大气PM2.5与急性心肌梗死入院人数的时间序列研究
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摘要
目的探讨石家庄市PM2.5与急性心肌梗死入院人数之间的相关性及其时间序列研究。方法收集石家庄地区因患急性心肌梗死疾病在2013年1月1日～2013年12月31日期间于河北医科大学第二医院入院的人数以及石家庄市环保部门对外公布的PM2.5研究性监测数据,分别描述两者的时间分布情况,建立回归分析模型,将PM2.5的滞后性考虑入内,分析PM2.5浓度与急性心肌梗死入院人数之间的相关性。结果入选的急性心肌梗死入院人数共计1229人次,石家庄市环保部门对外公布的PM2.5的研究性监测数据日均浓度为265.78μg/m3,急性心肌梗死的入院人数随着大气PM2.5浓度的提升随之增加,回归模型显示,PM2.5浓度与急性心肌梗死入院人数呈现正相关性,时间序列研究得出,这种正相关性具有一定的滞后性,以滞后3天的效应最为显著。结论石家庄市PM2.5浓度与急性心肌梗死入院人数呈现正相关性,并具有一定的滞后性,以滞后3天的效应最为显著。
Objective Discusses the relevance and the time-series studies between PM2.5 and acute myocardial infarction admissions in Shijiazhuang.Methods The total number of patients with acute myocardial infarction who visit at the Second Hospital of Hebei Medical University in Shijiazhuang from January 1, 2013 to December 31, 2013 are collected,as well as daily PM2.5 research monitoring data of ambient air quality announced by Shijiazhuang environmental protection department, Secondly,time distribution were described respectively, then the variables from the regression model were created, and PM2.5 lag should be into the consideration, Thirdly, analysis the correlation between PM2.5 concentration and the number of admissions for acute myocardial infarction.Results The total numbers of acute myocardial infarction patients are 1229, daily average concentration of PM2.5 research monitoring data of ambient air quality announced by Shijiazhuang environmental protection department is 265.78μg/m3,auto-regression model shows that PM2.5 levels were positively correlated with the incidence of acute myocardial infarction, the incidence increased with the increasing concentration, and there is a certain lag in the correlation, the 3 day lag effect is the most significant.Conclusion PM2.5 concentration in Shijiazhuang were positively correlated with the incidence of acute myocardial infarction, and the incidence increased with the increasing concentration, and appears a certain lag, the 3 day lag effect is the most significant.
Objective Discusses the relevance and the time-series studies between PM2.5 and acute myocardial infarction admissions in Shijiazhuang.Methods The total number of patients with acute myocardial infarction who visit at the Second Hospital of Hebei Medical University in Shijiazhuang from January 1, 2013 to December 31, 2013 are collected,as well as daily PM2.5 research monitoring data of ambient air quality announced by Shijiazhuang environmental protection department, Secondly,time distribution were described respectively, then the variables from the regression model were created, and PM2.5 lag should be into the consideration, Thirdly, analysis the correlation between PM2.5 concentration and the number of admissions for acute myocardial infarction.Results The total numbers of acute myocardial infarction patients are 1229, daily average concentration of PM2.5 research monitoring data of ambient air quality announced by Shijiazhuang environmental protection department is 265.78μg/m3,auto-regression model shows that PM2.5 levels were positively correlated with the incidence of acute myocardial infarction, the incidence increased with the increasing concentration, and there is a certain lag in the correlation, the 3 day lag effect is the most significant.Conclusion PM2.5 concentration in Shijiazhuang were positively correlated with the incidence of acute myocardial infarction, and the incidence increased with the increasing concentration, and appears a certain lag, the 3 day lag effect is the most significant.
引文
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[13]Araujo JA,Barajas B,Kleinman M,et al.Ambient particulate pollutants in the ultrafine range promote early atherosclerosis and systemic oxidative stress[J].Circ Res,2008,102(5):589-596
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[15]Gardner SY,Lehmann JR,Costa DL.Oil fly ash.induced elevation of plasmafibrinogenlevelsin rats[J].ToxicolSci,2000,56:175-180.
[16]Ghio AJ,Hall A,Bassett MA.et a1.Exposure to concentrated ambient particles alters hematologic indices in humans[J].Inhal Toxicot,2003,15:1465-1478.
[17]emmar A,Hoylaerts MF,Hoet PH,et a1.Possible mechanisms of the areciovascular effects of inhaled particles:systemic translocation and prothrombotic effects[J].Toxicol Lett,2004,149:243-253.
[2]Peters A,Dockery DW,Muller JE,et a1.Increased particulate air pollution and the triggering of myocardial infarction[J].Circulation,2001,103:2810-2815.
[3]Peters A,Liu E,Verrier RL,et a1.Air pollution and cardiac ardaythmia[J].Epidemiology,2000,11:1-17.
[4]Sarnet JM,Dominici F,Curriero FC,el a1.Fine particulate air pollution and mortality in 20 US cities.1987-1994[J].N Engl JMed,2000,343:1742-1749
[5]Zanobetti A,Schwartz J,Samoli E,et a1.The temporal pattern of respiratory and heart disease mortality in response to air pollution[J].Environ Health Perspect,2003,111:1188-1193.
[6]杨敏娟,潘小川.北京市大气污染与居民心脑血管疾病死亡的时间序列分析[J].环境与健康杂志,2008,25(4):294-297.
[7]van Eeden SF,Yeung A.Quinlam K,et a1.Systemic response to ambient particulate matter:relevance to chronic obstructive pulmonary disease[J].Proc Am Thorac Soc,2005,2:61-67.
[8]RUCKERL R,GREVEN S,LJUNGMAN P,et a1.Air pollution and inflamation(interleukin-6,C-reactive protein,fibrinogen)in myocardial infarction survivors[J].Environ Health Perspect,2007,115(7):1072-1080.
[9]van Eeden SF,Tan WC,Suwa T,et at.Cytnkines involved in the systemic inflammatory response induced by exposure to particulate matter air pollutions(PMl o)[J].Am J Respir Crit Care Med,2001,164:826-830.
[10]Lindmark E,Diderhohn E.Wallantin L,et ai.Relationship between interleukin 6 and mortality in patients with unstable coronary artery disease:effects ofan early invasive strategy[J].JAMA.200l,286:2107-2113.
[11]Ramage L.Guy K.Expression of C-reactive protein and heat-shock protein-70 in the lung epithelial cell line A549,in response to PMl0exposure[J].Inhal Toxic01.2004,16:447-452.
[12]Bartoli CR,Wellenius GA,Diaz EA,et a1.Mechanisms of inhaled fine particulate air pollution-induced arterial blood pressure changes[J].Environ Health Perspeet,2009,117(3):361-366.
[13]Araujo JA,Barajas B,Kleinman M,et al.Ambient particulate pollutants in the ultrafine range promote early atherosclerosis and systemic oxidative stress[J].Circ Res,2008,102(5):589-596
[14]Weissberg PL.Atherogenesis current understanding of the cause of ather-om.Heart,2000,83(1):247-253.
[15]Gardner SY,Lehmann JR,Costa DL.Oil fly ash.induced elevation of plasmafibrinogenlevelsin rats[J].ToxicolSci,2000,56:175-180.
[16]Ghio AJ,Hall A,Bassett MA.et a1.Exposure to concentrated ambient particles alters hematologic indices in humans[J].Inhal Toxicot,2003,15:1465-1478.
[17]emmar A,Hoylaerts MF,Hoet PH,et a1.Possible mechanisms of the areciovascular effects of inhaled particles:systemic translocation and prothrombotic effects[J].Toxicol Lett,2004,149:243-253.