Australia - TGA

Australia- Therapeutic Goods Administration

Of paramount importance is the finding that the vast majority of studies do not demonstrate NP skin penetration; the current weight of evidence suggests that TiO₂and ZnO NPs do not reach viable skin cells (even in compromised skin) or the general circulation, but rather remain on the skin surface and in the outer layer of the stratum corneum, a surface layer of non-viable, keratinized cells. It is therefore highly likely that if sunscreens are used as is intended, NPs from sunscreens applied dermally will not achieve significant concentrations in the systemic circulation.

Consequently, it is highly unlikely that NPs will induce the cytotoxic responses or pathological outcomes outlined in this review in the in vitroand animal studies, respectively. The data from the reviewed in vitroexperiments should be interpreted with caution given that the findings from studies conducted in cell lines are of limited value in assessing the potential toxicity NPs pose to humans from topically applied sunscreens. Similarly, the limitations of the reviewed animal studies, where NPs were administered at relatively high concentrations through exposure routes that are not relevant in the context of sunscreen use and at high frequency, should also be acknowledged. Given the majority of studies found no evidence of skin penetration of NPs when applied dermally, it is highly unlikely that the high systemic NP concentrations attained in these experimental animals would be achieved in people, even if accidental intake occurred via these non-dermal routes. Therefore, any deductions made regarding the safety of topically applied sunscreens in humans by extrapolating these findings in animals to humans, are of limited value.

It is also crucial to emphasize that NPs present in sunscreens are modified to reduce their potential to generate ROS, which largely mediate NP-induced cytotoxicity and genotoxicity. During the manufacturing process the surface of the NPs may be coated to reduce the formation of ROS, even after UV exposure. Sunscreens may also contain antioxidants in order to neutralise ROS generated by NPs. Additionally, endogenous protective mechanisms, such as antioxidant activity mediated by a range of intracellular enzymes and factors, will likely protect against the damaging effects of oxidative stress generated by any exposure to nanoparticles. Minimal dermal penetration of NPs is likely to be adequately counteracted by these natural cellular defences.

In conclusion, on current evidence, neither TiO₂ nor ZnO NPs are likely to cause harm when used as ingredients in sunscreens. The current state of knowledge strongly indicates that the minor risks potentially associated with NPs in sunscreens are vastly outweighed by the benefits that NP-containing sunscreens afford against skin damage and, importantly, skin cancer.