Diesel Exhaust May Impair the Functioning of Blood Vessels, Leading to Heart Attack or Stroke
19 December 2005
A new study published in Circulation, the Journal of the American Heart Association, has found that inhaling diesel exhaust at levels typically found in large cities may disrupt normal blood vessel and clotting activity. This may prove to be a mechanism linking air pollution to the pathogenesis of heart attack and stroke.
In the study, researchers found that exposure to diesel exhaust for one hour during exercise caused a significant decrease in blood vessels’ natural ability to dilate. Exposure to air pollution also decreased levels of an enzyme that helps prevent clots from forming.
Air pollution contributes to death and illness involving the heart and blood vessels. Short-term exposure to air pollution can worsen existing problems and lead to hospitalization for heart attack and other heart and lung conditions. Long-term repeated exposure increases the risk of death from coronary heart disease, abnormal heart rhythms and heart failure.
The link between air pollution and heart disease is strongest for fine-particle pollutants, of which the combustion of fossil fuels in road transportation is a major source. But the underlying factors responsible for air pollution’s effects on the heart and blood vessels have remained largely unknown. In previous work, the group has reported abnormal blood vessel function in cigarette smokers.
Cigarette smoke is an important indoor air pollutant. We hypothesized that the particles derived from burning diesel oil are likely to be just as harmful as particles derived from burning tobacco.—Nicholas Mills
In a double-blind, randomized, cross-over study, 30 healthy men were exposed to diluted diesel exhaust (300 µg/m3 particulate concentration) or filtered air for 1 hour during intermittent exercise.
The diesel exhaust was generated from an idling diesel engine. The particle concentration of 300 µg/m3 is comparable to curbside exposure on a busy street in a large city.
Two and six hours after being in the exposure chamber, the men received infusions of vasodilating drugs in one arm. Researchers measured blood flow in the infused and non-infused arms. They also drew blood before each exposure and two and six hours afterward. The researchers measured blood levels of tissue plasminogen activator (t-PA), a naturally occurring enzyme that dissolves blood clots, and plasminogen activator inhibitor type 1 (PAI-1), a substance that counterbalances the activity of t-PA to help maintain normal clotting activity.
The vasodilators caused dose-related increases in forearm blood flow after exposure to filtered air and diesel exhaust. Forearm blood flow decreased significantly two hours after diesel exposure, and the reduced response to the vasodilators persisted at six hours. Infusion of the natural hormone bradykinin releases t-PA from the blood vessel wall, but this vascular response was significantly reduced six hours after diesel exposure.
Diesel exhaust consists of a complex mixture of particles and gases. Before we can advocate the widespread use of particle traps in diesel engines, we need to verify that combustion derived particles are the responsible component. If we do that, then it is likely that retrofit exhaust treatments will reduce pollution exposure and benefit public health.—Nicholas Mills
Co-authors are Håkan Törnqvist, M.D.; Simon D. Robinson, MRCP; Manuel Gonzalez, M.D.; Kareen Darnley; William MacNee, M.D.; Nicholas A. Boon, M.D.; Ken Donaldson, Ph.D.; Anders Blomberg, M.D., Ph.D.; Thomas Sandstrom, M.D., Ph.D.; and David E. Newby, D.M., Ph.D.
The study was funded by the British Heart Foundation.
Mills is the recipient of a Michael Davies/British Cardiac Society Research Fellowship.
Diesel Exhaust Inhalation Causes Vascular Dysfunction and Impaired Endogenous Fibrinolysis; Nicholas L. Mills, Håkan Törnqvist, Simon D. Robinson, Manuel Gonzalez, Kareen Darnley, William MacNee, Nicholas A. Boon, Ken Donaldson, Anders Blomberg, Thomas Sandstrom, and David E. Newby; Circulation 2005 112: 3930 - 3936, doi:10.1161/CIRCULATIONAHA.105.588962
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