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Cardiovascular Effects in Adults with Metabolic Syndrome Exposed to Concentrated Ultrafine Air Pollution Particles
Citation:
BAILEY, C., A. RAPPOLD, M. T. SCHMITT, D. DIAZ SANCHEZ, M. S. CARRAWAY, AND R. B. DEVLIN. Cardiovascular Effects in Adults with Metabolic Syndrome Exposed to Concentrated Ultrafine Air Pollution Particles. Presented at American Thoracic Society (ATS) Annual Meeting, San Francisco, CA, May 18 - 23, 2012.
Impact/Purpose:
Our findings suggest individuals with metabolic syndrome may be more susceptible to the adverse effects associated with air pollution exposure.
Description:
RATIONALE: Epidemiologic studies report associations between ambient air pollution particulate matter (PM) and various indices of cardiopulmonary morbidity and mortality. A leading hypothesis contends that smaller ultrafine (UF) particles induce a greater physiologic response because they can be carried deep inside the lung during inspiration. Individuals with existing cardiovascular disease (CV) or diabetes have been shown in epidemiologic studies to have an increased risk of mortality and morbidity associated with PM. Recent panel studies in diabetics report changes in heart rate variability (HRV), vascular endothelial dysfunction, and vascular inflammation associated with exposure to PM. Some have suggested that peripheral vessel disease and endothelial cell dysfunction associated with diabetes may playa role in their enhanced responsiveness to air pollutants. The objective of this study was to characterize the cardiovascular (CV) effects of concentrated ambient ultrafine particles (lJFCAP) in people with metabolic syndrome, who have an increased risk ofdeveloping CV disease or diabetes. METHODS: Twenty subjects (mean age 48.1 (33-63)) with metabolic syndrome participated in the study; they were defined as having 3 of the following: abdominal obesity, elevated triglycerides, reduced high-density lipoprotein cholesterol, elevated blood pressure (or a history ofhigh blood pressure requiring medication), and elevated fasting glucose. In a randomized, single-blind crossover manner the subjects were exposed to filtered air or UFCAP (mean concentration 170,578 particle/cc and mean mass concentration 118.39 ug/m3 for 2 hr. Measurements were taken before, immediately after, and 20hr after exposure. Cardiac responses were assessed by comparing the time and frequency domains of HRV as well as repolarization changes. Changes in plasma components were also assessed. After normalization to preexposure levels, data are reported as percentage changes from baseline filtered air exposure levels. RESULTS: At 20hr post-exposure, UFCAP reduced the high-frequency to low-frequency ratio (27.9±11.9%), increased the normalized low-frequency domain (9.7±4.17%), and decreased the normalized high-frequency domain (16.8±8.26 %). UFCAP exposure prolonged measures of ventricular repolarization, (i.e. the QT interval corrected for heart rate was prolonged by 0.78 ±0.26%) immediately after exposure and this persisted 20 hr after exposure. UFCAP exposure also decreased plasma low-density lipoprotein (2.72±1.46%) 20 hr after exposure. CONCLUSIONS: Two hour exposure to UFCAP induced acute cardiac and plasma lipid changes in middle-aged individuals with metabolic syndrome. Our findings suggest individuals with metabolic syndrome may be more susceptible to the adverse effects associated with air pollution exposure. This abstract of a proposed presentation does not necessarily reflect EPA policy.