Academic journal article Environmental Health Perspectives

Endothelial Dysfunction: Associations with Exposure to Ambient Fine Particles in Diabetic Individuals

Academic journal article Environmental Health Perspectives

Endothelial Dysfunction: Associations with Exposure to Ambient Fine Particles in Diabetic Individuals

Article excerpt

BACKGROUND: Exposure to fine airborne particulate matter [[less than or equal to] 2.5 [micro]m in aerodynamic diameter ([PM.sub.2.5])] has been associated with cardiovascular and hematologic effects, especially in older people with cardiovascular disease. Some epidemiologic studies suggest that with diabetes also may be a particularly susceptible population.

OBJECTIVES: The purpose of this study was to analyze the short-term effects of ambient [PM.sub.2.5] on markers of endothelial function in diabetic volunteers.

METHODS: We conducted a prospective panel study in 22 people with type 2 diabetes mellitus in Chapel Hill, North Carolina (USA), from November 2004 to December 2005. We acquired daily measurements of [PM.sub.2.5] and meteorologic data at central monitoring sites. On 4 consecutive days, we measured endothelial function by brachial artery ultrasound in all participants and by pulsewave measurements in a subgroup. Data were analyzed using additive mixed models with a random participant effect and adjusted for season, day of the week, and meteorology.

RESULTS: Flow-mediated dilatation decreased in association with [PM.sub.2.5] during the first 24 hr, whereas small-artery elasticity index decreased with a delay of 1 and 3 days. These [PM.sub.2.5]-associated decrements in endothelial function were greater among participants with a high body mass index, high glycosylated hemoglobin A 1c, low adiponection, or the null polymorphism of glutathione S-transferase M1. However, high levels of myeloperoxidase on the examination day led to strongest effects on endothelial dysfunction.

CONCLUSIONS: These data demonstrate that [PM.sub.2.5] exposure may cause immediate endothelial dysfunction. Clinical characteristics associated with insulin resistance were associated with enhanced effects of PM on endothelial function. In addition, participants with greater oxidative potential seem to be more susceptible.

KEY WORDS: air pollution, diabetes, endothelial dysfunction, environmental epidemiology, particulate matter. Environ Health Perspect 116:1666-1674 (2008). doi:10.1289/ehp.11666 available via[Online 31 July 2008]


Numerous epidemiologic studies have reported associations between exposure to ambient levels of particulate matter (PM) and various indices of acute cardiopulmonary morbidity and mortality [U.S. Environmental Protection Agency (EPA) 2004]. Ambient PM exposure at current levels has been implicated in the onset and exacerbation of lung and heart disease (U.S. EPA 2004). Although the primary mode of entry into the body is through the respiratory system, the greatest population-attributable risk from air pollution is due to cardiovascular disease.

Epidemiologic data suggest that individuals with diabetes may be at higher risk from effects of PM (O'Neill et al. 2007; Zanobetti and Schwartz 2001, 2002). Several parallels exist between the pathophysiologic effects of diabetes and the cardiovascular, hematologic, and autonomic responses to airborne PM. Moreover, evidence indicates that diabetes and insulin resistance are associated with endothelial dysfunction (Caballero 2003; Feener and King 2001; Hsueh and Quinones 2003; Schram et al. 2004), which suggests that people with diabetes may be particularly susceptible to the effects of PM.

Flow-mediated dilatation (FMD) of the brachial artery is a noninvasive method of assessing endothelial function that has been widely employed in clinical studies of vascular biology. The technique uses high-definition ultrasound to measure brachial artery diameter before and after in increase in shear stress that is induced by reactive hyperemia. The arterial dilatation, quantified as the percent change in arterial diameter, reflects local endothelial release of nitric oxide (NO). This endothelial-dependent response to increased shear stress can be contrasted to the endothelium-independent dilatation observed with nitroglycerin. …

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