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

• Main Authors: Siri A. N. Holme, Torben Sigsgaard, Jørn A. Holme, Gitte Juel Holst
• Format: Article
• Language: English
• Published: BMC 2020-08-01
• Series: Particle and Fibre Toxicology
• Subjects: Air pollution; Particulate matter; Cardiovascular disease; Atherosclerosis; Lipoproteins; High-density-lipoprotein
• Online Access: http://link.springer.com/article/10.1186/s12989-020-00367-x

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 (PM2.5–0.1) 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. Graphical abstract