Pub Date : 2026-02-06DOI: 10.1016/j.envint.2026.110129
Sabrina Günsche, Matthew A. Borg, Olga Anikeeva, Blesson M. Varghese, Yannan Li, Dinesh Bhandari, Jing Li, Haoran Yang, Yihan Shi, Jingwen Liu, Keith Dear, Bertram Ostendorf, Nigel Stocks, Danny Liew, Peng Bi
{"title":"Mortality, morbidity and healthcare costs of short-term high temperatures and heatwaves exposure in older populations: a global systematic review and meta-analysis","authors":"Sabrina Günsche, Matthew A. Borg, Olga Anikeeva, Blesson M. Varghese, Yannan Li, Dinesh Bhandari, Jing Li, Haoran Yang, Yihan Shi, Jingwen Liu, Keith Dear, Bertram Ostendorf, Nigel Stocks, Danny Liew, Peng Bi","doi":"10.1016/j.envint.2026.110129","DOIUrl":"https://doi.org/10.1016/j.envint.2026.110129","url":null,"abstract":"","PeriodicalId":308,"journal":{"name":"Environment International","volume":"59 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146134219","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}
Pub Date : 2026-02-06DOI: 10.1016/j.envint.2026.110131
Karl O’Sharkey, Sanjali Mitra, Ting Chow, Amanda Goodrich, Kathryn Conlon, Miriam Nuño, Deborah H. Bennett, Sean Raffuse, Mohammad Astaneh, Yusheng Zhao, Michael Kleeman, Beate Ritz, Rebecca J. Schmidt
Background
Wildfire smoke is an increasingly prevalent source of air pollution and contains a complex mixture of neurotoxic constituents that could affect neurodevelopment, yet its potential role in autism spectrum disorder (ASD) etiology remains unexplored. We examined associations between wildfire-specific PM2.5 exposures and ASD risk in California births, considering exposure timing, intensity, and background air pollution.
Methods
We analyzed 8.6 million births in California from 2001 to 2019, linking records to ASD diagnoses in California Department of Developmental Services records through 2022. Wildfire-related PM2.5 exposures, including biomass burning and wildland-urban-interface (WUI) source tracers, were estimated for preconception, pregnancy, and post-pregnancy periods. Exposure metrics included continuous, percentile-based, and episode-based indicators. Logistic regression was used to estimate odds ratios, adjusting for sociodemographic covariates. Stratified analyses were conducted by background PM2.5, urbanicity, diagnostic era, and sex.
Results
Continuous wildfire-specific exposures during the pregnancy-period were weakly associated with ASD, but stronger effects emerged at high exposure percentiles and during intense wildfire episodes (≥35 µg/m3). Associations were most pronounced among children in the lowest quartile of prenatal background PM2.5, with odds of ASD increasing by 50% for those in the > 90th percentile of wildfire PM2.5 during pregnancy. WUI-related PM2.5 was associated with ASD in metro areas, suggesting unique toxicity. Effects were stronger in non-metro regions, with the exception of WUI-related PM2.5, for births occurring after the implementation of DSM-5, and in White children. Sex differences were minimal, but showed stronger effect estimates for WUI-related PM2.5 and high exposure episodes for males.
Conclusion
Wildfire smoke exposure during pregnancy may increase ASD risk, particularly in low background air pollution and rural settings. High-intensity wildfire events were most strongly associated with ASD, underscoring the need for targeted policies, such as vegetation management, land use planning, and indoor filtration upgrades in the context of increasing wildfire frequency and severity.
{"title":"Prenatal exposure to wildfire-related PM2.5 and autism spectrum disorder in children born in California between 2001–2019","authors":"Karl O’Sharkey, Sanjali Mitra, Ting Chow, Amanda Goodrich, Kathryn Conlon, Miriam Nuño, Deborah H. Bennett, Sean Raffuse, Mohammad Astaneh, Yusheng Zhao, Michael Kleeman, Beate Ritz, Rebecca J. Schmidt","doi":"10.1016/j.envint.2026.110131","DOIUrl":"https://doi.org/10.1016/j.envint.2026.110131","url":null,"abstract":"<h3>Background</h3>Wildfire smoke is an increasingly prevalent source of air pollution and contains a complex mixture of neurotoxic constituents that could affect neurodevelopment, yet its potential role in autism spectrum disorder (ASD) etiology remains unexplored. We examined associations between wildfire-specific PM<sub>2.5</sub> exposures and ASD risk in California births, considering exposure timing, intensity, and background air pollution.<h3>Methods</h3>We analyzed 8.6 million births in California from 2001 to 2019, linking records to ASD diagnoses in California Department of Developmental Services records through 2022. Wildfire-related PM<sub>2.5</sub> exposures, including biomass burning and wildland-urban-interface (WUI) source tracers, were estimated for preconception, pregnancy, and post-pregnancy periods. Exposure metrics included continuous, percentile-based, and episode-based indicators. Logistic regression was used to estimate odds ratios, adjusting for sociodemographic covariates. Stratified analyses were conducted by background PM<sub>2.5</sub>, urbanicity, diagnostic era, and sex.<h3>Results</h3>Continuous wildfire-specific exposures during the pregnancy-period were weakly associated with ASD, but stronger effects emerged at high exposure percentiles and during intense wildfire episodes (≥35 µg/m<sup>3</sup>). Associations were most pronounced among children in the lowest quartile of prenatal background PM<sub>2.5</sub>, with odds of ASD increasing by 50% for those in the > 90th percentile of wildfire PM<sub>2.5</sub> during pregnancy. WUI-related PM<sub>2.5</sub> was associated with ASD in metro areas, suggesting unique toxicity. Effects were stronger in non-metro regions, with the exception of WUI-related PM<sub>2.5</sub>, for births occurring after the implementation of DSM-5, and in White children. Sex differences were minimal, but showed stronger effect estimates for WUI-related PM<sub>2.5</sub> and high exposure episodes for males.<h3>Conclusion</h3>Wildfire smoke exposure during pregnancy may increase ASD risk, particularly in low background air pollution and rural settings. High-intensity wildfire events were most strongly associated with ASD, underscoring the need for targeted policies, such as vegetation management, land use planning, and indoor filtration upgrades in the context of increasing wildfire frequency and severity.","PeriodicalId":308,"journal":{"name":"Environment International","volume":"1 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146121996","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}
Uranium (U) contamination of water sources, arising from anthropogenic activities such as mining and nuclear fallout, poses a significant global threat to water quality and public health. Ingestion of U-contaminated water and food results in bioaccumulation, primarily within the kidneys and bones, leading to severe nephrotoxicity and potential long-term health consequences. Addressing this challenge, we present a novel bio-intervention strategy leveraging a genetically engineered probiotic for the prevention of U absorption at its primary entry point—the gastrointestinal tract. We engineered Escherichia coliNissle 1917 (EcN) to express a high-affinity uranyl-binding protein (U09), generating the EcN-U strain. EcN-U sequestered soluble uranyl ions (UO22+) within the gut lumen via selective and efficient binding, leading to fecal excretion and prevention of systemic absorption. In a murine model of acute UO22+ exposure, EcN-U pre-treatment significantly enhanced survival rates. Furthermore, in chronic exposure models utilizing mice, rats, and beagle dogs, EcN-U pre-treatment demonstrably reduced U accumulation in target organs by approximately 80%. Concurrently, this intervention alleviated oxidative stress biomarkers, restored gut microbiota homeostasis, and mitigated intestinal histopathological damage. Our findings establish engineered probiotics as a pragmatic and potent strategy for environmental health protection, offering a proactive and viable solution for public health risk mitigation associated with waterborne uranium contamination.
{"title":"Engineered probiotics for the in vivo mitigation of waterborne uranium toxicity and bioaccumulation","authors":"Haidong Li, Feifei Zhang, Chenya Wang, Zhencun Cui, Yina Liu, Zhenhua Song, Lingyan Yuan, Xiaolei Chen, Yumin Wu, Wangsuo Wu, Longlong Tian","doi":"10.1016/j.envint.2026.110127","DOIUrl":"https://doi.org/10.1016/j.envint.2026.110127","url":null,"abstract":"Uranium (U) contamination of water sources, arising from anthropogenic activities such as mining and nuclear fallout, poses a significant global threat to water quality and public health. Ingestion of U-contaminated water and food results in bioaccumulation, primarily within the kidneys and bones, leading to severe nephrotoxicity and potential long-term health consequences. Addressing this challenge, we present a novel bio-intervention strategy leveraging a genetically engineered probiotic for the prevention of U absorption at its primary entry point—the gastrointestinal tract. We engineered<!-- --> <em>Escherichia coli</em> <em>Nissle</em> 1917 (EcN) to express a high-affinity uranyl-binding protein (U09), generating the EcN-U strain. EcN-U sequestered soluble uranyl ions (UO<sub>2</sub><sup>2+</sup>) within the gut lumen via selective and efficient binding, leading to fecal excretion and prevention of systemic absorption. In a murine model of acute<!-- --> <!-- -->UO<sub>2</sub><sup>2+</sup> exposure, EcN-U pre-treatment significantly enhanced survival rates. Furthermore, in chronic exposure models utilizing mice, rats, and beagle dogs, EcN-U pre-treatment demonstrably reduced U accumulation in target organs by approximately 80%. Concurrently, this intervention alleviated oxidative stress biomarkers, restored gut microbiota homeostasis, and mitigated intestinal histopathological damage. Our findings establish engineered probiotics as a pragmatic and potent strategy for environmental health protection, offering a proactive and viable solution for public health risk mitigation associated with waterborne uranium contamination.","PeriodicalId":308,"journal":{"name":"Environment International","volume":"39 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146129657","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}
Pub Date : 2026-02-05DOI: 10.1016/j.envint.2026.110123
Sara D. Adar, Boya Zhang, Jennifer D’Souza, Adam A. Szpiro, Anjelica Gangaram, Jennifer Weuve, Carlos F. Mendes de Leon, Kayleigh P. Keller, Meredith Pedde, Jinkook Lee, Joel D. Kaufman, Jessica Faul, Kenneth M. Langa, Richard A. Hirth
Background
Air pollution is associated with poor health, including chronic diseases, cognitive declines, and physical limitations in late life. The financial burdens of these exposures are likely underestimated due to a reliance on indirect estimates not generated by individual-level data and the exclusion of out-of-pocket expenses and long-term care costs.
Methods
We used repeated measures of Medicare-linked survey data from respondents in the Health and Retirement Study (HRS), a nationally-representative, population-based, cohort study in the United States. We included all respondents aged ≥ 67 years who were enrolled in fee-for-service coverage between 2006 and 2016 to characterize associations between air pollution and Medicare and out-of-pocket healthcare spending. We estimated 10-year average concentrations of four key air pollutants (PM2.5, PM10-2.5, NO2, O3) for each respondent using residential histories and spatiotemporal models. We summarized Medicare and out-of-pocket (OOP) spending ($2016) for medical services, personal services, and prescription drugs for each respondent per month. Associations between 10-year average air pollution and monthly healthcare spending were assessed per interquartile range of exposure using linear and quantile regression, adjusting for confounding and accounting for survey design.
Results
Among 11,160 respondents (72 ± 7yrs), the mean annual total healthcare spending in Medicare and out-of-pocket spending were $16,680 and $3,156, respectively. Higher levels of PM10-2.5 and NO2 were associated with upward shifts in annual healthcare spending with $614 (95% CI: $324, $904) and $1,047 (95% CI: $580, $1,515) higher spending at the 90th percentile and $138 (95% CI: $113, $163) and $162 (95% CI: $123, $201) higher median spending, respectively. In contrast, associations with PM2.5 were not robust to the adjustment of co-pollutants, and O3 was associated with lower spending.
Conclusion
Interventions to reduce PM10-2.5 and NO2 may mitigate societal and personal healthcare spending for older adults, particularly for those with high medical needs.
{"title":"Air pollution predicts healthcare spending among older adults in the United States","authors":"Sara D. Adar, Boya Zhang, Jennifer D’Souza, Adam A. Szpiro, Anjelica Gangaram, Jennifer Weuve, Carlos F. Mendes de Leon, Kayleigh P. Keller, Meredith Pedde, Jinkook Lee, Joel D. Kaufman, Jessica Faul, Kenneth M. Langa, Richard A. Hirth","doi":"10.1016/j.envint.2026.110123","DOIUrl":"https://doi.org/10.1016/j.envint.2026.110123","url":null,"abstract":"<h3>Background</h3>Air pollution is associated with poor health, including chronic diseases, cognitive declines, and physical limitations in late life. The financial burdens of these exposures are likely underestimated due to a reliance on indirect estimates not generated by individual-level data and the exclusion of out-of-pocket expenses and long-term care costs.<h3>Methods</h3>We used repeated measures of Medicare-linked survey data from respondents in the Health and Retirement Study (HRS), a nationally-representative, population-based, cohort study in the United States. We included all respondents aged ≥ 67 years who were enrolled in fee-for-service coverage between 2006 and 2016 to characterize associations between air pollution and Medicare and out-of-pocket healthcare spending. We estimated 10-year average concentrations of four key air pollutants (PM<sub>2.5</sub>, PM<sub>10-2.5</sub>, NO<sub>2</sub>, O<sub>3</sub>) for each respondent using residential histories and spatiotemporal models. We summarized Medicare and out-of-pocket (OOP) spending ($2016) for medical services, personal services, and prescription drugs for each respondent per month. Associations between 10-year average air pollution and monthly healthcare spending were assessed per interquartile range of exposure using linear and quantile regression, adjusting for confounding and accounting for survey design.<h3>Results</h3>Among 11,160 respondents (72 ± 7yrs), the mean annual total healthcare spending in Medicare and out-of-pocket spending were $16,680 and $3,156, respectively. Higher levels of PM<sub>10-2.5</sub> and NO<sub>2</sub> were associated with upward shifts in annual healthcare spending with $614 (95% CI: $324, $904) and $1,047 (95% CI: $580, $1,515) higher spending at the 90th percentile and $138 (95% CI: $113, $163) and $162 (95% CI: $123, $201) higher median spending, respectively. In contrast, associations with PM<sub>2.5</sub> were not robust to the adjustment of co-pollutants, and O<sub>3</sub> was associated with lower spending.<h3>Conclusion</h3>Interventions to reduce PM<sub>10-2.5</sub> and NO<sub>2</sub> may mitigate societal and personal healthcare spending for older adults, particularly for those with high medical needs.","PeriodicalId":308,"journal":{"name":"Environment International","volume":"1 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146115962","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}
Ubiquitous environmental nano-plastics (NPs) can enter organisms via multiple pathways, posing potential health risks; however, the adverse effects of gestational polystyrene NPs (PS-NPs) exposure on adult offspring reproductive function and underlying mechanisms remain unclear. The adverse outcome pathway (AOP) framework models toxic events from molecular to organismal levels. This study employed multi-omics analysis to construct a putative partial-AOP network revealing insights into the mechanism of intergenerational reproductive impairment of PS-NPs in adult offspring. Gestational PS-NPs exposure induced testicular structural damage and abnormal spermatogenesis in adult male offspring. The testicular transcriptomic and serum metabolomic data integration, validation and the omics-anchored AOP network construction highlighted four molecular events in adult male offspring following gestational PS-NPs exposure: increased arachidonic acid release, elevated reactive oxygen species levels, increased palmitic acid levels, and decreased lysophosphatidyl choline levels. These molecular events might be implicated in a series of cellular key events (KEs), ranging from cellular damage and impaired proliferation to cell death. These cellular KEs could contribute to testicular cell reduction and organ-level KEs—testicular injury, reduced androgen secretion, and impaired spermatogenesis—culminating in the adverse outcome of reproductive dysfunction. This putative network characterizes the molecular and histopathological landscape of reproductive impairment in adult male offspring associated with gestational PS-NPs exposure, and provides clues for elucidating the intergenerational toxicity mechanisms of PS-NPs.
{"title":"Plastic poisoning the next generation: omics-anchored partial-adverse outcome pathway affords a glimpse into how gestational polystyrene nano-plastics exposure compromises adult male offspring reproduction","authors":"Ruxuan Zhang, Hongou Wang, Moxuan Zhao, Yue Zhang, Jinglong Xue, Xinyue Luo, Junhong Xie, Ruiyang Zhang, Xi Yang, Wei Ge, Lihua Ren, Xianqing Zhou","doi":"10.1016/j.envint.2026.110126","DOIUrl":"https://doi.org/10.1016/j.envint.2026.110126","url":null,"abstract":"Ubiquitous environmental nano-plastics (NPs) can enter organisms via multiple pathways, posing potential health risks; however, the adverse effects of gestational polystyrene NPs (PS-NPs) exposure on adult offspring reproductive function and underlying mechanisms remain unclear. The adverse outcome pathway (AOP) framework models toxic events from molecular to organismal levels. This study employed multi-omics analysis to construct a putative partial-AOP network revealing insights into the mechanism of intergenerational reproductive impairment of PS-NPs in adult offspring. Gestational PS-NPs exposure induced testicular structural damage and abnormal spermatogenesis in adult male offspring. The testicular transcriptomic and serum metabolomic data integration, validation and the omics-anchored AOP network construction highlighted four molecular events in adult male offspring following gestational PS-NPs exposure: increased arachidonic acid release, elevated reactive oxygen species levels, increased palmitic acid levels, and decreased lysophosphatidyl choline levels. These molecular events might be implicated in a series of cellular key events (KEs), ranging from cellular damage and impaired proliferation to cell death. These cellular KEs could contribute to testicular cell reduction and organ-level KEs—testicular injury, reduced androgen secretion, and impaired spermatogenesis—culminating in the adverse outcome of reproductive dysfunction. This putative network characterizes the molecular and histopathological landscape of reproductive impairment in adult male offspring associated with gestational PS-NPs exposure, and provides clues for elucidating the intergenerational toxicity mechanisms of PS-NPs.","PeriodicalId":308,"journal":{"name":"Environment International","volume":"159 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146122245","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}
Pub Date : 2026-02-05DOI: 10.1016/j.envint.2026.110130
Rebecca Cole, Leire Luque García, Gillian Flower, Arturo de la Cruz Libardi, Mikhail Sofiev, Pierre Masselot, Antonio Gasparrini
Objective
Evidence linking pollen exposure to asthma exacerbations is limited and inconsistent across regions, pollen types, and age groups. We assessed the association between pollen concentrations and asthma-related hospital admissions across England at high spatial resolution.
Materials and methods
We use unplanned asthma admissions records (2008–2022) from Hospital Episode Statistics, linked to 10-km gridded data on alder and birch pollen. Tree pollen exposure was categorised as low, medium, or high. Age-specific case time series analyses were conducted using conditional Poisson regression, controlling for temperature and air pollutants (PM2.5 and NO2). Analyses were restricted to January–August, when tree pollen is present.
Results
Elevated asthma admission risk was associated with both pollen types, with a non-linear exposure–response that increased sharply at low levels and attenuated at higher exposures. For alder pollen, relative risks (RRs) across all ages were 1.014 (95%CI: 0.998, 1.031) for low, 1.026 (1.007, 1.046) for medium, and 1.019 (0.995, 1.044) for high exposure. For birch, RRs were 1.016 (0.996, 1.037), 1.041 (1.019, 1.06), and 1.032 (1.005, 1.060), respectively. Risks were mostly limited to children, with medium alder pollen exposure associated with RRs of 1.047 (0.993, 1.105) and 1.112 (1.066, 1.159), and birch with RRs of 1.131 (1.066, 1.201) and 1.079 (1.029, 1.131) in 0–4 and 5–14-year-olds, respectively. No evidence of association was found in older groups.
Conclusion
Moderate tree pollen levels are associated with increased asthma admissions in younger populations in England. Further work is needed to understand group and individual susceptibility.
{"title":"Tree pollen and asthma-related hospital admissions in England: a national case time series analysis","authors":"Rebecca Cole, Leire Luque García, Gillian Flower, Arturo de la Cruz Libardi, Mikhail Sofiev, Pierre Masselot, Antonio Gasparrini","doi":"10.1016/j.envint.2026.110130","DOIUrl":"https://doi.org/10.1016/j.envint.2026.110130","url":null,"abstract":"<h3>Objective</h3>Evidence linking pollen exposure to asthma exacerbations is limited and inconsistent across regions, pollen types, and age groups. We assessed the association between pollen concentrations and asthma-related hospital admissions across England at high spatial resolution.<h3>Materials and methods</h3>We use unplanned asthma admissions records (2008–2022) from Hospital Episode Statistics, linked to 10-km gridded data on alder and birch pollen. Tree pollen exposure was categorised as low, medium, or high. Age-specific case time series analyses were conducted using conditional Poisson regression, controlling for temperature and air pollutants (PM<sub>2.5</sub> and NO<sub>2</sub>). Analyses were restricted to January–August, when tree pollen is present.<h3>Results</h3>Elevated asthma admission risk was associated with both pollen types, with a non-linear exposure–response that increased sharply at low levels and attenuated at higher exposures. For alder pollen, relative risks (RRs) across all ages were 1.014 (95%CI: 0.998, 1.031) for low, 1.026 (1.007, 1.046) for medium, and 1.019 (0.995, 1.044) for high exposure. For birch, RRs were 1.016 (0.996, 1.037), 1.041 (1.019, 1.06), and 1.032 (1.005, 1.060), respectively. Risks were mostly limited to children, with medium alder pollen exposure associated with RRs of 1.047 (0.993, 1.105) and 1.112 (1.066, 1.159), and birch with RRs of 1.131 (1.066, 1.201) and 1.079 (1.029, 1.131) in 0–4 and 5–14-year-olds, respectively. No evidence of association was found in older groups.<h3>Conclusion</h3>Moderate tree pollen levels are associated with increased asthma admissions in younger populations in England. Further work is needed to understand group and individual susceptibility.","PeriodicalId":308,"journal":{"name":"Environment International","volume":"56 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146129675","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}
Pub Date : 2026-02-05DOI: 10.1016/j.envint.2026.110111
Xuehan Zheng, Haochun Shi, Boyang Li, Jianan Li, Yan Liu, Jiahui Liang, Lili Chen, Karl Fent, Kun Zhang, Han Wang, Jiayin Dai, Yanbin Zhao
The circadian clock coordinates daily oscillations of essential physiological and behavioral processes in organisms. Conversely, aberrant circadian rhythms, triggered by external cues such as circadian disruptive compounds, have been linked with various chronic diseases and aging. To search for environmental molecules that perturb circadian rhythms, we conducted a high-throughput screening of environmental compounds utilizing an integrated, multi-tiered approach combining reduced transcriptomic analysis, behavioral monitoring, and time-course gene expression profiling. This strategy enabled us to analyze 84 environmental compounds, covering over 750 gene expression signatures, and prioritized compounds with significant circadian disruptive potentials. We identified 16 compounds that exerted the most pronounced transcriptional effects on circadian system, with steroid hormones (e.g. dexamethasone and triamcinolone), biocides (triclosan and prochloraz), and metallic compounds (AgNO3 and AgNPs), emerging as the key classes of circadian disruptors. Functional enrichment analyses revealed that these compounds modulate core circadian regulatory networks (e.g. per, cry, nr1d, bmal families) and downstream biological processes such as transcriptional regulation, mRNA splicing, and metabolic homeostasis. In addition, behavioral assays conducted for eleven representative compounds and time-course gene expression profiling performed for three compounds further demonstrated significant alterations in locomotor activity rhythms and molecular circadian dynamics, including dihydrotestosterone, prochloraz and AgNO3, emphasizing their disruptive effects at both physiological and transcriptional levels. Collectively, the circadian disruptors identified in this study provide novel insights into the potential risks of these compounds to ecological and human health.
{"title":"Identification of toxic substances considering circadian disruption: an integrated approach combining reduced transcriptomic analysis, behavioral monitoring, and time-course gene expression profiling","authors":"Xuehan Zheng, Haochun Shi, Boyang Li, Jianan Li, Yan Liu, Jiahui Liang, Lili Chen, Karl Fent, Kun Zhang, Han Wang, Jiayin Dai, Yanbin Zhao","doi":"10.1016/j.envint.2026.110111","DOIUrl":"https://doi.org/10.1016/j.envint.2026.110111","url":null,"abstract":"The circadian clock coordinates daily oscillations of essential physiological and behavioral processes in organisms. Conversely, aberrant circadian rhythms, triggered by external cues such as circadian disruptive compounds, have been linked with various chronic diseases and aging. To search for environmental molecules that perturb circadian rhythms, we conducted a high-throughput screening of environmental compounds utilizing an integrated, multi-tiered approach combining reduced transcriptomic analysis, behavioral monitoring, and time-course gene expression profiling. This strategy enabled us to analyze 84 environmental compounds, covering over 750 gene expression signatures, and prioritized compounds with significant circadian disruptive potentials. We identified 16 compounds that exerted the most pronounced transcriptional effects on circadian system, with steroid hormones (e.g. dexamethasone and triamcinolone), biocides (triclosan and prochloraz), and metallic compounds (AgNO<sub>3</sub> and AgNPs), emerging as the key classes of circadian disruptors. Functional enrichment analyses revealed that these compounds modulate core circadian regulatory networks (e.g. <em>per</em>, <em>cry</em>, <em>nr1d</em>, <em>bmal</em> families) and downstream biological processes such as transcriptional regulation, mRNA splicing, and metabolic homeostasis. In addition, behavioral assays conducted for eleven representative compounds and time-course gene expression profiling performed for three compounds further demonstrated significant alterations in locomotor activity rhythms and molecular circadian dynamics, including dihydrotestosterone, prochloraz and AgNO<sub>3</sub>, emphasizing their disruptive effects at both physiological and transcriptional levels. Collectively, the circadian disruptors identified in this study provide novel insights into the potential risks of these compounds to ecological and human health.","PeriodicalId":308,"journal":{"name":"Environment International","volume":"30 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146121897","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}
Pub Date : 2026-02-04DOI: 10.1016/j.envint.2026.110114
Danka Matijašević, Nemanja Kljajević, Milka Malešević, Lazar Gardijan, Stefan Stanovčić, Branko Jovčić, Katarina Novović
Antimicrobial resistance (AMR) and air pollution are critical global health challenges, but their interplay remains poorly understood, particularly in Europe. Serbia, characterized by extensive antibiotic use, high prevalence of multidrug-resistant isolates and severe air pollution, provides a relevant model to study airborne AMR dissemination. During the heating season, air samples were collected at eight locations in Belgrade, representing industrial, traffic loaded and background environments. Shotgun metagenomics, co-occurrence networks and NMDS ordinations were applied to investigate the relationships between atmospheric pollutants, antibiotic resistance genes (ARGs), biocide resistance genes (BRGs), metal resistance genes (MRGs) and mobile genetic elements (MGEs). Autumn microbiomes were dominated by Lactococcus spp., whereas winter lacked such dominance. ARGs associated with antibiotic inactivation accounted for > 50% in autumn and > 75% in winter, with β-lactam resistance (blaTEM) predominating in both seasons. Winter resistomes also showed more consistent patterns of BRGs and MRGs, with multibiocide/acid and multimetal resistance prevailing. Integron analysis revealed predominance of class 1 integrons (intI1) commonly associated with Escherichia coli. Plasmid-related contigs were most similar to sequences reported in Acinetobacter baumannii and E. coli, while plasmid signatures related to Lactococcus lactis were also detected in autumn. Crucially, the network analysis revealed a seasonal restructuring of the airborne resistome. Autumn networks displayed fragmented structure, showing antagonism between Lactococcus and Escherichia, whereas winter networks coalesced into a densely interconnected superhub that could facilitate horizontal gene transfer and co-selection of resistance determinants. These findings suggest that prolonged air pollution and seasonality jointly shape airborne resistomes, reinforcing the need for integrated environmental and AMR surveillance in highly polluted urban areas.
{"title":"Heating-season dynamics of the airborne microbiome, resistome and mobilome in Belgrade, Serbia","authors":"Danka Matijašević, Nemanja Kljajević, Milka Malešević, Lazar Gardijan, Stefan Stanovčić, Branko Jovčić, Katarina Novović","doi":"10.1016/j.envint.2026.110114","DOIUrl":"https://doi.org/10.1016/j.envint.2026.110114","url":null,"abstract":"Antimicrobial resistance (AMR) and air pollution are critical global health challenges, but their interplay remains poorly understood, particularly in Europe. Serbia, characterized by extensive antibiotic use, high prevalence of multidrug-resistant isolates and severe air pollution, provides a relevant model to study airborne AMR dissemination. During the heating season, air samples were collected at eight locations in Belgrade, representing industrial, traffic loaded and background environments. Shotgun metagenomics, co-occurrence networks and NMDS ordinations were applied to investigate the relationships between atmospheric pollutants, antibiotic resistance genes (ARGs), biocide resistance genes (BRGs), metal resistance genes (MRGs) and mobile genetic elements (MGEs). Autumn microbiomes were dominated by <em>Lactococcus</em> spp., whereas winter lacked such dominance. ARGs associated with antibiotic inactivation accounted for > 50% in autumn and > 75% in winter, with β-lactam resistance (<em>bla</em><sub>TEM</sub>) predominating in both seasons. Winter resistomes also showed more consistent patterns of BRGs and MRGs, with multibiocide/acid and multimetal resistance prevailing. Integron analysis revealed predominance of class 1 integrons (<em>intI1</em>) commonly associated with <em>Escherichia coli</em>. Plasmid-related contigs were most similar to sequences reported in <em>Acinetobacter baumannii</em> and <em>E. coli</em>, while plasmid signatures related to <em>Lactococcus lactis</em> were also detected in autumn. Crucially, the network analysis revealed a seasonal restructuring of the airborne resistome. Autumn networks displayed fragmented structure, showing antagonism between <em>Lactococcus</em> and <em>Escherichia</em>, whereas winter networks coalesced into a densely interconnected superhub that could facilitate horizontal gene transfer and co-selection of resistance determinants. These findings suggest that prolonged air pollution and seasonality jointly shape airborne resistomes, reinforcing the need for integrated environmental and AMR surveillance in highly polluted urban areas.","PeriodicalId":308,"journal":{"name":"Environment International","volume":"57 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146110886","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}
Cobalt is a critical raw material for consumer electronic products such as electric vehicles and mobile communication devices. Currently, its recovery rate remains relatively low, resulting in a large amount of waste cobalt entering soil and groundwater environments, which poses a potential threat to human health. Previous studies have mostly focused on the effects of acute cobalt exposure. However, the in vivo metabolic mechanism of long-term low-dose cobalt exposure remains unclear, and the long-term toxic effects of cobalt on the heart await further investigation. Based on the existing model framework, this study constructed a cobalt Physiologically Based Pharmacokinetic (PBPK) model incorporating a heart compartment, filling the research gap in this field. Meanwhile, the study calibrated the parameters of the PBPK model by integrating the specific exposure scenarios and dietary exposure characteristics of the Chinese population, and conducted model evaluation and evaluation using epidemiological data of the Chinese population. With the help of Monte Carlo simulation (MCS) technology, this study conducted an in-depth analysis of the inter-individual exposure and metabolic characteristics. The results showed that the deviation between the cobalt concentrations in blood, urine, liver, kidneys, and heart of the Chinese population predicted by the model and the measured values was basically controlled within a 2-fold range. The cobalt PBPK model constructed in this study provides a key tool for the accurate risk assessment and practical application of cobalt exposure in the Chinese population, and also offers a referable research paradigm for accurate risk assessment under the specific characteristics of different ethnic groups.
钴是电动汽车和移动通信设备等消费电子产品的关键原材料。目前，其回收率仍然较低，导致大量废钴进入土壤和地下水环境，对人类健康构成潜在威胁。以前的研究主要集中在急性钴暴露的影响上。然而，长期低剂量钴暴露的体内代谢机制尚不清楚，钴对心脏的长期毒性作用有待进一步研究。本研究在现有模型框架的基础上，构建了含心脏隔室的钴生理药代动力学（PBPK）模型，填补了该领域的研究空白。同时，结合中国人群的具体暴露情景和饮食暴露特征，对PBPK模型参数进行校准，并利用中国人群的流行病学数据进行模型评价和评价。本研究借助蒙特卡罗模拟（Monte Carlo simulation， MCS）技术，对个体间暴露和代谢特征进行了深入分析。结果表明，模型预测的中国人群血、尿、肝、肾、心钴浓度与实测值的偏差基本控制在2倍范围内。本研究构建的钴PBPK模型为中国人群钴暴露的准确风险评估和实际应用提供了关键工具，也为不同族群具体特征下的准确风险评估提供了可借鉴的研究范式。
{"title":"Development of a physiologically based pharmacokinetic (PBPK) model for cobalt in the Chinese population based on population exposure data","authors":"Xingyu Zhan, Wen Gu, Miaoying Shi, Chenglei Qi, Fuchang Deng, Xu Zhang, Guoqing Xiong, Jing Yang, Yican Wang, Mengyao Wang, Jiajun Xiao, Song Tang, Yufei Dai","doi":"10.1016/j.envint.2026.110132","DOIUrl":"https://doi.org/10.1016/j.envint.2026.110132","url":null,"abstract":"Cobalt is a critical raw material for consumer electronic products such as electric vehicles and mobile communication devices. Currently, its recovery rate remains relatively low, resulting in a large amount of waste cobalt entering soil and groundwater environments, which poses a potential threat to human health. Previous studies have mostly focused on the effects of acute cobalt exposure. However, the in vivo metabolic mechanism of long-term low-dose cobalt exposure remains unclear, and the long-term toxic effects of cobalt on the heart await further investigation. Based on the existing model framework, this study constructed a cobalt Physiologically Based Pharmacokinetic (PBPK) model incorporating a heart compartment, filling the research gap in this field. Meanwhile, the study calibrated the parameters of the PBPK model by integrating the specific exposure scenarios and dietary exposure characteristics of the Chinese population, and conducted model evaluation and evaluation using epidemiological data of the Chinese population. With the help of Monte Carlo simulation (MCS) technology, this study conducted an in-depth analysis of the inter-individual exposure and metabolic characteristics. The results showed that the deviation between the cobalt concentrations in blood, urine, liver, kidneys, and heart of the Chinese population predicted by the model and the measured values was basically controlled within a 2-fold range. The cobalt PBPK model constructed in this study provides a key tool for the accurate risk assessment and practical application of cobalt exposure in the Chinese population, and also offers a referable research paradigm for accurate risk assessment under the specific characteristics of different ethnic groups.","PeriodicalId":308,"journal":{"name":"Environment International","volume":"1 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146115995","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}
Pub Date : 2026-02-04DOI: 10.1016/j.envint.2026.110117
D. Sarigiannis, O. Anesti, N. Papaioannou, A. Karakoltzidis, S. Karakitsios
{"title":"Computational standards and tools for exposome-wide association studies linking the human exposome with health outcomes","authors":"D. Sarigiannis, O. Anesti, N. Papaioannou, A. Karakoltzidis, S. Karakitsios","doi":"10.1016/j.envint.2026.110117","DOIUrl":"https://doi.org/10.1016/j.envint.2026.110117","url":null,"abstract":"","PeriodicalId":308,"journal":{"name":"Environment International","volume":"91 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146110895","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}
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