Environmental Epidemiology最新文献

{"title":"Cumulative residential greenness and childhood body mass index.","authors":"Jo Davies, Lucy J Griffiths, Theodora Pouliou, Rowena Bailey, Richard Fry, Ronan A Lyons, Gareth Stratton, Amy Mizen","doi":"10.1097/EE9.0000000000000421","DOIUrl":"10.1097/EE9.0000000000000421","url":null,"abstract":"<p><strong>Background: </strong>Childhood obesity is a complex and multifaceted public health issue. Several studies have found that children living in greener neighborhoods have a lower body mass index (BMI); however, evidence on longitudinal exposure remains limited. This study examined the relationship between Enhanced Vegetation Index (EVI), green space, and children's weight status using linked environmental and national health data.</p><p><strong>Methods: </strong>We derived annual EVI values from Landsat 8 satellite imagery (30 m resolution) within 300 m of a child's residence in Wales from 2008 to 2019. Mean EVI exposure was calculated for the 4 years preceding BMI measurement. We utilized 2017 Ordnance Survey Open Greenspace data to identify green spaces within 800 m of a child's residence. BMI obtained from the Child Measurement Programme for Wales (2012/13 to 2018/19) for children aged 4-5 years was used to define healthy versus overweight/obesity. We used logistic regression to evaluate associations between residential greenness, green spaces, and childhood weight status.</p><p><strong>Results: </strong>The final cohort consisted of 200,237 children. A one-unit increase in EVI was associated with a 20% higher likelihood of being overweight or obese (OR = 1.20, 95% CI = 1.05, 1.37). For every additional green space within 800 m, the likelihood of having an unhealthy weight increased by 0.3%.</p><p><strong>Conclusions: </strong>Our findings suggest that EVI and access to green spaces should be interpreted with care, as they may not capture how young children interact with nearby green environments. Future work investigating the impact of greenness and greenspace on child weight status should use measures tailored to more accurately represent age-specific behaviors.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"9 5","pages":"e421"},"PeriodicalIF":3.8,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466902/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145184967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Temporal changes in the high-temperature-mortality association in the Netherlands and the potential impact of the implementation of the national heat plan.","authors":"Jochem O Klompmaker, Werner I Hagens","doi":"10.1097/EE9.0000000000000424","DOIUrl":"10.1097/EE9.0000000000000424","url":null,"abstract":"<p><strong>Background: </strong>To mitigate the health impact of high temperatures, heat plans (HPs) have become widespread around the world. Our aim was to evaluate the temperature-mortality associations and estimate the temperature-related deaths in the Netherlands in the years before (2000-2009) and after (2010-2019) the first activation of the national HP.</p><p><strong>Methods: </strong>We obtained data about daily all-cause mortality (2000-2019) for the entire Dutch population, and by age, sex, neighborhood socioeconomic status, and urbanization. We linked the daily maximum temperature based on 23 monitoring stations across the Netherlands. Time-series Poisson regression models with a distributed lag nonlinear model, adjusted for long-term and seasonal trends and day of the week, were used to assess relative risks (RRs, 95% confidence intervals [CIs]) in the warm months (May-September). Temperature-attributable mortality fractions for high-temperature exposures and potential HP days were calculated.</p><p><strong>Results: </strong>We observed positive associations between daily maximum temperature and mortality in 2000-2009 and in 2010-2019. Associations of high temperatures (28.9 °C-95th percentile) were weaker in 2010-2019 (RR: 1.07, 95% CI: 1.05, 1.09) than in 2000-2009 (RR: 1.17, 95% CI: 1.15, 1.20). The attenuation in temperature-mortality risk was strongest for the elderly, women, and individuals living in low-socioeconomic status neighborhoods. The estimated mortality attributable fractions of high temperatures (≥28.9 °C) were lower in 2010-2019 (0.72, 95% CI: 0.60, 0.84) than in 2000-2009 (1.21%, 95% CI: 1.07, 1.33).</p><p><strong>Conclusion: </strong>The impact of high temperatures on mortality attenuated in the Netherlands. This might be due to the implementation of the national HP, but other factors may have played a role as well.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"9 5","pages":"e424"},"PeriodicalIF":3.8,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466905/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145184963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal environmental risk for adolescent attention, thought, and substance use problems: A mixtures approach to coexposure and psychiatric comorbidities.","authors":"Jaime Benavides, Jacob W Cohen, Lawrence G Chillrud, Gali Cohen, Mariah DeSerisy, Bruce Ramphal, Jeff Goldsmith, Marianthi-Anna Kioumourtzoglou, Amy E Margolis","doi":"10.1097/EE9.0000000000000417","DOIUrl":"10.1097/EE9.0000000000000417","url":null,"abstract":"<p><strong>Background: </strong>Prospective studies suggest that prenatal exposure to chemical neurotoxicants and maternal stress increase risk for psychiatric problems. However, most studies have focused on childhood outcomes, leaving adolescence-a critical period for the emergence or worsening of psychiatric symptoms-relatively understudied. The complexity of prenatal coexposures and adolescent psychiatric comorbidities, particularly among structurally marginalized populations with high exposure burdens, remains poorly understood.</p><p><strong>Objectives: </strong>We aimed to investigate correlated features in prenatal chemical and psychosocial exposures and in adolescent behavioral outcomes in a sample of economically disadvantaged urban youth.</p><p><strong>Methods: </strong>Principal Component Pursuit, a pattern recognition technique, coupled with factor analysis identified profiles of prenatal chemical and psychosocial exposures and of adolescent behavioral outcomes. Linear regression tested associations between exposure and behavioral profiles, accounting for potential confounders.</p><p><strong>Results: </strong>Three prenatal exposure profiles were identified: one combining exposure to air pollutants, polycyclic aromatic hydrocarbons-DNA adducts, and psychosocial stressors, and two others separating exposure to endocrine-disrupting chemicals by molecular weight. Three adolescent behavioral profiles reflected two phenotypes: one characterized by attention problems only; two others characterized by attention, thought, substance use, and self-control problems, differentiated by informant (self vs. parent). The prenatal exposure profile involving air pollution and stress was associated with the phenotype of self-reported attention, thought, substance use, and self-control problems (<i>β</i> = 0.21, 95% confidence interval = 0.02, 0.40).</p><p><strong>Discussion: </strong>Principal Component Pursuit identified consistent patterns of multidimensional prenatal exposures and adolescent behavioral symptoms. Results support prior studies linking prenatal exposures associated with economic disadvantage to complex, self-reported transdiagnostic psychiatric problems in adolescence.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"9 5","pages":"e417"},"PeriodicalIF":4.2,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12417012/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145029246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of tailpipe-related and nontailpipe-related air pollution exposure with neuroimaging outcomes.","authors":"Ryan M Andrews, Stephanie T Grady, Neelum T Aggarwal, Todd L Beck, Klodian Dhana, Denis Evans, Pauline Maillard, Sarah Rothbard, Elizabeth A Stuart, Adam A Szpiro, Saarika Virkar, Sara D Adar, Charles S DeCarli, Joel D Kaufman, Kumar B Rajan, Jennifer Weuve","doi":"10.1097/EE9.0000000000000413","DOIUrl":"10.1097/EE9.0000000000000413","url":null,"abstract":"<p><strong>Background: </strong>Long-term exposure to air pollution may be related to neural atrophy or cerebrovascular pathology. A major source of air pollution is vehicle traffic, which is modifiable. In this study, we estimated associations between four traffic-related air pollutants and five neuroimaging biomarkers.</p><p><strong>Methods: </strong>We analyzed data from a subset (N = 817) of participants in the Chicago Health and Aging Project (1993-2012) who underwent a structural magnetic resonance imaging (MRI) scan between 2002 and 2012. Using previously developed air pollution models, we predicted participant-level exposure to the tailpipe pollutants oxides of nitrogen (NO_X) and nitrogen dioxide (NO₂), plus the nontailpipe pollutants copper and zinc found in coarse particulate matter (PM_10-2.5,Cu and PM_10-2.5,Zn, respectively) over the 3 years before each participants' first MRI scan date. Using linear regression, we estimated cross-sectional, covariate-adjusted associations between each pollutant with total cerebral volume, total hippocampal volume, total lateral ventricle volume, total white matter hyperintensity volume, and cortical thickness. These models incorporated inverse probability weights to account for potential selection biases driven by differences between participants who did and did not undergo an MRI scan after being offered one.</p><p><strong>Results: </strong>Exposure to NO_X and NO₂ was associated with less cortical thickness on average (-0.06 mm, 95% confidence interval [CI] = -0.09, -0.02 per 7.8 ppb NO_X; -0.04 mm, 95% CI = -0.07, -0.01 per 2.7 ppb NO₂). All other associations were consistent with no effect.</p><p><strong>Conclusion: </strong>These results are not indicative of large adverse associations between traffic-related air pollution exposures and indicators of neural atrophy or cerebrovascular pathology.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"9 5","pages":"e413"},"PeriodicalIF":3.8,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12384963/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144947204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The occurrence of appendicitis varies according to latitudes and seasons: A French national retrospective study.","authors":"Jean-François Hamel, Chloé Saint-Dizier, Antoine Lamer, Dune Allard, Tino Bienvenu, Mathieu Levaillant, Aurélien Venara","doi":"10.1097/EE9.0000000000000412","DOIUrl":"10.1097/EE9.0000000000000412","url":null,"abstract":"<p><strong>Background: </strong>Recent reports indicate that the occurrence of appendicitis follows a seasonal pattern and that there is an association between increased incidence and warmer weather. It is noteworthy that a reduction in the incidence of appendicitis has been observed in the Northern Hemisphere. The objective of this study is to present the epidemiological profile of appendicitis at the national level in France.</p><p><strong>Methods: </strong>This retrospective observational study, based on data from the French National Discharge Database, encompasses all hospitalizations for appendicitis diagnosis between 2013 and 2022. The progression of appendicitis over time was assessed through time-series models. The incidence of appendicitis was also compared depending on year, gender, age, and latitude.</p><p><strong>Results: </strong>It is noteworthy that the incidence of appendectomy in France exhibited a significant decrease between 2013 and 2022, with an average reduction of 2.1% annually. There was a significant decrease in the number of appendectomies performed on patients ≤20, while there was an increase in those >60. Furthermore, there was a seasonal pattern in the incidence of appendicitis, with a peak during the summer months. The seasonality remained consistent over time. Furthermore, there was a south-north gradient, with a higher number of appendectomies performed in the south.</p><p><strong>Conclusion: </strong>Seasonality (summer vs. winter) and latitude (south vs. north) could be considered as a proxy for temperature. However, temperature alone cannot explain the observed variations in appendicitis occurrence, since the latter decreases over time, in parallel with global warming. It is likely that other environmental and ecological parameters may be responsible for these variations.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"9 4","pages":"e412"},"PeriodicalIF":3.8,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12309809/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144752711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations of prenatal per- and polyfluoroalkyl substances with whole blood folate levels in pregnant women in the Health Outcomes and Measures of the Environment (HOME) Study.","authors":"Harin Lee, Amber M Hall, Antonia M Calafat, Aimin Chen, Zia Fazili, Bruce P Lanphear, Christine M Pfeiffer, Kimberly Yolton, Joseph M Braun","doi":"10.1097/EE9.0000000000000406","DOIUrl":"10.1097/EE9.0000000000000406","url":null,"abstract":"<p><strong>Background: </strong>Folate plays a critical role during pregnancy, preventing neural tube defects and possibly adverse neurodevelopment. Per- and polyfluoroalkyl substances (PFAS) are synthetic chemicals that may decrease folate levels. Although some studies have found associations between PFAS and folate, we are unaware of studies conducted in pregnant women. To address this knowledge gap, we evaluated associations between PFAS and whole blood folate (WBF) in pregnant women.</p><p><strong>Methods: </strong>We used data from 288 pregnant women in the Health Outcomes and Measures of the Environment (HOME) Study, a pregnancy and birth cohort in the Cincinnati Ohio area. We measured eight serum PFAS and WBF concentrations at 16 weeks' gestation. We used linear regression to estimate the effect of each PFAS on WBF, and quantile-based g-computation and Bayesian kernel machine regression (BKMR) to investigate the joint effect of PFAS on WBF, adjusting for parity, prenatal vitamin intake, maternal race/ethnicity, household income, maternal age, and second trimester smoking status in all models. In addition, we investigated interactions between PFAS using BKMR.</p><p><strong>Results: </strong>We did not observe inverse associations of individual PFAS or their mixture with WBF, nor interactions between PFAS in the BKMR model in pregnant women.</p><p><strong>Conclusion: </strong>Future studies could consider WBF measures in late pregnancy to evaluate other periods of susceptibility. Furthermore, as people are exposed to multiple PFAS, future studies should continue to consider joint PFAS exposure.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"9 4","pages":"e406"},"PeriodicalIF":3.8,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12212838/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Examining the association between gestational phenol exposure and infant non-nutritive suck in two Environmental influences on Child Health Outcomes cohorts.","authors":"Megan L Woodbury, Andréa Aguiar, Sarah Dee Geiger, Max T Aung, Shukhan Ng, Morgan Hines, Alaina Martens, Deborah J Watkins, Gredia Huerta-Montañez, José F Cordero, John D Meeker, Akram N Alshawabkeh, Susan L Schantz, Emily Zimmerman","doi":"10.1097/EE9.0000000000000399","DOIUrl":"10.1097/EE9.0000000000000399","url":null,"abstract":"<p><strong>Background: </strong>Non-nutritive suck (NNS) is a measure of neurofunction sensitive to environmental exposures in utero. This study aimed to evaluate the relationship between gestational phenol exposure and NNS patterning.</p><p><strong>Methods: </strong>Mother-infant pairs from two diverse prospective cohorts were enrolled in the Environmental influences on Child Health Outcomes Program. Phenols were measured in prenatal maternal urine samples and adjusted for specific gravity. NNS was sampled in 1-8-week-old infants using a custom pacifier for ~5 minutes. Associations of 11 phenols and triclocarban with 5 NNS outcomes were assessed individually and as a mixture using generalized linear models adjusted for cohort, child sex and assessment age, and maternal age and education.</p><p><strong>Results: </strong>Altogether, 215 mother-infant pairs were included. Bisphenol-F was related to a lower NNS frequency. Triclosan was associated with a higher NNS frequency. Propylparaben, 2,4-dichlorophenol, and 2,5-dichlorophenol were associated with lower NNS amplitude. Benzophenone-3, 2,4-dichlorophenol, and 2,5-dichlorophenol were related to more NNS bursts/minute. Propylparaben was associated with more NNS cycles/bursts. Seven phenols were included in mixture analyses: 2,4-dichlorophenol, 2,5-dichlorophenol, benzophenone-3, bisphenol-A, bisphenol-S, methylparaben, and propylparaben. Both Bayesian kernel machine regression and quantile g-computation showed that higher concentrations of the mixture were associated with lower amplitude but more bursts/minute and cycles/burst. Propylparaben was important in the overall mixture effect on amplitude, whereas benzophenone-3 was important in the relationship with bursts/minute.</p><p><strong>Conclusions: </strong>Gestational phenol exposure is linked to altered NNS patterning in neonates. Future work should further investigate phenol mixture effects, potential mechanisms, and the association of altered NNS with neurodevelopment.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"9 4","pages":"e399"},"PeriodicalIF":3.8,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12169973/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144309747","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessing bias in measuring power outage exposure with simulations.","authors":"Heather McBrien, Daniel Mork, Marianthi-Anna Kioumourtzoglou, Joan A Casey","doi":"10.1097/EE9.0000000000000403","DOIUrl":"10.1097/EE9.0000000000000403","url":null,"abstract":"<p><strong>Background: </strong>New national power outage exposure data have become available since 2020, which can support epidemiologic studies of power outage and health outcomes, but exposure assessment challenges remain. Two sources of bias could affect results: available datasets are missing large percentages of observations, and the health-relevant duration of power outages remains unknown. Here, we aimed to determine if existing datasets can produce usable effect estimates in epidemiologic studies despite missing data, and quantify bias introduced by incorrect assumptions about the health-relevant duration of power outages.</p><p><strong>Methods: </strong>Based on existing data from PowerOutage.us, we conducted simulations representing a county-level study. We simulated and then estimated the effect of daily power outage exposure on hospitalization rates. We measured the magnitude and direction of bias introduced in the presence of incorrect assumptions about the health-relevant power outage duration and when increasing amounts of exposure data were missing.</p><p><strong>Results: </strong>When the health-relevant power outage duration was underestimated, results were substantially biased towards the null (mean bias: -64.7%, SD: 34.9). Overestimation of the health-relevant power outage duration resulted in smaller bias (mean bias: -6.7%, SD: 30.6). When 80% or more of county-level person-time of power outage data were missing in 80% of study counties, results were severely biased towards the null (mean bias: -54.4%, SD: 39.8).</p><p><strong>Conclusions: </strong>Our results show that while some bias is likely, sensitivity analyses and careful choices of health-relevant duration can help researchers leverage available power outage data to produce low bias effect estimates in epidemiologic studies of power outages and health outcomes.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"9 4","pages":"e403"},"PeriodicalIF":3.8,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12160736/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144301385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between gestational environmental chemical mixtures and folate exposures with autistic behaviors in a Canadian birth cohort.","authors":"Joshua D Alampi, Bruce P Lanphear, Amanda J MacFarlane, Joseph M Braun, Youssef Oulhote, Jillian Ashley-Martin, Tye E Arbuckle, Aimin Chen, Gina Muckle, Lawrence C McCandless","doi":"10.1097/EE9.0000000000000402","DOIUrl":"10.1097/EE9.0000000000000402","url":null,"abstract":"<p><strong>Background: </strong>Prenatal exposure to environmental chemicals may be associated with autism or autistic-like behaviors. Previous studies suggest that these associations are stronger when folic acid (FA) supplementation is lower.</p><p><strong>Methods: </strong>We used data from the Maternal-Infant Research on Environmental Chemicals study, a Canadian pregnancy and birth cohort (2008-2011). We considered five separate chemical mixtures (measured during the first trimester of pregnancy): metals, organochlorine pesticides, per- and polyfluoroalkyl substances (PFAS), polychlorinated biphenyls (PCBs), and persistent organic pollutants (POPs; including organochlorine pesticides, PFAS, PCBs, and one polybrominated diphenyl ether congener). Autistic-like behaviors were documented in 601 3-4-year-old children with the social responsiveness scale-2 (SRS-2), where higher T-scores denote more behaviors. We used quantile g-computation to estimate the mixture-SRS-2 associations and assessed whether gestational FA supplementation and plasma total folate concentrations modified these associations.</p><p><strong>Results: </strong>The PFAS mixture was associated with decreased SRS-2 T-scores (Ψ = -0.5; 95% confidence interval [CI] = -1.1, 0.1). The metal-SRS-2 associations were stronger in the positive direction among participants with high (>1,000 μg/d) FA supplementation (Ψ = 2.4; 95% CI = 0.8, 3.9) versus those with adequate (400-1,000 μg/d) supplementation (Ψ = -0.2; 95% CI = -1.1, 0.7) (p-interaction = 0.003). Plasma total folate concentrations similarly modified these associations (p-interaction = 0.01). The associations between the PFAS, PCB, and POP mixtures and SRS-2 T-scores were stronger in the positive direction among participants with low (<400 μg/d) versus adequate FA supplementation. This was not observed when assessing modification by plasma total folate concentrations.</p><p><strong>Conclusion: </strong>Our results suggest that the metal mixture is more strongly associated with autistic-like behaviors among participants with higher folate exposure, and the PFAS, PCB, and POP mixtures are more strongly associated with autistic-like behaviors among participants with low FA supplementation.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"9 4","pages":"e402"},"PeriodicalIF":3.8,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12160746/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144301386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disparities in the association of ambient air pollution with childhood asthma incidence in the ECHO consortium: A US-wide multi-cohort study.","authors":"Veronica A Wang, Rima Habre, Patrick H Ryan, Brent A Coull, Soma Datta, Heike Luttmann-Gibson, Jeff Blossom, Allan C Just, Joel Schwartz, Jeff D Yanosky, Izzuddin M Aris, Aruna Chandran, Amii M Kress, Carrie Breton, Shohreh F Farzan, Carlos A Camargo, Donghai Liang, Assiamira Ferrera, Alicia K Peterson, Jean M Kerver, Catherine J Karr, Leslie D Leve, Dana Dabelea, Margaret R Karagas, Deborah H Bennett, Flory L Nkoy, Judy Aschner, T Michael O'Shea, Nathan Lothrop, Cindy T McEvoy, Emily A Knapp, Holly B Schuh, Rachel L Miller, Diane R Gold, Antonella Zanobetti","doi":"10.1097/EE9.0000000000000398","DOIUrl":"10.1097/EE9.0000000000000398","url":null,"abstract":"<p><strong>Background: </strong>Characterization of US sociodemographic disparities in air pollution respiratory effects has often been limited by lack of participant diversity, geography, exposure characterization, and small sample size.</p><p><strong>Methods: </strong>We included 34 sites comprising 23,234 children (born 1981-2021) from the Environmental influences on Child Health Outcomes (ECHO) Program with data on asthma diagnosis until age 10 (182,008 person-years). Predicted annual exposure to fine particulate matter (1988-2021), nitrogen dioxide (2000-2016), and ground ozone (2000-2016) were assigned based on residential histories. For each pollutant, we fitted time-varying Cox models adjusted for time trend, site, and several area- and individual-level sociodemographic features that were separately considered as modifiers via an interaction with exposure.</p><p><strong>Results: </strong>The hazard ratio of incident asthma by age 10 years was 1.19 (95% CI = 1.10, 1.28), 1.19 (95% CI = 1.05, 1.34), and 1.11 (95% CI = 1.01, 1.22) of an interquartile range increase in prior-year exposure to fine particulate matter (6.17 µg/m³), nitrogen dioxide (15.37 ppb), and ozone (6.87 ppb), respectively. For both fine particulate and nitrogen dioxide, children from areas with a higher proportion of Black residents or with a higher population density had greater pollution-associated risks of incident asthma. For ozone, asthma risks were enhanced in less dense areas.</p><p><strong>Conclusions: </strong>US efforts to mitigate childhood asthma risk by reducing air pollution would benefit from addressing root structural causes of vulnerability and susceptibility, including spatial patterning in air pollution sources and exposures as well as social and economic disadvantage.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"9 4","pages":"e398"},"PeriodicalIF":4.2,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12160752/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144301387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}