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EC number: 295-765-2 | CAS number: 92128-68-2
- 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
Toxicological Summary
- Administrative data
- Workers - Hazard via inhalation route
- Workers - Hazard via dermal route
- Workers - Hazard for the eyes
- Additional information - workers
- General Population - Hazard via inhalation route
- General Population - Hazard via dermal route
- General Population - Hazard via oral route
- General Population - Hazard for the eyes
- Additional information - General Population
Administrative data
Workers - Hazard via inhalation route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- DNEL (Derived No Effect Level)
- Value:
- 8.4 mg/m³
Acute/short term exposure
- Hazard assessment conclusion:
- no-threshold effect and/or no dose-response information available
DNEL related information
Local effects
Long term exposure
- Hazard assessment conclusion:
- no-threshold effect and/or no dose-response information available
Acute/short term exposure
- Hazard assessment conclusion:
- no-threshold effect and/or no dose-response information available
DNEL related information
Workers - Hazard via dermal route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- DNEL (Derived No Effect Level)
- Value:
- 23.7 mg/kg bw/day
DNEL related information
- Overall assessment factor (AF):
- 1
Acute/short term exposure
- Hazard assessment conclusion:
- no-threshold effect and/or no dose-response information available
DNEL related information
Local effects
Long term exposure
- Hazard assessment conclusion:
- no-threshold effect and/or no dose-response information available
Acute/short term exposure
- Hazard assessment conclusion:
- no-threshold effect and/or no dose-response information available
Workers - Hazard for the eyes
Additional information - workers
Compositional information:
These hydrocarbon streams meet the regulatory definition of UVCB substances, with inherent variations in composition present due to differences in manufacturing history. This variability is documented in the Category Justification, which lists the chemical marker substances present along with an indicative concentration range for each e.g.
Benzene: <0.1 – 0.9%
1,3-Butadiene: <0.1 – 3%
Isoprene: >1– 25[a]
Toluene: <0.1 – 4%
Pentane: < 30%
Intrinsic hazards of marker substances and associated DN(M)ELs:
The following hazard information and DNELs are available for marker substances present in this Category.
Benzene
Benzene causes adverse effects on the haematopoietic system of animals and in humans after repeated dose exposure via oral or inhalation routes. Long term experimental carcinogenicity bioassays have shown that it is a carcinogen producing a variety of tumours in animals (including lymphomas and leukaemia). Human epidemiological studies provide clear and consistent evidence of a causal association between benzene exposure and acute myelogenous (non-lymphocytic) leukemia (AMLor ANLL). An effect on bone marrow leading to subsequent changes in human blood cell populations is believed to underpin this response.
In accordance with REACH guidance, a science-based Binding Occupational Exposure Limit value (BOELV) can be used in place of a formal DN(M)EL providing no new scientific information exists which challenges the validity of the BOELV. While some information regarding a NOAEC for effects of benzene on human bone marrow (Schnatter et al, 2010; NOAEC = 11.18 mg/m3[b]) post-date the BOELV, a DNEL based on these bone marrow findings would be higher (and hence offer less protection) than the BOELV. The BOELV will therefore be used as the basis of the DN(M)EL for long-term systemic effects associated with benzene, including carcinogenicity.
Worker – long-term systemic inhalation DNEL
The BOELV will be used with no further modification
DN(M)ELl-t inhalation = 3.25 mg/m3
Worker - long-term systemic dermal DNEL
The dermal DNEL for benzene is based on the internal dose achieved by a worker undertaking light work and exposed to the BOELV for 8 hr, assuming 50% uptake by the lung and 1% by skin for benzene uptake from petroleum streams. The value of 1% is based on experiments with compromised skin and with repeated exposure (Blank and McAuliffe, 1985; Maibach and Anjo, 1981) as well as the general observation that vehicle effects may alter the dermal penetration of aromatic compounds through the skin (Tsuruta et al, 1996).
Dermal NOAEL= BOELV x wRV8-hour[c] x [ABSinhal-human/ABSdermal-human]
= 3.25 x 0.144 x [50 / 1]
DN(M)ELl-t dermal = 23.4 mg/kg bw/d
In summary, the following DNELs apply to benzene:
|
Worker |
|
|
Inhalation |
Dermal |
DN(M)EL |
DN(M)EL |
|
Benzene |
3.25 |
23.4 |
1,3-Butadiene
1,3-Butadiene is a multi-species carcinogen. In the mouse, it is a potent multi-organ carcinogen. Tumours develop after short durations of exposure, at low exposure concentrations and the carcinogenic response includes rare types of tumours. In the rat, fewer tumour types, mostly benign develop at exposure concentrations of 100 to1000-times higher than in the mouse. In humans, 1,3-butadiene is a recognised carcinogen. A positive association was demonstrated between workplace exposure to butadiene for men employed in the styrene-butadiene rubber industry and lymphohaematopoietic cancer (leukemia). Various models have established a dose response-relationship for cumulative exposure to 1,3-butadiene, especially concentrations above 100 ppm. The estimates for occupational and population human risk are based on these models.
Worker – long-term systemic inhalation DNEL
The association between 1,3-butadiene exposure and leukemia has been extensively modeled using Cox and Poisson regression models and the excess risk of leukemia determined. The preferred model for workers is the Cox continuous model (Cheng et al, 2007) as employed by Sielken et al (2008), using the exposure metric that excluded exposure that occurred more than 40 years ago or excluded the 5% of workers with the highest cumulative 1,3-butadiene exposures and included as covariate, the cumulative number of exposures to 1,3-butadiene concentrations > 100 ppm (the number of High Intensity Tasks [HITs]). This model incorporates dose descriptors and assessment factors and therefore further corrected dose descriptors and overall assessment factors are not required. The estimate of the excess risk of death from leukemia as a result of exposure to a DMEL of 2.21 mg/m3 (1 ppm) is 0.33 x 10-4 (with an upper bound of 0.66 x 10-4 based on a one-sided 95% upper confidence limit for the regression parameter).
This estimate is less than 0.4 x 10-4, which has been proposed as a future limit for acceptable occupational risk (AGS, 2008). Regression coefficients from other Cox regression models reported by Cheng et al (2007) and TCEQ (2008), and estimates from Poisson regression models, indicate that other risk estimates are generally close to 0.4 x 10-4, even if based on regression models that do not adjust for 1,3-butadiene HITs. All of the estimates are considerably lower than the current limit for acceptable occupational risk of 4 x 10-4 that has recently been proposed (AGS,2008).
Other routes
1,3-Butadiene is a gas at room temperature and therefore exposure by the dermal route is not relevant.
In summary, the following DNELs apply to 1,3-butadiene:
|
Worker |
|
|
Inhalation |
Dermal |
DN(M)EL |
Not relevant |
|
1,3-Butadiene |
2.21 |
Isoprene
An IOELV has not been established for isoprene. However, in accordance with REACH guidance (Appendix R.8-13) and since no new scientific information has been obtained under REACH which does not support the use of the German national occupational exposure level for this purpose, the established MAK (MAK, 46. Lieferung, 2009) of 3 ppm (equivalent to 8.4 mg/m3) - 8 hrTWAwill be proposed for the inhalation DNEL for workers.
The registrant proposes using the national OEL (German MAK value) in place of a DN(M)EL. It was concluded by the MAK Commission that a maximum admissible concentration (MAK) can be established for humans. The MAK Commission considered the carcinogenic and genotoxic effects of isoprene to be low (MAK, 46 Lieferung 2009), and if MAK values are not exceeded, there would be no appreciable increase of carcinogenic risk in humans expected. Isoprene was classified as a category 5 carcinogenic substance inGermany(no appreciable increase of carcinogenic risk in humans is expected if MAK values are not exceeded).
Isoprene has been shown to be carcinogenic to mice and rats. When inhaled in concentrations of 70 ppm and above, isoprene was found to induce tumours in a range of tissues including lung, liver, Harderian gland, forestomach, lymphoreticular system of male mice. At 70 ppm, statistically significant increases were only reported for increased incidences of Harderian and pituitary adenomas in female mice. No statistically significant increases in tumours were reported at a dose level of 10ppm (Placke et al. 1996). Inhalation by rats of concentrations above the lowest tested value of 220 ppm caused a significantly increased incidence of mammary gland, testicular and kidney tumours in males, and mammary gland tumours in females (NTP 1999). At the lowest dose tested, 220ppm, a statistically significant increase in only mammary gland fibroadenoma was observed in females.
Isoprene is metabolized by cytochrome P450 to two monoepoxides metabolites, which can then be metabolized further to the diepoxide metabolite methyl-1,2:3,4-diepoxybutane. It has been demonstrated that the diepoxide, rather than isoprene itself, is the mutagenic agent in bacterial test systems. In vivo studies have shown isoprene to be genotoxic to mice, and it is presumed that the carcinogenic effects in the mouse and rat long-term studies are due to a genotoxic mode-of-action involving the reactive epoxide metabolites, particular the diepoxide.
Isoprene is produced endogenously in the body from several sources, including intermediates in cholesterol metabolism, peroxidation of squalene, and decomposition of prenylated proteins. It has been reported that the amounts of isoprene exhaled within a 24-hour period were determined to be 0.36 to 9.36 mg (Conkle et al., 1975) and 2 to 4 mg (Gelmont et al., 1981). The mean endogenous blood concentration of isoprene was 37 ± 25 nmol/L. Therefore, to determine a DMEL for isoprene, the target organ levels of the reactive metabolites (mono- and diepoxide metabolites) of isoprene should be known in order to determine the excess carcinogenic risk posed by exposure to isoprene in the workplace and/or in the environment. However, the required in vitro and in vivo data to determine the body burden of the isoprene metabolites, in animals or humans, are not available.
An alternative approach is to use the AUC blood levels of isoprene for body burden[d]. Using a physiological toxicokinetic model, the endogenous body burden of isoprene was calculated using measured values of isoprene concentration in exhaled air (Csanady and Filser, 2001; Filser et al., 1996). This can then be compared with values resulting from exogenous isoprene exposures, such as in the workplace environment. For a workplace exposure limit, the MAK value was determined as the value of exogenous isoprene that correlated to the blood AUC for a lifetime (80 years) of endogenous isoprene formation.
The blood AUC for an exposure of 3 ppm for 8 hours a day over a period of 40 years would be equivalent to a lifetime exposure within the standard deviation of average endogenous concentration (see toxicokinetics under section 5.1 above). As a consequence, an exposure of 3 ppm is not considered to present a significant increase in carcinogenic risk (MAK, 46 Leiferung 2009). The MAK value for isoprene has been defined as 3 ppm and this value is considered appropriate to propose a DNEL for repeat dose inhalation exposure of workers.
Workers – long-term systemic dermal DNEL
The dermal NOAEL is extrapolated from the MAK value of 8.4 mg/m3. The MAK value is the exposure concentration at which the predicted blood AUC for isoprene resulting from a typical 40 year work period would not exceed one standard deviation above the mean endogenous blood AUC over an 80 year lifetime. The blood AUC levels were estimated using a physiological toxicokinetic (PT) model based on mouse, rat and human data.
In order to calculate the dermal DNEL from the inhalation DNEL using route-to-route extrapolation, the net inhalation uptake or dose must be determined. The inhalation DNEL is derived from blood AUC levels and is not equivalent to the dose.
To determine the net inhalation uptake per 8-hour day from an exposure concentration of 3 ppm (8.4 mg/m3), the following calculations were made:
Filser et al. (1996) determined the rates of isoprene metabolism (umol/hr/kg bw) in humans, rats, and mice at steady-state over a range of atmospheric concentrations to validate a PT model for isoprene. Metabolism of isoprene is linear up to 50 ppm. At the isoprene exposure concentration of interest 8.4 mg/m3 (3 ppm), the rate of metabolism (umol/hr/kg bw) can be determined and subtracted from the rate of metabolism at 0 mg/m3 (0 ppm).
At an exposure concentration of 3 ppm, the rate of isoprene metabolism is 0.13 umol/hr/kg bw.
For an 8-hr workday, net inhalation uptake (or dose) is: 0.13 umol/hr/kg bw x 8 hr = 1.04 umol/kg or 71 ug/kg[e].
DNELl-t dermal= 71 ug/kg/absorption factor[f]
= 71 / 0.003
= 23667 ug/kg
= 23.7 mg/kg.
Workers – long-term systemic inhalation DNEL
The MAK will be used
DN(M)ELl-t inhalation = 8.4 mg/m3
In summary, the following DNELs apply to isoprene:
|
Worker |
|
|
Inhalation |
Dermal |
DN(M)EL |
DN(M)EL |
|
Isoprene |
8.40 |
23.7 |
Toluene
Toluene exposure can produce central nervous system pathology in animals after high oral doses. Repeated inhalation exposure can produce ototoxicity in the rat and high concentrations are associated with local toxicity (nasal erosion). In humans neurophysiological effects and disturbances of auditory function and colour vision have been reported, particularly when exposures are not well controlled and/or associated with noisy environments.
Documentation supporting the IOELV (SCOEL, 2001) concluded that an exposure limit of 50 ppm (192 mg/m3) would protect against chronic effects hence, in accordance with REACH guidance and since no new scientific information has been obtained under REACH which contradicts use of the IOELV for this purpose, the established IOELV of 50 ppm (192[g]mg/m3) – 8 hrTWA(EU, 2006) will be used as the starting point for calculating the chronic dermal DNEL for workers.
Worker – long-term systemic inhalation DNEL
The IOELV will be used with no further modification
DNELl-t inhalation = IOELV = 192 mg/m3
Worker – long-term systemic dermal DNEL
The dermal DNEL for toluene is based on the internal dose achieved by a worker undertaking light work and exposed to the IOELV for 8 hr, assuming 50% uptake by the lung and 3.6% uptake by skin (ten Berge, 2009).
As the IOELV is based on worker life-time exposure no assessment factor is needed.
Dermal NOAEL = IOELV x wRV8-hour x [50/3.6]
= [192 x 0.144 x 13.89]
DNELl-t dermal = 384 mg/kg bw/d
In summary, the following DNELs apply to toluene:
|
Worker |
|
|
Inhalation |
Dermal |
DN(M)EL |
DN(M)EL |
|
Toluene |
192 |
384 |
Pentane
Pentane is a simple asphyxiant with an IOELV of 3000 mg/3 (EU, 2006). No DN(M)EL will therefore be derived.
Other components
2-methyl-2-butene
2 -Methyl-2 -butene may be present in some C5 non-cyclics streams at up to 18%. Since 2-methyl-2-butene is concluded to be an in vivo mutagen (Cat 3, R68 under DSD) with no relevant dose-response information and no cancer information, neither a DMEL nor a DNEL can be derived.A qualitative assessment is therefore considered. Since 2-methyl-2-butene is assigned the R-phrase R68 (possible risk of irreversible effects) it is allocated to the high hazard category on the basis that exposure to such substances should be strictly contained because they may cause serious health effects for which a dose threshold is not usually identifiable (TGD Section E.3.4).
With the strict control measures for a non-threshold mutagen, applying the RMMs/OCs as stipulated for the high hazard category, exposure control is considered to be sufficient and will cover any other relevant effects for which DNELs can be derived, for all routes of exposure.
In accordance with REACH guidance, it is concluded that this qualitative risk characterisation is sufficient and there is no need to conduct a quantitative risk assessment.
Substance selection for risk characterization
Risk characterization will be based on the premise that a marker substance with a low DN(M) EL present at high concentration in a stream will possess a greater relative hazard potential than a marker substance with a higher DN(M) EL present at the same or lower concentration. It will also focus on the potential of the markers to cause serious long-term health effects rather than on short-term or irritation-related changes.
In the case of this stream, the hazardous marker substances present are ranked as follows:
WORKERS
Marker substance |
Indicative concentration |
Inhalation |
Dermal |
||
DN(M)EL |
Relative hazard potential |
DN(M)EL |
Relative hazard potential |
||
Isoprene |
≤ 25 |
8.4 |
3.0 |
23.7 |
1.05 |
1,3-Butadiene |
≤ 3 |
2.21 |
0.90 |
na[h] |
na |
Benzene |
≤0.9 |
3.25 |
0.28 |
23.4 |
<0.01 |
Toluene |
≤4 |
192 |
0.02 |
384 |
0.01 |
2-Methyl-2-butene |
≤18 |
+ |
+ |
+ |
+ |
+ Apply RMMs/OCs, no quantitative DN(M)EL necessary
For workers: Based on this analysis, demonstration of “safe use” for hazards associated with the presence of 25% isoprene will also provide adequate protection against hazards arising from benzene, 1,3-butadiene and toluene that are also present.
The long-term inhalation and dermal DNELs for isoprene will therefore be used for worker risk characterization.
References
Blank IH, McAuliffe DJ (1985). Penetration of benzene through human skin. J. Invest. Dermatol. 85, 522–526.
Cheng H;Sathiakumar N;Graff J;Matthews R;Delzell E (2007). 1,3-Butadiene and leukemia among synthetic rubber industry workers: exposure-response relationships Chem Biol Interact, 166,15-24.
Committee on Hazardous Substances (AGS). (2008). Guide for the quantification of cancer risk figures after exposure to carcinogenic hazardous substances for establishing limit values at the workplace. 1. Edition.Dortmund: Bundesanstalt für Arbeitsschutz und Arbeitsmedizin. Available http://www.baua.de/nn_21712/en/Publications/Expert-Papers/Gd34,xv=vt.pdf
EU (1993). Occupational exposure limits: Criteria document for benzene. Report EUR 14491 en, ISSN 1018-5593, Commission of the European Communities, pp126.
EU (1999). Council Directive 1999/38/EC of 29 April 1999 amending for the second time Directive 90/394/EECon the protection of workers from the risks related to exposure to carcinogens at work and extending it to mutagens. Official Journal of the European Communities, L138, 66-69,1 June 1999.
EU (2006). Directive 2006/15/EC of 7 February 2006 establishing a second list of indicative occupational exposure limit values in implementation of Council Directive 98/24/EC and amending Directives 91/322/EECand 2000/39/EC. Official Journal of the European Union, l 38, 36-39.
EU (2008). Annex XV Transitional Dossier: Styrene. echa.europa.eu/doc/trd_substances/styrene/RAR/trd_rar_uk_styrene.rtf
MAK Commission (2009) MAK, 46 Lieferung
Maibach HI, Anjo DM (1981). Percutaneous penetration of benzene and benzene contained in solvents used in the rubber industry. Arch. Environ. Health 36, 256–260.
SCOEL (2001).Recommendation from the Scientific Committee on Occupational Exposure Limits for toluene 108-88-3 http://ec.europa.eu/social/BlobServlet?docId=3816&langId=en
Sielken RL, Valdez-Flores C, Gargas ML, Kirman CR, Teta MJ, Delzell E (2007). Cancer risk assessment for 1,3-butadiene: dose-response modeling from an epidemiological perspective. Chem Biol Interact 166, 140-149.
Sielken RL, Valdez-Flores C, Delzell E (2008). Quantitative Risk Assessment of Exposures to Butadiene in European Union Occupational Settings Based on the University of Alabama at Birmingham Epidemiological Study: All Leukemia, Acute Myelogenous Leukemia, Chronic Lymphocytic Leukemia, and Chronic Myelogenous Leukemia. Unpublished report to Lower Olefins Sector Group,Brussels,Belgium.
Susten AS et al(1990). In vivo percutaneous absorption studies of volatile organic solvents in hairless mice II; Toluene, ethylbenzene and aniline. J. Appl. Toxicol. 10: 217-225.
ten Berge, W (2009). A simple dermal absorption model: Derivation and application. Chemosphere, 75, 1440-1445.
TCEQ (2008) TexasCommission on Environmental Quality. Development Support Document. 1,3-Butadiene. Chief Engineer’s Office. Available: http://tceq.com/assets/public/implementation/tox/dsd/final/butadiene,_1-3-_106-99-0_final.pdf
Tsuruta H (1996). Skin absorption of solvent mixtures-effect of vehicle on skin absorption of toluene. Ind. Health 34, 369–378.
WHO (2000). Air Quality Guidelines forEurope, Second Edition. WHO regional publications, European series; No. 91.
Footnotes
[a] No upper limit set in CJD; 25% used as a “worst case” upper bound to exposure estimation modelling
[b] Data reported as 3.5 ppm, and converted to mg/m3using tool available fromhttp://www.cdc.gov/niosh/docs/2004-101/calc.htm
[c] worker respiratory volume (wRV) is 50% greater than the resting standard respiratory volume of 0.2 L/min/kg bw (wRV8-hour= (0.2 L/min/kg bw x 1.5 x 60 x 8) / 1000 = 0.144 m3/kg bw
[d] AUC: The area under the plasma concentration versus time curve is used to quantitate exposure (concentration times time) for toxicology assessment. AUC is used in non-compartmental pharmacokinetic parameter estimation.
[e] Note that this is a lower-bound estimate of the dose by other routes because some will also be exhaled. For endogenous isoprene, 90% is metabolized into epoxide metabolites and 10% is exhaled.
[f] An absorption of 0.3% was determined by a model (ten Berge, 2009) which predicted a maximum flux of 0.0000638 mg/cm2/min (see IUCLID endpoint record),
[g] mg/m3 values quoted in this document are as reported in the publication or calculated using a conversion at 25°C as used by ACGIH (http://www.cdc.gov/niosh/docs/2004-101/calc.htm).It is recognized that SCOEL used a different calculation
[h] Butadiene is a gas hence no dermal DNEL is quantifiable
General Population - Hazard via inhalation route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- DNEL (Derived No Effect Level)
- Value:
- 8.4 mg/m³
Acute/short term exposure
DNEL related information
Local effects
Acute/short term exposure
DNEL related information
General Population - Hazard via dermal route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- DNEL (Derived No Effect Level)
- Value:
- 71 mg/kg bw/day
Acute/short term exposure
DNEL related information
General Population - Hazard via oral route
Systemic effects
Long term exposure
- Hazard assessment conclusion:
- DNEL (Derived No Effect Level)
- Value:
- 0.213 mg/kg bw/day
Acute/short term exposure
DNEL related information
General Population - Hazard for the eyes
Additional information - General Population
General population DNELS
No DNELs have been developed for the general population since there are no consumer applications for these streams.
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.
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