Environmental Health最新文献

{"title":"Attributing heatwave mortality to human-induced climate change in Greece: a case-crossover and attribution analysis for 2000-2019.","authors":"Di Xi, Dimitris Evangelopoulos, Clair Barnes, Evangelos Chandakas, Constantine Vardavas, Paraskevi Katsaounou, Paolo Vineis, Filippos T Filippidis, Garyfallos Konstantinoudis","doi":"10.1186/s12940-026-01320-9","DOIUrl":"10.1186/s12940-026-01320-9","url":null,"abstract":"<p><strong>Background: </strong>Heatwaves increasingly threaten public health in the Mediterranean region, and Greece is among the hardest hit countries. Yet evidence on long-term adaptation, spatial vulnerability, and the contribution of human-induced climate change to heatwave-related mortality in Greece remains limited.</p><p><strong>Methods: </strong>We analysed 2,144,957 all-cause deaths in Greece (2000-2019) in people older than 65 years using a time-stratified case-crossover design. We derived population-weighted daily maximum temperatures at NUTS3 level from ERA5 reanalysis and WorldPop. We applied six heatwave definitions (HD1-HD6) varying by duration (≥ 2 or ≥ 3 days) and thresholds (90th, 95th, 99th percentiles). We fitted Bayesian hierarchical Poisson models to estimate heatwave-mortality associations varying by space and time. We additionally adjusted for relative humidity and national holidays. We then combined these estimates with probabilistic climate-attribution methods to quantify the number and proportion of heatwave-related deaths attributable to human-induced climate change.</p><p><strong>Results: </strong>Heatwaves raised mortality consistently, with relative risks from 1.08 (95% CrI (Credible Interval): 1.07-1.09; HD1) to 1.15 (1.12-1.19; HD6). Risks increased with heatwave intensity and duration, with particularly high risks observed among females and older adults. We did not detect a consistent temporal decline in risk or marked spatial heterogeneity. Human-induced climate change accounted for 46-80% of heatwave-related deaths across definitions. The proportion attributable to climate change rose over time.</p><p><strong>Conclusions: </strong>Heatwaves already impose a major mortality burden in Greece, with more than half driven by anthropogenic climate change and little evidence of population-level adaptation. These findings call for rapid emissions reductions and targeted adaptation, including stronger heat-health warning systems and protection of vulnerable groups.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":" ","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13640306/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148419505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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}

{"title":"Correction: Relevance and challenges of exposome studies for environmental health research.","authors":"Rémy Slama, Valérie Siroux, Martine Vrijheid, Xavier Basagaña","doi":"10.1186/s12940-026-01317-4","DOIUrl":"10.1186/s12940-026-01317-4","url":null,"abstract":"","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"25 1","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13352748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148419584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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}

{"title":"Lead exposure and risk of ADHD and conduct disorders in children: evidence from a retrospective cohort in Philadelphia, PA.","authors":"Xuewen Pei, Katarzyna Kordas, Meng Wang, Muwu Xu, Jing Nie, Amy Hequembourg, Adil I Khan, John Turella, Marina Oktapodas Feiler","doi":"10.1186/s12940-026-01318-3","DOIUrl":"10.1186/s12940-026-01318-3","url":null,"abstract":"<p><strong>Background: </strong>Childhood lead exposure remains a significant public health concern, particularly in urban settings with persistent socioeconomic disadvantage. Although prior studies have linked lead exposure to adverse neurodevelopmental outcomes, evidence using clinically diagnosed neurobehavioral disorders at contemporary low blood lead levels (BLLs) is limited.</p><p><strong>Methods: </strong>We conducted a retrospective cohort study of children aged 11 years or younger who received care through the Temple University Health System in Philadelphia, Pennsylvania, between 2010 and 2020. BLLs were obtained from electronic health records and analyzed as continuous measures and dichotomized at 3.5 µg/dL. Attention-deficit/hyperactivity disorder (ADHD) and conduct disorders were identified using international classification diagnoses (ICD) codes, and only incident diagnoses occurring after blood lead measurement were considered. Multivariable logistic regression models were fit adjusted for individual- and neighborhood-level sociodemographic factors selected using a directed acyclic graph framework. Sex-stratified analyses were conducted to assess effect modification.</p><p><strong>Results: </strong>Among 13,989 children included in the ADHD analysis, 751 (5.4%) were diagnosed with ADHD. Among 14,098 children included in the conduct disorder analysis, 247 (1.8%) were diagnosed with a conduct disorder. Higher log₁₀-transformed continuous BLLs were associated with increased odds of ADHD diagnosis (adjusted OR 1.51; 95% CI 1.37, 1.67). Children with BLLs ≥ 3.5 µg/dL had higher odds of ADHD (adjusted OR 1.84; 95% CI 1.56, 2.16) compared with those with BLLs < 3.5 µg/dL, with stronger associations observed among males than females. Associations between log₁₀-transformed continuous BLLs and conduct disorders were positive but not statistically significant (adjusted OR 1.12; 95% CI 0.95, 1.31), and no sex-specific associations were observed.</p><p><strong>Conclusion: </strong>Childhood lead exposure was associated with increased risk of ADHD in this urban clinical population, including at blood lead levels at or above the current reference value set by the Centers for Disease Control and Prevention, emphasizing the importance of continued prevention efforts. These findings underscore the ongoing neurodevelopmental risks of low-level lead exposure and highlight the disproportionate burden placed on children residing in socioeconomically disadvantaged urban communities.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":" ","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555946/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148316271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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}

{"title":"Observational and genetically-informed characterization of Gulf War Illness symptoms in 1990-1991 Gulf War deployed Veterans and non-deployed Gulf War Era Veterans.","authors":"Jun He, Gita A Pathak, Brenda Cabrera-Mendoza, Dan Qiu, Kelson Zawack, Lea Steele, Rachel Quaden, Kelly M Harrington, Elizabeth J Gifford, Mihaela Aslan, Drew A Helmer, Elizabeth R Hauser, Renato Polimanti","doi":"10.1186/s12940-026-01316-5","DOIUrl":"10.1186/s12940-026-01316-5","url":null,"abstract":"<p><strong>Background: </strong>Gulf War Illness (GWI) has been identified in more than 20% of Veterans following military service in the 1990-1991 Gulf War (GW). Unfortunately, after several decades, GWI pathogenesis remains unclear and the patterns of GWI symptom co-occurrence are still poorly understood.</p><p><strong>Methods: </strong>This population-based case-control study included 34,179 (16% females; 34% GW deployed; mean age 61 years) Veterans enrolled in the Million Veteran Program (MVP) who were active-duty military personnel in 1990-1991. We analyzed 14 GWI symptoms in GW-deployed and non-deployed GW-Era Veterans. Multivariable generalized linear models were used to estimate GWI symptom associations with demographic factors and deployment status. Correlation, factor, and network analyses were performed to examine the underlying structure of GWI symptoms. In addition, polygenic risk score and one-sample Mendelian randomization analyses were conducted to evaluate the genetically inferred effects of health-related traits on symptom factors.</p><p><strong>Results: </strong>Among 14 GWI symptoms, joint pain had the highest prevalence in both GW deployed (86%) and non-deployed GW-Era Veterans (79%). The median age of symptom onset ranged from 38 to 46 years among deployed Veterans and from 45 to 54 years among non-deployed Veterans. Factor analysis identified a five-factor latent structure as the best-fit model for GWI symptoms, and latent class analysis classified Veterans into seven symptom classes. The network of GWI symptoms showed that fatigue had the largest closeness and betweenness and had more edges in deployed Veterans. Younger age, female sex, non-European descent, lower educational attainment, enlisted rank, and GW deployment, as well as multiple GW-related exposures in deployed Veterans, were associated with increased GWI symptom burden. Genetic liability to multiple health-related outcomes, including type 2 diabetes (T2D) and posttraumatic stress disorder (PTSD), showed putative causal effects on GWI-symptom factors, with the T2D effect being larger in deployed Veterans and the PTSD effect being larger in non-deployed Veterans.</p><p><strong>Conclusions: </strong>The present findings demonstrate differences in symptom onset between deployed and non-deployed GW Veterans. They also reinforce the importance of symptom clusters of relevance to GWI, associations between deployment-specific exposures and symptom burden, and different genetic linkages underlying symptoms for deployed and non-deployed groups.</p><p><strong>Trial registration: </strong>Not applicable.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":" ","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13479420/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148224104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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}

{"title":"Air pollution and disease progression among patients with primary glomerular disease: an expanded study with extended follow-up.","authors":"Jonathan P Troost, Abhijit V Kshirsagar, William E Smoyer, Jon Klein, Michael L Merchant, Margaret Helmuth, Laura H Mariani, Matthias Kretzler, Abigail R Smith, Forrest Lacey, Lawrence S Engel, Howard Trachtman, Cassandra R O'Lenick","doi":"10.1186/s12940-026-01312-9","DOIUrl":"10.1186/s12940-026-01312-9","url":null,"abstract":"<p><strong>Background: </strong>Air pollution is increasingly recognized as a risk factor for progression of kidney disease; however, few studies have examined its impact among patients with primary glomerular disorders. To address this knowledge gap, we previously reported positive associations between fine particulate matter ≤ 2.5μm in aerodynamic diameter (PM_2.5) and black carbon with kidney disease progression in an observational cohort of children and adults (n = 925) with primary glomerular diseases, namely minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, and IgA nephropathy. In the current study, we leverage the same cohort to (1) identify additional air pollutants that may be associated with kidney disease progression using data from the National Center for Atmospheric Research (NCAR); (2) determine whether the association between baseline air pollution exposure and kidney disease progression is maintained over a longer follow-up period; and (3) assess whether associations identified in our previously published findings remain when using NCAR pollutant data.</p><p><strong>Methods: </strong>In this retrospective cohort study, we obtained air pollutant concentration data from NCAR based on participant residential census tract at enrollment. For each census tract and pollutant, we aggregated daily pollutant concentrations to annual averages. We used Cox proportional hazards models to estimate associations between average baseline pollutant exposure and time to kidney disease progression, defined as a 40% decline in estimated glomerular filtration rate (eGFR) or occurrence of kidney failure (eGFR) < 15 ml/min/1.73 m²) during follow-up. Hazard ratios (HR) represented a doubling of exposure.</p><p><strong>Results: </strong>Use of NCAR data supported our previous findings of adverse effects of PM_2.5 and black carbon on the progression of glomerular disease. Moreover, using the NCAR data we identified novel associations with NO₂ exposure, HR 1.12 [1.01, 1.26] and specific components of PM_2.5, including organic matter, HR 1.17 [1.01, 1.37] and an increased risk of disease progression. When considering a longer follow-up period, associations between baseline exposures and kidney outcomes persisted, but were attenuated suggesting a need for recent, interval-specific risk assessment, inclusion of acute exposures, and enhanced spatial resolution of exposures.</p><p><strong>Conclusion: </strong>Our findings highlight the importance of the systematic assessment including spatial and temporal variation of a broad range of air pollution components to determine the impact of exposure on short- and long-term outcomes in patients with primary glomerular disease (word count: 368).</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":" ","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13455273/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148162172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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}

{"title":"Not just splitting hairs-monitoring environmental chemical exposures, their biological effects and their social determinants with hair shafts and follicles: a narrative review.","authors":"Marie Robert, Alba Iglesias-González, Rawan Nour, Ke Zhou, Brice M R Appenzeller, Martine Bellanger, Pierre-Alexandre Vidi","doi":"10.1186/s12940-026-01315-6","DOIUrl":"10.1186/s12940-026-01315-6","url":null,"abstract":"<p><p>Humans encounter a wide range of natural and synthetic chemicals throughout their lifespan and these exposures have a complex impact on health outcomes. Epidemiological studies provide compelling evidence linking chemical exposure to neurological disorders and various cancers. However, establishing causality between specific pollutants, or their mixtures, and health outcomes is challenging due to long disease latencies. Functional biomarkers in exposed subjects provide rapid predictions of the impact of environmental exposures. Notably, genome alterations, including DNA breaks and epigenetic modifications, are hallmark features of cancers, premature aging, and neurological diseases. Biomonitoring studies show that individual chemical exposures are specific. These differences highlight disparities across socioeconomic groups. They also present opportunities to associate specific environmental factors and disease development, as well as socioeconomic determinants of exposures and their consequences. This review focuses on biomonitoring environmental chemical exposures and their effects with hair and hair follicles. Pollutants detected in the hair matrix reflect cumulative internal exposures over specific time periods, while biomarkers can be analyzed in plucked hair follicles. These mini organs contain proliferating and stem/progenitor cells, which are critical to understanding the onset of various diseases. We propose an integrated approach that combines socioeconomic indicators, chemical analyses in hair, and biological assessments of matching hair follicles to evaluate the exposome and its effects on the genome. We discuss the state of the art of these approaches, their current limitations, and the perspectives they offer.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":" ","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13449329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148155642","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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}

{"title":"Placental CYP450 gene dysregulation by maternal PFAS: a novel mechanism linking prenatal exposure to altered toddler growth.","authors":"Xiuxia Song, Zhaofeng Zhang, Xiaoyu Zhou, Hong Liang, Yao Chen, Weiqiang Zhu, Wei Yuan, Jing Du, Ziliang Wang, Maohua Miao","doi":"10.1186/s12940-026-01302-x","DOIUrl":"10.1186/s12940-026-01302-x","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Maternal per- and polyfluoroalkyl substances (PFAS) exposure has been linked to adverse health effects on offspring, but the mechanisms remain unclear. The present study investigates the relationship between maternal PFAS exposure and the expression of placental cytochrome P450 enzymes (CYP19A1, CYP2J2, and CYP2E1), and explores the potential role of these enzymes in linking maternal PFAS exposure to offspring development.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;We included 350 mother-infant pairs from the Jiashan birth cohort. Thirteen PFAS compounds were measured in maternal plasma collected at 8-16 weeks of gestation, while the expression levels of the three CYP genes were quantified in placental tissues collected at delivery. Offspring weight and length were measured at birth and at 1, 3, 6, 8, 12, and 24 months of age, and their ponderal index (PI) was computed. Multivariable linear regression was used to examine associations between plasma concentrations of individual PFAS and placental CYP gene expression. Quantile-based g-computation was used to examine the association of the PFAS mixture with placental CYP gene expression. A linear mixed model was used to examine the associations of maternal PFAS and placental CYP expression levels with repeated PI measurements from birth to 24 months. Multilevel mediation analysis was conducted to explore the potential mediating role of CYP genes.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Consistent inverse associations between maternal PFAS exposure and the three placental CYP genes expression in female placentas were observed. Specifically, statistically significant decreases were observed in the associations between all PFAS compounds and CYP2J2 expression with β- estimates for the highest exposure versus the lowest from -0.255 to -0.174, as well as between the highest exposure of perfluorotridecanoic acid (PFTrDA) and CYP19A1 expression (β = -0.279, 95% CI: -0.55, -0.007). In contrast, for male fetuses, significant associations were found between the highest exposure of perfluorohexane sulfonate (PFHxS) and increased CYP19A1 expression (β = 0.404, 95%CI: 0.131,0.677), and between the middle of perfluoroundecanoic acid (PFUdA), perfluorododecanoic acid (PFDoA), PFTrDA, and perfluoroheptanoic acid (PFHPA) and decreased CYP2E1 expression (β&lt;sub&gt;PFUdA&lt;/sub&gt; = -0.286, 95% CI: -0.511,-0.061; β&lt;sub&gt;PFDoA&lt;/sub&gt; = -0.270, 95% CI: -0.495,-0.045;β&lt;sub&gt;PFTrDA&lt;/sub&gt; = -0.236, 95% CI: -0.466,-0.006; and β&lt;sub&gt;PFHpA&lt;/sub&gt; = -0.344, 95% CI: -0.571,-0.117, respectively). The PFAS mixture was associated with decreased the three CYP genes expression in the placenta of female fetuses, but no association was observed in male placentas. Additionally, placental CYP19A1 expression was associated with a decrease in girls' PI and an increase in boys' PI, respectively. However, no mediating role of CYP19A1 in the relationship between PFTrDA and PI in girls or between PFHxS and PI in boys was observed, as the ind","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":" ","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13445925/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148148896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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}

{"title":"Preconception and early-pregnancy exposure to ambient air pollution and trajectories of depressive symptoms during pregnancy.","authors":"Yuhong Hu, Tingyu Yang, Sandrah P Eckel, Xinci Chen, Zhongzheng Niu, Claudia M Toledo-Corral, Nathan Pavlovic, Fred Lurmann, Brendan Grubbs, Laila Al-Marayati, Erika Garcia, Santiago Morales, Jill Johnston, Genevieve F Dunton, Rima Habre, Shohreh F Farzan, Carrie Breton, Theresa M Bastain","doi":"10.1186/s12940-026-01314-7","DOIUrl":"10.1186/s12940-026-01314-7","url":null,"abstract":"<p><strong>Background: </strong>Prenatal depression shows diverse patterns in severity and progression. While air pollution has been linked to depression risk, its impact on the course of prenatal depression remains understudied. The study objectives were to (1) identify distinct trajectories of depressive symptoms across pregnancy, and (2) to evaluate whether preconception and early-pregnancy air pollution exposure impacts membership in trajectory groups.</p><p><strong>Methods: </strong>This study followed 542 predominantly low-income Hispanic/Latina participants in the MADRES cohort. We assessed depressive symptoms using the Center for Epidemiologic Studies-Depression (CES-D) scale at 1st, 2nd, and 3rd trimester visits. Daily residential concentrations of PM_2.5, PM₁₀, NO₂, and O₃ were estimated using inverse-distance squared spatial interpolation from monitoring data. We used latent growth mixture modeling (LGMM) to identify trajectory classes and multinomial logistic regression to estimate adjusted relative risk ratios (RRRs) of membership in each class relative to the lowest group with averaged air pollution levels over preconception and early pregnancy.</p><p><strong>Results: </strong>We identified four distinct trajectories: moderate-to-high symptoms (7.4%), consistently-moderate symptoms (14.6%), moderate-to-low symptoms (34.7%), and consistently-low symptoms (43.4%). Higher proportions of Black mothers and those not cohabitating were found in the two highest symptom trajectories. Participants with an interquartile range higher early-pregnancy NO₂ (10.28 ppb) had a 3.82-fold higher relative risk (95% CI: 1.50-9.73) of following the moderate-to-high versus consistently-low-symptom trajectory. Similar elevated risks were observed for PM_2.5 (RRR = 1.61; 95%CI: 1.08-2.40) and PM₁₀ (RRR = 1.84; 95% CI: 1.01-3.35).</p><p><strong>Conclusion: </strong>Early-pregnancy exposure to ambient air pollution is associated with increased risk of moderate-to-high depressive symptoms across pregnancy.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":" ","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13455309/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148148925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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}

{"title":"Lessons learned from longitudinal biomonitoring and birth cohort studies: informing the future of reproductive health research in Canada.","authors":"Jillian Ashley-Martin, Mandy Fisher, Cheryl Khoury, Aranee Sathiyamoorthy, Michael M Borghese, Gillian England-Mason, Tyler Pollock, Tye E Arbuckle, Lauren A Wise, Joseph M Braun, Amy Metcalfe, Jessie P Buckley, Mark R Palmert, Christina Ricci, Erica Phipps, Gopal Banerjee, Erin Fuller, Linda Booij, Kathyrn Hopperton, Hope Weiler, Amanda J MacFarlane, Jesse Bertinato, Dorothea F K Rawn, Eric Lavigne, Amalie Timmermann, Emily Oken, Christina Wolfson, Ragnhild Eek Brandlistuen, Robin Shutt","doi":"10.1186/s12940-026-01313-8","DOIUrl":"10.1186/s12940-026-01313-8","url":null,"abstract":"<p><p>Longitudinal biomonitoring studies during preconception, pregnancy and early childhood are highly valuable tools for assessing environmental chemical exposures during sensitive windows and their effects on health and development. For the past 15 years, the Maternal-Infant Research on Environmental Chemicals (MIREC) Research Platform has been Canada's flagship study of the long-term effects of early life exposure to environmental chemicals. In light of the evolving scientific and legislative landscapes and need to address emerging research questions, MIREC Platform researchers at Health Canada consulted with scientific investigators of other cohort studies to inform the development of a future preconception or pregnancy longitudinal biomonitoring study. This effort included 1) hybrid consultation meetings on Dec 6, 2024 (Toronto, ON) and Jan 21, 2025 (Ottawa, ON) and 2) a virtual seminar series from October 2024 to June 2025 hosted by the Health Canada MIREC team. Our objective here is to share lessons learned from this consultation. We report on key lessons learned related to the themes of: 1) participant engagement, recruitment and retention, 2) validity and causal inference, and 3) study longevity. While the ultimate goal of this consultation was to inform future longitudinal biomonitoring studies in Canada, the content is largely generalizable and relevant to others planning, modifying, or evaluating observational research in reproductive and environmental epidemiology.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"25 1","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13220497/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148053381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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}

{"title":"Relevance and challenges of exposome studies for environmental health research.","authors":"Rémy Slama, Valérie Siroux, Martine Vrijheid, Xavier Basagaña","doi":"10.1186/s12940-026-01299-3","DOIUrl":"10.1186/s12940-026-01299-3","url":null,"abstract":"<p><p>The exposome encompasses all environmental exposures humans undergo from conception. We frame exposome studies according to four broad aims essential for environmental health research. First, a descriptive aim, consisting in assessing exposure patterns, including correlations between exposures and their within-subject variability. This descriptive aim includes \"environmental justice\" studies of associations between the exposome and sociodemographic factors. A second - etiologic - aim is to describe the subclinical and clinical effects of the exposome (hazard identification). A third aim is the quantification of the exposome health impact (e.g., in life years lost at the population level) and the ranking of exposures in terms of population disease burden (exposome disease burden or risk assessment). A fourth (intervention) aim corresponds to the identification of approaches to modify the exposome, as a way to improve health. With the large increase in the number of chemicals quantifiable in a small volume of a biospecimen, the main challenge of descriptive exposome studies is population representativeness. Regarding the etiologic aim, by simultaneously showing associations of a given biological parameter with hundreds of exposures, exposome studies effectively limit publication bias and selective reporting of results, which are a strong concern in single-exposure studies. They nonetheless face several challenges, related to the curse of dimensionality, the correlation between exposures, the breadth vs. depth tension… Increasing the number of exposures considered implies to simultaneously increase study population sizes, aiming for cohorts of 100,000 subjects or more. The accuracy of exposure assessment should simultaneously be improved, e.g., by collecting repeated biospecimens within each subject, assessing exposures at various ages and decreasing limits of quantification. Classical exposome statistical designs such as ExWAS (exposome-wide association studies) are subject to a high false positive rate. Models adapted to sparse data allowing to control for confounding by co-exposures appear more efficient. The results from exposome descriptive and etiologic studies can be combined to feed exposome disease burden assessments. These can in turn help prioritize exposures for which efficient interventions need to be identified. The approaches outlined in this work could help exposome research contribute more strongly to environmental health research and to the associated risk management decisions.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":" ","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13242124/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148053335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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}