tio2 water treatment factory

2: Clarification mechanism of coagulant

Chemical coagulation is a process in which chemical agents (coagulants) are added to water treatment to make colloidal dispersion system destabilize and agglomerate. In the coagulation process, small suspended particles and colloidal impurities are aggregated into larger solid particles to separate particulate impurities from water, which is called coagulation clarification.

After adding coagulant into water, colloidal particles and other small particles can be polymerized into larger flocs through the comprehensive action of mixing, coagulation and flocculation. The whole process of coagulation and flocculation is called coagulation.

(1) Destabilization and condensation of colloids

Adding electrolyte to water can compress the electric double layer and destabilize the colloid. The main mechanism is that the electric double layer of colloidal particles in water is compressed or neutralized by adding aluminum salt or iron salt coagulant. The coagulant and raw water are mixed rapidly and evenly, and a series of chemical reactions are produced to destabilize. This process takes a short time, generally about 1 min. Some cationic polymers can also play a role in the destabilization and condensation of colloids in water. These polymers have a long chain structure and positive charge in water. Their destabilization and condensation of colloids in water is due to the interaction of van der Waals force adsorption and electrostatic attraction.

(2) Flocculation and formation of floc (alum)

The particle size of the initial flocculate formed by colloid destabilization and coagulation in water is generally more than 1 m. at this time, Brownian motion can no longer push them to collide and form larger particles. In order to make the initial flocs collide with each other to form large flocs, it is necessary to input additional energy into the water to produce a velocity gradient. Sometimes it is necessary to add organic polymer flocculant into water, and the adsorption bridging effect of long chain molecules of flocculant is used to improve the probability of collision and adhesion. Flocculation efficiency usually increases with the increase of flocculate concentration and flocculation time.

Compared with polyaluminum chloride, polyaluminum chloride has the advantages of high density, fast settling speed and wide pH adaptability; the coagulation effect is less affected by temperature than that of polyaluminum sulfate; however, when adding ferric salt, it should be noted that when the equipment is not in normal operation, the iron ions will make the effluent color, and may pollute the subsequent desalination equipment.

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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 TiO2, 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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