Lead Exposure and Cardiovascular Dysfunction: Molecular Insights and Clinical Evidence

Abstract

Exposure to lead (Pb) continues to be a significant environmental health problem and is now known to play a significant role in cardiovascular disease (CVD). The aim of this review is to highlight the current knowledge regarding the molecular mechanisms and clinical implications of cardiovascular toxicity of lead. The main routes of exposure to lead are inhalation and ingestion, it is a long-term source of internal exposure because it is bioaccumulated in soft tissues and bone. Lead can cause oxidative stress, endothelial dysfunction, disruption of calcium signaling, chronic inflammation, mitochondrial impairment, and epigenetic changes all of which lead to vascular and myocardial injury. Lead exposure has been consistently associated with increased cardiovascular mortality, heart failure, stroke, coronary artery disease, and hypertension in epidemiological studies. Interestingly, there is no safe threshold for blood lead levels (BLL) since adverse CV effects have been reported at levels < 5µg/dl. In order to implement effective prevention strategies, to better define the risk of cardiovascular dysfunction, and to diminish the burden of cardiovascular dysfunction caused by environmental exposure, the complex relationship between the exposure to lead and cardiovascular dysfunction has to be understood.