Pub Date : 2024-06-21eCollection Date: 2024-08-01DOI: 10.1097/EE9.0000000000000316
Megan G Bragg, Irena Gorski-Steiner, Ashley Song, Jorge E Chavarro, Jaime E Hart, Loni P Tabb, Marc G Weisskopf, Heather Volk, Kristen Lyall
Background: Maternal nutrient intake may moderate associations between environmental exposures and children's neurodevelopmental outcomes, but few studies have assessed joint effects. We aimed to evaluate whether prenatal nutrient intake influences the association between air pollutants and autism-related trait scores.
Methods: We included 126 participants from the EARLI (Early Autism Risk Longitudinal Investigation, 2009-2012) cohort, which followed US pregnant mothers who previously had a child with autism. Bayesian kernel machine regression and traditional regression models were used to examine joint associations of prenatal nutrient intake (vitamins D, B12, and B6; folate, choline, and betaine; and total omega 3 and 6 polyunsaturated fatty acids, reported via food frequency questionnaire), air pollutant exposure (particulate matter <2.5 μm [PM2.5], nitrogen dioxide [NO2], and ozone [O3], estimated at the address level), and children's autism-related traits (measured by the Social Responsiveness Scale [SRS] at 36 months).
Results: Most participants had nutrient intakes and air pollutant exposures that met US standards. Bayesian kernel machine regression mixture models and traditional regression models provided little evidence of individual or joint associations of nutrients and air pollutants with SRS scores or of an association between the overall mixture and SRS scores.
Conclusion: In this cohort with a high familial likelihood of autism, we did not observe evidence of joint associations between air pollution exposures and nutrient intake with autism-related traits. Future work should examine the use of these methods in larger, more diverse samples, as our results may have been influenced by familial liability and/or relatively high nutrient intakes and low air pollutant exposures.
{"title":"Prenatal air pollution and children's autism traits score: Examination of joint associations with maternal intake of vitamin D, methyl donors, and polyunsaturated fatty acids using mixture methods.","authors":"Megan G Bragg, Irena Gorski-Steiner, Ashley Song, Jorge E Chavarro, Jaime E Hart, Loni P Tabb, Marc G Weisskopf, Heather Volk, Kristen Lyall","doi":"10.1097/EE9.0000000000000316","DOIUrl":"10.1097/EE9.0000000000000316","url":null,"abstract":"<p><strong>Background: </strong>Maternal nutrient intake may moderate associations between environmental exposures and children's neurodevelopmental outcomes, but few studies have assessed joint effects. We aimed to evaluate whether prenatal nutrient intake influences the association between air pollutants and autism-related trait scores.</p><p><strong>Methods: </strong>We included 126 participants from the EARLI (Early Autism Risk Longitudinal Investigation, 2009-2012) cohort, which followed US pregnant mothers who previously had a child with autism. Bayesian kernel machine regression and traditional regression models were used to examine joint associations of prenatal nutrient intake (vitamins D, B12, and B6; folate, choline, and betaine; and total omega 3 and 6 polyunsaturated fatty acids, reported via food frequency questionnaire), air pollutant exposure (particulate matter <2.5 μm [PM<sub>2.5</sub>], nitrogen dioxide [NO<sub>2</sub>], and ozone [O<sub>3</sub>], estimated at the address level), and children's autism-related traits (measured by the Social Responsiveness Scale [SRS] at 36 months).</p><p><strong>Results: </strong>Most participants had nutrient intakes and air pollutant exposures that met US standards. Bayesian kernel machine regression mixture models and traditional regression models provided little evidence of individual or joint associations of nutrients and air pollutants with SRS scores or of an association between the overall mixture and SRS scores.</p><p><strong>Conclusion: </strong>In this cohort with a high familial likelihood of autism, we did not observe evidence of joint associations between air pollution exposures and nutrient intake with autism-related traits. Future work should examine the use of these methods in larger, more diverse samples, as our results may have been influenced by familial liability and/or relatively high nutrient intakes and low air pollutant exposures.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"8 4","pages":"e316"},"PeriodicalIF":3.3,"publicationDate":"2024-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11196080/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141450140","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}
Pub Date : 2024-06-04eCollection Date: 2024-06-01DOI: 10.1097/EE9.0000000000000313
Stephanie Tuminello, Yibeltal Arega Ashebir, Chanel Schroff, Sitharam Ramaswami, Nedim Durmus, Yu Chen, Matija Snuderl, Yongzhao Shao, Joan Reibman, Alan A Arslan
Background: Increased incidence of cancer has been reported among World Trade Center (WTC)-exposed persons. Aberrant DNA methylation is a hallmark of cancer development. To date, only a few small studies have investigated the relationship between WTC exposure and DNA methylation. The main objective of this study was to assess the DNA methylation profiles of WTC-exposed community members who remained cancer free and those who developed breast cancer.
Methods: WTC-exposed women were selected from the WTC Environmental Health Center clinic, with peripheral blood collected during routine clinical monitoring visits. The reference group was selected from the NYU Women's Health Study, a prospective cohort study with blood samples collected before 9 November 2001. The Infinium MethylationEPIC array was used for global DNA methylation profiling, with adjustments for cell type composition and other confounders. Annotated probes were used for biological pathway and network analysis.
Results: A total of 64 WTC-exposed (32 cancer free and 32 with breast cancer) and 32 WTC-unexposed (16 cancer free and 16 with prediagnostic breast cancer) participants were included. Hypermethylated cytosine-phosphate-guanine probe sites (defined as β > 0.8) were more common among WTC-exposed versus unexposed participants (14.3% vs. 4.5%, respectively, among the top 5000 cytosine-phosphate-guanine sites). Cancer-related pathways (e.g., human papillomavirus infection, cGMP-PKG) were overrepresented in WTC-exposed groups (breast cancer patients and cancer-free subjects). Compared to the unexposed breast cancer patients, 47 epigenetically dysregulated genes were identified among WTC-exposed breast cancers. These genes formed a network, including Wnt/β-catenin signaling genes WNT4 and TCF7L2, and dysregulation of these genes contributes to cancer immune evasion.
Conclusion: WTC exposure likely impacts DNA methylation and may predispose exposed individuals toward cancer development, possibly through an immune-mediated mechanism.
背景:据报道,受世界贸易中心(WTC)影响的人群癌症发病率增加。DNA 甲基化异常是癌症发展的一个标志。迄今为止,只有少数几项小型研究调查了世贸中心暴露与 DNA 甲基化之间的关系。本研究的主要目的是评估受世界贸易中心影响的社区成员中未患癌症者和患乳腺癌者的 DNA 甲基化情况:方法:从世界贸易中心环境健康中心诊所选取受世界贸易中心影响的妇女,在常规临床监测访问中采集外周血。参照组选自纽约大学妇女健康研究(NYU Women's Health Study),该研究是一项前瞻性队列研究,在 2001 年 11 月 9 日前采集血样。Infinium MethylationEPIC 阵列用于全局 DNA 甲基化分析,并对细胞类型组成和其他混杂因素进行了调整。注释探针用于生物通路和网络分析:共纳入了 64 名接触过世界贸易中心的参与者(32 人未患癌症,32 人患有乳腺癌)和 32 名未接触过世界贸易中心的参与者(16 人未患癌症,16 人患有诊断前乳腺癌)。高甲基化胞嘧啶-磷酸鸟嘌呤探针位点(定义为β > 0.8)在暴露于 WTC 的参与者中比未暴露于 WTC 的参与者中更为常见(在前 5000 个胞嘧啶-磷酸鸟嘌呤位点中分别为 14.3% 和 4.5%)。与癌症相关的途径(如人类乳头瘤病毒感染、cGMP-PKG)在受到 WTC 暴露的群体(乳腺癌患者和无癌症受试者)中所占比例过高。与未暴露的乳腺癌患者相比,暴露于 WTC 的乳腺癌患者中发现了 47 个表观遗传失调基因。这些基因形成了一个网络,其中包括Wnt/β-catenin信号基因WNT4和TCF7L2,这些基因的失调有助于癌症免疫逃避:结论:接触世界贸易中心可能会影响 DNA 甲基化,并可能通过免疫介导机制使接触者易患癌症。
{"title":"Genome-wide DNA methylation profiles and breast cancer among World Trade Center survivors.","authors":"Stephanie Tuminello, Yibeltal Arega Ashebir, Chanel Schroff, Sitharam Ramaswami, Nedim Durmus, Yu Chen, Matija Snuderl, Yongzhao Shao, Joan Reibman, Alan A Arslan","doi":"10.1097/EE9.0000000000000313","DOIUrl":"10.1097/EE9.0000000000000313","url":null,"abstract":"<p><strong>Background: </strong>Increased incidence of cancer has been reported among World Trade Center (WTC)-exposed persons. Aberrant DNA methylation is a hallmark of cancer development. To date, only a few small studies have investigated the relationship between WTC exposure and DNA methylation. The main objective of this study was to assess the DNA methylation profiles of WTC-exposed community members who remained cancer free and those who developed breast cancer.</p><p><strong>Methods: </strong>WTC-exposed women were selected from the WTC Environmental Health Center clinic, with peripheral blood collected during routine clinical monitoring visits. The reference group was selected from the NYU Women's Health Study, a prospective cohort study with blood samples collected before 9 November 2001. The Infinium MethylationEPIC array was used for global DNA methylation profiling, with adjustments for cell type composition and other confounders. Annotated probes were used for biological pathway and network analysis.</p><p><strong>Results: </strong>A total of 64 WTC-exposed (32 cancer free and 32 with breast cancer) and 32 WTC-unexposed (16 cancer free and 16 with prediagnostic breast cancer) participants were included. Hypermethylated cytosine-phosphate-guanine probe sites (defined as <i>β</i> > 0.8) were more common among WTC-exposed versus unexposed participants (14.3% vs. 4.5%, respectively, among the top 5000 cytosine-phosphate-guanine sites). Cancer-related pathways (e.g., human papillomavirus infection, cGMP-PKG) were overrepresented in WTC-exposed groups (breast cancer patients and cancer-free subjects). Compared to the unexposed breast cancer patients, 47 epigenetically dysregulated genes were identified among WTC-exposed breast cancers. These genes formed a network, including Wnt/β-catenin signaling genes <i>WNT4</i> and <i>TCF7L2</i>, and dysregulation of these genes contributes to cancer immune evasion.</p><p><strong>Conclusion: </strong>WTC exposure likely impacts DNA methylation and may predispose exposed individuals toward cancer development, possibly through an immune-mediated mechanism.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"8 3","pages":"e313"},"PeriodicalIF":3.3,"publicationDate":"2024-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11152787/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141260394","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}
Pub Date : 2024-04-04eCollection Date: 2024-04-01DOI: 10.1097/EE9.0000000000000295
Kritika Anand, Gagandeep Kaur Walia, Siddhartha Mandal, Jyothi S Menon, Ruby Gupta, Nikhil Tandon, K M Venkat Narayan, Mohammed K Ali, Viswanathan Mohan, Joel D Schwartz, Dorairaj Prabhakaran
Background: Exposure to ambient PM2.5 is known to affect lipid metabolism through systemic inflammation and oxidative stress. Evidence from developing countries, such as India with high levels of ambient PM2.5 and distinct lipid profiles, is sparse.
Methods: Longitudinal nonlinear mixed-effects analysis was conducted on >10,000 participants of Centre for cArdiometabolic Risk Reduction in South Asia (CARRS) cohort in Chennai and Delhi, India. We examined associations between 1-month and 1-year average ambient PM2.5 exposure derived from the spatiotemporal model and lipid levels (total cholesterol [TC], triglycerides [TRIG], high-density lipoprotein cholesterol [HDL-C], and low-density lipoprotein cholesterol [LDL-C]) measured longitudinally, adjusting for residential and neighborhood-level confounders.
Results: The mean annual exposure in Chennai and Delhi was 40 and 102 μg/m3 respectively. Elevated ambient PM2.5 levels were associated with an increase in LDL-C and TC at levels up to 100 µg/m3 in both cities and beyond 125 µg/m3 in Delhi. TRIG levels in Chennai increased until 40 µg/m3 for both short- and long-term exposures, then stabilized or declined, while in Delhi, there was a consistent rise with increasing annual exposures. HDL-C showed an increase in both cities against monthly average exposure. HDL-C decreased slightly in Chennai with an increase in long-term exposure, whereas it decreased beyond 130 µg/m3 in Delhi.
Conclusion: These findings demonstrate diverse associations between a wide range of ambient PM2.5 and lipid levels in an understudied South Asian population. Further research is needed to establish causality and develop targeted interventions to mitigate the impact of air pollution on lipid metabolism and cardiovascular health.
{"title":"Longitudinal associations between ambient PM<sub>2.5</sub> exposure and lipid levels in two Indian cities.","authors":"Kritika Anand, Gagandeep Kaur Walia, Siddhartha Mandal, Jyothi S Menon, Ruby Gupta, Nikhil Tandon, K M Venkat Narayan, Mohammed K Ali, Viswanathan Mohan, Joel D Schwartz, Dorairaj Prabhakaran","doi":"10.1097/EE9.0000000000000295","DOIUrl":"10.1097/EE9.0000000000000295","url":null,"abstract":"<p><strong>Background: </strong>Exposure to ambient PM<sub>2.5</sub> is known to affect lipid metabolism through systemic inflammation and oxidative stress. Evidence from developing countries, such as India with high levels of ambient PM<sub>2.5</sub> and distinct lipid profiles, is sparse.</p><p><strong>Methods: </strong>Longitudinal nonlinear mixed-effects analysis was conducted on >10,000 participants of Centre for cArdiometabolic Risk Reduction in South Asia (CARRS) cohort in Chennai and Delhi, India. We examined associations between 1-month and 1-year average ambient PM<sub>2.5</sub> exposure derived from the spatiotemporal model and lipid levels (total cholesterol [TC], triglycerides [TRIG], high-density lipoprotein cholesterol [HDL-C], and low-density lipoprotein cholesterol [LDL-C]) measured longitudinally, adjusting for residential and neighborhood-level confounders.</p><p><strong>Results: </strong>The mean annual exposure in Chennai and Delhi was 40 and 102 μg/m<sup>3</sup> respectively. Elevated ambient PM<sub>2.5</sub> levels were associated with an increase in LDL-C and TC at levels up to 100 µg/m<sup>3</sup> in both cities and beyond 125 µg/m<sup>3</sup> in Delhi. TRIG levels in Chennai increased until 40 µg/m<sup>3</sup> for both short- and long-term exposures, then stabilized or declined, while in Delhi, there was a consistent rise with increasing annual exposures. HDL-C showed an increase in both cities against monthly average exposure. HDL-C decreased slightly in Chennai with an increase in long-term exposure, whereas it decreased beyond 130 µg/m<sup>3</sup> in Delhi.</p><p><strong>Conclusion: </strong>These findings demonstrate diverse associations between a wide range of ambient PM<sub>2.5</sub> and lipid levels in an understudied South Asian population. Further research is needed to establish causality and develop targeted interventions to mitigate the impact of air pollution on lipid metabolism and cardiovascular health.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"8 2","pages":"e295"},"PeriodicalIF":3.3,"publicationDate":"2024-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11008625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140850045","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}
Pub Date : 2024-02-02eCollection Date: 2024-02-01DOI: 10.1097/EE9.0000000000000293
Zin Wai Htay, Chris Fook Sheng Ng, Yoonhee Kim, Youn-Hee Lim, Masao Iwagami, Masahiro Hashizume
Background: Previous studies have indicated that renal disease mortality is sensitive to ambient temperatures. However, most have been limited to the summer season with inconclusive evidence for changes in population vulnerability over time.
Objective: This study aims to examine the association between short-term exposure to ambient temperatures and mortality due to renal diseases in Japan, and how this association varied over time.
Methods: We conducted a two-stage, time-stratified case-crossover study from 1979 to 2019 across 47 prefectures of Japan. We obtained the data of daily mortality counts for all renal diseases, acute renal failure, and chronic renal disease. We fitted a conditional quasi-Poisson regression model with a distributed lag nonlinear model. A random-effects meta-analysis was applied to calculate national averages. We performed additional analyses by four subperiods, sex, and age groups.
Results: We analyzed 997,590 renal mortality cases and observed a reversed J-shaped association. Lower temperatures were associated with increased mortality in all renal disease categories. The cumulative relative risks at 2.5th percentile compared to the minimum mortality temperature percentile were 1.34 (95% confidence interval [CI] = 1.29, 1.40), 1.51 (95% CI = 1.33, 1.71), and 1.33 (95% CI = 1.24, 1.43) for all renal, acute renal failure, and chronic renal disease mortality, respectively. The associations were observed in individuals of both sexes and aged 65 years and above. The associations of kidney mortality with low temperature remained consistent, while the associations with high temperature were pronounced in the past, but not in recent periods.
Conclusions: Protection for individuals with impaired renal function from exposure to low temperatures during cold seasons is warranted.
{"title":"Associations between short-term exposure to ambient temperature and renal disease mortality in Japan during 1979-2019: A time-stratified case-crossover analysis.","authors":"Zin Wai Htay, Chris Fook Sheng Ng, Yoonhee Kim, Youn-Hee Lim, Masao Iwagami, Masahiro Hashizume","doi":"10.1097/EE9.0000000000000293","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000293","url":null,"abstract":"<p><strong>Background: </strong>Previous studies have indicated that renal disease mortality is sensitive to ambient temperatures. However, most have been limited to the summer season with inconclusive evidence for changes in population vulnerability over time.</p><p><strong>Objective: </strong>This study aims to examine the association between short-term exposure to ambient temperatures and mortality due to renal diseases in Japan, and how this association varied over time.</p><p><strong>Methods: </strong>We conducted a two-stage, time-stratified case-crossover study from 1979 to 2019 across 47 prefectures of Japan. We obtained the data of daily mortality counts for all renal diseases, acute renal failure, and chronic renal disease. We fitted a conditional quasi-Poisson regression model with a distributed lag nonlinear model. A random-effects meta-analysis was applied to calculate national averages. We performed additional analyses by four subperiods, sex, and age groups.</p><p><strong>Results: </strong>We analyzed 997,590 renal mortality cases and observed a reversed J-shaped association. Lower temperatures were associated with increased mortality in all renal disease categories. The cumulative relative risks at 2.5th percentile compared to the minimum mortality temperature percentile were 1.34 (95% confidence interval [CI] = 1.29, 1.40), 1.51 (95% CI = 1.33, 1.71), and 1.33 (95% CI = 1.24, 1.43) for all renal, acute renal failure, and chronic renal disease mortality, respectively. The associations were observed in individuals of both sexes and aged 65 years and above. The associations of kidney mortality with low temperature remained consistent, while the associations with high temperature were pronounced in the past, but not in recent periods.</p><p><strong>Conclusions: </strong>Protection for individuals with impaired renal function from exposure to low temperatures during cold seasons is warranted.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"8 1","pages":"e293"},"PeriodicalIF":3.6,"publicationDate":"2024-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10852400/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139722034","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}
Pub Date : 2024-02-01DOI: 10.1097/EE9.0000000000000294
[This corrects the article DOI: 10.1097/EE9.0000000000000269.].
[此处更正了文章 DOI:10.1097/EE9.0000000000000269]。
{"title":"Erratum: Assessing heat effects on respiratory mortality and location characteristics as modifiers of heat effects at a small area scale in Central-Northern Europe: Erratum.","authors":"","doi":"10.1097/EE9.0000000000000294","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000294","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1097/EE9.0000000000000269.].</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"8 1","pages":"e294"},"PeriodicalIF":3.6,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10852360/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139725651","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}
Pub Date : 2024-01-12DOI: 10.1097/EE9.0000000000000285
Neal Fann, A. Zanobetti, Daniel Mork, William Steinhardt, Ana G. Rappold
Fine particle pollution is a well-established risk to human health. Observational epidemiology generally treats events as though they are independent of one another and so do not examine the role air pollution may play in promoting the progression of disease. Multistate survival models account for the complex pathway of disease to death. We employ a multistate survival model to characterize the role of chronic exposure to PM2.5 in affecting the rate at which Medicare beneficiaries transition to first hospitalization for cardiovascular disease and then subsequently death. We use an open cohort of Medicare beneficiaries and PM2.5 concentrations estimated with photochemical model predictions, satellite-based observations, land-use data, and meteorological variables. The multistate model included three transitions: (1) entry to cardiovascular hospital admission; (2) entry to death; and (3) cardiovascular hospital admission to death. The transition intensity was modeled using a Cox proportional hazards model. For a 1 µg/m3 increase in annual mean PM2.5, we estimate a nationally pooled hazard ratio of 1.022 (95% confidence interval [CI] = 1.018, 1.025) for the transition from entry to first cardiovascular hospital admission; 1.054 (95% CI = 1.039, 1.068) for the transition from entry to death; 1.036 (95% CI = 1.027, 1.044) for the transition from first cardiovascular hospital admission to death. The hazard ratios exhibited some heterogeneity within each of nine climatological regions and for each of the three transitions. We find evidence for the role of PM in both promoting chronic illness and increasing the subsequent risk of death.
{"title":"Applying a multistate survival model to explore the role of fine particles in promoting frailty in the Medicare cohort","authors":"Neal Fann, A. Zanobetti, Daniel Mork, William Steinhardt, Ana G. Rappold","doi":"10.1097/EE9.0000000000000285","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000285","url":null,"abstract":"Fine particle pollution is a well-established risk to human health. Observational epidemiology generally treats events as though they are independent of one another and so do not examine the role air pollution may play in promoting the progression of disease. Multistate survival models account for the complex pathway of disease to death. We employ a multistate survival model to characterize the role of chronic exposure to PM2.5 in affecting the rate at which Medicare beneficiaries transition to first hospitalization for cardiovascular disease and then subsequently death. We use an open cohort of Medicare beneficiaries and PM2.5 concentrations estimated with photochemical model predictions, satellite-based observations, land-use data, and meteorological variables. The multistate model included three transitions: (1) entry to cardiovascular hospital admission; (2) entry to death; and (3) cardiovascular hospital admission to death. The transition intensity was modeled using a Cox proportional hazards model. For a 1 µg/m3 increase in annual mean PM2.5, we estimate a nationally pooled hazard ratio of 1.022 (95% confidence interval [CI] = 1.018, 1.025) for the transition from entry to first cardiovascular hospital admission; 1.054 (95% CI = 1.039, 1.068) for the transition from entry to death; 1.036 (95% CI = 1.027, 1.044) for the transition from first cardiovascular hospital admission to death. The hazard ratios exhibited some heterogeneity within each of nine climatological regions and for each of the three transitions. We find evidence for the role of PM in both promoting chronic illness and increasing the subsequent risk of death.","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"12 1","pages":"e285"},"PeriodicalIF":3.6,"publicationDate":"2024-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139437745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-12DOI: 10.1097/EE9.0000000000000289
Elvira S. Fleury, J. Kuiper, J. Buckley, G. Papandonatos, K. Cecil, Aimin Chen, Charles B. Eaton, Heidi J Kalkwarf, B. Lanphear, K. Yolton, Joseph M. Braun
Background: Exposure to per- and polyfluoroalkyl substances (PFAS) throughout gestation and childhood may impact cardiometabolic risk. Methods: In 179 HOME Study participants (Cincinnati, OH; recruited 2003–2006), we used latent profile analysis to identify two distinct patterns of PFAS exposure from serum concentrations of four PFAS measured at birth and ages 3, 8, and 12 years. We assessed the homeostatic model of insulin resistance, triglycerides-to-high-density lipoprotein cholesterol ratio, leptin-to-adiponectin ratio, systolic blood pressure, visceral fat, and hemoglobin A1c levels at age 12 years. We used multivariable linear regression to assess the association of membership in the longitudinal PFAS mixture exposure group with a summary measure of overall cardiometabolic risk and individual components. Results: One PFAS exposure profile (n = 66, 39%) had higher geometric means of all PFAS across all visits than the other. Although adjusted associations were null in the full sample, child sex modified the association of longitudinal PFAS mixture exposure group with overall cardiometabolic risk, leptin-to-adiponectin ratio, systolic blood pressure, and visceral fat (interaction term P values: 0.02–0.08). Females in the higher exposure group had higher cardiometabolic risk scores (ß = 0.43; 95% CI = −0.08, 0.94), systolic blood pressures (ß = 0.6; 95% CI = 0.1, 1.1), and visceral fat (ß = 0.44; 95% CI = −0.13, 1.01); males had lower cardiometabolic risk scores (ß = −0.52; 95% CI = −1.06, −0.06), leptin-to-adiponectin ratios (ß = −0.7; 95% CI = −1.29, −0.1), systolic blood pressures (ß = −0.14; 95% CI = −0.7, 0.41), and visceral fat (ß = −0.52; 95% CI = −0.84, −0.19). Conclusions: Exposure to this PFAS mixture throughout childhood may have sex-specific effects on adolescent cardiometabolic risk.
背景:妊娠期和儿童期接触全氟和多氟烷基物质(PFAS)可能会影响心脏代谢风险。研究方法在 179 名 "HOME 研究 "参与者(俄亥俄州辛辛那提市;2003-2006 年招募)中,我们使用潜在特征分析,从出生时和 3、8、12 岁时测量的四种 PFAS 血清浓度中识别出两种不同的 PFAS 暴露模式。我们评估了胰岛素抵抗的稳态模型、甘油三酯与高密度脂蛋白胆固醇的比率、瘦素与脂联素的比率、收缩压、内脏脂肪以及 12 岁时的血红蛋白 A1c 水平。我们使用多变量线性回归法评估了纵向全氟辛烷磺酸混合物暴露组的成员资格与总体心脏代谢风险和单个成分的综合测量值之间的关联。结果一种 PFAS 暴露情况(n = 66,39%)在所有访问中的所有 PFAS 几何平均数均高于另一种情况。虽然调整后的关联在全样本中为零,但儿童性别改变了纵向 PFAS 混合暴露组与总体心脏代谢风险、瘦素与脂联素比率、收缩压和内脏脂肪的关联(交互项 P 值:0.02-0.08)。暴露程度较高组的女性具有较高的心脏代谢风险评分(ß = 0.43;95% CI = -0.08,0.94)、收缩压(ß = 0.6;95% CI = 0.1,1.1)和内脏脂肪(ß = 0.44;95% CI = -0.13,1.01);男性具有较低的心脏代谢风险评分(ß = -0.52; 95% CI = -1.06, -0.06)、瘦素与脂联素比率(ß = -0.7; 95% CI = -1.29, -0.1)、收缩压(ß = -0.14; 95% CI = -0.7, 0.41)和内脏脂肪(ß = -0.52; 95% CI = -0.84, -0.19)。结论童年时期接触这种全氟辛烷磺酸混合物可能会对青少年的心脏代谢风险产生性别特异性影响。
{"title":"Evaluating the association between longitudinal exposure to a PFAS mixture and adolescent cardiometabolic risk in the HOME Study","authors":"Elvira S. Fleury, J. Kuiper, J. Buckley, G. Papandonatos, K. Cecil, Aimin Chen, Charles B. Eaton, Heidi J Kalkwarf, B. Lanphear, K. Yolton, Joseph M. Braun","doi":"10.1097/EE9.0000000000000289","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000289","url":null,"abstract":"Background: Exposure to per- and polyfluoroalkyl substances (PFAS) throughout gestation and childhood may impact cardiometabolic risk. Methods: In 179 HOME Study participants (Cincinnati, OH; recruited 2003–2006), we used latent profile analysis to identify two distinct patterns of PFAS exposure from serum concentrations of four PFAS measured at birth and ages 3, 8, and 12 years. We assessed the homeostatic model of insulin resistance, triglycerides-to-high-density lipoprotein cholesterol ratio, leptin-to-adiponectin ratio, systolic blood pressure, visceral fat, and hemoglobin A1c levels at age 12 years. We used multivariable linear regression to assess the association of membership in the longitudinal PFAS mixture exposure group with a summary measure of overall cardiometabolic risk and individual components. Results: One PFAS exposure profile (n = 66, 39%) had higher geometric means of all PFAS across all visits than the other. Although adjusted associations were null in the full sample, child sex modified the association of longitudinal PFAS mixture exposure group with overall cardiometabolic risk, leptin-to-adiponectin ratio, systolic blood pressure, and visceral fat (interaction term P values: 0.02–0.08). Females in the higher exposure group had higher cardiometabolic risk scores (ß = 0.43; 95% CI = −0.08, 0.94), systolic blood pressures (ß = 0.6; 95% CI = 0.1, 1.1), and visceral fat (ß = 0.44; 95% CI = −0.13, 1.01); males had lower cardiometabolic risk scores (ß = −0.52; 95% CI = −1.06, −0.06), leptin-to-adiponectin ratios (ß = −0.7; 95% CI = −1.29, −0.1), systolic blood pressures (ß = −0.14; 95% CI = −0.7, 0.41), and visceral fat (ß = −0.52; 95% CI = −0.84, −0.19). Conclusions: Exposure to this PFAS mixture throughout childhood may have sex-specific effects on adolescent cardiometabolic risk.","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"1 7","pages":"e289"},"PeriodicalIF":3.6,"publicationDate":"2024-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139438031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-10DOI: 10.1097/EE9.0000000000000284
Harry D. Momo, Christian S. Alvarez, M. Purdue, Barry I. Graubard, K. McGlynn
Background: Nonalcoholic fatty liver disease (NAFLD) is the most common liver disorder worldwide and a leading cause of liver-related mortality. Prior studies have linked per- and polyfluoroalkyl substances (PFAS) exposure to liver dysfunction and alterations in metabolic pathways, but the extent of a PFAS-NAFLD relationship is unclear. Thus, the aim of the current study was to examine whether there were associations between PFAS exposures and NAFLD in the US adult population over a 16-year period. Methods: Data from 10,234 persons who participated in the National Health and Nutrition Examination Survey between 2003 and 2018 were analyzed. Odds ratios and 95% confidence intervals were calculated using multivariable logistic regression for the associations between PFAS and NAFLD, defined by the Hepatic Steatosis Index (NAFLD-HSI), the Fatty Liver Index (NAFLD-FLI), and by Transient Elastography with Controlled Attenuation Parameter (NAFLD-TE-CAP). Results: Overall, there was a significant inverse association between total PFAS and NAFLD-HSI (P-trend = 0.04). Significant inverse associations were also found between perfluorohexane sulfonic acid (PFHxS) and NAFLD-HSI (P-trend = 0.04), and NAFLD-FLI (P-trend = 0.03). Analysis by time period, 2003–2010 versus 2011–2018, found that while inverse associations were more apparent during the latter period when total PFAS (P-trend = 0.02), PFHxS (P-trend = 0.04), and perfluorooctanoic acid (PFOA) (P-trend = 0.03) were inversely associated with NAFLD-HSI and PFOA was inversely associated with NAFLD-FLI (P-trend = 0.05), there were no significant interaction effects. No significant associations between the PFAS and NAFLD-TE-CAP were found. Conclusions: The current study found no evidence of a positive association between the most common PFAS and NAFLD in the US population.
{"title":"Associations of per- and polyfluoroalkyl substances and nonalcoholic fatty liver disease in the United States adult population, 2003–2018","authors":"Harry D. Momo, Christian S. Alvarez, M. Purdue, Barry I. Graubard, K. McGlynn","doi":"10.1097/EE9.0000000000000284","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000284","url":null,"abstract":"Background: Nonalcoholic fatty liver disease (NAFLD) is the most common liver disorder worldwide and a leading cause of liver-related mortality. Prior studies have linked per- and polyfluoroalkyl substances (PFAS) exposure to liver dysfunction and alterations in metabolic pathways, but the extent of a PFAS-NAFLD relationship is unclear. Thus, the aim of the current study was to examine whether there were associations between PFAS exposures and NAFLD in the US adult population over a 16-year period. Methods: Data from 10,234 persons who participated in the National Health and Nutrition Examination Survey between 2003 and 2018 were analyzed. Odds ratios and 95% confidence intervals were calculated using multivariable logistic regression for the associations between PFAS and NAFLD, defined by the Hepatic Steatosis Index (NAFLD-HSI), the Fatty Liver Index (NAFLD-FLI), and by Transient Elastography with Controlled Attenuation Parameter (NAFLD-TE-CAP). Results: Overall, there was a significant inverse association between total PFAS and NAFLD-HSI (P-trend = 0.04). Significant inverse associations were also found between perfluorohexane sulfonic acid (PFHxS) and NAFLD-HSI (P-trend = 0.04), and NAFLD-FLI (P-trend = 0.03). Analysis by time period, 2003–2010 versus 2011–2018, found that while inverse associations were more apparent during the latter period when total PFAS (P-trend = 0.02), PFHxS (P-trend = 0.04), and perfluorooctanoic acid (PFOA) (P-trend = 0.03) were inversely associated with NAFLD-HSI and PFOA was inversely associated with NAFLD-FLI (P-trend = 0.05), there were no significant interaction effects. No significant associations between the PFAS and NAFLD-TE-CAP were found. Conclusions: The current study found no evidence of a positive association between the most common PFAS and NAFLD in the US population.","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"4 13","pages":"e284"},"PeriodicalIF":3.6,"publicationDate":"2024-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139439892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-09DOI: 10.1097/EE9.0000000000000286
Talia D. Pikounis, Kassaundra L. Amann, B. P. Jackson, T. Punshon, D. Gilbert-Diamond, S. Korrick, M. R. Karagas, K. L. Cottingham
Background: Early-life exposure to nonessential (toxic) and essential trace elements can influence child development. Although infant formula powders and the water used to reconstitute them can contain higher concentrations of many elements compared with human milk, the influence of feeding mode on reliable biomarkers of infant exposure has rarely been demonstrated. Methods: We evaluated associations between urinary biomarkers and feeding mode (exclusively human milk, exclusively formula, or combination-fed) for four toxic (arsenic, cadmium, nickel, and uranium) and three essential elements (cobalt, molybdenum, and selenium) using general linear models. Results: A total of 462 participants from the rural New Hampshire Birth Cohort Study were on average 6 weeks old between July 2012 and March 2019 and had urine samples, 3-day food diaries, and relevant covariate data available. In adjusted models, urinary arsenic was 5.15 (95% confidence interval = 4.04, 6.58), molybdenum was 19.02 (14.13–25.59), and selenium was 1.51 (1.35–1.68) times higher in infants fed exclusively with formula compared with infants fed exclusively with human milk. By contrast, urinary uranium was 0.59 (0.46–0.75) and cobalt was 0.78 (0.65–0.95) times lower with formula feeding than human milk feeding. Conclusion: Our findings suggest that infant exposure to several potentially toxic elements varies by feeding mode, as concentrations of reliable urinary biomarkers were higher with formula or human milk, depending on the element. Importantly, exposure to arsenic increased with household tap water arsenic regardless of feeding mode, suggesting that all infants could be at risk in populations with high concentrations of arsenic in drinking water.
{"title":"Urinary biomarkers of exposure to toxic and essential elements: A comparison of infants fed with human milk or formula","authors":"Talia D. Pikounis, Kassaundra L. Amann, B. P. Jackson, T. Punshon, D. Gilbert-Diamond, S. Korrick, M. R. Karagas, K. L. Cottingham","doi":"10.1097/EE9.0000000000000286","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000286","url":null,"abstract":"Background: Early-life exposure to nonessential (toxic) and essential trace elements can influence child development. Although infant formula powders and the water used to reconstitute them can contain higher concentrations of many elements compared with human milk, the influence of feeding mode on reliable biomarkers of infant exposure has rarely been demonstrated. Methods: We evaluated associations between urinary biomarkers and feeding mode (exclusively human milk, exclusively formula, or combination-fed) for four toxic (arsenic, cadmium, nickel, and uranium) and three essential elements (cobalt, molybdenum, and selenium) using general linear models. Results: A total of 462 participants from the rural New Hampshire Birth Cohort Study were on average 6 weeks old between July 2012 and March 2019 and had urine samples, 3-day food diaries, and relevant covariate data available. In adjusted models, urinary arsenic was 5.15 (95% confidence interval = 4.04, 6.58), molybdenum was 19.02 (14.13–25.59), and selenium was 1.51 (1.35–1.68) times higher in infants fed exclusively with formula compared with infants fed exclusively with human milk. By contrast, urinary uranium was 0.59 (0.46–0.75) and cobalt was 0.78 (0.65–0.95) times lower with formula feeding than human milk feeding. Conclusion: Our findings suggest that infant exposure to several potentially toxic elements varies by feeding mode, as concentrations of reliable urinary biomarkers were higher with formula or human milk, depending on the element. Importantly, exposure to arsenic increased with household tap water arsenic regardless of feeding mode, suggesting that all infants could be at risk in populations with high concentrations of arsenic in drinking water.","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"53 50","pages":"e286"},"PeriodicalIF":3.6,"publicationDate":"2024-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139441964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-09DOI: 10.1097/EE9.0000000000000291
H. Hsu, Jamil M. Lane, L. Schnaas, Brent A. Coull, Erika Osorio-Valencia, Y. Chiu, Ander Wilson, Allan C. Just, I. Kloog, David Bellinger, M. Téllez-Rojo, Robert O. Wright
Introduction: Neurotoxicity resulting from air pollution is of increasing concern. Considering exposure timing effects on neurodevelopmental impairments may be as important as the exposure dose. We used distributed lag regression to determine the sensitive windows of prenatal exposure to fine particulate matter (PM2.5) on children’s cognition in a birth cohort in Mexico. Methods: Analysis included 553 full-term (≥37 weeks gestation) children. Prenatal daily PM2.5 exposure was estimated using a validated satellite-based spatiotemporal model. McCarthy Scales of Children’s Abilities (MSCA) were used to assess children’s cognitive function at 4–5 years old (lower scores indicate poorer performance). To identify susceptibility windows, we used Bayesian distributed lag interaction models to examine associations between prenatal PM2.5 levels and MSCA. This allowed us to estimate vulnerable windows while testing for effect modification. Results: After adjusting for maternal age, socioeconomic status, child age, and sex, Bayesian distributed lag interaction models showed significant associations between increased PM2.5 levels and decreased general cognitive index scores at 31–35 gestation weeks, decreased quantitative scale scores at 30–36 weeks, decreased motor scale scores at 30–36 weeks, and decreased verbal scale scores at 37–38 weeks. Estimated cumulative effects (CE) of PM2.5 across pregnancy showed significant associations with general cognitive index (CE^ = −0.35, 95% confidence interval [CI] = −0.68, −0.01), quantitative scale (CE^ = −0.27, 95% CI = −0.74, −0.02), motor scale (CE^ = −0.25, 95% CI = −0.44, −0.05), and verbal scale (CE^ = −0.2, 95% CI = −0.43, −0.02). No significant sex interactions were observed. Conclusions: Prenatal exposure to PM2.5, particularly late pregnancy, was inversely associated with subscales of MSCA. Using data-driven methods to identify sensitive window may provide insight into the mechanisms of neurodevelopmental impairment due to pollution.
导言:空气污染导致的神经毒性日益受到关注。考虑暴露时间对神经发育障碍的影响可能与暴露剂量同样重要。我们使用分布式滞后回归法确定了墨西哥出生队列中产前暴露于细颗粒物(PM2.5)对儿童认知的敏感窗口。研究方法分析对象包括 553 名足月儿(妊娠期≥37 周)。产前每日PM2.5暴露量是通过一个经过验证的卫星时空模型估算出来的。麦卡锡儿童能力量表(MSCA)用于评估儿童在4-5岁时的认知功能(分数越低表示表现越差)。为了确定易感窗口,我们使用贝叶斯分布式滞后交互模型来检验产前 PM2.5 水平与 MSCA 之间的关联。这使我们能够估计易感窗口,同时测试效应修正。结果在对母亲年龄、社会经济地位、儿童年龄和性别进行调整后,贝叶斯分布式滞后交互模型显示,PM2.5水平升高与妊娠31-35周时一般认知指数评分下降、30-36周时定量量表评分下降、30-36周时运动量表评分下降和37-38周时言语量表评分下降之间存在显著关联。整个孕期PM2.5的估计累积效应(CE)显示与一般认知指数(CE^ = -0.35,95%置信区间[CI] = -0.68,-0.01)、定量表(CE^ = -0.27,95% CI = -0.74,-0.02)、运动量表(CE^ = -0.25,95% CI = -0.44,-0.05)和言语量表(CE^ = -0.2,95% CI = -0.43,-0.02)有显著关联。没有观察到明显的性别交互作用。结论产前暴露于PM2.5,尤其是孕晚期,与MSCA的分量表呈反比关系。使用数据驱动的方法来确定敏感窗口可能有助于深入了解污染导致神经发育障碍的机制。
{"title":"Sensitive development windows of prenatal air pollution and cognitive functioning in preschool age Mexican children","authors":"H. Hsu, Jamil M. Lane, L. Schnaas, Brent A. Coull, Erika Osorio-Valencia, Y. Chiu, Ander Wilson, Allan C. Just, I. Kloog, David Bellinger, M. Téllez-Rojo, Robert O. Wright","doi":"10.1097/EE9.0000000000000291","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000291","url":null,"abstract":"Introduction: Neurotoxicity resulting from air pollution is of increasing concern. Considering exposure timing effects on neurodevelopmental impairments may be as important as the exposure dose. We used distributed lag regression to determine the sensitive windows of prenatal exposure to fine particulate matter (PM2.5) on children’s cognition in a birth cohort in Mexico. Methods: Analysis included 553 full-term (≥37 weeks gestation) children. Prenatal daily PM2.5 exposure was estimated using a validated satellite-based spatiotemporal model. McCarthy Scales of Children’s Abilities (MSCA) were used to assess children’s cognitive function at 4–5 years old (lower scores indicate poorer performance). To identify susceptibility windows, we used Bayesian distributed lag interaction models to examine associations between prenatal PM2.5 levels and MSCA. This allowed us to estimate vulnerable windows while testing for effect modification. Results: After adjusting for maternal age, socioeconomic status, child age, and sex, Bayesian distributed lag interaction models showed significant associations between increased PM2.5 levels and decreased general cognitive index scores at 31–35 gestation weeks, decreased quantitative scale scores at 30–36 weeks, decreased motor scale scores at 30–36 weeks, and decreased verbal scale scores at 37–38 weeks. Estimated cumulative effects (CE) of PM2.5 across pregnancy showed significant associations with general cognitive index (CE^ = −0.35, 95% confidence interval [CI] = −0.68, −0.01), quantitative scale (CE^ = −0.27, 95% CI = −0.74, −0.02), motor scale (CE^ = −0.25, 95% CI = −0.44, −0.05), and verbal scale (CE^ = −0.2, 95% CI = −0.43, −0.02). No significant sex interactions were observed. Conclusions: Prenatal exposure to PM2.5, particularly late pregnancy, was inversely associated with subscales of MSCA. Using data-driven methods to identify sensitive window may provide insight into the mechanisms of neurodevelopmental impairment due to pollution.","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"121 9","pages":"e291"},"PeriodicalIF":3.6,"publicationDate":"2024-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139444376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}