Pub Date : 2024-11-01Epub Date: 2024-11-19DOI: 10.1289/EHP16591
Michael S Bloom, Juliana M Clark, John L Pearce, Pamela L Ferguson, Roger B Newman, James R Roberts, William A Grobman, Anthony C Sciscione, Daniel W Skupski, Kelly Garcia, John E Vena, Kelly J Hunt
{"title":"Erratum: \"Impact of Skin Care Products on Phthalates and Phthalate Replacements in Children: The ECHO-FGS\".","authors":"Michael S Bloom, Juliana M Clark, John L Pearce, Pamela L Ferguson, Roger B Newman, James R Roberts, William A Grobman, Anthony C Sciscione, Daniel W Skupski, Kelly Garcia, John E Vena, Kelly J Hunt","doi":"10.1289/EHP16591","DOIUrl":"10.1289/EHP16591","url":null,"abstract":"","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 11","pages":"119001"},"PeriodicalIF":10.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142667612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p><strong>Background: </strong>Planetary and human health are highly intertwined; our current food system is associated with high greenhouse gas emissions (GHGE) and burden of disease.</p><p><strong>Objective: </strong>The aim of this study was to investigate the associations of diet-related GHGE with all-cause and cause-specific mortality in Japan.</p><p><strong>Methods: </strong>This study included 58,031 Japanese adults (35,078 women and 22,953 men) 40-79 y of age who participated in the Japan Collaborative Cohort Study during the period 1988-1990. Diet-related GHGE was calculated from dietary intake estimated by a validated food frequency questionnaire and previously developed GHGE tables of each food and beverage. Participants were classified into quintiles of diet-related GHGE per kg food/d. Hazard ratios (HRs) of all-cause and cause-specific mortality were calculated using the Cox proportional hazard and restricted cubic spline models.</p><p><strong>Results: </strong>The average diet-related GHGE was <math><mrow><mn>1,522</mn><mrow><msub><mrow><mtext> </mtext><mi>g</mi><mtext>-</mtext><mtext>CO</mtext></mrow><mrow><mn>2</mn></mrow></msub></mrow><mtext>-eq</mtext><mo>/</mo><mi>kg</mi><mtext> food</mtext><mo>/</mo><mi>d</mi></mrow></math>. Over a period of 19.3 y (955,819 person-years) of median follow-up, 11,508 deaths were documented. After adjusting for lifestyle and medical history, in comparison with the fourth quintiles of diet-related GHGE, the first and fifth quintiles were associated with a higher risk of all-cause mortality: multivariable HR of all-cause mortality was 1.11 [95% confidence interval (CI): 1.05, 1.18] and 1.09 (95% CI: 1.03, 1.17) for the lowest and highest GHGE, respectively; those of cardiovascular disease mortality were 1.23 (95% CI: 1.10, 1.38) and 1.22 (95% CI: 1.08, 1.37), respectively. The diet-related GHGE range with the lowest HR of all-cause mortality was <math><mrow><mn>1,400</mn><mo>-</mo><mn>1,600</mn><mrow><msub><mrow><mtext> </mtext><mi>g</mi><mtext>-</mtext><mtext>CO</mtext></mrow><mrow><mn>2</mn></mrow></msub></mrow><mtext>eq</mtext><mo>/</mo><mi>kg</mi></mrow></math> food/d (<math><mrow><mi>p</mi></mrow></math> for nonlinearity <math><mrow><mo><</mo><mn>0.001</mn></mrow></math>). Replacing one serving of red meat with one serving of pulses was inversely associated with all-cause mortality (<math><mrow><mtext>HR</mtext><mo>=</mo><mn>0.96</mn></mrow></math>; 95% CI: 0.93, 0.99) and GHGE (mean change, <math><mrow><mo>-</mo><mn>347</mn><mrow><msub><mrow><mtext> </mtext><mi>g</mi><mtext>-</mtext><mtext>CO</mtext></mrow><mrow><mn>2</mn></mrow></msub></mrow><mtext>-eq</mtext><mo>/</mo><mi>kg</mi><mo>/</mo><mi>d</mi></mrow></math>; 95% CI: <math><mrow><mo>-</mo><mn>353</mn></mrow></math>, <math><mrow><mo>-</mo><mn>342</mn></mrow></math>).</p><p><strong>Discussion: </strong>Diet-related GHGE was associated with all-cause and cardiovascular disease mortality in a U-shaped fashion. This finding could be useful
{"title":"Association between Diet-Related Greenhouse Gas Emissions and Mortality among Japanese Adults: The Japan Collaborative Cohort Study.","authors":"Daiki Watanabe, Kotatsu Maruyama, Akiko Tamakoshi, Isao Muraki","doi":"10.1289/EHP14935","DOIUrl":"10.1289/EHP14935","url":null,"abstract":"<p><strong>Background: </strong>Planetary and human health are highly intertwined; our current food system is associated with high greenhouse gas emissions (GHGE) and burden of disease.</p><p><strong>Objective: </strong>The aim of this study was to investigate the associations of diet-related GHGE with all-cause and cause-specific mortality in Japan.</p><p><strong>Methods: </strong>This study included 58,031 Japanese adults (35,078 women and 22,953 men) 40-79 y of age who participated in the Japan Collaborative Cohort Study during the period 1988-1990. Diet-related GHGE was calculated from dietary intake estimated by a validated food frequency questionnaire and previously developed GHGE tables of each food and beverage. Participants were classified into quintiles of diet-related GHGE per kg food/d. Hazard ratios (HRs) of all-cause and cause-specific mortality were calculated using the Cox proportional hazard and restricted cubic spline models.</p><p><strong>Results: </strong>The average diet-related GHGE was <math><mrow><mn>1,522</mn><mrow><msub><mrow><mtext> </mtext><mi>g</mi><mtext>-</mtext><mtext>CO</mtext></mrow><mrow><mn>2</mn></mrow></msub></mrow><mtext>-eq</mtext><mo>/</mo><mi>kg</mi><mtext> food</mtext><mo>/</mo><mi>d</mi></mrow></math>. Over a period of 19.3 y (955,819 person-years) of median follow-up, 11,508 deaths were documented. After adjusting for lifestyle and medical history, in comparison with the fourth quintiles of diet-related GHGE, the first and fifth quintiles were associated with a higher risk of all-cause mortality: multivariable HR of all-cause mortality was 1.11 [95% confidence interval (CI): 1.05, 1.18] and 1.09 (95% CI: 1.03, 1.17) for the lowest and highest GHGE, respectively; those of cardiovascular disease mortality were 1.23 (95% CI: 1.10, 1.38) and 1.22 (95% CI: 1.08, 1.37), respectively. The diet-related GHGE range with the lowest HR of all-cause mortality was <math><mrow><mn>1,400</mn><mo>-</mo><mn>1,600</mn><mrow><msub><mrow><mtext> </mtext><mi>g</mi><mtext>-</mtext><mtext>CO</mtext></mrow><mrow><mn>2</mn></mrow></msub></mrow><mtext>eq</mtext><mo>/</mo><mi>kg</mi></mrow></math> food/d (<math><mrow><mi>p</mi></mrow></math> for nonlinearity <math><mrow><mo><</mo><mn>0.001</mn></mrow></math>). Replacing one serving of red meat with one serving of pulses was inversely associated with all-cause mortality (<math><mrow><mtext>HR</mtext><mo>=</mo><mn>0.96</mn></mrow></math>; 95% CI: 0.93, 0.99) and GHGE (mean change, <math><mrow><mo>-</mo><mn>347</mn><mrow><msub><mrow><mtext> </mtext><mi>g</mi><mtext>-</mtext><mtext>CO</mtext></mrow><mrow><mn>2</mn></mrow></msub></mrow><mtext>-eq</mtext><mo>/</mo><mi>kg</mi><mo>/</mo><mi>d</mi></mrow></math>; 95% CI: <math><mrow><mo>-</mo><mn>353</mn></mrow></math>, <math><mrow><mo>-</mo><mn>342</mn></mrow></math>).</p><p><strong>Discussion: </strong>Diet-related GHGE was associated with all-cause and cardiovascular disease mortality in a U-shaped fashion. This finding could be useful","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 11","pages":"117002"},"PeriodicalIF":12.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11542713/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01Epub Date: 2024-11-08DOI: 10.1289/EHP14634
Ying Liu, Xiaochun Ma, Yifei Le, Jiafan Feng, Mengting Xu, Wanyue Wang, Cui Wang
<p><strong>Background: </strong>Environmental chemical exposures have been associated with metabolic outcomes, and typically, their binding to nuclear hormone receptors is considered the molecular initiating event (MIE) for a number of outcomes. However, more studies are needed to understand the influence of such exposures on cell membrane-bound adiponectin receptors (AdipoRs), which are critical metabolic regulators.</p><p><strong>Objective: </strong>We aimed to clarify the potential interactions between AdipoRs and environmental chemicals, specifically organophosphorus flame retardants (OPFRs), and the resultant effects.</p><p><strong>Methods: </strong>Employing <i>in silico</i> simulation, cell thermal shift, and noncompetitive binding assays, we screened eight OPFRs for interactions with AdipoR1 and AdipoR2. We tested two key events underlying AdipoR modulation upon OPFR exposure in a liver cell model. The Toxicological Prioritization Index (ToxPi)scoring scheme was used to rank OPFRs according to their potential to disrupt AdipoR-associated metabolism. We further examined the inhibitory effect of OPFRs on AdipoR signaling activation in mouse models.</p><p><strong>Results: </strong>Analyses identified pi-pi stacking and pi-sulfur interactions between the aryl-OPFRs 2-ethylhexyl diphenyl phosphate (EHDPP), triphenyl phosphate (TPhP), and tricresyl phosphate (TCP) and the transmembrane cavities of AdipoR1 and AdipoR2. Cell thermal shift assays showed a <math><mrow><mo>></mo><mn>3</mn><mo>°</mo><mi>C</mi></mrow></math> rightward shift in the AdipoR proteins' melting curves upon exposure to these three compounds. Although the binding sites differed from adiponectin, results suggest that aryl-OPFRs noncompetitively inhibited the binding of the endogenous peptide ligand ADP355 to the receptors. Analyses of key events underlying AdipoR modulation revealed that glucose uptake was notably lower, whereas lipid content was higher in cells exposed to aryl-OPFRs. EHDPP, TCP, and TPhP were ranked as the top three disruptors according to the ToxPi scores. A noncompetitive binding between these aryl-OPFRs and AdipoRs was also observed in wild-type (WT) mice. In db/db mice, the finding of lower blood glucose levels after ADP355 injection was diminished in the presence of a typical aryl-OPFR (TCP). WT mice exposed to TCP demonstrated lower AdipoR1 signaling, which was marked by lower phosphorylated AMP-activated protein kinase (pAMPK) and a higher expression of gluconeogenesis-related genes. Moreover, WT mice exposed to ADP355 demonstrated higher levels of pAMPK protein and peroxisome proliferator-activated receptor-<math><mi>α</mi></math> messenger RNA. This was accompanied by higher glucose disposal and by lower levels of long-chain fatty acids and hepatic triglycerides; these metabolic improvements were negated upon TCP co-treatment.</p><p><strong>Conclusions: </strong><i>In silico</i>, <i>in vitro</i>, and <i>in vivo</i> assays suggest that aryl-OPFRs act
{"title":"Organophosphorus Flame Retardants and Metabolic Disruption: An <i>in Silico</i>, <i>in Vitro</i>, and <i>in Vivo</i> Study Focusing on Adiponectin Receptors.","authors":"Ying Liu, Xiaochun Ma, Yifei Le, Jiafan Feng, Mengting Xu, Wanyue Wang, Cui Wang","doi":"10.1289/EHP14634","DOIUrl":"10.1289/EHP14634","url":null,"abstract":"<p><strong>Background: </strong>Environmental chemical exposures have been associated with metabolic outcomes, and typically, their binding to nuclear hormone receptors is considered the molecular initiating event (MIE) for a number of outcomes. However, more studies are needed to understand the influence of such exposures on cell membrane-bound adiponectin receptors (AdipoRs), which are critical metabolic regulators.</p><p><strong>Objective: </strong>We aimed to clarify the potential interactions between AdipoRs and environmental chemicals, specifically organophosphorus flame retardants (OPFRs), and the resultant effects.</p><p><strong>Methods: </strong>Employing <i>in silico</i> simulation, cell thermal shift, and noncompetitive binding assays, we screened eight OPFRs for interactions with AdipoR1 and AdipoR2. We tested two key events underlying AdipoR modulation upon OPFR exposure in a liver cell model. The Toxicological Prioritization Index (ToxPi)scoring scheme was used to rank OPFRs according to their potential to disrupt AdipoR-associated metabolism. We further examined the inhibitory effect of OPFRs on AdipoR signaling activation in mouse models.</p><p><strong>Results: </strong>Analyses identified pi-pi stacking and pi-sulfur interactions between the aryl-OPFRs 2-ethylhexyl diphenyl phosphate (EHDPP), triphenyl phosphate (TPhP), and tricresyl phosphate (TCP) and the transmembrane cavities of AdipoR1 and AdipoR2. Cell thermal shift assays showed a <math><mrow><mo>></mo><mn>3</mn><mo>°</mo><mi>C</mi></mrow></math> rightward shift in the AdipoR proteins' melting curves upon exposure to these three compounds. Although the binding sites differed from adiponectin, results suggest that aryl-OPFRs noncompetitively inhibited the binding of the endogenous peptide ligand ADP355 to the receptors. Analyses of key events underlying AdipoR modulation revealed that glucose uptake was notably lower, whereas lipid content was higher in cells exposed to aryl-OPFRs. EHDPP, TCP, and TPhP were ranked as the top three disruptors according to the ToxPi scores. A noncompetitive binding between these aryl-OPFRs and AdipoRs was also observed in wild-type (WT) mice. In db/db mice, the finding of lower blood glucose levels after ADP355 injection was diminished in the presence of a typical aryl-OPFR (TCP). WT mice exposed to TCP demonstrated lower AdipoR1 signaling, which was marked by lower phosphorylated AMP-activated protein kinase (pAMPK) and a higher expression of gluconeogenesis-related genes. Moreover, WT mice exposed to ADP355 demonstrated higher levels of pAMPK protein and peroxisome proliferator-activated receptor-<math><mi>α</mi></math> messenger RNA. This was accompanied by higher glucose disposal and by lower levels of long-chain fatty acids and hepatic triglycerides; these metabolic improvements were negated upon TCP co-treatment.</p><p><strong>Conclusions: </strong><i>In silico</i>, <i>in vitro</i>, and <i>in vivo</i> assays suggest that aryl-OPFRs act ","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 11","pages":"117003"},"PeriodicalIF":12.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11548883/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01Epub Date: 2024-11-14DOI: 10.1289/EHP14513
Tamarra James-Todd, Kathryn S Tomsho, Symielle A Gaston, Kevin C Elliott, Chandra L Jackson
Background: In environmental epidemiology, we use an array of tools from various, related disciplines to answer key questions about environmental exposures in relation to health outcomes. Typically, we ask questions related to what, who, where, when, and how. We value these questions because they contribute to novel scientific discovery and our understanding of disease etiology linked to environmental exposures. In addition, these questions help us better understand who might be at highest risk of exposure and subsequent risk of disease. Although necessary for the goals of environmental epidemiology, these questions are insufficient for addressing environmental health disparities. Specifically, these questions may be able to help us describe exposure-health outcome associations but are limited in their ability to move beyond identification to intervening on observed disparities to achieve environmental health equity.
Objectives: We sought to emphasize the need to value and routinely add the key question of "Why?" in environmental epidemiological studies. In asking this additional critical question, we can identify and incorporate the structural determinants and drivers of environmental exposure disparities and determine whether these factors are linked to existing and historically recalcitrant health disparities. Further, we can design effective studies that build on existing frameworks to address the fundamental causes of environmental health disparities.
Discussion: This commentary underscores the need to routinely incorporate "why" questions in the practice of environmental epidemiology. By asking and addressing "Why?" we can employ better, more solution-oriented study designs, improve data collection, and enhance our ability to collaborate with diverse study populations through trust-building and community-engaged research. Incorporating these approaches will move environmental epidemiology forward from mostly documenting to actively addressing environmental health disparities. https://doi.org/10.1289/EHP14513.
{"title":"Asking Why Is Necessary to Address Health Disparities: A Critical Approach for Solution-Oriented Environmental Epidemiological Research.","authors":"Tamarra James-Todd, Kathryn S Tomsho, Symielle A Gaston, Kevin C Elliott, Chandra L Jackson","doi":"10.1289/EHP14513","DOIUrl":"10.1289/EHP14513","url":null,"abstract":"<p><strong>Background: </strong>In environmental epidemiology, we use an array of tools from various, related disciplines to answer key questions about environmental exposures in relation to health outcomes. Typically, we ask questions related to what, who, where, when, and how. We value these questions because they contribute to novel scientific discovery and our understanding of disease etiology linked to environmental exposures. In addition, these questions help us better understand who might be at highest risk of exposure and subsequent risk of disease. Although necessary for the goals of environmental epidemiology, these questions are insufficient for addressing environmental health disparities. Specifically, these questions may be able to help us describe exposure-health outcome associations but are limited in their ability to move beyond identification to intervening on observed disparities to achieve environmental health equity.</p><p><strong>Objectives: </strong>We sought to emphasize the need to value and routinely add the key question of \"Why?\" in environmental epidemiological studies. In asking this additional critical question, we can identify and incorporate the structural determinants and drivers of environmental exposure disparities and determine whether these factors are linked to existing and historically recalcitrant health disparities. Further, we can design effective studies that build on existing frameworks to address the fundamental causes of environmental health disparities.</p><p><strong>Discussion: </strong>This commentary underscores the need to routinely incorporate \"why\" questions in the practice of environmental epidemiology. By asking and addressing \"Why?\" we can employ better, more solution-oriented study designs, improve data collection, and enhance our ability to collaborate with diverse study populations through trust-building and community-engaged research. Incorporating these approaches will move environmental epidemiology forward from mostly documenting to actively addressing environmental health disparities. https://doi.org/10.1289/EHP14513.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 11","pages":"115001"},"PeriodicalIF":10.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11563029/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142616682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01Epub Date: 2024-11-12DOI: 10.1289/EHP16404
Ziwei Gao, Jiachen Qi, Wei Ye
{"title":"Comment on \"Associations between Changes in Exposure to Air Pollutants due to Relocation and the Incidence of 14 Major Disease Categories and All-Cause Mortality: A Natural Experiment Study\".","authors":"Ziwei Gao, Jiachen Qi, Wei Ye","doi":"10.1289/EHP16404","DOIUrl":"10.1289/EHP16404","url":null,"abstract":"","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 11","pages":"118001"},"PeriodicalIF":10.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11556394/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142616688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01Epub Date: 2024-11-08DOI: 10.1289/EHP15224
Wendee Nicole
The integrated approach tackles a perfect storm of poverty, invasive rats, deforestation, and climate change that is contributing to the increase in bubonic plague cases.
这种综合方法解决了导致鼠疫病例增加的贫困、鼠类入侵、森林砍伐和气候变化等问题。
{"title":"Madagascar's Plague: One Health Research Aims to Slow Its Spread.","authors":"Wendee Nicole","doi":"10.1289/EHP15224","DOIUrl":"10.1289/EHP15224","url":null,"abstract":"<p><p>The integrated approach tackles a perfect storm of poverty, invasive rats, deforestation, and climate change that is contributing to the increase in bubonic plague cases.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 11","pages":"112001"},"PeriodicalIF":12.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11548884/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01Epub Date: 2024-11-06DOI: 10.1289/EHP14334
Youran Tan, Stephanie M Eick, Anne L Dunlop, Dana Boyd Barr, Kaitlin R Taibl, Kyle Steenland, Kurunthachalam Kannan, Morgan Robinson, Che-Jung Chang, Parinya Panuwet, Volha Yakimavets, Carmen J Marsit, P Barry Ryan, Donghai Liang
<p><strong>Background: </strong>Longitudinal trends in per- and polyfluoroalkyl substances (PFAS) serum concentrations across pregnancy have not been thoroughly examined, despite evidence linking prenatal PFAS exposures with adverse birth outcomes.</p><p><strong>Objectives: </strong>We sought to characterize longitudinal PFAS concentrations across pregnancy and to examine the maternal-fetal transfer ratio among participants in a study of risk and protective factors for adverse birth outcomes among African Americans.</p><p><strong>Methods: </strong>In the Atlanta African American Maternal-Child cohort (2014-2020), we quantified serum concentrations of four PFAS in 376 participants and an additional eight PFAS in a subset of 301 participants during early (8-14 weeks gestation) and late pregnancy (24-30 weeks gestation). Among these, PFAS concentrations were also measured among 199 newborns with available dried blood spot (DBS) samples. We characterized the patterns, variability, and associations in PFAS concentrations at different time points across pregnancy using intraclass correlation coefficients (ICCs), maternal-newborn pairs transfer ratios, linear mixed effect models, and multivariable linear regression, adjusting for socioeconomic and prenatal predictors.</p><p><strong>Results: </strong>Perfluorohexane sulfonic acid (PFHxS), perfluorooctane sulfonic acid (PFOS), perfluorooctanoic acid (PFOA), and perfluorononanoic acid (PFNA) were detected in <math><mrow><mo>></mo><mn>95</mn><mo>%</mo></mrow></math> of maternal samples, with PFHxS and PFOS having the highest median concentrations. We observed high variability in PFAS concentrations across pregnancy time points (<math><mrow><mtext>ICC</mtext><mo>=</mo><mn>0.03</mn><mo>-</mo><mn>0.59</mn></mrow></math>). All median PFAS concentrations increased from early to late pregnancy, except for PFOA and N-methyl perfluorooctane sulfonamido acetic acid (NMFOSAA), which decreased [paired <math><mi>t</mi></math>-test for all PFAS <math><mrow><mi>p</mi><mo><</mo><mn>0.05</mn></mrow></math> except for PFOA and perfluorobutane sulfonic acid (PFBS)]. Prenatal serum PFAS were weakly to moderately correlated with newborn DBS PFAS (<math><mrow><mo>-</mo><mn>0.05</mn><mo><</mo><mtext>rho</mtext></mrow></math> <math><mrow><mo><</mo><mn>0.49</mn></mrow></math>). The median maternal-fetal PFAS transfer ratio was lower for PFAS with longer carbon chains. After adjusting for socioeconomic and prenatal predictors, in linear mixed effect models, the adjusted mean PFAS concentrations significantly increased during pregnancy, except for PFOA. In multivariable linear regression, PFAS concentrations in early pregnancy significantly predicted the PFAS concentrations in late pregnancy and in newborns.</p><p><strong>Discussion: </strong>We found that the concentrations of most PFAS increased during pregnancy, and the magnitude of variability differed by individual PFAS. Future studies are needed to understand the influence of
{"title":"A Prospective Analysis of Per- and Polyfluoroalkyl Substances from Early Pregnancy to Delivery in the Atlanta African American Maternal-Child Cohort.","authors":"Youran Tan, Stephanie M Eick, Anne L Dunlop, Dana Boyd Barr, Kaitlin R Taibl, Kyle Steenland, Kurunthachalam Kannan, Morgan Robinson, Che-Jung Chang, Parinya Panuwet, Volha Yakimavets, Carmen J Marsit, P Barry Ryan, Donghai Liang","doi":"10.1289/EHP14334","DOIUrl":"10.1289/EHP14334","url":null,"abstract":"<p><strong>Background: </strong>Longitudinal trends in per- and polyfluoroalkyl substances (PFAS) serum concentrations across pregnancy have not been thoroughly examined, despite evidence linking prenatal PFAS exposures with adverse birth outcomes.</p><p><strong>Objectives: </strong>We sought to characterize longitudinal PFAS concentrations across pregnancy and to examine the maternal-fetal transfer ratio among participants in a study of risk and protective factors for adverse birth outcomes among African Americans.</p><p><strong>Methods: </strong>In the Atlanta African American Maternal-Child cohort (2014-2020), we quantified serum concentrations of four PFAS in 376 participants and an additional eight PFAS in a subset of 301 participants during early (8-14 weeks gestation) and late pregnancy (24-30 weeks gestation). Among these, PFAS concentrations were also measured among 199 newborns with available dried blood spot (DBS) samples. We characterized the patterns, variability, and associations in PFAS concentrations at different time points across pregnancy using intraclass correlation coefficients (ICCs), maternal-newborn pairs transfer ratios, linear mixed effect models, and multivariable linear regression, adjusting for socioeconomic and prenatal predictors.</p><p><strong>Results: </strong>Perfluorohexane sulfonic acid (PFHxS), perfluorooctane sulfonic acid (PFOS), perfluorooctanoic acid (PFOA), and perfluorononanoic acid (PFNA) were detected in <math><mrow><mo>></mo><mn>95</mn><mo>%</mo></mrow></math> of maternal samples, with PFHxS and PFOS having the highest median concentrations. We observed high variability in PFAS concentrations across pregnancy time points (<math><mrow><mtext>ICC</mtext><mo>=</mo><mn>0.03</mn><mo>-</mo><mn>0.59</mn></mrow></math>). All median PFAS concentrations increased from early to late pregnancy, except for PFOA and N-methyl perfluorooctane sulfonamido acetic acid (NMFOSAA), which decreased [paired <math><mi>t</mi></math>-test for all PFAS <math><mrow><mi>p</mi><mo><</mo><mn>0.05</mn></mrow></math> except for PFOA and perfluorobutane sulfonic acid (PFBS)]. Prenatal serum PFAS were weakly to moderately correlated with newborn DBS PFAS (<math><mrow><mo>-</mo><mn>0.05</mn><mo><</mo><mtext>rho</mtext></mrow></math> <math><mrow><mo><</mo><mn>0.49</mn></mrow></math>). The median maternal-fetal PFAS transfer ratio was lower for PFAS with longer carbon chains. After adjusting for socioeconomic and prenatal predictors, in linear mixed effect models, the adjusted mean PFAS concentrations significantly increased during pregnancy, except for PFOA. In multivariable linear regression, PFAS concentrations in early pregnancy significantly predicted the PFAS concentrations in late pregnancy and in newborns.</p><p><strong>Discussion: </strong>We found that the concentrations of most PFAS increased during pregnancy, and the magnitude of variability differed by individual PFAS. Future studies are needed to understand the influence of ","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 11","pages":"117001"},"PeriodicalIF":10.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11540153/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142590264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01Epub Date: 2024-11-04DOI: 10.1289/EHP15844
Wendee Nicole
Gut microbes appeared to play a role in the obesity outcomes observed in mice fed manufactured polystyrene microspheres.
肠道微生物似乎在喂食人造聚苯乙烯微球的小鼠中观察到的肥胖结果中起了作用。
{"title":"Gut Check: Microbiota and Obesity in Mice Exposed to Polystyrene Microspheres.","authors":"Wendee Nicole","doi":"10.1289/EHP15844","DOIUrl":"10.1289/EHP15844","url":null,"abstract":"<p><p>Gut microbes appeared to play a role in the obesity outcomes observed in mice fed manufactured polystyrene microspheres.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 11","pages":"114001"},"PeriodicalIF":10.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11534003/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-01Epub Date: 2024-10-28DOI: 10.1289/EHP14806
Frederic T Lu, Disha Gupta, Nancy Fiedler, Usha Satish, Kathleen G Black, Alicia Legard, Adriana De Resende, Changjiang Guo, Andrew J Gow, Howard M Kipen
{"title":"Mechanisms Underlying Acute Cognitive Impairment following Carbon Dioxide Inhalation in a Randomized Crossover Trial.","authors":"Frederic T Lu, Disha Gupta, Nancy Fiedler, Usha Satish, Kathleen G Black, Alicia Legard, Adriana De Resende, Changjiang Guo, Andrew J Gow, Howard M Kipen","doi":"10.1289/EHP14806","DOIUrl":"10.1289/EHP14806","url":null,"abstract":"","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 10","pages":"107702"},"PeriodicalIF":10.1,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11515854/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142521435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jennifer L Ish, Che-Jung Chang, Deborah B Bookwalter, Rena R Jones, Katie M O'Brien, Joel D Kaufman, Dale P Sandler, Alexandra J White
{"title":"Outdoor Air Pollution Exposure and Ovarian Cancer Incidence in a United States-Wide Prospective Cohort Study.","authors":"Jennifer L Ish, Che-Jung Chang, Deborah B Bookwalter, Rena R Jones, Katie M O'Brien, Joel D Kaufman, Dale P Sandler, Alexandra J White","doi":"10.1289/EHP14729","DOIUrl":"10.1289/EHP14729","url":null,"abstract":"","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"132 10","pages":"107701"},"PeriodicalIF":10.1,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11444316/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142364909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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