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Simulating the impact of greenspace exposure on metabolic biomarkers in a diverse population living in San Diego, California: A g-computation application. 模拟绿地暴露对加利福尼亚州圣迭戈市不同人群代谢生物标志物的影响:g计算应用。
IF 3.3 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2024-08-07 eCollection Date: 2024-08-01 DOI: 10.1097/EE9.0000000000000326
Anaïs Teyton, Nivedita Nukavarapu, Noémie Letellier, Dorothy D Sears, Jiue-An Yang, Marta M Jankowska, Tarik Benmarhnia

Introduction: Growing evidence exists that greenspace exposure can reduce metabolic syndrome risk, a growing public health concern with well-documented inequities across population subgroups. We capitalize on the use of g-computation to simulate the influence of multiple possible interventions on residential greenspace on nine metabolic biomarkers and metabolic syndrome in adults (N = 555) from the 2014-2017 Community of Mine Study living in San Diego County, California.

Methods: Normalized difference vegetation index (NDVI) exposure from 2017 was averaged across a 400-m buffer around the participants' residential addresses. Participants' fasting plasma glucose, total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglyceride concentrations, systolic and diastolic blood pressure, hemoglobin A1c (%), waist circumference, and metabolic syndrome were assessed as outcomes of interest. Using parametric g-computation, we calculated risk differences for participants being exposed to each decile of the participant NDVI distribution compared to minimum NDVI. Differential health impacts from NDVI exposure by sex, ethnicity, income, and age were examined.

Results: We found that a hypothetical increase in NDVI exposure led to a decrease in hemoglobin A1c (%), glucose, and high-density lipoprotein cholesterol concentrations, an increase in fasting total cholesterol, low-density lipoprotein cholesterol, and triglyceride concentrations, and minimal changes to systolic and diastolic blood pressure, waist circumference, and metabolic syndrome. The impact of NDVI changes was greater in women, Hispanic individuals, and those under 65 years old.

Conclusions: G-computation helps to simulate the potential health benefits of differential NDVI exposure and identifies which subpopulations can benefit most from targeted interventions aimed at minimizing health disparities.

导言:越来越多的证据表明,接触绿地可以降低代谢综合征的风险,这是一个日益受到关注的公共健康问题,不同人口亚群之间的不平等现象有据可查。我们利用 g 计算来模拟居住绿地的多种可能干预措施对加利福尼亚州圣地亚哥县 2014-2017 年 "矿区社区研究 "中成年人(N = 555)的九种代谢生物标志物和代谢综合征的影响:对参与者住址周围 400 米缓冲区内 2017 年归一化差异植被指数(NDVI)的暴露量进行平均。参与者的空腹血浆葡萄糖、总胆固醇、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇和甘油三酯浓度、收缩压和舒张压、血红蛋白 A1c (%)、腰围和代谢综合征作为相关结果进行评估。利用参数 g 计算方法,我们计算了暴露于参与者 NDVI 分布中每个十分位数的参与者与最小 NDVI 相比的风险差异。我们还研究了不同性别、种族、收入和年龄的 NDVI 暴露对健康的不同影响:我们发现,假设增加 NDVI 暴露会导致血红蛋白 A1c (%)、葡萄糖和高密度脂蛋白胆固醇浓度下降,空腹总胆固醇、低密度脂蛋白胆固醇和甘油三酯浓度上升,收缩压和舒张压、腰围和代谢综合征的变化很小。NDVI变化对女性、西班牙裔和65岁以下人群的影响更大:G计算有助于模拟不同的NDVI暴露对健康的潜在益处,并确定哪些亚人群可从旨在最大限度减少健康差异的针对性干预措施中获益最多。
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引用次数: 0
Reviewing umbrella reviews of systematic reviews of original studies on the effects of air pollution on disease. 对有关空气污染对疾病影响的原始研究的系统综述进行总体审查。
IF 3.3 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2024-08-06 eCollection Date: 2024-08-01 DOI: 10.1097/EE9.0000000000000324
Bert Brunekreef, Kurt Straif, Neil Pearce
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引用次数: 0
Short-term exposures to temperature and risk of sudden cardiac death in women: A case-crossover analysis in the Nurses' Health Study. 短期温度暴露与女性心脏性猝死风险:护士健康研究》中的病例交叉分析。
IF 3.3 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2024-07-08 eCollection Date: 2024-08-01 DOI: 10.1097/EE9.0000000000000322
Jaime E Hart, Cindy R Hu, Jeff D Yanosky, Isabel Holland, Hari S Iyer, William Borchert, Francine Laden, Christine M Albert

Background: Sudden cardiac death (SCD) is a major source of mortality and is the first manifestation of heart disease for most cases. Thus, there is a definite need to identify risk factors for SCD that can be modified on the population level. Short-term exposures to temperature have been implicated as a potential risk factor. Our objective was to determine if short-term temperature exposures were associated with increased risk of SCD in a US-based time-stratified case-crossover study.

Methods: A total of 465 cases of SCD were identified among participants of the prospective Nurses' Health Study (NHS). Control days were selected from all other matching days of the week within the same month as the case day. Average ambient temperature on the current day (Lag0) and preceding 27 days (Lags1-27) was determined at the residence level using 800-m resolution estimates. Conditional logistic distributed lag nonlinear models (DLNMs) were used to assess the relative risk (RR) of the full range of temperature exposures over the lag period.

Results: Warmer exposures in the days before event and colder temperatures 21-28 days prior were associated with increased risks of SCD. These results were driven by associations in regions other than the Northeast and among married women.

Conclusions: Both warm and cold ambient temperatures are suggestively associated with risks of SCD among middle-aged and older women living across the United States.

背景:心脏性猝死(SCD)是导致死亡的主要原因,也是大多数心脏病患者的首发症状。因此,亟需确定可在人群中改变的 SCD 风险因素。短期暴露于温度被认为是一个潜在的风险因素。我们的目的是在一项基于美国的时间分层病例交叉研究中确定短期温度暴露是否与 SCD 风险增加有关:方法:在前瞻性护士健康研究(NHS)的参与者中共发现了 465 例 SCD 病例。对照日选自与病例日同月的一周中所有其他匹配日。当日(Lag0)和前 27 天(Lags1-27)的平均环境温度是使用 800 米分辨率估算值在居住地水平上确定的。条件逻辑分布式滞后非线性模型(DLNM)用于评估滞后期内所有温度暴露的相对风险(RR):事件发生前几天的气温较高和发生前 21-28 天的气温较低与 SCD 风险增加有关。这些结果与东北部以外地区和已婚妇女的相关性有关:在美国各地生活的中老年妇女中,温暖和寒冷的环境温度都与 SCD 风险有提示性关联。
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引用次数: 0
Choices of morbidity outcomes and concentration-response functions for health risk assessment of long-term exposure to air pollution. 长期暴露于空气污染的健康风险评估中发病率结果和浓度反应函数的选择。
IF 3.3 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2024-06-25 eCollection Date: 2024-08-01 DOI: 10.1097/EE9.0000000000000314
Francesco Forastiere, Joseph V Spadaro, Carla Ancona, Zorana Jovanovic Andersen, Ilaria Cozzi, Sophie Gumy, Dejan Loncar, Pierpaolo Mudu, Sylvia Medina, Roman Perez Velasco, Heather Walton, Jiawei Zhang, Michal Krzyzanowski
<p><strong>Background: </strong>Air pollution health risk assessment (HRA) has been typically conducted for all causes and cause-specific mortality based on concentration-response functions (CRFs) from meta-analyses that synthesize the evidence on air pollution health effects. There is a need for a similar systematic approach for HRA for morbidity outcomes, which have often been omitted from HRA of air pollution, thus underestimating the full air pollution burden. We aimed to compile from the existing systematic reviews and meta-analyses CRFs for the incidence of several diseases that could be applied in HRA. To achieve this goal, we have developed a comprehensive strategy for the appraisal of the systematic reviews and meta-analyses that examine the relationship between long-term exposure to particulate matter with an aerodynamic diameter smaller than 2.5 µm (PM<sub>2.5</sub>), nitrogen dioxide (NO<sub>2</sub>), or ozone (O<sub>3</sub>) and incidence of various diseases.</p><p><strong>Methods: </strong>To establish the basis for our evaluation, we considered the causality determinations provided by the US Environmental Protection Agency Integrated Science Assessment for PM<sub>2.5</sub>, NO<sub>2</sub>, and O<sub>3</sub>. We developed a list of pollutant/outcome pairs based on these assessments and the evidence of a causal relationship between air pollutants and specific health outcomes. We conducted a comprehensive literature search using two databases and identified 75 relevant systematic reviews and meta-analyses for PM<sub>2.5</sub> and NO<sub>2</sub>. We found no relevant reviews for long-term exposure to ozone. We evaluated the reliability of these studies using an adaptation of the AMSTAR 2 tool, which assesses various characteristics of the reviews, such as literature search, data extraction, statistical analysis, and bias evaluation. The tool's adaptation focused on issues relevant to studies on the health effects of air pollution. Based on our assessment, we selected reviews that could be credible sources of CRF for HRA. We also assessed the confidence in the findings of the selected systematic reviews and meta-analyses as the sources of CRF for HRA. We developed specific criteria for the evaluation, considering factors such as the number of included studies, their geographical distribution, heterogeneity of study results, the statistical significance and precision of the pooled risk estimate in the meta-analysis, and consistency with more recent studies. Based on our assessment, we classified the outcomes into three lists: list A (a reliable quantification of health effects is possible in an HRA), list B+ (HRA is possible, but there is greater uncertainty around the reliability of the CRF compared to those included on list A), and list B- (HRA is not recommended because of the substantial uncertainty of the CRF).</p><p><strong>Results: </strong>In our final evaluation, list A includes six CRFs for PM<sub>2.5</sub> (asthma in children,
背景:空气污染健康风险评估(HRA)通常是根据综合了空气污染健康影响证据的荟萃分析中的浓度反应函数(CRF),对所有病因和特定病因的死亡率进行评估。有必要采用类似的系统方法对发病率结果进行健康影响评估,因为在空气污染健康影响评估中往往忽略了发病率结果,从而低估了全部空气污染负担。我们的目标是从现有的系统综述和荟萃分析中汇编可用于 HRA 的几种疾病发病率的 CRF。为实现这一目标,我们制定了一套综合策略,用于评估研究长期暴露于空气动力学直径小于 2.5 µm 的颗粒物(PM2.5)、二氧化氮(NO2)或臭氧(O3)与各种疾病发病率之间关系的系统综述和荟萃分析:为了建立评估的基础,我们考虑了美国环境保护局综合科学评估报告中关于 PM2.5、二氧化氮和臭氧的因果关系判定。根据这些评估以及空气污染物与特定健康结果之间的因果关系证据,我们制定了污染物/结果对列表。我们使用两个数据库进行了全面的文献检索,确定了 75 篇关于 PM2.5 和 NO2 的相关系统综述和荟萃分析。我们没有发现关于长期暴露于臭氧的相关综述。我们使用 AMSTAR 2 工具的改编版对这些研究的可靠性进行了评估,该工具可评估综述的各种特性,如文献检索、数据提取、统计分析和偏差评估。该工具的改编侧重于与空气污染对健康影响的研究相关的问题。根据评估结果,我们选择了可作为 HRA 通用报告格式可靠来源的综述。我们还评估了所选系统综述和荟萃分析结果作为 HRA CRF 来源的可信度。我们制定了具体的评估标准,考虑的因素包括纳入研究的数量、地理分布、研究结果的异质性、荟萃分析中汇总风险估计值的统计学意义和精确性以及与近期研究的一致性。根据评估结果,我们将结果分为三个列表:列表 A(在健康影响评估中可以对健康影响进行可靠的量化)、列表 B+(可以进行健康影响评估,但与列表 A 中的结果相比,通用报告格式的可靠性存在更大的不确定性)和列表 B-(由于通用报告格式存在很大的不确定性,因此不建议进行健康影响评估):在我们的最终评估中,列表 A 包括 PM2.5 的六个 CRF(儿童哮喘、慢性阻塞性肺病、缺血性心脏病事件、中风、高血压和肺癌)和 NO2 的三个结果(儿童和成人哮喘以及儿童急性下呼吸道感染)。PM2.5的另外三个结果(糖尿病、痴呆症和自闭症谱系障碍)被列入清单B+。推荐的通用报告格式与疾病的发病率(发病)有关。国际疾病分类》第 10 次修订版的代码、年龄范围和建议的浓度范围也有具体说明,以确保 HRA 的一致性和适用性。由于缺乏相关的系统综述,因此没有对臭氧提出具体建议:本研究中提出的建议,包括从现有系统综述中选择的通用报告格式,有助于开展可靠的健康风险评估,并有助于公共卫生和环境政策中的循证决策。随着新证据的出现和方法论的发展,未来的研究应继续更新和完善这些建议。
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引用次数: 0
Genome-wide DNA methylation profiles and breast cancer among World Trade Center survivors. 全基因组 DNA 甲基化图谱与世贸中心幸存者中的乳腺癌。
IF 3.6 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2024-06-04 eCollection Date: 2024-06-01 DOI: 10.1097/EE9.0000000000000313
Stephanie Tuminello, Yibeltal Arega Ashebir, Chanel Schroff, Sitharam Ramaswami, Nedim Durmus, Yu Chen, Matija Snuderl, Yongzhao Shao, Joan Reibman, Alan A Arslan

Background: Increased incidence of cancer has been reported among World Trade Center (WTC)-exposed persons. Aberrant DNA methylation is a hallmark of cancer development. To date, only a few small studies have investigated the relationship between WTC exposure and DNA methylation. The main objective of this study was to assess the DNA methylation profiles of WTC-exposed community members who remained cancer free and those who developed breast cancer.

Methods: WTC-exposed women were selected from the WTC Environmental Health Center clinic, with peripheral blood collected during routine clinical monitoring visits. The reference group was selected from the NYU Women's Health Study, a prospective cohort study with blood samples collected before 9 November 2001. The Infinium MethylationEPIC array was used for global DNA methylation profiling, with adjustments for cell type composition and other confounders. Annotated probes were used for biological pathway and network analysis.

Results: A total of 64 WTC-exposed (32 cancer free and 32 with breast cancer) and 32 WTC-unexposed (16 cancer free and 16 with prediagnostic breast cancer) participants were included. Hypermethylated cytosine-phosphate-guanine probe sites (defined as β > 0.8) were more common among WTC-exposed versus unexposed participants (14.3% vs. 4.5%, respectively, among the top 5000 cytosine-phosphate-guanine sites). Cancer-related pathways (e.g., human papillomavirus infection, cGMP-PKG) were overrepresented in WTC-exposed groups (breast cancer patients and cancer-free subjects). Compared to the unexposed breast cancer patients, 47 epigenetically dysregulated genes were identified among WTC-exposed breast cancers. These genes formed a network, including Wnt/β-catenin signaling genes WNT4 and TCF7L2, and dysregulation of these genes contributes to cancer immune evasion.

Conclusion: WTC exposure likely impacts DNA methylation and may predispose exposed individuals toward cancer development, possibly through an immune-mediated mechanism.

背景:据报道,受世界贸易中心(WTC)影响的人群癌症发病率增加。DNA 甲基化异常是癌症发展的一个标志。迄今为止,只有少数几项小型研究调查了世贸中心暴露与 DNA 甲基化之间的关系。本研究的主要目的是评估受世界贸易中心影响的社区成员中未患癌症者和患乳腺癌者的 DNA 甲基化情况:方法:从世界贸易中心环境健康中心诊所选取受世界贸易中心影响的妇女,在常规临床监测访问中采集外周血。参照组选自纽约大学妇女健康研究(NYU Women's Health Study),该研究是一项前瞻性队列研究,在 2001 年 11 月 9 日前采集血样。Infinium MethylationEPIC 阵列用于全局 DNA 甲基化分析,并对细胞类型组成和其他混杂因素进行了调整。注释探针用于生物通路和网络分析:共纳入了 64 名接触过世界贸易中心的参与者(32 人未患癌症,32 人患有乳腺癌)和 32 名未接触过世界贸易中心的参与者(16 人未患癌症,16 人患有诊断前乳腺癌)。高甲基化胞嘧啶-磷酸鸟嘌呤探针位点(定义为β > 0.8)在暴露于 WTC 的参与者中比未暴露于 WTC 的参与者中更为常见(在前 5000 个胞嘧啶-磷酸鸟嘌呤位点中分别为 14.3% 和 4.5%)。与癌症相关的途径(如人类乳头瘤病毒感染、cGMP-PKG)在受到 WTC 暴露的群体(乳腺癌患者和无癌症受试者)中所占比例过高。与未暴露的乳腺癌患者相比,暴露于 WTC 的乳腺癌患者中发现了 47 个表观遗传失调基因。这些基因形成了一个网络,其中包括Wnt/β-catenin信号基因WNT4和TCF7L2,这些基因的失调有助于癌症免疫逃避:结论:接触世界贸易中心可能会影响 DNA 甲基化,并可能通过免疫介导机制使接触者易患癌症。
{"title":"Genome-wide DNA methylation profiles and breast cancer among World Trade Center survivors.","authors":"Stephanie Tuminello, Yibeltal Arega Ashebir, Chanel Schroff, Sitharam Ramaswami, Nedim Durmus, Yu Chen, Matija Snuderl, Yongzhao Shao, Joan Reibman, Alan A Arslan","doi":"10.1097/EE9.0000000000000313","DOIUrl":"10.1097/EE9.0000000000000313","url":null,"abstract":"<p><strong>Background: </strong>Increased incidence of cancer has been reported among World Trade Center (WTC)-exposed persons. Aberrant DNA methylation is a hallmark of cancer development. To date, only a few small studies have investigated the relationship between WTC exposure and DNA methylation. The main objective of this study was to assess the DNA methylation profiles of WTC-exposed community members who remained cancer free and those who developed breast cancer.</p><p><strong>Methods: </strong>WTC-exposed women were selected from the WTC Environmental Health Center clinic, with peripheral blood collected during routine clinical monitoring visits. The reference group was selected from the NYU Women's Health Study, a prospective cohort study with blood samples collected before 9 November 2001. The Infinium MethylationEPIC array was used for global DNA methylation profiling, with adjustments for cell type composition and other confounders. Annotated probes were used for biological pathway and network analysis.</p><p><strong>Results: </strong>A total of 64 WTC-exposed (32 cancer free and 32 with breast cancer) and 32 WTC-unexposed (16 cancer free and 16 with prediagnostic breast cancer) participants were included. Hypermethylated cytosine-phosphate-guanine probe sites (defined as <i>β</i> > 0.8) were more common among WTC-exposed versus unexposed participants (14.3% vs. 4.5%, respectively, among the top 5000 cytosine-phosphate-guanine sites). Cancer-related pathways (e.g., human papillomavirus infection, cGMP-PKG) were overrepresented in WTC-exposed groups (breast cancer patients and cancer-free subjects). Compared to the unexposed breast cancer patients, 47 epigenetically dysregulated genes were identified among WTC-exposed breast cancers. These genes formed a network, including Wnt/β-catenin signaling genes <i>WNT4</i> and <i>TCF7L2</i>, and dysregulation of these genes contributes to cancer immune evasion.</p><p><strong>Conclusion: </strong>WTC exposure likely impacts DNA methylation and may predispose exposed individuals toward cancer development, possibly through an immune-mediated mechanism.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"8 3","pages":"e313"},"PeriodicalIF":3.6,"publicationDate":"2024-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11152787/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141260394","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}
引用次数: 0
Longitudinal associations between ambient PM2.5 exposure and lipid levels in two Indian cities. 印度两个城市的环境 PM2.5 暴露与血脂水平之间的纵向联系。
IF 3.3 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2024-04-04 eCollection Date: 2024-04-01 DOI: 10.1097/EE9.0000000000000295
Kritika Anand, Gagandeep Kaur Walia, Siddhartha Mandal, Jyothi S Menon, Ruby Gupta, Nikhil Tandon, K M Venkat Narayan, Mohammed K Ali, Viswanathan Mohan, Joel D Schwartz, Dorairaj Prabhakaran

Background: Exposure to ambient PM2.5 is known to affect lipid metabolism through systemic inflammation and oxidative stress. Evidence from developing countries, such as India with high levels of ambient PM2.5 and distinct lipid profiles, is sparse.

Methods: Longitudinal nonlinear mixed-effects analysis was conducted on >10,000 participants of Centre for cArdiometabolic Risk Reduction in South Asia (CARRS) cohort in Chennai and Delhi, India. We examined associations between 1-month and 1-year average ambient PM2.5 exposure derived from the spatiotemporal model and lipid levels (total cholesterol [TC], triglycerides [TRIG], high-density lipoprotein cholesterol [HDL-C], and low-density lipoprotein cholesterol [LDL-C]) measured longitudinally, adjusting for residential and neighborhood-level confounders.

Results: The mean annual exposure in Chennai and Delhi was 40 and 102 μg/m3 respectively. Elevated ambient PM2.5 levels were associated with an increase in LDL-C and TC at levels up to 100 µg/m3 in both cities and beyond 125 µg/m3 in Delhi. TRIG levels in Chennai increased until 40 µg/m3 for both short- and long-term exposures, then stabilized or declined, while in Delhi, there was a consistent rise with increasing annual exposures. HDL-C showed an increase in both cities against monthly average exposure. HDL-C decreased slightly in Chennai with an increase in long-term exposure, whereas it decreased beyond 130 µg/m3 in Delhi.

Conclusion: These findings demonstrate diverse associations between a wide range of ambient PM2.5 and lipid levels in an understudied South Asian population. Further research is needed to establish causality and develop targeted interventions to mitigate the impact of air pollution on lipid metabolism and cardiovascular health.

背景:已知暴露于环境 PM2.5 会通过全身炎症和氧化应激影响脂质代谢。印度等发展中国家的环境 PM2.5 水平较高,但其血脂状况却截然不同,这方面的证据还很稀少:我们对印度钦奈和德里的南亚减少代谢风险中心(CARRS)队列中超过 10,000 名参与者进行了纵向非线性混合效应分析。我们研究了时空模型得出的1个月和1年平均环境PM2.5暴露量与纵向测量的血脂水平(总胆固醇[TC]、甘油三酯[TRIG]、高密度脂蛋白胆固醇[HDL-C]和低密度脂蛋白胆固醇[LDL-C])之间的关系,并对居住地和邻近地区的混杂因素进行了调整:钦奈和德里的年平均暴露量分别为 40 和 102 μg/m3。在这两个城市,当环境 PM2.5 水平达到 100 微克/立方米时,低密度脂蛋白胆固醇(LDL-C)和总胆固醇(TC)会升高,而在德里,当环境 PM2.5 水平超过 125 微克/立方米时,低密度脂蛋白胆固醇(LDL-C)和总胆固醇(TC)会升高。在钦奈,无论短期还是长期暴露,TRIG 水平在 40 µg/m3 之前都会上升,然后趋于稳定或下降,而在德里,随着年暴露量的增加,TRIG 水平持续上升。两个城市的 HDL-C 都随着月平均暴露量的增加而增加。在钦奈,随着长期暴露量的增加,高密度脂蛋白胆固醇略有下降,而在德里,当暴露量超过 130 µg/m3 时,高密度脂蛋白胆固醇就会下降:这些研究结果表明,在研究不足的南亚人群中,环境 PM2.5 与血脂水平之间存在多种关联。需要进一步研究,以确定因果关系,并制定有针对性的干预措施,减轻空气污染对脂质代谢和心血管健康的影响。
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引用次数: 0
Associations between short-term exposure to ambient temperature and renal disease mortality in Japan during 1979-2019: A time-stratified case-crossover analysis. 1979-2019年日本短期暴露于环境温度与肾病死亡率之间的关系:时间分层病例交叉分析。
IF 3.6 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2024-02-02 eCollection Date: 2024-02-01 DOI: 10.1097/EE9.0000000000000293
Zin Wai Htay, Chris Fook Sheng Ng, Yoonhee Kim, Youn-Hee Lim, Masao Iwagami, Masahiro Hashizume

Background: Previous studies have indicated that renal disease mortality is sensitive to ambient temperatures. However, most have been limited to the summer season with inconclusive evidence for changes in population vulnerability over time.

Objective: This study aims to examine the association between short-term exposure to ambient temperatures and mortality due to renal diseases in Japan, and how this association varied over time.

Methods: We conducted a two-stage, time-stratified case-crossover study from 1979 to 2019 across 47 prefectures of Japan. We obtained the data of daily mortality counts for all renal diseases, acute renal failure, and chronic renal disease. We fitted a conditional quasi-Poisson regression model with a distributed lag nonlinear model. A random-effects meta-analysis was applied to calculate national averages. We performed additional analyses by four subperiods, sex, and age groups.

Results: We analyzed 997,590 renal mortality cases and observed a reversed J-shaped association. Lower temperatures were associated with increased mortality in all renal disease categories. The cumulative relative risks at 2.5th percentile compared to the minimum mortality temperature percentile were 1.34 (95% confidence interval [CI] = 1.29, 1.40), 1.51 (95% CI = 1.33, 1.71), and 1.33 (95% CI = 1.24, 1.43) for all renal, acute renal failure, and chronic renal disease mortality, respectively. The associations were observed in individuals of both sexes and aged 65 years and above. The associations of kidney mortality with low temperature remained consistent, while the associations with high temperature were pronounced in the past, but not in recent periods.

Conclusions: Protection for individuals with impaired renal function from exposure to low temperatures during cold seasons is warranted.

背景:以往的研究表明,肾病死亡率对环境温度很敏感。然而,大多数研究仅限于夏季,没有确凿证据表明随着时间的推移,人群的易感性会发生变化:本研究旨在探讨短期暴露于环境温度与日本肾脏疾病死亡率之间的关联,以及这种关联随时间的变化情况:从 1979 年到 2019 年,我们在日本 47 个都道府县开展了一项分两个阶段、时间分层的病例交叉研究。我们获得了所有肾脏疾病、急性肾衰竭和慢性肾脏疾病的每日死亡率数据。我们利用分布式滞后非线性模型拟合了一个条件准泊松回归模型。采用随机效应荟萃分析法计算全国平均值。我们还按四个子时期、性别和年龄组进行了额外分析:我们分析了 997,590 例肾脏病死亡病例,观察到一种反向的 J 型关联。在所有肾病类别中,温度越低死亡率越高。与最低死亡温度百分位数相比,2.5 百分位数的累积相对风险在所有肾病、急性肾衰竭和慢性肾病死亡率中分别为 1.34(95% 置信区间 [CI] = 1.29,1.40)、1.51(95% CI = 1.33,1.71)和 1.33(95% CI = 1.24,1.43)。在 65 岁及以上的男性和女性中都观察到了这种关联。肾脏死亡率与低温的相关性保持一致,而与高温的相关性在过去很明显,但在近期则不明显:结论:在寒冷季节,肾功能受损者应避免暴露在低温环境中。
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引用次数: 0
Erratum: Assessing heat effects on respiratory mortality and location characteristics as modifiers of heat effects at a small area scale in Central-Northern Europe: Erratum. 勘误:在中北欧小范围内评估高温对呼吸系统死亡率的影响以及作为高温影响调节因素的地点特征:勘误。
IF 3.6 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2024-02-01 DOI: 10.1097/EE9.0000000000000294

[This corrects the article DOI: 10.1097/EE9.0000000000000269.].

[此处更正了文章 DOI:10.1097/EE9.0000000000000269]。
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引用次数: 0
Applying a multistate survival model to explore the role of fine particles in promoting frailty in the Medicare cohort 应用多州生存模型探索细颗粒物在促进医疗保险队列虚弱中的作用
IF 3.6 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2024-01-12 DOI: 10.1097/EE9.0000000000000285
Neal Fann, A. Zanobetti, Daniel Mork, William Steinhardt, Ana G. Rappold
Fine particle pollution is a well-established risk to human health. Observational epidemiology generally treats events as though they are independent of one another and so do not examine the role air pollution may play in promoting the progression of disease. Multistate survival models account for the complex pathway of disease to death. We employ a multistate survival model to characterize the role of chronic exposure to PM2.5 in affecting the rate at which Medicare beneficiaries transition to first hospitalization for cardiovascular disease and then subsequently death. We use an open cohort of Medicare beneficiaries and PM2.5 concentrations estimated with photochemical model predictions, satellite-based observations, land-use data, and meteorological variables. The multistate model included three transitions: (1) entry to cardiovascular hospital admission; (2) entry to death; and (3) cardiovascular hospital admission to death. The transition intensity was modeled using a Cox proportional hazards model. For a 1 µg/m3 increase in annual mean PM2.5, we estimate a nationally pooled hazard ratio of 1.022 (95% confidence interval [CI] = 1.018, 1.025) for the transition from entry to first cardiovascular hospital admission; 1.054 (95% CI = 1.039, 1.068) for the transition from entry to death; 1.036 (95% CI = 1.027, 1.044) for the transition from first cardiovascular hospital admission to death. The hazard ratios exhibited some heterogeneity within each of nine climatological regions and for each of the three transitions. We find evidence for the role of PM in both promoting chronic illness and increasing the subsequent risk of death.
细颗粒物污染对人类健康的危害已得到证实。观察流行病学通常将各种事件视为相互独立的,因此不会研究空气污染在促进疾病进展方面可能发挥的作用。多态生存模型考虑了从疾病到死亡的复杂路径。我们采用多州生存模型来描述长期暴露于 PM2.5 在影响医疗保险受益人首次因心血管疾病住院并随后死亡的速度方面所起的作用。我们使用了医疗保险受益人的开放队列以及通过光化学模型预测、卫星观测、土地使用数据和气象变量估算的 PM2.5 浓度。多州模型包括三个过渡:(1) 进入心血管病医院;(2) 进入心血管病医院至死亡;(3) 进入心血管病医院至死亡。过渡强度采用 Cox 比例危险模型进行建模。对于年均PM2.5每增加1微克/立方米,我们估计从入院到首次入住心血管病医院的全国汇总危险比为1.022(95% 置信区间 [CI] = 1.018, 1.025);从入院到死亡的危险比为1.054(95% CI = 1.039, 1.068);从首次入住心血管病医院到死亡的危险比为1.036(95% CI = 1.027, 1.044)。在九个气候区中,每个气候区的危险比以及三种转变的危险比都表现出一定的异质性。我们发现了可吸入颗粒物在促进慢性疾病和增加后续死亡风险方面发挥作用的证据。
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引用次数: 0
Evaluating the association between longitudinal exposure to a PFAS mixture and adolescent cardiometabolic risk in the HOME Study 评估 "居家 "研究中纵向接触全氟辛烷磺酸混合物与青少年心脏代谢风险之间的关系
IF 3.6 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2024-01-12 DOI: 10.1097/EE9.0000000000000289
Elvira S. Fleury, J. Kuiper, J. Buckley, G. Papandonatos, K. Cecil, Aimin Chen, Charles B. Eaton, Heidi J Kalkwarf, B. Lanphear, K. Yolton, Joseph M. Braun
Background: Exposure to per- and polyfluoroalkyl substances (PFAS) throughout gestation and childhood may impact cardiometabolic risk. Methods: In 179 HOME Study participants (Cincinnati, OH; recruited 2003–2006), we used latent profile analysis to identify two distinct patterns of PFAS exposure from serum concentrations of four PFAS measured at birth and ages 3, 8, and 12 years. We assessed the homeostatic model of insulin resistance, triglycerides-to-high-density lipoprotein cholesterol ratio, leptin-to-adiponectin ratio, systolic blood pressure, visceral fat, and hemoglobin A1c levels at age 12 years. We used multivariable linear regression to assess the association of membership in the longitudinal PFAS mixture exposure group with a summary measure of overall cardiometabolic risk and individual components. Results: One PFAS exposure profile (n = 66, 39%) had higher geometric means of all PFAS across all visits than the other. Although adjusted associations were null in the full sample, child sex modified the association of longitudinal PFAS mixture exposure group with overall cardiometabolic risk, leptin-to-adiponectin ratio, systolic blood pressure, and visceral fat (interaction term P values: 0.02–0.08). Females in the higher exposure group had higher cardiometabolic risk scores (ß = 0.43; 95% CI = −0.08, 0.94), systolic blood pressures (ß = 0.6; 95% CI = 0.1, 1.1), and visceral fat (ß = 0.44; 95% CI = −0.13, 1.01); males had lower cardiometabolic risk scores (ß = −0.52; 95% CI = −1.06, −0.06), leptin-to-adiponectin ratios (ß = −0.7; 95% CI = −1.29, −0.1), systolic blood pressures (ß = −0.14; 95% CI = −0.7, 0.41), and visceral fat (ß = −0.52; 95% CI = −0.84, −0.19). Conclusions: Exposure to this PFAS mixture throughout childhood may have sex-specific effects on adolescent cardiometabolic risk.
背景:妊娠期和儿童期接触全氟和多氟烷基物质(PFAS)可能会影响心脏代谢风险。研究方法在 179 名 "HOME 研究 "参与者(俄亥俄州辛辛那提市;2003-2006 年招募)中,我们使用潜在特征分析,从出生时和 3、8、12 岁时测量的四种 PFAS 血清浓度中识别出两种不同的 PFAS 暴露模式。我们评估了胰岛素抵抗的稳态模型、甘油三酯与高密度脂蛋白胆固醇的比率、瘦素与脂联素的比率、收缩压、内脏脂肪以及 12 岁时的血红蛋白 A1c 水平。我们使用多变量线性回归法评估了纵向全氟辛烷磺酸混合物暴露组的成员资格与总体心脏代谢风险和单个成分的综合测量值之间的关联。结果一种 PFAS 暴露情况(n = 66,39%)在所有访问中的所有 PFAS 几何平均数均高于另一种情况。虽然调整后的关联在全样本中为零,但儿童性别改变了纵向 PFAS 混合暴露组与总体心脏代谢风险、瘦素与脂联素比率、收缩压和内脏脂肪的关联(交互项 P 值:0.02-0.08)。暴露程度较高组的女性具有较高的心脏代谢风险评分(ß = 0.43;95% CI = -0.08,0.94)、收缩压(ß = 0.6;95% CI = 0.1,1.1)和内脏脂肪(ß = 0.44;95% CI = -0.13,1.01);男性具有较低的心脏代谢风险评分(ß = -0.52; 95% CI = -1.06, -0.06)、瘦素与脂联素比率(ß = -0.7; 95% CI = -1.29, -0.1)、收缩压(ß = -0.14; 95% CI = -0.7, 0.41)和内脏脂肪(ß = -0.52; 95% CI = -0.84, -0.19)。结论童年时期接触这种全氟辛烷磺酸混合物可能会对青少年的心脏代谢风险产生性别特异性影响。
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Environmental Epidemiology
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