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The aquatic toxicity of the substance zirconium dichloride oxide (a 'water soluble' zirconium compound) is evaluated using data for zirconium dichloride oxide as well as data from read across substances such as zirconium acetate (another 'water soluble' zirconium compound), zirconium basic carbonate (a sparingly soluble zirconium compound) and zirconium dioxide (an insoluble zirconium compound). Read across from insoluble or sparingly soluble zirconium substances is considered acceptable because stirring experiments performed with zirconium dichloride oxide in aquatic test media (e.g., Harris, 2014; Vryenhoef, 2014) indicated that zirconium from the 'water soluble' zirconium dichloride oxide does not stay in solution at environmentally relevant pH levels. Rapid hydrolysis occurs, resulting in precipitation of zirconium hydroxides or zirconium dioxide. Further, heavy complexing will occur with phosphates, which results in 100% precipitation whenever phosphate is present in excess. Complexation with carbonates may also result in progressive precipitation with increasing pH levels. As a result, at environmentally relevant conditions, zirconium dichloride oxide cannot be considered as a water soluble compound. Overall, zirconium is not bioavailable in the aquatic environment and therefore no adverse effects are to be expected in aquatic organisms.

Further argumentation for the read across approach is given in the read across document attached to IUCLID Section 13.

Zirconium dichloride oxide is concluded not to be toxic (acutely) to fish and aquatic invertebrates. The studies that were used for endpoint coverage (performed with zirconium dichloride oxide and/or read across substances) were performed according to internationally accepted guidelines and did not report any adverse effects (mortality in fish, immobilization in daphnids) at the limit test concentration of 100 mg/L or upon exposure to a 100% v/v saturated solution. In algal growth experiments with read across substances, it was demonstrated that the observed growth inhibition was concurrent with phosphate depletion. Toxicity to algae is therefore due to phosphate deprivation as no primary toxic effects have been observed. Although no phosphate monitoring was performed during the algal growth inhibition study with zirconium dichloride oxide (Vryenhoef, 2014), here too, the observed effect on growth of algae exposed to the 100% v/v saturated solution can be assumed to be due to phosphate deprivation. This is supported by the fact that no dissolved zirconium could be detected at levels > LOQ (11 µg Zr/L) in any of the test solutions. Further confirmation for this is provided by the study of Kumar and Rai (1978), where it was demonstrated that dosing additional phosphate to the test medium countered the effect on growth. Phosphate deprivation is a secondary effect which is not considered relevant at a normal environmental scale. Therefore, no effects on algae are expected in the environment either. Finally, based on read across from zirconium acetate, another 'water soluble' zirconium compound with similar behaviour in the aquatic environment as zirconium dichloride oxide, the substance is not expected to cause any adverse effects in aquatic microorganisms either.