Why Physicians Who Treat Hypertension Should Know More About Air Pollution

Abstract

Exposure to ambient levels of particulate matter (PM) air pollution increases the risk of a host of cardiovascular diseases and events. One potential mechanism explaining this association is that acute exposure to PM at high concentrations is capable of raising blood pressure within hours to days. Epidemiologic studies confirm that even commonly encountered levels of airborne pollutants can result in a prohypertensive response in humans. Several biologic pathways may be involved, including autonomic nervous system imbalance and arterial vascular dysfunction/vasoconstriction due to systemic oxidative stress/inflammation triggered by PM inhalation. The clinical importance of this vasopressor response and its relative role in promoting cardiovascular events associated with PM remain unclear. Because air pollution exposure is ubiquitous throughout the world, however, all health care providers and especially those who treat hypertension should be aware of this emerging and important biologic relationship.

Air Pollution and the Development of Posttransplant Chronic Lung Allograft Dysfunction

“…PM 10 contains a sizable proportion of biologic materials such as endotoxin, pollen and fungi as well as ground material and debris, in addition to the particles that comprise PM 2.5 , (37) and is generally regarded as a poor measure of TRAP. Thus, it would be difficult to extrapolate these observations of the health effects of PM 10 exposure to TRAP.…”

Particulate matter, air quality and climate: lessons learned and future needs

“…The strongest effects were observed for cardiovascular mortality (Gehring et al, 2006). PM long-term exposure was also associated with diabetes and cardiovascular and respiratory diseases (Martinelli et al, 2013), including atherosclerosis (Hoffmann et al, 2007), hypertensive episodes (Brook et al, 2007), arrhythmia (Rich et al, 2005) and asthma (Gehring et al, 2010). Kassomenos et al (2011) developed a neural network approach to estimate the significance of PM exposure in hospital admission for cardiovascular and respiratory diseases.…”

Particulate Matter, Hypertension, and the Metabolic Syndrome

“…Furthermore, they showed that ROS generated through this pathway in response to PM -activated RhoA/Rho -kinase (Sun et al, 2008 ). PM 2.5 has previously been shown to regulate ROS generation through an NADPH oxidase -dependent mechanism in a variety of cell types and may represent an important upstream pathway by which PM 2.5 may potentiate effects of AII (Brook, 2007 ;Mills et al, 2007 ;Dvonch et al, 2009 ). Since AII is well known to regulate NADPH oxidases, this may well represent an important upstream pathway by which PM 2.5 exerts additive effects on AII -mediated BP and CV remodeling (Briet et al, 2007 ;Choi et al, 2007 ).…”

“…It has also been hypothesized that changes in ANS balance favoring sympathetic activity (via direct β -receptor activation) and/or the associated alteration in skeletal muscle microvascular nutrientrich blood fl ow may both further impair insulin sensitivity. Reduced nitric oxide bioavailability, vasoconstriction, and endothelial dysfunction have all been associated with air pollution exposure and may be causally related to the development of 374 CHAPTER 18 PARTICULATE MATTER, HYPERTENSION, AND THE METABOLIC SYNDROME insulin resistance (Brook, 2005(Brook, , 2007. Finally, it is possible that soluble PM components may reach skeletal muscle cells and adipocytes via the circulation.…”

“…Short -term elevations in PM < 2.5 μ m in diameter (PM 2.5 ) are associated with an increased risk for acute myocardial infarction (MI), stroke, and heart failure Pope and Dockery, 2006 ;Brook, 2008 ). One important biological mechanism contributing to these associations is an air pollution -mediated pro -hypertensive response (Brook, 2007 ). Epidemiological studies demonstrate that present -day levels of PM are capable of elevating arterial blood pressure (BP) within a period of a few days (Linn et al, 1999 ;Brauer et al, 2001 ;Ibald -Mulli et al, 2001, 2004Zanobetti et al, 2004 ;Chuang et al, 2005 ;Santos et al, 2005 ;Harrabi et al, 2006 ;Madsen and Nafstad, 2006 ;Choi et al, 2007 ;Liu et al, 2007 ;McCracken et al, 2007 ;Auchincloss et al, 2008 ;Dvonch et al, 2009 ;Brook et al, 2010 ).…”