Environmental Health最新文献

{"title":"Banned here, sold elsewhere: globalization, e-commerce and the continuing circulation of asbestos-containing products.","authors":"Alessandro Francesco Gualtieri, Alessandro Cavallo","doi":"10.1186/s12940-026-01348-x","DOIUrl":"10.1186/s12940-026-01348-x","url":null,"abstract":"<p><p>Despite widespread recognition of its carcinogenicity and bans in many countries, asbestos remains a persistent global public health challenge. Regulatory fragmentation, transnational trade, and the rapid expansion of digital marketplaces continue to facilitate the circulation of asbestos-containing materials (ACM) across national borders. While all forms of asbestos, including chrysotile are prohibited in several jurisdictions, chrysotile is still mined, manufactured, and extensively used in major economies, including Russia and China, and remains incorporated into construction materials throughout large parts of Asia, the Middle East, and other regions. This regulatory asymmetry undermines national bans and compromises efforts to achieve zero exposure. In this Comment, we examine the consequences of the absence of a global asbestos ban and the continued failure to include chrysotile in Annex III of the Rotterdam Convention. We discuss how these regulatory gaps contribute to unrecognized exposure among the general population, create legal and economic liabilities for industries, and exacerbate environmental health risks in conflict zones and during large-scale construction and demolition activities. To illustrate the practical implications of these shortcomings, we present a case study demonstrating the ease with which asbestos-containing consumer products can be purchased through international e-commerce platforms. Laboratory analyses confirmed the presence of regulated chrysotile fibres in heat-resistant gloves purchased online, highlighting substantial deficiencies in product disclosure, regulatory enforcement, and cross-border accountability. This finding demonstrates how digital trade can bypass existing regulatory safeguards and expose unsuspecting consumers to carcinogenic materials. Asbestos should no longer be viewed as a legacy hazard but as an evolving global risk sustained by economic globalization, regulatory inconsistency, and technological change. Addressing this challenge will require coordinated international action, greater supply-chain transparency, and regulatory frameworks capable of responding to the realities of twenty-first century commerce.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"25 1","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13663101/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149180148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Residential indoor air monitoring to assess long-term exposure to air pollution in susceptible populations for epidemiology: overview and early findings.","authors":"Sun-Young Kim, Kyumin Kim, Seokmin Ji, Miyoun Shin, Hyunji Kim, Young Shin Park, Soyoung Han, Soyoun Bae, Younghyun Kim, Eehyun Park, Jiyoung Hwang, Seung-Hyun Cho, Hee-Young Yoon, Jin Woo Song","doi":"10.1186/s12940-026-01334-3","DOIUrl":"10.1186/s12940-026-01334-3","url":null,"abstract":"<p><p>While there has been accumulating evidence of the association between long-term exposure to air pollution and various health endpoints, most epidemiological studies relied on ambient air pollution which showed substantial deviation from indoor. This difference could lead to biased or imprecise health effect estimates, particularly for susceptible populations who spend most time indoors. Although a few studies focused on indoor air pollution, most monitoring was limited to one-time and/or relatively short-term periods. We aimed to provide an overview of an indoor monitoring campaign that was designed to assess long-term exposure to residential indoor PM_2.5 for epidemiology and applied to 130 older adults with idiopathic pulmonary fibrosis in the Seoul Metropolitan Area, South Korea, for 2021-2023. Specifically, our design focused on (1) representation of long-term exposure, (2) identification of pollution sources, (3) assessment of infiltration, and (4) implementation of non-contact monitoring. Using RTI MicroPEMs, we measured concentrations of indoor PM_2.5 and chemical components for five days including weekdays and weekends in four seasons as well as household information. We also collected matched outdoor samples to assess infiltration, and applied non-contact monitoring using postal mails for repeat visits. Our preliminary analyses of indoor hourly PM_2.5 measurements (mean: 14.90 µg/m³ [standard deviation: 36.12]) showed temporal patterns with higher concentrations in winter (20.17 [50.54]) than in summer (11.19 [32.76]) and during the daytime than nighttime. Indoor concentrations were lower than outdoor (20.44 [SD: 61.63]) with consistent seasonal patterns but contrasted hourly patterns. Thirty-six chemical components of PM_2.5 showed mostly similar temporal patterns to those of PM_2.5 with lower concentrations and smaller differences between indoors and outdoors in summer that in other seasons. The infiltration factor characterized by median indoor to outdoor ratios of sulfur, nickel, and iron were 51-70%. Average PM_2.5 concentrations tended to be high at households with cooking activities (15.14 vs. 10.96 µg/m³ at those without), humidifiers (19.19 vs. 13.16), pets (24.09 vs. 13.35), and smokers (16.76 vs. 11.79). Our indoor monitoring approach provides a practical guidance to future indoor monitoring studies that intend to assess the health effect of PM_2.5.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"25 1","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13587424/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148988282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The association of long-term air pollution with a composite neurodegenerative risk score among Chinese elderly: evidence from the CHARLS.","authors":"Ruoyu Gui, Wei Zhou, Jinsong Deng, Leiyu Shi, Gang Sun","doi":"10.1186/s12940-026-01335-2","DOIUrl":"10.1186/s12940-026-01335-2","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;The relationship between long-term exposure to air pollution and the risk of neurodegenerative diseases has drawn increasing attention. However, the relative effects of various pollutants and the potential role of systemic inflammation remain unclear. This study aims to explore the association between various air pollutants and the comprehensive risk score of neurodegenerative diseases in the middle-aged and elderly population in China, and to examine the effect modification of baseline high-sensitivity C-reactive protein (hs-CRP) and white blood cell count (WBC).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;The data were sourced from the China Longitudinal Study of Health and Retirement (CHARLS) and the National Earth System Science Data Center. The average concentrations of fine particulate matter (PM&lt;sub&gt;2.5&lt;/sub&gt;), inhalable particulate matter (PM10), nitrogen dioxide (NO&lt;sub&gt;2&lt;/sub&gt;), and ozone (O&lt;sub&gt;3&lt;/sub&gt; ) from 2012 to 2015 were obtained through processing by the ArcGIS platform. The outcome was the comprehensive risk score and its ternary scale constructed by grip strength, the Central Depression Scale (CES-D-10), the Mini-Mental State Examination (MMSE), and instrumental activities of daily living (IADL) at the follow-up in 2015. A two-stage analysis was adopted: Firstly, multiple linear regression (OLS) was used to analyze the association between pollutants and continuous scores; Then, ordered Logistic regression was applied. After adjusting for the baseline score in 2011, age, gender, education, urban and rural residence, and the number of chronic diseases, the association between pollutants and risk levels was analyzed, and age stratification analysis of pollutants was conducted (30-59 years old, 60-74 years old, ≥75 years old). The effect modification effect was examined by incorporating the interaction term between pollutants and baseline inflammatory markers into the model.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;OLS regression analysis showed that long-term PM2.5 exposure was significantly associated with an elevated comprehensive neurodegenerative risk score (adjusted β = 0.010, 95% CI: 0.008-0.016), while the associations with PM10, NO2, and O3 were not significant. Ordered Logistic regression analysis showed that, after adjusting for covariates, only PM2.5 was significantly associated with a higher neurodegenerative risk score grade (OR= 1.52, 95% CI: 1.01-2.31), and this association was specific to the 60-74 age group. Baseline hs-CRP and WBC levels had no significant effect modification on the association between pollutants and the comprehensive risk score of neurodegeneration (P &gt; 0.05).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;In the study population, long-term PM2.5 exposure was associated with an elevated comprehensive neurodegenerative risk score, especially among the elderly aged 60-74. No significant modifying effect of baseline inflammatory levels on this association was found. The research results suggest tha","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"25 1","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13570525/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148955163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic exposure to aflatoxin B1, ochratoxin A, and citrinin in women and children and associated health risk characterization: blood biomonitoring evidence from rural Bangladesh.","authors":"Nicholas N A Kyei, Benedikt Cramer, Hans-Ulrich Humpf, Michael Kuhn, Shafinaz Sobhan, Jannik Veerkamp, Sabine Gabrysch","doi":"10.1186/s12940-026-01330-7","DOIUrl":"10.1186/s12940-026-01330-7","url":null,"abstract":"<p><p>Dietary exposure to mycotoxins-including aflatoxins (AFs), ochratoxin A (OTA), and citrinin (CIT)-represents an important health risk, particularly in low-resource settings with widespread food contamination. This study investigates mycotoxin exposure among 719 participants (433 women and 286 children) of a cluster-randomized trial in rural Bangladesh, using residual blood samples collected during the 2019 endline survey. A total of 712 whole blood and 578 serum samples were analyzed by ultra-high-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS). Serum aflatoxin B1 (AFB₁)-lysine adducts were quantified following enzymatic digestion and solid-phase extraction. To evaluate potential health risks, we estimated probable daily intake (PDI) from blood concentrations of frequently detected mycotoxins. All whole blood samples contained at least two mycotoxins, and 84% of participants were co-exposed to at least three mycotoxins. Biomarkers for the main blood-relevant mycotoxins were frequently detected, with OTA detected in 100% of whole blood samples and its isomer, 2'R-ochratoxin A (2'R-OTA), detected in 98%, CIT in 91%, and Enniatin B (EnB) in 92%, while AFB₁-lysine-a biomarker of chronic exposure to the potent carcinogen AFB₁-was detected in nearly one-quarter of women and 4% of children with serum samples. Beauvericin was detected in 6% of samples. The PDI of OTA exceeded health-based guidance values in 80% of women and 99% of children, while the PDI of CIT was of concern for 12% of women and 27% of children. These findings demonstrate widespread co-exposure to multiple mycotoxins, with OTA, CIT, and AFB₁ posing notable risks, underscoring the urgent need for targeted interventions to protect vulnerable populations.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"25 1","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13563859/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148955105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mediating role of telomere shortening in dioxin-like polychlorinated biphenyls associated cognitive decline in children.","authors":"Lulu Liu, Jia Wang, Hua Chang, Yue Hu, Hongyan Zhang, Heng Wei, Yang Zhou, Xiufei Teng","doi":"10.1186/s12940-026-01319-2","DOIUrl":"10.1186/s12940-026-01319-2","url":null,"abstract":"<p><strong>Background: </strong>Dioxin-like polychlorinated biphenyls (DL-PCBs) are persistent environmental pollutants known to induce oxidative stress and inflammation, which may accelerate telomere shortening and affect neurodevelopment. We hypothesized that DL-PCB exposure contributes to cognitive deficits in children by accelerating telomere attrition, which in turn impairs brain function.</p><p><strong>Methods: </strong>We analyzed serum DL-PCB levels, leukocyte telomere length (LTL), and cognitive performance in 1756 primary school children (aged 7-10 years) from Shenyang, China. Twelve DL-PCB congeners were measured, and cognitive outcomes were assessed using a standardized test battery, including the n-back task (Two-Back and Three-Back) and the Attentional Network Test (ANT). LTL was quantified via qRT-PCR. Linear mixed models, mixture analyses (Quartile g-computation analysis (g-comp), Generalized Weighted Quantile Sum regression (gWQS), Bayesian Kernel Machine Regression (BKMR) ), and mediation analysis were applied, adjusting for relevant covariates.</p><p><strong>Results: </strong>Serum concentrations of PCB77, PCB126, and PCB189 were significantly associated with shorter LTL after Bonferroni correction (β = -0.041 for PCB189 per IQR increase, adjusted p = 0.001). PCB81 and PCB189 showed robust negative associations with superior working memory (Three-Back task; adjusted p < 0.05), while basic working memory (Two-Back) exhibited no significant associations. Inattentiveness (HRT-SE) was negatively associated with PCB157, PCB167, PCB169, and PCB189 in crude models, but these associations were attenuated after correction. Mixture analyses confirmed that DL-PCB mixtures were strongly associated with shorter LTL (g-comp β = -0.104, p < 0.001; gWQS β = -0.055, p < 0.001), as well as poorer superior working memory and inattentiveness. Mediation analysis revealed that LTL explained approximately 5-10% of the total effect of PCB77, PCB81, PCB169, and PCB189 on superior working memory and inattentiveness.</p><p><strong>Conclusion: </strong>Overall, early-life DL-PCB exposure is associated with telomere shortening and impaired higher-order cognitive function, with LTL acting as a partial mediator.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"25 1","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13536866/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879669","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Less air pollution previously related to clean air and climate policies is linked to improved cognitive scores over time in NYC children.","authors":"Frederica Perera, Yuqi Miao, Shuang Wang, Molly Algermissen, Julie Herbstman","doi":"10.1186/s12940-026-01328-1","DOIUrl":"https://doi.org/10.1186/s12940-026-01328-1","url":null,"abstract":"<p><strong>Background: </strong>Prenatal and postnatal exposure to air pollution has been associated in multiple epidemiological studies with adverse neurodevelopmental outcomes in children, including in New York City cohorts. Studies are lacking on changes in associations between air quality and neurodevelopmental outcomes over recent decades that have been marked by improvement in air quality. Here we investigated whether decreased prenatal exposure to air pollution, previously linked to clean air and climate policies in New York City, benefited cognitive development in children participating in cohort studies of the Columbia Center for Children's Environmental Health between 1998 and 2020. Information from such studies can benefit public health policy.</p><p><strong>Methods: </strong>We utilized data on prenatal exposure to fine particulate matter (PM2.5), nitrogen dioxide (NO₂) and polycyclic aromatic hydrocarbons (PAH) in successive longitudinal cohort studies. PM2.5 and NO₂ were available in the first two cohorts (1998-2016); PAH were monitored in three cohorts (1998-2020). Children were assessed for cognitive development at ages 1, 2, and 3 using the Bayley Scales of Infant and Toddler Development (BSID-II), which provided Mental Development Index (MDI) scores. To test associations between air pollutant exposures and MDI, we used linear regression, adjusting for demographic and other factors that contribute to neurodevelopment and/or changed over time.</p><p><strong>Results: </strong>Across the cohorts, levels of prenatal exposure to PM2.5, NO₂, and PAH decreased significantly; and there was a significant upward trend in MDI scores (N = 1109). Overall, when combining samples from cohorts, the pollutants were significantly and inversely associated with MDI at 1, 2, and 3 years. In the cohort-specific analyses, significant inverse associations between prenatal exposure to PM2.5, NO₂, PAH and 3-year MDI were seen in the larger initial cohort (N > 700, enrolled between 1998 and 2006) that experienced the highest exposure and the greatest decrease in levels of air pollutants. Weaker, albeit inverse, associations were observed between PM2.5 and cognitive development of children in the later cohort (2008-2016) who experienced lower exposure.</p><p><strong>Conclusions: </strong>These results indicate that, during the period of the largest reduction in air pollution levels, previously associated with air pollution and climate policies enacted in NYC, children's scores on cognitive tests improved, providing new evidence that such policies are beneficial to children's neurodevelopment.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"25 1","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13483841/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148789558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Conflicting views in experimental carcinogenesis: a commentary on design and methodological deficiencies in the follow-up validation studies on radiofrequency radiation.","authors":"Ronald L Melnick, Joel M Moskowitz, Paul Héroux","doi":"10.1186/s12940-026-01324-5","DOIUrl":"10.1186/s12940-026-01324-5","url":null,"abstract":"<p><p>Conflicting views in experimental carcinogenesis often arise due to differences in study design among reported studies. For carcinogenicity assessments, regulatory agencies, such as the US Food and Drug Administration (FDA), and intergovernmental advisory organizations, such as the Organization for Economic Co-operation and Development (OECD), specify the use of at least three dose levels plus control group for trend analyses, with the highest dose inducing a measurable toxic response. In addition, there needs to be a sufficient number of animals per group to have adequate power to detect a true carcinogenic effect. Departure from such recommendations can weaken the interpretations of study results. We examine here two recent carcinogenicity studies from Japan and Korea that were conducted following the positive carcinogenicity study of radiofrequency radiation (RFR) in experimental animals by the National Toxicology Program (NTP). The Japan and Korea follow-up studies used fewer animals per group, a single RFR exposure group, and a lower exposure level than the NTP study. Not surprisingly, while the NTP study revealed the carcinogenicity of RFR, the Japanese and Korean studies, which had reduced statistical power compared to the NTP study, issued conclusions conflicting with those of the more substantial NTP study on the health effects of RFR. In general, carcinogenicity studies with weaker doses, fewer exposure groups, and reduced statistical power should not be used to test the validity of more robust studies.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"25 1","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13417848/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148618814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bisphenol A and cancer: a critical review of the epidemiologic literature with an emphasis on exposure assessment.","authors":"Neela Guha, Gwendolyn Osborne, M Elizabeth Marder, Martha S Sandy, Meng Sun, Nancy Firchow, Vincent J Cogliano","doi":"10.1186/s12940-026-01306-7","DOIUrl":"10.1186/s12940-026-01306-7","url":null,"abstract":"<p><strong>Background: </strong>Bisphenol A (BPA) is a high production volume chemical that has been used for decades in numerous consumer and industrial applications. Daily exposure to BPA is likely; it is readily detected in >90% of the general population despite being rapidly metabolized and excreted. BPA's toxicity, including endocrine disrupting activity, has sparked public health concern. We comprehensively reviewed the epidemiologic literature on the carcinogenicity of BPA and highlighted exposure assessment considerations that impact study interpretation.</p><p><strong>Methods: </strong>Multiple biomedical databases were searched through February 2025 for peer-reviewed cancer epidemiology studies that assessed associations with BPA exposure. Studies of the following designs (or a variant) were included: cohort, case-control, cross-sectional. A detailed bias assessment was conducted with guidance from the Report on Carcinogens Handbook and the International Agency for Research on Cancer Monographs Preamble.</p><p><strong>Results: </strong>Of the 139 records identified, 43 epidemiological studies were reviewed; all were conducted in the general population. We focused the review on cancers of the breast and prostate because they had the highest number of cohort or case-control studies, but all cancer sites were summarized in the appendix for completeness. Generally, there were mixed results for associations with BPA. Interpretation was hampered by the high potential for exposure measurement error and the inability to characterize past BPA exposure, necessary to assess cancer outcomes with long latency. The majority of studies relied on biomonitoring using short-term biomarkers of recent BPA exposure, and measured BPA in urine at a single time point post-diagnosis; this failed to capture the critical time window of susceptibility, rule out reverse causation, or characterize temporal variation in BPA exposure.</p><p><strong>Conclusions: </strong>The epidemiologic evidence was inadequate to evaluate the carcinogenicity of BPA - mainly due to exposure measurement error and misclassification, limited number of studies by cancer site, and heterogeneity in the results and study methodology. The inadequate evidence base cannot rule out potential carcinogenicity of BPA in humans. Future studies conducted within highly exposed occupational cohorts, with prospective and longitudinal collection of quantitative exposure data (e.g., BPA levels) and assessment of cancer outcomes or acute endpoints involved in established mechanisms of carcinogenesis (e.g., receptor mediated effects) are likely to be informative.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"25 1","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13393274/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148561076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations between wildland fire smoke PM_2.5 and maternal blood pressure.","authors":"Patrick S Reuther, Sam D Faulstich, William J Metcalf, Calvin S Riss, Howard H Chang, Lyndsey A Darrow, Barrett M Welch, Heather A Holmes, Matthew J Strickland","doi":"10.1186/s12940-026-01323-6","DOIUrl":"10.1186/s12940-026-01323-6","url":null,"abstract":"<p><strong>Background: </strong>Wildland fires are a significant source of pollution that can cause sudden changes in ground-level ambient fine particulate matter (PM_2.5), an exposure that has been associated with gestational blood pressure increases. However, estimating the health risks specific to wildland fire smoke PM_2.5 is often encumbered by limitations to smoke plume modeling.</p><p><strong>Methods: </strong>We utilized a novel approach to estimate and characterize wildland fire smoke PM_2.5 in Reno, Nevada, USA, an area prone to seasonal smoke from wildland fires. Daily, 24-h averaged, plume-specific wildland fire smoke PM_2.5 concentrations were estimated at two air quality monitoring stations, and each plume was categorized by both the intensity of the source fire (high vs. low intensity) and the primary fuel type (forest, shrub/scrub, grassland, and other). Using electronic medical records (2012-2019), we identified a set of healthcare encounters of pregnant individuals, assigned these encounters to the air quality monitor closest to the maternal residential address at the time of the encounter and estimated the acute effects (0 to 3 day lag periods) of wildland fire smoke PM_2.5 on maternal systolic and diastolic blood pressure measures across gestational periods using a multi-level linear regression model.</p><p><strong>Results: </strong>We evaluated 132,570 clinical encounters with a blood pressure measurement over 22,399 pregnancies (median 4.0 measures per pregnancy). Overall, we found null associations between wildland fire smoke PM_2.5 and maternal blood pressure, regardless of the lag period. However, there was evidence that suggested associations could differ between gestational exposure periods, as positive associations not meeting statistical significance criteria were observed for almost all first trimester exposures. Associations did not differ by fire intensity or fuel type.</p><p><strong>Discussion: </strong>We did not find evidence for short-term associations between wildland fire smoke PM_2.5 and maternal blood pressure. Similar to other studies in the field, challenges to modeling smoke plumes and subjects altering their behavior during smoke events may be impacting the analyses.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":" ","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13663054/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148497435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations of prenatal exposure to per- and polyfluoroalkyl substances (PFAS) and childhood vaccine-induced immunity.","authors":"Anna Smith, Pi-I D Lin, Sheryl L Rifas-Shiman, Diane R Gold, Marie-France Hivert, Emily Oken, Andres Cardenas","doi":"10.1186/s12940-026-01322-7","DOIUrl":"10.1186/s12940-026-01322-7","url":null,"abstract":"<p><strong>Background: </strong>Plasma per- and polyfluoroalkyl substances (PFAS) are associated with immune dysfunction, including childhood antibody response. We evaluated whether first trimester maternal plasma PFAS concentrations are associated with mid-childhood MMR (measles, mumps, rubella) and DTaP (diphtheria, tetanus, pertussis) antibody titers.</p><p><strong>Methods: </strong>We measured six PFAS (EtFOSSA, MeFOSSA, PFHxS, PFNA, PFOA, PFOS) in first trimester plasma from participants in the longitudinal Project Viva cohort, recruited 1999-2002 in eastern Massachusetts. We measured mid-childhood plasma MMR and DTaP antibody titers. We restricted the analytical sample to children fully vaccinated, according to 2007 United States Center for Disease Control guidelines and used covariate-adjusted quantile g-computation and regression analyses to estimate associations (n = 333-416).</p><p><strong>Results: </strong>Median [interquartile range (IQR)] age at antibody titer blood draw was 7.7 years (7.4, 8.4), and children received their most recent MMR or DTaP dose at median (IQR) 4.3 years (4.1, 5.0). The PFAS mixture was associated with lower antibody titers, except for measles, although none of the associations reached statistical significance. A one unit (ng/mL) increase in EtFOSSA was associated with higher measles antibody titers [β = 0.02, 95% confidence interval (CI) = 0.01, 0.04 antibody (Ab) index]. A one ng/mL increase in MeFOSSA was associated with - 6.8% (95% CI: -11.9, -1.3) lower pertussis antibody titers. There was evidence of effect modification by infant sex for prenatal PFOS and childhood pertussis antibody titers, with higher prenatal PFOS associated with lower antibody titers in females and higher in males, although neither association reached statistical significance.</p><p><strong>Conclusions: </strong>While the prenatal PFAS mixture was not significantly associated with childhood antibody titers in our cohort, we observed individual associations between EtFOSSA and higher measles antibody titers and MeFOSSA and lower pertussis antibody titers. Overall, we found limited evidence of associations between first trimester plasma PFAS and mid-childhood antibody titers in our cohort.</p><p><strong>Trial registration: </strong>Clinical trial number: not applicable.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":" ","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13647844/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148445221","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}