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Temperature, Crime, and Violence: A Systematic Review and Meta-Analysis. 温度、犯罪和暴力:系统回顾与元分析》。
IF 10.4 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-10-15 DOI: 10.1289/ehp14300
Hayon Michelle Choi,Seulkee Heo,Damien Foo,Yimeng Song,Rory Stewart,Jiyoung Son,Michelle L Bell
BACKGROUNDHeat is known to affect many health outcomes, but more evidence is needed on the impact of rising temperatures on crime and/or violence.OBJECTIVESWe conducted a systematic review with meta-analysis regarding the influence of hot temperatures on crime and/or violence.METHODSIn this systematic review and meta-analysis, we evaluated the relationship between increase in temperature and crime and/or violence for studies across the world and generated overall estimates. We searched MEDLINE and Web of Science for articles from the available database start year (1946 and 1891, respectively) to 6 November 2023 and manually reviewed reference lists of identified articles. Two investigators independently reviewed the abstracts and full-text articles to identify and summarize studies that analyzed the relationship between increasing temperature and crime, violence, or both and met a priori eligibility criteria. PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines were used to extract information from included articles. Some study results were combined using a profile likelihood random-effects model for meta-analysis for a subset of outcomes: violent crime (assault, homicide), property crime (theft, burglary), and sexual crime (sexual assault, rape). This review is registered at PROSPERO, CRD42023417295.RESULTSWe screened 16,634 studies with 83 meeting the inclusion criteria. Higher temperatures were significantly associated with crime, violence, or both. A 10°C (18°F) increase in short-term mean temperature exposure was associated with a 9% [95% confidence interval (CI): 7%, 12%] increase in the risk of violent crime (I2=30.93%; eight studies). Studies had differing definitions of crime and/or violence, exposure assessment methods, and confounder assessments.DISCUSSIONOur findings summarize the evidence supporting the association between elevated temperatures, crime, and violence, particularly for violent crimes. Associations for some categories of crime and/or violence, such as property crimes, were inconsistent. Future research should employ larger spatial/temporal scales, consistent crime and violence definitions, advanced modeling strategies, and different populations and locations. https://doi.org/10.1289/EHP14300.
背景众所周知,高温会影响许多健康结果,但关于气温升高对犯罪和/或暴力的影响还需要更多的证据。目的我们就高温对犯罪和/或暴力的影响进行了系统综述和荟萃分析。方法在本系统综述和荟萃分析中,我们评估了世界各地研究中气温升高与犯罪和/或暴力之间的关系,并得出了总体估计值。我们在 MEDLINE 和 Web of Science 上检索了从可用数据库起始年(分别为 1946 年和 1891 年)到 2023 年 11 月 6 日的文章,并人工审阅了已识别文章的参考文献列表。两名调查人员独立审阅了文章摘要和全文,以确定并总结分析气温升高与犯罪、暴力或两者之间关系的研究,这些研究符合先验资格标准。采用 PRISMA(系统综述和 Meta 分析首选报告项目)指南从收录的文章中提取信息。对部分研究结果采用剖面似然随机效应模型进行荟萃分析:暴力犯罪(袭击、凶杀)、财产犯罪(盗窃、入室盗窃)和性犯罪(性侵犯、强奸)。结果我们筛选了 16634 项研究,其中 83 项符合纳入标准。气温升高与犯罪、暴力或两者均有明显关联。短期平均气温升高 10°C (18°F) 与暴力犯罪风险增加 9% [95% 置信区间 (CI):7%, 12%] 相关(I2=30.93%;8 项研究)。我们的研究结果总结了支持温度升高、犯罪和暴力(尤其是暴力犯罪)之间关联的证据。某些类别的犯罪和/或暴力(如财产犯罪)之间的关联并不一致。未来的研究应采用更大的空间/时间尺度、一致的犯罪和暴力定义、先进的建模策略以及不同的人群和地点。https://doi.org/10.1289/EHP14300。
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引用次数: 0
Mechanisms Underlying Acute Cognitive Impairment following Carbon Dioxide Inhalation in a Randomized Crossover Trial. 在一项随机交叉试验中,吸入二氧化碳后出现急性认知功能障碍的机理。
IF 10.1 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-10-01 Epub Date: 2024-10-28 DOI: 10.1289/EHP14806
Frederic T Lu, Disha Gupta, Nancy Fiedler, Usha Satish, Kathleen G Black, Alicia Legard, Adriana De Resende, Changjiang Guo, Andrew J Gow, Howard M Kipen
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引用次数: 0
Outdoor Air Pollution Exposure and Ovarian Cancer Incidence in a United States-Wide Prospective Cohort Study. 一项全美前瞻性队列研究中的室外空气污染暴露与卵巢癌发病率。
IF 10.1 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-10-01 DOI: 10.1289/EHP14729
Jennifer L Ish, Che-Jung Chang, Deborah B Bookwalter, Rena R Jones, Katie M O'Brien, Joel D Kaufman, Dale P Sandler, Alexandra J White
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引用次数: 0
Words Matter: Reflective Science Communication and Tradeoffs in Environmental Health Research. 言之有物:环境健康研究中的反思性科学交流与权衡。
IF 10.1 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-10-01 Epub Date: 2024-10-30 DOI: 10.1289/EHP14527
Kevin C Elliott, Heather B Patisaul, Robert M Sargis, Laura N Vandenberg

Background: 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.

Objectives: 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.

Discussion: 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).

Conclusions: Researchers who seek to responsibly communicate societally relevant work can employ several strategies to mitigate difficult tradeoffs, including a) striving for sensitivity to the social context and its relationship to their framing choices, b) choosing to avoid some frames, c) employing frames that alleviate ethical tensions, d) fostering education to alleviate harms, e) developing interdisciplinary and community collaborations, and f) working with institutions like scientific societies and journals to develop guidance on responsible communication practices. https://doi.org/10.1289/EHP14527.

背景:科学家在传播与社会相关的信息时,面临着错误信息、虚假信息、炒作和虚假信息盛行的挑战。因此,他们常常面临着如何以对社会负责的方式开展工作的艰难抉择:我们借鉴科学传播和框架设计方面的文献,确定了环境健康科学家在决定如何传播其工作时所面临的取舍,并提出了处理这些取舍的策略。我们以环境内分泌干扰素对人类健康影响的研究为案例,来说明这些挑战和策略:在讨论干扰内分泌的化学品对性发育、神经发育和肥胖的影响时,我们研究了四种主要框架(即包装信息的方式,可引起人们对某一问题或主题的关注)。我们展示了这些框架如何在有益(例如,让公众关注环境健康威胁并促进解决环境污染问题的行动)的同时产生有害影响(例如,助长对特定群体的污名化或宣扬有害的政治意识形态):寻求以负责任的方式传播与社会相关的工作的研究人员可以采用几种策略来减轻困难的权衡,包括 a) 努力提高对社会背景及其与他们的框架选择之间关系的敏感性;b) 选择避免某些框架;c) 采用缓解伦理紧张关系的框架;d) 促进教育以减轻危害;e) 发展跨学科和社区合作;f) 与科学协会和期刊等机构合作,制定负责任的传播实践指南。https://doi.org/10.1289/EHP14527。
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引用次数: 0
Exposure to Air Pollutants and Myocardial Infarction Incidence: A UK Biobank Study Exploring Gene-Environment Interaction. 空气污染物暴露与心肌梗死发病率:探索基因与环境相互作用的英国生物库研究》。
IF 10.1 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-10-01 Epub Date: 2024-10-10 DOI: 10.1289/EHP14291
Yudiyang Ma, Dankang Li, Feipeng Cui, Jianing Wang, Linxi Tang, Yingping Yang, Run Liu, Junqing Xie, Yaohua Tian
<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
背景:揭示基因与环境之间的相互作用可为早期疾病预防提供新的视角。然而,目前人们对遗传易感性和空气污染与心肌梗死(MI)风险之间相互作用的了解仍然有限。此外,空气污染物对心肌梗死发病风险的潜在长期影响还需要在社区人群中获得更多确凿证据:我们研究了遗传易感性和暴露于空气污染物对心肌梗死发病率的相互作用:该研究纳入了456,354名英国生物库参与者样本和英国环境、食品和农村事务部(2006-2021年)的年平均空气污染(PM2.5、PM10、二氧化氮和氮氧化物)数据。研究人员采用 Cox 比例危险模型来探讨长期暴露于空气污染物后的心肌梗死发病率。通过计算多基因风险评分(PRS)量化遗传风险,本研究进一步研究了遗传风险与暴露于空气污染物之间在心肌梗死发病过程中的加法和乘法效应:在 456 354 名参与者中,在 12.08 年的中位随访期间观察到 9 114 例心肌梗死事件。具体而言,PM2.5 的危险比(每四分位间范围)为 1.12(95% CI:1.10,1.13),PM10 为 1.20(95% CI:1.19,1.22),二氧化氮为 1.13(95% CI:1.12,1.15),氮氧化物为 1.12(95% CI:1.11,1.13)。就联合效应而言,在所有研究参与者中,高 PRS 和高空气污染暴露水平的参与者患心肌梗死的风险最大(255% 至 324%)。值得注意的是,在环境空气污染暴露和遗传风险对心肌梗死发病率的影响中,发现了乘法和加法的相互作用:讨论:环境空气污染物暴露和遗传易感性对心肌梗死发病风险存在相互作用。此外,这两种暴露的共同影响大于每个因素单独的影响。https://doi.org/10.1289/EHP14291。
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Furthermore, the potential long-term influence of air pollutants on MI incidence risk warrants more conclusive evidence in a community population.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Objective: &lt;/strong&gt;We investigated interactions between genetic predisposition and exposure to air pollutants on MI incidence.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;This study incorporated a sample of 456,354 UK Biobank participants and annual mean air pollution (&lt;math&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;msub&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;mi&gt;PM&lt;/mi&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;mn&gt;2.5&lt;/mn&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;/msub&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;/math&gt;, &lt;math&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;msub&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;mi&gt;PM&lt;/mi&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;mn&gt;10&lt;/mn&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;/msub&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;/math&gt;, &lt;math&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;msub&gt;&lt;mrow&gt;&lt;mi&gt;NO&lt;/mi&gt;&lt;/mrow&gt;&lt;mrow&gt;&lt;mn&gt;2&lt;/mn&gt;&lt;/mrow&gt;&lt;/msub&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;/math&gt;, and &lt;math&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;msub&gt;&lt;mrow&gt;&lt;mi&gt;NO&lt;/mi&gt;&lt;/mrow&gt;&lt;mrow&gt;&lt;mi&gt;x&lt;/mi&gt;&lt;/mrow&gt;&lt;/msub&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;/math&gt;) 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.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;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 &lt;math&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;msub&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;mi&gt;PM&lt;/mi&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;mn&gt;2.5&lt;/mn&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;/msub&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;/math&gt;, 1.20 (95% CI: 1.19, 1.22) for &lt;math&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;msub&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;mi&gt;PM&lt;/mi&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;mn&gt;10&lt;/mn&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;/msub&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;/math&gt;, 1.13 (95% CI: 1.12, 1.15) for &lt;math&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;msub&gt;&lt;mrow&gt;&lt;mi&gt;NO&lt;/mi&gt;&lt;/mrow&gt;&lt;mrow&gt;&lt;mn&gt;2&lt;/mn&gt;&lt;/mrow&gt;&lt;/msub&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;/math&gt;, and 1.12 (95% CI: 1.11, 1.13) for &lt;math&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;msub&gt;&lt;mrow&gt;&lt;mi&gt;NO&lt;/mi&gt;&lt;/mrow&gt;&lt;mrow&gt;&lt;mi&gt;x&lt;/mi&gt;&lt;/mrow&gt;&lt;/msub&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;/math&gt;. 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 (&lt;math&gt;&lt;mrow&gt;&lt;mo&gt;∼&lt;/mo&gt;&lt;mn&gt;255&lt;/mn&gt;&lt;mo&gt;%&lt;/mo&gt;&lt;/mrow&gt;&lt;/math&gt; to 324%). Remarkably, both multiplicative and additive interactions were detected in the ambient air pollutants exposure and genetic risk on the incidence of MI.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Discussion: &lt;/strong&gt;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}
引用次数: 0
Associations between Fine Particulate Matter Components, Their Sources, and Cognitive Outcomes in Children Ages 9-10 Years Old from the United States. 美国 9-10 岁儿童细颗粒物成分、来源与认知结果之间的关系。
IF 10.1 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-10-01 Epub Date: 2024-10-30 DOI: 10.1289/EHP14418
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
<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><
背景:新近的文献表明,空气污染中的细颗粒物[空气动力学直径≤2.5μm(PM2.5)]及其成分与各种神经发育结果有关。然而,很少有研究对不同来源的 PM2.5 混合物成分与儿童认知结果的关系进行评估:这项横断面研究调查了美国各地 PM2.5 成分混合物的环境浓度与 9 至 10 岁儿童神经认知能力的关系,并探讨了这些关联的潜在特定来源效应:利用时空混合模型,根据青少年大脑认知发展(ABCD)研究中儿童参与者的居住地址估算出 PM2.5 中 15 种化学成分的年浓度。一般认知能力、执行功能和学习/记忆力评分来自美国国立卫生研究院工具箱。我们采用正矩阵因式分解法,根据 15 个成分确定了 PM2.5 的六个主要来源,包括地壳、硫酸铵、生物质燃烧、交通、硝酸铵和工业/剩余燃料燃烧。然后,我们利用加权量化总和(WQS)和线性回归模型研究了PM2.5成分混合物、其潜在来源与儿童认知分数之间的关系:结果:混合物模型揭示了累积暴露量与所有三个结果领域认知能力下降之间的关系,包括硝酸铵、硅和钙所产生的有害影响的共同重叠。利用已确定的六种暴露源,确定了硝酸铵与学习和记忆、交通与执行功能以及地壳和工业混合物与一般认知能力之间的负相关。交通与一般能力以及生物质燃烧与执行功能之间也存在意想不到的正相关关系:讨论:这项研究表明,室外 PM2.5 暴露与儿童认知能力之间存在微妙的联系,包括与单个化学品以及这些暴露的特定来源有关的认知能力的重要差异。https://doi.org/10.1289/EHP14418。
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However, few studies have evaluated how &lt;math&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;msub&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;mi&gt;PM&lt;/mi&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;mn&gt;2.5&lt;/mn&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;/msub&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;/math&gt; component mixtures from distinct sources relate to cognitive outcomes in children.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Objectives: &lt;/strong&gt;This cross-sectional study investigated how ambient concentrations of &lt;math&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;msub&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;mi&gt;PM&lt;/mi&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;mn&gt;2.5&lt;/mn&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;/msub&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;/math&gt; 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.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Using spatiotemporal hybrid models, annual concentrations of 15 chemical components of &lt;math&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;msub&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;mi&gt;PM&lt;/mi&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;mn&gt;2.5&lt;/mn&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;/msub&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;/math&gt; 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 &lt;math&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;msub&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;mi&gt;PM&lt;/mi&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;mn&gt;2.5&lt;/mn&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;/msub&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;/math&gt; 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 &lt;math&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;msub&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;mi&gt;PM&lt;/mi&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;mn&gt;2.5&lt;/mn&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;/msub&gt;&lt;/mrow&gt;&lt;/mrow&gt;&lt;/math&gt; components' mixture, their potential sources, and children's cognitive scores.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;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.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Discussion: &lt;/strong&gt;This work suggests nuanced associations between outdoor &lt;math&gt;&lt;mrow&gt;&lt;mrow&gt;&lt;msub&gt;&lt;","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}
引用次数: 0
Trends in NHANES Biomonitored Exposures in California and the United States following Enactment of California's Proposition 65. 加州 65 号提案颁布后加州和美国 NHANES 生物监测暴露趋势。
IF 10.1 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-10-01 Epub Date: 2024-10-21 DOI: 10.1289/EHP13956
Kristin E Knox, Megan R Schwarzman, Ruthann A Rudel, Claudia Polsky, Robin E Dodson

Background: 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?

Objective: 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.

Methods: 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.

Results: 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.

Discussion: 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.

背景:有毒化学品在美国商业中的普遍存在促使一些州通过法律来减少化学品的接触。加利福尼亚州的第 65 号提案(Proposition 65)就是一项影响广泛的法律,该提案列出了一份可致癌、对发育有害或具有生殖毒性的化学品清单。该法律旨在阻止企业使用这些化学品,并最大限度地减少消费者的接触。然而,一个关键问题仍然没有答案:提案 65 是否减少了人群对所列化学品的暴露?我们利用疾病控制和预防中心 (CDC) 提供的全国生物监测数据,评估提案 65 对人群暴露的影响:我们评估了美国国家健康与营养调查 (NHANES) 参与者血液和尿液中 37 种化学品(包括邻苯二甲酸盐、酚类、挥发性有机化合物、金属、多环芳烃和全氟辛烷磺酸)浓度的变化与 65 号提案列出化学品时间的关系。其中,11 种在生物监测期之前被列入,11 种在生物监测期期间被列入,4 种在生物监测期之后被列入。其余 11 种虽然未被列入名单,但与列入 65 号提案的化学品密切相关。在有 65 号提案上市日期前后的生物监测数据的情况下,我们使用差分模型估算了加州人与非加州人的浓度随时间的变化。我们使用量子回归法估算了暴露量随时间的变化,以及加州人与非加州人在第 25、75 和 95 百分位数上的差异:我们发现,随着时间的推移,全国范围内生物监测化学品的浓度普遍下降,与这些化学品是否被列入 65 号提案清单无关。双酚 A (BPA) 的浓度中位数在双酚 A 被列入 65 号提案后下降了 15%,而未被列入提案但与之密切相关的双酚 S (BPS) 的浓度在同一时期上升了 20%,这表明存在化学替代现象。加利福尼亚人的生物监测化学品水平普遍低于美国其他地区的人口:讨论:我们的研究结果表明,科学和监管部门的日益关注以及公众对提案 65 所列化学品危害的认识,促使产品配方发生变化,从而在全国范围内减少了对这些化学品的接触。双酚和几种邻苯二甲酸盐的趋势表明,制造商用密切相关但未列入清单的化学品替代了某些列入清单的化学品,从而增加了对替代品的接触。我们的研究结果对减少有毒物质暴露的政策设计、为政策干预提供信息的生物监测计划以及未来对影响化学品暴露的监管和市场力量的研究都有意义。https://doi.org/10.1289/EHP13956。
{"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}
引用次数: 0
Erratum: "Dioxins vs. PFAS: Science and Policy Challenges". 勘误:"二恶英与全氟辛烷磺酸:科学与政策挑战"。
IF 10.1 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-10-01 Epub Date: 2024-10-25 DOI: 10.1289/EHP16380
Alex J George, Linda S Birnbaum
{"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}
引用次数: 0
Reconceptualizing and Defining Exposomics within Environmental Health: Expanding the Scope of Health Research. 重新认识和定义环境健康中的暴露学:扩大健康研究范围。
IF 10.4 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-09-27 DOI: 10.1289/ehp14509
Caspar W Safarlou,Karin R Jongsma,Roel Vermeulen
BACKGROUNDExposomics, the study of the exposome, is flourishing, but the field is not well defined. The term "exposome" refers to all environmental influences and associated biological responses throughout the lifespan. However, this definition is very similar to that of the term "environment"-the external elements and conditions that surround and affect the life and development of an organism. Consequently, the exposome seems to be nothing more than a synonym for the environment, and exposomics a synonym for environmental research. As a result, some have rebranded their "standard" environmental health research with the neologistic exposome term, whereas others ignore or seek to abandon the seemingly redundant concept of the exposome.OBJECTIVESWe argue that exposomics needs to sharpen its mission focus to counteract this apparent redundancy. Exposomics should be defined as a research program in environmental health aimed at enabling a comprehensive and discovery-driven approach to identifying environmental determinants of human health. Similar to the aim of the Human Genome Project, exposomics aims to analyze the complete complexity of exposures and their corresponding biological responses. Exposomics' primary premise is that the existence of undiscovered, potentially interconnected, nongenetic (environmental) risk factors for health necessitates a comprehensive discovery-driven analysis approach.DISCUSSIONWe argue that exposomics researchers should adopt our reconceptualization of exposomics and focus on the productiveness and integrity of their research program: its purpose and principles. We suggest that exposomics researchers should coordinate the writing of reviews that assess the program's productiveness and integrity, as well as provide a platform for exposomics researchers to define their vision for the field. https://doi.org/10.1289/EHP14509.
背景暴露组学(Exposomics)是对暴露组的研究,目前正在蓬勃发展,但该领域还没有明确的定义。所谓 "暴露组",是指在人的一生中受到的所有环境影响以及相关的生物反应。然而,这一定义与 "环境 "一词的定义非常相似--即围绕并影响生物体生命和发育的外部因素和条件。因此,暴露体似乎只不过是环境的同义词,而暴露组学则是环境研究的同义词。因此,有些人将 "标准 "的环境健康研究与新造的 "暴露体 "一词重新组合,而另一些人则忽视或试图放弃 "暴露体 "这一看似多余的概念。暴露组学应被定义为环境健康领域的一项研究计划,旨在以发现为导向的综合方法来确定人类健康的环境决定因素。与人类基因组计划的目标类似,暴露组学旨在分析暴露的全部复杂性及其相应的生物反应。我们认为,暴露量子学研究人员应采用我们对暴露量子学的重新认识,并重点关注其研究计划的有效性和完整性:研究计划的目的和原则。我们建议,暴露组学研究人员应协调撰写评论,以评估该计划的成效和完整性,并为暴露组学研究人员提供一个平台,以确定他们对该领域的愿景。https://doi.org/10.1289/EHP14509。
{"title":"Reconceptualizing and Defining Exposomics within Environmental Health: Expanding the Scope of Health Research.","authors":"Caspar W Safarlou,Karin R Jongsma,Roel Vermeulen","doi":"10.1289/ehp14509","DOIUrl":"https://doi.org/10.1289/ehp14509","url":null,"abstract":"BACKGROUNDExposomics, the study of the exposome, is flourishing, but the field is not well defined. The term \"exposome\" refers to all environmental influences and associated biological responses throughout the lifespan. However, this definition is very similar to that of the term \"environment\"-the external elements and conditions that surround and affect the life and development of an organism. Consequently, the exposome seems to be nothing more than a synonym for the environment, and exposomics a synonym for environmental research. As a result, some have rebranded their \"standard\" environmental health research with the neologistic exposome term, whereas others ignore or seek to abandon the seemingly redundant concept of the exposome.OBJECTIVESWe argue that exposomics needs to sharpen its mission focus to counteract this apparent redundancy. Exposomics should be defined as a research program in environmental health aimed at enabling a comprehensive and discovery-driven approach to identifying environmental determinants of human health. Similar to the aim of the Human Genome Project, exposomics aims to analyze the complete complexity of exposures and their corresponding biological responses. Exposomics' primary premise is that the existence of undiscovered, potentially interconnected, nongenetic (environmental) risk factors for health necessitates a comprehensive discovery-driven analysis approach.DISCUSSIONWe argue that exposomics researchers should adopt our reconceptualization of exposomics and focus on the productiveness and integrity of their research program: its purpose and principles. We suggest that exposomics researchers should coordinate the writing of reviews that assess the program's productiveness and integrity, as well as provide a platform for exposomics researchers to define their vision for the field. https://doi.org/10.1289/EHP14509.","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"52 1","pages":"95001"},"PeriodicalIF":10.4,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142328839","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}
引用次数: 0
Invited Perspective: The Exposome-An Exciting Opportunity for Collaboration, Not Competition. 特邀观点:博览会--合作而非竞争的良机。
IF 10.4 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-09-27 DOI: 10.1289/ehp15504
Christopher P Wild
{"title":"Invited Perspective: The Exposome-An Exciting Opportunity for Collaboration, Not Competition.","authors":"Christopher P Wild","doi":"10.1289/ehp15504","DOIUrl":"https://doi.org/10.1289/ehp15504","url":null,"abstract":"","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"87 1","pages":"91302"},"PeriodicalIF":10.4,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142329090","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}
引用次数: 0
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Environmental Health Perspectives
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