Air pollution may increase heart disease risk: study
Changes in HDL levels may already appear after brief and medium-length exposures to air pollution, researchers said.
Washington: Traffic-related air pollution may increase cardiovascular disease risk by lowering levels of high-density lipoprotein (HDL), commonly known as "good" cholesterol, new research has warned.
Scientists have long known that air pollution increases the risk of developing cardiovascular diseases including atherosclerosis and heart failure, but are uncertain how the two are connected. The connection may be explained by a reduction in the
number of small, cholesterol-depleted HDL particles, leaving the average amount of cholesterol in HDL particles higher on a per-particle basis, said Griffith Bell, from the University of Washington School of Public Health in the US.
Recent evidence suggests that the number and functionality of HDL particles may be a better gauge of HDL's heart-healthy effects than their cholesterol content. In a study of 6,654 middle-aged and older US adults from diverse ethnic backgrounds, participants living in areas with high levels of traffic-related air pollution tended to have lower HDL levels. Researchers found that higher exposure to black carbon (a marker of traffic-related pollution) averaged over a one year period was significantly associated with a lower "good" cholesterol level.
Higher particulate matter exposure over three months was associated with a lower HDL particle number. Men and women responded to air pollutants differently: HDL was lower at higher pollution exposure for both sexes, but the magnitude was greater in women.
The lower levels of HDL observed with high levels of air pollution "may put individuals at a higher risk for cardiovascular disease down the line," Bell said.
Changes in HDL levels may already appear after brief and medium-length exposures to air pollution, researchers said. "Our study helps strengthen the biological plausibility
of the link between traffic-related air pollution and cardiovascular disease," Bell added.
The study was published in the journal Arteriosclerosis, Thrombosis, and Vascular Biology.