More air pollutants, fewer HDL particles
Association of Air Pollution Exposures With High-Density Lipoprotein Cholesterol and Particle Number: The Multi-Ethnic Study of AtherosclerosisBell G, Mora S, Greenland P, et al. - Arterioscler Thromb Vasc Biol. 2017;37:published online ahead of print
Although HDL-C is inversely associated with cardiovascular events, there is no evidence showing that HDL-C elevations are associated with a clinical benefit [1,2]. One reason could be that the measurement of HDL particle number (HDL-P) may better reflect the cardio-protective effects of HDL compared with HDL-C [3,4]. Ambient air pollution, which may negatively influence the HDL concentrations through inflammation and oxidative stress, is associated with atherosclerosis, heart failure and cardiovascular death [5,6].
In this analysis of the MESA study (Multi-Ethnic Study of Atherosclerosis Air Pollution), the associations between long- and short-term concentrations of the traffic-related air pollutants PM2.5 or black carbon (BC) and HDL-c or HDL-P were evaluated in a multi-ethnic cohort of 6654 adults without cardiovascular disease. Long-term exposure periods were averaged to 12 months, 3 months and 2 weeks prior to examination. Short-term averaging periods estimate average PM2.5 exposure on the day of blood draw, the day before blood draw, and a moving average of the previous 5 days of PM2.5 exposure
- In the 2-week averaging period, there was a significant difference in HDL-C for a 5 μg/m3 higher PM2.5 (0.86 mg/dL, 95% CI −1.38 to −0.34) when adjusting for age, sex, race/ethnicity and site only, which became non-significant after adjustment for other covariates.
- The short-term (0–5 days prior to blood draw) PM2.5 exposure or outdoor PM2.5 exposure were not significantly associated with HDL-C.
- At the 1-year averaged time period, a 0.7×10−6 m−1 higher BC was significantly associated with a −1.68 mg/dL (95% CI −2.86 to −0.50, P=0.001) lower HDL-C when adjusted for covariates.
- There was a significant inverse association between medium-term (3-month and 2-week) PM2.5 concentrations and HDL-P, but not in the 1-year period.
- A 5 μg/m3 higher 3-month average PM2.5 concentration was associated with a −0.64 μmol/L (95% CI −1.02 to −0.26) lower HDL-P and a 5 μg/m3 higher 2-week average PM2.5 was associated with a −0.29 μmol/L (95% CI −0.57 to −0.01) lower HDL-P.
- In the short-term PM2.5 analysis, there was a significant inverse association between higher PM2.5 in the 5 days before blood draw and HDL-P (−0.21 μmol/L per 5 μg/m3, 95% CI −0.38 to −0.04). Averaging periods that included fewer days before the blood draw had no association with HDL-P.
- Adjusted for 3-day average PM2.5, a 5 μg/m3 higher PM2.5 over the 3-month time period was associated with a −0.50 (95% CI −0.92 to −0.09) change in HDL-P.
- A 0.7×10−6 m−1 higher 1-year BC exposure was associated with −0.55 μmol/L (95% CI −1.13 to 0.03) lower HDL-P.
- There was a significant interaction between gender and the association between BC and HDL-C (P for interaction <0.001), with the association stronger in women for BC and HDL-C (−2.63 mg/dL, 95% CI −4.46 to −0.81) compared with men (−0.65 mg/dL, 95% CI −2.14 to 0.84).
In a large, multi-ethnic cohort without cardiovascular disease, exposure to high levels of the traffic-related pollutants PM2.5 (3 months) and BC (1 year) was associated with changes in several measures of HDL. Moreover, short-term exposure was associated with lower HDL-P. These findings suggest that the negative influence of air pollutants on HDL, may explain the increased cardiovascular risk under these environmental conditions.