Air, noise pollution raise cardiovascular risk

Washington: Both air and noise pollution may increase an individual`s risk of developing cardiovascular disease, according to a study in which both factors were considered simultaneously.

Using data from the Heinz Nixdorf Recall study, an ongoing population study from three neighbouring cities in the Ruhr region of Germany, study leader Barbara Hoffmann, MD, MPH, a professor of environmental epidemiology at the IUF Leibniz Research Institute for Environmental Medicine in Germany and her colleagues assessed the long-term exposure to fine particulate matter with an aerodynamic diameter <2.5 micrometre (PM2.5) and long-term exposure to traffic noise in 4238 study participants (mean age 60 years, 49.9 percent male). The exposure to air pollutants was determined by using the EURopean Air Pollution Disperson, or EURAD, model. Exposure to traffic noise was calculated using European Union models of outdoor traffic noise levels. These levels were quantified as weighted 24-hour mean exposure (Lden) and nighttime exposure (Lnight). To determine the association of the two variables with cardiovascular risk, the researchers looked at thoracic aortic calcification (TAC), a measure of subclinical atherosclerosis. TAC was quantified using non-contrast enhanced electron beam computed tomography. Using multiple linear regression, the researchers controlled for other cardiovascular risk factors, including age, gender, education, unemployment, smoking status and history, exposure to second-hand smoke, physical activity, alcohol use and body mass index. After controlling for these variables, the researchers found that fine-particle air pollution was associated with an increase in TAC burden by 19.9 percent (95 percent CI 8.2; 32.8 percent) per 2.4microgram/m3. (To put that increase in perspective: in the United States, the Environmental Protection Agency recently revised the overall limit downward from 15 to 12microgram/m3). The researchers also found that nighttime traffic noise pollution increased TAC burden by 8 percent (95 percent CI 0.8; 8.9 percent) per 5 dB. (An average living room would typically have a noise level of about 40 A-weighted decibels. Mean exposure to traffic noise over 24 hours was not associated with increased TAC. Among subgroups of participants, the researchers found even stronger associations. The interaction of PM2.5 and TAC was clearer among those younger than 65, participants with prevalent coronary artery disease and those taking statins. In contrast, the effect of Lnight was stronger in participants who were not obese, did not have coronary artery disease and did not take statins. ANI