PM2.5 and cardiovascular Diseases

   Cardiovascular Diseases

Epidemiological studies have shown a clear association between PM2.5 and cardiovascular diseases, including arrhythmia [123],

 cardiac arrest [124], coronary artery disease [125], heart failure [126,127], venous thromboembolism [128], and cerebrovascular disease [129] 

Acute exposure has been linked to such cardiovascular diseases. Individuals presenting with myocardial infarction were more like to have been in traffic 1–2 h prior [130].

 Although it is difficult to control for confounding variables such as noise and stress, correcting for activity intensity had no effect on the connection. The confounding relationship between pollution and cardiovascular health provides a prediction of cardiovascular health, noises, such as railway and air traffic, are highly connected with cardiovascular health [131]. 

However, with respect to considering the health effects of PM2.5, the confounding variables are not included to determine the PM2.5 effects of cardiovascular diseases.

 Subsequent investigations have further corroborated this link, which is independent of the mode of transportation used [132]. 

Epidemiological studies have associated air pollution with various end points underpinning cardiovascular conditions. Atherosclerosis in a variety of arterial beds has been linked to urban air pollution [133].

 Although there is some variation, PM exposure is linked to a slight but significant increase in blood pressure (typically 5 mmHg for an interquartile increase due to PM2.5) [134]. 

The constriction or reduced vasodilation of resistance arteries, which occurs after exposure to PM, elevates blood pressure. Although not all studies have identified significant connections, exposure to PM2.5 and traffic (e.g., distance from major road to residential address) has been related to increased arterial stiffness [135,136,137].

 Oxidative stress is the primary hierarchical response to PM exposure in humans, followed by other variables. Toll-like receptors (TLR2/TLR4) and nucleotide binding receptors are involved in this response and may be directly or indirectly activated by secondary mediators, including ROS [138,139,140]. 

The induction of ROS may lead to the activation of MAPK pathways, NF-κb, and AP1, which increases the synthesis of inflammatory proteins and brings about alterations in membrane permeability and mitochondrial dysfunction [141,142].

 Inflammatory markers induced by PM2.5 directly act on the heart and induce cardiac tissue remodeling and function alteration, leading to the development of cardiac diseases. Current evidence suggests that translocated PM2.5 causes both systemic inflammation and sympathetic activation in the cardiovascular system. PM2.5 causes systemic inflammation and elevates catecholamines, leading to an acute or chronic phase response of hypercoagulable state (suppression of fibrinolysis and activation of coagulation), vasoconstriction, increase in blood pressure, endothelial dysfunction, cardiac electrical changes, imbalance of cardiac ANS [143].

 Sympathetic activation increases catecholamine production, leading to endothelial dysfunction, increase in heart rate, and promotes vasoconstriction and hypertension [144]. The combined effects of systemic inflammation and sympathetic activation on their molecular targets lead to ischemic or thrombotic events, cardiac arrhythmia, and heart failure [145].

 The biological pathways whereby PM2.5 promotes cardiovascular impairments are illustrated (Figure 3). The effects of PM2.5 exposure on catecholamine levels show that PM2.5 exposure is a major disruptor of the cardiac autonomic nervous system (ANS). Little is known about how PM2.5 exposure affects the cardiovascular system, thus further study is needed to discover the negative health consequences linked with PM2.5 exposure [145]

.Changes in inflammatory pathways and ER stress have been identified as the key mechanisms by which PM2.5 promotes IR and T2DM and activates their pathophysiological responses [143,144,145]. 

Modulation of visceral adipose inflammation, hepatic lipid metabolism, glucose utilization in skeletal muscle, and CC-chemokine receptor 2-dependent pathways were discovered to play a significant role in PM2.5-mediated IR. Furthermore, PM2.5 has been shown to activate unfolded protein response (UPR), an intracellular ER stress signal that governs cell metabolism and survival in vivo, by phosphorylating inositol-requiring enzyme 1 alpha in hepatic cells [144]. 

Additionally, UPR or UPR-mediated ER stress has been linked to inflammatory pathways and has been shown to contribute to the generation of inflammatory mediators. Inflammatory mediators might activate or spread intracellular UPR [145].

 As a result of the combination between inflammation

 and ER stress, a positive feedback loop may form, amplifying the effects of PM2.5 on DM.

Ref

Int J Environ Res Public Health. 2022 Jun 19;19(12):7511. doi: 10.3390/ijerph19127511

Recent Insights into Particulate Matter (PM2.5)-Mediated Toxicity in Humans: An Overview

Prakash Thangavel 1, Duckshin Park 2,*, Young-Chul Lee 1,3,*

Editor: Paul B Tchounwou