Background: Although longer working hours are associated with lower sleep quality, it is still necessary to work a certain number of hours to make a living. In this study, we investigated the relationship between working hours and sleep quality in a community setting. We then explored how to manage work style while maintaining the sleep quality of workers without markedly reducing working hours.
Methods: 4388 day-time workers in various occupations living in Ota ward in Tokyo were included in the analysis. The relationship between working hours and sleep quality measured by the Athens Insomnia Scale was examined by ANOVA and linear regression models. Effect modification by work style (work end time, shift in working start and end time, current work from home status, change in work place) on the relationship between working hours and sleep quality was investigated by multivariate linear regression models.
Results: Longer working hours were significantly associated with lower sleep quality. The magnitude of the relationship between long working hours and low sleep quality was significantly larger when work end time was later (p for trend of interaction < 0.01) and when working start and end time were shifted later (vs no change, p for interaction = 0.03). The relationship was marginally greater when the proportion of work from home was increased (vs no change, p for interaction = 0.07).
Conclusions: A relationship between longer working hours and lower sleep quality was observed among workers. Leaving work earlier or optimizing the work environment at home may diminish the adverse effect of long working hours on sleep quality.
背景:虽然较长的工作时间与较低的睡眠质量有关,但人们仍需要工作一定的时间来维持生计。在这项研究中,我们调查了社区环境中工作时间与睡眠质量之间的关系。方法:分析对象包括居住在东京都大田区的 4388 名不同职业的日间工作者。通过方差分析和线性回归模型研究了工作时间与雅典失眠量表测量的睡眠质量之间的关系。通过多变量线性回归模型研究了工作方式(工作结束时间、工作开始和结束时间的转变、目前在家工作的状态、工作地点的改变)对工作时间与睡眠质量之间关系的影响:结果:工作时间越长,睡眠质量越低。工作时间长与睡眠质量低之间的关系,在工作结束时间较晚(交互作用趋势的 p < 0.01)以及工作开始和结束时间较晚(相对于无变化,交互作用的 p = 0.03)时明显更大。当在家工作的比例增加时,两者之间的关系略大(与无变化相比,交互作用的 p = 0.07):结论:在工人中观察到了工作时间延长与睡眠质量下降之间的关系。提前下班或优化在家的工作环境可减少长时间工作对睡眠质量的不利影响。
{"title":"Relationship between working hours and sleep quality with consideration to effect modification by work style: a community-based cross-sectional study.","authors":"Aya Yoshida, Keiko Asakura, Haruhiko Imamura, Sachie Mori, Minami Sugimoto, Takehiro Michikawa, Yuji Nishiwaki","doi":"10.1265/ehpm.23-00252","DOIUrl":"10.1265/ehpm.23-00252","url":null,"abstract":"<p><strong>Background: </strong>Although longer working hours are associated with lower sleep quality, it is still necessary to work a certain number of hours to make a living. In this study, we investigated the relationship between working hours and sleep quality in a community setting. We then explored how to manage work style while maintaining the sleep quality of workers without markedly reducing working hours.</p><p><strong>Methods: </strong>4388 day-time workers in various occupations living in Ota ward in Tokyo were included in the analysis. The relationship between working hours and sleep quality measured by the Athens Insomnia Scale was examined by ANOVA and linear regression models. Effect modification by work style (work end time, shift in working start and end time, current work from home status, change in work place) on the relationship between working hours and sleep quality was investigated by multivariate linear regression models.</p><p><strong>Results: </strong>Longer working hours were significantly associated with lower sleep quality. The magnitude of the relationship between long working hours and low sleep quality was significantly larger when work end time was later (p for trend of interaction < 0.01) and when working start and end time were shifted later (vs no change, p for interaction = 0.03). The relationship was marginally greater when the proportion of work from home was increased (vs no change, p for interaction = 0.07).</p><p><strong>Conclusions: </strong>A relationship between longer working hours and lower sleep quality was observed among workers. Leaving work earlier or optimizing the work environment at home may diminish the adverse effect of long working hours on sleep quality.</p>","PeriodicalId":11707,"journal":{"name":"Environmental Health and Preventive Medicine","volume":"29 ","pages":"19"},"PeriodicalIF":4.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10965413/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140179477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Methylmercury (MeHg), the causative agent of Minamata disease, damages the cranial nervous system and causes specific sensory disturbances, especially hypoesthesia, in the extremities. However, recent reports demonstrate that patients with chronic Minamata disease conversely develop neuropathic pain in the lower extremities. Studies on our established Minamata disease model rats showed that MeHg-mediated neurodegeneration might induce neuropathic pain by over time through inducing rewiring with neuronal activation in the somatosensory cortex via microglial activation in the spinal dorsal horn.
Methods: In this study, the effects of gabapentin, a potentially effective treatment for neuropathic pain, was evaluated using this Minamata disease model rats. To further elucidate the mechanism of its medicinal effects, histochemical and biochemical analyses of the nervous system of Minamata disease model rats were conducted.
Results: Gabapentin treatment restored the reduction in the pain threshold caused by MeHg exposure in rats. Histochemical and biochemical analyses revealed that gabapentin showed no effect on MeHg-induced neurodegeneration in entire nervous system and microglial activation in the spinal dorsal horn. However, it was shown that gabapentin may reduce excessive synaptogenesis through its antagonist action on the alpha2-delta-1 subunit of calcium channels in the somatosensory cortex.
Conclusions: These results indicate that gabapentin may alleviated neuropathic pain in MeHg poisoning, as typified by Minamata disease, by reversibly modulation synaptic rewiring in the somatosensory cortex.
{"title":"Gabapentin improves neuropathic pain in Minamata disease model rats.","authors":"Masatake Fujimura","doi":"10.1265/ehpm.24-00035","DOIUrl":"10.1265/ehpm.24-00035","url":null,"abstract":"<p><strong>Background: </strong>Methylmercury (MeHg), the causative agent of Minamata disease, damages the cranial nervous system and causes specific sensory disturbances, especially hypoesthesia, in the extremities. However, recent reports demonstrate that patients with chronic Minamata disease conversely develop neuropathic pain in the lower extremities. Studies on our established Minamata disease model rats showed that MeHg-mediated neurodegeneration might induce neuropathic pain by over time through inducing rewiring with neuronal activation in the somatosensory cortex via microglial activation in the spinal dorsal horn.</p><p><strong>Methods: </strong>In this study, the effects of gabapentin, a potentially effective treatment for neuropathic pain, was evaluated using this Minamata disease model rats. To further elucidate the mechanism of its medicinal effects, histochemical and biochemical analyses of the nervous system of Minamata disease model rats were conducted.</p><p><strong>Results: </strong>Gabapentin treatment restored the reduction in the pain threshold caused by MeHg exposure in rats. Histochemical and biochemical analyses revealed that gabapentin showed no effect on MeHg-induced neurodegeneration in entire nervous system and microglial activation in the spinal dorsal horn. However, it was shown that gabapentin may reduce excessive synaptogenesis through its antagonist action on the alpha2-delta-1 subunit of calcium channels in the somatosensory cortex.</p><p><strong>Conclusions: </strong>These results indicate that gabapentin may alleviated neuropathic pain in MeHg poisoning, as typified by Minamata disease, by reversibly modulation synaptic rewiring in the somatosensory cortex.</p>","PeriodicalId":11707,"journal":{"name":"Environmental Health and Preventive Medicine","volume":"29 ","pages":"31"},"PeriodicalIF":4.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11157338/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141199749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Francisco Díaz-Martínez, Miguel F Sánchez-Sauco, Laura T Cabrera-Rivera, Claudia A Ortín-Fernández, Esteban Orenes-Piñero, Juan A Ortega-García
Background: Substance abuse is a global problem that cuts across all sectors of society and requires innovative solutions that go beyond conventional treatments. Contact with nature could be a complementary tool to address drug-related problems. This review aimed to assess the impact of natural environments on drug-related outcomes.
Method: 8205 articles were screened between 2013 and 2023 from 6 databases, of which 21 met the inclusion criteria.
Results: Most studies (12) focused on treatment, followed by incidence/consumption (7), prevention (5) and mortality (1). The main drugs studied were drugs in general (12), followed by alcohol (6), tobacco (6), and other drugs, including cannabis and opioids (4). The results of 85% of the studies showed positive outcomes, supporting the effectiveness of nature-based interventions for drug dependence. While some studies produced neutral or negative results.
Conclusion: The use of nature-based interventions for the prevention and treatment of drug addiction shows considerable potential. However, more research is needed to understand the underlying mechanisms and to improve evidence-based interventions. Integrating health and environmental policies is essential to promote a holistic approach to drug strategies at the national and international levels.
{"title":"Harnessing the healing power of nature: a review of natural interventions in substance abuse treatment and prevention.","authors":"Francisco Díaz-Martínez, Miguel F Sánchez-Sauco, Laura T Cabrera-Rivera, Claudia A Ortín-Fernández, Esteban Orenes-Piñero, Juan A Ortega-García","doi":"10.1265/ehpm.24-00145","DOIUrl":"10.1265/ehpm.24-00145","url":null,"abstract":"<p><strong>Background: </strong>Substance abuse is a global problem that cuts across all sectors of society and requires innovative solutions that go beyond conventional treatments. Contact with nature could be a complementary tool to address drug-related problems. This review aimed to assess the impact of natural environments on drug-related outcomes.</p><p><strong>Method: </strong>8205 articles were screened between 2013 and 2023 from 6 databases, of which 21 met the inclusion criteria.</p><p><strong>Results: </strong>Most studies (12) focused on treatment, followed by incidence/consumption (7), prevention (5) and mortality (1). The main drugs studied were drugs in general (12), followed by alcohol (6), tobacco (6), and other drugs, including cannabis and opioids (4). The results of 85% of the studies showed positive outcomes, supporting the effectiveness of nature-based interventions for drug dependence. While some studies produced neutral or negative results.</p><p><strong>Conclusion: </strong>The use of nature-based interventions for the prevention and treatment of drug addiction shows considerable potential. However, more research is needed to understand the underlying mechanisms and to improve evidence-based interventions. Integrating health and environmental policies is essential to promote a holistic approach to drug strategies at the national and international levels.</p>","PeriodicalId":11707,"journal":{"name":"Environmental Health and Preventive Medicine","volume":"29 ","pages":"64"},"PeriodicalIF":4.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11570648/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142616750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Organophosphate flame retardants (OPFRs) are commonly used in various consumer products to prevent fire hazards. However, OPFRs have been linked to several health problems, including cancer. This study aimed to investigate the association between urine levels of OPFRs and endometrial cancer (EC), and to explore the correlation between concentrations of parent OPFR compounds and their metabolites.
Methods: Urine samples from 76 EC patients and 76 healthy controls were collected and analyzed for the levels of five common parent OPFRs and their respective metabolites. Propensity score matching was applied to account for differences in baseline characteristics between the two participant groups. Significantly higher levels of OPFRs in EC patients were identified, and logistic regression models were used to determine whether elevated OPFRs were associated with EC and to explore whether any lifestyle behaviors contributed to the increased OPFR levels. Spearman's rank correlation coefficients between the concentrations of the parent compounds and their metabolites were calculated.
Results: Out of the ten OPFRs studied, the median urine levels of bis(1,3-dichloro-2-propyl) phosphate (BDCPP), tris(2-butoxyethyl) phosphate (TBEP), and di-(2-butoxyethyl) phosphate (DBEP) were significantly higher in EC patients compared to healthy controls. After matching 41 patients with 41 controls, multiple logistic regression analysis revealed that only BDCPP (OR 4.274; 95% CI 1.172-15.592) was an independent factor associated with EC. A lifestyle questionnaire survey found that urine BDCPP levels were related to age (OR 4.294; 95% CI 1.015-18.164), meals eaten out (OR 4.238; 95% CI 1.454-12.354), and consumption of chilled-ready meals (OR 0.118; 95% CI 0.014-0.985). A positive correlation was only observed between the concentrations of TBEP and its metabolite DBEP; other correlations were not significant.
Conclusion: We concluded that higher urine BDCPP level was an independent factor associated with EC, and higher BDCPP levels were related to aging, more meals eaten out, and fewer chilled-ready meals. These findings highlight the potential hazard of long-term OPFR exposure on the development of EC.
背景:有机磷阻燃剂(OPFR)通常用于各种消费品,以防止火灾危险。然而,有机磷阻燃剂与包括癌症在内的多种健康问题有关。本研究旨在调查尿液中 OPFRs 水平与子宫内膜癌(EC)之间的关联,并探讨 OPFR 母体化合物及其代谢物浓度之间的相关性:收集了76名子宫内膜癌患者和76名健康对照者的尿液样本,分析了五种常见母体OPFR及其代谢物的水平。为了考虑两组参与者基线特征的差异,采用了倾向得分匹配法。研究发现,心血管疾病患者的 OPFR 水平明显较高,因此采用逻辑回归模型来确定 OPFR 的升高是否与心血管疾病有关,并探讨是否有任何生活方式导致 OPFR 水平升高。计算了母体化合物及其代谢物浓度之间的斯皮尔曼等级相关系数:结果:在所研究的十种 OPFRs 中,与健康对照组相比,EC 患者尿液中磷酸二(1,3-二氯-2-丙基)酯(BDCPP)、磷酸三(2-丁氧基乙基)酯(TBEP)和磷酸二(2-丁氧基乙基)酯(DBEP)的中位数水平明显较高。在对41名患者和41名对照组进行配对后,多元逻辑回归分析表明,只有BDCPP(OR 4.274;95% CI 1.172-15.592)是与EC相关的独立因素。生活方式问卷调查发现,尿液中的 BDCPP 水平与年龄(OR 4.294;95% CI 1.015-18.164)、在外就餐(OR 4.238;95% CI 1.454-12.354)和食用冷藏即食食品(OR 0.118;95% CI 0.014-0.985)有关。仅观察到 TBEP 及其代谢物 DBEP 的浓度之间存在正相关;其他相关性不显著:我们得出的结论是,尿液中 BDCPP 含量较高是诱发心血管疾病的一个独立因素,而 BDCPP 含量较高与年龄增长、外出就餐次数较多和冷藏即食食品较少有关。这些发现凸显了长期暴露于 OPFR 对诱发心肌梗死的潜在危害。
{"title":"Lifestyle factors and urine levels of organophosphorus flame retardants in endometrial cancer: insights from a case-control study.","authors":"Yu-Che Ou, Fu-Jen Cheng, Wan-Ting Huang, Wen-Chin Lee, Hung-Chun Fu, Chen-Hsuan Wu, Ying-Yi Chen, Kuo-Chung Lan, Xuan-Ping Liou, Hao Lin, Chia-Te Kung","doi":"10.1265/ehpm.24-00175","DOIUrl":"10.1265/ehpm.24-00175","url":null,"abstract":"<p><strong>Background: </strong>Organophosphate flame retardants (OPFRs) are commonly used in various consumer products to prevent fire hazards. However, OPFRs have been linked to several health problems, including cancer. This study aimed to investigate the association between urine levels of OPFRs and endometrial cancer (EC), and to explore the correlation between concentrations of parent OPFR compounds and their metabolites.</p><p><strong>Methods: </strong>Urine samples from 76 EC patients and 76 healthy controls were collected and analyzed for the levels of five common parent OPFRs and their respective metabolites. Propensity score matching was applied to account for differences in baseline characteristics between the two participant groups. Significantly higher levels of OPFRs in EC patients were identified, and logistic regression models were used to determine whether elevated OPFRs were associated with EC and to explore whether any lifestyle behaviors contributed to the increased OPFR levels. Spearman's rank correlation coefficients between the concentrations of the parent compounds and their metabolites were calculated.</p><p><strong>Results: </strong>Out of the ten OPFRs studied, the median urine levels of bis(1,3-dichloro-2-propyl) phosphate (BDCPP), tris(2-butoxyethyl) phosphate (TBEP), and di-(2-butoxyethyl) phosphate (DBEP) were significantly higher in EC patients compared to healthy controls. After matching 41 patients with 41 controls, multiple logistic regression analysis revealed that only BDCPP (OR 4.274; 95% CI 1.172-15.592) was an independent factor associated with EC. A lifestyle questionnaire survey found that urine BDCPP levels were related to age (OR 4.294; 95% CI 1.015-18.164), meals eaten out (OR 4.238; 95% CI 1.454-12.354), and consumption of chilled-ready meals (OR 0.118; 95% CI 0.014-0.985). A positive correlation was only observed between the concentrations of TBEP and its metabolite DBEP; other correlations were not significant.</p><p><strong>Conclusion: </strong>We concluded that higher urine BDCPP level was an independent factor associated with EC, and higher BDCPP levels were related to aging, more meals eaten out, and fewer chilled-ready meals. These findings highlight the potential hazard of long-term OPFR exposure on the development of EC.</p>","PeriodicalId":11707,"journal":{"name":"Environmental Health and Preventive Medicine","volume":"29 ","pages":"63"},"PeriodicalIF":4.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11570647/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142616755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Aristolochic acid nephropathy (AAN) is a rapidly progressive interstitial nephropathy caused by Aristolochic acid (AA). AAN is associated with the development of nephropathy and urothelial carcinoma. It is estimated that more than 100 million people worldwide are at risk of developing AAN. However, the underlying mechanisms driving renal deterioration in AAN remain poorly understood, and the treatment options are limited.
Methods: We obtained GSE27168 and GSE136276 series matrix data from the Gene Expression Omnibus (GEO) related to AAN. Using the R Studio environment, we applied the limma package and WGCNA package to identify co-differently expressed genes (co-DEGs). By GO/KEGG/GSVA analysis, we revealed common biological pathways. Subsequently, co-DEGs were subjected to the String database to construct a protein-protein interaction (PPI) network. The MCC algorithms implemented in the Cytohubba plugin were employed to identify hub genes. The hub genes were cross-referenced with the transcription factor (TF) database to identify hub TFs. Immune infiltration analysis was performed to identify key immune cell groups by utilizing CIBERSORT. The expressions of AAN-associated hub TFs were verified in vivo and in vitro. Finally, siRNA intervention was performed on the two TFs to verify their regulatory effect in AAN.
Results: Our analysis identified 88 co-DEGs through the "limma" and "WGCNA" R packages. A PPI network comprising 53 nodes and 34 edges was constructed with a confidence level >0.4. ATF3 and c-JUN were identified as hub TFs potentially linked to AAN. Additionally, expressions of ATF3 and c-JUN positively correlated with monocytes, basophils, and vessels, and negatively correlated with eosinophils and endothelial cells. We observed a significant increase in protein and mRNA levels of these two hub TFs. Furthermore, it was found that siRNA intervention targeting ATF3, but not c-JUN, alleviated cell damage induced by AA. The knockdown of ATF3 protects against oxidative stress and inflammation in the AAN cell model.
Conclusion: This study provides novel insights into the role of ATF3 in AAN. The comprehensive analysis sheds light on the molecular mechanisms and identifies potential biomarkers and drug targets for AAN treatment.
背景:马兜铃酸肾病(AAN)是一种由马兜铃酸(AA)引起的快速进展性间质性肾病。AAN 与肾病和尿路癌的发生有关。据估计,全球有 1 亿多人面临罹患 AAN 的风险。然而,人们对导致 AAN 肾功能恶化的潜在机制仍知之甚少,治疗方案也很有限:我们从基因表达总库(Gene Expression Omnibus,GEO)中获得了与 AAN 相关的 GSE27168 和 GSE136276 系列矩阵数据。利用 R Studio 环境,我们使用 limma 软件包和 WGCNA 软件包来识别共差异表达基因(co-DEGs)。通过 GO/KEGG/GSVA 分析,我们发现了共同的生物学通路。随后,共差异表达基因被纳入 String 数据库,以构建蛋白质-蛋白质相互作用(PPI)网络。我们使用 Cytohubba 插件中的 MCC 算法来识别中心基因。将中心基因与转录因子(TF)数据库进行交叉比对,以确定中心 TF。利用 CIBERSORT 进行了免疫浸润分析,以确定关键的免疫细胞群。在体内和体外验证了 AAN 相关枢纽 TF 的表达。最后,对这两个TFs进行了siRNA干预,以验证它们在AAN中的调控作用:我们的分析通过 "limma "和 "WGCNA "R软件包确定了88个共DEGs。我们构建了一个由 53 个节点和 34 条边组成的 PPI 网络,其置信度大于 0.4。ATF3和c-JUN被确定为可能与AAN相关的枢纽TF。此外,ATF3 和 c-JUN 的表达与单核细胞、嗜碱性粒细胞和血管呈正相关,与嗜酸性粒细胞和内皮细胞呈负相关。我们观察到这两种枢纽 TF 的蛋白和 mRNA 水平都有明显增加。此外,我们还发现靶向 ATF3 的 siRNA(而非 c-JUN)能减轻 AA 引起的细胞损伤。在AAN细胞模型中,敲除ATF3可保护细胞免受氧化应激和炎症的影响:本研究为了解 ATF3 在 AAN 中的作用提供了新的视角。综合分析揭示了分子机制,并确定了治疗 AAN 的潜在生物标志物和药物靶点。
{"title":"Identification and analysis of differently expressed transcription factors in aristolochic acid nephropathy.","authors":"Yi-Feng Wu, Zhi-Yao Tang, Yi-Xuan Deng, Kun Liu, Xu-Rui Gu, Guang-Liang Zhou, Yu-Jie Huang, Xiao-Qing Lin, Lin-Yun Zhou, Xiao-Cong Zuo","doi":"10.1265/ehpm.23-00245","DOIUrl":"10.1265/ehpm.23-00245","url":null,"abstract":"<p><strong>Background: </strong>Aristolochic acid nephropathy (AAN) is a rapidly progressive interstitial nephropathy caused by Aristolochic acid (AA). AAN is associated with the development of nephropathy and urothelial carcinoma. It is estimated that more than 100 million people worldwide are at risk of developing AAN. However, the underlying mechanisms driving renal deterioration in AAN remain poorly understood, and the treatment options are limited.</p><p><strong>Methods: </strong>We obtained GSE27168 and GSE136276 series matrix data from the Gene Expression Omnibus (GEO) related to AAN. Using the R Studio environment, we applied the limma package and WGCNA package to identify co-differently expressed genes (co-DEGs). By GO/KEGG/GSVA analysis, we revealed common biological pathways. Subsequently, co-DEGs were subjected to the String database to construct a protein-protein interaction (PPI) network. The MCC algorithms implemented in the Cytohubba plugin were employed to identify hub genes. The hub genes were cross-referenced with the transcription factor (TF) database to identify hub TFs. Immune infiltration analysis was performed to identify key immune cell groups by utilizing CIBERSORT. The expressions of AAN-associated hub TFs were verified in vivo and in vitro. Finally, siRNA intervention was performed on the two TFs to verify their regulatory effect in AAN.</p><p><strong>Results: </strong>Our analysis identified 88 co-DEGs through the \"limma\" and \"WGCNA\" R packages. A PPI network comprising 53 nodes and 34 edges was constructed with a confidence level >0.4. ATF3 and c-JUN were identified as hub TFs potentially linked to AAN. Additionally, expressions of ATF3 and c-JUN positively correlated with monocytes, basophils, and vessels, and negatively correlated with eosinophils and endothelial cells. We observed a significant increase in protein and mRNA levels of these two hub TFs. Furthermore, it was found that siRNA intervention targeting ATF3, but not c-JUN, alleviated cell damage induced by AA. The knockdown of ATF3 protects against oxidative stress and inflammation in the AAN cell model.</p><p><strong>Conclusion: </strong>This study provides novel insights into the role of ATF3 in AAN. The comprehensive analysis sheds light on the molecular mechanisms and identifies potential biomarkers and drug targets for AAN treatment.</p>","PeriodicalId":11707,"journal":{"name":"Environmental Health and Preventive Medicine","volume":"29 ","pages":"30"},"PeriodicalIF":4.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11157247/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141080688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yizhang Xia, Chunli Shi, Yang Li, Shijuan Ruan, Xianyan Jiang, Wei Huang, Yu Chen, Xufang Gao, Rong Xue, Mingjiang Li, Hongying Sun, Xiaojuan Peng, Renqiang Xiang, Jianyu Chen, Li Zhang
Background: There are few multi-city studies on the association between temperature and mortality in basin climates. This study was based on the Sichuan Basin in southwest China to assess the association of basin temperature with non-accidental mortality in the population and with the temperature-related mortality burden.
Methods: Daily mortality data, meteorological and air pollution data were collected for four cities in the Sichuan Basin of southwest China. We used a two-stage time-series analysis to quantify the association between temperature and non-accidental mortality in each city, and a multivariate meta-analysis was performed to obtain the overall cumulative risk. The attributable fractions (AFs) were calculated to access the mortality burden attributable to non-optimal temperature. Additionally, we performed a stratified analyses by gender, age group, education level, and marital status.
Results: A total of 751,930 non-accidental deaths were collected in our study. Overall, 10.16% of non-accidental deaths could be attributed to non-optimal temperatures. A majority of temperature-related non-accidental deaths were caused by low temperature, accounting for 9.10% (95% eCI: 5.50%, 12.19%), and heat effects accounted for only 1.06% (95% eCI: 0.76%, 1.33%). The mortality burden attributable to non-optimal temperatures was higher among those under 65 years old, females, those with a low education level, and those with an alternative marriage status.
Conclusions: Our study suggested that a significant association between non-optimal temperature and non-accidental mortality. Those under 65 years old, females, and those with a low educational level or alternative marriage status had the highest attributable burden.
{"title":"Association between temperature and mortality: a multi-city time series study in Sichuan Basin, southwest China.","authors":"Yizhang Xia, Chunli Shi, Yang Li, Shijuan Ruan, Xianyan Jiang, Wei Huang, Yu Chen, Xufang Gao, Rong Xue, Mingjiang Li, Hongying Sun, Xiaojuan Peng, Renqiang Xiang, Jianyu Chen, Li Zhang","doi":"10.1265/ehpm.23-00118","DOIUrl":"10.1265/ehpm.23-00118","url":null,"abstract":"<p><strong>Background: </strong>There are few multi-city studies on the association between temperature and mortality in basin climates. This study was based on the Sichuan Basin in southwest China to assess the association of basin temperature with non-accidental mortality in the population and with the temperature-related mortality burden.</p><p><strong>Methods: </strong>Daily mortality data, meteorological and air pollution data were collected for four cities in the Sichuan Basin of southwest China. We used a two-stage time-series analysis to quantify the association between temperature and non-accidental mortality in each city, and a multivariate meta-analysis was performed to obtain the overall cumulative risk. The attributable fractions (AFs) were calculated to access the mortality burden attributable to non-optimal temperature. Additionally, we performed a stratified analyses by gender, age group, education level, and marital status.</p><p><strong>Results: </strong>A total of 751,930 non-accidental deaths were collected in our study. Overall, 10.16% of non-accidental deaths could be attributed to non-optimal temperatures. A majority of temperature-related non-accidental deaths were caused by low temperature, accounting for 9.10% (95% eCI: 5.50%, 12.19%), and heat effects accounted for only 1.06% (95% eCI: 0.76%, 1.33%). The mortality burden attributable to non-optimal temperatures was higher among those under 65 years old, females, those with a low education level, and those with an alternative marriage status.</p><p><strong>Conclusions: </strong>Our study suggested that a significant association between non-optimal temperature and non-accidental mortality. Those under 65 years old, females, and those with a low educational level or alternative marriage status had the highest attributable burden.</p>","PeriodicalId":11707,"journal":{"name":"Environmental Health and Preventive Medicine","volume":"29 ","pages":"1"},"PeriodicalIF":4.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10788187/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139466333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Many studies have reported that the Omicron variant is less pathogenic than the Delta variant and the wild-type. Epidemiological evidence regarding the risk of severe COVID-19 from the wild-type to the Omicron variant has been lacking.
Methods: Study participants were COVID-19 patients aged 18 and older without previous COVID-19 infection who were notified to the Nara Prefecture Chuwa Public Health Center from January 2020 to March 2023, during the periods from the wild-type to the Omicron variant. The outcome variable was severe COVID-19 (i.e., ICU admission or COVID-19-related death). The explanatory variable was SARS-CoV-2 variant type or the number of COVID-19 vaccinations. Covariates included gender, age, risk factors for aggravation, and the number of general hospital beds per population. The generalized estimating equations of negative binomial regression models were used to estimate the adjusted incidence proportion (AIP) with 95% confidence interval (CI) for severe COVID-19.
Results: Among 77,044 patients included in the analysis, 14,556 (18.9%) were unvaccinated and 520 (0.7%) developed severe COVID-19. Among unvaccinated patients, the risk of severe COVID-19 increased in the Alpha/Delta variants and decreased in the Omicron variant compared to the wild-type (AIP [95% CI] was 1.55 [1.06-2.27] in Alpha/Delta and 0.25 [0.15-0.40] in Omicron), but differed by age. Especially in patients aged ≥80, there was no significant difference in the risk of severe COVID-19 between the wild-type and the Omicron variant (AIP [95% CI] = 0.59 [0.27-1.29]). Regarding the preventive effect of vaccines, among all study participants, the number of vaccinations was significantly associated with the prevention of severe COVID-19, regardless of variant type. After stratified analyses by age, patients aged ≥80 remained a significant association for all variant types. On the other hand, the number of vaccinations had no association in Omicron BA.5 of patients aged 18-64.
Conclusions: Patients aged ≥80 had less reduction in risk of severe COVID-19 during the Omicron variant period, and a greater preventive effect of vaccines against severe COVID-19, compared to younger people. Our findings suggest that booster vaccination is effective and necessary for older people, especially aged ≥80.
{"title":"Risk of severe COVID-19 in unvaccinated patients during the period from wild-type to Omicron variant: real-world evidence from Japan.","authors":"Kimiko Tomioka, Kenji Uno, Masahiro Yamada","doi":"10.1265/ehpm.23-00274","DOIUrl":"10.1265/ehpm.23-00274","url":null,"abstract":"<p><strong>Background: </strong>Many studies have reported that the Omicron variant is less pathogenic than the Delta variant and the wild-type. Epidemiological evidence regarding the risk of severe COVID-19 from the wild-type to the Omicron variant has been lacking.</p><p><strong>Methods: </strong>Study participants were COVID-19 patients aged 18 and older without previous COVID-19 infection who were notified to the Nara Prefecture Chuwa Public Health Center from January 2020 to March 2023, during the periods from the wild-type to the Omicron variant. The outcome variable was severe COVID-19 (i.e., ICU admission or COVID-19-related death). The explanatory variable was SARS-CoV-2 variant type or the number of COVID-19 vaccinations. Covariates included gender, age, risk factors for aggravation, and the number of general hospital beds per population. The generalized estimating equations of negative binomial regression models were used to estimate the adjusted incidence proportion (AIP) with 95% confidence interval (CI) for severe COVID-19.</p><p><strong>Results: </strong>Among 77,044 patients included in the analysis, 14,556 (18.9%) were unvaccinated and 520 (0.7%) developed severe COVID-19. Among unvaccinated patients, the risk of severe COVID-19 increased in the Alpha/Delta variants and decreased in the Omicron variant compared to the wild-type (AIP [95% CI] was 1.55 [1.06-2.27] in Alpha/Delta and 0.25 [0.15-0.40] in Omicron), but differed by age. Especially in patients aged ≥80, there was no significant difference in the risk of severe COVID-19 between the wild-type and the Omicron variant (AIP [95% CI] = 0.59 [0.27-1.29]). Regarding the preventive effect of vaccines, among all study participants, the number of vaccinations was significantly associated with the prevention of severe COVID-19, regardless of variant type. After stratified analyses by age, patients aged ≥80 remained a significant association for all variant types. On the other hand, the number of vaccinations had no association in Omicron BA.5 of patients aged 18-64.</p><p><strong>Conclusions: </strong>Patients aged ≥80 had less reduction in risk of severe COVID-19 during the Omicron variant period, and a greater preventive effect of vaccines against severe COVID-19, compared to younger people. Our findings suggest that booster vaccination is effective and necessary for older people, especially aged ≥80.</p>","PeriodicalId":11707,"journal":{"name":"Environmental Health and Preventive Medicine","volume":"29 ","pages":"10"},"PeriodicalIF":4.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10937246/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140049069","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: High blood pressure (HBP) and diabetes mellitus (DM) are two of the most prevalent cardiometabolic disorders globally, especially among individuals with lower socio-economic status (SES). Studies have linked residential greenness to decreased risks of HBP and DM. However, there has been limited evidence on whether SES may modify the associations of residential greenness with HBP and DM.
Methods: Based on a national representative cross-sectional study among 44,876 adults, we generated the normalized difference vegetation index (NDVI) at 1 km spatial resolution to characterize individuals' residential greenness level. Administrative classification (urban/rural), nighttime light index (NLI), individual income, and educational levels were used to characterize regional urbanicity and individual SES levels.
Results: We observed weaker inverse associations of NDVI with HBP and DM in rural regions compared to urban regions. For instance, along with per interquartile range (IQR, 0.26) increment in residential NDVI at 0∼5 year moving averages, the ORs of HBP were 1.04 (95%CI: 0.94, 1.15) in rural regions and 0.85 (95%CI: 0.79, 0.93) in urban regions (P = 0.003). Along with the decrease in NLI levels, there were continuously decreasing inverse associations of NDVI with DM prevalence (P for interaction <0.001). In addition, weaker inverse associations of residential NDVI with HBP and DM prevalence were found among individuals with lower income and lower education levels compared to their counterparts.
Conclusions: Lower regional urbanicity and individual SES could attenuate the associations of residential greenness with odds of HBP and DM prevalence.
{"title":"Lower regional urbanicity and socioeconomic status attenuate associations of green spaces with hypertension and diabetes mellitus: a national representative cross-sectional study in China.","authors":"Wanzhou Wang, Chao Yang, Jinwei Wang, Fulin Wang, Ze Liang, Yueyao Wang, Feifei Zhang, Chenyu Liang, Chenshuang Li, Yiqun Lan, Shuangcheng Li, Pengfei Li, Ying Zhou, Luxia Zhang, Lieyun Ding","doi":"10.1265/ehpm.24-00121","DOIUrl":"10.1265/ehpm.24-00121","url":null,"abstract":"<p><strong>Background: </strong>High blood pressure (HBP) and diabetes mellitus (DM) are two of the most prevalent cardiometabolic disorders globally, especially among individuals with lower socio-economic status (SES). Studies have linked residential greenness to decreased risks of HBP and DM. However, there has been limited evidence on whether SES may modify the associations of residential greenness with HBP and DM.</p><p><strong>Methods: </strong>Based on a national representative cross-sectional study among 44,876 adults, we generated the normalized difference vegetation index (NDVI) at 1 km spatial resolution to characterize individuals' residential greenness level. Administrative classification (urban/rural), nighttime light index (NLI), individual income, and educational levels were used to characterize regional urbanicity and individual SES levels.</p><p><strong>Results: </strong>We observed weaker inverse associations of NDVI with HBP and DM in rural regions compared to urban regions. For instance, along with per interquartile range (IQR, 0.26) increment in residential NDVI at 0∼5 year moving averages, the ORs of HBP were 1.04 (95%CI: 0.94, 1.15) in rural regions and 0.85 (95%CI: 0.79, 0.93) in urban regions (P = 0.003). Along with the decrease in NLI levels, there were continuously decreasing inverse associations of NDVI with DM prevalence (P for interaction <0.001). In addition, weaker inverse associations of residential NDVI with HBP and DM prevalence were found among individuals with lower income and lower education levels compared to their counterparts.</p><p><strong>Conclusions: </strong>Lower regional urbanicity and individual SES could attenuate the associations of residential greenness with odds of HBP and DM prevalence.</p>","PeriodicalId":11707,"journal":{"name":"Environmental Health and Preventive Medicine","volume":"29 ","pages":"47"},"PeriodicalIF":4.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11391273/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142153375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xiqiang Zhang, Longchao Wu, Yu Li, Ze Tao, Na Li, Haoyang Zhang, Ming Ren, Kexin Wang
Background: Vascular intestinal disease is a major health concern that often requires emergency surgery in patients with intestinal obstruction, perforation, or bowel necrosis. We aimed to provide data on the incidence, prevalence, mortality and disability-adjusted life years (DALYs) of vascular intestinal diseases from 1990 to 2021, thereby contributing to the development of health policies.
Methods: Using standardized methods from the 2021 Global Burden of Disease study, we analyzed the incidence, prevalence, mortality, and DALYs of vascular intestinal disease from the perspectives of the sociodemographic index (SDI), regional, and country, along with the corresponding estimated annual percentage changes. Additionally, we used join-point regression to identify the key time points for disease burden changes.
Results: In 2021, a total of 169,432 cases [95% uncertainty interval (UI): 155,127-185,189] of vascular intestinal disease were identified worldwide. The age-standardized incidence rate decreased from 18.81 (95% UI: 16.07-21.73) in 1990 to 15.98 (95% UI: 13.99-19.10) in 2021. In 2021, the age-standardized mortality rate was 1.12/100,000 people (95% UI: 1.00-1.21). Over the 32-year period, the global DALYs rate declined by 1.44 (95% Confidence Interval: -1.55 to -1.34). Within the five SDI regions, the high-middle SDI areas recorded the peak standardized mortality rates in 2021. Regionally, the greatest increase in incidence occurred in North Africa and the Middle East. Canada recorded the greatest national incidence rate [58.35 (95% UI: 50.05-67.37)] in 2021 among 204 countries, while Russia exhibited the highest related mortality [5.64/100,000 people (95% UI: 5.19-6.11)] and DALYs rate [101.48/100,000 people (95% UI: 93.83-109.66)].
Conclusions: Despite a global decline in the burden of vascular intestinal disease from 1990 to 2021, significant regional and national disparities persist and the disease burden among the elderly has increased.
{"title":"The global burden of vascular intestinal diseases: results from the 2021 Global Burden of Disease Study and projections using Bayesian age-period-cohort analysis.","authors":"Xiqiang Zhang, Longchao Wu, Yu Li, Ze Tao, Na Li, Haoyang Zhang, Ming Ren, Kexin Wang","doi":"10.1265/ehpm.24-00206","DOIUrl":"10.1265/ehpm.24-00206","url":null,"abstract":"<p><strong>Background: </strong>Vascular intestinal disease is a major health concern that often requires emergency surgery in patients with intestinal obstruction, perforation, or bowel necrosis. We aimed to provide data on the incidence, prevalence, mortality and disability-adjusted life years (DALYs) of vascular intestinal diseases from 1990 to 2021, thereby contributing to the development of health policies.</p><p><strong>Methods: </strong>Using standardized methods from the 2021 Global Burden of Disease study, we analyzed the incidence, prevalence, mortality, and DALYs of vascular intestinal disease from the perspectives of the sociodemographic index (SDI), regional, and country, along with the corresponding estimated annual percentage changes. Additionally, we used join-point regression to identify the key time points for disease burden changes.</p><p><strong>Results: </strong>In 2021, a total of 169,432 cases [95% uncertainty interval (UI): 155,127-185,189] of vascular intestinal disease were identified worldwide. The age-standardized incidence rate decreased from 18.81 (95% UI: 16.07-21.73) in 1990 to 15.98 (95% UI: 13.99-19.10) in 2021. In 2021, the age-standardized mortality rate was 1.12/100,000 people (95% UI: 1.00-1.21). Over the 32-year period, the global DALYs rate declined by 1.44 (95% Confidence Interval: -1.55 to -1.34). Within the five SDI regions, the high-middle SDI areas recorded the peak standardized mortality rates in 2021. Regionally, the greatest increase in incidence occurred in North Africa and the Middle East. Canada recorded the greatest national incidence rate [58.35 (95% UI: 50.05-67.37)] in 2021 among 204 countries, while Russia exhibited the highest related mortality [5.64/100,000 people (95% UI: 5.19-6.11)] and DALYs rate [101.48/100,000 people (95% UI: 93.83-109.66)].</p><p><strong>Conclusions: </strong>Despite a global decline in the burden of vascular intestinal disease from 1990 to 2021, significant regional and national disparities persist and the disease burden among the elderly has increased.</p>","PeriodicalId":11707,"journal":{"name":"Environmental Health and Preventive Medicine","volume":"29 ","pages":"71"},"PeriodicalIF":4.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11653002/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Current experimental evidence supports that ethylene oxide (EO) exposure-related pathophysiologies may affect glucose metabolism, but few population-based studies have explored the potential links.
Methods: This study used cross-sectional data from 15560 participants in the National Health and Nutrition Examination Survey (NHANES) from 2017 to 2020. EO exposure levels were calculated by testing hemoglobin adducts of EO (HbEO) via a modified Edman reaction. We focused on the association of EO exposure with prediabetes and diabetes as well as indicators of impaired glucose metabolism and further analyzed the potential pathogenic mechanisms. Statistics included logistic regression, generalized additive model fitting, penalized spline method, two-piecewise linear regression, recursive algorithm, mediation analysis, and Pearson's analysis.
Results: EO exposure was associated with changes in glucose metabolic indicators and increased prevalence of prediabetes and diabetes, showing age-consistency and being more pronounced in obese and non-smoking populations. For each one pmol/g Hb, one SD, or two-fold SD increase in log2-HbEO, the risk of prediabetes increased by 12%, 16%, and 33%, with an increased risk of diabetes by 18%, 26%, and 61%, respectively. Dose-response curves revealed that this positive correlation was approximately linear with prediabetes and "J" shaped with diabetes. When log2-HbEO > 8.03 pmol/g Hb, the risk of diabetes would be further increased. Pearson's correlation revealed that EO exposure was associated with reduced fasting insulin and elevated HbA1c in the prediabetic stage. While in the diabetes stage, EO exposure was correlated with elevated fasting glucose, HbA1c, and HOMA-IR, suggesting an exacerbation of diabetes progression by EO exposure. A potential mechanism that the early stages of impaired glucose metabolism may be initiated by EO-related inflammation and oxidative stress damaging pancreatic β-cells, resulting in decreased insulin secretion. These speculations were partially supported by mediation analysis and mediators' Pearson analysis.
Conclusion: Elevated ethylene oxide exposure increases the incidence of impaired glucose metabolism in the general U.S. population and a potential intervention may be to effectively suppress inflammation and oxidative stress imbalances.
{"title":"Ethylene oxide exposure increases impaired glucose metabolism in the US general population: a national cross-sectional study.","authors":"Yuqi Zhao, Deliang Liu, Xiaogao Pan, Yuyong Tan","doi":"10.1265/ehpm.24-00199","DOIUrl":"10.1265/ehpm.24-00199","url":null,"abstract":"<p><strong>Background: </strong>Current experimental evidence supports that ethylene oxide (EO) exposure-related pathophysiologies may affect glucose metabolism, but few population-based studies have explored the potential links.</p><p><strong>Methods: </strong>This study used cross-sectional data from 15560 participants in the National Health and Nutrition Examination Survey (NHANES) from 2017 to 2020. EO exposure levels were calculated by testing hemoglobin adducts of EO (HbEO) via a modified Edman reaction. We focused on the association of EO exposure with prediabetes and diabetes as well as indicators of impaired glucose metabolism and further analyzed the potential pathogenic mechanisms. Statistics included logistic regression, generalized additive model fitting, penalized spline method, two-piecewise linear regression, recursive algorithm, mediation analysis, and Pearson's analysis.</p><p><strong>Results: </strong>EO exposure was associated with changes in glucose metabolic indicators and increased prevalence of prediabetes and diabetes, showing age-consistency and being more pronounced in obese and non-smoking populations. For each one pmol/g Hb, one SD, or two-fold SD increase in log2-HbEO, the risk of prediabetes increased by 12%, 16%, and 33%, with an increased risk of diabetes by 18%, 26%, and 61%, respectively. Dose-response curves revealed that this positive correlation was approximately linear with prediabetes and \"J\" shaped with diabetes. When log2-HbEO > 8.03 pmol/g Hb, the risk of diabetes would be further increased. Pearson's correlation revealed that EO exposure was associated with reduced fasting insulin and elevated HbA1c in the prediabetic stage. While in the diabetes stage, EO exposure was correlated with elevated fasting glucose, HbA1c, and HOMA-IR, suggesting an exacerbation of diabetes progression by EO exposure. A potential mechanism that the early stages of impaired glucose metabolism may be initiated by EO-related inflammation and oxidative stress damaging pancreatic β-cells, resulting in decreased insulin secretion. These speculations were partially supported by mediation analysis and mediators' Pearson analysis.</p><p><strong>Conclusion: </strong>Elevated ethylene oxide exposure increases the incidence of impaired glucose metabolism in the general U.S. population and a potential intervention may be to effectively suppress inflammation and oxidative stress imbalances.</p>","PeriodicalId":11707,"journal":{"name":"Environmental Health and Preventive Medicine","volume":"29 ","pages":"68"},"PeriodicalIF":4.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11631556/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}