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Environmental Cardiology: Pollution and Heart Disease (Issues in Toxicology, 8) - Hardcover

 
9781849730051: Environmental Cardiology: Pollution and Heart Disease (Issues in Toxicology, 8)

Inhaltsangabe

Although it is widely recognized that environmental factors such as smoking, diet, exercise, and socioeconomic status affect the risk of cardiovascular disease, recent work showing the effects of other environmental factors provides a more complete assessment of the situation. This view has emerged from three developments. Firstly, there has been a sudden explosion in the prevalence of diabetes and obesity which indicates a strong environmental component. Secondly, there is an accumulation of evidence suggesting that most cases of these diseases could be prevented by healthy lifestyle choices. Finally, studies have shown that exposure to environmental pollutants has a significant effect on heart disease risk. This book is the first to provide a comprehensive account of the effects of pollutants on heart disease and to integrate this area of research within the overall theme of environmental cardiology. The introductory chapter outlines the effects of different aspects of the environment on heart disease and provides a context for the discussion that follows. Subsequent chapters give an overview of the effects of particulate matter and discuss the epidemiological studies supporting the link. The book then goes on to cover the effects of pollution on different aspects of cardiovascular disease (hypertension, stroke, heart failure, ischemic heart disease and atherogenesis). Because of a close association between diabetes and heart disease, a discussion of the effects of particulate matter on diabetes is also included. Later chapters discuss the effects of individual pollutants such as vehicular emissions, metals and aldehydes. A review on manufactured nanoparticles is incorporated because these particles represent an important new threat to cardiovascular health. The understanding that emerges from this monograph suggests that we must be more alert to the effects of the environment and develop strategies that target, not only the diseased individual, but also the unhealthy, disease-causing environment. It is essential reading for cardiologists, epidemiologists, urban planners and pollution control specialists.

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Environmental Cardiology: Pollution and Heart Disease is the first landmark publication to provide a comprehensive multidisciplinary review on the emerging field of environmental cardiology and current research linking pollutant exposure to heart disease. The book begins with an introductory chapter on the environmental basis of cardiovascular disease and the role of the environment in evolution. It provides a new classification for the different categories of the human environment and provides an in-depth analysis of the role of the natural, social and personal environments in modifying and transmitting the risk for heart disease. Subsequent chapters discuss how exposure to particulate air pollutants, vehicular exhaust, manufactured nanoparticles and pollutants such as metals, arsenic and environmental aldehydes affect the risk of developing cardiovascular disease. Both experimental and epidemiological evidence are discussed as well as the impact of exposure to air pollution on hypertension, atherogenesis, ischemic heart disease and heart failure. There is also new evidence supporting a link between exposure to environmental pollutants and stoke, obesity and diabetes. The understanding that emerges from this book suggests that we must be more alert to the effects of the environment and develop strategies that target, not only the diseased individual, but also the unhealthy, disease-causing environment. It is essential reading for cardiologists, epidemiologists, urban planners and pollution control specialists.

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Environmental Cardiology

Pollution and Heart Disease

By Aruni Bhatnagar

The Royal Society of Chemistry

Copyright © 2011 Royal Society of Chemistry
All rights reserved.
ISBN: 978-1-84973-005-1

Contents

Chapter 1 Environmental Basis of Cardiovascular Disease A. Bhatnagar, 1,
Chapter 2 Cardiovascular Effects of Particulate-Matter Air Pollution: An Overview and Perspectives J. A. Araujo and R. D. Brook, 76,
Chapter 3 Air Pollution and Atherosclerosis: Epidemiologic Studies V. C. Van Hee and J. D. Kaufman, 105,
Chapter 4 Hypertension and Vascular Toxicity of PM Z. Ying and S. Rajagopalan, 121,
Chapter 5 Air Pollution and Diabetes E. H. Wilker and J. D. Schwartz, 143,
Chapter 6 Ambient Particulate Matter and the Risk of Stroke G. A. Wellenius, D. R. Gold and M. A. Mittleman, 159,
Chapter 7 Environmental Pollutants and Heart Failure S. D. Prabhu, 177,
Chapter 8 Ultrafine Particles and Atherosclerosis J. A. Araujo, 198,
Chapter 9 Air Pollution and Ischemic Heart Disease A. Peters, 220,
Chapter 10 Vehicular Emissions and Cardiovascular Disease M. Campen and A. Lund, 234,
Chapter 11 Manufactured Nanoparticles G. S. Kang, P. A. Gillespie and L. C. Chen, 253,
Chapter 12 Metals in Environmental Cardiovascular Diseases A. Barchowsky, 272,
Chapter 13 Environmental Aldehydes and Cardiovascular Disease D. J. Conklin, P. Haberzettl, J. Lee and S. Srivastava, 301,
Subject Index, 371,


CHAPTER 1

Environmental Basis of Cardiovascular Disease


1.1 Introduction

The term cardiovascular disease (CVD) refers to a group of illnesses caused by the disorders of the heart, blood vessels and blood flow. The most common cause of cardiovascular diseases is atherosclerosis, which is the hardening of arteries due to the formation of an atheromatous plaque. Abrupt changes in blood flow in atherosclerotic vessels result in acute myocardial infarction and stroke, which are the major clinical manifestations of chronic changes in the vessel wall. In the heart, ischemic injury due to atherosclerotic disease often leads to arrhythmia, hypertrophy, cardiomyopathy and heart failure. Heart disease is accompanied by chronic metabolic and physiological changes that precede and contribute to its clinical manifestations. These include metabolic changes such as high cholesterol (hypercholesterolemia) and insulin resistance and physiological changes such as an increase in blood pressure (hypertension) and changes in cardiac contractility. Although the causes of diabetes are not well understood, diabetes primarily affects the heart and blood vessels and is, therefore, considered to be a major CVD risk factor. Therefore diabetes and obesity are included in this discussion of heart disease.

Significant CVD is also associated with rheumatic disease, which is due to myocardial damage caused by streptococcal bacteria and congenital malformation of the structures of the heart or blood vessels. Several other types of congenital CVD are also common. These defects could be overt, resulting from gross malformation of major blood vessels or myocardial tissue in the fetus, or they may be more subtle, leading to an increase in susceptibility to stress or exercise. Congenital defects or prolonged hypertension and infectious diseases could also result in the dilation and rupture of the aorta leading to aortic aneurysm and dissection. Additionally, cardiovascular disorder associated with deep vein thrombosis and pulmonary embolism could result from blood clots in the leg veins that can dislodge and move to the heart and the lungs.

As a group, CVD is the leading cause of death world-wide (Figure 1.1). According to the WHO in 2004, CVD accounted for nearly 30% of all deaths worldwide. It killed twice as many people as infectious and parasitic disease and 3 times as many people as all forms of cancer. Globally, most (43–45%) cardiovascular deaths are due to coronary heart disease (CHD) or ischemic heart disease (IHD), whereas stroke accounts for 33% of CVD. A similar distribution of CVD deaths has been reported for countries such as the US (Figure 1.2).

These statistics suggest that heart disease is the major cause of mortality world-wide. Although the prevalence of heart disease varies considerably (vide infra) it still remains a major cause of death in all human populations regardless of their geographic location or ethnicity. It shows no preference for gender or economic status. Both men and women appear to be equally susceptible. World-wide, more women (31.5%) than men (26.8%) die of heart disease. Even in low-income countries (per capita ≤$825) IHD is the number two leading cause of death (9.4%), second only to deaths caused by lower respiratory infections (11.2%), whereas in middle and high income countries ($10, 066 or more) IHD and cerebrovascular disease account for 25 to 28% of all deaths (WHO, 2005). What is more alarming is that the prevalence of heart disease in increasing. The WHO estimates that 80% of all current CVD deaths are in developing, low- and middle-income countries and it is estimated that by 2010, CVD will be the leading cause of death in developing, low-income countries as well. In developed countries, the emergent epidemics of diabetes and obesity are threatening to erode the pattern of recent gains in health. In the US, the increase in obesity alone has been forecasted to slow down the increase in life expectancy that has been steadily increasing since the early 20th century. Thus, CVD is the most frequent cause of death throughout the world, independent of economic status, gender, or ethnic differences.

The universally high burden of CVD and the extraordinarily high rates of CVD mortality across all communities, suggests that humans as a species are particularly prone to heart disease. It may be argued that CVD is an inevitable consequence of aging, that blood pressure and cholesterol levels inexorably increase with age and that if an individual survives middle age without succumbing to infectious disease, sporadic cancers, accidents or violence, their most likely fate is cardiovascular death. This view is consistent with data showing that the risk of dying from CVD increases with age. In the US, the percentage of population with CVD increases from 14.9 and 8.7% for men and women of 20–39 years of age to 78.8 and 84.7% for men and women more than 80 years of age. It has been suggested that because heart disease develops more often in old individuals, it is not subject to direct selective pressure, i.e. that natural selection during evolution is unable to weed out these diseases as they do not affect reproductive success. Natural selection, it is believed, tends to maintain the frequency of genes that increase reproductive success even if the genes have other effects that increase disease susceptibility in older age. However, as we shall see, these arguments do not take into account the important role of the environment, which affects not only the long-range evolutionary susceptibility to disease, but also the proximate causes that lead to the disease development in a specific individual. Moreover, changes in the environment can modify (slow down or accelerate) age-dependent changes in the heart and blood vessels. In addition, a changing environment could continuously alter the context within which the effects of a gene manifest. Thus, a gene could be beneficial in one environment but not the other. As a result, changes in the environment could impart maladaptive predilection to a previously well-adapted genetic...

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