Effects of Particulate Matter on Inflammation and Thrombosis: Past Evidence for Future Prevention

Abstract

Ambient air pollution has become a common problem worldwide. Exposure to pollutant particles causes many health conditions, having a particular impact on pulmonary and cardiovascular disease. Increased understanding of the pathological processes related to these conditions may facilitate the prevention of the adverse impact of air pollution on our physical health. Evidence from in vitro, in vivo, and clinical studies has consistently shown that exposure to particulate matter could induce the inflammatory responses such as IL-6, TNF-α, IL-1β, as well as enhancing the oxidative stress. These result in vascular injury, adhesion molecule release, platelet activation, and thrombin generation, ultimately leading to a prothrombotic state. In this review, evidence on the effects of particulate matter on inflammation, oxidative stress, adhesion molecules, and coagulation pathways in enhancing the risk of thrombosis is comprehensively summarized and discussed. The currently available outcomes of interventional studies at a cellular level and clinical reports are also presented and discussed.

Joint Exposure to Ambient Air Pollutants, Genetic Risk, and Ischemic Stroke: A Prospective Analysis in UK Biobank

“…49 Therefore, it is plausible that similar mechanisms underlie the observed relationships between air pollution and vascular traits. One possible pathway was that exposure to air pollution could lead to oxidative stress, systemic inflammation, and autonomic imbalance, [50][51][52] which further increase endothelial dysfunction and decrease B-type natriuretic peptide, 53,54 and then elevate blood pressure and decrease cardiac output. 55,56 Prolonged or repeated stimulation of these pathways might further precipitate the progression of endothelial dysfunction, atherosclerosis, and diastolic dysfunction, ultimately culminating in thrombosis and elevated risk of stroke.…”

Palliative effects of carnosol on lung‐deposited pollutant particles‐induced thrombogenicity and vascular injury in mice

“… 38 It has been shown that exposure to particulate air pollution impairs vascular homeostasis, and elevates the expression of vascular inflammatory biomarkers, comprising ICAM‐1 and VCAM‐1, and P‐selectin. 38 ICAM‐1, VCAM‐1 and P‐selectin exert a central role in thrombogenicity through the promotion of interactions between WBCs endothelial cells and WBCs platelets in inflammatory reactions. 38 E‐selectin is essential for the primary rolling interaction and ensuing adhesion of WBCs in the inflamed endothelium, in addition to the transmigration of inflammatory cells to areas of inflammation.…”

“… 38 ICAM‐1, VCAM‐1 and P‐selectin exert a central role in thrombogenicity through the promotion of interactions between WBCs endothelial cells and WBCs platelets in inflammatory reactions. 38 E‐selectin is essential for the primary rolling interaction and ensuing adhesion of WBCs in the inflamed endothelium, in addition to the transmigration of inflammatory cells to areas of inflammation. It has reported that exposure to particulate air pollution induces the upregulation of VCAM‐1, ICAM‐1, P‐selectin, and E‐selectin.…”

Exposome in ischaemic heart disease: beyond traditional risk factors

“… 63–66 Oxidative stress and the interplay between interleukin-6 and tissue factor appear to be additional mechanisms in pollution-mediated thrombosis, together with an emerging role for circulating microvesicles and epigenetic changes. 67 , 68 Air pollution enhances the thrombotic response, as shown in an experimental model through intratracheal exposure to diesel exhaust particles, which induced platelet activation within an hour 67 ; and in human, where inhalation of PM increased platelet–leucocyte aggregates. 69–71 The thrombotic response appears to be mediated by platelet activation through direct contact in the lung or translocation of ultrafine PM, as well as through mediators released into the circulation as a result of PM-induced lung inflammation 69 , 70 ( Figure 3 ).…”

“…Epigenetic modifications of the molecular circadian rhythms lead to cardiovascular dysfunction, triggering systemic inflammatory responses, detrimentally affecting the immune system, and increasing superoxide and endothelial NO synthase uncoupling in blood vessels. 55 , 67 , 74 Recent data advance the concept that environmental factors may exert cardiovascular effects via epigenetic alteration of circadian targets. 94 , 95 , 99 , 100 In an important study comparing chronic ambient inhalational air pollution exposure, PM2.5 caused peripheral insulin resistance, circadian rhythm dysfunction, and metabolic and brown adipose tissue (BAT) dysfunction, similar to light at night (however with no additive interaction between PM2.5 and night-time light).…”