Environmental Health Perspectives最新文献

{"title":"Exposure to Size-Fractioned\u0000Ambient Particles Associated\u0000with Alterations in Gut Microbiome and Pro-Atherosclerotic Biomarkers\u0000in Young Adults","authors":"Xinghou He,Bin Zhang,Erlu Zhao,Yan Fang,Jiahui Liu,Yutong Zhu,Huiying Xu,Qian Zhao,Xiaoming Song,Tong Wang,Hongbing Xu,Wei Huang","doi":"10.1021/ehp.6c00374","DOIUrl":"https://doi.org/10.1021/ehp.6c00374","url":null,"abstract":"Abstract Background: Ambient fine and ultrafine particles are linked to the progression of atherosclerotic cardiovascular diseases, wherein gut microbiome may play a critical role. However, the underlying mechanisms and relevant metabolic pathways are not yet fully understood. Objectives: To identify the features and metabolic pathways of gut microbiome, and to explore their potential roles in the pro-inflammatory and pro-atherosclerotic effects of particles in size ranges of 5–560 nm (measured as number concentration, PNC5–560). Methods: We conducted a longitudinal panel study of 152 young adults in Beijing, China, with four monthly clinical examinations between September 2019 and January 2020. Gut microbiome, fecal metabolome, and circulating pro-inflammatory and pro-atherosclerotic biomarkers were measured. Linear mixed-effects models were used to examine the associations linking short-term PNC5–560 exposure to health indicators. We further evaluated whether gut microbiota could mediate changes in these biomarkers and identified the underlying metabolic pathways. Results: Major sources of PNC5–560 in the study area were identified as diesel vehicle emissions (37.9%), gasoline vehicle emissions (39.4%), nucleation (9.2%), and secondary aerosols (11.9%). Per interquartile range increment in PNC5–560 over the preceding 7 days was associated with significant elevations in circulating pro-inflammatory and pro-atherosclerotic biomarkers, with effect estimates ranging from 2.1% (95% CI: 0.4%, 3.8%) to 198.6% (95% CI: 29.3%, 365.8%). PNC5–560 exposure was also associated with decreased gut microbial α-diversity (e.g., Shannon, Simpson, and Chao1) and altered taxonomic composition. Several microbial species (e.g., Solibaculum mannosilyticum, Bacteroides stercoris, and Bifidobacterium longum) were identified as potential mediators of the effects of PNC5–560 on pro-inflammatory and pro-atherosclerotic responses, with mediation proportions up to 9.8% (95% CI: 0.8, 38.3) and 4.8% (95% CI: 0.09, 22.5), respectively. Functional analyses further revealed that these mediating effects involved perturbations in nucleotide and amino acid metabolism pathways. Conclusions: This study provides evidence suggesting that gut microbiome may regulate nucleotide and amino acid metabolism, thereby partially mediating the detrimental cardiovascular effects of size-fractioned ambient particles.","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"137 1","pages":""},"PeriodicalIF":10.4,"publicationDate":"2026-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148894977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations of Green\u0000Space and Air Pollution Mixture\u0000with Heterogeneous Biological Aging Patterns","authors":"Guoqiang Ma,Jing Xu,Yishu Li,Yuefei Wu,Qian Li,Xuan Cao,Zitong Zhao,Jingyan Gao,Lijun Gao,Lina Yan,Xiaolin Zhang","doi":"10.1021/ehp.6c00004","DOIUrl":"https://doi.org/10.1021/ehp.6c00004","url":null,"abstract":"Abstract Evidence on associations between green space, air pollution mixture, and heterogeneous biological aging patterns remains limited. We investigated the opposing effects of green space and air pollution mixture on biological aging patterns using an accelerated longitudinal design based on repeated-measures data from 11,760 adults (aged 20–65 years) in a high-pollution Chinese city. Biological age acceleration (BAA) was derived via the Klemera-Doubal method. Group-based trajectory modeling identified three stable BAA profiles, labeled as “slow”, “moderate”, and “accelerated” aging, which were primarily distinguished by overall BAA magnitude rather than divergent slopes over age. Multinomial generalized linear mixed models and weighted quantile sum regression were applied to assess environmental associations. Higher green space (500 m normalized difference vegetation index (NDVI)) was associated with lower odds of membership in the “accelerated aging” trajectory (OR: 0.84; 95% CI: 0.75, 0.95). Even under limited exposure contrast in this high-pollution setting, higher exposures to PM2.5, PM10, SO2, and O3 were associated with higher odds of membership in the accelerated aging trajectory. The air pollution mixture showed a consistent positive association (OR: 1.16; 95% CI: 1.08, 1.24), driven primarily by O3 and PM10. Mediation analysis revealed that 25.0% of the protective association of green space was mediated by reduced pollution exposure. These findings highlight green space as a vital resilience resource, supporting synergistic urban greening and pollution control strategies to promote healthy aging.","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"16 1","pages":""},"PeriodicalIF":10.4,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148894979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"External Validation of STopTox: A Novel Alternative\u0000Method (NAM) for Acute Systemic and Topical Toxicity","authors":"Ricardo Scheufen Tieghi,Cleber C. Melo-Filho,Holli-Joi Martin,José Teófilo Moreira-Filho,Tripp LaPratt,Dave Allen,Judy Strickland,Alexander Tropsha,Nicole Kleinstreuer,Eugene N. Muratov","doi":"10.1021/ehp.6c01195","DOIUrl":"https://doi.org/10.1021/ehp.6c01195","url":null,"abstract":"","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"51 1","pages":"494-497"},"PeriodicalIF":10.4,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148896060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Invited Perspective: How Do Green- and Bluespaces Reduce Heat-Related Health Risks? Gaining New Insights from Street-View Imagery, Deep Learning Models, and Smartphone Data","authors":"Li Yi, Peter James","doi":"10.1021/ehp.6c00547","DOIUrl":"https://doi.org/10.1021/ehp.6c00547","url":null,"abstract":"","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"46 1","pages":""},"PeriodicalIF":10.4,"publicationDate":"2026-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148687903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Household Fuel Use and Kidney Disease-Related Mortality: The Golestan Cohort Study.","authors":"Michele Sassano, Monireh Sadat Seyyedsalehi, Sudabeh Alatab, Hossein Poustchi, Mahdi Sheikh, Arash Etemadi, Reza Malekzadeh, Paolo Boffetta","doi":"10.1021/EHP.6c00520","DOIUrl":"10.1021/EHP.6c00520","url":null,"abstract":"<p><strong>Background: </strong>A large proportion of the global population uses solid fuels for household purposes, and limited evidence from previous studies suggests that it might be associated with reduced renal function.</p><p><strong>Objectives: </strong>To investigate the association between household use of different types of fuels and kidney disease-related mortality.</p><p><strong>Methods: </strong>We analyzed data from the Golestan Cohort Study, a population-based prospective cohort study conducted in northeastern Iran, with 50 045 individuals aged 40-75 years enrolled in the period 2004-2008 and followed through April 2023. Information about household fuel use was collected using validated questionnaires. We estimated adjusted hazard ratios (HRs) and corresponding 95% confidence intervals (CIs) using Cox proportional hazards models. The outcome of interest was death due to any kidney disease, excluding kidney cancer (ICD-10 codes: N00-N19 and N25-N29).</p><p><strong>Results: </strong>During 724,063.62 person-years of follow-up, 262 participants died due to kidney disease. The risk of kidney disease-related mortality was higher with increasing duration of biomass use for cooking or house heating (HR for every 10-year increase: 1.20; 95% CI: 1.04-1.37), while it was not associated with increased duration of using kerosene (10-y HR: 1.09; 95% CI: 0.95-1.24) or gas (10-y HR: 1.00; 95% CI: 0.86-1.16). Estimates for lifetime duration of fuel burning for both cooking and house heating (exclusive fuel use) did not differ according to whether used heating stoves were chimney-equipped or not for kerosene, while they differed for biomass (10-y HR, chimney-equipped: 1.06 [95% CI: 0.95-1.18]; 10-y HR, not chimney-equipped: 1.19 [95% CI: 1.06-1.34]; <i>P</i> _difference = 0.025).</p><p><strong>Discussion: </strong>The findings of our study suggest that burning biomass for household purposes under poor ventilating conditions is associated with kidney disease-related mortality.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 4","pages":"485-493"},"PeriodicalIF":10.9,"publicationDate":"2026-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13445265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multibehavioral Phenotyping in Early-Life-Stage Zebrafish for Identifying Disruptors of Nonassociative Learning.","authors":"David Leuthold, Nadia K Herold, Jana Nerlich, Kristina Bartmann, Ilka Scharkin, Stefan J Hallermann, Nicole Schweiger, Ellen Fritsche, Tamara Tal","doi":"10.1021/EHP.6c00394","DOIUrl":"10.1021/EHP.6c00394","url":null,"abstract":"<p><p><b>BACKGROUND</b>: The vertebrate nervous system is vulnerable to chemical toxicity, and the widespread release of chemicals into the environment outstrips the capacity to assess their safety. The zebrafish (<i>Danio rerio</i>) is a powerful vertebrate model that can bridge the gap between <i>in vitro</i>- and mammalian-based <i>in vivo</i> studies. However, the behavior-rich repertoire of larval zebrafish, a 3R-compliant model amenable to higher throughput chemical screens, has yet to be fully deployed to identify and characterize chemical compounds that cause neurotoxicity. <b>OBJECTIVE</b>: We sought to establish a multibehavioral phenotyping approach in larval zebrafish to identify and mechanistically elucidate neuroactive chemicals, with particular focus on chemical compounds that affect nonassociative habituation learning. <b>METHODS</b>: We devised a battery of automated behavioral assays in larval zebrafish. The battery captures stereotypical visual and acoustic behaviors including habituation, a form of nonassociative learning. To elucidate mechanisms underlying exposure-induced behavioral alterations in zebrafish, <i>in silico</i> target predictions, pharmacological interventions, patch-clamp recordings in cultured mouse cortical neurons, and human multineurotransmitter (hMNR) assay in 3D BrainSpheres were used. <b>RESULTS</b>: Known pharmacological modulators of habituation in zebrafish evoked distinct behavioral patterns. By screening chemicals positive for <i>ex vivo N</i>-methyl-d-aspartate receptor (NMDAR) modulation, we identified chlorophene, a biocide that caused sedation, paradoxical excitation, and reduced habituation in zebrafish. Using <i>in silico</i> target predictions and pharmacological interventions, we discovered that chlorophene acts via gamma-aminobutyric acid A receptors (GABA_ARs), a previously unknown target site. Orthogonal validation in cultured mouse cortical neurons and human stem cell-derived BrainSpheres confirmed chlorophene's interaction with GABA_ARs. Chlorophene's behavioral profile resembled that of flupirtine, a Kv7 potassium channel (M-current) activator, suggesting that habituation deficits stem from M-current rather than GABA_AR modulation. <b>CONCLUSIONS</b>: These studies combined a series of behavior assays in a phenotypically rich, rapid, and inexpensive nonmammalian vertebrate test system to screen chemicals for neurotoxicity. Together with <i>in silico</i> target predictions and mouse- and human-based models, our findings establish multibehavioral phenotyping in zebrafish as a powerful toolkit for neurotoxicity testing and mechanism identification, with relevance for humans.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 4","pages":"465-484"},"PeriodicalIF":10.9,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13445272/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exposures to Drinking Water Contaminants in Community Water Systems and Risk of Ovarian Cancer in the California Teachers Study Cohort.","authors":"Maya Spaur, Lauren M Hurwitz, Danielle N Medgyesi, Alexander P Keil, Laura E Beane Freeman, Jared A Fisher, Jessica M Madrigal, Samantha Ammons, Emma S Spielfogel, Komal Bangia, Paul S Albert, Tiffany R Sanchez, James V Lacey, Rena R Jones, Mary H Ward","doi":"10.1021/EHP.6c00169","DOIUrl":"10.1021/EHP.6c00169","url":null,"abstract":"<p><strong>Background: </strong>Several drinking water contaminants are known or suspected carcinogens; however, there are only a few investigations of drinking water exposure and ovarian cancer. We evaluated associations between regulated contaminants in community water systems (CWS) and ovarian cancer risk in the California Teachers Study, a prospective cohort of female California educators.</p><p><strong>Methods: </strong>Participants were cancer-free, without bilateral oophorectomy, living in California at baseline (1995-1996) with geocoded addresses linked to a CWS (<i>N</i> = 91,127, 92%), with follow-up through 2020 (mean = 19.0 years). Among participants with a residential duration at enrollment of at least 10 years, we computed 15-year (1990-2005) averages of log2-transformed arsenic, nitrate, total trihalomethanes (TTHM) (<i>N</i> = 59,881), and uranium concentrations (<i>N</i> = 56,314). We estimated hazard ratios (HRs, 95% CIs) for all epithelial ovarian cancers (<i>n</i> = 413) and the high-grade serous histotype (<i>n</i> = 199), using Cox proportional hazards regression, adjusting for age, body mass index, menopause status, oral contraceptive use, and parity. We evaluated the mixture effect (per IQR in log2 concentrations) using quantile-based g-computation.</p><p><strong>Results: </strong>Almost all women (>99%) had average exposures below regulatory limits for all contaminants. In single contaminant analyses, a doubling in average uranium concentrations was associated with all ovarian cancer (HR_perlog2 = 1.07, CI 1.00-1.15), whereas a doubling in nitrate was associated with the high-grade serous histotype (HR_perlog2 = 1.09, 95% CI 1.01, 1.17). Findings were similar in models adjusted for other contaminants. We observed positive but imprecise associations for arsenic and TTHM in single-contaminant and contaminant-adjusted analyses. HRs per increase in the mixture were 1.34 (0.95, 1.88) and 1.77 (1.09, 2.87) for all ovarian cancer and the high-grade serous histotype, respectively. Uranium was the largest contributor (56%) to the mixture effect for all ovarian cancers, and nitrate was the largest contributor (48%) for the high-grade serous histotype.</p><p><strong>Conclusions: </strong>Novel associations between drinking water contaminants and ovarian cancer risk at levels below regulatory limits warrant further investigation.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 4","pages":"452-464"},"PeriodicalIF":10.9,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13445266/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A New Mouse Model for Ozone Health Effects Research.","authors":"Gregory J Smith, Robert M Immormino, Martin T Ferris, Sarah A Lester, Timothy P Moran, Jack R Harkema, Samir N P Kelada","doi":"10.1021/EHP.6c00312","DOIUrl":"10.1021/EHP.6c00312","url":null,"abstract":"<p><strong>Background: </strong>Exposure to the ambient air pollutant ozone (O₃) is associated with adverse respiratory health outcomes. Rodent models have been used to identify mechanisms of response to O₃, but their utility has been questioned owing to species differences in physiologic response, most notably exposure-induced hypothermia, which renders rodents relatively resistant to O₃ compared to humans.</p><p><strong>Objectives: </strong>First, to test whether a recombinant inbred mouse strain from the Collaborative Cross population, CC002/Unc, provides a sensitive model of ozone response by benchmarking it to the most commonly used inbred strain, C57BL/6J. Second, to identify the genetic basis of CC002/Unc's sensitivity.</p><p><strong>Methods: </strong>We examined the responses of CC002/Unc and C57BL/6J mice to either acute (0.4 or 0.8 ppm O₃ 4 h) or repeated (0.8 ppm O₃ × 4 h/day × 3 or 9 weekdays) O₃ exposure. Then, we mapped quantitative trait loci (QTL) for responses to 9 days of O₃ in a CC002/Unc × CC005/TauUnc (O₃-resistant) backcross population.</p><p><strong>Results: </strong>CC002/Unc was far more responsive to acute O₃ than C57BL/6J, exhibiting significant inflammation following a single 0.4 ppm O₃ exposure and greater inflammation and injury after 0.8 ppm O₃. Enhanced sensitivity of CC002/Unc mice was associated with decreased breathing frequency and diminished hypothermic responses. Following repeated exposure, C57BL/6J lungs appeared normal, while CC002/Unc lungs had eosinophilic inflammation and centriacinar fibrosis. We identified five QTL for airway eosinophilia, including a large-effect QTL on chromosome 11 that accounts for 18% of phenotypic variation and contains genes with plausible links to aberrant immune responses.</p><p><strong>Discussion: </strong>The CC002/Unc strain provides an improved model to study the effects of acute and repeated O₃ exposure due to its enhanced sensitivity vs C57BL/6J and more human-like thermoregulatory response. Further genetic analysis to pinpoint causal genes underlying CC002/Unc's susceptibility will provide new insights into mechanisms of O₃-induced lung disease.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 4","pages":"438-451"},"PeriodicalIF":10.9,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13445267/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Linking \"Big\" Geospatial and Health Data: Implications for Research in Environmental Epidemiology.","authors":"Andrea R Titus, Tarik Benmarhnia, Lorna E Thorpe","doi":"10.1021/EHP.6c00321","DOIUrl":"10.1021/EHP.6c00321","url":null,"abstract":"<p><strong>Background: </strong>Environmental epidemiology studies increasingly integrate \"big\" geospatial and health data sets to examine associations between environmental factors and health outcomes. Using such data sets ─ and linking between them ─ presents a number of complexities with regard to study design and analytic approaches. These complexities are often magnified with the integration of additional contextual data representing other neighborhood characteristics including socioeconomic factors. Guidance regarding the design of environmental health studies that leverage \"big\" geospatial and health outcome data is limited and fragmented.</p><p><strong>Objective: </strong>Drawing on methodological literature and case studies, this commentary outlines common challenges related to geospatial and health data linkages, posing a series of guiding questions and considerations for investigators conducting environmental health studies, particularly analyses with an etiological focus.</p><p><strong>Discussion: </strong>Recommendations include: 1) using a target trial approach to guide causal analysis, 2) aligning measures with hypothesized causal mechanisms, 3) exploring opportunities to \"groundtruth\" and validate data, and 4) prioritizing interdisciplinary science. The goal of the commentary is to consolidate insights from multiple disciplines ─ including exposure science, epidemiology, and sociology ─ to provide a foundation for etiologic research focused on advancing environmental health for all populations.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 4","pages":"375-382"},"PeriodicalIF":10.9,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13445273/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exposure to Organophosphate Ester Flame Retardants and Plasticizers during Pregnancy and Autism-Related Outcomes in the ECHO Cohort.","authors":"Jennifer L Ames, Assiamira Ferrara, Juanran Feng, Stacey Alexeeff, Lyndsay A Avalos, Emily S Barrett, Theresa M Bastain, Deborah H Bennett, Jessie P Buckley, Courtney C Carignan, Patricia Cintora, Akhgar Ghassabian, Monique M Hedderson, Ixel Hernandez-Castro, Kurunthachalam Kannan, Margaret R Karagas, Catherine J Karr, Jordan R Kuiper, Donghai Liang, Kristen Lyall, Cindy T McEvoy, Rachel Morello-Frosch, Thomas G O'Connor, Jiwon Oh, Alicia K Peterson, Lesliam Quiros-Alcala, Sheela Sathyanarayana, Susan Schantz, Rebecca J Schmidt, Anne P Starling, Tracey J Woodruff, Heather E Volk, Yeyi Zhu, Lisa A Croen","doi":"10.1021/EHP.6c00247","DOIUrl":"https://doi.org/10.1021/EHP.6c00247","url":null,"abstract":"<p><p><b>BACKGROUND</b>: Organophosphate ester flame retardants and plasticizers (OPEs) have myriad uses in industry and consumer products. Increasing human exposure to OPEs has raised concerns about their potential effects on child neurodevelopment during the pregnancy. <b>Objective:</b> We investigated whether OPE urinary concentrations during pregnancy were associated with child's autism-related outcomes. <b>METHODS:</b> We included 4159 mother-child pairs from 15 cohorts in the NIH Environmental influences on Child Health Outcomes (ECHO) Consortium, with children born from 2006-2020 (median age [interquartile range]: 6 [4,10] years). Nine OPE biomarkers were measured in urine samples collected mid- to late pregnancy. Dilution-adjusted biomarkers were modeled continuously, categorically (high [>median], moderate [≤median], nondetect), or as detect/nondetect depending on their detection frequency. We assessed child autism-related traits via a) parent report on the Social Responsiveness Scale (SRS) and b) clinical autism diagnosis. We examined associations of OPEs with child outcomes, including modification by child sex, using generalized estimating equations to account for clustering by ECHO cohort. <b>RESULTS:</b> Compared with nondetectable concentrations, high exposure to bis-(butoxyethyl) phosphate (BBOEP) was associated with higher autistic trait scores (adj-β 0.97, 95% confidence interval [CI]: 0.42, 1.52) and greater odds of autism diagnosis (adjusted odds ratio [adj-OR]: 1.27, 95% CI: 1.07, 1.50). Bis-(1-chloro-2-propyl) phosphate (BCPP) showed associations with autistic trait scores (BCPP adj-β for high exposure vs nondetect: 0.34, 95% CI: -0.46, 1.13; BCPP adj-β for moderate exposure vs nondetect: 0.72, 95% CI: 0.24, 1.20). High exposure to bis-(2-chloroethyl) phosphate (BCETP) was associated with lower odds of autism diagnosis (adj-OR: 0.76, 95% CI: 0.60, 0.95). Other OPEs showed no associations in adjusted models. Associations between BBOEP and higher autistic trait scores were stronger in males than females. <b>DISCUSSION:</b> Prenatal exposure to OPEs, specifically BCPP and BBOEP, may be associated with a higher risk of autism diagnosis and related traits in childhood.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 4","pages":"423-437"},"PeriodicalIF":10.9,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13445271/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}