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EC number: 203-468-6
CAS number: 107-15-3
In repeated dose studies, decreased body weights and water and feed consumption has been observed, and are probably related to the irritating nature of EDA and it’s high pH. Hepatocellular pleomorphism has been observed and also increased AST and ALS values.
dose group: Diet
and water consumption significantly reduced in the high dose female
rats. Significant reduction in body weight gain of both sexes in the
high dose group; significant reduction in absolute weights of liver and
heart (both sexes), adrenal and brain (female), kidney and spleen (male)
in the high dose group; increase of relative weight of brain (both
sexes), spleen and heart (female) and testis in the high dose group.
Significant elevation of alkaline phosphatase activity in males and
elevation of alanine aminotransferase activity in males and females of
high dose groups. Increased
mean corpuscular volumes in males and females. Significant
increase of mean corpuscular hemoglobin and significant depression of
hematocrit and hemoglobin values; significant depression of red blood
cell counts, serum glucose level and urinary pH (from 6.0 to 5.0) and
significant elevation of aspartate aminotransferase activity in both
sexes of the high dose group; hepatocellular pleomorphism in 7/10 female
and 2/10 male (control: 0/10 of each sex) in high dose group,
hepatocellular degeneration and significant increased
prevalence of tracheitis in male of the high dose group.
dose group: Water
consumption significantly reduced in female rats. Significant elevation
of alanine aminotransferase activity in males of intermediate dose
mean corpuscular volumes in females.
Low dose group: Water
consumption significantly reduced in female rats. Significant
elevation of alkaline phosphatase activity in males, this effect was not
noted in the intermediate dose group.
In a three month dietary study, male and female rats were fed targeted
doses of 0, 50, 250 or 1000 mg/kg/day of EDA-2HCl . There were no deaths
and no abnormal clinical signs noted during the study. Body weight gains
were significantly decreased in the high dose group which affected a
number of absolute and relative organ weights in both males and females. Water
consumption was comparable to control values at all dose levels in males
but was decreased in a dose-response manner in female rats at all 3 dose
132 ppm: The death of
4/30 animals was attributed to lung infection (not substance-related);
slight depilation; body weight gain and relative weights of liver and
kidney were not affected; no substance-related macroscopic or histologic
225 ppm: The death of
16/30 was substance-related and another 10 death were considered not to
be substance-related; the 4 rats which survived showed significantly
lower weight gain and higher relative weights of liver and kidney;
cloudy swelling of the liver and of the loop and convoluted tubules of
the kidney; lung congestion was observed in exposed as well as in
control rats in similar proportions.
484 ppm: All rats died within 20 days of initial exposure; depilation
was first observed on the 6th day of exposure; cloudy swelling of the
liver (in 23/28 animals), cloudy swelling and degeneration of convoluted
tubules (in 7/28 animals); congestion of the lung (in 17/28 animals) and
of the adrenal cortex (in 5/28 animals).
59 ppm: No effect on weight gain or organ weights. No depilation. No
significant damage to examined tissues; lung, liver and kidney.
In a 6 week study four exposure groups of 30 Sherman rats (15 female/15
male) were exposed to EDA vapour 7 h /day for 5 days per week. Each
exposure group had a control group. The NOAEC was 144 mg/m³ air
Mean survival time of
the exposure group for substance 2 (598 days) was shorter than that of
the singly housed control group (626 days); no treatment-related
macroscopic or histopathologic findings; one mouse of the exposure group
had a dermal fibrosis at application site and another one had a mammary
adenocarcinoma. One sebaceous adenoma of the skin of the thorax was
noted in the control group individually housed.
In the exposure group
for substance 1, 1 mouse had a myxosarcoma at the base of the tail, and
11 animals had mild to moderate dermal fibrosis, suggesting skin
irritation. Survival time did not differ from negative control groups.
3-methylcholanthrene group, 39 of 40 mice had skin tumors including 37
with confirmed squamous cell carcinomas.
The dermal oncogenic potential of
ethylenediamine (EDA) was assessed by applying 25 µ1 of a I% solution in
deionized water to the skin of 50 male C3H/HeJ mice. This was the
highest concentration not producing irritation or weight changes in a
preliminary 2-week study. Two EDA samples (Nos. 1 and 2) from different
production sources were tested. Applications were made thrice weekly
until the death of the animals. A negative control group received
deionized water only. This group and the EDA-treated groups were
individually housed. A fourth group of 40 mice, housed 5 per cage,
received 0.1% 3-methylcholanthrene (MC) in acetone as a positive control
substance. A fifth group of 40 mice, housed 5 per cage, also received
deionized water to determine the effect of group housing on survival. No
skin tumors were observed in the EDA-treated groups. In the positive
control group, however, 39 animals (98%) had skin tumors including 37
(92%) with confirmed squamous cell carcinomas. Eleven mice (22%) which
received EDA No. 1 had dermal fibrosis indicative of probable skin
irritation in this group; there was no such lesion in the controls.
No skin tumors were observed in the EDA
treated animals. In the positive control group 98% of the animals had
Ethylenediamine sample was oncogenic (carcinogenic) to the skin or
systemically under the conditions of this study.
In a dermal
carcinogenicity study, the maximum tolerated dose for local effects was
applied to the back of 50 male mice three times weekly throughout their
lifespan. There were no treatment-related systemic macroscopic or
There are three oral repeat dose
studies, the key study being a reasonable modern 90 day dietary study,
with Ethylenediamine dihydrochloride. A NOAEL was determined at
22mg/kg/day after adjustment to the dose level as Ethylenediamine
base. There is also a 2 year cancer bioassay which had a NOAEL of
9mg/kg/day but this may have been higher as the next dose level was
45mg/kg/day as Ethylenediamine base. The third oral study was
investigated specific effects on the eyes at significantly higher dose
with no NOAEL. There is a very old 6 week inhalation study which
established a NOAEC of 144 mg/m3 and dermal study which had a NOAEL at
the only dose tested of 8mg/kg/day.
Based on this the key value is the
22mg/kg day NOAEL from the 90 day dietary study.
The classification for repeat dose
toxicity for a 90 day study is based of serious adverse systemic effects
seen at dose levels of 100mg/kg or less. In the 90 day study the only
serious probably none reversible effects were seen at the highest dose
level of 456mg/kg/day with relatively minor effects at 114mg/kg/day as
ethylendiamine base. As the top dose where the serious adverse effects
were seen was well above the 100mg/kg upper limit for a classification
of STOT (Specific Target Organ Toxicity) at Category 2. Based on this,
no classification for repeat dose toxicity if required under the EU CLP
and GHS criteria.
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