More air pollutants, fewer HDL particles

Association of Air Pollution Exposures With High-Density Lipoprotein Cholesterol and Particle Number: The Multi-Ethnic Study of Atherosclerosis

Literature - Bell 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

Main results

  • 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.


1. Boden WE, Probstfield JL, Anderson T, et al; AIM-HIGH Investigators. Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. N Engl J Med. 2011;365:2255–2267.

2. Barter PJ, Caulfield M, Eriksson M, et al; ILLUMINATE Investigators. Effects of torcetrapib in patients at high risk for coronary events. N Engl J Med. 2007;357:2109–2122.

3. Mora S, Glynn RJ, Ridker PM. High-density lipoprotein cholesterol, size, particle number, and residual vascular risk after potent statin therapy. Circulation. 2013;128:1189–1197.

4. Mackey RH, Greenland P, Goff DC Jr, et al. High-density lipoprotein cholesterol and particle concentrations, carotid atherosclerosis, and coronary events: MESA (multi-ethnic study of atherosclerosis). J Am Coll Cardiol. 2012;60:508–516.

5. Brook RD, Rajagopalan S, Pope CA 3rd, et al; American Heart Association Council on Epidemiology and Prevention, Council on the Kidney in Cardiovascular Disease, and Council on Nutrition, Physical Activity and Metabolism. Particulate matter air pollution and cardiovascular disease: An update to the scientific statement from the American Heart Association. Circulation. 2010;121:2331–2378.

6. Puett RC, Hart JE, Yanosky JD, et al. Chronic fine and coarse particulate exposure, mortality, and coronary heart disease in the Nurses’ Health Study. Environ Health Perspect. 2009;117:1697–1701.

Find this article online at Arterioscler Thromb Vasc Biol.

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