Why Diesel Particulates Cause Cardiovascular Disease

Particulates in diesel exhaust are a substantial cause of the negative health effects traced to air pollution, above all in traffic environments. Diesel exhaust contains a number of extremely tiny particles about 1/10,000 mm in diameter, with chemical compounds bound to the surface that have been suggested to lie behind the ability of these particles to cause harmful health effects.

Individuals with lung or heart disease are especially vulnerable and are impacted most negatively during periods with high levels of air pollution. In his dissertation, Håkan Törnqvist studied the effects of diesel exhaust on healthy individuals and respective patient groups with chronic obstructive lung disease (COL) and coronary disease with atherosclerosis in the coronary artery.

The aim of the studies in the dissertation was to use controlled exposure studies to try to elucidate the mechanisms that explain why diesel exhaust particulates in polluted air cause increased morbidity in both lung and heart diseases. The studies were carried out in an exposure chamber, where the individuals were exposed for one hour to, respectively, diesel exhaust with a particulate concentration of about 300 µg/m3 and filtered air. The two exposures were in random order, so the individuals served as their own controls.

The dissertation work studied whether exposure to diesel exhaust would lead to a deterioration of the lung function and increased inflammation of the airways as measured by induced sputum (coughing samples) in patients with moderately severe but stable COL. Analysis of the cough samples could not reveal any increase in inflammation of the airways, not was there any deterioration of the lung function. Studies of the these same patients were also used to determine whether exposure to diesel exhaust can lead to increased general inflammation, can impact the capacity of the blood to coagulate, or can cause damage to the lung epithelia as measured in the blood. No general increase in blood coagulation or signs of increased inflammation in the blood could be found.

The thesis also addressed the question of whether exposure to diesel exhaust can affect the vascular function in a group of healthy individuals 2 and 6 hours after exposure. In this group exposure to diesel exhaust decreased two important and complementary blood-vessel functions: the regulation of the width of the blood vessels and the body’s own ability to dissolve blood clots (fibrinolysis). What’s more, the study illuminated the late course of events involved in the blood-vessel effects triggered by diesel exhaust in healthy individuals in the test. As much as 24 hours after their exposure to exhaust, the capacity of their blood vessels to expand was disturbed. Moreover there were signs of systemic inflammation, measured as an increase in inflammatory markers in the blood.

The final study in the dissertation targeted individuals with clinically fully stable coronary artery disease. The issue was whether exposure to diesel exhaust can affect the heart, decrease vessel mobility, and hamper the capacity to dissolve blood clots. A lowered capacity to dissolve blood clots was observed, together with an impaired ability of blood vessels to expand. The most important finding, however, was that after exposure to diesel exhaust patients evinced EKG signs that were consistent with a shortage of oxygen in the heart muscle. This effect was general, that is, not limited to any particular blood vessel in the heart, and it was observed despite the fact that the patients were fully stable in their coronary artery disease and were under optimal medical treatment.

The dissertation clarifies previously unknown mechanisms that can explain why air pollution in particulate form causes heart attacks, stroke, and increased mortality. It shows that diesel exhaust cause a rapid deterioration of the function of blood vessels that persists as long as 24 hours after exposure. The EKG findings in heart patients indicate acute heart effects that are consistent with increased risk of heart attack in connection with exposure to traffic.