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}
Pub Date : 2023-12-29DOI: 10.1097/EE9.0000000000000282
A. Veludo, M. Röösli, M. A. Dalvie, Petra Stuchlík Fišerová, R. Prokes, P. Příbylová, P. Šenk, Jiří Kohoutek, Mufaro Mugari, Jana Klánová, Anke Huss, D. Figueiredo, H. Mol, Jonatan Dias, C. Degrendele, S. Fuhrimann
Background: Children in agricultural areas are exposed to organophosphate (OP) and pyrethroid (PYR) insecticides. This explorative study investigated child exposure to OPs and PYRs, comparing temporal and spatial exposure variability within and among urine, wristbands, and dust samples. Methods: During spraying season 2018, 38 South African children in two agricultural areas (Grabouw/Hex River Valley) and settings (farm/village) participated in a seven-day study. Child urine and household dust samples were collected on days 1 and 7. Children and their guardians were wearing silicone wristbands for seven days. Intraclass correlation coefficients (ICCs) evaluated temporal agreements between repeated urine and dust samples, Spearman rank correlations (Rs) evaluated the correlations among matrices, and linear mixed-effect models investigated spatial exposure predictors. A risk assessment was performed using reverse dosimetry. Results: Eighteen OPs/PYRs were targeted in urine, wristbands, and dust. Levels of chlorpyrifos in dust (ICC = 0.92) and diethylphosphate biomarker in urine (ICC = 0.42) showed strong and moderate temporal agreement between day 1 and day 7, respectively. Weak agreements were observed for all others. There was mostly a weak correlation among the three matrices (Rs = −0.12 to 0.35), except for chlorpyrifos in dust and its biomarker 3,5,6-trichloro-2-pyridinol in urine (Rs = 0.44). No differences in exposure levels between living locations were observed. However, 21% of the urine biomarker levels exceeded the health-risk threshold for OP exposure. Conclusions: Observed high short-term variability in exposure levels during spraying season highlights the need for repeated sampling. The weak correlation between the exposure matrices points to different environmental and behavioral exposure pathways. Exceeding risk thresholds for OP should be further investigated.
{"title":"Child exposure to organophosphate and pyrethroid insecticides measured in urine, wristbands, and household dust and its implications for child health in South Africa: A panel study","authors":"A. Veludo, M. Röösli, M. A. Dalvie, Petra Stuchlík Fišerová, R. Prokes, P. Příbylová, P. Šenk, Jiří Kohoutek, Mufaro Mugari, Jana Klánová, Anke Huss, D. Figueiredo, H. Mol, Jonatan Dias, C. Degrendele, S. Fuhrimann","doi":"10.1097/EE9.0000000000000282","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000282","url":null,"abstract":"Background: Children in agricultural areas are exposed to organophosphate (OP) and pyrethroid (PYR) insecticides. This explorative study investigated child exposure to OPs and PYRs, comparing temporal and spatial exposure variability within and among urine, wristbands, and dust samples. Methods: During spraying season 2018, 38 South African children in two agricultural areas (Grabouw/Hex River Valley) and settings (farm/village) participated in a seven-day study. Child urine and household dust samples were collected on days 1 and 7. Children and their guardians were wearing silicone wristbands for seven days. Intraclass correlation coefficients (ICCs) evaluated temporal agreements between repeated urine and dust samples, Spearman rank correlations (Rs) evaluated the correlations among matrices, and linear mixed-effect models investigated spatial exposure predictors. A risk assessment was performed using reverse dosimetry. Results: Eighteen OPs/PYRs were targeted in urine, wristbands, and dust. Levels of chlorpyrifos in dust (ICC = 0.92) and diethylphosphate biomarker in urine (ICC = 0.42) showed strong and moderate temporal agreement between day 1 and day 7, respectively. Weak agreements were observed for all others. There was mostly a weak correlation among the three matrices (Rs = −0.12 to 0.35), except for chlorpyrifos in dust and its biomarker 3,5,6-trichloro-2-pyridinol in urine (Rs = 0.44). No differences in exposure levels between living locations were observed. However, 21% of the urine biomarker levels exceeded the health-risk threshold for OP exposure. Conclusions: Observed high short-term variability in exposure levels during spraying season highlights the need for repeated sampling. The weak correlation between the exposure matrices points to different environmental and behavioral exposure pathways. Exceeding risk thresholds for OP should be further investigated.","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"6 14","pages":"e282"},"PeriodicalIF":3.6,"publicationDate":"2023-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139148131","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 : 2023-12-15DOI: 10.1097/EE9.0000000000000283
L. Mcguinn, Iván Gutiérrez-Avila, M. Rosa, Allan C. Just, Brent Coull, I. Kloog, Marcela Tamayo Ortiz, H. Harari, Sandra Martinez, Erika Osorio-Valencia, M. Téllez-Rojo, Daniel N. Klein, Rosalind J. Wright, Robert O. Wright
Background: Fine particulate matter (PM2.5) exposure has been linked to anxiety and depression in adults; however, there is limited research in the younger populations, in which symptoms often first arise. Methods: We examined the association between early-life PM2.5 exposure and symptoms of anxiety and depression in a cohort of 8–11-year-olds in Mexico City. Anxiety and depressive symptoms were assessed using the Spanish versions of the Revised Children’s Manifest Anxiety Scale and Children’s Depression Inventory. Daily PM2.5 was estimated using a satellite-based exposure model and averaged over several early and recent exposure windows. Linear and logistic regression models were used to estimate the change in symptoms with each 5-µg/m3 increase in PM2.5. Models were adjusted for child’s age, child’s sex, maternal age, maternal socioeconomic status, season of conception, and temperature. Results: Average anxiety and depressive symptom T-scores were 51.0 (range 33–73) and 53.4 (range 44–90), respectively. We observed consistent findings for exposures around the fourth year of life, as this was present for both continuous and dichotomized anxiety symptoms, in both independent exposure models and distributed lag modeling approaches. This window was also observed for elevated depressive symptoms. An additional consistent finding was for PM2.5 exposure during early pregnancy in relation to both clinically elevated anxiety and depressive symptoms, this was seen in both traditional and distributed lag modeling approaches. Conclusion: Both early life and recent PM2.5 exposure were associated with higher mental health symptoms in the child highlighting the role of PM2.5 in the etiology of these conditions.
{"title":"Association between prenatal and childhood PM2.5 exposure and preadolescent anxiety and depressive symptoms","authors":"L. Mcguinn, Iván Gutiérrez-Avila, M. Rosa, Allan C. Just, Brent Coull, I. Kloog, Marcela Tamayo Ortiz, H. Harari, Sandra Martinez, Erika Osorio-Valencia, M. Téllez-Rojo, Daniel N. Klein, Rosalind J. Wright, Robert O. Wright","doi":"10.1097/EE9.0000000000000283","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000283","url":null,"abstract":"Background: Fine particulate matter (PM2.5) exposure has been linked to anxiety and depression in adults; however, there is limited research in the younger populations, in which symptoms often first arise. Methods: We examined the association between early-life PM2.5 exposure and symptoms of anxiety and depression in a cohort of 8–11-year-olds in Mexico City. Anxiety and depressive symptoms were assessed using the Spanish versions of the Revised Children’s Manifest Anxiety Scale and Children’s Depression Inventory. Daily PM2.5 was estimated using a satellite-based exposure model and averaged over several early and recent exposure windows. Linear and logistic regression models were used to estimate the change in symptoms with each 5-µg/m3 increase in PM2.5. Models were adjusted for child’s age, child’s sex, maternal age, maternal socioeconomic status, season of conception, and temperature. Results: Average anxiety and depressive symptom T-scores were 51.0 (range 33–73) and 53.4 (range 44–90), respectively. We observed consistent findings for exposures around the fourth year of life, as this was present for both continuous and dichotomized anxiety symptoms, in both independent exposure models and distributed lag modeling approaches. This window was also observed for elevated depressive symptoms. An additional consistent finding was for PM2.5 exposure during early pregnancy in relation to both clinically elevated anxiety and depressive symptoms, this was seen in both traditional and distributed lag modeling approaches. Conclusion: Both early life and recent PM2.5 exposure were associated with higher mental health symptoms in the child highlighting the role of PM2.5 in the etiology of these conditions.","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"26 25","pages":"e283"},"PeriodicalIF":3.6,"publicationDate":"2023-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139000665","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 : 2023-12-14DOI: 10.1097/EE9.0000000000000287
Alexander J Northrop, Nina M. Flores, V. Do, Perry E. Sheffield, Joan A. Casey
Background: In the past decade, electrical power disruptions (outages) have increased in the United States, especially those attributable to weather events. These outages have a range of health impacts but are largely unstudied in children. Here, we investigated the association between outages and unintentional injury hospitalizations, a leading cause of childhood morbidity. Methods: The study setting was New York State (NYS) from 2017 to 2020. Outage exposure was defined as ≥10%, ≥20%, and ≥50% of customers from a power operating locality without power, ascertained from NYS Department of Public Service records and stratified by rural, urban non-New York City (NYC), and NYC regions. Outcome daily block group-level pediatric injury hospitalization data was from the Statewide Planning and Research Cooperative System (SPARCS). We leveraged a case-crossover study design with logistic conditional regression. Results: We identified 23,093 unintentional injury hospitalizations in children <18 years with complete block group and exposure data. Most hospitalizations occurred in urban regions (90%), whereas outages were more likely in rural than urban areas. In urban non-NYC regions, outages ≥4 hours were associated with 30% increased odds of all-cause unintentional injury hospitalizations when ≥50% of customers were without power. Analyses by injury subtype revealed increasing point estimates as the proportion of customers exposed increased. These results, however, had wide confidence intervals. Conclusions: Outage exposure differed significantly across rural, urban non-NYC, and NYC regions across New York. Especially at the highest outage threshold, we observed an increased risk of pediatric unintentional injury hospitalizations.
{"title":"Power outages and pediatric unintentional injury hospitalizations in New York State","authors":"Alexander J Northrop, Nina M. Flores, V. Do, Perry E. Sheffield, Joan A. Casey","doi":"10.1097/EE9.0000000000000287","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000287","url":null,"abstract":"Background: In the past decade, electrical power disruptions (outages) have increased in the United States, especially those attributable to weather events. These outages have a range of health impacts but are largely unstudied in children. Here, we investigated the association between outages and unintentional injury hospitalizations, a leading cause of childhood morbidity. Methods: The study setting was New York State (NYS) from 2017 to 2020. Outage exposure was defined as ≥10%, ≥20%, and ≥50% of customers from a power operating locality without power, ascertained from NYS Department of Public Service records and stratified by rural, urban non-New York City (NYC), and NYC regions. Outcome daily block group-level pediatric injury hospitalization data was from the Statewide Planning and Research Cooperative System (SPARCS). We leveraged a case-crossover study design with logistic conditional regression. Results: We identified 23,093 unintentional injury hospitalizations in children <18 years with complete block group and exposure data. Most hospitalizations occurred in urban regions (90%), whereas outages were more likely in rural than urban areas. In urban non-NYC regions, outages ≥4 hours were associated with 30% increased odds of all-cause unintentional injury hospitalizations when ≥50% of customers were without power. Analyses by injury subtype revealed increasing point estimates as the proportion of customers exposed increased. These results, however, had wide confidence intervals. Conclusions: Outage exposure differed significantly across rural, urban non-NYC, and NYC regions across New York. Especially at the highest outage threshold, we observed an increased risk of pediatric unintentional injury hospitalizations.","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"331 1","pages":"e287"},"PeriodicalIF":3.6,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138974134","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 : 2023-12-01DOI: 10.1097/EE9.0000000000000267
Ellen Martinson, Howard Chang, R. D’Souza, S. Ebelt, N. Scovronick
Background: Here, we investigate the association between outdoor temperature and fatal police shootings in the United States between 2015 and 2021. Methods: We conducted a time-stratified case-crossover study. Data on fatal police shootings were from the Washington Post’s Fatal Force database and temperature data were from Daymet. Results: A 5°C increase in maximum same-day temperature was associated with a 1.033 (95% CI = 1.002, 1.065) increased odds of a fatal police shooting. In stratified analyses, the strongest associations were observed in victims who were armed (OR, 1.052 [95% CI = 1.017, 1.088), White (OR, 1.052 [95% CI = 1.006, 1.100), or aged 45+ (OR, 1.110 [95% CI = 1.044, 1.181]). In additional subgroup analyses, relative risks were also generally higher among those who were armed. Conclusions: There is evidence of an association between outdoor temperature and fatal police shootings in the United States, particularly when the victims were reported as armed. This study cannot determine if the associations are a result of any specific causes (e.g., increased police aggression or other factors).
背景:在这里，我们调查了2015年至2021年间美国室外温度与致命警察枪击事件之间的关系。方法:采用时间分层病例交叉研究。警方致命枪击事件的数据来自《华盛顿邮报》的致命力量数据库，气温数据来自Daymet。结果:当天最高气温每升高5°C，发生警察致命枪击的几率增加1.033 (95% CI = 1.002, 1.065)。在分层分析中，在武装人员(OR, 1.052 [95% CI = 1.017, 1.088])、白人(OR, 1.052 [95% CI = 1.006, 1.100])和45岁以上(OR, 1.110 [95% CI = 1.044, 1.181])的受害者中观察到最强的相关性。在其他亚组分析中，武装人员的相对风险也普遍较高。结论:有证据表明，在美国，室外温度与致命的警察枪击事件之间存在关联，特别是当受害者被报道为持有武器时。这项研究无法确定这种关联是否由任何特定原因(例如，警察的攻击性增加或其他因素)造成。
{"title":"Association between outdoor temperature and fatal police shootings in the United States, 2015–2021","authors":"Ellen Martinson, Howard Chang, R. D’Souza, S. Ebelt, N. Scovronick","doi":"10.1097/EE9.0000000000000267","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000267","url":null,"abstract":"Background: Here, we investigate the association between outdoor temperature and fatal police shootings in the United States between 2015 and 2021. Methods: We conducted a time-stratified case-crossover study. Data on fatal police shootings were from the Washington Post’s Fatal Force database and temperature data were from Daymet. Results: A 5°C increase in maximum same-day temperature was associated with a 1.033 (95% CI = 1.002, 1.065) increased odds of a fatal police shooting. In stratified analyses, the strongest associations were observed in victims who were armed (OR, 1.052 [95% CI = 1.017, 1.088), White (OR, 1.052 [95% CI = 1.006, 1.100), or aged 45+ (OR, 1.110 [95% CI = 1.044, 1.181]). In additional subgroup analyses, relative risks were also generally higher among those who were armed. Conclusions: There is evidence of an association between outdoor temperature and fatal police shootings in the United States, particularly when the victims were reported as armed. This study cannot determine if the associations are a result of any specific causes (e.g., increased police aggression or other factors).","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"52 s38","pages":"e267"},"PeriodicalIF":3.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138627698","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 : 2023-12-01DOI: 10.1097/EE9.0000000000000279
Lara Stucki, Staffan Betnér, Jenny Selander, M. Lõhmus, A. Åkesson, C. Eriksson
Background: Recent evidence suggests environmental health inequalities both within and between European countries and socially deprived groups may be more susceptible to pollution. However, evidence is still inconclusive and additional studies are warranted. This study aims to investigate sociodemographic inequalities in long-term residential exposure to air pollution, road traffic noise, and greenness, taking lifestyle and degree of urbanization into account. Methods: In total 20,407 women, born 1914–48 residing in Uppsala County, Sweden, were followed between 1997 and 2017. Time-varying sociodemographic variables were obtained from registers, and questionnaires provided lifestyle information. Generalized estimating equations were used to compute beta-coefficients (β) and 95% confidence intervals (95% CI) for associations between sociodemographic and lifestyle variables and spatial-temporal modeled particulate matter (PM2.5, PM10), nitrogen dioxide (NO2), road traffic noise and greenness. All models were additionally stratified by urbanization type. Results: Urban area residency was the most important predictor of high exposure to air pollution and noise, and to low greenness. For instance, β for NO2 was −2.92 (95% CI = −3.00, −2.83) and −3.10 (95% CI = −3.18, −3.01) µg/m3 in suburban and rural areas, respectively, compared with urban areas. For greenness, the opposite held true with corresponding β of 0.059 (95% CI = 0.056, 0.062) and 0.095 (95% CI = 0.092, 0.098). Within urban areas, elderly, unmarried and well-educated women had the highest environmental burden. However, less pronounced, and even reversed associations were found in suburban and rural areas. Conclusion: This study provides evidence of a mixed pattern of environmental health inequalities across sociodemographic groups in urban areas.
背景:最近的证据表明，欧洲国家内部和国家之间以及社会贫困群体之间的环境卫生不平等可能更容易受到污染的影响。然而，证据仍然不确定，需要进一步的研究。本研究的目的是在考虑生活方式和城市化程度的情况下，调查长期居住暴露于空气污染、道路交通噪音和绿化方面的社会人口不平等。方法:在1997年至2017年期间，共有20,407名女性，出生于1914 - 1948年，居住在瑞典乌普萨拉县。随时间变化的社会人口变量从登记册中获得，调查问卷提供生活方式信息。使用广义估计方程计算社会人口学和生活方式变量与时空模拟颗粒物(PM2.5、PM10)、二氧化氮(NO2)、道路交通噪声和绿化之间的关联的β系数(β)和95%置信区间(95% CI)。所有模型均按城市化类型进行分层。结果:城区居住是空气污染和噪声高暴露和绿化低的最重要预测因子。例如，与城市地区相比，郊区和农村地区NO2的β分别为- 2.92 (95% CI = - 3.00， - 2.83)和- 3.10 (95% CI = - 3.18， - 3.01)µg/m3。对于绿色，相反的情况是正确的，相应的β为0.059 (95% CI = 0.056, 0.062)和0.095 (95% CI = 0.092, 0.098)。在城市地区，老年、未婚和受过良好教育的妇女的环境负担最重。然而，在郊区和农村地区发现的关联不那么明显，甚至是相反的。结论:本研究提供了城市地区不同社会人口群体环境卫生不平等混合模式的证据。
{"title":"Sociodemographic inequalities in long-term exposure to air pollution, road traffic noise, and greenness: A population-based cohort study of women","authors":"Lara Stucki, Staffan Betnér, Jenny Selander, M. Lõhmus, A. Åkesson, C. Eriksson","doi":"10.1097/EE9.0000000000000279","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000279","url":null,"abstract":"Background: Recent evidence suggests environmental health inequalities both within and between European countries and socially deprived groups may be more susceptible to pollution. However, evidence is still inconclusive and additional studies are warranted. This study aims to investigate sociodemographic inequalities in long-term residential exposure to air pollution, road traffic noise, and greenness, taking lifestyle and degree of urbanization into account. Methods: In total 20,407 women, born 1914–48 residing in Uppsala County, Sweden, were followed between 1997 and 2017. Time-varying sociodemographic variables were obtained from registers, and questionnaires provided lifestyle information. Generalized estimating equations were used to compute beta-coefficients (β) and 95% confidence intervals (95% CI) for associations between sociodemographic and lifestyle variables and spatial-temporal modeled particulate matter (PM2.5, PM10), nitrogen dioxide (NO2), road traffic noise and greenness. All models were additionally stratified by urbanization type. Results: Urban area residency was the most important predictor of high exposure to air pollution and noise, and to low greenness. For instance, β for NO2 was −2.92 (95% CI = −3.00, −2.83) and −3.10 (95% CI = −3.18, −3.01) µg/m3 in suburban and rural areas, respectively, compared with urban areas. For greenness, the opposite held true with corresponding β of 0.059 (95% CI = 0.056, 0.062) and 0.095 (95% CI = 0.092, 0.098). Within urban areas, elderly, unmarried and well-educated women had the highest environmental burden. However, less pronounced, and even reversed associations were found in suburban and rural areas. Conclusion: This study provides evidence of a mixed pattern of environmental health inequalities across sociodemographic groups in urban areas.","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"36 1‐2","pages":"e279"},"PeriodicalIF":3.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138626049","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}
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