Particulate air pollution, systemic oxidative stress, inflammation, and atherosclerosis

Abstract

Air pollution has been associated with significant adverse health effects leading to increased overall morbidity and mortality of worldwide significance. Epidemiological studies have shown that the largest portion of air pollution-related mortality is due to cardiovascular diseases, predominantly those of ischemic nature. Human studies suggest an association with atherosclerosis and increasing experimental animal data support that this association is likely to be causal. While both gasses and particles have been linked to detrimental health effects, more evidence implicates the particulate matter (PM) components as major responsible for a large portion of the proatherogenic effects. Multiple experimental approaches have revealed the ability of PM components to trigger and/or enhance free radical reactions in cells and tissues, both ex vivo as well as in vivo. It appears that exposure to PM leads to the development of systemic prooxidant and proinflammatory effects that may be of great importance in the development of atherosclerotic lesions. This article reviews the epidemiological studies, experimental animal, and cellular data that support the association of air pollutants, especially the particulate components, with systemic oxidative stress, inflammation, and atherosclerosis. It also reviews the use of transcriptomic studies to elucidate molecular pathways of importance in those systemic effects.

Controlled Exposure of Healthy Young Volunteers to Ozone Causes Cardiovascular Effects

“…PM air pollution has recently been reported to be able to oxidize cholesterol, presumably by translocation of particles from the lung into the circulatory system. 43 A second proposed mechanism has been the spillover of pollutantinduced mediators from the lung into the blood, which could interact with vascular or cardiac cells. Ozone is known to cause robust increases in a number of pulmonary markers, including proinflammatory cytokines, eicosanoids, tPA, and fibrinogen.…”

Using Machine Learning to Estimate Global PM2.5 for Environmental Health Studies

“…In recent years, researchers are finding it worthwhile to investigate a link of PM 2.5 exposure with adverse birth outcomes, 21,22 epigenetic alteration, [23][24][25][26][27][28][29][30][31][32][33][34][35][36] infant mortality, [37][38][39][40][41][42] athero sclerosis, [43][44][45] stroke, 46-50 rheumatic autoimmune diseases, 51,52 central nervous system disorders, [53][54][55][56][57] and diabetes. [58][59][60] Since many of these health conditions are interlinked, comprehensive studies are required to better understand the impact of PM 2.5 .…”

Particulate Matter and Cardiovascular Health Effects

“…These lipids are derived from plasma low-density lipoprotein (LDL) particles that travel into the arterial wall and get trapped in the subendothelial space where they can be oxidatively modified (Steinberg 1997;Araujo, Barajas et al 2008). Several studies using different PM size fractions (PM 10 , PM 2.5 , UFP) to expose different animal models (apoE -/-mice, LDL-R -/-mice and hyperlipidemic rabbits) via different modes of exposure (inhalation of CAPs, oropharyngeal/intratracheal instillation) converge to demonstrate that PM exposure leads to enhanced atherosclerotic lesions or plaques with altered composition, suggesting that the associations encountered in epidemiological studies are very likely to be causal (Araujo 2011a). …”