
About 95% of ethylbenzene produced is employed for the production
of styrene. Ethylbenzene is a constituent (15-20%) of commercial
xylene ("mixed xylenes"), and hence used as a component of solvents,
as a diluent in paints and lacquers, and as a solvent in the rubber
and chemical manufacturing industries.
Ethylbenzene ("mixed xylenes") can also be added to motor fuels.
A typical ethylbenzene content of a reformate is about 4% (by volume)
4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION AND TRANSFORMATION
4.1 Transport and distribution between media
The majority of ethylbenzene released into the environment passes
directly into the atmosphere or into surface water.
It can be predicted from physico-chemical properties that, when
ethylbenzene is released into air, the major part remains in the
atmosphere and only small amounts are found in water, soil and
sediment. If it is assumed that all ethylbenzene is continuously
released to the atmosphere, the Level III generic fugacity model
consisting of homogeneous compartments of air, water, soil and
sediment predicts that over 99% of ethylbenzene would be distributed
in the atmosphere at steady state. Ethylbenzene discharged to the
atmosphere has very little potential for entering other media.
Precipitation from the atmosphere can occur. The key processes
determining overall fate are reaction in the air and advection (Mackay
et al., 1992).
Ethylbenzene has a low water solubility (152 mg/litre at 20°C)
and a relatively high vapour pressure (1.24 kPa at 20°C). This means
that only a very small proportion of ethylbenzene in the atmosphere is
likely to be removed by precipitation. This is shown by the fact that
it has been detected only at low levels in rain water samples (see
section 5, Table 3). Ethylbenzene may adsorb to atmospheric
particulates and be removed along with the particles by precipitation
or dry deposition.
Transport and distribution of a substance in the aquatic
environment are dependent on its solubility, movement of the water,
exchanges at the air-water interfaces, adsorption to sediment and
particulate matter, and bioconcentration in aquatic organisms. The
residence time in water is also dependent upon the type of
environmental conditions encountered, such as temperature, wind speed,
currents, ice cover, etc.
For ethylbenzene, the half-life at 20°C in a river 1 m deep,
flowing at 1 m/sec and with a wind velocity of 3 m/sec, calculated
according to the method described by Thomas (1982) for high volatility
compounds, is 3.1 h. The half-lives in a marine mesocosm were 20 days
at 8-16°C in the spring, 2.1 days at 20-22°C in the summer and 13 days
at 3-7°C in the winter (Wakeham et al., 1983). Volatilization was a
dominant factor. The increased turnover time during summer was also
probably due to biodegradation. The seasonal variations between
winter and spring may have largely been due to changes in hydrodynamic
conditions as a result of changes in wind-driven turbulence.
If it is assumed that ethylbenzene is continuously released only
into the water compartment, the Level III generic fugacity model
predicts that approximately 93% of ethylbenzene would be distributed
into the water at steady state, 4.5% into the atmosphere, 2.5% into
the sediment and 1% into the soil. The key processes determining
overall fate are reaction in water and evaporation (Mackay et al.,
It has been estimated (Callahan, 1979) from a computed Henry's
Law constant of 6.44 × 10-3 atmos.m3.mol-1 that the volatility of
ethylbenzene from water will be very similar to that of toluene
(Henry's Law constant = 6.68 × 10-3 atmos.m3.mol-1). Thus,
ethylbenzene can be expected to have a half-life for volatilization
from still water at a depth of 1 m of about 5 to 6 h (Mackay &
Leinonen, 1975). A measured value of the Henry's Law constant of
8.43 × 10-3 atmos.m3.mol-1 (Mackay et al., 1979) supports this
If it is assumed that ethylbenzene is only released to the soil
compartment, the Level III generic fugacity model indicates that
approximately 1% of ethylbenzene should be distributed into water,
4.9% into the atmosphere, 94.7% into the soil and >1% into the
sediment. The soil acts only as a reservoir. The soil concentration
is controlled almost entirely by the rate at which it can evaporate
(Mackay et al., 1992).
In a study by Jaynes & Boyd (1991), the sorption isotherms of
ethylbenzene and some other volatile organic compounds on organo-clays
indicated that sorption occurred by partition interactions with the
hexadecyltrimethylammonium (HDTMA)-derived organic phase.
Mineral-charge effects on sorption of ethylbenzene were evident.
Greater sorption of ethylbenzene and other alkylbenzenes by high-
charge HDTMA clays was attributed to the ability of the large basal
spacings to accommodate larger solute molecules (Jaynes & Boyd, 1991).
Several studies of soil-water partitioning for ethylbenzene have
been reported. In one study a value of 1.01 (log value) was found for
the soil-water partition coefficient (Kp) for a soil of 4.02
(± 0.06)% organic carbon content (Vowles & Mantoura, 1987). Pussemier
et al. (1990) reported a soil organic carbon-water partition
coefficient (Koc) of 2.41 (log value). Roy & Griffin (1985)
estimated log Koc values of 2.60 and 2.87 derived from equations
using solubility and Kow data, respectively. The soil organic
matter-water partition coefficient (Kom) was measured as 1.98 (log
value) for a soil containing 1.9% organic matter (Chiou et al., 1983).
Lee et al. (1989) reported log Kom values ranging from 1.73 to 1.97
for untreated soil and from 2.37 to 3.23 for soil treated with organic
cations. It is likely that ethylbenzene will be adsorbed to soil to
some extent. Roy & Griffin (1985) predicted that ethylbenzene would
have low mobility in water-saturated soil, based on the predicted Koc
values. However, Howard (1989) stated that the range of soil-water
partition coefficients suggests that ethylbenzene is adsorbed
moderately by soil and will probably leach through soil. The presence
of ethylbenzene in bank infiltrate water suggests that there is a high
probability of it leaching through soil. Other factors influencing
the movement of ethylbenzene through soil to groundwater include soil
type, soil porosity, amount of rainfall, depth of groundwater and
extent of degradation.
The competitive adsorption of ethylbenzene and water on bentonite
was studied by Rhue et al. (1989) using a technique that allowed the
amount of adsorbed water and the alkylbenzene to be measured
independently. Results indicated that ethylbenzene adsorption on the
clay was not affected by water at relative humidities near 0.23 but
was reduced significantly at values near 0.5.
Laboratory studies indicate that volatilization of ethylbenzene
occurs rapidly from sludge-treated soil (100% removal of an initial
concentration of 50 mg/kg occurred within 6 days) (Water Pollution
It has been reported that sorption isotherms of ethylbenzene and
some other nonionic organic compounds by maize (Zea mays) residues
and soil are linear. Sorption coefficients of the corn residues were
from 35 to 60 times greater than for surface soil (1.9% organic
matter), demonstrating the high sorptive capability of these residues
(Boyd et al., 1990).
Annable et al. (1993) studied the reduction of gasoline component
(including ethylbenzene) leaching potential by soil venting. Results
from columns vented for different periods of time showed vented soil
to be effective at reducing constituent concentrations in leachate
ultimately to about 1 µg/litre.
Clapp et al. (1994) compared the performance of activated sludge
(AS) and fixed-film processes with biological aerated filter (BAF)
fermenters for removal of priority pollutants, including ethylbenzene.
They found that the AS and BAF fermenters achieved comparable VOC
removal, and stripping rates were slightly higher for the AS
fermenters; degradation rates were slightly higher for the BAF
The physical-chemical properties of ethylbenzene indicate that
only small amounts should be found in sediment.
22.214.171.124 Aerobic degradation
Ethylbenzene has been shown to be biodegradable in aquatic
systems. In simulations of spring and summer conditions in a coastal
bay, half-lives of 20 days and 2.1 days, respectively, were obtained
for ethylbenzene. Both volatilization and biodegradation were
responsible for removal (Wakeham et al., 1983). The reduction in
half-life in the summer was thought to represent an increase in
microbial degradation. An adaptation period was found to be important
for microbial degradation to take place. It was concluded that
microbial degradation becomes important under warm conditions, with
high biological activity, for the removal of ethylbenzene from the
aquatic environment. Howard (1991) report a half-life for aqueous
biodegradation, in an unacclimated system, of 3 to 10 days.
In an inherent biodegradability test (OECD 302 C), ethylbenzene
was degraded by 81 to 126% biological oxygen demand (BOD) in 2 weeks
(CITI, 1992). In another biodegradability test, ECETOC (1986)
reported that the BOD of ethylbenzene was determined after 6, 9 and 20
days and that biodegradation corresponding to 32, 36 and 45% of the
theoretical oxygen demand (TOD) was found. Pitter & Chudoba (1990)
reported a BOD5/TOD ratio of 0.29 for ethylbenzene.
Ethylbenzene, as part of the water-soluble fraction of gas oil,
has been shown to be degraded to 1-phenylethanol by the autochthonous
microflora of clean groundwater. After an initial lag phase of 3 to 4
days, complete disappearance of ethylbenzene (from an initial
concentration of 45 µg/litre) occurred within 12 days at 10°C
(Kappeler & Wuhrmann, 1978a,b).
Ethylbenzene was shown to be removed in core samples from an area
that had been previously contaminated with unleaded gasoline.
Complete degradation occurred within three weeks on incubation of
ethylbenzene in core samples that had previously had hydrogen peroxide
added, whereas a small amount of ethylbenzene remained after three
weeks in the previously gasoline-contaminated and uncontaminated core
samples (Thomas et al., 1990).
In static experiments, where ethylbenzene was incubated in the
dark for 7 days with settled domestic wastewater as microbial
inoculum, followed by 3 weekly subcultures from the medium,
ethylbenzene was shown to be 100% degraded within 7 days in the
initial inoculum and the three subsequent subcultures when the initial
ethylbenzene concentration was 5 mg/litre. At an initial ethylbenzene
concentration of 10 mg/litre, 69% degradation of ethylbenzene occurred
within 7 days in the initial culture, rising to 100% degradation
within 7 days in the third subculture, indicating that gradual
adaptation was needed for degradation of the higher concentration
(Tabak et al., 1981).
Soil bacteria have been shown to be capable of using ethylbenzene
as a sole carbon source. Microbial oxidative degradation has been
shown to proceed via hydroxylation of the aromatic ring to give
2,3-dihydroxy-1-ethylbenzene (Gibson et al., 1973). A similar
intermediate has been postulated in the degradation of ethylbenzene by
Pseudomonas sp. NCIB 10643 cultures. The 2,3-dihydroxy intermediate
was suggested to undergo further degradation by meta cleavage of the
aromatic ring (Smith & Ratledge, 1989).
Nocardia tartaricans has been shown to be capable of converting
ethylbenzene to 1-phenylethanol and acetophenone in a shake flask
culture using hexadecane as the source of carbon and energy (Cox &
Bestetti & Galli (1984) showed that Pseudomonas fluorescens can
utilize ethylbenzene as sole carbon source. Degradation appeared to
occur by meta cleavage of the ring, with formation of the semi-
aldehyde. Utkin et al. (1991) have also recently shown that a species
of Pseudomonas is capable of growing on ethylbenzene as the
sole source of carbon. Products observed included 1-phenylethanol,
2-phenylethanol, phenylacetate, salicylate, 2-hydroxyphenylacetate and
126.96.36.199 Anaerobic degradation
In a study to simulate the anaerobic degradation of landfill
leachate on aquifer material that was known to support methanogenesis,
no significant degradation of ethylbenzene was observed over the first
20 weeks of the experiment. However after 40 weeks the concentration
of ethylbenzene was found to be 26% of the original value, and after
120 weeks the concentration was < 1% of the original value (Wilson et
Ethylbenzene, at a concentration of 500 mg/litre, was not found
to be metabolized by or toxic to enriched methane-producing cultures
(Chou et al., 1978).
Ethylbenzene has been shown to undergo anaerobic degradation by
aquifer microorganisms under denitrifying conditions in the presence
of nitrate. A lag period of around 30 days was observed before
biodegradation of ethylbenzene occurred, but total removal of
ethylbenzene occurred within the 56-day test period. Using aquifer
material that had been previously contaminated with jet fuel, little
degradation of ethylbenzene occurred over the 180-day test period, but
this was enhanced by addition of nitrate (Hutchins et al., 1991a,b).
Kuhn et al. (1988) also studied the degradation of ethylbenzene under
denitrifying conditions using nitrate as the sole electron acceptor.
In their experiment an aquifer column was used which was capable of
degrading m-xylene. The concentration of ethylbenzene was only
slightly reduced during passage through the column, and the authors
concluded that microbial mineralization of ethylbenzene was unlikely
under denitrifying conditions. However, they did point out that the
experiment was only carried out for 6 days. A longer experimental
period might have allowed another microbial population to grow within
the column that could have been capable of degrading ethylbenzene.
Ethylbenzene, as a component of crude oil contamination of anoxic
groundwater, has been found to be degraded in the anoxic region, but
the rate of disappearance was found to increase significantly in the
more oxygenated parts of the aquifer (Cozzarelli et al., 1990).
4.2.2 Abiotic degradation
Ethylbenzene does not absorb UV-visible radiation appreciably at
wavelengths longer than 290 nm. This means that it is unlikely to be
directly photolysed in the troposphere or in solution, as the earth's
ozone layer absorbs radiation at wavelengths less than 290 nm (Crookes
& Howe, 1992). Mabey et al. (1982) stated that direct photolysis of
ethylbenzene is not environmentally significant.
Atmospheric oxidation of ethylbenzene is rapid and proceeds via
free-radical chain processes. The most important oxidant is the
hydroxyl radical, but ethylbenzene is also reactive with other species
found in the atmosphere, such as alkoxy radicals, peroxy radicals,
ozone and nitrogen oxides. Estimates for the half-life of
ethylbenzene in the atmosphere have been made from smog chamber
experiments and from knowledge of the reaction rate constant for
reaction with hydroxyl radicals. Atkinson (1985) reviewed the
available hydroxyl radical reaction rate constant data and recommended
a kOH value of 7.5 × 10-12 molecule-1.cm3.sec-1 at 25°C for
reaction with ethylbenzene.
A study by Callahan (1979) produced an atmospheric half-life of
around 15 h for ethylbenzene. Another report gave a figure of 51%
loss of ethylbenzene due to reaction with hydroxyl radicals in one day
(12 sunlight hours) (Singh et al., 1981, 1983). An atmospheric
lifetime of 14 sunlight hours has been quoted based on a value of kOH
(Singh et al., 1986). An important point when considering these data
is that the half-life calculated depends on several factors, including
temperature and also the actual concentration of hydroxyl radicals in
the atmosphere. It is known that the concentration of hydroxyl
radicals depends greatly on the amount of sunlight available; thus a
typical figure is around 2 × 106 molecules/cm3 in summer months,
falling by a factor of approximately 2 in winter months (Singh et al.,
1986). At night the concentration of hydroxyl radicals is negligible.
Even so, it can be seen that ethylbenzene is removed from the
atmosphere quite readily by reaction with hydroxyl radicals. It is
also possible that ethylbenzene will be removed from aquatic systems
by similar types of reactions, as hydroxyl radicals are known to exist
in aquatic systems.
It is considered unlikely that ethylbenzene will hydrolyse under
typical conditions found in the environment.
Ethylbenzene has an octanol-water partition coefficient of 3.13
(log value), which indicates that bioaccumulation of ethylbenzene
could take place. Using this partition coefficient, an estimated
bioconcentration factor (BCF) of 2.16 (log value) can be calculated
In goldfish, a measured BCF of 1.19 (log value) has been reported
(Ogata et al., 1984). No details of exposure concentrations or length
of exposure were given.
When the manila clam (Tapes semidecussata) was exposed to
ethylbenzene at a concentration of 0.08 mg/litre in water containing
other petroleum hydrocarbons, the concentration found in the tissue
was 0.37 mg/kg after 8 days. Depuration occurred rapidly after
exposure ceased, tissue concentrations being below the limit of
detection (< 0.13 mg/kg) after 15 days (Nunes & Benville, 1979).
The low measured BCF values indicate that biomagnification of
ethylbenzene through the aquatic food chain is unlikely. No aquatic
food chain magnification was predicted from the model calculations and
empirical observations by Thomann (1989).
5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE
5.1 Environmental levels
Measured levels of ethylbenzene in air are presented in Table 2.
Mean levels of ethylbenzene ranging from 0.74 to 100 µg/m3 have been
measured at urban sites. Industrial releases and vehicle emissions
are the principal sources of ethylbenzene. Levels found at rural
sites are generally < 2 µg/m3.
Ethylbenzene levels for indoor air are included in section 5.2.1.
5.1.2 Surface water and sediment
The levels of ethylbenzene found in surface water are shown in
Table 3. These are generally less than 0.1 µg/litre in non-industrial
areas. In industrial and urban areas ethylbenzene concentrations of
up to 15 µg/litre have been reported.
In 1985, 21 water samples and 21 bottom sediment samples were
collected at 7 sites in Japan and were analysed for the presence of
ethylbenzene. None of the water samples contained ethylbenzene; 3 of
the sediment samples from one site contained ethylbenzene
concentrations of 0.9 to 2.7 µg/kg dry weight. The detection limit
was 0.02 µg/litre for water and 0.8 µg/kg dry weight for bottom
sediment. In 1986, ethylbenzene was detected in 7 out of 133 samples
of surface water at 5 out of 46 sites (0.03-1.1 µg/litre) and in
28 out of 120 samples of bottom sediment at 15 out of 40 sites
(0.5-28 µg/kg dry weight). The detection limit was 0.03 µg/litre for
water and 0.5 µg/kg dry weight for sediment (EAJ, 1989).
Staples et al. (1985) reviewed the US EPA's STORET water quality
database and reported that median levels of ethylbenzene in ambient
surface water were less than 5.0 µg/litre between 1980 and 1982.
Ethylbenzene was detected in 10% of the 1101 samples collected during
this period. The median ethylbenzene concentration in sediment was
5.0 µg/kg dry weight, the compound being detected in 11% of the 350
In a study of the Tees Estuary, United Kingdom, levels of
ethylbenzene between 1 and 5 µg/kg were found in river sediment from a
heavily industrialized area (Whitby et al., 1982).
Table 2. Concentrations of ethylbenzene in air
Sampling source Concentration (µg/m3) References
Rural 0.23-1.6 (range of means) Petersson (1982), Clark et al. (1984b), Jüttner (1988), Lanzerstorfer
& Puxbaum (1990), Kawata & Fujeda (1993)
Urban 0.74-100 (range of means) Grob & Grob (1971), Bos et al. (1977), Louw et al. (1977), Singh et
(maximum value, 360) al. (1981; 1982; 1986), Nelson & Quigley (1982), Harkov et al. (1983),
De Bortoli et al. (1984), Clark et al. (1984a), Guicherit & Schulting
(1985), Jonsson et al. (1985), Hunt et al. (1986), Bruckmann et al.
(1988), Lanzerstorfer & Puxbaum (1990), Chan et al. (1991a), Derwent
(personal communication to the IPCS, 1991),
Industrial/residential site 22.0 (annual mean) Bruckmann et al. (1988)
near a rubber factory
Industrial site near 10.8 (annual mean) Bruckmann et al. (1988)
Industrial site 94 (mean) Kroneld (1989)
near automotive 52 (< 1.6 km away) Sexton & Westberg (1980)
painting plant 11.5 (6.4 km away)
5 (17.6 km away)
Near to car plant 86 Petersson (1982)
27.8 (1 km away)
Road tunnels 2.1-48.2 Bos et al. (1977), Hampton et al. (1983), Dannecker et al. (1990)
Motorway 147 (mean) Thorburn & Colenutt (1979)
Table 3. Concentrations of ethylbenzene in water
Sampling source Concentration Reference
Non-industrial river sites < 0.1 Waggott (1981), McFall et al. (1985), SAC (1989)
Industrial/urban river sites 1.9-15 Gomez-Belinchon et al. (1991)
(range of means)
Estuary (industrial area) ND-1.8 Whitby et al. (1982)
Seawater 0.0018-0.026 Gschwend et al. (1982), Gomez-Belinchon
(range of means) et al. (1991)
Sea near offshore oil 0.07 Sauer (1981)
Rainwater 0.0006-0.009 Kawamura & Kaplan (1983), Pankow et al. (1984)
Uncontaminated NDb-0.07 Kenrick et al. (1985)
Contaminated 30-2000 Tester & Harker (1981), Van Duijvenbooden &
Kooper (1981), Stuermer et al. (1982), Rao et al.
Water-table at a solvent up to 28 000 Cline & Viste (1985)
Table 3. (Cont'd)
Sampling source Concentration Reference
Effluent from wastewater/ NDc-14 Kennicutt et al. (1984); Namkung & Rittmann
sewage treatment works (1987); Feiler et al. (1979); Michael et al.
(1991); Gossett et al. (1983)
Landfill leachate 1.7-2310 Först et al. (1984); Reinhard et al. (1984);
Van Duijvenbooden & Kooper (1981); Cline &
a ND = not detected
b detection limit = 0.01 µg/litre
c detection limit not stated
A sludge characterization study for a slip containing wastewater
sludge situated in Baltimore Harbour, USA, was performed. The slip
contained an estimated 14 100 m3 of sludge, which averaged 20% solids
(by weight). Organic compounds were found to be the primary
constituents in the sludge, the highest concentrations being
represented by benzene, ethylbenzene, toluene and xylenes (Mott &
The levels of ethylbenzene in groundwater are summarized in Table
Ethylbenzene levels in uncontaminated groundwater are generally
< 0.1 µg/litre. However, much higher levels have been reported for
groundwater contaminated via waste disposal, fuel spillage and
industrial facilities. At a solvent recovery facility, ethylbenzene
concentrations of up to 28 000 µg/litre were measured.
Lesage et al. (1990) detected ethylbenzene in 3% of anoxic
groundwater samples at a concentration of 2 µg/litre. Goodenkauf &
Atkinson (1986) analysed 63 wells and detected ethylbenzene in only
one at a concentration of 0.99 µg/litre; the detection limit was
0.5 µg/litre. Ethylbenzene was found in 3 out of 466 groundwater
samples collected in the USA in 1982. The maximum concentration was
1.1 µg/litre and the detection limit 0.5 µg/litre (Cotruvo, 1985).
5.1.4 Urban run-off, effluent and landfill leachate
The levels of ethylbenzene in effluent from wastewater/sewage
treatment plants and landfill leachate are summarized in Table 3.
When Perry et al. (1979) analysed a range of industrial effluent
samples, 19 contained < 10 µg/litre, 4 contained 10-100 µg/litre and
2 contained > 100 µg/litre. Staples et al. (1985) reported that
ethylbenzene was detected in 7.4% of 1368 industrial effluent samples
collected between 1980 and 1983, the median concentration being less
than 3.0 µg/litre.
Cole et al. (1984) detected ethylbenzene in 4% of urban run-off
samples. Concentrations ranged from 1-2 µg/litre; however, no
detection limits were stated.
ATSDR (1990) reported that ethylbenzene was detected in 9.22%
soil samples from 1177 sites. The geometric mean of these samples was
Several species of aquatic organisms have been analysed for
ethylbenzene (Table 4).
Table 4. Levels of ethylbenzene in aquatic species (Gossett et al., 1983)
Species Ethylbenzene level
µg/kg wet weight
Pacific sanddab (Citharichthys xanthostigma) (liver) <0.3
scorpion fish (Scorpaena guttata) (liver) <0.3
Dover sole (Microstomus pacificus) (liver) 0.3
white croaker (Genyonemus lineatus) (liver) 4
shrimp (muscle) <0.3
invertebrate (whole body) <0.3
NOTE: No detection limits were stated; organisms were collected from an
area near to the discharge zone of a waste treatment plant; ethylbenzene
levels of 14 µg/litre in effluent and 0.5 µg/kg (dryweight) in sediment
were measured in the area at the time of sampling.
In 1986, ethylbenzene was detected in 43 out of 138 fish samples
at 16 out of 42 sites in Japan, the concentrations ranging from 1.0 to
9.8 µg/kg wet weight. The detection limit was 1 µg/kg wet weight
Staples et al. (1985) reviewed the US EPA's STORET water quality
database and reported that ethylbenzene was not detected in 97 biota
samples (detection limit, 0.025 mg/kg wet weight).
Lockhart et al. (1992) reported data on ethylbenzene levels in
freshwater fish sampled in the Canadian Arctic in 1985 and 1986. Mean
ethylbenzene concentrations ranged from 2.45 to 49.6 µg/kg in muscle
tissue and from 1.81 to 46.3 µg/kg in liver tissue for burbot. In
whitefish muscle tissue samples, mean ethylbenzene concentrations
ranged from 7.46 to 104 µg/kg.
5.2 General population exposure
5.2.1 Environmental sources
The magnitude of natural releases into the environment has not
Although ethylbenzene is ubiquitous in rural and urban
atmospheres, levels in urban areas are elevated due to vehicular and
industrial emissions. Ethylbenzene was not detectable in some rural
samples, while those taken on busy urban streets contained levels up
to 99 µg/m3 (23.1 ppb) (ATSDR, 1990).
The Environmental Protection Agency (USA) conducted a study of
ethylbenzene levels in public access buildings and found that
concentration, which was 387 µg/m3 (90 ppb) at the time construction
was completed, declined to 39 µg/m3 (9 ppb) following several months
of occupation of the building. This indicated that building materials
and/or finishings, such as paints, carpets and adhesives, were likely
sources of emissions (Pellizzari et al., 1984). Subsequent emission
studies using inhalation chambers revealed that ethylbenzene was
emitted from glued carpet at a mean level of 6.4 (± 3.2) µg/m3,
corresponding to an emission rate of 77 (± 39) ng/min per m2 (Wallace
et al., 1987c). Hodgson et al. (1991) studied the emissions of
volatile organic compounds in a new office building over a period of
14 months. Ethylbenzene levels in the building ranged from 7.0 to
11.8 µg/m3, as compared to 1.8 µg/m3 in the outdoor air. The
authors suggested that motor vehicles in the underground carpark of
the building were one of the major sources of ethylbenzene, but this
area was not specifically monitored.
Wallace et al. (1987a,b) monitored ethylbenzene in breathing-zone
air, exhaled air and ambient air samples taken from some of the home
backyards of 400 residents of an industrial/chemical manufacturing
area (the cities of Bayonne and Elizabeth, New Jersey, USA). Median
levels of ethylbenzene ranged from 4.6 to 7.1 µg/m3 for breathing-
zone air, 1.3 to 2.9 µg/m3 for exhaled air and 2.2 to 4.0 µg/m3
for backyard air. Personal air monitoring conducted at home
yielded high ethylbenzene levels, believed to be due to the presence
of the chemical in tobacco smoke. The maximum geometric mean
ethylbenzene exposure of people living in homes with smokers (13
µg/m3) was approximately 1.5 times the geometric mean of people
living in homes without smokers (8 µg/m3). Wallace et al. (1987a)
found the geometric mean level of ethylbenzene in the expired air of
smokers (n=200) to be 2 to 3 times higher than in that of non-smokers
(n=322). Wallace et al. (1987a) estimated that the total amount of
ethylbenzene in the mainstream smoke of a single cigarette, containing
16 mg of tar and nicotine, was 8 µg.
In another study, the blood concentration of ethylbenzene was
measured in 13 non-smokers and 14 cigarette smokers, all living in an
urban area. The concentration of ethylbenzene in blood ranged from
175 to 2284 ng/litre and 378 to 2697 ng/litre, respectively
(Hajimiragha et al., 1989).
Fellin & Otson (1993) monitored indoor air for ethylbenzene in
754 randomly selected Canadian residences in 1986. Mean ethylbenzene
concentrations were 6.46 µg/m3 in winter, 8.15 µg/m3 in spring, 4.35
µg/m3 in summer and 13.97 µg/m3 in autumn.
Wallace et al. (1989) carried out a study on seven volunteers who
performed 25 common activities thought to increase personal exposure
to volatile organic compounds during a 3-month period. Monitoring
personal, indoor and outdoor air levels, as well as exhaled breath,
revealed that painting and using a carburettor cleaner resulted in an
80-fold increase in ethylbenzene exposure. Combustion sources
(including cigarette smoke), gasoline vapours and consumer products
containing ethylbenzene increased exposures by up to 6 times over the
Chan et al. (1991b) studied exposure of commuters in Boston, USA
to ethylbenzene. These individuals spent 1.3 to 1.7 h per day (5% to
7% of the day) commuting and this contributed 10-20% of their total
daily ethylbenzene exposure. The results showed that the highest
exposures were associated with commuting by car (5.8 µg/m3) and that
the use of car heaters resulted in even higher in-vehicle levels of
ethylbenzene. Heater use resulted in a passenger compartment mean
ethylbenzene level of 8 µg/m3, whereas non-use resulted in 3.7
µg/m3. The authors postulated that heaters can increase influx of
both the vehicle's own exhaust and general roadway exhaust.
Coal-fired power stations have been found to emit ethylbenzene
along with other volatile organic compounds (Garcia, 1992).
Bevan et al. (1991) monitored exposure to vehicle emissions while
commuting by bicycle on urban roads in Southampton, United Kingdom and
compared it with ethylbenzene exposure for a typical suburban area.
Mean ethylbenzene levels on urban roads were 30.3 µg/m3 compared with
15.1 µg/m3 for suburban areas. The authors reported that 2 metres
from the exhaust of a stationary idling vehicle the mean ethylbenzene
level was 137 µg/m3.
Ashley et al. (1994) analysed the blood ethylbenzene
concentration of 631 non-occupationally exposed people in the USA.
The mean and median levels were 0.11 and 0.06 µg/litre, respectively,
and the detection limit was 0.02 µg/litre.
Kawai et al. (1992) evaluated urinalysis and blood analysis as
means of detecting human exposure to ethylbenzene and some other
volatile organic compounds, using 143 exposed and 20 non-exposed
workers. They found that both solvent concentration in blood and
metabolite concentration in urine correlated significantly with the
concentration of the solvent in air.
Pellizzari et al. (1982) analysed volatile organic compounds in
human milk samples taken from lactating women living in urban areas of
the USA and found ethylbenzene in all eight samples. Ethylbenzene has
also been detected in human axillary volatiles (Labows et al., 1979).
However, both these studies were based solely on qualitative scans of
the mass spectra peaks from GC/MS analysis; no detection limits were
Ethylbenzene has been detected in several types of dried legumes.
Levels of between 0 and 11 µg/kg (mean 5 µg/kg) in beans, 13 µg/kg in
split peas and 5 µg/kg in lentils were measured (Lovegren et al.,
Although ethylbenzene has been detected in the skin of roasted
guinea hens (at a level of 2 µg/kg) by Noleau & Toulemonde (1988), the
authors did not state whether the source of the ethylbenzene was
directly from the skin or the cooking process.
Otson et al. (1982) found that ethylbenzene levels in Canadian
treated potable water ranged from <1 to 10 µg/litre. Westrick et al.
(1984) reported that ethylbenzene was detected in 8 out of 945 samples
of finished (undefined) water from groundwater supplies. The levels
ranged from 0.74 to 12 µg/litre. Coleman et al. (1984) analysed
drinking-water from Cincinnati, USA and found an ethylbenzene level
of 0.036 µg/litre.
Durst & Laperle (1990) studied the migration of ethylbenzene from
polystyrene containers into stored deionized water. The water samples
were stored for up to 90 days at temperatures ranging from 24 to 66°C.
Migration of ethylbenzene increased with time and storage temperature.
The levels in the water samples ranged from 16 µg/litre on day 1 to 41
µg/litre at 24°C, 48 µg/litre at 38°C and 107 µg/litre at 52°C.
Ethylbenzene levels of up to 209 µg/litre were detected on day 8 at
5.3 Occupational exposure during manufacture, formulation or use
Occupational exposure to ethylbenzene alone is rare.
Simultaneous exposure to other organic solvents usually occurs.
The following ethylbenzene exposure levels have been reported
from various occupational settings: exposure to gasoline, mean
concentration of less than 0.08 mg/m3 (Rappaport et al., 1987);
exposure to jet fuel, mean concentrations of 0.02 mg/m3 (4 h) and
0.07 mg/m3 (15 min) and maximum concentrations of 1.3 mg/m3 (4 h)
and 8.0 mg/m3 (15 min) (Holm et al., 1987); exposure in petroleum and
chemical factories, mean concentration of 7.7 mg/m3 (Inoue et al.,
1995); exposure while varnishing vehicles, average concentration of 17
mg/m3 (Angerer & Wulf, 1985); exposure during paint-rolling and
brushing, maximum concentration of 3.2 mg/m3 (Verhoeff et al.,
1988); exposure in a petroleum company and a pharmaceutical factory,
concentration range of 0.05-23 mg/m3 (Lu & Zhen, 1989).
During painting operations, ethylbenzene and some other volatile
organic compounds were detected in the working atmosphere at
concentrations ranging from 0.1 to 69.1 ppm (Vincent et al., 1994).
5.3.1 Biological monitoring
Determination of mandelic acid in urine has been recommended as a
biomarker of exposure to ethylbenzene. In studies by Bardodej &
Bardodejová (1970) and by Gromieck & Piotrowski (1984), exposure to
ethylbenzene at 430 mg/m3 (100 ppm) for 8 h resulted in 13 mmol/litre
and 7.8 mmol/litre, respectively, of mandelic acid in the
end-of-exposure urine samples. A value of 1.5 g mandelic acid per g
creatinine (about 10 mmol/litre) in the post-shift urine has been
proposed as a Biological Exposure Index (ACGIH, 1985-1986).
In specific analysis (e.g., by gas chromatography), the urinary
level of mandelic acid is negligible (less than 0.2 mmol/litre) in the
general population. However, certain drugs may be metabolized to
mandelic acid (Aitio et al., 1994).
Monitoring of personal exposure has shown that low ethylbenzene
concentrations of approximately 8.6 mg/m3 (2 ppm) correlate
significantly (correlation coefficients of 0.6-0.7) with urinary
phenylglyoxylic acid concentration, suggesting that measurements of
this acid in the urine could be used for biomonitoring (Inoue et al.,
6. KINETICS AND METABOLISM IN LABORATORY ANIMALS AND HUMANS
6.1.1 Skin absorption
One human subject was exposed for 2 h to ethylbenzene vapour at
concentrations ranging from 650 to 1300 mg/m3 in an exposure chamber.
The exposed skin accounted for 90-95% of the total skin area. Clean
breathing air was provided by means of a gas-tight respirator. The
mandelic acid concentration in urine, before, during and up to 6 h
after exposure, was within physiological limits (approximately 2.7
mg/litre). The authors concluded that the skin is not a relevant
route of entry into the body for ethylbenzene vapours (Gromiec &
The possible absorption of liquid ethylbenzene across human sin
has also been studied (Dutkiewicz & Tyras, 1967). Ethylbenzene
(0.2 ml=174 mg) was applied in a watch glass tightly fixed on the
forearm. The exposed skin area was 17.3 cm2. After 10-15 min the
contents of the watch glass space was extracted with ethanol and the
recovered amount of ethylbenzene determined spectrophotometrically.
On the basis of the quantity of ethylbenzene not recovered, the mean
absorption rate for seven people was calculated to be 28 mg/cm2 per
hour (range 22-33 mg cm2 per hour).
The penetration rate of ethylbenzene through excised rat skin has
been determined in a penetration chamber. One ml of ethylbenzene was
applied to 2.55 cm2 skin. After a 6-h application period, the
penetration rate was found to be about 0.99 nmoles/cm2 per min
(6 µg/cm2 per hour (Tsuruta, 1982).
Percutaneous absorption of ethylbenzene has been studied in
hairless mice (11 animals) (Susten et al., 1990). 14C-ring-labelled
ethylbenzene (in a volume of 5 µl) was injected into a chamber glued
onto the back skin (0.8 cm2), and the animals were housed in
metabolism cages for 4 h. During that period exhaled breath samples
were collected. At the end of 4 h, the animals were killed and the
absorbed dose was measured in the excreta and carcass. A total of
95.2 (± 1)% of the nominal dose was recovered. The absorption rate
was calculated to be 0.037 (± 0.0315) mg/cm2 per min (2.2 ± 1.9
mg/cm2 per hour).
Dermal absorption of volatile organic chemicals from aqueous
solutions has been studied in male Fischer-344 rats. For 24 h the
rats were exposed (3.1 cm2 dorsal shaved skin) to 2 ml (in a glass
exposure cell) of one-third saturated, two-thirds saturated, or a
fully saturated solution of ethylbenzene. Blood samples were obtained
at 0, 0.5, 1, 2, 4, 8, 12 and 24 h. The peak blood level (exposure to
neat ethylbenzene) was 5.6 mg/litre. The level reached a maximum
within 4 h and then either remained at about the same level for the
duration of the exposure or decreased. The blood levels were directly
related to the exposure concentrations (Morgan et al., 1991).
The data concerning skin permeability of ethylbenzene in humans
(Dutkievicz and Tyras, 1967) is not consistent with the animal data.
The reliability of the estimated fluxes of ethylbenzene through human
skin must be questioned because they are many times higher than the
measured fluxes through rat skin, whereas from studies of in vitro
percutaneous absorption it is known that rat skin is more permeable
than human skin (mean ratio about 3) for several chemicals (Barber et
6.1.2 Absorption via inhalation
When volunteers (number not given) were exposed to 99, 185, 198
or 365 mg/m3 (23, 43, 46 or 85 ppm) ethylbenzene for 8 h, 64% of the
inhaled ethylbenzene was taken up by the respiratory tract (Bardodej &
Bardodejova, 1966). In another study, six volunteers were exposed
under controlled conditions for 8 h to 18, 34, 80, 150 or 200 mg/m3.
The retention of ethylbenzene in the lungs (difference in
concentration between inhaled and exhaled air) was 49% (± 5%)
independent of the exposure concentration (Gromiec & Piotrowski,
When volunteers were exposed to 430 mg/m3 or 870 mg/m3 of
"industrial xylene" (containing 40% ethylbenzene and 60% xylenes) for
2 h, about 60% was taken up, independent of concentration. If the
workload increased during exposure, the retention dropped to 50%
(Ĺstrand et al., 1978).
In a study by Chin et al. (1980a), rats (male, Harlan-Wistar)
were exposed to 14C-labelled ethylbenzene at a concentration of 1000
mg/m3 for 6 h. Assuming a ventilation rate of 100 ml/min, each rat
had an estimated intake of 36 mg ethylbenzene, of which 44% was
6.1.3 Absorption after oral intake
Toxicity studies in various animal species show indirectly that
ethylbenzene is absorbed after oral administration (Wolf et al., 1956,
NTP, 1992). Moreover, in one study, ethylbenzene appeared to be
rapidly and well absorbed from the gastro-intestinal tract since more
than 80% of the administered radioactively labelled compound was
recovered in urine within 48 h (Climie et al., 1983).
When volunteers (n=12) were exposed for 2 h to 100 or 200 ppm
"industrial xylene", the amount of ethylbenzene taken up correlated
with the amount of body fat ("industrial xylene" consisted of 40.4%
ethylbenzene, 49.4% m-xylene, 8.8% o-xylene and 1.4% p-xylene).
The concentration of ethylbenzene ranged from 4 to 8 mg/kg in
subcutaneous adipose tissue 30 min after exposure. There was,
however, a negative correlation between the concentration in the
adipose tissue and the estimated relative amount of fat (Engström &
The ethylbenzene concentration in the subcutaneous fat of workers
in a styrene polymerization plant was less than 0.8 mg/kg. The level
of exposure to ethylbenzene was reported to be below 17 mg/m3 (4
ppm). The 25 workers were exposed to a variety of other chemicals as
well (Wolff et al., 1977).
When rats were exposed to 1000 mg/m3 14C-ring-labelled
ethylbenzene for 6 h, 0.2% of this radioactivity was found 42 h later
in the tissues, mainly in the liver, gastrointestinal tract, fat and
the carcass (Chin et al., 1980a).
In a study by Engström et al., (1985), male Wistar rats (n = 20)
were exposed to 215, 1290 or 2580 mg ethylbenzene/m3 (50, 300 or 600
ppm) for 6 h/day, and 5 days/week for up to 16 weeks. The
concentration of ethylbenzene in perirenal fat was measured in weeks
2, 5 and 9. There were no consistent changes in ethylbenzene levels
during the course of exposure. After 16 weeks the amount of
ethylbenzene in perirenal fat was 8.5, 167.7 and 262.2 mg/kg fat at
the three exposure levels, respectively.
6.3 Metabolic transformation
Metabolic pathways of ethylbenzene based on urinary metabolites
have been proposed for humans (Fig. 1) and for rats (Fig. 2). The
main metabolic pathway is oxidation of the side chain, both in humans
and in animals. However, it has been demonstrated that there are both
qualitative and quantitative inter-species differences in the
metabolites produced (Engström et al., 1984; Engström 1984b). In
humans, the main metabolites of ethylbenzene are mandelic and
phenylglyoxylic acids. In several animal species the metabolic
transformation continues to benzoic acid, leading to excretion of
hippuric acid after conjugation with glycine. This conjugate is
generally one of the main urinary metabolites, together with mandelic
acid, in rats and dogs (Chin et al., 1980b). Hydroxylation of the
aromatic nucleus is a minor pathway. In the rabbit this phenolic
pathway accounts for less than 2% of the ethylbenzene absorbed (Kiese
& Lenk, 1974).
Ethylbenzene is metabolized by the microsomal cytochrome P-450
enzyme system. Although specific isozymes have not been unequivocally
identified, enzyme induction studies suggest that CYP2B1/2, CYP1A1/2
and CYP2E1 may be involved (see section 7.8).
Four male volunteers were exposed to 655 mg/m3 (150 ppm)
ethylbenzene for 4 h and urine was collected for 24 h. Mandelic acid
(71.5%) and phenylglyoxylic acid (19.1%) were the main metabolites,
but smaller amounts of 1-phenylethanol, p-hydroxyacetophenone,
m-hydroxyacetophenone, 1-phenyl-1,2-ethandiol, 4-ethylphenol,
omega-hydroxyacetophenone and acetophenone were also found. Ring
oxidation accounted for 4.0%. Simultaneous exposure to 150 ppm
m-xylene did not alter the urinary metabolite pattern, but it
delayed excretion and decreased the amounts of metabolites excreted
(Engström et al., 1984). Mandelic acid (64%) and phenylglyoxylic aid
(25%) were found to be the main urinary excretion products in
volunteers after an 8-h exposure to 99-365 mg/m3 (23-85 ppm)
ethylbenzene (Bardodej & Bardodejová, 1970).
When two volunteers were exposed by inhalation to 430 mg/m3 (100
ppm) ethylbenzene for 4 h, most of the mandelic acid was excreted as
the R-enantiomer (Drummond et al., 1989).
In a study by Korn et al. (1992), urinary samples from workers
exposed to ethylbenzene, toluene and xylenes were analysed. The
average urinary concentration of phenylglyoxylic acid was 50.1
mg/litre. The concentration of mandelic acids was 135.2 mg/litre, of
which 127.8 mg/litre was R-mandelic acid and 7.3 mg/litre was
S-mandelic acid. The R/S ratio was independent of the air
concentration of ethylbenzene, which varied between 6.4 and 142 mg/m3
(1.5 and 33 ppm).
Four female histology laboratory assistants were exposed to a
mixture of xylenes (75%) and ethylbenzene (25%). The air concentration
of the solvent was 160-179 mg/m3, and the concentration of
ethylbenzene in blood collected at the end of the working day was
reported to be 0.5 to 0.8 mg/litre. The 24-h excretion of
2-ethylphenol in urine varied between 4.4 and 6.0 mg corresponding to
1 to 1.5% of the retained ethylbenzene (Angerer & Lehnert, 1979). The
findings by Angerer & Lehnert (1979) that ethylbenzene is metabolized
to 2-ethylphenol could not be verified by Engström et al. (1984).
Male Wistar rats (6 per group) were exposed for 6 h to
ethylbenzene at 1290 or 2580 mg/m3 (300 or 600 ppm). The urine was
collected for 48 h from the onset of exposure. Altogether, 14
different metabolites from ethylbenzene were identified. The main
metabolites were 1-phenylethanol, mandelic acid and benzoic acid, each
of which accounted for about 25%. Only 13% (low dose) and 6% (high
dose) of the estimated absorbed doses were eliminated during the 6-h
exposure. Over the 48-h period, the corresponding values were 83% and
59%, respectively. The metabolic pattern was similar, irrespective of
the exposure level (Engström, 1984b).
In another study, male Wistar rats (20 per group) were exposed to
215, 1290 or 2580 mg ethylbenzene/m3 (50, 300 or 600 ppm) for 6
h/day, 5 days/week, for up to 16 weeks. Urinary excretion of some of
the metabolites was measured in weeks 2, 5 and 9. A significant
dose-related percentage decrease of phenylglyoxylic acid and hippuric
acid plus benzoic acid was found. A corresponding increase of
1-phenylethanol and omega-hydroxyacetophenone excretion was also
noted. The total amount of metabolites in urine collected during the
24 h after onset of exposure remained, however, constant at each
exposure level throughout the study (Engström et al., 1985).
When a single oral dose of 318 mg ethylbenzene/kg body weight was
administered to rabbits, the main urinary metabolites found were
hippuric acid and methylphenylglucuronic acid, which together
represented 60-70% of the dose, while mandelic acid and phenaceturic
acid were minor metabolites (El Masry et al., 1956).
It has been established in in vivo studies that experimental
animals convert ethylbenzene mainly to the R-enantiomer of mandelic
acid (Drummond et al., 1990). In an in vitro study it was found
that ethylbenzene is hydroxylated by cytochrome P-450cam (from
Escherichera coli) almost exclusively at the secondary ethyl carbon
with about a 2:1 ratio of R:S products (Filipovic et al., 1992).
The rates of metabolism of ethylbenzene have been studied in
vitro in rabbit liver and lung. Organs from five female animals
were used, but details of the experimental procedures were not
reported. For the liver (mean weight 76 g) the rate of metabolism was
453 nmol/g tissue per 10 min (34.4 µmol per liver per 10 min or 11.7
nmol per nmol cytochrome P-450 per 10 min). The corresponding figures
for lung (mean weight 7.7 g), were 680 nmol, 5.3µmol and 200.1 nmol,
respectively. Thus, lung tissue may significantly contribute to the
body clearance of ethylbenzene in rabbits (Sato & Nakajima, 1987).
6.4 Elimination and excretion
In humans, ethylbenzene is mainly excreted in the urine as
mandelic and phenylglyoxylic acids (Bardodej & Bardodejová, 1970;
Ĺstrand et al., 1978; Engström et al., 1984; Gromiec & Piotrowski,
1984). Only up to 5% of retained ethylbenzene is estimated to be
exhaled without transformation (Ĺstrand et al., 1978). The
elimination half-lives of ethylbenzene in exhaled air and urine have
been estimated to be 0.5-3 h and 8 h, respectively (Wolff, 1976). In
human volunteers exposed to 100 or 200 ppm "industrial xylene" for
2 h, there was no decline in the concentration of xylenes plus
ethylbenzene in the gluteal subcutaneous adipose tissue between 30 min
and 22 h after exposure (Engström & Bjurström, 1978). The elimination
of mandelic acid has been found to be biphasic, with half-lives of 3.1
and 24.5 h (Gromiec & Piotrowski, 1984).
The elimination kinetics for 10 volatile organic compounds,
including ethylbenzene, has been studied in human volunteers exposed
to a variety of consumer products. Breath samples were collected
post-exposure and analysed by GC/MS. The half-lives for the 10
chemicals varied from a few hours to 1-2 days. The authors concluded
that volatile organic compounds exhibit relatively short residence
times in the body (Pellizzari et al., 1992).
Male Harlan-Wistar rats exposed to 14C-ring-labelled
ethylbenzene (1000 mg/m3) for 6 h excreted 82% of the radioactivity
in the urine, 8.2% in expired air (0.03% as CO2) and 0.7% in faeces.
After 42 h, 0.2% remained in the tissues. The remaining 8.3% could not
be accounted for (Chin et al., 1980a).
7. EFFECTS ON LABORATORY MAMMALS AND IN VITRO TEST SYSTEMS
7.1 Single exposure
Single high exposures to ethylbenzene cause irritation of the
mucous membranes and central nervous system effects. The results from
single exposure in vivo studies are summarized in Table 5.
Table 5. Single exposure of animals to ethylbenzenea
Species Route Dose Parameter Reference
Rat oral 3.5 g/kg LD50 Wolf et al. (1956)
Rat oral 4.7 g/kg LD50 Smyth et al. (1962)
Rat inhalation 9.37 g/m3 (2180 ppm) Minimum Molnár et al. (1986)
Rat inhalation 17.2 g/m3 (4000 ppm) 1 h LC10 Smyth et al. (1962)
Rat inhalation 17.2 g/m3 (4000 ppm) 4 h LC50 Smyth et al. (1962)
Rat inhalation 34.4 g/m3 (8000 ppm) 1 h LC100 Smyth et al. (1962)
Rabbit dermal 77.4 g/kg LD50 Smyth et al. (1962)
a Additional information is given in the following reviews: DFG (1985), ECETOC (1986).
7.2 Short-term exposure
In a short-term study, six male rats (Sprague Dawley) were
exposed for 6 h/day during 3 consecutive days to 8.6 g/m3 (2000 ppm)
ethylbenzene. The animals were killed 16-18 h after the last
exposure. Small increases in dopamine and noradrenaline levels and
turnover in various parts of the hypothalamus and the median eminence
were reported. Ethylbenzene was also found to produce selective
reduction in prolactin and corticosterone secretion and selective
increase in dopamine turnover within the dopamine-cholecystokinin-8-
immuno-reactive nerve terminals of the nucleus accumbens (posterior
part) (Andersson et al., 1981).
When eight male rabbits (New Zealand) were exposed 12 h daily for
7 days to 3.22 g/m3 (750 ppm) ethylbenzene, there was a marked
(p<0.05) depletion of striatal and tuberoinfundibular dopamine. Such
an effect was also caused by intraperitoneal dosing of rabbits (eight
per group) with mandelic or phenylglyoxylic acid (4 mmol/kg per day
for 3 days) in saline (Romanelli et al., 1986).
In a 4-week inhalation study Fischer-344 rats (five of each sex
per group) were exposed to ethylbenzene for 6 h/day, 5 days per week,
at exposure levels of 0, 426, 1643 or 3363 mg/m3 (0, 99, 382 or 782
ppm). At the two highest exposure levels, sporadic lacrimation and
salivation, as well as significantly (p<0.05) increased liver
weights, were seen. At the highest exposure level, there was a small
increase in leukocyte counts and, in males, a marginal increase in
platelet counts (Cragg et al., 1989).
In the same study, mice (B6C3F1) of both sexes were similarly
exposed. At 1643 and 3363 mg ethylbenzene/m3, females showed
significantly (p<0.01) increased absolute and relative liver weights.
In males a significantly (p<0.05) increased relative liver-to-brain
weight ratio was seen. Male and female rabbits (New Zealand White)
were also used in this study. The exposure levels were 0, 1643, 3363
and 6923 mg/m3 (0, 382, 782 and 1610 ppm). At the highest exposure
level females gained weight more slowly than controls but neither sex
exhibited gross or microscopic organ changes (Cragg et al., 1989).
No changes in mortality pattern were seen in the three species.
There were no changes in clinical chemistry parameters in rats or
rabbits. Mice were not subjected to clinical chemistry or
haematological examinations due to the small volume of blood that
could be collected. For similar reasons, urinalyses were performed
for rats (no change) but not for mice. Rabbits were excluded from
urinalysis for logistical reasons. No changes in gross or microscopic
pathology were noted in any of over 30 tissues from each of the three
species when the animals were exposed at the highest concentration
(Cragg et al., 1989).
7.3 Long-term exposure
7.3.1 Oral exposure
Matched groups of 10 Wistar female rats were given daily
ethylbenzene doses of 0, 13.6, 136, 408 or 680 mg/kg by stomach tube
5 days a week for 6 months. The two highest dosages induced slight
increases in liver and kidney weights and slight cloudy swelling of
parenchymal liver cells and of the tubular epithelium in the kidney
(Wolf et al., 1956).
7.3.2 Inhalation exposure
In a 13-week National Toxicology Program study, groups of 10 rats
(F-344/N) and 10 mice (B6C3F1) of each sex were exposed for 6 h (plus
10 min to reach 90% of the target chamber concentration) per day,
5 days per week for 92 (female rats), 93 (male rats), 97 (female mice)
or 98 (male mice) days, at ethylbenzene concen-trations of 0, 430,
1075, 2150, 3225 or 4300 mg/m3 (0, 100, 250, 500, 750 or 1000 ppm).
Blood for clinical chemistry and haematological examination was
collected on study days 4 and 23 and again at week 13 from both male
and female rats. Dose-related increases in absolute liver weight were
seen in both sexes of mice exposed to the two highest dose levels, and
the relative kidney weight of female mice exposed to 4300 mg/m3 was
greater than that of the controls. Increased absolute and relative
liver and kidney weights were seen in male rats exposed to the two
highest dose levels. Increased absolute liver and kidney weights were
seen in female rats exposed to the three highest dose levels, but no
increased relative liver and kidney weights were seen. No chemically
related histopathological changes were observed in any rat or mouse
tissues. Clinical chemistry results were negative (NTP, 1992).
In another study, groups of five male rats (Wistar) were exposed
for 6 h/day, 5 days/week to ethylbenzene concentrations of 0, 215,
1290 or 2580 mg/m3 (0, 50, 300 or 600 ppm) and sacrificed after 2, 5,
9 or 16 weeks of exposure. At 2580 mg/m3 liver cells showed a slight
proliferation of smooth endoplasmic reticulum, slight degranulation
and splitting of rough endoplasmic reticulum, and enlarged
mitochondria. At the same dose level, liver microsomal protein, but
not cytochrome P-450, concentration was slightly increased. There was
also an increase in NADPH-cytochrome c reductase, 7-ethoxycoumarin-
O-deethylase and UDPG-transferase activities in the liver. In the
kidney only the two latter enzymes showed dose-related increases.
Urinary excretion of thioethers was measured to ascertain the
generation of electrophilic intermediates during ethylbenzene
metabolism. Excretion of thioethers increased in a dose-dependent
manner, with some fluctuation over the course of 7 weeks, reaching
about eight times the control level at 2580 mg ethylbenzene/m3.
However, there was no decrease in hepatic or renal levels of
glutathione (GSH), indicating that the cells were able to maintain the
intra-cellular homeostasis of GSH during exposure (Elovaara et al.,
In inhalation experiments, matched groups of 10-25 male and
female Wistar rats, 5-10 guinea-pigs, 1-2 rabbits and 1-2 rhesus
monkeys of either sex or both sexes were all exposed 7 h/day, 5
days/week, for up to 6 months. The exposure levels were 0, 1720 and
2580 mg/m3 (0, 400 and 600 ppm) for 186 days, 5375 mg/m3 (1250 ppm)
for 214 days (no monkeys) or 9460 mg/m3 (2200 ppm) for 144 days (rats
only). Slight effects were seen in rats: increased liver and kidney
weights at 1720 mg/m3; increased liver and kidney weights at 2580
mg/m3; and small histopathological changes (cloudy swelling) in liver
and kidney at 5375 and 9460 mg/m3 (Wolf et al. 1956).
In guinea-pigs and monkeys slightly increased liver weights were
noted in the 2580 mg/m3 group only. At the same exposure level,
small histopathological effects in the testes, described as
degeneration of the germinal epithelium, were seen in rabbits and
monkeys. At 5375 mg/m3 a slight growth depression was noted in
guinea-pigs. The no-observed-effect level (all four species) was
considered to be about 860 mg/m3 (200 ppm) (Wolf et al., 1956). It
should be noted, however, that Cragg et al. (1989) found no
histopathological effects in the testes of rats and rabbits exposed to
up to 3363 mg/m3 (782 ppm) for 4 weeks, and the lack of toxicity was
confirmed by NTP (1992).
7.4 Skin and eye irritation, sensitization
Inhalation for 3 min of ethylbenzene at a concentration of 4300
mg/m3 caused slight nasal irritation in guinea-pigs, and an 8-min
exposure caused eye irritation as well. At 8600 mg/m3 a 1-min
exposure was enough to cause both effects (Cavender, 1993).
Two drops of undiluted ethylbenzene placed in the eyes of rabbits
resulted in slight conjunctival irritation but no effects on the
cornea (Wolf et al., 1956). A slight conjunctival irritation with
some reversible corneal injury was reported in rabbits in a study by
Smyth et al. 1962.
Undiluted ethylbenzene has been shown to produce moderate
irritation when applied to the uncovered skin of rabbits (Smyth et
al., 1962). The application of undiluted ethylbenzene to the ear and
to the shaved abdomen of rabbits up to 20 times during a 4-week period
resulted in moderate irritation. There was erythema and oedema with
superficial necrosis and exfoliation of large patches of skin (Wolf et
No animal sensitization studies have been reported.
7.5 Reproductive toxicity, embryotoxicity and teratogenicity
In an inhalation study, rats (Wistar or Sprague-Dawley) and
rabbits (New Zealand White) were exposed to 430 or 4300 mg/m3 (100 or
1000 ppm) ethylbenzene for 6 to 7 h/day on gestation days 1 to 19
(rats) or 1 to 24 (rabbits). All pregnant animals were sacrificed on
the day before term (day 21 for rats, day 30 for rabbits). The
rabbits had a significantly (p<0.05) reduced number of live pups per
litter at both exposure levels, but the number of implantations per
litter and the number of dead or resorbed fetuses per litter did not
differ from those of the controls. Maternal toxicity in rats exposed
to 4300 mg/m3 was reflected in increased liver, kidney and spleen
weights. There was a significant (p<0.05) increase in the incidence
of extra ribs in both of the exposed rat groups (Hardin et al., 1981).
In a further study, rats (CFY) were exposed to ethylbenzene
concentrations of 600, 1200 or 2400 mg/m3 continuously (24 h/day)
from day 7 to day 15 of pregnancy. They were then killed on day 21.
Mice (CFLP) were exposed for three periods of 4 h per day to 500
mg/m3 on days 6-15 of pregnancy and killed on day 18. Rabbits (New
Zealand White) were exposed continuously on days 7-20 of gestation to
500 or 1000 mg/m3 and were killed at day 30. The maternal toxic
effects (not specified) in mice and rats were moderate and
dose-dependent. In both species ethylbenzene caused skeletal growth
retardation, extra ribs and reduced fetal growth rate at the highest
concentration. In rabbits, the highest dose concentration caused mild
maternal toxic effects (decreased weight gain) and reduction in the
number of fetuses due to abortion (Ungváry & Tátrai, 1985).
When rats (F-344/N) and mice (B6C3F1) were exposed to
ethylbenzene at concentrations of 0, 430, 2150 and 4300 mg/m3 (0,
100, 500 and 1000 ppm), 6 h per day, 5 days per week, for 13 weeks,
there were no changes in sperm or vaginal cytology (NTP, 1992).
Rat embryos were explanted on day 9 of gestation and cultured in
rat serum with added xylene (containing 18% ethylbenzene) at
concentrations up to 1.0 ml/litre serum. Dose-dependent retardation
of growth and development was seen but there were no observable
teratogenic effects (Brown-Woodman et al., 1991).
No multigeneration and reproductive studies on ethylbenzene have
7.6 Mutagenicity and related end-points
In a National Toxicology Program study, ethylbenzene was not
mutagenic in Salmonella tests and did not induce chromosomal
aberrations or sister chromatid exchange in Chinese hamster ovary
(CHO) cells in vitro, although it did induce trifluorothymidine
resistance in mouse lymphoma cells at the highest concentration tested
(80 mg/litre). There was no increase of micronuclei in the peripheral
blood of mice exposed to ethylbenzene (NTP, 1992).
In several other studies ethylbenzene did not induce point
mutations (with or without added metabolic activation system). In
addition, it did not cause an increase in the spontaneous
recessive-lethal frequency in the Drosophila recessive-lethal test,
nor had it any chromosomal effects in vitro (Donner et al., 1980;
Florin et al., 1980; Dean et al., 1985). Ethylbenzene had a marginal
effect on sister chromatid exchange in human lymphocytes in vitro
when a high (10 mmol/litre) concentration was used (Norppa & Vainio,
1983). In addition, in the TK+/- test in mouse lymphoma cells there
was a slight effect at a high concentration (80 mg/litre) (McGregor et
al., 1988). This study is obviously the same as the one subsequently
reported by NTP (1992).
No excess of chromosomal aberrations in bone marrow cells was
seen in rats after up to 18 weeks of exposure (6 h/day, 5 days/week)
to 300 ppm of a xylene mixture containing 18.3% ethylbenzene (Donner
et al., 1980).
In a carcinogenicity study, rats (Sprague-Dawley) were exposed to
one of several aromatic hydrocarbons, including ethylbenzene. Groups
of rats (40 of each sex) were exposed to 500 mg ethylbenzene (in olive
oil) per kg body weight by gavage, 4 or 5 days per week for 104 weeks.
Results were determined after 141 weeks. The first malignant tumour,
a nephroblastoma, was observed after 33 weeks. The total number of
malignant tumours was 31 in the 77 animals of the exposed group alive
at 33 weeks compared with an incidence of 23 of 94 animals in the
control group. The authors concluded that ethylbenzene caused an
increase in the incidence of total malignant tumours, although there
was no increase in the incidence of any specific type of tumour
(Maltoni et al., 1985). It is difficult to draw any firm conclusion
from this study because of inadequate reporting.
7.8 Other special studies
Ethylbenzene was found to have low acute cytotoxicity in vitro
on Ehrlich ascites cells (Holmberg & Malmfors, 1974).
The effects of ethylbenzene have been studied in four in vitro
test systems: decreased cell growth in Ascites sarcoma BP 8 cells;
decreased oxidative metabolism in hamster brown fat cells; cell
membrane damage of human embryonic lung fibroblasts; and inhibition of
ciliary activity in chicken embryo trachea. On a 0-9 point scale
(equivalent to 0-100%) the activity of these four systems scored 4, 6,
8 and 8, respectively (Curvall et al., 1984).
The activity of cytochrome CYP2E1 can be monitored in microsomal
preparations by p-nitrophenol hydroxylation. When rabbit (white
male New Zealand) liver microsomes were treated with up to 0.25 mM
ethylbenzene an inhibition of p-nitrophenol hydroxylation was seen
(Koop & Laethem, 1992).
In a study by Pyykkö et al. (1987), Sprague-Dawley male rats were
given ethylbenzene dissolved in corn oil intraperitoneally in a single
dose of 5 mmol/kg (530 mg/kg body weight). The rats were killed 24 h
later and the livers and lungs removed. In the liver 7-ethoxycoumarin-
0-deethylase (a marker of CYP2B1/2) was induced 4-fold; no induction
was found in the lung. Ethylbenzene also induced 7-ethoxyresorufin-
0-deethylase (a marker of CYP1A1/2) both in the liver (4-fold)
and the lung (2.5 fold). These findings are common to many aromatic
Alterations in the levels of specific cytochrome P-450 isozymes
were measured by Western immunoblotting techniques using rabbit
anti-rat polyclonal antibodies for cytochrome CYP1A1, CYP2B1 and
CYP2E1 on rat liver microsomes. The rats, male and female Holtzman
rats, were given 10 mmoles ethylbenzene per kg body weight for 3 days
and killed 24 h after the last injection. Ethylbenzene was shown to
induce CYP2B1/2B2 to a greater extent in male rats, while cytochrome
CYP2E1 was only induced in female rats. The level of cytochrome
CYP1A1 was not affected by ethylbenzene (Sequeira et al., 1992).
In another study (Gut et al., 1993), Wistar male rats were
exposed in a dynamic inhalation apparatus to 4 mg ethylbenzene/litre
air, 20 h per day, for 4 days. The rats were then killed and liver
microsomes prepared. By use of Western immunoblotting techniques it
was shown that cytochrome CYP2B1 was induced and the cytochrome CYP2E1
levels were decreased.
In a sensory irritation test, groups of four male mice
(Swiss-Webster) were exposed for 30 min to ethylbenzene at
concentrations of 1.76, 3.7, 8.06, 17.07 or 41.45 g/m3 (410, 860,
1875, 3970 or 9640 ppm). The RD50 value, i.e. the concentration
necessary to depress the respiratory rate by 50%, was calculated to be
17.46 g/m3 (4060 ppm) (95% confidence interval 10.6-28.6 g/m3;
2480-6660 ppm). The respiratory rate decreased due to sensory
irritation of the upper respiratory tract (Damgĺrd Nielsen & Alarie,
1982). In a similar test male mice (Swiss F1) were exposed for about
5 min to different concentrations of ethylbenzene. At least four
different concentrations were used and there were six mice for each
concentration. In this study the RD50 value was calculated to be
6.16 g/m3 (1432 ppm) (De Ceaurriz et al., 1981).
7.9 Factors modifying toxicity
Rats (Sprague-Dawley) were exposed for 2 h to 774 mg/m3 (180
ppm) ethylbenzene. One of two corresponding animals received 20 mmol
ethanol/kg body weight in physiological saline intraperitoneally
before exposure to ethylbenzene. Ethanol enhanced significantly (1.4
fold) the blood levels of inhaled ethylbenzene (Römer et al., 1986).
8. EFFECTS ON HUMANS
8.1 Volunteer studies
A dermal maximization test conducted on 25 volunteers at a
concentration of 10% ethylbenzene in petrolatum produced no skin
sensitization reaction (ECETOC, 1986).
In a review of studies from the 1930s, it was stated that
exposure to 21.5 g/m3 (5000 ppm) ethylbenzene for a few seconds gives
intolerable irritation of nose, eyes and throat. A few seconds of
exposure to 4.3 g/m3 (1000 ppm) initially gives eye irritation which
diminishes after a few minutes of exposure (Damgĺrd Nielsen & Alarie,
In a study on ethylbenzene metabolism in man it was incidentally
reported that, when the exposure was above the occupational limit
value (8 h; 430 mg/m3,100 ppm), complaints of fatigue, sleepiness,
headache and irritation of the eyes and respiratory tract were
reported (Bardodej & Bardodejová, 1970).
Healthy male subjects were exposed to technical xylene
(containing 20.7% ethylbenzene) for 2 h with or without a 100-watt
workload on an ergometer cycle. The air concentration of technical
xylene was 435 or 1300 mg/m3. During work at the higher exposure
level, evidence of performance decrement was observed in three of the
five performance tests: reaction time addition test (p<0.05),
short-term memory (p<0.05) and choice reaction time (p<0.10)
(Gamberale et al., 1978).
8.2 Occupational exposure
A number of epidemiological studies have been carried out on
groups occupationally exposed to mixtures of solvents, including
ethylbenzene. In these studies it is difficult to attribute the
effects to ethylbenzene or any other single chemical present.
Ethylbenzene occurs in mixed xylenes (at up to 30%) and effects of
occupational exposure to mixed xylenes are usually presented as
effects of xylenes and not of ethylbenzene.
A cross-sectional epidemiological study showed no strong evidence
of adverse neurobehavioural effects in 105 house painters when
compared with 53 workers from various professions (non-painters). The
concentration of ethylbenzene at the workplace was up to 12.9 mg/m3
(3 ppm). Other solvents present were ethyl acetate, toluene, butyl
acetate, methyl isobutyl ketone and xylene. In two neurobehavioural
tests significant differences were found between painters and controls
(the tests were "change of personality" and "short-term memory
capacity"). In a subgroup of painters with repeated prenarcotic
symptoms at the workplace, the differences were more pronounced
(Triebig et al., 1988).
In a study involving 35 spray painters, employed for between 2
and 26 years, erythrocyte and haemoglobin levels were slightly (but
not statistically significantly) lower than those of the controls.
The concentration of ethylbenzene was 17.2 mg/m3 (4 ppm) (Angerer &
In a medical surveillance report of some 200 ethylbenzene-
production workers, mandelic acid concentrations in urine were
measured twice a year for 20 years. Mandelic acid concentration
in the samples never exceeded 3.25 mmol/litre (=497 mg/litre), and the
mean value was 0.20-0.30 mmol/litre. According to the authors, a
post-shift urine mandelic acid concentration of 6.25 mmol/litre is
equivalent to an air concentration of 200 mg/m3. Therefore, the
measured maximum and mean mandelic acid values were considered to be
equivalent to air ethylbenzene concentrations of about 86 and 8.6
mg/m3 (20 and 2 ppm), respectively. None of the workers examined
over the last 10 years showed any effects on the levels of
haemoglobin, leucocytes or platelets, nor did they have a changed
haematocrit or alanine aminotransferase activity (Bardodej & Círek,
Minor changes in evoked potential and nerve conduction velocity
were found in 22 workers exposed to ethylbenzene at concentrations of
0.43-17.2 mg/m3 (0.1-4 ppm) for 4-20 years. They were also exposed
to styrene (about 1.5 ppm) (Lu & Zhen, 1989).
9. EFFECTS ON OTHER ORGANISMS IN THE LABORATORY AND FIELD
Ethylbenzene has been shown to inhibit the respiration of sewage
sludge utilizing biogenic substrates. Two screening tests were used,
RIKA and OECD 209. The concentration of ethylbenzene used was at the
limit of solubility in the medium (approximately 150 mg/litre), and
inhibitions of the respiration rate of 30% (ACCEDE 209) and 100%
(RIKA) were observed (Volskay & Grady, 1990).
Bringmann & Kühn (1980) studied the effect of ethylbenzene on
bacteria. A toxicity threshold of 12 mg/litre for Pseudomonas putida
was obtained in a cell multiplication inhibition test.
9.2 Aquatic organisms
Numerous acute toxicity tests have been carried out on
ethylbenzene. Organisms that have been studied include protozoans
(Bringmann & Kühn, 1980), algae (US EPA, 1978; Bringmann & Kühn, 1980;
Galassi et al., 1988; Masten et al. 1994), water fleas (LeBlanc, 1980;
Bringmann & Kühn, 1982; Abernethy et al., 1986; Galassi et al., 1988;
Vigano, 1993), diatoms (US EPA, 1978; Masten et al., 1994), copepods,
grass shrimp (Potera, 1975), bay shrimps (Benville & Korn, 1977),
mysid shrimps (US EPA, 1978; Masten et al., 1994), Dungeness crabs
(Caldwell et al., 1976) and Pacific oysters (LeGore, 1974). Fish that
have been studied include rainbow trout (Mayer & Ellersieck, 1986;
Galassi et al., 1988), guppy (Pickering & Henderson, 1966; Galassi et
al., 1988), bluegill (Pickering & Henderson, 1966; Buccafusco et al.,
1981), fathead minnow, goldfish (Pickering & Henderson, 1966), channel
catfish (Mayer & Ellersieck, 1986), Atlantic silverside (Masten et
al., 1994), striped bass (Benville & Korn, 1977) and sheepshead minnow
(US EPA, 1978; Heitmuller et al., 1981).
Many of the test results are not comparable, owing to
inconsistent exposure conditions, resulting from emulsions, open
static systems and systems with large air spaces. Aquatic toxicity
results from consistent exposure conditions, which are comparable, are
shown in Table 6.
No information regarding chronic exposure of aquatic organisms to
ethylbenzene has been reported.
Table 6. Toxicity of ethylbenzene to aquatic organisms
Species Age/size Stat/flowa Temperature Salinity pH Parameterc Concentration Reference
(°C) (0/00) (mg/litre)d
Alga stat 72-h EC50 4.6 Galassi et al. (1988)
(Selenastrum stat 19-21 48-h EC50 7.2 (3.4-15.1) Masten et al. (1994)
capricornutum) stat 19-21 96-h EC50 3.6 (1.7-7.6) Masten et al. (1994)
Water flea < 24 h statb 24-h LC50 2.2 Galassi et al. (1988)
(Daphnia magna) statb 21-25 48-h LC50 2.1e Abernethy et al. (1986)
< 24 h statb 48-h LC50 1.81-2.38 Viganň (1993)
(Skeletonema statb 19-21 48-h EC50 7.5 (5.0-11.2) Masten et al. (1994)
costatum) statb 19-21 72-h EC50 4.9 (2.4-9.8) Masten et al. (1994)
statb 19-21 96-h EC50 7.7 (5.9-10.0) Masten et al. (1994)
Mysid shrimp < 24 h flow 24-26 20 8.0 48-h LC50 >5.2 Masten et al. (1994)
(Mysidopsis < 24 h flow 24-26 20 8.0 96-h LC50 2.6 (2.0-3.3) Masten et al. (1994)
Rainbow trout stat 96-h LC50 4.2 Galassi et al. (1988)
Guppy stat 96-h LC50 9.2 Galassi et al. (1988)
Table 6. (Cont'd)
Species Age/size Stat/flowa Temperature Salinity pH Parameterc Concentration Reference
(°C) (0/00) (mg/litre)d
Atlantic silverside 3-15 mg flow 21-23 20 48-h LC50 6.4 (5.8-7.5) Masten et al. (1994)
(Menidia menidia) 3-15 mg flow 21-23 20 96-h LC50 5.1 (4.4-5.7) Masten et al. (1994)
a in all cases a closed system was used; stat = static conditions (water unchanged for the duration of the test);
flow = flow-through conditions (ethylbenzene concentration in water continously maintained)
b air space was eliminated
c the EC50 for algae was based on growth inhibition
d test concentrations were measured, unless stated otherwise
e nominal test concentration;
9.3 Terrestrial organisms
An LC50 value of 47 µg per cm2 of contact area was obtained for
earthworms exposed to ethylbenzene adsorbed on filter paper in glass
vials (Neuhauser et al., 1986). Callahan et al. (1994) reported a
2-day LC50 value of 4.93 µg/kg for Eisenia foetida in a contact
No toxicity data on plants, birds and wild mammals have been
10. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE ENVIRONMENT
10.1 Evaluation of human health risks
The acute and chronic toxicities of ethylbenzene are low. The
toxic effects in humans and animals relate to depression of the
central nervous system (CNS) and to irritation of the mucous membranes
and eyes. No data concerning carcinogenic or reproductive effects
have been reported. Ethylbenzene does not have significant mutagenic
properties or teratogenic effects.
Exposure to more than 430 mg/m3 (100 ppm) causes symptoms of CNS
depression and irritation in humans.
A 20-year medical surveillance study of 200 workers showed no
indications of effects in routine blood tests. The maximum exposure,
estimated from the urinary concentration of mandelic acid, was less
than about 86 mg/m3 (20 ppm) and the mean value about 8.6 mg/m3
In a 13-week animal study, increased liver weight was the only
dose-related biological finding in male rats. This was seen at a
concentration of 3225 mg/m3 (750 ppm) or more.
The definition and aim of the use of a guidance value for the
general population have been described by IPCS (1994).
On the basis of biological significance criteria cited above, a
no-observed-effect level (NOEL) of 2150 mg/m3 (500 ppm) was defined.
The no-observed-adverse-effect level would be higher than 4300 mg/m3
(1000 ppm) (highest concentration used), since the increase in liver
weight was not associated with any histopathological findings. A NOEL
of 2150 mg/m3 (500 ppm) was used as the basis for determining the
guidance value. The following uncertainty factors were used: 10 for
interspecies variability; 5 for intraspecies variability (effect seen
in males only); and 2 for lack of chronic toxicity data. This gives a
guidance value of 22 mg/m3 (5 ppm).
From the medical surveillance study the NOEL could be estimated
to be between 8.6 mg/m3 (2 ppm) (mean value) and 86 mg/m3 (20 ppm)
(maximum value). However, since no dose-response relationship was
derived, this study is not suitable for the estimation of a guidance
value. Furthermore, no effects would be expected at this exposure
level, which is almost the same as the guidance value.
Humans are exposed to ethylbenzene principally by inhalation,
where the substance is rapidly absorbed into the body. Exposure by
skin absorption or ingestion may also occur. Ethylbenzene is not
considered to bioaccumulate.
Table 7 gives the estimated weekly ethylbenzene dose resulting
from different types of exposure. A guidance value of 22 mg/m3
(5 ppm) ethylbenzene is approximately equivalent to a weekly ethyl-
benzene dose of 2000 mg. This is 100 times higher than the worst
exposure situation of the general population.
Table 7. Estimated weekly ethylbenzene dose from different types of exposures
Type of exposure Reported concentration Weekly total amount Dose mg/week
in media inhaled, ingested
Inhalation (means)b 0.74-100 µg/m3 140 m3 0.07-10c
Ingestion (food) 13 µg/kgd 7 kg 0.1
Drinking- or groundwaterb 0.07-1.1 µg/litree 14 litres 0.01
30.0 µg/litref 0.42
Inhalation (mean)g 10 mg/m3 300c
Inhalation (max)g 100 mg/m3 50 m3 3000c
Inhalationh 430 mg/m3 12700c
Smokers 8 µg/cigarettei 140 cigarettes/week 1.1
a Based on a breathing rate of 20 m3/day
b Values from Tables 2 and 3
c Retention 60%
d Lovegren et al. (1979) (highest reported value)
e Highest reported values of uncontaminated groundwater
f Lowest reported value of contaminated groundwater
g Bardodej & Círek (1988)
h Corresponds to occupational exposure limits in several countries
i Wallace et al. (1987a)
A 2-year carcinogenicity study has been performed by the National
Toxicology Program (USA) but the results are not yet available.
10.2 Evaluation of effects on the environment
Ethylbenzene is found in air, water, soil, sediment, biota and
groundwater. It is released primarily into air and water from various
natural and anthropogenic sources. The atmosphere is the major sink
for ethylbenzene. Ethylbenzene is rapidly photo-oxidized in the
atmosphere and this may contribute to photo-chemical smog formation.
In water, the key processes determining overall fate are
volatilization and biodegradation.
The log octanol/water partition coefficient is 3.13, indicating a
potential for bioaccumulation. However, the limited evidence
available shows that ethylbenzene bioconcentration factors are low for
fish and molluscs. Elimination from aquatic organisms appears to be
rapid. Biomagnification through the food chain is unlikely.
Mean levels of ethylbenzene in air ranging from 0.74 to 100
µg/m3 have been measured at urban sites. Industrial releases and
vehicle emissions are the principal sources of ethylbenzene. Levels
found at rural sites are generally <2 µg/m3. The levels of
ethylbenzene in surface water are generally less than 0.1 µg/litre in
non-industrial areas. In industrial and urban areas ethylbenzene
concentrations of up to 15 µg/litre have been reported. Urban
run-off, effluent and landfill leachate are sources of local
contamination. Ethylbenzene levels in sediment are generally < 0.5
µg/kg. Levels of ethylbenzene between 1 and 5 µg/kg have been found
in sediments from heavily industrialized areas. Ethylbenzene levels
in uncontaminated groundwater are generally < 0.1 µg/litre. However,
much higher levels have been reported for groundwater contaminated via
waste disposal, fuel spillage and industrial facilities.
Acute toxicity studies on aquatic organisms show ethylbenzene to
be of moderate toxicity. The lowest acute toxicity values are 4.6
mg/litre for algae (72-h EC50), 1.8 mg/litre for daphnids (48-h LC50)
and 4.2 mg/litre for fish (96-h LC50). There are no chronic toxicity
studies on aquatic organisms.
There is limited information regarding the toxicity of
ethylbenzene to bacteria and earthworms. There are no data for
terrestrial plants, birds or wild mammals.
On the basis of available data, it is concluded that ethylbenzene
is unlikely to be found at levels in the environment that will cause
adverse effects on aquatic and terrestrial ecosystems, except in cases
of spills or point-source emissions.
Ethylbenzene has low toxicity. Its vapour irritates the mucous
membranes to a limited extent and causes prenarcotic effects on the
central nervous system.
With respect to the general population, a tentative guidance
value of 22 mg/m3 (5 ppm) for ethylbenzene in inhaled air has been
derived, although information on certain important toxicity end-points
are unavailable. This value would correspond to a weekly absorbed
dose (daily ventilation of 20 m3 with 60% retention) of about 2000
mg. It is at least 200 times higher than the dose received in the
most polluted living environment reported. Hence, no harmful effects
on the general population would be expected. However, it should be
noted that the guidance value of 22 mg/m3 (5 ppm) is about 10 times
higher than the odour threshold (about 2.2 mg/m3; 0.5 ppm), and so
exposure at that level may cause annoyance. On the other hand, odour
detection may be considered to be a safeguard against excessive
Ethylbenzene is a non-persistent chemical and is degraded
primarily by photooxidation and biodegradation. Volatilization to the
atmosphere is rapid. Photooxidation reactions of ethylbenzene may
contribute to photochemical smog formation.
Limited evidence suggests that bioaccumulation is low in aquatic
organisms. Ethylbenzene is unlikely to cause adverse effects in
aquatic or terrestrial ecosystems except in cases of spills or
12. FURTHER RESEARCH
a) To fill the data gaps that currently limit the toxicological
evaluation of ethylbenzene, an appropriate rodent carcinogenicity
study and a reproductive toxicity study are needed. (The former
study has been conducted but the study report has not yet been
b) There is little information on the long-term effects of
ethylbenzene in humans and, in particular, no dose-response or
dose-effect data are at hand. Epidemiological studies of
populations occupationally exposed to ethylbenzene should be
encouraged. In this context, the use of ethylbenzene metabolites
in urine as a marker of exposure can be of special value because
the method determines the internal doses that individuals receive
via all routes of exposure. Because ethylbenzene is a central
nervous system depressant, and because some studies suggest that
high doses of the substance or its metabolites may affect the
metabolism of some neurotransmitters in the brain, epidemiological
studies should address the central nervous system as a potential
target organ. Moreover, since ethylbenzene is almost invariably
only one of the components in solvent mixtures at the workplace,
study designs that address possible interactions between
ethylbenzene and other solvents are desirable.
c) Further mechanistic studies are needed.
13. PREVIOUS EVALUATION BY INTERNATIONAL BODIES
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L'éthylbenzčne est un hydrocarbure aromatique qui s'obtient par
une réaction d'alkylation mettant en jeu le benzčne et l'éthylčne.
Aux Etats-Unis, on estime sa production annuelle ŕ environ 5 millions
de tonnes. En 1983, l'Europe occidentale en a produit environ 3
millions de tonnes. Il se présente sous la forme d'un liquide
incolore dégageant une odeur douceâtre qui rappelle l'essence. On
l'utilise principalement pour la production de styrčne. Ajouté ŕ du
xylčne technique, il sert également de solvant pour les peintures et
les vernis et on l'emploie aussi dans l'industrie chimique et dans
celle du caoutchouc. Il est présent dans le pétrole brut, les
produits raffinés dérivés du pétrole et dans leurs produits de
L'éthylbenzčne n'est pas persistant car il se décompose dans
l'environnement, principalement par photo-oxydation et par dégradation
biologique. Il est possible que la photo-oxydation de l'éthylbenzčne
dans l'atmosphčre contribue ŕ la formation du smog photochimique.
Le logarithme du coéfficient de partage entre l'octanol et l'eau
est égal ŕ 3,13, ce qui indique que le composé se pręte ŕ une
bioaccumulation. Cependant, les données limitées dont on dispose
montrent que le facteur de bioaccumulation de l'éthylbenzčne est
faible pour les mollusques et les poissons. Apparemment, il est vite
éliminé par les organismes aquatiques.
A la campagne, la concentration d'éthylbenzčne dans l'air est
généralement inférieure ŕ 2 µg/m3. Sur des sites urbains, on a
trouvé des teneurs moyennes allant de 0,74 ŕ 100 µg/m3. La
concentration d'éthylbenzčne présente dans les eaux superficielles
est généralement inférieure ŕ 0,1 µg/litre dans les zones non
industrialisées. En revanche, dans les zones urbaines ou
industrialisées, la concentration peut atteindre 15 µg/litre. Dans
les sédiments, la concentration est en général inférieure ŕ
0,5 µg/litre, encore que l'on ait signalé des valeurs comprises entre
1 et 5 µg/litre dans des sédiments provenant de régions fortement
industrialisées. Dans les eaux souterraines non contaminées, la
concentration est habituellement inférieure ŕ 0,1 µg/litre, mais elle
est beaucoup plus élevée dans les eaux contaminées.
L'éthylbenzčne présente une toxicité aiguë modérée pour les
algues, les invertébrés aquatiques et les poissons. La valeur de la
CE50 ŕ 72 h est de 4,6 mg/litre pour l'algue Selenastrum
capricornutum, la CL50 ŕ 48 h est de 1,8 mg/litre pour Daphnia
magna, et on a une CL50 ŕ 96 h de 4,2 mg/litre pour la truite
arc-en-ciel. On ne possčde aucune donnée sur l'exposition chronique
des organismes aquatiques ŕ l'éthylbenzčne.
En ce qui concerne les bactéries et les lombrics, les données
toxicologiques sont limitées. Il n'en n'existe aucune sur les
végétaux terrestres, les oiseaux ou les mammifčres sauvages.
Chez l'homme, l'exposition ŕ l'éthylbenzčne se produit
principalement par inhalation; 40 ŕ 60% du composé sont retenus dans
les poumons. L'éthylbenzčne est fortement métabolisé, principalement
en acides mandélique et phénylglyoxylique. On peut utiliser les
métabolites présents dans les urines pour surveiller l'exposition
Qu'elle soit aiguë ou chronique, la toxicité de l'éthylbenzčne
est faible pour l'homme et les animaux. Il exerce des effets toxiques
sur le systčme nerveux central et il est irritant pour les muqueuses
et les yeux. Le seuil de concentration pour ces effets chez l'homme a
été estimé ŕ environ 430-860 mg/m3 (100-200 ppm) lors d'une seule
exposition de courte durée.
Des rats et des souris ŕ qui on avait fait inhaler pendant 13
semaines de l'éthylbenzčne ŕ des concentrations allant jusqu'ŕ 4300
mg/m3, n'ont présenté aucune lésion histopathologique. La dose sans
effet observable (critčre retenu: l'augmentation du poids du foie) a
été estimée ŕ 2150 mg/m3 (500 ppm).
L'éthylbenzčne stimule les enzymes des microsomes hépatiques. Il
n'est ni mutagčne ni tératogčne pour le rat ou le lapin. On ne dispose
d'aucune donnée au sujet de ses effets toxiques éventuels sur
l'appareil reproducteur ni sur son pouvoir cancérogčne.
Une valeur-guide de 22 mg/litre (5 ppm) a été calculée ŕ partir
des résultats fournis par les études sur l'animal. On estime que la
population générale est exposée ŕ des concentrations inférieures ŕ
cette valeur, męme dans les cas les plus graves. On a constaté qu'une
exposition de longue durée en milieu professionnel, ŕ des concentration
de cet ordre, n'avait aucun effet nocif sur la santé des travailleurs
El etilbenceno es un hidrocarburo aromático que se obtiene por
alkilación del benceno y del etileno. La producción estimada en los
Estados Unidos de América es de unos cinco millones de toneladas por
ańo, y en Europa occidental fue de aproximadamente tres millones de
toneladas en 1983. El etilbenceno es un líquido incoloro de olor
dulce semejante al de la gasolina. Se utiliza principalmente para la
producción de estireno. También se utiliza en el xileno técnico como
disolvente de pinturas y lacas, así como en la industria del caucho y
en la fabricación de sustancias químicas. Se encuentra en el petróleo
crudo, en los productos de petróleo refinados y en productos de
El etilbenceno es una sustancia química no persistente, que se
degrada principalmente por fotooxidación y biodegradación. Su
volatilización en la atmósfera es rápida. La reacción de foto-
oxidación del etilbenceno en la atmósfera puede contribuir a la
formación de niebla fotoquímica.
El logaritmo del coeficiente de reparto octanol-agua es 3,13, lo
que indica posibilidad de bioacumulación. Sin embargo, los limitados
indicios disponibles muestran que los factores de bioconcentración del
etilbenceno son bajos para peces y moluscos. La eliminación por los
organismos acuáticos parece ser rápida.
Los niveles de etilbenceno en el aire en puntos rurales son
generalmente inferiores a 2 µg/m3. En puntos urbanos se han
registrado niveles medios de etilbenceno que oscilan entre 0,74 y 100
µg/m3. Los niveles de etilbenceno detectados en las aguas
superficiales son generalmente inferiores a 0,1 µg/litro en zonas no
industriales. Se han comunicado concentraciones de etilbenceno de
hasta 15 µg/litro en zonas industriales y urbanas. Los niveles de
etilbenceno en sedimentos son generalmente inferiores a 0,5 µg/kg,
aunque en sedimentos de zonas muy industrializadas se han encontrado
niveles de 1 a 5 µg/kg. Las concentraciones en aguas subterráneas no
contaminadas son generalmente inferiores a 0,1 µg/litro, pero son
mucho más elevadas en aguas subterráneas contaminadas.
La toxicidad aguda del etilbenceno para las algas, los
invertebrados acuáticos y los peces es moderada. Los valores de
toxicidad aguda más bajos son de 4,6 mg/litro para el alga
Selenastrum capricornutum (CE50 a las 72 horas, sobre la base de la
inhibición del crecimiento), 1,8 mg/litro para Daphnia magna (CL50
a las 48 horas) y 4,2 mg/litro para la trucha irisada (CL50 a las 96
horas). No se dispone de información sobre la exposición crónica de
los organismos acuáticos al etilbenceno.
Hay información limitada sobre la toxicidad del etilbenceno para
las bacterias y para las lombrices. No hay datos relativos a las
plantas terrestres, las aves y los mamíferos silvestres.
La exposición humana al etilbenceno se produce principalmente por
inhalación; el 40-60% del etilbenceno inhalado se retiene en los
pulmones. El etilbenceno se metaboliza extensamente, transformándose
sobre todo en ácidos mandélico y fenilglioxílico. Estos metabolitos
urinarios pueden utilizarse para vigilar la exposición humana.
El etilbenceno tiene una toxicidad aguda y crónica baja tanto
para los animales como para el hombre. Es tóxico para el sistema
nervioso central e irrita las mucosas y los ojos. El umbral para esos
efectos en el ser humano después de exposiciones únicas breves se
estimó en aproximadamente 430-860 mg/m3 (100-200 ppm).
La inhalación de etilbenceno por ratas y ratones durante 13
semanas en concentraciones de hasta 4300 mg/m3 (1000 ppm) no dio
lugar a lesiones histopatológicas. El nivel sin efectos observados,
sobre la base de un aumento del peso del hígado en las ratas, fue de
2150 mg/m3 (500 ppm).
El etilbenceno es un inductor de las enzimas microsómicas
hepáticas. No es mutagénico ni teratogénico en ratas y conejos. No
se dispone de información sobre la toxicidad reproductiva ni la
carcinogenicidad del etilbenceno.
Se ha calculado un valor de orientación de 22 mg/m3 (5 ppm) a
partir de estudios realizados en animales. La exposición estimada de
la población general (incluso en la peor de las situaciones) es
inferior a ese valor de orientación. La exposición ocupacional a
largo plazo a concentraciones de etilbenceno estimadas en este orden
de magnitud no ocasionaron efectos adversos en la salud de los