Environmental Health Perspectives最新文献

{"title":"Assessing the potential impacts of California Senate Bill 27 (SB27) on the antimicrobial susceptibility of <i>Escherichia coli</i> from raw meat.","authors":"Vanessa Quinlivan, Daniel E Park, Maliha Aziz, Joan A Casey, Meghan Davis, Qi Hu, Gabriel Innes, Keeve Nachman, Ann Nyaboe, Magdalena Pomichowski, Hanna-Grace Rabanes, Annie Roberts, Erika Roloff, Harpreet S Takhar, Sara Y Tartof, Cindy Liu, Lance Price","doi":"10.1289/EHP16115","DOIUrl":"10.1289/EHP16115","url":null,"abstract":"<p><strong>Background: </strong>Antimicrobial use in food-animal production selects for antimicrobial-resistant <i>Escherichia coli (E. coli)</i> that can be transmitted to humans via contaminated meat products. California Senate Bill 27 (SB27), which took effect on January 1, 2018, restricts the use of medically important antimicrobials in California food-animal production. Over time, SB27 could reduce the prevalence of antimicrobial-resistant <i>E. coli</i> on meat produced in California.</p><p><strong>Objectives: </strong>We aimed to assess whether the implementation of SB27 was associated with significant decreases in resistance to medically important antimicrobials among <i>E. coli</i> strains contaminating raw chicken produced in California.</p><p><strong>Methods: </strong>We purchased raw chicken products in Southern California, including those produced in and outside of California, from 2017 to 2021 and cultured them for <i>E. coli</i>. Susceptibility to 19 antimicrobials was determined using the disk diffusion method. Changes in antimicrobial susceptibility over the course of the study were evaluated using the Mann-Kendall test.</p><p><strong>Results: </strong>We observed significant decreases in resistance to multiple classes of antimicrobials in <i>E. coli</i> isolated from retail chicken meat from 2017 to 2021. Resistance to penicillins had a relative decrease of 14-18% annually in E. coli from chicken raised in California but not from chicken raised outside California, potentially indicating that SB27 was effective. Resistance to multiple other classes of antimicrobials saw an absolute decrease of up to 8% in chicken produced both inside and outside California.</p><p><strong>Discussion: </strong>Our findings suggest that the downward trends in antimicrobial resistance among E. coli populations from California-produced chicken products reflect national trends. It is possible that the California SB27 legislation helped motivate industry-wide decreases in antimicrobial use among broiler chicken producers. Alternatively, the changes observed in California may have been driven by industry-wide trends independent of SB27. The lack of publicly available data regarding actual antimicrobial use in California and non-California broiler chicken production limits our ability to make stronger conclusions about our observations. https://doi.org/10.1289/EHP16115.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"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":"10.1289/EHP15204","DOIUrl":"https://doi.org/10.1289/EHP15204","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 during pregnancy 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 using multiple informant models. A group-based trajectory modelling (GBTM) combined with multinomial logistic regression model were 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 \"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. While 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 gestation and 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 mid-gestational 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. https://doi.org/10.1289/EHP15204.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Association of Arsenic Exposure and Metabolism Biomarkers with Subclinical Measures of Liver Disease: a cross-sectional investigation in the Multi-Ethnic Study of Atherosclerosis.","authors":"Hui-Chen Wu, Ronald A Glabonjat, Kathrin Schilling, William A Anderson, Siyue Gao, Arce Domingo Relloso, Nancy LoIacono, Monique Slowly, Anne E Nigra, Tiffany Sanchez, Marisa H Sobel, Marta Galvez-Fernandez, Matthew J Budoff, Mary V Gamble, Ana Navas-Acien, Mariana Lazo","doi":"10.1289/EHP16728","DOIUrl":"10.1289/EHP16728","url":null,"abstract":"<p><strong>Background: </strong>Long-term exposure to arsenic (As) can cause many health effects and As metabolism is key in the detoxification and elimination of As. We hypothesize that hepatic steatosis might affect As metabolism efficiency. We evaluated the association of As exposure and As metabolism biomarkers with hepatic steatosis.</p><p><strong>Methods: </strong>In this cross-sectional analysis, we analyzed data from 3,577 participants in the Multi-Ethnic Study of Atherosclerosis (MESA), an ethnically diverse US adult population, with urinary metals and liver CT scan data available. We measured total As and As species in urine, and summarized As methylation biomarkers as inorganic (iAs%), monomethylarsonic acid (MMA%), and dimethylarsinic acid (DMA%). The ratio of liver-to-spleen (L/S) Hounsfield units (HU) < 1.0 and liver attenuation < 40 HU were used to assess the presence and severity of liver fat content. We used logistic regression to estimate the odds ratio (OR) (95%CI) of steatosis per higher interquartile range (IQR) of log-transformed total urinary As levels (ΣAs, μg/L), and per 5% higher in log-transformed As species (iAs%, MMA%, DMA%).</p><p><strong>Results: </strong>The adjusted ORs (95%CI) for L/S < 1.0 were 1.09 (0.91, 1.30) per higher IQR of ΣAs, and 0.80 (0.68, 0.95), 0.69 (0.61, 0.77), and 1.24 (1.15, 1.34) per 5% higher iAs%, MMA%, and DMA%, respectively. The corresponding ORs (95% CI) for HU < 40 were 0.99 (0.75, 1.30) per higher IQR of increase ΣAs, and 0.70 (0.50, 0.91), 0.65 (0.55, 0.78), and 1.31 (1.16, 1.48) per 5% higher iAs%, MMA%, and DMA%, respectively. The associations were consistent by self-reported race/ethnicity and sex.</p><p><strong>Conclusions: </strong>Arsenic methylation capacity, but not exposure, was associated with the prevalence of hepatic steatosis. Studies are needed to examine the longitudinal association between the progression of hepatic steatosis with As metabolism biomarkers and As-related disease. https://doi.org/10.1289/EHP16728.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":" ","pages":""},"PeriodicalIF":9.8,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144257678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pesticide Exposure Estimation across Census Tracts in Washington State: Identifying Vulnerable Areas and Populations.","authors":"Solmaz Amiri, Jeffrey M Bryant, Daniel H Farber, Ofer Amram, Jennifer C Sabel","doi":"10.1289/EHP15686","DOIUrl":"https://doi.org/10.1289/EHP15686","url":null,"abstract":"<p><strong>Introduction: </strong>Disparities in exposure to and harm associated with pesticides are established. However, high resolution spatial data on exposure to pesticides are lacking.</p><p><strong>Purpose: </strong>To describe the development of a pesticide metric for Washington State and to evaluate the associations between pesticide exposure and sociodemographic characteristics of census tracts.</p><p><strong>Methods: </strong>We used the US cropland dataset to quantify the location and size of agricultural land. These data were overlayed with state- and county-level estimated annual agricultural pesticide use to estimate pesticide exposure at the census tract level. Sociodemographic characteristics of census tracts were from the US Centers for Disease Control and Prevention's Social Vulnerability Index (SVI). Generalized additive models evaluated the associations between pesticide exposure and each of the SVI variables.</p><p><strong>Results: </strong>The median exposure to pesticides was 1.5 lbs/sq mi. Significant associations were observed between exposure to pesticides and higher percentage of population below poverty, populations unemployed, populations 65 and older, non-Hispanic white populations, those with limited English language proficiency, mobile homes, and group quarters.</p><p><strong>Conclusions: </strong>The results inform public health and policy efforts to identify areas and populations that are most vulnerable to pesticide exposure and improve the health and wellbeing of farmworkers and populations residing near agricultural areas. https://doi.org/10.1289/EHP15686.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"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, Lisa Marie Frohn, Matthias Ketzel, Anja Olsen, Lau Caspar Thygesen, Mette Sørensen","doi":"10.1289/EHP16554","DOIUrl":"https://doi.org/10.1289/EHP16554","url":null,"abstract":"<p><strong>Background: </strong>The evidence linking long-term exposure to air pollution and 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 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 (N = 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 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 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 contribute to COPD risk, with variations depending on the pollutant type. Further research is needed to validate these findings across different populations and geographical settings. https://doi.org/10.1289/EHP16554.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144257677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pre-disease biomarkers of persistent organic pollutants (POPs) and amyotrophic lateral sclerosis (ALS) risk in Finland.","authors":"Ian W Tang, Paul Knekt, Panu Rantakokko, Markku Heliövaara, Harri Rissanen, Päivi Ruokojärvi, Rajarshi Mukherjee, Marc G Weisskopf","doi":"10.1289/EHP16539","DOIUrl":"10.1289/EHP16539","url":null,"abstract":"<p><strong>Background: </strong>Persistent organic pollutants (POPs) are toxic chemicals that bioaccumulate and were used in pesticides and industrial products/processes. POP-exposed occupations and environmental exposure to POPs have been associated with amyotrophic lateral sclerosis (ALS), but no study has evaluated the association with ALS when measuring POPs in samples collected before ALS onset.</p><p><strong>Objectives: </strong>This study examined the relationship between pre-disease POP exposure and ALS risk.</p><p><strong>Methods: </strong>We conducted a nested case-control study pooling three Finnish cohorts (n=56,862). During a median follow-up of 27 years, 97 incident ALS cases were identified (mean age at ALS=68). Within each cohort, two controls per case were selected by individual matching for age, sex, municipality, and serum freeze-thaw cycles. Thirteen polychlorinated biphenyls (PCB) and nine organochlorine pesticides (OCP) were determined in serum samples collected at baseline and stored at -20C. We considered these POPs both in groups (similar congener, isomer, metabolite groups) and separately. Odds ratios and 95% confidence intervals were estimated using a conditional logistic model in a two-stage approach, further adjusting for smoking, occupation, marital status, BMI, and serum cholesterol level in primary models.</p><p><strong>Results: </strong>In the main model hexachlorobenzene (HCB) showed a positive association with ALS occurrence. In contrast, Σnon-dioxin-like (NDL) PCB and ΣDDT were significantly inversely associated with ALS incidence. Most other POP groups were non-significantly inversely associated with ALS risk. In co-pollutant models, the only notable changes were that Σdioxin-like PCB and ΣHCH showed large non-significant, elevated, ORs, suggesting some negative co-pollutant confounding. There were some suggestions of stronger findings when limiting to some subgroups.</p><p><strong>Discussion: </strong>We found little evidence that POPs were associated with ALS, but we identified a suggestive positive association with HCB and HCH. ΣNDL PCB and ΣDDT were inversely associated with ALS. This could suggest protective mechanisms or uncontrolled confounding by neuroprotective factors (e.g. fish oils). https://doi.org/10.1289/EHP16539.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":" ","pages":""},"PeriodicalIF":9.8,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144247065","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ambient temperature and injury-related emergency department visits in China and its Provinces: a large national case-crossover study.","authors":"Guanhao He, Yuan Wang, Tao Liu, Xiao Deng, Jianxiong Hu, Yuliang Er, Pengpeng Ye, Qijiong Zhu, Ye Jin, Cuirong Ji, Ziqiang Lin, Fengrui Jing, Leilei Duan, Wenjun Ma","doi":"10.1289/EHP16878","DOIUrl":"https://doi.org/10.1289/EHP16878","url":null,"abstract":"<p><strong>Background: </strong>Temperature-related risks on non-accidental morbidity or mortality have been well documented. However, limited studies have investigated the injury morbidity risk and burden attributed to ambient temperature.</p><p><strong>Objective: </strong>The current study aimed to assess the injury morbidity risk and burden attributed to ambient temperature in China.</p><p><strong>Methods: </strong>A time-stratified case-crossover study was conducted in 31 provincial-level administrations across mainland China, and 11.5 million injury-related emergency department visits recorded in National Injury Surveillance System (NISS) during 2006-2021 were included in the study. An injury case refers to a patient who takes the first visit to the outpatient or emergency department in NISS due to an injury. Daily meteorological data were collected from the fifth generation of European ReAnalysis-Land. A two-stage approach, including a conditional logistic regression and a multilevel meta-analysis, was applied to estimate the temperature-injury association, which were then applied to assess the morbidity burden attributable to temperature.</p><p><strong>Results: </strong>We observed that injury risk increased 1.2% (95%CI: 1.0%-1.4%) for a 1 °C increase in daily mean temperature with higher risk for males, children aged 0-4, and residents in tropical and subtropical zone. We also found that animal injury, violence and attack, and injury in agricultural area were more susceptible to temperature. Compared to the 2020s, we projected 5.7 times increase of injury cases and 10.4 times of attributable fraction due to temperature change driven by global warming in the 2090s under SSP5-8.5 scenario in China. Our findings might be informative for injury prevention in the context of climate change in China.</p><p><strong>Conclusion: </strong>Our findings identify susceptible populations, regions and mechanism-specific injuries when exposure to ambient temperature, which could be informative for injury prevention in the context of climate change in China. https://doi.org/10.1289/EHP16878.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144247062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"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":"10.1289/EHP16607","DOIUrl":"10.1289/EHP16607","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 causative mechanisms behind these correlations, particularly considering the increasing frequency of wildfires and the resulting air quality impacts. https://doi.org/10.1289/EHP16607.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":" ","pages":""},"PeriodicalIF":10.9,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144257679","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary exposure to per- and polyfluoroalkyl substances and health risk assessment in 7-year-old children in Shandong, China.","authors":"Yan Zhang, Qian Yao, Rong Shi, Jingguang Li, Angela Vinturache, Guanghe Wang, Xiaoning Lei, Yuxin Wang, Ying Tian, Yu Gao","doi":"10.1289/EHP15157","DOIUrl":"https://doi.org/10.1289/EHP15157","url":null,"abstract":"<p><strong>Background: </strong>Dietary intake, especially foods of animal-origin, is an important source of per- and polyfluoroalkyl substances (PFAS) exposure to the general population. However, the distribution of legacy and emerging PFAS in different food categories is unclear, as well as their potential health risk for children.</p><p><strong>Objectives: </strong>To investigate dietary sources of PFAS and evaluate the risk for 7-year-old children in Laizhou Wan, a region with high PFAS exposure in Shandong, China.</p><p><strong>Methods: </strong>We sampled participants from the Laizhou Wan Birth Cohort study. We administered a dietary questionnaire to the parents of 7-year-old children and measured PFAS compounds in the serum of the children (n = 154) and meat and seafood samples (n = 45). We calculated the Mann-Whitney U test to compare serum PFAS levels between children who frequently consumed a specific type of marine fish or shrimp/shellfish and those who did not. Children's dietary PFAS intake was calculated through multiplying food consumption and PFAS concentrations, and health risks were assessed by comparing the intake of PFAS with health-based guideline values.</p><p><strong>Results: </strong>In seafood, perfluorooctanic acid (PFOA) (0.52 ng/g wet weight (ww)), perfluoro-6-methylheptanesulfonic acid (iso-PFOS) (0.02 ng/g ww), and 6:2 chlorinated polyfluoroethersulfonic acid (0.06 ng/g ww) had the highest median concentrations among 10 linear PFAS, 8 branched isomers of PFOA and perfluorooctanesulfonic acid (PFOS), and 3 alternatives, respectively. Particularly, PFOA levels (median, 87.80 ng/g) in <i>Zoarces slongatus</i> (one type of marine fish), were approximately 10-100 times of those in other seafood species. Children who frequently consumed <i>Zoarces slongatus</i> had higher serum PFAS levels, especially PFOA, than those who did not. Seafood intake accounted for more than 80% of the total estimated daily intake of PFAS. The dietary estimated weekly intake values of four PFAS (PFOA, PFOS, perfluorononanoic acid, and perfluorohexanesulfonic acid) for children (7.4 ng/kg of body weight (bw)/week) exceeded the tolerable weekly intake (4.4 ng/kg bw/week) as recommended by the European Food Safety Authority.</p><p><strong>Conclusion: </strong>Seafood was widely contaminated by both legacy PFAS and their alternatives in Laizhou Wan area. Intake of seafood, especially <i>Zoarces slongatus</i>, may contribute greatly to PFAS exposure in 7-year-old children. Avoiding intake of high PFAS polluted seafood may be an important strategy to protect local children. https://doi.org/10.1289/EHP15157.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144247063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In utero per - and polyfluoroalkyl substances (PFAS) exposure and changes in infant T helper cell development among UPSIDE-ECHO cohort participants.","authors":"Darline Castro Meléndez, Nathan Laniewski, Todd A Jusko, Xing Qiu, B Paige Lawrence, Zorimar Rivera-Núñez, Jessica Brunner, Meghan Best, Allison Macomber, Alena Leger, Kurunthachalam Kannan, Richard Kermit Miller, Emily S Barrett, Thomas G O'Connor, Kristin Scheible","doi":"10.1289/EHP16726","DOIUrl":"10.1289/EHP16726","url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Objectives: </strong>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.</p><p><strong>Methods: </strong>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 (n=200). All models included a PFAS and age interaction and were adjusted for parity, infant sex, and pre-pregnancy body mass index.</p><p><strong>Results: </strong>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. TEXT.</p><p><strong>Discussion: </strong>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 risk of adverse immune-related health outcomes in children are warranted. https://doi.org/10.1289/EHP16726.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":" ","pages":""},"PeriodicalIF":9.8,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144257676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}