Phthalic acid esters (PAEs) exhibit ubiquitous contamination across aquatic systems, yet their spatiotemporal dynamics and associated risks remain poorly characterized. To address this, this study measured the concentrations of 13 PAEs in river samples collected from various locations along the Jinjiang River in Chengdu at different times, as well as in tap water samples from five different floors of a building and bottled water from five brands. Additionally, ecological risks were assessed using SSD curves, and health risks were evaluated based on USEPA‐validated health risk models. The results indicated that surface water ΣPAEs ranged from 0.016 to 9.36 μg/L, with DBP (9.36 ± 2.46 μg/L) and DIBP (5.66 ± 1.49 μg/L) being the primary contributors, and significantly higher concentrations were observed upstream (most p < 0.05). Bottled and tap water ΣPAEs ranged from 0.015 to 7.42 and 0.019 to 7.79 μg/L, respectively, both dominated by DBP (bottled: 7.41 ± 0.35; tap: 7.79 ± 0.35 μg/L). Natural mineral bottled water showed the highest ΣPAEs, whereas ΣPAEs in tap water decreased with increasing building floor height. Furthermore, ecological risks to shellfish were identified, yet human health risks (oral/dermal) for adults/children remained low across all water types. Despite the high detection rates of PAEs, the dangers of population exposure were minimal. However, natural mineral bottled water and tap water from lower floors require prioritized monitoring due to higher PAE levels in surface water associated with human activities.
{"title":"Profiles of Phthalic Acid Esters ( PAEs ) in Various Water Matrices and the Associated Ecological and Health Risk Assessments","authors":"Qian Wang, Li Huang, Wei Huang, Qingkun Yang, Ling Wu, Qiurong He, Zunzhen Zhang, Xiu Huang, Jing Zhang","doi":"10.1002/tox.24580","DOIUrl":"https://doi.org/10.1002/tox.24580","url":null,"abstract":"Phthalic acid esters (PAEs) exhibit ubiquitous contamination across aquatic systems, yet their spatiotemporal dynamics and associated risks remain poorly characterized. To address this, this study measured the concentrations of 13 PAEs in river samples collected from various locations along the Jinjiang River in Chengdu at different times, as well as in tap water samples from five different floors of a building and bottled water from five brands. Additionally, ecological risks were assessed using SSD curves, and health risks were evaluated based on USEPA‐validated health risk models. The results indicated that surface water ΣPAEs ranged from 0.016 to 9.36 μg/L, with DBP (9.36 ± 2.46 μg/L) and DIBP (5.66 ± 1.49 μg/L) being the primary contributors, and significantly higher concentrations were observed upstream (most <jats:italic>p</jats:italic> < 0.05). Bottled and tap water ΣPAEs ranged from 0.015 to 7.42 and 0.019 to 7.79 μg/L, respectively, both dominated by DBP (bottled: 7.41 ± 0.35; tap: 7.79 ± 0.35 μg/L). Natural mineral bottled water showed the highest ΣPAEs, whereas ΣPAEs in tap water decreased with increasing building floor height. Furthermore, ecological risks to shellfish were identified, yet human health risks (oral/dermal) for adults/children remained low across all water types. Despite the high detection rates of PAEs, the dangers of population exposure were minimal. However, natural mineral bottled water and tap water from lower floors require prioritized monitoring due to higher PAE levels in surface water associated with human activities.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"377 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145485028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
William E. Mullen, Jackson E. Stewart, Rahatul Islam, Salik Hussain, Dharendra Thapa
A majority of deaths associated with air pollution are attributed to cardiovascular and heart diseases. Carbon black that represents the carbon core of particulate matter, a major component of air pollution, has been shown to result in cardiac mitochondrial dysfunction. The goal of this study was to identify mechanisms that potentially regulate cardiac mitochondrial function in acute carbon black exposure. Specifically, we examined whether lysine acetylation, a post‐translational modification, impacts cardiac mitochondrial function and contributes to mitochondrial dysfunction observed with carbon black exposure. C57BL/6J animals exposed to 10 mg/m 3 CB for 3 h resulted in a significant increase in acetylation of fatty acid oxidation proteins—long and short chain acyl‐CoA dehydrogenase and hydroxyacyl‐CoA dehydrogenase—which correlated with decreased enzymatic activities. Further, a significant decrease in fatty acid import protein carnitine palmitoyl‐transferase 1b was observed. An increase in acetylation of electron transport chain complexes I and V along with increased Complex V activity was observed in carbon black exposed animals. This decrease in import and utilization of fatty acid metabolism was counteracted by an increase in protein and activity level of glucose oxidation protein pyruvate dehydrogenase. These findings suggest that acute exposure to carbon black results in a switch in substrate utilization from fatty acids to glucose that in turn feeds the electron transport chain process in the exposed heart. Finally, these findings present the potential role of lysine acetylation mediated regulation of mitochondrial dysfunction in the acute carbon black exposed model.
{"title":"Acute Inhalation Exposure to Ultrafine Carbon Black Alters Mitochondrial Substrate Utilization in the Heart","authors":"William E. Mullen, Jackson E. Stewart, Rahatul Islam, Salik Hussain, Dharendra Thapa","doi":"10.1002/tox.24582","DOIUrl":"https://doi.org/10.1002/tox.24582","url":null,"abstract":"A majority of deaths associated with air pollution are attributed to cardiovascular and heart diseases. Carbon black that represents the carbon core of particulate matter, a major component of air pollution, has been shown to result in cardiac mitochondrial dysfunction. The goal of this study was to identify mechanisms that potentially regulate cardiac mitochondrial function in acute carbon black exposure. Specifically, we examined whether lysine acetylation, a post‐translational modification, impacts cardiac mitochondrial function and contributes to mitochondrial dysfunction observed with carbon black exposure. C57BL/6J animals exposed to 10 mg/m <jats:sup>3</jats:sup> CB for 3 h resulted in a significant increase in acetylation of fatty acid oxidation proteins—long and short chain acyl‐CoA dehydrogenase and hydroxyacyl‐CoA dehydrogenase—which correlated with decreased enzymatic activities. Further, a significant decrease in fatty acid import protein carnitine palmitoyl‐transferase 1b was observed. An increase in acetylation of electron transport chain complexes I and V along with increased Complex V activity was observed in carbon black exposed animals. This decrease in import and utilization of fatty acid metabolism was counteracted by an increase in protein and activity level of glucose oxidation protein pyruvate dehydrogenase. These findings suggest that acute exposure to carbon black results in a switch in substrate utilization from fatty acids to glucose that in turn feeds the electron transport chain process in the exposed heart. Finally, these findings present the potential role of lysine acetylation mediated regulation of mitochondrial dysfunction in the acute carbon black exposed model.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"603 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145404581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}