Zirconium sulphate

Ecotoxicological Summary

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 sulfate 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 demonstrated in algal growth inhibition experiments with read across substances. The fact that in an algal growth inhibition test with zirconium sulfate no measurable zirconium concentrations > LOQ (20 µg Zr/L) could be detected in any of the treatments whereas 53% reduction of growth rate was observed in the 100% v/v saturated solution supports 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 sulfate is not toxic to aquatic organisms.

Similarly, microorganisms in a sewage treatment plant are not expected to be exposed to zirconium (sulfate), 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. 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, except for a short-term toxicity study to terrestrial plants, yielding only unbound NOEC values. Therefore, no PNEC values for soil and sediment can be derived applying the assessment factor either. Since zirconium sulfate 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 with 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 sulfate, 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 the limit test concentration of 100 mg/L or upon exposure to a 100% v/v saturated solution. Only for algae, growth inhibition was observed at this limit test concentration for zirconium sulfate as well as for two read across substances, however, 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.