Adverse effects of air pollution-derived fine particulate matter on cardiovascular homeostasis and disease

Abstract

Air pollution is a rapidly growing major health concern around the world. Atmospheric particulate matter that has a diameter of less than 2.5 µm (PM_2.5) refers to an air pollutant composed of particles and chemical compounds that originate from various sources. While epidemiological studies have established the association between PM_2.5 exposure and cardiovascular diseases, the precise cellular and molecular mechanisms by which PM_2.5 promotes cardiovascular complications are yet to be fully elucidated. In this review, we summarize the various sources of PM_2.5, its components, and the concentrations of ambient PM_2.5 in various settings. We discuss the experimental findings to date that evaluate the potential adverse effects of PM_2.5 on cardiovascular homeostasis and function, and the possible therapeutic options that may alleviate PM_2.5-driven cardiovascular damage.

Figure 1.. Preparation and administration of PM_2.5 for in vitro and in vivo studies

Two methods exist for preparation of PM_2.5 for experimental usage. (A) One method is to collect ambient PM_2.5 on ultra-fine filters using a high-volume air sampler; cut the filters adhering PM_2.5 into small pieces; immerse the pieces in sterile distilled water and perform ultrasonic sonication; vacuum-freeze dry the particles to obtain powder from; and then perform chromatography and spectrometry to analyze the components and composition. (B) Alternatively, PM products are available for purchase from the National Institute of Standards and Technology (NIST) Standard Reference Materials (SRM). Products NIST SRM 1650B, 2876, and 2975 fit the definition of PM_2.5 (particulate matter with diameter of less than 2.5 μm).

Figure 2.. Adverse cardiovascular effects of PM_2.5

Plausible pathophysiological mechanisms linking PM_2.5 exposure and cardiovascular disorders, categorized into cardiac and vascular disorders, include pathological fibrosis; cardiac autonomic dysfunction; contractile dysfunction and electrophysiological abnormalities; inflammation; oxidative stress; autophagy; and atherosclerosis, thrombosis, and vascular remodeling.