Journal of Exposure Science and Environmental Epidemiology最新文献

{"title":"Volatile hydrocarbon exposures and immune-related illnesses among Deepwater Horizon oil spill workers.","authors":"Opal P Patel, Kaitlyn G Lawrence, Christine G Parks, Patricia A Stewart, Mark R Stenzel, Caroline P Groth, Gurumurthy Ramachandran, Sudipto Banerjee, Tran B Huynh, Braxton Jackson, Dale P Sandler, Lawrence S Engel","doi":"10.1038/s41370-024-00738-y","DOIUrl":"https://doi.org/10.1038/s41370-024-00738-y","url":null,"abstract":"<p><strong>Background: </strong>Despite evidence from experimental studies linking some petroleum hydrocarbons to markers of immune suppression, limited epidemiologic research exists on this topic.</p><p><strong>Objective: </strong>The aim of this cross-sectional study was to examine associations of oil spill related chemicals (benzene, toluene, ethylbenzene, xylene, and n-hexane (BTEX-H)) and total hydrocarbons (THC) with immune-related illnesses as indicators of potential immune suppression.</p><p><strong>Methods: </strong>Subjects comprised 8601 Deepwater Horizon (DWH) oil spill clean-up and response workers who participated in a home visit (1-3 years after the DWH spill) in the Gulf Long-term Follow-up (GuLF) Study. Cumulative exposures to THC and individual BTEX-H constituents during the oil spill clean-up were estimated using a job-exposure matrix linking air measurement data to detailed participant work histories. Study outcomes included post-spill occurrence and/or frequency of illnesses ascertained at the home visit, including colds, flu, cold sores, pneumonia, and shingles. Frequent cold and frequent flu were defined as ≥4 colds and ≥2 episodes of flu since the spill, respectively. We examined an aggregate outcome of frequent colds, any flu, cold sores, or pneumonia since the spill. In single pollutant models, we used multivariable log-binomial regression to estimate prevalence ratios (PR) and 95% confidence intervals (CI) for associations between quartiles of THC and BTEX-H exposures with each outcome. We used quantile g-computation to estimate the joint effect of the BTEX-H mixture.</p><p><strong>Results: </strong>We observed positive associations of increasing quartiles of THC and BTEX-H with all outcomes except shingles, with evidence of an exposure-response for most outcomes. Strongest associations were observed for frequent flu (range of PR: 1.41-1.67). The BTEX-H mixture was associated with small to modest elevations in PRs for most outcomes.</p><p><strong>Impact statement: </strong>This study is the first to our knowledge to demonstrate an association between oil spill BTEX-H exposures and multiple immune-related illnesses as measures of potential immune suppression. Increasing oil spill-related volatile hydrocarbon exposures may increase the risk of multiple immune-related illnesses, especially frequent cold and frequent flu. Future research on this topic using more robust measures of immune function would advance existing evidence on this relationship.</p>","PeriodicalId":15684,"journal":{"name":"Journal of Exposure Science and Environmental Epidemiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142894779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurodevelopmental costs of noise pollution–is history rhyming again?","authors":"Peter M. Bingham","doi":"10.1038/s41370-024-00725-3","DOIUrl":"10.1038/s41370-024-00725-3","url":null,"abstract":"","PeriodicalId":15684,"journal":{"name":"Journal of Exposure Science and Environmental Epidemiology","volume":"35 1","pages":"34-36"},"PeriodicalIF":4.1,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142881842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal exposure to endocrine disrupting chemicals and the association with behavioural difficulties in 7-year-old children in the SELMA study.","authors":"Marlene Stratmann, Fatih Özel, Maria Marinopoulou, Christian Lindh, Hannu Kiviranta, Chris Gennings, Carl-Gustaf Bornehag","doi":"10.1038/s41370-024-00739-x","DOIUrl":"https://doi.org/10.1038/s41370-024-00739-x","url":null,"abstract":"<p><strong>Background: </strong>Endocrine disrupting chemicals (EDCs) can cross the placenta and thereby expose the fetus, which may lead to developmental consequences. It is still unclear which chemicals are of concern regarding neurodevelopment and specifically behaviour, when being exposed to a mixture.</p><p><strong>Objective: </strong>The objective is to determine associations between prenatal exposure to EDCs and behavioural difficulties. Furthermore, we investigated sex-specific associations and determined chemicals of concern in significant regressions.</p><p><strong>Methods: </strong>Associations between prenatal exposure to EDCs (both as single compounds and their mixtures) and behavioural outcomes using the Strengths and Difficulties Questionnaire (SDQ) were estimated in 607 mother-child pairs in the Swedish Environmental Longitudinal, Mother and Child, Asthma and Allergy (SELMA) study. Levels for chemical compounds were measured in either urine or serum (median of 10 weeks of gestation). Associations were estimated for the total SDQ score (quasipoisson regression) and a 90th percentile cut-off (logistic regression). Exposure for EDC mixtures (phenols, phthalates, PFAS and persistent chlorinated) was studied using weighted quantile sum (WQS) regression with deciles and with and without repeated holdout validation techniques. The models were adjusted for selected covariates.</p><p><strong>Results: </strong>The odds for behavioural difficulties increased in girls with higher chemical exposures (OR 1.77, 95% CI 1.67, 1.87) using the full sample and borderline for the validation set (OR 1.31, 95% CI 0.93, 1.85) with 94/100 positive betas in the 100 repeated holdout validations. Chemicals of concern for girls are mostly short-lived chemicals and more specifically plasticizers. No pattern of significant associations was detected for boys.</p><p><strong>Significance: </strong>There is an indication of increased behavioural difficulties for girls in the SELMA population with higher exposure to mixtures of EDCs. Using the repeated holdout validation techniques, the inference is more stable, reproducible and generalisable. Prenatal exposure to mixtures of environmental chemicals should be considered when assessing the safety of chemicals.</p><p><strong>Impact: </strong>Growing evidence points towards a \"mixture effect\" where different environmental chemicals might act jointly where individual compounds may be below a level of concern, but the combination may have an effect on human health. We are constantly exposed to a complicated mixture pattern that is individual for every person as this mixture depends on personal choices of lifestyle, diet and housing to name a few. Our study suggests that prenatal exposure to EDCs might adversely affect the behaviour of children and especially girls. Hence, risk assessment needs to improve and sex-specific mechanisms should be included in assessments.</p>","PeriodicalId":15684,"journal":{"name":"Journal of Exposure Science and Environmental Epidemiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Noise causes cardiovascular disease: it’s time to act","authors":"Thomas Münzel,&nbsp;Andreas Daiber,&nbsp;Nicole Engelmann,&nbsp;Martin Röösli,&nbsp;Marin Kuntic,&nbsp;Jamie L. Banks","doi":"10.1038/s41370-024-00732-4","DOIUrl":"10.1038/s41370-024-00732-4","url":null,"abstract":"Chronic transportation noise is an environmental stressor affecting a substantial portion of the population. The World Health Organization (WHO) and various studies have established associations between transportation noise and cardiovascular disease (CVD), such as myocardial infarction, stroke, heart failure, and arrhythmia. The WHO Environmental Noise Guidelines and recent reviews confirm a heightened risk of cardiovascular incidents with increasing transportation noise levels. We present a narrative review of the evidence from epidemiologic studies and translation studies on the adverse cardiovascular effects of transportation noise. We describe the results of a recent Umbrella+ review that combines the evidence used in the 2018 WHO Environmental Noise Guidelines with more recent (post-2015) high-quality systematic reviews of original studies. High-quality systematic reviews were included based on the quality of literature search, risk of bias assessment, and meta-analysis methodology using AMSTAR 2. Epidemiologic studies show that exposure to high levels of road traffic noise for several years lead to numerous adverse health outcomes, including premature deaths, ischemic heart disease (IHD), chronic sleep disturbances, and increased annoyance. Mechanistically, noise exposure triggers oxidative stress, inflammation, endothelial dysfunction, and circadian rhythm disruptions. These processes involve the activation of NADPH oxidase, mitochondrial dysfunction, and nitric oxide synthase uncoupling, leading to vascular and cardiac damage. Studies indicate that chronic noise exposure does not result in habituation, and susceptible individuals, such as those with pre-existing CVD, are particularly vulnerable.","PeriodicalId":15684,"journal":{"name":"Journal of Exposure Science and Environmental Epidemiology","volume":"35 1","pages":"24-33"},"PeriodicalIF":4.1,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41370-024-00732-4.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142807028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chemical exposomics in biobanked plasma samples and associations with breast cancer risk factors.","authors":"Jessica Edlund, Kalliroi Sdougkou, Stefano Papazian, Wendy Yi-Ying Wu, Jonathan W Martin, Sophia Harlid","doi":"10.1038/s41370-024-00736-0","DOIUrl":"https://doi.org/10.1038/s41370-024-00736-0","url":null,"abstract":"<p><strong>Background: </strong>The chemical exposome includes exposure to numerous environmental and endogenous molecules, many of which have been linked to reproductive outcomes due to their endocrine-disrupting properties. As several breast cancer risk factors, including age and parity, are related to reproduction, it is imperative to investigate the interplay between such factors and the chemical exposome prior to conducting large scale exposome-based breast cancer studies.</p><p><strong>Objective: </strong>This pilot study aimed to provide an overview of the chemical exposome in plasma samples from healthy women and identify associations between environmental exposures and three risk factors for breast cancer: age, parity, and age at menarche.</p><p><strong>Material and methods: </strong>Plasma samples (n = 161), were selected based on reproductive history from 100 women participating in the Northern Sweden Health and Disease Study, between 1987 and 2006. Samples were analyzed by liquid chromatography high-resolution mass spectrometry (LC-HRMS) for 77 priority target analytes including contaminants and hormones, with simultaneous untargeted profiling of the chemical exposome and metabolome. Linear mixed effects models were applied to test associations between risk factors and chemical levels.</p><p><strong>Results: </strong>Fifty-five target analytes were detected in at least one individual and over 94,000 untargeted features were detected across all samples. Among untargeted features, 430 could be annotated and were broadly classified as environmental (246), endogenous (167) or ambiguous (17). Applying mixed effect models to features detected in at least 70% of the samples (16,778), we found seven targeted analytes (including caffeine and various per- and poly-fluoroalkyl substances) and 38 untargeted features, positively associated with age. The directionality of these associations reversed for parity, decreasing with increasing births. Seven separate targeted analytes were associated with age at menarche.</p><p><strong>Significance: </strong>This study demonstrates how a comprehensive chemical exposome approach can be used to inform future research prioritization regarding associations between known and unknown substances, reproduction, and breast cancer risk.</p><p><strong>Impact statement: </strong>This study illustrates how chemical exposomics of long-term stored blood samples offers valuable insights to discover chemical exposures and their potential links to disease in humans, particularly those related to reproduction and breast cancer risk factors.</p>","PeriodicalId":15684,"journal":{"name":"Journal of Exposure Science and Environmental Epidemiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of chelation on bone Pb stores in Pb poisoned children.","authors":"Aaron J Specht, Yanfen Lin, Jian Xu, Aisha S Dickerson, Chonghuai Yan, Howard Hu, Marc G Weisskopf, Linda H Nie","doi":"10.1038/s41370-024-00735-1","DOIUrl":"https://doi.org/10.1038/s41370-024-00735-1","url":null,"abstract":"<p><strong>Background: </strong>Lead exposure remains a key problem for children during development. One treatment for lead poisoning is chelation - a topic that remains controversial with varied results. Bone lead serves as a marker of total body burden of lead and encompasses between 60-90% of lead storage in children.</p><p><strong>Objective: </strong>In this study, we aimed to identify the change in bone lead as a result of chelation therapy in a group of lead poisoned children (blood lead >25 µg/dL).</p><p><strong>Methods: </strong>Upon diagnosis with lead poisoning at Xinhua Hospital in Shanghai, China, children were recruited to our study, had their bone lead levels measured, and underwent one-week of intravenous, in-patient ethylenediaminetetraacetic acid chelation treatment. Up to three clinical visits with the same treatment protocol and bone lead measurements were completed over the two-year study. We measured biomarkers of lead exposure for children exposed via various potential sources, including home contaminants, local industrial emissions, traditional medicines, or lead cookware.</p><p><strong>Results: </strong>We observed significant differences with bone lead after chelation therapy (p < 0.0001), even after calculating a conservative model for theoretical decay from known bone turnover (p = 0.01). The difference identified between our observed change in bone lead and literature established bone lead change significantly increased with more chelation treatments. A significant reduction in bone lead was observed following chelation treatment of children with lead poisoning - a difference that increased more with more chelation.</p><p><strong>Significance: </strong>Study results indicate that chelation treatment is effective in reducing bone lead stores in children with initial blood lead levels greater than 25 µg/dL.</p><p><strong>Impact statement: </strong>Lead exposure in children is a consistent problem - drastically impacting health across the life span. After exposure, lead stores in the bone of children serving as a potential endogenous source of exposure for years to decades. Our study demonstrated that chelation therapy, while reducing blood lead levels, additionally reduced bone lead levels. A reduction in bone lead would effectively reduce the potential for endogenous release of lead and restrict the damage done by lead exposure.</p>","PeriodicalId":15684,"journal":{"name":"Journal of Exposure Science and Environmental Epidemiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142769372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Additive effect of high transportation noise exposure and socioeconomic deprivation on stress-associated neural activity, atherosclerotic inflammation, and cardiovascular disease events","authors":"Shady Abohashem,&nbsp;Wesam Aldosoky,&nbsp;Omar Hahad,&nbsp;Giovanni Civieri,&nbsp;Alula Assefa,&nbsp;Hui Chong Lau,&nbsp;Krystel Abi-Karam,&nbsp;Maria Khalil,&nbsp;Lainie Louis-Jame,&nbsp;Sadeer Al-Kindi,&nbsp;Ahmed Tawakol,&nbsp;Michael T. Osborne","doi":"10.1038/s41370-024-00734-2","DOIUrl":"10.1038/s41370-024-00734-2","url":null,"abstract":"Noise exposure and lower socioeconomic status (SES) are both independently linked to increased cardiovascular disease (CVD) risk. Although these factors frequently coexist, their combined impact and the underlying pathophysiological mechanisms remain poorly understood. This study aimed to evaluate the joint effects of high transportation noise exposure and lower SES on major adverse cardiovascular events (MACE) and the role of the neural-arterial axis in mediating this relationship. We retrospectively analyzed data from 507 individuals who underwent clinical 18F-FDG-PET/CT imaging at a single center. SES was evaluated using local median income (as a primary measure) and area deprivation index (ADI, as a secondary measure). Participants were classified into three groups based on transportation noise exposure and income/ADI: low noise/higher SES, high noise or lower SES, and high noise/lower SES. Cox models assessed MACE risks. Linear regression models evaluated associations with stress-related neural activity (SNA) and arterial inflammation (ArtI). The combination of high noise exposure and low income (vs. neither exposure) associated with increased MACE risk (HR [95% CI]: 5.597 [2.201–14.233], p &lt; 0.001). SNA (standardized β [95% CI]: 0.389 [0.192–0.586], p &lt; 0.001) and ArtI (0.151 [0.005–0.298], p = 0.043) were greater in this group. Mediation analysis showed that the neural-arterial axis contributes to increased exposure-related MACE risk and accounts for 8% of the overall effect. Similar results were found with ADI. Our study uniquely demonstrates how combined high transportation noise and lower socioeconomic status additively increases cardiovascular disease risk through specific biological pathways, particularly via effects on stress-associated neural activity and arterial inflammation. As such, the research offers novel insights into the interplay between environmental and socioeconomic factors in cardiovascular health. This underscores an urgent need for integrated public health strategies that address both noise pollution and socioeconomic disparities and provides a foundation for targeted interventions aimed at reducing the burden of cardiovascular disease in vulnerable populations.","PeriodicalId":15684,"journal":{"name":"Journal of Exposure Science and Environmental Epidemiology","volume":"35 1","pages":"62-69"},"PeriodicalIF":4.1,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142693032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Air pollution mixture exposure during pregnancy and postpartum psychological functioning: racial/ethnic- and fetal sex-specific associations.","authors":"Yueh-Hsiu Mathilda Chiu, Brent A Coull, Ander Wilson, Hsiao-Hsien Leon Hsu, Naim Xhani, Farida Nentin, Barbara C Deli, Joel Schwartz, Elena Colicino, Robert O Wright, Rosalind J Wright","doi":"10.1038/s41370-024-00726-2","DOIUrl":"10.1038/s41370-024-00726-2","url":null,"abstract":"<p><strong>Background: </strong>Prenatal air pollution (AP) exposure has been linked to postpartum psychological functioning, impacting health outcomes in both women and children. Extant studies primarily focused on individual pollutants.</p><p><strong>Objective: </strong>To assess the association between prenatal exposure to a mixture of seven AP components and postpartum psychological functioning using daily exposure data and data-driven statistical methods.</p><p><strong>Methods: </strong>Analyses included 981 women recruited at 24.0 ± 9.9 weeks gestation and followed longitudinally. We estimated prenatal daily exposure levels for constituents of fine particles [elemental carbon (EC), organic carbon (OC), nitrate (NO₃^-), sulfate (SO₄^2-), ammonium (NH₄⁺)], nitrogen dioxide (NO₂), and ozone (O₃) using validated global 3-D chemical-transport models and satellite-based hybrid models based on residential addresses. Edinburgh Postnatal Depression Scale (EPDS) was administered to participants to derive a total EPDS score and the subconstruct scores for anhedonia and depressive symptoms. A distributed lag model (DLM) was employed within Bayesian Kernel Machine Regression (BKMR) to develop time-weighted exposure profile for each pollutant. These exposures were then input into a Weighted Quantile Sum (WQS) regression to estimate an overall mixture effect, adjusted for maternal age, education, race/ethnicity, season of delivery, and delivery year. Effect modification by race/ethnicity and fetal sex was also examined.</p><p><strong>Results: </strong>Women were primarily Hispanic (51%) and Black (32%) reporting ≤12 years of education (58%). Prenatal exposure to an AP mixture was significantly associated with increased anhedonia subscale z-scores, particularly in Hispanics (β = 0.07, 95%CI = 0.004-0.13, per unit increase in WQS index). It was also borderline associated with increased total EPDS (β = 0.11, 95%CI = 0.00-0.22) and depressive symptom subscale (β = 0.09, 95%CI = -0.02 to 0.19) z-scores, particularly among Hispanic women who gave birth to a male infant. Sulfate (SO₄^2-), O₃ and OC were major contributors to these associations.</p><p><strong>Impact: </strong>This study utilizes an advanced data-driven approach to examine the temporally- and mixture-weighted effects of prenatal air pollution exposure on postpartum psychological functioning. We found that exposure to a prenatal air pollution mixture predicted poorer postpartum psychological functioning, particularly anhedonia symptoms in Hispanic women. Findings underscore the importance of considering both exposure mixtures as well as potential modifying factors to better help identify particular pollutants that drive effects and susceptible populations, which can inform more effective intervention strategies.</p>","PeriodicalId":15684,"journal":{"name":"Journal of Exposure Science and Environmental Epidemiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12092737/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681715","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal ozone exposure and risk of intellectual disability.","authors":"Sara E Grineski, Roger Renteria, Amanda Bakian, Timothy W Collins, James VanDerslice, Camden J Alexander, Deborah Bilder","doi":"10.1038/s41370-024-00729-z","DOIUrl":"10.1038/s41370-024-00729-z","url":null,"abstract":"<p><strong>Background: </strong>Knowledge of relationships between tropospheric ozone and mental and developmental health outcomes is currently inconclusive, with the largest knowledge gaps for children. This gap is important to address as evidence suggests that climate change will worsen ozone pollution.</p><p><strong>Objective: </strong>We examine the association of average ozone exposure during the preconception period, and first, second and third trimesters of pregnancy on the odds of intellectual disability (ID) in Utah children.</p><p><strong>Methods: </strong>For the period of 2002-2020, we assembled daily, tract-level ozone concentration data, data on ID case status, and data on cases' full siblings and population controls. We analyzed the data using generalized estimating equations.</p><p><strong>Results: </strong>Ozone was positively associated with the odds of ID in cases vs. their siblings (in the preconception, first, second and third trimester exposure windows, all p < 0.05, n = 1042) and vs. population controls (only in the second trimester exposure window, p < 0.05, n = 5179). The strength of the association was largest during the second trimester in both analyses. A second trimester average ozone level increase of 10 ppb was associated with a 55.3% increase in the odds of ID relative to full siblings (95% confidence interval [CI]: 1.171-2.058) and a 22.8% increase in the odds of ID relative to population controls (CI: 1.054-1.431). Findings were robust to different subsets of sibling controls as well as several sensitivity analyses.</p><p><strong>Significance: </strong>Results document that ozone has a measurable relationship with children's cognitive development in Utah.</p><p><strong>Impact statement: </strong>Evidence suggests that climate change will worsen ozone pollution. The potential amplifying effect of climate change on ozone is more certain than it is for fine particulate matter. This means that ozone and health research will remain relevant into the future. Currently, several systematic reviews and meta-analyses have concluded that knowledge about ozone and cognitive health is insufficient, especially for children. Using two different study designs, we find that prenatal ozone exposure is associated with risk of intellectual disability in children.</p>","PeriodicalId":15684,"journal":{"name":"Journal of Exposure Science and Environmental Epidemiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12085709/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142667965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Environmental public health research at the U.S. Environmental Protection Agency: A blueprint for exposure science in a connected world.","authors":"Lindsay W Stanek, Wayne E Cascio, Timothy M Barzyk, Michael S Breen, Nicole M DeLuca, Shannon M Griffin, Lisa Jo Melnyk, Jeffrey M Minucci, Kent W Thomas, Nicolle S Tulve, Christopher P Weaver, Elaine A Cohen Hubal","doi":"10.1038/s41370-024-00720-8","DOIUrl":"https://doi.org/10.1038/s41370-024-00720-8","url":null,"abstract":"<p><p>Exposure science plays an essential role in the U.S. Environmental Protection Agency's (U.S. EPA) mission to protect human health and the environment. The U.S. EPA's Center for Public Health and Environmental Assessment (CPHEA) within the Office of Research and Development (ORD) provides the exposure science needed to characterize the multifaceted relationships between people and their surroundings in support of national, regional, local and individual-level actions. Furthermore, exposure science research must position its enterprise to tackle the most pressing public health challenges in an ever-changing environment. These challenges include understanding and confronting complex human disease etiologies, disparities in the social environment, and system-level changes in the physical environment. Solutions will sustainably balance and optimize the health of people, animals, and ecosystems. Our objectives for this paper are to review the role of CPHEA exposure science research in various recent decision-making contexts, to present current challenges facing U.S. EPA and the larger exposure science field, and to provide illustrative case examples where CPHEA exposure science is demonstrating the latest methodologies at the intersection of these two motivations. This blueprint provides a foundation for applying exposomic tools and approaches to holistically understand real-world exposures so optimal environmental public health protective actions can be realized within the broader context of a One Health framework. IMPACT STATEMENT: The U.S. EPA's Center for Public Health and Environmental Assessment exposure research priorities reside at the intersection of environmental decision contexts and broad public health challenges. The blueprint provides a foundation for advancing the tools and approaches to holistically understand real-world exposures so optimal environmental protection actions can be realized. A One Health lens can help shape exposure research for maximum impact to support solutions that are transdisciplinary and must engage multiple sectors.</p>","PeriodicalId":15684,"journal":{"name":"Journal of Exposure Science and Environmental Epidemiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142643930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}