Kevin C Elliott, Heather B Patisaul, Robert M Sargis, Laura N Vandenberg
{"title":"Words Matter: Reflective Science Communication and Tradeoffs in Environmental Health Research.","authors":"Kevin C Elliott, Heather B Patisaul, Robert M Sargis, Laura N Vandenberg","doi":"10.1289/EHP14527","DOIUrl":"10.1289/EHP14527","url":null,"abstract":"<p><strong>Background: </strong>Scientists who communicate societally relevant information face challenging contexts in which misinformation, disinformation, hype, and spin are prevalent. As a result, they often face difficult decisions about how to frame their work in a socially responsible manner.</p><p><strong>Objectives: </strong>Drawing from the literature on science communication and framing, we identify tradeoffs that environmental health scientists face when deciding how to communicate their work, and we propose strategies for handling these tradeoffs. We use research on the human health effects of environmental endocrine disruptors as a case study to illustrate these challenges and strategies.</p><p><strong>Discussion: </strong>We examine four major frames (i.e., ways of packaging information that draw attention to facets of an issue or topic) in discussions of the effects of endocrine-disrupting chemicals on sexual and neural development and obesity. We show how these frames can be beneficial (e.g., focusing public attention on environmental health threats and promoting actions to address environmental pollution) while simultaneously having harmful effects (e.g., contributing to stigmatization of particular groups or the promotion of harmful political ideologies).</p><p><strong>Conclusions: </strong>Researchers who seek to responsibly communicate societally relevant work can employ several strategies to mitigate difficult tradeoffs, including <i>a</i>) striving for sensitivity to the social context and its relationship to their framing choices, <i>b</i>) choosing to avoid some frames, <i>c</i>) employing frames that alleviate ethical tensions, <i>d</i>) fostering education to alleviate harms, <i>e</i>) developing interdisciplinary and community collaborations, and <i>f</i>) working with institutions like scientific societies and journals to develop guidance on responsible communication practices. https://doi.org/10.1289/EHP14527.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 10","pages":"105001"},"PeriodicalIF":10.1,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11524408/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142544484","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":"Exposure to Air Pollutants and Myocardial Infarction Incidence: A UK Biobank Study Exploring Gene-Environment Interaction.","authors":"Yudiyang Ma, Dankang Li, Feipeng Cui, Jianing Wang, Linxi Tang, Yingping Yang, Run Liu, Junqing Xie, Yaohua Tian","doi":"10.1289/EHP14291","DOIUrl":"10.1289/EHP14291","url":null,"abstract":"<p><strong>Background: </strong>Unraveling gene-environment interaction can provide a novel insight into early disease prevention. Nevertheless, current understanding of the interplay between genetic predisposition and air pollution in relation to myocardial infarction (MI) risk remains limited. Furthermore, the potential long-term influence of air pollutants on MI incidence risk warrants more conclusive evidence in a community population.</p><p><strong>Objective: </strong>We investigated interactions between genetic predisposition and exposure to air pollutants on MI incidence.</p><p><strong>Methods: </strong>This study incorporated a sample of 456,354 UK Biobank participants and annual mean air pollution (<math><mrow><mrow><msub><mrow><mrow><mi>PM</mi></mrow></mrow><mrow><mrow><mn>2.5</mn></mrow></mrow></msub></mrow></mrow></math>, <math><mrow><mrow><msub><mrow><mrow><mi>PM</mi></mrow></mrow><mrow><mrow><mn>10</mn></mrow></mrow></msub></mrow></mrow></math>, <math><mrow><mrow><msub><mrow><mi>NO</mi></mrow><mrow><mn>2</mn></mrow></msub></mrow></mrow></math>, and <math><mrow><mrow><msub><mrow><mi>NO</mi></mrow><mrow><mi>x</mi></mrow></msub></mrow></mrow></math>) from the UK Department for Environment, Food and Rural Affairs (2006-2021). The Cox proportional hazards model was employed to explore MI incidence after chronic air pollutants exposure. By quantifying genetic risk through the calculation of polygenic risk score (PRS), this study further examined the interactions between genetic risk and exposure to air pollutants in the development of MI on both additive and multiplicative scales.</p><p><strong>Results: </strong>Among 456,354 participants, 9,114 incident MI events were observed during a median follow-up of 12.08 y. Chronic exposure to air pollutants was linked with an increased risk of MI occurrence. Specifically, the hazard ratios (per interquartile range) were 1.12 (95% CI: 1.10, 1.13) for <math><mrow><mrow><msub><mrow><mrow><mi>PM</mi></mrow></mrow><mrow><mrow><mn>2.5</mn></mrow></mrow></msub></mrow></mrow></math>, 1.20 (95% CI: 1.19, 1.22) for <math><mrow><mrow><msub><mrow><mrow><mi>PM</mi></mrow></mrow><mrow><mrow><mn>10</mn></mrow></mrow></msub></mrow></mrow></math>, 1.13 (95% CI: 1.12, 1.15) for <math><mrow><mrow><msub><mrow><mi>NO</mi></mrow><mrow><mn>2</mn></mrow></msub></mrow></mrow></math>, and 1.12 (95% CI: 1.11, 1.13) for <math><mrow><mrow><msub><mrow><mi>NO</mi></mrow><mrow><mi>x</mi></mrow></msub></mrow></mrow></math>. In terms of the joint effects, participants with high PRS and high level of air pollution exposure exhibited the greatest risk of MI among all study participants (<math><mrow><mo>∼</mo><mn>255</mn><mo>%</mo></mrow></math> to 324%). Remarkably, both multiplicative and additive interactions were detected in the ambient air pollutants exposure and genetic risk on the incidence of MI.</p><p><strong>Discussion: </strong>There were interactions between exposure to ambient air pollutants and genetic susceptibility o","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 10","pages":"107002"},"PeriodicalIF":10.1,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11466320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142399728","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}
Kirthana Sukumaran, Katherine L Botternhorn, Joel Schwartz, Jim Gauderman, Carlos Cardenas-Iniguez, Rob McConnell, Daniel A Hackman, Kiros Berhane, Hedyeh Ahmadi, Shermaine Abad, Rima Habre, Megan M Herting
{"title":"Associations between Fine Particulate Matter Components, Their Sources, and Cognitive Outcomes in Children Ages 9-10 Years Old from the United States.","authors":"Kirthana Sukumaran, Katherine L Botternhorn, Joel Schwartz, Jim Gauderman, Carlos Cardenas-Iniguez, Rob McConnell, Daniel A Hackman, Kiros Berhane, Hedyeh Ahmadi, Shermaine Abad, Rima Habre, Megan M Herting","doi":"10.1289/EHP14418","DOIUrl":"10.1289/EHP14418","url":null,"abstract":"<p><strong>Background: </strong>Emerging literature suggests that fine particulate matter [with aerodynamic diameter <math><mrow><mo>≤</mo><mn>2.5</mn><mspace></mspace><mi>μ</mi><mi>m</mi></mrow></math> (<math><mrow><mrow><msub><mrow><mrow><mi>PM</mi></mrow></mrow><mrow><mrow><mn>2.5</mn></mrow></mrow></msub></mrow></mrow></math>)] air pollution and its components are linked to various neurodevelopmental outcomes. However, few studies have evaluated how <math><mrow><mrow><msub><mrow><mrow><mi>PM</mi></mrow></mrow><mrow><mrow><mn>2.5</mn></mrow></mrow></msub></mrow></mrow></math> component mixtures from distinct sources relate to cognitive outcomes in children.</p><p><strong>Objectives: </strong>This cross-sectional study investigated how ambient concentrations of <math><mrow><mrow><msub><mrow><mrow><mi>PM</mi></mrow></mrow><mrow><mrow><mn>2.5</mn></mrow></mrow></msub></mrow></mrow></math> component mixtures relate to neurocognitive performance in 9- to 10-year-old children, as well as explored potential source-specific effects of these associations, across the US.</p><p><strong>Methods: </strong>Using spatiotemporal hybrid models, annual concentrations of 15 chemical components of <math><mrow><mrow><msub><mrow><mrow><mi>PM</mi></mrow></mrow><mrow><mrow><mn>2.5</mn></mrow></mrow></msub></mrow></mrow></math> were estimated based on the residential address of child participants from the Adolescent Brain Cognitive Development (ABCD) Study. General cognitive ability, executive function, and learning/memory scores were derived from the NIH Toolbox. We applied positive matrix factorization to identify six major <math><mrow><mrow><msub><mrow><mrow><mi>PM</mi></mrow></mrow><mrow><mrow><mn>2.5</mn></mrow></mrow></msub></mrow></mrow></math> sources based on the 15 components, which included crustal, ammonium sulfate, biomass burning, traffic, ammonium nitrate, and industrial/residual fuel burning. We then utilized weighted quantile sum (WQS) and linear regression models to investigate associations between <math><mrow><mrow><msub><mrow><mrow><mi>PM</mi></mrow></mrow><mrow><mrow><mn>2.5</mn></mrow></mrow></msub></mrow></mrow></math> components' mixture, their potential sources, and children's cognitive scores.</p><p><strong>Results: </strong>Mixture modeling revealed associations between cumulative exposure and worse cognitive performance across all three outcome domains, including shared overlap in detrimental effects driven by ammonium nitrates, silicon, and calcium. Using the identified six sources of exposure, source-specific negative associations were identified between ammonium nitrates and learning & memory, traffic and executive function, and crustal and industrial mixtures and general cognitive ability. Unexpected positive associations were also seen between traffic and general ability as well as biomass burning and executive function.</p><p><strong>Discussion: </strong>This work suggests nuanced associations between outdoor <math><mrow><mrow><msub><","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 10","pages":"107009"},"PeriodicalIF":10.1,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11524409/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142544483","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}
Kristin E Knox, Megan R Schwarzman, Ruthann A Rudel, Claudia Polsky, Robin E Dodson
{"title":"Trends in NHANES Biomonitored Exposures in California and the United States following Enactment of California's Proposition 65.","authors":"Kristin E Knox, Megan R Schwarzman, Ruthann A Rudel, Claudia Polsky, Robin E Dodson","doi":"10.1289/EHP13956","DOIUrl":"10.1289/EHP13956","url":null,"abstract":"<p><strong>Background: </strong>The prevalence of toxic chemicals in US commerce has prompted some states to adopt laws to reduce exposure. One with broad reach is California's Proposition 65 (Prop 65), which established a list of chemicals that cause cancer, developmental harm, or reproductive toxicity. The law is intended to discourage businesses from using these chemicals and to minimize consumer exposure. However, a key question remains unanswered: Has Prop 65 reduced population-level exposure to the listed chemicals?</p><p><strong>Objective: </strong>We used national biomonitoring data from the Centers for Disease Control and Prevention (CDC) to evaluate the impact of Prop 65 on population-level exposures.</p><p><strong>Methods: </strong>We evaluated changes in blood and urine concentrations of 37 chemicals (including phthalates, phenols, VOCs, metals, PAHs, and PFAS), among US National Health and Nutrition Examination Survey (NHANES) participants in relation to the time of chemicals' Prop 65 listing. Of these, 11 were listed prior to, 11 during, and 4 after the biomonitoring period. The remaining 11 were not listed but were closely related to a Prop 65-listed chemical. Where biomonitoring data were available from before and after the date of Prop 65 listing, we estimated the change in concentrations over time for Californians compared with non-Californians, using a difference-in-differences model. We used quantile regression to estimate changes in exposure over time, as well as differences between Californians and non-Californians at the 25th, 75th, and 95th percentiles.</p><p><strong>Results: </strong>We found that concentrations of biomonitored chemicals generally declined nationwide over time irrespective of their inclusion on the Prop 65 list. Median bisphenol A (BPA) concentrations decreased 15% after BPA's listing on Prop 65, whereas concentrations of the nonlisted but closely related bisphenol S (BPS) increased 20% over this same period, suggesting chemical substitution. Californians generally had lower levels of biomonitored chemicals than the rest of the US population.</p><p><strong>Discussion: </strong>Our findings suggest that increased scientific and regulatory attention, as well as public awareness of the harms of Prop 65-listed chemicals, prompted changes in product formulations that reduced exposure to those chemicals nationwide. Trends in bisphenols and several phthalates suggest that manufacturers replaced some listed chemicals with closely related but unlisted chemicals, increasing exposure to the substitutes. Our findings have implications for the design of policies to reduce toxic exposures, biomonitoring programs to inform policy interventions, and future research into the regulatory and market forces that affect chemical exposure. https://doi.org/10.1289/EHP13956.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 10","pages":"107007"},"PeriodicalIF":10.1,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11493239/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142460950","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: \"Dioxins vs. PFAS: Science and Policy Challenges\".","authors":"Alex J George, Linda S Birnbaum","doi":"10.1289/EHP16380","DOIUrl":"https://doi.org/10.1289/EHP16380","url":null,"abstract":"","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 10","pages":"109001"},"PeriodicalIF":10.1,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11504291/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142497395","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":"Long-Term Exposure to Polystyrene Microspheres and High-Fat Diet-Induced Obesity in Mice: Evaluating a Role for Microbiota Dysbiosis.","authors":"Zhian Zhai, Ying Yang, Sheng Chen, Zhenlong Wu","doi":"10.1289/EHP13913","DOIUrl":"10.1289/EHP13913","url":null,"abstract":"<p><strong>Background: </strong>Microplastics (MPs) have become a global environmental problem, emerging as contaminants with potentially alarming consequences. However, long-term exposure to polystyrene microspheres (PS-MS) and its effects on diet-induced obesity are not yet fully understood.</p><p><strong>Objectives: </strong>We aimed to investigate the effect of PS-MS exposure on high-fat diet (HFD)-induced obesity and underlying mechanisms.</p><p><strong>Methods: </strong>In the present study, C57BL/6J mice were fed a normal diet (ND) or a HFD in the absence or presence of PS-MS via oral administration for 8 wk. Antibiotic depletion of the microbiota and fecal microbiota transplantation (FMT) were performed to assess the influence of PS-MS on intestinal microbial ecology. We performed 16S rRNA sequencing to dissect microbial discrepancies and investigated the dysbiosis-associated intestinal integrity and inflammation in serum.</p><p><strong>Results: </strong>Compared with HFD mice, mice fed the HFD with PS-MS exhibited higher body weight, liver weight, metabolic dysfunction-associated steatotic liver disease (MASLD) activity scores, and mass of white adipose tissue, as well as higher blood glucose and serum lipid concentrations. Furthermore, 16S rRNA sequencing of the fecal microbiota revealed that mice fed the HFD with PS-MS had greater <math><mi>α</mi></math>-diversity and greater relative abundances of <i>Lachnospiraceae</i>, <i>Oscillospiraceae</i>, <i>Bacteroidaceae</i>, <i>Akkermansiaceae</i>, <i>Marinifilaceae</i>, <i>Deferribacteres</i>, and <i>Desulfovibrio</i>, but lower relative abundances of <i>Atopobiaceae</i>, <i>Bifidobacterium</i>, and <i>Parabacteroides</i>. Mice fed the HFD with PS-MS exhibited lower expression of MUC2 mucin and higher levels of lipopolysaccharide and inflammatory cytokines [tumor necrosis factor-<math><mi>α</mi></math> (TNF-<math><mi>α</mi></math>), interleukin-6 (IL-6), IL-1<math><mi>β</mi></math>, and IL-17A] in serum. Correlation analyses revealed that differences in the microbial flora of mice exposed to PS-MS were associated with obesity. Interestingly, microbiota-depleted mice did not show the same PS-MS-associated differences in Muc2 and Tjp1 expression in the distal colon, expression of inflammatory cytokines in serum, or obesity outcomes between HFD and HFD + PS-MS. Importantly, transplantation of feces from HFD + PS-MS mice to microbiota-depleted HFD-fed mice resulted in a lower expression of mucus proteins, higher expression of inflammatory cytokines, and obesity outcomes, similar to the findings in HFD + PS-MS mice.</p><p><strong>Conclusions: </strong>Our findings provide a new gut microbiota-driven mechanism for PS-MS-induced obesity in HFD-fed mice, suggesting the need to reevaluate the adverse health effects of MPs commonly found in daily life, particularly in susceptible populations. https://doi.org/10.1289/EHP13913.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 9","pages":"97002"},"PeriodicalIF":10.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11370995/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142125185","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}
Yunjia Lai, Muhammet Ay, Carolina Duarte Hospital, Gary W Miller, Souvarish Sarkar
{"title":"Seminar: Functional Exposomics and Mechanisms of Toxicity-Insights from Model Systems and NAMs.","authors":"Yunjia Lai, Muhammet Ay, Carolina Duarte Hospital, Gary W Miller, Souvarish Sarkar","doi":"10.1289/EHP13120","DOIUrl":"10.1289/EHP13120","url":null,"abstract":"<p><strong>Background: </strong>Significant progress has been made over the past decade in measuring the chemical components of the exposome, providing transformative population-scale frameworks in probing the etiologic link between environmental factors and disease phenotypes. While the analytical technologies continue to evolve with reams of data being generated, there is an opportunity to complement exposome-wide association studies (ExWAS) with functional analyses to advance etiologic search at organismal, cellular, and molecular levels.</p><p><strong>Objectives: </strong>Exposomics is a transdisciplinary field aimed at enabling discovery-based analysis of the nongenetic factors that contribute to disease, including numerous environmental chemical stressors. While advances in exposure assessment are enhancing population-based discovery of exposome-wide effects and chemical exposure agents, functional screening and elucidation of biological effects of exposures represent the next logical step toward precision environmental health and medicine. In this work, we focus on the use, strategies, and prospects of alternative approaches and model systems to enhance the current human exposomics framework in biomarker search and causal understanding, spanning from bench-based nonmammalian organisms and cell culture to computational new approach methods (NAMs).</p><p><strong>Discussion: </strong>We visit the definition of the functional exposome and exposomics and discuss a need to leverage alternative models as opposed to mammalian animals for delineating exposome-wide health effects. Under the \"three Rs\" principle of reduction, replacement, and refinement, model systems such as roundworms, fruit flies, zebrafish, and induced pluripotent stem cells (iPSCs) are advantageous over mammals (e.g., rodents or higher vertebrates). These models are cost-effective, and cell-specific genetic manipulations in these models are easier and faster, compared to mammalian models. Meanwhile, <i>in silico</i> NAMs enhance hazard identification and risk assessment in humans by bridging the translational gaps between toxicology data and etiologic inference, as represented by <i>in vitro</i> to <i>in vivo</i> extrapolation (IVIVE) and integrated approaches to testing and assessment (IATA) under the adverse outcome pathway (AOP) framework. Together, these alternatives offer a strong toolbox to support functional exposomics to study toxicity and causal mediators underpinning exposure-disease links. https://doi.org/10.1289/EHP13120.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 9","pages":"94201"},"PeriodicalIF":10.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11373422/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142125187","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}
Ge Chen, Zhengmin Min Qian, Junguo Zhang, Xiaojie Wang, Zilong Zhang, Miao Cai, Lauren D Arnold, Chad Abresch, Chuangshi Wang, Yiming Liu, Qi Fan, Hualiang Lin
{"title":"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":"Ge Chen, Zhengmin Min Qian, Junguo Zhang, Xiaojie Wang, Zilong Zhang, Miao Cai, Lauren D Arnold, Chad Abresch, Chuangshi Wang, Yiming Liu, Qi Fan, Hualiang Lin","doi":"10.1289/EHP14367","DOIUrl":"10.1289/EHP14367","url":null,"abstract":"<p><strong>Background: </strong>Though observational studies have widely linked air pollution exposure to various chronic diseases, evidence comparing different exposures in the same people is limited. This study examined associations between changes in air pollution exposure due to relocation and the incidence and mortality of 14 major diseases.</p><p><strong>Methods: </strong>We included 50,522 participants enrolled in the UK Biobank from 2006 to 2010. Exposures to particulate matter with a diameter <math><mrow><mo>≤</mo><mn>2.5</mn><mspace></mspace><mi>μ</mi><mi>m</mi></mrow></math> (<math><mrow><mrow><msub><mrow><mrow><mi>PM</mi></mrow></mrow><mrow><mrow><mn>2.5</mn></mrow></mrow></msub></mrow></mrow></math>), particulate matter with a diameter <math><mrow><mo>≤</mo><mn>10</mn><mspace></mspace><mi>μ</mi><mi>m</mi></mrow></math> (<math><mrow><mrow><msub><mrow><mrow><mi>PM</mi></mrow></mrow><mrow><mrow><mn>10</mn></mrow></mrow></msub></mrow></mrow></math>), nitrogen oxides (<math><mrow><mrow><msub><mrow><mi>NO</mi></mrow><mrow><mi>x</mi></mrow></msub></mrow></mrow></math>), nitrogen dioxide (<math><mrow><mrow><msub><mrow><mi>NO</mi></mrow><mrow><mn>2</mn></mrow></msub></mrow></mrow></math>), and sulfur dioxide (<math><mrow><mrow><msub><mrow><mi>SO</mi></mrow><mrow><mn>2</mn></mrow></msub></mrow></mrow></math>) were estimated for each participant based on their residential address and relocation experience during the follow-up. Nine exposure groups were classified based on changes in long-term exposures due to residential mobility. Incidence and mortality of 14 major diseases were identified through linkages to hospital inpatient records and death registries. Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for incidence and mortality of the 14 diseases of interest.</p><p><strong>Results: </strong>During a median follow-up of 12.6 years, 29,869 participants were diagnosed with any disease of interest, and 3,144 died. Significantly increased risk of disease and all-cause mortality was observed among individuals who moved from a lower to higher air polluted area. Compared with constantly low exposure, moving from low to moderate <math><mrow><mrow><msub><mrow><mrow><mi>PM</mi></mrow></mrow><mrow><mrow><mn>2.5</mn></mrow></mrow></msub></mrow></mrow></math> exposure was associated with increased risk of all 14 diseases but not for all-cause mortality, with adjusted HRs (95% CIs) ranging from 1.18 (1.05, 1.33) to 1.48 (1.30, 1.69); moving from low to high <math><mrow><mrow><msub><mrow><mrow><mi>PM</mi></mrow></mrow><mrow><mrow><mn>2.5</mn></mrow></mrow></msub></mrow></mrow></math> areas increased risk of all 14 diseases: infections [1.37 (1.19, 1.58)], blood diseases [1.57 (1.34, 1.84)], endocrine diseases [1.77 (1.50, 2.09)], mental and behavioral disorders [1.93 (1.68, 2.21)], nervous system diseases [1.51 (1.32, 1.74)], ocular diseases [1.76 (1.56, 1.98)], ear disorders [1.58 (1.35, 1.86)],","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 9","pages":"97012"},"PeriodicalIF":10.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11441638/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142344003","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}
Behnan Albahsahli, Anna Dimitrova, Nadine Kadri, Tarik Benmarhnia, Tala Al-Rousan
{"title":"Mapping Climate-Related Hazards along Migration Routes: A Mixed Methods Study of Hypertensive Syrian and Iraqi Refugees Resettled in San Diego, California.","authors":"Behnan Albahsahli, Anna Dimitrova, Nadine Kadri, Tarik Benmarhnia, Tala Al-Rousan","doi":"10.1289/EHP14632","DOIUrl":"10.1289/EHP14632","url":null,"abstract":"","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 9","pages":"97701"},"PeriodicalIF":10.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11370993/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142125186","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}
Mercedes A Bravo, Daniel R Kowal, Dominique Zephyr, Joseph Feldman, Katherine Ensor, Marie Lynn Miranda
{"title":"Spatial Variability in Relationships between Early Childhood Lead Exposure and Standardized Test Scores in Fourth Grade North Carolina Public School Students (2013-2016).","authors":"Mercedes A Bravo, Daniel R Kowal, Dominique Zephyr, Joseph Feldman, Katherine Ensor, Marie Lynn Miranda","doi":"10.1289/EHP13898","DOIUrl":"10.1289/EHP13898","url":null,"abstract":"<p><strong>Background: </strong>Exposure to lead during childhood is detrimental to children's health. The extent to which the association between lead exposure and elementary school academic outcomes varies across geography is not known.</p><p><strong>Objective: </strong>Estimate associations between blood lead levels (BLLs) and fourth grade standardized test scores in reading and mathematics in North Carolina using models that allow associations between BLL and test scores to vary spatially across communities.</p><p><strong>Methods: </strong>We link geocoded, individual-level, standardized test score data for North Carolina public school students in fourth grade (2013-2016) with detailed birth records and blood lead testing data retrieved from the North Carolina childhood blood lead state registry on samples typically collected at 1-6 y of age. BLLs were categorized as: <math><mrow><mn>1</mn><mspace></mspace><mi>μ</mi><mi>g</mi><mo>/</mo><mtext>dL</mtext></mrow></math> (reference), <math><mrow><mn>2</mn><mspace></mspace><mi>μ</mi><mi>g</mi><mo>/</mo><mtext>dL</mtext></mrow></math>, <math><mrow><mn>3</mn><mo>-</mo><mn>4</mn><mspace></mspace><mi>μ</mi><mi>g</mi><mo>/</mo><mtext>dL</mtext></mrow></math> and <math><mrow><mo>≥</mo><mn>5</mn><mspace></mspace><mi>μ</mi><mi>g</mi><mo>/</mo><mtext>dL</mtext></mrow></math>. We then fit spatially varying coefficient models that incorporate information sharing (smoothness), across neighboring communities via a Gaussian Markov random field to provide a global estimate of the association between BLL and test scores, as well as census tract-specific estimates (i.e., spatial coefficients). Models adjusted for maternal- and child-level covariates and were fit separately for reading and math.</p><p><strong>Results: </strong>The average BLL across the 91,706 individuals in the analysis dataset was <math><mrow><mn>2.84</mn><mspace></mspace><mi>μ</mi><mi>g</mi><mo>/</mo><mtext>dL</mtext></mrow></math>. Individuals were distributed across 2,002 (out of 2,195) census tracts in North Carolina. In models adjusting for child sex, birth weight percentile for gestational age, and Medicaid participation as well as maternal race/ethnicity, educational attainment, marital status, and tobacco use, BLLs of <math><mrow><mn>2</mn><mspace></mspace><mi>μ</mi><mi>g</mi><mo>/</mo><mtext>dL</mtext></mrow></math>, <math><mrow><mn>3</mn><mo>-</mo><mn>4</mn><mspace></mspace><mi>μ</mi><mi>g</mi><mo>/</mo><mtext>dL</mtext></mrow></math> and <math><mrow><mo>≥</mo><mn>5</mn><mspace></mspace><mi>μ</mi><mi>g</mi><mo>/</mo><mtext>dL</mtext></mrow></math> were associated with overall lower reading test scores of <math><mrow><mo>-</mo><mn>0.28</mn></mrow></math> [95% confidence interval (CI): <math><mrow><mo>-</mo><mn>0.43</mn></mrow></math>, <math><mrow><mo>-</mo><mn>0.12</mn></mrow></math>], <math><mrow><mo>-</mo><mn>0.53</mn></mrow></math> (<math><mrow><mo>-</mo><mn>0.69</mn></mrow></math>, <math><mrow><mo>-</mo><mn>0.38</mn></mrow></math>), ","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 9","pages":"97003"},"PeriodicalIF":10.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11370994/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142125188","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}