Artikel
Long- and short-term residential exposure to PM2.5 and blood markers of systemic inflammation and coagulation
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Veröffentlicht: | 2. September 2009 |
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Introduction: Epidemiologic and experimental studies link elevated levels of particulate matter (PM) to systemic inflammation and coagulation, which have been hypothesized to contribute to air pollution-induced atherogenesis. There are only few studies on long-term exposures yielding controversial results. We examined the association of long-term exposure to fine particulate matter with several blood markers of inflammation and coagulation, controlling for short-term exposures to fine PM and temperature.
Methods: We used baseline data (2000–2003) from the Heinz Nixdorf Recall Study, a population-based prospective cohort of 4814 participants living in three adjacent cities in Germany. A chemistry transport model was applied to model daily surface concentrations of PM2.5 on a grid of 1 km2. We used multiple linear regression analysis to investigate the association between the mean PM2.5 of the 365 days prior to the blood draw at each participant’s residence with acute phase reactants (high-sensitivity C-reactive protein (hs-CRP), fibrinogen), markers of bone marrow response (white blood cells (WBC)) and thrombotic activity (platelets, plasminogen activator inhibitor-1 (PAI-1)).
Results: We found long-term effects for all blood markers, except for WBC. After adjustment (N=3809) for socioeconomic status, lifestyle-related characteristics, current medication, short-term exposure to PM2.5 and meteorology, an increase in PM2.5 of 2.4 µg/m³ (interquartile range) was associated with hs-CRP (10.0% increase; 95% CI 4.6 to 15.6%), fibrinogen (1.49% increase; 95% CI 0.45 to 2.53%), PAI-1 (3.4% increase; 95% CI 0.72 to 7.7%), and platelet count (4*109/L increase; 95% CI: 1*109/L to 6*109/L). Effect estimates were generally stronger in men than in women. No consistent effect of short-term PM2.5 (averaged over 4 days prior to the blood draw) was found.
Discussion: This study indicates that long-term residential exposure to high levels of PM2.5 are independently of short-term exposures associated with markers of systemic inflammation and thrombotic activity, which could contribute to the development and progression of atherosclerosis.