Cadmium

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For people not occupationally exposed to cadmium (Cd), dietary intake is the main route of exposure to cadmium. This is shown by Table 10.2, listing data on the routes of exposure and the daily intake by adults. Smoking of 20 cigarettes per day causes an intake of 4 |g of cadmium. In comparison with dietary intake, this does not seem to be too much. However, one should take into account that the absorption of Cd is much lower after oral intake (4 to 8%) than on inhalatory exposure (15 to 40%).

Cd is present in nearly all foodstuffs. In noncontaminated regions, food usually contains less than 0.1 mg Cd/kg. High concentrations (1 to 10 mg/kg) can be found in the organs of cattle, in seafood, and in some mushroom species.

Like most inorganic contaminants, Cd is only absorbed to a small extent from the gastrointestinal tract. Its ability to accumulate in the body may be accounted for by its long biological half-life.

After uptake from the gastro-intestinal tract, Cd is bound to the low molecular weight protein metallothionein (Mt) in the cells of the intestinal wall and in the liver. Mt plays a key role in the homeostases of trace elements such as Zn and Cu in the organism, and in the detoxication of nonessential metals such as Cd, Hg, and Pt. Cd-Mt complexes are gradually released from the intestinal wall and the liver into systemic circulation. After renal excretion by glomerular filtration, the complexes are reabsorbed by the renal proximal tubule cell. It is believed that free ionic Cd resulting from lysosomal degradation of Cd-Mt causes damage to the kidneys.

Several factors are known to affect the absorption of Cd and its distribution over the body. The latter, for example, is determined by the Cd content of the diet. At low doses, Cd accumulates mainly in the kidneys. After high doses, the intestinal Mt-pool is saturated and free Cd will reach the liver. As a result, acute oral toxicity has been observed mainly in the liver and the erythropoietic system, while long-term exposure to low Cd levels (orally and inhalatory) has been found to result in toxic effects in the lungs, kidneys, and bones. It is important to note that in most long-term animal studies where renal and other effects were examined, the renal effects preceded or occurred simultaneously with the other effects.

Also, many dietary factors are known to influence the absorption and distribution of Cd in humans. Various metals may interfere very efficiently with the uptake of Cd.

High-fiber and low-fat diets with adequate mineral levels of calcium, zinc, iron, and phosphorus are known to lead to a lower total body retention of Cd than diets high in fat with a marginal mineral status.

Cadmium has been shown to interfere with the metabolism of vitamin D, calcium, and collagen. These effects manifest themselves as osteoporosis and osteomalacia in humans as well as in animals. An illustrative example is the Itai Itai bone disease ("ouch ouch" disease). This disease occurred as an epidemic among the inhabitants of the Fuchu area in Japan, who for a long time ingested rice that was highly contaminated with Cd (300 to 2000 |g Cd per day). The etiology of this disease points to a combination of factors. Not only the exposure to Cd, but also a deficient diet (low in protein, calcium, and vitamin D) were found to be responsible for the development of this disease in that particular area.

In occupational settings and in studies in rodents, it has appeared that long-term inhalatory exposure to Cd is associated with an increase in prostate cancer and lung cancer. However, the potential carcinogenicity of cadmium has not been clearly shown in oral studies.

In addition to the dose and dietary factors, the speciation of Cd in the diet appears to be an important factor in determining its uptake from food. There is a clear need for data on the form in which Cd is present in food. In animal tissues, Cd occurs mainly as metallothionein complexes. Foods originating from plants are an even more important source of dietary Cd than food of animal origin. In plants, Cd is bound to phytochelatins, proteins that have several properties in common with metallothioneins. Information on the toxicological risks due to the oral intake of Cd bound to metallothionein is limited. Cd and Cd-Mt differ in intensity of toxicity. After parenteral administration, Cd-Mt is more nephrotoxic than inorganic Cd. This seems not to be the case after oral administration. It has been suggested that after a low intake, the metabolic routes of both Cd forms are similar. After uptake from the gastro-intestinal tract, Cd may be released from Cd-Mt. After a high intake, there seems to be a difference in metabolic fate, leading to a higher availability of Cd after intake of inorganic Cd. A difference in Cd availability between foods will certainly have important consequences for the evaluation of risks due to Cd intake and the estimation of tolerable Cd levels in different types of food. The kidneys are the critical organs for long-term oral exposure to Cd, and renal effects always precede or occur simultaneously with other effects. Epidemiological studies in occupational settings have shown that 10% of a population of industrial workers at the age of 45 shows symptoms of renal dysfunction once the renal Cd concentration has reached a level of 200 mg/kg kidney cortex. For the general population, it has been calculated that this level will be reached in 45-year old individuals after a daily dietary Cd intake of ±400 |g. (Table 10.3).

Table 10.3 Calculated average cadmium kidney cortex concentration at age 45 for non-smokers with cadmium intake via food only

Average daily cadmium

100

200

300

400

500

600

700

intake at age 50

Geometric mean cadmium

61

102

143

183

224

265

305

concentration in kidney

cortex* (mg/kg)

Estimated proportion (%)

A

2.7

11

22

34

44

53

60

with kidney cortex cadmium

B

1.8

7.8

17

26

35

44

51

above their individual-

critical concentration

A: PCC50 = 250 mg Cd/kg and PCC10 = 180 mg Cd/kg, log-normal distribution of critical concentrations. B: PCC50 = 300 mg Cd/kg and PCC10 = 200 mg Cd/kg, log-normal distribution of critical concentrations. * Assumed to have a log-normal distribution with geometric SD of 2. Source: Friberg et al., 1985, 1986.

A: PCC50 = 250 mg Cd/kg and PCC10 = 180 mg Cd/kg, log-normal distribution of critical concentrations. B: PCC50 = 300 mg Cd/kg and PCC10 = 200 mg Cd/kg, log-normal distribution of critical concentrations. * Assumed to have a log-normal distribution with geometric SD of 2. Source: Friberg et al., 1985, 1986.

kidney cortex -Cd mg/kg wet weight

10 20 30 40 50 60 70 80 age

Norway o------o former Yugoslavia

Figure 10.1 Average concentration of cadmium in kidney cortex in relation to age. Results from 12 different studies in 10 countries are summarized. The averages are based on data from smokers, non-smokers, females, and males combined. Source: Friberg et al., 1985, 1986.

The FAO/WHO provisional tolerable daily intake (see Chapter 16, Section 16.3.2.1) of Cd, 70 |g, leads to kidney cortex concentrations of 40 to 60 mg/kg (compare these figures with the actual renal Cd concentrations in 10 countries, given in Figure 10.1).

Differences in Cd availability resulting from the intake of different forms of Cd or the effects of other dietary factors are not taken into account in the estimation of tolerances. Another factor contributing to the Cd retention in the body is the smoking behavior of the population. A cigarette contains 0.8 to 2 |g Cd, from which 25 to 40% is absorbed on inhalation. This means that smokers may have higher Cd tissue levels than non-smokers (Figure 10.2).

kidney cortex - A Cd mg/kg wet weight

Belgium India Japan Sweden former USA

Yugoslavia

mean age 56.7 55.5 39.4 42.7 49.3 51.8 51.4 58.4 49.6 53.8 30-59

Belgium India Japan Sweden former USA

Yugoslavia

mean age 56.7 55.5 39.4 42.7 49.3 51.8 51.4 58.4 49.6 53.8 30-59

current and former smoker non-smoker

Figure 10.2 Cadmium kidney cortex concentration (geometric mean values) in relation to smoking habits among subjects (30 to 69 years of age) studied in Belgium, India, Japan, and (former) Yugoslavia. Also included in the figure are data from Sweden and the US (subjects aged 30 to 59). Source: Friberg et al., 1985, 1986.

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