Pub Date : 2024-11-01DOI: 10.1016/j.envint.2024.109092
Yuanyuan Zheng , Lu Wang , Jianing Wu , Li Xiang , Yafei Gao , Hao Chen , Hongwen Sun , Yuanjiang Pan , Hongzhi Zhao
Fluorotelomer sulfonates (FTSs) are widely used as novel substitutes for perfluorooctane sulfonate, inevitably leading to FTSs accumulation in various environmental media and subsequent exposure to humans. This accumulation eventually poses environmental hazards and health risks. However, their toxicity mechanisms remain unclear. Herein, the mechanisms of two FTSs (6:2 and 8:2 FTS) induced toxicity in human hepatocellular carcinoma cells were investigated via non-targeted metabolomics and lipidomics based on liquid chromatography–high resolution mass spectrometry. Our results revealed that amino acid, purine, acylcarnitine and lipid levels were significantly perturbed by 6:2 and 8:2 FTS exposure. The effects of 8:2 FTS exposure were largely characterized by up-regulation of pyruvate metabolism pathway and down-regulation of purine metabolism pathway, whereas the opposite trends were induced by 6:2 FTS exposure. The opposite trends were confirmed by the mRNA expression levels of four key genes (glyoxalase 1, adenylosuccinate lyase, inosine monophosphate dehydrogenase 1 (IMPDH1) and IMPDH2) determined by real-time PCR. Common lipid perturbations included significantly increased ceramide/sphingomyelin ratios, and obvious accumulation of hexosylceramides and lysoglycerophospholipids. 6:2 FTS exposure induced sharp accumulation of glycerides, including monoglycerides, diglycerides and triglycerides. 8:2 FTS exposure induced decreased levels of acylcarnitines and fatty acids. Both of 6:2 and 8:2 FTS exposure induced increased levels of intracellular reactive oxygen species, an imbalance in energy metabolism homeostasis, and mitochondrial dysfunction. The results of integrated omics analysis are expected to serve as valuable information for the health risk assessment of 6:2 FTS and 8:2 FTS.
{"title":"Integrated non-targeted metabolomics and lipidomics reveal mechanisms of fluorotelomer sulfonates-induced toxicity in human hepatocytes","authors":"Yuanyuan Zheng , Lu Wang , Jianing Wu , Li Xiang , Yafei Gao , Hao Chen , Hongwen Sun , Yuanjiang Pan , Hongzhi Zhao","doi":"10.1016/j.envint.2024.109092","DOIUrl":"10.1016/j.envint.2024.109092","url":null,"abstract":"<div><div>Fluorotelomer sulfonates (FTSs) are widely used as novel substitutes for perfluorooctane sulfonate, inevitably leading to FTSs accumulation in various environmental media and subsequent exposure to humans. This accumulation eventually poses environmental hazards and health risks. However, their toxicity mechanisms remain unclear. Herein, the mechanisms of two FTSs (6:2 and 8:2 FTS) induced toxicity in human hepatocellular carcinoma cells were investigated via non-targeted metabolomics and lipidomics based on liquid chromatography–high resolution mass spectrometry. Our results revealed that amino acid, purine, acylcarnitine and lipid levels were significantly perturbed by 6:2 and 8:2 FTS exposure. The effects of 8:2 FTS exposure were largely characterized by up-regulation of pyruvate metabolism pathway and down-regulation of purine metabolism pathway, whereas the opposite trends were induced by 6:2 FTS exposure. The opposite trends were confirmed by the mRNA expression levels of four key genes (<em>glyoxalase 1</em>, <em>adenylosuccinate lyase</em>, <em>inosine monophosphate dehydrogenase 1</em> (<em>IMPDH1</em>) and <em>IMPDH2</em>) determined by real-time PCR. Common lipid perturbations included significantly increased ceramide/sphingomyelin ratios, and obvious accumulation of hexosylceramides and lysoglycerophospholipids. 6:2 FTS exposure induced sharp accumulation of glycerides, including monoglycerides, diglycerides and triglycerides. 8:2 FTS exposure induced decreased levels of acylcarnitines and fatty acids. Both of 6:2 and 8:2 FTS exposure induced increased levels of intracellular reactive oxygen species, an imbalance in energy metabolism homeostasis, and mitochondrial dysfunction. The results of integrated omics analysis are expected to serve as valuable information for the health risk assessment of 6:2 FTS and 8:2 FTS.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"193 ","pages":"Article 109092"},"PeriodicalIF":10.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142452444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.envint.2024.109104
Stefania Romeo , Anna Sannino , Maria Rosaria Scarfì , Susanna Lagorio , Olga Zeni
<div><h3>Background</h3><div>Over the last decades, great concern has been raised about possible adverse effects to human health due to exposures to radiofrequency electromagnetic fields (RF-EMF, 100 kHz – 300 GHz) emitted by wireless communication technologies. In 2011 the International Agency for Research on Cancer classified RF-EMF as possibly carcinogenic to humans, highlighting that the evidence was weak and far from conclusive. Updated systematic reviews of the scientific literature on this topic are lacking, especially for mechanistic studies.</div></div><div><h3>Objectives</h3><div>To perform a systematic review of the scientific literature on genotoxic effects induced by RF-EMF in <em>in vitro</em> experimental models. The overall aim is to assess the confidence and level of evidence of the induced effects in mammalian cell cultures.</div></div><div><h3>Methods</h3><div>Full details regarding the eligibility criteria, information sources, and methods developed to assess risk of bias in the included study, are reported in our published protocol (<span><span>Romeo et al. 2021</span></span>). The databases NCBI PubMed, Web of Science, and EMF-Portal were used as information sources (last searched on 31st December 2022). In developing the systematic review, we followed the guidelines provided by the National Toxicology Program-Office of Health Assessment and Translation (NTP-OHAT), adapted to the evaluation of <em>in vitro</em> studies. A narrative synthesis of the body of evidence was performed by tabulating data classified according to meaningful groups (endpoints) and sub-groups (exposure parameters). This report, abstract included, conforms to the PRISMA 2020 (Preferred Reporting Items for Systematic reviews and Meta-Analyses) guidelines.</div></div><div><h3>Results</h3><div>Out of 7750 unique records identified, 159 articles were eligible for inclusion. From the extracted data, we identified 1111 experiments (defined as independent specific combinations of diverse biological and electromagnetic parameters). The large majority (80%) of experiments reviewed did not show statistically significant genotoxic effects of RF-EMF exposures, and most “positive” studies were rated as of moderate to low quality, with negative ratings in the key bias domains. A qualitative evidence appraisal was conducted at the endpoint level, and then integrated across endpoints.</div></div><div><h3>Discussion</h3><div>To the best of our knowledge, this is the first systematic review of the scientific literature on genotoxic effects in mammalian cell cultures in relation to RF-EMF exposure, which confirms and strengthens conclusions from previous syntheses of this specific topic thanks to the use of transparently reported methods, pre-defined inclusion criteria, and formal assessment of susceptibility to bias. Limitations of the evidence included the frequent reporting of findings in graphical display only, and the large heterogeneity of experimental data, which p
{"title":"Genotoxicity of radiofrequency electromagnetic fields on mammalian cells in vitro: A systematic review with narrative synthesis","authors":"Stefania Romeo , Anna Sannino , Maria Rosaria Scarfì , Susanna Lagorio , Olga Zeni","doi":"10.1016/j.envint.2024.109104","DOIUrl":"10.1016/j.envint.2024.109104","url":null,"abstract":"<div><h3>Background</h3><div>Over the last decades, great concern has been raised about possible adverse effects to human health due to exposures to radiofrequency electromagnetic fields (RF-EMF, 100 kHz – 300 GHz) emitted by wireless communication technologies. In 2011 the International Agency for Research on Cancer classified RF-EMF as possibly carcinogenic to humans, highlighting that the evidence was weak and far from conclusive. Updated systematic reviews of the scientific literature on this topic are lacking, especially for mechanistic studies.</div></div><div><h3>Objectives</h3><div>To perform a systematic review of the scientific literature on genotoxic effects induced by RF-EMF in <em>in vitro</em> experimental models. The overall aim is to assess the confidence and level of evidence of the induced effects in mammalian cell cultures.</div></div><div><h3>Methods</h3><div>Full details regarding the eligibility criteria, information sources, and methods developed to assess risk of bias in the included study, are reported in our published protocol (<span><span>Romeo et al. 2021</span></span>). The databases NCBI PubMed, Web of Science, and EMF-Portal were used as information sources (last searched on 31st December 2022). In developing the systematic review, we followed the guidelines provided by the National Toxicology Program-Office of Health Assessment and Translation (NTP-OHAT), adapted to the evaluation of <em>in vitro</em> studies. A narrative synthesis of the body of evidence was performed by tabulating data classified according to meaningful groups (endpoints) and sub-groups (exposure parameters). This report, abstract included, conforms to the PRISMA 2020 (Preferred Reporting Items for Systematic reviews and Meta-Analyses) guidelines.</div></div><div><h3>Results</h3><div>Out of 7750 unique records identified, 159 articles were eligible for inclusion. From the extracted data, we identified 1111 experiments (defined as independent specific combinations of diverse biological and electromagnetic parameters). The large majority (80%) of experiments reviewed did not show statistically significant genotoxic effects of RF-EMF exposures, and most “positive” studies were rated as of moderate to low quality, with negative ratings in the key bias domains. A qualitative evidence appraisal was conducted at the endpoint level, and then integrated across endpoints.</div></div><div><h3>Discussion</h3><div>To the best of our knowledge, this is the first systematic review of the scientific literature on genotoxic effects in mammalian cell cultures in relation to RF-EMF exposure, which confirms and strengthens conclusions from previous syntheses of this specific topic thanks to the use of transparently reported methods, pre-defined inclusion criteria, and formal assessment of susceptibility to bias. Limitations of the evidence included the frequent reporting of findings in graphical display only, and the large heterogeneity of experimental data, which p","PeriodicalId":308,"journal":{"name":"Environment International","volume":"193 ","pages":"Article 109104"},"PeriodicalIF":10.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142519781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.envint.2024.109120
Quan Zhang , Liuqing Yang , Huiyun Wang , Chengwang Wu , Rui Cao , Meirong Zhao , Guanyong Su , Cui Wang
The ubiquitous presence of organophosphate esters (OPEs) in the environment has prompted growing concerns about their potential health risks, particularly their endocrine-disrupting effects. This study comprehensively evaluated the endocrine-disrupting properties of six emerging OPEs: five aryl-OPEs (2-ethylhexyl diphenyl phosphate (EHDPP), tris (2-biphenylyl) phosphate (TBPP), resorcinol bis (diphenyl phosphate) (RDP), 4-hydroxyphenyl diphenyl phosphate (para-OH-TPHP), and 3-hydroxyphenyl diphenyl phosphate (meta-OH-TPHP) and one alkyl-OPE, triallyl phosphate (TAP). Our findings revealed that all tested aryl-OPEs exhibited antagonistic effects on one or more hormone receptors. Importantly, para-OH-TPHP demonstrated the most potent antagonistic activity, inhibiting estrogen receptor α (ERα), thyroid hormone receptor β (TRβ), glucocorticoid receptor (GR), and mineralocorticoid receptor (MR) with the concentration of test compounds showing 20 % relative inhibitory concentration (RIC20) value below 10−6 mol/L (M). RDP antagonized ERα and cortical receptors (GR and MR), TBPP affected TRβ and GR, while EHDPP and meta-OH-TPHP targeted MR. Regarding steroidogenesis, para-OH-TPHP significantly inhibited genes for estrogen (cyp19) and cortisol synthesis (cyp11b2), and along with meta-OH-TPHP, EHDPP, TAP, and RDP downregulated cyp11a1, a rate-limiting enzyme in hormone synthesis. All compounds caused malformations and swimming abnormalities in zebrafish embryos/larvae at concentrations of 10−7 M or higher, with para-OH-TPHP showing nearly 50 % peak induction. Furthermore, the six compounds tested influenced genes associated with the hypothalamic-pituitary–gonadal (HPG) axis in both zebrafish larvae and adult female zebrafish, in addition to affecting the reproductive behavior of zebrafish. A weighted scoring system was employed to rank the endocrine-disrupting potency of the OPEs, with para-OH-TPHP exhibiting the highest risk, followed by EHDPP, RDP, TBPP, meta-OH-TPHP, and TAP. Collectively, our results highlight the significant endocrine-disrupting effects of emerging OPEs, underscoring the urgent need for further research to assess their potential health implications.
{"title":"A comprehensive evaluation of the endocrine-disrupting effects of emerging organophosphate esters","authors":"Quan Zhang , Liuqing Yang , Huiyun Wang , Chengwang Wu , Rui Cao , Meirong Zhao , Guanyong Su , Cui Wang","doi":"10.1016/j.envint.2024.109120","DOIUrl":"10.1016/j.envint.2024.109120","url":null,"abstract":"<div><div>The ubiquitous presence of organophosphate esters (OPEs) in the environment has prompted growing concerns about their potential health risks, particularly their endocrine-disrupting effects. This study comprehensively evaluated the endocrine-disrupting properties of six emerging OPEs: five aryl-OPEs (2-ethylhexyl diphenyl phosphate (EHDPP), tris (2-biphenylyl) phosphate (TBPP), resorcinol bis (diphenyl phosphate) (RDP), 4-hydroxyphenyl diphenyl phosphate (<em>para</em>-OH-TPHP), and 3-hydroxyphenyl diphenyl phosphate (<em>meta</em>-OH-TPHP) and one alkyl-OPE, triallyl phosphate (TAP). Our findings revealed that all tested aryl-OPEs exhibited antagonistic effects on one or more hormone receptors. Importantly, <em>para</em>-OH-TPHP demonstrated the most potent antagonistic activity, inhibiting estrogen receptor α (ERα), thyroid hormone receptor β (TRβ), glucocorticoid receptor (GR), and mineralocorticoid receptor (MR) with the concentration of test compounds showing 20 % relative inhibitory concentration (RIC<sub>20</sub>) value below 10<sup>−6</sup> mol/L (M). RDP antagonized ERα and cortical receptors (GR and MR), TBPP affected TRβ and GR, while EHDPP and <em>meta</em>-OH-TPHP targeted MR. Regarding steroidogenesis, <em>para</em>-OH-TPHP significantly inhibited genes for estrogen (<em>cyp19</em>) and cortisol synthesis (<em>cyp11b2</em>), and along with <em>meta</em>-OH-TPHP, EHDPP, TAP, and RDP downregulated <em>cyp11a1</em>, a rate-limiting enzyme in hormone synthesis. All compounds caused malformations and swimming abnormalities in zebrafish embryos/larvae at concentrations of 10<sup>−7</sup> M or higher, with <em>para</em>-OH-TPHP showing nearly 50 % peak induction. Furthermore, the six compounds tested influenced genes associated with the hypothalamic-pituitary–gonadal (HPG) axis in both zebrafish larvae and adult female zebrafish, in addition to affecting the reproductive behavior of zebrafish. A weighted scoring system was employed to rank the endocrine-disrupting potency of the OPEs, with <em>para</em>-OH-TPHP exhibiting the highest risk, followed by EHDPP, RDP, TBPP, <em>meta</em>-OH-TPHP, and TAP. Collectively, our results highlight the significant endocrine-disrupting effects of emerging OPEs, underscoring the urgent need for further research to assess their potential health implications.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"193 ","pages":"Article 109120"},"PeriodicalIF":10.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142562261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.envint.2024.109100
Jason G. Su , Eahsan Shahriary , Emma Sage , John Jacobsen , Katherine Park , Arash Mohegh
California’s diverse geography and meteorological conditions necessitate models capturing fine-grained patterns of air pollution distribution. This study presents the development of high-resolution (100 m) daily land use regression (LUR) models spanning 1989–2021 for nitrogen dioxide (NO2), fine particulate matter (PM2.5), and ozone (O3) across California. These machine learning LUR algorithms integrated comprehensive data sources, including traffic, land use, land cover, meteorological conditions, vegetation dynamics, and satellite data. The modeling process incorporated historical air quality observations utilizing continuous regulatory, fixed site saturation, and Google Streetcar mobile monitoring data. The model performance (adjusted R2) for NO2, PM2.5, and O3 was 84 %, 65 %, and 92 %, respectively.
Over the years, NO2 concentrations showed a consistent decline, attributed to regulatory efforts and reduced human activities on weekends. Traffic density and weather conditions significantly influenced NO2 levels. PM2.5 concentrations also decreased over time, influenced by aerosol optical depth (AOD), traffic density, weather, and land use patterns, such as developed open spaces and vegetation. Industrial activities and residential areas contributed to higher PM2.5 concentrations. O3 concentrations exhibited no significant annual trend, with higher levels observed on weekends and lower levels associated with traffic density due to the scavenger effect. Weather conditions and land use, such as commercial areas and water bodies, influenced O3 concentrations.
To extend the prediction of daily NO2, PM2.5, and O3 to 1989, models were developed for predictors such as daily road traffic, normalized difference vegetation index (NDVI), Ozone Monitoring Instrument (OMI)–NO2, monthly AOD, and OMI-O3. These models enabled effective estimation for any period with known daily weather conditions.
Longitudinal analysis revealed a consistent NO2 decline, regulatory-driven PM2.5 decreases countered by wildfire impacts, and spatially variable O3 concentrations with no long-term trend. This study enhances understanding of air pollution trends, aiding in identifying lifetime exposure for statewide populations and supporting informed policy decisions and environmental justice advocacy.
{"title":"Development of over 30-years of high spatiotemporal resolution air pollution models and surfaces for California","authors":"Jason G. Su , Eahsan Shahriary , Emma Sage , John Jacobsen , Katherine Park , Arash Mohegh","doi":"10.1016/j.envint.2024.109100","DOIUrl":"10.1016/j.envint.2024.109100","url":null,"abstract":"<div><div>California’s diverse geography and meteorological conditions necessitate models capturing fine-grained patterns of air pollution distribution. This study presents the development of high-resolution (100 m) daily land use regression (LUR) models spanning 1989–2021 for nitrogen dioxide (NO<sub>2</sub>), fine particulate matter (PM<sub>2.5</sub>), and ozone (O<sub>3</sub>) across California. These machine learning LUR algorithms integrated comprehensive data sources, including traffic, land use, land cover, meteorological conditions, vegetation dynamics, and satellite data. The modeling process incorporated historical air quality observations utilizing continuous regulatory, fixed site saturation, and Google Streetcar mobile monitoring data. The model performance (adjusted R<sup>2</sup>) for NO<sub>2</sub>, PM<sub>2.5</sub>, and O<sub>3</sub> was 84 %, 65 %, and 92 %, respectively.</div><div>Over the years, NO<sub>2</sub> concentrations showed a consistent decline, attributed to regulatory efforts and reduced human activities on weekends. Traffic density and weather conditions significantly influenced NO<sub>2</sub> levels. PM<sub>2.5</sub> concentrations also decreased over time, influenced by aerosol optical depth (AOD), traffic density, weather, and land use patterns, such as developed open spaces and vegetation. Industrial activities and residential areas contributed to higher PM<sub>2.5</sub> concentrations. O<sub>3</sub> concentrations exhibited no significant annual trend, with higher levels observed on weekends and lower levels associated with traffic density due to the scavenger effect. Weather conditions and land use, such as commercial areas and water bodies, influenced O<sub>3</sub> concentrations.</div><div>To extend the prediction of daily NO<sub>2</sub>, PM<sub>2.5</sub>, and O<sub>3</sub> to 1989, models were developed for predictors such as daily road traffic, normalized difference vegetation index (NDVI), Ozone Monitoring Instrument (OMI)–NO2, monthly AOD, and OMI-O3. These models enabled effective estimation for any period with known daily weather conditions.</div><div>Longitudinal analysis revealed a consistent NO<sub>2</sub> decline, regulatory-driven PM<sub>2.5</sub> decreases countered by wildfire impacts, and spatially variable O<sub>3</sub> concentrations with no long-term trend. This study enhances understanding of air pollution trends, aiding in identifying lifetime exposure for statewide populations and supporting informed policy decisions and environmental justice advocacy.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"193 ","pages":"Article 109100"},"PeriodicalIF":10.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142519789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Monomethylmercury (MMHg) is a potent neurotoxin that poses a threat to human health. MMHg cycles in all spheres of the Earth but the sources and fate of atmospheric MMHg are unclear. Here, we develop a global model for atmospheric MMHg, which integrates the presently available data and indicates the limitations of the current study. Constrained by the observations in the atmosphere, the global atmospheric MMHg from all sources is 1009 (205–2474 as an uncertainty range) Mg/yr, with the largest sources from the in-cloud methylation of divalent mercury (475 Mg/yr) and MMHg sea spray (395 Mg/yr). MMHg has a short lifetime of 1.9 days in the troposphere due to rapid photo-demethylation. Our model indicates a net loss of marine MMHg to the atmosphere and thus a detoxifying effect on MMHg contamination in marine fish. However, it suggests additional MMHg deposition to the land, particularly in densely populated coastal areas, introducing a new risk pathway that needs to be considered in mercury exposure assessment. The atmosphere plays a non-negligible role in the biogeochemical cycle and human health, which requires further study and consideration in implementing the global Minamata Convention.
{"title":"Atmospheric monomethylmercury: Inferred sources constrained by observations and implications for human exposure","authors":"Peipei Wu , Zhengcheng Song , Peng Zhang , Shaojian Huang , Tengfei Yuan , Yanxu Zhang","doi":"10.1016/j.envint.2024.109127","DOIUrl":"10.1016/j.envint.2024.109127","url":null,"abstract":"<div><div>Monomethylmercury (MMHg) is a potent neurotoxin that poses a threat to human health. MMHg cycles in all spheres of the Earth but the sources and fate of atmospheric MMHg are unclear. Here, we develop a global model for atmospheric MMHg, which integrates the presently available data and indicates the limitations of the current study. Constrained by the observations in the atmosphere, the global atmospheric MMHg from all sources is 1009 (205–2474 as an uncertainty range) Mg/yr, with the largest sources from the in-cloud methylation of divalent mercury (475 Mg/yr) and MMHg sea spray (395 Mg/yr). MMHg has a short lifetime of 1.9 days in the troposphere due to rapid photo-demethylation. Our model indicates a net loss of marine MMHg to the atmosphere and thus a detoxifying effect on MMHg contamination in marine fish. However, it suggests additional MMHg deposition to the land, particularly in densely populated coastal areas, introducing a new risk pathway that needs to be considered in mercury exposure assessment. The atmosphere plays a non-negligible role in the biogeochemical cycle and human health, which requires further study and consideration in implementing the global <em>Minamata Convention</em>.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"193 ","pages":"Article 109127"},"PeriodicalIF":10.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142588469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.envint.2024.109110
Xuewei Huang , Zhouyi Wang , Fang Lei , Weifang Liu , Lijin Lin , Tao Sun , Yuanyuan Cao , Xingyuan Zhang , Jingjing Cai , Hongliang Li
Urban environments and cardiovascular health are closely linked, yet only a few specific exposures have been explored in isolation and mostly adopting cross-sectional design. The influence of socioeconomic status and genetic predisposition also remains unclear. Hence, leveraging the UK Biobank data (n = 206,681), we conducted a prospective analysis of 213 urban environmental variables and their association with atherosclerotic cardiovascular disease (ASCVD). The ExWAS and regularized Cox models analyses highlighted air pollution, industrial sites, and complex street networks as primary environmental risk factors. Instead, land-use density of leisure, public services, infrastructure and residential, and drinking water hardness showed a negative association with ASCVD risk. By integrating sparse canonical correlation and mediation analyses, we found distinct urban environment patterns through diverse pathways influence ASCVD. The environment characterized by pollution and complex streets impact ASCVD through adverse mental health (mediation proportion:30.7 %, 95 % CI:22.4 %-44.0 %), while highly-developed community and high-water hardness environment via cardiometabolic status (22.6 %, 95 % CI:19.7 %-26.0 %). Further, we found low socioeconomic status amplifies disadvantaged urban environment effects on ASCVD, yet there were no similar findings for ASCVD genetic predisposition. This research deepened our understanding of city-cardiovascular health links and the role of socioeconomic status, with implications for urban planning and public health interventions.
{"title":"Association of urban environments with Atherosclerotic cardiovascular disease: A prospective cohort study in the UK Biobank","authors":"Xuewei Huang , Zhouyi Wang , Fang Lei , Weifang Liu , Lijin Lin , Tao Sun , Yuanyuan Cao , Xingyuan Zhang , Jingjing Cai , Hongliang Li","doi":"10.1016/j.envint.2024.109110","DOIUrl":"10.1016/j.envint.2024.109110","url":null,"abstract":"<div><div>Urban environments and cardiovascular health are closely linked, yet only a few specific exposures have been explored in isolation and mostly adopting cross-sectional design. The influence of socioeconomic status and genetic predisposition also remains unclear. Hence, leveraging the UK Biobank data (n = 206,681), we conducted a prospective analysis of 213 urban environmental variables and their association with atherosclerotic cardiovascular disease (ASCVD). The ExWAS and regularized Cox models analyses highlighted air pollution, industrial sites, and complex street networks as primary environmental risk factors. Instead, land-use density of leisure, public services, infrastructure and residential, and drinking water hardness showed a negative association with ASCVD risk. By integrating sparse canonical correlation and mediation analyses, we found distinct urban environment patterns through diverse pathways influence ASCVD. The environment characterized by pollution and complex streets impact ASCVD through adverse mental health (mediation proportion:30.7 %, 95 % CI:22.4 %-44.0 %), while highly-developed community and high-water hardness environment via cardiometabolic status (22.6 %, 95 % CI:19.7 %-26.0 %). Further, we found low socioeconomic status amplifies disadvantaged urban environment effects on ASCVD, yet there were no similar findings for ASCVD genetic predisposition. This research deepened our understanding of city-cardiovascular health links and the role of socioeconomic status, with implications for urban planning and public health interventions.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"193 ","pages":"Article 109110"},"PeriodicalIF":10.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142562258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.envint.2024.109109
Hang Huang , Pengyu Lei , Haiyang Yu , Jiao Du , Baihui Wu , Hanbing Wang , Qinsi Yang , Yongwei Cheng , Da Sun , Lijun Wan
Micro/Nano plastics (MNPs) pollutants are widespread in the environment, raising significant concerns about their biosafety. Emerging studies indicate that the urinary system is a primary accumulation site for MNPs, leading to severe tissue and functional damage. This review aims to summarize recent research on the potential hazards that MNPs may pose to the urinary system, highlighting the mechanisms of toxicity and the current state of knowledge. Studies have shown that MNPs enter the human body through drinking water, the food chain, inhalation, and skin contact. They may penetrate the bloodstream via the digestive, respiratory, and skin systems, subsequently dispersing to various organs, including the urinary system. The potential accumulation of MNPs in the urinary system might induce cellular oxidative stress, inflammation, apoptosis, autophagy, the “intestine-kidney axis”, and other possible toxic mechanisms. These processes could disrupt kidney metabolic functions and promote tissue fibrosis, thereby potentially increasing the risk of urinary system diseases. Despite ongoing research, the understanding of MNPs’ impact on the urinary system remains limited. Therefore, this review provides a comprehensive overview of MNPs’ potential toxicity mechanisms in the urinary system, highlights key challenges, and outlines future research directions. It offers a theoretical basis for the development of effective protective measures and policies.
{"title":"Micro/nano plastics in the urinary system: Pathways, mechanisms, and health risks","authors":"Hang Huang , Pengyu Lei , Haiyang Yu , Jiao Du , Baihui Wu , Hanbing Wang , Qinsi Yang , Yongwei Cheng , Da Sun , Lijun Wan","doi":"10.1016/j.envint.2024.109109","DOIUrl":"10.1016/j.envint.2024.109109","url":null,"abstract":"<div><div>Micro/Nano plastics (MNPs) pollutants are widespread in the environment, raising significant concerns about their biosafety. Emerging studies indicate that the urinary system is a primary accumulation site for MNPs, leading to severe tissue and functional damage. This review aims to summarize recent research on the potential hazards that MNPs may pose to the urinary system, highlighting the mechanisms of toxicity and the current state of knowledge. Studies have shown that MNPs enter the human body through drinking water, the food chain, inhalation, and skin contact. They may penetrate the bloodstream via the digestive, respiratory, and skin systems, subsequently dispersing to various organs, including the urinary system. The potential accumulation of MNPs in the urinary system might induce cellular oxidative stress, inflammation, apoptosis, autophagy, the “intestine-kidney axis”, and other possible toxic mechanisms. These processes could disrupt kidney metabolic functions and promote tissue fibrosis, thereby potentially increasing the risk of urinary system diseases. Despite ongoing research, the understanding of MNPs’ impact on the urinary system remains limited. Therefore, this review provides a comprehensive overview of MNPs’ potential toxicity mechanisms in the urinary system, highlights key challenges, and outlines future research directions. It offers a theoretical basis for the development of effective protective measures and policies.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"193 ","pages":"Article 109109"},"PeriodicalIF":10.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142566187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.envint.2024.109087
Song Liu , Jing Wei , Xicheng Li , Lei Shu , Jiaming Zhang , Tzung-May Fu , Xin Yang , Lei Zhu
The recognized importance of ambient fine particulate matter (PM2.5), ozone (O3), and nitrogen dioxide (NO2) on human health has prompted the world to enact increasingly strict regulations on anthropogenic nitrogen oxides (NOx) emissions. However, the health concerns from soil NOx, potentially driven by fertilizer input but conventionally categorized as natural sources, remain less studied. Here, we emphasize the underappreciated roles of soil NOx emissions on health burden attributable to short-term PM2.5, O3, and NO2 exposure. Globally, we quantify acute health effects using machine-learning-based daily exposure estimates and identify influences of soil NOx emissions based on chemical transport model simulations. We find that 72.3% of the globe is affected by soil NOx emissions, whose contributions to short-term PM2.5, O3, and NO2 pollution lead to 13.9 (95% Confidence Interval [CI]: 9.1–18.8), 26.0 (18.2–34.2), and 13.9 (10.3–17.5) thousand premature mortality, respectively, in 2019. With distinct variations in regions, seasons, and pollutants, soil NOx-originated air pollution poses a global health concern, particularly for developing regions and intensively agricultural areas. In response to the intensive fertilizer use, South Asia, Southern Sub-Saharan Africa, and Central Europe witness the largest soil NOx-related health burden of up to 1.6 (95% CI: 1.1–2.1) mortality per 100k population. The overall health risk peaks in May, with O3 pollution typically dominating the soil NOx-attributable health burden during warm seasons and NO2 or PM2.5 during cold months. Our study highlights the necessity of dynamically adapted agricultural strategies for health-oriented multi-pollutant control, among which the improved use of synthetic fertilizers deserves priority under the ever-changing climate.
{"title":"Underappreciated roles of soil nitrogen oxide emissions on global acute health burden","authors":"Song Liu , Jing Wei , Xicheng Li , Lei Shu , Jiaming Zhang , Tzung-May Fu , Xin Yang , Lei Zhu","doi":"10.1016/j.envint.2024.109087","DOIUrl":"10.1016/j.envint.2024.109087","url":null,"abstract":"<div><div>The recognized importance of ambient fine particulate matter (PM<sub>2.5</sub>), ozone (O<sub>3</sub>), and nitrogen dioxide (NO<sub>2</sub>) on human health has prompted the world to enact increasingly strict regulations on anthropogenic nitrogen oxides (NO<sub><em>x</em></sub>) emissions. However, the health concerns from soil NO<sub><em>x</em></sub>, potentially driven by fertilizer input but conventionally categorized as natural sources, remain less studied. Here, we emphasize the underappreciated roles of soil NO<sub><em>x</em></sub> emissions on health burden attributable to short-term PM<sub>2.5</sub>, O<sub>3</sub>, and NO<sub>2</sub> exposure. Globally, we quantify acute health effects using machine-learning-based daily exposure estimates and identify influences of soil NO<sub><em>x</em></sub> emissions based on chemical transport model simulations. We find that 72.3% of the globe is affected by soil NO<sub><em>x</em></sub> emissions, whose contributions to short-term PM<sub>2.5</sub>, O<sub>3</sub>, and NO<sub>2</sub> pollution lead to 13.9 (95% Confidence Interval [CI]: 9.1–18.8), 26.0 (18.2–34.2), and 13.9 (10.3–17.5) thousand premature mortality, respectively, in 2019. With distinct variations in regions, seasons, and pollutants, soil NO<sub><em>x</em></sub>-originated air pollution poses a global health concern, particularly for developing regions and intensively agricultural areas. In response to the intensive fertilizer use, South Asia, Southern Sub-Saharan Africa, and Central Europe witness the largest soil NO<sub><em>x</em></sub>-related health burden of up to 1.6 (95% CI: 1.1–2.1) mortality per 100k population. The overall health risk peaks in May, with O<sub>3</sub> pollution typically dominating the soil NO<sub><em>x</em></sub>-attributable health burden during warm seasons and NO<sub>2</sub> or PM<sub>2.5</sub> during cold months. Our study highlights the necessity of dynamically adapted agricultural strategies for health-oriented multi-pollutant control, among which the improved use of synthetic fertilizers deserves priority under the ever-changing climate.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"193 ","pages":"Article 109087"},"PeriodicalIF":10.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142536531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.envint.2024.109099
Zelin Yan , Panpan Wang , Hanyu Wang , Jing Zhang , Yanyan Zhang , Yuchen Wu , Hongwei Zhou , Yan Li , Zhangqi Shen , Gongxiang Chen , Ruichao Li , Rong Zhang
Plasmid-mediated tigecycline resistance genes, notably the tet(X) and tmexCD-toprJ genes, have garnered considerable attention due to their transferability. This study aims to investigate the prevalence and resistance mechanisms associated with tet(X) and tmexCD-toprJ in flies, which are important reservoirs of antimicrobial resistance genes. A total of 52 tigecycline resistant bacterial isolates were collected, among which 40 (76.9 %) and 12 (23.1 %) were positive for tet(X) and tmexCD-toprJ, respectively. Tigecycline resistant bacteria were isolated from diverse geographical locations in China, with tet(X4)-positive Escherichia coli and tmexCD1-toprJ1-positive Klebsiella pneumoniae dominant among the isolates. The prevalence of tet(X) in rural area was significantly higher than that in urban area (2.7 % vs. 0.3 %; P < 0.001), while the prevalence of tmexCD1-toprJ1 shows no significant difference between urban and rural areas (0.2 % vs. 0.6 %; P > 0.05). Most tet(X)-positive strains (n = 40, 100.0 %), and 11(91.7 %) of the tmexCD1-toprJ1-positive strains exhibited multi-drug resistance. The IncFIB(Mar)/IncHI1B hybrid plasmid carrying tmexCD1-toprJ1 was identified by whole-genome sequencing analysis, which dominated the transmission of tmexCD1-toprJ1 in K. pneumoniae. Genetic context analysis showed that tmexCD1-toprJ1 was related locally to IS26, and IS26 may exacerbate the spread of tmexCD1-toprJ1 in different bacteria. In addition, the genetic structure of tmexCD1-toprJ1 also contains several antimicrobial resistance genes, including aph(3′)-Ic, sul1, blaDHA-1, blaCTX-M−5, etc., conferring resistance to aminoglycosides, sulfonamides, and carbapenems. This study provides insights into the epidemiology and transmission dynamics of tigecycline resistance genes, informing targeted intervention strategies to mitigate antimicrobial resistance dissemination.
{"title":"Emergence and genomic epidemiology of tigecycline resistant bacteria of fly origin across urban and rural China","authors":"Zelin Yan , Panpan Wang , Hanyu Wang , Jing Zhang , Yanyan Zhang , Yuchen Wu , Hongwei Zhou , Yan Li , Zhangqi Shen , Gongxiang Chen , Ruichao Li , Rong Zhang","doi":"10.1016/j.envint.2024.109099","DOIUrl":"10.1016/j.envint.2024.109099","url":null,"abstract":"<div><div>Plasmid-mediated tigecycline resistance genes, notably the <em>tet</em>(X) and <em>tmexCD-toprJ</em> genes, have garnered considerable attention due to their transferability. This study aims to investigate the prevalence and resistance mechanisms associated with <em>tet</em>(X) and <em>tmexCD-toprJ</em> in flies, which are important reservoirs of antimicrobial resistance genes. A total of 52 tigecycline resistant bacterial isolates were collected, among which 40 (76.9 %) and 12 (23.1 %) were positive for <em>tet</em>(X) and <em>tmexCD-toprJ</em>, respectively. Tigecycline resistant bacteria were isolated from diverse geographical locations in China, with <em>tet</em>(X4)-positive <em>Escherichia coli</em> and <em>tmexCD1-toprJ1</em>-positive <em>Klebsiella pneumoniae</em> dominant among the isolates. The prevalence of <em>tet</em>(X) in rural area was significantly higher than that in urban area (2.7 % vs. 0.3 %; <em>P</em> < 0.001), while the prevalence of <em>tmexCD1-toprJ1</em> shows no significant difference between urban and rural areas (0.2 % vs. 0.6 %; P > 0.05). Most <em>tet</em>(X)-positive strains (n = 40, 100.0 %), and 11(91.7 %) of the <em>tmexCD1</em>-<em>toprJ1-</em>positive strains exhibited multi-drug resistance. The IncFIB(Mar)/IncHI1B hybrid plasmid carrying <em>tmexCD1</em>-<em>toprJ1</em> was identified by whole-genome sequencing analysis, which dominated the transmission of <em>tmexCD1</em>-<em>toprJ1</em> in <em>K. pneumoniae</em>. Genetic context analysis showed that <em>tmexCD1</em>-<em>toprJ1</em> was related locally to IS<em>26</em>, and IS<em>26</em> may exacerbate the spread of <em>tmexCD1</em>-<em>toprJ1</em> in different bacteria. In addition, the genetic structure of <em>tmexCD1-toprJ1</em> also contains several antimicrobial resistance genes, including <em>aph(3′)-Ic</em>, <em>sul1</em>, <em>bla</em><sub>DHA-1</sub>, <em>bla</em><sub>CTX-M−5</sub>, etc., conferring resistance to aminoglycosides, sulfonamides, and carbapenems. This study provides insights into the epidemiology and transmission dynamics of tigecycline resistance genes, informing targeted intervention strategies to mitigate antimicrobial resistance dissemination.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"193 ","pages":"Article 109099"},"PeriodicalIF":10.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142489223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.envint.2024.109132
Xuchao Dai , Weikang Chen , Guangyuan Liu , Feidi Li , Shuren Sun , Qi Chen , Gang Chen , Mengqi Zhang , Zhenfeng Wang , Wenyuan Li , Hong Huang , Jingping Li
Background
The association between greenness exposure and semen quality and the underlying mechanism are unclear.
Objectives
To assess the association between greenness exposure and semen quality and whether the association is mediated by air pollutant exposure.
Methods
We collected data from 10,273 men in Zhejiang, China, whose wives received assisted reproductive technology from 2015 to 2021. The mean exposure concentrations of air pollutants and greenness indices (normalized difference vegetation index (NDVI) and the soil-adjusted vegetation index (SAVI)) in the 300 m, 400 m, 800 m, and 1000 m buffer zones were assessed from 0–90 days prior to semen testing on the basis of the patient’s residential address. A multivariate linear mixed-effects model was used to evaluate the associations, and mediation analysis was used to investigate the influences of air pollutant exposure and body mass index (BMI) on the associations.
Results
The average (standard deviation) age of the participants was 33.1 (5.2) years. After adjusting for confounders, progressive motility was positively associated with the NDVI400m (β (95 % CI): 1.744 (0.834, 2.655)) and SAVI400m (β (95 % CI): 1.484 (0.591, 2.377)). Furthermore, we found that NO2 and CO exposure significantly mediated part of the association between greenness exposure and progressive motility. Similar results are observed in the sensitivity analysis.
Conclusions
Our results suggest that greater greenness exposure is associated with higher semen quality and can be partially mediated by lower NO2 and CO exposure levels.
{"title":"Association between residential greenness exposure and semen quality: A retrospective study in China","authors":"Xuchao Dai , Weikang Chen , Guangyuan Liu , Feidi Li , Shuren Sun , Qi Chen , Gang Chen , Mengqi Zhang , Zhenfeng Wang , Wenyuan Li , Hong Huang , Jingping Li","doi":"10.1016/j.envint.2024.109132","DOIUrl":"10.1016/j.envint.2024.109132","url":null,"abstract":"<div><h3>Background</h3><div>The association between greenness exposure and semen quality and the underlying mechanism are unclear.</div></div><div><h3>Objectives</h3><div>To assess the association between greenness exposure and semen quality and whether the association is mediated by air pollutant exposure.</div></div><div><h3>Methods</h3><div>We collected data from 10,273 men in Zhejiang, China, whose wives received assisted reproductive technology from 2015 to 2021. The mean exposure concentrations of air pollutants and greenness indices (normalized difference vegetation index (NDVI) and the soil-adjusted vegetation index (SAVI)) in the 300 m, 400 m, 800 m, and 1000 m buffer zones were assessed from 0–90 days prior to semen testing on the basis of the patient’s residential address. A multivariate linear mixed-effects model was used to evaluate the associations, and mediation analysis was used to investigate the influences of air pollutant exposure and body mass index (BMI) on the associations.</div></div><div><h3>Results</h3><div>The average (standard deviation) age of the participants was 33.1 (5.2) years. After adjusting for confounders, progressive motility was positively associated with the NDVI<sub>400m</sub> (β (95 % CI): 1.744 (0.834, 2.655)) and SAVI<sub>400m</sub> (β (95 % CI): 1.484 (0.591, 2.377)). Furthermore, we found that NO<sub>2</sub> and CO exposure significantly mediated part of the association between greenness exposure and progressive motility. Similar results are observed in the sensitivity analysis.</div></div><div><h3>Conclusions</h3><div>Our results suggest that greater greenness exposure is associated with higher semen quality and can be partially mediated by lower NO<sub>2</sub> and CO exposure levels.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"193 ","pages":"Article 109132"},"PeriodicalIF":10.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142594178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}