Environmental Health Perspectives最新文献

{"title":"In Utero Per- and Polyfluoroalkyl Substances (PFAS) Exposure and Changes in Infant T Helper Cell Development among UPSIDE-ECHO Cohort Participants.","authors":"Darline Castro-Melendez, Nathan Laniewski, Todd Jusko, Xing Qiu, B Paige Lawrence, Zorimar Rivera-Núñez, Brunner Jessica, Meghan Best, Allison Macomber, Alena Leger, Kurunthachalam Kannan, Richard K Miller, Emily S Barret, Thomas G O'Connor, Kristin Scheible","doi":"10.1021/EHP.6c00037","DOIUrl":"10.1021/EHP.6c00037","url":null,"abstract":"<p><p><b>BACKGROUND</b>: Environmental exposures to toxicants, such as per- and polyfluoroalkyl substances (PFAS), during gestation can disrupt immune development, causing long-term impacts on a child's ability to generate a well-regulated, protective immune response. T-cells coordinate with all immune cell types to orchestrate both cellular and antibody-mediated responses. While there is compelling evidence that PFAS alters immunity in humans, the specific effects of early life PFAS exposure on infant T-cell development are unreported. Because of their central role in immunity, altered T-cell development in infants would have implications on immune responses broadly and long-term. <b>OBJECTIVES</b>: We seek to model longitudinal changes in the frequency of functionally distinct CD4+ T-cell subpopulations from birth through 12 months and their association with in utero PFAS exposure. <b>METHODS</b>: Maternal-infant dyads were recruited as part of the UPSIDE-ECHO cohort during the first trimester between 2015 and 2019 in Rochester, New York; dyads were followed through the infant's first birthday. Maternal PFAS concentrations (PFOS, PFOA, PFNA, PFHXS and PFDA) were quantified in serum during the second trimester using high-performance liquid chromatography and tandem mass spectrometry. Infant lymphocyte frequencies were assessed at birth, 6- and 12-months using mass cytometry and high-dimensional clustering methods. Linear mixed-effects models were employed to analyze the relationship between maternal PFAS concentrations and CD4+ T-cell subpopulations (<i>n</i> = 200). All models included a PFAS and age interaction and were adjusted for parity, infant sex, and prepregnancy body mass index. <b>RESULTS</b>: In utero PFAS exposure correlated with multiple CD4+ T-cell subpopulations in infants. The greatest effect sizes were seen in T follicular helper (Tfh) and T-helper 2 (Th2) cells at 12 months. A log₂-unit increase in PFOS was associated with lower Tfh [0.17% (95% CI: -0.30, -0.40)] and greater Th2 [0.27% (95% CI: 0.18, 0.35)] cell percentages at 12 months. Similar trends were observed for PFOA, PFNA, PFHXS, and PFDA. <b>DISCUSSION</b>: Maternal PFAS exposures correlate with cell-specific changes in the infant T-cell compartment, including key CD4+ T-cell subpopulations that play central roles in coordinating well-regulated protective immunity. Future studies into the role of PFAS-associated T-cell distribution and the risk of adverse immune-related health outcomes in children are warranted.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 4","pages":"408-422"},"PeriodicalIF":10.9,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13445270/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683911","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 Start.","authors":"Joel D Kaufman","doi":"10.1021/EHP.6c00320","DOIUrl":"10.1021/EHP.6c00320","url":null,"abstract":"","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 1","pages":"1-2"},"PeriodicalIF":10.9,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13250798/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148224130","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":"Source-Specific Air Pollution and Risk of Chronic Obstructive Pulmonary Disease: A Pooled Cohort Study.","authors":"Manuella Lech Cantuaria, Aslak Harbo Poulsen, Ole Raaschou-Nielsen, Étienne Audureau, Ralph Epaud, Sophie Lanone, Jørgen Brandt, Lise Marie Frohn, Matthias Ketzel, Anja Olsen, Lau Caspar Thygesen, Mette Sørensen","doi":"10.1021/EHP.6c00128","DOIUrl":"10.1021/EHP.6c00128","url":null,"abstract":"<p><strong>Background: </strong>The evidence linking long-term exposure to air pollution and the development of chronic obstructive pulmonary disease (COPD) is still controversial. Furthermore, most studies have investigated associations with particulate matter (PM) and nitrogen dioxide (NO₂), disregarding their emission source and other relevant air pollutants, such as ultrafine particles (UFP) and elemental carbon (EC).</p><p><strong>Objectives: </strong>This study aimed to assess associations between long-term residential exposure to PM_2.5, NO₂, UFP, and EC and the risk of COPD, distinguishing the effects of air pollution from local traffic and other sources.</p><p><strong>Methods: </strong>We pooled data from two large Danish cohorts, the Diet, Cancer, and Health cohort and the Danish National Health Survey. For all participants (<i>N</i> = 159,769), we estimated long-term air pollution exposure to total, local traffic, and other contributions, based on complete address histories. We used Cox proportional hazards models to estimate associations between 10-year time-weighted averaged air pollution and incident COPD, adjusting for demographic, socioeconomic, and lifestyle factors, including smoking. We evaluated the possible modification of these associations by sex, smoking status, and previous asthma diagnosis.</p><p><strong>Results: </strong>Long-term exposures to PM_2.5, NO₂, UFP, and EC were associated with higher risk of COPD. The highest hazard ratio (HR) per interquartile range of total contributions was observed for PM_2.5 (HR: 1.11 [95% confidence interval: 1.05, 1.17]), followed by NO₂ (1.08 [1.04, 1.13]), UFP (1.05 [0.99, 1.11]), and EC (1.02 [1.00, 1.05]), after full adjustment. PM_2.5 from other sources than local traffic was more strongly associated with COPD than PM_2.5 from local traffic, while for UFP and EC, the contributions from local traffic seemed to be the most harmful. Effect modification analyses showed stronger associations among women, never smokers, and those with an asthma diagnosis.</p><p><strong>Discussion: </strong>Our findings suggest that air pollution from local traffic and other sources contributes to COPD risk, with variations depending on the pollutant type. Further research is needed to validate these findings across different populations and geographical settings.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 4","pages":"386-396"},"PeriodicalIF":10.9,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13445269/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683929","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":"Wildfire-Season Fine Particulate Matter Exposure and Associations with Influenza and Influenza-like-Illness Risk in the Western USA.","authors":"Ava Orr, Nisha B Alden, Elizabeth Austin, Zeina Jaffar, Jonathon Knudson, Jon Graham, Christopher T Migliaccio, Curtis Noonan, Shawn Urbanski, Maximilian Wegener, Erin L Landguth","doi":"10.1021/EHP.6c00326","DOIUrl":"10.1021/EHP.6c00326","url":null,"abstract":"<p><strong>Background: </strong>Influenza remains a significant public health threat with pandemic potential. Understanding environmental factors influencing virus spread and severity is critical, particularly as wildfires become more frequent and intense. While temperature and humidity's roles in virus seasonality and persistence are well understood, the impacts of air pollution ─ especially wildfire-specific particulate matter (PM_2.5) ─ on respiratory infections are less explored.</p><p><strong>Objectives: </strong>This study aimed to investigate the association between wildfire PM_2.5 exposure and influenza or influenza-like illness (ILI) incidence. Specifically, we assessed (1) the long-term impact of PM_2.5 exposure during the preceding wildfire season on influenza/ILI risk in the following flu season, and (2) the effects of short-term PM_2.5 exposure during the active flu season.</p><p><strong>Methods: </strong>We utilized ILI and influenza data from state health departments in six Western U.S. states (Arizona, Colorado, Montana, Nevada, Oregon, and Washington) from 2010 to 2019. We applied generalized linear distributed lag models to assess the impact of PM_2.5 exposure during the preceding wildfire season on influenza or ILI risk in the subsequent flu season, as well as the effect of short-term PM_2.5 exposure during the current flu season.</p><p><strong>Results: </strong>Long-term exposure to wildfire PM_2.5 was associated with increased influenza risk in states with influenza data: Arizona ([Rate Ratio (RR) = 1.061 (1.026-1.100)]), Colorado [RR = 1.067 (1.056-1.078)], Montana [RR = 1.038 (1.013-1.063)], and Oregon [RR = 1.049 (1.041-1.057)], per 10 μg/m³ PM_2.5 increase. However, the states with only ILI data did not follow this pattern, revealing no observed effect in Nevada [RR = 1.005 (0.920-1.097)] and a negative effect in Washington [RR = 0.884 (0.842-0.919)]. Similarly, but to a lesser degree, short-term PM_2.5 exposure effects were noted in states with only influenza data but not ILI data.</p><p><strong>Discussion: </strong>Our findings underscore a positive association between wildfire-specific PM_2.5 and influenza risk in states with influenza data, suggesting a differential effect of PM_2.5 on respiratory infections. This study supports further investigation into the causative mechanisms behind these correlations, particularly considering the increasing frequency of wildfires and the resulting air quality impacts.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 4","pages":"397-407"},"PeriodicalIF":10.9,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13445268/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683904","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":"Expanded Tox21 Biological Assay Panel for the Prediction of Drug-Induced Liver Injury and Cardiotoxicity.","authors":"Tuan Xu, Masato Ooka, Jinghua Zhao, Srilatha Sakamuru, Deborah K Ngan, Li Zhang, Shu Yang, Jameson Travers, Menghang Xia, Tongan Zhao, Carleen Klumpp-Thomas, Hu Zhu, Mathew D Hall, Stephen Ferguson, Natalie D Shaw, David M Reif, Anton Simeonov, Ruili Huang","doi":"10.1021/EHP.6c00052","DOIUrl":"10.1021/EHP.6c00052","url":null,"abstract":"<p><strong>Background: </strong>Toxicology in the 21st Century (Tox21) assay data provide a valuable resource for the prediction of <i>in vivo</i> toxicity using machine learning models. However, the performances of these models previously developed using the pre-existing Tox21 assay data were less than ideal, likely due to insufficient coverage of the biological response space by the assay targets.</p><p><strong>Objectives: </strong>This study aimed to assess whether expanding the Tox21 portfolio with new assays that probe under-represented targets/pathways related to unanticipated adverse drug effects could improve the predictive capacity of <i>in vitro</i> assay data for <i>in vivo</i> toxicity such as drug-induced liver injury (DILI) and cardiotoxicity (DICT).</p><p><strong>Methods: </strong>Models were constructed using data from the pre-existing panel of 36 assay targets and the expanded panel of 49 assay targets. A feature selection approach was used to determine the optimal number of assays needed for each model. The models were then applied to predict the potential hepatotoxicity and cardiotoxicity of compounds in the Tox21 10K compound library.</p><p><strong>Results: </strong>For both DILI and DICT prediction, the best-performing models developed using the expanded assay panel required a smaller number of assays to achieve the same level of performance compared to those based on the pre-existing assays. Models constructed by combining both assay data (pre-existing + expanded) and chemical structure consistently outperformed those constructed based on assay data alone but showed similar performance to those constructed based on chemical structure. The compounds predicted to have the highest toxic potential were experimentally verified to demonstrate the effectiveness of our models in identifying new potentially toxic compounds.</p><p><strong>Discussion: </strong>The expansion of the Tox21 assay panel has significantly enhanced the predictive capacity of assay data for predicting the DILI and DICT potential. This improvement underscores the importance of a diverse and comprehensive <i>in vitro</i> assay portfolio in advancing safety assessment.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 3","pages":"361-374"},"PeriodicalIF":10.9,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13347643/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148419612","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":"Prenatal Exposure to Ambient Air Pollution and Fetal Growth Trajectories in Wuhan, China.","authors":"Chen Hu, Hongxiu Liu, Yang Peng, Jie Hu, Wei Xia, Shunqing Xu, Yuanyuan Li","doi":"10.1021/EHP.6c00033","DOIUrl":"10.1021/EHP.6c00033","url":null,"abstract":"<p><strong>Background: </strong>While numerous studies have examined associations between prenatal air pollution exposure and fetal growth measures, investigations assessing longitudinal growth trajectories across multiple time points during mid-to-late pregnancy remain limited.</p><p><strong>Objectives: </strong>The aim of this study is to explore the effects of prenatal exposure to air pollution on fetal growth trajectories.</p><p><strong>Methods: </strong>From a prospective birth cohort in Wuhan, China, recruited from 2013 to 2016, we included a total of 4283 eligible pregnant women. At 16, 24, 31, and 38 weeks of gestation, we collected ultrasound measurements, including biparietal diameter (BPD), abdominal circumference (AC), femur length (FL), and estimated fetal weight (EFW). Exposure to air pollution during pregnancy was estimated for the participants' residential addresses using a spatial interpolation method. Associations between air pollutants and fetal growth parameters across four exposure windows were examined by using multiple informant models. Group-based trajectory modeling (GBTM) combined with a multinomial logistic regression model was used to explore the effect of air pollution exposure on fetal growth trajectories.</p><p><strong>Results: </strong>Four trajectory groups for AC, FL, and EFW, and three trajectory groups for BPD were selected based on GBTM. Compared with the reference trajectory group, exposure to higher PM_2.5 during weeks 1-16 was significantly associated with lower odds of being in the \"fast growth group\" for AC (OR = 0.68, 95% CI: 0.55, 0.84) and EFW (OR = 0.71, 95% CI: 0.56, 0.91). Exposures to PM_2.5, PM₁₀, NO₂, SO₂, and CO during 1-16 weeks were negatively associated with AC, FL, and EFW at 16 weeks as well as BPD, FL, and EFW at 24 weeks. Similar negative associations were observed between air pollution exposure during 25-38 weeks and AC and EFW at 38 weeks.</p><p><strong>Discussion: </strong>Our study provided evidence of negative associations between air pollution exposure during 1-16 weeks of gestation and the fast growth trajectory group. In addition, we observed distinct lagged associations between air pollution and fetal growth, with early pregnancy exposure negatively related to early and midgestational growth, and mid-to-late pregnancy exposure negatively related to growth in the late window. These results underscore the importance of identifying critical windows of susceptibility during pregnancy and support early intervention strategies to mitigate adverse fetal developmental outcomes.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 3","pages":"351-360"},"PeriodicalIF":10.9,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13347642/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148419723","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":"The Role of Gut Microbiota in the Association between Air Pollution and Cognitive Function in Older Adults.","authors":"Wenhao Qi, Mengmeng Kong, Xia Meng, Zhonghan Sun, Zhendong Mei, Yanni Pu, Xiaofeng Zhou, Qichu Wang, Jian-Ge Qiu, Bing-Hua Jiang, Jie Shen, Changzheng Yuan, John S Ji, Xiaofeng Wang, Haidong Kan, Yan Zheng","doi":"10.1021/EHP.6c00026","DOIUrl":"10.1021/EHP.6c00026","url":null,"abstract":"<p><strong>Background: </strong>Growing evidence links air pollution to cognitive dysfunction in older adults. The gut microbiome and circulating metabolites present an important yet unexplored pathway given their crucial role in the gut-brain axis.</p><p><strong>Objectives: </strong>We aimed to explore the potential roles of gut bacteria, fungi, microbial functional potentials, and circulating metabolites in the association of residential PM_2.5 and O₃ exposure with cognitive dysfunction.</p><p><strong>Methods: </strong>We analyzed gut microbiome data from 1,027 older adults using metagenome and internal transcribed spacer sequencing to profile bacterial and fungal taxa, functional pathways, and enzyme abundances. Targeted metabolomics quantified 195 circulating metabolites, such as amino acids and organic acids. Annual average ambient PM_2.5 and O₃ exposures were estimated by using satellite-based models. Cognitive outcomes, including mild cognitive impairment and cognitive decline, were assessed using the Mini-Mental State Examination and Hasegawa Dementia Scale. Statistical analyses included Microbiome Multivariable Association with Linear Models (with a false discovery rate threshold of 0.25) for microbial associations and multivariate regression for metabolites and cognitive outcomes.</p><p><strong>Results: </strong>Higher PM_2.5 and O₃ exposures were associated with disturbances in microbial composition, altered taxonomic profiles (e.g., decreased abundances of <i>Blautia obeum</i> and <i>Gordonibacter pamelaeae</i>), and disrupted functional pathways, particularly those regulating 2-oxoglutarate. These findings were partially replicated in an independent population. Higher air pollution levels were associated with increased circulating levels of 2-oxoglutarate and l-glutamine (key metabolites in neurodegenerative progression), which were further linked to higher odds of concurrent mild cognitive impairment (OR: 1.39-1.56) and an increased 2-year risk of cognitive decline (OR: 1.26-1.37). These associations were partially mediated by air pollution-related changes in microbial anaerobic energy metabolism pathways, especially involving 2-oxoglutarate metabolism and the enzyme aspartate transaminase.</p><p><strong>Conclusions: </strong>Our findings highlight the role of the gut microbiome and microbial metabolites in mediating the detrimental impact of air pollution on cognitive health in older adults, providing new insights into the underlying etiology for future hypothesis generation.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 3","pages":"335-350"},"PeriodicalIF":10.9,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13347636/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148419703","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":"Effects of Extreme Heat Exposure on Heatstroke and Liver Injury in Mice: The Role of PPARα.","authors":"Guoqing Zhang, Lisha Zhao, Jiahui Wang, Kunyi Wang, Xiuyu Ji, Renjie Hu, Tong Hou, Lu Zhang, Ran Li, Qinghua Sun, Kezhong Zhang, Cuiqing Liu","doi":"10.1021/EHP.6c00267","DOIUrl":"10.1021/EHP.6c00267","url":null,"abstract":"<p><p><b>BACKGROUND:</b> Liver injury is a frequent complication of heatstroke and constitutes a direct cause of death. However, only a few studies examined the mechanism underlying heatstroke-induced liver injury. <b>OBJECTIVE:</b> We aimed to evaluate the role of peroxisome proliferator-activated receptor α (PPARα) in heatstroke-induced liver injury and to explore the potential mechanisms. <b>METHODS:</b> Male C57BL/6N mice were subjected to a control (22 ± 1 °C) or extreme heat temperature (39.5 ± 0.5 °C) to induce a heatstroke-associated liver injury animal model. PPARα agonist, ferroptosis inhibitor, and AAV8-mediated PPARα overexpression were administered to the mice to investigate the role of PPARα and ferroptosis in the heatstroke-induced liver injury. Serum was collected for liver function evaluation. Liver tissues were applied for morphological observation, staining detection, ferroptosis examination, and mechanistic exploration. <b>RESULTS:</b> Compared with the control group, extreme heat exposure-induced temperature dysregulation, impaired liver function, and morphological damage in mice. Proteomics screened PPARα as a protein of interest, with its level being significantly decreased in response to extreme heat exposure. Both PPARα activation and overexpression attenuated extreme heat-induced heatstroke and liver injury. Hmox1 was next screened and higher Hmox1 expression was identified, accompanied by elevated markers of ferroptosis including prostaglandin-endoperoxide synthase 2 (Ptgs2), malondialdehyde (MDA), lipid peroxidation (LPO) and Fe²⁺ levels. Ferroptosis inhibition mitigated heatstroke and liver injury induced by heat exposure. In the setting of extreme heat exposure, PPARα activation suppressed Hmox1 expression and the levels of ferroptosis markers. It not only induced differences in the expression of members of iron generation, efflux and uptake process and reduced hepatic intracellular Fe²⁺ accumulation, but also stimulated expression of molecules for countering lipid peroxidation including Nrf2-SLC7A11-GPX4 axis and FSP1 signaling. <b>DISCUSSION:</b> PPARα played an essential role in extreme heat exposure-induced heatstroke and liver injury, and PPARα intervention conferred protection against it via inhibition of ferroptosis.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 1","pages":"110-123"},"PeriodicalIF":10.9,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13151047/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147962612","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":"Prenatal Air Pollution Exposure and Autism Spectrum Disorder in the ECHO Consortium.","authors":"Akhgar Ghassabian, Aisha S Dickerson, Yuyan Wang, Joseph M Braun, Deborah H Bennett, Lisa A Croen, Kaja Z LeWinn, Heather H Burris, Rima Habre, Kristen Lyall, Jean A Frazier, Hannah C Glass, Stephen R Hooper, Robert M Joseph, Catherine J Karr, Rebecca J Schmidt, Chloe Friedman, Margaret R Karagas, Annemarie Stroustrup, Jennifer K Straughen, Anne L Dunlop, Jody M Ganiban, Leslie D Leve, Rosalind J Wright, Cindy T McEvoy, Alison E Hipwell, Angelo P Giardino, Hudson P Santos, Hannah Krause, Emily Oken, Carlos A Camargo, Jiwon Oh, Christine Loftus, T Michael O'Shea, Thomas G O'Connor, Adam Szpiro, Heather E Volk","doi":"10.1021/EHP.6c00106","DOIUrl":"10.1021/EHP.6c00106","url":null,"abstract":"<p><strong>Background: </strong>The relationship between prenatal exposure to low-level air pollution and child autism spectrum disorder (ASD) is unclear.</p><p><strong>Objective: </strong>To examine associations of prenatal air pollution exposure with autism.</p><p><strong>Methods: </strong>We analyzed data from 8,035 mother-child pairs from 44 United States cohorts in the Environmental influences on Child Health Outcomes (ECHO) Cohort. Fine particulate matter (PM_2.5), nitrogen dioxide (NO₂), and 8-h-max ozone (O₃) levels were estimated at residential addresses during pregnancy. Parents rated children's autism-related traits using the Social Responsiveness Scale (SRS) (mean age 9.4 years, SD = 3.6) and reported physician-diagnosed ASD. We examined associations of the three air pollutants with SRS scores (10th, 50th, and 90th quantiles) using quantile regression and with ASD diagnosis using logistic regression. Models were run within census divisions, and coefficients were pooled in a meta-analysis.</p><p><strong>Results: </strong>Average (SD) pregnancy exposures were 9.3 μg/m³ (2.7) for PM_2.5, 21.8 ppb (8.8) for NO₂, and 40.3 ppb (5.5) for O₃, with variations across census divisions. The median SRS T-score was 46 (IQR = 41 to 52), and 444 children (5.5%) had an ASD diagnosis. Higher PM_2.5 was associated with higher SRS scores at the 10th quantile (β = 0.74, 95% CI: 0.09, 1.40) but not at the median or highest quantile. The association between PM_2.5 and ASD diagnosis was highly heterogeneous, with associations present in the South Central, Mountain, and Pacific census divisions. Heterogeneity was also high in the association between NO₂ and SRS at the median and only in the mid-Atlantic, West North Central, and South Atlantic census divisions. Higher O₃ was associated with higher SRS scores at the median (β per IQR increment = 0.83, 95% CI: 0.05, 1.61) and highest quantile (β = 2.19, 95% CI: 0.06, 4.32) in the meta-analysis. Higher O₃ also was associated with ASD.</p><p><strong>Discussion: </strong>Associations with ASD outcomes were present even at low levels of air pollutants.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 3","pages":"324-334"},"PeriodicalIF":10.9,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13347653/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148419653","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":"Deep Tubewell Use and Child Diarrhea in Rural Bangladesh: Results from a Prospective Community Surveillance Study.","authors":"Varun Goel, Mia Ziade, Brianna Chan, Md Yunus, Md Taslim Ali, Md Al Fazal Khan, Md Nurul Alam, Asg Faruque, Shahabuddin Babu, Md Masnoon Kabir, Paul L Delamater, Marc L Serre, Mark D Sobsey, Md Sirajul Islam, Michael Emch","doi":"10.1021/EHP.6c00045","DOIUrl":"10.1021/EHP.6c00045","url":null,"abstract":"<p><strong>Background: </strong>Diarrheal diseases remain a leading cause of mortality and morbidity among under-five children in South Asia. In rural Bangladesh, deep tubewells that tap into low-arsenic deep aquifers have been installed to provide microbially safe and arsenic-free drinking water at the source. However, unlike more widely used shallow tubewells, deep tubewells are sparsely distributed, and households often travel farther for drinking-water consumption from such wells. Hence, benefits from deep tubewells may be abated by higher levels of microbial contamination during water handling and storage that could increase the risk of diarrheal diseases.</p><p><strong>Objectives: </strong>We examined the association between deep tubewell use and diarrheal disease risk in under-five children and investigated the role of social and environmental factors on modifying the association.</p><p><strong>Methods: </strong>We implemented community diarrheal disease surveillance across households with under-five children using deep and shallow tubewells in Matlab, Bangladesh from March 2018 to October 2019. We used Generalized Estimating Equations (GEE) to estimate the association between deep tubewell versus shallow tubewell use and diarrheal disease prevalence.</p><p><strong>Results: </strong>Children in households using deep tubewells had diarrheal disease prevalence 0.83 times that of children in households using shallow tubewells (95% confidence interval (CI): 0.71-0.96). Protective effects of deep tubewell use on diarrhea risk were observed among children in households that drank from wells within their household compound (risk ratio (RR) = 0.70, 95% CI: 0.54 - 0.91), were in flood-prone areas (RR = 0.83, 95% CI: 0.75 - 0.92), and used unimproved latrines (RR = 0.62, 95% CI: 0.43-0.89). Deep tubewell use was more protective against diarrhea than shallow tubewell use during the dry season (RR = 0.71, 95% CI: 0.52-0.97).</p><p><strong>Conclusions: </strong>Despite concerns, using deep tubewells may not translate to higher diarrhea risk among under-five children and may reduce diarrhea further, especially in social and environmental contexts associated with higher groundwater microbial contamination.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 3","pages":"312-323"},"PeriodicalIF":10.9,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13347651/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148419620","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}