Environmental Health Perspectives最新文献

{"title":"TIDieR-WASH: A Guideline for Reporting Implementation of Water, Sanitation, and Hygiene Interventions.","authors":"Jonny Crocker, Emily Ogutu, Jedidiah S Snyder, Antoinette Kome, Ben Tidwell, Jan Willem Rosenboom, Jesse Shapiro, Jessy Samuyachi Mahongo, Kelly T Alexander, Michael E Gnilo, Om Prasad Gautam, Sara Hoffman, Sovattha Neou, Matthew C Freeman","doi":"10.1289/EHP14780","DOIUrl":"10.1289/EHP14780","url":null,"abstract":"<p><strong>Introduction: </strong>Accurate information on context and implementation of public health interventions is necessary to replicate, adapt, and scale effective interventions and to interpret evaluations. Reporting the context and implementation of water, sanitation, and hygiene (WASH) interventions has been inconsistent and incomplete.</p><p><strong>Methods: </strong>To improve the reporting of WASH interventions, we developed the Template for Intervention Description and Replication for WASH (TIDieR-WASH) checklist and guide, by adapting and expanding the original TIDieR guide. We performed a scoping review of existing implementation reporting guidelines, and of current implementation reporting in WASH evaluations, to develop a list of candidate items to include in this checklist. We then used a 4-stages of review by international experts to reach consensus.</p><p><strong>Results: </strong>The resulting 14-item checklist comprises: <i>a</i>) name, <i>b</i>) theory of change, <i>c</i>) prior evidence, <i>d</i>) location and setting, <i>e</i>) context, <i>f</i>) suitability, <i>g</i>) implementers, <i>h</i>) recipients, <i>i</i>) targeting, <i>j</i>) activities, <i>k</i>) intervention dose, <i>l</i>) fidelity, <i>m</i>) costs, and <i>n</i>) materials. Definitions, explanations, examples, and instructions for use are reported in this article.</p><p><strong>Discussion: </strong>The checklist can be applied to all types of evaluations of WASH interventions, including direct service provision, behavior change, and systems strengthening interventions. We deliberately developed this guidance document to be accessible and relevant to practitioners and researchers. Adoption of this checklist will support transparent reporting of WASH implementation for research and practice. As with other sectors that have used TIDieR checklists, clear implementation reporting can assist with evidence synthesis, adaptation, and policy guidance. https://doi.org/10.1289/EHP14780.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 11","pages":"117006"},"PeriodicalIF":10.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11604158/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142738876","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between Diet-Related Greenhouse Gas Emissions and Mortality among Japanese Adults: The Japan Collaborative Cohort Study.","authors":"Daiki Watanabe, Kotatsu Maruyama, Akiko Tamakoshi, Isao Muraki","doi":"10.1289/EHP14935","DOIUrl":"10.1289/EHP14935","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Planetary and human health are highly intertwined; our current food system is associated with high greenhouse gas emissions (GHGE) and burden of disease.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Objective: &lt;/strong&gt;The aim of this study was to investigate the associations of diet-related GHGE with all-cause and cause-specific mortality in Japan.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;This study included 58,031 Japanese adults (35,078 women and 22,953 men) 40-79 y of age who participated in the Japan Collaborative Cohort Study during the period 1988-1990. Diet-related GHGE was calculated from dietary intake estimated by a validated food frequency questionnaire and previously developed GHGE tables of each food and beverage. Participants were classified into quintiles of diet-related GHGE per kg food/d. Hazard ratios (HRs) of all-cause and cause-specific mortality were calculated using the Cox proportional hazard and restricted cubic spline models.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;The average diet-related GHGE was &lt;math&gt;&lt;mrow&gt;&lt;mn&gt;1,522&lt;/mn&gt;&lt;mrow&gt;&lt;msub&gt;&lt;mrow&gt;&lt;mtext&gt; &lt;/mtext&gt;&lt;mi&gt;g&lt;/mi&gt;&lt;mtext&gt;-&lt;/mtext&gt;&lt;mtext&gt;CO&lt;/mtext&gt;&lt;/mrow&gt;&lt;mrow&gt;&lt;mn&gt;2&lt;/mn&gt;&lt;/mrow&gt;&lt;/msub&gt;&lt;/mrow&gt;&lt;mtext&gt;-eq&lt;/mtext&gt;&lt;mo&gt;/&lt;/mo&gt;&lt;mi&gt;kg&lt;/mi&gt;&lt;mtext&gt; food&lt;/mtext&gt;&lt;mo&gt;/&lt;/mo&gt;&lt;mi&gt;d&lt;/mi&gt;&lt;/mrow&gt;&lt;/math&gt;. Over a period of 19.3 y (955,819 person-years) of median follow-up, 11,508 deaths were documented. After adjusting for lifestyle and medical history, in comparison with the fourth quintiles of diet-related GHGE, the first and fifth quintiles were associated with a higher risk of all-cause mortality: multivariable HR of all-cause mortality was 1.11 [95% confidence interval (CI): 1.05, 1.18] and 1.09 (95% CI: 1.03, 1.17) for the lowest and highest GHGE, respectively; those of cardiovascular disease mortality were 1.23 (95% CI: 1.10, 1.38) and 1.22 (95% CI: 1.08, 1.37), respectively. The diet-related GHGE range with the lowest HR of all-cause mortality was &lt;math&gt;&lt;mrow&gt;&lt;mn&gt;1,400&lt;/mn&gt;&lt;mo&gt;-&lt;/mo&gt;&lt;mn&gt;1,600&lt;/mn&gt;&lt;mrow&gt;&lt;msub&gt;&lt;mrow&gt;&lt;mtext&gt; &lt;/mtext&gt;&lt;mi&gt;g&lt;/mi&gt;&lt;mtext&gt;-&lt;/mtext&gt;&lt;mtext&gt;CO&lt;/mtext&gt;&lt;/mrow&gt;&lt;mrow&gt;&lt;mn&gt;2&lt;/mn&gt;&lt;/mrow&gt;&lt;/msub&gt;&lt;/mrow&gt;&lt;mtext&gt;eq&lt;/mtext&gt;&lt;mo&gt;/&lt;/mo&gt;&lt;mi&gt;kg&lt;/mi&gt;&lt;/mrow&gt;&lt;/math&gt; food/d (&lt;math&gt;&lt;mrow&gt;&lt;mi&gt;p&lt;/mi&gt;&lt;/mrow&gt;&lt;/math&gt; for nonlinearity &lt;math&gt;&lt;mrow&gt;&lt;mo&gt;&lt;&lt;/mo&gt;&lt;mn&gt;0.001&lt;/mn&gt;&lt;/mrow&gt;&lt;/math&gt;). Replacing one serving of red meat with one serving of pulses was inversely associated with all-cause mortality (&lt;math&gt;&lt;mrow&gt;&lt;mtext&gt;HR&lt;/mtext&gt;&lt;mo&gt;=&lt;/mo&gt;&lt;mn&gt;0.96&lt;/mn&gt;&lt;/mrow&gt;&lt;/math&gt;; 95% CI: 0.93, 0.99) and GHGE (mean change, &lt;math&gt;&lt;mrow&gt;&lt;mo&gt;-&lt;/mo&gt;&lt;mn&gt;347&lt;/mn&gt;&lt;mrow&gt;&lt;msub&gt;&lt;mrow&gt;&lt;mtext&gt; &lt;/mtext&gt;&lt;mi&gt;g&lt;/mi&gt;&lt;mtext&gt;-&lt;/mtext&gt;&lt;mtext&gt;CO&lt;/mtext&gt;&lt;/mrow&gt;&lt;mrow&gt;&lt;mn&gt;2&lt;/mn&gt;&lt;/mrow&gt;&lt;/msub&gt;&lt;/mrow&gt;&lt;mtext&gt;-eq&lt;/mtext&gt;&lt;mo&gt;/&lt;/mo&gt;&lt;mi&gt;kg&lt;/mi&gt;&lt;mo&gt;/&lt;/mo&gt;&lt;mi&gt;d&lt;/mi&gt;&lt;/mrow&gt;&lt;/math&gt;; 95% CI: &lt;math&gt;&lt;mrow&gt;&lt;mo&gt;-&lt;/mo&gt;&lt;mn&gt;353&lt;/mn&gt;&lt;/mrow&gt;&lt;/math&gt;, &lt;math&gt;&lt;mrow&gt;&lt;mo&gt;-&lt;/mo&gt;&lt;mn&gt;342&lt;/mn&gt;&lt;/mrow&gt;&lt;/math&gt;).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Discussion: &lt;/strong&gt;Diet-related GHGE was associated with all-cause and cardiovascular disease mortality in a U-shaped fashion. This finding could be useful","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 11","pages":"117002"},"PeriodicalIF":12.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11542713/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated Studies on Male Reproductive Toxicity of Decabromodiphenyl Ethane in Zebrafish Spermatozoa <i>Ex Vivo</i>, Male Zebrafish <i>in Vivo</i>, and GC-1 Cells <i>in Vitro</i>.","authors":"Lihua Yang, Yindan Zhang, Jianghuan Hua, Guili Song, Fan Li, Na Zheng, Taotao Zhang, Zhixiang Xu, Xinxin Ren, Biran Zhu, Yanna Han, Yongyong Guo, Jian Han, Bingsheng Zhou","doi":"10.1289/EHP14426","DOIUrl":"10.1289/EHP14426","url":null,"abstract":"<p><strong>Background: </strong>Legacy brominated flame retardants have been recognized as risky factors leading to declined sperm quality. The widespread utilization of decabromodiphenyl ethane (DBDPE) as a replacement for decabromodiphenyl ether has given rise to considerable concern over its potential risks to reproductive health.</p><p><strong>Objectives: </strong>The objectives were to quickly determine whether DBDPE affects sperm quality upon <i>ex vivo</i> exposure, to reveal the reproductive outcomes and underlying molecular mechanisms using an <i>in vivo</i> zebrafish model exposed to DBDPE, and to validate the potential impact on DNA damage and energy metabolism balance <i>in vitro</i>.</p><p><strong>Methods: </strong>Zebrafish spermatozoa were treated with DBDPE (0.01, 0.1, 1, <math><mrow><mn>10</mn><mspace></mspace><mi>μ</mi><mi>M</mi></mrow></math>) for 3 h, and the spermatozoa motility and fertilization ability with normal eggs were evaluated. Then adult male zebrafish were treated with DBDPE (0.1, 1, 10, and <math><mrow><mn>100</mn><mtext> nM</mtext></mrow></math>) for 2 months, and their reproductive performance was examined. Four-dimensional label-free proteome and phosphoproteome were performed in zebrafish testes, and the findings were validated by multiple indicators. Finally, mouse spermatogonial GC-1 cells were treated with DBDPE (0.1, <math><mrow><mn>1</mn><mspace></mspace><mi>μ</mi><mi>M</mi></mrow></math>) for 72 h, and DNA damage was examined, as well as the energy production of glycolysis and oxidative phosphorylation.</p><p><strong>Results: </strong><i>Ex vivo</i> exposure to DBDPE caused lower motility and fertilization rates of zebrafish spermatozoa. <i>In vivo</i> exposure to DBDPE caused lower sperm motility and abnormal spermatogenesis in male zebrafish testes. Integrated whole-proteome and phosphoproteome analysis revealed DNA damage responses and energy metabolic disorders in zebrafish testes. A dosage window characterized by higher mitochondrial membrane potential (MMP) in combination with unchanged reactive oxygen species and apoptosis rates was observed in both zebrafish testes and GC-1 cells.</p><p><strong>Discussion: </strong>This study suggests that in zebrafish, DBDPE exposure could impair sperm quality and spermatogenesis, and the underlying mechanism could be related to DNA damage and energy metabolic reprogramming in testicular germ cells. https://doi.org/10.1289/EHP14426.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 11","pages":"117005"},"PeriodicalIF":10.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11580837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Invited Perspective: Climate Change and Maternal Mental Health-Looking beyond High-Income Countries.","authors":"Andrea G Buchwald, Sarah Boudova","doi":"10.1289/EHP16476","DOIUrl":"10.1289/EHP16476","url":null,"abstract":"","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 11","pages":"111301"},"PeriodicalIF":10.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11601094/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142727054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of Postpartum Temperature Exposure with Postpartum Depression: A Retrospective Cohort Study in Southern California.","authors":"Yi Sun, Kathryne S Headon, Wajeeha Umer, Anqi Jiao, Jeff M Slezak, Chantal C Avila, Vicki Y Chiu, David A Sacks, Kelly T Sanders, John Molitor, Tarik Benmarhnia, Jiu-Chiuan Chen, Darios Getahun, Jun Wu","doi":"10.1289/EHP14783","DOIUrl":"10.1289/EHP14783","url":null,"abstract":"<p><strong>Background: </strong>Postpartum depression (PPD) has been associated with biological, emotional, social, and environmental factors. However, evidence regarding the effect of temperature on PPD is extremely limited.</p><p><strong>Objectives: </strong>We aimed to examine the associations between postpartum temperature exposure and PPD.</p><p><strong>Methods: </strong>We conducted a retrospective cohort study using data from Kaiser Permanente Southern California electronic health records from 1 January 2008 through 31 December 2018. PPD was first assessed using the Edinburgh Postnatal Depression Scale (score <math><mrow><mo>≥</mo><mn>10</mn></mrow></math>) during the first year of the postpartum period and further identified by using both diagnostic codes and prescription medications. Historical daily ambient temperatures were obtained from the <math><mrow><mn>4</mn><mtext>-km</mtext></mrow></math> resolution gridMET dataset (https://www.climatologylab.org/gridmet.html) and linked to participants' residential addresses at delivery. Postpartum temperature exposures were measured by calculating various temperature metrics during the period from delivery to PPD diagnosis date. A time-to-event approach with a discrete-time logistic regression was applied to estimate the association between temperature exposure and time to PPD. Effect modification by maternal characteristics and other environmental factors was examined.</p><p><strong>Results: </strong>There were 46,114 (10.73%) PPD cases among 429,839 pregnancies (<math><mrow><mtext>mean</mtext><mo>±</mo><mtext>standard deviation</mtext></mrow></math> age <math><mrow><mo>=</mo><mn>30.22</mn><mo>±</mo><mn>5.75</mn></mrow></math> y). Increased PPD risks were positively associated with exposure to higher mean temperature [adjusted odds ratio (aOR) per interquartile range increment: 1.07; 95% confidence interval (CI): 1.05, 1.09] and diurnal temperature range (<math><mrow><mtext>aOR</mtext><mo>=</mo><mn>1.08</mn></mrow></math>; 95% CI: 1.06, 1.10); the associations were stronger for maximum temperature compared with minimum temperature. The temperature-related PPD risks were greater among African American, Asian, and Hispanic mothers and among mothers <math><mrow><mo>≥</mo><mn>25</mn></mrow></math> years of age compared with their counterparts. We also observed higher effects of temperature on PPD among mothers exposed to higher air pollution or lower green space levels and among mothers with lower air conditioning penetration rates.</p><p><strong>Conclusion: </strong>Maternal exposure to higher temperature and diurnal temperature variability during the postpartum period was associated with an increased risk of PPD. Effect modification by maternal age, race/ethnicity, air pollution, green space, and air conditioning penetration was identified. https://doi.org/10.1289/EHP14783.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 11","pages":"117004"},"PeriodicalIF":10.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11601096/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142726956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Organophosphorus Flame Retardants and Metabolic Disruption: An <i>in Silico</i>, <i>in Vitro</i>, and <i>in Vivo</i> Study Focusing on Adiponectin Receptors.","authors":"Ying Liu, Xiaochun Ma, Yifei Le, Jiafan Feng, Mengting Xu, Wanyue Wang, Cui Wang","doi":"10.1289/EHP14634","DOIUrl":"10.1289/EHP14634","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Environmental chemical exposures have been associated with metabolic outcomes, and typically, their binding to nuclear hormone receptors is considered the molecular initiating event (MIE) for a number of outcomes. However, more studies are needed to understand the influence of such exposures on cell membrane-bound adiponectin receptors (AdipoRs), which are critical metabolic regulators.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Objective: &lt;/strong&gt;We aimed to clarify the potential interactions between AdipoRs and environmental chemicals, specifically organophosphorus flame retardants (OPFRs), and the resultant effects.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Employing &lt;i&gt;in silico&lt;/i&gt; simulation, cell thermal shift, and noncompetitive binding assays, we screened eight OPFRs for interactions with AdipoR1 and AdipoR2. We tested two key events underlying AdipoR modulation upon OPFR exposure in a liver cell model. The Toxicological Prioritization Index (ToxPi)scoring scheme was used to rank OPFRs according to their potential to disrupt AdipoR-associated metabolism. We further examined the inhibitory effect of OPFRs on AdipoR signaling activation in mouse models.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Analyses identified pi-pi stacking and pi-sulfur interactions between the aryl-OPFRs 2-ethylhexyl diphenyl phosphate (EHDPP), triphenyl phosphate (TPhP), and tricresyl phosphate (TCP) and the transmembrane cavities of AdipoR1 and AdipoR2. Cell thermal shift assays showed a &lt;math&gt;&lt;mrow&gt;&lt;mo&gt;&gt;&lt;/mo&gt;&lt;mn&gt;3&lt;/mn&gt;&lt;mo&gt;°&lt;/mo&gt;&lt;mi&gt;C&lt;/mi&gt;&lt;/mrow&gt;&lt;/math&gt; rightward shift in the AdipoR proteins' melting curves upon exposure to these three compounds. Although the binding sites differed from adiponectin, results suggest that aryl-OPFRs noncompetitively inhibited the binding of the endogenous peptide ligand ADP355 to the receptors. Analyses of key events underlying AdipoR modulation revealed that glucose uptake was notably lower, whereas lipid content was higher in cells exposed to aryl-OPFRs. EHDPP, TCP, and TPhP were ranked as the top three disruptors according to the ToxPi scores. A noncompetitive binding between these aryl-OPFRs and AdipoRs was also observed in wild-type (WT) mice. In db/db mice, the finding of lower blood glucose levels after ADP355 injection was diminished in the presence of a typical aryl-OPFR (TCP). WT mice exposed to TCP demonstrated lower AdipoR1 signaling, which was marked by lower phosphorylated AMP-activated protein kinase (pAMPK) and a higher expression of gluconeogenesis-related genes. Moreover, WT mice exposed to ADP355 demonstrated higher levels of pAMPK protein and peroxisome proliferator-activated receptor-&lt;math&gt;&lt;mi&gt;α&lt;/mi&gt;&lt;/math&gt; messenger RNA. This was accompanied by higher glucose disposal and by lower levels of long-chain fatty acids and hepatic triglycerides; these metabolic improvements were negated upon TCP co-treatment.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;&lt;i&gt;In silico&lt;/i&gt;, &lt;i&gt;in vitro&lt;/i&gt;, and &lt;i&gt;in vivo&lt;/i&gt; assays suggest that aryl-OPFRs act ","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 11","pages":"117003"},"PeriodicalIF":12.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11548883/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum: \"Comment on 'Association of Domestic Water Hardness with All-Cause and Cause-Specific Cancers: Evidence from 447,996 UK Biobank Participants'\".","authors":"Hongcheng Luo, Haoliang Wu, Zhaohui He","doi":"10.1289/EHP16641","DOIUrl":"10.1289/EHP16641","url":null,"abstract":"","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 11","pages":"119002"},"PeriodicalIF":10.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11580833/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Asking Why Is Necessary to Address Health Disparities: A Critical Approach for Solution-Oriented Environmental Epidemiological Research.","authors":"Tamarra James-Todd, Kathryn S Tomsho, Symielle A Gaston, Kevin C Elliott, Chandra L Jackson","doi":"10.1289/EHP14513","DOIUrl":"10.1289/EHP14513","url":null,"abstract":"<p><strong>Background: </strong>In environmental epidemiology, we use an array of tools from various, related disciplines to answer key questions about environmental exposures in relation to health outcomes. Typically, we ask questions related to what, who, where, when, and how. We value these questions because they contribute to novel scientific discovery and our understanding of disease etiology linked to environmental exposures. In addition, these questions help us better understand who might be at highest risk of exposure and subsequent risk of disease. Although necessary for the goals of environmental epidemiology, these questions are insufficient for addressing environmental health disparities. Specifically, these questions may be able to help us describe exposure-health outcome associations but are limited in their ability to move beyond identification to intervening on observed disparities to achieve environmental health equity.</p><p><strong>Objectives: </strong>We sought to emphasize the need to value and routinely add the key question of \"Why?\" in environmental epidemiological studies. In asking this additional critical question, we can identify and incorporate the structural determinants and drivers of environmental exposure disparities and determine whether these factors are linked to existing and historically recalcitrant health disparities. Further, we can design effective studies that build on existing frameworks to address the fundamental causes of environmental health disparities.</p><p><strong>Discussion: </strong>This commentary underscores the need to routinely incorporate \"why\" questions in the practice of environmental epidemiology. By asking and addressing \"Why?\" we can employ better, more solution-oriented study designs, improve data collection, and enhance our ability to collaborate with diverse study populations through trust-building and community-engaged research. Incorporating these approaches will move environmental epidemiology forward from mostly documenting to actively addressing environmental health disparities. https://doi.org/10.1289/EHP14513.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 11","pages":"115001"},"PeriodicalIF":10.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11563029/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142616682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comment on \"Associations between Changes in Exposure to Air Pollutants due to Relocation and the Incidence of 14 Major Disease Categories and All-Cause Mortality: A Natural Experiment Study\".","authors":"Ziwei Gao, Jiachen Qi, Wei Ye","doi":"10.1289/EHP16404","DOIUrl":"10.1289/EHP16404","url":null,"abstract":"","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 11","pages":"118001"},"PeriodicalIF":10.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11556394/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142616688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Madagascar's Plague: One Health Research Aims to Slow Its Spread.","authors":"Wendee Nicole","doi":"10.1289/EHP15224","DOIUrl":"10.1289/EHP15224","url":null,"abstract":"<p><p>The integrated approach tackles a perfect storm of poverty, invasive rats, deforestation, and climate change that is contributing to the increase in bubonic plague cases.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 11","pages":"112001"},"PeriodicalIF":12.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11548884/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}