<div><h3>Background</h3><div>Synthetic phenols are widely used chemicals with potential neurodevelopmental toxicity. Human studies are often limited by small sample sizes and exposure misclassification. Identifying the biological pathways affected by these substances is crucial for understanding key drivers of toxicity. We aimed to study associations between prenatal exposure to synthetic phenols and child behaviour, exploring the potential mediating role of maternal steroid hormones.</div></div><div><h3>Methods</h3><div>We pooled data from two European cohorts: the Barcelona Life Study Cohort (BiSC; Barcelona, Spain, 2018–21, N=1080) and Suivi de l’Exposition à la Pollution Atmosphérique durant la Grossesse et Effets sur la Santé (SEPAGES; Grenoble, France, 2014–17, N=484). Mothers older than 18 years having a singleton pregnancy of less than 19 weeks gestational age were eligible for inclusion in the cohorts; those having multiple pregnancies were excluded. Repeated urine samples (up to 24 in BiSC; up to 42 in SEPAGES) collected in the second and third trimesters were pooled and analysed for 12 synthetic phenols. Child behavioural outcomes were assessed at 18 months in BiSC and 24 months in SEPAGES using the Child Behavior Checklist for Ages 1·5–5 (CBCL). Concentrations of total cortisol, total cortisone, and 11-dehydrocorticosterone—steroid hormones involved in the hypothalamic–pituitary–adrenal axis—were measured from maternal hair samples. Associations between phenol exposure and behavioural outcomes were estimated by adjusted linear regression analysis, and mediation by steroid hormones was assessed with regression-based causal mediation analysis within the counterfactual framework.</div></div><div><h3>Findings</h3><div>1024 mother–child pairs were included in the study: 607 from BiSC and 417 from SEPAGES. Maternal exposure to methylparaben in the third trimester of pregnancy was associated with higher internalising scores (change in score of 0·44 [95% CI 0·10–0·79] points) and externalising scores (0·67 [0·12–1·24]) in the CBCL. In boys, maternal exposure to bisphenol S in the third trimester was linked to increased internalising scores (0·92 [0·15 to 1·75]; p=0·019) and could be linked to increased externalising scores (1·14 [−0·09 to 2·44]; p=0·070). In girls, second-trimester butylparaben and propylparaben exposure were associated with lower internalising (−1·03 [−1·84 to −0·09], p=0·033) and externalising (−0·68 [−1·23 to −0·12]; p=0·019) scores. No mediation by steroid hormones was observed.</div></div><div><h3>Interpretation</h3><div>Prenatal exposure to phenols might influence early behavioural development, with sex-specific patterns. There was no strong evidence of mediation by maternal steroid hormones, suggesting the involvement of alternative pathways in the biological effects of phenols. Together with previous findings, these results highlight the need for stricter regulation of these compounds to reduce prenatal exposure.</div
背景：合成酚是一种应用广泛的化学物质，具有潜在的神经发育毒性。人体研究经常受到样本量小和暴露错误分类的限制。确定受这些物质影响的生物途径对于理解毒性的关键驱动因素至关重要。我们的目的是研究产前暴露于合成酚和儿童行为之间的关系，探索母体类固醇激素的潜在中介作用。方法：我们汇集了来自两个欧洲队列的数据：巴塞罗那生活研究队列（BiSC；巴塞罗那，西班牙，2018-21，N=1080）和Suivi de l'Exposition la Pollution atmosprique durant la Grossesse et Effets sur la sant （SEPAGES；格勒诺布尔，法国，2014-17，N=484）。年龄大于18岁且单胎妊娠小于19周的母亲有资格纳入队列；多胎妊娠者被排除在外。在妊娠中期和晚期收集的重复尿液样本（BiSC最多24份，SEPAGES最多42份）汇总并分析了12种合成酚。使用儿童行为检查表（CBCL）对18个月大的BiSC和24个月大的SEPAGES的儿童行为结果进行评估。总皮质醇、总可的松和参与下丘脑-垂体-肾上腺轴的11-脱氢皮质酮类固醇激素的浓度从母体头发样本中测量。通过调整线性回归分析估计苯酚暴露与行为结果之间的关系，并在反事实框架内使用基于回归的因果中介分析评估类固醇激素的中介作用。研究结果：1024对母子纳入研究：607对来自BiSC， 417对来自SEPAGES。孕妇在妊娠晚期接触对羟基苯甲酸甲酯与CBCL中较高的内化评分（0.44 [95% CI 0.10 - 0.79]分）和外化评分（0.67[0.12 - 1.24]）相关。在男孩中，母亲在妊娠晚期暴露于双酚S与内化得分增加有关（0.92[0.15至1.75];p= 0.019），并可能与外化得分增加有关（1.14[- 0.09至2.44];p= 0.070）。在女孩中，妊娠中期暴露于对羟基苯甲酸丁酯和对羟基苯甲酸丙酯与较低的内化（-1·03[-1·84至-0·09]，p= 0.033）和外化（-0·68[-1·23至-0·12]，p= 0.019）评分相关。未观察到类固醇激素的介导作用。解释：产前接触酚类物质可能影响早期行为发育，并具有性别特异性模式。没有强有力的证据表明母体类固醇激素介导，这表明酚类物质的生物学效应有其他途径参与。与先前的研究结果一起，这些结果强调了对这些化合物进行更严格监管以减少产前暴露的必要性。资助：法国食品、环境和职业健康与安全局、欧盟“地平线2020”研究和创新方案以及法国基金-法国基金会。
{"title":"Prenatal phenol exposure and child behaviour: insights into the hypothalamic–pituitary–adrenal axis from two prospective mother–child cohorts","authors":"Matthieu Rolland MSc , Mariona Bustamante PhD , Paulina Jedynak PhD , Cathrine Thomsen PhD , Amrit K Sakhi PhD , Maria Foraster PhD , Mireia Gascon PhD , Maria Dolores Gómez-Roig MD PhD , Elisa Llurba MD PhD , Ioar Rivas PhD , Isabelle Ouellet-Morin PhD , Muriel Ferrer MSc , Alex Morillas MSc , Sylvain Carras PhD , Sam Bayat MD PhD , Sarah Lyon-Caen MSc , Oscar J Pozo PhD , Martine Vrijheid PhD , Jordi Sunyer MD PhD , Rémy Slama PhD , Claire Philippat PhD","doi":"10.1016/j.lanplh.2025.101330","DOIUrl":"10.1016/j.lanplh.2025.101330","url":null,"abstract":"<div><h3>Background</h3><div>Synthetic phenols are widely used chemicals with potential neurodevelopmental toxicity. Human studies are often limited by small sample sizes and exposure misclassification. Identifying the biological pathways affected by these substances is crucial for understanding key drivers of toxicity. We aimed to study associations between prenatal exposure to synthetic phenols and child behaviour, exploring the potential mediating role of maternal steroid hormones.</div></div><div><h3>Methods</h3><div>We pooled data from two European cohorts: the Barcelona Life Study Cohort (BiSC; Barcelona, Spain, 2018–21, N=1080) and Suivi de l’Exposition à la Pollution Atmosphérique durant la Grossesse et Effets sur la Santé (SEPAGES; Grenoble, France, 2014–17, N=484). Mothers older than 18 years having a singleton pregnancy of less than 19 weeks gestational age were eligible for inclusion in the cohorts; those having multiple pregnancies were excluded. Repeated urine samples (up to 24 in BiSC; up to 42 in SEPAGES) collected in the second and third trimesters were pooled and analysed for 12 synthetic phenols. Child behavioural outcomes were assessed at 18 months in BiSC and 24 months in SEPAGES using the Child Behavior Checklist for Ages 1·5–5 (CBCL). Concentrations of total cortisol, total cortisone, and 11-dehydrocorticosterone—steroid hormones involved in the hypothalamic–pituitary–adrenal axis—were measured from maternal hair samples. Associations between phenol exposure and behavioural outcomes were estimated by adjusted linear regression analysis, and mediation by steroid hormones was assessed with regression-based causal mediation analysis within the counterfactual framework.</div></div><div><h3>Findings</h3><div>1024 mother–child pairs were included in the study: 607 from BiSC and 417 from SEPAGES. Maternal exposure to methylparaben in the third trimester of pregnancy was associated with higher internalising scores (change in score of 0·44 [95% CI 0·10–0·79] points) and externalising scores (0·67 [0·12–1·24]) in the CBCL. In boys, maternal exposure to bisphenol S in the third trimester was linked to increased internalising scores (0·92 [0·15 to 1·75]; p=0·019) and could be linked to increased externalising scores (1·14 [−0·09 to 2·44]; p=0·070). In girls, second-trimester butylparaben and propylparaben exposure were associated with lower internalising (−1·03 [−1·84 to −0·09], p=0·033) and externalising (−0·68 [−1·23 to −0·12]; p=0·019) scores. No mediation by steroid hormones was observed.</div></div><div><h3>Interpretation</h3><div>Prenatal exposure to phenols might influence early behavioural development, with sex-specific patterns. There was no strong evidence of mediation by maternal steroid hormones, suggesting the involvement of alternative pathways in the biological effects of phenols. Together with previous findings, these results highlight the need for stricter regulation of these compounds to reduce prenatal exposure.</div","PeriodicalId":48548,"journal":{"name":"Lancet Planetary Health","volume":"9 12","pages":"Article 101330"},"PeriodicalIF":21.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145745198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01Epub Date: 2025-11-27DOI: 10.1016/j.lanplh.2025.101375
Inge Schrijver MA , Prof Paul Behrens PhD , Rutger Hoekstra PhD , Prof René Kleijn PhD
Climate change has broad and deep impacts on people’s wellbeing; yet, these dynamics are largely excluded from integrated environment–society–economy (ESE) models. In this Review, we provide an overview of climate change–wellbeing impact pathways and explore which of these pathways have been quantified or modelled, or both. We assessed literature reviews and meta-analyses to describe how climate change affects specific wellbeing outcomes and which of these relationships are robust and amenable to parametrisation. We also conducted a review of 18 models that include one or more wellbeing impacts of climate change. Generally, more quantified pathways are available in the literature than those currently incorporated in ESE models. Temperature-related mortality, food security, and GDP are well represented in quantitative literature and to some extent in ESE models, whereas the impacts of climate change on infectious diseases; respiratory, cardiovascular, and neurological outcomes; mental health; adverse birth outcomes; occupational health and labour productivity; conflict; migration; poverty; air quality; and biodiversity loss have been quantified in the literature but are largely absent in ESE models. These relationships present promising steps towards a next generation of ESE models that could include more sophisticated interactions between environmental impacts and wellbeing.
{"title":"Inclusion of wellbeing impacts of climate change: a review of literature and integrated environment–society–economy models","authors":"Inge Schrijver MA , Prof Paul Behrens PhD , Rutger Hoekstra PhD , Prof René Kleijn PhD","doi":"10.1016/j.lanplh.2025.101375","DOIUrl":"10.1016/j.lanplh.2025.101375","url":null,"abstract":"<div><div>Climate change has broad and deep impacts on people’s wellbeing; yet, these dynamics are largely excluded from integrated environment–society–economy (ESE) models. In this Review, we provide an overview of climate change–wellbeing impact pathways and explore which of these pathways have been quantified or modelled, or both. We assessed literature reviews and meta-analyses to describe how climate change affects specific wellbeing outcomes and which of these relationships are robust and amenable to parametrisation. We also conducted a review of 18 models that include one or more wellbeing impacts of climate change. Generally, more quantified pathways are available in the literature than those currently incorporated in ESE models. Temperature-related mortality, food security, and GDP are well represented in quantitative literature and to some extent in ESE models, whereas the impacts of climate change on infectious diseases; respiratory, cardiovascular, and neurological outcomes; mental health; adverse birth outcomes; occupational health and labour productivity; conflict; migration; poverty; air quality; and biodiversity loss have been quantified in the literature but are largely absent in ESE models. These relationships present promising steps towards a next generation of ESE models that could include more sophisticated interactions between environmental impacts and wellbeing.</div></div>","PeriodicalId":48548,"journal":{"name":"Lancet Planetary Health","volume":"9 12","pages":"Article 101375"},"PeriodicalIF":21.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145641350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01Epub Date: 2025-11-03DOI: 10.1016/j.lanplh.2025.101324
Allison R Sherris PhD , Logan C Dearborn MPH , Dana E Goin PhD , Christine T Loftus PhD , Prof Adam A Szpiro PhD , Joan A Casey PhD , Sindana D Ilango PhD , Jyoti Angal PhD , Prof Deborah H Bennett PhD , Miatta A Buxton PhD , Prof Carlos A Camargo Jr MD DrPH , Prof Kecia N Carroll MD , Marissa L Childs PhD , Camille Cioffi PhD , Lisa A Croen PhD , Prof Dana Dabelea MD PhD , Stephanie M Eick PhD , Shohreh F Farzan PhD , Assiamira Ferrara MD PhD , Erika Garcia PhD , Amy M Padula PhD
<div><h3>Background</h3><div>Exposure to PM<sub>2·5</sub> from wildfire smoke during pregnancy has been implicated as a risk factor for preterm birth. We investigated this association in the prospective nationwide US Environmental Influences on Child Health Outcomes (ECHO) Cohort, focusing on prenatal wildfire PM<sub>2·5</sub> exposure intensity, duration, and timing.</div></div><div><h3>Methods</h3><div>In this cohort analysis, we included live singleton births recorded in the ECHO Cohort with available data on gestational age at birth and birthweight and dates of conception between Jan 1, 2006, and March 20, 2020. Census tract-level estimates of daily mean wildfire-derived PM<sub>2·5</sub> for the years 2006–20 from a previous machine learning model were linked to residential address history. We calculated the mean concentration of daily wildfire PM<sub>2·5</sub>, days with wildfire PM<sub>2·5</sub> (>0, ≥2·5, ≥5·0, and ≥10·0 μg/m<sup>3</sup>; termed smoke days) and consecutive smoke days (2, 3, or ≥4 days; termed smoke waves) above the prespecified concentration thresholds across pregnancy. Associations of cumlative pregnancy wildfire PM<sub>2·5</sub> exposure with preterm birth (delivery before 37 weeks of gestation) were analysed by adjusted pooled logistic regression in the nationwide ECHO sample and in the US West census region. Associations between smoke days in gestational weeks 0–35 and preterm birth were evaluated by logistic regression in the national sample.</div></div><div><h3>Findings</h3><div>We included 20 034 births from 30 ECHO Cohort study sites, with residences during pregnancy in all 48 contiguous US states and the District of Columbia. 1687 (8·4%) of the 20 034 infants were preterm. The mean daily wildfire PM<sub>2·5</sub> concentration during pregnancy was 0·36 μg/m<sup>3</sup> (SD 0·46), with exposure to a mean of 22·2 smoke days (SD 16·6) of any wildfire PM<sub>2·5</sub> concentration (>0 μg/m<sup>3</sup>). Estimates of association between wildfire PM<sub>2·5</sub> exposure metrics and preterm birth included the null in nationwide analyses; whereas, in the US West sample (N=5807), we estimated increased odds of preterm birth associated with mean daily wildfire PM<sub>2·5</sub> (odds ratio [OR] 1·139 per 1-μg/m<sup>3</sup> increase [95% CI 1·001–1·296]), exposure to smoke days with a wildfire PM<sub>2·5</sub> concentration of 5·0 μg/m<sup>3</sup> or greater (OR 1·018 per additional smoke day [1·003–1·032]) and 10·0 μg/m<sup>3</sup> or greater (OR 1·030 [1·006–1·054]), and exposure to ≥4-day smoke waves of 5·0 μg/m<sup>3</sup> or greater (OR 1·185 per additional smoke wave [1·044–1·347]) and 10·0 μg/m<sup>3</sup> or greater (OR 1·232 [1·029–1·475]). At the national level, by week of gestation, associations with preterm birth were observed in mid-pregnancy for smoke days with wildfire PM<sub>2·5</sub> concentrations above 0 μg/m<sup>3</sup>, of 2·5 μg/m<sup>3</sup> or greater, and of 5·0 μg/m<sup>3</sup> or greater, a
{"title":"Wildfire-specific fine particulate matter and preterm birth: a US ECHO Cohort analysis","authors":"Allison R Sherris PhD , Logan C Dearborn MPH , Dana E Goin PhD , Christine T Loftus PhD , Prof Adam A Szpiro PhD , Joan A Casey PhD , Sindana D Ilango PhD , Jyoti Angal PhD , Prof Deborah H Bennett PhD , Miatta A Buxton PhD , Prof Carlos A Camargo Jr MD DrPH , Prof Kecia N Carroll MD , Marissa L Childs PhD , Camille Cioffi PhD , Lisa A Croen PhD , Prof Dana Dabelea MD PhD , Stephanie M Eick PhD , Shohreh F Farzan PhD , Assiamira Ferrara MD PhD , Erika Garcia PhD , Amy M Padula PhD","doi":"10.1016/j.lanplh.2025.101324","DOIUrl":"10.1016/j.lanplh.2025.101324","url":null,"abstract":"<div><h3>Background</h3><div>Exposure to PM<sub>2·5</sub> from wildfire smoke during pregnancy has been implicated as a risk factor for preterm birth. We investigated this association in the prospective nationwide US Environmental Influences on Child Health Outcomes (ECHO) Cohort, focusing on prenatal wildfire PM<sub>2·5</sub> exposure intensity, duration, and timing.</div></div><div><h3>Methods</h3><div>In this cohort analysis, we included live singleton births recorded in the ECHO Cohort with available data on gestational age at birth and birthweight and dates of conception between Jan 1, 2006, and March 20, 2020. Census tract-level estimates of daily mean wildfire-derived PM<sub>2·5</sub> for the years 2006–20 from a previous machine learning model were linked to residential address history. We calculated the mean concentration of daily wildfire PM<sub>2·5</sub>, days with wildfire PM<sub>2·5</sub> (>0, ≥2·5, ≥5·0, and ≥10·0 μg/m<sup>3</sup>; termed smoke days) and consecutive smoke days (2, 3, or ≥4 days; termed smoke waves) above the prespecified concentration thresholds across pregnancy. Associations of cumlative pregnancy wildfire PM<sub>2·5</sub> exposure with preterm birth (delivery before 37 weeks of gestation) were analysed by adjusted pooled logistic regression in the nationwide ECHO sample and in the US West census region. Associations between smoke days in gestational weeks 0–35 and preterm birth were evaluated by logistic regression in the national sample.</div></div><div><h3>Findings</h3><div>We included 20 034 births from 30 ECHO Cohort study sites, with residences during pregnancy in all 48 contiguous US states and the District of Columbia. 1687 (8·4%) of the 20 034 infants were preterm. The mean daily wildfire PM<sub>2·5</sub> concentration during pregnancy was 0·36 μg/m<sup>3</sup> (SD 0·46), with exposure to a mean of 22·2 smoke days (SD 16·6) of any wildfire PM<sub>2·5</sub> concentration (>0 μg/m<sup>3</sup>). Estimates of association between wildfire PM<sub>2·5</sub> exposure metrics and preterm birth included the null in nationwide analyses; whereas, in the US West sample (N=5807), we estimated increased odds of preterm birth associated with mean daily wildfire PM<sub>2·5</sub> (odds ratio [OR] 1·139 per 1-μg/m<sup>3</sup> increase [95% CI 1·001–1·296]), exposure to smoke days with a wildfire PM<sub>2·5</sub> concentration of 5·0 μg/m<sup>3</sup> or greater (OR 1·018 per additional smoke day [1·003–1·032]) and 10·0 μg/m<sup>3</sup> or greater (OR 1·030 [1·006–1·054]), and exposure to ≥4-day smoke waves of 5·0 μg/m<sup>3</sup> or greater (OR 1·185 per additional smoke wave [1·044–1·347]) and 10·0 μg/m<sup>3</sup> or greater (OR 1·232 [1·029–1·475]). At the national level, by week of gestation, associations with preterm birth were observed in mid-pregnancy for smoke days with wildfire PM<sub>2·5</sub> concentrations above 0 μg/m<sup>3</sup>, of 2·5 μg/m<sup>3</sup> or greater, and of 5·0 μg/m<sup>3</sup> or greater, a","PeriodicalId":48548,"journal":{"name":"Lancet Planetary Health","volume":"9 12","pages":"Article 101324"},"PeriodicalIF":21.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145460480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01Epub Date: 2025-12-30DOI: 10.1016/j.lanplh.2025.101420
The Lancet Planetary Health
{"title":"In desperate need of systems change","authors":"The Lancet Planetary Health","doi":"10.1016/j.lanplh.2025.101420","DOIUrl":"10.1016/j.lanplh.2025.101420","url":null,"abstract":"","PeriodicalId":48548,"journal":{"name":"Lancet Planetary Health","volume":"9 12","pages":"Article 101420"},"PeriodicalIF":21.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145852482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01Epub Date: 2025-11-22DOI: 10.1016/j.lanplh.2025.101389
Thais Araújo Cavendish , Thiago Nogueira
{"title":"A call to action: climate leadership at the World Health Assembly","authors":"Thais Araújo Cavendish , Thiago Nogueira","doi":"10.1016/j.lanplh.2025.101389","DOIUrl":"10.1016/j.lanplh.2025.101389","url":null,"abstract":"","PeriodicalId":48548,"journal":{"name":"Lancet Planetary Health","volume":"9 12","pages":"Article 101389"},"PeriodicalIF":21.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145606893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01Epub Date: 2025-12-11DOI: 10.1016/j.lanplh.2025.101394
Yu Zhang PhD , Qi Sun PhD , Yi-Xin Wang PhD , Yang Sun MD , Prof Mariana F Fernández PhD , Carmen Messerlian PhD , Vicente Mustieles PhD
Background
Plastic pollution is a major environmental and health issue. To cover knowledge gaps, this study aimed to examine the association between population exposure to plasticiser mixtures and mortality, estimate the attributable public health burden, and explore potential nutritional mitigation measures.
Methods
This prospective population-based study included non-pregnant US adults aged 20 years or older free from cardiovascular diseases and cancer at baseline from the US National Health and Nutrition Examination Survey 2005–16. The main outcome was mortality status and cause of death, which was confirmed using ICD-9 and ICD-10 codes. Baseline urinary concentrations of eight phthalate metabolites and bisphenol A were selected a priori based on a comprehensive review of the toxicological and epidemiological evidence and modelled as a plasticiser mixture by quantile-based g-computation. Vitamin concentrations were examined as effect modifiers.
Findings
8378 adults were included. Over 71 127 person-years of follow-up (average 8·5 years per person), 633 deaths occurred. Each tertile increase in the mixture concentration was positively associated with all-cause mortality (hazard ratio 1·35, 95% CI 1·02–1·78), cancer mortality (1·79, 1·06–3·03), and cardiovascular disease mortality (1·83, 1·04–3·22). An estimated 10·31% (95% CI 0·78–20·38) of total deaths were attributable to a tertile increase in the mixture, equating to 256 471 annual excess deaths in the USA. The mixture association with all-cause, cancer, or cardiovascular disease mortality was observed only in individuals with serum vitamin D or red blood cell folate concentrations in the lowest tertile, but not in the upper tertiles.
Interpretation
Exposure to a mixture of common plasticisers was associated with increased all-cause, cancer, and cardiovascular disease mortality risk. Vitamin D and folate appeared to mitigate these associations. The findings underscore the need to reduce plasticiser exposure, optimise vitamin intake, and regulate chemicals by class.
Funding
Instituto de Salud Carlos III (Spain) and NextGeneration EU.
背景：塑料污染是一个重大的环境和健康问题。为了弥补知识空白，本研究旨在研究人群接触塑化剂混合物与死亡率之间的关系，估计可归因的公共卫生负担，并探索潜在的营养缓解措施。方法：这项基于人群的前瞻性研究纳入了2005- 2016年美国国家健康与营养调查中无心血管疾病和癌症的20岁或以上未怀孕的美国成年人。主要结果是死亡率状况和死亡原因，使用ICD-9和ICD-10代码进行确认。八种邻苯二甲酸盐代谢物和双酚A的基线尿液浓度是基于毒理学和流行病学证据的综合审查先验选择的，并通过基于分位数的g计算建模为塑化剂混合物。研究了维生素浓度作为效果调节剂。结果：纳入8378名成年人。在71 127人年的随访中（平均每人8.5年），发生了633例死亡。混合浓度每增加一分位数与全因死亡率（危险比1.35,95% CI 1.02 - 1.78）、癌症死亡率（1.79,1.06 - 3.03）和心血管疾病死亡率（1.83,1.04 - 3.22）呈正相关。估计总死亡人数的10.31% （95% CI 0.78 - 20.38）可归因于混合物的1 / 5增加，相当于美国每年的额外死亡人数为256471人。与全因、癌症或心血管疾病死亡率的混合关联仅在血清维生素D或红细胞叶酸浓度最低的个体中观察到，而在最高的个体中没有观察到。解释：暴露于常见增塑剂混合物与全因、癌症和心血管疾病死亡风险增加有关。维生素D和叶酸似乎减轻了这些关联。研究结果强调了减少塑化剂暴露、优化维生素摄入和按类别调节化学品的必要性。资助：卡洛斯三世研究所（西班牙）和下一代欧盟。
{"title":"Plasticisers chemical mixture, vitamin status, and mortality in US adults: a prospective population-based cohort","authors":"Yu Zhang PhD , Qi Sun PhD , Yi-Xin Wang PhD , Yang Sun MD , Prof Mariana F Fernández PhD , Carmen Messerlian PhD , Vicente Mustieles PhD","doi":"10.1016/j.lanplh.2025.101394","DOIUrl":"10.1016/j.lanplh.2025.101394","url":null,"abstract":"<div><h3>Background</h3><div>Plastic pollution is a major environmental and health issue. To cover knowledge gaps, this study aimed to examine the association between population exposure to plasticiser mixtures and mortality, estimate the attributable public health burden, and explore potential nutritional mitigation measures.</div></div><div><h3>Methods</h3><div>This prospective population-based study included non-pregnant US adults aged 20 years or older free from cardiovascular diseases and cancer at baseline from the US National Health and Nutrition Examination Survey 2005–16. The main outcome was mortality status and cause of death, which was confirmed using ICD-9 and ICD-10 codes. Baseline urinary concentrations of eight phthalate metabolites and bisphenol A were selected a priori based on a comprehensive review of the toxicological and epidemiological evidence and modelled as a plasticiser mixture by quantile-based g-computation. Vitamin concentrations were examined as effect modifiers.</div></div><div><h3>Findings</h3><div>8378 adults were included. Over 71 127 person-years of follow-up (average 8·5 years per person), 633 deaths occurred. Each tertile increase in the mixture concentration was positively associated with all-cause mortality (hazard ratio 1·35, 95% CI 1·02–1·78), cancer mortality (1·79, 1·06–3·03), and cardiovascular disease mortality (1·83, 1·04–3·22). An estimated 10·31% (95% CI 0·78–20·38) of total deaths were attributable to a tertile increase in the mixture, equating to 256 471 annual excess deaths in the USA. The mixture association with all-cause, cancer, or cardiovascular disease mortality was observed only in individuals with serum vitamin D or red blood cell folate concentrations in the lowest tertile, but not in the upper tertiles.</div></div><div><h3>Interpretation</h3><div>Exposure to a mixture of common plasticisers was associated with increased all-cause, cancer, and cardiovascular disease mortality risk. Vitamin D and folate appeared to mitigate these associations. The findings underscore the need to reduce plasticiser exposure, optimise vitamin intake, and regulate chemicals by class.</div></div><div><h3>Funding</h3><div>Instituto de Salud Carlos III (Spain) and NextGeneration EU.</div></div>","PeriodicalId":48548,"journal":{"name":"Lancet Planetary Health","volume":"9 12","pages":"Article 101394"},"PeriodicalIF":21.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145751952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01Epub Date: 2025-12-18DOI: 10.1016/j.lanplh.2025.101384
Huihuan Luo PhD , Tanchun Yu MS , Ya Gao BA , Yixiang Zhu PhD , Lu Zhou PhD , Anni Li MS , Peng Yin PhD , Prof Haidong Kan PhD , Prof Maigeng Zhou PhD , Prof Xiujuan Zhang PhD , Prof Renjie Chen PhD
<div><h3>Background</h3><div>Rising global temperatures and diabetes pose growing health risks worldwide. Individuals with diabetes are particularly vulnerable to heat, mainly because of impaired thermoregulation. However, the specific heat-related mortality risks associated with diabetes subtypes and complications remain poorly quantified.</div></div><div><h3>Methods</h3><div>We conducted a nationwide, individual-level, time-stratified case-crossover study encompassing 289 902 diabetes-related deaths across mainland China from 2013 to 2019. Death records for 2013–19 were sourced from the China Cause of Death Reporting System, a nationwide surveillance system. We used conditional logistic regression incorporating a distributed lag non-linear model to estimate temperature–mortality associations at the national level for overall diabetes, primary diabetes subtypes (type 1 and type 2), and specific complications (diabetic coma, diabetic ketoacidosis, diabetic nephropathy, and diabetes with peripheral vascular disease [PVD]). We examined how the associations varied across the temperate continental, temperate monsoon, and subtropical monsoon zones. The future heat-attributable diabetes mortality burden up to 2099 was projected under three shared socioeconomic pathways (SSP126 [low emissions], SSP245 [moderate emissions], and SSP585 [high emissions]). Additionally, we modelled several adaptation scenarios by assuming 10%, 30%, and 50% reductions in the exposure–response coefficients.</div></div><div><h3>Findings</h3><div>Exposure to extreme high temperatures (97·5th percentile [31·0°C]) compared with the minimum mortality temperature was associated with an increase in overall diabetes mortality (odds ratio [OR] 1·25, 95% CI 1·22–1·29) over a 0–6 day lag period, with the magnitude of risk higher in cooler regions. Heat-related mortality outcomes for diabetes subtypes and complications varied geographically. In warmer zones, individuals with type 2 diabetes were at higher risk of mortality than those with type 1 diabetes (eg, OR 1·21 [95% CI 1·16–1·26] <em>vs</em> 1·14 [1·04–1·26] in the subtropical monsoon zone [warmest region]), whereas the opposite held in cooler zones (1·31 [1·09–1·58] <em>vs</em> 1·65 [1·17–2·33] in the temperate continental zone [coldest region]). By climate zone, the most heat-sensitive complications were diabetic ketoacidosis and nephropathy, in the subtropical zone; PVD and nephropathy, in the temperate monsoon zone; and diabetic coma and PVD, in the temperate continental zone. We projected that by the 2090s, under a high emission scenario (SSP585), the heat-attributable fraction of diabetes deaths would reach 11·16% (empirical 95% CI 6·11–18·01). In the temperate continental zone, we projected a burden of 29·02% (7·53 to 44·58) of diabetes coma deaths attributable to heat, followed by PVD (28·65% [–22·60 to 46·95]) and nephropathy (17·40% [–4.41 to 31·27]). Population ageing and growth were projected to increase the burden of o
{"title":"Heat-related mortality burden of type 1 diabetes, type 2 diabetes, and diabetes complications in mainland China amid global warming: a nationwide, case-crossover study","authors":"Huihuan Luo PhD , Tanchun Yu MS , Ya Gao BA , Yixiang Zhu PhD , Lu Zhou PhD , Anni Li MS , Peng Yin PhD , Prof Haidong Kan PhD , Prof Maigeng Zhou PhD , Prof Xiujuan Zhang PhD , Prof Renjie Chen PhD","doi":"10.1016/j.lanplh.2025.101384","DOIUrl":"10.1016/j.lanplh.2025.101384","url":null,"abstract":"<div><h3>Background</h3><div>Rising global temperatures and diabetes pose growing health risks worldwide. Individuals with diabetes are particularly vulnerable to heat, mainly because of impaired thermoregulation. However, the specific heat-related mortality risks associated with diabetes subtypes and complications remain poorly quantified.</div></div><div><h3>Methods</h3><div>We conducted a nationwide, individual-level, time-stratified case-crossover study encompassing 289 902 diabetes-related deaths across mainland China from 2013 to 2019. Death records for 2013–19 were sourced from the China Cause of Death Reporting System, a nationwide surveillance system. We used conditional logistic regression incorporating a distributed lag non-linear model to estimate temperature–mortality associations at the national level for overall diabetes, primary diabetes subtypes (type 1 and type 2), and specific complications (diabetic coma, diabetic ketoacidosis, diabetic nephropathy, and diabetes with peripheral vascular disease [PVD]). We examined how the associations varied across the temperate continental, temperate monsoon, and subtropical monsoon zones. The future heat-attributable diabetes mortality burden up to 2099 was projected under three shared socioeconomic pathways (SSP126 [low emissions], SSP245 [moderate emissions], and SSP585 [high emissions]). Additionally, we modelled several adaptation scenarios by assuming 10%, 30%, and 50% reductions in the exposure–response coefficients.</div></div><div><h3>Findings</h3><div>Exposure to extreme high temperatures (97·5th percentile [31·0°C]) compared with the minimum mortality temperature was associated with an increase in overall diabetes mortality (odds ratio [OR] 1·25, 95% CI 1·22–1·29) over a 0–6 day lag period, with the magnitude of risk higher in cooler regions. Heat-related mortality outcomes for diabetes subtypes and complications varied geographically. In warmer zones, individuals with type 2 diabetes were at higher risk of mortality than those with type 1 diabetes (eg, OR 1·21 [95% CI 1·16–1·26] <em>vs</em> 1·14 [1·04–1·26] in the subtropical monsoon zone [warmest region]), whereas the opposite held in cooler zones (1·31 [1·09–1·58] <em>vs</em> 1·65 [1·17–2·33] in the temperate continental zone [coldest region]). By climate zone, the most heat-sensitive complications were diabetic ketoacidosis and nephropathy, in the subtropical zone; PVD and nephropathy, in the temperate monsoon zone; and diabetic coma and PVD, in the temperate continental zone. We projected that by the 2090s, under a high emission scenario (SSP585), the heat-attributable fraction of diabetes deaths would reach 11·16% (empirical 95% CI 6·11–18·01). In the temperate continental zone, we projected a burden of 29·02% (7·53 to 44·58) of diabetes coma deaths attributable to heat, followed by PVD (28·65% [–22·60 to 46·95]) and nephropathy (17·40% [–4.41 to 31·27]). Population ageing and growth were projected to increase the burden of o","PeriodicalId":48548,"journal":{"name":"Lancet Planetary Health","volume":"9 12","pages":"Article 101384"},"PeriodicalIF":21.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145806084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01Epub Date: 2025-12-24DOI: 10.1016/j.lanplh.2025.101391
Anand Bhopal MBChB PhD , Martin Hensher PhD , Andrea J MacNeill MD , Ole F Norheim MD PhD , Jodi D Sherman MD , Craig Mitton PhD
Priority setting in health care is a research and practice area at the intersection of medicine, ethics, and economics, which aims to systematically and transparently evaluate the value for money of health services to support fair resource allocation. Three widely accepted principles for fair priority setting are cost-effectiveness, priority to the worse off, and financial risk protection, with a wide range of other contested criteria. Conceptualising and navigating potential synergies and trade-offs between competing goals, and clearly communicating the values at stake, are the central tasks of priority setting. It is now increasingly clear that health care systems have substantial environmental effects that have been largely overlooked, and that the growing movement towards high-quality, low-polluting, and climate-resilient health systems has potentially far-reaching implications for resource allocation. This Personal View explores how priority setting tools can facilitate the transition to environmentally sustainable health care. We outline the key principles of priority setting in health care and explore how environmental sustainability can be incorporated into resource allocation tools, such as health technology assessment and multicriteria decision analysis, as well as budgetary processes, such as programme budgeting and marginal analysis. We conclude with some implications for wider health system transformation.
{"title":"Priority setting for environmentally sustainable health care: emerging approaches to fair resource allocation","authors":"Anand Bhopal MBChB PhD , Martin Hensher PhD , Andrea J MacNeill MD , Ole F Norheim MD PhD , Jodi D Sherman MD , Craig Mitton PhD","doi":"10.1016/j.lanplh.2025.101391","DOIUrl":"10.1016/j.lanplh.2025.101391","url":null,"abstract":"<div><div>Priority setting in health care is a research and practice area at the intersection of medicine, ethics, and economics, which aims to systematically and transparently evaluate the value for money of health services to support fair resource allocation. Three widely accepted principles for fair priority setting are cost-effectiveness, priority to the worse off, and financial risk protection, with a wide range of other contested criteria. Conceptualising and navigating potential synergies and trade-offs between competing goals, and clearly communicating the values at stake, are the central tasks of priority setting. It is now increasingly clear that health care systems have substantial environmental effects that have been largely overlooked, and that the growing movement towards high-quality, low-polluting, and climate-resilient health systems has potentially far-reaching implications for resource allocation. This Personal View explores how priority setting tools can facilitate the transition to environmentally sustainable health care. We outline the key principles of priority setting in health care and explore how environmental sustainability can be incorporated into resource allocation tools, such as health technology assessment and multicriteria decision analysis, as well as budgetary processes, such as programme budgeting and marginal analysis. We conclude with some implications for wider health system transformation.</div></div>","PeriodicalId":48548,"journal":{"name":"Lancet Planetary Health","volume":"9 12","pages":"Article 101391"},"PeriodicalIF":21.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145844451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01Epub Date: 2025-11-01DOI: 10.1016/j.lanplh.2025.101376
Erin Coughlan de Perez , Ahmed Ishtiaque Amin Chowdhury , Glecy Atienza , Sonia Binte Murshed , Ramon Christopher A Caballero , Dennis De La Torre , Aira Joy Delos Angeles , Desderius Haufiku , Alexa Samantha R Hernandez , Md. Monirul Islam , Kenneth Lekatsa , Selma Lendelvo , Tandi Litwayi , Makoala V Marake , Joalane Marunye , Mashfiqus Salehin , Kebitsamang Mothibe , Elena Naumova , Mothusi Nyofane , Garimoi Christopher Orach , Carolyn Van Sant
{"title":"Beyond the narrow lens: the power of an interdisciplinary approach to climate and health research and training","authors":"Erin Coughlan de Perez , Ahmed Ishtiaque Amin Chowdhury , Glecy Atienza , Sonia Binte Murshed , Ramon Christopher A Caballero , Dennis De La Torre , Aira Joy Delos Angeles , Desderius Haufiku , Alexa Samantha R Hernandez , Md. Monirul Islam , Kenneth Lekatsa , Selma Lendelvo , Tandi Litwayi , Makoala V Marake , Joalane Marunye , Mashfiqus Salehin , Kebitsamang Mothibe , Elena Naumova , Mothusi Nyofane , Garimoi Christopher Orach , Carolyn Van Sant","doi":"10.1016/j.lanplh.2025.101376","DOIUrl":"10.1016/j.lanplh.2025.101376","url":null,"abstract":"","PeriodicalId":48548,"journal":{"name":"Lancet Planetary Health","volume":"9 12","pages":"Article 101376"},"PeriodicalIF":21.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145446390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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