Effects of particulate matter on atherosclerosis: a link via high-density lipoprotein (HDL) functionality?

Abstract

Background: Exposure to air pollution has been associated with adverse effects on human health, and ultimately increased morbidity and mortality. This is predominantly due to hazardous effects on the cardiovascular system. Exposure to particulate matter (PM) is considered to be responsible for the most severe effects. Main body: Here we summarize current knowledge from existing epidemiological, clinical and animal studies on the influence of PM exposure on high-density lipoprotein (HDL) functionality and the potential initiation and progression of atherosclerosis. We highlight experimental studies that bring support to the causality and point to possible mechanistic links. Recent studies indicate that the functional properties of HDL are more important than the levels per se. Fine (PM 2.5-0.1) and ultrafine (UFP) PM are composed of chemicals as well as biological elements that are redox-active and may trigger pro-inflammatory responses. Experimental studies indicate that these properties and responses may promote HDL dysfunction via oxidative pathways. By affecting protein and lipid components of the HDL particle, its anti-atherosclerotic characteristics including cholesterol efflux capacity, as well as other anti-oxidative and anti-inflammatory features might be impaired. Conclusion: Current literature suggests that PM promotes HDL dysfunction via oxidative pathways. However, as relatively few studies so far have evaluated the impact of particulate air pollution on HDL functionality, more human epidemiological as well as experimental studies are needed to strengthen any possible causal relationship and determine any relevance to atherosclerosis.

Air Pollution Exposure Duration and Its Correlation with Triglyceride, HDL, and Atherogenic Index in Online Motorcycle Drivers

“…7 Another study conducted by Holme et al, a case study of the relationship between PM and HDL exposure, showed that exposure of fine particulate matter (PM2,5) and Ultrafine particulate matter (PM 0.1) caused a decrease in HDL levels through oxidative processes. 14 Research conducted by Fan et al, where the atherogenic index value of 112 samples compared to the total carbon, organic carbon, and elemental carbon components at PM2.5 showed that the three components of PM2.5 had a significant correlation the increase in atherogenic index value, total carbon. r=0.307, organic carbon r=0.287, elemental carbon r=0.252 (Fan et al, 2014).…”

Gut Metabolite Trimethylamine-N-Oxide in Atherosclerosis: From Mechanism to Therapy

“…TMAO can upregulate scavenger receptors, such as cluster of differentiation 36 (CD36) and scavenger receptor class A type 1 (SR-A1), and promote the formation of foam cells, leading to development and progression of atherosclerosis ( 7 ). As mentioned previously, the TMAO is similar to that of oxidized low density lipoprotein (ox-LDL), which can promote the differentiation of monocytes into macrophages that scavenge ox-LDL and transform into foam cells ( 63 ). TMAO can also promote endoplasmic reticulum stress (ERS) by up-regulating SR-1 receptors, while downregulating ATP-binding cassette transporter A1 in macrophages ( 64 ).…”

The critical role of endothelial function in fine particulate matter-induced atherosclerosis

“…PM 2.5 induces oxidative stress, increasing the apoptosis of foam cells via the mitochondrial apoptosis pathway [52]. PM 2.5 impairs HDL functions such as HDL-mediated cholesterol efflux, thus facilitating foam cell formation and accumulation [53]. Apoptotic cells are not quickly and efficiently engulfed and decomposed by phagocytes, resulting in secondary necrosis and the release of a large amount of pro-inflammatory cytokines and thus contributing to the development of the necrotic core [54].…”

“…Epidemiological evidence has shown that exposure to PM 2.5 reduces the anti-inflammatory and antioxidant capacity of high-density lipoprotein (HDL), and decreases the expression of antioxidant markers such as glutathione peroxidase (GSH) and superoxide dismutase (SOD) [67,129]. A review showed that particulate matter impairs HDL function via oxidative pathways [53]. Importantly, evidence has shown that exercise training enhances HDL functions, including cholesterol efflux capacity and antioxidant capacity, and protects against endothelial dysfunction induced by PM 2.5 [130] [111].…”