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The results showed that the risk of death from cardiovascular disease was almost six times higher in men with the highest levels of bone lead compared to men with the lowest levels. The risk of death from all causes was 2.

The results appeared independent of age, smoking, education, race, alcohol, physical activity, BMI, high density lipoprotein or total cholesterol levels, hypertension or diabetes.

They also note that, in addition to high blood pressure, exposure to lead has been associated with widened pulse-pressure an indicator of arterial stiffening and heart disease. The prime targets to lead toxicity are the heme synthesis enzymes, thiol-containing antioxidants and enzymes superoxide dismutase, catalase, glutathione peroxidase, glucose 6-phosphate dehydrogenase and antioxidant molecules like GSH. The low blood lead levels are sufficient to inhibit the activity of these enzymes and induce generation of reactive oxygen species and intensification oxidative stress.

The primary target of lead toxicity is the central nervous system. There are different cellular, intracellular and molecular mechanisms of lead neurotoxicity: The vascular endothelium is now regarded as the main target organ for the toxic effect of lead.

Lead affects the vasoactive function of endothelium through the increased production of reactive oxygen species, inactivation of endogenous nitric oxide and downregulation of soluble guanylate cyclase by reactive oxygen species, leading to a limiting nitric oxide availability, impairing nitric oxide signaling. Westpac Online Investing; Batch Advantage;. Westpac Choice is our most popular everyday account.

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