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The evidence base supporting a causal relationship between air pollution and increased risk for cardiovascular events continues to grow, but the underlying mechanism remains unclear. In a double-blind, randomized, crossover study to investigate the effect of air pollution on myocardial, vascular, and fibrinolytic function, 20 men with prior MI were exposed to dilute diesel exhaust (generated from an idling Volvo diesel engine and diluted with filtered air to make it comparable to concentrations occurring in urban road traffic) or filtered air.
All subjects experienced ischemia with exercise during both exposures, but mean maximum ST-segment depression was significantly greater during exposure to diesel exhaust than during exposure to filtered air. At 6 hours after exposure, neither endothelium-dependent nor endothelium-independent vasodilation was affected by exposure to exhaust, and no between-group differences in fibrinolytic or inflammatory markers were noted. However, bradykinin-induced release of endothelial tissue plasminogen activator decreased significantly 6 hours after exposure to exhaust.
Mills NL et al. Ischemic and thrombotic effects of dilute diesel-exhaust inhalation in men with coronary heart disease. N Engl J Med 2007 Sep 13; 357:1075-82.
Mittleman MA. Air pollution, exercise, and cardiovascular risk. N Engl J Med 2007 Sep 13; 357:1147-9.
Comment
This study shows that diesel exhaust, a complex mixture of gases and particulate matter, can worsen exercise-induced myocardial ischemia and impair endogenous fibrinolytic activity. The two distinct adverse effects may contribute to the toxic cardiovascular effects of air pollution. These findings reinforce the need to address this risk factor in our public health programs.