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EC number: 947-155-9 | 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
A carcinogenicity study was conducted on a structural analog of MTDID 44428. The results of the study were:
Not carcinogenic when tested according to via dermal exposure for 2 years.
Key value for chemical safety assessment
Carcinogenicity: via dermal route
Link to relevant study records
- Endpoint:
- carcinogenicity: dermal
- Type of information:
- experimental study
- Adequacy of study:
- key study
- Study period:
- April 1979 - may 1981
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: Male mice only and one dose was tested. Dosing and evaluation is consistent with a 2 year dermal study.
- Qualifier:
- no guideline available
- Principles of method if other than guideline:
- No guidelines were referenced in the protocol or report; however, the study was conducted in accordance with carcinogenicity assays at that time. This was a 2 year dermal carcinogenicity assay that was reviewed by the Quality Assurance Unit at Bushy Run Research Center. The fur on the back of each mouse was clipped on Tuesday and Thursday of each week. 25 microliters of the test article were applied three times per week throughout the study, using an Eppendorf automatic pipette and spreading the aliquot up the back of each mouse. Animals were observed daily for mortality and monthly for skin leisons. All animals were necropisied at the end of the in-life phase; the necropsy included a careful examination of the skin and internal cavities and the recording of observations. All suspect tumors and the dorsal skin of all non-autolyzed mice, with or without tumors, were fixed in 10% neutral buffered formalin. Slides were prepared from the dorsal skin of all mice and any suspect internal tumors Histopathologic examinations were performed and reported.
- GLP compliance:
- no
- Species:
- mouse
- Strain:
- C3H
- Sex:
- male
- Details on test animals or test system and environmental conditions:
- TEST ANIMALS
- Source: Jackson Laboratoris, Bar Harbor, Maine
- Age at study initiation: 74-9 Days
- Weight at study initiation: 21/1 to 27.5 g
- Fasting period before study:
- Housing: Group housing
- Diet (e.g. ad libitum): ad libitum
- Water (e.g. ad libitum): ad libitum
- Acclimation period: Two weeks
ENVIRONMENTAL CONDITIONS
- Temperature (°C):
- Humidity (%):
- Air changes (per hr):
- Photoperiod (hrs dark / hrs light):
IN-LIFE DATES: From: 9 April 1979 To: 1 May 1981 - Route of administration:
- dermal
- Vehicle:
- acetone
- Details on exposure:
- PREPARATION OF DOSING SOLUTIONS:
VEHICLE
- Justification for use and choice of vehicle (if other than water): Test article solubility
- Concentration in vehicle: 5% Test artcle in Acetone
TEST SITE
- Area of exposure: Back of mice
- % coverage:
- Type of wrap if used: None
- Time intervals for shavings or clipplings: Animals were clipped on Tuesdays and Thursdays
TEST MATERIAL
- Amount(s) applied (volume or weight with unit): 25 microliters
- Concentration (if solution): 5%
- Constant volume or concentration used: yes
VEHICLE
- Justification for use and choice of vehicle (if other than water): Test article solubility
- M/F ratio per cage: males Only - Analytical verification of doses or concentrations:
- yes
- Details on analytical verification of doses or concentrations:
- GC analysis was conducted to verify the dosing concentrations
- Duration of treatment / exposure:
- Test article was applied and was not washed after application
- Frequency of treatment:
- 3 times per week
- Remarks:
- Doses / Concentrations:
A single 5% concentration was used which equals a 1.25 microliter dose
Basis:
other: applied to the skin - No. of animals per sex per dose:
- 40
- Control animals:
- yes, concurrent vehicle
- Details on study design:
- - Dose selection rationale: Based on dose finding study, the 5% dose resulted in slight skin irriation and did not result in weight loss.
- Positive control:
- None
- Observations and examinations performed and frequency:
- CAGE SIDE OBSERVATIONS: Yes
- Time schedule: Daily
DETAILED CLINICAL OBSERVATIONS: Yes
- Time schedule: Monthly
DERMAL IRRITATION (if dermal study): Yes
- Time schedule for examinations: Daily
BODY WEIGHT: No data
OPHTHALMOSCOPIC EXAMINATION: No
HAEMATOLOGY: No
CLINICAL CHEMISTRY: No
URINALYSIS: No
NEUROBEHAVIOURAL EXAMINATION: No - Sacrifice and pathology:
- GROSS PATHOLOGY: Yes (see ATT 1)
HISTOPATHOLOGY: Yes (see ATT 2) - Other examinations:
- Mortality incidences were assessed by the product-limit method (Kaplan and Meire, 1958) and teh Mantel-Cox and Breslow statistics were used for testing the equality of teh survival curves (Mantel, 1966; Breslow, 1970)
- Body weight and weight changes:
- not specified
- Food consumption and compound intake (if feeding study):
- not specified
- Food efficiency:
- not specified
- Water consumption and compound intake (if drinking water study):
- not specified
- Ophthalmological findings:
- not examined
- Haematological findings:
- not examined
- Clinical biochemistry findings:
- not examined
- Urinalysis findings:
- not examined
- Behaviour (functional findings):
- not examined
- Organ weight findings including organ / body weight ratios:
- not specified
- Gross pathological findings:
- effects observed, treatment-related
- Histopathological findings: non-neoplastic:
- effects observed, treatment-related
- Histopathological findings: neoplastic:
- effects observed, treatment-related
- Relevance of carcinogenic effects / potential:
- The dermal carcinogenic potential of isooctyl acrylate was assessed by applying a 25 microliters of a 5% (v/v) dilution in acetone to the backs of 40 C3H/HeJ male mice. These mice were selected because of a low incidence of spontaneous skin tumors. A negative control group recieving acetone was dosed simultaneously. The dermal route of exposure was selected because this constitutes the most likely route of exposure to this substance.
A squamous cell carcinoma, not at the site of application, was found in the treated group of mice. In addition, an initially diagnosed dermal melanoma was found at the site of application in the treated group. Two nodules in the acetone control group in the acetone control group were diagnosed at a hematoma and fat necrosis. Skin alterations in the treatment group included hyperkeratosis, dermatitis and surface crusting.
The initially diagnosed melanoma wa reviewed by an additional pathologist who stated 'that the cells comprising this melanoma are well diifferentiated with no indication of nuclear or cytologic pleamorphism or atypia. The lesion is well circumscribed and confined to the dermis.' It was the pathologists opinion that this consttutes a benign lesion and would not be expected to invade or metastasize given non subsantative change in morphology if the animal had lived longer. (see attached letter)
The conclusion reached is that the test substance was not found to be carcinogenic. - Key result
- Dose descriptor:
- NOAEL
- Effect level:
- ca. 0.91 mg/kg bw/day
- Based on:
- test mat.
- Sex:
- male
- Basis for effect level:
- histopathology: neoplastic
- Remarks on result:
- other: Effect type: carcinogenicity (migrated information)
- Conclusions:
- The test substance, a 5% (v/v) Isooctyl acrylate in acetone, was not found to be carcinogenic in a two year dermal assay.
- Executive summary:
40 C3H/HeJ mice were treated for two years by applying 25 microliters of a 5% (v/v) in acetone solution to the back. Treated animals exhibited surface crusting, moderate dermatitis, hyperkeratosis, epidermal hyperplasia and melanosis at the treatment site. A benign dermal melanoma was diagnosed in tissue taken from the treatment site of one animal in the treated group. Isooctyl acrylate was not found to be carcinogenic in this study.
- Endpoint:
- carcinogenicity: dermal
- Type of information:
- read-across from supporting substance (structural analogue or surrogate)
- Adequacy of study:
- key study
- Justification for type of information:
- REPORTING FORMAT FOR THE ANALOGUE APPROACH
1. HYPOTHESIS FOR THE ANALOGUE APPROACH
The target chemical (MTDID 44428, CASRN 87015-11-0) and the source chemical (isooctyl acrylate (IOA) CAS 29590-42-9) are isomers that contain the same functional acrylate moiety attached to primarily C8 alkyl hydrocarbon chains (C7-C9, C8 rich for the source chemical) with variable branching. The source chemical differs from the target chemical in both the degree and position of branching of the alkyl ester group with the source chemical being branched at the terminal end of the alkyl chain while the target chemical is branched near the acrylate functional group. The acrylate group is expected to be metabolized in the same manner in both substances and the remaining alkyl chain will be metabolized and excreted via the same pathway. The source chemical and target chemical have the same molecular weight and very similar log Kow values (Target: 4.7-4.8, Source: 4.5-4.7). Similar ADME profiles are expected between the two substances as the metabolic pathway of acrylate esters has been well characterized. Acrylate and methacrylate functionalities are electrophilic and both may participate in Michael addition reactions. Metabolism is expected to occur through the same pathways, hydrolysis by carboxylesterases into two metabolites, an alcohol and an acrylic acid moiety with minor conjugation to gluthathione. Hydrolysis is similar across the acrylate family and enhances the elimination of the chemical upon exposure (McCarthy & Witz, 1997). Studies with n-butyl acrylate and 2-ethylhexyl acrylate confirm that the acrylic acid metabolite enters aerobic oxidation and in completely metabolized to CO2 with only a minor proportion be conjugated to glutathione and excreted in the urine as a N-acetyl cysteine conjugate (Sanders, JM et. al, 1988; Gut, I, et al. 1988). The previously mentioned studies have also demonstrated that enzymatic hydrolysis kinetic constants for methacrylate and acrylate esters are similar.
2. SOURCE AND TARGET CHEMICAL(S) (INCLUDING INFORMATION ON PURITY AND IMPURITIES)
Target Chemical
The target molecule, MTDID 44428 (CASRN 87015-11-0), is a multi-constituent substance defined as the reaction mass of octan-2-yl acrylate, octan-3-yl acrylate and octan-4-yl acrylate as represented by the following structures.
(see attached read-across justification document).
Molecular weight of the target chemical is 184.3
Source Chemical:
The source chemical, isooctyl acrylate (IOA) CAS 29590-42-9, is defined as a UVCB and is represented by the following structure (see attached read-across justification document).
The average molecular weight of the source substance is ca. 184.0. The source chemical differs from the target chemical in the degree and position of branching of the alkyl ester group with the source chemical having variable methyl branching along the alkyl chain while the target chemical is branched immediately adjacent to the acrylate functional group.
Purity and Impurities :
MTDID 44428 is a multi-constituent substance and the three acrylate constituents contribute >99% of the content. There are very low levels of residual reactants and reaction side products.
Isooctyl acrylate is a UVCB substance, based on the mixed-isomer nature of the material. As a UVCB substance, all components are considered part of the substance and the concept of impurities has little meaning. Acrylate ester content of IOA is >99 %, with very low levels of residual reactants and reaction side products. These non-acrylate components are substantially similar and do not impact the read-across of test results from IOA.
3. ANALOGUE APPROACH JUSTIFICATION
Analogue Approach Justification
The target chemical and source chemical are closely related alkyl acrylate compounds. They differ slightly in the structure of the alkyl ester portion of the molecule. MTDID 44428 contains a methyl, ethyl or propyl branch at the 1-carbon of the alkyl chain portion of the molecule, which is always C8 in total. IOA may have methyl or ethyl branches at one or more positions along the alkyl ester group. The carbon chain is predominantly C8 in total with lesser contributions of C7 and C9 (C8 on average).
The environmental toxicity of low molecular weight acrylate esters (aquatic mortality and immobilization) is by protein adduct formation via a Michael-type addition mechanism. In the environment, toxicity increases on a molar concentration basis with molecular weight (and concomitantly, hydrophobicity) due to increased ability of the molecule to reach its active site. The excess toxicity is mitigated in high molecular weight acrylate esters with log P > 5.
The mammalian toxicity of IOA and MTDID 44428 is also based on protein adduct formation via a Michael-type addition with the acrylate groups. Both the target and source chemical are weak dermal sensitizers (section 5) indicating that an equivalent mechanism of toxicity is at work for both substances based on identical functional groups and molecular weights and very similar log Kow values and water solubilities.
The number of hydrophobic carbons of IOA relative to MTDID 44428 is predicted to be similar resulting in very similar octanol water partition coefficient values. This was confirmed experimentally and the log Kow for IOA is 4.5-4.7 while the log Kow for MTDID 44428 is 4.7-4.8. Additionally, IOA and MTDID 44428 have very similar water solubility at 12.44 and 14.6 mg/L, respectively. IOA is expected to be metabolized via the same hydrolytic and enzymatic pathways as MTDID 44428, forming acrylic acid and isooctanol.
Similar mammalian metabolic pathways are expected for IOA and MTDID 44428 based on Sanders, et. al and Gut, et al. The source chemical and target chemical have the same molecular weight and very similar log Kow values. Similar ADME profiles are expected between the two substances as the metabolic pathway of acrylate esters has been well characterized. Acrylate and methacrylate functionalities are electrophilic and both may participate in Michael addition reactions. Metabolism is expected to occur through the same pathways, hydrolysis by carboxylesterases into two metabolites, an alcohol and an acrylic acid moiety with minor conjugation to gluthathione. Hydrolysis is similar across the acrylate family and enhances the elimination of the chemical upon exposure (McCarthy & Witz, 1997). Studies with n-butyl acrylate and 2-ethylhexyl acrylate confirm that the acrylic acid metabolite enters aerobic oxidation and in completely metabolized to CO2 with only a minor proportion be conjugated to glutathione and excreted in the urine as a N-acetyl cysteine conjugate (Sanders, JM et. al, 1988; Gut, I, et al. 1988). The previously mentioned studies have also demonstrated that enzymatic hydrolysis kinetic constants for methacrylate and acrylate esters are similar.
As can be seen in the table in section 5, the source and target substances have very similar environmental and mammalian hazard profiles for endpoints where each substance has experimental data. This further supports the hypothesis that the target and source substances are expected to behave similarly in mammalian and environmental systems with the same mechanism of action and that read-across of the data for higher-tier endpoints is appropriate in an effort to reduce unnecessary animal testing.
4. DATA MATRIX
See 'Other Information Including Tables' or attached justification.
Supporting References
Gut, I, Vodička, Cikrt, M, Sapota, A, and Kavan, I (1988) Distribution and elimination of (14C)-2-ehtylheyxyl acrylate radioactivity in rats. Archives of Toxicology 62:346-350.
McCarty, TJ and Witz, G (1997) Structure-activity relationships in the hydrolysis of acrylate and methacrylate esters by carboxylesterase in vitro. Toxicology 116: 153-158. - Reason / purpose for cross-reference:
- read-across source
- Body weight and weight changes:
- not specified
- Food consumption and compound intake (if feeding study):
- not specified
- Food efficiency:
- not specified
- Water consumption and compound intake (if drinking water study):
- not specified
- Ophthalmological findings:
- not examined
- Haematological findings:
- not examined
- Clinical biochemistry findings:
- not examined
- Urinalysis findings:
- not examined
- Behaviour (functional findings):
- not examined
- Organ weight findings including organ / body weight ratios:
- not specified
- Gross pathological findings:
- effects observed, treatment-related
- Histopathological findings: non-neoplastic:
- effects observed, treatment-related
- Histopathological findings: neoplastic:
- effects observed, treatment-related
- Relevance of carcinogenic effects / potential:
- The dermal carcinogenic potential of isooctyl acrylate was assessed by applying a 25 microliters of a 5% (v/v) dilution in acetone to the backs of 40 C3H/HeJ male mice. These mice were selected because of a low incidence of spontaneous skin tumors. A negative control group recieving acetone was dosed simultaneously. The dermal route of exposure was selected because this constitutes the most likely route of exposure to this substance.
A squamous cell carcinoma, not at the site of application, was found in the treated group of mice. In addition, an initially diagnosed dermal melanoma was found at the site of application in the treated group. Two nodules in the acetone control group in the acetone control group were diagnosed at a hematoma and fat necrosis. Skin alterations in the treatment group included hyperkeratosis, dermatitis and surface crusting.
The initially diagnosed melanoma wa reviewed by an additional pathologist who stated 'that the cells comprising this melanoma are well diifferentiated with no indication of nuclear or cytologic pleamorphism or atypia. The lesion is well circumscribed and confined to the dermis.' It was the pathologists opinion that this consttutes a benign lesion and would not be expected to invade or metastasize given non subsantative change in morphology if the animal had lived longer. (see attached letter)
The conclusion reached is that the test substance was not found to be carcinogenic. - Key result
- Dose descriptor:
- NOAEL
- Effect level:
- ca. 0.91 mg/kg bw/day (nominal)
- Based on:
- test mat.
- Sex:
- male
- Basis for effect level:
- histopathology: neoplastic
- Conclusions:
- Reading-across the results from the source substance (IOA), the target substance (MTDID 44428) is not carcinogenic.
- Executive summary:
The similarities between the structural, physical & chemical, toxicity, and predicted metabolic properties of the source and target substances presented above support the read-across hypothesis for genetic toxicity. The data are adequate and reliable scientific information to support the hypothesis. Therefore, based upon the data and considerations presented in the above sections, it can be concluded that the results of the carcinogenicity study with source substance will accurately predict the results for the target substance and are considered as adequate to fulfil the information requirement of Annex VIII, of the REACH Regulation for the target substance.
Referenceopen allclose all
SEE ATT 1 : IOA Frequency of Gross Findings
SEE ATT 2: IOA Frequency of Histologic Findings
READ-ACROSS DATA MATRIX
Target substance |
Source substance |
|
CHEMICAL NAME |
Reaction mass of octan-2-yl acrylate, octan-3-yl acrylate and octan-4-yl acrylate |
Isooctyl acrylate |
CAS# |
44914-03-6 |
29590-42-9 |
Molecular formula |
C11H20O2 |
C11H20O2 (on average) |
Molecular Weight |
184.3 |
184.3 (on average) |
Melting Point |
Experimental: <-35 °C |
Experimental: < -90 °C at 1004 hPa |
Boiling Point |
Experimental: 217.6 °C (normalized) |
Experimental: 196.8 °C at 1016 hPa |
Density |
Experimental: 0.8665 at 23 °C |
Experimental: 0.885 g/cm3 at 20.0 °C |
Vapour Pressure |
Experimental: .06 hPa at 18 °C |
Experimental: 1 hPa at 20 °C |
Partition Coefficient (log KOW) |
Experimental: 4.7-4.8 |
Experimental: 4.5 - 4.7 |
Water Solubility |
Experimental: Individual isomers had solubilites of 4-5 mg/L, total was 14.6 mg/L |
Experimental: 12.44 mg/L at 23.1 °C |
|
|
|
Stability in Water |
Experimental: t1/2at 25 °C, pH 9, 37.7-116 days t1/2at 25 °C, pH 7, 137 days - not determinable t1/2at 25 °C, pH 4, 154 days - not determinable. Hydrolysis product could be detected at pH 9 but not pH 7 and 4. Half-life increased from 2-octyl < 3-octyl < 4-octyl isomers. |
Adaptation, readily biodegradable |
Aerobic Biodegradation |
Experimental: 54.7% after 28 days, biodegradation essentially stopped at day 11 (OECD 301F)
67% after 28 days. No residual material could be detected in test chambers on day 28. In abiotic control, residual test material was 4.8% of initial result (OECD 302C) |
Experimental: 93-95% after 28 days (OECD 301D) |
Bioconcentration |
|
Not bioaccumulative |
Transport and Distribution |
Experimental: Koc 630 (OECD121) |
Experimental: Koc 650-3900 (OECD121) |
Henry's Law constant |
NDA |
Experimental: 1780 Pa*m3/mol at 23.1 °C |
Acute Toxicity to Fish (P. promelasunless noted) |
NDA |
Experimental: 96-hour LC50 0.67 mg/L (OECD 202) |
Chronic Toxicity to Fish |
NDA |
Waived |
Acute Toxicity to Aquatic Invertebrates (D. magna) |
NDA |
Experimental: 48-hour EC50 0.4 mg/L (OECD 202) |
Long-Term Toxicity to Aquatic Invertebrates (D. magna) |
NDA |
Experimental: 28-day NOEC 0.065 mg/L (OECD 202 rev 1984) |
Toxicity to Algae and Aquatic Plants (P. subcapitata) |
NDA |
QSAR result not read across |
Toxicity to Microorganisms (activated sludge respiration) |
Experimental: 3-hour EC50 >1000 mg/L (OECD 209) |
Experimental: 3-hour EC50 >1000 mg/L (OECD 209) |
Acute Oral Toxicity |
Experimental: Rat oral LD50 > 2,000 mg/kg |
Experimental: Rat oral LD50 > 5,000 mg/kg |
Acute Dermal Toxicity |
Read-across from source: Rabbit dermal LD50 > 2,000 mg/kg |
Experimental: Rabbit dermal LD50 > 2,000 mg/kg |
Acute Inhalation Toxicity |
Read-across from source: NDA |
Experimental: NDA |
Skin Irritation |
Experimental: Irritating (GHS Cat. 2) |
Experimental: Not irritating |
Eye Irritation |
Experimental: Not Irritating |
Experimental: Not irritating |
Skin Sensitization |
Experimental: Weak sensitizer (GHS Category 1B) |
Experimental: Weak sensitizer (GHS Category 1B) |
Ames Assay |
Experimental: Non-mutagenic |
Experimental: Non-mutagenic |
in vitroChromosome Aberration |
Read-across from source: Clastogenic at cytotoxic concentrations |
Experimental: Clastogenic at cytotoxic concentrations |
in vitroMouse Lymphoma Assay |
Read-across from source: Non-mutagenic |
Experimental: Non-mutagenic |
28 Day Oral Toxicity |
Read-across from source: NOAEL = 1,000 mg/kg/day |
Experimental: NOAEL = 1,000 mg/kg/day |
90 Day Oral Toxicity |
Read-across from source: NOAEL = 600 mg/kg/day |
Experimental: NOAEL = 600 mg/kg/day |
Reproductive/Developmental Screening Study (Dermal) |
Read-across from source: NOAEL = 20% Dermal Exposure |
Experimental: NOAEL = 20% Dermal Exposure |
Prenatal Developmental Study (Oral) |
Read-across from source: NOAEL = 1,000 mg/kg/day |
Experimental: NOAEL = 1,000 mg/kg/day |
Carcinogenicity (Dermal) |
Read-Across from source: Not Carcinogenic |
Experimental: Not Carcinogenic (5% Dermal Exposure) |
Justification for classification or non-classification
Based on the results of the study conducted on a structural analog, MTDID 44428 does not meet the criteria for classification.
Additional information
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.