| Abstract : The oxidation of the common pesticide chlorpyrifos (CPF) initiated by HO() radical and the risks of its degradation products were studied in the gaseous and aqueous phases via computational approaches. Oxidation mechanisms were investigated, including H-, Cl-, CH(3)- abstraction, HO()-addition, and single electron transfer. In both phases, HO()-addition at the C of the pyridyl ring is the most energetically favorable and spontaneous reaction, followed by H-abstraction reactions at methylene groups (i.e., at H19/H21 in the gas phase and H22/H28 in water). In contrast, other abstractions and electron transfer reactions are unfavorable. However, regarding the kinetics, the significant contribution to the oxidation of CPF is made from H-abstraction channels, mostly at the hydrogens of the methylene groups. CPF can be decomposed in a short time (5-8 h) in the gas phase, and it is more persistent in natural water with a lifetime between 24 days and 66 years, depending on the temperature and HO() concentration. Subsequent oxidation of the essential radical products with other oxidizing reagents, i.e., HO(), NO(2)(), NO(), and (3)O(2), gave primary neutral products P1-P15. Acute and chronic toxicity calculations estimate very toxic levels for CPF and two degradation products, P7(w) and P12(w), in aquatic systems. The neurotoxicity of these products was investigated by docking and molecular dynamics. P7(w) and P12(w) show the most significant binding scores with acetylcholinesterases, while P8(w) and P13(w) are with butyrylcholinesterase enzyme. Finally, molecular dynamics illustrate stable interactions between CPF degradants and cholinesterase enzyme over a 100 ns time frame and determine P7(w) as the riskiest degradant to the neural developmental system. |