Use of this information is subject to copyright laws and may require the permission of the owner of the information, as described in the ECHA Legal Notice.
EC number: 203-468-6
CAS number: 107-15-3
In a 2 -generation rat study there was no
evidence of reproductive toxicity or developmental toxicity up to and
including 227 mg EDA/kg bw/day.
In a two-generation reproduction study (Yang et al., 1984) there was no reproductive effect noted in any dose group as regards fertility, pup survival, number of pups born alive and number of pups weaned per litter; thus there was no evidence of reproductive toxicity at levels of 500 mg EDA.2HCl/kg/day in rats (recalculated as 227 mg/kg bw/day EDA base).
Growth retardation was observed in fetuses
from rats receiving 1000 mg/kg bw/day, levels which resulted in maternal
toxicity. However there was no evidence of a teratogenic effect. In
rabbits, maternal toxicity and embryotoxicity/ teratogenicity was absent
at the highest dose tested of 80 mg/kg bw/day. A higher dose could not
be tested as 20% mortality or more was seen at dose levels of 100 mg/kg
bw/day and higher.
There are both rat and rabbit
pre-natal developmental toxicity (teratology)studies. The rabbit study
consisted of New Zealand White rabbits, which were dosed by gavage with
Ethylenediamine dihydrochoride (EDA*2HCL) on gestation days 6 -19. The
dose levels were 0, 10, 40 and 80 mg/kg bw, calculated as
Ethylenediamine base. The top dose of 80 mg/kg bw/day was selected due
to 20% mortality in a dose ranging study at 100 mg/kg bw/day. In the
main study, there were no adverse effects on the mothers and no
indication of any developmental toxicity/teratogenicity in the foetuses.
In a rat teratology study
Ethylenediamine dihydrochoride was administered in the diet at 0, 50,
250 and 1000 mg/kg bw/day on days 6 -15 of gestation. These doses were
0, 25, 114 and 454 mg/kg bw/day calculated as Ethylenediamine
base. There was a significantly reduced body weight gain in the
intermediate and high dose groups together with reduced food
consumption. There were several findings in the offspring at the high
dose, such as reduced ossification, increased resorptions, decreased
foetal weight and length. The most important finding was an increased
incidence of missing and shortened innominate artery. By missing the
authors indicated that the right and left carotid branched off the
brachiocephalic artery, rather than it becoming the innominate after the
left carotid branches. So there is no innominate but this would not
affect blood supply. As a missing innominate artery had been observed
in offspring of rats on diets deficient in folic acid, further studies
were performed to determine if this effect was due to malnutrition due
to decreased diet consumption. A first step was to establish if the
reduced food consumption was due to palatability of the diet; 10
pregnant rats were dosed by gavage from days 6 -15 of gestation at 1000
mg/kg Ethylenediamine dihydrochloride (454 mg/kg bw/day calculated as
Ethylenediamine base).These rats showed reduced bodyweight gain and food
consumption, even though there was no ethylenediamine dihydrochoride in
the diet. The foetuses were not examined internally, but there was a
decrease in live foetuses/litter and an increase in resorptions.
This demonstrated that the reduced
food consumption seen in the dietary study was not due to palatability
of the diet. This study was followed by a paired feeding study where a
group of pregnant females were fed the same amount of control diet as
consumed by the rats who were receiving 1000 mg/kg EDA*2HCL (454 mg/kg
Ethylenediamine base). The pair fed controls had the same incidence of
missing innominate arteries as those fed Ethylenediamine; this was not
seen in a second, ad libitum fed control group. This indicated that this
effect was as suspected due to a folic acid deficiency caused by reduced
food consumption. The ethylenediamine dosed rats, however, still showed
shortened innominate arteries. The authors concluded that this
shortening was not a teratogenic effect as it would not result in a
functional deficit and, in addition, it may be reversible being a result
of the growth retardation seen together with reduced foetal weights
which only occurred in the presence of maternal toxicity.
The two generation study in rats
showed there were no adverse effects on reproduction either on fertility
or embryotoxicity from exposure to Ethylenediamine, administered in the
diet up to 500 mg EDA*2HCL/kg bw/day (227 mg/kg bw/day calculated as
There were no indications of any
developmental toxicity / teratogenicity seen in rabbits at a maximal
dose of 80 mg/kg bw/day of Ethylenediamine by gavage.
In the rat teratogenicity study there
were some findings interpreted as being due to malnutrition (low folic
acid) which was the case for the missing innominate arteries, due to
reduced maternal food consumption, caused by the ethylene diamine and
not due to palatability of the diet. Other findings of shortened
innominate arteries, delayed ossification etc. were considered to be due
to the delayed fetal development linked to the reduced foetal weight at
a maternally toxic dose level. The NOAEL for effects in the foetuses was
250 mg/kg EDA*2HCL (114 mg/kg bw/day calculated as Ethylenediamine
base); the maternal NOAEL was 23 mg EDA/kg bw/day.
Based on these findings it is
concluded that ethylene diamine would not require any classification
under the EU CLP(GHS) criteria for adverse effects on reproduction or
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.Reproduction or further distribution of this information may be subject to copyright protection. Use of the information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner.
Questo sito web si avvale di cookie affinché possiate usufruire della migliore esperienza sui nostri siti web.
Welcome to the ECHA website. This site is not fully supported in Internet Explorer 7 (and earlier versions). Please upgrade your Internet Explorer to a newer version.
Do not show this message again