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Controlled Exposure of Humans with Metabolic Syndrome to Concentrated Ultrafine Ambient Particulate Matter Causes Cardiovascular Effects
Citation:
Devlin, R., C. Bailey Smith, Mike T. Schmitt, Ana G. Rappold, A. Hinderliter, D. Graff, AND Martha Sue Carraway. Controlled Exposure of Humans with Metabolic Syndrome to Concentrated Ultrafine Ambient Particulate Matter Causes Cardiovascular Effects. TOXICOLOGICAL SCIENCES. Society of Toxicology, RESTON, VA, 140(1):61-72, (2014).
Impact/Purpose:
Numerous epidemiology studies have shown that exposure to ambient airborne particulate matter (PM) is associated with increased mortality and morbidity, especially in elderly people with cardiovascular disease (EPA 2009). Ambient PM is a complex mixture of organic and inorganic compounds adsorbed Onto a carbonaceous core. Its composition varies across time and space and depends on factors such as primary sources (e.g. traffic and power plant emissions, biomass burning, crustal or biological material), and meteorological and geographical conditions that are specific to the area in which it is sampled.
Description:
Background: Many studies have reported associations between PM2.5 and adverse cardiovascular effects. However there is increased concern that ultrafine PM (aerodynamic diameter less than 0.1 micron) may be disproportionately toxic relative to the 0.1 to 2.5 micron fraction of PM2.5. Because of its location and non-uniform dispersion it has been difficult for epidemiology studies to associate exposure to ultrafine PM with adverse health effects. Methods and Results: Thirty four individuals with metabolic syndrome were exposed for two hours to clean air and concentrated ambient ultrafine particles (UCAPS). Individuals carrying the null allele for GSTM1 (a prominent antioxidant gene) were identified by genotyping. Blood was obtained immediately prior to exposure, and at one hour and 20 hours afterward. Blood pressure and brachial artery ultrasound were measured at the same time points and blood pressure was also measured at 15 minute intervals during the exposure period. Holter monitoring was measured for 24 hours. The brachial artery diameter of GSTM1 null individuals exposed to UCAPS failed to return to its normal diameter following an ischemic stress. GSTM1 null individuals also had increased QRS complexity following exposure to UCAPS as well as increased QT duration. Blood plasminogen and thrombomodulin were decreased in the whole population following UCAPS exposure, while C reactive protein and SAA were increased. Conclusions: This controlled human exposure study is the first to show that ambient ultrafine particles can cause cardiovascular changes in people with metabolic syndrome, which affects nearly a quarter of the U.S. adult population.