TY - JOUR
T1 - Effects of Ambient Air Pollution on Hemostasis and Inflammation
AU - Rudez, Goran
AU - Janssen, NAH
AU - Kilinc, E
AU - Leebeek, Frank
AU - Gerlofs-Nijland, ME
AU - Spronk, HMH
AU - ten Cate, H
AU - Cassee, FR
AU - de Maat, Moniek
PY - 2009
Y1 - 2009
N2 - BACKGROUND: Air pollution has consistently been associated with increased morbidity and mortality due to respiratory and cardiovascular disease. Underlying biological mechanisms are not entirely clear, and hemostasis and inflammation are suggested to be involved. OBJECTIVES: Our aim was to study the association of the variation in local concentrations of airborne particulate matter (PM) with aerodynamic diameter < 10 mu m, carbon monoxide, nitrogen monoxide, nitrogen dioxide, and ozone with platelet aggregation, thrombin generation, fibrinogen, and C-reactive protein (CRP) levels in healthy individuals. METHODS: From 40 healthy volunteers, we collected 13 consecutive blood samples within a 1-year period and measured light-transmittance platelet aggregometry, thrombin generation, fibrinogen, and CRP. We performed regression analysis using generalized additive models to study the association between the hemostatic and inflammatory variables, and local environmental concentrations 0 air pollutants for time lags within 24 hr before blood sampling or 24-96 hr before blood sampling. RESULTS: In general, air pollutants were associated with platelet aggregation [average, +8% per interquartile range (IQR), p < 0.01] and thrombin generation (average, +1% per IQR, p < 0.015). Platelet aggregation was not affected by in vitro incubation of plasma with PM. We observed no relationship between any of the air pollutants and fibrinogen or CRP levels. CONCLUSIONS:. Air pollution increased platelet aggregation as well as coagulation activity but had no clear effect on systemic inflammation. These prothrombotic effects may partly explain the relationship between air pollution and the risk of ischemic cardiovascular disease.
AB - BACKGROUND: Air pollution has consistently been associated with increased morbidity and mortality due to respiratory and cardiovascular disease. Underlying biological mechanisms are not entirely clear, and hemostasis and inflammation are suggested to be involved. OBJECTIVES: Our aim was to study the association of the variation in local concentrations of airborne particulate matter (PM) with aerodynamic diameter < 10 mu m, carbon monoxide, nitrogen monoxide, nitrogen dioxide, and ozone with platelet aggregation, thrombin generation, fibrinogen, and C-reactive protein (CRP) levels in healthy individuals. METHODS: From 40 healthy volunteers, we collected 13 consecutive blood samples within a 1-year period and measured light-transmittance platelet aggregometry, thrombin generation, fibrinogen, and CRP. We performed regression analysis using generalized additive models to study the association between the hemostatic and inflammatory variables, and local environmental concentrations 0 air pollutants for time lags within 24 hr before blood sampling or 24-96 hr before blood sampling. RESULTS: In general, air pollutants were associated with platelet aggregation [average, +8% per interquartile range (IQR), p < 0.01] and thrombin generation (average, +1% per IQR, p < 0.015). Platelet aggregation was not affected by in vitro incubation of plasma with PM. We observed no relationship between any of the air pollutants and fibrinogen or CRP levels. CONCLUSIONS:. Air pollution increased platelet aggregation as well as coagulation activity but had no clear effect on systemic inflammation. These prothrombotic effects may partly explain the relationship between air pollution and the risk of ischemic cardiovascular disease.
U2 - 10.1289/ehp.0800437
DO - 10.1289/ehp.0800437
M3 - Article
C2 - 19590696
SN - 0091-6765
VL - 117
SP - 995
EP - 1001
JO - Environmental Health Perspectives
JF - Environmental Health Perspectives
IS - 6
ER -