Cardiovascular actions of lead and relationship to hypertension: a review.

Abstract

Chronic and acute lead poisoning cause overt, clinical symptoms of cardiac and vascular damage with potentially lethal consequences. Morphological, biochemical, and functional derangements of the heart have all been described in patients following exposure to excessive lead levels. Disturbances in cardiac electrical and mechanical activity and postmortem evidence of morphological and biochemical derangements of the myocardium have all been reported following excessive exposure to lead in humans. In addition, signs of vascular degeneration, abnormal vascular smooth muscle function, and altered vessel compliance have been described in humans chronically and acutely exposed to toxic lead levels. Similar cardiovascular complications have been detected following excessive lead exposure in experimental animals. Myocarditis, electrocardiographic disturbances, heightened catecholamine arrhythmogenicity, altered myocardial contractile responsiveness to inotropic stimulation, degenerative structural and biochemical changes affecting the musculature of the heart and vasculature, hypertension, hypercholesterolemia, atherosclerosis, and increased vascular reactivity to alpha-adrenergic agonists have been among the reported cardiovascular disturbances linked to lead poisoning. Less certain are the cardiovascular effects of subclinical lead poisoning. Although controversial, chronic low-level lead exposure has been linked to hypertension and other cardiovascular disturbances in both clinical and experimental studies. In general, it can be concluded that lead over a wide range of exposure intensities can induce significant changes in the function of the cardiovascular system. Evidence points to the involvement of multiple sites of action. Cardiac and vascular sites, as well as sites within the central nervous system, have all been implicated in the sequelae of cardiovascular effects. The exact pathogenic mechanisms that underlie the actions of lead in the cardiovascular system, however, have yet to be elucidated definitively.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Lead Is a Predictor of Homocysteine Levels in a Population-Based Study of Older Adults

“…Another meta-analysis of 20 prospective studies found that for an increase in serum homocysteine of 5 μmol/L, the OR for ischemic heart disease was increased (OR = 1.32; 95% CI, 1.19–1.45), as was the OR for stroke (OR = 1.59; 95% CI, 1.29–1.96) (Wald et al 2002). Other studies support the similarities between the cardiovascular effects of lead and homocysteine (Bautista et al 2002; Cheng et al 2001; Kopp et al 1988; Moller and Kristensen 1992; Nash et al 2003; Pocock et al 1988). …”

Lead and δ-Aminolevulinic Acid Dehydratase Polymorphism: Where Does It Lead? A Meta-Analysis

“…The effect of lead on blood pressure has also been widely investigated (Kopp et al 1988; Pirkle et al 1985). The available literature suggests that there is a positive, albeit weak association between systolic blood pressure and blood lead concentration.…”

Lead Levels and Ischemic Heart Disease in a Prospective Study of Middle-Aged and Elderly Men: the VA Normative Aging Study

“…Moreover, a substantial proportion of the population has had higher lead exposure from leaded gasoline and other sources such as soldered cans, paints, and tap water in the past (Pirkle et al 1994). The long-term consequences of lead exposure include circulatory diseases, kidney diseases, and neurologic disorders (Cheng et al 2001; Harlan 1988; Hertz-Picciotto and Croft 1993; Hu et al 1996a; Kopp et al 1988; Lin et al 2003; Martin et al 2006; Moller and Kristensen 1992; Nash et al 2003; Pirkle et al 1985; Schwartz 1991, 1995; Tsaih et al 2004). …”

“…Lead exposure has been associated with increased blood pressure and hypertension in cross-sectional as well as longitudinal studies (Cheng et al 2001; Harlan 1988; Hertz-Picciotto and Croft 1993; Hu et al 1996a; Kopp et al 1988; Martin et al 2006; Moller and Kristensen 1992; Nash et al 2003; Pirkle et al 1985; Schwartz 1991, 1995). More recently, there is evidence of increased mortality from circulatory causes in individuals with blood lead levels of 20–29 μg/dL in the past (Lustberg and Silbergeld 2002).…”