Pollution has ‘deleterious effects’ on CV health
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The deleterious effects of pollution on human CV health have garnered attention from both governmental agencies and nongovernmental researchers interested in understanding their pathophysiology and epidemiologic implications.
Pollution is associated with increased risk for CVD events such as stroke and MI as well as increased risk for CVD risk factors such as hypertension, type 2 diabetes and metabolic syndrome.
Globally, air pollution is the fourth leading risk factor for mortality and contributed to an estimated 6.7 million deaths in 2019. An estimated 91% of the global population resides in areas where air pollution levels exceed the limits established by WHO. Without corrective efforts, mortality rates due to air pollution are expected to increase as much as fourfold from 2010 to 2060.
A review article by Sanjay Rajagopalan, MD, chief of cardiovascular medicine for University Hospitals Harrington Heart & Vascular Institute, the Herman K. Hellerstein, MD Professor of Cardiovascular Research and director of the Case Cardiovascular Research Institute at Case Western Reserve University School of Medicine, and Philip J. Landrigan, MD, director of the Global Public Health Program and Global Pollution Observatory, Schiller Institute for Integrated Science and Society, Boston College, published in November in The New England Journal of Medicine offers a contemporaneous review of factors pertinent to the relationship between pollution and CV health. This commentary discusses the effects of four major intertwined facets of pollution: air pollutants, toxic metals, climate change and manufactured chemical pollutants. Figure 1 illustrates the effects of these four facets on CV health.
Air pollution
Air pollution is a heterogenous mixture of gases and particulate matter and is influenced by geographic, temporal and climatic factors. Particulate matter (PM), also known as particle pollution, is one of the six common air pollutants recognized by the U.S. Environmental Protection Agency. It is classified based on particle diameter as: ultrafine (PM0.1), fine (PM2.5) and coarse (PM10). Categories are denoted as PMx, where x represents the upper limit of the diameter of that PM in microns.
The link between PM and CVD is strongest for PM2.5 and can be depicted by a logarithmic curve between exposure and risk for stroke and ischemic heart disease. Short-term exposure to PM2.5 above the primary PM2.5 standards established by the U.S. National Ambient Air Quality Standards (NAAQS; ie, annual average standard, < 15 µg/m3; 24-hour standard, < 65 µg/m3) is associated with alterations in vascular tone, increasing risk for CVD. This helps explain the 0.1% to 1% increased risk for MI, stroke and CVD with every 10 µg/mm3 short-term increase in PM2.5 levels.
Meanwhile, long-term exposure to increased PM2.5, through a multitude of mechanisms such as autonomic imbalance, endothelial dysfunction, systemic inflammation, oxidative stress and thrombogenesis, is associated with increased risk for subclinical markers of CVD (eg, elevated carotid intima-medial thickness, coronary artery calcium, abdominal aortic calcification and left ventricular hypertrophy), clinical atherosclerotic disease and chronic kidney disease. One mechanism in which PM2.5 mediates oxidative stress is the increased production of free radicals, particularly in pulmonary tissue. In vitro studies demonstrate the pro-inflammatory effect and disrupted intracellular signaling caused by PM2.5 in pulmonary tissue.
The pathogenesis of some pollutants in precipitating CVD have been explicated, but many pollutants have an unknown pathophysiology mediating its deleterious effects on CV health. This problem is further muddled by disparate mechanisms mediating CVD in short- vs. long-term PM2.5 exposure. The few studies that have elucidated these mechanisms are not well publicized. Recent studies have associated radon exposure with increased risk for CVD, mediated by hypertensive disorders and oxidative stress. Elucidating the pathophysiology is a step forward, but there must be continued effort and greater publicity of these efforts in the future.
Source of pollution and area of impact
Beyond diameter and duration of exposure, pollution can be categorized by source (eg, anthropogenic or natural) and area of impact (ie, ambient or home). Rajagopalan and Landrigan emphasized the effects of anthropogenic PM; however, natural sources of PM do exist, either as primary particles (eg, sea salt, mineral dust, soot) directly emitted into the atmosphere or as secondary sources (eg, sulfur dioxide, nitrogen oxide and organic materials) formed from aerosolized precursors from natural sources or as secondary particles formed through the reaction of primary particles with various environmental compounds.
Natural sources account for approximately 18% of all PM2.5. Ambient air pollution is particularly important in middle- and high-income countries, with industrial and agricultural processes being primary contributors. In contrast, low-income countries are disproportionately burdened by home air pollution from house fuel combustion.
Toxic metal pollutants
Exposure to toxic metal pollutants such as lead, mercury, arsenic and cadmium portends an increased risk for CVD. Exposure to lead accounted for 21,000 deaths in the U.S. in 2019. Common sources of lead include paint — primarily, paint synthesized prior to 1978 — and batteries. Although previously thought to be safe at mean blood levels less than 40 µg/dL, exposure to lead at levels as low as 3 µg/dL has been associated with increased risk for CVD and hypertension.
Methylmercury, the toxic metabolite of mercury, is a potent neurotoxin produced in aqueous environments that bioconcentrates in predator species such as tuna. Important sources of polluting mercury vapors are the combustion of coal and gold mining, which causes mercury to precipitate in streams, ultimately promoting the biosynthesis of methylmercury. Exposure to methylmercury is implicated in CVD and nonfatal MI. Groundwater that is contaminated with naturally occurring arsenic is a common source of arsenic exposure, particularly in New England and the Southwest.
Arsenic exposure is associated with increased risk for CHD, peripheral artery disease and type 2 diabetes and is weakly associated with increased risk for stroke. The deleterious CV effects of arsenic exposure are thought to be mediated by oxidative damage and the host inflammatory response. Common sources of cadmium include tobacco smoke, occupational exposure and certain food sources (eg, some grains and vegetables). Finally, exposure to cadmium through tobacco smoke, workplace environment and consumption of foods grown in contaminated soil is associated with increased risk for CAD, PAD, stroke and CVD mortality.
An emphasis has been placed on public transportation to limit auto pollution and become “cleaner,” but the impact of air pollution produced by the combustion of fossil fuels on citizens who use public transit at high rates, such as those who travel by bus and those who live in urban areas where there is a high concentration of vehicles, is a growing area of concern for CV health. Although fossil fuel combustion is the primary cause of both climate change and air pollution, their relationship is more complex.
Climate change
Climate change contributes to air pollution through increased surface temperatures that have been associated with increased frequency and severity of wildfires, dust storms and ozonolysis. These environmental effects portend an increased risk for fatal MI and stroke. The impact of climate change on air pollution is particularly salient, as global surface temperatures are predicted to continue increasing, with estimates for 2100 as high as 5.4°C above current temperatures.
The increased surface temperatures will result in the increased production of toxic tropospheric ozone, which is created from heat and light reacting with nitrogen oxides and volatile organic compounds produced from fossil fuel combustion. Figure 2 illustrates the associations of wildfires, dust storms and ozone exposure with increased risk for fatal MI and stroke.
Manufactured chemical pollutants
Manufactured chemical pollutants, often called legacy chemicals due to their long half-lives, include halogenated hydrocarbons, perfluoroalkyl substances (PFAS) and plastic-associated chemicals. Many of these chemical pollutants were released during industrialization prior to the ban of production of such chemicals established under the Stockholm Convention on Persistent Organic Pollutants.
Halogenated hydrocarbons have long been recognized as environmental pollutants and were even addressed in Rachel Carson’s Silent Spring, the influential book published in 1962 warning of dangers to the environment. They are implicated in the development of dyslipidemia, insulin resistance and obesity. Sources of PFAS include water repellants and firefighting foams. They can be used to synthesize fluoropolymers that can confer various properties such as heat, water and oil resistance.
Bisphenol A (BPA) is a common plastic-associated chemical. It was a common compound found in personal care products, pharmaceuticals and paper products. Exposure to BPA is implicated in diabetes and obesity.
Pollution, like the diseases it is associated with, does not present uniform risk for all populations. There are geographic, socioeconomic and medical risk factors that modulate the degree of impact pollution has on promoting CVD. Deaths attributable to pollution are decreasing for higher-income countries, but they are increasing for middle- and lower-income countries. The decreased mortality in higher-income countries is attributed to legislative efforts and the availability of purification technologies. In these countries, aerosolization of cleaning products and pollutants released from gas combustion are the primary sources of household air pollution.
Meanwhile, in middle- and lower-income countries, there tends to be a greater contribution of household combustion reactions (eg, wood, dung) to household air pollution. Additionally, global warming does not increase surface temperatures uniformly. Different global regions are exposed to greater amounts of direct sunlight and have higher average surface temperatures than others. This contributes to a disparate burden of CVD mediated by global warming. Increased age, a diagnosis of established CVD, increased CVD risk factor burden, pulmonary disease and immunosuppression also increase the risk for CVD from pollution.
Primary prevention of CVD
Primary prevention of CVD from pollution can be categorized as legislative and nonlegislative. Legislative efforts are considered the gold standard, as they have the potential to derive the greatest degree of change. Previous legislative efforts have included the NAAQS, the Clean Air Act of 1970, the Stockholm Convention on Persistent Organic Pollutants and efforts of the EPA. To address the impact of increased emission of primary pollutants from industrial processes, a “polluter pays” principle was proposed; this principle would financially penalize corporations for increased emissions.
Nonlegislative efforts often involve efforts on the individual or small population level. Examples include avoiding high pollution routes to minimize personal exposure, carpooling to mitigate vehicular pollutant emission, usage of masks in high PM areas to minimize personal exposure and home air filtration systems to mitigate household exposure to both ambient and home air pollutants. The Table illustrates gaps in knowledge and future considerations to mitigate the deleterious effects of pollution on CV health.
Pollution is gaining recognition for the major CV risk factor it is. A substantial literature exists that links air pollution, toxic metals and chemical pollutants to increased CV morbidity and mortality. The medical community has a role to play in communicating these health effects. Going forward, there must be individual considerations for pollutant exposure, further legislative efforts to mitigate the impact of pollution on CV risk, and a greater effort to elucidate the pathophysiology of pollutants in mediating CVD.
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For more information:
Earl Goldsborough III is a medical student at the Johns Hopkins University School of Medicine. Twitter: @goldsboroughii.
Salvatore Esposito, ME, holds a Master’s degree in civil engineering and is currently applying to medical schools for the 2023 cycle.
Roger S. Blumenthal, MD, is director of the Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease and professor of medicine at Johns Hopkins University School of Medicine. He is also the editor of the Prevention section of the Cardiology Today Editorial Board. Twitter: @rblument1.
Alan P. Jacobsen, MB, BCh, BAO, is a cardiology fellow at Johns Hopkins Hospital. Twitter: @alanpjacobsen.
The authors can be reached at Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease, Division of Cardiology, Johns Hopkins University School of Medicine, 600 N. Wolfe St., Halsted 560, Baltimore, MD 21827.
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