{"title":"Couples exposure to neonicotinoid insecticides and its influence on in vitro fertilization/intracytoplasmic sperm injection outcomes.","authors":"Ziyu Liu, Hao Shi, Nijie Li, Zhenhan Xu, Xin Zhao, Guihua Liu, Xiaoyan Liang, Xing Yang","doi":"10.1186/s12940-025-01242-y","DOIUrl":"10.1186/s12940-025-01242-y","url":null,"abstract":"<p><p>Neonicotinoid insecticides (NEOs), recognized endocrine-disrupting compounds, are extensively utilized in agricultural and livestock practices, exhibiting global environmental persistence and bioaccumulation in human populations and wildlife. Accumulating experimental and epidemiological evidence implicates NEO exposure in reproductive dysfunction. This study investigated paired NEO concentrations in serum, female follicular fluid, and male seminal plasma from 211 couples undergoing assisted reproductive technology (ART), evaluating associations with reproductive outcomes. NEO concentrations were quantified using liquid chromatography-tandem mass spectrometry (LC–MS/MS), and associations with ART parameters, considering partner exposure metrics, were examined utilizing covariate-adjusted generalized linear models. Results revealed N-demethyl-acetamiprid (N-dm-ACE) was commonly detected across all matrices. Female serum clothianidin (CLO) demonstrated a significant inverse correlation with fertilization potential and good-quality embryo yield, while elevated serum N-dm-ACE concentrations were linked to diminished biochemical pregnancy probability. Within follicular fluid, CLO presence impaired fertilization and cleavage rates, and higher N-dm-ACE levels compromised good-quality embryo developmental competence. Additionally, THX detection in seminal plasma was linked to reduced cleavage rates and lower biochemical and clinical pregnancy rates. Negative dose–response relationships were observed between N-dm-ACE exposure in female serum and both biochemical and clinical pregnancies, and between N-dm-ACE levels in follicular fluid and cleavage rate and biochemical pregnancy. These results demonstrate that partner NEO exposure detrimentally influences pivotal ART success metrics, highlighting the critical importance of dual parental biomonitoring in reproductive toxicology research for clinical risk assessment. Comprehensive longitudinal cohort studies are warranted to substantiate these associations and elucidate mechanistic pathways.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"24 1","pages":"93"},"PeriodicalIF":7.3,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12709820/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145773964","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}
Anna K Maassel, Paige Brochu, Valerie S Harder, Taylor H Ricketts, Stephen J Teach, Keith J Robinson
{"title":"Wildfire smoke and pediatric asthma control in the Northeastern United States: a cross-sectional study.","authors":"Anna K Maassel, Paige Brochu, Valerie S Harder, Taylor H Ricketts, Stephen J Teach, Keith J Robinson","doi":"10.1186/s12940-025-01245-9","DOIUrl":"10.1186/s12940-025-01245-9","url":null,"abstract":"<p><strong>Background: </strong>Poor air quality due to smoke from distant wildfires is a growing risk for the Northeastern United States, a region largely unaffected by these events until recently. Despite this emerging threat, few studies have examined the effect of wildfire smoke on respiratory health in this region. We investigated the association between wildfire smoke exposure and pediatric asthma control in Vermont and upstate New York.</p><p><strong>Methods: </strong>We extracted data from the electronic health records of youth aged 3-21 years diagnosed with asthma within a single regional healthcare system and included three clinical measures of asthma control: Test for Respiratory and Asthma Control in Kids (3-4 years), Asthma Therapy Assessment Questionnaire (5-21 years), and the National Heart, Lung and Blood Institute (NHLBI) asthma control guidelines (3-21 years). We first compared asthma control in the smoke-affected summer of 2023 to the largely unaffected summers of 2022 and 2024 using regression models, controlling for pollen exposure. We then obtained airborne particulate matter (PM<sub>2.5</sub>) values within ZIP codes and used regression models to investigate the association between asthma control and PM<sub>2.5</sub> during the smoke-affected summer of 2023.</p><p><strong>Results: </strong>The study sample included 1,217 encounters (mean age 9.1 ± 4.4 years, 57% male). Asthma control was significantly worse in the severely smoke-affected summer of 2023 versus 2022 for two of the three clinical measures but was not different between 2023 and 2024 for any of the clinical measures. Within summer 2023, there were no significant associations between ZIP code-level PM<sub>2.5</sub> and asthma control for any of the three clinical measures.</p><p><strong>Conclusions: </strong>Wildfire smoke exposure in the Northeast was associated with decreased asthma control in this pediatric population, though not consistently across years and all clinical measures. As climate change drives longer and more intense wildfire seasons, continued monitoring is needed to understand the impact on pediatric respiratory health in this historically low-exposed region.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"24 1","pages":"91"},"PeriodicalIF":5.3,"publicationDate":"2025-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12696890/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145721823","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}
Heli Lehtomäki, Gunn Marit Aasvang, Gerhard Sulo, Bruce R Denby, Otto Olavi Hänninen, Michael Brauer, Gavin Pereira, Omid Dadras, Anette Kocbach Bølling
{"title":"Burden of disease attributable to PM<sub>2.5</sub> at low exposure levels: impact of methodological choices.","authors":"Heli Lehtomäki, Gunn Marit Aasvang, Gerhard Sulo, Bruce R Denby, Otto Olavi Hänninen, Michael Brauer, Gavin Pereira, Omid Dadras, Anette Kocbach Bølling","doi":"10.1186/s12940-025-01250-y","DOIUrl":"10.1186/s12940-025-01250-y","url":null,"abstract":"<p><strong>Background: </strong>Exposure to fine particles (PM<sub>2.5</sub>) has been associated with adverse health outcomes, even at low exposure levels (< 10 µg/m<sup>3</sup>). Burden of disease assessments can quantify these associations; however, their sensitivity to methodological choices limits comparability between studies.</p><p><strong>Methods: </strong>This study aimed to quantify the impact of methodological choices on disease burden attributable to low levels of ambient PM<sub>2.5</sub>, using Norway as a case study. Key methodological choices included (i) population exposure data, (ii) concentration-response curves, and (iii) population health data. Data from national and international sources were applied, including the global burden of disease (GBD) study. Attributable mortality and disability-adjusted life years (DALY) were estimated using burden of disease methodology. Additionally, the impact of choices related to concentration-response curves was assessed for higher exposure levels, using a scenario where exposure distributions were shifted to mean exposures up to 30 µg/m<sup>3</sup>.</p><p><strong>Results: </strong>Methodological choices related to the concentration-response curves had the largest impacts on the estimated attributable deaths, ranging from - 91% to 104% change relative to the reference estimate (1,448 deaths, 95% CI 502-1497). These choices had a smaller impact on higher exposure levels, varying from - 46% to 53%. The choice of exposure and population health data led to 40% differences in attributable death estimates. DALYs attributable to PM<sub>2.5</sub> were predominantly driven by years of life lost (YLL: 74%). The choice of relative risk (RR) for the concentration response curve caused around 30% variation in DALY estimates relative to the reference (11,730 DALYs; 5,980 - 16,790), with larger differences for ischemic heart disease (-44 to 79%).</p><p><strong>Conclusion: </strong>Attributable burden estimates for PM<sub>2.5</sub> are highly sensitive to key methodological choices, particularly at low exposure levels. Consequently, transparent reporting of the methodological choices and data sources in PM<sub>2.5</sub> health risk assessments are required to improve comparability and facilitate interpretations of the burden estimates.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":" ","pages":"4"},"PeriodicalIF":5.3,"publicationDate":"2025-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12802007/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145741223","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}
Nicole E Sieck, Menglu Liang, Hyeonjin Song, Hao He, Jochen G Raimann, Raul Cruz, Ross J Salawitch, Amy R Sapkota, Frank W Maddux, Len A Usvyat, Peter Kotanko, Amir Sapkota
{"title":"Risk of hospitalization and mortality across US climate regions following extreme heat exposure in patients with end-stage kidney disease (ESKD) receiving in-center hemodialysis: a space-time-stratified case-crossover analysis.","authors":"Nicole E Sieck, Menglu Liang, Hyeonjin Song, Hao He, Jochen G Raimann, Raul Cruz, Ross J Salawitch, Amy R Sapkota, Frank W Maddux, Len A Usvyat, Peter Kotanko, Amir Sapkota","doi":"10.1186/s12940-025-01249-5","DOIUrl":"10.1186/s12940-025-01249-5","url":null,"abstract":"<p><strong>Background: </strong>The impact of heat exposure on patients with end-stage kidney disease (ESKD) is of growing concern in the context of climate change. In this study, we investigated the association of heat exposure with hospitalization and mortality, and how the risk of these adverse health outcomes varied by climate region in the US.</p><p><strong>Methods: </strong>We obtained hospitalization and mortality data for patients with ESKD receiving in-center hemodialysis treatment between 2012 and 2018 at Fresenius Kidney Care facilities located within the contiguous US. We used the treatment facility location to assign heat exposure using maximum universal thermal climate index temperature data. We conducted a space-time-stratified case-crossover study using conditional Poisson regression with distributed lag nonlinear models to examine the effects of heat exposure at the 95th percentile of the region-specific temperature distribution for lags of three days. Stratified analyses were run to assess differences in associations across nine climate regions and three latitude bands.</p><p><strong>Results: </strong>The cumulative lag 0-3 risk of hospitalization associated with heat exposure was highest in the West (rate ratio [RR]: 1.099; 95% confidence interval [CI]: 1.041, 1.160), whereas the highest risk of mortality was observed in the Northwest region (RR: 1.097; 95% CI: 1.007, 1.195). We observed significant increases in the risk of hospitalization at the low- and mid-latitude bands and a significant increase in the risk of mortality in the mid-latitude band.</p><p><strong>Conclusion: </strong>We observed spatial heterogeneity across US climate regions. The strongest effects of heat exposure were observed in the Ohio Valley, South, and West regions for hospitalization and the Upper Midwest, Southeast, and Northwest regions for mortality. Findings may be used to inform targeted interventions to patients with ESKD residing in areas with higher risks of adverse health outcomes following heat exposure.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":" ","pages":"3"},"PeriodicalIF":5.3,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12797976/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145687133","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}
Maria Luiza Dos Santos Rodrigues Vaz, Ana Beatriz da Silva Sousa, Carolina Martins Ribeiro, Paula Maria Quaglio Bellozi, Angelica Amorim Amato
{"title":"A systematic review of exposure to endocrine disruptors and energy expenditure in mice.","authors":"Maria Luiza Dos Santos Rodrigues Vaz, Ana Beatriz da Silva Sousa, Carolina Martins Ribeiro, Paula Maria Quaglio Bellozi, Angelica Amorim Amato","doi":"10.1186/s12940-025-01207-1","DOIUrl":"10.1186/s12940-025-01207-1","url":null,"abstract":"<p><p>Exposure to endocrine disruptors (EDs) is associated with increased susceptibility to obesity and metabolic dysfunction in epidemiological and preclinical studies. Accumulating evidence supports that various EDs promote energy intake and fat storage, but little is known about how they affect energy expenditure (EE). This systematic review examined the effect of EDs on EE in murine models and on mitochondrial bioenergetics in cell-based studies. We included 12 in vivo studies, which assessed the effect of phytoestrogens, DDT, tolylfluanid, benzene, bisphenol A, bisphenol S, butyl-phthalate, deltamethrin, and the mixtures of 23 chemicals and of organophosphate flame retardants. DDT, tolylfluanid, benzene, and the mixtures of 23 chemicals and of flame retardants decreased; bisphenol A, bisphenol S, and butyl-phthalate had a neutral effect; and phytoestrogens and deltamethrin increased EE. The effects of some EDs were sexually dimorphic, dose-dependent, and interacted with diet. Nine cell-based studies were included and indicated that mitochondrial bioenergetics was impaired by tolylfluanid, bisphenol A, and DDT in muscle cells; by bisphenol AF, BDE-99, DDT, DDE, and the mixture of DDE, trans-nonachlor, and oxychlordane in adipocytes; by bisphenol A in hepatocytes; and by tributyltin in pluripotent cells. Our findings indicate that EDs affect EE in mice in a sexually dimorphic pattern and impair mitochondrial bioenergetics in cellular models which are representative of key tissues involved in energy balance. While further studies are needed to fully elucidate the impact of EDs on energy balance and mitochondrial function, this review underscores the plausibility of mitochondrial dysfunction and altered EE as key pathways linking ED exposure to metabolic diseases.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":" ","pages":"2"},"PeriodicalIF":5.3,"publicationDate":"2025-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12781358/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145676882","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":"Chained mediation of interleukins linking fluoride exposure to frailty: a cohort study of skeletal fluorosis patients in China.","authors":"Yun Lu, FuYu Tao, Ting Hu, Rourou Wang, Zhijuan Shao, Hongbing Ye, Guanghong Yang, Jingshu Li, Qingzhen Jia, Feng Hong, Peng Luo","doi":"10.1186/s12940-025-01240-0","DOIUrl":"10.1186/s12940-025-01240-0","url":null,"abstract":"<p><strong>Background: </strong>Chronic fluorosis, characterized by excessive exposure to fluoride, is associated with a greater risk of frailty in endemic populations. While fluoride correlates with inflammation and frailty, the mediating role of interleukins (ILs) remains unclear. This study investigated the potential multiple mediation pathways of ILs on the relationship between fluoride exposure and frailty in skeletal fluorosis patients.</p><p><strong>Methods: </strong>A multicenter cross-sectional cohort (N= 678; age: ≥40 years) from high-fluoride areas in China (2023-2024) was enrolled. Urine fluoride (uF) was used to assess exposure. Frailty was measured via the FRAIL scale, and serum ILs (IL-6, IL-8, IL-1β, and IFN-α) were measured via ELISA. Associations and potential mediating pathways were evaluated via chain mediation models (PROCESS macro, SPSS),which test IL-mediated pathways between uF and frailty and adjust for age/sex. Bootstrapping (5,000 resamples) was used to estimate 95% CIs.</p><p><strong>Results: </strong>Frailty prevalence (5.9%) surpassed that of the general population (2.3%). A high uF value was directly associated with frailty risk (β = 0.2856, P < 0.001). Two potential pathways were identified: the inflammatory cascade: uF→IL-6↑ (β= 0.2947) → IL-1β↑ (β= 0.3936) →frailty (β= 0.0893), and the indirect association accounted for 3.6% of the total effect. Muscle-nutrition depletion: IL-1β↑ → sarcopenia↑ (β= 0.1137)→ increased undernutrition risk↑ (β=-0.2148)→ frailty (β=-0.1990); the indirect association accounted for 4.2% of the total effect. IFN-α attenuated the association of fluoride with IL-1β (P = 0.0113) and was linked to lower frailty risk (β = -0.086, P < 0.01). CONCLUSIONS : The\"IL-6→IL-1β\" pathway is a potential mechanism for inflammation-related frailty, and nutritional interventions could disrupt the \"IL-1β→sarcopenia→malnutrition\" cycle. IFN-α has a protective effect on fluoride-induced inflammation.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"24 1","pages":"90"},"PeriodicalIF":5.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12667193/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145654028","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":"Children's environmental health, environmental justice and PM2.5 regulation in the US, 1997-2024.","authors":"Marianne Sullivan, Ellen Kohl","doi":"10.1186/s12940-025-01247-7","DOIUrl":"10.1186/s12940-025-01247-7","url":null,"abstract":"<p><p>INTRODUCTION: Children are uniquely susceptible to air pollution. US EPA is required to set National Ambient Air Quality standards that protect susceptible populations from air pollution within an “adequate margin.” Additionally, environmental justice communities are often disproportionately exposed to air pollution, therefore children living in these communities may experience increased vulnerability. PM2.5 contributes significantly to air pollution attributable morbidity and mortality. This research analyzes each PM2.5 rulemaking starting with the first in 1997 to determine for how children and children living in environmental justice communities were considered at each stage of the rulemaking process. METHODS: We used content analysis to analyze all EPA PM 2.5 rulemakings. Publicly available rulemaking documents were searched to determine how EPA assessed the weight of evidence for Children’s Environmental Health (CEH) endpoints and how this evidence was used in later stages of rulemaking. We also analyzed EPA’s consideration of children in environmental justice analyses related to rulemaking. We used word count analysis to examine the relative emphasis on CEH and environmental justice in rulemaking over time. Finally, we examined if CEH evidenced was prioritized in EPA’s rulemaking rationales. RESULTS: The evidence base for CEH and PM 2.5 has expanded since 1997 but there are a limited number of CEH health endpoints designated as causal or likely causal in EPA’s weight of evidence assessments. CEH health effects in PM 2.5 benefits assessments have primarily been limited to respiratory effects and infant mortality. Consideration of environmental justice was limited until 2012 but expanded in 2024, however children have not been included in environmental justice health effects analyses. When CEH evidence was prioritized in rulemaking rationales, standards were strengthened. CONCLUSIONS AND RECOMMENDATIONS: We find conflicting treatment of CEH in PM 2.5 standard setting. In some rulemakings CEH was prioritized while in others it was not. There has been limited consideration of environmental justice in PM 2.5 rulemaking and no rulemaking has accounted for the potential risk of adverse health effects for children living in environmental justice communities. EPA’s strict adherence to causal criteria for CEH endpoints, which can be difficult to study, may slow the adoption of protective standards. Further, policymakers should have access to more comprehensive data and information on PM2.5’s impact on CEH. Finally, due to its importance for lifelong health, we advocate for a consistent precautionary approach to CEH in NAAQs standard setting. </p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":" ","pages":"94"},"PeriodicalIF":7.3,"publicationDate":"2025-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12720475/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145630919","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}
Houman Kahroba, Julian Krauskopf, Jacco J Briedé, Tim Nawrot, Theo M de Kok
{"title":"Small extracellular vesicles: connecting early life exposure outcomes to air pollution during pregnancy to early childhood health.","authors":"Houman Kahroba, Julian Krauskopf, Jacco J Briedé, Tim Nawrot, Theo M de Kok","doi":"10.1186/s12940-025-01238-8","DOIUrl":"10.1186/s12940-025-01238-8","url":null,"abstract":"<p><p>Exposure to air pollution poses a serious threat to maternal and child health, particularly during critical developmental periods. Extracellular vesicles (EVs), as key mediators of intercellular communication, have emerged as a novel mechanism through which environmental exposures, including air pollutants, exert systemic effects. This review synthesizes current evidence on the role of small EVs (sEVs) in mediating the biological impacts of prenatal air pollution exposure, with a focus on their molecular profile, including the presence of signaling molecules like miRNAs and proteins, and their implications for childhood health outcomes. In this review, we explore mechanisms involving sEVs in transplacental exposure, signaling and epigenetic modifications, linking exposure to adverse developmental and health effects in early life. Furthermore, we highlight the potential of sEVs as biomarkers for exposure assessment and predictors of adverse health outcomes. Relevant studies were identified through a comprehensive literature search and systematic review of experimental and epidemiological evidence. By integrating insights from toxicology, epidemiology, and molecular biology, we identify specific needs for further research into sEVs, both as mechanistic mediators and diagnostic tools for air pollution-related health risks.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"24 1","pages":"89"},"PeriodicalIF":7.3,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12661761/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145630398","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}
Aimée Vester, Yingying Xu, Nicholas C Newman, Melinda C MacDougall, George D Papandonatos, Patrick J Parsons, Christopher D Palmer, Joseph M Braun, Bruce P Lanphear, Aimin Chen, Kim M Cecil, Kimberly Yolton
{"title":"Cumulative childhood lead exposure estimation and school-age IQ in a prospective birth cohort.","authors":"Aimée Vester, Yingying Xu, Nicholas C Newman, Melinda C MacDougall, George D Papandonatos, Patrick J Parsons, Christopher D Palmer, Joseph M Braun, Bruce P Lanphear, Aimin Chen, Kim M Cecil, Kimberly Yolton","doi":"10.1186/s12940-025-01244-w","DOIUrl":"10.1186/s12940-025-01244-w","url":null,"abstract":"<p><strong>Background: </strong>Lead is a well-known neurotoxicant with no identified safe level. Prior studies found that childhood lead exposure is associated with decreased intelligence quotient (IQ) scores. However, most studies rely on a limited number of blood lead measurements. In this prospective pregnancy and birth cohort, we estimated cumulative childhood lead exposure using repeated blood lead concentrations and regression calibration, allowing for more accurate assessment of lead burden over time and its association with IQ.</p><p><strong>Methods: </strong>This prospective study included 262 mother-child dyads from Greater Cincinnati enrolled in the Health Outcomes and Measures of the Environment (HOME) Study from 2003 to 2006. We obtained serial blood lead measurements and estimated cumulative childhood lead exposure using a regression calibration method. Outcome was assessed via Wechsler-based IQ testing at ages 5-12 years. We examined the association between estimated cumulative childhood lead exposure and child IQ using linear regression models.</p><p><strong>Results: </strong>Our cohort had low levels of estimated lifetime average lead exposure (geometric mean: 1.21 μg/dL). Overall, estimated lead exposure decreased from age 12 months to time of IQ test. Cumulative childhood lead exposure estimate was associated with decreased IQ at ages 5-12 years in unadjusted analyses, but not after adjusting for maternal IQ, household income, reported prenatal vitamin use, Home Observation for Measurement of the Environment score, and maternal serum cotinine. Sensitivity analyses additionally adjusting for prenatal total folate did not markedly change our results. We assessed early-life, school-age, or concurrent blood lead exposure estimate in place of cumulative childhood lead exposure estimate and observed a similar pattern of results.</p><p><strong>Conclusions: </strong>We used a regression calibration method to leverage robust, repeated lead exposure data in our prospective pregnancy and birth cohort. In this cohort with low levels of lead exposure, cumulative childhood lead exposure estimate was negatively associated with school-age IQ in unadjusted analyses but not adjusted analyses. We considered sociodemographic and maternal factors previously associated with cognitive development. Our results suggest these factors may confound the association between low-level child lead exposure and child IQ.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":" ","pages":"1"},"PeriodicalIF":5.3,"publicationDate":"2025-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12764035/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145631003","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}
Tuo Liu, Melissa A Furlong, Justin M Snider, Shawn Beitel, Catherine E Mullins, Douglas I Walker, Jaclyn M Goodrich, Derek J Urwin, Jamie Gabriel, Jeff Hughes, John J Gulotta, Miriam M Calkins, Yiwen Liu, Frank A von Hippel, Paloma Beamer, Jefferey L Burgess
{"title":"Evaluating urinary metabolic profiles with wildland-urban-interface (wui) fire exposure among male firefighters: a comparison with municipal structure fires (msf).","authors":"Tuo Liu, Melissa A Furlong, Justin M Snider, Shawn Beitel, Catherine E Mullins, Douglas I Walker, Jaclyn M Goodrich, Derek J Urwin, Jamie Gabriel, Jeff Hughes, John J Gulotta, Miriam M Calkins, Yiwen Liu, Frank A von Hippel, Paloma Beamer, Jefferey L Burgess","doi":"10.1186/s12940-025-01239-7","DOIUrl":"10.1186/s12940-025-01239-7","url":null,"abstract":"<p><strong>Background: </strong>Firefighters have frequent exposure to carcinogens and an increased risk of cancer. Wildland-urban interface (WUI) fires, which involve both structures and undeveloped wildland fuels, pose unique challenges to the health of firefighters. However, the extent of health risks associated with these fires remains underexplored.</p><p><strong>Objectives: </strong>This study aims to identify altered urine metabolites and metabolic processes among male firefighters that were associated with WUI fires as compared with municipal structure fires (MSF).</p><p><strong>Methods: </strong>Untargeted metabolomic profiling was applied to pre-exposure (baseline) and postfire urine samples collected from firefighters responding to WUI and MSF fires. Differential analysis was conducted by fitting linear mixed effects regression models on preprocessed ion intensity and exposure status while adjusting for demographic covariates. Differential metabolites by post-exposure status were identified using a false discovery rate (FDR) threshold of < 0.05. Pathway analysis was performed to identify pathways that were significantly perturbed at a Bonferroni adjusted p-value < 0.05 level. We conducted differential and pathway analyses in both the WUI and MSF cohorts and compared the two fire types in terms of the number of differentially expressed metabolites and patterns of metabolic pathway enrichment.</p><p><strong>Results: </strong>Eighty-five firefighters contributed paired baseline and post-fire samples from WUI events, and 98 firefighters contributed paired baseline and post-fire samples from MSF events. We performed metabolic profiling on baseline and postfire urine samples from WUI and MSF using four modes: HILIC(-), HILIC(+), C18(-), and C18(+) and identified metabolites against an in-house library. We identified 244, 297, 320, and 266 level-1 metabolites from the four respective modes. In the statistical analysis, the main model identified a total of 176 differential metabolites from WUI fires. For MSF, the model identified a total of 652 differential metabolites from the four respective modes. Most metabolites with significant changes after a WUI fire also changed significantly after an MSF event. Two metabolic pathways were significantly enriched after WUI fires, while 7 pathways were significantly enriched after MSF exposure and 2 pathways overlapped between the two types of fires.</p><p><strong>Conclusion: </strong>Fire exposure induces numerous metabolic perturbations in firefighters responding to WUI fires, potentially contributing to their elevated cancer risk. Although individual metabolites changed in a similar fashion across both WUI and MSF, MSF were associated with an increased number of metabolite changes and some of the enriched pathways differed between exposures to WUI fires vs. MSF. These findings suggest that WUI and MSF exposures may share common biological responses while also posing unique health risks to firefighter","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"24 1","pages":"88"},"PeriodicalIF":5.3,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12625405/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145539696","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}