These results suggest that inflammation as well as parts of the coagulation pathway may contribute to the association between particulate air pollution and coronary events.

Background-Daily variations in ambient particulate air pollution have been associated with cardiovascular mortality and morbidity. We therefore assessed the associations between levels of the 3 main modes of urban aerosol distribution and the occurrence of ST-segment depressions during repeated exercise tests. Methods and Results-Repeated biweekly submaximal exercise tests were performed during 6 months among adult subjects with stable coronary heart disease in Helsinki, Finland. Seventy-two exercise-induced ST-segment depressions Ͼ0.1 mV occurred during 342 exercise tests among 45 subjects. Simultaneously, particle mass Ͻ2.5 m (PM2.5) and the number concentrations of ultrafine particles (particle diameter 10 to 100 nm [NC 0.01-0.1 ]) and accumulation mode particles (100 to 1000 nm [NC 0.1-1 ]) were monitored at a central site. Levels of particulate air pollution 2 days before the clinic visit were significantly associated with increased risk of ST-segment depression during exercise test. The association was most consistent for measures of particles reflecting accumulation mode particles (odds ratio 3.29; 95% CI, 1.57 to 6.92 for NC 0.1-1 and 2.84; 95% CI, 1.42 to 5.66 for PM2.5), but ultrafine particles also had an effect (odds ratio 3.14; 95% CI, 1.56 to 6.32), which was independent of PM2.5. Also, gaseous pollutants NO 2 and CO were associated with an increased risk for ST-segment depressions. No consistent association was observed for coarse particles. The associations tended to be stronger among subjects who did not use ␤-blockers. Conclusions-The present results suggest that the effect of particulate air pollution on cardiovascular morbidity is at least partly mediated through increased susceptibility to myocardial ischemia. (Circulation. 2002;106:933-938.)

Epidemiological studies of the past decades have provided a strong body of evidence that elevated levels of ambient particulate air pollution (PM) are associated with increased cardiovascular and respiratory morbidity and mortality. Exacerbations of ischemic and/or arrhythmic cardiac diseases have been linked to PM exposure. At a workshop held at the GSF- National Center for Environment and Health in November 2003, relevant epidemiological and toxicological data of the past 5 years were compiled and potential biological pathways discussed. Available clinical and experimental evidence lends support to the following mechanisms mediating cardiovascular effects of inhaled ambient particles: (i) pulmonary and/or systemic inflammatory responses inducing endothelial dysfunction, a pro-coagulatory state and promotion of atherosclerotic lesions, (ii) dysfunction of the autonomic nervous system in response to direct reflexes from receptors in the lungs and/or to local or systemic inflammatory stimuli, and (iii) cardiac malfunction due to ischemic responses in the myocardium and/or altered ion-channel functions in myocardial cells. While an increasing number of studies addressing these questions support the notion that PM exposure is associated with cardiovascular effects, these studies at present provide only a fragmentary and at times inconclusive picture of the complex biological pathways involved. The available data are consistent with the occurrence of a systemic inflammatory response and an alteration of autonomic cardiac control, but evidence on endothelial dysfunction, pro-coagulatory states, and PM-related myocardial malfunction is as yet scarce. Further studies are therefore needed to substantiate our current understanding of the pathophysiological links between PM exposure and adverse cardiovascular outcomes.

Evidence from epidemiologic studies linking ambient concentrations of particulate matter to morbidity and mortality influenced the guidelines for air quality standards worldwide. With the improvement of measurement techniques, clearer effects were observed with smaller particle sizes. Based on these effects and results from animal studies on the potential toxicity of ultrafine particles, recent epidemiologic studies focus on the health effects of particles which are less than 100nm in diameter. However, most of the studies are ongoing and only few results have been available so far. Six panel studies with patients suffering from chronic pulmonary diseases have been performed in Germany, Finland and the United Kingdom. Overall, a decrease of peak expiratory flow (PEF) and an increase of daily symptoms and medication use was found for elevated daily particle concentrations. Effects were seen with both fine and ultrafine particles. One large study on daily mortality from Germany showed comparable effects of fine and ultrafine particles in all size classes considered. However, fine particles showed more immediate effects while ultrafine particles showed more delayed effects on mortality. The limited number of epidemiological studies suggest that there are health effects of fine and ultrafine particles which might be independent of each other. If these effects are confirmed by ongoing research, monitoring and regulation of particulate air pollution may need to be revised.