spacer U.S. Department of Health and Human Services U.S. Department of Health and Human Services U.S. Department of Health and Human Services spacer
National Institutes of Health
NIH Research Portfolio Online Reporting Tools (Report) Report, Data and Analyses of NIH Research Activities
NIH Recovery Act Investment Reports
ARRA Investments in Environmental Determinants of Cardiovascular Disease

Public Health Burden
Cardiovascular diseases (CVD) remain the number one cause of death and disability in the United States. While there are several well-established lifestyle risk factors for CVD, such as smoking, diet and physical activity, numerous environmental contaminants have also been shown or are suspected to contribute to CVD-related mortality and disability.  Such exposures include air pollution, heavy metals and organophosphate pesticides.  

Early Markers of Exposure Response
The development of atherosclerosis, the primary underlying pathogenic process of CVD, begins in early life and continues to progress over an individual’s lifetime, ultimately resulting in CVD in some individuals.  Scientists hypothesize chronic exposure to some environmental contaminants during childhood and adolescence may contribute to this process and lead to development of CVD later in life.  Studies using early markers of abnormal cardiovascular function will help clarify how early life environmental exposures may lead to future CVD risk.  Several ARRA funded grants are exploring early markers of environmental exposure response in relation to CVD and/or assessing the utility of these markers in studies of young adults and children.  These projects will:
  • Study the association between lifetime exposure to air pollution and carotid intima media thickness (CMIT), a measure of atherosclerosis, in college students and elementary-school children. 1,2
  • Evaluate the reliability of CIMT measurements as a measure of early atherosclerosis in research involving otherwise healthy young adults and children.2
  • Evaluate the use of arterial wall stiffness, another indicator of atherosclerosis, as a potentially valuable indicator of early cardiovascular disease progression in relation to lifetime air pollution.1
  • Assess the association between increased lead exposure and vascular function in response to acute stress in children.3
  • Attempt to develop potential biological markers to predict susceptibility to cardiovascular disease in an African American population exposed to pesticides in the South.4
Biological Mechanisms Contributing to CVD
Numerous mechanisms have been proposed to explain how environmental contaminants cause and/or exacerbate underlying CVD, but the exact mechanism(s) by which exposures lead to negative biological effects remain unclear.  A better understanding of the mechanisms by which specific environmental exposures impact cardiovascular function may improve public health communication and clinical interventions, and could ultimately lead to a reduction in CVD-related disease and disability.  Several ARRA funded grants are examining the biological mechanism by which environmental exposures impact cardiovascular function.  These studies will:      
  • Investigate the impact of short-term and long-term air pollution exposure on systemic inflammation, oxidative stress and atherogenesis in children.5
  • Examine the impact of environmental tobacco smoke (second-hand smoke) on inflammation, the function of blood vessel cells and oxidative stress in children and whether obesity intensifies these effects.6
  • Investigate how pesticide exposure impacts cholesterol metabolism and transport and may lead to the development of atherosclerosis.7
  • Investigate the impact of arsenic on vascular function to better understand the adverse cardiovascular impacts of arsenic exposures.8
  • Investigate the contribution of light/dark cycles on the progression of cardiovascular disease to better understand the biological basis for increased incidence of CVD in shift workers.9

  1. 3R01ES014708-04S1 -- Air Pollution, Intima-media Thickness, and Lung Function in College Students -- Avol, Edward (CA)
  2. 3R01ES014447-04S1 -- Air Pollution and Preclinical Atherosclerosis in Elementary-School children -- Avol, Edward (CA)
  3. 3R15ES015619-01S1 -- Lead and Vascular Reactivity to Stress in Children -- Gump, Brooks (NY)
  4. 3R21ES015107-03S1 -- Relationship of Blood Esterases, Pesticide Exposure and Cardiovascular Disease -- Chambers, Janice (MS)
  5. 1R21ES016637-01A1 -- Air Pollution, Systemic Inflammation, and Sub-Clinical Atheroslerosis in High-Altitude Children -- Armijos, Rodrigo X (TX)
  6. 1R21ES016883-01A1 -- Vascular Toxicities of Environmental Tobacco Particulates in Children -- Bauer, John A (OH)
  7. 3R15ES015348-01A1S1 -- Effect of organophosphate exposure on cholesteryl ester hydrolase- Ross, Mathew (MS)
  8. 3R01ES013781-02S1 -- Mechanisms of arsenic-induced vascular disease -- Barchowsky, Aaron (PA)
  9. 1RC1ES018636-01 -- Clock genes, environmental challenges and cardiopulmonary disease -- Esser, Karyn (KY)

Homespacer| Investment Reportsspacer| spacerFAQsspacer| spacerContact Usspacer| spacerRePORT Home

Office of Extramural Research spacer spacer spacer spacer spacer logo spacer spacer

Page Last Updated on June 30, 2018 NIH...Turning Discovery Into Health®