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Brüske, I. ; Hampel, R. ; Baumgärtner, Z.* ; Rückerl, R. ; Greven, S.* ; Koenig, W.* ; Peters, A. ; Schneider, A.E.

Ambient air pollution and lipoprotein-associated phospholipase A₂ in survivors of myocardial infarction.

Environ. Health Perspect. 119, 921-926 (2011)

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Increasing evidence suggests a proatherogenic role for lipoprotein-associated phospholipase A₂ (Lp-PLA2). A meta-analysis of published cohorts has shown that Lp-PLA2 is an independent predictor of coronary heart disease events and stroke. OBJECTIVE: In this study, we investigated whether the association between air pollution and cardiovascular disease might be partly explained by increased Lp-PLA2 mass in response to exposure. METHODS: A prospective longitudinal study of 200 patients who had had a myocardial infarction was performed in Augsburg, Germany. Up to six repeated clinical examinations were scheduled every 4-6 weeks between May 2003 and March 2004. Supplementary to the multicenter AIRGENE protocol, we assessed repeated plasma Lp-PLA2 concentrations. Air pollution data from a fixed monitoring site representing urban background concentrations were collected. We measured hourly means of particle mass [particulate matter (PM) < 10 µm (PM₁₀) and PM < 2.5 µm (PM(2.5)) in aerodynamic diameter] and particle number concentrations (PNCs), as well as the gaseous air pollutants carbon monoxide (CO), sulfur dioxide (SO₂), ozone (O₃), nitric oxide (NO), and nitrogen dioxide (NO₂). Data were analyzed using mixed models with random patient effects. RESULTS: Lp-PLA2 showed a positive association with PM₁₀, PM(2.5), and PNCs, as well as with CO, NO₂, NO, and SO₂ 4-5 days before blood withdrawal (lag 4-5). A positive association with O₃ was much more immediate (lag 0). However, inverse associations with some pollutants were evident at shorter time lags. CONCLUSION: These preliminary findings should be replicated in other study populations because they suggest that the accumulation of acute and subacute effects or the chronic exposure to ambient particulate and gaseous air pollution may result in the promotion of atherosclerosis, mediated, at least in part, by increased levels of Lp-PLA2.

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