Abstract:
Background: Associations between estimates of long-term population exposure to fine airborne particulate matter (PM2.5) and cardiovascular endpoints, especially mortality, have now been reported in several population cohort studies. More recently, several studies have linked PM2.5 with increases in blood pressure, but the components of PM2.5 primarily responsible for these changes in blood pressure are not well studied. Although a few studies have linked trace elements such as copper, zinc, and nickel with elevations in blood pressure, the effects of ambient vanadium on blood pressure are unknown. The purpose of this study is to determine if estimated PM2.5 vanadium exposure is associated with systolic and diastolic blood pressure.
Methods: The primary outcomes were cross-sectional measurements in 2005-2007 of seated systolic and diastolic blood pressure from 5517 participants aged 45-84 in the Multi-Ethnic Study of Atherosclerosis (MESA). Individual-level ambient exposure to vanadium was estimated using existing geospatial modeling predictions developed by MESA Air and the National Particle Components Toxicity (NPACT) Initiative. Incrementally richer regression models were used to adjust for the following covariates: age, gender, race/ethnicity, educational level, income, smoking status, alcohol use, blood lipids, body mass index, blood glucose, city region, and anti-hypertensive usage. Sensitivity analyses were conducted by restricting analysis to those not taking anti-hypertensive medications, and to those who had lived at one address since 1980. Additionally, some of the models included adjustment variables for other PM2.5 metals.
Results: In our primary model with adjustment for city region, mean systolic blood pressure (SBP) increased by 0.4 mm Hg per interquartile range (IQR) increase in vanadium (V) concentration, 95% CI [-1.1, 1.8]. There was no effect on mean diastolic blood pressure (DBP). The effect estimate for SBP was in negative direction when there was no adjustment for city region. The effect estimates for SBP and DBP became larger (1.4 mm Hg [-0.5, 3.3] and 1.1 mm Hg [0.1, 2.0]), respectively, in city-adjusted analyses after excluding subjects taking anti-hypertensive medications. The findings were somewhat sensitive to adjustments for other PM2.5 metals, depending on the metal.
Conclusion: These results indicate that exposure to vanadium may be associated with increases in both SBP and DBP. Because the findings were primarily seen in those not taking anti-hypertensive medications and were somewhat model-dependent, these findings need to be interpreted cautiously and replicated in other cohorts. Investigating potential effects of other PM2.5 components will also be of interest.