Environment & Health最新文献

{"title":"Reassessing Toxicity Claims of Micro- and Nanoplastics in Human Health Research.","authors":"Bing Yan, Guibin Jiang","doi":"10.1021/envhealth.6c00079","DOIUrl":"https://doi.org/10.1021/envhealth.6c00079","url":null,"abstract":"","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 4","pages":"560-562"},"PeriodicalIF":6.3,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13097157/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147782809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synergism between Distribution, Mechanistic and Omics Analyses in Studies on Assessing Environmental Exposure and Human Health Impact.","authors":"K W Michael Siu","doi":"10.1021/envhealth.5c00425","DOIUrl":"10.1021/envhealth.5c00425","url":null,"abstract":"","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 1","pages":"1-3"},"PeriodicalIF":6.3,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12813703/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146011882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic Reprogramming Bridges Environmental Exposure and Tinnitus Severity: Evidence from AI-Driven Serum Multiomics.","authors":"Tingting Qian, Ge Wang, Peifan Li, Nanfeng Zhang, Chongkai Lu, Yongzhen Wu, Xia Gao, Yi-Quan Tang, Huawei Li, Shan Sun","doi":"10.1021/envhealth.5c00512","DOIUrl":"https://doi.org/10.1021/envhealth.5c00512","url":null,"abstract":"<p><p>Tinnitus is a prevalent auditory disorder with poorly understood links between environmental exposure and disease, complicating objective diagnosis and intervention. In a graded observational cohort with documented occupational noise histories, we integrated serum metabolomics, lipidomics, and immunophenotyping with interpretable machine learning. Mediation analysis suggested that a panel of metabolites, including gamma-aminobutyric acid (GABA), fumaric acid, and sphingolipids, accounted for a substantial proportion of the association between noise exposure and tinnitus severity (indirect effect = 92%, <i>p</i> < 0.001). Lipidomic profiling indicated early sphingolipid perturbations, followed by patterns consistent with T helper 1 (Th1)-skewed immune activation and lower circulating GABA, outlining a putative \"Exposure-Metabolism-Immunity\" cascade. A CatBoost predictive model trained on these features stratified tinnitus severity with 84.8% accuracy and a mean absolute error of 0.174. In summary, our findings identify specific biomarker associations that link occupational noise exposure to the metabolic and immune signatures of tinnitus and generate hypotheses implicating GABAergic tone and sphingolipid metabolism as candidate pathways for future mechanistic and interventional studies.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 4","pages":"585-600"},"PeriodicalIF":6.3,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13097159/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147783335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Health Risks of Prenatal and Early-Life Microplastics Exposure: A Comprehensive Review.","authors":"Haopeng Zhang, Xiaomeng Ding, Huijuan Zheng, Qianwen Ma, Ting Zhang","doi":"10.1021/envhealth.5c00388","DOIUrl":"https://doi.org/10.1021/envhealth.5c00388","url":null,"abstract":"<p><p>Microplastics (MPs) and nanoplastics (NPs) are emerging environmental contaminants that have raised increasing concern regarding their potential health effects. During pregnancy and early life, developing organisms are particularly vulnerable due to immature biological barriers and the dynamic nature of organogenesis. This review summarizes current evidence on maternal and early life exposure routes to MPs and NPs, including oral ingestion, inhalation, dermal contact, and transplacental transfer. Laboratory and epidemiological studies have demonstrated that microplastics can cross the placental barrier, potentially impairing placental function, altering fetal growth, and compromising pregnancy outcomes. Experimental data from animal models and in vitro systems suggest that maternal MP exposure may contribute to adverse neonatal development via multiple mechanisms including oxidative stress, inflammation, endocrine disruption, and epigenetic alterations. These toxicological pathways have been implicated in neurodevelopmental abnormalities, reproductive dysfunction, and immune dysregulation, often in a sex-dependent manner. Despite increasing experimental evidence, major knowledge gaps remain regarding human exposure levels, dose-response relationships, and long-term health implications. Future research should focus on improving detection sensitivity, establishing standardized exposure models, and developing targeted risk assessment frameworks to evaluate microplastic-associated health risks during pregnancy and early development.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 4","pages":"567-584"},"PeriodicalIF":6.3,"publicationDate":"2025-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13097170/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147783340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cigarette Smoking-Regulated <i>PRKCE</i> Is Involved in Bladder Cancer Susceptibility through cGMP/PKG-Dependent Glycolysis.","authors":"Yanping Xiao, Jinyue Zhang, Yu Jia, Hui Song, Zhenguang Mao, Fang Gao, Rui Zheng","doi":"10.1021/envhealth.5c00411","DOIUrl":"10.1021/envhealth.5c00411","url":null,"abstract":"<p><p>The mechanism by which cigarette smoking affects bladder cancer susceptibility via glucose metabolism remains unclear. We identified bladder cancer-specific glucose metabolism-related genes (GMGs) using Molecular Signatures Database (MSigDB) and a case-control study (580 cases and 1,101 controls) through genetic association and interaction analyses with cigarette smoking. Among 811 GMGs, we observed that <i>PRKCE</i> rs4953292 G > A was significantly associated with increased bladder cancer risk [odds ratio (OR) = 1.19, 95% confidence interval (CI): 1.03-1.37, <i>P</i> _adj = 1.87 × 10^-2] and exhibited an interaction effect with cigarette smoking (<i>P</i> _interaction < 0.05). Smokers with rs4953292 A allele had higher bladder cancer risk than nonsmokers with G allele (<i>P</i> _trend < 9.09 × 10^-3). We performed functional experiments using 4-aminobiphenyl (4-ABP)-treated bladder cancer cells and found that the rs4953292 A allele combined with 4-ABP decreased <i>PRKCE</i> expression levels in bladder cancer cells, which could upregulate PKG and phosphorylate VASP within the cGMP-PKG signaling pathway, enhance glucose uptake, lactate generation, and extracellular acidification rate (ECAR) to reprogram glycolysis, thus promoting bladder cancer susceptibility. This study elucidates that cigarette smoking-regulated <i>PRKCE</i> facilitates bladder cancer susceptibility by mediating glycolytic reprogramming through activating the cGMP-PKG signaling pathway. The findings provide valuable predictors for bladder cancer susceptibility, aiding in prevention strategies.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 3","pages":"365-378"},"PeriodicalIF":6.3,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13010304/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147515096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pollutant Exposure Shapes Mitochondrial Bioenergetics in a Wild Seabird.","authors":"Guadalupe Lopez-Nava, Lucie Michel, Giacomo Dell'Omo, Petra Quillfeldt, Paco Bustamante, Stefania Casagrande","doi":"10.1021/envhealth.5c00297","DOIUrl":"https://doi.org/10.1021/envhealth.5c00297","url":null,"abstract":"<p><p>Laboratory studies show that mercury (Hg) and per- and polyfluoroalkyl substances (PFAS) can impair mitochondrial bioenergetics, which is a vital process for cellular energy production. However, their effects on wild, free-living organisms remain unexplored. Using red blood cells, we investigated how foraging habits, inferred from stable isotopes, and contaminant exposure were associated with mitochondrial bioenergetics in breeding Scopoli's shearwaters (<i>Calonectris diomedea</i>), a top marine predator in the Mediterranean Sea. We found higher concentrations of Hg, but not of total PFAS, in older individuals and in males compared to females. Our results also indicate dietary pollutant exposure: Hg, but not total PFAS, was higher in birds with a higher trophic position and in those foraging closer to shores. Additionally, higher Hg concentration was linked to higher mitochondrial proton leakage (LEAK), reflecting reduced efficiency to couple oxygen consumption to energy production. In contrast, specific PFAS were negatively associated with LEAK, suggesting a potential impairment in the regulation of mitochondrial membrane potential through proton conductance, a key mechanism protecting cells from oxidative stress. Our study highlights how foraging ecology shapes pollutant exposure and its consequences for mitochondria bioenergetics in an apex predator of conservation interest.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 4","pages":"782-799"},"PeriodicalIF":6.3,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13097166/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147783284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exposure to Nanoplastics Disrupts Neurotransmitter Release in Rat Hippocampal Neurons.","authors":"Ka Hei Ho, Xin Yi Yeo, Chungwon Park, Wing Tung Yung, Sunda Do, Jeongeun Lee, Kwang-Min Kim, Sangyong Jung, Hyokeun Park","doi":"10.1021/envhealth.5c00477","DOIUrl":"https://doi.org/10.1021/envhealth.5c00477","url":null,"abstract":"<p><p>Plastics are used broadly for various applications, and their degradation and fragmentation have led to widespread accumulation of nanoplastics in the environment. Although nanoplastics are ubiquitous and intractable in the environment and in organisms, their potential health impacts remain unclear. Emerging evidence showed that nanoplastics can cross the blood-brain barrier and accumulate in the brain. However, the effects of nanoplastics on neuronal health and functions in the brain are poorly understood. Here, we examined the effects of nanoplastic exposure on neurotransmitter release by measuring FM 4-64 (a lipophilic styryl dye) release from synaptic vesicles during electrical stimulation after exposing rat hippocampal neurons to 1-10 μg/mL of fluorescent polystyrene nanoplastics with an average diameter of 42 nm. We found that nanoplastics accumulated in the presynaptic terminal of hippocampal neurons and reduced stimulation-induced FM 4-64 release in a dose-dependent manner. Furthermore, nanoplastics decreased Ca²⁺ elevation in the presynaptic terminal of hippocampal neurons during electrical stimulation. Our results suggest that accumulated nanoplastics in the brain can impair neuronal functions by disrupting neurotransmitter release and Ca²⁺ dynamics in the presynaptic terminal of neurons, which could eventually lead to neurodegeneration.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 4","pages":"768-781"},"PeriodicalIF":6.3,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13096968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147783287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Coke Oven Emission Exposure Triggers Malignant Transformation of Lung Epithelial Cells by <i>SFTA1P</i>-Dependent Alteration of Acetyl-CoA Metabolism.","authors":"Qiang Ju, Xinmei Li, Zhaoxu Wu, Pimei Zhang, Hongguang Chen, Jing Ji, Wei Gao, Yuxin Zheng, Dianke Yu, Yanjie Zhao","doi":"10.1021/envhealth.5c00524","DOIUrl":"https://doi.org/10.1021/envhealth.5c00524","url":null,"abstract":"<p><p>Exposure to coke oven emissions (COEs) is an important environmental factor in lung cancer. A previous study revealed that 20 μg/mL COE exposure for 120 days could induce malignant transformation of lung epithelial cells. However, the underlying mechanism remains unclear. The epigenetic regulation of long noncoding RNAs (lncRNAs) plays an important role in carcinogenesis. Changes in lncRNA expression during COE-induced malignant transformation were detected, highlighting the importance of gene-environment interactions in cancer. Here, we identified that <i>SFTA1P</i> was downregulated in COE-induced malignant transformation of lung epithelial cells. Interestingly, this reduction was found to have a gradient effect on different stages of cells of COE exposure. Moreover, we found that downregulation of <i>SFTA1P</i> expression in lung cancer was related to patients' poor prognosis. Phenotypic studies have demonstrated that <i>SFTA1P</i> suppressed lung cancer cell proliferation in vitro and in vivo. Further mechanistic studies revealed that <i>SFTA1P</i> directly interacts with ACSS2, an important enzyme responsible for synthesizing acetyl-CoA, leading to abnormal acetyl-CoA metabolism and affecting COE-induced lung carcinogenesis. COE-induced malignant transformed cells or cells with the knockdown of <i>SFTA1P</i> showed significantly increased fatty acid and cholesterol levels, while normal lung epithelial cells or cells with overexpression of <i>SFTA1P</i> showed substantially decreased fatty acid and cholesterol levels. Moreover, transfection of ACSS2 into cells with overexpressing <i>SFTA1P</i> could rescue the <i>SFTA1P-</i>induced cell phenotype. Our findings link <i>SFTA1P-</i>regulated acetyl-CoA metabolism with COE-induced malignant transformation and imply that <i>SFTA1P</i> could be an important biomarker for early intervention and diagnosis of lung cancer.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 4","pages":"754-767"},"PeriodicalIF":6.3,"publicationDate":"2025-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13097155/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147783272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNA Methylation of <i>FAM50B</i>/<i>PTCHD3</i> Mediates the Relationships between Low Blood Lead Exposure and Neurobehavioral Development of 0-3 Aged Infants: A Prospective Birth Cohort Study in Southern China.","authors":"Cong Wan, Huimin Ma, Xiaowen Zeng, Guanghui Dong, Jian Chen, Jing You, Fei Cheng, Yuan Luo, Kevin C Jones, Gan Zhang, Zhiqiang Yu, Ping'an Peng","doi":"10.1021/envhealth.5c00459","DOIUrl":"https://doi.org/10.1021/envhealth.5c00459","url":null,"abstract":"<p><p>Lead, recognized by the World Health Organization as one of the 10 chemicals of major public health concern, ranks as the fourth leading environmental risk factor contributing to the global burden of disease. Nevertheless, the neurodevelopmental consequences of prenatal low-level lead exposure remain inadequately characterized, with limited understanding of its mechanistic underpinnings and a lack of robust biomarkers for susceptibility. In this birth cohort study, we quantified the concentrations of 27 metals along with DNA methylation levels at 12 gene regions in cord blood. Neurodevelopment was assessed longitudinally in infancy using the Ages and Stages Questionnaires (ASQ). Associations between metal exposures and neurodevelopmental outcomes were evaluated via three complementary statistical approaches: mixed-effect models, quantile g-computation, and Bayesian kernel machine regression. Among all metals examined, only lead (mean concentration of 15.3 μg/L) exhibited consistent and statistically significant negative associations with neurodevelopmental performance. A linear dose-response relationship was observed between lead levels and deficits in problem-solving, fine motor, and gross motor skills. Furthermore, we identified four CpG sites within <i>FAM50B</i> and <i>PTCHD3</i> that mediate the effects of lead exposure and demonstrated strong predictive capacity for neurodevelopmental outcomes using a random forest model. Our results provide novel evidence that even low-level prenatal lead exposure adversely affects early neurodevelopment and implicate <i>FAM50B</i>/<i>PTCHD3</i> methylation as both a promising biomarker of lead-related neurodevelopmental risk and a potential target for therapeutic intervention.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 4","pages":"742-753"},"PeriodicalIF":6.3,"publicationDate":"2025-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13097069/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147783319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"How Ambient Pollutants Accelerate Aging: Bridging Epigenetics, Age-Stratified Effects, and Public Health Interventions.","authors":"Ya-Qian Xu, Linghui Cai, Yaowen Nuo, Xiangwei Li","doi":"10.1021/envhealth.5c00542","DOIUrl":"https://doi.org/10.1021/envhealth.5c00542","url":null,"abstract":"","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 4","pages":"563-566"},"PeriodicalIF":6.3,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13096967/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147783308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}