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EC number: 939-516-4 | CAS number: -
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
Carcinogenicity
Administrative data
Description of key information
There are no data for polyglycerine. Data does exist for glycerine and the higher MW material. In the case of glycerine, the subchronic NOAEL was 8000-10,000 mg/kg bw based on the absence of treatment-related effects in high dose animals. In the case of the higher MW material, chronic toxicity/carcinogenicity data exists for polyglycerol polyricinoleate (PGPR). PGPR has been shown to be metabolized in the GI tract releasing polyglycerine(called Polyglycerine-Heavy in Justification document) which is excreted unchanged in the urine (diglycerine and triglycerine) and feces (higher MW glycerines) (Detailed in Sections 7.1.1 and 13). No carcinogenic effect was found for PGPR after feeding 5% to rats for 2 yr.
Key value for chemical safety assessment
Carcinogenicity: via oral route
Link to relevant study records
- Endpoint:
- carcinogenicity: oral
- Type of information:
- migrated information: read-across from supporting substance (structural analogue or surrogate)
- Adequacy of study:
- weight of evidence
- Study period:
- Prior to 1970
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: The study was conducted according to guideline and/or standard method but was non-GLP.
- Qualifier:
- according to guideline
- Guideline:
- other: Ministry of Health (1960) Carcinogenic risks in food additives and pesticides. Monthly Bulletin of the Ministry of Health 19, 108–112
- Deviations:
- not specified
- Principles of method if other than guideline:
- The studies carried out included a 2-yr rat feeding study in Colworth Wistar rats. The studies were conducted in the 1960s in accordance with guidelines and standards in operation at the time (Ministry of Health, 1960)
- GLP compliance:
- no
- Species:
- rat
- Strain:
- Wistar
- Sex:
- male/female
- Details on test animals or test system and environmental conditions:
- 120 Colworth Wistar rats (60 of each sex obtained from the breeding facility at the Unilever Colworth Laboratory, Sharnbrook, Bedford, UK) were randomly divided at 32–42 days old into test and control groups, each of 30 male and 30 female animals. The rats were housed in individual cages.
- Route of administration:
- oral: feed
- Vehicle:
- unchanged (no vehicle)
- Details on exposure:
- Test animals were fed a diet containing 2% PGPR for the first 10 wk and then 5% PGPR for the remainder of the 2-yr period. Control animals were fed the same diet except that groundnut oil replaced the PGPR. The composition of the purified diets which were fed ad lib. for 2 yr is shown in Table 1a and Table 1b. Water was also provided ad lib. to the rats.
- Analytical verification of doses or concentrations:
- not specified
- Details on analytical verification of doses or concentrations:
- No data.
- Duration of treatment / exposure:
- continuous for two years
- Frequency of treatment:
- continuous in diet
- Post exposure period:
- Not applicable
- Remarks:
- Doses / Concentrations:
diet containing 2% PGPR for the first 10 wk and then 5% PGPR for the remainder of the 2-yr period
Basis:
nominal in diet - No. of animals per sex per dose:
- 30 males and 30 females/dose level
- Control animals:
- other: groundnut oil replaced the PGPR
- Details on study design:
- Test animals were fed a diet containing 2% PGPR for the first 10 wk and then 5% PGPR for the remainder of the 2-yr period. Control animals were fed the same diet except that groundnut oil replaced the PGPR. Blood, collected after 80 wk from four rats of each sex fed PGPR or the control diet, and on all surviving animals at study termination was analysed for erythrocyte and leucocyte counts, haemoglobin concentrations and value, red cell fragility and prothrombin time. Each animal was subjected to gross examination at autopsy. The following organs were weighed and the organ/body weight ratios determined: adrenals, heart, kidney, spleen, liver, testes, thyroid and pituitary. These organs, together with the lung, ovary, uterus, thymus, stomach, intestine, caecum, bladder, lymph nodes, skin, mammary gland, tongue and any macroscopic abnormality were removed, fixed and processed for histological examination
- Positive control:
- No data.
- Observations and examinations performed and frequency:
- Animals were observed daily for clinical signs of toxicity or changes in behaviour, and were weighed weekly. Food consumption was measured three times weekly and evaluated as a weekly amount.
- Sacrifice and pathology:
- Liver function was examined after 84 and 103 wk using the bromosulfothalein excretion test. Kidney function was assessed at the same times by measuring urine concentration. Blood was collected by cardiac puncture under ether anaesthesia after 80 wk from four rats of each sex fed PGPR or the control diet, and on all surviving animals at study termination. Blood samples were analysed for erythrocyte and leucocyte counts, haemoglobin concentrations and value, red cell fragility and prothrombin time. Each animal was subjected to gross examination at autopsy. The following organs were weighed and the organ/body weight ratios determined: adrenals, heart, kidney, spleen, liver, testes, thyroid and pituitary. These organs, together with the lung, ovary, uterus, thymus, stomach, intestine, caecum, bladder, lymph nodes, skin, mammary gland, tongue and any macroscopic abnormality were removed, fixed and processed for histological examination.
- Other examinations:
- No additional information available
- Statistics:
- All records were examined separately for each sex by analysis of variance to assess the significance of any inter-group differences. Organ weights were also analysed if justified by an analysis of covariance on final body weight.
In the analysis of variance, the F-ratio test was used to test whether the treatments differed. Student's t-tests were then used to compare every treatment mean individually against the control. - Clinical signs:
- no effects observed
- Mortality:
- no mortality observed
- Body weight and weight changes:
- no effects observed
- Food consumption and compound intake (if feeding study):
- no effects observed
- Food efficiency:
- not specified
- Water consumption and compound intake (if drinking water study):
- not specified
- Ophthalmological findings:
- not specified
- Haematological findings:
- no effects observed
- Clinical biochemistry findings:
- no effects observed
- Description (incidence and severity):
- limited tests reported
- Urinalysis findings:
- no effects observed
- Behaviour (functional findings):
- not specified
- Organ weight findings including organ / body weight ratios:
- effects observed, treatment-related
- Description (incidence and severity):
- kidneys from male and female rats and livers from female (but not male) rats fed PGPR were heavier than those fed the control diet.
- Gross pathological findings:
- no effects observed
- Histopathological findings: non-neoplastic:
- no effects observed
- Histopathological findings: neoplastic:
- no effects observed
- Details on results:
- Rats in both treatment and control groups occasionally showed clinical signs of respiratory disease, which in some cases was accompanied by loss of body weight and reduced food consumption. The incidence of respiratory disease was most evident from wk 50 onwards. Bronchiectasis and emphysema were the main cause of death among animals in both test and control groups. The incidence of respiratory disease was comparable between treatment and control groups.
No statistical difference (P=0.05) was found for survival between PGPR-fed and control rats when those dying from non-treatment-related factors (death during blood sampling and from intestinal obstruction—hair ball) were excluded (survival figures are shown in Table 3).
No treatment-related adverse effects were found for body weight and food consumption (Table 4 and Table 5). Liver function tests (bromosulfothalein excretion) and blood analyses revealed no signs of treatment-related effects. Urinalysis revealed no difference in specific gravity at wk 84 but a significantly lower specific gravity for urine from PGPR fed rats at wk 103, but all values fell within the historical value range (data not shown). Organ weight measurements showed that kidneys from male and female rats and livers from female (but not male) rats fed PGPR were heavier than those fed the control diet (Table 6).
Histological assessment of tissues revealed no treatment-related effect (data not shown). The incidence of tumours was comparable between control and treated rats (Table 7). - Relevance of carcinogenic effects / potential:
- Although this is a study conducted in the 1960s, there was no evidence of a carcinogenic effect observed in rats fed 5% polyglycerol polyricinoleate in the diet.
- Dose descriptor:
- NOEL
- Effect level:
- 5 other: % in diet
- Based on:
- test mat.
- Sex:
- male/female
- Basis for effect level:
- other: There were no carcinogenic effects noted in rats fed 5% in the diet.
- Remarks on result:
- other: Effect type: carcinogenicity (migrated information)
- Conclusions:
- There was no evidence of a carcinogenic effect observed in rats fed 5% polyglycerol polyricinoleate in the diet. Organ weight analysis revealed an increase in liver and kidney weight in both male and female rats
- Executive summary:
The carcinogenic potential of the food emulsifier ADMUL WOL brand of polyglycerol polyricinoleate (PGPR) was evaluated in rats
and mice. Groups of 60 male and 60 female rats were given purified diets containing 5% of either PGPR or groundnut oil for 2 years.
No carcinogenic effect of PGPR was observed. In addition, dietary PGPR had no adverse effect on growth, food consumption,
longevity and haematology. Organ weight analysis revealed an increase in liver and kidney weight in both male and female rats.
Histological analysis of tissues revealed no treatment related adverse effects.
Reference
Table 3.Rat survival after 104 wk
Sex | PGPR diet | Control purified diet |
Male | 18/30 (60.0%) | 23/30 (76.7%) |
Female | 18/30 (60.0%) | 21/30 (70.0%) |
Total | 36/60 (60.0%) | 44/60 (73.3%) |
Table 4.Mean body weight gains of rats fed for 104 wk on PGPR or control diets
Mean body weight gains (g) | ||||
Males | Females | |||
Wk | PGPR diet | Purified diet (control) | PGPR diet | Purified diet (control) |
0–3 | 78.7 | 79.7 | 44.3 | 48.1 |
3–9 | 95.0 | 90.7 | 52.1 | 49.8 |
9–20 | 48.9 | 57.3 | 27.2 | 30.1 |
20–60 | 60.8 | 53.2 | 17.1 | 16.5 |
60–104 | −19.1 | −11.8 | 13.6 | 27.9 |
0–104 | 264.3 | 269.1 | 154.3 | 172.4 |
Table 5.Mean total food consumption by rats fed for 104 wk on PGPR or control diets
Mean total food consumption (g) | ||||
Males | Females | |||
Wk | PGPR diet | Purified diet (control) | PGPR diet | Purified diet (control) |
0–3 | 281.9 | 279.9 | 230.8 | 246.3 |
3–9 | 660.2 | 644.1 | 508.5 | 509.3 |
9–20 | 1255.3 | 1264.0 | 936.3 | 957.2 |
20–60 | 4060.8 | 3968.5 | 3140.9 | 3187.5 |
60–104 | 4595.6 | 4407.3 | 3699.6 | 3831.4 |
0–104 | 10853.8 | 10563.8 | 8516.1 | 8731.7 |
Table 6.Mean organ weights for rats fed for 104 wk on PGPR and control diets
Mean organ weight | ||||||||
Absolute weight (g±SD) | Weight (g/100 g rat body wt (±SD) | |||||||
Males | Females | Males | Females | |||||
Diet | PGPR | Purified control | PGPR | Purified control | PGPR | Purified control | PGPR | Purified control |
Liver | 12.18 (1.84) | 11.45 (1.61) | 9.15a(2.72) | 8.67 (1.72) | 3.38 (0.58) | 3.24 (0.32) | 3.92a(0.85) | 3.48 (0.47) |
Kidneys | 3.59a(0.61) | 3.19 (0.45) | 2.52a(0.50) | 2.37 (0.34) | 1.00a(0.17) | 0.90 (0.13) | 1.08a(0.20) | 0.95 (0.14) |
Heart | 1.39 (0.31) | 1.30 (0.23) | 1.00 (0.16) | 1.05 (0.23) | 0.38 (0.09) | 0.367 (0.09) | 0.43 (0.08) | 0.42 (0.09) |
Spleen | 0.95 (0.37) | 0.849 (0.28) | 0.60 (0.13) | 0.65 (0.180) | 0.26 (0.11) | 0.237 (0.10) | 0.26 (0.05) | 0.26 (0.07) |
Pituitary | 0.010 (0.001) | 0.008 (0.004) | 0.010 (0.044) | 0.011 (0.033) | 0.0027 (0.001) | 0.002 (0.001) | 0.004 (0.001) | 0.004 (0.002) |
Thyroid | 0.028 (0.005) | 0.029 (0.007) | 0.023 (0.005) | 0.024 (0.008) | 0.0079 (0.008) | 0.008 (0.002) | 0.010 (0.002) | 0.009 (0.003) |
Adrenals | 0.081 (0.014) | 0.078 (0.012) | 0.091 (0.026) | 0.098 (0.016) | 0.022 (0.004) | 0.022 (0.004) | 0.039 (0.010) | 0.0394 (0.007) |
Testes | 2.85 (0.71) | 2.56 (0.86) | — | — | 0.790 (0.192) | 0.724 (0.26) | — | — |
a Significantly different from control (P=0.05).
Table 7.Tumour incidence of rats fed PGPR or control diet
Animals killed after 104 wk | Animals dying during test | |||||||
Males | Females | Males | Females | |||||
Total no. of rats examined | PGPR | Control | PGPR | Control | PGPR | Control | PGPR | Control |
18 | 23 | 18 | 21 | 12 | 7 | 12 | 9 | |
Tumour incidence | ||||||||
Total primary tumours | 9(50.0%) | 9(39.1%) | 8(44.4%) | 11(52.4%) | 1(8.3%) | 2(28.6%) | 4(33.3%) | 2(22.2%) |
Rats with one tumour | 6 | 7 | 6 | 6 | 1 | 2 | 2 | 2 |
Rats with multiple tumours | 1 | 1 | 1 | 2 | 0 | 0 | 1 | 0 |
Tumour types | ||||||||
(a) Uterus | ||||||||
Adenocarcinoma | — | — | 1 | 0 | — | — | 0 | 0 |
Fibroma | — | — | 0 | 1 | — | — | 1 | 0 |
(b) Thymus | ||||||||
Thymoma | 0 | 1 | 0 | 1 | 0 | 0 | 2 | 0 |
(c) Thyroid | ||||||||
Adenoma | 4 | 5 | 2 | 3 | 0 | 0 | 0 | 0 |
(d) Pituitary | ||||||||
Adenoma | 3 | 2 | 5 | 6 | 1 | 1 | 1 | 0 |
(e) Testis | ||||||||
Adenoma (Leydig cell) | 2 | 0 | -- | -- | 0 | 0 | -- | -- |
(f) Mesentery | ||||||||
Lipoma | 0 | 1 | 0 | 0 | 0 | 0 | 0 | 0 |
(g) Stomach | ||||||||
Squamous cell papilloma | 0 | 0 | 0 | 0 | 0 | 1 | 0 | 0 |
(h) Tongue | ||||||||
Sarcoma | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 1 |
(i) Subcutaneous tissue | ||||||||
Fibrosarcoma | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 1 |
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed
- Study duration:
- chronic
- Species:
- rat
Carcinogenicity: via inhalation route
Endpoint conclusion
- Endpoint conclusion:
- no study available
Carcinogenicity: via dermal route
Endpoint conclusion
- Endpoint conclusion:
- no study available
Justification for classification or non-classification
There is no justification for classification based on data from available studies.
Additional information
There are no data for polyglycerine. Data do exist for glycerine or the higher MW material. In the case of glycerine, the chronic NOAEL was 8000-10,000 mg/kg bw based on the absence of treatment-related effects in high dose animals. In the case of the higher MW material, chronic toxicity/carcinogenicity data exist for polyglycerol polyricinoleate (PGPR). PGPR has been shown to be metabolized in the GI tract releasing polyglycerine (called Polyglycerine-Heavy in Justification document) which is excreted unchanged in the urine (diglycerine and triglycerine) and feces (higher MW glycerines) (Detailed in Sections 7.1.1 and 13). No carcinogenic effect was found for PGPR after feeding 5% to rats for 2 yr. In addition, PGPR had no adverse effect on growth, food consumption, survival, haematology or histological appearance of tissues. The changes in weight of liver and kidneys in PGPR-fed animals were consistent with those seen in previous studies and considered to be a result of metabolic compensation in response to the high level of PGPR ingested. As noted in Section 7.5, castor oil, used in the preparation of PGPR, likewise affects the liver probably due to an adaptive hypertrophy, without toxic damage, through the need to metabolize ricinoleic acid. Thus the subchronic effects observed with PGPR are believed to not be due to polyglycerine but rather attributed solely to the polyricinoleate portion of the molecule.
Justification for selection of carcinogenicity via oral route endpoint:
Data from polyglycerol (as part of polyglycerol polyricinoleate).
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