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. 2014 Jun 1;1(2):148-162.
doi: 10.1007/s40572-014-0011-2.

Arsenic Exposure and Subclinical Endpoints of Cardiovascular Diseases

Fen Wu  1 , Peter Molinaro  1 , Yu Chen  1
Affiliations

Arsenic Exposure and Subclinical Endpoints of Cardiovascular Diseases

Fen Wu et al. Curr Environ Health Rep. .

Abstract

Mechanistic evidence suggests that arsenic exposure from drinking water increases the production of reactive oxygen species and influences inflammatory responses and endothelial nitric oxide homeostasis. These arsenic-induced events may lead to endothelial dysfunction that increases the risk of atherosclerosis and cardiovascular disease. We reviewed accumulating epidemiologic evidence that evaluated the association between arsenic exposure and intermediate markers and subclinical measures that predict future cardiovascular risk. Cross-sectional studies have indicated positive associations between high or low-to-moderate levels of arsenic exposure with indices of subclinical atherosclerosis, QT interval prolongation, and circulating markers of endothelial dysfunction. The evidence is limited for other intermediate endpoints such as markers of oxidative stress and inflammation, QT dispersion, and lipid profiles. Prospective studies are needed to enhance the causal inferences of arsenic's effects on subclinical endpoints of cardiovascular disease, especially at lower arsenic exposure levels.

Keywords: QTc prolongation; arsenic exposure; cardiovascular disease; endothelial dysfunction; inflammation; oxidative stress; subclinical atherosclerosis; susceptibility.

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Conflict of interest statement

Compliance with Ethics Guidelines: Conflict of Interest: Fen Wu, Peter Molinaro, and Yu Chen declare that they have no conflict of interest.

Figures

Figure 1
Figure 1
Schematic depiction of epidemiologic evidence on possible mechanisms underlying the cardiovascular effects of arsenic exposure. Epidemiologic studies have demonstrated that arsenic may lead to cardiovascular diseases via its effects on subclinical endpoints which may be modified by individual susceptibility. Ox-LDL, oxidized low-density lipoproteins; CRP, C-reactive protein; PAI-1, plasminogen activator inhibitor-1; sICAM-1, soluble intercellular adhesion molecule 1; sVCAM-1, soluble vascular adhesion molecule 1; cIMT, carotid artery intima-media thickness; QTc, heart-rate corrected QT; QTD, QT dispersion; TDR, transmural dispersion of repolarizaton.
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