Yiqian Zeng,Gavin Rudge,Tsung Yu,Weiyi Chen,Ka Chun Chong,Yu Huang,G Neil Thomas,Xiang Qian Lao
BACKGROUNDThere is limited information on the association between walkability and health in Asian countries.OBJECTIVEOur study aims to investigate the association between neighborhood walkability and mortality in Taiwanese adults.METHODSWe selected 457,874 participants (≥18 years old) from Taiwan who joined a standard medical examination program between 1998 and 2016, and followed them until 31 July 2021. Three walkability measures were estimated within a walking distance of 640m of participant's addresses: points of interest (POI), transit stations, and impedance (restrictions to walking due to absence of intersections and physical barriers). Walkability measures were applied as continuous and categorical (tertiles) variables in data analyses. Mortality data was obtained from the National Death Registry maintained by the Ministry of Health and Welfare in Taiwan. A time-varying Cox regression model was used to investigate the association of neighborhood walkability with deaths from natural causes and specific causes.RESULTSThis study identified 24,744 deaths over a median follow up of 16.9 years. Compared with participants living with the first tertile for numbers of POI and transit stations, those living with higher numbers of POI and transit stations were associated with a lower risk of natural-cause mortality, with hazard ratios (HRs) (95% confidence intervals (CIs)) of 0.97 (0.94, 1.00) and 0.93 (0.90, 0.96) for second and third tertiles of numbers of POI, and 0.99 (0.96, 1.02) and 0.94 (0.92, 0.98) for second and third tertiles of numbers of transit station, respectively. Each unit increase in POI and transit stations were associated with a 3% [HR (95% CI): 0.97 (0.96, 0.99)] and 2% [HR (95% CI): 0.98 (0.97, 0.99)] reduced risk of natural-cause mortality, respectively. In addition, compared with living in areas with the first tertile of impedance, living with the third tertile of impedance was associated a higher risk of natural-cause mortality, with HRs (95%CI) of 1.01 (1.00, 1.03). One unit increase in impedance was associated with a 1% [HR (95% CI): 1.01 (1.00, 1.03)] increased risk of natural-cause mortality. We also found significantly inverse associations between three walkability measures with deaths from cardiovascular diseases, and between POI and death from chronic respiratory diseases.CONCLUSIONOur findings indicate that a higher level of neighborhood walkability was associated with a lower risk of mortality. Our data suggests it is important to take into account neighborhood walkability in urban planning and health guideline development. https://doi.org/10.1289/EHP15209.
{"title":"Pavements to Longevity: The Influence of Neighborhood Walkability on Mortality in Taiwan.","authors":"Yiqian Zeng,Gavin Rudge,Tsung Yu,Weiyi Chen,Ka Chun Chong,Yu Huang,G Neil Thomas,Xiang Qian Lao","doi":"10.1289/ehp15209","DOIUrl":"https://doi.org/10.1289/ehp15209","url":null,"abstract":"BACKGROUNDThere is limited information on the association between walkability and health in Asian countries.OBJECTIVEOur study aims to investigate the association between neighborhood walkability and mortality in Taiwanese adults.METHODSWe selected 457,874 participants (≥18 years old) from Taiwan who joined a standard medical examination program between 1998 and 2016, and followed them until 31 July 2021. Three walkability measures were estimated within a walking distance of 640m of participant's addresses: points of interest (POI), transit stations, and impedance (restrictions to walking due to absence of intersections and physical barriers). Walkability measures were applied as continuous and categorical (tertiles) variables in data analyses. Mortality data was obtained from the National Death Registry maintained by the Ministry of Health and Welfare in Taiwan. A time-varying Cox regression model was used to investigate the association of neighborhood walkability with deaths from natural causes and specific causes.RESULTSThis study identified 24,744 deaths over a median follow up of 16.9 years. Compared with participants living with the first tertile for numbers of POI and transit stations, those living with higher numbers of POI and transit stations were associated with a lower risk of natural-cause mortality, with hazard ratios (HRs) (95% confidence intervals (CIs)) of 0.97 (0.94, 1.00) and 0.93 (0.90, 0.96) for second and third tertiles of numbers of POI, and 0.99 (0.96, 1.02) and 0.94 (0.92, 0.98) for second and third tertiles of numbers of transit station, respectively. Each unit increase in POI and transit stations were associated with a 3% [HR (95% CI): 0.97 (0.96, 0.99)] and 2% [HR (95% CI): 0.98 (0.97, 0.99)] reduced risk of natural-cause mortality, respectively. In addition, compared with living in areas with the first tertile of impedance, living with the third tertile of impedance was associated a higher risk of natural-cause mortality, with HRs (95%CI) of 1.01 (1.00, 1.03). One unit increase in impedance was associated with a 1% [HR (95% CI): 1.01 (1.00, 1.03)] increased risk of natural-cause mortality. We also found significantly inverse associations between three walkability measures with deaths from cardiovascular diseases, and between POI and death from chronic respiratory diseases.CONCLUSIONOur findings indicate that a higher level of neighborhood walkability was associated with a lower risk of mortality. Our data suggests it is important to take into account neighborhood walkability in urban planning and health guideline development. https://doi.org/10.1289/EHP15209.","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"91 1","pages":""},"PeriodicalIF":10.4,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143893358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Bonnie N Young,Jennifer L Peel,Sarah Rajkumar,Kayleigh P Keller,Megan L Benka-Coker,Nicholas Good,Ethan S Walker,Robert D Brook,Tracy L Nelson,John Volckens,Christian L'Orange,Casey Quinn,Sebastian Africano,Anibal B Osorto Pinel,Maggie L Clark
BACKGROUNDType 2 diabetes is a rapidly growing global health challenge in low- and middle-income countries (LMICs), and evidence suggests that air pollution exposure contributes. Household air pollution from burning solid fuels for cooking is a major burden in LMICs but studies demonstrating associations between reductions in household air pollution and improvements in HbA1c, a biomarker of diabetes risk, are lacking. We previously reported substantial reductions in fine particulate matter (PM2.5) and black carbon concentrations following an intervention in rural Honduras with the Justa cookstove, a wood-burning stove with an engineered combustion chamber and chimney.OBJECTIVEIn a stepped-wedge randomized controlled trial among 230 Honduran women using traditional wood-burning stoves at baseline, we evaluated the effect of the Justa intervention on HbA1c and characterized the longitudinal associations between air pollution exposures and HbA1c.METHODSAt each of 6 visits over 3 years, we measured 24-hour PM2.5 and black carbon concentrations, and finger-stick HbA1c levels. We used linear mixed models in intent-to-treat (condition by assigned stove type), exposure-response (using 24-hour measures and modeled estimates of long-term exposures), and "per protocol" self-reported stove use analyses.RESULTSHbA1c was reduced for the Justa condition compared to the traditional stove condition, but estimates were small and not statistically significant (-0.03 percentage points, 95% confidence interval [CI]: -0.13, 0.07, n=1,208 observations). A slightly stronger effect was observed when using self-reported stove use in per protocol analyses. Exposure-response analyses demonstrated positive associations between HbA1c and air pollution (e.g., HbA1c was 0.22 percentage points higher (95% CI: 0.13, 0.30) per log-unit higher long-term average personal PM2.5).DISCUSSIONOur study provides novel evidence of exposure-response associations between household air pollution and HbA1c within a randomized cookstove trial, contributing to the evidence base necessary to support clean cooking policy initiatives. https://doi.org/10.1289/EHP15095.
{"title":"Impact of the wood-burning Justa cookstove on glycated hemoglobin (HbA1c): a stepped-wedge randomized trial in rural Honduras.","authors":"Bonnie N Young,Jennifer L Peel,Sarah Rajkumar,Kayleigh P Keller,Megan L Benka-Coker,Nicholas Good,Ethan S Walker,Robert D Brook,Tracy L Nelson,John Volckens,Christian L'Orange,Casey Quinn,Sebastian Africano,Anibal B Osorto Pinel,Maggie L Clark","doi":"10.1289/ehp15095","DOIUrl":"https://doi.org/10.1289/ehp15095","url":null,"abstract":"BACKGROUNDType 2 diabetes is a rapidly growing global health challenge in low- and middle-income countries (LMICs), and evidence suggests that air pollution exposure contributes. Household air pollution from burning solid fuels for cooking is a major burden in LMICs but studies demonstrating associations between reductions in household air pollution and improvements in HbA1c, a biomarker of diabetes risk, are lacking. We previously reported substantial reductions in fine particulate matter (PM2.5) and black carbon concentrations following an intervention in rural Honduras with the Justa cookstove, a wood-burning stove with an engineered combustion chamber and chimney.OBJECTIVEIn a stepped-wedge randomized controlled trial among 230 Honduran women using traditional wood-burning stoves at baseline, we evaluated the effect of the Justa intervention on HbA1c and characterized the longitudinal associations between air pollution exposures and HbA1c.METHODSAt each of 6 visits over 3 years, we measured 24-hour PM2.5 and black carbon concentrations, and finger-stick HbA1c levels. We used linear mixed models in intent-to-treat (condition by assigned stove type), exposure-response (using 24-hour measures and modeled estimates of long-term exposures), and \"per protocol\" self-reported stove use analyses.RESULTSHbA1c was reduced for the Justa condition compared to the traditional stove condition, but estimates were small and not statistically significant (-0.03 percentage points, 95% confidence interval [CI]: -0.13, 0.07, n=1,208 observations). A slightly stronger effect was observed when using self-reported stove use in per protocol analyses. Exposure-response analyses demonstrated positive associations between HbA1c and air pollution (e.g., HbA1c was 0.22 percentage points higher (95% CI: 0.13, 0.30) per log-unit higher long-term average personal PM2.5).DISCUSSIONOur study provides novel evidence of exposure-response associations between household air pollution and HbA1c within a randomized cookstove trial, contributing to the evidence base necessary to support clean cooking policy initiatives. https://doi.org/10.1289/EHP15095.","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"25 1","pages":""},"PeriodicalIF":10.4,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143893359","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Susan S Hoffman,John A Kaufman,Robert B Hood,Tamar Wainstock,Kathleen Hartnett,Hillary Barton,Melanie A Pearson,Metrecia L Terrell,Michele Marcus
BACKGROUNDThe Michigan Polybrominated Biphenyl (PBB) registry, followed since 1976, was created after a 1973 chemical manufacturing mistake. The flame retardant PBB was accidentally mixed into animal feed and distributed to Michigan farms for nearly a year, exposing farm residents and animal product consumers.OBJECTIVEWe synthesize knowledge to date on health effects of PBB exposure within the Michigan PBB Registry, and describe research findings in the context of literature on other persistent organic pollutants (POPs) and endocrine disrupting chemicals (EDCs).METHODSWe reviewed literature published from 1973-2025 on human health effects of PBB following the Michigan contamination using PubMed and Thompson Reuters (ISI) Web of Science databases. We excluded studies not in English; on exposures besides PBB; animal studies; reviews, abstracts, or letters to the editor; studies without a health outcome; and studies outside of Michigan or unrelated to the 1973 contamination. For each article, two researchers performed title and abstract screening, full article review, and data extraction.RESULTSWe included 79 publications out of 601 identified and screened. Early studies did not find many health outcomes associated with PBB, possibly because of methodological limitations. More recent studies on long-term and multigenerational impacts found an increased breast cancer risk, accelerated pubertal development and earlier menarche for girls exposed in utero, urogenital problems and slower pubertal development in boys exposed in utero, lower estrone 3-glucuronide and follicle-stimulating hormone among women exposed in childhood, and increased miscarriage risk among daughters of exposed women. Epigenetic and metabolomic research reported altered pathways related to estrogenic effects and immune function, and epigenetic alterations of spermatogenic cells.DISCUSSIONThis unique community-academic partnership has produced insights into multigenerational consequences of EDC/POP exposures across the lifecourse. The findings from this cohort underscore the broader relevance of critical windows of vulnerability, particularly during fetal development and childhood.. https://doi.org/10.1289/EHP15012.
密歇根州多溴联苯（PBB）登记制度是在1973年的一次化学制造错误之后建立的，自1976年开始实施。阻燃剂多溴联苯意外混入动物饲料，并分发到密歇根州的农场近一年，使农场居民和动物产品消费者暴露。目的：我们综合了密歇根州多氯联苯登记处迄今为止关于多氯联苯暴露对健康影响的知识，并在其他持久性有机污染物（POPs）和内分泌干扰物（EDCs）的文献背景下描述了研究结果。方法：我们使用PubMed和Thompson Reuters (ISI) Web of Science数据库回顾了1973-2025年发表的关于密歇根州污染后多氯联苯对人类健康影响的文献。我们排除了非英语研究；多氯联苯以外的暴露；动物实验;评论、摘要或给编辑的信；没有健康结果的研究；以及密歇根以外的研究或与1973年的污染无关的研究。对于每篇文章，两名研究人员进行标题和摘要筛选，全文审查和数据提取。结果从601篇文献中纳入79篇。早期的研究没有发现许多与PBB相关的健康结果，可能是由于方法上的限制。最近对长期和多代影响的研究发现，乳腺癌风险增加，子宫内暴露的女孩青春期发育加快，月经初潮提前，子宫内暴露的男孩出现泌尿生殖问题，青春期发育缓慢，儿童时期暴露的妇女雌激素- 3-葡萄糖醛酸盐和促卵泡激素水平较低，暴露妇女的女儿流产风险增加。表观遗传学和代谢组学研究报告了与雌激素效应和免疫功能相关的通路改变，以及生精细胞的表观遗传学改变。这种独特的社区-学术合作关系对EDC/POP暴露在整个生命过程中对几代人的影响产生了深刻的见解。该队列的研究结果强调了脆弱性关键窗口的广泛相关性，特别是在胎儿发育和儿童时期。https://doi.org/10.1289/EHP15012。
{"title":"A State of the Science Review of Human Health Effects of the Michigan Polybrominated Biphenyl Contamination after Five Decades.","authors":"Susan S Hoffman,John A Kaufman,Robert B Hood,Tamar Wainstock,Kathleen Hartnett,Hillary Barton,Melanie A Pearson,Metrecia L Terrell,Michele Marcus","doi":"10.1289/ehp15012","DOIUrl":"https://doi.org/10.1289/ehp15012","url":null,"abstract":"BACKGROUNDThe Michigan Polybrominated Biphenyl (PBB) registry, followed since 1976, was created after a 1973 chemical manufacturing mistake. The flame retardant PBB was accidentally mixed into animal feed and distributed to Michigan farms for nearly a year, exposing farm residents and animal product consumers.OBJECTIVEWe synthesize knowledge to date on health effects of PBB exposure within the Michigan PBB Registry, and describe research findings in the context of literature on other persistent organic pollutants (POPs) and endocrine disrupting chemicals (EDCs).METHODSWe reviewed literature published from 1973-2025 on human health effects of PBB following the Michigan contamination using PubMed and Thompson Reuters (ISI) Web of Science databases. We excluded studies not in English; on exposures besides PBB; animal studies; reviews, abstracts, or letters to the editor; studies without a health outcome; and studies outside of Michigan or unrelated to the 1973 contamination. For each article, two researchers performed title and abstract screening, full article review, and data extraction.RESULTSWe included 79 publications out of 601 identified and screened. Early studies did not find many health outcomes associated with PBB, possibly because of methodological limitations. More recent studies on long-term and multigenerational impacts found an increased breast cancer risk, accelerated pubertal development and earlier menarche for girls exposed in utero, urogenital problems and slower pubertal development in boys exposed in utero, lower estrone 3-glucuronide and follicle-stimulating hormone among women exposed in childhood, and increased miscarriage risk among daughters of exposed women. Epigenetic and metabolomic research reported altered pathways related to estrogenic effects and immune function, and epigenetic alterations of spermatogenic cells.DISCUSSIONThis unique community-academic partnership has produced insights into multigenerational consequences of EDC/POP exposures across the lifecourse. The findings from this cohort underscore the broader relevance of critical windows of vulnerability, particularly during fetal development and childhood.. https://doi.org/10.1289/EHP15012.","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"69 1","pages":""},"PeriodicalIF":10.4,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143889234","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Josh Naiman,Daniel Q Naiman,Judy S LaKind,Dana Boyd Barr
{"title":"Are NHANES data representative of the US population for chemicals with seasonal and regional use?","authors":"Josh Naiman,Daniel Q Naiman,Judy S LaKind,Dana Boyd Barr","doi":"10.1289/ehp17203","DOIUrl":"https://doi.org/10.1289/ehp17203","url":null,"abstract":"","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"17 1","pages":""},"PeriodicalIF":10.4,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143880207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BACKGROUNDAs immunity wanes and viral mutations continue, the risk of endemic SARS-CoV-2 breakthrough infections (BTIs) remains. Air pollution is considered a risk factor for respiratory infection, but evidence of its association with SARS-CoV-2 BTIs is limited.OBJECTIVESWe aimed to examine the effects of long-term exposure to air pollution on disease outcomes, immune responses, and antibody dynamics of SARS-CoV-2 BTIs.METHODSWe gathered data on self-reported SARS-CoV-2 infections through questionnaires and measured IgG antibody levels using serological assays from a total of 6,875 participants from the Yichang COVID-19 Antibody Longitudinal Survey cohort in China. Air pollutant exposure (PM2.5, PM10, PM1, SO2, NO2, O3, and CO) was quantified using validated models for the past five years (2018 to 2022). Logistic and linear regression models were applied to analyze the associations between air pollutant levels and SARS-CoV-2 BTIs, Long COVID, COVID-19 hospitalization, and antibody responses. Quantile g-computation was used to assess the combined effects of pollutant mixtures. A linear mixed model was used to evaluate the effect of air pollution on antibody dynamics.RESULTSPer interquartile range (IQR) increase in PM2.5, SO2, NO2, and CO, the adjusted odds ratios (ORs) for SARS-CoV-2 BTIs were 1.65(95% CI: 1.30, 2.08), 1.30 (95% CI: 1.12, 1.50), 1.63 (95% CI: 1.20, 2.20), and 1.24 (95% CI: 1.06, 1.45). The ORs for PM2.5 were 1.78 (95% CI: 1.07, 3.02) and 2.02 (95% CI: 1.18, 3.54) for Long COVID and hospitalization. Per IQR increase in PM1 and NO2, IgG antibody percentages decreased by -2.31% (95% CI: -4.49%, -0.13%) and -2.69% (95% CI: -5.35%, -0.03%). Effects were stronger in older adults, those with comorbidities, and the under-vaccinated. The combined effect on SARS-CoV-2 BTIs was mainly driven by PM2.5 (59.4%), while the impact on IgG response was largely attributed to NO2 (63.7%). Exposure to the highest levels of PM2.5 (p = 0.002), PM1 (p < 0.001), and NO2 (p = 0.002) was associated with a faster IgG decline than the lowest.DISCUSSIONLong-term exposure to air pollution increases the risk of SARS-CoV-2 BTIs and disease severity while weakening the immune response, particularly for vulnerable populations. https://doi.org/10.1289/EHP15660.
{"title":"Effects of Long-Term Air Pollution Exposure on Disease Outcomes and Hybrid Immune Responses in SARS-CoV-2 Breakthrough Infections: A Study of the Yichang COVID-19 Antibody Longitudinal Survey (YC-CALS) in China.","authors":"Xiaolong Yan,Yin Du,Ke Li,Xin Zhao,Hao Wang,Li Liu,Qi Wang,Jianhua Liu,Sheng Wei","doi":"10.1289/ehp15660","DOIUrl":"https://doi.org/10.1289/ehp15660","url":null,"abstract":"BACKGROUNDAs immunity wanes and viral mutations continue, the risk of endemic SARS-CoV-2 breakthrough infections (BTIs) remains. Air pollution is considered a risk factor for respiratory infection, but evidence of its association with SARS-CoV-2 BTIs is limited.OBJECTIVESWe aimed to examine the effects of long-term exposure to air pollution on disease outcomes, immune responses, and antibody dynamics of SARS-CoV-2 BTIs.METHODSWe gathered data on self-reported SARS-CoV-2 infections through questionnaires and measured IgG antibody levels using serological assays from a total of 6,875 participants from the Yichang COVID-19 Antibody Longitudinal Survey cohort in China. Air pollutant exposure (PM2.5, PM10, PM1, SO2, NO2, O3, and CO) was quantified using validated models for the past five years (2018 to 2022). Logistic and linear regression models were applied to analyze the associations between air pollutant levels and SARS-CoV-2 BTIs, Long COVID, COVID-19 hospitalization, and antibody responses. Quantile g-computation was used to assess the combined effects of pollutant mixtures. A linear mixed model was used to evaluate the effect of air pollution on antibody dynamics.RESULTSPer interquartile range (IQR) increase in PM2.5, SO2, NO2, and CO, the adjusted odds ratios (ORs) for SARS-CoV-2 BTIs were 1.65(95% CI: 1.30, 2.08), 1.30 (95% CI: 1.12, 1.50), 1.63 (95% CI: 1.20, 2.20), and 1.24 (95% CI: 1.06, 1.45). The ORs for PM2.5 were 1.78 (95% CI: 1.07, 3.02) and 2.02 (95% CI: 1.18, 3.54) for Long COVID and hospitalization. Per IQR increase in PM1 and NO2, IgG antibody percentages decreased by -2.31% (95% CI: -4.49%, -0.13%) and -2.69% (95% CI: -5.35%, -0.03%). Effects were stronger in older adults, those with comorbidities, and the under-vaccinated. The combined effect on SARS-CoV-2 BTIs was mainly driven by PM2.5 (59.4%), while the impact on IgG response was largely attributed to NO2 (63.7%). Exposure to the highest levels of PM2.5 (p = 0.002), PM1 (p < 0.001), and NO2 (p = 0.002) was associated with a faster IgG decline than the lowest.DISCUSSIONLong-term exposure to air pollution increases the risk of SARS-CoV-2 BTIs and disease severity while weakening the immune response, particularly for vulnerable populations. https://doi.org/10.1289/EHP15660.","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"76 1","pages":""},"PeriodicalIF":10.4,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143876471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mia C Mattioli,Katharine M Benedict,Shanna Miko,Catherine E Barrett,Alexis Roundtree,Sunkyung Kim,Sarah A Collier,Elizabeth Adam,Julia W Gargano,Jonathan S Yoder,Deborah A Vacs Renwick,Kenneth Rotert,Mike Sullivan,Sharon Sweeney,Michael Beach,Vincent R Hill
BACKGROUNDLow pressure events (LPEs), defined as a water service disruption that presumably lowers system water pressure, can cause drinking water contamination resulting in increased illness risk to consumers.OBJECTIVESExamine whether LPEs increase the risk for highly credible acute gastrointestinal illness (HCGI) and acute respiratory illness (ARI) and compare water quality in exposed and unexposed areas in the United States.METHODSA matched cohort study was conducted during 2015-2019. For each LPE, household survey exposed areas were matched 1:2 with unexposed areas based on water main size and material at the point of repair, as well as the housing type and demographic characteristics of the local population from the most recent census tract. Water samples were collected to monitor physicochemical and microbiological water quality parameters. Households (HHs) were surveyed about water use and illness during the 2 weeks after the LPE. Multivariable log-binomial models clustered on utility and LPE number were used to investigate associations between LPE exposure and HCGI and ARI.RESULTSFive water utilities reported 58 LPEs, including planned maintenance (76%) and emergency (24%) events. Controlling for livestock near home, private well presence, number of people in HH, and travel away from home, exposed HH were at higher risk of HCGI compared to unexposed HH (risk ratio =1.20; 95%CI: 1.05,1.37). No associations between LPE and ARI were detected. Certain LPEs characteristics like pipe material, size, and depth were associated with an increased HH HCGI risk. HHs experiencing LPEs where low disinfectant residual, high adenosine triphosphate, or general Bacteroidales were detected in water following an LPE repair were also at a higher risk for HCGI.CONCLUSIONSLPEs were associated with 20% higher risk of HCGI in HHs. Planned improvements to water distribution system infrastructure, adherence to industry standard distribution repair practices, and water monitoring following pipe repairs could supplement community alert systems to reduce illnesses from LPEs. https://doi.org/10.1289/EHP15564.
{"title":"Health Effects and Water Quality Following Low Pressure Events in Drinking Water Distribution Systems in the United States.","authors":"Mia C Mattioli,Katharine M Benedict,Shanna Miko,Catherine E Barrett,Alexis Roundtree,Sunkyung Kim,Sarah A Collier,Elizabeth Adam,Julia W Gargano,Jonathan S Yoder,Deborah A Vacs Renwick,Kenneth Rotert,Mike Sullivan,Sharon Sweeney,Michael Beach,Vincent R Hill","doi":"10.1289/ehp15564","DOIUrl":"https://doi.org/10.1289/ehp15564","url":null,"abstract":"BACKGROUNDLow pressure events (LPEs), defined as a water service disruption that presumably lowers system water pressure, can cause drinking water contamination resulting in increased illness risk to consumers.OBJECTIVESExamine whether LPEs increase the risk for highly credible acute gastrointestinal illness (HCGI) and acute respiratory illness (ARI) and compare water quality in exposed and unexposed areas in the United States.METHODSA matched cohort study was conducted during 2015-2019. For each LPE, household survey exposed areas were matched 1:2 with unexposed areas based on water main size and material at the point of repair, as well as the housing type and demographic characteristics of the local population from the most recent census tract. Water samples were collected to monitor physicochemical and microbiological water quality parameters. Households (HHs) were surveyed about water use and illness during the 2 weeks after the LPE. Multivariable log-binomial models clustered on utility and LPE number were used to investigate associations between LPE exposure and HCGI and ARI.RESULTSFive water utilities reported 58 LPEs, including planned maintenance (76%) and emergency (24%) events. Controlling for livestock near home, private well presence, number of people in HH, and travel away from home, exposed HH were at higher risk of HCGI compared to unexposed HH (risk ratio =1.20; 95%CI: 1.05,1.37). No associations between LPE and ARI were detected. Certain LPEs characteristics like pipe material, size, and depth were associated with an increased HH HCGI risk. HHs experiencing LPEs where low disinfectant residual, high adenosine triphosphate, or general Bacteroidales were detected in water following an LPE repair were also at a higher risk for HCGI.CONCLUSIONSLPEs were associated with 20% higher risk of HCGI in HHs. Planned improvements to water distribution system infrastructure, adherence to industry standard distribution repair practices, and water monitoring following pipe repairs could supplement community alert systems to reduce illnesses from LPEs. https://doi.org/10.1289/EHP15564.","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"48 1","pages":""},"PeriodicalIF":10.4,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143872097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jinwoo Kim,Mi-Jin Kang,So-Yeon Lee,Sang-Bum Hong,Ho Cheol Kim,Myung Hee Nam,Soo-Jong Hong
BACKGROUNDThe South Korean humidifier disinfectant-associated lung injury case was one of the worst disasters involving household chemical products, resulting in over 5,800 casualties. Despite the strong association between lung injury and humidifier disinfectants, the underlying pathogenic mechanisms remain unclear.OBJECTIVESWe investigated patients with humidifier disinfectant-associated lung injury to identify key metabolic signatures, aiming to gain insights into the underlying pathogenic mechanisms based on the characteristics of these metabolites.METHODSWe employed untargeted metabolomics to assess the differential enrichment of plasma metabolites in 80 South Korean children with lung injuries caused by exposure to humidifier disinfectant containing polyhexamethylene guanidine. The key metabolites identified were subsequently validated in an independent cohort of 132 South Korean adults.RESULTSIn the plasma of patients with humidifier disinfectant-associated lung injuries, we observed significantly higher levels of oxidized lipids compared to healthy controls, with these levels negatively correlating with lung function. These metabolic signatures differentiated humidifier disinfectant-associated lung injury from other respiratory diseases in children, such as asthma and bronchiolitis obliterans. The 47 key metabolites identified in children were validated in an independent adult cohort. Furthermore, the classification performance of these metabolic signatures for humidifier disinfectant-associated lung injury achieved an accuracy of 0.97, a precision of 0.95, an F1 score of 0.97, and a recall of 1.00.DISCUSSIONThese findings suggest a connection between humidifier disinfectant-associated lung injury and oxidative stress-induced lipid peroxidation. The oxidative stress signatures provide valuable insights into the underlying pathogenesis of humidifier disinfectant-associated lung injury and may serve as potential targets for biomarker development. https://doi.org/10.1289/EHP14984.
{"title":"Evaluating Metabolic Signatures in the Serum of South Korean Patients with Humidifier Disinfectant-Associated Lung Injury Identified through Untargeted Metabolomics.","authors":"Jinwoo Kim,Mi-Jin Kang,So-Yeon Lee,Sang-Bum Hong,Ho Cheol Kim,Myung Hee Nam,Soo-Jong Hong","doi":"10.1289/ehp14984","DOIUrl":"https://doi.org/10.1289/ehp14984","url":null,"abstract":"BACKGROUNDThe South Korean humidifier disinfectant-associated lung injury case was one of the worst disasters involving household chemical products, resulting in over 5,800 casualties. Despite the strong association between lung injury and humidifier disinfectants, the underlying pathogenic mechanisms remain unclear.OBJECTIVESWe investigated patients with humidifier disinfectant-associated lung injury to identify key metabolic signatures, aiming to gain insights into the underlying pathogenic mechanisms based on the characteristics of these metabolites.METHODSWe employed untargeted metabolomics to assess the differential enrichment of plasma metabolites in 80 South Korean children with lung injuries caused by exposure to humidifier disinfectant containing polyhexamethylene guanidine. The key metabolites identified were subsequently validated in an independent cohort of 132 South Korean adults.RESULTSIn the plasma of patients with humidifier disinfectant-associated lung injuries, we observed significantly higher levels of oxidized lipids compared to healthy controls, with these levels negatively correlating with lung function. These metabolic signatures differentiated humidifier disinfectant-associated lung injury from other respiratory diseases in children, such as asthma and bronchiolitis obliterans. The 47 key metabolites identified in children were validated in an independent adult cohort. Furthermore, the classification performance of these metabolic signatures for humidifier disinfectant-associated lung injury achieved an accuracy of 0.97, a precision of 0.95, an F1 score of 0.97, and a recall of 1.00.DISCUSSIONThese findings suggest a connection between humidifier disinfectant-associated lung injury and oxidative stress-induced lipid peroxidation. The oxidative stress signatures provide valuable insights into the underlying pathogenesis of humidifier disinfectant-associated lung injury and may serve as potential targets for biomarker development. https://doi.org/10.1289/EHP14984.","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"7 1","pages":""},"PeriodicalIF":10.4,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143872098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jessica M Madrigal,Britton Trabert,Danielle N Medgyesi,Jared A Fisher,Antonia M Calafat,Julianne Cook Botelho,Kayoko Kato,Paul S Albert,Debra T Silverman,Jonathan N Hofmann,Rena R Jones
{"title":"Pre-diagnostic serum concentrations of per- and polyfluoroalkyl substances and risk of endometrial cancer in a US cohort.","authors":"Jessica M Madrigal,Britton Trabert,Danielle N Medgyesi,Jared A Fisher,Antonia M Calafat,Julianne Cook Botelho,Kayoko Kato,Paul S Albert,Debra T Silverman,Jonathan N Hofmann,Rena R Jones","doi":"10.1289/ehp16569","DOIUrl":"https://doi.org/10.1289/ehp16569","url":null,"abstract":"","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"26 1","pages":""},"PeriodicalIF":10.4,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143866403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BACKGROUNDEnvironmental factors, such as fluctuations of climatic conditions and land cover, play a pivotal role in driving infectious disease epidemics, particularly those originating from wildlife reservoirs. Orthohantavirus puumalaense, hosted by bank voles in Europe, is the causative agent of a form of haemorrhagic fever and renal syndrome called nephropathia epidemica. Despite two decades of consistent presence in western Europe, nephropathia epidemica outbreaks still pose challenges due to localised periodic occurrences and a lack of understanding of its environmental drivers.OBJECTIVEOur study aims to bridge this gap by investigating the specific ecological and climatic factors influencing nephropathia epidemica outbreaks in western Europe.METHODSWe compiled monthly, serologically confirmed nephropathia epidemica case data obtained from public health authorities in Belgium, France, Germany, and the Netherlands for the period 2004-2012. Cases were geo-referenced to the finest available administrative unit. We selected 28 covariates, including climatic variables, land cover, tree species distributions, and human population, and implemented a Bayesian spatio-temporal model using integrated nested Laplace approximation (INLA) with zero-inflated Poisson distribution, including fixed effects and spatial, temporal, and non-structured random effects.RESULTSWe identified key triggers for nephropathia epidemica outbreaks, particularly climate-mediated changes in all seasons up to two years before, favouring tree mast impacting bank vole abundance. Our findings revealed that while land cover factors mostly determine hotspots locations, climatic fluctuation patterns rather tend to modulate outbreak intensity.DISCUSSIONCrucially, our model allows for the generation of yearly maps showcasing nephropathia epidemica incidence and risk factors, aiding in public health preparedness against climate change-induced disease emergence. This work represents a significant step towards developing targeted forecasting tools for Orthohantavirus puumalaense outbreaks, offering valuable insights for epidemic control strategies. https://doi.org/10.1289/EHP15457.
{"title":"Impact of environmental factors on the distribution patterns of nephropathia epidemica cases in western Europe.","authors":"Diana Erazo,Maria Fernanda Vincenti-Gonzalez,Guillaume Ghisbain,Mirko Faber,Chantal Reusken,Virginie Sauvage,William Wint,Herwig Leirs,Simon Dellicour,Katrien Tersago","doi":"10.1289/ehp15457","DOIUrl":"https://doi.org/10.1289/ehp15457","url":null,"abstract":"BACKGROUNDEnvironmental factors, such as fluctuations of climatic conditions and land cover, play a pivotal role in driving infectious disease epidemics, particularly those originating from wildlife reservoirs. Orthohantavirus puumalaense, hosted by bank voles in Europe, is the causative agent of a form of haemorrhagic fever and renal syndrome called nephropathia epidemica. Despite two decades of consistent presence in western Europe, nephropathia epidemica outbreaks still pose challenges due to localised periodic occurrences and a lack of understanding of its environmental drivers.OBJECTIVEOur study aims to bridge this gap by investigating the specific ecological and climatic factors influencing nephropathia epidemica outbreaks in western Europe.METHODSWe compiled monthly, serologically confirmed nephropathia epidemica case data obtained from public health authorities in Belgium, France, Germany, and the Netherlands for the period 2004-2012. Cases were geo-referenced to the finest available administrative unit. We selected 28 covariates, including climatic variables, land cover, tree species distributions, and human population, and implemented a Bayesian spatio-temporal model using integrated nested Laplace approximation (INLA) with zero-inflated Poisson distribution, including fixed effects and spatial, temporal, and non-structured random effects.RESULTSWe identified key triggers for nephropathia epidemica outbreaks, particularly climate-mediated changes in all seasons up to two years before, favouring tree mast impacting bank vole abundance. Our findings revealed that while land cover factors mostly determine hotspots locations, climatic fluctuation patterns rather tend to modulate outbreak intensity.DISCUSSIONCrucially, our model allows for the generation of yearly maps showcasing nephropathia epidemica incidence and risk factors, aiding in public health preparedness against climate change-induced disease emergence. This work represents a significant step towards developing targeted forecasting tools for Orthohantavirus puumalaense outbreaks, offering valuable insights for epidemic control strategies. https://doi.org/10.1289/EHP15457.","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"10 1","pages":""},"PeriodicalIF":10.4,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143866447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Joanna M Marroquin,Jenna R Krall,Karen Schliep,Leslie V Farland,Vimalkumar Krishnamoorthi,Kurunthachalam Kannan,Anna Z Pollack
BACKGROUNDPer- and polyfluoroalkyl substances (PFAS) exposure is widespread and has been linked with gynecologic disease. To our knowledge, no study has measured PFAS in endometrial tissue.METHODSEutopic endometrial tissue specimens (n=434) were collected from Investigating Mixtures of Pollutants and Endometriosis in Tissue (IMPLANT) Study participants undergoing laparoscopy or laparotomy for any indication (2007-2009). Nine PFAS were measured by HPLC-tandem MS (perfluorodecanoic acid [PFDA], perfluorohexane sulfonic acid [PFHxS], perfluorononanoic acid [PFNA], perfluorooctanoic acid [PFOA], perfluorooctane sulfonic acid [PFOS], perfluorododecanoic acid [PFDoDA], perfluoroheptanoic acid [PFHpA], perfluorooctanesulfonamide [PFOSA], and perfluoroundecanoic acid [PFUnDA]. Surgeons diagnosed endometriosis by gold-standard visualization and evaluated the endometriosis staging as moderate and severe (stage 3-4) compared to minimal and mild (stage 1-2), using American Society of Reproductive Medicine (ASRM) classification. We used modified Poisson regression models adjusted for age (continuous), race (white, all other race/ethnicities), smoking status (serum cotinine > ng/mL), study site (Utah, California), and body mass index (continuous) to obtain relative risks (RR) of endometriosis diagnosis and 95% confidence intervals (CI) for each PFAS. PFAS mixtures were evaluated using Bayesian Kernel Machine Regression.RESULTSParticipants were, on average, 33 ± 7 years old, and 75% of participants were non-Hispanic white. Of the 181 participants with an incident endometriosis diagnosis, 73% had ASRM stage 1-2, while 27% had stage 3-4. Median (IQR) eutopic endometrium tissue levels, in ng/g, were 6.58 (6.44) for PFOS, 1.93 (1.71) for PFOA, 0.65 (0.75) for PFHxS, 0.58 (0.52) for PFNA, 0.12 (0.18) for PFOSA. PFAS in the endometrial tissue was not associated with endometriosis. However, select PFAS in the eutopic tissue were associated with a risk of more advanced (stage 3 or 4 vs. 1 or 2) endometriosis [(PFOSA RR=1.25 (95% CI: 1.10-1.43), PFHxS RR=1.37 (95% CI: 1.12, 1.68), PFOS RR=1.36 (95% CI: 1.02, 1.81)].CONCLUSIONPFAS were widely detected in eutopic endometrial tissue. There was no evidence that PFAS in endometrial tissue were associated with a higher risk of endometriosis diagnosis. However, PFOS, PFOSA and PFHxS in the endometrial tissue were associated with risk of more severe stage of endometriosis. https://doi.org/10.1289/EHP15852.
{"title":"Per- and polyfluoroalkyl substances in eutopic endometrium tissue and risk of endometriosis: findings from the Investigating Mixtures of Pollutants and Endometriosis in Tissue (IMPLANT) Study.","authors":"Joanna M Marroquin,Jenna R Krall,Karen Schliep,Leslie V Farland,Vimalkumar Krishnamoorthi,Kurunthachalam Kannan,Anna Z Pollack","doi":"10.1289/ehp15852","DOIUrl":"https://doi.org/10.1289/ehp15852","url":null,"abstract":"BACKGROUNDPer- and polyfluoroalkyl substances (PFAS) exposure is widespread and has been linked with gynecologic disease. To our knowledge, no study has measured PFAS in endometrial tissue.METHODSEutopic endometrial tissue specimens (n=434) were collected from Investigating Mixtures of Pollutants and Endometriosis in Tissue (IMPLANT) Study participants undergoing laparoscopy or laparotomy for any indication (2007-2009). Nine PFAS were measured by HPLC-tandem MS (perfluorodecanoic acid [PFDA], perfluorohexane sulfonic acid [PFHxS], perfluorononanoic acid [PFNA], perfluorooctanoic acid [PFOA], perfluorooctane sulfonic acid [PFOS], perfluorododecanoic acid [PFDoDA], perfluoroheptanoic acid [PFHpA], perfluorooctanesulfonamide [PFOSA], and perfluoroundecanoic acid [PFUnDA]. Surgeons diagnosed endometriosis by gold-standard visualization and evaluated the endometriosis staging as moderate and severe (stage 3-4) compared to minimal and mild (stage 1-2), using American Society of Reproductive Medicine (ASRM) classification. We used modified Poisson regression models adjusted for age (continuous), race (white, all other race/ethnicities), smoking status (serum cotinine > ng/mL), study site (Utah, California), and body mass index (continuous) to obtain relative risks (RR) of endometriosis diagnosis and 95% confidence intervals (CI) for each PFAS. PFAS mixtures were evaluated using Bayesian Kernel Machine Regression.RESULTSParticipants were, on average, 33 ± 7 years old, and 75% of participants were non-Hispanic white. Of the 181 participants with an incident endometriosis diagnosis, 73% had ASRM stage 1-2, while 27% had stage 3-4. Median (IQR) eutopic endometrium tissue levels, in ng/g, were 6.58 (6.44) for PFOS, 1.93 (1.71) for PFOA, 0.65 (0.75) for PFHxS, 0.58 (0.52) for PFNA, 0.12 (0.18) for PFOSA. PFAS in the endometrial tissue was not associated with endometriosis. However, select PFAS in the eutopic tissue were associated with a risk of more advanced (stage 3 or 4 vs. 1 or 2) endometriosis [(PFOSA RR=1.25 (95% CI: 1.10-1.43), PFHxS RR=1.37 (95% CI: 1.12, 1.68), PFOS RR=1.36 (95% CI: 1.02, 1.81)].CONCLUSIONPFAS were widely detected in eutopic endometrial tissue. There was no evidence that PFAS in endometrial tissue were associated with a higher risk of endometriosis diagnosis. However, PFOS, PFOSA and PFHxS in the endometrial tissue were associated with risk of more severe stage of endometriosis. https://doi.org/10.1289/EHP15852.","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"7 1","pages":""},"PeriodicalIF":10.4,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143862026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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