Environment & Health最新文献

{"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, Yao Yao, Zhihong Huang, Zhihui Guo, Xinxin Tang, Xulong Chen, Xinjie Li, Yiming Ge, Bingjun Lu, Yujie Sha, Shaoyou Lu","doi":"10.1021/envhealth.4c00202","DOIUrl":"10.1021/envhealth.4c00202","url":null,"abstract":"<p><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"},"PeriodicalIF":0.0,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11934205/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143721664","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 Enrichment Exposure Alleviates Geriatric Depressive-Like Symptoms through Regulating Neurogenesis and Neuroinflammation.","authors":"Wei Zhang, Guangyu Jiang, Huiwen Kang, Jingyu Wang, Ziyan Liu, Ziyan Wang, Danyang Huang, Ai Gao","doi":"10.1021/envhealth.4c00186","DOIUrl":"10.1021/envhealth.4c00186","url":null,"abstract":"<p><p>Environmental enrichment (EE) is a significant approach to influencing brain function by altering the environment and changing living conditions and has been shown to modulate mood-related diseases, including depression. Among the elderly, depression is particularly prevalent and is often linked to social isolation. However, the specific role of EE in social isolation-related geriatric depression remains imprecise. This study was intended to explore the status of EE exposure in geriatric depression and to uncover its underlying mechanisms. We utilized 19-month-old male C57BL/6J mice, which are equivalent to humans aged 50-60 years, and induced depression through social isolation. After 2 weeks of social isolation, mice were identified as depressive by using the sugar preference test and then classified into either standard or enrichment environment groups for 4 weeks. Subsequently, conventional indices associated with depression, including neurogenesis, neurotrophic factors, and neuroinflammation, were measured. Results display that EE alleviated the depressive-like symptoms in elderly mice and enriched their social activities. Concurrently, EE regulated levels of certain neurotransmitters in the hippocampus, including the systems of glutamate, tyrosine, and histamine. Moreover, the ability of neurogenesis also increased in the hippocampus of EE mice. At the neuroinflammation level, the activation of Natural Killer (NK) cells and ARG1⁺ microglia is considered a major contributor to mediating the effects of EE-regulated geriatric depression. Collectively, these results underline the importance of EE in the treatment of geriatric depression and partially elucidate its underlying mechanism, offering valuable suggestions for treating social isolation--related depression via environmental modulation.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"3 3","pages":"259-270"},"PeriodicalIF":0.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11934201/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143721663","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 Enrichment Exposure Alleviates Geriatric Depressive-Like Symptoms through Regulating Neurogenesis and Neuroinflammation","authors":"Wei Zhang,&nbsp;Guangyu Jiang,&nbsp;Huiwen Kang,&nbsp;Jingyu Wang,&nbsp;Ziyan Liu,&nbsp;Ziyan Wang,&nbsp;Danyang Huang and Ai Gao*,&nbsp;","doi":"10.1021/envhealth.4c0018610.1021/envhealth.4c00186","DOIUrl":"https://doi.org/10.1021/envhealth.4c00186https://doi.org/10.1021/envhealth.4c00186","url":null,"abstract":"<p >Environmental enrichment (EE) is a significant approach to influencing brain function by altering the environment and changing living conditions and has been shown to modulate mood-related diseases, including depression. Among the elderly, depression is particularly prevalent and is often linked to social isolation. However, the specific role of EE in social isolation-related geriatric depression remains imprecise. This study was intended to explore the status of EE exposure in geriatric depression and to uncover its underlying mechanisms. We utilized 19-month-old male C57BL/6J mice, which are equivalent to humans aged 50–60 years, and induced depression through social isolation. After 2 weeks of social isolation, mice were identified as depressive by using the sugar preference test and then classified into either standard or enrichment environment groups for 4 weeks. Subsequently, conventional indices associated with depression, including neurogenesis, neurotrophic factors, and neuroinflammation, were measured. Results display that EE alleviated the depressive-like symptoms in elderly mice and enriched their social activities. Concurrently, EE regulated levels of certain neurotransmitters in the hippocampus, including the systems of glutamate, tyrosine, and histamine. Moreover, the ability of neurogenesis also increased in the hippocampus of EE mice. At the neuroinflammation level, the activation of Natural Killer (NK) cells and ARG1⁺ microglia is considered a major contributor to mediating the effects of EE-regulated geriatric depression. Collectively, these results underline the importance of EE in the treatment of geriatric depression and partially elucidate its underlying mechanism, offering valuable suggestions for treating social isolation--related depression via environmental modulation.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"3 3","pages":"259–270 259–270"},"PeriodicalIF":0.0,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.acs.org/doi/epdf/10.1021/envhealth.4c00186","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143667137","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":"Protein Biomarkers of DNA Damage in Yeast Cells for Genotoxicity Screening","authors":"Yushi Jin,&nbsp;Boyuan Xue and Xiaohong Zhou*,&nbsp;","doi":"10.1021/envhealth.4c0016010.1021/envhealth.4c00160","DOIUrl":"https://doi.org/10.1021/envhealth.4c00160https://doi.org/10.1021/envhealth.4c00160","url":null,"abstract":"<p >Providing an unbiased and comprehensive view of the DNA damage response in cells is critical in genotoxicity screening to identify substances that cause diverse types of DNA damage. Considering that <i>S. cerevisiae</i> is one of the most well-characterized model organisms in molecular and cellular biology, we created a map of the DNA damage response network containing the reported signaling pathways in yeast cells programmed to constitutively respond to DNA damage. A collection of GFP-fused <i>S. cerevisiae</i> yeast strains treated with typical genotoxic agents illuminated the cellular response to DNA damage, thereby identifying 15 protein biomarkers encompassing all eight documented DNA damage response pathways. Three statistical and one deep learning models were proposed to interpret the quantitative molecular toxicity end point, i.e. protein effect level index (PELI), by introducing weights of 15 biomarkers in genotoxicity assessment. The method based on standard deviation exhibited the best performance, with an <i>R</i>² of 0.916 compared to the SOS/umu test and an <i>R</i>² of 0.989 compared to the comet assay. The GFP-fused yeast-based proteomic assay has minute-level resolution of pathway activation data. It provides a concise alternative for fast, efficient, and mechanistic genotoxicity screening for various environmental and health applications.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"3 3","pages":"250–258 250–258"},"PeriodicalIF":0.0,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.acs.org/doi/epdf/10.1021/envhealth.4c00160","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143667136","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":"Protein Biomarkers of DNA Damage in Yeast Cells for Genotoxicity Screening.","authors":"Yushi Jin, Boyuan Xue, Xiaohong Zhou","doi":"10.1021/envhealth.4c00160","DOIUrl":"10.1021/envhealth.4c00160","url":null,"abstract":"<p><p>Providing an unbiased and comprehensive view of the DNA damage response in cells is critical in genotoxicity screening to identify substances that cause diverse types of DNA damage. Considering that <i>S. cerevisiae</i> is one of the most well-characterized model organisms in molecular and cellular biology, we created a map of the DNA damage response network containing the reported signaling pathways in yeast cells programmed to constitutively respond to DNA damage. A collection of GFP-fused <i>S. cerevisiae</i> yeast strains treated with typical genotoxic agents illuminated the cellular response to DNA damage, thereby identifying 15 protein biomarkers encompassing all eight documented DNA damage response pathways. Three statistical and one deep learning models were proposed to interpret the quantitative molecular toxicity end point, i.e. protein effect level index (PELI), by introducing weights of 15 biomarkers in genotoxicity assessment. The method based on standard deviation exhibited the best performance, with an <i>R</i> ² of 0.916 compared to the SOS/umu test and an <i>R</i> ² of 0.989 compared to the comet assay. The GFP-fused yeast-based proteomic assay has minute-level resolution of pathway activation data. It provides a concise alternative for fast, efficient, and mechanistic genotoxicity screening for various environmental and health applications.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"3 3","pages":"250-258"},"PeriodicalIF":0.0,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11934195/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143721671","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":"Disruption of Copper Redox Balance and Dysfunction under <i>In Vivo</i> and <i>In Vitro</i> Alzheimer's Disease Models.","authors":"Yiteng Xia, Karl W K Tsim, Wen-Xiong Wang","doi":"10.1021/envhealth.4c00175","DOIUrl":"10.1021/envhealth.4c00175","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a neurodegenerative disorder disease mainly caused by extracellular senile plaques (SP) formed by β-amyloid (Aβ1-42) protein deposits. Copper (Cu) is an essential metal involved in neural system, and its homeostasis is the key to maintain its proper function. Herein, the subcellular locations of Cu(I) and Cu(II) in human neurodegenerative disease SH-SY5Y cells and AD mouse brains were imaged. We found that the content of Cu(II) decreased while that of Cu(I) increased under Aβ exposure, which were further verified in the brain tissues of the AD mouse model, strongly suggesting the disruption of Cu homeostasis under Aβ exposure or AD. Remarkably, the mitochondrial and lysosomal Cu(II) decreased significantly, whereas Cu(I) decreased in mitochondria but increased in lysosome. Lysosomes digested the damaged mitochondria via mitophagy to remove excess Cu(I) and maintain Cu homeostasis. The Aβ induced Cu(I) in mitochondria resulted in an overformation of reactive oxygen species and altered the morphology of this organelle. Due to the oxidative stress, glutathione (GSH) was converted into glutathione disulfide (GSSG), and Cu(I) bound with GSH was further released into the cytoplasm and absorbed by the lysosome. Transcriptomic analysis showed that genes (ATP7A/B) related to Cu transportation were upregulated, whereas genes related to mitochondrial complex were down-regulated, representing the damage of this organelle. This study demonstrated that Aβ exposure caused the disruption of intracellular homeostasis by reducing Cu(II) to Cu(I) and damaging the mitochondria, which further triggered detoxification by the lysosome. Our finding provided new insights in Aβ and AD induced Cu redox transformation and toxicity.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"3 3","pages":"238-249"},"PeriodicalIF":0.0,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11934196/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143721641","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":"Disruption of Copper Redox Balance and Dysfunction under In Vivo and In Vitro Alzheimer’s Disease Models","authors":"Yiteng Xia,&nbsp;Karl W. K. Tsim and Wen-Xiong Wang*,&nbsp;","doi":"10.1021/envhealth.4c0017510.1021/envhealth.4c00175","DOIUrl":"https://doi.org/10.1021/envhealth.4c00175https://doi.org/10.1021/envhealth.4c00175","url":null,"abstract":"<p >Alzheimer’s disease (AD) is a neurodegenerative disorder disease mainly caused by extracellular senile plaques (SP) formed by β-amyloid (Aβ1–42) protein deposits. Copper (Cu) is an essential metal involved in neural system, and its homeostasis is the key to maintain its proper function. Herein, the subcellular locations of Cu(I) and Cu(II) in human neurodegenerative disease SH-SY5Y cells and AD mouse brains were imaged. We found that the content of Cu(II) decreased while that of Cu(I) increased under Aβ exposure, which were further verified in the brain tissues of the AD mouse model, strongly suggesting the disruption of Cu homeostasis under Aβ exposure or AD. Remarkably, the mitochondrial and lysosomal Cu(II) decreased significantly, whereas Cu(I) decreased in mitochondria but increased in lysosome. Lysosomes digested the damaged mitochondria via mitophagy to remove excess Cu(I) and maintain Cu homeostasis. The Aβ induced Cu(I) in mitochondria resulted in an overformation of reactive oxygen species and altered the morphology of this organelle. Due to the oxidative stress, glutathione (GSH) was converted into glutathione disulfide (GSSG), and Cu(I) bound with GSH was further released into the cytoplasm and absorbed by the lysosome. Transcriptomic analysis showed that genes (ATP7A/B) related to Cu transportation were upregulated, whereas genes related to mitochondrial complex were down-regulated, representing the damage of this organelle. This study demonstrated that Aβ exposure caused the disruption of intracellular homeostasis by reducing Cu(II) to Cu(I) and damaging the mitochondria, which further triggered detoxification by the lysosome. Our finding provided new insights in Aβ and AD induced Cu redox transformation and toxicity.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"3 3","pages":"238–249 238–249"},"PeriodicalIF":0.0,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.acs.org/doi/epdf/10.1021/envhealth.4c00175","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143667025","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":"Exposure to Manganese Induces Autophagy-Lysosomal Pathway Dysfunction-Mediated Tauopathy by Activating the cGAS-STING Pathway in the Brain.","authors":"Xin Zhang, Jingjing Liu, Shiyin Zhong, Zhimin Zhang, Qiongli Zhou, Jirui Yang, Xuhong Chang, Hui Wang","doi":"10.1021/envhealth.4c00176","DOIUrl":"10.1021/envhealth.4c00176","url":null,"abstract":"<p><p>Manganese (Mn) exposure leads to pathological accumulation of Tau-associated neurodegenerative disease and has become a major public health concern. However, the precise mechanism underlying this effect remains unclear. Here, the mechanism by which Mn induces dysfunction of autophagy-lysosomal pathway-mediated tauopathy by activating the cGAS-STING pathway was explored both <i>in vitro</i> and <i>in vivo</i>. Mn exposure induced tauopathy in microglia and in mice while activating the cGAS-STING pathway, inducing type I interferon production, and impairing the degradation function of the autophagy-lysosomal pathway. Importantly, inactivation of the cGAS-STING pathway rescued the degradation activity of the autophagy-lysosomal pathway, while tauopathy was markedly attenuated, as shown in both <i>cGAS</i>-knockout and <i>STING</i>-knockout BV2 microglia and in mice. Moreover, the autophagy inhibitor 3-methyladenine (3-MA) restored the impaired degradation activity of the autophagy-lysosomal pathway by inactivating the cGAS-STING pathway, thereby clearing Tau aggregation. Taken together, these results indicate that Mn exposure induces tauopathy by impairing the function of the autophagy-lysosomal pathway through the activation of the cGAS-STING pathway. Thus, this study identifies a novel mechanism by which Mn exposure induces Tau aggregation, which in turn triggers potential neurotoxicity, providing a foundation for future drug target research.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"3 2","pages":"199-212"},"PeriodicalIF":0.0,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11851216/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143516949","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":"Exposure to Manganese Induces Autophagy–Lysosomal Pathway Dysfunction-Mediated Tauopathy by Activating the cGAS–STING Pathway in the Brain","authors":"Xin Zhang,&nbsp;Jingjing Liu,&nbsp;Shiyin Zhong,&nbsp;Zhimin Zhang,&nbsp;Qiongli Zhou,&nbsp;Jirui Yang,&nbsp;Xuhong Chang and Hui Wang*,&nbsp;","doi":"10.1021/envhealth.4c0017610.1021/envhealth.4c00176","DOIUrl":"https://doi.org/10.1021/envhealth.4c00176https://doi.org/10.1021/envhealth.4c00176","url":null,"abstract":"<p >Manganese (Mn) exposure leads to pathological accumulation of Tau-associated neurodegenerative disease and has become a major public health concern. However, the precise mechanism underlying this effect remains unclear. Here, the mechanism by which Mn induces dysfunction of autophagy–lysosomal pathway-mediated tauopathy by activating the cGAS–STING pathway was explored both <i>in vitro</i> and <i>in vivo</i>. Mn exposure induced tauopathy in microglia and in mice while activating the cGAS–STING pathway, inducing type I interferon production, and impairing the degradation function of the autophagy–lysosomal pathway. Importantly, inactivation of the cGAS–STING pathway rescued the degradation activity of the autophagy–lysosomal pathway, while tauopathy was markedly attenuated, as shown in both <i>cGAS</i>-knockout and <i>STING</i>-knockout BV2 microglia and in mice. Moreover, the autophagy inhibitor 3-methyladenine (3-MA) restored the impaired degradation activity of the autophagy–lysosomal pathway by inactivating the cGAS–STING pathway, thereby clearing Tau aggregation. Taken together, these results indicate that Mn exposure induces tauopathy by impairing the function of the autophagy–lysosomal pathway through the activation of the cGAS–STING pathway. Thus, this study identifies a novel mechanism by which Mn exposure induces Tau aggregation, which in turn triggers potential neurotoxicity, providing a foundation for future drug target research.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"3 2","pages":"199–212 199–212"},"PeriodicalIF":0.0,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.acs.org/doi/epdf/10.1021/envhealth.4c00176","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143452529","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":"Methyl tert-Butyl Ether May Be a Potential Environmental Pathogenic Factor for Nonalcoholic Fatty Liver Disease: Results from NHANES 2017–2020","authors":"Fengtao Cui,&nbsp;Hanyun Wang,&nbsp;Mingxiao Guo,&nbsp;Yucheng Sun,&nbsp;Ye Xin,&nbsp;Wei Gao,&nbsp;Xingqiang Fang,&nbsp;Li Chen,&nbsp;Piye Niu* and Junxiang Ma*,&nbsp;","doi":"10.1021/envhealth.4c0014010.1021/envhealth.4c00140","DOIUrl":"https://doi.org/10.1021/envhealth.4c00140https://doi.org/10.1021/envhealth.4c00140","url":null,"abstract":"<p >Previous studies have shown that methyl <i>tert</i>-butyl ether (MTBE) could interfere with lipid metabolism. However, there is still a lack of epidemiological reports on the association between MTBE exposure and the risk of nonalcoholic fatty liver disease (NAFLD). In this study, a cross-sectional study was performed with data from the 2017–2020 cycles of the National Health and Nutrition Examination Survey (NHANES). The target population consisted of adults with reliable vibration controlled Transient elastography (VCTE) and blood MTBE concentration results. The hepatic steatosis and fibrosis were assessed by the values of the controlled attenuation parameter (CAP) and liver stiffness measurement (LSM), respectively. Generalized linear mixed model analysis was performed to evaluate the association between MTBE exposure and both steatosis and early liver fibrosis after adjustment for potential confounders. A total of 1303 subjects were enrolled and divided into NAFLD groups (CAP ≥ 248) and non-NAFLD groups (CAP &lt; 248) based on the values of CAP in this study. Generalized linear mixed analysis suggested that blood MTBE concentration was positively associated with NAFLD risk in whole populations (OR: 2.153, 95% confidence interval [CI], 1.176–3.940) and female populations (OR: 11.019, 95% CI: 2.069–58.676). Blood MTBE concentration still showed an obvious positive correlation with the NAFLD risk after excluding factors such as diet and exercise in whole populations. Similarly, a positive correlation between blood MTBE concentration and liver fibrosis was also observed, although the results did not show significant statistical differences. In conclusion, our results indicate that MTBE exposure might be a potential important environmental pathogenic factor for NAFLD.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"3 2","pages":"190–198 190–198"},"PeriodicalIF":0.0,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.acs.org/doi/epdf/10.1021/envhealth.4c00140","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143452543","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}