Association of ambient air pollution with blood markers of inflammation and coagulation: Results from a prospective panel study in Augsburg, Germany

Background: While there is compelling evidence that elevated concentrations of particulate matter are associated with cardiovascular disease exacerbation, the pathophysiological mechanisms remain unclear. Objective: To examine the effect of ambient air pollutants on blood markers of inflammation and coagulation in individuals with type 2 diabetes (T2DM) or impaired glucose tolerance (IGT) and in healthy people with a potential genetic predisposition on the detoxifying pathway. Materials and Methods: The study consisted of two panels of non-smoking individuals: 1) individuals with either T2DM (n=83) or IGT (n=104), and 2) individuals with potential genetic susceptibility (n=87). All study participants had blood withdrawn in up to seven repeated examinations, scheduled every 4–6 weeks at the same time on the same day of the week between 3/2007 and 12/2008 in Augsburg. In total, 1766 blood samples were investigated for soluble CD40 ligand (sCD40L), fibrinogen, myeloperoxidase (MPO), and plasminogen activator inhibitor-1 (PAI-1). Hourly means of were collected at a fixed monitoring site and 24 hour averages were calculated. Associations between air pollutants and blood markers were analyzed using additive mixed models adjusting for long-term time trend, air temperature, relative humidity, and barometric pressure. Results: In the panel with potential genetic susceptibility sCD40L and PAI-1 showed a negative association with all air pollutant averages within 24 hours before the blood withdrawal (lag 0). MPO was strongly positively associated with all air pollutants (lag of 0–2 days) whereas the effect for fibrinogen was weaker and had a longer time delay (lag of 1–3 days). Results: were less conclusive for the other panel except for fibrinogen. Conclusion: Early physiological responses in blood markers of inflammation and coagulation were associated with the exposure to ambient air pollutants suggesting that the biological pathway for aggravating atherosclerotic disease leads via systemic inflammation.