Objective In recent decades,China has implemented a series of policies to address air pollution.We aimed to assess the health effects of these policies on stroke burden attributable to ambient fine particulate matter(...Objective In recent decades,China has implemented a series of policies to address air pollution.We aimed to assess the health effects of these policies on stroke burden attributable to ambient fine particulate matter(PM_(2.5)).Methods Joinpoint regression was applied to explore the temporal tendency of stroke burden based on data from the Global Burden of Disease 2019 study.Results The age-standardized rates of disability-adjusted life year(DALY)for stroke attributable to ambient PM2.5 in China,increased dramatically during 1990-2012,subsequently decreased at an annual percentage change(APC)of-1.98[95% confidence interval(CI):-2.26,-1.71]during 2012-2019.For ischemic stroke(IS),the age-standardized DALY rates doubled from 1990 to 2014,and decreased at an APC of-0.83(95%CI:-1.33,-0.33)during 2014-2019.Intracerebral hemorrhage(ICH)showed a substantial increase in age-standardized DALY rates from 1990 to 2003,followed by declining trends,with APCs of-1.46(95%CI:-2.74,-0.16)during 2003-2007 and-3.33(95%CI:-3.61,-3.06)during 2011-2019,respectively.Conversely,the age-standardized DALY rates for subarachnoid hemorrhage(SAH)generally declined during 1990-2019.Conclusion Our results clarified the dynamic changes of the ambient PM_(2.5)-attributable stroke burden in China during 1990-2019,highlighting the health effects of air quality improvement policies.展开更多
Exposure to fine ambient particulate matter(PM_(2.5)) is known to be associated with cardiovascular disease. To uncover the molecular mechanisms involved in cardiovascular toxicity of PM_(2.5), we investigated alterat...Exposure to fine ambient particulate matter(PM_(2.5)) is known to be associated with cardiovascular disease. To uncover the molecular mechanisms involved in cardiovascular toxicity of PM_(2.5), we investigated alterations in the protein profile of human umbilical vein endothelial cells(HUVECs) treated with PM_(2.5) using two-dimensional electrophoresis in conjunction with mass spectrometry(MS). A total of 31 protein spots were selected as differentially expressed proteins and identified by matrix-assisted laser desorption/ionization-time of flight(MALDI-TOF) MS. The results demonstrated that DNA damage and cell apoptosis are important factors contributing to PM_(2.5)-mediated toxicity in HUVECs. It is further proposed that PM_(2.5) can inhibit superoxide dismutase(SOD) activity and increase reactive oxygen species(ROS) and malonaldehyde(MDA) production in a concentration-dependent manner. Induction of apoptosis and DNA damage through oxidative stress pathways may be one of the key toxicological events occurring in HUVECs under PM_(2.5) stress. These results indicated that the toxic mechanisms of PM_(2.5) on cardiovascular disease are related to endothelial dysfunction.展开更多
基金supported by National Key Research and Development Program of China(2018YFE0115300,2022YFC3600800,2017YFC0211706)Chinese Academy of Medical Sciences(CAMS)Innovation Fund for Medical Sciences(2021-I2M-1-010)+3 种基金National Natural Science Foundation of China(82073658,82070473)National High Level Hospital Clinical Research Funding(2022-GSP-GG-1,2022-GSP-GG-2)Research Unit of Prospective Cohort of Cardiovascular Diseases and Cancers,CAMS(2019RU038)National Clinical Research Center for Cardiovascular Diseases,Fuwai Hospital,CAMS(NCRC2020006)。
文摘Objective In recent decades,China has implemented a series of policies to address air pollution.We aimed to assess the health effects of these policies on stroke burden attributable to ambient fine particulate matter(PM_(2.5)).Methods Joinpoint regression was applied to explore the temporal tendency of stroke burden based on data from the Global Burden of Disease 2019 study.Results The age-standardized rates of disability-adjusted life year(DALY)for stroke attributable to ambient PM2.5 in China,increased dramatically during 1990-2012,subsequently decreased at an annual percentage change(APC)of-1.98[95% confidence interval(CI):-2.26,-1.71]during 2012-2019.For ischemic stroke(IS),the age-standardized DALY rates doubled from 1990 to 2014,and decreased at an APC of-0.83(95%CI:-1.33,-0.33)during 2014-2019.Intracerebral hemorrhage(ICH)showed a substantial increase in age-standardized DALY rates from 1990 to 2003,followed by declining trends,with APCs of-1.46(95%CI:-2.74,-0.16)during 2003-2007 and-3.33(95%CI:-3.61,-3.06)during 2011-2019,respectively.Conversely,the age-standardized DALY rates for subarachnoid hemorrhage(SAH)generally declined during 1990-2019.Conclusion Our results clarified the dynamic changes of the ambient PM_(2.5)-attributable stroke burden in China during 1990-2019,highlighting the health effects of air quality improvement policies.
基金Project supported by the Medical and Health Science and Technology Fund of Zhejiang Province(No.2016KYB224)the Scientific Research Fund of Zhejiang Chinese Medicine University(No.2015ZG17),China
文摘Exposure to fine ambient particulate matter(PM_(2.5)) is known to be associated with cardiovascular disease. To uncover the molecular mechanisms involved in cardiovascular toxicity of PM_(2.5), we investigated alterations in the protein profile of human umbilical vein endothelial cells(HUVECs) treated with PM_(2.5) using two-dimensional electrophoresis in conjunction with mass spectrometry(MS). A total of 31 protein spots were selected as differentially expressed proteins and identified by matrix-assisted laser desorption/ionization-time of flight(MALDI-TOF) MS. The results demonstrated that DNA damage and cell apoptosis are important factors contributing to PM_(2.5)-mediated toxicity in HUVECs. It is further proposed that PM_(2.5) can inhibit superoxide dismutase(SOD) activity and increase reactive oxygen species(ROS) and malonaldehyde(MDA) production in a concentration-dependent manner. Induction of apoptosis and DNA damage through oxidative stress pathways may be one of the key toxicological events occurring in HUVECs under PM_(2.5) stress. These results indicated that the toxic mechanisms of PM_(2.5) on cardiovascular disease are related to endothelial dysfunction.
