Pub Date : 2026-01-20DOI: 10.1016/j.etap.2026.104945
Yubeen Kim , Jisoo Song , Seung-Min Bae , Fuller W. Bazer , Gwonhwa Song , Wooyoung Jeong , Whasun Lim
Tolylfluanid is a phenylsulfamide fungicide commonly used to manage fungal diseases in crops; however, evidence has shown its unintended toxicity in non-target organisms. To elucidate its cellular impact, we investigated how tolylfluanid affects bovine mammary epithelial (MAC-T) cells. The results revealed that exposure to tolylfluanid suppressed MAC-T cell viability, enhanced apoptotic responses, and disrupted 3D spheroid development compared with the control group. The treatment provoked excessive generation of ROS, elevated mitochondrial calcium accumulation, and triggered a reduction in mitochondrial membrane potential. These alterations were accompanied by oxidative stress–mediated mitochondrial depolarization, which was alleviated when cells were co-treated with N-acetyl-L-cysteine. Western blotting and RT-qPCR further demonstrated that tolylfluanid activated PI3K and MAPK signaling and upregulated inflammation-related genes. Additionally, real-time oxygen consumption measurements reveal mitochondrial dysfunction following tolylfluanid. Altogether, these findings indicate that tolylfluanid exerts cytotoxic and pro-oxidative effects on MAC-T cells, suggesting possible implications for milk production efficiency in cattle.
{"title":"Tolylfluanid induces mitochondrial dysfunction through excessive ROS generation and inhibits cell growth in bovine mammary epithelial cells","authors":"Yubeen Kim , Jisoo Song , Seung-Min Bae , Fuller W. Bazer , Gwonhwa Song , Wooyoung Jeong , Whasun Lim","doi":"10.1016/j.etap.2026.104945","DOIUrl":"10.1016/j.etap.2026.104945","url":null,"abstract":"<div><div>Tolylfluanid is a phenylsulfamide fungicide commonly used to manage fungal diseases in crops; however, evidence has shown its unintended toxicity in non-target organisms. To elucidate its cellular impact, we investigated how tolylfluanid affects bovine mammary epithelial (MAC-T) cells. The results revealed that exposure to tolylfluanid suppressed MAC-T cell viability, enhanced apoptotic responses, and disrupted 3D spheroid development compared with the control group. The treatment provoked excessive generation of ROS, elevated mitochondrial calcium accumulation, and triggered a reduction in mitochondrial membrane potential. These alterations were accompanied by oxidative stress–mediated mitochondrial depolarization, which was alleviated when cells were co-treated with N-acetyl-<span>L</span>-cysteine. Western blotting and RT-qPCR further demonstrated that tolylfluanid activated PI3K and MAPK signaling and upregulated inflammation-related genes. Additionally, real-time oxygen consumption measurements reveal mitochondrial dysfunction following tolylfluanid. Altogether, these findings indicate that tolylfluanid exerts cytotoxic and pro-oxidative effects on MAC-T cells, suggesting possible implications for milk production efficiency in cattle.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"122 ","pages":"Article 104945"},"PeriodicalIF":4.2,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146014956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-20DOI: 10.1016/j.etap.2026.104943
Rahul Kumar , Ashwin Chinala , Rama R. Gullapalli
Cadmium (Cd) is an anthropogenic toxic heavy metal pollutant with a biological half-life on the order of decades. Chronic Cd exposures through industrial sources, cigarette smoke (1° and 2°), and contaminated food and/or water sources lead to progressive bioaccumulation, particularly in the human liver and kidneys. In hepatocytes, Cd is a potent inducer of mitochondrial dysfunction and oxidative stress. Cd exposures initiate a cascade of reactive oxygen species (ROS) production, triggering redox imbalances, acute and chronic inflammation, and, in extreme exposures, cellular death. While mitochondria are well recognized as central targets of Cd toxicity, the precise mechanisms linking Cd-induced mitochondrial damage driving chronic liver and metabolic diseases remains incompletely understood. Emerging evidence implicates Cd exposure as a direct inhibitor of the mitochondrial electron transport chain (ETC) complexes and disruption of calcium homeostasis as key, converging pathways of hepatocellular injury. And yet, their specific molecular underpinnings are still unknown. This review focuses on how Cd exposures perturb mitochondrial bioenergetics, calcium signaling, and lipid signaling and metabolism within the hepatocytes specifically. Subsequently, we examine how these molecular-level alterations may contribute to the pathogenesis of chronic liver disease. In this review article, we present a cohesive framework to highlight Cd exposures as a critical (and a model) environmental heavy metal driver of chronic hepatocellular mitochondrial injury. Prolonged heavy metal exposures (such as Cd) have significant implications for long-term human hepatic health and metabolic disorders, such as metabolic (dysfunction) associated liver injury (MASLD), a key emerging pandemic of chronic human liver disease.
{"title":"Understanding molecular mechanisms driving cadmium-induced mitochondrial dysfunction in human metabolic liver disease","authors":"Rahul Kumar , Ashwin Chinala , Rama R. Gullapalli","doi":"10.1016/j.etap.2026.104943","DOIUrl":"10.1016/j.etap.2026.104943","url":null,"abstract":"<div><div>Cadmium (Cd) is an anthropogenic toxic heavy metal pollutant with a biological half-life on the order of decades. Chronic Cd exposures through industrial sources, cigarette smoke (1° and 2°), and contaminated food and/or water sources lead to progressive bioaccumulation, particularly in the human liver and kidneys. In hepatocytes, Cd is a potent inducer of mitochondrial dysfunction and oxidative stress. Cd exposures initiate a cascade of reactive oxygen species (ROS) production, triggering redox imbalances, acute and chronic inflammation, and, in extreme exposures, cellular death. While mitochondria are well recognized as central targets of Cd toxicity, the precise mechanisms linking Cd-induced mitochondrial damage driving chronic liver and metabolic diseases remains incompletely understood. Emerging evidence implicates Cd exposure as a direct inhibitor of the mitochondrial electron transport chain (ETC) complexes and disruption of calcium homeostasis as key, converging pathways of hepatocellular injury. And yet, their specific molecular underpinnings are still unknown. This review focuses on how Cd exposures perturb mitochondrial bioenergetics, calcium signaling, and lipid signaling and metabolism within the hepatocytes specifically. Subsequently, we examine how these molecular-level alterations may contribute to the pathogenesis of chronic liver disease. In this review article, we present a cohesive framework to highlight Cd exposures as a critical (and a model) environmental heavy metal driver of chronic hepatocellular mitochondrial injury. Prolonged heavy metal exposures (such as Cd) have significant implications for long-term human hepatic health and metabolic disorders, such as metabolic (dysfunction) associated liver injury (MASLD), a key emerging pandemic of chronic human liver disease.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"122 ","pages":"Article 104943"},"PeriodicalIF":4.2,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146014950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-19DOI: 10.1016/j.etap.2026.104942
Kanghee Kim , Yooeun Chae , Yeong-Jin Kim , Seonggeun Zee , Sun-Hyun Park , Chang-Beom Park
Tire wear particles release the antioxidant N-(1,3-dimethylbutyl)-N′-phenyl-p-phenylenediamine (6PPD) and its oxidative products, notably 4-hydroxydiphenylamine (4-HDPA) and 6PPD-quinone (6PPD-Q), which pose unrecognized neurotoxic hazards to aquatic life. This study demonstrates that seven-day exposure of zebrafish larvae to environmentally relevant concentrations (30 and 300 µg/L) of these compounds leads to dose-dependent locomotor deficits, with up to a 42 % reduction in swimming speed at 300 µg/L. LC-MS/MS analysis confirmed accumulation of 6PPD, 4-HDPA, and 6PPD-Q in brain tissue, where they provoked oxidative stress, elevated reactive oxygen species, and dysregulated key antioxidant enzymes. Critically, dopaminergic dysfunction emerged as a central mechanism: downregulation of tyrosine hydroxylase (th2) and dopamine transporter (dat) expression coincided with depletion of brain dopamine and behavioral impairments. Suppression of corticotropin-releasing hormone further indicated broad neuroendocrine disruption. Despite preserved motor neuron morphology, apoptotic neuronal death increased, triggering compensatory neurotrophic and anti-apoptotic gene responses. By delineating this adverse outcome pathway, from chemical exposure and brain accumulation to oxidative injury, dopaminergic collapse, and locomotor impairment, our findings provide the mechanistic evidence of tire-derived antioxidant neurotoxicity in fish. These results underscore the urgent need to reassess 6PPD use in tire formulations, inform regulatory policies on tire wear particle emissions, and guide the design of safer alternative antioxidants to protect aquatic ecosystems.
{"title":"6PPD and its metabolites induce locomotor dysfunction in zebrafish through dopaminergic disruption with brain accumulation","authors":"Kanghee Kim , Yooeun Chae , Yeong-Jin Kim , Seonggeun Zee , Sun-Hyun Park , Chang-Beom Park","doi":"10.1016/j.etap.2026.104942","DOIUrl":"10.1016/j.etap.2026.104942","url":null,"abstract":"<div><div>Tire wear particles release the antioxidant N-(1,3-dimethylbutyl)-N′-phenyl-p-phenylenediamine (6PPD) and its oxidative products, notably 4-hydroxydiphenylamine (4-HDPA) and 6PPD-quinone (6PPD-Q), which pose unrecognized neurotoxic hazards to aquatic life. This study demonstrates that seven-day exposure of zebrafish larvae to environmentally relevant concentrations (30 and 300 µg/L) of these compounds leads to dose-dependent locomotor deficits, with up to a 42 % reduction in swimming speed at 300 µg/L. LC-MS/MS analysis confirmed accumulation of 6PPD, 4-HDPA, and 6PPD-Q in brain tissue, where they provoked oxidative stress, elevated reactive oxygen species, and dysregulated key antioxidant enzymes. Critically, dopaminergic dysfunction emerged as a central mechanism: downregulation of tyrosine hydroxylase (<em>th2</em>) and dopamine transporter (<em>dat</em>) expression coincided with depletion of brain dopamine and behavioral impairments. Suppression of corticotropin-releasing hormone further indicated broad neuroendocrine disruption. Despite preserved motor neuron morphology, apoptotic neuronal death increased, triggering compensatory neurotrophic and anti-apoptotic gene responses. By delineating this adverse outcome pathway, from chemical exposure and brain accumulation to oxidative injury, dopaminergic collapse, and locomotor impairment, our findings provide the mechanistic evidence of tire-derived antioxidant neurotoxicity in fish. These results underscore the urgent need to reassess 6PPD use in tire formulations, inform regulatory policies on tire wear particle emissions, and guide the design of safer alternative antioxidants to protect aquatic ecosystems.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"122 ","pages":"Article 104942"},"PeriodicalIF":4.2,"publicationDate":"2026-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146014954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nanoplastic fragments (NP) are a growing concern and using dog aortic endothelial cells (CnAEOC) and fluorescence microscopy, we observed an interaction between NP and cells, demonstrating a localization at the cytoplasmic level. Furthermore, the data collected show a disruption of both cell proliferation and metabolic activity. The results also show the induction of oxidative stress. In detail, NP caused an increase in the levels of ROS production and an inhibition of enzymatic defence systems. On the contrary, there was no alteration of the non-enzymatic defence mechanism. The analysis conducted to evaluate a possible induction of autophagy, a survival mechanism implemented by cells, following exposure to NP reported the absence of autophagy involvement in the model analysed. Finally, investigations were conducted regarding the involvement of NP in gene expression processes. Both RNA-seq and RT-PCR did not highlight differentially expressed genes in treated cells.
{"title":"Toxic effects of nanoplastics on a model of dog aortic cells","authors":"Giuseppina Basini , Martina Tambassi , Simona Bussolati , Francesca Grasselli , Anna Scalori , Erika Scaltriti , Stefano Grolli , Roberto Ramoni , Fausto Quintavalla , Melissa Berni","doi":"10.1016/j.etap.2026.104940","DOIUrl":"10.1016/j.etap.2026.104940","url":null,"abstract":"<div><div>Nanoplastic fragments (NP) are a growing concern and using dog aortic endothelial cells (CnAEOC) and fluorescence microscopy, we observed an interaction between NP and cells, demonstrating a localization at the cytoplasmic level. Furthermore, the data collected show a disruption of both cell proliferation and metabolic activity. The results also show the induction of oxidative stress. In detail, NP caused an increase in the levels of ROS production and an inhibition of enzymatic defence systems. On the contrary, there was no alteration of the non-enzymatic defence mechanism. The analysis conducted to evaluate a possible induction of autophagy, a survival mechanism implemented by cells, following exposure to NP reported the absence of autophagy involvement in the model analysed. Finally, investigations were conducted regarding the involvement of NP in gene expression processes. Both RNA-seq and RT-PCR did not highlight differentially expressed genes in treated cells.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"122 ","pages":"Article 104940"},"PeriodicalIF":4.2,"publicationDate":"2026-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145995620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-15DOI: 10.1016/j.etap.2026.104939
Evren Doruk ENGIN , Ayse Basak ENGIN , Atilla ENGIN
Suppression of nocturnal circadian melatonin signaling amplitude, disruption of the host's circadian clock through diet or phase shifts, and imbalances in the gut microbiome are significant factors that increase the incidence of breast cancer. After host-derived mature microRNAs (miRNAs) are secreted from intestinal epithelial cells, they pass to the microbiota as faecal or exosomal miRNAs and modify the epigenetic profile of the microbiome. Subsequently, the profile of host miRNAs is altered by metabolites, which are derived from intestinal bacteria. Bidirectional epigenetic modulations of host and microbiota trigger the activation of oncogenic transcriptional pathways in extraintestinal tissues. However, the effect of the mutual epigenetic interactions between the gut microbiota and the host on the development of extraintestinal cancer is not clear. The aim of this review is to discuss the factors influencing bidirectional epigenetic regulation mechanisms between microbial dysbiosis and the host in breast cancer.
{"title":"Bidirectional effect of intestinal microbiome and host in circadian rhythm disruption: Environmental factors and breast cancer development","authors":"Evren Doruk ENGIN , Ayse Basak ENGIN , Atilla ENGIN","doi":"10.1016/j.etap.2026.104939","DOIUrl":"10.1016/j.etap.2026.104939","url":null,"abstract":"<div><div>Suppression of nocturnal circadian melatonin signaling amplitude, disruption of the host's circadian clock through diet or phase shifts, and imbalances in the gut microbiome are significant factors that increase the incidence of breast cancer. After host-derived mature microRNAs (miRNAs) are secreted from intestinal epithelial cells, they pass to the microbiota as faecal or exosomal miRNAs and modify the epigenetic profile of the microbiome. Subsequently, the profile of host miRNAs is altered by metabolites, which are derived from intestinal bacteria. Bidirectional epigenetic modulations of host and microbiota trigger the activation of oncogenic transcriptional pathways in extraintestinal tissues. However, the effect of the mutual epigenetic interactions between the gut microbiota and the host on the development of extraintestinal cancer is not clear. The aim of this review is to discuss the factors influencing bidirectional epigenetic regulation mechanisms between microbial dysbiosis and the host in breast cancer.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"122 ","pages":"Article 104939"},"PeriodicalIF":4.2,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145994698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-10DOI: 10.1016/j.etap.2026.104938
Jennifer R. McCall , Kathryn T. Sausman , Ralph N. Mead
Per- and Polyfluoroalkyl substances (PFAS) are widespread environmental contaminants linked to various adverse health conditions, including immune dysregulation and inflammation, though cellular mechanisms remain poorly understood. In this study, we investigated the direct in vitro impact of long-chain/legacy PFOA and PFOS, byproduct NBP2, PFO4DA, and PFMOAA, and next generation HFPO-DA/”GenX” on THP-1 human monocyte function at the cellular level. While all PFAS activated THP-1 cells and altered immune function, it is important to note that they did so in very different and often contrasting ways. PFOS suppressed inflammatory cytokine release, while NBP2 and PFO4DA activated uncoordinated and simultaneous inflammatory and anti-inflammatory immune responses. PFOA, HFPO-DA/”GenX”, and PFMOAA increased markers of suppressive phenotypes often associated with tumor-associated macrophages. Taken together, our findings demonstrate that PFAS, even at non-lethal concentrations, can directly interfere with functional immune responses in cellular models by altering cytokine profiles and immune activation states.
{"title":"Per- and polyfluoroalkyl substances (PFAS) alter immune responses from THP-1 human monocytes","authors":"Jennifer R. McCall , Kathryn T. Sausman , Ralph N. Mead","doi":"10.1016/j.etap.2026.104938","DOIUrl":"10.1016/j.etap.2026.104938","url":null,"abstract":"<div><div>Per- and Polyfluoroalkyl substances (PFAS) are widespread environmental contaminants linked to various adverse health conditions, including immune dysregulation and inflammation, though cellular mechanisms remain poorly understood. In this study, we investigated the direct <em>in vitro</em> impact of long-chain/legacy PFOA and PFOS, byproduct NBP2, PFO4DA, and PFMOAA, and next generation HFPO-DA/”GenX” on THP-1 human monocyte function at the cellular level<em>.</em> While all PFAS activated THP-1 cells and altered immune function, it is important to note that they did so in very different and often contrasting ways. PFOS suppressed inflammatory cytokine release, while NBP2 and PFO4DA activated uncoordinated and simultaneous inflammatory and anti-inflammatory immune responses. PFOA, HFPO-DA/”GenX”, and PFMOAA increased markers of suppressive phenotypes often associated with tumor-associated macrophages. Taken together, our findings demonstrate that PFAS, even at non-lethal concentrations, can directly interfere with functional immune responses in cellular models by altering cytokine profiles and immune activation states.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"122 ","pages":"Article 104938"},"PeriodicalIF":4.2,"publicationDate":"2026-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145956536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-09DOI: 10.1016/j.etap.2026.104934
Paloma De Oro-Carretero, Natalia Melones-Peña, Emma Gracia-Lor , Jon Sanz-Landaluze
Non-steroidal anti-inflammatory (NSAIDs) pharmaceuticals are one of the most widely used drugs worldwide. Their consumption in Spain experienced an increase from 2020 due to the global pandemic COVID-19, according to prescription packaging sales. However, many of these pharmaceutical products are over-the-counter or not all of the amount sold is consumed. Therefore, wastewater-based epidemiology (WBE) was applied to provide objective and real-time information on their consumption. Seven pharmaceuticals were measured in untreated wastewater collected during one week between December 2020 and December 2021 from seven wastewater treatment plants (WWTPs) in different Spanish cities. The samples were analysed using an analytical methodology based on solid-phase extraction and gas chromatography tandem mass spectrometry with prior derivatization. The concentrations found were converted into population normalized daily consumption considering the daily flow rate, population and correction factors. Refined correction factors have been obtained by a systematic review of all accessible studies, considering the excretion factors of each substance and their stability in the sewer system. The results showed that pharmaceutical consumption was similar in the different WWTPs, with paracetamol, ibuprofen and acetylsalicylic acid being the most consumed with mean values of 7, 41 and 12 g/day/1000 inhabitants, respectively. The estimated NSAID consumption (MD), derived from wastewater analysis, aligned with the dispensing values (DCV), except for ibuprofen and diclofenac showing an overestimation of consumption. Principal component analysis (PCA) revealed the predominant days of the week for each compound. In addition, an increase in consumption was observed in the New Year's Eve week. Overall, these findings demonstrate that WBE provides a reliable and complementary approach for assessing real NSAID consumption patterns in the population.
{"title":"Wastewater-based epidemiology of non-steroidal anti-inflammatory drugs in six cities of Spain: Consumption patterns, seasonal trends, and the role of refined correction factors","authors":"Paloma De Oro-Carretero, Natalia Melones-Peña, Emma Gracia-Lor , Jon Sanz-Landaluze","doi":"10.1016/j.etap.2026.104934","DOIUrl":"10.1016/j.etap.2026.104934","url":null,"abstract":"<div><div>Non-steroidal anti-inflammatory (NSAIDs) pharmaceuticals are one of the most widely used drugs worldwide. Their consumption in Spain experienced an increase from 2020 due to the global pandemic COVID-19, according to prescription packaging sales. However, many of these pharmaceutical products are over-the-counter or not all of the amount sold is consumed. Therefore, wastewater-based epidemiology (WBE) was applied to provide objective and real-time information on their consumption. Seven pharmaceuticals were measured in untreated wastewater collected during one week between December 2020 and December 2021 from seven wastewater treatment plants (WWTPs) in different Spanish cities. The samples were analysed using an analytical methodology based on solid-phase extraction and gas chromatography tandem mass spectrometry with prior derivatization. The concentrations found were converted into population normalized daily consumption considering the daily flow rate, population and correction factors. Refined correction factors have been obtained by a systematic review of all accessible studies, considering the excretion factors of each substance and their stability in the sewer system. The results showed that pharmaceutical consumption was similar in the different WWTPs, with paracetamol, ibuprofen and acetylsalicylic acid being the most consumed with mean values of 7, 41 and 12 g/day/1000 inhabitants, respectively. The estimated NSAID consumption (MD), derived from wastewater analysis, aligned with the dispensing values (DCV), except for ibuprofen and diclofenac showing an overestimation of consumption. Principal component analysis (PCA) revealed the predominant days of the week for each compound. In addition, an increase in consumption was observed in the New Year's Eve week. Overall, these findings demonstrate that WBE provides a reliable and complementary approach for assessing real NSAID consumption patterns in the population.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"122 ","pages":"Article 104934"},"PeriodicalIF":4.2,"publicationDate":"2026-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145954691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-09DOI: 10.1016/j.etap.2026.104935
Anna Koubová , Worrayanee Thammatorn , Antonín Kouba , Vladimír Žlábek , Bent Speksnijder , Daniel Cerveny , Oksana Golovko
Pharmaceutical active compounds (PhACs) increasingly appear as complex mixtures in aquatic ecosystems, yet their bioconcentration in non-target organisms is poorly understood. This study examined tissue-specific distribution of five PhACs – bicalutamide, amitriptyline, furosemide, daidzein and sertraline – in signal crayfish (Pacifastacus leniusculus) after 96-hour exposure and an equal depuration period. Crayfish were subjected to environmentally relevant and 10-fold elevated mixture concentrations. Water and tissues (haemolymph, hepatopancreas, muscle) were analysed using ultra-high performance liquid chromatography–tandem mass spectrometry. Despite verified water concentrations and stable conditions, none of the compounds were quantifiable in tissues, except trace sertraline near the detection limit in some controls. The lack of detectable residues indicates minimal bioconcentration, likely due to physicochemical properties (low log Kow), rapid metabolism and efficient excretion. Results underscore the need for longer exposures and metabolite-focused studies to better assess environmental fate, tissue kinetics and potential risks of PhAC mixtures in freshwater invertebrates.
{"title":"Limited bioconcentration of water-associated pharmaceutical active compounds through short-term exposure in signal crayfish (Pacifastacus leniusculus)","authors":"Anna Koubová , Worrayanee Thammatorn , Antonín Kouba , Vladimír Žlábek , Bent Speksnijder , Daniel Cerveny , Oksana Golovko","doi":"10.1016/j.etap.2026.104935","DOIUrl":"10.1016/j.etap.2026.104935","url":null,"abstract":"<div><div>Pharmaceutical active compounds (PhACs) increasingly appear as complex mixtures in aquatic ecosystems, yet their bioconcentration in non-target organisms is poorly understood. This study examined tissue-specific distribution of five PhACs – bicalutamide, amitriptyline, furosemide, daidzein and sertraline – in signal crayfish (<em>Pacifastacus leniusculus</em>) after 96-hour exposure and an equal depuration period. Crayfish were subjected to environmentally relevant and 10-fold elevated mixture concentrations. Water and tissues (haemolymph, hepatopancreas, muscle) were analysed using ultra-high performance liquid chromatography–tandem mass spectrometry. Despite verified water concentrations and stable conditions, none of the compounds were quantifiable in tissues, except trace sertraline near the detection limit in some controls. The lack of detectable residues indicates minimal bioconcentration, likely due to physicochemical properties (low log <em>K</em><sub>ow</sub>), rapid metabolism and efficient excretion. Results underscore the need for longer exposures and metabolite-focused studies to better assess environmental fate, tissue kinetics and potential risks of PhAC mixtures in freshwater invertebrates.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"122 ","pages":"Article 104935"},"PeriodicalIF":4.2,"publicationDate":"2026-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145954677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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