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PM Health Effects: Biological Plausibility and Mechanisms
Robert Devlin
EPA National Health and Environmental Effects Research Laboratory,
Research Triangle Park, NC

Six years ago, there were several dozen epidemiology papers that reported associations between daily changes in ambient PM concentration and increased mortality and morbidity. However, very little was known about the underlying pathophysiological processes which might explain how someone could inhale a relatively small amount of particles and die within 24 hours. This presentation summarizes progress made by the PM Centers and EPA scientists in providing biological plausibility to the epidemiology studies through the identification of mechanisms by which PM causes adverse health effects. These studies have shown that PM can cause pulmonary inflammation and interfere with oxygen exchange deep within the lung. PM has also been shown to adversely affect the ability to fight off infections in the lung. Exposure to low levels of PM has been associated with myocardial infarctions and alterations in the autonomic nervous system control of the heart, potentially leading to fatal arrhythmias. PM has also been shown to cause systemic inflammation and to increase the likelihood of blood clot formation and atherosclerotic plaque progression. These studies provide co herence to the epidemiology studies and extended their observations, thus strengthening the science in sup-port of the PM standard. Although substantial progress has been made in this area of research, there are still significant areas of uncertainty. Future challenges include a better understanding of: (1) the cellular and mo-lecular mechanisms which underlie the pathophysiological changes caused by PM; (2) whether different PM components or PM derived from different sources operates through different mechanisms; and (3) whether PM causes injury to different susceptible populations by different mechanisms.


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