Fine particulate matter air pollution and atherosclerosis: Mechanistic insights

Biochim Biophys Acta. 2016 Dec;1860(12):2863-8. doi: 10.1016/j.bbagen.2016.04.030. Epub 2016 May 6.

Abstract

Background: Atherosclerosis is a progressive disease characterized by the accumulation of lipids and fibrous plaque in the arteries. Its etiology is very complicated and its risk factors primarily include genetic defects, smoking, hyperlipidemia, hypertension, lack of exercise, and infection. Recent studies suggest that fine particulate matter (PM2.5) air pollution may also contribute to the development of atherosclerosis.

Scope of review: The present review integrates current experimental evidence with mechanistic pathways whereby PM2.5 exposure can promote the development of atherosclerosis.

Major conclusions: PM2.5-mediated enhancement of atherosclerosis is likely due to its pro-oxidant and pro-inflammatory effects, involving multiple organs, different cell types, and various molecular mediators.

General significance: Studies about the effects of PM2.5inhalation on atherosclerosis may yield a better understanding of the link between air pollution and major cardiovascular diseases, and provide useful information for policy makers to determine acceptable levels of PM2.5 air quality. This article is part of a Special Issue entitled Air Pollution, edited by Wenjun Ding, Andrew J. Ghio and Weidong Wu.

Keywords: Air pollution; Atherosclerosis; Fine particulate matter; Inflammation; Oxidative stress.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Air Pollution / adverse effects*
  • Atherosclerosis / etiology*
  • Atherosclerosis / metabolism
  • Atherosclerosis / pathology
  • Foam Cells / drug effects
  • Foam Cells / metabolism
  • Foam Cells / pathology
  • Humans
  • Hyperlipidemias / physiopathology
  • Hypertension / physiopathology
  • Inhalation Exposure / adverse effects*
  • Lipoproteins, LDL / agonists
  • Lipoproteins, LDL / biosynthesis
  • Oxidative Stress
  • Particle Size
  • Particulate Matter / toxicity*
  • Plaque, Atherosclerotic / etiology*
  • Plaque, Atherosclerotic / metabolism
  • Plaque, Atherosclerotic / pathology
  • Reactive Oxygen Species / agonists*
  • Reactive Oxygen Species / metabolism
  • Risk Factors
  • Sedentary Behavior
  • Smoking / physiopathology

Substances

  • Lipoproteins, LDL
  • Particulate Matter
  • Reactive Oxygen Species
  • oxidized low density lipoprotein