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Data bank of environmental chemicals     |     The Finnish Environment Institute (SYKE)
 


29.3.2024

Data bank of environmental properties of chemicals


Chemical
Ethylene oxide
CAS-number :
75-21-8
 
Synonyms :
1,2-epoxyethane
alpha,beta-oxidoethane
dihydrooxirene
dimethyleneoxide
ethene oxide
Etyleenioksidi
oxane
oxirane.
 
Sumformula of the chemical :
C2H4O
EINECS-number :
2008499
 
Purity, % :
100 
 
Uses :
Intermediate in the production of various chemicals:
the antifreeze 1,2-ethanediol; polyethylene terephthalate
polyesters for fibres, films, and bottles; non-ionic surface
active agents; glycol ethers; ethanolamines; and choline.

A small fraction of the total consumption was used as an
antimicrobial sterilant or as an insecticidal fumigant
(WHO 1978, Glaser 1979).

Less than 0.02 % of this production was used for sterilization
in hospitals (Glaser 1979).

In Belgium small fraction was also used in the health care
and medical products industries (Wolfs et al. 1983).
 
State and appearance :
Colourless solution or gas.
 
Odor :
Ethereal (Jacobson et al.1956) (Hellman & Small 1974).

Odour threshold for perception: 470 mg/m3
Odour threshold for recognition: 900-1260 mg/m3.

Recognition level 1.5 mg/m3 in air
(Sax 1986).

Quality: sweet, olefinic
Hedonic tone: neutral
Threshold odour concetration
absolute: 260 ppm
50 % recognition: 500 ppm
100 % recognition: 500 ppm
Odour index 100 % recognition: 2 000
(Hellman & Small 1974).
 
Molecular weight :
44.06
 
Spesicif gravity (water=1) :
0.882 
 
Vapor density (air=1) :
1.52 
 
Density, kg/m3 :
870  20 °C
 
Conversion factor, 1 ppm in air=_mg/m3 :
1.8  mg/m3 at 25 °C
 
Vapor pressure, mmHg :
1095  20 °C
200  -19.5 °C
 
Melting point, °C :
-111 
 
Boiling point, °C :
10.4 
 
Flashing point, °C :
-18 
 
Log octanol/water coefficient, log Pow :
-0.3  Sangster 1989
 
Volatilization :
Evaporation from water is a significant removal process. 
Under
specific concentrations, a half-life of 1 hr was found for
the evaporation of ethylene oxide from water (WHO 1985).
 
Mobility :
The main pathway of entry of ethylene oxide into the
environment is through its escape into the atmosphere due to
evaporation and with vented gases during production, handling,
storage, transport, and use. 
Most of the ethyleneoxide applied
as a sterilant or fumigant will enter the atmosphere (Bogyo 
et al. 1980).
 
Other physicochemical properties :
Very flammable, combustion imminent.

Toxic combustion products: hazardous.

Explosiveness: Reactive under confinement, extreme caution.

Vapor forms explosive mixtures with air over wide range. 
May
rearrange chemically and/or polymerize violently with evolution
of heat in contact with catalytic surfaces.

Misciple, 25 °C.
 
Photochemical degradation in air :
Photooxidation half-life in air:
38.2d - 382d,
based upon measured rate constant for reaction with hydroxyl 
radical (Howard 1991).
 
Other reactions in atmosphere :
At ambient levels, ethylene oxide will be removed from the
atmosphere via oxidation by hydroxyl radicals. 
On the basis of
a theoretical rate constant for this reaction, the atmospheric
residence time of ethylene oxide was estimated to be 5.8 days
(Cupitt 1980).

However, experimental data have shown the residence time
to be 100 - 215 days, depending on the hydroxyl radical
concentration and the ambient temperature (US EPA 1985).

Because of its high water solubility, ethylene oxide
levels in air will also be reduced through washout by rain
(Conway et al.1982).

The photochemical reactivity of ethylene oxide, in terms of its
ozone forming ability, is low (Joshi et al.1982).
 
Hydrolysis in water :
Hydrolysis to 1,2-ethanediol results in detoxification.

The toxicity of 2-chloroethanol for aquatic organisms resembles
that of ethylene oxide,though 2-chloroethanol seems to be more
toxic for Daphnia magna. 
Nevertheless, under environmental
conditions,the conversion of ethylene oxide to 2-chloroethanol
or 1,2-ethanediol will be slow (WHO 1985).

First-order hydrolysis half-life:
285 hours at 25°C (11.9 days),
(t1/2 at pH 7), based upon measured first-order and base and
acid catalyzed hydrolysis rate constants (Howard 1991).
 
Hydrolysis in acid :
Acid rate constant 9.3. x 1-3s-1 at 25°C,
(t1/2=251 hours (10.5 days) at pH 5), based upon measured 
first-order and base and acid catalyzed hydrolysis rate 
constants (Howard 1991).
 
Hydrolysis in base :
Base rate constant 1.0 x 10-4M-1s-1 at 25°C,
(t1/2=285 hours (11.9 days) at pH 9), based upon measured
first-order and base and acid catalyzed hydrolysis rate 
constants (Howard 1991).
 
Chemical oxygen demand, g O2/g :
1.74  5 days, Bridie et al. 1979
 
Other chemical degradation processes :
In the environment, chemical degradation in water through ionic
reactions appears to be comparativily slow. 
In neutral, fresh
water at 25 °C, ethylene oxide is broken down to form
1,2-ethanediol with a half-life of 14 days (Conway et al.1983).

At 0 °C, the half-life is 309 days. 
The reaction  is
acid-base-catalysed (Virtanen 1963).

In the presence of halide ions, 2-haloethanol will also be
formed. 
In neutral water of 3 % salinity, at 25 °C,
77 % of ethylene oxide was found to react to form
1,2-ethanediol and 23 %, to form 2-chloroethanol with
a half-life of 9 days (Conway et al.1983).
 
Biochemical oxygen demand, g O2/g :
0.06  5 days, Bridie et al. 1979
 
Half-life in air, days :
38.2  38.2d - 382d,
382  based upon photooxidation half-life in air,
  Howard 1991
 
Half-life in soil, days :
10.5  10.5d - 11.9d,
11.9  scientific judgement based upon hydrolysis
  half-lives at pH 7 and 9 (high t1/2) and pH 5
  (low t1/2),
  Howard 1991
 
Half-life in water, days :
10.5  10.5d - 11.9d,
11.9  in surface water, scientific judgement based upon
  hydrolysis half-lives at pH 7 and 9 (high t1/2)
  and pH 5 (low t1/2),
10.5  10.5d - 11.9d,
11.9  in ground water, scientific judgement based upon
  hydrolysis half-lives at pH 7 and 9 (high t1/2)
  and pH 5 (low t1/2),
  Howard 1991
 
Aerobic degradation in water :
Ethylene oxide and its possible metabolites can be biodegraded
slowly by aerobic microorganisms. 
Biological oxygen demands of
3 - 5 % and 52 % of the theoretical oxygen demand were
determined for ethylene oxide after 5 and 20 days,
respectivily, using a domestic sewage seed (Bridie et al.1979b)
(Conway et al.1983).

Aerobic half-life:
4w - 6mo,
scientific judgement based upon unacclimated aerobic aqueous
screening test data (Howard 1991).
 
Anaerobic degradation in water :
Anaerobic half-life:
16w - 24mo,
scientific judgement based upon estimated aerobic 
biodegradation half-life (Howard 1991).
 
Metabolism in mammals :
Available animal data indicate 2 possible pathways for the
metabolism of ethylene oxide, i.e., hydrolysis and
glutathione-conjugation (WHO 1985).

In dogs, peak levels of 13 and 33 mg 1,2-ethandiol/litre
blood-plasma were measured between 1 and 3 hr after intravenous
administration of 25 or 75 mg ethylene oxide in water /kg body
weight, respectively. 
As the half-life for hydrolysis is about
60 hr at 40 °C in neutral fresh water (Virtanen 1963).

The involvement of an epoxide-hydrolase has been suggested, but
this has not yet been confirmed. 
The peak concentration of
1,2-ethanediol at 25 mg ethylene oxide /kg body weight
represented approximately 25 % of the dose of ethylene oxide.

Within 24 hr, 7 - 24 % of the dose was excreted in the urine
as 1,2-ethanediol. 
No other compound-related metabolites were
indentified (Martis et al. 1982).

The results of studies on rats, rabbits, and monkeys have shown
that some 1,2-ethanediol is metabolized but that most of it is
excreted unchanged in the urine (Gessner et al. 1961)
(McChessney et al. 1971).

When a single dose of 2 mg labelled ethylene oxide in
propanediol /kg body weight was applied  intraperitoneally to
rats, 43 % of the administered radioactivity was excreted in
the urine within 50 hr (41 % within 24 hr) of exposure, 9 % as
S-(2-hydroxyethyl)cysteine and 33 % as
N-acetyl-S-(2-hydroxyethyl)cysteine, both products of
glutathione-conjugation. 
Via the lungs, 1.5 % was excreted as
CO2 and 1 % as unmetabolized ethylene oxide. 
(Jones & Wells
1981).

The involvement of glutathione-epoxide-S-transferase has not
been investigated further. 
In vitra glutathione-conjugation of
the homologue propyleneoxide was shown to proceed only in the
presence of an enzyme (Fjellstedt et al. 1973).

In rabbits, no effect  was found on liver-glutathione and
blood-glutathione levels, after 12 weeks af exposure to
concentrations of ethylene oxide at 18, 90, or 450 mg/m3, for
5 days per week, 6 hr per day (Yager & Bentz 1982).

As ethylene oxide can react  with chloride-ions, and this
reaction is acid-catalysed, 2-chloroethanol might be expected
to be a metabolite, especially after oral administration.

However, neither 2-chloroethanol, not its metabolites have been
found in the plasma, tissues, or urine of species exposed to
ethylene oxide (Johnson 1967) ( Grunow & Altman 1982).

Ehrenberg et al. 
(1974) found  that an average of 74 % of
labelled ethylene oxide inhaled by mice, was excreted in the
urine within 24 hr in the form of unidentified metabolites, and
only 4 % within the next 24 hr. 
Thus, on the basis of this and
previously presented excretion data, excretion of metabolites
of ethylene oxide mainly takes place via the urine, within 24
hr following exposure.
 
Other information of bioaccumulation :
Potential for accumulation negative (Sax 1986).
 
LD50 values to mammals in oral exposure, mg/kg :
330  orl-rat, Smyth et al. 1941
280  orl-mice, Woodard & Woodard 1971
365  280 - 365
  > 10000 mg/kg, orl, 1,2-ethanediol
  --
270  14d, orl-gpg, Sax 1986
72  orl-rat
 
LD50 values to mammals in non-oral exposure , mg/kg :
  * 5210 mg/kg,1,2-ethanediol,rat,
  * intravenous,Woodard & Woodard 1971
  --
290  ivn-mus, Sax 1986
 
LC50 values to mammals in inhalation exposure, mg/m3 :
1500  4-hr, ihl-mus, Jacobson et al.1956
1730  dog
2630  rat
 
LC50 values to mammals in inhalation exposure, ppm :
4000  4hr, ihl-rat, Sax 1986
836  4hr, ihl-mus
973  4hr, ihl-dog
1462  4hr, ihl-rat
960  4hr, ihl-dog
 
LDLo values to mammals in non-oral exposure , mg/kg :
444  ivn-dog, Sax 1986
100  ipr-mus
175  ivn-rbt
 
TDLo values to mammals in non-oral exposure , mg/kg :
225  ivn-mus, 10-12d preg, teratogenic
450  ivn-mus, 8-10d preg, teratogenic
450  ivn-mus, 10-12d preg, teratogenic
292  scu-mus, 95W-I, tumorigenic
  Sax 1986
 
TCLo values to mammals in inhalation exposure, mg/kg :
3.6  ihl-rat, 24hr, 60d male, teratogenic
  Sax 1986
 
TCLo values to mammals in inhalation exposure, ppm :
100  ihl-rat, 6hr, 6-15d preg, teratogenic
12500  ihl-hmn, 10s
500  ihl-wmn, 2min
  Sax 1986
 
Effects on physiology of mammals :
Acute exposures:(oral, intravenous and inhalation studies)
In mortality studies, the lungs and nervous system are the main
targets in rodents and dogs. 
In dynamic inhalation exposure
studies on guinea-pigs (Waite et al.1930),(Jacobson et al.1956)
rats, mice and dogs, nasal irritation was the first
clinical effect. 
Respiratory problems occured ranging from
gasping to laboured breathing. 
Dogs exhibited laboured
breathing, vomited, and suffered convulsions. 
Guinea-pigs,
exposed to a concentration of 13000 mg ethylene oxide /m3, for
2.5 hr, were found lying on their sides, unable to stand, and
quiet. 
Gross pathological changes in animals that did not
survive included moderate congestion in the lungs of dogs,
minor patchy oedema in the lungs of rats, and congestion with
oedema in the lungs of guinea-pigs. 
In rats, moderate
congestion with petecchial haemorrhage of the trachea was also
observed. 
Lobural pneumonia and hyperaemia of the liver and
kidneys were observed in guinea-pigs. 
Parenchymatous changes in
the kidney of guinea-pigs were seen at 2300 mg/m3.

Ataxia, prostration, laboured breathing, and occasional toxic
convulsions were effects shown by rats and mice at lethal oral
or intravenous doses of ethyleneoxide (Woodard & Woodard 1971).

Rabbits were exposed for 2 hr via polyvinyl chloride
endotracheal tubes containing 0 - 600 mg ethylene oxide /kg
material. 
There were no deaths, but rabbits receiving the tubes
with the highest residues showed increased incidences of
hyperaemia, oedema, leukocyte infiltration, and epithelial
erosion of the larynx and trachea (Star et al.1980).

Acute effects on eyes and skin:
Concentrations above 1 % ethylene oxide  established into the
conjunctival sac of rabbits, caused reversible changes in
conjunctiva such as hyperaemia and swelling, and irreversible
opacity, both in the cornea and in the lens. 
Possible reaction
products, 2-chloroethanol and 1,2-ethanediol, were less
irritating to eye (McDonald et al.1973).

Skin irritation with hyperaemia, oedema, and scar formation was
observed from 6 min after application of pads of cotton,
moistened with solutions of 100 or 500 g ethylene oxide /l
water, on the shaved skin of rabbits, under a plastic cover
(Hollingsworth et al. 1956).

Liquid ethylene oxide is apparently without adverse effects on
rabbit and human skin, on single mild exposures, if the
material evaporates rapidly. 
If large amounts of material are
involved, evaporation may cause sufficient cooling to cause a
lesion similar to frost bite (Hine & Rowe 1981).

Short-term studies: (inhalation exposure) Surviving rats showed
increased relative lung weights after 26 - 27 weeks at 200 and
370 mg/m3. 
At 370 mg/m3, haemorrhages, hyperaemia, emphysema,
and local alveolar collapse were observed in these lungs. 
Lungs
of male rabbits also showed hyperaemia and slight oedema at 370
mg/m3. 
Gross respiratory tract irritation was apparent in all
species at 1510 mg/m3. 
Delayed reversible effects were observed
on the peripheral nervous system. 
Monkeys and rabbits exhibited
paralysis of the hind legs at 370 mg/m3 and, together with
rats, at 640 mg/m3. 
This was accompanied by atrophy of the
muscles of the hind legs, except in rabbits at 370 mg/m3. 
The
effects on the peripheral nervous system were investigated
further in monkeys, and loss of both sensory and motor function
was noted at levels 370 mg/m3 and 640 mg/m3. 
Significant
increases in body weight were also observed in rats, at levels
of 200 mg/m3 or more. 
Rats showed slight but significant
increases in the relative weights of kidney ans liver at 370
mg/m3 (Hollingsworth et al. 1956).

Groups og mice were exposed to concentrations 0 - 425 mg/m3,
for 6 hr/day, and 5 days per week. 
The exposures lasted for 10
- 11 weeks. 
No effects were observed in relation to survival,
body weight, clinical signs, white blood cell count, serum
clinical chemistry, urinanalysis, and histopathology. 
At the
highest exposure level, changes at terminal sacrifice uncluded
an increased relative liver weight in female mice, and a
decreased testicular weight in males. 
A decreased relative
spleen weightwas observed at 187 and 425 mg/m3
(Snellings et al. 1984a).

Short-term studies: (oral exposure) Rats received 15 doses of
100 mg/kg ethylene oxide in 21 days. 
There was marked loss in
body weight, gastric irritation, and slight liver damage
(Hollingsworth et al. 1956).

Long-term inhalation studies: Rats were exposed to actual
ethylene oxide concentrations of 18 - 173 mg/m3 for 6 hr per
day, 5 days a week over 25 months. 
The mortality rates
increased significantly from the 22nd and 23rd  month, at the
highest exposure. 
Body weights were depressed. 
In females, the
relative liver weight were increased. 
Relative spleen weight
were increased in rats that developed leukaemia. 
Haematological
changes were found in rats that at all doses. 
Non-neoplastic
histopathological changes odserved included an elevated
frequency of focal fatty metamorphosis of the adrenal cortices
in both sexes and bone marrow hyperplasia in females at 173
mg/m3. 
Also  mild skeletal muscular atrophy was observed.
 
Effects on reproduction of mammals :
Rats and guinea-pigs were exposed to vapour concentrations of
370 and 640 mg ethylene oxide /m3, for 7 hr per day, 5 days per
week, for up to 32 weeks. 
Among other effects, degeneration of
testes tubules was observed at the higher exposure level in
guinea-pigs, while at 370 mg/m3, there was a decrease in the
relative weights of testes in rats and guinea-pigs, which was
not statistically significant (Hollingsworth et al.1956).

Significantly decreased absolute testicular weights were
observed in mice exposed to ethylene oxide at a concentration
of 425 mg/m3, for 6 hr/day, 5 days per week, over 10 - 11 weeks
(Snellings et al. 1984a).

However the testicular effects may have been secondary to toxic
effects (e.g., growth inhibition). 
Rats exposed repeatedly to
concentrations of ethyleneoxide of up to 182 mg/m3, for 6
hr/day, 5 days per week, over 25 months, did not show any
histopathological effects on the reproductive tissues
(Snellings et al. 1981).

When monkeys were exposed to concentrations of ethylene oxide
at 90 and 180 mg/m3, for 7 hr/day, 5 days per week, over 2
years, spermatogenic functions were found to differ from those
of controls. 
At both exposure levels, sperm motility and sperm
count were decreased and the sperm drive range was increased,
but there was no increase in effect with increase in dose.

The incidence of abnormal sperm heads did not change
(Lynch et al. 1984c).

Rats were exposed to concentrations of ethylene oxide of 18,
58, or 173 mg/m3, for 6 hr/day, 5 days per week, over 12 weeks.

After mating females were further exposed for 7 days/week, up
to 3 weeks after delivery, with the exception of the first 5
days of lactation. 
Effects on the reproductive performance were
detected. 
The number of pups per litter was decreased at 173
mg/m3, as well as the number of implantation sites per female,
and the number of fetuses born per implantation site. 
The
number of females with a gestation period longer then 22 days
was also increased at this concentration, but no effects were
noted on the average length of the gestation period. 
Neither
parents nor pups showed signs of toxicity from ethylene oxide.

The percentages of pregnant females and fertile males were not
affected (Snellings et al. 1982a).

The potential of ethylene oxide to cause teratogenic or adverse
reproductivity effects has been examined in 4 animal species
(mice, rats, rabbits, and monkeys) by 2 routes of
administration. 
Results from these studies showed that ethylene
oxide is toxic to reproductive function in both males (reduced
sperm number and sperm motility, and an increased time to
traverse a linear path) and females (depression of fetal weight
gain, fetal death, and fetal malformation). 
The levels needed
to produce these fetal effects approach or equal the dose
needed to produce maternal toxicity. 
The results of animal
studies suggest possible reproductive impairment in human males
but are inadequate for assessing the fetal risk. 
Data on
reproductive effects in human beings are insufficient; one
study (Hemminki et al. 1982) suggests an increase in
spontaneous abortion  rate in women occupationally exposed to
ethylene oxide. 
However, the reported time-weighted average air
concentrations may not reflect the exposure levels  that
induced the effect (WHO  1985).
 
Other information of mammals :
Short-term studies:(inhalation exposure)
Guinea-pigs, rabbits, and monkeys tolerated 90 and 200 mg/m3,
and rats tolerated exposure to 90 mg/m3 without adverse effects
on general appearance, behaviour, mortality rate, growth,
body and organ weight, gross and histopathology. 
Rats showed
eleveted mortality rates from 370 mg/m3, rabbits from 640
mg/m3, and all exposed animals died at 1510 mg/m3. 
Secondary
respiratory infection caused the deaths of an appreciable
number of rats and mice in these studies (Hollingsworth et al
1956).
 
Health effects :
Moderately toxic by inhalation. 
Characteristic ether odour
irritating in high concentrations. 
Anesthetic. 
Can cause
pulmonary edema. 
Max allowable concentration is 100 ppm. 3000
ppm may be tolerated for 60 minutes max. 50000 - 100000 ppm
fatal within few minutes. 
Strong irritant and and inhalative
poison. -  
Chronic irritant (Sax 1986).

Skin and eye irritation data:
skn, hmn, 1 %, 7 s;
eye, rbt, 18 mg, 6 hr, moderate
(Sax 1986).
 
Carcinogenicity :
Ethylene oxide has induced following effects:
Inhalation exposure:
- neoplasms in rats(Snellings et al. 1981, 1984b)
- increased incidence of mononuclear cell leukaemia in rats
(Snellings et al. 1981, 1984b, Lynch et al. 1984a)

- primary brain tumours in rats(mainly gliomas and malignant
reticular tumours) (Snellings et al. 1981, 1984b)

- peritoneal mesotheliomas in rats, originating from the testi-
cular mesothelium and of mixed-cell gliomas in the brain
(Lynch et al. 1984a).

Oral exposure:
- elevated incidences of tumours in the forestomach in rats
- elevated incidences of squamous cell carcinomas in rats
- invasive growth, metastases, fibrosarcomas in rats
- elevated incidences of hyperplasia, hyperkeratosis,
papillomas and carcinomas in the forestomach of rats.

(Dunkelberg 1982).

Subcutaneous exposure:
- elevated incidence of tumours only at the injection site
though the mortality rate was increased (mice).
- increased incidence of sarcomas, mainly fibrosarcomas in mice
(Dunkelberg 1981).

Dermal exposure:
- no skin tumours were found, nor was there any sign of skin
irritation, when mice received ethyleneoxide in acetone,brush-
ed on the clipped dorsal uncovered skin. 
It was assumed that
ethyleneoxide evaporated rapidly from the skin.

(Van Duuren et al. 1965)
 
Mutagenicity :
Almost all reports available demonstrate the mutagenic action
of ethylene oxide.Ethylene oxide is an alkylating agent.It has
induced gene mutations in all plants, bacteria, fungi, insects,
and mammalian cells investigated in vitro, with and without
metabolic activation. 
Chromosome damage and sister chromatid
exchanges were observed in plants,insects, and mammalian
somatic cells exposed in vivo and in vitro
(Fomenko & Strekalova 1973,Embree & Hine 1975, Strekalova et
al. 1975,Appelgren et al.1977,Cumming & Michaud 1979, Generoso
et al. 1980, Pero et al. 1981,Lyarskii et al. 1983).

Negative results were observed on a few occasions only
(Appelgren et al. 1977, Kligerman et al. 1983).

Known to cause mutations and chromosome aberrations. 
Positive
both in barley spikes and neurospora and reversions (Sax 1986).

Mutagen data:
mmo, sat, 0.040 mmol/plate;
cyt, dmg, par, 55 mmol/l;
mmo, nsc, 140 mmol/l, 10 min;
mnt, rat, ivn, 200 mg/kg;
cyt, rat, ihl, 0.001 mg/l, 17 weeks;
dlt, rat, ihl, 1000 ppm, 4 hr;
dns, mus, ihl, 300 ppm;
dlt, mus, ipr, 150 mg/kg;
trn, mus, ipr, 30 mg/kg, 25D-I;
sce, rbt, ihl, 50 ppm, 12W-I
(Sax 1986).
 
Teratogenicity :
Rats were exposed to concentrations of ethylene oxide of 18,
58, or 173 mg/m3, for 6 hr/day, on days 6 - 15 of gestation.

Maternal behaviour was normal, and there were no deaths. 
The
only effect on the fetuses was a 5 - 8 % decrease in weight
at 180 mg/m3
(Snellings et al. 1982b.)

Rats were exposed to concentrations of ethylene oxide of 0 and
270 mg/m3, for 7 hr/day, on days 7 - 16 of gestation (group 1)
or on days 1 - 16 of gestation (group 2) or during 3 weeks
before mating (5 days per week), and on days 1 - 16 of gestation
(group 3). 
No dams died, but body weights were decreased in
group 3. 
In all exposed groups, the relative and absolute
weight of kidney and spleen were increased. 
The results of
histopathological examination did not show any abnormalities.

There was a significant increase in resorptions per litter
and per implantation site in group 3, with no significant
effect on the number of implants, live fetuses,and pregnancies. 

In all exposed groups, weights and lengths of the fetuses were
decreased. 
Reduced ossification of sternebrae and primary skull
was observed (Hackett et al. 1982).

Female mice received, intraveneously, doses of 0, 75, or 150 mg
ethylene oxide /kg body weight in an aqueous dextrose solution
on days 4 - 6, 6 - 8, 8 - 10, or 10 - 12 of pregnancy. 
Dams
exposed on days 6 - 8 of pregnancy did not show toxic signs.

In the other groups, at the highest dose, toxic signs such as
weakness, laboured respiration, and tremor were observed with
a mortality rate of 19 - 48 %. 
In the group without signs of
maternal toxicity, fetotoxicity was observed at 150 mg/kg, as
shown by a 20 % decrease in mean fetal weight. 
Fetal
malformation were shown in 19.3 % of fetuses in exposed litters 
compared with 2 % in control groups. 
These malformations were 
mainly fused cervical arches. 
In addition, fused thoracic 
arches, scrambled and fused sternebrae, and fused, branched, or 
missing thoracic ribs were observed (Laborde & Kimmel 1980).
 
Maximum longterm immission concentration in air for plants,mg/m3 :
VDI 2306
 
Maximum longterm immission concentration in air for plants,ppm :
VDI 2306
 
LC50 values to crustaceans, mg/l :
212  48 hr, Daphnia magna, Conway et al.1983
  > 10000 mg/l, 1,2-ethanediol
  100 mg/l, 2-chloroethanol
 
LC50 values to fishes, mg/l :
84  96 hr,Pimephales promelas, Conway et al.
  * 1983
  > 10000 mg/l, 1,2-ethanediol
  90 mg/l, 2-chloroethanol
90  24 hr,Carassius auratus,Bridie et
  * al. 1979a
  > 5000 mg/l, 1,2-ethanediol

References
1702Appelgren, L.-E., Eneroth, G. & Grant, C. 1977. Studies on ethylene oxide: whole-body autoradiography and dominant lethal test in mice. In: Clinical toxicology. Proceedings of the Meeting held at Edinburgh, June 1976, European Society of Toxicology. Amsterdam. Excerpta Medica. Vol. 18. pp. 315 - 317.
1675Bogyo, S., Lande, S.S., Meyland, W.M., Howard, P.H. & Santodonato, J. 1980. Investigation of selected potential environmental contaminants: epoxides. Syracuse, New York, Center for Chemical Hazard Assessment, Syracuse Research Corporation (Report No. EPA 560/11-80-005, PB 80- 183197).
182Bridie, A.L. et al. 1979. The acute toxicity of some petrochemicals to goldfish. Water Res. 13: 623.
1680Bridie, A.L., Wolff, C.J.M. & Winter, M. 1979. BOD and COD of some petrochemicals. Water Res. 13: 627 - 630.
1678Conway , R.A., Waggy, G.T., Spiegel, M.H. & Berglund, R.L. 1983. Environmental fate and effects of ethylene oxide. Environ. Sci. Technol. 17: 107 - 112.
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