Lithopone factory: Natrosol has some characteristics

A 2022 review on past studies of titanium dioxide and rat lung cancer, for instance, said the original study was under extreme conditions and its effects were not replicated in other animal species. Additionally, the review concluded that the few studies which did directly focus on titanium dioxide's impact on humans did not end up showing any increased cancer risk.

The properties of lithopone are very suitable for use in the production of coatings. Because the ingredients of lithopone are zinc sulfide and barium sulfate, and the more zinc sulfide content, the stronger its covering power. This indicates a paint product with strong white covering power. It is different from water in that it reacts with acid but does not react with alkali. It has a wide range of uses. Because its structural properties are similar to titanium dioxide and its price is relatively cheap, it can also be used as a substitute for some titanium dioxide. Lithopone can be used for coloring paints, inks, pigments, rubber, paper, leather, enamel, etc.

However, most dermatologists will warn their patients not to rely on mineral makeup alone in order to be protected by the sun’s rays. This is because there can be quite a bit of variation with mineral foundation – not only with how much we apply but how much titanium dioxide the foundation contains.

Lithopone manufacturer: Application areas

Another important application of titanium dioxide is in the production of sunscreen and other skincare products. Titanium dioxide is a key ingredient in many sunscreens due to its ability to reflect and scatter ultraviolet (UV) radiation, providing protection against harmful UV rays. Manufacturers of titanium dioxide for sunscreen products often use special coatings and surface treatments to enhance its UV-blocking properties.

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.