Cadmium

Classification:

Cadmium is a chemical element.

Cas:

7440-43-9

Synonyms/Trade Names:

: C.I. 77180, Colloidal Cadmium.

Chemistry/Composition:

Cd. It can contain impurities of Fe, Cu, or Zn .

Structure:

Almost hexagonal closed packing.

Crystallographic Constants:

c:a = 1.886

Crystal Group:

Hexagonal.

Color:

Normally, white.

Optical Properties:

Opaque.

Pleochroism:

None.

Powder Diagram:

2.35 2.81 2.58 1.90 (5-674).

Natural Sources:

Cadmium ores are mined in Australia, Poland, Russia, and the USA.

Medical Importance:

Key Hazards:

Intoxication, carcinogenic.

Involved Organs:

Lung, kidneys, skeleton, gastrointestinal tract.

Exposure/Epidemiology:

Cadmium is used in the manufacture of alloys, in alkaline accumulator production, electroplating, atomic reactors, welding of steel, paints, as stabilizing agent in plastics, and in aluminum soldering. Cd is found in tobacco smoke. World production of Cd was 16 500 tons in 1972. Since 1960, about 90 cases of Cd-induced lung Diseases (without carcinoma) have been reported. In the USA, about 500 000 workers may be exposed to Cd.

Thresholds:

TWA STEL
mg/m3 mg/m3
Australia 0.05
Belgium 0.05
Czechoslovakia 0.05 0.1
Denmark 0.01
Finland 0.02
Great Britain 0.05
Russia 0.01 0.05
Japan 6
Sweden 6
Switzerland 0.02 (dust)
United States: ACGIH 0.05
United States: NIOSH/OSHA 0.2

Etiology/Pathophysiology:

Cd is inhaled (lungs) or absorbed by the gastrointestinal tract (25% of amount absorbed). The dust is deposited in the alveoli and absorbed (>90%). Normally, most of the dust is cleared by the mucociliary system. Cd induces an inhibitory effect to a-1-antitrypsin. Exact data of absorption via the lung do not exist; however, it is assumed that about 25-50% of the inhaled Cd is absorbed. In the blood, most of the Cd is bound to erythrocytes and proteins. The liver and kidneys store Cd for a long time and excrete it slowly. The decay time amounts to 20 years. Cd bonds with metallothionine and reacts with sulfhydryl groups. It does not cross the placenta.

Lung Diseases:

Cadmium fumes are cytotoxic to the pneumocytes, macrophages, and histiocytes, and induce emphysema and bronchitis. Cd-exposed persons have an increased risk of lung cancer. In addition to the acute lung intoxication, Cd-induced osteoporosis and kidney diseases are known (Itai-itai disease).

Clinical Presentation:

In acute exposure, the symptoms start with throat irritation and dyspnea some hours after exposure, possibly followed by lung edema. Death occurs in 16% of the injured patients. In chronic exposure, Cd induces an irregular emphysema. In acute intoxication, the patients present with fever, headache, cough, vomitus, and diarrhoea some hours after intoxication, followed by tachypnea, and severe lung edema with cyanosis and pain after 5-20 hours. In chronic intoxications, the symptoms include proteinuria, rhinitis, dyspnea, emphysema, and a painful osteomalacia.

Radiology:

Chest radiographs show hilar shadows.

Lung Function:

A mild obstruction may be seen. In advanced stages, cadmium induces emphysema.

Bronchoalveolar Lavage:

The lavage fluid can contain an increased number of macrophages and granulocytes, and an abnormal T4/T8 ratio.

Pathology:

Gross::

Acute intoxication induces heavy wet lungs of yellowish-reddish color. Chronic stages induce large emphysematous cysts with focal fibrosis and scarring.

Histology:

Acute intoxication induces necrosis, desquamation, hyperplasia and dysplasia of the pneumocytes. The alveoli contain fibrinoid material, mixed inflammatory infiltrates, and macrophages. Necrosis of the bronchioles and alveolar ducts is present. Chronic stages are characterized by partial resolution of the exudate, which is followed by marked proliferation of the pneumocytes and emphysematous eradication of the peribronchiolar interstitial tissue. The end stage presents with empty enlarged air spaces, which are irregularly distributed in both lungs.

Prognosis:

The acute intoxication has a lethality of 15%.

Additional Diseases:

Nose:

Ulcers and chronic rhinitis may occur.

Kidney:

The so-called renal-tubular syndrome has been reported from Cd-exposed workers. A higher rate of kidney stones was found in Cd workers (Ca-phosphatstone).

Skeleton:

Irregularly formed bone lesions may be induced by Cd.

Prostate:

In the USA, the EPA has included Cd as a potentially carcinogenic substance for prostate cancer.

Remarks:

Cd is an enzyme-bound element in some strains of diatoms (Thalassiosira weissflogii).

References:

search Pubmed for Cadmium


Alessio L, Odone P, Bertelli G, Foa V: Cadmium. In: Commission of the European Community (Ed): Human biological monitoring of industrial chemicals series. Luxemburg (1983)
Armstrong R, Chettle DR, Scott MC, Blindt M, Mason HJ: Longitudinal study of exposure to cadmium. Br J Ind Med 49 (1992) 556-559
Blot WJ: Lung cancer and occupational exposures. In: M Mizell, P Correa (Eds): Lung cancer: causes and prevention. Verlag Chemie Int, Weinheim (1984) 47-64
Dail DH, Hammar SP: Pulmonary Pathology. Springer, New York (1988)
Dunhill M S : Pulmonary pathology. Churchill Livingstone, Edinburgh (1982)
Fraser RG, Paré JAP: Diagnosis of diseases of the chest. WB Saunders, London, Toronto (1979)
Friberg L, Kjellstrom T, Nordberg GF: Cadmium. In: L Friberg, GF Nordberg, VB Vouk (Eds): Handbook on the toxicology of metals. Elsevier, Amsterdam, New York (1990)
IARC: Overall evaluations of carcinogenicity: an updating of IARC monographs volumes 1 to 42. IARC Mono Eval Carcinog Risk Human Suppl 7 (1987)
IARC: Cancer: causes, occurrence and control. IARC Sci Publ 100 (1990)
Kahan E, Derazne E, Lilancboim J, Askenazi R, Ribak J: Adverse effects on workers exposed to Cadmium. Am J Ind Med 21 (1992) 527-537
Kayser K: Analytical lung Pathology. Springer, Heidelberg, New York (1992)
Kazantzis G: Cadmium mortality assessment. Am J Ind Med 20 (1991) 701-704
Kollmeier H, Seemann J, Wittig P, Rothe G, Müller KM: Cadmium in human lung tissues. Int Arch Occup Environ Health 62 (1990) 373-377
Leduc D, De Francquen P, Jacobovitz D, Vandenweyer R, Lauwerys R, De Vuyst P: Association of cadmium exposure with rapidly progressive emphysema in a smoker. Thorax 48 (1993) 570-571
Lewis RJ: Carcinogenically active chemicals. Van Nostrand Reinhold, New York (1991)
Nemery B: Metal toxicity and the respiratory tract. Eur Respir J 3 (1990) 202-219
Peerzada N, McMorrow L, Skiliros S, Guinea M, Ryan P: Distribution of heavy metals in Gove Harbour, Northern Territory, Australia. Sci Total Environ 92 (1990) 1-12
Reichel G: Auf anorganische Stäube mit geringem oder fehlendem Quarzgehalt zurückgehende Lungenveränderungen. In: WT Ulmer (Ed): Handbuch der inneren Medizin, Bd IV: Pneumokoniosen. Springer, Heidelberg (1978) 468-508
Roels H, Bernard AM, Cardenas A, Buchet JP, Lauwerys RR, Hotter G: Markers of early renal changes induced by industrial pollutants. III Application to workers exposed to cadmium. Br J Ind Med 50 (1993) 37-48
Rose CS, Heywood PG, Constanzo RM: Olfactroy impairment after chronic occupational cadmium exposure. J Occup Med 34 (1992) 600-605
Sartor FA, Rondia DJ, Claeys FD, Staessen JA, Lauwerys RR: Impact of environmental cadmium pollution on cadmium exposure and body burden. Arch Environ Health 47 (1992) 347-363
Staessen J, Amery A, Bernard A, Bruaux P: Blood pressure, the prevalence of cardiovascular diseases, and exposure to cadmium: a population study. Am J Epidemiol 134 (1991) 257-267
Thun MJ, Elinder CG, Friberg L: Scientific basis for an occupational standard for cadmium. Am J Ind Med 20 (1991) 629-642
Valentin H, Lehnert G, Petry H, Weber G, Wittgens H, Woitowitz HJ: Arbeitsmedizin Vol 2. Thieme, Stuttgart (1985)
Wilson JD, Braunwald E, Isselbach KJ, Petersdorf RG, Martin JB, Fauci AS, Root RK: Harrison’s principles of internal medicine. 12th Edition. McGraw Hill, New York (1991)
Wirth W, Gloxhuber C: Toxikologie. Thieme, Stuttgart (1985)
Zwennis WCM, Franssen AC: Assessment of occupational exposure to cadmium in The Netherlands, 1980-1989. Am J Ind Med 21 (1992) 793-805