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EC number: 200-338-0
CAS number: 57-55-6
Based on the lack of (pre-)neoplastic lesions in available long-term studies with rats and dogs, monopropylene glycol is not carcinogenic.
Based on the lack of increased tumor
incidence, pre-neoplastic lesions or hyperplasia in available chronic
toxicity studies, classification of monopropylene glycol as carcinogenic
is not warranted in accordance with Directive
67/548/EEC and EU Classification, Labeling and Packaging of Substances
and Mixtures (CLP) Regulation (EC) No. 1272/2008.
carcinogenicity studies with monopropylene glycol were available for
assessment. However, two long-term studies with rats, using 2 years and
140 days exposure duration, and 104 -week study with dogs administered
monopropylene glycol either in diet or in drinking water were available
for assessment. Gaunt et al., 1972, administered diets containing 0,
6250, 12500, 25000 and 50000 ppm monopropylene glycol to groups 30 male
and 30 female weanling rats for 2 years. No adverse effects and no
histopathological changes, including (pre-)neoplastic lesions, were
noted at the highest tested dose, resulting in NOAELs of 1700 mg/kg
bw/day and 2100 mg/kg bw/day for male and female rats, respectively,
based on the determined daily average food intake.
In the old study of
Seidenfeld et al., 1932, with only limited parameters examined, groups
of 5 rats were administered propylene glycol in drinking water as 0, 1,
2, 5, 10, 25 and 50% solutions for 140 days, corresponding to average
daily doses of 1600, 3680, 7700, 13200, 21000 and 37000 mg/kg bw/day,
respectively. Histopathological examination was performed on kidneys,
hearts, spleens and livers. All animals given 25% or 50% propylene
glycol in water died within the first 9 days of treatment. No adverse
effects were noted in other dose groups, resulting in NOAEL of = 13200
In the 104-week study
with dogs reported by Weil et al., 1971, groups of 5 male and 5 female
beagle dogs were fed diets containing propylene glycol at dosage levels
of 5000 and 2000 mg/kg bw for 2 years.
A second series of animals was given an isocaloric amount of dextrose
mixed with food (2540 and 6350 mg/kg bw/day) and served as another set
of controls. Micropathology was performed at the end of the study
period. Apart from a slight increase in bone marrow activity in female
dogs from the high dose group, histopathological lesions occurred
with comparable severity and incidence in the treated, control and
equicaloric control groups. The change in bone marrow activity
was considered a physiological, rather than a toxicological, response.
Overall, there were no adverse,
treatment-related histopathological changes linked to
chronic ingestion of propylene glycol.
In a limited
study of Stenbäck et al. (1974), groups of 50 female Swiss mice were
treated twice a week with 0.02 ml of either neat monopropylene glycol or
its 50% or 10% solution in acetone, by dropping the liquid on the dorsal
skin between the flanks on a 1-inch square area which was shaved
regularly. Mice were allowed to die spontaneously or killed when
moribound. Complete autopsies were performed on all animals and the skin
and all grossly observed tumors and other lesions were examined
histopathologically. The authors concluded that no substance-caused
increase in tumor evidence was evidenced in any group and monopropylene
glycol is not carcinogenic by dermal route of exposure.
two well-conducted and reported drinking water carcinogenicity studies
with rats and mice are available on a structural homologue of
monopropylene glycol, dipropylene glycol (National
Toxicology Program, 2004b). As
available toxicokinetic data indicate that monopropylene glycol is
formed as a metabolite of dipropylene glycol upon its uptake by the
body, it is considered acceptable to use the data on dipropylene glycol
to assess the carcinogenic potential of monopropylene glycol. A full
justification for read across is contained in a separate document
attached to chapter 13 of the lead registrants IUCLID dossier.
In the rat study, the exposure
concentrations for the 2-year drinking water study were 0, 2,500,
10,000, and 40,000 ppm, corresponding to actual average ingested doses
of 115 , 470 and 3040 mg/kg bw/day in males and 140, 530 and 2330 mg/kg
bw/day in females. In the study with mice, the used exposure levels were
0, 10000, 20000 and 40000 ppm, corresponding to average ingested doses
of 735, 1220 and 2390 mg/kg bw/day (males) and 575, 1040 and 1950 mg/kg
bw/day (females). In the rat study, dipropylene glycol-related
non-neoplastic lesions were found in the kidney, liver, and nose. In the
mice study, no compound-related neoplasms or non-neoplastic lesions were
observed; only the reduced body weights. In conclusion, no evidence of
carcinogenic activity of dipropylene glycol was observed in either rats
or mice in the 2 -year drinking water study. These results provide
additional evidence that its metabolite monopropylene glycol is also not
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.
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