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Friday, 11 February 2011 03:51

Cadmium

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Gunnar Nordberg

Occurrence and Uses

Cadmium (Cd) has many chemical and physical similarities to zinc and occurs together with zinc in nature. In minerals and ores, cadmium and zinc generally have a ratio of 1:100 to 1:1,000.

Cadmium is highly resistant to corrosion and has been widely used for electroplating of other metals, mainly steel and iron. Screws, screw nuts, locks and various parts for aircraft and motor vehicles are frequently treated with cadmium in order to withstand corrosion. Nowadays, however, only 8% of all refined cadmium is used for platings and coatings. Cadmium compounds (30% of the use in developed countries) are used as pigments and stabilizers in plastics, and cadmium is also used in certain alloys (3%). Rechargeable, small portable cadmium-containing batteries, used, for example, in mobile telephones, comprise a rapidly increasing usage of cadmium (55% of all cadmium in industrialized countries in 1994 was used in batteries).

Cadmium occurs in various inorganic salts. The most important is cadmium stearate, which is used as a heat stabilizer in polyvinyl chloride (PVC) plastics. Cadmium sulphide and cadmium sulphoselenide are used as yellow and red pigments in plastics and colours. Cadmium sulphide is also used in photo- and solar cells. Cadmium chloride acts as a fungicide, an ingredient in elecroplating baths, a colourant for pyrotechnics, an additive to tinning solution and a mordant in dyeing and printing textiles. It is also used in the production of certain photographic films and in the manufacture of special mirrors and coatings for electronic vacuum tubes. Cadmium oxide is an elecroplating agent, a starting material for PVC heat stabilizers and a component of silver alloys, phosphors, semiconductors and glass and ceramic glazes.

Cadmium can represent an environmental hazard, and many countries have introduced legislative actions aimed towards decreasing the use and subsequent environmental spread of cadmium.

Metabolism and accumulation

Gastrointestinal absorption of ingested cadmium is about 2 to 6% under normal conditions. Individuals with low body iron stores, reflected by low concentrations of serum ferritin, may have considerably higher absorption of cadmium, up to 20% of a given dose of cadmium. Significant amounts of cadmium may also be absorbed via the lung from the inhalation of tobacco smoke or from occupational exposure to atmospheric cadmium dust. Pulmonary absorption of inhaled respirable cadmium dust is estimated at 20 to 50%. After absorption via the gastrointestinal tract or the lung, cadmium is transported to the liver, where production of a cadmium-binding low-molecular-weight protein, metallothionein, is initiated.

About 80 to 90% of the total amount of cadmium in the body is considered to be bound to metallothionein. This prevents the free cadmium ions from exerting their toxic effects. It is likely that small amounts of metallothionein-bound cadmium are constantly leaving the liver and being transported to the kidney via the blood. The metallothionein with the cadmium bound to it is filtered through the glomeruli into the primary urine. Like other low-molecular-weight proteins and amino acids, the metallothionein-cadmium complex is subsequently reabsorbed from the primary urine into the proximal tubular cells, where digestive enzymes degrade the engulfed proteins into smaller peptides and amino acids. Free cadmium ions in the cells result from degradation of metallothionein and initiate a new synthesis of metallothionein, binding the cadmium, and thus protecting the cell from the highly toxic free cadmium ions. Kidney dysfunction is considered to occur when the metallothionein-producing capacity of the tubular cells is exceeded.

The kidney and liver have the highest concentrations of cadmium, together containing about 50% of the body burden of cadmium. The cadmium concentration in the kidney cortex, before cadmium-induced kidney damage occurs, is generally about 15 times the concentration in liver. Elimination of cadmium is very slow. As a result of this, cadmium accumulates in the body, the concentrations increasing with age and length of exposure. Based on organ concentration at different ages the biological half-life of cadmium in humans has been estimated in the range of 7 to 30 years.

Acute toxicity

Inhalation of cadmium compounds at concentrations above 1 mg Cd/m3 in air for 8 hours, or at higher concentrations for shorter periods, may lead to chemical pneumonitis, and in severe cases pulmonary oedema. Symptoms generally occur within 1 to 8 hours after exposure. They are influenza-like and similar to those in metal fume fever. The more severe symptoms of chemical pneumonitis and pulmonary oedema may have a latency period up to 24 hours. Death may occur after 4 to 7 days. Exposure to cadmium in the air at concentrations exceeding 5 mg Cd/m3 is most likely to occur where cadmium alloys are smelted, welded or soldered. Ingestion of drinks contaminated with cadmium at concentrations exceeding 15 mg Cd/l gives rise to symptoms of food poisoning. Symptoms are nausea, vomiting, abdominal pains and sometimes diarrhoea. Sources of food contamination may be pots and pans with cadmium-containing glazing and cadmium solderings used in vending machines for hot and cold drinks. In animals parenteral administration of cadmium at doses exceeding 2 mg Cd/kg body weight causes necrosis of the testis. No such effect has been reported in humans.

Chronic toxicity

Chronic cadmium poisoning has been reported after prolonged occupational exposure to cadmium oxide fumes, cadmium oxide dust and cadmium stearates. Changes associated with chronic cadmium poisoning may be local, in which case they involve the respiratory tract, or they may be systemic, resulting from absorption of cadmium. Systemic changes include kidney damage with proteinuria and anaemia. Lung disease in the form of emphysema is the main symptom at heavy exposure to cadmium in air, whereas kidney dysfunction and damage are the most prominent findings after long-term exposure to lower levels of cadmium in workroom air or via cadmium-contaminated food. Mild hypochromic anaemia is frequently found among workers exposed to high levels of cadmium. This may be due to both increased destruction of red blood cells and to iron deficiency. Yellow discolouration of the necks of teeth and loss of sense of smell (anosmia) may also be seen in cases of exposure to very high cadmium concentrations.

Pulmonary emphysema is considered a possible effect of prolonged exposure to cadmium in air at concentrations exceeding 0.1 mg Cd/m3. It has been reported that exposure to concentrations of about 0.02 mg Cd/m3 for more than 20 years can cause certain pulmonary effects. Cadmium-induced pulmonary emphysema can reduce working capacity and may be the cause of invalidity and life shortening. With long-term low-level cadmium exposure the kidney is the critical organ (i.e., the organ first affected). Cadmium accumulates in renal cortex. Concentrations exceeding 200 µg Cd/g wet weight have previously been estimated to cause tubular dysfunction with decreased reabsorption of proteins from the urine. This causes tubular proteinuria with increased excretion of low-molecular-weight proteins such as
α,α-1-microglobulin (protein HC), β-2-microglobulin and retinol binding protein (RTB). Recent research suggests, however, that tubular damage may occur at lower levels of cadmium in kidney cortex. As the kidney dysfunction progresses, amino acids, glucose and minerals, such as calcium and phosphorus, are also lost into the urine. Increased excretion of calcium and phosphorous may disturb bone metabolism, and kidney stones are frequently reported by cadmium workers. After long-term medium-to-high levels of exposure to cadmium, the kidney’s glomeruli may also be affected, leading to a decreased glomerular filtration rate. In severe cases uraemia may develop. Recent studies have shown the glomerular dysfunction to be irreversible and dose dependent. Osteomalacia has been reported in cases of severe chronic cadmium poisoning.

In order to prevent kidney dysfunction, as manifested by β-2-microglobulinuria, particularly if the occupational exposure to cadmium fumes and dust is likely to last for 25 years (at 8 hours workday and 225 workdays/year), it is recommended that the average workroom concentration of respirable cadmium should be kept below 0.01 mg/m3.

Excessive cadmium exposure has occurred in the general population through ingestion of contaminated rice and other foodstuffs, and possibly drinking water. The itai-itai disease, a painful type of osteomalacia, with multiple fractures appearing together with kidney dysfunction, has occurred in Japan in areas with high cadmium exposure. Though the pathogenesis of itai-itai disease is still under dispute, it is generally accepted that cadmium is a necessary aetiological factor. It should be stressed that cadmium-induced kidney damage is irreversible and may grow worse even after exposure has ceased.

Cadmium and cancer

There is strong evidence of dose-response relationships and an increased mortality from lung cancer in several epidemiological studies on cadmium-exposed workers. The interpretation is complicated by concurrent exposures to other metals which are known or suspected carcinogens. Continuing observations of cadmium-exposed workers have, however, failed to yield evidence of increased mortality from prostatic cancer, as initially suspected. The IARC in 1993 assessed the risk of cancer from exposure to cadmium and concluded that it should be regarded as a human carcinogen. Since then additional epidemiological evidence has come forth with somewhat contradictory results, and the possible carcinogenicity of cadmium thus remains unclear. It is nevertheless clear that cadmium possesses strong carcinogenic properties in animal experiments.

Safety and Health Measures

The kidney cortex is the critical organ with long-term cadmium exposure via air or food. The critical concentration is estimated at about 200 µg Cd/g wet weight, but may be lower, as stated above. In order to keep the kidney cortex concentration below this level even after lifelong exposure, the average cadmium concentration in workroom air (8 hours per day) should not exceed 0.01 mg Cd/m3.

Work processes and operations which may release cadmium fumes or dust into the atmosphere should be designed to keep concentration levels to a minimum and, if practicable, be enclosed and fitted with exhaust ventilation. When adequate ventilation is impossible to maintain (e.g., during welding and cutting), respirators should be carried and air should be sampled to determine the cadmium concentration. In areas with hazards of flying particles, chemical splashes, radiant heat and so on (e.g., near electroplating tanks and furnaces), workers should wear appropriate safety equipment, such as eye, face, hand and arm protection and impermeable clothing. Adequate sanitary facilities should be supplied, and workers should be encouraged to wash before meals and to wash thoroughly and change clothes before leaving work. Smoking, eating and drinking in work areas should be prohibited. Tobacco contaminated with cadmium dust from workrooms can be an important exposure route. Cigarettes and pipe tobacco should not be carried in the workroom. Contaminated exhaust air should be filtered, and persons in charge of dust collectors and filters should wear respirators while working on the equipment.

To ensure that excessive accumulation of cadmium in the kidney does not occur, cadmium levels in blood and in urine should be checked regularly. Cadmium levels in blood are mainly an indication of the last few months exposure, but can be used to assess body burden a few years after exposure has ceased. A value of 100 nmol Cd/l whole blood is an approximate critical level if exposure is regular for long periods. Cadmium values in urine can be used to estimate the cadmium body burden, providing kidney damage has not occurred. It has been estimated by the WHO that 10 nmol/mmol creatinine is the concentration below which kidney dysfunction should not occur. Recent research has, however, shown that kidney dysfunction may occur already at around 5 nmol/mmol creatinine.

Since the mentioned blood and urinary levels are levels at which action of cadmium on kidney has been observed, it is recommended that control measures be applied whenever the individual concentrations of cadmium in urine and/or in blood exceed 50 nmol/l whole blood or
3 nmol/mmol creatinine respectively. Pre-employment medical examinations should be given to workers who will be exposed to cadmium dust or fumes. Persons with respiratory or kidney disorders should avoid such work. Medical examination of cadmium-exposed workers should be carried out at least once every year. In workers exposed to cadmium for longer periods, quantitative measurements of ß-2-microglobulin or other relevant low-molecular-weight proteins in urine should be made regularly. Concentrations of ß-2-microglobulin in urine should normally not exceed 34 µg/mmol creatinine.

Treatment of cadmium poisoning

Persons who have ingested cadmium salts should be made to vomit or given gastric lavage; persons exposed to acute inhalation should be removed from exposure and given oxygen therapy if necessary. No specific treatment for chronic cadmium poisoning is available, and symptomatic treatment has to be relied upon. As a rule the administration of chelating agents such as BAL and EDTA is contraindicated since they are nephrotoxic in combination with cadmium.

 

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Contents

Preface
Part I. The Body
Part II. Health Care
Part III. Management & Policy
Part IV. Tools and Approaches
Part V. Psychosocial and Organizational Factors
Part VI. General Hazards
Part VII. The Environment
Part VIII. Accidents and Safety Management
Part IX. Chemicals
Metals: Chemical Properties and Toxicity
Resources
Minerals and Agricultural Chemicals
Using, Storing and Transporting Chemicals
Part X. Industries Based on Biological Resources
Part XI. Industries Based on Natural Resources
Part XII. Chemical Industries
Part XIII. Manufacturing Industries
Part XIV. Textile and Apparel Industries
Part XV. Transport Industries
Part XVI. Construction
Part XVII. Services and Trade
Part XVIII. Guides

Metals: Chemical Properties and Toxicity Additional Resources

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Metals: Chemical Properties and Toxicity References

Agency for Toxic Substances and Disease Registry (ATSDR). 1995. Case Studies in Environmental Medicine: Lead Toxicity. Atlanta: ATSDR.

Brief, RS, JW Blanchard, RA Scala, and JH Blacker. 1971. Metal carbonyls in the petroleum industry. Arch Environ Health 23:373–384.

International Agency for Research on Cancer (IARC). 1990. Chromium, Nickel and Welding. Lyon: IARC.

National Institute for Occupational Safety and Health (NIOSH). 1994. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 94-116. Cincinnati, OH: NIOSH.

Rendall, REG, JI Phillips and KA Renton. 1994. Death following exposure to fine particulate nickel from a metal arc process. Ann Occup Hyg 38:921–930.

Sunderman, FW, Jr., and A Oskarsson,. 1991. Nickel. In Metals and their compounds in the environment, edited by E Merian, Weinheim, Germany: VCH Verlag.

Sunderman, FW, Jr., A Aitio, LO Morgan, and T Norseth. 1986. Biological monitoring of nickel. Tox Ind Health 2:17–78.

United Nations Committee of Experts on the Transport of Dangerous Goods. 1995. Recommendations on the Transport of Dangerous Goods, 9th edition. New York: United Nations.