What is titanium dioxide? Why is it used in food products?

0.1% Max

Different dermal cell types have been reported to differ in their sensitivity to nano-sized TiO₂ . Kiss et al. exposed human keratinocytes (HaCaT), human dermal fibroblast cells, sebaceous gland cells (SZ95) and primary human melanocytes to 9 nm-sized TiO₂ particles at concentrations from 0.15 to 15 μg/cm² for up to 4 days. The particles were detected in the cytoplasm and perinuclear region in fibroblasts and melanocytes, but not in kerati-nocytes or sebaceous cells. The uptake was associated with an increase in the intracellular Ca²⁺ concentration. A dose- and time-dependent decrease in cell proliferation was evident in all cell types, whereas in fibroblasts an increase in cell death via apoptosis has also been observed. Anatase TiO₂ in 20–100 nm-sized form has been shown to be cytotoxic in mouse L929 fibroblasts. The decrease in cell viability was associated with an increase in the production of ROS and the depletion of glutathione. The particles were internalized and detected within lysosomes. In human keratinocytes exposed for 24 h to non-illuminated, 7 nm-sized anatase TiO_2, a cluster analysis of the gene expression revealed that genes involved in the “inflammatory response” and “cell adhesion”, but not those involved in “oxidative stress” and “apoptosis”, were up-regulated. The results suggest that non-illuminated TiO₂ particles have no significant impact on ROS-associated oxidative damage, but affect the cell-matrix adhesion in keratinocytes in extracellular matrix remodelling. In human keratinocytes, Kocbek et al. investigated the adverse effects of 25 nm-sized anatase TiO₂ (5 and 10 μg/ml) after 3 months of exposure and found no changes in the cell growth and morphology, mitochondrial function and cell cycle distribution. The only change was a larger number of nanotubular intracellular connections in TiO₂-exposed cells compared to non-exposed cells. Although the authors proposed that this change may indicate a cellular transformation, the significance of this finding is not clear. On the other hand, Dunford et al. studied the genotoxicity of UV-irradiated TiO₂ extracted from sunscreen lotions, and reported severe damage to plasmid and nuclear DNA in human fibroblasts. Manitol (antioxidant) prevented DNA damage, implying that the genotoxicity was mediated by ROS.

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We’re most often exposed to E171 through the foods we ingest. We find E171 in many food products, like popsicles, ice cream, gum, and more. Another way we ingest E171 is through pharmaceutical drugs. Many pills and capsules contain E171 as an inactive ingredient.  

Fig. 4. Hemolysis (%) values of samples, A: 0.2 mg/mL P25TiO₂NPs; B: 0.02 mg/mL P25TiO₂NPs; C: 0.2 mg/mL VitaminB2@P25TiO₂NPs; D: 0.02 mg/mL VitaminB2@P25TiO₂NPs after 3 h of irradiation (red) and 6 h (blue). SD <5 for all samples and p <0.05 between C-D and A-B.

Sulphate process. The ilmenite is reacted with sulphuric acid giving titanium sulphate and ferric oxide. After separation of ferric oxide, addition of alkali allows precipitation of hydrous titanium dioxide. The washed precipitate is calcined in a rotary kiln to render titanium dioxide. The nucleation and calcination conditions determine the crystalline structure of titanium dioxide (e.g. rutile or anatase).

Promotion of noncancerous tumors

Following the filtration, the precipitate is washed thoroughly to remove any impurities and excess reagents. This is a crucial step, as thorough washing ensures that no contaminants interfere with the final mass measurement. Once washed, the precipitate is dried in an oven at a controlled temperature to remove moisture, ensuring that the mass recorded reflects only the titanium content.

“Lithopone Market by Application: Global Opportunity Analysis and Industry Forecast, 2020-2027”

But despite all these cries of alarm, five years on from the original study no further testing into the safety of Titanium Dioxide in our food supply

The Evolution and Impact of Anatase Titanium Dioxide Manufacturers