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Could dirty air cause diabetes?

February 2, 2009

Diabetes is a growing epidemic, and it has become arguably one of the biggest health challenges of our time. Currently, more than 23 million Americans have diabetes, and the Centers for Disease Control and Prevention estimate that in the last 15 years, the number of people in the United States with diabetes has more than doubled. Diabetes is increasing at an alarming rate in Europe as well, and it is fast becoming a major health threat in developing countries such as India and China. Despite its high prevalence, however, diabetes remains somewhat of a mystery. Although type 1 diabetes mellitus could be attributed to insufficient insulin release by the ?-cells of the pancreas, the origins of type 2 diabetes mellitus (which accounts for >90% of the cases of diabetes) remain obscure. Insulin resistance is a cardinal feature of type 2 diabetes mellitus; however, it is not clear how whole-body insulin resistance develops, which specific tissues are affected first and which ones later, and how metabolic changes in individual tissues contribute to the overall development of the disease and its many secondary complications.

Environmental cardiology: studying mechanistic links between pollution and heart disease

September 28, 2006

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.