Particulate Matter Air Pollution: Effects on the Cardiovascular System

Abstract

Air pollution is a complex mixture of gaseous and particulate components, each of which has detrimental effects on human health. While the composition of air pollution varies greatly depending on the source, studies from across the world have consistently shown that air pollution is an important modifiable risk factor for significantly increased morbidity and mortality. Moreover, clinical studies have generally shown a greater impact of particulate matter (PM) air pollution on health than the gaseous components. PM has wide-ranging deleterious effects on human health, particularly on the cardiovascular system. Both acute and chronic exposure to PM air pollution is associated with increased risk of death from cardiovascular diseases including ischemic heart disease, heart failure, and ischemic/thrombotic stroke. Particulate matter has also been shown to be an important endocrine disrupter, contributing to the development of metabolic diseases such as obesity and diabetes mellitus, which themselves are risk factors for cardiovascular disease. While the epidemiological evidence for the deleterious effects of PM air pollution on health is increasingly accepted, newer studies are shedding light on the mechanisms by which PM exerts its toxic effects. A greater understanding of how PM exerts toxic effects on human health is required in order to prevent and minimize the deleterious health effects of this ubiquitous environmental hazard. Air pollution is a growing public health problem and mortality due to air pollution is expected to double by 2050. Here, we review the epidemiological evidence for the cardiovascular effects of PM exposure and discuss current understanding about the biological mechanisms, by which PM exerts toxic effects on cardiovascular system to induce cardiovascular disease.

Adverse organogenesis and predisposed long-term metabolic syndrome from prenatal exposure to fine particulate matter

“…Although ultrafine particles contribute only to a small fraction of the total ambient PM mass, they are typically present in high concentrations in the urban atmosphere (3,(29)(30)(31) and have a high probability to deposit in the pulmonary system after inhalation than large particles (32,33). Through blood circulation and endocytosis, ultrafine particles likely enter organs beyond the lungs, such as the reproductive tract, heart, liver, spleen, kidneys, brain, and BAT (34,35). The large surface area, high redox capacity, and ability to form radical species for ultrafine particles likely induce inflammatory effects, cause cellular DNA damage, and interfere with cell metabolism and function (27,36).…”

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

“…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].…”

A community‐engaged approach to investigate cardiovascular‐associated inflammation among American Indian women: A research protocol

“…Although the exact biological pathways underlying the cardiovascular health effects of PM inhalation remain largely debatable, both oxidative stress and systemic inflammation have been purported to play major independent and interactive roles (Hamanaka & Mutlu, ). PM‐induced oxidative stress has been shown to activate the autonomic nervous system, producing a sympathetic response involving adverse physiological changes (e.g., hypertension and impaired heart rate variability [HRV]) which can compromise cardiovascular health (Hamanaka & Mutlu, ; Morishita, Thompson, & Brook, ). Ambient PM exposure has also been shown to be associated with an immunological response involving the release of proinflammatory cytokines, such as CRP, IL‐6 (Du et al, ; Hamanaka & Mutlu, ; Ridker, Hennekens, Buring, & Rifai, ; Shrivastava, Singh, Raizada, & Singh, ), and other types of immune cells (e.g., white blood cells) circulating within the blood (Steenhoff et al, ).…”

“…PM‐induced oxidative stress has been shown to activate the autonomic nervous system, producing a sympathetic response involving adverse physiological changes (e.g., hypertension and impaired heart rate variability [HRV]) which can compromise cardiovascular health (Hamanaka & Mutlu, ; Morishita, Thompson, & Brook, ). Ambient PM exposure has also been shown to be associated with an immunological response involving the release of proinflammatory cytokines, such as CRP, IL‐6 (Du et al, ; Hamanaka & Mutlu, ; Ridker, Hennekens, Buring, & Rifai, ; Shrivastava, Singh, Raizada, & Singh, ), and other types of immune cells (e.g., white blood cells) circulating within the blood (Steenhoff et al, ). Key biological markers, including CRP, Amyloid A, and IL‐6, have been used as nonspecific measures of inflammatory status in epidemiologic studies of CVD in women (Ridker et al, ; Shrivastava et al, ).…”

“…Given the exceedingly high levels of environmental air pollutants in Robeson County, arising largely from agriculture, manufacturing, and the proximity to major interstates (e.g., Interstate 95), a focused effort is needed to uncover how this known-yet invisible-driver of CVD risk, morbidity and mortality is related to cardiovascular-associated inflammation in American Indian women (Hamanaka & Mutlu, 2018;Mannucci, Harari, Martinelli, & Franchini, 2015;Parker, Kravets, & Vaidyanathan, 2018;Robeson County Health Department, 2014). Particulate matter (PM), a composite of solid particles and liquid droplets suspended in air, is classified into two major categories: coarse particles (PM 10-2.5 ) and fine particles (PM 2.5 ; Hamanaka & Mutlu, 2018). PM is closely linked to CVD, as reflected in a range of illness-relevant biomarkers, including C-reactive protein (CRP) and interleukin-6 (IL-6), involved in systemic inflammation (Adams, Greenbaum, Shaikh, van Erp, & Russell, 2015;Du, Xu, Chu, Guo, & Wang, 2016;Pope et al, 2016;Tsai et al, 2012;Wu, Jin, & Carlsten, 2018).…”