• Cigarettes are a significant source of cadmium exposure for the smoking population because tobacco leaves contain large amounts of cadmium (Morrow 2001).
It has been estimated that tobacco smokers are exposed to 1.7 μg cadmium per
cigarette, and about 10% is inhaled when smoked (Morrow 2001; NTP 2005).
• Occupations in which the highest potential exposures occur include cadmium
production and refining, Ni–Cd battery manufacture, cadmium pigment manufacture and formulation, cadmium alloy production, mechanical plating, zinc
smelting, brazing with a silver–cadmium–silver alloy solder, and polyvinyl
chloride compounding (IARC 1993).
• Contamination of children’s jewelry with cadmium can have long-term effects by
introducing a toxicant that can remain in a child’s body (Mead 2010).
4 Toxicity of Cadmium in the Environment
Cadmium has no known biological function in animals and humans but mimics other
divalent metals that are essential to diverse biological functions. Cadmium was
found to be competitive with zinc and copper and to a lesser extent to iron (Pond
et al. 1995). It can cross various biological membranes by different mechanisms
(e.g., metal transporters) and once inside the cells binds to ligands with exceptional
affinity (e.g., metallothioneins), thereby reducing the absorption of copper and, to a
lesser extent, of zinc. Especially, the liver and kidneys contain metallothioneins,
which accumulate cadmium throughout the animal life. However, cadmium is not
easily cleared by the cells, with a biological half-life estimated to be 10–30 years,
and the poor efficiency of cellular export systems explains the long residence time of
this element in storage tissues such as the intestine, liver, and kidneys (EFSA 2009).
4.1 Health Impact on Human Beings
4.1.1 Effect on the Kidney
The kidney is the critical organ of intoxication after long-term exposure to cadmium.
Initial sign of renal lesion is tubular damage resulting in an increased urinary
excretion of low molecular weight proteins, particularly α 2 -, β 2 -, and γ-globulins.
In severe cases effects on renal function are manifested by glucosuria, aminoaciduria, hypercalciuria, hyperphosphateuria, and polyuria due to decreased concentration capacity (Friberg et al. 1974). All these conditions ultimately results
in nephropathy that is the major cause of mortality in workers exposed to cadmium
toxicity (Fig. 15.3).
A number of studies in different areas over the years have looked at the effects of
cadmium on the kidney in the environmentally exposed populations (Cai et al. 1990;
Jung et al. 1993; Nordberg et al. 1997). In Japan many areas were contaminated with
cadmium as a result of discharges from numerous nonferrous metal mines and
15 Cadmium as an Environmental Pollutant: Ecotoxicological Effects, Health. . .
363
It has been estimated that tobacco smokers are exposed to 1.7 μg cadmium per
cigarette, and about 10% is inhaled when smoked (Morrow 2001; NTP 2005).
• Occupations in which the highest potential exposures occur include cadmium
production and refining, Ni–Cd battery manufacture, cadmium pigment manufacture and formulation, cadmium alloy production, mechanical plating, zinc
smelting, brazing with a silver–cadmium–silver alloy solder, and polyvinyl
chloride compounding (IARC 1993).
• Contamination of children’s jewelry with cadmium can have long-term effects by
introducing a toxicant that can remain in a child’s body (Mead 2010).
4 Toxicity of Cadmium in the Environment
Cadmium has no known biological function in animals and humans but mimics other
divalent metals that are essential to diverse biological functions. Cadmium was
found to be competitive with zinc and copper and to a lesser extent to iron (Pond
et al. 1995). It can cross various biological membranes by different mechanisms
(e.g., metal transporters) and once inside the cells binds to ligands with exceptional
affinity (e.g., metallothioneins), thereby reducing the absorption of copper and, to a
lesser extent, of zinc. Especially, the liver and kidneys contain metallothioneins,
which accumulate cadmium throughout the animal life. However, cadmium is not
easily cleared by the cells, with a biological half-life estimated to be 10–30 years,
and the poor efficiency of cellular export systems explains the long residence time of
this element in storage tissues such as the intestine, liver, and kidneys (EFSA 2009).
4.1 Health Impact on Human Beings
4.1.1 Effect on the Kidney
The kidney is the critical organ of intoxication after long-term exposure to cadmium.
Initial sign of renal lesion is tubular damage resulting in an increased urinary
excretion of low molecular weight proteins, particularly α 2 -, β 2 -, and γ-globulins.
In severe cases effects on renal function are manifested by glucosuria, aminoaciduria, hypercalciuria, hyperphosphateuria, and polyuria due to decreased concentration capacity (Friberg et al. 1974). All these conditions ultimately results
in nephropathy that is the major cause of mortality in workers exposed to cadmium
toxicity (Fig. 15.3).
A number of studies in different areas over the years have looked at the effects of
cadmium on the kidney in the environmentally exposed populations (Cai et al. 1990;
Jung et al. 1993; Nordberg et al. 1997). In Japan many areas were contaminated with
cadmium as a result of discharges from numerous nonferrous metal mines and
15 Cadmium as an Environmental Pollutant: Ecotoxicological Effects, Health. . .
363