Role of oxidative stress in cardiovascular disease outcomes following exposure to ambient air pollution

Abstract

Exposure to ambient air pollution is associated with adverse cardiovascular outcomes. These are manifested through several, likely overlapping, pathways including at the functional level, endothelial dysfunction, atherosclerosis, pro-coagulation and alterations in autonomic nervous system balance and blood pressure. At numerous points within each of these pathways, there is potential for cellular oxidative imbalances to occur. The current review examines epidemiological, occupational and controlled exposure studies and research employing healthy and diseased animal models, isolated organs and cell cultures in assessing the importance of the pro-oxidant potential of air pollution in the development of cardiovascular disease outcomes. The collective body of data provides evidence that oxidative stress (OS) is not only central to eliciting specific cardiac endpoints, but is also implicated in modulating the risk of succumbing to cardiovascular disease, sensitivity to ischemia/reperfusion injury and the onset and progression of metabolic disease following ambient pollution exposure. To add to this large research effort conducted to date, further work is required to provide greater insight into areas such as (a) whether an oxidative imbalance triggers and/or worsens the effect and/or is representative of the consequence of disease progression, (b) OS pathways and cardiac outcomes caused by individual pollutants within air pollution mixtures, or as a consequence of inter-pollutant interactions and (c) potential protection provided by nutritional supplements and/or pharmacological agents with antioxidant properties, in susceptible populations residing in polluted urban cities.

Vanadium Derivative Exposure Promotes Functional Alterations of VSMCs and Consequent Atherosclerosis via ROS/p38/NF-κB-Mediated IL-6 Production

“…Although the causes of vascular diseases are complex, it is being recognized that environmental factors such as PM can play a significant role [6,33]. Metals in PM are considered to contribute to the particle's toxic effects.…”

“…Metals in PM are considered to contribute to the particle's toxic effects. Numerous epidemiological studies link PM metal exposure to an increased risk of vascular diseases and cardiovascular mortality [5,6]. Vanadium is classified as a group 5 transition metal and is a redox-sensitive element.…”

“…The main underlying cause of cardiovascular diseases is atherosclerosis, which is recognized as a chronic inflammatory disease [4]. Evidence has indicated that exposure to PM air pollution elicits numerous pathological and biological responses, including systemic inflammation and oxidants, which increases the relative risk of cardiovascular mortality [2,[5][6][7]. Although the toxic effects of PM on cardiovascular disease are usually assessed by its particle mass, there is increasing evidence that the chemical composition and size/morphology of PM may be a major contributor to its pathotoxicity toward the cardiovascular system [6,8].…”

Development of a chromatographic method to study oxidative potential of airborne particulate matter

“…, ROO . , and non-radical species such as O3 and H2O2 in the ELF 20 (Kelly and Fussell, 2017;Sies et al, 2017). Although quinones and TMs are widely recognized as being redox-active, other redox-active chemicals, such as those in humic-like substances, are also anticipated to pose OP (Charrier and Anastasio, 2012;Verma et al, 2015;Dou et al, 2015;Gonzalez et al, 2017).…”

Snow scavenging and phase partitioning of nitrated and oxygenated aromatic hydrocarbons in polluted and remote environments in central Europe and the European Arctic

“…Many N/OPAHs are suggested to be more mutagenic than their parent species and are also classified as possible carcinogens (Finlayson-Pitts and Pitts, 2000;Lammel, 2015). Moreover, quinones, a prominent sub-class of OPAHs, are precursors of environmentally persistent free radicals (Borrowman et al, 2016) and reactive oxygen species (Chung et al, 2006;Charrier et al, 2014), inducing oxidative stress and inflammatory reactions in organisms, which may lead to cellular damage, respiratory and 20 cardiovascular disease (Lodovici and Bigagli, 2011;Møller et al, 2014;Kelly and Fussell, 2017).…”