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EC number: 231-869-6 | CAS number: 7773-01-5
- 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
Neurotoxicity
Administrative data
Description of key information
Human epidemiological data reviewed by Gut, 2009, attached.
Key value for chemical safety assessment
Effect on neurotoxicity: via inhalation route
Endpoint conclusion
- Endpoint conclusion:
- adverse effect observed
- Dose descriptor:
- NOAEC
- 21.5 µg/m³
- Species:
- other: human
- Quality of whole database:
- The review covers publically available human epidemiological reports and data up to 2009. The value cited is not impacted by animal data.
Additional information
A fair body of evidence stemming from human (epidemiological) cohort studies indicates that occupational and to a lesser extent environmental manganese exposures induce neurotoxic effects in man. This report aims at i) the evaluation of data relating to the neurotoxicity of inorganic manganese compounds, ii) the analyses of exposure-effect relationships between some inorganic manganese manganese and neurofunctional alterations, and m) the identification of a no observable adverse effect level (NOAEL) for the major route of manganese exposure, i.e. inhalation.
The aggregated data from a recent meta-analytical analysis (Meyer-Baron et al., 2009) taking into account thirteen human cohort studies examining a total of 958 exposed and 815 unexposed study participants revealed mean concentrations of inhalable manganese in the range from 50 to 1590 µg/m3, and mean concentrations of manganese in blood ranged from 8.1 to 48.4 µg/L.
The overall effects displayed a negative impact of manganese on neurofunctional performance parameters. Significant overall effects were obtained for six test variables; as aggregated in the study by Meyer-Baron et al. (2009) their effect sizes ranged from - 0.23 to - 0.36. Four of the variables measured motor speed and two of them speed of information processing. The evidence of cognitive and motor performance effects is in accordance with the knowledge about accumulation of manganese in the basal ganglia and the effect of manganese on the neurotransmitter dopamine, and supported indirectly by data from several high dose manganese studies in laboratory animal revealing neuronal injury.
Inconsistencies in the relationship between effect sizes and the concentration of manganese, in blood or urine, were identified in several human cohort studies. In contrast, consistent exposure-effect relationships have been identified when respirable manganese was used as the exposure parameter. Under these conditions, the analysis of exposure-effect relationships showed that larger effect sizes were generally associated with higher concentrations of respirable manganese.
A number of suitable occupational cohort studies were identified for the extraction of a reliable NOAEL value for respirable manganese-induced neurotoxicity in humans. Thus, the analysis of the studies by Gibbs el al. (1999, NOAEL = 66 µg/m3), Deschamps et al. (2001, (NOAEL = 57 µg/m3), and Young et al. (2005, NOAEL = 58 µg/m3) yielded with reasonable reliability an overall NOAEL of 60 µg/m3for neurotoxicity of respirable manganese in humans. Moreover, Myers et al. (IEH/IOM Report (2004)) calculated a NOAEL in the range of 40 — 80 g/m3.
In addition, the study by Roels et al. (1992) yielded a “study observed effect level (“sOEL")" of 215 µg/m3for respirable manganese (MnO2). Considering this value as representative of a LOAEL and applying a transformation factor of 0.1 for the conversion of a LOAEL to a NOAEL (IEH/IOM Report (2004)) may yield the equivalent of a NOAEL calculated from these data of 21.5 µg/m3, a value slightly below that abstracted from the other studies above.
For a full review see the attached document (Gut, 2009).
Justification for selection of effect on neurotoxicity via inhalation route endpoint:
Weight of evidence based on a review of all avaialble studies by Gut, 2009 (see discussion below and the attached document).
Justification for classification or non-classification
It is proposed to classify MnCl2 under GHS as STOT RE2. H373, based on known effects in animals (manganese sulphate) and humans (occupational exposures to managenese) on the nervous system.
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