Cadmium chronic poisoning

Cadmium, 5, 925-1022 acute poisoning, 5,1000 binding to metallothioneins, 6, 673 chronic poisoning, 5, 1000 gravimetry, 1,532 masking, 1,538 metallothioneins, 5,1021 poisoning... 

The most severe form of chronic cadmium (Cd) poisoning caused by prolonged oral Cd ingestion is Itai-itai disease, which developed in numerous inhabitants of the Jinzu River basin in Toyama Prefecture, Japan in the 1950s (Figure 20.7). For the first time, cadmium pollution was shown to have severe consequences on human health, particularly in women. The most important effects were softening of the bones and kidney failure. The name of the disease is derived from the painful screams (Japanese /to/) caused by the severe pain in the... 

Cadmium, 925-1022 acute poisoning, 1000 chronic poisoning, 1000 metallothioneins, 1021 poisoning therapy, 1001 toxicology, 999 Cadmium complexes alcohols, 964 amides, 944 amine oxides, 964 amines, 933 amino acids, 938... 

For this reason, heavy metals and metal ions that are used as additives in plastics and rubber (as colorants, stabilisers, plasticisers and so on) should be monitored carefully, and their use as well as the amounts used should be well known and regulated. In addition to their existence in some of the additives used in plastics and rubbers, toxic heavy metals most of which are considered chronic poisons, such as arsenic, lead, mercury, cadmium, nickel, zinc and chromium, are frequently encountered in industrial processing and other manufacturing operations (their main industrial sources include paint, ink, plastic, rubber and plastic film production, leather tanning, wood preserving, battery manufacturing, and so on). 

Reports on chronic effects of cadmium on human liver function are rare. In experimental animals, liver also accumulates substantial amounts of cadmium after both acute and chronic poisoning (Kotsonis and Klaassen 1977, 1978), which results in hepatic injury with both types of exposure (Dudley et al. 1982 Stowe et al. 1972 Faeder et al. 1977). Dudley et al. (1982) demonstrated that liver is a target organ after acute exposure and that the liver injury may play a role in the lethality of animals soon after exposure. The prominent morphological changes after an acute high dose of cadmium... 

RBP has been found in relatively large amounts in the urine from patients with tubular proteinuria (Peterson and Berggard, 1971). Much is known about urinary protein excretion of Japanese patients with chronic cadmium poisoning (Kanai-er al., 1972a,b). These patients manifest tubular proteinuria and the excretion of considerable amounts of low-molecular-weight proteins, including RBP. The urinary excretion of RBP has been induced in a rabbit (Muto et al., 1976) and in a rhesus monkey (Nomiyama et al., 1981) by chronic poisoning with cadmium. Studies of the role of the kidney in RBP metabolism have also been carried out in rats with various kinds of experimentally induced renal lesions (Peterson et al., 1974). These various reported observations are all consistent with the above postulated role of the kidney in RBP metabolism. 

Friberg, L. (1957) Deposition and distribution of cadmium in man in chronic poisoning Arch. Ind. Health 16, 27-29. 

The Japanese disease itai-itai (ouch-ouch) is a particular syndrome caused by chronic cadmium poisoning. It leads to fractures of long bones due to decalcification, and to muscular dystrophy. The first time the disease was... 

Cadmium (Cd) is a non-essensial metal used in industry as an anti-corrosive agent, and is found as a contaminant in food and also in cigarette smoke. The most serious consequence of chronic Cd poisoning is lung- and prostate cancer but the first effect during chronic intake is kidney damage, manifested by marked proteinuria [164]. Under chronic exposure, cadmium is primarily taken up by the liver, where it induces synthesis of metallothionein (MT) and induces formation of cadmium-metallothionein complexes. 

The functional changes in chronic lead nephropathy appear to be less specific than those observed in acute poisoning. As in other forms of interstitial nephritis, proteinuria and glycosuria are initially absent. In contrast to cadmium nephropathy, the excretion of a large array of urinary marker proteins such as retinal binding protein, lysozyme, and iriicroglobulin [33, 34] is not increased in the absence of a reduced GFR. 

Friberg L. Flealth hazards in the manufacture of alkaline accumulators with special reference to chronic cadmium poisoning. Act Med Sea nd 1950 138 (su ppl. 240) 1-124. 

Piscator M. Proteinuria in chronic cadmium poisoning. I. An electrophoretic and chemical study of urinary and serum proteins from workers with chronic cadmium poisoning. Arch Environ Health 1962 4 607-621. 

Piscator M.The nephropathy of chronic cadmium poisoning. In Cadmium. Foulkes EC (editor). Springer-Verlag, Berlin 1986 p. 179-194. 

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