|Monthly Tech-Tip |
Compounds: cadmium oxide; cadmium carbonate; cadmium chloride; cadmium sulfate; cadmium sulfide.
Uses: The metal is used in electroplating, in solder for aluminium, as a constituent of easily fusible alloys, as a deoxidizer in nickel plating, in process engraving, in cadmium-nickel batteries, and in reactor control rods.
Cadmium compounds are employed as TV phosphors, as pigments in glazes and enamels, in dyeing and printing, and in semi-conductors and rectifiers.
Exposure: Cadmium is well-absorbed by inhalation but, poorly by ingestion.
It is not absorbed by the skin. Aside from occupational exposure, it is also present in :
2-Cigarette smoke (the main source of contamination in the general population).
3-Urban atmospheric air (levels may be high in the vicinity of cadmium producing facilities)
4-Lichen and moss ( they concentrate cadmium as well as other heavy metals).
1-Metal fume fever:
Inhalation of cadmium oxide fumes, produced when cadmium metal and cadmium compounds are heated to high temperature, causes flu-like symptoms better known as Ã‚Â« metal fume fever Ã‚Â», a benign condition. Treatment is entirely symptomatic.
More severe exposures may cause lung damage and ultimately death.
Cadmium oxide fume is a severe pulmonary irritant; cadmium dust is a less potent irritant than cadmium fume because it has a larger particle size.
Inhalation exposure to high levels of cadmium fumes or dust is intensely irritating to respiratory tissue. Particle size appears to be a more important determinant of toxicity than chemical form. However, most acute intoxications have been caused by inhalation of cadmium fume at concentrations that did not provide sufficient warning symptoms of irritation so that workers could leave the contaminated workplace.
Concentrations of fume responsible for fatalities have been 40 to 50 mg/m3 for 1 hour or 9 mg/m3 for 5 hours. There have been non-fatal cases at lower concentrations.
Pulmonary symptoms and clinical signs reflect lesions ranging from nasopharyngeal and bronchial irritation to pulmonary oedema, and death.
There also may be possibly : headache, chills, muscle aches, nausea, vomiting, and diarrhea.
Among survivors , the subsequent course is unpredictable ; most cases resolve slowly, but respiratory symptoms may linger for several weeks, and impairment of pulmonary function may persists for months.
Chronic exposure to cadmium, by inhalation or ingestion, results in renal damage which may continue to progress even after exposure ceases.
Long-term inhalation exposure at low levels leads to decreased lung function and emphysema.
Even if absorbtion by ingestion is low, chronic exposure to high levels of cadmium in food has caused bone disorders, including osteoporosis and osteamalacia. Long term ingestion, by a Japanese population, of water and food contaminated with cadmium, was associated with a crippling condition, Ã‚Â« itai-itai Ã‚Â» (ouch-ouch) disease. The affliction is characterized by pain in the back and joints, osteomalacia (adult rickets), bone fractures, and occasional renal failure, and most often affects women with multiple risk factors such as multiparity and poor nutrition.
Other consequences of cadmium exposure are: anemia, yellow discoloration of the teeth, rhinitis, occasional ulceration of the nasal septum, damage to the olfactory nerve, and anosmia.
Carcinogenesis and mutagenesis:
Several inorganic cadmium compounds cause malignant tumors in animals.
Occupational exposure to cadmium has been implicated in a significant increase of lung and prostate cancer. The IARC has determined that there is sufficient evidence in humans for the carcinogenicity of cadmium and cadmium compounds. It also appears that cadmium has the capability to alter genetic materials, particularly chromosomes.
The important thing is your level of exposure to cadmium, it may vary if you are a pottery factory worker, a teacher, a full-time studio potter or a part-time. It certainly depends also on the amount used over a given period of time. In the wet state (in glazes), these compounds are certainly much less hazardous than as dust (main route of entry being inhalation).
Factories can afford the monitoring of cadmium exposure but it is not the same for artists and crafts persons.
The ACGIH threshold limit value time-weighted average (TLV-TWA) for elemental cadmium and compounds as Cd is 0.01 mg/m3 for total particulate dust (while it is 10mg/m3 for titanium dioxide in Quebec); or 0.002 mg/m3 for the respirable fraction of dust , there is an A 2 suspected human carcinogen designation for both forms.
Good housekeeping of your studio is important. Avoidance of processes generating unnecessary dust is also important.
Depending on the severity of exposure, local ventilation should be used and the aspired air should be vented outside to avoid producing dust from work tables and the floor.
The wearing of an approved dust mask when the exposure seems hazardous is mandatory.
It should be forbidden to drink, eat or smoke in the workshop.
The diagnosis of the intoxication is based on:
2 -Search for proteinuria, in order to screen for a beginning renal impairment, like:
a-Beta-2 microglobulin (a low molecular weight protein),
b -The retinol carrying protein (a low molecular weight protein),
c-Alpha-1 globulin (a low molecular weight protein),
d-Albumine (a high molecular weight protein).
3-Measurements in biological tissues, such as blood and urine, more particularly to assess the chronic intoxication risk.
A large part of absorbed cadmium is retained in the body and its excretion is very slow. The very long biological half-life of cadmium allows to assess excessive impregnation several years after cessation of exposure.
When there are repeated increases in one of the urinary proteins, a thorough investigation of the renal function more must be carried out.
Biological monitoring tests for populations exposed to cadmium in the industry & the environment
|Parameter||Tissue||Normal value||Maximal allowable concentration||Significance|
|Cadmium||Blood||<0.5 Ã‚Âµg/L||5 Ã‚Âµg/L||Recent exposure|
|Cadmium||Urine||<2 Ã‚Âµg/g creatinine||<5 Ã‚Âµg/g creatinine||Body burden**|
|BÃƒÂªta-2 micro-globulin*||Urine||<300 Ã‚Âµg/g creatinine||Tubular impairment|
|Retinol carrying protein||Urine||<300 Ã‚Âµg/g creatinine||Tubular impairment|
|Albumin||Urine||<20 mg/g creatinine||Glomerular impairment|
* unstable if urinary pH < 5.6
** in case of moderate exposure and in the absence of renal damage
Dissodic calcium ETDA may be used in the treatment of the acute intoxication but one must be very careful in the presence of renal impairment. No chelating agent can be proposed for the treatment of the chronic intoxication.
1-Chemical Hazards of the Workplace, Proctor & Hughes, last edition.
2-Hazardous Materials Toxicology, Sullivan & Krieger, last edition.
3-EncyclopÃƒÂ©die MÃƒÂ©dico-Chirurgicale, Toxicologie-Pathologie Professionnelle. Paris, Juillet 2001.
4-Occupational & Environmental Medicicne, Ladou J., last edition
|Materials||Ferro 239416 Yellow Stain|
Article by Edouard Bastarache
Edouard Bastarache is a well known doctor that has written many articles on the subject of toxicity of ceramic materials and books on technical aspects of ceramics. He writes in both English and French.
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By Edouard Bastarache