Fate, transformation and toxicological implications of environmental diclofenac: Role of mineralogy and solar flux.

Diclofenac is an emerging surface water contaminant, yet the environmental impact of its degradation products remains elusive. The current study focuses on mineralogy-controlled diclofenac photo-degradation and its potential health impacts. Under irradiated conditions, we studied the effects of kaolinite, hematite, and anatase on diclofenac degradation. Our results showed that kaolinite doubled the diclofenac degradation rate, which can be attributed to the high catalytic effect, mediated via increased surface area and pore size of mineral surface in the low pH. Conversely, anatase, a crystal phase of titanium dioxide (TiO2), diminished the diclofenac degradation compared to treatments without TiO2. Hematite, on the other hand, showed no effect on diclofenac degradation. Photo-degradation products also varied with the mineral surface. We further assessed in vitro toxicological effects of photo-degraded products on two human cell lines, HEK293T and HepG2. Biological assays confirmed that photo-degraded compound 6 (1-(2,6-dichlorophenyl)indolin-2-one) decreased HEK293T cell survival significantly (p < 0.05) when compared to diclofenac in all concentrations. At lower concentrations, inhibition of HEK293T cells caused by compounds 4 (2-(8-chloro-9H-carbazol-1-yl)acetic acid), and 5 (2-(9H-carbazol-1-yl)acetic acid) was greater than diclofenac. Compound 7 (1-phenylindolin-2-one) was toxic only at 250 µM. Additionally, compound 6 decreased HepG2 cell viability significantly when compared to diclofenac. Overall, our data highlighted that mineralogy plays a vital role in environmental diclofenac transformation and its photo-degraded products. Some photo-degraded compounds can be more cytotoxic than the parent compound, diclofenac.

Heterogeneous Photocatalysis of Amoxicillin under Natural Conditions and High-Intensity Light: Fate, Transformation, and Mineralogical Impacts.

The ß-Lactam antibiotic amoxicillin is among the most widely used antibiotics in human and veterinary medicine. Consequently, amoxicillin is abundant in natural waters and can undergo diverse abiotic reactions to form degradation compounds under environmental conditions. Yet, little is known about these decay pathways and mineralogical impacts on environmental amoxicillin degradation. The current study focuses on understanding the mineralogical influences of amoxicillin degradation under ecological conditions. We studied the role of anatase and kaolinite on amoxicillin degradation under irradiated and non-irradiated conditions. Anatase increases amoxicillin degradation by 4.5-fold in the presence of light compared to just being exposed to sunlight. Interestingly, anatase also showed a higher degradation rate under dark than light controls. Conversely, kaolinite diminishes the amoxicillin degradation under irradiation. The formation of degradation compounds was mineralogy-controlled, while no mineralization was observed. Further, we irradiated amoxicillin with a high-intensity light to evaluate its removal from wastewater. The formation of varying amoxicillin degradation products with high-intensity light will limit its removal from wastewater. Our study emphasizes that the mineralogical impact on amoxicillin degradation is diverse, and the role of anatase is significant. Consequently, the increased addition of manufactured titanium nanoparticles to the environment can further enhance these effects.

A toxicological study on photo-degradation products of environmental ibuprofen: Ecological and human health implications.

Increasing quantities of pharmaceutical waste in the environment have disrupted the balance of ecosystems, and may have subsequent effects on human health. Although a handful of previous studies have shown the impacts of pharmaceutically active compounds on the environment, the toxicological effects of their degradation products remain largely unknown. In the current study, the photo-degradation products of environmental ibuprofen were assessed for both ecotoxicological and human health effects using a series of in vitro assays. Here, six of the major degradation products are synthesized with high purity (>98%) and characterized with 1HNMR, 13CNMR, FT-IR and HRMS. To evaluate human health effects, three gut microbiota species, Lactobacillus acidophilus, Enterococcus faecalis and Escherichia coli, and two human cell lines, HEK293T and HepG2, are exposed to various concentrations of ibuprofen and its degradation products. On L. acidophilus, the ibuprofen degradation product (±)-(2R,3R)-2-(4-isobutylphenyl)-5-methylhexan-3-ol shows a greater toxic effect while ibuprofen enhances its growth at lower concentrations. At higher concentrations, ibuprofen shows at least a 2-fold higher toxicity compared to that of its degradation products. However, E. faecalis shows little or no effect upon exposure to these compounds. An induction of the SOS response in E. coli is observed but limited to only ibuprofen and 4-acetylbenzoic acid. In human cell line studies, survival of both HEK293T and HepG2 cell lines is profoundly impaired by the photo-degradation products of (±)- (2R,3R)-2-(4-isobutylphenyl)-5-methylhexan-3-ol, (±)-(2R,3S)-2-(4-isobutylphenyl)-5-methylhexan-3-ol, and (±)-1-(4-(1-hydroxy-2methylpropyl)phenyl)ethan-1-one. In this work, the bioluminescence bacterium, Aliivibrio fischeri, is used as a model to assess environmental impact. Both ibuprofen and its degradation products inhibit the growth of this gram-negative bacteria with the primary compound showing the most significant impact. Overall, our results highlight that some of the degradation products of ibuprofen can be more toxic to human kidney cell line and liver cell line than the parent compound while ibuprofen can be more toxic to human gut microbiota and A. fischeri than ibuprofen degradation products.