Environment & Health最新文献

{"title":"Impacts of Gestational F-53B Exposure on Fetal Neurodevelopment: Insights from Placental and Thyroid Hormone Disruption","authors":"Sujuan Zhao,&nbsp;Yumeng Sun,&nbsp;Jiayao Duan,&nbsp;Tianxu Zhang,&nbsp;Yuchun Xiao,&nbsp;Yumin Zhu,&nbsp;Yibo Jia,&nbsp;Wenjue Zhong and Lingyan Zhu*,&nbsp;","doi":"10.1021/envhealth.4c0015810.1021/envhealth.4c00158","DOIUrl":"https://doi.org/10.1021/envhealth.4c00158https://doi.org/10.1021/envhealth.4c00158","url":null,"abstract":"<p >It has been evidenced that chlorinated polyfluoroalkyl ether sulfonic acids (Cl-PFESAs) have strong potential cross the placental barrier, but their adverse effects on offspring remain unclear. In this study, pregnant mice received daily intraperitoneal injections of chlorinated polyfluorinated ether sulfonate (Cl-PFESA; commercially known as F-53B, primarily comprising 6:2 Cl-PFESA and 8:2 Cl-PFESA) at dosages of 40 and 200 μg/kg from gestational days 6 to 17. Following gestational exposure, distinct accumulation of 6:2 and 8:2 Cl-PFESAs was observed in both the placenta and fetal brain, confirming their penetration across the placental and fetal blood-brain barriers. Maternal exposure to F-53B disrupted the placental 11β-hydroxysteroid dehydrogenase type 2 (<i>hsd11b2</i>) barrier, characterized by hypermethylation of its promoter, decreased blood sinusoids in labyrinth layer, and downregulation of the nutrient transport genes, thereby severely impairing the placenta’s protective and nutrient transfer functions. Concomitantly, significant fetal intrauterine growth restriction indicated by decreased fetal weight and crown-rump length was observed. Additionally, changes in thyroid hormones, along with transcriptional and DNA methylation alterations in the promoter regions of transthyretin (<i>ttr</i>) and deiodinase 3 (<i>dio</i>3) genes, were noted in the placenta. These epigenetic changes might affect the maternal-fetal transport of thyroid hormones, possibly leading to disrupted thyroid function in the F1 generation. With the decreased nutrient transport capacity of the placenta, T4 levels in the fetus are significantly reduced, resulting in significant fetal neurodevelopmental abnormalities, reduced nerve cell proliferation (Ki67), and damage to synaptic plasticity. This study reveals unveil the hidden dangers of F-53B, highlighting its neurotoxic effects on fetal development through the disruption of thyroid hormone transport across the placenta.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"3 3","pages":"308–320 308–320"},"PeriodicalIF":0.0,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.acs.org/doi/epdf/10.1021/envhealth.4c00158","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143666880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impacts of Gestational F-53B Exposure on Fetal Neurodevelopment: Insights from Placental and Thyroid Hormone Disruption.","authors":"Sujuan Zhao, Yumeng Sun, Jiayao Duan, Tianxu Zhang, Yuchun Xiao, Yumin Zhu, Yibo Jia, Wenjue Zhong, Lingyan Zhu","doi":"10.1021/envhealth.4c00158","DOIUrl":"10.1021/envhealth.4c00158","url":null,"abstract":"<p><p>It has been evidenced that chlorinated polyfluoroalkyl ether sulfonic acids (Cl-PFESAs) have strong potential cross the placental barrier, but their adverse effects on offspring remain unclear. In this study, pregnant mice received daily intraperitoneal injections of chlorinated polyfluorinated ether sulfonate (Cl-PFESA; commercially known as F-53B, primarily comprising 6:2 Cl-PFESA and 8:2 Cl-PFESA) at dosages of 40 and 200 μg/kg from gestational days 6 to 17. Following gestational exposure, distinct accumulation of 6:2 and 8:2 Cl-PFESAs was observed in both the placenta and fetal brain, confirming their penetration across the placental and fetal blood-brain barriers. Maternal exposure to F-53B disrupted the placental 11β-hydroxysteroid dehydrogenase type 2 (<i>hsd11b2</i>) barrier, characterized by hypermethylation of its promoter, decreased blood sinusoids in labyrinth layer, and downregulation of the nutrient transport genes, thereby severely impairing the placenta's protective and nutrient transfer functions. Concomitantly, significant fetal intrauterine growth restriction indicated by decreased fetal weight and crown-rump length was observed. Additionally, changes in thyroid hormones, along with transcriptional and DNA methylation alterations in the promoter regions of transthyretin (<i>ttr</i>) and deiodinase 3 (<i>dio</i>3) genes, were noted in the placenta. These epigenetic changes might affect the maternal-fetal transport of thyroid hormones, possibly leading to disrupted thyroid function in the F1 generation. With the decreased nutrient transport capacity of the placenta, T4 levels in the fetus are significantly reduced, resulting in significant fetal neurodevelopmental abnormalities, reduced nerve cell proliferation (Ki67), and damage to synaptic plasticity. This study reveals unveil the hidden dangers of F-53B, highlighting its neurotoxic effects on fetal development through the disruption of thyroid hormone transport across the placenta.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"3 3","pages":"308-320"},"PeriodicalIF":0.0,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11934197/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143721666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations between Per- and Polyfluoroalkyl Substances Exposures and Bone Mineral: A Systematic Review and Best Evidence Synthesis","authors":"Kai Tao,&nbsp;Bin Zeng,&nbsp;Linghui Deng,&nbsp;Wei Zhang,&nbsp;Xianghong Zhou,&nbsp;Yuming Jin,&nbsp;Zilong Zhang,&nbsp;Weichao Huang,&nbsp;Xiaoli Zou,&nbsp;Yu Zhan,&nbsp;Ping Lu,&nbsp;Shi Qiu,&nbsp;Lu Yang* and Qiang Wei*,&nbsp;","doi":"10.1021/envhealth.4c0014310.1021/envhealth.4c00143","DOIUrl":"https://doi.org/10.1021/envhealth.4c00143https://doi.org/10.1021/envhealth.4c00143","url":null,"abstract":"<p >Per- and polyfluoroalkyl substances (PFAS) are persistent environmental pollutants known for their bioaccumulative nature. Reduced bone mineral density (BMD) is associated with an increased risk of developing osteoporosis. This pioneering study aims to assess the effects of different PFAS compounds on bone mineral. We conducted searches on online databases. Inclusion criteria included the presence of associations between perfluorooctanoic acid (PFOA), perfluorooctanesulfonate (PFOS), perfluorohexanesulfonic acid (PFHxS), perfluorononanoic acid (PFNA), and perfluorodecanoic acid (PFDA) and BMD, BMD z-score, and bone mineral content (BMC). Meta-analyses were performed. Best evidence synthesis (BES) was performed to summarize the results. The results of BES showed that the evidence of PFOS, PFOA and PFNA with reduced bone mineral were moderate. The variability in methods for assessing bone mineral and sex differences are potential sources of heterogeneity in the results. Meta analysis showed that PFOA was associated with BMD (β −0.01, 95% CI −0.01 to −0.00; <i>I</i>² = 0%). Subgroup analysis by sex showed that PFOS (β −0.01, 95% CI −0.01 to −0.00; <i>I</i>² = 50%), PFOA (β −0.01, 95% CI −0.01 to +0.00; <i>I</i>² = 29%) were negatively correlated with BMD. This systematic review and BES revealed negative correlations between exposure to PFOS, PFOA, PFNA and bone mineral. Sex emerged as a potential factor affecting the negative effects of PFAS on bone mineral. The damage of PFAS to bone mineral still requires further exploration.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"3 4","pages":"363–372 363–372"},"PeriodicalIF":0.0,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.acs.org/doi/epdf/10.1021/envhealth.4c00143","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143842293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of Per- and Polyfluoroalkyl Substance Exposure with Coronary Stenosis and Prognosis in Acute Coronary Syndrome","authors":"Haoran Li,&nbsp;Ming Yang,&nbsp;Jiaxin Zhao,&nbsp;Zhenzhen Tan,&nbsp;Longfei Li,&nbsp;Ziwen An,&nbsp;Yi Liu,&nbsp;Xuehui Liu,&nbsp;Xiaoguang Zhang,&nbsp;Jingchao Lu,&nbsp;Ang Li* and Huicai Guo*,&nbsp;","doi":"10.1021/envhealth.4c0016610.1021/envhealth.4c00166","DOIUrl":"https://doi.org/10.1021/envhealth.4c00166https://doi.org/10.1021/envhealth.4c00166","url":null,"abstract":"<p >Per- and polyfluoroalkyl substances (PFAS) have been associated with an increased risk of acute coronary syndromes (ACS), but the influence on the degree of coronary stenosis and prognosis is unclear. This study enrolled 571 newly diagnosed ACS cases and investigated the association of 12 PFAS with coronary stenosis severity and prognosis. Coronary stenosis was assessed via Gensini score (GS) and number of lesioned vessels (LVN). Prognosis was estimated by tracking major adverse cardiovascular events (MACE). Statistical analyses included ordered logistic regression, Cox regression, threshold effect models, Bayesian kernel machine regression, and quantile g-computation models. The adverse outcome pathway (AOP) framework was applied to reveal the underlying mechanism. The results showed positive association between perfluorooctanesulfonic acid (PFOS) and coronary stenosis, with an odds ratio (95% confidence interval, CI) of 1.33 (1.06, 1.67) for GS and 1.36 (1.08, 1.71) for LVN. PFOS significantly increased the incidence of poor prognosis, with hazard ratios (95% CI) of 1.96 (1.34, 2.89) for MACE. Threshold effects were observed for PFAS on coronary stenosis and prognosis, with PFOS thresholds of 4.65 ng/mL for GS, 4.54 ng/mL for LVN, and 5.14 ng/mL for MACE, and 5.03 ng/mL for nonfatal myocardial infarction. PFAS mixture exposure increased the occurrence of MACE and nonfatal myocardial infarction. The AOP framework shows that PFAS may impact protein binding, the cytoskeleton, multicellular biological processes, and heart function. In summary, our study revealed the adverse effects of PFAS on the degree of coronary stenosis and prognosis in ACS and identified potentially relevant molecular loci.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"3 3","pages":"291–307 291–307"},"PeriodicalIF":0.0,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.acs.org/doi/epdf/10.1021/envhealth.4c00166","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143666885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of Per- and Polyfluoroalkyl Substance Exposure with Coronary Stenosis and Prognosis in Acute Coronary Syndrome.","authors":"Haoran Li, Ming Yang, Jiaxin Zhao, Zhenzhen Tan, Longfei Li, Ziwen An, Yi Liu, Xuehui Liu, Xiaoguang Zhang, Jingchao Lu, Ang Li, Huicai Guo","doi":"10.1021/envhealth.4c00166","DOIUrl":"10.1021/envhealth.4c00166","url":null,"abstract":"<p><p>Per- and polyfluoroalkyl substances (PFAS) have been associated with an increased risk of acute coronary syndromes (ACS), but the influence on the degree of coronary stenosis and prognosis is unclear. This study enrolled 571 newly diagnosed ACS cases and investigated the association of 12 PFAS with coronary stenosis severity and prognosis. Coronary stenosis was assessed via Gensini score (GS) and number of lesioned vessels (LVN). Prognosis was estimated by tracking major adverse cardiovascular events (MACE). Statistical analyses included ordered logistic regression, Cox regression, threshold effect models, Bayesian kernel machine regression, and quantile g-computation models. The adverse outcome pathway (AOP) framework was applied to reveal the underlying mechanism. The results showed positive association between perfluorooctanesulfonic acid (PFOS) and coronary stenosis, with an odds ratio (95% confidence interval, CI) of 1.33 (1.06, 1.67) for GS and 1.36 (1.08, 1.71) for LVN. PFOS significantly increased the incidence of poor prognosis, with hazard ratios (95% CI) of 1.96 (1.34, 2.89) for MACE. Threshold effects were observed for PFAS on coronary stenosis and prognosis, with PFOS thresholds of 4.65 ng/mL for GS, 4.54 ng/mL for LVN, and 5.14 ng/mL for MACE, and 5.03 ng/mL for nonfatal myocardial infarction. PFAS mixture exposure increased the occurrence of MACE and nonfatal myocardial infarction. The AOP framework shows that PFAS may impact protein binding, the cytoskeleton, multicellular biological processes, and heart function. In summary, our study revealed the adverse effects of PFAS on the degree of coronary stenosis and prognosis in ACS and identified potentially relevant molecular loci.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"3 3","pages":"291-307"},"PeriodicalIF":0.0,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11934203/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143721614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Environmental Health and Safety Implications of the Interplay Between Microplastics and the Residing Biofilm.","authors":"Xiaohan Wu, Fei He, Xueran Xu, Leilei Wu, Jinyu Rong, Sijie Lin","doi":"10.1021/envhealth.4c00148","DOIUrl":"10.1021/envhealth.4c00148","url":null,"abstract":"<p><p>The increasing prevalence of microplastics in the environment has raised concerns about their potential environmental and health implications. Biofilms readily colonize microplastics upon their entry into the environment, altering their surface characteristics. While most studies have explored how biofilms influence the adsorption and transportation of other contaminants by microplastics, the reciprocal interplay between microplastics and biofilms and the resulting ecological risks remain understudied. This review comprehensively reviews the impact of microplastic properties on biofilm formation and composition, including the microbial community structure. We then explore the dynamic interactions between microplastics and biofilms, examining how biofilms alter the physicochemical properties, migration, and deposition of microplastics. Furthermore, we emphasize the potential of biofilm-colonized microplastics to influence the environmental fate of other pollutants. Lastly, we discuss how biofilm-microplastic interactions may modify the bioavailability, biotoxicity, and potential health implications of microplastics.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"3 2","pages":"118-132"},"PeriodicalIF":0.0,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11851218/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143516948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Environmental Health and Safety Implications of the Interplay Between Microplastics and the Residing Biofilm","authors":"Xiaohan Wu,&nbsp;Fei He,&nbsp;Xueran Xu,&nbsp;Leilei Wu,&nbsp;Jinyu Rong and Sijie Lin*,&nbsp;","doi":"10.1021/envhealth.4c0014810.1021/envhealth.4c00148","DOIUrl":"https://doi.org/10.1021/envhealth.4c00148https://doi.org/10.1021/envhealth.4c00148","url":null,"abstract":"<p >The increasing prevalence of microplastics in the environment has raised concerns about their potential environmental and health implications. Biofilms readily colonize microplastics upon their entry into the environment, altering their surface characteristics. While most studies have explored how biofilms influence the adsorption and transportation of other contaminants by microplastics, the reciprocal interplay between microplastics and biofilms and the resulting ecological risks remain understudied. This review comprehensively reviews the impact of microplastic properties on biofilm formation and composition, including the microbial community structure. We then explore the dynamic interactions between microplastics and biofilms, examining how biofilms alter the physicochemical properties, migration, and deposition of microplastics. Furthermore, we emphasize the potential of biofilm-colonized microplastics to influence the environmental fate of other pollutants. Lastly, we discuss how biofilm–microplastic interactions may modify the bioavailability, biotoxicity, and potential health implications of microplastics.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"3 2","pages":"118–132 118–132"},"PeriodicalIF":0.0,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.acs.org/doi/epdf/10.1021/envhealth.4c00148","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143452531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Independent and Combined Associations between Metals Exposure and Inflammatory Markers among the General U.S. Adults.","authors":"Xinrui Feng, Yaoyu Luo, Min Zheng, Xiaojie Sun, Xiantao Shen","doi":"10.1021/envhealth.4c00097","DOIUrl":"10.1021/envhealth.4c00097","url":null,"abstract":"<p><p>Exposure to metals can trigger a series of diseases by dysregulating the human immune system, but there is still a lack of systematic studies assessing the independent and combined effects of exposure to metals on immune function in the general population, particularly concerning inflammation markers. This cross-sectional study was designed to mainly examine the associations between urinary metal mixtures and inflammatory markers, including white blood cell (WBC), platelet count (PLT), mean platelet volume (MPV), MPV/PLT ratio (MPR), platelet-to-lymphocyte ratio (PLR), and neutrophil-to-lymphocyte ratio (NLR). A total of 3451 participants aged ≥20 years were selected from the 2013-2016 National Health and Nutrition Examination Survey. Generalized linear models were used to investigate the relationships of exposure to single metals on inflammatory markers. Associations between coexposure to multiple metals and inflammatory markers were determined using weighted quantile sum regression and quantile g-computation. Barium, cadmium, lead, thallium, and cobalt showed significant associations with MPV, PLR, and NLR. Metal mixtures showed a negative association with MPV, while they had positive associations with PLR and NLR. Overall, our study highlights the significant effects of multiple metals exposure on inflammation markers, including MPV, PLR, and NLR, among U.S. adults. Thereinto, uranium, cadmium, and cobalt were identified as major contributors. Further prospective studies representative of other countries are warranted to either validate or refute our findings.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"3 3","pages":"282-290"},"PeriodicalIF":0.0,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11934204/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143721667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gestational Exposure to Endocrine-Disrupting Chemicals of Emerging Concern and the Risk of Developing Gestational Diabetes Mellitus: A Comprehensive Investigation of Sex-Specific and Trimester-Specific Associations","authors":"Jinfeng Fu,&nbsp;Yao Yao,&nbsp;Zhihong Huang,&nbsp;Zhihui Guo,&nbsp;Xinxin Tang,&nbsp;Xulong Chen,&nbsp;Xinjie Li,&nbsp;Yiming Ge,&nbsp;Bingjun Lu,&nbsp;Yujie Sha and Shaoyou Lu*,&nbsp;","doi":"10.1021/envhealth.4c0020210.1021/envhealth.4c00202","DOIUrl":"https://doi.org/10.1021/envhealth.4c00202https://doi.org/10.1021/envhealth.4c00202","url":null,"abstract":"<p >Gestational diabetes mellitus (GDM) is a type of diabetes that arises during pregnancy, leading to long-term adverse consequences for maternal health and fetal development. However, the specific role of endocrine-disrupting chemicals (EDCs) in the pathogenesis of GDM remains controversial. This prospective cohort study sought to investigate how coexposure to bisphenols, parabens, triclosan (TCS), benzophenone-type UV filters, and neonicotinoids (NEOs) affects the odds of GDM. Quantile-based g-computation and Bayesian kernel machine regression showed a significant inverse relationship between EDC mixtures and the reduced risk of GDM (OR = 0.34, 95% CI: 0.13–0.87), which was mainly explained by bisphenol (OR = 0.49, 95% CI: 0.29–0.80) and paraben (OR = 0.60, 95% CI: 0.40–0.91) exposure. Bisphenol S (BPS), bisphenol Z (BPZ), ethylparaben (EtP), propylparaben (PrP), and butylparaben (BuP) were identified as key contributors to the joint effect. In addition, subgroup analyses suggested that the bisphenols-GDM association was more pronounced in younger/normal-weight participants. The sex-specific impact of exposure to bisphenols on the development of GDM was observed, whereas the second trimester represented a critical window for EDC exposure. Continued research efforts, focusing on causal pathways and nonmonotonic relationships, will be crucial to elucidate the complex influence of EDC exposure on the development of GDM.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"3 3","pages":"271–281 271–281"},"PeriodicalIF":0.0,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.acs.org/doi/epdf/10.1021/envhealth.4c00202","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143667138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Independent and Combined Associations between Metals Exposure and Inflammatory Markers among the General U.S. Adults","authors":"Xinrui Feng,&nbsp;Yaoyu Luo,&nbsp;Min Zheng,&nbsp;Xiaojie Sun* and Xiantao Shen*,&nbsp;","doi":"10.1021/envhealth.4c0009710.1021/envhealth.4c00097","DOIUrl":"https://doi.org/10.1021/envhealth.4c00097https://doi.org/10.1021/envhealth.4c00097","url":null,"abstract":"<p >Exposure to metals can trigger a series of diseases by dysregulating the human immune system, but there is still a lack of systematic studies assessing the independent and combined effects of exposure to metals on immune function in the general population, particularly concerning inflammation markers. This cross-sectional study was designed to mainly examine the associations between urinary metal mixtures and inflammatory markers, including white blood cell (WBC), platelet count (PLT), mean platelet volume (MPV), MPV/PLT ratio (MPR), platelet-to-lymphocyte ratio (PLR), and neutrophil-to-lymphocyte ratio (NLR). A total of 3451 participants aged ≥20 years were selected from the 2013–2016 National Health and Nutrition Examination Survey. Generalized linear models were used to investigate the relationships of exposure to single metals on inflammatory markers. Associations between coexposure to multiple metals and inflammatory markers were determined using weighted quantile sum regression and quantile g-computation. Barium, cadmium, lead, thallium, and cobalt showed significant associations with MPV, PLR, and NLR. Metal mixtures showed a negative association with MPV, while they had positive associations with PLR and NLR. Overall, our study highlights the significant effects of multiple metals exposure on inflammation markers, including MPV, PLR, and NLR, among U.S. adults. Thereinto, uranium, cadmium, and cobalt were identified as major contributors. Further prospective studies representative of other countries are warranted to either validate or refute our findings.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"3 3","pages":"282–290 282–290"},"PeriodicalIF":0.0,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.acs.org/doi/epdf/10.1021/envhealth.4c00097","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143667139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}