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EC number: 203-458-1
CAS number: 107-06-2
Dominant lethal screening:
Statistically significant effects in the ratio of dead to
live fetuses were observed in both generations. However, these effects,
which were both increases and decreases compared to controls, did not
appear to be dose related.
Maternal ingestion of the test compound produced no
apparent adverse reproductive effects or increased incidence of fetal
visceral or skeletal anomalies.
A multigeneration reproduction study was modified to
include screening for lethal and teratogenic effects of 1,2
-dichloroethane in drinking solution (Emulphor: deionized water, 1:99,
v/v). Male and female (10 and 30/dose level, respectively) ICR Swiss
mice received 1,2 -dichloroethane at concentrations of 0, 0.03, 0.09 or
0.29 mg/mL. These concentrations were designed to yield daily doses of
0, 5, 15 or 50 mg/kg bw/d. No taste aversion was evident. There appeared
to be no dose-dependent effects on fertility, gestation, viability, or
lactation indices. Pup survival and weight gain were not adversely
affected. 1,2 -dichlororethane failed to produce significant dominant
lethal mutations or terata in either of the two generations tested.
In a 2-year “repeated dose one-generation study”
with male and female rats fed 1,2 -dichloroethane in the diet at 250 and
500 mg/kg feed, no differences in parental fertility, litter data, and
pup data (survival, body weights) compared to controls were seen during
F0 -pregnancies from number 1 through 5. NOAELs for both parental and F1
reproductive effects were estimated to be the top dose in the range of
50 mg/kg bw/d, taking into account substance losses due to evaporation
(Alumot et al., 1975). This result was confirmed by a similarly designed
two-generation study in male and female ICR mice having received
comparable doses of DCE in drinking water of 5 – 50 mg/kg bw/d for 5
weeks during premating of the F0 and 11 weeks of the F1 generation.
Adult mice (F0 and F1b) showed no significant changes in water
consumption, body weight or fertility index and gestation index (number
of females with live litters/number of females pregnant) but
'inexplicable' sporadic increases in mortality occurred (details not
given). Among the offspring of F0 and F1b animals (F1a, F1b, F2a), no
significant changes were seen in mean litter size, mean post-natal body
weights (measured on days 7, 14 and 21), or survival (measured on days 4
and 21) and it was reported that there was no evidence of dose-dependent
gross pathology or congenital external, visceral or skeletal
malformations although no details or data were given. According to the
results of the two-generation study in mice, the NOAEL for general and
parental toxicity as well as for the F1 and F2 offspring was 50 mg/kg
bw/d in each case (Lane et al., 1982).
The reproductive toxicity of 1,2 -dichloroethane was also
investigated in a one-generation study in male and female rats after
inhalation exposure to 0, 25, 75 or 150 ppm (corresponding to 0, 103,
308 or 617 mg/m³) for 60 exposures (5/wk, 6 h/d) during the premating
period and another 116 exposures (7/wk; 6 h/d) for the remainder, but
sparing the pregnancy and lactation period for the F0-females. Neither
the parental nor the F1 animals revealed any treatment-related changes
in clinical and pathological parameters or reproductive performance
(Murray et al., 1980 ; Rao et al., 1980). NOAELs from this study were
150 ppm for both parental animals and F1-offsprings and also for signs
of general toxicity.
All three studies failed to exhibit clear toxic signs at
the doses applied. Therefore, evaluation as to reproduction performances
was only possible under this restriction.
The reproductive toxicity of 1,2-dichloroethane was
investigated in a one-generation study in male and female Sprague-Dawley
rats after inhalation exposure to 0, 25, 75 or 150 ppm (corresponding to
0, 103, 308 or 617 mg/m³), respectively. The premating period was 60
days for both sexes and the mating regimen was one male each with one
female for a period of four days to produce the F1a-generation. The
F1a-generation was necropsied between postnatal day 21 and 25. Seven
days after the last F1a litter was sacrificed parental animals were
remated and the produced F1b-litter was necropsied between postnatal
days 21 and 25 as well. Maternal exposure was discontinued only from
gestation day 21 until lactation day four. Adult animals did not reveal
any clinical signs of intoxication and no treatment-related changes in
food consumption or body weights were reported. Relative organ weights
of liver, kidneys, testes, uterus and ovaries of all dose groups were
comparable to controls, too. In the offspring (both F1 generations) no
changes in the fertility indices, in the number of pups/litter,
gestation survival, pup survival indices on days, 1, 7, 14 and 21, sex
ratio at day 21, neonatal body weight and growth was observable. No
substance related macroscopical and histopathological changes of liver
and kidneys and external, visceral and skeletal malformations or
retardations/variations were evident in both F1 -generations (Murray et
al., 1980 ; Rao et al., 1980). The NOAEL derived from this study was 150
ppm for both parental animals and F1 -offsprings and signs of general
In four oral or inhalation studies in rats and rabbits, intrauterine development of embryos and fetuses was not significantly affected up to maternally toxic doses.
Developmental toxicity/teratogenicity studies were
performed in rats and rabbits by the inhalation and oral route of
In two well conducted studies using pregnant SD rats
either exposed to 150, 200, 250 or 300 ppm (6h/d) or to 118, 158, 198 or
238 mg/kg bw/d (corn oil, gavage) from day 6 through 20 p.c., no
treatment-related differences were seen in mean litter size, foetuses
per litter, in numbers of implantations, incidence of resorptions,
foetal body weight and the incidence of malformations length, sex ratio
as compared to controls at maternally non-toxic doses/concentrations of
either exposure regimen, except some embryolethal effects (increase in
non-viable implants and resorption sites per litter), significant in the
oral dose-groups of 200 mg/kg bw/d and higher (p< 0.05). Distinct
maternal toxicity was indicated by intermittent delayed body weight
gains and expressed by a decrease in the absolute body weight gain of
dams and by three and two stillborn/not viable litters delivered at 240
mg/kg bw/d and 300 ppm, respectively (Payan et al., 1995).
Accordingly, the NOAELs(inhalation/oral) were at 250 ppm
and 158 mg/kg bw/d for maternal general toxicity, and 300 ppm for
embryo-/fetotoxicity/teratogenicity, and at 238 mg/kg bw/d for
fetotoxicity/teratogenicity, but at 158 mg/kg bw/d for embryotoxicity,
In the limited inhalation rat study by Rao et al. (1980)
using only two concentrations of 100 and 300 ppm, the NOAEL was 100 ppm
for maternal and developmental toxicity, while the high exposure level
showed overt toxicity (10/16 dams dead). An intermediate, less
maternally toxic levels appeared to be missing in order to identify the
appropriate NOAEL. In the respective inhalation study conducted in
rabbits (Rao et al., 1980), the NOAEL for developmental effects was at
300 ppm with unclear maternal toxicity, as several dams died at either
exposure level without signs of intoxication.
In principal, the observations of the latter were in line
with those of the more comprehensive studies by Payan et al. (1995).
Overall, three generation studies by the oral or
inhalation route in rats and mice gave no evidence of impairment of the
parental reproductive performance and pre- and postnatal viability and
development of the progeny. In four oral or inhalation studies in rats
and rabbits, intrauterine development of embryos and fetuses was not
significantly affected up to maternally toxic doses. Based on Directive
67/548/EEC and on Regulation 1272/2008 (CLP, GHS), 1,2-dichloroethane
was not classified as reproductive or developmental toxicant.
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