Cadmium exposure in the population: from health risks to strategies of prevention

Abstract

We focus on the recent evidence that elucidates our understanding about the effects of cadmium (Cd) on human health and their prevention. Recently, there has been substantial progress in the exploration of the shape of the Cd concentrationresponse function on osteoporosis and mortality. Environmental exposure to Cd increases total mortality in a continuous fashion without evidence of a threshold, independently of kidney function and other classical factors associated with mortality including age, gender, smoking and social economic status. Pooled hazard rates of two recent environmental population based cohort studies revealed that for each doubling of urinary Cd concentration, the relative risk for mortality increases with 17% (95% CI 4.2-33.1%; P \ 0.0001). Tubular kidney damage starts at urinary Cd concentrations ranging between 0.5 and 2 lg urinary Cd/g creatinine, and recent studies focusing on bone effects show increased risk of osteoporosis even at urinary Cd below 1 lg Cd/g creatinine. The non-smoking adult population has urinary Cd concentrations close to or higher than 0.5 lg Cd/g creatinine. To diminish the transfer of Cd from soil to plants for human consumption, the bioavailability of soil Cd for the plants should be reduced (external bioavailability) by maintaining agricultural and garden soils pH close to neutral (pH-H 2 O of 7.5; pH-KCL of 6.5). Reducing the systemic bioavailability of intestinal Cd can be best achieved by preserving a balanced iron status. The latter might especially be relevant in groups with a lower intake of iron, such as vegetarians, and women in reproductive phase of life. In exposed populations, house dust loaded with Cd is an additional relevant exposure route. In view of the insidious etiology of health effects associated with low dose exposure to Cd and the current European Cd intake which is close to the tolerable weekly intake, one should not underestimate the importance of the recent epidemiological evidence on Cd toxicity as to its medical and public health implications.

CAX‐ing a wide net: Cation/H+ transporters in metal remediation and abiotic stress signalling

“…Improved sequestration of metals such as Cd 2+ in the root tissues of plants can reduce Cd 2+ levels in edible tissues, as Cd 2+ exposure is a major hazard to human health (Nawrot et al . 2010). Root‐specific expression of CAX transporters mitigates Cd 2+ content in tobacco leaves (Korenkov et al .…”

The Mechanism of the Osteoprotective Action of a Polyphenol-Rich Aronia melanocarpa Extract during Chronic Exposure to Cadmium is Mediated by the Oxidative Defense System

“…Recently, the possibility of using natural plant ingredients for protection against the dangerous action of xenobiotics to which humans are exposed throughout their lifetime, including Cd, which is one of the most toxic heavy metals, has been of special interest to researchers [1][2][3][4][5][6][7][8][9]. Evidence that even relatively low exposure to Cd contributes to osteoporosis and bone fractures [10][11][12] together with forecasts that the general populationʼs exposure to this element will increase [2] are reasons that growing attention has been focused on searching for an effective means of protection from the unfavorable action of this xenobiotic, including damage to the skeleton.…”

“…Evidence that even relatively low exposure to Cd contributes to osteoporosis and bone fractures [10][11][12] together with forecasts that the general populationʼs exposure to this element will increase [2] are reasons that growing attention has been focused on searching for an effective means of protection from the unfavorable action of this xenobiotic, including damage to the skeleton. It seems that polyphenols, being the most abundant bioactive components in our diet [13,14], are a promising group of compounds playing a role in this protection [3][4][5][6][7][8][9]15].…”

Harmful Interactions of Non-Essential Heavy Metals with Cells of the Innate Immune System

“…Although the exact components of cigarette smoke which promote biofilm formation have not been established, it is noteworthy that nickel, which like Cd, Pb and V is also present in tobacco has been reported to promote biofilm formation by Escherichia coli in vitro [109,110]. Alternative sources of exposure to Cd, Pb and V include industrial and environmental pollution, high risk occupations and contaminated food such as fish [111,112]. an unusual mechanism involving the inactivation of the neutrophil/ monocyte chemoattractants, IL8 and the complement cleavage product, C5a.…”