UV/H 2 O 2 advanced oxidation for abatement of organophosphorous pesticides and the effects on various toxicity screening assays

• Published in: Chemosphere (Oxford) Vol. 182; p. 477
• Main Authors: Parker, Austa M, Lester, Yaal, Spangler, Emily K, von Gunten, Urs, Linden, Karl G
• Format: Journal Article
• Language: English
• Published: England 01.09.2017
• Subjects: Hydrogen Peroxide - chemistry; Hydroxyl Radical - chemistry; Models, Theoretical; Mutagens - analysis; Mutagens - radiation effects; Mutagens - toxicity; Organophosphorus Compounds - analysis; Organophosphorus Compounds - radiation effects; Organophosphorus Compounds - toxicity; Oxidation-Reduction; Pesticides - analysis; Pesticides - radiation effects; Pesticides - toxicity; Toxicity Tests; Ultraviolet Rays; Water Pollutants, Chemical - analysis; Water Pollutants, Chemical - radiation effects; Water Pollutants, Chemical - toxicity; Water Purification - methods; Transformation products; UV/HO; Neurotoxicity; Advanced oxidation; Genotoxicity; Organophosphorous insecticides; Estrogenicity
• ISSN: 1879-1298

Advanced oxidation processes (AOPs) are utilized due to their ability to treat emerging contaminants with the fast reacting and non-selective hydroxyl radical (OH). Organophosphorous insecticides are common drinking water contaminants, with 12 different compounds of this class being found on the US EPA's most recent Candidate Contaminant List (CCL4). The use of the AOP UV/H O for the treatment of organophosphorous insecticides was explored in this study, by coupling biological and analytical tools to follow the abatement of the target compounds. Four insecticides were explored for advanced oxidation treatment: acephate, dicrotophos, fenamiphos, and methamidophos. All four compounds were fast reacting with OH, all reacting with second order rate constants ≥5.5 × 10  M s . Three major endpoints of toxicity were studied: estrogenicity, genotoxicity (mutagenicity) and neurotoxicity. None of the target compounds showed any estrogenic activity, while all compounds showed an active genotoxic (mutagenic) response (AMES II assay) and most compounds had some level of neurotoxic activity. AOP treatment did not induce any estrogenic activity, and reduced the compounds' neurotoxicity and genotoxicity in all but one case. Methamidophos degradation by UV/H O resulted in an increase in genotoxicity, likely due to the formation of toxic transformation products. The increase in toxicity gradually decreased with time, possibly due to hydrolysis of the transformation products formed. This study provides insights into parent compound abatement and the changes in toxicity due to transformation products.