Special Report For reprint orders, please contact: reprints@futuremedicine.com The role of air pollution on ST-elevation myocardial infarction: a narrative mini review Mohammad Amin Shahrbaf ‡,1 , Mohammad Parsa Mahjoob ‡,1 , Isa Khaheshi * ,1,2 , Mohammad Ali Akbarzadeh 1 , Elham Barkhordari 1 , Mohammadreza Naderian 3 & Farbod Zahed Tajrishi 4 1 Cardiovascular Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran 2 Modarres Hospital, Kaj square, Sa’adat Abad Ave, Tehran, Iran, 1998734383 3 Non-Communicable Diseases Research Center, Endocrinology & Metabolism Population Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran 4 Faculty of Medicine, Babol University of Medical Sciences, Babol, Iran *Author for correspondence: Tel.: + 98 212 208 3106; isa.khaheshi@gmail.com ‡ Authors contributed equally ST-elevation myocardial infarction (STEMI) is one of the potential causes of death worldwide. In spite of substantial advances in its diagnosis and treatment, STEMI is still considered as a major public health dilemma in developed and particularly developing countries. One of the triggering factors of STEMI is sup- posed to be air pollutants like gaseous pollutants including, sulfur dioxide, nitric dioxide, carbon monox- ide, ozone and particulate matters (PM) including, PM under 2.5 μm (PM 2.5 ) and PM under 10 μm (PM 10 ). Air pollution can trigger STEMI with various mechanisms such as increasing infammatory factors and changing the heart rate or blood viscosity. In this article, we aimed to explore research in the feld and discuss the relationship between air pollution and STEMI. First draft submitted: 20 August 2017; Accepted for publication: 23 May 2018; Published online: 22 June 2018 Keywords: air pollution • coronary artery disease • myocardial infarction • ST-elevation myocardial infarction Myocardial infarction (MI) is one of the most considerable cardiovascular problems with no social or geographical limitations [1–3]. Over the recent years, some studies have indicated that mortality and hospitalization due to MI are associated with air pollution exposure [4,5]. Ambient air pollution consists of particulate matter (PM) and gaseous pollutants such as sulfur dioxide (SO 2 ), carbon monoxide (CO), nitric dioxide (NO 2 ) and ozone (O 3 ). PM is categorized into two groups: PM 2.5 particles with a diameter of less than 2.5 μm and PM 10 particles having a diameter of less than 10 μm. PM 2.5 and NO 2 generally result from fossil fuel combustion and the transportation system, whereas PM 10 can be produced from natural processes [6]. PM size seems to be having a relationship with cardiovascular morbidity and mortality [7,8]. Previous studies have reported raised blood pressure and decreased heart rate variability during highly polluted periods [9]. These effects are in concurrence with other reports on cardiovascular effects of urban air pollution exposure [10–12]. Today, WHO reports air pollution as a prominent cause of avoidable death [13], which is responsible for reducing life expectancy to approximately 6 months per 10 μg/m 3 increment of PM 10 [14]. In addition to pulmonary and carcinogenic effects of air pollution, exposure to it has been associated with an increased risk of cardiovascular events and death [15]. A recent meta-analysis has demonstrated that a 10 μg/m 3 increase in PM 10 increased coronary events by 12% [16]. A similar increase in acute coronary syndrome (ACS) was observed with 5 μg/m 3 increases in PM 2.5 , suggesting that fine particulate matter has even more obvious cardiovascular toxicity [16]. In addition to air particles, the role of gaseous air pollutants remains controversial, with an inconsistent relationship found between MI and exposure to O 3 and NO 2 [17,18]. Future Cardiol. (Epub ahead of print) ISSN 1479-6678 10.2217/fca-2017-0078 C  2018 Future Medicine Ltd