Impact of Particulate Air Pollution on Cardiovascular Health
Abstract
Purpose of Review
Air pollution is established as an independent risk factor for cardiovascular diseases (CVDs). Ambient particulate matter (PM), a principal component of air pollutant, has been considered as a main culprit of the adverse effects of air pollution on human health.
Recent Findings
Extensive epidemiological and toxicological studies have demonstrated particulate air pollution is positively associated with the development of CVDs. Short-term PM exposure can trigger acute cardiovascular events while long-term exposure over years augments cardiovascular risk to an even greater extent and can reduce life expectancy by a few years. Inhalation of PM affects heart rate variability, blood pressure, vascular tone, blood coagulability, and the progression of atherosclerosis. The potential molecular mechanisms of PM-caused CVDs include direct toxicity to the cardiovascular system or indirect injury by inducing systemic inflammation and oxidative stress in circulation.
Summary
This review mainly focuses on the acute and chronic effects of ambient PM exposure on the development of cardiovascular diseases and the possible mechanisms for PM-induced increases in cardiovascular morbidity and mortality. Additionally, we summarized some appropriate interventions to attenuate PM air pollution-induced cardiovascular adverse effects, which may promote great benefits to public health.
Keywords
Particulate matter Cardiovascular disease Oxidative stress Inflammation InterventionAbbreviations
- CVDs
Cardiovascular diseases
- PM
Particulate matter
- PM10
PM with an aerodynamic diameter less than 10 μm
- PM2.5–10
PM with an aerodynamic diameter 2.5–10 μm
- PM2.5
PM with an aerodynamic diameter less than 2.5 μm
- UFPs/PM0.1
PM with an aerodynamic diameter less than 0.1 μm
- BC
Black carbon
- DEP
Diesel exhaust particles
- HRV
Heart rate variability
- CHF
Congestive heart failure
- CHD
Coronary heart disease
- RRs
Relative risk ratios
- HRs
Hazard ratios
- IL
Interleukin
- TNF-α
Tumor necrosis factor-α
- GM-CSF
Granulocyte macrophage colony-stimulating factor
- CRP
C-reactive protein
- ROS
Reactive oxygen species
- t-PA
Tissue plasminogen activator
- PAI-1
Plasminogen activator inhibitor
- FMD
Flow-mediated dilation
- PUFAs
Polyunsaturated fatty acids
- GSTM1
Glutathione S-transferase M1
Notes
Compliance with Ethical Standards
Conflict of Interest
The authors declare no conflicts of interest relevant to this manuscript.
Human and Animal Rights and Informed Consent
This article does not contain any studies with human or animal subjects performed by any of the authors.
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