Metal pollutants and cardiovascular disease: Mechanisms and consequences of exposure

Abstract

Introduction There is epidemiological evidence that metal contaminants may play a role in the development of atherosclerosis and its complications. Moreover, a recent clinical trial of a metal chelator had a surprisingly positive result in reducing cardiovascular events in a secondary prevention population, strengthening the link between metal exposure and cardiovascular disease (CVD). This is, therefore, an opportune moment to review evidence that exposure to metal pollutants, such as arsenic, lead, cadmium, and mercury, are significant risk factors for CVD. Methods We reviewed the English-speaking medical literature to assess and present the epidemiological evidence that 4 metals having no role in the human body (xenobiotic), mercury, lead, cadmium, and arsenic, have epidemiologic and mechanistic links to atherosclerosis and CVD. Moreover, we briefly review how the results of the Trial to Assess Chelation Therapy strengthen the link between atherosclerosis and xenobiotic metal contamination in humans. Conclusions There is strong evidence that xenobiotic metal contamination is linked to atherosclerotic disease and is a modifiable risk factor.

Mortality for chronic-degenerative diseases in Tuscany: Ecological study comparing neighboring areas with substantial differences in environmental pollution

“…Moreover, some heavy metals may also affect traditional cardiovascular risk factors. For instance, chronic lead overload (both evaluated by its blood and bone levels) is associated to arterial hypertension and dyslipidemia [22]. As a result, an increase in vascular inflammation and endothelial damage markers [24] and early carotid atherosclerotic changes [25] have been reported in chronically exposed subjects to heavy metals.…”

“…The hypothesis that metal environment contamination might represent a common risk factor for this heterogeneous group of diseases deserves a few comments. Strong epidemiological studies support a causal link between chronic environmental exposure to xenobiotic metals (arsenic, lead, cadmium and mercury) and cardiovascular morbidity [22,23]. All heavy metals may reduce antioxidant cellular pool, increasing the intracellular concentration of reactive oxygen species and promoting lipid peroxidation and both cell membrane and DNA damages.…”

Disruption of iron homeostasis and resultant health effects upon exposure to various environmental pollutants: A critical review

“…Li et al, 2006). Meanwhile, heavy metals could generate free radicals, such as reactive oxygen species (ROS), through binding with glutathione (Solenkova et al, 2014) and metallothionein (MT) (Sato and Kondoh, 2002), thus driving oxidative stress and incurring detrimental effects on cells (Farina et al, 2013). Thereby, the following events may occur to break concerted iron balance.…”

“…Once these heavy metals enter the body, they bind to proteins that contain sulfhydryl groups (e.g., glutathione), due to their electrophilic properties. Depletion of glutathione will increase intracellular oxidative stress (Solenkova et al, 2014), which further induces lipid peroxidation, protein oxidation, DNA oxidation and other toxic effects (Solenkova et al, 2014). Moreover, heavy metals can bind to nitrogenand oxygen-containing groups or compete with the essential metal ions in enzyme molecules, and thus cause conformational and functional changes of these biomolecules and thereby disturb the in vivo metal homeostasis (Koedrith and Seo, 2011).…”

Assessment of the levels of cadmium and lead in soil and vegetable samples from selected dumpsites in the Kumasi Metropolis of Ghana

“…Based on dose-response analyses, it has been established that provisional tolerable weekly intake (PTWI) of 25000 mgkg -1 body weight is associated with a decrease of at least 3 IQ points in children and an increase in systolic blood pressure of approximately 3 mmHg (0.4 kPa) in adults (WHO/FAO, 2011;Solenkova et al, 2014;Tellez-Plaza et al, 2012). The rate of absorption of Pb into the bloodstream ranges from 3 to 80% (WHO/FAO, 2011;Marsh and Bailey, 2013;Sabath and Robles-Osorio, 2012).…”