Pharmaceuticals are a group of contaminants of emerging concern in aquatic environments. In drinking water disinfection, pharmaceuticals may be transformed by chlorine to halogenated disinfection byproducts (DBPs), and some pharmaceutical-derived DBPs could be more toxic than the parent compounds. The effective control of pharmaceuticals and the associated DBPs has become one of the priorities in securing safe drinking water. This thesis evaluated the significance of pharmaceuticals in the formation of halogenated DBPs (as represented by total organic halogen (TOX)) and their toxicity (as represented by developmental toxicity) in chlorinated drinking water in the absence and presence of natural organic matter (NOM). The control of pharmaceutical-derived DBPs by a new approach was also p...[ Read more ]

Pharmaceuticals are a group of contaminants of emerging concern in aquatic environments. In drinking water disinfection, pharmaceuticals may be transformed by chlorine to halogenated disinfection byproducts (DBPs), and some pharmaceutical-derived DBPs could be more toxic than the parent compounds. The effective control of pharmaceuticals and the associated DBPs has become one of the priorities in securing safe drinking water. This thesis evaluated the significance of pharmaceuticals in the formation of halogenated DBPs (as represented by total organic halogen (TOX)) and their toxicity (as represented by developmental toxicity) in chlorinated drinking water in the absence and presence of natural organic matter (NOM). The control of pharmaceutical-derived DBPs by a new approach was also proposed. The results showed that the contributions of pharmaceuticals to the TOX formation were 0.5–20.2% and 0.41–16.5% in bromide-free and bromide-containing water samples, respectively, at initial total pharmaceutical concentrations of 1–50 μg/L each. Compared with NOM, although pharmaceuticals contributed only a small portion of the TOX in the chlorinated drinking water, they contributed significantly to the toxicity of the water. The toxicity index of the chlorinated pharmaceutical sample increased from 5.8 to 62.9 with increasing the total pharmaceutical concentration from 0.03 to 0.31 mg/L as C, while the toxicity index of the chlorinated NOM sample increased only from 5.0 to 16.6 with increasing the initial NOM concentration from 1.0 to 3.0 mg/L as C. More interestingly, antagonism on the developmental toxicity was observed for the combination of NOM-derived DBPs and pharmaceutical-derived DBPs, although the mechanisms behind remained to be explored. In addition, two models were developed and validated with the experimental data, and they were successfully used in the estimation of the TOX formation and the developmental toxicity in chlorination of pharmaceuticals and NOM at various environmentally relevant concentrations. During the TOX measurement, it was found that quenching agents (e.g., sodium sulfite, sodium thiosulfate, and ascorbic acid) significantly affected the measured TOX concentrations, and this effect was impacted by the species of pharmaceuticals, and the type and dose of the quenching agent. To improve the accuracy for quantifying halogenated products formed from chlorination of pharmaceuticals, exact-quenching with ascorbic acid toward the free chlorine residual (i.e., at an ascorbic acid to free chlorine molar ratio of 1:1) was recommended. In terms of DBP control, it was demonstrated that the new approach (i.e., chlorination prior to granular activated carbon (GAC) adsorption) successfully removed halogenated DBPs in chlorination of source waters containing both NOM and pharmaceuticals. Compared with the traditional approach (i.e., GAC adsorption prior to chlorination), the new approach more significantly reduced the concentrations of halogenated DBPs, especially for brominated DBPs, which could be explained by the higher affinity (indicated K_ow) of intermediates than that of the parent precursors; Also, the new approach more significantly reduced the developmental toxicity of the chlorinated water samples. Finally, a new group of polymeric DBPs along with a new pathway via the radical-mediated coupling reaction during chlorination of a particular pharmaceutical (i.e., acetaminophen) were identified via experiments and quantum chemical calculations. Effects of NOM and bromide on this reaction pathway were also discussed. This thesis disclosed the nonnegligible roles of pharmaceuticals in DBP formation and toxicity in chlorinated drinking water, and it offered a promising approach to effectively control pharmaceutical- and NOM-derived DBPs and reduce the related toxicity by sequential use of chlorination and GAC adsorption.