Environmental Epidemiology最新文献

{"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}

{"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}

{"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 (Lag₀) and preceding 27 days (Lags_1-27) 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.</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}

{"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":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;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&lt;sub&gt;2.5&lt;/sub&gt;), nitrogen dioxide (NO&lt;sub&gt;2&lt;/sub&gt;), or ozone (O&lt;sub&gt;3&lt;/sub&gt;) and incidence of various diseases.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;To establish the basis for our evaluation, we considered the causality determinations provided by the US Environmental Protection Agency Integrated Science Assessment for PM&lt;sub&gt;2.5&lt;/sub&gt;, NO&lt;sub&gt;2&lt;/sub&gt;, and O&lt;sub&gt;3&lt;/sub&gt;. 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&lt;sub&gt;2.5&lt;/sub&gt; and NO&lt;sub&gt;2&lt;/sub&gt;. 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).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;In our final evaluation, list A includes six CRFs for PM&lt;sub&gt;2.5&lt;/sub&gt; (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}

{"title":"Prenatal air pollution and children's autism traits score: Examination of joint associations with maternal intake of vitamin D, methyl donors, and polyunsaturated fatty acids using mixture methods.","authors":"Megan G Bragg, Irena Gorski-Steiner, Ashley Song, Jorge E Chavarro, Jaime E Hart, Loni P Tabb, Marc G Weisskopf, Heather Volk, Kristen Lyall","doi":"10.1097/EE9.0000000000000316","DOIUrl":"10.1097/EE9.0000000000000316","url":null,"abstract":"<p><strong>Background: </strong>Maternal nutrient intake may moderate associations between environmental exposures and children's neurodevelopmental outcomes, but few studies have assessed joint effects. We aimed to evaluate whether prenatal nutrient intake influences the association between air pollutants and autism-related trait scores.</p><p><strong>Methods: </strong>We included 126 participants from the EARLI (Early Autism Risk Longitudinal Investigation, 2009-2012) cohort, which followed US pregnant mothers who previously had a child with autism. Bayesian kernel machine regression and traditional regression models were used to examine joint associations of prenatal nutrient intake (vitamins D, B12, and B6; folate, choline, and betaine; and total omega 3 and 6 polyunsaturated fatty acids, reported via food frequency questionnaire), air pollutant exposure (particulate matter <2.5 μm [PM_2.5], nitrogen dioxide [NO₂], and ozone [O₃], estimated at the address level), and children's autism-related traits (measured by the Social Responsiveness Scale [SRS] at 36 months).</p><p><strong>Results: </strong>Most participants had nutrient intakes and air pollutant exposures that met US standards. Bayesian kernel machine regression mixture models and traditional regression models provided little evidence of individual or joint associations of nutrients and air pollutants with SRS scores or of an association between the overall mixture and SRS scores.</p><p><strong>Conclusion: </strong>In this cohort with a high familial likelihood of autism, we did not observe evidence of joint associations between air pollution exposures and nutrient intake with autism-related traits. Future work should examine the use of these methods in larger, more diverse samples, as our results may have been influenced by familial liability and/or relatively high nutrient intakes and low air pollutant exposures.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"8 4","pages":"e316"},"PeriodicalIF":3.3,"publicationDate":"2024-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11196080/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141450140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"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":3.3,"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}

{"title":"Longitudinal associations between ambient PM_2.5 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_2.5 is known to affect lipid metabolism through systemic inflammation and oxidative stress. Evidence from developing countries, such as India with high levels of ambient PM_2.5 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_2.5 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.</p><p><strong>Results: </strong>The mean annual exposure in Chennai and Delhi was 40 and 102 μg/m³ respectively. Elevated ambient PM_2.5 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.</p><p><strong>Conclusion: </strong>These findings demonstrate diverse associations between a wide range of ambient PM_2.5 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.</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}

{"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}

{"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}

{"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}