2011 Progress Report: Cardiovascular Effects of Urban and Rural Coarse Particulate Matter in Obese and Lean AdultsEPA Grant Number: R833740
Title: Cardiovascular Effects of Urban and Rural Coarse Particulate Matter in Obese and Lean Adults
Investigators: Brook, Robert D. , Brook, Jeffrey R. , Dvonch, Joseph T. , Gold, Diane R. , Kaciroti, Niko , Keeler, Gerald J. , Silverman, Frances , Urch, Bruce
Institution: University of Michigan - Ann Arbor , Harvard University , University of Toronto
EPA Project Officer: Chung, Serena
Project Period: March 1, 2008 through February 28, 2011 (Extended to February 28, 2014)
Project Period Covered by this Report: March 1, 2011 through February 29,2012
Project Amount: $1,199,500
RFA: Sources, Composition, and Health Effects of Coarse Particulate Matter (2006) RFA Text | Recipients Lists
Research Category: Air , Air Quality and Air Toxics , Particulate Matter
Coarse particulate matter (PM10-2.5) is a heterogeneous mixture of crustal materials, trace metals/elements, and bio-aerosols. The components vary considerably due to location differences in primary sources. Despite fewer studies than for fine particulate matter (PM), epidemiological evidence suggests that coarse PM may also be associated with an increased risk for acute cardiovascular (CV) events. In order to support the biological plausibility that coarse PM exposure is causally linked to CV disease, it is essential to demonstrate that it can rapidly trigger adverse biological responses in humans capable of acutely promoting CV events. The overall hypothesis is that short-term exposure to both urban and rural coarse PM is capable of promoting pro-vasoconstrictive vascular dysfunctions and CV autonomic imbalance. This proposal aims to demonstrate that short-term concentrated ambient coarse PM (CAP) inhalation (1) triggers pro-vasoconstrictive vascular dysfunctions related to (mediated by) CV autonomic imbalance; and (2) that these responses occur to a greater degree in obese than in lean adults; and (3) we aim to elucidate the constituents/sources responsible for the CV responses and to perform detailed characterizations of differences in rural vs. urban coarse PM to improve the epidemiological understanding of coarse PM.
In years 1-3 we completed the purchasing of all necessary research equipment and validated the medical and air pollution research protocols to be employed. The assembly of the new mobile exposure facility (AIRCARE-2) was completed by April 2011. The original protocol was modified (as described in detail in the year 3 annual report) to include novel outcomes for cardiovascular and metabolic parameters. Study subjects were enrolled and human exposures began in May 2011. Human exposures and air pollution characterizations actively continue. As of end of June 2012, we will have completed 35 subjects (70 total exposures including CAP and filtered air (FA)) with the plan to complete all exposures at both the rural (Dexter) and urban (Dearborn) locations (150 total exposures, CAP and FA) by the end of February 2013.
Our plan is to continue human exposures at this rural location through completion of 50 subjects (100 total exposures including CAP and FA). We will then move the facility to Dearborn and complete 50 total exposures at this urban location (CAP only). Several novel metabolic outcomes including insulin sensitivity and HDL functionality are being investigated as secondary endpoints. We anticipate being capable of analyzing these data during year 4 as hypothesis-generating results. This protocol will be the first to investigate the vascular effects of coarse PM. In addition, the susceptibility of an obese sub-population and the relative CV and metabolic toxicity of 2 differing coarse PM exposures (derived from a rural versus urban location) comprised of differing constituents and from differing sources will be explored. It is expected that exposures to both rural and urban coarse PM will cause arterial vasoconstriction and raise BP and that obese individuals will have a greater adverse response via mechanisms involving autonomic imbalance. These results will provide biological plausibility that coarse PM, even of varying composition and sources, is capable of triggering CV events. Moreover, the extensive coarse PM characterization will in-itself enhance our level of understanding of coarse PM epidemiology in 2 environments.