Ambient fine particulate air pollution triggers ST-elevation myocardial infarction, but not non-ST elevation myocardial infarction: a case-crossover study

被引:103
作者
Gardner, Blake [1 ]
Ling, Frederick [1 ]
Hopke, Philip K. [2 ]
Frampton, Mark W. [3 ]
Utell, Mark J. [3 ]
Zareba, Wojciech [1 ]
Cameron, Scott J. [1 ]
Chalupa, David [3 ]
Kane, Cathleen [4 ]
Kulandhaisamy, Suresh [1 ]
Topf, Michael C. [1 ]
Rich, David Q. [4 ]
机构
[1] Univ Rochester, Med Ctr, Dept Med, Div Cardiol, Rochester, NY 14642 USA
[2] Clarkson Univ, Inst Sustainable Environm, Potsdam, NY USA
[3] Univ Rochester, Med Ctr, Dept Med, Div Pulm & Crit Care Med, Rochester, NY 14642 USA
[4] Univ Rochester, Sch Med & Dent, Dept Publ Hlth Sci, Rochester, NY 14627 USA
来源
PARTICLE AND FIBRE TOXICOLOGY | 2014年 / 11卷
关键词
Myocardial infarction; Acute coronary syndrome; Epidemiology; Air pollution; DIESEL-EXHAUST INHALATION; ULTRAFINE PARTICLES; EXPOSURE; TERM; INFLAMMATION; ASSOCIATION; THROMBOSIS; MARKERS; EVENTS; RISK;
D O I
10.1186/1743-8977-11-1
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
Background: We and others have shown that increases in particulate air pollutant (PM) concentrations in the previous hours and days have been associated with increased risks of myocardial infarction, but little is known about the relationships between air pollution and specific subsets of myocardial infarction, such as ST-elevation myocardial infarction (STEMI) and non ST-elevation myocardial infarction (NSTEMI). Methods: Using data from acute coronary syndrome patients with STEMI (n = 338) and NSTEMI (n = 339) and case-crossover methods, we estimated the risk of STEMI and NSTEMI associated with increased ambient fine particle (<2.5 um) concentrations, ultrafine particle (10-100 nm) number concentrations, and accumulation mode particle (100-500 nm) number concentrations in the previous few hours and days. Results: We found a significant 18% increase in the risk of STEMI associated with each 7.1 mu g/m(3) increase in PM2.5 concentration in the previous hour prior to acute coronary syndrome onset, with smaller, non-significantly increased risks associated with increased fine particle concentrations in the previous 3, 12, and 24 hours. We found no pattern with NSTEMI. Estimates of the risk of STEMI associated with interquartile range increases in ultrafine particle and accumulation mode particle number concentrations in the previous 1 to 96 hours were all greater than 1.0, but not statistically significant. Patients with pre-existing hypertension had a significantly greater risk of STEMI associated with increased fine particle concentration in the previous hour than patients without hypertension. Conclusions: Increased fine particle concentrations in the hour prior to acute coronary syndrome onset were associated with an increased risk of STEMI, but not NSTEMI. Patients with pre-existing hypertension and other cardiovascular disease appeared particularly susceptible. Further investigation into mechanisms by which PM can preferentially trigger STEMI over NSTEMI within this rapid time scale is needed.
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