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DOI: 10.13140/2.1.1165.4082 · Available from: Patrick De Boever, Sep 26, 2015
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    ABSTRACT: Background: Microcirculation plays an important role in the physiology of cardiovascular health. Air pollution is an independent risk factor for the development and progression of cardiovascular diseases, but the number of studies on the relation between air pollution and the micro-circulation is limited. Objectives: We examined the relationship between short-term changes in air pollution and microvascular changes. Methods: We measured retinal microvasculature using fundus image analysis in a panel of 84 healthy adults (52% female), 22-63 years of age, during January-May 2012. Blood vessels were measured as central retinal arteriolar/venular equivalent (CRAE/CRVE), with a median of 2 measurements (range, 1-3). We used monitoring data on particulate air pollution (PM10) and black carbon (BC). Mixed-effect models were used to estimate associations between CRAE/CRVE and exposure to PM10 and BC using various exposure windows. Results: CRAE and CRVE were associated with PM10 and BC concentrations, averaged over the 24 hr before the retinal examinations. Each 10-μg/m3 increase in PM10 was associated with a 0.93-μm decrease (95% CI: -1.42, -0.45; p = 0.0003) in CRAE and a 0.86-μm decrease (95% CI: -1.42, -0.30; p = 0.004) in CRVE after adjusting for individual characteristics and time varying conditions such as ambient temperature. Each 1-μg/m3 increase in BC was associated with a 1.84-μm decrease (95% CI: -3.18, -0.51; p < 0.001) in CRAE. Conclusions: Our findings suggest that the retinal microvasculature responds to short-term changes in air pollution levels. These results support a mechanistic pathway through which air pollution can act as a trigger of cardiovascular events at least in part through effects on the microvasculature.
    Environmental Health Perspectives 06/2013; DOI:10.1289/ehp.1205721 · 7.98 Impact Factor
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    ABSTRACT: In 2004, the first American Heart Association scientific statement on "Air Pollution and Cardiovascular Disease" concluded that exposure to particulate matter (PM) air pollution contributes to cardiovascular morbidity and mortality. In the interim, numerous studies have expanded our understanding of this association and further elucidated the physiological and molecular mechanisms involved. The main objective of this updated American Heart Association scientific statement is to provide a comprehensive review of the new evidence linking PM exposure with cardiovascular disease, with a specific focus on highlighting the clinical implications for researchers and healthcare providers. The writing group also sought to provide expert consensus opinions on many aspects of the current state of science and updated suggestions for areas of future research. On the basis of the findings of this review, several new conclusions were reached, including the following: Exposure to PM <2.5 microm in diameter (PM(2.5)) over a few hours to weeks can trigger cardiovascular disease-related mortality and nonfatal events; longer-term exposure (eg, a few years) increases the risk for cardiovascular mortality to an even greater extent than exposures over a few days and reduces life expectancy within more highly exposed segments of the population by several months to a few years; reductions in PM levels are associated with decreases in cardiovascular mortality within a time frame as short as a few years; and many credible pathological mechanisms have been elucidated that lend biological plausibility to these findings. It is the opinion of the writing group that the overall evidence is consistent with a causal relationship between PM(2.5) exposure and cardiovascular morbidity and mortality. This body of evidence has grown and been strengthened substantially since the first American Heart Association scientific statement was published. Finally, PM(2.5) exposure is deemed a modifiable factor that contributes to cardiovascular morbidity and mortality.
    Circulation 06/2010; 121(21):2331-78. DOI:10.1161/CIR.0b013e3181dbece1 · 14.43 Impact Factor
  • Direct and indirect effects of particulate matter on the cardiovascular system . Toxicol Lett 208 293-299.