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Hot dip galvanizing, also known as hot dip zinc and hot dip galvanizing, is an effective way of metal corrosion prevention, mainly used in various industries of metal structure facilities. It is to immerse the steel parts after rust removal into the molten zinc liquid at about 500℃, so that the surface of the steel member is attached with zinc layer, so as to play the purpose of anticorrosion.

When pickling, we should pay great attention to the acid has a strong corrosion, so when adding acid, we must pour acid into water, and it is along the wall of the cylinder, not a splash down, so as not to cause splash. Remember the order of pouring acid, acid into water rather than water into acid, water into acid will cause splashing and boiling, when pouring acid must wear protective glasses, must ensure that there are no non-professional onlookers, so as not to cause some risk of splashing acid.

Titanium dioxide is used a food colour (E171) and, as with all food colours, its technological function is to make food more visually appealing, to give colour to food that would otherwise be colourless, or to restore the original appearance of food. Titanium dioxide is also present in cosmetics, paints, and medicines.

For people in occupational settings that increase the risk of titanium dioxide exposure, taking protective measures is helpful. This may include wearing protective equipment, such as respirators, and using ventilation systems.

Lithopone Market Outlook - 2020–2027

≤0.3

Chemical formula: BaO5S2Zn2

Durabo White, 24.5 per cent zinc sulphide, 51 per cent barium sulphate, 18 per cent white clay, 5.5 per cent infusorial earth.

 (1) Konaka et al. 1999. (2) Serpone et al. 2006. (3) Brezova et al. 2004. (4) Dunford et al. 1997. (5) Warner et al. 1997. (6) Salinaro et al. 1997. (7) Maness et al. 1999.

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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There’s also concern that exposure to the mineral over time, even in small amounts, can build up in the body, particularly in the kidneys, spleen and liver. Although most of the mineral is excreted in feces, there is evidence that a small percentage may remain in bodily organs.