Weixu Tang,Jianjian Wei,Shuting Wang,Qiang Cheng,Aroob Abid,Jia Gu,Min Zheng,Dehua Ma
This study aims to identify the highly non-specific toxicity by-products during ozonation of three cresols in wastewater. In ozonated effluents, biotoxicity increased along with increasing reaction time, followed by gradual decrease. The peak biotoxicity for ozonated o -cresol ( o -C), m -cresol ( m -C), and p -cresol ( p -C) was estimated to be 17.4, 14.8 and 5.5 times higher than that of untreated wastewater, respectively. A redox-directed approach with high-resolution mass spectrometry and toxicity prediction revealed that monomeric para-benzoquinones ( p -BQs), hydroxylated p -BQs, and dimeric p -BQs in ozonated cresols were the primary contributors to the increased toxicity. Calculations based on density functional theory indicated formation pathways of p -BQs byproducts, e.g., the formation of 2-methyl- p -benzoquinone was likely induced by ozone molecules rather than hydroxyl radicals in ozonated o -C and m -C, and the formation of p -benzoquinone during ozonation of p -C was attributed to the oxidation of methyl group to carboxyl group and subsequent decarboxylation initiated by hydroxyl radicals. Electron paramagnetic resonance and spin density calculation showed that the presence of carbon-centered cresoxyl radicals was responsible for dimeric p -BQs formation. Collectively, these results underscore significant contribution of non-halogenated p -BQs to non-specific toxicity increase in ozonated effluents.
Vision is the primary sensory function for most animals and is also a sensitive toxic target of environmental pollutants. A new class of organophosphate flame retardants (OPFRs) termed emerging OPFRs (eOPFRs) with limited toxicological information is rapidly developed into the substitutes of traditional OPFRs. In this study, we investigated the visual toxicity of triphenyl phosphate (TPHP, one traditional OPFR) and cresyl diphenyl phosphate (CDP, one emerging OPFR) on zebrafish larvae at environmentally relevant concentrations (3 and 30 nM). After 5 days of exposure, an opposite toxicity was found between the two OPFRs, manifested in the light perception and the gene expressions of visual opsins. CDP caused a weak reaction to light and overall inhibition of opsin expression (0.7- to 0.8-fold) in the larvae, while TPHP tended to stimulate these events (1.2- to 2.4-fold). Besides, we identified a key transcription factor, tbx2a, that was significantly disrupted in both OPFRs’ exposure. The differing ways in which both OPFRs bind to Tbx2a may be the reason behind their opposite effects. These findings provided new clues for the toxicological mechanisms of OPFRs and revisited the question regarding safe substitutes for those emerging contaminants.