Heavy Metal Poisoning and Cardiovascular Disease

Eman M. Alissa, Gordon A. Ferns

Journal of Toxicology · 2011 · 486 citations · 159 references

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Concepts

TL;DR

Cardiovascular disease is a growing global health problem, and while traditional risk factors explain only part of its mortality, environmental exposures such as chronic heavy metal contamination—whose mechanisms remain unclear but may involve oxidative stress—are increasingly recognized as important contributors. This review summarizes heavy‑metal homeostasis, evidence linking them to cardiovascular disease, proposes potential mechanisms, and highlights the need for further mechanistic and prospective studies to clarify their role. Heavy metals may raise cardiovascular risk through impaired antioxidant metabolism and oxidative stress, though the precise mechanisms remain to be fully elucidated.

Abstract

Cardiovascular disease (CVD) is an increasing world health problem. Traditional risk factors fail to account for all deaths from CVD. It is mainly the environmental, dietary and lifestyle behavioral factors that are the control keys in the progress of this disease. The potential association between chronic heavy metal exposure, like arsenic, lead, cadmium, mercury, and CVD has been less well defined. The mechanism through which heavy metals act to increase cardiovascular risk factors may act still remains unknown, although impaired antioxidants metabolism and oxidative stress may play a role. However, the exact mechanism of CVD induced by heavy metals deserves further investigation either through animal experiments or through molecular and cellular studies. Furthermore, large-scale prospective studies with follow up on general populations using appropriate biomarkers and cardiovascular endpoints might be recommended to identify the factors that predispose to heavy metals toxicity in CVD. In this review, we will give a brief summary of heavy metals homeostasis, followed by a description of the available evidence for their link with CVD and the proposed mechanisms of action by which their toxic effects might be explained. Finally, suspected interactions between genetic, nutritional and environmental factors are discussed.

References

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