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EC number: 255-255-2 | CAS number: 41198-08-7
- 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
Key value for chemical safety assessment
Carcinogenicity: via oral route
Link to relevant study records
- Endpoint:
- carcinogenicity: oral
- Type of information:
- experimental study
- Adequacy of study:
- key study
- Study period:
- 13 March 1978 to 16 January 1980
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: Non GLP / no guideline followed
- Qualifier:
- no guideline followed
- Qualifier:
- equivalent or similar to guideline
- Guideline:
- OECD Guideline 451 (Carcinogenicity Studies)
- Deviations:
- not applicable
- GLP compliance:
- no
- Species:
- mouse
- Strain:
- CD-1
- Sex:
- male/female
- Route of administration:
- oral: feed
- Vehicle:
- unchanged (no vehicle)
- Analytical verification of doses or concentrations:
- yes
- Duration of treatment / exposure:
- 24 months
- Frequency of treatment:
- continuous (diet)
- Post exposure period:
- None
- Remarks:
- Doses / Concentrations:0, 1, 30, 100 ppmBasis:nominal in diet
- Remarks:
- Doses / Concentrations:Males: 0, 0.1421, 4.5442, 14.2427 mg/kg dietBasis:actual ingested
- Remarks:
- Doses / Concentrations:Females: 0, 0.1911, 5.7736, 19.1857 mg/kg dietBasis:actual ingested
- No. of animals per sex per dose:
- 65 animals/sex/group
- Control animals:
- yes, plain diet
- Relevance of carcinogenic effects / potential:
- In terms of carcinogenic potential, Profenofos was concluded not to possess any carcinogenic potential.
- Dose descriptor:
- NOEL
- Effect level:
- ca. 30 ppm
- Sex:
- male/female
- Basis for effect level:
- other: (equivalent to 4.5 mg/kg diet). Based on significant inhibition of brain cholinesterase activity (25%) in females at 100 ppm
- Remarks on result:
- other: Effect type: toxicity (migrated information)
- Dose descriptor:
- NOAEL
- Effect level:
- ca. 100 ppm
- Sex:
- male/female
- Basis for effect level:
- other: (equivalent to ~14 mg/kg diet). No carcinogenic effect observed
- Remarks on result:
- other: Effect type: carcinogenicity (migrated information)
- Conclusions:
- In conclusion, profenofos was concluded not to be carcinogenic. Whilst a dietary levels in excess of 1ppm (0.14 mg/kg diet) resulted in clearly significant inhibition of plasma and erythrocyte cholinesterase activities, a 25% inhibition in brain cholinesterase acitivity was only observed at 100 ppm in females. Therefore, in accordance with the JMPR review, as brain cholinesterase acitivity is considered the preferential marker for inhibition, the NOEL is considered 30 ppm (~4.5 mg/kg diet).
- Executive summary:
Mice (65 animals/sex/group) were treated with Profenofos at dietary levels of 0, 1, 30 or 100 ppm for 85 weeks (males: equivalent to 0, 0.14, 4.5 and 14.2 mg/kg diet) or 96 weeks (females: equivalent to 0, 0.19, 5.77 and 19.19 mg/kg diet). Five animals/sex/group were sacrificed at week 53 and subjected to a full necropsy, with plasma, erythrocyte and brain cholinesterase activity determined.
Treatment did not adversely affect survival rates. Survival of male mice treated with 0, 1, 30 and 100 ppm was 63, 55, 66 and 30% respectively. The corresponding figures for females were 65, 68, 75 and 79% respectively. There were no treatment related effects with respect to clinical signs, body weights, food consumption, incidences of tumour formation, gross pathology or histopathology.
Statistically significant decreases in erythrocyte and plasma cholinesterase values for the 30 and 100 ppm male and females at week 53 and termination were observed. No sex differences were observed in terms of either plasma or erythrocyte inhibition. Brain cholinesterase activity was significantly decreased in females (25%) at termination in the 100 ppm group, in males whilst a 15% inhibition in brain cholinesterase activity was observed at week 53, at termination an increase in activity was present. Therefore the decrease was not considered biologically relevant.
In conclusion, profenofos was concluded not to be carcinogenic. Whilst a dietary levels in excess of 1ppm (0.14 mg/kg diet) resulted in clearly significant inhibition of plasma and erythrocyte cholinesterase activities, a 25% inhibition in brain cholinesterase acitivity was only observed at 100 ppm in females. Therefore, in accordance with the JMPR review, as brain cholinesterase acitivity is considered the preferential marker for inhibition, the NOEL is considered 30 ppm (~4.5 mg/kg diet).
References:
JMPR (2007). Pesticide residues in food. Joint FAO/WHO meeting on pesticide residues. Report of the Joint Meeting of the FAO Panel of Experts on Pesticide Residues in Food and the Environment and the WHO Core Assessment Group on Pesticide Residues. Geneva, Switzerland, 18 -27 September 2007.
- Endpoint:
- carcinogenicity: oral
- Type of information:
- experimental study
- Adequacy of study:
- supporting study
- Study period:
- 6 January 1978 to 17 January 1980
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: Non GLP, no guideline followed
- GLP compliance:
- no
- Species:
- rat
- Strain:
- Fischer 344
- Sex:
- male/female
- Route of administration:
- oral: feed
- Vehicle:
- unchanged (no vehicle)
- Analytical verification of doses or concentrations:
- yes
- Duration of treatment / exposure:
- 24 months
- Frequency of treatment:
- Continuous
- Post exposure period:
- 4 weeks
- Remarks:
- Doses / Concentrations:0, 0.3, 10, 100 ppmBasis:nominal in diet
- Remarks:
- Doses / Concentrations:Males: 0, 0.017, 0.559, 5.685 mg/kg dietBasis:actual ingested
- Remarks:
- Doses / Concentrations:Females: 0, 0.2, 0.694, 6.951 mg/kg dietBasis:actual ingested
- No. of animals per sex per dose:
- 60 rats/sex/group. An additional 10 animals/sex/group were included for the vehicle and high dose group, with 5 animals/sex/gp killed at week 52 (interim sacrfice) and an addition 5 animals/sex/gp switched to a basal diet and observed for 4 weeks (recovery), before being sacrificed at week 57.
- Control animals:
- yes, plain diet
- Relevance of carcinogenic effects / potential:
- In terms of carcinogenic potential, Profenofos was concluded not to possess any carcinogenic potential.
- Dose descriptor:
- NOAEL
- Effect level:
- ca. 100 ppm
- Sex:
- male/female
- Basis for effect level:
- other: (equivalent to ~6 mg/kg diet). No biologically relevant inhibition in cholinesterase activity observed
- Remarks on result:
- other: Effect type: toxicity (migrated information)
- Dose descriptor:
- NOAEL
- Effect level:
- ca. 100 ppm
- Sex:
- male/female
- Basis for effect level:
- other: (equivalent to ~6 mg/kg diet). No carcinogenic effect observed
- Remarks on result:
- other: Effect type: carcinogenicity (migrated information)
- Conclusions:
- The author concluded the NOEL was 0.3 ppm, based on inhibition of plasma and erythrocyte cholinesterase at 10 ppm and greater. Howewver, it is biologically plausible to infer from a previous JMPR review (1991) that the NOAEL can be considered to be 100 ppm, the highest dose administered. This is based the following: variable and inconsistent erythrocyte cholinesterase inhibition never exceeding 20%, which was fully reversible at the end of the treatment period. Initially, brain cholinesterase activities were statisically significantly inhibited in females fed 100 ppm (equivalent to 6 mg/kg diet) at week 105, with inhbition not reaching the required 20% to be considered biologically relevant (11% inhibition achieved). Following reevaluation inconjunction with historical control values, these differences were not considered statistically significant. Finally, following a 10 -fold increase in dose (10 ppm to 100ppm) the level of inhibition in one sex only increased by ~2%. Therefore the biological relevance is questionable. In terms of carcinogenic potential, Profenofos was concluded not to possess any carcinogenic potential.
- Executive summary:
Rats (60/sex/group) were fed Profenofos Technical at dietary levels of 0, 0.3, 10 or 100 ppm for 2 years. These dietary levels were equivalent to 0, 0.02, 0.56, 5.69 mg/kg diet for males and 0, 0.02, 0.07, 7.0 mg/kg diet for females, respectively. An additional 10 rats/sex were also included in the control and high dose groups respectively. OF the latter, 5 rats/sex/group were sacrificed at 52 weeks (interim sacrifice) and 5 rats/sex/group were placed on control feed after 52 weeks so that recovery could be investigated. These rats were then sacrificed during week 63.
There were no treatment related increases in mortality; survival rates in all groups for both genders were above 70%. No clinical signs of toxicity were observed and bodyweights were not affected at any dose level. For females in the high dose group, there was an increased in food consumption. An increase in thyroid gland perifollicular cell hyperplasia was observed in males (4/70 controls vs. 10/70 high dose group) and an increase in liver neoplastic nodules in females (1/70 controls vs. 3/60 low dose, 2/60 mid dose and 6/70 high dose). These histopathological findings were not considered to be treatment related or to be suggestive of an oncogenic effect. No increase in liver carcinomas occurred.
The author concluded the NOEL was 0.3 ppm, based on inhibition of plasma and erythrocyte cholinesterase at 10 ppm and greater. However, it is biologically plausible to infer from a previous JMPR review (1991) that the NOAEL can be considered to be 100 ppm (equivalent to 6 mg/kg diet), the highest dose administered. This is based the following: variable and inconsistent erythrocyte cholinesterase inhibition never exceeding 20%, which was fully reversible at the end of the treatment period. Initially, brain cholinesterase activities were statistically significantly inhibited in females fed 100 ppm at week 105, with inhibition not reaching the required 20% to be considered biologically relevant (11% inhibition achieved). Following re-evaluation in conjunction with historical control values, these differences were not considered statistically significant. Finally, following a 10 -fold increase in dose (10 ppm to 100ppm) the level of inhibition in one sex only increased by ~2%. Therefore the biological relevance is questionable.
In terms of carcinogenic potential, Profenofos was concluded not to possess any carcinogenic potential.
References:
JMPR (1991). Pesticide residues in food - 1990 evaluations. Part II Toxicology. World Health Organisation, WHO/PCS/91.47, Geneva, 1991.JMPR (2007). Pesticide residues in food. Joint FAO/WHO meeting on pesticide residues. Report of the Joint Meeting of the FAO Panel of Experts on Pesticide Residues in Food and the Environment and the WHO Core Assessment Group on Pesticide Residues. Geneva, Switzerland, 18 -27 September 2007.
Referenceopen allclose all
OBSERVATIONS:
Clinical signs of toxicity:
No test material related clinical signs were noted.
Mortality:
Statistical analysis of the survival data for male animals from weeks 0-85 and from female animals from weeks 0-97 revealed no significant differences between the control and treated animals. Additional analysis conducted in conjunction with the analysis of tumour incidence data also revealed no difference among groups.
Table 7.7-1: Survival rates
Group (ppm) / Study week |
Males |
Females |
||||||
0 |
1 |
30 |
100 |
0 |
5 |
20 |
60 |
|
24 |
65/65 |
62/65 |
62/65 |
64/64a |
64/65 |
65/65 |
65/65 |
64/65 |
48 |
63/65 |
60/65 |
62/65 |
63/65 |
64/65 |
64/65 |
62/65 |
62/64b |
72c |
48/60 |
38/60 |
43/59d |
43/59 |
43/60 |
45/60 |
39/60 |
47/58b |
Terminatione (% survival) |
38 (63) |
33 (55) |
39 (66) |
18 (30) |
39 (65) |
41 (68) |
45 (75) |
46 (79) |
a 1 animal missing at week 4
b one accidental death
c 5 animals/gp sacrificed at week 52 as per study design
d 1 animal missing at week 72
e Week 85 for males, week 97 for females
Palpable masses:
No treatment related differences were seen in the incidence of palpable nodules, tissue masses or wart like lesions.
Bodyweight and bodyweight gains:
No treatment related differences observed
Food consumption:
No treatment related differences observed
Blood analysis:
Statistically significant decreases in erythrocyte and plasma cholinesterase values for the 30 and 100 ppm male and females at week 53 and termination were observed. No sex differences were observed in terms of either plasma or erythrocyte inhibition. Brain cholinesterase activity was significantly decreased in females (25%) at termination in the 100 ppm group, in males whilst a 15% inhibition in brain cholinesterase activity was observed at week 53, at termination an increase in activity was present. Therefore the decrease was not considered biologically relevant.
Table 7.7-2: AChE %inhibition
Dose |
Time |
Plasma |
RBC |
Brain |
|||||||||
(ppm) |
(weeks) |
Male |
Sig |
Female |
Sig |
Male |
Sig |
Female |
Sig |
Male |
Sig |
Female |
Sig |
1 |
53 |
3 |
NS |
-89 |
NS |
9 |
NS |
5 |
NS |
5 |
NS |
0 |
NS |
1 |
Term. |
15 |
NS |
-93 |
NS |
-4 |
NS |
0 |
NS |
-54 |
NS |
-6 |
NS |
30 |
53 |
38 |
* |
55 |
* |
58 |
* |
49 |
* |
1 |
NS |
7 |
NS |
30 |
Term. |
42 |
* |
68 |
* |
68 |
* |
54 |
* |
-44 |
NS |
5 |
NS |
100 |
53 |
52 |
* |
46 |
* |
73 |
* |
66 |
* |
15 |
NS |
4 |
NS |
100 |
Term. |
64 |
* |
76 |
* |
74 |
* |
74 |
* |
-31 |
NS |
25 |
* |
* statistically significant (p<0.05)
OBSERVATIONS:
Clinical signs of toxicity:
No test material related clinical signs were noted.
Mortality:
Statistical analysis of survival data from weeks 0-104 did not reveal any significant differences between the control and treated males and females.
Table 7.7 -3: Survival rates
Group (ppm) / Study week |
Males |
Females |
||||||
0 |
0.3 |
10 |
100 |
0 |
0.3 |
10 |
60 |
|
26 |
70/70 |
59/60 |
59/60 |
69/70 |
69/69 |
60/60 |
60/60 |
69/70 |
54 |
64/65 |
59/60 |
59/60 |
58/65 |
63/64 |
59/60 |
59/60 |
57/65 |
82 |
57/60 |
57/60 |
58/60 |
55/60 |
54/59 |
59/60 |
56/60 |
55/60 |
Termination (% survival) |
51 (85) |
54 (90) |
48 (80) |
50 (83) |
45 (76) |
43 (72) |
46 (78) |
41 (68 |
Palpable masses:
An increase in thyroid gland perifollicular cell hyperplasia was observed in males (4/70 controls vs. 10/70 high dose group) and an increase in liver neoplastic nodules in females (1/70 controls vs. 3/60 low dose, 2/60 mid dose and 6/70 high dose). These histopathological findings were not considered to be treatment related or to be suggestive of an oncogenic effect. No increase in liver carcinomas occurred.
BODY WEIGHT AND BODY WEIGHT GAIN:
Bodyweights and gains were not affected.
FOOD CONSUMPTION
Statistically significant increased in food consumption was observed in females at it the high dose group compared to the controls. The same effect was not observed in males.
BLOOD ANALYSIS:
Haematological and clinical chemistry values were unremarkable, with the exception of the inhibition in cholinesterase activities (discussed below).
Table 7.7-2: AChE % inhibition
Dose |
Time |
Plasma |
RBC |
Brain |
|||||||||
(ppm) |
(weeks) |
Male |
Sig |
Female |
Sig |
Male |
Sig |
Female |
Sig |
Male |
Sig |
Female |
Sig |
0.3 |
13 |
12 |
* |
2.5 |
NS |
5.7 |
* |
4.8 |
NS |
- |
- |
- |
- |
0.3 |
26 |
-23.2 |
* |
-6.9 |
* |
-5.9 |
NS |
-9.8 |
* |
- |
- |
- |
- |
0.3 |
52 |
1.9 |
NS |
0 |
NS |
-5.3 |
NS |
7.7 |
NS |
- |
- |
- |
- |
0.3 |
78 |
14.8 |
* |
1.2 |
NS |
-4.7 |
NS |
6.2 |
NS |
- |
- |
- |
- |
0.3 |
105 |
17.9 |
NS |
2.3 |
NS |
-4.5 |
NS |
10 |
* |
1.4 |
NS |
5.7 |
NS |
10 |
13 |
27.9 |
* |
24.3 |
* |
31.1 |
* |
31.3 |
* |
- |
- |
- |
- |
10 |
26 |
-8.6 |
NS |
13.6 |
NS |
25.7 |
* |
16.3 |
* |
- |
- |
- |
- |
10 |
52 |
15.2 |
* |
9.2 |
* |
23.1 |
* |
23.4 |
* |
- |
- |
- |
- |
10 |
78 |
23 |
* |
13.7 |
* |
22.2 |
* |
21.6 |
* |
- |
- |
- |
- |
10 |
105 |
23.1 |
NS |
25.5 |
* |
11.9 |
* |
18.6 |
NS |
1.4 |
NS |
8.9 |
* |
100 |
13 |
30.4 |
NS |
57.9 |
* |
66.8 |
* |
64 |
* |
- |
- |
- |
- |
100 |
26 |
35.3 |
* |
58.1 |
* |
67.2 |
* |
60.9 |
* |
- |
- |
- |
- |
100 |
52 |
37.7 |
* |
49.6 |
* |
69.4 |
* |
66.3 |
* |
-1.9 |
NS |
6.3 |
NS |
100 |
78 |
49.7 |
* |
54 |
* |
70.6 |
* |
60.7 |
* |
- |
- |
- |
- |
100 |
105 |
62.4 |
* |
62.4 |
* |
58.2 |
* |
58.6 |
* |
4.2 |
NS |
11.5 |
* |
In the low dose group (0.3 ppm) no statistically significant inhibition of plasma cholinesterase was observed, with levels of inhibition never exceeding 18%. In the 100 ppm group statistically significant inhibition was generally observed at all time points, with %inhibition ranging from 30 to 62% for males and 50 to 62% for females.
Erythrocyte inhibition at the low dose was noted, but never exceeded 10% for either gender. At 10 ppm statistically significant inhibition was observed at all time points. Inhibition reached 31% at week 13, and appeared to recover to some extent at termination. At 100 ppm inhibition ranged from 30 to 62% and 58 to 71% in males and females respectively. The effects on plasma and erythrocyte inhibition were fully reversible after 4 weeks recovery following a 52 week administration period.
Statically significant inhibition in brain cholinesterase activity was observed in females only at both the 10 and 100 ppm (105 week time point) groups, however the level of inhibition never exceeded 12%.
Following re-evaluation of brain cholinesterase activities with study control values after combination with historical control values revealed that these differences were not statistically significant.
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed
- Dose descriptor:
- NOAEL
- 4.5 mg/kg bw/day
- Study duration:
- subchronic
- Species:
- mouse
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 was no evidence of carcinogenicity in studies with Profenofos; therefore Profenofos has not been classified as carcinogenic.
Additional information
Of the two available carcinogenicity studies available Profenofos did not adversely affect survival, there were no clinical signs of toxicity, no increase in the incidence of tumour formation and no treatment-related changes in either gross pathology or histopathology. Plasma and erythrocyte cholinesterase activity were significantly reduced in mice and rats given Profenofos in the diet at 30 ppm (equal to 4.5 mg/kg diet) and 100 ppm (equal to 5.7 mg/kg diet) respectively. In female mice a statistically significant inhibition of brain cholinesterase activity (25%) at termination was observed in the 100 ppm group, equal to 5.7 mg/kg diet. Therefore in accordance with the recent JMPR guidelines, the NOAEL for toxicity in the mouse study was based on available brain cholinesterase data, with the NOAEL considered to be 4.5 mg/kg diet. No carcinogenic effect was observed.
In the 2 year rat study the author concluded that the NOAEL was 0.3 ppm, based on statistically significant inhibition of both plasma and erythrocyte cholinesterase activity. In light of the JMPR review, the NOAEL was revaluated. It is biologically plausible to infer that the NOAEL can be considered to be 100 ppm, the highest dose administered. This is based the following: variable and inconsistent erythrocyte cholinesterase inhibition never exceeding 20%, which was fully reversible at the end of the treatment period. Initially, brain cholinesterase activities were statistically significantly inhibited in females fed 100 ppm at week 105, with inhibition not reaching the required 20% to be considered biologically relevant (11% inhibition achieved). Following re-evaluation in conjunction with historical control values, these differences were not considered statistically significant. Finally, following a 10 -fold increase in dose (10 ppm to 100ppm) the level of inhibition in one sex only increased by ~2%. Therefore the biological relevance is questionable.
Profenofos was not considered to be carcinogenic up to the highest dose tested. Overt toxicity was not observed despite the level erythrocyte cholinesterase inhibition exceeding 70% and brain cholinesterase inhibition exceeding 11% in both studies.
The data were sufficient to conclude that Profenofos was not carcinogenic in mice or rats.
References:
JMPR (2007). Pesticide residues in food. Joint FAO/WHO meeting on pesticide residues. Report of the Joint Meeting of the FAO Panel of Experts on Pesticide Residues in Food and the Environment and the WHO Core Assessment Group on Pesticide Residues. Geneva, Switzerland, 18 -27 September 2007.
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