Environmental Cardiology

Abstract

Abstract-Environmental factors are considered key determinants of cardiovascular disease. Although lifestyle choices such as smoking, diet, and exercise are viewed as major environmental influences, the contribution of pollutants and environmental chemicals is less clear. Accumulating evidence suggests that exposure to pollutants and chemicals could elevate the risk of cardiovascular disease. Many epidemiological studies report that exposure to fine particles present in ambient air is associated with an increase in cardiovascular mortality. Statistically significant relationships between particulate air pollution and ischemic heart disease, arrhythmias, and heart failure have been reported. Animal studies show that exposure to ambient air particles increases peripheral thrombosis and atherosclerotic lesion formation. Exposures to arsenic, lead, cadmium, pollutant gases, solvents, and pesticides have also been linked to increased incidence of cardiovascular disease. Mechanistically, these effects have been attributed to changes in the synthesis or reactivity of nitric oxide that may be caused by environmental oxidants or increased endogenous production of reactive oxygen species. Additional studies are urgently needed to: identify the contribution of individual pollutants to specific aspects of cardiovascular disease; establish causality; elucidate the underlying physiological and molecular mechanisms; estimate the relative susceptibility of diseased and healthy individuals and that of specific population groups; and determine whether pollutant exposure are risk correlates, that is, whether they influence major risk factors, such as hypertension, cholesterol, or diabetes, or whether they contribute to the absolute risk of heart disease. Collectively, these investigations could contribute to the emergent field of environmental cardiology.

Dietary methyl-consuming compounds and metabolic syndrome

“…Chronic exposure to arsenic has been recognized to cause various types of human diseases, including metabolic syndrome, T2D, CVD and various cancers, [40][41][42][43][44] which may contribute to the prevalence of metabolic syndrome in arsenic-polluted areas. The mechanism underlying arsenic toxicity is believed to be due to methyl depletion-induced aberrant DNA methylation, and excessive ROS generation and subsequent oxidative cell injury.…”

“…35 The increased appetite may lead to an increase in energy intake and subsequent obesity. As a result, the long-term persistent b-cell compensation together with the oxidative b-cell damage may eventually induce b-cell failure and T2D, which may account for the associations between arsenic [42][43][44] or niacin 34,35 exposure and the prevalence of metabolic syndrome and its related diseases.…”

Short‐term effects of air pollution on cardiovascular diseases: outcomes and mechanisms

“…Because of their small size, ultrafine particles are deposited deep in the lung alveoli and can reach the blood stream. Particulate matter is the type of air pollutant that causes the most numerous and serious effects on human health, because of the broad range of different toxic substances that it contains; it may thus be considered the most relevant indicator of the impact on health of global air pollution [12,13].…”

Tobacco Industry Efforts Undermining Evidence Linking Secondhand Smoke With Cardiovascular Disease

“…136 Because the OSHA proposal 27 addressed all indoor air pollution, not just SHS, the tobacco industry's actions have repercussions on regulating other pollutants and environmental chemicals that have significance in the emergent field of environmental cardiology. 137 Simply eliminating SHS exposure through regulatory policies immediately reduces morbidity and mortality from CVD. Smoke-free workplaces reduce absolute smoking prevalence by 3.8% and reduce cigarette consumption among continuing smokers by Ϸ3 cigarettes a day.…”