Background: Long-term exposure to fine particulate matter (PM2.5) may lead to increased blood pressure (BP). The role of industry- and traffic-specific PM2.
View Article and Find Full Text PDFBackground: Land-use regression (LUR) and dispersion models (DM) are commonly used for estimating individual air pollution exposure in population studies. Few comparisons have however been made of the performance of these methods.
Objectives: Within the European Study of Cohorts for Air Pollution Effects (ESCAPE) we explored the differences between LUR and DM estimates for NO2, PM10 and PM2.
Background: Long-term exposures to particulate matter air pollution (PM2.5 and PM10) and high traffic load have been associated with markers of systemic inflammation. Epidemiological investigations have focused primarily on total PM, which represents a mixture of pollutants originating from different sources.
View Article and Find Full Text PDFAims: Living close to high traffic has been linked to subclinical atherosclerosis, however it is not clear, whether fine particulate matter (PM) air pollution or noise, two important traffic-related exposures, are responsible for the association. We investigate the independent associations of long-term exposure to fine PM and road traffic noise with thoracic aortic calcification (TAC), a reliable measure of subclinical atherosclerosis.
Methods And Results: We used baseline data (2000-2003) from the German Heinz Nixdorf Recall Study, a population-based cohort of 4814 randomly selected participants.
Objectives: The aim of this study was to investigate the association of long-term residential exposure to fine particles with carotid intima-media thickness (CIMT).
Background: Experimental and epidemiological evidence suggest that long-term exposure to air pollution might have a causal role in atherogenesis, but epidemiological findings are still inconsistent. We investigate whether urban particulate matter (PM) air pollution is associated with CIMT, a marker of subclinical atherosclerosis.
Daily to monthly variations in fine particulate matter have been linked to systemic inflammatory responses. It has been hypothesized that smaller particles resulting from combustion processes confer higher toxicity. We aim to analyze the association between short-term exposure to ultrafine and fine particles and systemic inflammation.
View Article and Find Full Text PDFTraffic is one of the major sources of environmental pollution in metropolitan areas, emitting pollutants such as particulate matter and noise. Epidemiological evidence links both particulate matter (PM) and noise to cardiovascular disease and increased cardiovascular mortality. Short-term exposure to traffic may trigger acute cardiovascular events.
View Article and Find Full Text PDFBackground: Long-term exposure to urban air pollution may accelerate atherogenesis, but mechanisms are still unclear. The induction of a low-grade systemic inflammatory state is a plausible mechanistic pathway.
Objectives: We analyzed the association of residential long-term exposure to particulate matter (PM) and high traffic with systemic inflammatory markers.
Background: Long-term exposure to particulate air pollution has been associated with increased cardiovascular disease. Biologic pathways for this association are not fully understood.
Methods: We examined the association of urban air pollution with atherosclerosis of the peripheral vascular bed, using baseline data (2000-2003) from 4348 participants in a population-based cohort study in the German Ruhr Area.
Aims: Long-term exposure to urban air pollution may accelerate atherogenesis and increase cardiopulmonary mortality. We aim to examine the relationship between the long-term residential exposure to traffic and prevalence of coronary heart disease (CHD).
Methods And Results: We used baseline data from the German Heinz Nixdorf RECALL study, a population-based, prospective cohort study.