Pub Date : 2024-08-07eCollection Date: 2024-08-01DOI: 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.
{"title":"Simulating the impact of greenspace exposure on metabolic biomarkers in a diverse population living in San Diego, California: A g-computation application.","authors":"Anaïs Teyton, Nivedita Nukavarapu, Noémie Letellier, Dorothy D Sears, Jiue-An Yang, Marta M Jankowska, Tarik Benmarhnia","doi":"10.1097/EE9.0000000000000326","DOIUrl":"10.1097/EE9.0000000000000326","url":null,"abstract":"<p><strong>Introduction: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>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.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"8 4","pages":"e326"},"PeriodicalIF":3.3,"publicationDate":"2024-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11309718/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141906241","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}
Pub Date : 2024-08-06eCollection Date: 2024-08-01DOI: 10.1097/EE9.0000000000000324
Bert Brunekreef, Kurt Straif, Neil Pearce
{"title":"Reviewing umbrella reviews of systematic reviews of original studies on the effects of air pollution on disease.","authors":"Bert Brunekreef, Kurt Straif, Neil Pearce","doi":"10.1097/EE9.0000000000000324","DOIUrl":"10.1097/EE9.0000000000000324","url":null,"abstract":"","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"8 4","pages":"e324"},"PeriodicalIF":3.3,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11305730/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141901338","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}
Pub Date : 2024-07-08eCollection Date: 2024-08-01DOI: 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.
{"title":"Short-term exposures to temperature and risk of sudden cardiac death in women: A case-crossover analysis in the Nurses' Health Study.","authors":"Jaime E Hart, Cindy R Hu, Jeff D Yanosky, Isabel Holland, Hari S Iyer, William Borchert, Francine Laden, Christine M Albert","doi":"10.1097/EE9.0000000000000322","DOIUrl":"10.1097/EE9.0000000000000322","url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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 (Lag<sub>0</sub>) and preceding 27 days (Lags<sub>1-27</sub>) 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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>Both warm and cold ambient temperatures are suggestively associated with risks of SCD among middle-aged and older women living across the United States.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"8 4","pages":"e322"},"PeriodicalIF":3.3,"publicationDate":"2024-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11233109/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141563016","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}
Pub Date : 2024-06-25eCollection Date: 2024-08-01DOI: 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。
{"title":"Choices of morbidity outcomes and concentration-response functions for health risk assessment of long-term exposure to air pollution.","authors":"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","doi":"10.1097/EE9.0000000000000314","DOIUrl":"10.1097/EE9.0000000000000314","url":null,"abstract":"<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,","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"8 4","pages":"e314"},"PeriodicalIF":3.3,"publicationDate":"2024-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11265782/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141751404","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}
Pub Date : 2024-06-04eCollection Date: 2024-06-01DOI: 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}
Pub Date : 2024-04-04eCollection Date: 2024-04-01DOI: 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.
{"title":"Longitudinal associations between ambient PM<sub>2.5</sub> exposure and lipid levels in two Indian cities.","authors":"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","doi":"10.1097/EE9.0000000000000295","DOIUrl":"10.1097/EE9.0000000000000295","url":null,"abstract":"<p><strong>Background: </strong>Exposure to ambient PM<sub>2.5</sub> is known to affect lipid metabolism through systemic inflammation and oxidative stress. Evidence from developing countries, such as India with high levels of ambient PM<sub>2.5</sub> and distinct lipid profiles, is sparse.</p><p><strong>Methods: </strong>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 PM<sub>2.5</sub> 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.</p><p><strong>Results: </strong>The mean annual exposure in Chennai and Delhi was 40 and 102 μg/m<sup>3</sup> respectively. Elevated ambient PM<sub>2.5</sub> levels were associated with an increase in LDL-C and TC at levels up to 100 µg/m<sup>3</sup> in both cities and beyond 125 µg/m<sup>3</sup> in Delhi. TRIG levels in Chennai increased until 40 µg/m<sup>3</sup> 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/m<sup>3</sup> in Delhi.</p><p><strong>Conclusion: </strong>These findings demonstrate diverse associations between a wide range of ambient PM<sub>2.5</sub> 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.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"8 2","pages":"e295"},"PeriodicalIF":3.3,"publicationDate":"2024-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11008625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140850045","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}
Pub Date : 2024-02-02eCollection Date: 2024-02-01DOI: 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.
{"title":"Associations between short-term exposure to ambient temperature and renal disease mortality in Japan during 1979-2019: A time-stratified case-crossover analysis.","authors":"Zin Wai Htay, Chris Fook Sheng Ng, Yoonhee Kim, Youn-Hee Lim, Masao Iwagami, Masahiro Hashizume","doi":"10.1097/EE9.0000000000000293","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000293","url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Objective: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>Protection for individuals with impaired renal function from exposure to low temperatures during cold seasons is warranted.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"8 1","pages":"e293"},"PeriodicalIF":3.6,"publicationDate":"2024-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10852400/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139722034","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}
Pub Date : 2024-02-01DOI: 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]。
{"title":"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.","authors":"","doi":"10.1097/EE9.0000000000000294","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000294","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1097/EE9.0000000000000269.].</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"8 1","pages":"e294"},"PeriodicalIF":3.6,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10852360/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139725651","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}
Pub Date : 2024-01-12DOI: 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.
{"title":"Applying a multistate survival model to explore the role of fine particles in promoting frailty in the Medicare cohort","authors":"Neal Fann, A. Zanobetti, Daniel Mork, William Steinhardt, Ana G. Rappold","doi":"10.1097/EE9.0000000000000285","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000285","url":null,"abstract":"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.","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"12 1","pages":"e285"},"PeriodicalIF":3.6,"publicationDate":"2024-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139437745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-12DOI: 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。
{"title":"Evaluating the association between longitudinal exposure to a PFAS mixture and adolescent cardiometabolic risk in the HOME Study","authors":"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","doi":"10.1097/EE9.0000000000000289","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000289","url":null,"abstract":"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.","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"1 7","pages":"e289"},"PeriodicalIF":3.6,"publicationDate":"2024-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139438031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}