Recently, data from the population-based MESA has shown that retinal arteriolar caliber were narrower and venular caliber were wider among persons living in areas with increased long- and short-term exposure to PM2.5 [1]. Three gram/m3 increases in PM2.5 concentration was associated with arteriole narrowing equivalent to those seen with an age increase of seven years, a more traditional cardiovascular risk factor. These results
suggest that important vascular changes occur with small increases in long- and short-term air pollution exposures. Wider venular diameter with chronic air pollution exposure are consistent with similar investigations into the effects of smoking on retinal microvascular structure [18,19,23,26,28,40,48,60], and may be mediated Selleck PD98059 in part by similar, inflammation-related mechanisms. Long-term exposure to air pollution is known to promote inflammation and endothelial dysfunction [9,49], and may lead to disruptions of microvascular autoregulatory function and venular
widening within the retina. Practically, these findings are important in that subclinical microvascular changes (arteriolar narrowing and venular widening) were reported in individuals exposed to PM2.5 levels well below established regulatory thresholds [1]. These data may Y-27632 order provide information necessary to establish safer and more accurate regulatory air quality standards. Recent work with regard to selected modifiable risk factors and the retinal microcirculation have added to Ceramide glucosyltransferase expanding evidence relating modifiable lifestyle and environmental risk factors to adverse cardiovascular outcomes. It appears that exposure to modifiable risk factors
may affect systemic physiology, which is reflected in retinal microvascular structure. As an easily accessible site in which the human microcirculation can be visualized non-invasively and quantified, the potential use of retinal imaging as a biomarker indicating reversible pathophysiologic processes within the systemic circulation is promising. Nevertheless, evidence showing that quantitative assessment of retinal microvasculature may provide prognostic information beyond current traditional risk factors is very limited. Currently, there have been no established reference levels for age, gender, or disease status, which therefore still limits the utility of retinal imaging as a tool to monitor cardiovascular and metabolic risk in asymptomatic patients or those who have other traditional, positive risk factors. More longitudinal studies are also needed to determine if changes in retinal microvascular structure can revert to normal with various interventions. Retinal imaging may provide clinicians with a personalized and specific marker to measure the effects of specific interventions on disease progression.