Cardiovascular Effects of Air Pollutants

75 Cardiovascular Effects of Air Pollutants



Wayne E. Cascio, Milan J. Hazucha, Susan Lyon Stone, Robert B. Devlin


Risk factors for atherosclerotic coronary artery disease—including hypertension, lipid abnormalities, diabetes mellitus, obesity, physical inactivity, and tobacco use—provide targets for the prevention or progression of heart disease (see Chapters 46, 61, 65, 70, 73, and 74). Yet these risk factors account for only approximately 50% to 75% of cases of ischemic heart disease and cardiac events. For this reason it is logical to assume that other factors contribute independently or modify the known risk factors to produce vascular disease and trigger cardiac events. Air pollution is the best-studied environmental factor known to impact hospitalizations and deaths from heart disease. Of the various air pollutants, the evidence for a causative role in cardiovascular diseases is strongest for particles derived from combustion. Indeed, the World Health Organization estimates that more than 2 million premature deaths each year are attributed to urban outdoor air pollution and indoor air pollution from the burning of solid fuels. However, the effects of air pollutants on the cardiovascular system are generally not appreciated by patients or their health care providers. The major air pollutants include particulate matter (PM), ozone (O3), nitrogen oxides, carbon monoxide (CO), and sulfur dioxide (SO2). This chapter reviews the links between air pollution and cardiovascular disease, describes plausible physiologic mechanisms accounting for these effects, and provides an educational resource for physicians and patients to decrease exposure and risk.



History


During the twentieth century, three notable extreme air pollution episodes focused the attention of the public and governments on air pollution’s adverse public health impact. These events occurred in the Meuse Valley, Belgium; Donora, Pennsylvania; and London, England, as a consequence of weather conditions that trapped combustion products and other pollutants from coal fires, vehicles, power plants, and industrial emissions. The best known of these events was the Great London smog. In London, between 5 December and 9 December 1952, a cold air inversion trapped combustion products of the entire city of 8.3 million persons and its industry, resulting in an extreme air pollution episode claiming more than 10,000 lives. During this event, daily mortality increased nearly fourfold, and the mortality rate remained significantly higher than usual for several weeks after the air pollution event had resolved. Surprisingly, these additional deaths that continued to mount were not explained solely by pulmonary disease. Instead a majority of deaths were attributed to cardiovascular etiologies. These important historical events had a profound impact on local and governmental responses to air pollution and contributed significantly to the passing of the Clean Air Act in the United States in 1963, which has been updated and modified several times since. Through the Clean Air Act, the U.S. Environmental Protection Agency (EPA) has statutory responsibility to regulate ambient air pollutants, including PM, CO, nitrogen dioxide (NO2), O3, SO2, and lead. The levels of permissible air pollutants are established by the doses at which a measurable health risk is anticipated, allowing for an adequate margin of safety. This risk assessment is based on scientific data updated every 5 years and published as the U.S. National Ambient Air Quality Integrative Science Assessment. While urban air pollution continues to be a significant challenge overall, since the implementation of the Clean Air Act, the quality of the air in the United States has improved continuously. The improvement in air quality has translated into decreased overall mortality and cardiopulmonary mortality associated with exposure to air pollutants. Yet, despite the remarkable progress made in air quality, health risks of air pollution remain because intermittent increases in air pollution persist, the risk extends to relatively low levels encountered by most persons in the United States, and some people are more sensitive and vulnerable to the effects of air pollution, particularly elderly people with cardiovascular disease.



Particulate Matter


Airborne PM is not a single compound but a mixture of materials having a carbonaceous core and associated constituents such as organic compounds, acids, metals, crustal components, and biologic materials, including pollen, spores, and endotoxins. Combustion processes, such as those in vehicles and power plants, account for most human-generated PM. Importantly, particles generated by mechanical processes, windblown dust, and wildfires also contribute to the mass of PM. Particles are classified as “ultrafine,” “fine” or “coarse” based on their size. Ultrafine particles have an equivalent aerodynamic diameter smaller than 0.1 µm (about one one-thousandth the diameter of a human hair). Fine particles (PM2.5) have a diameter of 2.5 µm or less. Coarse particles (PM2.5–10) have a diameter between 2.5 and 10 µm. Only particles smaller than 10 µm in diameter are respirable (Fig. 75-1, upper). Ultrafine and fine fractions are more likely to be produced by combustion, whereas the coarse fraction is more likely to contain crustal and biologic material. Outdoor PM readily penetrates into homes and buildings depending on building stock and use of air conditioning and heating, and thus increases in outdoor PM can result in increased indoor levels of PM. Cooking, smoking, dusting, and vacuuming also contribute to indoor PM, although not much is known about cardiovascular effects induced by exposure to indoor sources of air pollution in the United States. The national air quality standard for the allowable level of PM2.5 averaged over 24 hours is 35 µg/m3, and the annual average is 15 µg/m3. The standard for PM10 averaged over 24 hours is 150 µg/m3.


image

Figure 75-1 Cardiovascular effects of air pollutants.


AV, atrioventricular; CO, carbon monoxide; NO2, nitrogen dioxide; O3, ozone; SA, sinoatrial; SO2, sulfur dioxide.


Generally it is agreed that PM exposure, even at low concentrations, influences cardiovascular events and mortality rates, yet some skepticism exists. In part, uncertainty over the cardiovascular effects of some pollutants is due to the reliance on epidemiologic data showing positive but weak associations between fluctuating levels of air pollution and cardiovascular health, difficulty assessing exposure accurately, and significant confounding from many factors including but not limited to other pollutants, meteorologic factors, and medications. Also, the strong intercorrelation among outdoor air pollutants to increase cardiovascular risk makes it difficult to attribute observed cardiovascular effects to specific air pollution components. Nevertheless, time-series and cross-sectional epidemiologic studies show a positive association between exposure to airborne PM and cardiovascular morbidity and mortality rates. The association seems to be strongest with fine particles and in the eastern United States. Deeper penetration of fine particles into the lung before deposition may contribute to the apparent biologic activity of these particles. These findings implicate the aerodynamic diameter, regional sources, and composition of PM as factors that affect health.


The causal link between inhaled particles depositing on respiratory surfaces and cardiovascular health effects remains poorly understood. PM air pollution is associated with acute coronary syndrome (unstable angina and myocardial infarction), deep venous thrombosis, rhythm disturbances, stroke, and worsening of heart failure. Biochemical and physiologic responses of exposure to ambient air PM include changes in blood proteins, including acute-phase reactants, coagulation proteins, and proinflammatory cytokines; endothelial function; and neural modulation of the heart. Such changes would be expected to increase the risk of cardiovascular events secondary to thrombosis and arrhythmia (Fig. 75-1).


Possible cardiovascular effects associated with PM exposure can be categorized as short-term (hours or days) or long-term (years). Exposure to PM can increase heart rate and blood pressure, and can decrease oxygen saturation within hours. PM also affects pulmonary oxygen transport and neural modulation of the sinus node and the vascular system, although the magnitude of these changes is small. An increase in heart rate might be caused by an increase in sympathetic input to the heart or a decrease in parasympathetic input. Exposure to PM decreases cardiac vagal input, as suggested by a decrease in heart rate variability (HRV). Yet the association between changes in HRV and ambient PM concentrations is inconsistent. Whether the differences relate to the chemical composition of PM, other associated pollutants, age, gender, genetic background, concurrent cardiac disease, medications, or the HRV methodology is not known. Nor is it known whether change in HRV associated with PM exposure represents an independent measure of risk.

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Jun 12, 2016 | Posted by in CARDIOLOGY | Comments Off on Cardiovascular Effects of Air Pollutants

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