Cardiovascular Responses to Particulate Air Pollution

Description

Objectives/Hypothesis:

The primary objective of this study is to systematically study the adverse effects and the injury mechanisms of the criteria pollutants on cardiovascular health. The specific objectives and related testing hypotheses are listed below:

Criteria pollutants and clinical manifestations of cardiovascular effects:
Whether the exposures to each individual air pollutant prior to the clinical examination are associated with higher frequency of arrhythmia? Whether the associations are independent of other gaseous copollutants? Whether the PM-arrhythmia association is synergistically modified by the exposure to other gaseous copollutants? Whether previous history of cardiovascular disease modifies the above relationships? Whether the air pollution and arrhythmia association differs by age, sex, social economic status, and ethnicity?

Criteria pollutants and the development of individually validated cardiovascular diseases (CVD):
Whether the incident rates of validated cardiovascular events (sudden cardiac death, myocardium infarction [MI], coronary heart disease [CHD], and stroke) are associated with high levels of each individual air pollutant? Whether the associations are independent of other gaseous copollutants? Whether the PM-cardiac events association is synergistically modified by the exposure to other gaseous copollutants? Whether previous history of cardiovascular disease modifies the above relationships? Whether the above associations differ by age, sex, social economic status, and ethnicity?

Criteria pollutants and cardiac autonomic control - potential physiological mechanism 1:
Whether the exposures to each individual ambient air pollutant prior to the clinical examination are associated with poor cardiac autonomic control, assessed by heart rate variability? Whether the associations are independent of other gaseous copollutants? Whether the PM-poor cardiac autonomic control association is synergistically modified by the exposure to other gaseous copollutants? Whether previous history of cardiovascular disease modifies the above relationships? Whether the above associations differ by age, sex, social economic status, and ethnicity?

Criteria pollutants and cardiovascular reactivity - potential physiological mechanism 2:
Whether the exposures to each individual ambient air pollutant prior to the clinical examination are associated with higher cardiovascular reactivity, assessed by postural changes of blood pressure and heart rate? Whether the associations are independent of other gaseous copollutants? Whether the PM-cardiac reactivity association is synergistically modified by the exposure to other gaseous copollutants? Whether previous history of cardiovascular disease modifies the above relationships? Whether the air pollution and higher cardiovascular reactivity association differs by age, sex, social economic status, and ethnicity?

Criteria pollutants and inflammatory /hemostatic markers - potential physiological mechanism 3:
Whether the exposures to each individual ambient air pollutant prior to the clinical examination are associated with higher levels of inflammation / hemostatic factors? Whether the associations are independent of other gaseous copollutants? Whether the PM-inflammation/hemostatic factors associations are synergistically modified by the exposure to other gaseous copollutants? Whether previous history of cardiovascular disease modifies the above relationships? Whether the air pollution and higher levels of inflammation/hemostatic factors association differs by age, sex, social economic status, and ethnicity?

Approach:

This study will be conducted as an ancillary study to the Atherosclerosis Risk in Communities (ARIC) study. The ARIC study, sponsored by the National Heart, Lung and Lung Institute (NHLBI), is an ongoing, bi-racial population-based cohort study of cardiovascular and pulmonary diseases in 15,792 men and women randomly selected from the residents of four U.S. communities. The baseline examination of this cohort was conducted in 1987-1989, followed by yearly contacts and re-examinations every three years. All initial ARIC cohort participants will be eligible for this study. We will assess major exposures at the communities where the study participants were residing over the entire study period (1987-1998). We will abstract ambient air pollution data from the AIRS database, and to create the exposure data for each study participant according to their randomly assigned exam date and community of residences. These exposure data will be combined with the cardiovascular health data already collected by the ARIC investigators. We will perform our analyses to contrast the mean levels or the proportion of cardiovascular responses (the dependent variables) across the levels of air pollution exposures. Since each of the ARIC cohort examinations lasted for three years, with a total of four such examinations, we will have enough variations in the exposure levels to perform cohort examination specific analysis, as well as combining all four cohort examinations adjusting for repeated measures of the dependent variables. All statistical associations between the air pollution exposures and cardiovascular responses will be adjusted for weather factors and other established cardiovascular risk factors, using multivariable regression methods.

The primary pollutant is particulate matter (PM10 and TSP), followed by O3, SO2, CO, and NO2.

The primary cardiovascular health outcomes include:

The occurrence of arrhythmia from regular 2-minute ECG.