Airborne PM and Cardiovascular Disease
Associations between episodes of particulate matter (PM) air pollution and hospital admissions for cardiopulmonary disease have been documented worldwide. Exascerbations of chronic bronchitis, asthma, COPD, and pneumonia are logically connected with the known pro-inflammatory effects of a variety of anthropomorphic pollutants including Ozone, SO2, NO2, Carbon particles (black smoke) and the complex particulate mixtures of combustion products resulting from vehicular emissions. Less clear is the relationship between episodes of heightened air pollution and mortality from cardiovascular disease. While the interaction between inhaled irritants and chronic lung disease has received considerable research interest, epidemiologic studies suggest that cardiovascular effects are acute in response to short periods of high pollutant concentrations. There is even a distinction in some studies between the time course of cardiac disease and acute pulmonary complications such as asthma or aggravation of bronchitis. While pulmonary effects tend to have a “lag” period of one or two days post exposure, cardiac effects are more immediate.
The physiologic basis of association between acute PM exposure and cardiac mortality remains largely unknown. The pathology behind the cardiac deaths reported in epidemiologic studies is often not available for analysis. While some analyses use ischemic heart disease or myocardial infarction statistics, others report all causes of cardiovascular deaths presumably including congestive heart failure and arrythmia. In one study where this distinction was evaluated, 70% of the increase in cardiac deaths were due to myocardial infarction. A more recent study confirms the strong risk association between fine PM and myocardial ischemia and demonstrates a higher PM association with cardiac rather than pulmonary associated mortality. An associated question is whether the relationship to PM exposure is simply a result of hastened death of patients who are terminally ill. Latency analysis suggests otherwise. Data from a large European multicity study demonstrates an even greater mortality rate associated with PM 10 levels in a distributed lag model of 40 days compared with short term one and two day analysis.
Several recent studies emphasize the potential importance of systemic circulation of ultrafine particulate air pollution. Intratracheally administered diesel exhaust particles undergo systemic circulation in hamsters and lead to activation of the clotting system. Human volunteers exposed to carbon black also show systemic circulation of carbon particulates. Environmentally derived particulates accumulate in the brain of naturally exposed dogs and experimentally exposed rats. Significant hepatic accumulation of ultrafine carbon or iridium particles has also been demonstrated in short term inhalation studies. We are studying the mechanisms of endothelial transport of ultrafine particles. For more information see the Air Quality Research Center website.
Environmental Cardiology
Transmission Electron Micrograph of Iron Oxide particles in Endothelial cell culture suggest transport through caveolae
