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":null,"pages":null},"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":null,"pages":null},"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 : 2024-06-25eCollection 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
Background: 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 (PM2.5), nitrogen dioxide (NO2), or ozone (O3) and incidence of various diseases.
Methods: To establish the basis for our evaluation, we considered the causality determinations provided by the US Environmental Protection Agency Integrated Science Assessment for PM2.5, NO2, and O3. 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 PM2.5 and NO2. 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).
Results: In our final evaluation, list A includes six CRFs for PM2.5 (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":null,"pages":null},"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":null,"pages":null},"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 : 2024-05-17DOI: 10.1097/EE9.0000000000000311
Che-Jung Chang, Katie M. O’Brien, J. Kresovich, J. Nwanaji-Enwerem, Zongli Xu, S. Gaston, Chandra L. Jackson, Dale P. Sandler, Jack A. Taylor, Alexandra J White
Background: Hair products may be a source of harmful chemicals and have been linked to age-related health outcomes. We investigated whether the use of hair products is related to epigenetic age in a sample of Black (both Hispanic and non-Hispanic) and non-Hispanic White women. Methods: In a subset of 4358 participants aged 35–74 years from the Sister Study, we estimated cross-sectional associations between self-reported use of four chemical hair products (permanent dye, semipermanent dye, straighteners/relaxers, and hair permanents/body waves) in the year before enrollment (2003–2009) and three DNA methylation-based measures of epigenetic age (DunedinPACE, GrimAge age acceleration [GrimAgeAccel], and PhenoAge age acceleration [PhenoAgeAccel]) using survey-weighted multivariable linear regressions. Associations were estimated both overall and by self-identified race and ethnicity, adjusting for chronological age, socioeconomic and lifestyle factors, body mass index, menopausal status, and DNA methylation platform. Results: Associations between the use of hair products and the three epigenetic age measures were largely null. Use of hair permanents/body waves was modestly associated with higher DunedinPACE among all participants (βever-never = 0.010; 95% confidence interval [CI] = 0.001, 0.019) and with lower PhenoAgeAccel among Black women (βever-never = −1.53; 95% CI = −2.84, −0.21). Conclusion: In this US-based study, we found little evidence of associations between chemical hair product use and epigenetic age in Black and non-Hispanic White women. Observed associations were modest and largely not supported by dose–response relationships or were inconsistent across epigenetic age measures. Previously observed associations between chemical hair product use and aging-related health outcomes may not be explained by the biological aging pathways captured by DunedinPACE, GrimAgeAccel, or PhenoAgeAccel. Alternative biological pathways are worth investigating in racially diverse samples.
{"title":"Associations between use of chemical hair products and epigenetic age: Findings from the Sister Study","authors":"Che-Jung Chang, Katie M. O’Brien, J. Kresovich, J. Nwanaji-Enwerem, Zongli Xu, S. Gaston, Chandra L. Jackson, Dale P. Sandler, Jack A. Taylor, Alexandra J White","doi":"10.1097/EE9.0000000000000311","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000311","url":null,"abstract":"Background: Hair products may be a source of harmful chemicals and have been linked to age-related health outcomes. We investigated whether the use of hair products is related to epigenetic age in a sample of Black (both Hispanic and non-Hispanic) and non-Hispanic White women. Methods: In a subset of 4358 participants aged 35–74 years from the Sister Study, we estimated cross-sectional associations between self-reported use of four chemical hair products (permanent dye, semipermanent dye, straighteners/relaxers, and hair permanents/body waves) in the year before enrollment (2003–2009) and three DNA methylation-based measures of epigenetic age (DunedinPACE, GrimAge age acceleration [GrimAgeAccel], and PhenoAge age acceleration [PhenoAgeAccel]) using survey-weighted multivariable linear regressions. Associations were estimated both overall and by self-identified race and ethnicity, adjusting for chronological age, socioeconomic and lifestyle factors, body mass index, menopausal status, and DNA methylation platform. Results: Associations between the use of hair products and the three epigenetic age measures were largely null. Use of hair permanents/body waves was modestly associated with higher DunedinPACE among all participants (βever-never = 0.010; 95% confidence interval [CI] = 0.001, 0.019) and with lower PhenoAgeAccel among Black women (βever-never = −1.53; 95% CI = −2.84, −0.21). Conclusion: In this US-based study, we found little evidence of associations between chemical hair product use and epigenetic age in Black and non-Hispanic White women. Observed associations were modest and largely not supported by dose–response relationships or were inconsistent across epigenetic age measures. Previously observed associations between chemical hair product use and aging-related health outcomes may not be explained by the biological aging pathways captured by DunedinPACE, GrimAgeAccel, or PhenoAgeAccel. Alternative biological pathways are worth investigating in racially diverse samples.","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141126339","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 : 2024-05-17DOI: 10.1097/EE9.0000000000000312
Xinyue Liu, Alique G. Berberian, Sophia Wang, Lara J. Cushing
Background: Hurricane Harvey made landfall in August 2017 and resulted in catastrophic flooding in Houston, Texas. Prior studies of hurricanes and preterm birth have found conflicting results. We tested the hypotheses that exposure to Hurricane Harvey was associated with a higher risk of spontaneous pre- and early-term birth and assessed vulnerable subpopulations. Methods: We conducted a retrospective study of singleton births using administrative birth records in the nine-county greater Houston area from 2015 to 2019. We estimated the likelihood of pre- and early-term births using logistic regression, comparing births occurring during or within 1, 2, or 4 weeks of Hurricane Harvey to unexposed reference periods encompassing the same dates 2 years prior and after. Stratified models assessed effect modification by degree of flooding, birth parent age, high- vs. low-risk pregnancy, race/ethnicity, and prenatal care. Results: Among 15,564 births, we found no association between exposure to Hurricane Harvey and spontaneous preterm birth within 1 week adjusted (odds ratio [OR], 1.06; 95% confidence interval [CI] = 0.91, 1.25) but a 14% higher odds of spontaneous early-term birth (OR, 1.14; 95% CI = 1.04, 1.25). The odds of early-term birth were even higher in neighborhoods with severe flooding (OR, 1.21; 95% CI = 1.05, 1.38), segregated neighborhoods (OR, 1.23; 95% CI = 1.03, 1.47), and among foreign-born Hispanics (OR, 1.21; 95% CI = 1.04, 1.53) and pregnant people receiving no prenatal care (OR, 1.37; 95% CI = 1.03, 1.82). Effect estimates were attenuated or null when considering 2-week or 4-week lags to define exposure. Conclusions: Hurricane Harvey was associated with higher odds of spontaneous early-term birth up to 1 week later, especially among socially marginalized populations.
{"title":"Hurricane Harvey and the risk of spontaneous preterm and early-term birth","authors":"Xinyue Liu, Alique G. Berberian, Sophia Wang, Lara J. Cushing","doi":"10.1097/EE9.0000000000000312","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000312","url":null,"abstract":"Background: Hurricane Harvey made landfall in August 2017 and resulted in catastrophic flooding in Houston, Texas. Prior studies of hurricanes and preterm birth have found conflicting results. We tested the hypotheses that exposure to Hurricane Harvey was associated with a higher risk of spontaneous pre- and early-term birth and assessed vulnerable subpopulations. Methods: We conducted a retrospective study of singleton births using administrative birth records in the nine-county greater Houston area from 2015 to 2019. We estimated the likelihood of pre- and early-term births using logistic regression, comparing births occurring during or within 1, 2, or 4 weeks of Hurricane Harvey to unexposed reference periods encompassing the same dates 2 years prior and after. Stratified models assessed effect modification by degree of flooding, birth parent age, high- vs. low-risk pregnancy, race/ethnicity, and prenatal care. Results: Among 15,564 births, we found no association between exposure to Hurricane Harvey and spontaneous preterm birth within 1 week adjusted (odds ratio [OR], 1.06; 95% confidence interval [CI] = 0.91, 1.25) but a 14% higher odds of spontaneous early-term birth (OR, 1.14; 95% CI = 1.04, 1.25). The odds of early-term birth were even higher in neighborhoods with severe flooding (OR, 1.21; 95% CI = 1.05, 1.38), segregated neighborhoods (OR, 1.23; 95% CI = 1.03, 1.47), and among foreign-born Hispanics (OR, 1.21; 95% CI = 1.04, 1.53) and pregnant people receiving no prenatal care (OR, 1.37; 95% CI = 1.03, 1.82). Effect estimates were attenuated or null when considering 2-week or 4-week lags to define exposure. Conclusions: Hurricane Harvey was associated with higher odds of spontaneous early-term birth up to 1 week later, especially among socially marginalized populations.","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141126532","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 : 2024-04-16DOI: 10.1097/ee9.0000000000000307
Otienoh Oguge, Joshua Nyamondo, Noah Adera, Lydia Okolla, Beldine Okoth, Stephen Anyango, Augustine Afulo, A. Kumie, Jonathan Samet, Kiros Berhane
Continuous ambient air quality monitoring in Kenya has been limited, resulting in a sparse data base on the health impacts of air pollution for the country. We have operated a centrally located monitor in Nairobi for measuring fine particulate matter (PM2.5), the pollutant that has demonstrated impact on health. Here, we describe the temporal levels and trends in PM2.5 data for Nairobi and evaluate associated health implications. We used a centrally located reference sensor, the beta attenuation monitor (BAM-1022), to measure hourly PM2.5 concentrations over a 3-year period (21 August 2019 to 20 August 2022). We used, at minimum, 75% of the daily hourly concentration to represent the 24-hour concentrations for a given calendar day. To estimate the deaths attributable to air pollution, we used the World Health Organization (WHO) AirQ+ tool with input as PM2.5 concentration data, local mortality statistics, and population sizes. The daily (24-hour) mean (±SEM) PM2.5 concentration was 19. 2 ± 0.6 (µg/m3). Pollutant levels were lowest at 03:00 and, peaked at 20:00. Sundays had the lowest daily concentrations, which increased on Mondays and remained high through Saturdays. By season, the pollutant concentrations were lowest in April and highest in August. The mean annual concentration was 18.4 ± 7.1 (µg/m3), which was estimated to lead to between 400 and 1,400 premature deaths of the city’s population in 2021 hence contributing 5%–8% of the 17,432 adult deaths excluding accidents when referenced to WHO recommended 2021 air quality guideline for annual thresholds of 5 µg/m3. Fine particulate matter air pollution in Nairobi showed daily, day-of-week, and seasonal fluctuations consistent with the anthropogenic source mix, particularly from motor vehicles. The long-term population exposure to PM2.5 was 3.7 times higher than the WHO annual guideline of 5 µg/m3 and estimated to lead to a substantial burden of attributable deaths. An updated regulation targeting measures to reduce vehicular emissions is recommended.
{"title":"Fine particulate matter air pollution and health implications for Nairobi, Kenya","authors":"Otienoh Oguge, Joshua Nyamondo, Noah Adera, Lydia Okolla, Beldine Okoth, Stephen Anyango, Augustine Afulo, A. Kumie, Jonathan Samet, Kiros Berhane","doi":"10.1097/ee9.0000000000000307","DOIUrl":"https://doi.org/10.1097/ee9.0000000000000307","url":null,"abstract":"\u0000 \u0000 Continuous ambient air quality monitoring in Kenya has been limited, resulting in a sparse data base on the health impacts of air pollution for the country. We have operated a centrally located monitor in Nairobi for measuring fine particulate matter (PM2.5), the pollutant that has demonstrated impact on health. Here, we describe the temporal levels and trends in PM2.5 data for Nairobi and evaluate associated health implications.\u0000 \u0000 \u0000 \u0000 We used a centrally located reference sensor, the beta attenuation monitor (BAM-1022), to measure hourly PM2.5 concentrations over a 3-year period (21 August 2019 to 20 August 2022). We used, at minimum, 75% of the daily hourly concentration to represent the 24-hour concentrations for a given calendar day. To estimate the deaths attributable to air pollution, we used the World Health Organization (WHO) AirQ+ tool with input as PM2.5 concentration data, local mortality statistics, and population sizes.\u0000 \u0000 \u0000 \u0000 The daily (24-hour) mean (±SEM) PM2.5 concentration was 19. 2 ± 0.6 (µg/m3). Pollutant levels were lowest at 03:00 and, peaked at 20:00. Sundays had the lowest daily concentrations, which increased on Mondays and remained high through Saturdays. By season, the pollutant concentrations were lowest in April and highest in August. The mean annual concentration was 18.4 ± 7.1 (µg/m3), which was estimated to lead to between 400 and 1,400 premature deaths of the city’s population in 2021 hence contributing 5%–8% of the 17,432 adult deaths excluding accidents when referenced to WHO recommended 2021 air quality guideline for annual thresholds of 5 µg/m3.\u0000 \u0000 \u0000 \u0000 Fine particulate matter air pollution in Nairobi showed daily, day-of-week, and seasonal fluctuations consistent with the anthropogenic source mix, particularly from motor vehicles. The long-term population exposure to PM2.5 was 3.7 times higher than the WHO annual guideline of 5 µg/m3 and estimated to lead to a substantial burden of attributable deaths. An updated regulation targeting measures to reduce vehicular emissions is recommended.\u0000","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140694622","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 : 2024-04-12DOI: 10.1097/ee9.0000000000000306
Tanya E. Libby, S. Ilango, C. Leary, E. Semmens, Claire E Adam, Annette L. Fitzpatrick, J. Kaufman, A. Hajat
Growing evidence links air pollution exposure to the risk of dementia. We hypothesized that hypertension may partially mediate this effect. We previously documented an association between air pollution and dementia in the Ginkgo Evaluation of Memory Study, a randomized, placebo-controlled trial of 3069 adults ≥75 years across four US sites who were evaluated for dementia every 6 months from 2000–2008. We utilized a two-stage regression approach for causal mediation analysis to decompose the total effect of air pollution on dementia into its natural direct and indirect effect through prevalent hypertension. Exposure to air pollution in the 10 or 20 years before enrollment was assigned using estimates from fine-scale spatial-temporal models for PM2.5, PM10, and NO2. We used Poisson regression models for hypertension and Cox proportional hazard models for time-to-incident all-cause dementia, adjusting for a priori confounders. Participants were free of mild cognitive impairment at baseline (n = 2564 included in analyses); 69% had prevalent hypertension at baseline. During follow-up, 12% developed all-cause dementia (Alzheimer’s disease [AD] = 212; vascular dementia with or without AD [VaD/AD mixed] = 97). We did not find an adverse effect of any air pollutant on hypertension. Hypertension was associated with VaD/AD mixed (HR, 1.92 [95% CI = 1.14, 3.24]) but not AD. We did not observe mediation through hypertension for the effect of any pollutant on dementia outcomes. The lack of mediated effect may be due to other mechanistic pathways and the minimal effect of air pollution on hypertension in this cohort of older adults.
{"title":"An assessment of the mediating role of hypertension in the effect of long-term air pollution exposure on dementia","authors":"Tanya E. Libby, S. Ilango, C. Leary, E. Semmens, Claire E Adam, Annette L. Fitzpatrick, J. Kaufman, A. Hajat","doi":"10.1097/ee9.0000000000000306","DOIUrl":"https://doi.org/10.1097/ee9.0000000000000306","url":null,"abstract":"\u0000 \u0000 Growing evidence links air pollution exposure to the risk of dementia. We hypothesized that hypertension may partially mediate this effect.\u0000 \u0000 \u0000 \u0000 We previously documented an association between air pollution and dementia in the Ginkgo Evaluation of Memory Study, a randomized, placebo-controlled trial of 3069 adults ≥75 years across four US sites who were evaluated for dementia every 6 months from 2000–2008. We utilized a two-stage regression approach for causal mediation analysis to decompose the total effect of air pollution on dementia into its natural direct and indirect effect through prevalent hypertension. Exposure to air pollution in the 10 or 20 years before enrollment was assigned using estimates from fine-scale spatial-temporal models for PM2.5, PM10, and NO2. We used Poisson regression models for hypertension and Cox proportional hazard models for time-to-incident all-cause dementia, adjusting for a priori confounders.\u0000 \u0000 \u0000 \u0000 Participants were free of mild cognitive impairment at baseline (n = 2564 included in analyses); 69% had prevalent hypertension at baseline. During follow-up, 12% developed all-cause dementia (Alzheimer’s disease [AD] = 212; vascular dementia with or without AD [VaD/AD mixed] = 97). We did not find an adverse effect of any air pollutant on hypertension. Hypertension was associated with VaD/AD mixed (HR, 1.92 [95% CI = 1.14, 3.24]) but not AD. We did not observe mediation through hypertension for the effect of any pollutant on dementia outcomes.\u0000 \u0000 \u0000 \u0000 The lack of mediated effect may be due to other mechanistic pathways and the minimal effect of air pollution on hypertension in this cohort of older adults.\u0000","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140711235","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 : 2024-04-12DOI: 10.1097/ee9.0000000000000309
Emily J. Hemstock, Ashley Bigaran, S. Allgood, Amanda J. Wheeler, M. Dalton, Grant J. Williamson, Caroline X. Gao, Michael J. Abramson, Kazuaki Negishi, F. Johnston, G. Zosky
Chronic, low-intensity air pollution exposure has been consistently associated with increased atherosclerosis in adults. However, there was limited research regarding the implications of acute, high-intensity air pollution exposure during childhood. We aimed to determine whether there were any associations between early-life exposure to such an episode and early-life vascular function changes. We conducted a prospective cohort study of children (<9 years old) who lived in the vicinity of the Hazelwood coal mine fire (n = 206). Vascular function was measured using noninvasive diagnostic methods including carotid intima-media thickness and pulse wave velocity (PWV). Exposure estimates were calculated from prognostic models and location diaries during the exposure period completed by each participant’s parent. Linear mixed-effects models were used to determine whether there were any associations between exposure and changes in vascular outcomes at the 3- and 7-year follow-ups and over time. At the 7-year follow-up, each 10 μg/m3 increase in daily PM2.5 in utero was associated with increased PWV (β = 0.13 m/s; 95% confidence interval [CI] = 0.02, 0.24; P = 0.02). The association between in utero exposure to daily PM2.5 was not altered by adjustment for covariates, body mass index, and maternal fire stress. Each 1 µg/m3 increase in background PM2.5 was associated with increased PWV (β = 0.68 m/s; 95% CI = 0.10, 1.26; P = 0.025), in children from the in utero exposure group. There was a trend toward smaller PWV (β = −0.17 m/s; 95% CI = −0.366, 0.02) from the 3- to 7-year follow-up clinic suggesting that the deficits observed previously in children exposed postnatally did not persist. There was a moderate improvement in vascular stiffness of children exposed to PM2.5 from a local coal mine fire in infancy. There was a mild increase in vascular stiffness in children exposed to PM2.5 from a local coal mine fire while their mothers were pregnant.
{"title":"Increased vascular stiffness in children exposed in utero but not children exposed postnatally to emissions from a coal mine fire","authors":"Emily J. Hemstock, Ashley Bigaran, S. Allgood, Amanda J. Wheeler, M. Dalton, Grant J. Williamson, Caroline X. Gao, Michael J. Abramson, Kazuaki Negishi, F. Johnston, G. Zosky","doi":"10.1097/ee9.0000000000000309","DOIUrl":"https://doi.org/10.1097/ee9.0000000000000309","url":null,"abstract":"\u0000 \u0000 Chronic, low-intensity air pollution exposure has been consistently associated with increased atherosclerosis in adults. However, there was limited research regarding the implications of acute, high-intensity air pollution exposure during childhood. We aimed to determine whether there were any associations between early-life exposure to such an episode and early-life vascular function changes.\u0000 \u0000 \u0000 \u0000 We conducted a prospective cohort study of children (<9 years old) who lived in the vicinity of the Hazelwood coal mine fire (n = 206). Vascular function was measured using noninvasive diagnostic methods including carotid intima-media thickness and pulse wave velocity (PWV). Exposure estimates were calculated from prognostic models and location diaries during the exposure period completed by each participant’s parent. Linear mixed-effects models were used to determine whether there were any associations between exposure and changes in vascular outcomes at the 3- and 7-year follow-ups and over time.\u0000 \u0000 \u0000 \u0000 At the 7-year follow-up, each 10 μg/m3 increase in daily PM2.5 in utero was associated with increased PWV (β = 0.13 m/s; 95% confidence interval [CI] = 0.02, 0.24; P = 0.02). The association between in utero exposure to daily PM2.5 was not altered by adjustment for covariates, body mass index, and maternal fire stress. Each 1 µg/m3 increase in background PM2.5 was associated with increased PWV (β = 0.68 m/s; 95% CI = 0.10, 1.26; P = 0.025), in children from the in utero exposure group. There was a trend toward smaller PWV (β = −0.17 m/s; 95% CI = −0.366, 0.02) from the 3- to 7-year follow-up clinic suggesting that the deficits observed previously in children exposed postnatally did not persist.\u0000 \u0000 \u0000 \u0000 There was a moderate improvement in vascular stiffness of children exposed to PM2.5 from a local coal mine fire in infancy. There was a mild increase in vascular stiffness in children exposed to PM2.5 from a local coal mine fire while their mothers were pregnant.\u0000","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140710507","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 : 2024-04-04eCollection 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":"https://doi.org/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":null,"pages":null},"PeriodicalIF":3.6,"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}
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