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: 203-466-5
CAS number: 107-13-1
In general, no overt signs of intoxication was noted and
mortality only occurred in the 2000 ppm dose group, in which 2/18 rats
died from severe bilateral adrenal hemorrhage and necrosis. Decreased
water and food intake was observed in both the 2000 and the 500 ppm
drinking water groups and following 100 mg/kg bw twice daily by gavage.
Adrenal weights were decreased in 7, 14, and 21 day studies in rats
receiving 500 and 2000 ppm in drinking water, accompanied in the 2000
ppm group by polyuria. Pair-fed controls to the 2000 ppm group also
showed a decreased relative adrenal weight, but urinary output was
normal. However, animals given the equivalent of 2000 ppm (100 mg/kg bw
twice daily) by gavage showed an enlargement of the adrenals, again
accompanied by polyuria. Following 60 days administration in drinking
water, there was also a significant increase in adrenal weight that was
particularly prominent in the group given 60 mg/kg bw (equivalent to 500
ppm) daily. Histological examination of the adrenals from rats
administered 500 and 2000 ppm in drinking water for 7, 14, or 21 days
revealed atrophy in the adrenal cortex (especially the zona
fasciculata). In contrast, cellular hyperplasia with normal size or
slightly shrunken cells was seen in the adrenals from rats given
equivalent amounts by gavage and in animals administered 500 ppm in
drinking water for 60 days.
Plasma levels of corticosterone showed a dose-dependent
decrease in rats administered 100, 500 or 2000 ppm in drinking water,
with larger decreases being seen when acrylontrile was administered by
gavage. The decrease noted in the 2000 ppm group (14 days
administration) was even more marked in pair-fed controls. Plasma
aldosterone levels were less affected by administration of acrylonitrile
Effects were only seen at high levels and after prolonged exposure. A
significant decrease was observed only after administration by gavage of
60 mg/kg bw for 60 days.
Other effects reported in these studies were increased
liver weights following a 21-day administration period, with a decrease
being reported after 60 days. Kidneys were enlarged in the 100 ppm group
after 60 days of administration and in the 500 ppm group after 21 days.
Hyperplasia was observed in regions of the gastric mucosa of rats
receiving 100 and 500 ppm in drinking water for at least 21 days.
Treatment-related effects occurred consistently at the 100 ppm level via
drinking water, with 20 ppm representing a NOAEL (equivalent to an
intake of 4 mg/kg bw/d).
The stated aim of this study was to investigate the sub-acute and
sub-chronic toxicity of acrylonitrile to the adrenals, stomach and
duodenum by correlating biochemical, functional and morphologic
investigations, and to elucidate the mechanism of toxicity of
acrylonitrile. Rats were exposed to 0, 0.0001% (1 ppm), 0.002%, 0.01%,
0.05% or 0.2% acrylonitrile in drinking water, or to the same dose level
administered by gavage, for 7, 21 or 60 days. Acrylonitrile caused a
time- and dose-dependent decrease in plasma corticosterone levels;
aldosterone was affected only by the high dose level and prolonged time
of exposure. Young rats were noted to be more susceptible than adults to
this action of acrylonitrile. The adrenal cortex, especially the zona
fasciculata, was atrophic in rats exposed through drinking water. At
dose levels of 0.05% and 0.2%, administration also caused decreased food
intake and body weight gain. The adrenals were enlarged with a
hyperplastic zona fasciculata after daily gavage doses of acrylonitrile.
Ingestion of the chemical did not interfere with compensatory
enlargement of the adrenal gland following unilateral adrenalectomy. On
the other hand, the ACTH-induced elevation of corticosterone plasma
concentration was significantly attenuated by acrylonitrile in drinking
water. Electron microscopy of the adrenal glands revealed no consistent
changes in the steroid-producing cells. The authors postulate that
accelerated turnover of circulating corticoids and/or interference with
the secretion or action of ACTH may primarily be responsible for the
decreased plasma levels of corticosterone and aldosterone in rats that
ingest acrylonitrile. The mucosa in the stomach at the junction of the
forestomach and glandular region of animals that had ingested
acrylonitrile was hyperplastic. The corpus also showed regional mucosal
hyperplasia. Changes were associated with an elevated concentration of
non-protein sulphydryls mostly in the mucosa of the glandular stomach. A
similar, less prominent elevation also occurred in the proximal
duodenum. The results of the study suggest that the effects of
acrylonitrile on the adrenals were in part attributable to its inherent
toxicity and the consequences of decreased food and especially water
intake (probably due to its unpalatability in drinking water even at 20
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.
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