J Korean Med Assoc.  2015 Nov;58(11):1044-1059. 10.5124/jkma.2015.58.11.1044.

Guidelines for the prevention and management of cardiovascular disease associated with fine dust/Asian dust exposure

• Kim IS
• Jang JY
• Kim TH
• Park J
• Shim J
• Kim JB
• Byun YS
• Sung JH
• Yoon YW
• Kim JY
• Cho YJ
• Kim C
• Joung B

• KMID: 2195134
• DOI: http://doi.org/10.5124/jkma.2015.58.11.1044

Abstract

Epidemiological studies have demonstrated an increased risk for cardiovascular events in relation to both short- and long-term exposure to ambient particulate matter (PM). Several plausible mechanistic pathways have been described, including an enhanced propensity for arrhythmias, systemic inflammatory responses, and the chronic promotion of atherosclerosis. On the basis of this review, several new findings were reached, including the following: exposure to PM including PM <2.5 microm in diameter can trigger cardiovascular disease-related mortality; longer-term exposure (e.g., a few years) increases the risk for cardiovascular mortality; reductions in PM levels are associated with decreases in cardiovascular mortality within a period as short as a few years; and many credible pathological mechanisms have been elucidated that lend biological plausibility to these findings. It is the opinion of the writing group that the overall evidence is consistent with a causal relationship between PM exposure and cardiovascular morbidity and mortality. Finally, PM exposure is deemed a modifiable factor that contributes to cardiovascular morbidity and mortality. The purpose of this statement is to develop evidence-based practical guidelines for healthcare professionals and regulatory agencies with a comprehensive review of the literature on air pollution and cardiovascular disease and a specific focus on the clinical implications.

Keyword

Air pollution; Particulate matter; Yellow dust; Cardiovascular diseases

MeSH Terms

Air Pollution
Arrhythmias, Cardiac
Atherosclerosis
Cardiovascular Diseases*
Delivery of Health Care
Dust*
Epidemiologic Studies
Mortality
Particulate Matter
Writing
Dust
Particulate Matter

Figure

• 

  Figure 1 Particle size distribution constitutes particulate matter air pollution [2]. RBC, red blood cell; PM10, particulate matter <10 µm in diameter; PM10-2.5, particulate matter 2.5 to 10 µm in diameter; PM2.5, particulate matter <2.5 µm in diameter; PM0.1, particulate matter <0.1 µm in diameter.

• 

  Figure 2 Three biophysiological pathways related with PM exposure [2]. These pathways shows pathophysiological mechanism of cardio-vascular diseases after PM exposure. Pathway 1: release of pro-inflammatory cytokines or cells originated from bronchioles/alveoli (ex, cytokines, activated immunological cells, or platelets) or vasoactive molecules (ex, histamine). Pathway 2: particular interactions with pulmonary receptors and nervous systems that results systemic disturbances manifested as imbalance of ANS or arrhythmogenic potentials. Pathway 3: transmission of PM, UFP or particles (organic/inorganic compounds) into blood stream and systemic spread. PM, particulate matter; ANS, autonomic nervous system; MPO, myeloperoxidase; PAI, plasminogen activator inhibitor; PSNS, parasympathetic nervous system; SNS, sympathetic nervous system; UFP, ultrafine particles; WBC, white blood cell; IL, interleukin; TNF, tumor necrosis factor; ROS, reactive oxygen species; BP, blood pressure; CRP, C-reactive protein; HRV, heart rate variability; HDL, high-density lipoprotein; PAI, plasminogen activator inhibitor.

• 

  Figure 3 Cohort studies of risks by 10 µg/m3 of PM2.5 or PM10 incremental [2,424748495051525354565758]. PM2.5, particulate matter <2.5 µm in diameter; PM10, particulate matter <10 µm in diameter; CPD, cardio-pulmonary disease; CI, confidence interval; CVD, cardio-vascular disease; IHD, ischemic heart disease; ACS, American Cancer Society; LA, Los Angeles; AHSMOG, Adventist Health Study of Smog; VA, veterans affairs; CA, California; PAARC, pollution atmosphe´rique et affections respiratoires chroniques.

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