J Aerosol Med 2000 Winter; 13(4): 335–54
Pope CA 3rd
Brigham Young University,
Provo, Utah 84602, USA. email@example.com
In the last 10 years there has been an abundance of new epidemiological studies on health effects of particulate air pollution. The overall evidence suggests that fine particulate pollution can be an important risk factor for cardiopulmonary disease. Long-term, repeated exposure to fine particulate air pollution may increase the risk of chronic respiratory disease and the risk of cardiopulmonary mortality. Short-term exposures exacerbate existing cardiovascular and pulmonary disease and increase the risk of becoming symptomatic, requiring medical attention, or even dying. This paper outlines the results of the basic epidemiologic studies and briefly reviews and discusses recent studies that have looked at specific physiologic health endpoints in addition to lung function.
A few recent, mostly exploratory pilot studies, have observed particulate pollution associations with blood plasma viscosity, heart rate, heart rate variability, and indicators of bone marrow stimulation. A systemic response to particulate-related pulmonary inflammation remains somewhat speculative. The epidemiologic evidence, nevertheless, seems consistent with the hypothesis that particle-induced pulmonary inflammation, cytokine release, and altered cardiac autonomic function may be part of the pathophysiological mechanisms or pathways linking particulate pollution with cardiopulmonary disease.