Rassegna bibliografica

Particle and Fibre Toxicology. Vol. 11, Iss. 1, 3, 6, January 2014

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


Riassunto

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 μg/m3 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.

Keywords

Air pollution, Myocardial infarction; Acute coronary syndrome; Epidemiology

Articoli correlati che potrebbero interessarti

Platelet activation independent of pulmonary inflammation contributes to diesel exhaust particulate-induced promotion of arterial thrombosis

Particle and Fibre Toxicology. Vol. 13, Iss. 6 January 2016

Acute exposure to wood smoke from incomplete combustion - indications of cytotoxicity

Particle and Fibre Toxicology. Vol. 12, Iss. 33,34 October 2015

Air Pollution Impact on Pregnancy Outcomes in Como, Italy

Journal of Occupational and Environmetal Medicine. Vol. 58, Iss. 1, January 2016