A Systematic Review of the Association between Air Pollution and Cardiovascular Parameters: Blood Pressure, Arterial Stiffness, and Endothelial Function
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Abstract
Exposure to air pollution is hypothesized to influence blood pressure, arterial stiffness, and endothelial function, all independent predictors of cardiovascular disease. Systematic literature search for articles reporting exposure to particulate matter (PM) or gaseous pollutants (carbon monoxide, ozone, sulfur dioxide, nitrogen oxide, and nitrogen dioxide) on blood pressure, arterial stiffness, and endothelial function. Short-term exposures studies presented heterogeneous results: 17 of 31 papers supported a rise in blood pressure after exposure to PM, and five of 13 studies of gaseous pollutants; impaired endothelial function in response to PM (six of 11 papers) and gaseous pollutants (three of six studies); and arterial stiffness after PM exposure in three of six studies. Blood pressure data from long-term air pollution studies were more consistent: Seven of nine PM and five of six gaseous exposure studies reported blood pressure elevation. Three studies reported arterial stiffness, with heterogeneous results. A single study was identified reporting PM impaired dilatation. This supports an association between long-term exposure to certain gaseous pollutants, particularly sulfur dioxide (SO2), and PM with increased blood pressure, arterial stiffness, and possibly endothelial dysfunction. Acute exposure can impair endothelial function and may affect blood pressure, but not measures of vascular stiffness. The implication for researchers is that acute versus long-term air pollution conveys different patterns of confounding on these cardiovascular measures. Regarding population-based prevention strategies, data support air quality as potentially a modifiable risk factor in the development of cardiovascular diseases.
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