Matthew Gee and Dr. C. Arden Pope III, Economics Department

Exposure to elevated concentrations of ambient particulate matter (PM) has been implicated as a risk factor for cardiovascular disease and mortality. Short-term elevated PM exposures and related inflammation may contribute to acute complications of atherosclerosis by accelerating the progression of atherosclerosis, and triggering plaque rupture. Empirical evidence (Brook et al. 2002) suggests that endothelial dysfunction promoted by systemic inflammation related to PM exposure may lie at the heart of the problem. Our experiment examines the effect of short-term exposure to elevated PM levels on endothelial function using a non-invasive procedure called peripheral arterial tonometry (PAT). Using the Endo-PAT 2000 (Itamar Med. Ltd., Caesarea, Israel), we measured the reactive hyperemia index (RHI), a measure of endothelial function, of twelve healthy, non-smoking, college-aged subjects. Measurements were taken six times over two six hour periods in both controlled exposure and controlled clean room environments. During the exposure period, pollution from a coal furnace was used to maintain PM concentrations between 150-200 µg/m3 in the exposure room. Data from the Endo-PAT measurements were collected and analyzed using regression analysis. Controlling for time trends, temperature, baseline heart rate, and individual specific fix effects, PM exposure was not significantly correlated with a change in endothelial function. Future research examining the effects of aged particles on endothelial function need to be conducted because they occur more frequently in outdoor environments.

Exposure to elevated concentrations of ambient particulate matter (PM) has been implicated as a risk factor for cardiovascular disease and mortality. Repeated long-term exposure to PM contributes to pulmonary and systemic oxidative stress, inflammation, atherosclerosis and increased risk of ischemic heart disease and death (Pope and Dockery 2006). Short-term elevated PM exposures and related inflammation may also contribute to acute complications of atherosclerosis by increasing the risk of atherosclerotic plaque rupture, thrombosis, and the acceleration of acute ischemic events. The endothelium is a layer of thin flat cells lining the interior surface of blood vessels and is directly involved with regulation of vascular tone (vasodilation and vasoconstriction), the control of blood fluidity and coagulation (thrombosis and fibrinolysis) and the regulation of inflammatory processes. Endothelial dysfunction is characterized by the loss of proper function of the endothelium and associated with the initiation of atherosclerosis, stable and unstable angina, myocardial infarction and ischemic stroke. Historically endothelial function has been difficult to measure because of the expense and invasive nature of the procedure. With new developments in peripheral arterial tonometry technology endothelial function can now be measured with a simple non-invasive

Based on recent research into the health effects of air pollution (Pope and Dockery 2006, Brook et al. 2002), we hypothesized that short-term exposure to PM would result in a measurable decrease in endothelial function.

The study was approved by the Internal Review Board for Human Studies Committee of Brigham Young University and was performed on the Brigham Young University campus. Subjects signed a consent form and were healthy 18 to 30 year old non-smokers with no risk factors for cardiovascular disease. Subjects were fed at regular intervals during each visit. Pre-exposure blood pressure and PAT measurements were taken upon arrival. Each participant received four, three hour exposures on two separate days. Exposure periods consisted of three hours in an environment with PM concentrations between 150-200µg/m3 and three hours with PM concentrations < 10µg/m3. Exposure periods were crossed-over on the second day to control for diurnal variation. PAT measurements were taken following each exposure period (figure 1). Figure 2 depicts a PAT measurement with the Endo-Pat 2000 (Itamar Med. Ltd., Caesarea, Israel).

The results from four different regression models are presented below in Table 1. All models included an indicator variable for exposure. Estimates of the exposure effect on RHI were insignificant in all four models. Additionally, models 1, 3, and 4 controlled for individual fixed effects as well as a diurnal time trend. The diurnal time trend was found to be significant in each of these models. Models were also estimated using controls for baseline heart rate and temperature. Coefficient estimates on exposure were somewhat sensitive to additional controls, but were insignificant in all four models. Figure 1 illustrates the change in RHI between the baseline (1), exposure (2), and clean room (3) periods.

The results from the models fail to reject the null-hypotheses that exposure effect estimates are significantly different from zero. Consistent with the results of Brook et al. (2002) for fresh particles our results suggest that personal exposure to elevated concentrations of ambient fine particulate matter may not be associated with a significant change in endothelial function. Empirical evidence from Brook et al. (2002) suggests that personal exposure to aged particles (particles exposed to UV radiation, which include O3) is positively correlated with vasoconstriction and endothelial dysfunction. Further research using a similar study design, but with aged particles is needed to examine these effects further. Additionally, current literature suggest that exposure to fine particulate matter may alter autonomic function (Pope and Dockery 2006).