Pub Date : 2025-12-02DOI: 10.1016/j.envint.2025.109972
Anita Houeto , Anne-Sophie Evrard , Claire Perrin , Fanny Artaud , Adélie Boileau , Mathieu Hellot , Pierre Jamard , Fanny Mietlicki , Céline Domergue , Valérie Janillon , Bruno Vincent , Thomas Coudon , Lény Grassot , Delphine Praud , Guy Fagherazzi , Gianluca Severi , Élodie Faure
Background
It has been suggested that exposure to transportation noise is associated with an increased risk of type 2 diabetes (T2D), but only a few prospective cohort studies have investigated this hypothesis for railway and aircraft noise. In the BROUHAHA study, we examined this association using data from the E3N-Generations cohort of French women.
Methods
We included 18,926 women residing in the Île-de-France or Auvergne-Rhône-Alpes regions (France) between 2000 and 2014. Annual average Lden (day-evening-night level) and Ln (night level) values were estimated for road traffic, railway, and aircraft noise using strategic noise maps. Incident T2D cases were identified through follow-up questionnaires and validated using drug reimbursement insurance databases. Cox proportional hazards models were used to calculate adjusted hazard ratios (HRs) and 95 % confidence intervals (CI).
Results
A 10 dB(A) increase in road traffic noise exposure was associated with a moderate increase in T2D risk (Lden: HR = 1.08, 95 %CI: 1.00, 1.18; Ln: HR = 1.12, 95 %CI: 1.01, 1.25). Adjustment for NO2 and PM2.5 slightly increased the estimated HRs. No association was observed between railway or aircraft noise and T2D incidence.
Conclusion
In this prospective cohort study of French women, exposure to road traffic noise was associated with a moderate increase in T2D risk, independently of NO2 and PM2.5 exposure. This association was slightly stronger for night-time noise exposure than for day-evening-night exposure.
{"title":"Association between transportation noise exposure and type 2 diabetes risk in a French prospective cohort: the E3N-generations cohort","authors":"Anita Houeto , Anne-Sophie Evrard , Claire Perrin , Fanny Artaud , Adélie Boileau , Mathieu Hellot , Pierre Jamard , Fanny Mietlicki , Céline Domergue , Valérie Janillon , Bruno Vincent , Thomas Coudon , Lény Grassot , Delphine Praud , Guy Fagherazzi , Gianluca Severi , Élodie Faure","doi":"10.1016/j.envint.2025.109972","DOIUrl":"10.1016/j.envint.2025.109972","url":null,"abstract":"<div><h3>Background</h3><div>It has been suggested that exposure to transportation noise is associated with an increased risk of type 2 diabetes (T2D), but only a few prospective cohort studies have investigated this hypothesis for railway and aircraft noise. In the BROUHAHA study, we examined this association using data from the E3N-Generations cohort of French women.</div></div><div><h3>Methods</h3><div>We included 18,926 women residing in the Île-de-France or Auvergne-Rhône-Alpes regions (France) between 2000 and 2014. Annual average L<sub>den</sub> (day-evening-night level) and L<sub>n</sub> (night level) values were estimated for road traffic, railway, and aircraft noise using strategic noise maps. Incident T2D cases were identified through follow-up questionnaires and validated using drug reimbursement insurance databases. Cox proportional hazards models were used to calculate adjusted hazard ratios (HRs) and 95 % confidence intervals (CI).</div></div><div><h3>Results</h3><div>A 10 dB(A) increase in road traffic noise exposure was associated with a moderate increase in T2D risk (L<sub>den</sub>: HR = 1.08, 95 %CI: 1.00, 1.18; L<sub>n</sub>: HR = 1.12, 95 %CI: 1.01, 1.25). Adjustment for NO<sub>2</sub> and PM<sub>2.5</sub> slightly increased the estimated HRs. No association was observed between railway or aircraft noise and T2D incidence.</div></div><div><h3>Conclusion</h3><div>In this prospective cohort study of French women, exposure to road traffic noise was associated with a moderate increase in T2D risk, independently of NO<sub>2</sub> and PM<sub>2.5</sub> exposure. This association was slightly stronger for night-time noise exposure than for day-evening-night exposure.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"207 ","pages":"Article 109972"},"PeriodicalIF":9.7,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145658097","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 : 2025-12-02DOI: 10.1016/j.envint.2025.109976
Zhebin Yu , Irene Fontes Marques , Simon Kebede Merid , Kimberley Burrows , Ana Goncalves Soares , Andrei Pyko , Mikael Ögren , Göran Pershagen , Johanna Lepeule , Norun Hjertager Krog , Gunn Marit Aasvang , Michelle S.W. Kusters , Maria Foraster , Mariona Bustamante , Miriam Leskien , Elisabeth Thiering , Ahmed Elhakeem , Annette Peters , Gerard H. Koppelman , Ulrike Gehring , Olena Gruzieva
Road traffic noise exposure has been associated with multiple adverse outcomes in epidemiological studies. However, the underlying biological mechanisms remain unclear. The aim of this study was to investigate the association between road traffic noise exposure and cord blood and child blood DNA methylation (DNAm).
Data from six European studies (BAMSE, Generation R, HELIX, INMA, LISA, PIAMA) were used to perform the discovery epigenome-wide meta-analysis. Prenatal, infancy, and recent road traffic noise exposure was assessed at the residential addresses. Blood DNAm was measured using the Illumina 450 K or EPIC arrays. To identify differentially methylated positions (DMPs), we fitted robust linear regression models for each cohort, and the results were subsequently meta-analyzed. Differentially methylated regions (DMRs) were identified using Comb-p and DMRcate. Findings were then looked-up in the independent ALSPAC cohort, in which noise was measured categorically.
A total of 1477 newborns with DNAm data in cord blood, and 1129 and 2065 with DNAm in child blood (age 4–6 and age 8–10 years, respectively) were included in the discovery meta-analysis. We did not observe genome-wide significant (False Discovery Rate (FDR) < 0.05) DMPs associated with road traffic noise exposure. However, 46 DMPs reached suggestive significance (P < 1 × 10–5) across different time windows. One CpG site (cg09400092, annotated to SSTR1) associated with recent noise exposure at age 8–10 years was also significantly associated in the ALSPAC cohort (same direction of association with P = 0.00165). In addition, we identified a total of 93 FDR significant DMRs, of which 14 were nominally significant in the ALSPAC study.
In conclusion, we observed suggestive evidence of an association between road traffic noise exposure and DNAm in child blood. This may indicate that differential DNAm plays a role in the biological mechanism underlying health effects of noise exposure.
{"title":"Road traffic noise exposure and blood DNA methylation at birth and in childhood: An epigenome-wide meta-analysis","authors":"Zhebin Yu , Irene Fontes Marques , Simon Kebede Merid , Kimberley Burrows , Ana Goncalves Soares , Andrei Pyko , Mikael Ögren , Göran Pershagen , Johanna Lepeule , Norun Hjertager Krog , Gunn Marit Aasvang , Michelle S.W. Kusters , Maria Foraster , Mariona Bustamante , Miriam Leskien , Elisabeth Thiering , Ahmed Elhakeem , Annette Peters , Gerard H. Koppelman , Ulrike Gehring , Olena Gruzieva","doi":"10.1016/j.envint.2025.109976","DOIUrl":"10.1016/j.envint.2025.109976","url":null,"abstract":"<div><div>Road traffic noise exposure has been associated with multiple adverse outcomes in epidemiological studies. However, the underlying biological mechanisms remain unclear. The aim of this study was to investigate the association between road traffic noise exposure and cord blood and child blood DNA methylation (DNAm).</div><div>Data from six European studies (BAMSE, Generation R, HELIX, INMA, LISA, PIAMA) were used to perform the discovery epigenome-wide <em>meta</em>-analysis. Prenatal, infancy, and recent road traffic noise exposure was assessed at the residential addresses. Blood DNAm was measured using the Illumina 450 K or EPIC arrays. To identify differentially methylated positions (DMPs), we fitted robust linear regression models for each cohort, and the results were subsequently <em>meta</em>-analyzed. Differentially methylated regions (DMRs) were identified using Comb-p and DMRcate. Findings were then looked-up in the independent ALSPAC cohort, in which noise was measured categorically.</div><div>A total of 1477 newborns with DNAm data in cord blood, and 1129 and 2065 with DNAm in child blood (age 4–6 and age 8–10 years, respectively) were included in the discovery <em>meta</em>-analysis. We did not observe genome-wide significant (False Discovery Rate (FDR) < 0.05) DMPs associated with road traffic noise exposure. However, 46 DMPs reached suggestive significance (P < 1 × 10<sup>–5</sup>) across different time windows. One CpG site (cg09400092, annotated to <em>SSTR1</em>) associated with recent noise exposure at age 8–10 years was also significantly associated in the ALSPAC cohort (same direction of association with P = 0.00165). In addition, we identified a total of 93 FDR significant DMRs, of which 14 were nominally significant in the ALSPAC study.</div><div>In conclusion, we observed suggestive evidence of an association between road traffic noise exposure and DNAm in child blood. This may indicate that differential DNAm plays a role in the biological mechanism underlying health effects of noise exposure.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"207 ","pages":"Article 109976"},"PeriodicalIF":9.7,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145657793","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 : 2025-12-02DOI: 10.1016/j.envint.2025.109973
Menglin Liu , Jinping Wu , Hao Yu , Yuwei Wang , Shujun Yi , Liping Yang , Jinglan Feng , Zhiguo Cao , Lingyan Zhu
6:2 fluorotelomer carboxylic acid (6:2 FTCA), as a novel alternative to perfluorooctanoic acid (PFOA), has been widely detected in aquatic environments, while little is known about its bioaccumulation and biotransformation in fish. This study investigated the tissue-specific distribution and biotransformation of 6:2 FTCA in zebrafish during a 21-day exposure in water. The concentration of 6:2 FTCA was highest in the liver, then was in the intestine, gill, brain and muscle. The result consistently indicated that liver was the primary site for 6:2 FTCA biotransformation, subsequently intestine through in vivo and in vitro experiments. 6:2 FTCA experienced similar biotransformation pathway in the liver and intestine and produced 6:2 fluorotelomer unsaturated carboxylic acid (6:2 FTUCA) and C4-C7 perfluorocarboxylic acids (PFCAs) by removing HF, α- and β-oxidation. The significant increase of CYP450 enzyme and the molecular docking results demonstrated that CYP450 enzyme played a crucial role in 6:2 FTCA transformation in the liver. However, in the intestine, beyond CYP450 enzyme, intestinal microbiota also participated the biotransformation of 6:2 FTCA, especially the genera Paracoccus, Gemmobacter and Pelomonas, which could secrete metabolic enzymes and abundance significantly increased after exposure to 6:2 FTCA. This study revealed the potential of the intestine in metabolizing environmental pollutants and provided profound insights into the biotransformation of 6:2 FTCA in aquatic organisms.
{"title":"First insight into in vivo and in vitro biotransformation of 6:2 fluorotelomer carboxylic acid (6:2 FTCA) in zebrafish (Danio rerio)","authors":"Menglin Liu , Jinping Wu , Hao Yu , Yuwei Wang , Shujun Yi , Liping Yang , Jinglan Feng , Zhiguo Cao , Lingyan Zhu","doi":"10.1016/j.envint.2025.109973","DOIUrl":"10.1016/j.envint.2025.109973","url":null,"abstract":"<div><div>6:2 fluorotelomer carboxylic acid (6:2 FTCA), as a novel alternative to perfluorooctanoic acid (PFOA), has been widely detected in aquatic environments, while little is known about its bioaccumulation and biotransformation in fish. This study investigated the tissue-specific distribution and biotransformation of 6:2 FTCA in zebrafish during a 21-day exposure in water. The concentration of 6:2 FTCA was highest in the liver, then was in the intestine, gill, brain and muscle. The result consistently indicated that liver was the primary site for 6:2 FTCA biotransformation, subsequently intestine through <em>in vivo</em> and <em>in vitro</em> experiments. 6:2 FTCA experienced similar biotransformation pathway in the liver and intestine and produced 6:2 fluorotelomer unsaturated carboxylic acid (6:2 FTUCA) and C4-C7 perfluorocarboxylic acids (PFCAs) by removing HF, <em>α-</em> and <em>β-</em>oxidation. The significant increase of CYP450 enzyme and the molecular docking results demonstrated that CYP450 enzyme played a crucial role in 6:2 FTCA transformation in the liver. However, in the intestine, beyond CYP450 enzyme, intestinal microbiota also participated the biotransformation of 6:2 FTCA, especially the genera <em>Paracoccus</em>, <em>Gemmobacter</em> and <em>Pelomonas</em>, which could secrete metabolic enzymes and abundance significantly increased after exposure to 6:2 FTCA. This study revealed the potential of the intestine in metabolizing environmental pollutants and provided profound insights into the biotransformation of 6:2 FTCA in aquatic organisms.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"207 ","pages":"Article 109973"},"PeriodicalIF":9.7,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145657659","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 : 2025-12-01DOI: 10.1016/j.envint.2025.109951
Yi Zhang , Li Chen , Xinli Song , Ruolin Wang , Jianuo Jiang , Jieyu Liu , Zhiying Song , Jinghong Liang , Yinghua Ma , Jun Ma , Junqing Xie , Yi Song , Yanhui Dong
Childhood hypertension is a growing public health concern, predisposing affected individuals to long-term cardiovascular complications. The cardiovascular and metabolic effects of exposure to bisphenol A (BPA) substitutes, emerging endocrine-disrupting chemicals, remain poorly understood in children. This study investigated associations between childhood BPA substitutes exposure and blood pressure, focusing on the modifying role of latent insulin resistance (LIR) and potential lipid metabolic pathways. A total of 747 children from a prospective cohort in Xiamen, China, were included. Associations between repeated bisphenol measurements and blood pressure were assessed using mixed-effects models and generalized estimating equations. A random subsample underwent lipidomic profiling; participants were grouped by bisphenol exposure and triglyceride-glucose (TyG) index. Differentially expressed lipids were identified, tested for associations with blood pressure, and analyzed by enrichment and mediation approaches. Exposure to bisphenol AF and AP was positively associated with higher systolic blood pressure z-scores (β = 0.075 and 0.144, both P < 0.001) and with increased risk of elevated and high blood pressure (OR = 1.218 and 1.364, P < 0.001 and = 0.002; OR = 1.281 and 1.539, both P < 0.001). Children with concurrently higher bisphenol AF or AP exposure and TyG exhibited lipid dysregulation, which was associated with increased childhood blood pressure. Dysregulated lipids were predominantly enriched in lysoglycerophospholipids and lipid-mediated signaling pathways. Specific lipids, including two glycerolipids and five glycerophospholipids, potentially mediated the association between bisphenol AF/AP × LIR and blood pressure, with indirect effects ranging from 0.114 to 0.626. In conclusion, bisphenol AP and AF were significantly associated with elevated childhood blood pressure. LIR amplified these adverse effects, partly through lipidomic perturbations, highlighting glycerophospholipid and glycerolipid metabolism as potential pathways underlying this association.
{"title":"Synergistic effects of bisphenol A and its substitutes with latent insulin resistance on childhood blood pressure and the potential role of lipid metabolism","authors":"Yi Zhang , Li Chen , Xinli Song , Ruolin Wang , Jianuo Jiang , Jieyu Liu , Zhiying Song , Jinghong Liang , Yinghua Ma , Jun Ma , Junqing Xie , Yi Song , Yanhui Dong","doi":"10.1016/j.envint.2025.109951","DOIUrl":"10.1016/j.envint.2025.109951","url":null,"abstract":"<div><div>Childhood hypertension is a growing public health concern, predisposing affected individuals to long-term cardiovascular complications. The cardiovascular and metabolic effects of exposure to bisphenol A (BPA) substitutes, emerging endocrine-disrupting chemicals, remain poorly understood in children. This study investigated associations between childhood BPA substitutes exposure and blood pressure, focusing on the modifying role of latent insulin resistance (LIR) and potential lipid metabolic pathways. A total of 747 children from a prospective cohort in Xiamen, China, were included. Associations between repeated bisphenol measurements and blood pressure were assessed using mixed-effects models and generalized estimating equations. A random subsample underwent lipidomic profiling; participants were grouped by bisphenol exposure and triglyceride-glucose (TyG) index. Differentially expressed lipids were identified, tested for associations with blood pressure, and analyzed by enrichment and mediation approaches. Exposure to bisphenol AF and AP was positively associated with higher systolic blood pressure z-scores (<em>β</em> = 0.075 and 0.144, both P < 0.001) and with increased risk of elevated and high blood pressure (<em>OR</em> = 1.218 and 1.364, <em>P</em> < 0.001 and = 0.002; <em>OR</em> = 1.281 and 1.539, both <em>P</em> < 0.001). Children with concurrently higher bisphenol AF or AP exposure and TyG exhibited lipid dysregulation, which was associated with increased childhood blood pressure. Dysregulated lipids were predominantly enriched in lysoglycerophospholipids and lipid-mediated signaling pathways. Specific lipids, including two glycerolipids and five glycerophospholipids, potentially mediated the association between bisphenol AF/AP × LIR and blood pressure, with indirect effects ranging from 0.114 to 0.626. In conclusion, bisphenol AP and AF were significantly associated with elevated childhood blood pressure. LIR amplified these adverse effects, partly through lipidomic perturbations, highlighting glycerophospholipid and glycerolipid metabolism as potential pathways underlying this association.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"206 ","pages":"Article 109951"},"PeriodicalIF":9.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145575307","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 : 2025-12-01DOI: 10.1016/j.envint.2025.109960
Yibo Jia, Rouyi Wang, Yumin Zhu, Lingyan Zhu
The binding affinity with human liver-fatty acid binding protein (Kd FABP) is a key parameter to characterize the accumulation potential of per- and polyfluoroalkyl substances (PFAS) in animal liver. However, the vast number of PFAS, combined with the limited available commercial standards, makes it a major challenge to measure their Kd FABP. In this study, the Kd FABP of 44 PFAS standards, and 72 PFAS extracted and semi-quantified in environmental samples by suspect screening analysis were measured using ultrafiltration methods. Several machine learning regression algorithms were developed to predict the Kd FABP, and extreme gradient boosting regression exhibited the best performance. Of note, intrinsic molecular descriptors, such as AATS0d, AATS8pe, VR1_A, ATSC1d, and AATSC2Z were found to be the primary factors to affect the binding affinities. The optimized model was then applied to predict the Kd FABP values of 9117 PFAS listed by U.S. EPA. DTXSID40896722, which features perfluorinated branches connected through sulfonyl linkages, exhibits the lowest Kd FABP value. Additionally, by combining the predicted Kd FABP of 76,216 artificial-intelligence-generated PFAS, it was found that chemical fragments containing carbon–fluorine and ether moieties are conducive for the binding. This study holds significant importance in de novo design of environmentally friendly PFAS.
{"title":"High-throughput prediction of PFAS binding affinities with human liver-fatty acid binding protein using machine learning and QSAR model","authors":"Yibo Jia, Rouyi Wang, Yumin Zhu, Lingyan Zhu","doi":"10.1016/j.envint.2025.109960","DOIUrl":"10.1016/j.envint.2025.109960","url":null,"abstract":"<div><div>The binding affinity with human liver-fatty acid binding protein (<em>K</em><sub>d FABP</sub>) is a key parameter to characterize the accumulation potential of per- and polyfluoroalkyl substances (PFAS) in animal liver. However, the vast number of PFAS, combined with the limited available commercial standards, makes it a major challenge to measure their <em>K</em><sub>d FABP</sub>. In this study, the <em>K</em><sub>d FABP</sub> of 44 PFAS standards, and 72 PFAS extracted and semi-quantified in environmental samples by suspect screening analysis were measured using ultrafiltration methods. Several machine learning regression algorithms were developed to predict the <em>K</em><sub>d FABP</sub>, and extreme gradient boosting regression exhibited the best performance. Of note, intrinsic molecular descriptors, such as AATS0d, AATS8pe, VR1_A, ATSC1d, and AATSC2Z were found to be the primary factors to affect the binding affinities. The optimized model was then applied to predict the <em>K</em><sub>d FABP</sub> values of 9117 PFAS listed by U.S. EPA. DTXSID40896722, which features perfluorinated branches connected through sulfonyl linkages, exhibits the lowest <em>K</em><sub>d FABP</sub> value. Additionally, by combining the predicted <em>K</em><sub>d FABP</sub> of 76,216 artificial-intelligence-generated PFAS, it was found that chemical fragments containing carbon–fluorine and ether moieties are conducive for the binding. This study holds significant importance in <em>de novo</em> design of environmentally friendly PFAS.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"206 ","pages":"Article 109960"},"PeriodicalIF":9.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145593321","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 : 2025-12-01DOI: 10.1016/j.envint.2025.109930
Yaerim Kim , Inae Lee , Jeonghwan Lee , Gowoon Lee , Jin Hyuk Paek , Seungyeup Han , Younglim Kho , Chun Soo Lim , Kyungho Choi , Jung Pyo Lee
Background
Per- and polyfluoroalkyl substances (PFAS) are persistent environmental pollutants increasingly linked to hypertension. However, the modifying effects of kidney function and metabolic health remain unclear. This study examined the associations between serum PFAS concentrations and hypertension, with a particular focus on kidney function and metabolic status as potential effect modifiers.
Methods
Data were obtained from the Korean National Environmental Health Survey (KoNEHS, 2018–2020), which included adults aged 19 years or older with available serum PFAS, blood pressure, and kidney function data. Adjusted odds ratios for hypertension were estimated using multivariable logistic regression across PFAS quartiles, with stratified analyses by kidney function and metabolic status.
Results
Among 2,993 participants, elevated levels of perfluorooctanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDeA), and total PFAS were associated with higher hypertension risk. Associations were more evident in individuals in the higher eGFR group, whereas effect estimates were attenuated in those with lower eGFR. In quartile-based analyses, positive exposure–response trends were observed for most PFAS, supporting the consistency of associations across exposure levels. Associations were stronger in participants with favorable metabolic profiles (e.g., without central obesity, normal triglycerides, high high-density lipoprotein cholesterol, normoglycemia) but attenuated in those with metabolic abnormalities.
Conclusions
PFAS exposure is associated with an increased risk of hypertension, particularly among those in the higher eGFR range and favorable metabolic profiles. These findings highlight the need to consider related disease phenotypes when assessing PFAS-associated cardiovascular toxicity and emphasize the importance of exposure mitigation in the healthy general population.
{"title":"Differential impact of per- and polyfluoroalkyl substances exposure on hypertension risk by kidney function and metabolic status","authors":"Yaerim Kim , Inae Lee , Jeonghwan Lee , Gowoon Lee , Jin Hyuk Paek , Seungyeup Han , Younglim Kho , Chun Soo Lim , Kyungho Choi , Jung Pyo Lee","doi":"10.1016/j.envint.2025.109930","DOIUrl":"10.1016/j.envint.2025.109930","url":null,"abstract":"<div><h3>Background</h3><div>Per- and polyfluoroalkyl substances (PFAS) are persistent environmental pollutants increasingly linked to hypertension. However, the modifying effects of kidney function and metabolic health remain unclear. This study examined the associations between serum PFAS concentrations and hypertension, with a particular focus on kidney function and metabolic status as potential effect modifiers.</div></div><div><h3>Methods</h3><div>Data were obtained from the Korean National Environmental Health Survey (KoNEHS, 2018–2020), which included adults aged 19 years or older with available serum PFAS, blood pressure, and kidney function data. Adjusted odds ratios for hypertension were estimated using multivariable logistic regression across PFAS quartiles, with stratified analyses by kidney function and metabolic status.</div></div><div><h3>Results</h3><div>Among 2,993 participants, elevated levels of perfluorooctanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDeA), and total PFAS were associated with higher hypertension risk. Associations were more evident in individuals in the higher eGFR group, whereas effect estimates were attenuated in those with lower eGFR. In quartile-based analyses, positive exposure–response trends were observed for most PFAS, supporting the consistency of associations across exposure levels. Associations were stronger in participants with favorable metabolic profiles (e.g., without central obesity, normal triglycerides, high high-density lipoprotein cholesterol, normoglycemia) but attenuated in those with metabolic abnormalities.</div></div><div><h3>Conclusions</h3><div>PFAS exposure is associated with an increased risk of hypertension, particularly among those in the higher eGFR range and favorable metabolic profiles. These findings highlight the need to consider related disease phenotypes when assessing PFAS-associated cardiovascular toxicity and emphasize the importance of exposure mitigation in the healthy general population.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"206 ","pages":"Article 109930"},"PeriodicalIF":9.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145593901","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 : 2025-12-01DOI: 10.1016/j.envint.2025.109969
Yimeng He, Hefa Cheng, Shu Tao
Animal manures and organic fertilizers often contain elevated residues of transition metals (e.g., Cu and Zn) and antibiotics, and their complexation complicates the phytotoxicity evaluation and risk attribution in agricultural ecosystems. This study systematically elucidated the toxicity and detoxification mechanisms of copper-ciprofloxacin complexes (CuCIP2+, CuCIP2+, and CuCIP22+) in lettuce (Lactuca sativa L.). Exposure to copper-ciprofloxacin complexes caused significant reduction in plant growth and physiological parameters, including chlorophyll content, antioxidant enzyme activity, and membrane integrity, with CuCIP2+ exhibited the highest acute toxicity. Integrated transcriptomic and metabolomic analyses reveal that these complexes could induce systemic oxidative stress, activate the stress responsive signaling pathways, and trigger coordinated metabolic reprogramming associated with antioxidant defense and energy compensation. These responses result from a reactive oxygen species (ROS)-centered metabolic feedback loop that includes lipid peroxidation signaling, flavonoid-mediated antioxidant defense, and glycolysis-driven energy compensation. The distinct physiological and molecular responses induced by copper-ciprofloxacin complexes, in contrast to those of free Cu(II) and CIP, are indicative of their involvement in disrupting plant’s redox homeostasis and stress-related signaling pathways. These findings demonstrate that the complexes of transition metals and antibiotics could induce distinct toxicological effects and indicate the need for considering their interaction in ecological risk evaluation.
{"title":"Molecular mechanisms of toxicity and detoxification of copper-ciprofloxacin complexes in lettuce (Lactuca sativa L.)","authors":"Yimeng He, Hefa Cheng, Shu Tao","doi":"10.1016/j.envint.2025.109969","DOIUrl":"10.1016/j.envint.2025.109969","url":null,"abstract":"<div><div>Animal manures and organic fertilizers often contain elevated residues of transition metals (e.g., Cu and Zn) and antibiotics, and their complexation complicates the phytotoxicity evaluation and risk attribution in agricultural ecosystems. This study systematically elucidated the toxicity and detoxification mechanisms of copper-ciprofloxacin complexes (CuCIP<sup>2+</sup>, CuCIP<sub>2</sub><sup>+</sup>, and CuCIP<sub>2</sub><sup>2+</sup>) in lettuce (<em>Lactuca sativa</em> L.). Exposure to copper-ciprofloxacin complexes caused significant reduction in plant growth and physiological parameters, including chlorophyll content, antioxidant enzyme activity, and membrane integrity, with CuCIP<sup>2+</sup> exhibited the highest acute toxicity. Integrated transcriptomic and metabolomic analyses reveal that these complexes could induce systemic oxidative stress, activate the stress responsive signaling pathways, and trigger coordinated metabolic reprogramming associated with antioxidant defense and energy compensation. These responses result from a reactive oxygen species (ROS)-centered metabolic feedback loop that includes lipid peroxidation signaling, flavonoid-mediated antioxidant defense, and glycolysis-driven energy compensation. The distinct physiological and molecular responses induced by copper-ciprofloxacin complexes, in contrast to those of free Cu(II) and CIP, are indicative of their involvement in disrupting plant’s redox homeostasis and stress-related signaling pathways. These findings demonstrate that the complexes of transition metals and antibiotics could induce distinct toxicological effects and indicate the need for considering their interaction in ecological risk evaluation.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"207 ","pages":"Article 109969"},"PeriodicalIF":9.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145657768","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 : 2025-12-01DOI: 10.1016/j.envint.2025.109968
Ce Wang , Yi Qi , Guangcan Zhu , Yi Yang , Jianfeng Xie , Haibo Qiu
Extensive epidemiological evidence has evaluated the effect of a single climate-induced environmental stressor on cause-specific mortality. However, this exposure pattern often fails to reflect the real-world context of simultaneous exposure to multiple stressors. The conventional additive models face several methodological limitations—high susceptibility to multicollinearity, low predictive accuracy, and a lack of straightforward interpretability of risk estimation—which challenge comprehensive health risk assessment. We establish a Sequence-to-Sequence architecture combined with local feature attribution method to investigate the effect of ambient temperature on the association between coexisting meteorological factors and air pollutants and mortality for Jiangsu Province, China from 2014 through 2019. The model usually generated satisfactory performance in capturing the temporal trajectory of deaths of non-accidental causes (NAC), cardio-cerebrovascular diseases (CD), and respiratory diseases (RD) with extreme outcomes. Quantitative insights in temperature-related excess deaths at given temperature benefited from optimal local explanations. E.g., annually, an average of 20 300, 12 661, 2 511 excess deaths of NAC, CD, and RD, respectively, were associated with non-optimal temperatures over the entire study period; corresponding statistics of 1 192, 806, and 98 were attributable to extreme low temperatures, and those of 3 604, 2 238 and 480 were attributable to temperature drops. The magnitude and pattern of interaction effects even from the same pairwise features might differ by cause-specific mortality in each city. Our findings highlight the significance of simultaneous exposure in tailored public health policies. The methodology would have good performance with data availability in risk assessments at national and global scale.
{"title":"A new perspective of simultaneous exposure of risk factors to explore the role of ambient temperature associated with mortality","authors":"Ce Wang , Yi Qi , Guangcan Zhu , Yi Yang , Jianfeng Xie , Haibo Qiu","doi":"10.1016/j.envint.2025.109968","DOIUrl":"10.1016/j.envint.2025.109968","url":null,"abstract":"<div><div>Extensive epidemiological evidence has evaluated the effect of a single climate-induced environmental stressor on cause-specific mortality. However, this exposure pattern often fails to reflect the real-world context of simultaneous exposure to multiple stressors. The conventional additive models face several methodological limitations—high susceptibility to multicollinearity, low predictive accuracy, and a lack of straightforward interpretability of risk estimation—which challenge comprehensive health risk assessment. We establish a Sequence-to-Sequence architecture combined with local feature attribution method to investigate the effect of ambient temperature on the association between coexisting meteorological factors and air pollutants and mortality for Jiangsu Province, China from 2014 through 2019. The model usually generated satisfactory performance in capturing the temporal trajectory of deaths of non-accidental causes (NAC), cardio-cerebrovascular diseases (CD), and respiratory diseases (RD) with extreme outcomes. Quantitative insights in temperature-related excess deaths at given temperature benefited from optimal local explanations. E.g., annually, an average of 20 300, 12 661, 2 511 excess deaths of NAC, CD, and RD, respectively, were associated with non-optimal temperatures over the entire study period; corresponding statistics of 1 192, 806, and 98 were attributable to extreme low temperatures, and those of 3 604, 2 238 and 480 were attributable to temperature drops. The magnitude and pattern of interaction effects even from the same pairwise features might differ by cause-specific mortality in each city. Our findings highlight the significance of simultaneous exposure in tailored public health policies. The methodology would have good performance with data availability in risk assessments at national and global scale.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"206 ","pages":"Article 109968"},"PeriodicalIF":9.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145619379","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 : 2025-12-01DOI: 10.1016/j.envint.2025.109924
Paulien Cleys , Lucas Panneel , Philippe G. Jorens , Antonius Mulder , Adrian Covaci
Plasticizers are chemicals added to plastic polymers, such as polyvinyl chloride, to enhance their flexibility and durability. Di-(2-ethylhexyl) phthalate (DEHP) was the most used plasticizer due to its low cost and enhanced physical stability. However, adverse health effects have been attributed to phthalates and their metabolites. As a result, alternative plasticizers such as tri-(2-ethylhexyl) trimellitate (TOTM), have been developed to replace DEHP, mainly based on physicochemical properties and toxicity studies. In this study, the exposure to TOTM in the Neonatal Intensive Care Unit (NICU) was studied by analysing 8 TOTM urinary metabolites in 190 urine samples from 83 NICU patients and 8 term maternity ward patients. Overall, TOTM metabolites had a higher detection frequency and median concentration in NICU neonates compared to term patients confirming the exposure to TOTM leaching from medical devices. Highest concentrations were found for 5Cx-1-MEPTM, 5OH-2-MEHTM and 2-MEHTM for NICU patients receiving parenteral nutrition and respiratory support, reaching maximum concentrations of 1055 ng/mL, 285 ng/mL and 2931 ng/mL, respectively. These findings are even more remarkable considering the low leaching potential of TOTM from plastic medical devices and the low urinary excretion factors of TOTM metabolites obtained from pharmacokinetic studies. The estimated daily intake for thirteen premature patients exceeded the adult-based DNEL proposed by ECHA, indicating potential TOTM exposure above safe levels for this fragile NICU population, with possible negative health effects that are still insufficiently studied. Since this reference value does not account for the reduced metabolic and renal capacities of premature neonates, the actual risk for these patients may be underestimated.
{"title":"Biomonitoring tri-(2-ethylhexyl) trimellitate (TOTM) exposure in the Neonatal Intensive Care Unit: Investigating potential sources and exposure levels","authors":"Paulien Cleys , Lucas Panneel , Philippe G. Jorens , Antonius Mulder , Adrian Covaci","doi":"10.1016/j.envint.2025.109924","DOIUrl":"10.1016/j.envint.2025.109924","url":null,"abstract":"<div><div>Plasticizers are chemicals added to plastic polymers, such as polyvinyl chloride, to enhance their flexibility and durability. Di-(2-ethylhexyl) phthalate (DEHP) was the most used plasticizer due to its low cost and enhanced physical stability. However, adverse health effects have been attributed to phthalates and their metabolites. As a result, alternative plasticizers such as tri-(2-ethylhexyl) trimellitate (TOTM), have been developed to replace DEHP, mainly based on physicochemical properties and toxicity studies. In this study, the exposure to TOTM in the Neonatal Intensive Care Unit (NICU) was studied by analysing 8 TOTM urinary metabolites in 190 urine samples from 83 NICU patients and 8 term maternity ward patients. Overall, TOTM metabolites had a higher detection frequency and median concentration in NICU neonates compared to term patients confirming the exposure to TOTM leaching from medical devices. Highest concentrations were found for 5Cx-1-MEPTM, 5OH-2-MEHTM and 2-MEHTM for NICU patients receiving parenteral nutrition and respiratory support, reaching maximum concentrations of 1055 ng/mL, 285 ng/mL and 2931 ng/mL, respectively. These findings are even more remarkable considering the low leaching potential of TOTM from plastic medical devices and the low urinary excretion factors of TOTM metabolites obtained from pharmacokinetic studies. The estimated daily intake for thirteen premature patients exceeded the adult-based DNEL proposed by ECHA, indicating potential TOTM exposure above safe levels for this fragile NICU population, with possible negative health effects that are still insufficiently studied. Since this reference value does not account for the reduced metabolic and renal capacities of premature neonates, the actual risk for these patients may be underestimated.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"206 ","pages":"Article 109924"},"PeriodicalIF":9.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145593389","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 : 2025-12-01DOI: 10.1016/j.envint.2025.109955
Noémie Letellier , Caitlin G. Jones-Ngo , Michael W. Cheung , Rosana Aguilera , Joan A. Casey , Jennifer Monroe Zakaras , Rebecca Sugrue , Arianne Teherani , Neeta Thakur , Harold Collard , Sheri D. Weiser , Tarik Benmarhnia
Background
As the health burden attributable to wildfire activity increases under climate change, it is crucial to determine which subgroups face heightened vulnerability to wildfire smoke. Marginalized communities may experience disproportionate risk from overlapping individual and community vulnerability factors. We leverage recent developments in machine learning methods for high-dimensional settings to construct detailed profiles of California communities disproportionately impacted by wildfire smoke across 27 potential effect modifiers.
Methods
We used daily 2006–2019 data on hospital admissions and emergency department (ED) visits for cardio-respiratory diseases in California. We applied a time-stratified case-crossover study design to analyze the effect of wildfire-specific fine particulate matter (PM2.5) on cardio-respiratory diseases. Then, we investigated heterogeneous effects using a generalized random forest approach, which can handle a large set of individual-level (age, sex, race/ethnicity) and area-level (e.g., poverty level, racial/ethnic segregation) factors to construct vulnerability profiles for each Air Basin, representing areas with similar meteorological and geographic conditions.
Results
A 10 µg/m3 increase in wildfire PM2.5 concentration (2-day moving average) was associated with an increased risk of hospital admissions and ED visits related to respiratory diseases (OR = 1.014, 95 % confidence interval = 1.012–1.016). No association was found for cardiovascular diseases. Associations between exposure to wildfire PM2.5 and respiratory diseases varied strongly by individual- (age, sex, race/ethnicity) and area-level factors (such as A/C prevalence, Black/White dissimilarity index). The importance of these effect modifiers, and vulnerability profiles, changed across Air Basins.
Conclusions
Machine learning can characterize the complex heterogeneity in wildfire smoke-related health impacts.
{"title":"Using generalized random forests to characterize vulnerability to adverse health outcomes following wildfire smoke exposure in California","authors":"Noémie Letellier , Caitlin G. Jones-Ngo , Michael W. Cheung , Rosana Aguilera , Joan A. Casey , Jennifer Monroe Zakaras , Rebecca Sugrue , Arianne Teherani , Neeta Thakur , Harold Collard , Sheri D. Weiser , Tarik Benmarhnia","doi":"10.1016/j.envint.2025.109955","DOIUrl":"10.1016/j.envint.2025.109955","url":null,"abstract":"<div><h3>Background</h3><div>As the health burden attributable to wildfire activity increases under climate change, it is crucial to determine which subgroups face heightened vulnerability to wildfire smoke. Marginalized communities may experience disproportionate risk from overlapping individual and community vulnerability factors. We leverage recent developments in machine learning methods for high-dimensional settings to construct detailed profiles of California communities disproportionately impacted by wildfire smoke across 27 potential effect modifiers.</div></div><div><h3>Methods</h3><div>We used daily 2006–2019 data on hospital admissions and emergency department (ED) visits for cardio-respiratory diseases in California. We applied a time-stratified case-crossover study design to analyze the effect of wildfire-specific fine particulate matter (PM<sub>2.5</sub>) on cardio-respiratory diseases. Then, we investigated heterogeneous effects using a generalized random forest approach, which can handle a large set of individual-level (age, sex, race/ethnicity) and area-level (e.g., poverty level, racial/ethnic segregation) factors to construct vulnerability profiles for each Air Basin, representing areas with similar meteorological and geographic conditions.</div></div><div><h3>Results</h3><div>A 10 µg/m<sup>3</sup> increase in wildfire PM<sub>2.5</sub> concentration (2-day moving average) was associated with an increased risk of hospital admissions and ED visits related to respiratory diseases (OR = 1.014, 95 % confidence interval = 1.012–1.016). No association was found for cardiovascular diseases. Associations between exposure to wildfire PM<sub>2.5</sub> and respiratory diseases varied strongly by individual- (age, sex, race/ethnicity) and area-level factors (such as A/C prevalence, Black/White dissimilarity index). The importance of these effect modifiers, and vulnerability profiles, changed across Air Basins.</div></div><div><h3>Conclusions</h3><div>Machine learning can characterize the complex heterogeneity in wildfire smoke-related health impacts.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"206 ","pages":"Article 109955"},"PeriodicalIF":9.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145567594","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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