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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. 产前空气污染与儿童自闭症特质得分:使用混合方法研究与母亲摄入维生素 D、甲基供体和多不饱和脂肪酸的共同关系。
IF 3.3 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2024-06-21 eCollection Date: 2024-08-01 DOI: 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.

背景:母亲的营养摄入量可能会缓和环境暴露与儿童神经发育结果之间的关联,但很少有研究对联合效应进行评估。我们旨在评估产前营养素摄入量是否会影响空气污染物与自闭症相关特质评分之间的关联:我们纳入了来自 EARLI(早期自闭症风险纵向调查,2009-2012 年)队列的 126 名参与者,该队列追踪了曾有过自闭症患儿的美国孕妇。贝叶斯核机回归和传统回归模型被用来研究产前营养素摄入量(维生素 D、B12 和 B6;叶酸、胆碱和甜菜碱;总欧米茄 3 和 6 多不饱和脂肪酸,通过食物频率问卷报告)、空气污染物暴露量(颗粒物 2.5]、二氧化氮[NO2]和臭氧[O3],按地址水平估算),以及儿童的自闭症相关特征(通过 36 个月时的社会反应量表[SRS]测量):结果:大多数参与者的营养摄入量和空气污染物暴露量均符合美国标准。贝叶斯核机器回归混合物模型和传统回归模型几乎不能证明营养素和空气污染物与 SRS 评分之间存在单独或联合关联,也不能证明总体混合物与 SRS 评分之间存在关联:结论:在这个自闭症家族遗传可能性很高的队列中,我们没有观察到空气污染暴露和营养素摄入与自闭症相关特征之间存在联合关联的证据。由于我们的结果可能受到家族遗传因素和/或相对较高的营养素摄入量和较低的空气污染物暴露量的影响,因此未来的工作应研究在更大规模、更多样化的样本中使用这些方法。
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引用次数: 0
Genome-wide DNA methylation profiles and breast cancer among World Trade Center survivors. 全基因组 DNA 甲基化图谱与世贸中心幸存者中的乳腺癌。
IF 3.3 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2024-06-04 eCollection Date: 2024-06-01 DOI: 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。
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引用次数: 0
Longitudinal associations between ambient PM2.5 exposure and lipid levels in two Indian cities. 印度两个城市的环境 PM2.5 暴露与血脂水平之间的纵向联系。
IF 3.3 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2024-04-04 eCollection Date: 2024-04-01 DOI: 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.

背景:已知暴露于环境 PM2.5 会通过全身炎症和氧化应激影响脂质代谢。印度等发展中国家的环境 PM2.5 水平较高,但其血脂状况却截然不同,这方面的证据还很稀少:我们对印度钦奈和德里的南亚减少代谢风险中心(CARRS)队列中超过 10,000 名参与者进行了纵向非线性混合效应分析。我们研究了时空模型得出的1个月和1年平均环境PM2.5暴露量与纵向测量的血脂水平(总胆固醇[TC]、甘油三酯[TRIG]、高密度脂蛋白胆固醇[HDL-C]和低密度脂蛋白胆固醇[LDL-C])之间的关系,并对居住地和邻近地区的混杂因素进行了调整:钦奈和德里的年平均暴露量分别为 40 和 102 μg/m3。在这两个城市,当环境 PM2.5 水平达到 100 微克/立方米时,低密度脂蛋白胆固醇(LDL-C)和总胆固醇(TC)会升高,而在德里,当环境 PM2.5 水平超过 125 微克/立方米时,低密度脂蛋白胆固醇(LDL-C)和总胆固醇(TC)会升高。在钦奈,无论短期还是长期暴露,TRIG 水平在 40 µg/m3 之前都会上升,然后趋于稳定或下降,而在德里,随着年暴露量的增加,TRIG 水平持续上升。两个城市的 HDL-C 都随着月平均暴露量的增加而增加。在钦奈,随着长期暴露量的增加,高密度脂蛋白胆固醇略有下降,而在德里,当暴露量超过 130 µg/m3 时,高密度脂蛋白胆固醇就会下降:这些研究结果表明,在研究不足的南亚人群中,环境 PM2.5 与血脂水平之间存在多种关联。需要进一步研究,以确定因果关系,并制定有针对性的干预措施,减轻空气污染对脂质代谢和心血管健康的影响。
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引用次数: 0
Associations between short-term exposure to ambient temperature and renal disease mortality in Japan during 1979-2019: A time-stratified case-crossover analysis. 1979-2019年日本短期暴露于环境温度与肾病死亡率之间的关系:时间分层病例交叉分析。
IF 3.6 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2024-02-02 eCollection Date: 2024-02-01 DOI: 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.

背景:以往的研究表明,肾病死亡率对环境温度很敏感。然而,大多数研究仅限于夏季,没有确凿证据表明随着时间的推移,人群的易感性会发生变化:本研究旨在探讨短期暴露于环境温度与日本肾脏疾病死亡率之间的关联,以及这种关联随时间的变化情况:从 1979 年到 2019 年,我们在日本 47 个都道府县开展了一项分两个阶段、时间分层的病例交叉研究。我们获得了所有肾脏疾病、急性肾衰竭和慢性肾脏疾病的每日死亡率数据。我们利用分布式滞后非线性模型拟合了一个条件准泊松回归模型。采用随机效应荟萃分析法计算全国平均值。我们还按四个子时期、性别和年龄组进行了额外分析:我们分析了 997,590 例肾脏病死亡病例,观察到一种反向的 J 型关联。在所有肾病类别中,温度越低死亡率越高。与最低死亡温度百分位数相比,2.5 百分位数的累积相对风险在所有肾病、急性肾衰竭和慢性肾病死亡率中分别为 1.34(95% 置信区间 [CI] = 1.29,1.40)、1.51(95% CI = 1.33,1.71)和 1.33(95% CI = 1.24,1.43)。在 65 岁及以上的男性和女性中都观察到了这种关联。肾脏死亡率与低温的相关性保持一致,而与高温的相关性在过去很明显,但在近期则不明显:结论:在寒冷季节,肾功能受损者应避免暴露在低温环境中。
{"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}
引用次数: 0
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. 勘误:在中北欧小范围内评估高温对呼吸系统死亡率的影响以及作为高温影响调节因素的地点特征:勘误。
IF 3.6 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2024-02-01 DOI: 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]。
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引用次数: 0
Applying a multistate survival model to explore the role of fine particles in promoting frailty in the Medicare cohort 应用多州生存模型探索细颗粒物在促进医疗保险队列虚弱中的作用
IF 3.6 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2024-01-12 DOI: 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.
细颗粒物污染对人类健康的危害已得到证实。观察流行病学通常将各种事件视为相互独立的,因此不会研究空气污染在促进疾病进展方面可能发挥的作用。多态生存模型考虑了从疾病到死亡的复杂路径。我们采用多州生存模型来描述长期暴露于 PM2.5 在影响医疗保险受益人首次因心血管疾病住院并随后死亡的速度方面所起的作用。我们使用了医疗保险受益人的开放队列以及通过光化学模型预测、卫星观测、土地使用数据和气象变量估算的 PM2.5 浓度。多州模型包括三个过渡:(1) 进入心血管病医院;(2) 进入心血管病医院至死亡;(3) 进入心血管病医院至死亡。过渡强度采用 Cox 比例危险模型进行建模。对于年均PM2.5每增加1微克/立方米,我们估计从入院到首次入住心血管病医院的全国汇总危险比为1.022(95% 置信区间 [CI] = 1.018, 1.025);从入院到死亡的危险比为1.054(95% CI = 1.039, 1.068);从首次入住心血管病医院到死亡的危险比为1.036(95% CI = 1.027, 1.044)。在九个气候区中,每个气候区的危险比以及三种转变的危险比都表现出一定的异质性。我们发现了可吸入颗粒物在促进慢性疾病和增加后续死亡风险方面发挥作用的证据。
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引用次数: 0
Evaluating the association between longitudinal exposure to a PFAS mixture and adolescent cardiometabolic risk in the HOME Study 评估 "居家 "研究中纵向接触全氟辛烷磺酸混合物与青少年心脏代谢风险之间的关系
IF 3.6 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2024-01-12 DOI: 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}
引用次数: 0
Associations of per- and polyfluoroalkyl substances and nonalcoholic fatty liver disease in the United States adult population, 2003–2018 2003-2018年美国成年人口中全氟和多氟烷基物质与非酒精性脂肪肝的关系
IF 3.6 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2024-01-10 DOI: 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.
背景:非酒精性脂肪肝(NAFLD非酒精性脂肪肝(NAFLD)是全球最常见的肝脏疾病,也是肝脏相关死亡的主要原因。先前的研究已将接触全氟和多氟烷基物质(PFAS)与肝功能异常和代谢途径的改变联系起来,但 PFAS 与非酒精性脂肪肝的关系程度尚不清楚。因此,本研究的目的是检测美国成年人在 16 年间接触的 PFAS 与非酒精性脂肪肝之间是否存在关联。研究方法:对 2003 年至 2018 年期间参加全国健康与营养调查的 10234 人的数据进行了分析。采用多变量逻辑回归法计算了PFAS与非酒精性脂肪肝之间的相关性的患病率和95%置信区间,非酒精性脂肪肝的定义包括肝脏脂肪变性指数(NAFLD-HSI)、脂肪肝指数(NAFLD-FLI)和瞬态弹性成像与控制衰减参数(NAFLD-TE-CAP)。结果显示总体而言,PFAS 总量与 NAFLD-HSI 之间存在明显的反向关系(P-趋势 = 0.04)。全氟己烷磺酸(PFHxS)与非酒精性脂肪肝-HSI(P-trend = 0.04)和非酒精性脂肪肝-FLI(P-trend = 0.03)之间也存在明显的反比关系。按时间段(2003-2010年与2011-2018年)分析发现,虽然在后一时期,PFAS总量(P-trend = 0.02)、PFHxS(P-trend = 0.04)和全氟辛酸(PFOA)(P-trend = 0.03)与非酒精性脂肪肝-HSI呈反向关系,PFOA与非酒精性脂肪肝-FLI呈反向关系(P-trend = 0.05),但两者之间没有显著的交互作用。PFAS与NAFLD-TE-CAP之间未发现明显关联。结论:本研究没有发现证据表明美国人群中最常见的 PFAS 与非酒精性脂肪肝之间存在正相关关系。
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引用次数: 0
Urinary biomarkers of exposure to toxic and essential elements: A comparison of infants fed with human milk or formula 暴露于有毒和必需元素的尿液生物标志物:母乳喂养和配方奶喂养婴儿的比较
IF 3.6 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2024-01-09 DOI: 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.
背景:生命早期接触非必需(有毒)和必需微量元素会影响儿童的发育。尽管与母乳相比,婴儿配方粉和用于重组配方粉的水可能含有更高浓度的多种元素,但喂养模式对婴儿暴露的可靠生物标志物的影响却很少得到证实。研究方法我们使用一般线性模型评估了四种有毒元素(砷、镉、镍和铀)和三种必需元素(钴、钼和硒)的尿液生物标志物与喂养方式(完全母乳喂养、完全配方粉喂养或混合喂养)之间的关系。研究结果新罕布什尔州农村出生队列研究共有 462 名参与者,他们在 2012 年 7 月至 2019 年 3 月期间出生,平均年龄为 6 周岁,有尿液样本、3 天食物日记和相关协变量数据。在调整后的模型中,与纯母乳喂养的婴儿相比,纯配方奶喂养的婴儿尿砷含量高出 5.15(95% 置信区间 = 4.04,6.58)倍,钼含量高出 19.02(14.13-25.59)倍,硒含量高出 1.51(1.35-1.68)倍。相比之下,配方奶喂养的婴儿尿中铀的含量为 0.59(0.46-0.75)倍,钴的含量为 0.78(0.65-0.95)倍。结论我们的研究结果表明,婴儿暴露于几种潜在有毒元素的情况因喂养方式而异,因为可靠的尿液生物标志物的浓度因元素而异,配方奶或人奶的浓度更高。重要的是,无论采用哪种喂养方式,砷的暴露量都会随着家庭自来水砷含量的增加而增加,这表明在饮用水中砷浓度较高的人群中,所有婴儿都可能面临风险。
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引用次数: 0
Sensitive development windows of prenatal air pollution and cognitive functioning in preschool age Mexican children 产前空气污染敏感发育窗口与学龄前墨西哥儿童的认知功能
IF 3.6 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2024-01-09 DOI: 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。
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引用次数: 0
期刊
Environmental Epidemiology
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