Pub Date : 2026-01-16DOI: 10.1016/j.envint.2026.110067
Xuan Chen , Gerard Hoek , Paul Frijters , Georgia M.C. Dyer , Stefan Gössling , Sasha Khomenko , Haneen Khreis , Eline Kolb , Natalie Mueller , Brigit Staatsen , Rafael Costa Simões De Vasconcelos , Daniel Saldanha Resendes , Elise van Kempen , Mathew P. White , Roel Vermeulen , Mark Nieuwenhuijsen , Ulrike Gehring
Introduction
Environmental Health Impact Assessments (HIAs) can inform decisions about the health effects of policy-related changes in environmental exposures. Conventional health impact metrics, focusing on mortality, morbidity, and disability, neglect subjective well-being. We explored the need and feasibility of integrating well-being indicators such as happiness and life satisfaction into quantitative environmental HIAs.
Methods
Building on a multidisciplinary expert workshop and existing literature, we addressed (1) definitions and indicators of well-being, (2) pathways linking environmental exposures (air pollution, noise, extreme temperatures, and green space) to well-being, and (3) the strength of epidemiological evidence for these associations. We evaluated the challenges of integrating well-being indicators into environmental HIAs, and provided an exploratory example.
Results
We argue that including well-being in HIAs offers a more comprehensive view of health, aligning with policy goals focused on enhancing citizen’s well-being. The literature identifies plausible pathways linking exposures to well-being, whilst epidemiological evidence for associations between environmental exposures and well-being is limited, but suggestive. We propose conducting exploratory HIAs integrating well-being, especially for green space (n = 16 epidemiological studies) and air pollution (n = 18). We outline two practical integration strategies: (1) report well-being impacts separately as Well-being-Adjusted Life Years, and (2) incorporate well-being into existing health indicators such as Quality-Adjusted Life Years or Disability-Adjusted Life Years.
Conclusions
Inclusion of well-being into quantitative environmental HIAs presents a more comprehensive representation of health and well-being beyond indicators focusing on morbidity and mortality. However, the epidemiological evidence base regarding environmental exposures and well-being warrants further expansion.
{"title":"Toward integrating subjective well-being in environmental health impact assessments for healthy urban living: a conceptual and methodological exploration","authors":"Xuan Chen , Gerard Hoek , Paul Frijters , Georgia M.C. Dyer , Stefan Gössling , Sasha Khomenko , Haneen Khreis , Eline Kolb , Natalie Mueller , Brigit Staatsen , Rafael Costa Simões De Vasconcelos , Daniel Saldanha Resendes , Elise van Kempen , Mathew P. White , Roel Vermeulen , Mark Nieuwenhuijsen , Ulrike Gehring","doi":"10.1016/j.envint.2026.110067","DOIUrl":"10.1016/j.envint.2026.110067","url":null,"abstract":"<div><h3>Introduction</h3><div>Environmental Health Impact Assessments (HIAs) can inform decisions about the health effects of policy-related changes in environmental exposures. Conventional health impact metrics, focusing on mortality, morbidity, and disability, neglect subjective well-being. We explored the need and feasibility of integrating well-being indicators such as happiness and life satisfaction into quantitative environmental HIAs.</div></div><div><h3>Methods</h3><div>Building on a multidisciplinary expert workshop and existing literature, we addressed (1) definitions and indicators of well-being, (2) pathways linking environmental exposures (air pollution, noise, extreme temperatures, and green space) to well-being, and (3) the strength of epidemiological evidence for these associations. We evaluated the challenges of integrating well-being indicators into environmental HIAs, and provided an exploratory example.</div></div><div><h3>Results</h3><div>We argue that including well-being in HIAs offers a more comprehensive view of health, aligning with policy goals focused on enhancing citizen’s well-being. The literature identifies plausible pathways linking exposures to well-being, whilst epidemiological evidence for associations between environmental exposures and well-being is limited, but suggestive. We propose conducting exploratory HIAs integrating well-being, especially for green space (n = 16 epidemiological studies) and air pollution (n = 18). We outline two practical integration strategies: (1) report well-being impacts separately as Well-being-Adjusted Life Years, and (2) incorporate well-being into existing health indicators such as Quality-Adjusted Life Years or Disability-Adjusted Life Years.</div></div><div><h3>Conclusions</h3><div>Inclusion of well-being into quantitative environmental HIAs presents a more comprehensive representation of health and well-being beyond indicators focusing on morbidity and mortality. However, the epidemiological evidence base regarding environmental exposures and well-being warrants further expansion.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110067"},"PeriodicalIF":9.7,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145995541","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 : 2026-01-16DOI: 10.1016/j.envint.2026.110079
Melissa Fiffer , Mercedes A. Bravo , Dominique Zephyr , Joshua L. Tootoo , Charlotte Roscoe , Grete Wilt , Rafiga Gasymova , Peter James , Marie Lynn Miranda
Introduction
Studies show that prenatal neighborhood greenness is positively associated with birthweight. However, few go beyond a pregnancy-long greenness average or consider air pollution co-exposures. We used time-varying greenness and air pollution estimates to explore sensitive windows and subpopulations.
Methods
We examined Michigan (U.S.) birth records between 2007 and 2016 (n = 798,071). We derived the Normalized Difference Vegetation Index (NDVI) from Landsat images (30 m2 resolution) to estimate greenness within 270 m and 1230 m radial buffers around each mother’s address, to represent greenness immediately surrounding addresses and within a short walk, respectively, in the three seasons before birth. We joined estimated weekly 1 km2 gridded PM2.5, NO2, and O3 concentrations, and fit distributed lag models to assess trimester-specific greenness, weekly air pollution, and birthweight, adjusting for temperature, seasonality, maternal factors, and gestational age. We examined whether the NDVI-birthweight association varied by socioeconomic status, and whether the air pollution-birthweight association varied by NDVI tertile.
Results
In adjusted models, an IQR (0.2 unit) increase in NDVI within a 270 m buffer was associated with a 12.3 g (95% CI: 9.7 g, 15.0 g) higher birthweight. Positive associations were observed in all trimesters, and across all maternal education and neighborhood median household income levels. PM2.5-birthweight associations (IQR = 5 μg/m3) were largest in the lowest NDVI tertile (PM2.5: −21.3 g, 95% CI: −31.1 g, −11.5 g).
Conclusions
Birthweight is positively associated with residential greenness in all trimesters after co-adjusting for air pollutants. Addresses surrounded by the least greenness had the strongest inverse PM2.5-birthweight association. Nature-based solutions may attenuate air pollution’s negative impacts.
{"title":"Prenatal greenness, air pollution, and birthweight: Assessing sensitive windows of exposure and sub-populations in a multi-exposure setting","authors":"Melissa Fiffer , Mercedes A. Bravo , Dominique Zephyr , Joshua L. Tootoo , Charlotte Roscoe , Grete Wilt , Rafiga Gasymova , Peter James , Marie Lynn Miranda","doi":"10.1016/j.envint.2026.110079","DOIUrl":"10.1016/j.envint.2026.110079","url":null,"abstract":"<div><h3>Introduction</h3><div>Studies show that prenatal neighborhood greenness is positively associated with birthweight. However, few go beyond a pregnancy-long greenness average or consider air pollution co-exposures. We used time-varying greenness and air pollution estimates to explore sensitive windows and subpopulations.</div></div><div><h3>Methods</h3><div>We examined Michigan (U.S.) birth records between 2007 and 2016 (n = 798,071). We derived the Normalized Difference Vegetation Index (NDVI) from Landsat images (30 m<sup>2</sup> resolution) to estimate greenness within 270 m and 1230 m radial buffers around each mother’s address, to represent greenness immediately surrounding addresses and within a short walk, respectively, in the three seasons before birth. We joined estimated weekly 1 km<sup>2</sup> gridded PM<sub>2.5</sub>, NO<sub>2</sub>, and O<sub>3</sub> concentrations, and fit distributed lag models to assess trimester-specific greenness, weekly air pollution, and birthweight, adjusting for temperature, seasonality, maternal factors, and gestational age. We examined whether the NDVI-birthweight association varied by socioeconomic status, and whether the air pollution-birthweight association varied by NDVI tertile.</div></div><div><h3>Results</h3><div>In adjusted models, an IQR (0.2 unit) increase in NDVI within a 270 m buffer was associated with a 12.3 g (95% CI: 9.7 g, 15.0 g) higher birthweight. Positive associations were observed in all trimesters, and across all maternal education and neighborhood median household income levels. PM<sub>2.5</sub>-birthweight associations (IQR = 5 μg/m<sup>3</sup>) were largest in the lowest NDVI tertile (PM<sub>2.5</sub>: −21.3 g, 95% CI: −31.1 g, −11.5 g).</div></div><div><h3>Conclusions</h3><div>Birthweight is positively associated with residential greenness in all trimesters after co-adjusting for air pollutants. Addresses surrounded by the least greenness had the strongest inverse PM<sub>2.5</sub>-birthweight association. Nature-based solutions may attenuate air pollution’s negative impacts.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110079"},"PeriodicalIF":9.7,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145995534","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 : 2026-01-16DOI: 10.1016/j.envint.2026.110070
Benjamin Sachse , Sebastian Schmeisser , Jan van Benthem , Raffaella Corvi , Eugenia Dogliotti , Norman Ertych , Roland Frötschl , Ulrike Gündel , Kristin Herrmann , George Johnson , Carsten Kneuer , Jeannette König , Hans-Jörg Martus , Stefan Pfuhler , Stephanie Smith-Roe , Helga Stopper , Paul White , Tanja Schwerdtle , Andreas Hensel , Tewes Tralau
Genotoxicity plays an important role in chemical safety assessment, as genetic alterations can lead to severe and irreversible health consequences. To date, the assessment of genotoxicity has mostly been limited to hazard identification, followed by rigorous risk mitigation measures if a substance is found to be mutagenic, regardless of potency, the underlying mechanism, and cellular biology. While this regulatory hazard-based approach is straightforward, it is unsatisfactory when exposure to genotoxic substances cannot be completely avoided and/or regulatory measures lead to misperceptions of risk and undesirable socioeconomic side effects. The latter becomes particularly obvious in light of natural genotoxicants, e.g. occurring in plant-based food, and for substances that are difficult to replace but come with a high socioeconomic value but little potency and exposure. Hence, there is an increasing demand for a paradigm shift towards a quantitative interpretation of genotoxicity data in regulatory risk assessment. However, moving away from the traditional hazard-based assessment and doing so safely requires a collective effort of all relevant stakeholders. To this end, the German Federal Institute for Risk Assessment (BfR) organised an international symposium, at which experts from regulatory authorities, academia and industry discussed the opportunities and challenges involved. Here, we present key issues to be considered for a successful implementation of quantitative approaches. In situations where exposure to genotoxic substances cannot be completely avoided, e.g. occurrence of contaminants, quantitative approaches offer the opportunity to better characterise the associated risks and thus enable risk managers to make more informed decisions.
{"title":"Quantitative evaluation of genotoxicity data for risk assessment and regulatory decision-making: Time for a paradigm shift","authors":"Benjamin Sachse , Sebastian Schmeisser , Jan van Benthem , Raffaella Corvi , Eugenia Dogliotti , Norman Ertych , Roland Frötschl , Ulrike Gündel , Kristin Herrmann , George Johnson , Carsten Kneuer , Jeannette König , Hans-Jörg Martus , Stefan Pfuhler , Stephanie Smith-Roe , Helga Stopper , Paul White , Tanja Schwerdtle , Andreas Hensel , Tewes Tralau","doi":"10.1016/j.envint.2026.110070","DOIUrl":"10.1016/j.envint.2026.110070","url":null,"abstract":"<div><div>Genotoxicity plays an important role in chemical safety assessment, as genetic alterations can lead to severe and irreversible health consequences. To date, the assessment of genotoxicity has mostly been limited to hazard identification, followed by rigorous risk mitigation measures if a substance is found to be mutagenic, regardless of potency, the underlying mechanism, and cellular biology. While this regulatory hazard-based approach is straightforward, it is unsatisfactory when exposure to genotoxic substances cannot be completely avoided and/or regulatory measures lead to misperceptions of risk and undesirable socioeconomic side effects. The latter becomes particularly obvious in light of natural genotoxicants, <em>e.g.</em> occurring in plant-based food, and for substances that are difficult to replace but come with a high socioeconomic value but little potency and exposure. Hence, there is an increasing demand for a paradigm shift towards a quantitative interpretation of genotoxicity data in regulatory risk assessment. However, moving away from the traditional hazard-based assessment and doing so safely requires a collective effort of all relevant stakeholders. To this end, the German Federal Institute for Risk Assessment (BfR) organised an international symposium, at which experts from regulatory authorities, academia and industry discussed the opportunities and challenges involved. Here, we present key issues to be considered for a successful implementation of quantitative approaches. In situations where exposure to genotoxic substances cannot be completely avoided, <em>e.g.</em> occurrence of contaminants, quantitative approaches offer the opportunity to better characterise the associated risks and thus enable risk managers to make more informed decisions.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110070"},"PeriodicalIF":9.7,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145993405","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 : 2026-01-16DOI: 10.1016/j.envint.2026.110071
Kara L. Fry, Xiaochi Liu, Maryam Moslehi, John Leeder, Mark Patrick Taylor, Jennifer Martin, Antti T. Mikkonen
{"title":"Chemicals in homes and gardens: understanding sources, exposure and risk","authors":"Kara L. Fry, Xiaochi Liu, Maryam Moslehi, John Leeder, Mark Patrick Taylor, Jennifer Martin, Antti T. Mikkonen","doi":"10.1016/j.envint.2026.110071","DOIUrl":"https://doi.org/10.1016/j.envint.2026.110071","url":null,"abstract":"","PeriodicalId":308,"journal":{"name":"Environment International","volume":"40 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145995535","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 : 2026-01-14DOI: 10.1016/j.envint.2026.110048
Jin Xu , Xiuhong Liu , Shiyong Zhang , Jiaxin Li , Qing Yang
Most pollutants in the environment exist in complex forms, and exploring the impact of a single pollutant lacks wide applicability. The co-exposure of microplastics (MPs) and NaClO in wastewater treatment plants (WWTPs) is a widespread occurrence. At present, relevant reports on the impact of individual NaClO or MPs on antibiotic resistance genes (ARGs) have been established. Herein, this study investigated the fate of antibiotic-resistant bacteria (ARB) and ARGs after exposure to MPs with or without NaClO stress. In this study, the total ARG abundance increased by 11.83% under MPs stress, and further increases by 17.89% under NaClO stress with MPs co-exposure. The mechanism was that the presence of NaClO promoted the selective enrichment of potential ARB and ARGs on the MPs-biofilm. The surface morphology of the MPs was changed and the attached biofilm became thicker, which provided a suitable environment for the proliferation of ARB and the spread of ARGs. Vertical gene transfer (VGT) and horizontal gene transfer (HGT) of ARGs were facilitated by MPs under NaClO stress. Specifically, the VGT of ARGs was facilitated via enhanced bacterial cell proliferation (by 132.66%), and relevant functional genes are also increased. HGT of ARGs is promoted by the increasing relative abundance of mobile genetic elements (MGEs). ARG-carrying plasmids are also demonstrated that MPs promoted HGT of ARGs in the presence of NaClO. The increase in oxidative stress, cell membrane permeability, and Type IV secretion system (T4SS) collaboration facilitated the HGT of ARGs. In summary, co-exposure to NaClO and MPs promote VGT and HGT of ARGs through the variation in MPs structure and the enhancement of MPs-biofilms. Furthermore, the presence of MPs restrained the disinfection effect of NaClO, with an inhibition rate higher than 50%.
{"title":"Sodium hypochlorite residual in the environment facilitated the spread of antibiotic resistance genes: through microplastics as a medium","authors":"Jin Xu , Xiuhong Liu , Shiyong Zhang , Jiaxin Li , Qing Yang","doi":"10.1016/j.envint.2026.110048","DOIUrl":"10.1016/j.envint.2026.110048","url":null,"abstract":"<div><div>Most pollutants in the environment exist in complex forms, and exploring the impact of a single pollutant lacks wide applicability. The co-exposure of microplastics (MPs) and NaClO in wastewater treatment plants (WWTPs) is a widespread occurrence. At present, relevant reports on the impact of individual NaClO or MPs on antibiotic resistance genes (ARGs) have been established. Herein, this study investigated the fate of antibiotic-resistant bacteria (ARB) and ARGs after exposure to MPs with or without NaClO stress. In this study, the total ARG abundance increased by 11.83% under MPs stress, and further increases by 17.89% under NaClO stress with MPs co-exposure. The mechanism was that the presence of NaClO promoted the selective enrichment of potential ARB and ARGs on the MPs-biofilm. The surface morphology of the MPs was changed and the attached biofilm became thicker, which provided a suitable environment for the proliferation of ARB and the spread of ARGs. Vertical gene transfer (VGT) and horizontal gene transfer (HGT) of ARGs were facilitated by MPs under NaClO stress. Specifically, the VGT of ARGs was facilitated via enhanced bacterial cell proliferation (by 132.66%), and relevant functional genes are also increased. HGT of ARGs is promoted by the increasing relative abundance of mobile genetic elements (MGEs). ARG-carrying plasmids are also demonstrated that MPs promoted HGT of ARGs in the presence of NaClO. The increase in oxidative stress, cell membrane permeability, and Type IV secretion system (T4SS) collaboration facilitated the HGT of ARGs. In summary, co-exposure to NaClO and MPs promote VGT and HGT of ARGs through the variation in MPs structure and the enhancement of MPs-biofilms. Furthermore, the presence of MPs restrained the disinfection effect of NaClO, with an inhibition rate higher than 50%.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110048"},"PeriodicalIF":9.7,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145993407","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}
Early-life exposure to phthalates, widely used in consumer products, may induce developmental lung adaptations and predispose to respiratory morbidity throughout childhood. We assessed the associations of fetal phthalate exposure with wheezing, asthma, and lung function from birth to adolescence.
Methods
We performed 1-stage individual participant data meta-analyses with data from six European birth cohorts (3,745 mother–child pairs) to assess associations of pregnancy-averaged maternal urinary concentrations of 7 phthalate metabolites and 3 phthalate groups (high- and low-molecular-weight phthalate metabolites and sum of di-2-ethylhexyl phthalate metabolites) with wheezing in infancy (0–1 years) and at preschool age (1–5 years), and asthma and lung function at school age (5–12 years).
Results
Higher maternal pregnancy urine phthalate concentrations were not associated with wheezing in infancy or preschool age. Higher maternal pregnancy urine mono-benzyl phthalate concentrations were associated with an increased risk of asthma at school age (odds ratio (95% confidence interval): 1.13 (1.01–1.26) per natural log interquartile range unit increase in concentration), but not with wheezing or lung function and attenuated into non-significance after multiple testing correction. Higher maternal pregnancy concentrations of mono-2-ethyl-5-hydroxyhexyl phthalate, mono-iso-butyl phthalate, mono-n-butyl phthalate and low-molecular-weight phthalate metabolites were associated with higher FEV1, FEV1/FVC and FEF75 z-scores after multiple testing correction.
Conclusion
Fetal exposure to higher phthalate concentrations is associated with lung function adaptations, while overall no consistent associations were observed with childhood wheezing or asthma. Future studies are needed to assess the causality of the observed associations, to identify the underlying mechanisms, and to assess potential respiratory consequences in adult life.
{"title":"Fetal phthalate exposure and asthma outcomes from infancy to adolescence: Individual participant data meta-analysis in the EU Child Cohort Network","authors":"Tarik Karramass , Liesbeth Duijts , Demetris Avraam , Sophia Blaauwendraad , Paula Carrasco , Nuria Güil-Oumrait , Amaia Irizar , Manik Kadawathagedara , Marianna Karachaliou , Maria-Jose Lopez-Espinosa , Antonis Myridakis , Elke Rouxel , Amrit Kaur Sakhi , Cathrine Thomsen , Chloe Vainqueur , Martine Vrijheid , Charline Warembourg , Marieke Welten , Carlos Zabaleta , Leonardo Trasande , Vincent Jaddoe","doi":"10.1016/j.envint.2026.110069","DOIUrl":"10.1016/j.envint.2026.110069","url":null,"abstract":"<div><h3>Objective</h3><div>Early-life exposure to phthalates, widely used in consumer products, may induce developmental lung adaptations and predispose to respiratory morbidity throughout childhood. We assessed the associations of fetal phthalate exposure with wheezing, asthma, and lung function from birth to adolescence.</div></div><div><h3>Methods</h3><div>We performed 1-stage individual participant data <em>meta</em>-analyses with data from six European birth cohorts (3,745 mother–child pairs) to assess associations of pregnancy-averaged maternal urinary concentrations of 7 phthalate metabolites and 3 phthalate groups (high- and low-molecular-weight phthalate metabolites and sum of di-2-ethylhexyl phthalate metabolites) with wheezing in infancy (0–1 years) and at preschool age (1–5 years), and asthma and lung function at school age (5–12 years).</div></div><div><h3>Results</h3><div>Higher maternal pregnancy urine phthalate concentrations were not associated with wheezing in infancy or preschool age. Higher maternal pregnancy urine mono-benzyl phthalate concentrations were associated with an increased risk of asthma at school age (odds ratio (95% confidence interval): 1.13 (1.01–1.26) per natural log interquartile range unit increase in concentration), but not with wheezing or lung function and attenuated into non-significance after multiple testing correction. Higher maternal pregnancy concentrations of mono-2-ethyl-5-hydroxyhexyl phthalate, mono-<em>iso</em>-butyl phthalate, mono-n-butyl phthalate and low-molecular-weight phthalate metabolites were associated with higher FEV<sub>1,</sub> FEV<sub>1</sub>/FVC and FEF<sub>75</sub> z-scores after multiple testing correction.</div></div><div><h3>Conclusion</h3><div>Fetal exposure to higher phthalate concentrations is associated with lung function adaptations, while overall no consistent associations were observed with childhood wheezing or asthma. Future studies are needed to assess the causality of the observed associations, to identify the underlying mechanisms, and to assess potential respiratory consequences in adult life.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110069"},"PeriodicalIF":9.7,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145962751","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 : 2026-01-14DOI: 10.1016/j.envint.2026.110074
Zhenlong Wang , Ji Lu , Xiumin Wang , Wei An , Ya Zhao , Bing Han , Hui Tao , Jie Liu , Jianhua Guo , Jinquan Wang
Pet ownership offers physical and mental health benefits, but the risks of antibiotic resistance genes (ARGs) transmission between pets and humans remain underexplored. In this study, we used metagenomics analysis of fecal samples to compare resistome profiles among four groups: owned cats and their owners, and caged cats and non-cat owners. Our findings show significant similarities in gut microbial composition, ARGs, and mobile genetic elements (MGEs) between owned cats and their owners, identifying 73 shared core ARGs and 80 shared MGEs. In contrast, caged cats and non-cat owners shared only 30 ARGs and 73 MGEs. Long-term contact was positively correlated with a higher number of shared ARGs (from 20 + to 60 + ) and MGEs (from 10 + to 40 + ), as well as increased resistome risk (2.47- to 4.92-fold) between pet cats and owners. The gut microbiota played a key role in shaping the ARGs and MGEs profiles, with Escherichia coli and Klebsiella pneumoniae identified as primary carriers, each genome harboring 20 to 62 ARGs and 6 to 29 MGEs. ARGs transfer events were more frequent between pet cats and their owners than in other groups. These findings underscore a potential risk of shared antimicrobial resistance between companion animals and humans within the studied population in China.
{"title":"Long-term pet ownership promotes resistome similarity between cats and their owners","authors":"Zhenlong Wang , Ji Lu , Xiumin Wang , Wei An , Ya Zhao , Bing Han , Hui Tao , Jie Liu , Jianhua Guo , Jinquan Wang","doi":"10.1016/j.envint.2026.110074","DOIUrl":"10.1016/j.envint.2026.110074","url":null,"abstract":"<div><div>Pet ownership offers physical and mental health benefits, but the risks of antibiotic resistance genes (ARGs) transmission between pets and humans remain underexplored. In this study, we used metagenomics analysis of fecal samples to compare resistome profiles among four groups: owned cats and their owners, and caged cats and non-cat owners. Our findings show significant similarities in gut microbial composition, ARGs, and mobile genetic elements (MGEs) between owned cats and their owners, identifying 73 shared core ARGs and 80 shared MGEs. In contrast, caged cats and non-cat owners shared only 30 ARGs and 73 MGEs. Long-term contact was positively correlated with a higher number of shared ARGs (from 20 + to 60 + ) and MGEs (from 10 + to 40 + ), as well as increased resistome risk (2.47- to 4.92-fold) between pet cats and owners. The gut microbiota played a key role in shaping the ARGs and MGEs profiles, with <em>Escherichia coli</em> and <em>Klebsiella pneumoniae</em> identified as primary carriers, each genome harboring 20 to 62 ARGs and 6 to 29 MGEs. ARGs transfer events were more frequent between pet cats and their owners than in other groups. These findings underscore a potential risk of shared antimicrobial resistance between companion animals and humans within the studied population in China.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110074"},"PeriodicalIF":9.7,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145993406","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 : 2026-01-14DOI: 10.1016/j.envint.2026.110060
Yuanyuan Mo, Peng Xiao, Lemian Liu, Jun Zuo, Huihuang Chen, Erik Jeppesen, Guogui Chen, Xuan Gu, Yong-Guan Zhu, Jun Yang
Understanding the large-scale distribution mechanisms of bacterial pathogens is critical for predicting their ecology and associated human health risks under climate change. Here, we investigate the biogeographical patterns and community assembly of bacterial pathogens across 59 lakes and reservoirs in eastern China. We identify the low-latitude region as a significant bacterial pathogen hotspot, primarily dominated by the genus Acinetobacter. The assembly of pathogen communities is co-driven by spatial, environmental, and climatic factors, with spatial processes exerting the strongest effects. Importantly, we reveal precipitation as a key climatic factor that simultaneously enhances pathogen diversity and promotes potential dispersal. Genera such as Acinetobacter, Sphingomonas, and Stenotrophomonas are identified as highly dispersal-prone. Generally, under future precipitation scenarios, our models project that increased precipitation will significantly enhance both the abundance and richness of pathogens. This expansion is predicted to further intensify pathogen hotspots in low-latitude regions and accelerate the spread of potential health risks. These results establish a critical link between hydrological cycles and pathogen biogeography, mediated through dispersal. Our study provides new insights for developing integrated surveillance frameworks that combine hydrological monitoring with a 'One Health' approach to address the escalating ecological and public health threats from climate-driven pathogen reshaping.
{"title":"Climate change-driven dispersal of pathogenic bacteria in large-scale lakes and reservoirs.","authors":"Yuanyuan Mo, Peng Xiao, Lemian Liu, Jun Zuo, Huihuang Chen, Erik Jeppesen, Guogui Chen, Xuan Gu, Yong-Guan Zhu, Jun Yang","doi":"10.1016/j.envint.2026.110060","DOIUrl":"https://doi.org/10.1016/j.envint.2026.110060","url":null,"abstract":"<p><p>Understanding the large-scale distribution mechanisms of bacterial pathogens is critical for predicting their ecology and associated human health risks under climate change. Here, we investigate the biogeographical patterns and community assembly of bacterial pathogens across 59 lakes and reservoirs in eastern China. We identify the low-latitude region as a significant bacterial pathogen hotspot, primarily dominated by the genus Acinetobacter. The assembly of pathogen communities is co-driven by spatial, environmental, and climatic factors, with spatial processes exerting the strongest effects. Importantly, we reveal precipitation as a key climatic factor that simultaneously enhances pathogen diversity and promotes potential dispersal. Genera such as Acinetobacter, Sphingomonas, and Stenotrophomonas are identified as highly dispersal-prone. Generally, under future precipitation scenarios, our models project that increased precipitation will significantly enhance both the abundance and richness of pathogens. This expansion is predicted to further intensify pathogen hotspots in low-latitude regions and accelerate the spread of potential health risks. These results establish a critical link between hydrological cycles and pathogen biogeography, mediated through dispersal. Our study provides new insights for developing integrated surveillance frameworks that combine hydrological monitoring with a 'One Health' approach to address the escalating ecological and public health threats from climate-driven pathogen reshaping.</p>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"110060"},"PeriodicalIF":9.7,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146111625","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 : 2026-01-13DOI: 10.1016/j.envint.2026.110068
Amanda J. Goodrich , Deborah H. Bennett , Michael J. Kleeman , Daniel J. Tancredi , Yunin J. Ludeña , Irva Hertz-Picciotto , Rebecca J. Schmidt
Background
Particulate matter (PM) composition varies by source components and size. While studies show prenatal and early life exposure to total PM2.5 mass to be associated with autism spectrum disorder (ASD), little is known about the role of ultrafine (PM0.1) and fine PM specific components, especially PM0.1.
Objectives
We investigated associations between prenatal and early life exposure to size-resolved PM components and ASD in the CHARGE case–control study.
Methods
We analyzed 1,281 children (751 ASD, 530 typically developing) from the CHARGE study (enrolled 2003–2020). Daily PM0.1 and PM2.5 component concentrations were estimated using a chemical transport model with 4- or 24-km km resolution (for 95% and 5% of addresses, respectively) and bias correction. Daily exposures were averaged over preconception, pregnancy, and the first year of life, and log transformed. Using logistic regression, we estimated PM0.1 odds ratios (ORs) for ASD per interquartile range (IQR) increase in each component, adjusting for confounders, PM2.5 remainder, and NO2.
Results
First-year PM0.1 iron, manganese, black carbon, and sodium were consistently associated with increased odds of ASD (OR (95% CI): 1.60 (1.21, 2.12), 1.27 (1.04, 1.55), 1.54 (1.00, 2.38), and 1.92 (1.24, 2.99), respectively). Similar results were observed with first-year PM0.1-2.5 iron and manganese (OR (95% CI): 1.54 (1.13, 2.09) and 1.46 (1.07, 2.01), respectively).
Discussion
Our findings suggest that exposure to specific PM components during early life, especially in the ultrafine fraction, contribute to ASD risk, with less consistent evidence for prenatal exposures, underscoring the importance of particle composition and exposure timing.
{"title":"Fine and ultrafine particulate matter components and autism spectrum disorder (ASD)","authors":"Amanda J. Goodrich , Deborah H. Bennett , Michael J. Kleeman , Daniel J. Tancredi , Yunin J. Ludeña , Irva Hertz-Picciotto , Rebecca J. Schmidt","doi":"10.1016/j.envint.2026.110068","DOIUrl":"10.1016/j.envint.2026.110068","url":null,"abstract":"<div><h3>Background</h3><div>Particulate matter (PM) composition varies by source components and size. While studies show prenatal and early life exposure to total PM<sub>2.5</sub> mass to be associated with autism spectrum disorder (ASD), little is known about the role of ultrafine (PM<sub>0.1</sub>) and fine PM specific components, especially PM<sub>0.1</sub>.</div></div><div><h3>Objectives</h3><div>We investigated associations between prenatal and early life exposure to size-resolved PM components and ASD in the CHARGE case–control study.</div></div><div><h3>Methods</h3><div>We analyzed 1,281 children (751 ASD, 530 typically developing) from the CHARGE study (enrolled 2003–2020). Daily PM<sub>0.1</sub> and PM<sub>2.5</sub> component concentrations were estimated using a chemical transport model with 4- or 24-km km resolution (for 95% and 5% of addresses, respectively) and bias correction. Daily exposures were averaged over preconception, pregnancy, and the first year of life, and log transformed. Using logistic regression, we estimated PM<sub>0.1</sub> odds ratios (ORs) for ASD per interquartile range (IQR) increase in each component, adjusting for confounders, PM<sub>2.5</sub> remainder, and NO<sub>2</sub>.</div></div><div><h3>Results</h3><div>First-year PM<sub>0.1</sub> iron, manganese, black carbon, and sodium were consistently associated with increased odds of ASD (OR (95% CI): 1.60 (1.21, 2.12), 1.27 (1.04, 1.55), 1.54 (1.00, 2.38), and 1.92 (1.24, 2.99), respectively). Similar results were observed with first-year PM<sub>0.1-2.5</sub> iron and manganese (OR (95% CI): 1.54 (1.13, 2.09) and 1.46 (1.07, 2.01), respectively).</div></div><div><h3>Discussion</h3><div>Our findings suggest that exposure to specific PM components during early life, especially in the ultrafine fraction, contribute to ASD risk, with less consistent evidence for prenatal exposures, underscoring the importance of particle composition and exposure timing.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110068"},"PeriodicalIF":9.7,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145962754","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 : 2026-01-12DOI: 10.1016/j.envint.2026.110065
Ji-Seok Han , Heejin Park , Tae-Yang Jung , Woojin Kim , Han Young Eom , Yong-Bum Kim , Jae-Woo Cho , Wan-Jung Im , Min Heui Yoo , Sung-Ae Hyun , Byoung-Seok Lee
Perfluoroheptanoic acid (PFHpA), a short-chain perfluoroalkyl used in various industrial applications, is highly persistent and raises concerns about ecological and human health. However, in vivo toxicity data are limited. This study evaluated PFHpA toxicity in male and female Sprague-Dawley rats given oral doses of 20, 40, and 80 mg/kg/day for 26 weeks. During administration, body weights, clinical observations, and neurobehavioral assessments were conducted, followed by clinical pathology and histopathology after the final sacrifice. Additionally, PFHpA concentrations were measured in the serum of all rats at week 26. At the end of the dosing period, serum concentrations of PFHpA were higher in male rats than in females. Males receiving 80 mg/kg/d exhibited centrilobular hepatocellular hypertrophy in the liver, follicular cell hypertrophy in the thyroid, increased liver weight, elevated blood urea nitrogen, and decreased total bilirubin levels. Squamous cell hyperplasia in the forestomach, indicative of localized irritant effects, was observed in all PFHpA-treated groups. Thyroid hormone assays revealed lower total thyroxine levels in the high-dose group than in the control group in both sexes (P < 0.001). The main changes observed in PFHpA-treated groups appeared to be rat-specific hepatic adaptations rather than adverse effects, as no mortality, clinical symptoms, or body weight loss occurred. We concluded that the toxicological impact of PFHpA is negligible in standard lab rats. This novel finding can inform stakeholders in the industrial, medical, and political fields, especially regarding public health management.
{"title":"Comprehensive 26-week subchronic toxicity assessment of perfluoroheptanoic acid in Sprague–Dawley rats: implications for human health","authors":"Ji-Seok Han , Heejin Park , Tae-Yang Jung , Woojin Kim , Han Young Eom , Yong-Bum Kim , Jae-Woo Cho , Wan-Jung Im , Min Heui Yoo , Sung-Ae Hyun , Byoung-Seok Lee","doi":"10.1016/j.envint.2026.110065","DOIUrl":"10.1016/j.envint.2026.110065","url":null,"abstract":"<div><div>Perfluoroheptanoic acid (PFHpA), a short-chain perfluoroalkyl used in various industrial applications, is highly persistent and raises concerns about ecological and human health. However, in vivo toxicity data are limited. This study evaluated PFHpA toxicity in male and female Sprague-Dawley rats given oral doses of 20, 40, and 80 mg/kg/day for 26 weeks. During administration, body weights, clinical observations, and neurobehavioral assessments were conducted, followed by clinical pathology and histopathology after the final sacrifice. Additionally, PFHpA concentrations were measured in the serum of all rats at week 26. At the end of the dosing period, serum concentrations of PFHpA were higher in male rats than in females. Males receiving 80 mg/kg/d exhibited centrilobular hepatocellular hypertrophy in the liver, follicular cell hypertrophy in the thyroid, increased liver weight, elevated blood urea nitrogen, and decreased total bilirubin levels. Squamous cell hyperplasia in the forestomach, indicative of localized irritant effects, was observed in all PFHpA-treated groups. Thyroid hormone assays revealed lower total thyroxine levels in the high-dose group than in the control group in both sexes (P < 0.001). The main changes observed in PFHpA-treated groups appeared to be rat-specific hepatic adaptations rather than adverse effects, as no mortality, clinical symptoms, or body weight loss occurred. We concluded that the toxicological impact of PFHpA is negligible in standard lab rats. This novel finding can inform stakeholders in the industrial, medical, and political fields, especially regarding public health management.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110065"},"PeriodicalIF":9.7,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145956871","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}