Pub Date : 2026-02-04DOI: 10.1016/j.envint.2026.110119
Stephanie M. Engel, Tengfei Li, Emily J. Werder, Chih-Wei Liu, Diana C. Pacyga, Jake Thistle, Weiyan Yin, Julia E. Rager, Zhengwang Wu, Zehui Sun, Li Wang, Andrea Bankoski, John H. Gilmore, Joseph Piven, Gang Li, Hongtu Zhu, Kun Lu, Weili Lin
{"title":"Early life phthalate and replacement plasticizer exposures and changes in early childhood brain functional connectivity and structural morphology","authors":"Stephanie M. Engel, Tengfei Li, Emily J. Werder, Chih-Wei Liu, Diana C. Pacyga, Jake Thistle, Weiyan Yin, Julia E. Rager, Zhengwang Wu, Zehui Sun, Li Wang, Andrea Bankoski, John H. Gilmore, Joseph Piven, Gang Li, Hongtu Zhu, Kun Lu, Weili Lin","doi":"10.1016/j.envint.2026.110119","DOIUrl":"https://doi.org/10.1016/j.envint.2026.110119","url":null,"abstract":"","PeriodicalId":308,"journal":{"name":"Environment International","volume":"58 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146110896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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}
Widely used personal care product (PCP) chemicals can disrupt the function of thyroid hormones. Pregnancy-induced vulnerability heightens the risk of PCPs on maternal thyroid health, but their individual, joint, and longitudinal impacts have been underexplored. Moreover, the risk assessment regarding maternal thyroid-impairing effects of PCPs has been lacking from epidemiological and mechanistic insights. In this study, we conducted an integrated risk assessment of PCPs on maternal thyroid functions, synthesizing evidence from 47 epidemiological, 18 in vivo, and 19 in vitro evidences from four major databases. Besides, a separate cohort analysis was prospectively performed among 803 pregnant women to explore associations between real-world PCP exposure and thyroid function. Serum samples in the second trimester (T2) were analyzed for PCP profiles by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Anti-thyroid peroxidase antibodies (ATPO), thyroid stimulating hormone (TSH), and free thyroxine (FT4) during T2 and the third trimester (T3) were measured using immunoassays. The targeted risk assessment of environmental chemicals (TRAEC) strategy yielded a middle-level risk score of 5.01 for PCPs, with category-specific scores of 5.47 for phthalates, 4.85 for per- and polyfluoroalkyl substances (PFASs), and 4.12 for bisphenols. The cohort results revealed significant associations between bisphenol S (BPS), monobutyl phthalate (MEHP), dimethyl phthalate (DMP), di-n-pentyl phthalate (DnPP), dicyclohexyl phthalate (DCHP) , Sodium perfluoro-1-octanesulfonate (L-PFOS), and perfluoro-n-undecanoic acid (PFUdA) with thyroid function markers during T2 and T3. Mixed-exposure models showed negative associations of PCPs with TSH during T2, with PFUdA, DMP, DCHP, and BPS identified as key contributors. These findings highlighted the potential risk of PCP exposure as determined by the TRAEC strategy. In conclusion, PCP exposure may contribute to maternal thyroid dysfunction with trimester-specific effects. Our findings highlighted the need to mitigate PCP-related exposures during pregnancy and improve maternal thyroid health.
{"title":"Association of exposure to personal care product chemicals with maternal thyroid health: a prospective cohort study integrated with targeted risk assessment for environmental chemicals strategy","authors":"Mazhar Sultan, Ziye Xia, Feng Zhu, Jiali Chen, Chao Dong, Qiuyun Yu, Farah Kafauit, Salimata Yakubu, Xuan Ma, Natasha Chitakwa, Aizhen Wang, Quanquan Guan, Yankai Xia","doi":"10.1016/j.envint.2026.110121","DOIUrl":"https://doi.org/10.1016/j.envint.2026.110121","url":null,"abstract":"Widely used personal care product (PCP) chemicals can disrupt the function of thyroid hormones. Pregnancy-induced vulnerability heightens the risk of PCPs on maternal thyroid health, but their individual, joint, and longitudinal impacts have been underexplored. Moreover, the risk assessment regarding maternal thyroid-impairing effects of PCPs has been lacking from epidemiological and mechanistic insights. In this study, we conducted an integrated risk assessment of PCPs on maternal thyroid functions, synthesizing evidence from 47 epidemiological, 18 <em>in vivo,</em> and 19 <em>in vitro</em> evidences from four major databases. Besides, a separate cohort analysis was prospectively performed among 803 pregnant women to explore associations between real-world PCP exposure and thyroid function. Serum samples in the second trimester (T2) were analyzed for PCP profiles by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Anti-thyroid peroxidase antibodies (ATPO), thyroid stimulating hormone (TSH), and free thyroxine (FT4) during T2 and the third trimester (T3) were measured using immunoassays. The targeted risk assessment of environmental chemicals (TRAEC) strategy yielded a middle-level risk score of 5.01 for PCPs, with category-specific scores of 5.47 for phthalates, 4.85 for per- and polyfluoroalkyl substances (PFASs), and 4.12 for bisphenols. The cohort results revealed significant associations between bisphenol S (BPS), monobutyl phthalate (MEHP), dimethyl phthalate (DMP), di-n-pentyl phthalate (DnPP), dicyclohexyl phthalate (DCHP) , Sodium perfluoro-1-octanesulfonate (L-PFOS), and perfluoro-n-undecanoic acid (PFUdA) with thyroid function markers during T2 and T3. Mixed-exposure models showed negative associations of PCPs with TSH during T2, with PFUdA, DMP, DCHP, and BPS identified as key contributors. These findings highlighted the potential risk of PCP exposure as determined by the TRAEC strategy. In conclusion, PCP exposure may contribute to maternal thyroid dysfunction with trimester-specific effects. Our findings highlighted the need to mitigate PCP-related exposures during pregnancy and improve maternal thyroid health.","PeriodicalId":308,"journal":{"name":"Environment International","volume":"80 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2026-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146097833","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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 : 2026-02-02DOI: 10.1016/j.envint.2026.110116
Teemu Lepistö, Jarkko V. Niemi, Laura Salo, Ville Silvonen, Mohamed Elsayed, Milja Jäppi, Teresia Stranden, Katariina Kylämäki, Sami D. Harni, Piia Sormunen, Hanna E. Manninen, Hilkka Timonen, Topi Rönkkö
Airports have been identified as major sources of ultrafine particles, which have gained increasing attention due to their linkage with adverse health effects. To better understand the exposure, impacts and needed regulatory actions related to airport-originated pollution, the characteristics, dynamics and dispersion of these emissions should be known. In this study, we investigate particle pollution from a medium-large international airport (Helsinki-Vantaa, Finland) by utilising a stationary measurement site near the airport and mobile laboratory measurements up to 10 km away from the determined airport reference location. We report particle number concentration (PNC) and size distributions (1.2 nm–2.5 µm), emission factors as well as dispersion of particles larger than 2.5 nm, 4 nm, 10 nm and 23 nm, BC, PM2.5 and lung deposited surface area (LDSAal). Furthermore, data from a long-term air quality monitoring site and 12 PNC sensor sites up to 15 km away are used to investigate the long-term impacts of the airport. Finally, we estimate the airport’s contribution to yearly averaged PNC and LDSAal in the surrounding areas. Overall, the studied airport is a major source of ultrafine particles: The downwind PNC> 10 nm exceeded the World Health Organization’s definition for high short-term PNC (20 000 #/cm3) up to a 4.4 km distance, and 500–5 000 #/cm3 yearly increases of PNC>10 nm at 2–5 km distances were estimated. The high contribution of particles smaller than 10 nm and nanocluster aerosols (<3 nm) suggest an important role of (semi-)volatile compounds in the airport emissions
{"title":"Dispersion of ultrafine particle pollution from an international airport: Characteristics and short- and long-term effects in surrounding areas","authors":"Teemu Lepistö, Jarkko V. Niemi, Laura Salo, Ville Silvonen, Mohamed Elsayed, Milja Jäppi, Teresia Stranden, Katariina Kylämäki, Sami D. Harni, Piia Sormunen, Hanna E. Manninen, Hilkka Timonen, Topi Rönkkö","doi":"10.1016/j.envint.2026.110116","DOIUrl":"https://doi.org/10.1016/j.envint.2026.110116","url":null,"abstract":"Airports have been identified as major sources of ultrafine particles, which have gained increasing attention due to their linkage with adverse health effects. To better understand the exposure, impacts and needed regulatory actions related to airport-originated pollution, the characteristics, dynamics and dispersion of these emissions should be known. In this study, we investigate particle pollution from a medium-large international airport (Helsinki-Vantaa, Finland) by utilising a stationary measurement site near the airport and mobile laboratory measurements up to 10 km away from the determined airport reference location. We report particle number concentration (PNC) and size distributions (1.2 nm–2.5 µm), emission factors as well as dispersion of particles larger than 2.5 nm, 4 nm, 10 nm and 23 nm, BC, PM<sub>2.5</sub> and lung deposited surface area (LDSA<sup>al</sup>). Furthermore, data from a long-term air quality monitoring site and 12 PNC sensor sites up to 15 km away are used to investigate the long-term impacts of the airport. Finally, we estimate the airport’s contribution to yearly averaged PNC and LDSA<sup>al</sup> in the surrounding areas. Overall, the studied airport is a major source of ultrafine particles: The downwind PNC<sub>> 10 nm</sub> exceeded the World Health Organization’s definition for high short-term PNC (20 000 #/cm<sup>3</sup>) up to a 4.4 km distance, and 500–5 000 #/cm<sup>3</sup> yearly increases of PNC<sub>>10 nm</sub> at 2–5 km distances were estimated. The high contribution of particles smaller than 10 nm and nanocluster aerosols (<3 nm) suggest an important role of (semi-)volatile compounds in the airport emissions","PeriodicalId":308,"journal":{"name":"Environment International","volume":"8 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2026-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146097840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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 : 2026-02-01DOI: 10.1016/j.envint.2026.110096
D. Lopez-Rodriguez , G. Guerrero-Limón , N. Chèvre
With over 350,000 chemicals and mixtures currently registered for production and use worldwide, around 83% of authorized chemicals lack adequate toxicity data, leaving the majority of chemicals poorly characterized. International agencies urge scientists to develop screening methods to explore, identify, and predict chemical hazards, supporting the prioritization of chemical risk assessment. Here, Tree Manifold Approximation and Projection (TMAP) were applied, with the aim of reducing the dimensionality of large toxicological dataset, providing the foundations to data imputation methods allowing to get an understanding of chemical modes of action. Specifically, TMAP was implemented using MHFP6 fingerprints and the NORMAN SusDat database, which contains over 100,000 compounds. To ensure that the TMAP layout preserves chemical structural similarity, a quantitative parameter optimization procedure was developed. The defined optimal parameter set allowed us to define the embeddings that preserves the most structural similarity among nearest connected neighbors, with similarity progressively decreasing as the distance between nodes increases. Leveraging this approach, a graph-based spatial imputation function was generated to obtain insights into the potential ecotoxicity mechanisms of data poor chemicals using physicochemical properties and CTD toxicogenomic data. The relevance and meaningfulness of TMAP chemical space was explored for Daphnia magna, Pimephales promelas and Algae. Chemical classes known to be structurally similar were found to be grouped together in the TMAP chemical space, while heterogeneous classes were found to be sparse. Data imputation allowed for the identification of known and potential chemical mechanisms of action. Indeed, acetylcholinesterase and transthyretin were confirmed as major mechanisms of action of organothiophosphate and brominated flame retardant toxicity in Daphnia magna and Pimephales promelas, respectively. Overall, transdisciplinary toxicological databases combined with TMAP, stand out as a computationally efficient and suitable method to explore and analyze large datasets, allowing for the inference of associations between chemical structures and chemical hazard identification and other potential applications of this hypotheses-generating tool.
{"title":"A chemical space model for the exploration of eco-toxicological data","authors":"D. Lopez-Rodriguez , G. Guerrero-Limón , N. Chèvre","doi":"10.1016/j.envint.2026.110096","DOIUrl":"10.1016/j.envint.2026.110096","url":null,"abstract":"<div><div>With over 350,000 chemicals and mixtures currently registered for production and use worldwide, around 83% of authorized chemicals lack adequate toxicity data, leaving the majority of chemicals poorly characterized. International agencies urge scientists to develop screening methods to explore, identify, and predict chemical hazards, supporting the prioritization of chemical risk assessment. Here, Tree Manifold Approximation and Projection (TMAP) were applied, with the aim of reducing the dimensionality of large toxicological dataset, providing the foundations to data imputation methods allowing to get an understanding of chemical modes of action. Specifically, TMAP was implemented using MHFP6 fingerprints and the NORMAN SusDat database, which contains over 100,000 compounds. To ensure that the TMAP layout preserves chemical structural similarity, a quantitative parameter optimization procedure was developed. The defined optimal parameter set allowed us to define the embeddings that preserves the most structural similarity among nearest connected neighbors, with similarity progressively decreasing as the distance between nodes increases. Leveraging this approach, a graph-based spatial imputation function was generated to obtain insights into the potential ecotoxicity mechanisms of data poor chemicals using physicochemical properties and CTD toxicogenomic data. The relevance and meaningfulness of TMAP chemical space was explored for <em>Daphnia magna</em>, <em>Pimephales promelas</em> and <em>Algae</em>. Chemical classes known to be structurally similar were found to be grouped together in the TMAP chemical space, while heterogeneous classes were found to be sparse. Data imputation allowed for the identification of known and potential chemical mechanisms of action. Indeed, acetylcholinesterase and transthyretin were confirmed as major mechanisms of action of organothiophosphate and brominated flame retardant toxicity in <em>Daphnia magna</em> and <em>Pimephales promelas</em>, respectively. Overall, transdisciplinary toxicological databases combined with TMAP, stand out as a computationally efficient and suitable method to explore and analyze large datasets, allowing for the inference of associations between chemical structures and chemical hazard identification and other potential applications of this hypotheses-generating tool.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110096"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146034186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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}
Per- and polyfluoroalkyl substances (PFAS) pose significant health risks to vulnerable populations such as pregnant women and children. Evidence on prenatal PFAS exposure and childhood respiratory allergic diseases (RAD) is scarce, particularly regarding how this relationship might be modified by prenatal PM2.5 exposure.
Objective
To assess the association between prenatal PFAS exposure and the risk of childhood RAD and evaluate whether prenatal PM2.5 exposure modifies this association.
Methods
We conducted a population-based prospective cohort study of 4,166 mother–child pairs from the Shanghai Birth Cohort Consortium to investigate this relationship. Data on RAD (including asthma and allergic rhinitis) in children under 8 years of age were collected from medical records or validated questionnaires. Concentrations of seven PFAS were measured in maternal blood collected during early pregnancy using ultra-high performance liquid chromatography/triple quadrupole tandem mass spectrometry. Generalized linear regression models were used to assess the associations between PFAS and childhood RAD after adjusting for potential confounders.
Results
Among the participants, 1,003 (23.9%) children were diagnosed with RAD. PFOA exhibited the highest median concentration (11.97 ng/mL), followed by PFOS (9.68 ng/mL). A doubling increment in PFOA was associated with an increased adjusted odds ratio (aOR) for childhood RAD (1.21, 95% CI: 1.03 to 1.41). The molar sum of five carboxylate PFAS (∑PFCAs) were also significantly associated with elevated RAD risk (aOR = 1.21, 95% CI: 1.03 to 1.42). Additionally, we observed that higher prenatal PM2.5 exposure appeared to enhance the adverse effects of PFAS on RAD, with a significant interaction specifically noted for PFOA in relation to allergic rhinitis (aOR = 1.35, 95% CI: 1.07 to 1.72).
Conclusion
Prenatal exposure to individual and PFAS mixture was associated with an increased risk of childhood RAD, particularly allergic rhinitis. Children born to mothers with high PM2. 5 levels during pregnancy were more susceptible. Reducing prenatal PFAS and PM2.5 exposure may reduce the public health burden of childhood RAD.
{"title":"Prenatal PFAS exposure and childhood respiratory allergic diseases: Findings from Shanghai Birth cohort Consortium","authors":"Yabin Hu, Qian Chen, Jianya Xi, Yingya Zhao, Liyi Zhang, Yuyan Gui, Wei Yuan, Maohua Miao, Yu Gao, Ying Tian, Huijing Shi, Hong Liang, Jun Zhang, Yunhui Zhang","doi":"10.1016/j.envint.2026.110118","DOIUrl":"https://doi.org/10.1016/j.envint.2026.110118","url":null,"abstract":"<h3>Background</h3>Per- and polyfluoroalkyl substances (PFAS) pose significant health risks to vulnerable populations such as pregnant women and children. Evidence on prenatal PFAS exposure and childhood respiratory allergic diseases (RAD) is scarce, particularly regarding how this relationship might be modified by prenatal PM<sub>2.5</sub> exposure.<h3>Objective</h3>To assess the association between prenatal PFAS exposure and the risk of childhood RAD and evaluate whether prenatal PM<sub>2.5</sub> exposure modifies this association.<h3>Methods</h3>We conducted a population-based prospective cohort study of 4,166 mother–child pairs from the Shanghai Birth Cohort Consortium to investigate this relationship. Data on RAD (including asthma and allergic rhinitis) in children under 8 years of age were collected from medical records or validated questionnaires. Concentrations of seven PFAS were measured in maternal blood collected during early pregnancy using ultra-high performance liquid chromatography/triple quadrupole tandem mass spectrometry. Generalized linear regression models were used to assess the associations between PFAS and childhood RAD after adjusting for potential confounders.<h3>Results</h3>Among the participants, 1,003 (23.9%) children were diagnosed with RAD. PFOA exhibited the highest median concentration (11.97 ng/mL), followed by PFOS (9.68 ng/mL). A doubling increment in PFOA was associated with an increased adjusted odds ratio (aOR) for childhood RAD (1.21, 95% CI: 1.03 to 1.41). The molar sum of five carboxylate PFAS (∑PFCAs) were also significantly associated with elevated RAD risk (aOR = 1.21, 95% CI: 1.03 to 1.42). Additionally, we observed that higher prenatal PM<sub>2</sub>.<sub>5</sub> exposure appeared to enhance the adverse effects of PFAS on RAD, with a significant interaction specifically noted for PFOA in relation to allergic rhinitis (aOR = 1.35, 95% CI: 1.07 to 1.72).<h3>Conclusion</h3>Prenatal exposure to individual and PFAS mixture was associated with an increased risk of childhood RAD, particularly allergic rhinitis. Children born to mothers with high PM<sub>2</sub>. <sub>5</sub> levels during pregnancy were more susceptible. Reducing prenatal PFAS and PM<sub>2.5</sub> exposure may reduce the public health burden of childhood RAD.","PeriodicalId":308,"journal":{"name":"Environment International","volume":"65 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146110887","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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 : 2026-02-01DOI: 10.1016/j.envint.2026.110072
Jamshid Faraji , Gerlinde A.S. Metz
Environmental factors can have profound influences on biological systems, particularly through their effects on epigenetic processes. Epigenetics provides a powerful framework for understanding the regulation of gene expression through the interplay between genetic predispositions, inherited epigenetic marks, and lifelong environmental influences. This review proposes that even subtle epigenetic changes may initiate cascading effects on gene regulation and biological systems, ultimately contributing to significant phenotypic outcomes, including the modification of developmental trajectories, disease susceptibility, and adaptive responses. The reversible and adaptable nature of epigenetic modifications enables organisms to respond dynamically to a wide range of stimuli throughout their lifespan. Conversely, maladaptive epigenetic regulation can be associated with pathologies, including cancer, diabetes, neurodegenerative disorders, and adverse mental health outcomes. Thus, epigenetic markers represent a promising target for risk prediction, prevention and therapeutic intervention. In this narrative review, we discuss the wide-ranging implications of epigenetic theories underlying gene-environment interactions. Furthermore, we examine the evolving expectations of the scientific community and the public regarding epigenetic theories, which may shape future research directions and drive therapeutic innovation in health and disease. Epigenetic concepts are poised to bridge the gap between genetic predispositions and environmental influences, offering novel insights into complex biological processes and their outcomes.
{"title":"Environmental epigenetics: new horizons in redefining biological and health outcomes","authors":"Jamshid Faraji , Gerlinde A.S. Metz","doi":"10.1016/j.envint.2026.110072","DOIUrl":"10.1016/j.envint.2026.110072","url":null,"abstract":"<div><div>Environmental factors can have profound influences on biological systems, particularly through their effects on epigenetic processes. Epigenetics provides a powerful framework for understanding the regulation of gene expression through the interplay between genetic predispositions, inherited epigenetic marks, and lifelong environmental influences. This review proposes that even subtle epigenetic changes may initiate cascading effects on gene regulation and biological systems, ultimately contributing to significant phenotypic outcomes, including the modification of developmental trajectories, disease susceptibility, and adaptive responses. The reversible and adaptable nature of epigenetic modifications enables organisms to respond dynamically to a wide range of stimuli throughout their lifespan. Conversely, maladaptive epigenetic regulation can be associated with pathologies, including cancer, diabetes, neurodegenerative disorders, and adverse mental health outcomes. Thus, epigenetic markers represent a promising target for risk prediction, prevention and therapeutic intervention. In this narrative review, we discuss the wide-ranging implications of epigenetic theories underlying gene-environment interactions. Furthermore, we examine the evolving expectations of the scientific community and the public regarding epigenetic theories, which may shape future research directions and drive therapeutic innovation in health and disease. Epigenetic concepts are poised to bridge the gap between genetic predispositions and environmental influences, offering novel insights into complex biological processes and their outcomes.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110072"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145995908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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}
Haloketones (HKs) are an emerging class of unregulated drinking water disinfection byproducts (DBPs) that are primarily responsible for drinking water cytotoxicity and also exhibit genotoxicity and carcinogenicity. We determined the concentrations of 11 HKs in drinking water and conducted quantitative and comparative analyses of their toxicity. Nine HKs were detected in drinking water from Nanning City in Southwest China, with median concentrations ranging from 0.03 to 3.32 μg/L. 1,1,3-Tribromopropanone and 1-bromo-1,1-dichloropropanone were identified in drinking water for the first time in China. The descending rank order of HK cytotoxicity was 1,3-dichloropropanone > bromopropanone > 1,1,3-tribromopropanone > 1,1,3-trichloropropanone ≈ chloropropanone > 1,1-dichloropropanone > 1,1,3,3-tetrachloropropanone > 1-bromo-1,1-dichloropropanone ≈ 1,1,3,3-tetrabromopropanone > 1,1,1-trichloropropanone ≈ 1,1-dibromopropanone (F10,208 = 4672.689, P < 0.001). The rank order for HK genotoxicity was 1,3-dichloropropanone > bromopropanone > chloropropanone > 1,1-dibromopropanone > 1,1,3-trichloropropanone ≈ 1,1,3-tribromopropanone > 1-bromo-1,1-dichloropropanone ≈ 1,1,3,3-tetrachloropropanone > 1,1,3,3-tetrabromopropanone > 1,1-dichloropropanone ≈ 1,1,1-trichloropropanone (F10,66 = 7028.528, P < 0.001). The rank order for HK thiol reactivity was 1,1-dibromopropanone ≈ 1,3-dichloropropanone ≈ chloropropanone ≈ bromopropanone ≈ 1-bromo-1,1-dichloropropanone ≈ 1,1,3-tribromopropanone > 1,1,3,3-tetrabromopropanone > 1,1,3-trichloropropanone ≈ 1,1,3,3-tetrachloropropanone ≈ 1,1-dichloropropanone ≈ 1,1,1-trichloropropanone (F10,154 = 473.640, P < 0.001). Quantitative structure activity relationship models indicated that HK toxicity was closely correlated with hydrophobicity, boiling point, and topological properties. HKs exhibited higher cytotoxicity and genotoxicity than regulated haloacetic acids and trihalomethanes. In particular, 1,3-dichloropropanone showed higher toxicity than nitrogenous DBPs. Further studies are required to expand the investigation of HK pollution, elucidate their formation and toxic mechanisms, and evaluate the potential human health risks.
{"title":"Occurrence and toxicity of haloketones: emerging class of disinfection byproducts in drinking water of Nanning City, Southwest China","authors":"Yuwen Huang , Zan Sheng , Qiuyan Wei , Mingliang Wu , Jingyi Xiao , Qing Zhong , Zhanmou Liu , Mengting Yang , Xiao Wei","doi":"10.1016/j.envint.2026.110097","DOIUrl":"10.1016/j.envint.2026.110097","url":null,"abstract":"<div><div>Haloketones (HKs) are an emerging class of unregulated drinking water disinfection byproducts (DBPs) that are primarily responsible for drinking water cytotoxicity and also exhibit genotoxicity and carcinogenicity. We determined the concentrations of 11 HKs in drinking water and conducted quantitative and comparative analyses of their toxicity. Nine HKs were detected in drinking water from Nanning City in Southwest China, with median concentrations ranging from 0.03 to 3.32 μg/L. 1,1,3-Tribromopropanone and 1-bromo-1,1-dichloropropanone were identified in drinking water for the first time in China. The descending rank order of HK cytotoxicity was 1,3-dichloropropanone > bromopropanone > 1,1,3-tribromopropanone > 1,1,3-trichloropropanone ≈ chloropropanone > 1,1-dichloropropanone > 1,1,3,3-tetrachloropropanone > 1-bromo-1,1-dichloropropanone ≈ 1,1,3,3-tetrabromopropanone > 1,1,1-trichloropropanone ≈ 1,1-dibromopropanone (<em>F</em><sub>10,208</sub> = 4672.689, <em>P</em> < 0.001). The rank order for HK genotoxicity was 1,3-dichloropropanone > bromopropanone > chloropropanone > 1,1-dibromopropanone > 1,1,3-trichloropropanone ≈ 1,1,3-tribromopropanone > 1-bromo-1,1-dichloropropanone ≈ 1,1,3,3-tetrachloropropanone > 1,1,3,3-tetrabromopropanone > 1,1-dichloropropanone ≈ 1,1,1-trichloropropanone (<em>F</em><sub>10,66</sub> = 7028.528, <em>P</em> < 0.001). The rank order for HK thiol reactivity was 1,1-dibromopropanone ≈ 1,3-dichloropropanone ≈ chloropropanone ≈ bromopropanone ≈ 1-bromo-1,1-dichloropropanone ≈ 1,1,3-tribromopropanone > 1,1,3,3-tetrabromopropanone > 1,1,3-trichloropropanone ≈ 1,1,3,3-tetrachloropropanone ≈ 1,1-dichloropropanone ≈ 1,1,1-trichloropropanone (<em>F</em><sub>10,154</sub> = 473.640, <em>P</em> < 0.001). Quantitative structure activity relationship models indicated that HK toxicity was closely correlated with hydrophobicity, boiling point, and topological properties. HKs exhibited higher cytotoxicity and genotoxicity than regulated haloacetic acids and trihalomethanes. In particular, 1,3-dichloropropanone showed higher toxicity than nitrogenous DBPs. Further studies are required to expand the investigation of HK pollution, elucidate their formation and toxic mechanisms, and evaluate the potential human health risks.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110097"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146014685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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 : 2026-02-01DOI: 10.1016/j.envint.2026.110095
Arce Domingo-Relloso , Katlyn E. McGraw , Irene Martinez-Morata , Yuchen Zhang , Kathrin Schilling , Ronald A. Glabonjat , Ziqing Wang , Kiros Berhane , Brent A. Coull , Marta Galvez-Fernandez , Miranda R. Jones , Wendy S. Post , Joel Kaufman , Tiffany R. Sanchez , Maria Tellez-Plaza , Graham R. Barr , Steven Shea , Ana Navas-Acien , Linda Valeri
Metals are associated with cardiovascular disease (CVD), but the underlying pathways remain largely unclear. We evaluated the potential intermediate role of coronary artery calcification (CAC) trajectory on the association between urinary metals and incident CVD, accounting for competing risks by death from other causes. We used data from 6,459 participants of the Multi-Ethnic Study of Atherosclerosis (MESA). CAC was measured longitudinally using the spatially weighted calcium score in five exams, starting in 2000. Participants were followed for CVD events through 2019. Cadmium, cobalt, copper, uranium, tungsten, and zinc were measured in urine at the baseline visit (2000–2002). We used a causal inference algorithm with a path-specific effects approach for longitudinal mediation analysis to evaluate the intermediate role of CAC on the association between metals and incident CVD. The association with incident CVD mediated through the CAC trajectory was statistically significant for cadmium, cobalt, copper, tungsten, and zinc. The number of CVD cases (95% CI) per 100,000 person-years attributable to an interquartile range (IQR) increase in metal levels through the longitudinal trajectory of CAC was 44 (20, 72) for cadmium, 21 (6, 39) for cobalt, 19 (2, 36) for copper, 18 (2, 38) for tungsten, and 43 (26, 62) for zinc. This study supports that part of the association between urinary metals and CVD is attributable to changes in CAC over time. In particular, half of the association between urinary cadmium and CVD might be mediated by longitudinal changes in CAC. This study could inform strategies for early detection and prevention of CVD based on urinary metal levels.
{"title":"The role of coronary artery calcification in metal-related cardiovascular disease","authors":"Arce Domingo-Relloso , Katlyn E. McGraw , Irene Martinez-Morata , Yuchen Zhang , Kathrin Schilling , Ronald A. Glabonjat , Ziqing Wang , Kiros Berhane , Brent A. Coull , Marta Galvez-Fernandez , Miranda R. Jones , Wendy S. Post , Joel Kaufman , Tiffany R. Sanchez , Maria Tellez-Plaza , Graham R. Barr , Steven Shea , Ana Navas-Acien , Linda Valeri","doi":"10.1016/j.envint.2026.110095","DOIUrl":"10.1016/j.envint.2026.110095","url":null,"abstract":"<div><div>Metals are associated with cardiovascular disease (CVD), but the underlying pathways remain largely unclear. We evaluated the potential intermediate role of coronary artery calcification (CAC) trajectory on the association between urinary metals and incident CVD, accounting for competing risks by death from other causes. We used data from 6,459 participants of the Multi-Ethnic Study of Atherosclerosis (MESA). CAC was measured longitudinally using the spatially weighted calcium score in five exams, starting in 2000. Participants were followed for CVD events through 2019. Cadmium, cobalt, copper, uranium, tungsten, and zinc were measured in urine at the baseline visit (2000–2002). We used a causal inference algorithm with a path-specific effects approach for longitudinal mediation analysis to evaluate the intermediate role of CAC on the association between metals and incident CVD. The association with incident CVD mediated through the CAC trajectory was statistically significant for cadmium, cobalt, copper, tungsten, and zinc. The number of CVD cases (95% CI) per 100,000 person-years attributable to an interquartile range (IQR) increase in metal levels through the longitudinal trajectory of CAC was 44 (20, 72) for cadmium, 21 (6, 39) for cobalt, 19 (2, 36) for copper, 18 (2, 38) for tungsten, and 43 (26, 62) for zinc. This study supports that part of the association between urinary metals and CVD is attributable to changes in CAC over time. In particular, half of the association between urinary cadmium and CVD might be mediated by longitudinal changes in CAC. This study could inform strategies for early detection and prevention of CVD based on urinary metal levels.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110095"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146022150","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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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