Studies on Advanced Oxidation Processes for the Removal of Acetamiprid from Wastewater

Pollution of water with pesticides has become a threat to the man, material and environment. The pesticides released to the environment reach the water bodies through run off. Industrial wastewater from pesticide manufacturing industries contains pesticides at higher concentration and hence a major source of water pollution. Pesticides create a lot of health and environmental hazards which include diseases like cancer, liver and kidney disorders, reproductive disorders, fatal death, birth defects etc. Conventional wastewater treatment plants based on biological treatment are not efficient to remove these compounds to the desired level. Most of the pesticides are phyto-toxic i.e., they kill the microorganism responsible for the degradation and are recalcitrant in nature. Advanced oxidation process (AOP) is a class of oxidation techniques where hydroxyl radicals are employed for oxidation of pollutants. AOPs have the ability to totally mineralise the organic pollutants to CO2 and water. Different methods are employed for the generation of hydroxyl radicals in AOP systems. Acetamiprid is a neonicotinoid insecticide widely used to control sucking type insects on crops such as leafy vegetables, citrus fruits, pome fruits, grapes, cotton, ornamental flowers. It is now recommended as a substitute for organophosphorous pesticides. Since its use is increasing, its presence is increasingly found in the environment. It has high water solubility and is not easily biodegradable. It has the potential to pollute surface and ground waters. Here, the use of AOPs for the removal of acetamiprid from wastewater has been investigated. Five methods were selected for the study based on literature survey and preliminary experiments conducted. Fenton process, UV treatment, UV/ H2O2 process, photo-Fenton and photocatalysis using TiO2 were selected for study. Undoped TiO2 and TiO2 doped with Cu and Fe were prepared by sol-gel method. Characterisation of the prepared catalysts was done by X-ray diffraction, scanning electron microscope, differential thermal analysis and thermogravimetric analysis. Influence of major operating parameters on the removal of acetamiprid has been investigated. All the experiments were designed using central compoiste design (CCD) of response surface methodology (RSM). Model equations were developed for Fenton, UV/ H2O2, photo-Fenton and photocatalysis for predicting acetamiprid removal and total organic carbon (TOC) removal for different operating conditions. Quality of the models were analysed by statistical methods. Experimental validations were also done to confirm the quality of the models. Optimum conditions obtained by experiment were verified with that obtained using response optimiser. Fenton Process is the simplest and oldest AOP where hydrogen peroxide and iron are employed for the generation of hydroxyl radicals. Influence of H2O2 and Fe2+ on the acetamiprid removal and TOC removal by Fenton process were investigated and it was found that removal increases with increase in H2O2 and Fe2+ concentration. At an initial concentration of 50 mg/L acetamiprid, 200 mg/L H2O2 and 20 mg/L Fe2+ at pH 3 was found to be optimum for acetamiprid removal. For UV treatment effect of pH was studied and it was found that pH has not much effect on the removal rate. Addition of H2O2 to UV process increased the removal rate because of the hydroxyl radical formation due to photolyis of H2O2. An H2O2 concentration of 110 mg/L at pH 6 was found to be optimum for acetamiprid removal. With photo-Fenton drastic reduction in the treatment time was observed with 10 times reduction in the amount of reagents required. H2O2 concentration of 20 mg/L and Fe2+ concentration of 2 mg/L was found to be optimum at pH 3. With TiO2 photocatalysis improvement in the removal rate was noticed compared to UV treatment. Effect of Cu and Fe doping on the photocatalytic activity under UV light was studied and it was observed that Cu doping enhanced the removal rate slightly while Fe doping has decreased the removal rate. Maximum acetamiprid removal was observed for an optimum catalyst loading of 1000 mg/L and Cu concentration of 1 wt%. It was noticed that mineralisation efficiency of the processes is low compared to acetamiprid removal efficiency. This may be due to the presence of stable intermediate compounds formed during degradation Kinetic studies were conducted for all the treatment processes and it was found that all processes follow pseudo-first order kinetics. Kinetic constants were found out from the experimental data for all the processes and half lives were calculated. The rate of reaction was in the order, photo- Fenton>UV/ H2O2>Fenton> TiO2 photocatalysis>UV. Operating cost was calculated for the processes and it was found that photo-Fenton removes the acetamiprid at lowest operating cost in lesser time. A kinetic model was developed for photo-Fenton process using the elementary reaction data and mass balance equations for the species involved in the process. Variation of acetamiprid concentration with time for different H2O2 and Fe2+ concentration at pH 3 can be found out using this model. The model was validated by comparing the simulated concentration profiles with that obtained from experiments. This study established the viability of the selected AOPs for the removal of acetamiprid from wastewater. Of the studied AOPs photo- Fenton gives the highest removal efficiency with lowest operating cost within shortest time.

Adrenergic and muscarinic receptor subtypes functional regulation during diabetogenesis: Effect of curcumin and vitamin D3 pre-treatment

In the present study, the initial phase was directed to confirm the effects of curcumin and vitamin D3 in preventing or delaying diabetes onset by studying the blood glucose and insulin levels in the pre-treated and diabetic groups. Behavioural studies were conducted to evaluate the cognitive and motor function in experimental rats. The major focus of the study was to understand the cellular and neuronal mechanisms that ensure the prophylactic capability of curcumin and vitamin D3. To elucidate the mechanisms involved in conferring the antidiabetogenesis effect, we examined the DNA and protein profiles using radioactive incorporation studies for DNA synthesis, DNA methylation and protein synthesis. Furthermore the gene expression studies of Akt-1, Pax, Pdx-1, Neuro D1, insulin like growth factor-1 and NF-κB were done to monitor pancreatic beta cell proliferation and differentiation. The antioxidant and antiapoptotic actions of curcumin and vitamin D3 were examined by studying the expression of antioxidant enzymes - SOD and GPx, and apoptotic mediators like Bax, caspase 3, caspase 8 and TNF-α. In order to understand the signalling pathways involved in curcumin and vitamin D3 action, the second messengers, cAMP, cGMP and IP3 were studied along with the expression of vitamin D receptor in the pancreas. The neuronal regulation of pancreatic beta cell maintenance, proliferation and insulin release was studied by assessing the adrenergic and muscarinic receptor functional regulation in the pancreas, brain stem, hippocampus and hypothalamus. The receptor number and binding affinity of total muscarinic, muscarinic M1, muscarinic M3, total adrenergic, α adrenergic and β adrenergic receptor subtypes were studied in pancreas, brain stem and hippocampus of experimental rats. The mRNA expression of muscarinic and adrenergic receptor subtypes were determined using Real Time PCR. Immunohistochemistry studies using confocal microscope were carried out to confirm receptor density and gene expression results. Cell signalling alterations in the pancreas and brain regions associated with diabetogenesis and antidiabetogenesis were assessed by examining the gene expression profiles of vitamin D receptor, CREB, phospholipase C, insulin receptor and GLUT. This study will establish the anti-diabetogenesis activity of curcumin and vitamin D3 pre-treatment and will attempt to understand the cellular, molecular and neuronal control mechanism in the onset of diabetes.Administration of MLD-STZ to curcumin and vitamin D3 pre-treated rats induced only an incidental prediabetic condition. Curcumin and vitamin D3 pretreated groups injected with MLD-STZ exhibited improved circulating insulin levels and behavioural responses when compared to MLD-STZ induced diabetic group. Activation of beta cell compensatory response induces an increase in pancreatic insulin output and beta cell mass expansion in the pre-treated group. Cell signalling proteins that regulate pancreatic beta cell survival, insulin release, proliferation and differentiation showed a significant increase in curcumin and vitamin D3 pre-treated rats. Marked decline in α2 adrenergic receptor function in pancreas helps to relent sympathetic inhibition of insulin release. Neuronal stimulation of hyperglycemia induced beta cell compensatory response is mediated by escalated signalling through β adrenergic, muscarinic M1 and M3 receptors. Pre-treatment mediated functional regulation of adrenergic and cholinergic receptors, key cell signalling proteins and second messengers improves pancreatic glucose sensing, insulin gene expression, insulin secretion, cell survival and beta cell mass expansion in pancreas. Curcumin and vitamin D3 pre-treatment induced modulation of adrenergic and cholinergic signalling in brain stem, hippocampus and hypothalamus promotes insulin secretion, beta cell compensatory response, insulin sensitivity and energy balance to resist diabetogenesis. Pre-treatment improved second messenger levels and the gene expression of intracellular signalling molecules in brain stem, hippocampus and hypothalamus, to retain a functional neuronal response to hyperglycemia. Curcumin and vitamin D3 protect pancreas and brain regions from oxidative stress by their indigenous antioxidant properties and by their ability to stimulate cellular free radical defence system. The present study demonstrates the role of adrenergic and muscarinic receptor subtypes functional regulation in curcumin and vitamin D3 mediated anti-diabetogenesis. This will have immense clinical significance in developing effective strategies to delay or prevent the onset of diabetes.