首页 > 最新文献

Environmental Epidemiology最新文献

英文 中文
Ecological studies of COVID-19 and air pollution: How useful are they? COVID-19和空气污染的生态学研究:它们有多有用?
IF 3.6 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2022-02-04 eCollection Date: 2022-02-01 DOI: 10.1097/EE9.0000000000000195
Paul J Villeneuve, Mark S Goldberg

Background: Results from ecological studies have suggested that air pollution increases the risk of developing and dying from COVID-19. Drawing causal inferences from the measures of association reported in ecological studies is fraught with challenges given biases arising from an outcome whose ascertainment is incomplete, varies by region, time, and across sociodemographic characteristics, and cannot account for clustering or within-area heterogeneity. Through a series of analyses, we illustrate the dangers of using ecological studies to assess whether ambient air pollution increases the risk of dying from, or transmitting, COVID-19.

Methods: We performed an ecological analysis in the continental United States using county-level ambient concentrations of fine particulate matter (PM2.5) between 2000 and 2016 and cumulative COVID-19 mortality counts through June 2020, December 2020, and April 2021. To show that spurious associations can be obtained in ecological data, we modeled the association between PM2.5 and the prevalence of human immunodeficiency virus (HIV). We fitted negative binomial models, with a logarithmic offset for county-specific population, to these data. Natural cubic splines were used to describe the shape of the exposure-response curves.

Results: Our analyses revealed that the shape of the exposure-response curve between PM2.5 and COVID-19 changed substantially over time. Analyses of COVID-19 mortality through June 30, 2021, suggested a positive linear relationship. In contrast, an inverse pattern was observed using county-level concentrations of PM2.5 and the prevalence of HIV.

Conclusions: Our analyses indicated that ecological analyses are prone to showing spurious relationships between ambient air pollution and mortality from COVID-19 as well as the prevalence of HIV. We discuss the many potential biases inherent in any ecological-based analysis of air pollution and COVID-19.

背景:生态学研究结果表明,空气污染增加了患COVID-19和死于COVID-19的风险。从生态学研究中报告的关联度量中得出因果推论充满了挑战,因为结果的确定不完整,因地区、时间和社会人口特征而异,并且不能解释聚类或区域内异质性。通过一系列分析,我们说明了利用生态研究来评估环境空气污染是否会增加COVID-19死亡或传播风险的危险。方法:我们使用2000年至2016年期间美国大陆县级环境细颗粒物(PM2.5)浓度和2020年6月、2020年12月和2021年4月的累积COVID-19死亡率计数进行了生态分析。为了证明在生态数据中可以获得虚假的关联,我们建立了PM2.5与人类免疫缺陷病毒(HIV)流行之间的关联模型。我们对这些数据进行了负二项模型的拟合,并对特定县的人口进行了对数偏移。采用自然三次样条曲线来描述暴露-响应曲线的形状。结果:我们的分析显示,PM2.5与COVID-19之间的暴露-响应曲线的形状随着时间的推移发生了很大变化。对截至2021年6月30日的COVID-19死亡率的分析表明,这是一种正线性关系。相比之下,使用县级PM2.5浓度和艾滋病毒流行率观察到相反的模式。结论:我们的分析表明,生态分析容易显示环境空气污染与COVID-19死亡率以及艾滋病毒流行之间的虚假关系。我们讨论了任何基于生态的空气污染和COVID-19分析中固有的许多潜在偏差。
{"title":"Ecological studies of COVID-19 and air pollution: How useful are they?","authors":"Paul J Villeneuve,&nbsp;Mark S Goldberg","doi":"10.1097/EE9.0000000000000195","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000195","url":null,"abstract":"<p><strong>Background: </strong>Results from ecological studies have suggested that air pollution increases the risk of developing and dying from COVID-19. Drawing causal inferences from the measures of association reported in ecological studies is fraught with challenges given biases arising from an outcome whose ascertainment is incomplete, varies by region, time, and across sociodemographic characteristics, and cannot account for clustering or within-area heterogeneity. Through a series of analyses, we illustrate the dangers of using ecological studies to assess whether ambient air pollution increases the risk of dying from, or transmitting, COVID-19.</p><p><strong>Methods: </strong>We performed an ecological analysis in the continental United States using county-level ambient concentrations of fine particulate matter (PM<sub>2.5</sub>) between 2000 and 2016 and cumulative COVID-19 mortality counts through June 2020, December 2020, and April 2021. To show that spurious associations can be obtained in ecological data, we modeled the association between PM<sub>2.5</sub> and the prevalence of human immunodeficiency virus (HIV). We fitted negative binomial models, with a logarithmic offset for county-specific population, to these data. Natural cubic splines were used to describe the shape of the exposure-response curves.</p><p><strong>Results: </strong>Our analyses revealed that the shape of the exposure-response curve between PM<sub>2.5</sub> and COVID-19 changed substantially over time. Analyses of COVID-19 mortality through June 30, 2021, suggested a positive linear relationship. In contrast, an inverse pattern was observed using county-level concentrations of PM<sub>2.5</sub> and the prevalence of HIV.</p><p><strong>Conclusions: </strong>Our analyses indicated that ecological analyses are prone to showing spurious relationships between ambient air pollution and mortality from COVID-19 as well as the prevalence of HIV. We discuss the many potential biases inherent in any ecological-based analysis of air pollution and COVID-19.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e195"},"PeriodicalIF":3.6,"publicationDate":"2022-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ac/52/ee9-6-e195.PMC8835551.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39927692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 6
The EXIMIOUS project-Mapping exposure-induced immune effects: connecting the exposome and the immunome. EXIMIOUS项目-暴露诱导免疫效应制图:连接暴露体和免疫组。
IF 3.6 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2022-02-01 DOI: 10.1097/EE9.0000000000000193
Steven Ronsmans, Karin Sørig Hougaard, Tim S Nawrot, Michelle Plusquin, François Huaux, María Jesús Cruz, Horatiu Moldovan, Steven Verpaele, Murali Jayapala, Michael Tunney, Stéphanie Humblet-Baron, Hubert Dirven, Unni Cecilie Nygaard, Birgitte Lindeman, Nur Duale, Adrian Liston, Esben Meulengracht Flachs, Kenneth Kastaniegaard, Matthias Ketzel, Julia Goetz, Jeroen Vanoirbeek, Manosij Ghosh, Peter H M Hoet

Immune-mediated, noncommunicable diseases-such as autoimmune and inflammatory diseases-are chronic disorders, in which the interaction between environmental exposures and the immune system plays an important role. The prevalence and societal costs of these diseases are rising in the European Union. The EXIMIOUS consortium-gathering experts in immunology, toxicology, occupational health, clinical medicine, exposure science, epidemiology, bioinformatics, and sensor development-will study eleven European study populations, covering the entire lifespan, including prenatal life. Innovative ways of characterizing and quantifying the exposome will be combined with high-dimensional immunophenotyping and -profiling platforms to map the immune effects (immunome) induced by the exposome. We will use two main approaches that "meet in the middle"-one starting from the exposome, the other starting from health effects. Novel bioinformatics tools, based on systems immunology and machine learning, will be used to integrate and analyze these large datasets to identify immune fingerprints that reflect a person's lifetime exposome or that are early predictors of disease. This will allow researchers, policymakers, and clinicians to grasp the impact of the exposome on the immune system at the level of individuals and populations.

免疫介导的非传染性疾病(如自身免疫性疾病和炎症性疾病)是慢性疾病,其中环境暴露与免疫系统之间的相互作用起着重要作用。在欧洲联盟,这些疾病的流行率和社会成本正在上升。EXIMIOUS联盟聚集了免疫学、毒理学、职业健康、临床医学、暴露科学、流行病学、生物信息学和传感器开发方面的专家,将研究11个欧洲研究人群,涵盖整个生命周期,包括产前生活。对暴露体进行表征和量化的创新方法将与高维免疫分型和分析平台相结合,以绘制暴露体诱导的免疫效应(免疫组)。我们将采用两种“中间衔接”的主要方法——一种从接触物开始,另一种从健康影响开始。基于系统免疫学和机器学习的新型生物信息学工具将用于整合和分析这些大型数据集,以识别反映一个人一生暴露或疾病早期预测的免疫指纹。这将使研究人员、政策制定者和临床医生能够在个人和人群水平上掌握暴露体对免疫系统的影响。
{"title":"The EXIMIOUS project-Mapping exposure-induced immune effects: connecting the exposome and the immunome.","authors":"Steven Ronsmans,&nbsp;Karin Sørig Hougaard,&nbsp;Tim S Nawrot,&nbsp;Michelle Plusquin,&nbsp;François Huaux,&nbsp;María Jesús Cruz,&nbsp;Horatiu Moldovan,&nbsp;Steven Verpaele,&nbsp;Murali Jayapala,&nbsp;Michael Tunney,&nbsp;Stéphanie Humblet-Baron,&nbsp;Hubert Dirven,&nbsp;Unni Cecilie Nygaard,&nbsp;Birgitte Lindeman,&nbsp;Nur Duale,&nbsp;Adrian Liston,&nbsp;Esben Meulengracht Flachs,&nbsp;Kenneth Kastaniegaard,&nbsp;Matthias Ketzel,&nbsp;Julia Goetz,&nbsp;Jeroen Vanoirbeek,&nbsp;Manosij Ghosh,&nbsp;Peter H M Hoet","doi":"10.1097/EE9.0000000000000193","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000193","url":null,"abstract":"<p><p>Immune-mediated, noncommunicable diseases-such as autoimmune and inflammatory diseases-are chronic disorders, in which the interaction between environmental exposures and the immune system plays an important role. The prevalence and societal costs of these diseases are rising in the European Union. The EXIMIOUS consortium-gathering experts in immunology, toxicology, occupational health, clinical medicine, exposure science, epidemiology, bioinformatics, and sensor development-will study eleven European study populations, covering the entire lifespan, including prenatal life. Innovative ways of characterizing and quantifying the exposome will be combined with high-dimensional immunophenotyping and -profiling platforms to map the immune effects (immunome) induced by the exposome. We will use two main approaches that \"meet in the middle\"-one starting from the exposome, the other starting from health effects. Novel bioinformatics tools, based on systems immunology and machine learning, will be used to integrate and analyze these large datasets to identify immune fingerprints that reflect a person's lifetime exposome or that are early predictors of disease. This will allow researchers, policymakers, and clinicians to grasp the impact of the exposome on the immune system at the level of individuals and populations.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e193"},"PeriodicalIF":3.6,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/99/cb/ee9-6-e193.PMC8835560.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39927691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 6
Chronic fine particulate matter exposure, habitual exercise, and dyslipidemia: A longitudinal cohort study. 慢性细颗粒物暴露、习惯性运动和血脂异常:一项纵向队列研究。
IF 3.6 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2022-01-05 eCollection Date: 2022-02-01 DOI: 10.1097/EE9.0000000000000190
Yi Qian Zeng, Ly-Yun Chang, Cui Guo, Changqing Lin, Yacong Bo, Martin C S Wong, Tony Tam, Alexis K H Lau, Xiang Qian Lao

Background: Physical activity may increase the intake of air pollutants due to a higher ventilation rate, which may exacerbate the adverse health effects. This study investigated the combined effects of habitual exercise and long-term exposure to fine particulate matter (PM2.5) on the incidence of dyslipidemia in a large longitudinal cohort in Taiwan.

Methods: A total of 121,948 adults (≥18 years) who received at least two medical examinations from 2001 to 2016 were recruited, yielding 407,821 medical examination records. A satellite-based spatiotemporal model was used to estimate the 2-year average PM2.5 concentration (i.e., the year of and the year before the medical examination) at each participant's address. Information on habitual exercise within 1 month before the medical examination was collected using a standard self-administered questionnaire. A Cox regression model with time-dependent covariates was used to investigate the combined effects.

Results: Compared with inactivity, moderate and high levels of exercise were associated with a lower incidence of dyslipidemia, with hazard ratios (HRs) (95% confidence intervals [CIs]) of 0.91 (0.88, 0.94) and 0.73 (0.71, 0.75), respectively. Participants with a moderate (22.37-25.96 μg/m3) or high (>25.96 μg/m3) level of PM2.5 exposure had a higher incidence of dyslipidemia than those with a low level of PM2.5 exposure (≤22.37 μg/m3), with HRs (95% CIs) of 1.36 (1.32, 1.40), and 1.90 (1.81, 1.99), respectively. We observed a statistically significant, but minor, interaction effect of PM2.5 exposure and exercise on the development of dyslipidemia, with an overall hazard ratios (95% CI) of 1.08 (1.05, 1.10), indicating that an incremental increase in the level of exercise was associated with an 8% increase in the risk of dyslipidemia associated with every 10 μg/m3 increase in PM2.5 exposure. However, the negative association between habitual exercise and dyslipidemia remained, regardless of the level of PM2.5 exposure, suggesting that the benefits of increased habitual exercise outweighed the adverse effects of the increase in PM2.5 intake during exercise.

Conclusions: Increased levels of exercise and reduced levels of PM2.5 exposures were associated with a lower incidence of dyslipidemia. Although an increase in habitual exercise slightly increased the risk of dyslipidemia associated with PM2.5 exposure, the benefits of the increased habitual exercise outweighed the risks. Our findings suggest that habitual exercise is an effective approach for dyslipidemia prevention, even for people residing in relatively polluted areas.

背景:由于较高的通风量,体育活动可能增加空气污染物的摄入量,这可能加剧对健康的不利影响。本研究以台湾为研究对象,探讨习惯运动与长期暴露于细颗粒物(PM2.5)对血脂异常发生率的影响。方法:招募2001 - 2016年至少接受过两次体检的成人(≥18岁)121948人,获得体检记录407821份。使用基于卫星的时空模型估计每个参与者地址的2年平均PM2.5浓度(即体检当年和体检前一年)。使用标准的自我管理问卷收集体检前1个月内的习惯性运动信息。采用含时间相关协变量的Cox回归模型对联合效应进行研究。结果:与不运动相比,中度和高水平运动与较低的血脂异常发生率相关,其风险比(hr)(95%可信区间[ci])分别为0.91(0.88,0.94)和0.73(0.71,0.75)。中等(22.37 ~ 25.96 μg/m3)或高(>25.96 μg/m3) PM2.5暴露水平的参与者血脂异常发生率高于低(≤22.37 μg/m3) PM2.5暴露水平的参与者,其hr (95% ci)分别为1.36(1.32,1.40)和1.90(1.81,1.99)。我们观察到PM2.5暴露和运动对血脂异常发展的交互作用具有统计学意义,但影响较小,总体风险比(95% CI)为1.08(1.05,1.10),表明PM2.5暴露每增加10 μg/m3,运动水平的增加与血脂异常风险增加8%相关。然而,无论PM2.5暴露水平如何,习惯性运动与血脂异常之间的负相关仍然存在,这表明增加习惯性运动的好处超过了运动期间PM2.5摄入量增加的不利影响。结论:运动水平的增加和PM2.5暴露水平的降低与血脂异常发生率的降低有关。尽管增加习惯性锻炼会略微增加与PM2.5暴露相关的血脂异常的风险,但增加习惯性锻炼的好处大于风险。我们的研究结果表明,习惯性运动是预防血脂异常的有效方法,即使对于居住在相对污染地区的人也是如此。
{"title":"Chronic fine particulate matter exposure, habitual exercise, and dyslipidemia: A longitudinal cohort study.","authors":"Yi Qian Zeng,&nbsp;Ly-Yun Chang,&nbsp;Cui Guo,&nbsp;Changqing Lin,&nbsp;Yacong Bo,&nbsp;Martin C S Wong,&nbsp;Tony Tam,&nbsp;Alexis K H Lau,&nbsp;Xiang Qian Lao","doi":"10.1097/EE9.0000000000000190","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000190","url":null,"abstract":"<p><strong>Background: </strong>Physical activity may increase the intake of air pollutants due to a higher ventilation rate, which may exacerbate the adverse health effects. This study investigated the combined effects of habitual exercise and long-term exposure to fine particulate matter (PM<sub>2.5</sub>) on the incidence of dyslipidemia in a large longitudinal cohort in Taiwan.</p><p><strong>Methods: </strong>A total of 121,948 adults (≥18 years) who received at least two medical examinations from 2001 to 2016 were recruited, yielding 407,821 medical examination records. A satellite-based spatiotemporal model was used to estimate the 2-year average PM<sub>2.5</sub> concentration (i.e., the year of and the year before the medical examination) at each participant's address. Information on habitual exercise within 1 month before the medical examination was collected using a standard self-administered questionnaire. A Cox regression model with time-dependent covariates was used to investigate the combined effects.</p><p><strong>Results: </strong>Compared with inactivity, moderate and high levels of exercise were associated with a lower incidence of dyslipidemia, with hazard ratios (HRs) (95% confidence intervals [CIs]) of 0.91 (0.88, 0.94) and 0.73 (0.71, 0.75), respectively. Participants with a moderate (22.37-25.96 μg/m<sup>3</sup>) or high (>25.96 μg/m<sup>3</sup>) level of PM<sub>2.5</sub> exposure had a higher incidence of dyslipidemia than those with a low level of PM<sub>2.5</sub> exposure (≤22.37 μg/m<sup>3</sup>), with HRs (95% CIs) of 1.36 (1.32, 1.40), and 1.90 (1.81, 1.99), respectively. We observed a statistically significant, but minor, interaction effect of PM<sub>2.5</sub> exposure and exercise on the development of dyslipidemia, with an overall hazard ratios (95% CI) of 1.08 (1.05, 1.10), indicating that an incremental increase in the level of exercise was associated with an 8% increase in the risk of dyslipidemia associated with every 10 μg/m<sup>3</sup> increase in PM<sub>2.5</sub> exposure. However, the negative association between habitual exercise and dyslipidemia remained, regardless of the level of PM<sub>2.5</sub> exposure, suggesting that the benefits of increased habitual exercise outweighed the adverse effects of the increase in PM<sub>2.5</sub> intake during exercise.</p><p><strong>Conclusions: </strong>Increased levels of exercise and reduced levels of PM<sub>2.5</sub> exposures were associated with a lower incidence of dyslipidemia. Although an increase in habitual exercise slightly increased the risk of dyslipidemia associated with PM<sub>2.5</sub> exposure, the benefits of the increased habitual exercise outweighed the risks. Our findings suggest that habitual exercise is an effective approach for dyslipidemia prevention, even for people residing in relatively polluted areas.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e190"},"PeriodicalIF":3.6,"publicationDate":"2022-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a4/99/ee9-6-e190.PMC8835602.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39926771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Estimating long-term average household air pollution concentrations from repeated short-term measurements in the presence of seasonal trends and crossover. 在季节性趋势和交叉存在的情况下,通过重复短期测量估算长期平均家庭空气污染浓度。
IF 3.6 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2021-12-20 eCollection Date: 2022-02-01 DOI: 10.1097/EE9.0000000000000188
Joshua P Keller, Maggie L Clark

Estimating long-term exposure to household air pollution is essential for quantifying health effects of chronic exposure and the benefits of intervention strategies. However, typically only a small number of short-term measurements are made. We compare different statistical models for combining these short-term measurements into predictions of a long-term average, with emphasis on the impact of temporal trends in concentrations and crossover in study design. We demonstrate that a linear mixed model that includes time adjustment provides the best predictions of long-term average, which have lower error than using household averages or mixed models without time, for a variety of different study designs and underlying temporal trends. In a case study of a cookstove intervention study in Honduras, we further demonstrate how, in the presence of strong seasonal variation, long-term average predictions from the mixed model approach based on only two or three measurements can have less error than predictions based on an average of up to six measurements. These results have important implications for the efficiency of designs and analyses in studies assessing the chronic health impacts of long-term exposure to household air pollution.

估计长期暴露于室内空气污染对于量化长期暴露对健康的影响和干预策略的益处至关重要。然而,通常只进行少量的短期测量。我们比较了不同的统计模型,将这些短期测量结合到长期平均值的预测中,重点是浓度的时间趋势的影响和研究设计中的交叉。我们证明,对于各种不同的研究设计和潜在的时间趋势,包括时间调整的线性混合模型提供了长期平均值的最佳预测,其误差低于使用家庭平均值或不含时间的混合模型。在洪都拉斯炉灶干预研究的案例研究中,我们进一步证明,在存在强烈季节性变化的情况下,仅基于两个或三个测量的混合模型方法的长期平均预测如何比基于多达六个测量的平均预测误差更小。这些结果对评估长期暴露于室内空气污染的慢性健康影响的研究的设计和分析的效率具有重要意义。
{"title":"Estimating long-term average household air pollution concentrations from repeated short-term measurements in the presence of seasonal trends and crossover.","authors":"Joshua P Keller,&nbsp;Maggie L Clark","doi":"10.1097/EE9.0000000000000188","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000188","url":null,"abstract":"<p><p>Estimating long-term exposure to household air pollution is essential for quantifying health effects of chronic exposure and the benefits of intervention strategies. However, typically only a small number of short-term measurements are made. We compare different statistical models for combining these short-term measurements into predictions of a long-term average, with emphasis on the impact of temporal trends in concentrations and crossover in study design. We demonstrate that a linear mixed model that includes time adjustment provides the best predictions of long-term average, which have lower error than using household averages or mixed models without time, for a variety of different study designs and underlying temporal trends. In a case study of a cookstove intervention study in Honduras, we further demonstrate how, in the presence of strong seasonal variation, long-term average predictions from the mixed model approach based on only two or three measurements can have less error than predictions based on an average of up to six measurements. These results have important implications for the efficiency of designs and analyses in studies assessing the chronic health impacts of long-term exposure to household air pollution.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e188"},"PeriodicalIF":3.6,"publicationDate":"2021-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/7d/cb/ee9-6-e188.PMC8835562.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39926769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 4
Early environmental quality and life-course mental health effects: The Equal-Life project. 早期环境质量和终生心理健康影响:平等生活项目。
IF 3.6 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2021-12-16 eCollection Date: 2022-02-01 DOI: 10.1097/EE9.0000000000000183
Irene van Kamp, Kerstin Persson Waye, Katja Kanninen, John Gulliver, Alessandro Bozzon, Achilleas Psyllidis, Hendriek Boshuizen, Jenny Selander, Peter van den Hazel, Marco Brambilla, Maria Foraster, Jordi Julvez, Maria Klatte, Sonja Jeram, Peter Lercher, Dick Botteldooren, Gordana Ristovska, Jaakko Kaprio, Dirk Schreckenberg, Maarten Hornikx, Janina Fels, Miriam Weber, Ella Braat-Eggen, Julia Hartmann, Charlotte Clark, Tanja Vrijkotte, Lex Brown, Gabriele Bolte

Background: There is increasing evidence that a complex interplay of factors within environments in which children grows up, contributes to children's suboptimal mental health and cognitive development. The concept of the life-course exposome helps to study the impact of the physical and social environment, including social inequities, on cognitive development and mental health over time.

Methods: Equal-Life develops and tests combined exposures and their effects on children's mental health and cognitive development. Data from eight birth-cohorts and three school studies (N = 240.000) linked to exposure data, will provide insights and policy guidance into aspects of physical and social exposures hitherto untapped, at different scale levels and timeframes, while accounting for social inequities. Reasoning from the outcome point of view, relevant stakeholders participate in the formulation and validation of research questions, and in the formulation of environmental hazards. Exposure assessment combines GIS-based environmental indicators with omics approaches and new data sources, forming the early-life exposome. Statistical tools integrate data at different spatial and temporal granularity and combine exploratory machine learning models with hypothesis-driven causal modeling.

Conclusions: Equal-Life contributes to the development and utilization of the exposome concept by (1) integrating the internal, physical and social exposomes, (2) studying a distinct set of life-course effects on a child's development and mental health (3) characterizing the child's environment at different developmental stages and in different activity spaces, (4) looking at supportive environments for child development, rather than merely pollutants, and (5) combining physical, social indicators with novel effect markers and using new data sources describing child activity patterns and environments.

背景:越来越多的证据表明,儿童成长环境中各种因素的复杂相互作用,导致儿童的心理健康和认知发展欠佳。终生接触的概念有助于研究物质和社会环境,包括社会不平等,对长期认知发展和心理健康的影响。方法:平等生活开发和测试综合暴露及其对儿童心理健康和认知发展的影响。来自8个出生队列和3个学校研究(N = 24万)的数据与暴露数据相关联,将为迄今尚未开发的不同规模水平和时间框架的身体和社会暴露方面提供见解和政策指导,同时考虑到社会不平等。从结果的角度推理,相关利益相关者参与研究问题的制定和验证,并参与环境危害的制定。暴露评估将基于gis的环境指标与组学方法和新数据源相结合,形成了生命早期暴露。统计工具集成了不同时空粒度的数据,并将探索性机器学习模型与假设驱动的因果模型相结合。结论:平等生活通过以下方式促进暴露体概念的发展和利用:(1)整合内部、身体和社会暴露体;(2)研究对儿童发展和心理健康的一套不同的生命历程影响;(3)描述儿童在不同发展阶段和不同活动空间的环境特征;(4)关注儿童发展的支持性环境,而不仅仅是污染物;具有新颖效果标记的社会指标,并使用新的数据来源描述儿童活动模式和环境。
{"title":"Early environmental quality and life-course mental health effects: The Equal-Life project.","authors":"Irene van Kamp,&nbsp;Kerstin Persson Waye,&nbsp;Katja Kanninen,&nbsp;John Gulliver,&nbsp;Alessandro Bozzon,&nbsp;Achilleas Psyllidis,&nbsp;Hendriek Boshuizen,&nbsp;Jenny Selander,&nbsp;Peter van den Hazel,&nbsp;Marco Brambilla,&nbsp;Maria Foraster,&nbsp;Jordi Julvez,&nbsp;Maria Klatte,&nbsp;Sonja Jeram,&nbsp;Peter Lercher,&nbsp;Dick Botteldooren,&nbsp;Gordana Ristovska,&nbsp;Jaakko Kaprio,&nbsp;Dirk Schreckenberg,&nbsp;Maarten Hornikx,&nbsp;Janina Fels,&nbsp;Miriam Weber,&nbsp;Ella Braat-Eggen,&nbsp;Julia Hartmann,&nbsp;Charlotte Clark,&nbsp;Tanja Vrijkotte,&nbsp;Lex Brown,&nbsp;Gabriele Bolte","doi":"10.1097/EE9.0000000000000183","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000183","url":null,"abstract":"<p><strong>Background: </strong>There is increasing evidence that a complex interplay of factors within environments in which children grows up, contributes to children's suboptimal mental health and cognitive development. The concept of the life-course exposome helps to study the impact of the physical and social environment, including social inequities, on cognitive development and mental health over time.</p><p><strong>Methods: </strong>Equal-Life develops and tests combined exposures and their effects on children's mental health and cognitive development. Data from eight birth-cohorts and three school studies (N = 240.000) linked to exposure data, will provide insights and policy guidance into aspects of physical and social exposures hitherto untapped, at different scale levels and timeframes, while accounting for social inequities. Reasoning from the outcome point of view, relevant stakeholders participate in the formulation and validation of research questions, and in the formulation of environmental hazards. Exposure assessment combines GIS-based environmental indicators with omics approaches and new data sources, forming the early-life exposome. Statistical tools integrate data at different spatial and temporal granularity and combine exploratory machine learning models with hypothesis-driven causal modeling.</p><p><strong>Conclusions: </strong>Equal-Life contributes to the development and utilization of the exposome concept by (1) integrating the internal, physical and social exposomes, (2) studying a distinct set of life-course effects on a child's development and mental health (3) characterizing the child's environment at different developmental stages and in different activity spaces, (4) looking at supportive environments for child development, rather than merely pollutants, and (5) combining physical, social indicators with novel effect markers and using new data sources describing child activity patterns and environments.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e183"},"PeriodicalIF":3.6,"publicationDate":"2021-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/91/af/ee9-6-e183.PMC8835570.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39624143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 11
The destruction of Gaza's infrastructure is exacerbating environmental health impacts. 加沙基础设施的破坏加剧了对环境健康的影响。
IF 3.6 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2021-12-16 eCollection Date: 2022-02-01 DOI: 10.1097/EE9.0000000000000186
Adnan Al-Hindi, Amira Aker, Wael K Al-Delaimy
{"title":"The destruction of Gaza's infrastructure is exacerbating environmental health impacts.","authors":"Adnan Al-Hindi,&nbsp;Amira Aker,&nbsp;Wael K Al-Delaimy","doi":"10.1097/EE9.0000000000000186","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000186","url":null,"abstract":"","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e186"},"PeriodicalIF":3.6,"publicationDate":"2021-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/1d/9b/ee9-6-e186.PMC8835639.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39624142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
The influence of outdoor PM2.5 concentration at workplace on nonaccidental mortality estimates in a Canadian census-based cohort. 工作场所室外PM2.5浓度对加拿大人口普查队列中非意外死亡率估计的影响。
IF 3.6 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2021-12-03 eCollection Date: 2021-12-01 DOI: 10.1097/EE9.0000000000000180
Tanya Christidis, Lauren L Pinault, Dan L Crouse, Michael Tjepkema

Background: Associations between mortality and exposure to ambient air pollution are usually explored using concentrations of residential outdoor fine particulate matter (PM2.5) to estimate individual exposure. Such studies all have an important limitation in that they do not capture data on individual mobility throughout the day to areas where concentrations may be substantially different, leading to possible exposure misclassification. We examine the possible role of outdoor PM2.5 concentrations at work for a large population-based mortality cohort.

Methods: Using the 2001 Canadian Census Health and Environment Cohort (CanCHEC), we created a time-weighted average that incorporates employment hours worked in the past week and outdoor PM2.5 concentration at work and home. We used a Cox proportional hazard model with a 15-year follow-up (2001 to 2016) to explore whether inclusion of workplace estimates had an impact on hazard ratios for mortality for this cohort.

Results: Hazard ratios relying on outdoor PM2.5 concentration at home were not significantly different from those using a time-weighted estimate, for the full cohort, nor for those who commute to a regular workplace. When exploring cohort subgroups according to neighborhood type and commute distance, there was a notable but insignificant change in risk of nonaccidental death for those living in car-oriented neighborhoods, and with commutes greater than 10 km.

Conclusions: Risk analyses performed with large cohorts in low-pollution environments do not seem to be biased if relying solely on outdoor PM2.5 concentrations at home to estimate exposure.

背景:死亡率与暴露于环境空气污染之间的关系通常通过住宅室外细颗粒物(PM2.5)浓度来评估个体暴露。这些研究都有一个重要的局限性,因为它们没有捕捉到个人全天在浓度可能有很大差异的地区的流动性数据,从而可能导致暴露错误分类。我们研究了室外PM2.5浓度在工作场所对大型人群死亡率队列的可能作用。方法:利用2001年加拿大人口普查健康与环境队列(CanCHEC),我们创建了一个时间加权平均值,其中包括过去一周的工作时间和工作场所和家中的室外PM2.5浓度。我们使用Cox比例风险模型进行了为期15年的随访(2001年至2016年),以探讨纳入工作场所评估是否对该队列的死亡率风险比产生影响。结果:在整个队列中,依赖于家中室外PM2.5浓度的风险比与使用时间加权估计的风险比没有显著差异,对于那些通勤到常规工作场所的人也是如此。当根据社区类型和通勤距离探索队列亚组时,居住在以汽车为导向的社区和通勤距离大于10公里的人群的非意外死亡风险有显著但不显著的变化。结论:在低污染环境中对大量人群进行的风险分析,如果仅仅依靠家中室外PM2.5浓度来估计暴露量,似乎并不存在偏差。
{"title":"The influence of outdoor PM<sub>2.5</sub> concentration at workplace on nonaccidental mortality estimates in a Canadian census-based cohort.","authors":"Tanya Christidis,&nbsp;Lauren L Pinault,&nbsp;Dan L Crouse,&nbsp;Michael Tjepkema","doi":"10.1097/EE9.0000000000000180","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000180","url":null,"abstract":"<p><strong>Background: </strong>Associations between mortality and exposure to ambient air pollution are usually explored using concentrations of residential outdoor fine particulate matter (PM<sub>2.5</sub>) to estimate individual exposure. Such studies all have an important limitation in that they do not capture data on individual mobility throughout the day to areas where concentrations may be substantially different, leading to possible exposure misclassification. We examine the possible role of outdoor PM<sub>2.5</sub> concentrations at work for a large population-based mortality cohort.</p><p><strong>Methods: </strong>Using the 2001 Canadian Census Health and Environment Cohort (CanCHEC), we created a time-weighted average that incorporates employment hours worked in the past week and outdoor PM<sub>2.5</sub> concentration at work and home. We used a Cox proportional hazard model with a 15-year follow-up (2001 to 2016) to explore whether inclusion of workplace estimates had an impact on hazard ratios for mortality for this cohort.</p><p><strong>Results: </strong>Hazard ratios relying on outdoor PM<sub>2.5</sub> concentration at home were not significantly different from those using a time-weighted estimate, for the full cohort, nor for those who commute to a regular workplace. When exploring cohort subgroups according to neighborhood type and commute distance, there was a notable but insignificant change in risk of nonaccidental death for those living in car-oriented neighborhoods, and with commutes greater than 10 km.</p><p><strong>Conclusions: </strong>Risk analyses performed with large cohorts in low-pollution environments do not seem to be biased if relying solely on outdoor PM<sub>2.5</sub> concentrations at home to estimate exposure.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e180"},"PeriodicalIF":3.6,"publicationDate":"2021-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/13/86/ee9-5-e180.PMC8663884.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39589214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Epidemiology and biological plausibility in assessing causality. 评价因果关系的流行病学和生物学合理性。
IF 3.6 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2021-11-11 eCollection Date: 2021-12-01 DOI: 10.1097/EE9.0000000000000177
David A Savitz
One of the well-accepted principles of epidemiology is the need to draw upon ancillary evidence from biological research in the selection of topics to pursue, design of studies, and especially, the interpretation of the results. In environmental epidemiology, understanding the biological pathways by which the exposure of concern may affect health often has a great value in framing research questions and guiding the studies that are done but calls for deeper reflection of how that ancillary biological information should (and should not) be used. Biological evidence of potential health harm may motivate epidemiologic studies and help to guide exposure assessment to maximize the likelihood of identifying an etiologic relationship if one is present. Decisions regarding exposure aggregation (lumping or splitting), duration of exposure, the timing of exposure in relation to disease occurrence, exploration of dose-response patterns (thresholds and ceilings), and other chemical and physical features of exposure to be examined in epidemiologic studies benefit from drawing on knowledge from pertinent biological research. Similarly, the choice of specific disease entities should be informed by knowledge of biological mechanisms in the analogous decisions regarding grouping, timing of onset, distinctive features of the disease (e.g., subsets of cancer with a shared etiology), and clinical manifestations. Markers of susceptibility that could result in effect-modification may be gleaned from biological research as well as candidate confounders. The product of this knowledge drawn from work done in other fields, if considered in advance, is an enhanced ability to design and conduct epidemiologic studies in which the measure of association is most likely to identify any causal effects that are present, that is, more valid studies. If positive or negative associations are found, they would be seen as concordant with expectations based on biology and if null associations are found, this would provide meaningful evidence that the plausible etiologic relationship is not likely to be present. But the dividing line between using biological evidence to optimize the design of studies and the use of biological evidence to render a verdict on the validity of the study calls for a closer look. The consideration of biological plausibility in the interpretation of the study results, as advocated by Sir Austin Bradford Hill1 raises some concerns when considering why measured associations may or may not reflect a causal effect. To the extent that the epidemiologic research is informed by sound biological insights, we will benefit from having focused on the most pertinent exposure and disease measures, minimizing exposure and disease misclassification, and isolating the most highly susceptible subgroups. Once we have gleaned all that we can from ancillary biological research on the topic, however, the epidemiologic study must stand on its merits in order to approximate the caus
{"title":"Epidemiology and biological plausibility in assessing causality.","authors":"David A Savitz","doi":"10.1097/EE9.0000000000000177","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000177","url":null,"abstract":"One of the well-accepted principles of epidemiology is the need to draw upon ancillary evidence from biological research in the selection of topics to pursue, design of studies, and especially, the interpretation of the results. In environmental epidemiology, understanding the biological pathways by which the exposure of concern may affect health often has a great value in framing research questions and guiding the studies that are done but calls for deeper reflection of how that ancillary biological information should (and should not) be used. Biological evidence of potential health harm may motivate epidemiologic studies and help to guide exposure assessment to maximize the likelihood of identifying an etiologic relationship if one is present. Decisions regarding exposure aggregation (lumping or splitting), duration of exposure, the timing of exposure in relation to disease occurrence, exploration of dose-response patterns (thresholds and ceilings), and other chemical and physical features of exposure to be examined in epidemiologic studies benefit from drawing on knowledge from pertinent biological research. Similarly, the choice of specific disease entities should be informed by knowledge of biological mechanisms in the analogous decisions regarding grouping, timing of onset, distinctive features of the disease (e.g., subsets of cancer with a shared etiology), and clinical manifestations. Markers of susceptibility that could result in effect-modification may be gleaned from biological research as well as candidate confounders. The product of this knowledge drawn from work done in other fields, if considered in advance, is an enhanced ability to design and conduct epidemiologic studies in which the measure of association is most likely to identify any causal effects that are present, that is, more valid studies. If positive or negative associations are found, they would be seen as concordant with expectations based on biology and if null associations are found, this would provide meaningful evidence that the plausible etiologic relationship is not likely to be present. But the dividing line between using biological evidence to optimize the design of studies and the use of biological evidence to render a verdict on the validity of the study calls for a closer look. The consideration of biological plausibility in the interpretation of the study results, as advocated by Sir Austin Bradford Hill1 raises some concerns when considering why measured associations may or may not reflect a causal effect. To the extent that the epidemiologic research is informed by sound biological insights, we will benefit from having focused on the most pertinent exposure and disease measures, minimizing exposure and disease misclassification, and isolating the most highly susceptible subgroups. Once we have gleaned all that we can from ancillary biological research on the topic, however, the epidemiologic study must stand on its merits in order to approximate the caus","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e177"},"PeriodicalIF":3.6,"publicationDate":"2021-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8663842/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39589211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Ambient temperature and stillbirth risks in northern Sweden, 1880-1950. 1880-1950年瑞典北部的环境温度和死产风险。
IF 3.6 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2021-11-04 eCollection Date: 2021-12-01 DOI: 10.1097/EE9.0000000000000176
Lena Karlsson, Johan Junkka, Erling Häggström Lundevaller, Barbara Schumann

Background: Climate vulnerability of the unborn can contribute to adverse birth outcomes, in particular, but it is still not well understood. We investigated the association between ambient temperature and stillbirth risk among a historical population in northern Sweden (1880-1950).

Methods: We used digitized parish records and daily temperature data from the study region covering coastal and inland communities some 600 km north of Stockholm, Sweden. The data included 141,880 births, and 3,217 stillbirths, corresponding to a stillbirth rate of 22.7 (1880-1950). The association between lagged temperature (0-7 days before birth) and stillbirths was estimated using a time-stratified case-crossover design. Incidence risk ratios (IRR) with 95% confidence intervals were computed, and stratified by season and sex.

Results: We observed that the stillbirth risk increased both at low and high temperatures during the extended summer season (April to September), at -10°C, and the IRR was 2.3 (CI 1.28, 4.00) compared to the minimum mortality temperature of +15°C. No clear effect of temperature during the extended winter season (October to March) was found. Climate vulnerability was greater among the male fetus compared to the female counterparts.

Conclusion: In this subarctic setting before and during industrialization, both heat and cold during the warmer season increased the stillbirth risk. Urbanization and socio-economic development might have contributed to an uneven decline in climate vulnerability of the unborn.

背景:未出生胎儿的气候脆弱性尤其可能导致不良的出生结果,但人们对其仍未充分了解。我们调查了瑞典北部历史人口(1880-1950)环境温度与死产风险之间的关系。方法:我们使用数字化教区记录和来自瑞典斯德哥尔摩北部约600公里的沿海和内陆社区的日温度数据。数据包括141880例新生儿和3217例死产,对应的死产率为22.7%(1880-1950)。使用时间分层病例交叉设计估计滞后温度(出生前0-7天)与死产之间的关系。计算95%置信区间的发病率风险比(IRR),并按季节和性别分层。结果:我们观察到,在延长的夏季(4月至9月),在-10°C的低温和高温下,死产风险均增加,与+15°C的最低死亡温度相比,IRR为2.3 (CI 1.28, 4.00)。在延长的冬季(10月至3月),温度没有明显的影响。与女性胎儿相比,男性胎儿的气候脆弱性更大。结论:在工业化前和工业化期间的亚北极环境中,温暖季节的高温和低温都增加了死胎的风险。城市化和社会经济发展可能导致未出生婴儿气候脆弱性的不均衡下降。
{"title":"Ambient temperature and stillbirth risks in northern Sweden, 1880-1950.","authors":"Lena Karlsson,&nbsp;Johan Junkka,&nbsp;Erling Häggström Lundevaller,&nbsp;Barbara Schumann","doi":"10.1097/EE9.0000000000000176","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000176","url":null,"abstract":"<p><strong>Background: </strong>Climate vulnerability of the unborn can contribute to adverse birth outcomes, in particular, but it is still not well understood. We investigated the association between ambient temperature and stillbirth risk among a historical population in northern Sweden (1880-1950).</p><p><strong>Methods: </strong>We used digitized parish records and daily temperature data from the study region covering coastal and inland communities some 600 km north of Stockholm, Sweden. The data included 141,880 births, and 3,217 stillbirths, corresponding to a stillbirth rate of 22.7 (1880-1950). The association between lagged temperature (0-7 days before birth) and stillbirths was estimated using a time-stratified case-crossover design. Incidence risk ratios (IRR) with 95% confidence intervals were computed, and stratified by season and sex.</p><p><strong>Results: </strong>We observed that the stillbirth risk increased both at low and high temperatures during the extended summer season (April to September), at -10°C, and the IRR was 2.3 (CI 1.28, 4.00) compared to the minimum mortality temperature of +15°C. No clear effect of temperature during the extended winter season (October to March) was found. Climate vulnerability was greater among the male fetus compared to the female counterparts.</p><p><strong>Conclusion: </strong>In this subarctic setting before and during industrialization, both heat and cold during the warmer season increased the stillbirth risk. Urbanization and socio-economic development might have contributed to an uneven decline in climate vulnerability of the unborn.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e176"},"PeriodicalIF":3.6,"publicationDate":"2021-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/27/10/ee9-5-e176.PMC8663868.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39589210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
Ambient air pollution associated with lower academic achievement among US children: A nationwide panel study of school districts. 环境空气污染与美国儿童较低的学习成绩有关:一项全国学区小组研究。
IF 3.6 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2021-11-03 eCollection Date: 2021-12-01 DOI: 10.1097/EE9.0000000000000174
Wenxin Lu, Daniel A Hackman, Joel Schwartz

Background: Ambient air pollution is an important environmental exposure and has been linked with impaired cognitive function. Few studies have investigated its impact on children's academic performance on a nationwide level. We hypothesize that higher ambient air pollution concentrations will be associated with lower average academic test scores.

Methods: We investigated three prevalent ambient air pollutants: PM2.5, NO2 and ozone, and their associations with the average academic test scores, at the Geographic School District (GSD) level, of the third to eighth grade students in the United States from 2010 to 2016. We applied multivariate linear regression and controlled for urbanicity, socioeconomic status, student racial/ethnic compositions, and individual intercepts for each district-grade level and each year.

Results: We found that an interquartile range increase in PM2.5 concentrations was associated with a 0.007 (95% confidence interval: 0.005, 0.009) SD lower average math test scores, and a 0.004 (95% confidence interval: 0.002, 0.005) SD lower average English language/arts test scores. Similar associations were observed for NO2 and ozone on math, and for NO2 on English language/arts. The magnitudes of these associations are equivalent to the effects of short-term reductions of thousands of dollars in district median household income. The reductions in test scores were larger for GSDs with higher socioeconomic status, though most associations remained negative at all socioeconomic levels.

Conclusions: Our results show that ambient air pollution within a GSD is associated with lower academic performance among children. Further improving air quality may benefit children's overall academic achievement and socioeconomic attainment across the lifespan.

背景:环境空气污染是一种重要的环境暴露,与认知功能受损有关。很少有研究在全国范围内调查它对儿童学习成绩的影响。我们假设较高的环境空气污染浓度与较低的平均学业考试成绩有关。方法:我们调查了三种常见的环境空气污染物:PM2.5、NO2和臭氧,以及它们与2010年至2016年美国地理学区(GSD)水平三至八年级学生平均学业考试成绩的关系。我们应用了多元线性回归,并控制了城市化程度、社会经济地位、学生种族/民族组成和每个地区年级水平和每年的个人截距。结果:我们发现PM2.5浓度的四分位数范围增加与平均数学考试成绩降低0.007(95%置信区间:0.005,0.009)个标准差相关,与平均英语语言/艺术考试成绩降低0.004(95%置信区间:0.002,0.005)个标准差相关。在数学和英语语言/艺术方面,二氧化氮和臭氧也观察到类似的关联。这些关联的程度相当于地区家庭收入中位数短期减少数千美元的影响。在社会经济地位较高的gsd中,考试成绩的下降幅度更大,尽管在所有社会经济水平上大多数关联仍然是负相关的。结论:我们的研究结果表明,GSD内的环境空气污染与儿童较低的学习成绩有关。进一步改善空气质量可能有利于儿童一生的整体学业成绩和社会经济成就。
{"title":"Ambient air pollution associated with lower academic achievement among US children: A nationwide panel study of school districts.","authors":"Wenxin Lu,&nbsp;Daniel A Hackman,&nbsp;Joel Schwartz","doi":"10.1097/EE9.0000000000000174","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000174","url":null,"abstract":"<p><strong>Background: </strong>Ambient air pollution is an important environmental exposure and has been linked with impaired cognitive function. Few studies have investigated its impact on children's academic performance on a nationwide level. We hypothesize that higher ambient air pollution concentrations will be associated with lower average academic test scores.</p><p><strong>Methods: </strong>We investigated three prevalent ambient air pollutants: PM<sub>2.5</sub>, NO<sub>2</sub> and ozone, and their associations with the average academic test scores, at the Geographic School District (GSD) level, of the third to eighth grade students in the United States from 2010 to 2016. We applied multivariate linear regression and controlled for urbanicity, socioeconomic status, student racial/ethnic compositions, and individual intercepts for each district-grade level and each year.</p><p><strong>Results: </strong>We found that an interquartile range increase in PM<sub>2.5</sub> concentrations was associated with a 0.007 (95% confidence interval: 0.005, 0.009) SD lower average math test scores, and a 0.004 (95% confidence interval: 0.002, 0.005) SD lower average English language/arts test scores. Similar associations were observed for NO<sub>2</sub> and ozone on math, and for NO<sub>2</sub> on English language/arts. The magnitudes of these associations are equivalent to the effects of short-term reductions of thousands of dollars in district median household income. The reductions in test scores were larger for GSDs with higher socioeconomic status, though most associations remained negative at all socioeconomic levels.</p><p><strong>Conclusions: </strong>Our results show that ambient air pollution within a GSD is associated with lower academic performance among children. Further improving air quality may benefit children's overall academic achievement and socioeconomic attainment across the lifespan.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e174"},"PeriodicalIF":3.6,"publicationDate":"2021-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/56/8b/ee9-5-e174.PMC8663889.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39589209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 6
期刊
Environmental Epidemiology
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1