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We've used titanium dioxide safely for decades. However, recently its safety was called into question. 
 
At CRIS, we've explored the safety of titanium dioxide for nearly half a decade, including conducting double-blind research to test the safety of food-grade titanium dioxide (E171). Our study shows that when exposed to food-grade titanium dioxide in normal conditions, research animals did not experience adverse health outcomes.
 
It's important to emphasize that in a National Institutes of Health study, experimental animals were exposed to titanium dioxide in amounts as high as 5% of their diet for a lifetime and showed no evidence of adverse effects. 
 
A handful of studies greatly influenced the decisions made by the European Food Safety Authority (EFSA). Unfortunately, these studies did not consider that titanium dioxide exposure comes from food, not drinking water. Additionally, CRIS researchers could not reproduce the adverse outcomes identified by the studies through typical food ingestion. Regardless, the EFSA banned E171 as a food ingredient and for use in other capacities in the summer of 2022.
 
In 2022, the United States, United Kingdom, and Canada maintained that the scientific evidence supports that titanium dioxide (E171) is safe for humans to use and consume.

A few non-dietary studies have reported adverse effects in the gastrointestinal tract of laboratory animals given food-grade TiO₂. However, these same effects were not seen when the same or higher doses of food-grade TiO₂ were administered in the animals' diet. Dietary studies best reflect how humans are exposed to TiO₂ from food. Thus, the Food Directorate placed the most emphasis on the results of these studies in the state of the science report.

It's also worth noting that even prior to the EU decision, France had already outlawed titanium dioxide in food back in January 2020.

As mentioned above, these oxide NPs are harmful in part because both anatase and rutile forms are semiconductors and produce ROS. Particularly, P25 kind has band-gap energies estimated of 3.2 and 3.0 eV, equivalent to radiation wavelengths of approximately 388 and 414 nm, respectively. Irradiation at these wavelengths or below produces a separation of charge, resulting in a hole in the valence band and a free electron in the conduction band, due to the electron movement from the valence to conduction bands. These hole–electron pairs generate ROS when they interact with H₂O or O₂ [43,44]. It was described that they can cause an increase in ROS levels after exposure to UV-visible light [45]. The NBT assay in the studied samples showed that bare P25TiO₂NPs produce a large amount of ROS, which is drastically reduced by functionalization with vitamin B2 (Fig. 5). This vitamin, also known as riboflavin, was discovered in 1872 as a yellow fluorescent pigment, [46] but its function as an essential vitamin for humans was established more than sixty years later, and its antioxidant capacity was not studied until the end of the XX century [47,48]. This antioxidant role in cells is partially explained because the glutathione reductase enzyme (GR) requires it for good functionality. This enzyme is the one in charge of the conversion of oxidized glutathione to its reduced form which acts as a powerful inner antioxidant and can quench the ROS [49,50]. The cost of this action is that the glutathione is converted to the oxidized form and needs to be recovered by the GR. Consequently, the cells need more vitamin B2. Another glutathione action is the protection against hydroperoxide. This activity is also mediated by riboflavin. Therefore, local delivery of this vitamin seems to significantly help the cells in their fight to keep the oxidative balance, once they are exposed to high levels of ROS.