Environmental health research aims to identify environmental conditions suitable for the healthy living and reproduction of human beings.Through the interdisciplinary research bridging environmental sciences and healt...Environmental health research aims to identify environmental conditions suitable for the healthy living and reproduction of human beings.Through the interdisciplinary research bridging environmental sciences and health/medical sciences,the impacts of physical,chemical,and biological environmental factors on human health are investigated.This includes identifying environmental factors detrimental to human health,evaluating human exposure characteristics to environmental factors,clarifying causal relationships between environmental exposure and health effects,analyzing the underlying biochemical mechanisms,linking environmental factors to the onset and progression of diseases,establishing exposure-response relationships,and determining effect thresholds.Ultimately,the results of environmental health research can serve as a scientific basis for formulating environmental management strategies and guiding prevention and intervention measures at both the public and individual levels.This paper summarizes the recent advances and future perspectives of environmental health research in China,as reported by a group of Chinese scientists who recently attended a workshop in Hainan,China.While it is not intended to provide a comprehensive review of this expansive field,it offers a glimpse into the significant progress made in understanding the health impacts of environmental factors over the past decade.Looking ahead,it is imperative not only to sustain efforts in studying the health effects of traditional environmental pollution,but also to prioritize research on the health impacts of emerging pollutants and climate change.展开更多
Chlorinated polyfluorinated ether sulfonate(F-53B),a chromium-fog depressant widely utilized as an alternative to perfluorooctanesulfonate,can transfer from mother to fetus.Recent research has demonstrated that prenat...Chlorinated polyfluorinated ether sulfonate(F-53B),a chromium-fog depressant widely utilized as an alternative to perfluorooctanesulfonate,can transfer from mother to fetus.Recent research has demonstrated that prenatal exposure to F-53B results in synaptic damage in weaning mice.However,the mechanism underpinning F-53B-triggered synaptic damage during fetal development remains unclear.This study aims to investigate the role of the protein kinase A(PKA)/cAMP response element-binding protein(CREB)pathway,a crucial signaling mechanism known as“synaptic switch”,in the early neurotoxicity of F-53B exposure both in vivo and in vitro.Here,C57BL/6 fetal mice were subjected to exposure to F-53B(0,4,and 40μg/L)from gestation days(GD)0 to 14 to evaluate nerve injury prior to delivery.HT22 neurons exposed to F-53B(0,0.016,0.08,0.4,2,and 10μmol/L)for 24 h were utilized to elucidate the underlying mechanism.Our results demonstrated that F-53B significantly increased the fluorescence intensity of Nestin(a neural stem cell marker)in the fetal brain hippocampus(GD14).Subsequently,we found that F-53B downregulated the expression of synaptic plasticity markers(SYP,GAP43,and BDNF)in the fetal brain and HT22 neurons.Further molecular docking analysis revealed that F-53B fits into the ligand-binding pockets of PKA and CREB1.Results showed that F-53B inhibited the translocation of PKA protein from the cytoplasm to the neuronal nuclei and reduced the levels of PKA,CREB1,p-PKA(α/β/γ)-Thr197,and p-CREB1-S133 in the nucleus.Furthermore,the expression of synaptic plasticity markers altered by F-53B could be reversed by a PKA agonist and was intensified by a PKA antagonist.In summary,our findings suggest that intrauterine exposure to F-53B can weaken the expression of synaptic plasticity markers in the fetal brain,with this neurotoxicity being mediated by the cytoplasmic retention of PKA.展开更多
Evidence from animal experiments has shown that chlorinated polyfluoroalkyl ether sulfonic acids(Cl-PFESAs)can induce vision dysfunction in zebrafish.However,environmental epidemiological evidence supporting this hypo...Evidence from animal experiments has shown that chlorinated polyfluoroalkyl ether sulfonic acids(Cl-PFESAs)can induce vision dysfunction in zebrafish.However,environmental epidemiological evidence supporting this hypothesis remains limited.In our case−control study,samples collected from 270 individuals(135 controls and 135 cases)from the Isomers of C8 Health Project data were analyzed for Cl-PFESAs.We also repeated our analysis on zebrafish to support our findings in humans and to decipher the mechanism underlying Cl-PFESA eye toxicity.The serum levels of per-and polyfluoroalkyl substances(PFASs)and alternatives were significantly higher in the cases than in the controls.Higher serum Cl-PFESA levels were associated with greater odds of eye diseases,and the trend showed a statistically significant dose-dependent relationship.The Shapley additive explanations(SHAP)value indicated that 8:2 Cl-PFESA was the dominant eye disease risk factor among the 13 studied PFASs.In zebrafish experiments,Cl-PFESAs induced eye toxicity in adult zebrafish by oxidative damage and cell apoptosis.Compared to the control group,there was significantly reduced thicknesses of the inner plexiform layer(IPL),outer plexiform layer(OPL),and retinal tissue in the zebrafish exposed to Cl-PFESAs.Our study provides human clinical and animal experimental data,showing that exposure to PFASs increases the odds of the development of eye toxicity.展开更多
基金supported by the Ministry of Science and Technology of China(No.2022YFC3702600).
文摘Environmental health research aims to identify environmental conditions suitable for the healthy living and reproduction of human beings.Through the interdisciplinary research bridging environmental sciences and health/medical sciences,the impacts of physical,chemical,and biological environmental factors on human health are investigated.This includes identifying environmental factors detrimental to human health,evaluating human exposure characteristics to environmental factors,clarifying causal relationships between environmental exposure and health effects,analyzing the underlying biochemical mechanisms,linking environmental factors to the onset and progression of diseases,establishing exposure-response relationships,and determining effect thresholds.Ultimately,the results of environmental health research can serve as a scientific basis for formulating environmental management strategies and guiding prevention and intervention measures at both the public and individual levels.This paper summarizes the recent advances and future perspectives of environmental health research in China,as reported by a group of Chinese scientists who recently attended a workshop in Hainan,China.While it is not intended to provide a comprehensive review of this expansive field,it offers a glimpse into the significant progress made in understanding the health impacts of environmental factors over the past decade.Looking ahead,it is imperative not only to sustain efforts in studying the health effects of traditional environmental pollution,but also to prioritize research on the health impacts of emerging pollutants and climate change.
基金supported by the National Science Foundation of China(No.82073503,82173471,82003409,82103823)the Natural Science Foundation of Guangdong Province(No.2021B1515020015,2021A1515012212)the Guangzhou Science and Technology Plan Project(No.2024A04J6476).
文摘Chlorinated polyfluorinated ether sulfonate(F-53B),a chromium-fog depressant widely utilized as an alternative to perfluorooctanesulfonate,can transfer from mother to fetus.Recent research has demonstrated that prenatal exposure to F-53B results in synaptic damage in weaning mice.However,the mechanism underpinning F-53B-triggered synaptic damage during fetal development remains unclear.This study aims to investigate the role of the protein kinase A(PKA)/cAMP response element-binding protein(CREB)pathway,a crucial signaling mechanism known as“synaptic switch”,in the early neurotoxicity of F-53B exposure both in vivo and in vitro.Here,C57BL/6 fetal mice were subjected to exposure to F-53B(0,4,and 40μg/L)from gestation days(GD)0 to 14 to evaluate nerve injury prior to delivery.HT22 neurons exposed to F-53B(0,0.016,0.08,0.4,2,and 10μmol/L)for 24 h were utilized to elucidate the underlying mechanism.Our results demonstrated that F-53B significantly increased the fluorescence intensity of Nestin(a neural stem cell marker)in the fetal brain hippocampus(GD14).Subsequently,we found that F-53B downregulated the expression of synaptic plasticity markers(SYP,GAP43,and BDNF)in the fetal brain and HT22 neurons.Further molecular docking analysis revealed that F-53B fits into the ligand-binding pockets of PKA and CREB1.Results showed that F-53B inhibited the translocation of PKA protein from the cytoplasm to the neuronal nuclei and reduced the levels of PKA,CREB1,p-PKA(α/β/γ)-Thr197,and p-CREB1-S133 in the nucleus.Furthermore,the expression of synaptic plasticity markers altered by F-53B could be reversed by a PKA agonist and was intensified by a PKA antagonist.In summary,our findings suggest that intrauterine exposure to F-53B can weaken the expression of synaptic plasticity markers in the fetal brain,with this neurotoxicity being mediated by the cytoplasmic retention of PKA.
基金supported by the National Key Research and Development Program of China(2018YFC1004300,2018YFC1004301,and 2018YFE0106900)the National Natural Science Foundation of China(82173471,82003409,82103823,and 82073503)+1 种基金the Natural Science Foundation of Guangdong Province(2021A1515012212,2021A1515011754,2021B1515020015,2020A1515011131,2019A050510017,2018B05052007,and 2017A090905042)the Guangxi Key Research and Development Plan(GUIKEAB18050024).
文摘Evidence from animal experiments has shown that chlorinated polyfluoroalkyl ether sulfonic acids(Cl-PFESAs)can induce vision dysfunction in zebrafish.However,environmental epidemiological evidence supporting this hypothesis remains limited.In our case−control study,samples collected from 270 individuals(135 controls and 135 cases)from the Isomers of C8 Health Project data were analyzed for Cl-PFESAs.We also repeated our analysis on zebrafish to support our findings in humans and to decipher the mechanism underlying Cl-PFESA eye toxicity.The serum levels of per-and polyfluoroalkyl substances(PFASs)and alternatives were significantly higher in the cases than in the controls.Higher serum Cl-PFESA levels were associated with greater odds of eye diseases,and the trend showed a statistically significant dose-dependent relationship.The Shapley additive explanations(SHAP)value indicated that 8:2 Cl-PFESA was the dominant eye disease risk factor among the 13 studied PFASs.In zebrafish experiments,Cl-PFESAs induced eye toxicity in adult zebrafish by oxidative damage and cell apoptosis.Compared to the control group,there was significantly reduced thicknesses of the inner plexiform layer(IPL),outer plexiform layer(OPL),and retinal tissue in the zebrafish exposed to Cl-PFESAs.Our study provides human clinical and animal experimental data,showing that exposure to PFASs increases the odds of the development of eye toxicity.
