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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

Diss Factsheets

Administrative data

Link to relevant study record(s)

Description of key information

For the purposes of human risk assessment, oral absorption of praseodymium oxide is estimated at 0.1%, inhalation absorption is estimated at 1% and dermal absorption is estimated at 0.1%.

Key value for chemical safety assessment

Bioaccumulation potential:
no bioaccumulation potential
Absorption rate - oral (%):
0.1
Absorption rate - dermal (%):
0.1
Absorption rate - inhalation (%):
1

Additional information

Executive summary

Praseodymium oxide is a brown powder, with a molecular weight of 1021.4 g/mol and a melting point of 2183ºC. The D50 particle sizes for praseodymium oxide range between 2 and 50 μm. The physico-chemical properties of praseodymium oxide (sparingly soluble in water at 1.27 mg/L and with a large molecular weight >1000 g/mol) would suggest that absorption into the body by any route is likely to be extremely low.

Due to a limited availability of toxicokinetic data for praseodymium oxide, the relevant information for other soluble and poorly soluble praseodymium compounds are used to perform a qualitative assessment of the absorption, distribution/metabolism and elimination/excretion of praseodymium compounds.

Due to its very low water solubility, the absorption after oral, dermal or inhalation exposure to praseodymium oxide is expected to be very limited, as evidenced in the available oral mammalian toxicology studies where a lack of systemic adverse toxicity was demonstrated in the bolus dosing regimens up to 1000 mg/kg bw/day, the highest dose level recommended in the regulatory required repeated dose toxicity studies under REACH. The available oral gavage toxicokinetic study in mice shows a fast elimination of praseodymium oxide from the whole blood once it enters the circulatory system.

Based on the information available for soluble praseodymium compounds via intravenous or intramuscular administrations in rodents, praseodymium is distributed and deposited in the liver and bones and potentially enhances liver metabolism capacity. The incorporation in liver is expected to occur via removal of colloidal precipitates from the blood stream by phagocytic cells and consequent storage, for instance in lysosomes in the liver. Upon exposure via inhalation and under conditions of lung overload and insufficient clearance, macrophage-mediated translocation of solid material to lung-associated lymph nodes (and from there to other organs) is expected to occur. Bile is considered to be the main route of excretion. This may however be applicable to only a limited extent for praseodymium oxide since its absorption after oral, dermal or inhalation exposure is expected to be minimal.

For the purposes of human risk assessment, oral absorption of praseodymium oxide is estimated at 0.1%, inhalation absorption is estimated at 1% and dermal absorption is estimated at 0.1%.

The full toxicokinetic report is attached in section 13 of this dataset.