Zirconium dinitrate oxide

Ecotoxicological Summary

Hazard for aquatic organisms

Freshwater

Hazard assessment conclusion:

no hazard identified

Marine water

Hazard assessment conclusion:

no hazard identified

STP

Hazard assessment conclusion:

no hazard identified

Sediment (freshwater)

Hazard assessment conclusion:

no hazard identified

Sediment (marine water)

Hazard assessment conclusion:

no hazard identified

Hazard for air

Air

Hazard assessment conclusion:

no hazard identified

Hazard for terrestrial organisms

Soil

Hazard assessment conclusion:

no hazard identified

Hazard for predators

Secondary poisoning

Hazard assessment conclusion:

no potential for bioaccumulation

Additional information

PNEC values for the aquatic compartment cannot be derived. The available acute ecotoxicity tests in fish and daphnids show EC50 or LC50 values which are higher than 100 mg/L (based on added test substance) or > 100 % v/v saturated solution. When zirconium dinitrate oxide is dissolved in a buffered aqueous solution (such as a natural surface water), precipitation of zirconium as zirconium hydroxide/zirconium dioxide (pH dependent), zirconium carbonate (pH dependent) and/or zirconium phosphate will occur. The precipitation of zirconium phosphate in algal test media seems to result in some growth inhibition due to phosphate deprivation (i.e., a secondary effect). This was observed in algal growth inhibition experiments with several read across substances. The results from these experiments support the assumption that the observed effects are not due to primary exposure to bioavailable zirconium, but rather due to a secondary effect such as phosphate deprivation. This effect is however not considered environmentally relevant as it may only occur extremely locally. Overall, in view of the extremely low bioavailability of zirconium in environmentally relevant media at environmentally relevant conditions, it can be concluded that zirconium from zirconium dinitrate oxide is not harmful or toxic to aquatic organisms.

Similarly, microorganisms in a sewage treatment plant are not expected to be exposed to zirconium, as zirconium will have been removed from the water column through hydrolysis and carbonate and/or phosphate complexation before reaching the biological treatment step. Often a pH increase step is included for metal precipitation as one of the (first) waste water treatment steps in on-site waste water treatment plants. If such as step is included the removal efficiency will be 100%. Moreover, no adverse effects have been observed in an activated sludge respiration inhibition study performed with the read across substance zirconium acetate. Therefore no PNEC needs to be derived.

As no PNEC aquatic could be derived, no PNEC values for soil and sediment can be derived either by using the equilibrium partitioning method. No toxicity data are available for sediment or soil organisms, therefore, no PNEC values for soil and sediment can be derived applying the assessment factor method either. Since zirconium dinitrate oxide is not considered hazardous to the environment, no chemical safety assesment needs to be conducted and therefore no PNECs need to be derived for these compartments.

No long-term oral or dietary avian toxicity studies are available. A repeated dose toxicity study in rats (OECD 422 study performed with the read across substance zirconium acetate, another 'water soluble' zirconium compound) did not observe any significant adverse effects up to and including the highest tested dose (NOAEL >= 1000 mg/kg bw/day, based on anhydrous test compound). Therefore no PNEC oral can be derived. This route is considered not relevant anyway as it can be reasonably assumed that zirconium will not bioaccumulate in the food chain.

Conclusion on classification

The substance does not need to be classified for environmental hazards, based on the available information for zirconium dinitrate oxide, used in combination with information from read across substances. In none of the studies used to cover the aquatic toxicity endpoints, adverse effects have been observed up to and including at the limit test concentration of 100 mg/L. Only for algae, growth inhibition was observed, however, in the tests in which phosphate levels were monitored, the observed inhibition was concurrent with phosphate depletion from the test medium (through heavy complexation with zirconium), and was hence considered a phosphate deprivation effect, which is not considered relevant at a normal environmental scale. Since there were no signs of primary toxicity, the effect in algae was not considered relevant for hazard assessment or classification purposes.