gms | German Medical Science

Background: Ambient air pollution concentrations have been associated with cardiovascular morbidity and mortality. Lipoprotein-associated phospholipase (Lp-PLA2) plays a critical role in atherogenesis and was described as a novel risk factor for cardiovascular disease. The present study examines the influence of ambient air pollution on Lp-PLA2 levels.

Methods: A prospective longitudinal study of 200 post myocardial infarction (MI) survivors was performed in Augsburg, Germany. Six repeated measurements of Lp-PLA2 levels (total 1143) were scheduled for each patient between May 2003 and March 2004. Hourly data on particle number concentrations (PNC), mass concentrations of less than 10µm (PM10) and 2,5 µm (PM2,5), were collected at a central measurement site, gaseous pollutants and meteorological data were obtained from local networks. A confounder model was built adjusting for meteorology, time-invariant and time-varying covariates. Data were analyzed with a mixed effects model.

Results: The results of the association between air pollutants and Lp-PLA2 are presented as percent changes of arithmetic mean for Lp-PLA2 level based on an increase of one interquartile range in air pollutants. First negative (lag0, lag1, lag2) and then delayed positive (lag3 and lag4) associations between Lp-PLA2 levels and concentrations of several markers of urban air pollution (PNC, PM10, NO, CO, SO2) were observed. However most effects only achieved statistical significance on the same day (lag0) and on day 4 (lag4) before the blood withdrawal. The strongest increase per interquartile range (IQR) on Lp-PLA2 (4.6; 95%CI: 1.24, 7.95) resulted on day 4 from the ultrafine particles, a marker of traffic combustion processes.

Conclusions: We hypothesize that Lp-PLA2 increases through oxidative stress caused by particle pollution.