electrochemical deposition of Cd from solution
Werner
electrochemistry.
When you take for example a solution containing Cd-ions and you
introduce a cupper elektrode and a Cd-elektrode (and a saltbridge if
needed), then the cupper will deposit and the Cd will go into solution
generating energy (correct me if I'm wrong). Would it be possible to
apply a current so that the reaction goes into the oter direction to
give deposition of Cd2+ on the Cd-electrode and Cu go into solution?
Would it be possible to deposit Cd2+ on a Cd-elektrode using a
Pt-electrode and H2-gas or other methods to prevent other metal-ions
(from the metal-electrode- going into solution? Or working with two
cells only connected with a saltbridge?
Any comments greatly appreciated !!
Werner
Rob Copcutt
Cd plating was very common 30+ years ago and then someone discovered
that it is EXTREMELY toxic. All you need to do is to make the thing you
want to plate the cathode, an inert anode and cadmium in solution.
hanson
news:3BE6B12F...@cam.ac.uk...
> Werner wrote:
> >
> > I wonder if it is possible to deposit Cd2+ from a solution by
> > electrochemistry.
>
> that it is EXTREMELY toxic. All you need to do is to make the thing you
> want to plate the cathode, an inert anode and cadmium in solution.
Cadmium's EXTREMELY OVER EXAGGERATED toxicity is nothing but classical
enviro shit hype. Nothing else. Cad has not caused any chronic problems to
public health in or from the Cad plating industry. There certainly may have
been a few acute Cad poisonings from careless work habits in the industry.
For over 100 years 1/3 of all of the bolts and nuts in the entire world
were Cad plated. Where are all the Cad caused cancer- and disease- victims,
the enviro turds warned us of and threatened us with? Show me one!
Cad plated parts are still widely available in the US. It comes in a soft
silvery white version or as a corrosion protection enhanced iridescent
golden coating. Cad is still used because it offers a corrosion resistance
to ferrous parts far superior to Zinc electroplate and is at least as good
as Tin and Zn/Ni coats, which are much more costly.
Cad could not be replaced, so far, in certain applications where friction
and el. conductivity is important. It is said that Cad has a slipperiness
(metal to metal friction)exceeding that of Teflon. It's particular "smeary"
softness makes the Cad coating self healing against scratches. Certain
Mil-specs still demand Cad over "enviro-substitutes. Any and all classical
car & engine restorers do pay big bucks to have their parts replated with
Cad to be certified as "original condition".
You can easily electroplate Cad from solutions, ranging from pH 3 (CdSO4)
to pH 12, (Na2Cd(CN)4), at RT, in concentrations of 10 - 120 gr/lt Cd.
Adding a few ppm of Ni2+ or Co2+ and an amine as brightener will give
mirror-like coatings. Make the anodes from graphite for pH <8 or from steel
for pH > 8. DC current @ 1.5 to 9 Volts.
Remember, environmentalism is nothing but sanitation driven to pathological
extremes, ...promulgated by opportunistic ex-communists and misogynic,
unemployable perverts, who have succeeded in generating enviro taxes,
permit fees and user surcharges from which these useless, cocksucking
motherfuckers draw their welfare checks. --- The Cad industry, like all
other industries have not suffered, of course. They simply passed the
enviro costs along to the users. That's how the environmentalists fuck the
general public, by making you pay more, so that they can live. ..off your
back.
hanson
Tom Walz
I admire and respect your opinions. I even agree with you to a great
extent. However, We have developed substitutes for Cadmium in
braze alloys based on the following which references dangers of
Cadmium.
Tom
OCCUPATIONAL DISEASES
A Guide to Their Recognition
Revised Edition - June 1977
US DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE
National Institute for Occupational Safety and Health
CADMIUM AND COMPOUNDS
Description
Cd, Cadmium, is a bluish-white metal. The only cadmium mineral,
greeockite, is rare; however, small amounts of cadmium are found in
zinc, copper, and lead ores. It is generally produced as a by-product
of these metals, particularly zinc. cadmium is insoluble in water but
is soluble in acids.
Synonyms
None.
Potential Occupational Exposures
Cadmium is highly corrosion resistant and is used as a protective
coating for iron, steel, and copper; it is generally applied by
electroplating, but hot dipping and spraying are possible. Cadmium may
be alloyed with copper, nickel, gold, silver, bismuth, and aluminum
too for easily fusible compounds. These alloys may be used as coating
for other materials, welding electrodes, solders, etc. It is also
utilized in electrodes of alkaline storage batteries, as a neutron
absorber in nuclear reactors, a stabilizer for polyvinyl chloride
plastics, a deoxidizer in nickel plating, an amalgam in dentistry, in
the manufacturer of fluorescent lamps, semiconductors, photocells, and
jewelry, in process engraving, in the automobile and aircraft
industries, and to charge Jones reductors.
Various cadmium compounds find use as fungicides, insecticides,
nematocides, polymerization catalysts, pigments, paints, and glass;
they are used in the photographic industry and in glazes. Cadmium is
also a contaminant of superphosphate fertilizers.
Exposure may occur during the smelting and refining of
cadmium-containing zinc, lead, and copper ores, and during spacing,
welding, cutting, brazing, soldering, heat treating, melting, alloying
and salvage operations which require burning of cadmium-containing
material.
A partial list of occupations in which exposure may occur includes:
Alloy makers Pesticide workers
Battery makers Solder workers
Dental Amalgam makers Textile printers
Engravers Welders
Metalizers zinc refiners
Paint makers
Permissible Exposure Limits The Federal standard for cadmium fume is
0.1 mg/m3 (as Cd) as an 8-hour TWA with an acceptable ceiling of 3
mg/m3. For cadmium dust, that standard is 0.2 mg/m3 (Cd) as an 8-hour
TWA with an acceptable maximum ceiling of 0.6 mg/m3 . NIOSH has
recommended a TWA limit of 40 mg/m3 with a ceiling limit of 200 mg in
a 5-minute sampling period.
Routes of Entry
Inhalation or ingestion of fumes or dust.
Harmful Effects
Local - Cadmium is an irritant to the respiratory tract. Prolonged
exposure can cause anosmia and a yellow stain or ring that gradually
appears in the necks of the teeth. Cadmium compounds are poorly
absorbed from the intestinal tract, but relatively well absorbed by
inhalation. Skin absorption appears negligible. Once absorbed Cd has a
very long half-life and is retained in the kidney and liver.
Systemic - Acute toxicity is almost caused by inhalation of cadmium
fumes or dust which are produced when cadmium is heated. There is
generally a latent period of a few hours after exposure before
symptoms develop. During the ensuing period, symptoms may appear
progressively. The earliest symptom is slight irritation of the upper
respiratory tract. This may be followed over the next few hours by
cough, pain in the chest, sweating, and chills which resemble the
symptoms of nonspecific upper respiratory infection. Eight to 24 hours
following acute exposure severe pulmonary irritation may develop, with
pain in the chest, dyspnea, cough, and generalized weakness. Dyspnea
may become more pronounced as pulmonary edema develops. The mortality
rate in acute cases is about 15%. Patients who survive may develop
emphysema and corpulmonale; recovery can be prolonged.
Chronic cadmium poisoning has been reported after prolonged exposure
to cadmium oxide fumes, cadmium oxide dust, cadmium sulfides, and
cadmium stearates. Heavy smoking has been reported to considerably
increase tissue Cd levels. In some cases, only the respiratory tract
is affected. In others, the effects may be systemic due to absorption
of the cadmium. Lung damage often results in a characteristic form of
emphysema which in some instances is not preceded by a history of
chronic bronchitis or coughing. This type of emphysema can be
extremely disabling. Some studies have not shown these effects.
Systemic changes due to cadmium absorption include damage to the
kidneys with proteinuria, anemia, and elevated sedimentation rate. Of
these, proteinuria (low molecular weight) is the most typical. In
advanced stages of the disease, these may be increased urinary
excretion of amino acids, glucose, calcium, and phosphates. These
changes may lead to the formation of renal calculi. If the exposure is
discontinued, there is usually no progression of the kidney damage.
Mild hypochromic anemia is another systemic condition sometimes found
in chronic exposure to cadmium.
In studies with experimental animals, cadmium has produced damage to
the liver and central nervous system, testicular atrophy, teratogenic
effects in rodents after intravenous injection of cadmium, decrease in
total red cells, sarcomata, and testicular neoplasms. Hypertensive
effects have also been produced. None of these conditions, however,
has been found in man resulting from occupational exposure to cadmium.
Heavy smoking would appear to increase the risk of cumulative toxic
effects.
Medical Surveillance
In preemployment physical examinations, emphasis should be given to a
history of or the actual presence of significant kidney disease,
smoking history, and respiratory disease. A chest X-ray and baseline
pulmonary function study is recommended. Periodic examinations should
emphasize the respiratory system, including pulmonary function tests,
kidneys, and blood.
Special Tests
A low molecular weight proteinuria may be the earliest indication of
renal toxicity. The trichloroacetic acid test may pick this up, but
more specific quantitive studies would be preferable. If renal disease
due to cadmium is present, there may also be increased excretion of
calcium, amino acids, glucose, and phosphates.
Personal Protective Methods
Most important is the requirement that each worker be adequately
protected by the use of effective respiratory protection: Either by
dust masks, vapor canister respirators, or supplied air respirators.
Clothing should be changed after each shift and clean work clothing
issued each day. Food should not be eaten in contaminated work areas.
Workers should shower after each shift before changing to street
clothes.
The Analytical Toxicology of Industrial Inorganic Poisons
Morris B. Jacobs, Ph.D.
1967 - Interscience Publishers
CADMIUM
It has been shown that cadmium is a poison entirely analogous to
arsenic and mercury. It does not have a noxious effect merely because
of the state of subdivision of the cadmium compounds inhaled. Cadmium
melts at 320.9°C, a few degrees lower than lead. Its major use is in
cadmium electroplating.
As a result of increased use of cadmium for industrial purposes the
industrial hygienist has been presented with another problem. Among
the industrial processes in which cadmium poisoning may occur are the
smelting of cadmium ores, working up or residues, production of
cadmium compounds, spraying of cadmium-plated pipe, cadmium-plating
process - particularly of marine hardware and other fittings which
were formerly zinc-coated - and melting the metal.
In industry, cadmium poisoning usually occurs from the accidental
absorption of cadmium fumes or dusts through the respiratory system.
It seldom occurs by ingestion.
The generally accepted maximum safe permissible working concentration
of cadmium fume dust is 0.1 mg/m3.
INDUSTRIAL TOXICOLOGY
Hamilton and Hardy - Third Edition
(State of Washington - Department of Labor and Industries)
(Industrial Safety and Health Division)
CADMIUM
Industrial Uses
Cadmium, which was for a long time a rare metal in industry, has
become widely used in the manufacturer of alloys and for
electroplating. When imports are necessary, the United States obtains
cadmium chiefly from Canada and Mexico. Cadmium is extracted from zinc
ores in the course of smelting and in a constituent of the so-called
blue powder, a condensation product which has up to 4 or 5 percent of
cadmium. Cadmium is also found in the sludge after the electrolytic
recovery of zinc. It is used in alloys, but more extensively for the
electroplating of metal since it resists corrosion better than nickel
or steel. X
Cadmium is used in making storage batteries. “Cadmium
lithopone,” as well as the cadmium yellows, is used as a
pigment.
While the chief use of cadmium is as an ingredient in alloys and in
electroplating, the following are also uses for cadmium; in bearing
metals, in ceramics, in process engraving, in cadmium vapor lamps, and
for rustproofing tools and other iron and steel articles such as
marine hardware, previously coated with zinc. In France, ferronickel
storage batteries have a negative anode made of cadmium. There is
little manufacturer of cadmium storage batteries in the United States.
The presence of cadmium has to be considered, not only in the
manufacturer of paints, but in the spraying of pigments and in welding
metal when the metal or the welding rod contains cadmium.
Photoelectric cells, made by coating small steel plates with selenium,
are sprayed with metallic cadmium. More recent potentially hazardous
uses of cadmium may arise with its use in nuclear reactors because of
its neutron absorbing properties. cadmium may be sprayed onto graphite
or may be used in rods for this purpose.
Prodan (1932) stated that the greatest industrial hazards were in the
smelting of ores, the working up of residues, the handling of
“blue powder,” production of compounds, spraying of
pigments, welding alloys, and melting the metal. Fairhall (1945)
considered that industrial cadmium poisoning was not due for the most
part to the electroplating process but to the subsequent firing or
welding of cadmium-plating material. He added that cadmium was little
used as a metal, but the overheating and oxidation of cadmium metal
was an important source of industrial cadmium poisoning.
Recently, solders containing in varying amounts with copper, lead,
tin, zinc, and silver, especially silver solders, known to be widely
used, have been a source of poisoning. Such hazards exist chiefly
because of ignorance of the toxic potential of cadmium so that no
precautions are taken. Batteries made with cadmium and nickel are used
in airplanes, missiles, and refrigerated cars. Certain cadmium
compounds are used in photography. Stokinger (1963) reports the use of
diethyl cadmium in the manufacturer of tetraethyl lead as an additive
to gasoline. Remelting of scrap and the use of a blowtorch in working
cadmium plated steel popes are dangerous, often because the presence
of cadmium is not suspected.
Industrial and experimental evidence shows cadmium to be one of the
most hazardous metals. It has a significant vapor pressure at its
melting point; a concentration of 5,000 times the safe limit vale can
be produced. Freshly generated fumes of cadmium have been shown to be
more acutely poisonous than “old” settled fumes that are
inhaled as a dust.
Worker Illness
The United States Public Health Report, vol. 57 of 1942, published a
review of cadmium poisoning. This report included an ancient
observation of Stockhusen describing gastrointestinal disturbances in
foundry workers exposed to cadmium fumes. Tracinski (1888) (Hamilton
and Hardy, 1949, p. 146) published a report in which he described the
industrial diseases of zinc smelters in Upper Silesia. Irritation of
the upper respiratory tract, as well as indigestion, vomiting, and
diarrhea were reported. The chief exposure, poorly controlled, was to
5 percent of cadmium as a fume with some SO2. G. Arbour Stephens
(1920-1921) drew attention to cadmium poisoning in Welsh zinc smelters
also characterized by intestinal symptoms. He reported recovery of
cadmium but not lead from the liver of an aged smelter-worker in Wales
whose autopsy showed marked evidence of chronic interstitial
nephritis, as well. In eight autopsies of smelter workers, Stephens
found significant amounts of cadmium. A case reported by Schwartz
(Hamilton and Hardy, 1948, p. 147) was caused by melting cadmium and
inhaling the fumes leading to chronic respiratory symptoms diagnosed
as bronchitis with bouts of bronchopneumonia. One report described the
illness of three servants who polished silverware with cadmium
carbonate and brushed off the dry powder, one of them doing this work
for a day and a half, the others for only half a day (Hamilton and
Hardy, 1949, PP.147-148). All three suffered from dizziness, dyspnea,
vomiting, and diarrhea. One worker was profoundly prostrated with
colic, incessant vomiting and diarrhea.
Ross (1944), writing from England, reported an accident which affected
twenty-three workers at once. Since finely divided cadmium is
inflammable and when ignited will produce cadmium oxide, smoking is
strictly forbidden in industries where such material is handled in
quantity. As a result of the breaking of this rule, cadmium dust was
ignited by a lighted cigarette with resultant dangerous exposure of
the workers to cadmium oxide. The victims complained of irritation of
the eyes, headache, vertigo, dryness of the throat, constriction of
the chest. After three hours, the exposed workers complained of
nausea, epigastric pain, and dyspnea.
Two series of cases of French workers who were exposed to cadmium as
cadmium hydroxide in the manufacturer of storage batteries and
developed chronic illnesses attracted attention in the 1940’s
(reported in detail in the next section).
The Indiana Bureau of Industrial Hygiene reported in 1943 two cases of
severe acute cadmium poisoning caused by the fumes from the use of a
blowtorch on cadmium-plated steel pipe. After using the blowtorch for
four hours, the two workmen became violently ill with vomiting, pains
in the chest, and difficult breathing. One recovered; the other died
four day later “of severe chest involvement.” Johnstone
(Hamilton and Johnstone, 1945, p.616) reported a case which
illustrates the fact that industrial cadmium poisoning produces a
clinical picture resembling that following nitrous fume poisoning. His
patient became acutely ill after using an acetylene torch on the
inside walls of a furnace in which cadmium residues had been recovered
from scrap metal. The patient had severe dyspnea, constant cough, and
chest pain, which came on soon after his job was finished. A patchy
bronchopneumonia was seen on x-ray, and at autopsy nine days later the
lungs were edematous with areas of consolidation. In 1945 the Kansas
City Area Industrial Hygiene Service investigated symptoms of
respiratory distress reported by workers in a silver manufacturing
plant. In the process of silver soldering, it was discovered that
samples of the solder contained from 18 percent to as high as 70
percent of cadmium. Elkins told HLH of a fatal case of cadmium
poisoning investigated by the Massachusetts Division of Occupational
Hygiene. The victim was a helper in a brass foundry. He and a fellow
employee, without protection or warning of the dangers involved,
melted cadmium to be poured into molds and small castings. The metal
became overheated, giving off dense fumes which filled the shop and
caused both employees and two onlookers to cough. The worker who died
stayed to skim the metal after it was removed from the fire. In spite
of coughing and bouts of vomiting which continued through the night
following the accident, the sick worker went back to his job the next
day. He died six days after the accident with what the attending
physician called “bronchial pneumonia.”
Chronic Cadmium Poisoning
Industrial hygienists in the United States considered until recently
that there was little evidence for the existence of a clinical picture
of chronic cadmium poisoning of occupational origin. The 1920 history
of Stephens’ aged smelter-worker, whose liver at autopsy after
ten years of illness contained 0.91 grain of cadmium per pound, is
evidence that disability may arise from industrial exposures too
slight to produce the violent symptoms of acute poisoning. In 1942
Lafitte and Gros (Hamilton and Hardy, 1949, pp. 150-151) described a
series of cases in workers exposed to cadmium in unstated amounts
whose clinical complaints the authors felt presented a unique clinical
syndrome due to chronic cadmium intoxication. After periods of
exposure varying from five to fourteen years, these workers of both
sexes developed pain in the lower back and legs. Without treatment and
with exposure continued, the workers became unable to walk. On X-ray,
scapula, femur, and ileum, showed lines of pseudofracture known ad
Milkman’s syndrome. The only other regular finding was an anemia
of the iron-deficiency type. Treatment with Vitamin D, calcium, and
parathyroid substance resulted in cure. A similar report from France
was made by Barthelmy and Moline in 1946 ( Hamilton and Hardy, 1949,
p. 151). In France the negative anode of ferronickel batteries is made
of cadmium. Workers in this industry, after exposure to operations
involving cadmium for more than six years, presented a clinical
picture like that described by Lafitte and Gros. Gervais and Delpech
(1964) reported in detail clinical findings in eight cases of cadmium
workers with evidence of abnormal findings of the skeleton. Several
cases suffered pathologic fractures, and in all cases bone changes
were visible on X-ray. Exposure to cadmium lasted from twelve to
thirty years. No other etiology was discovered and the authors
concluded that the cadmium had caused serious metabolic changes. These
French reports are of great interest currently, in light of the
Japanese cadmium induced disease of the bone named Itai-itai disease
(Nilsson, 1970), occurring in workers in rice fields near a mine
producing zinc, lead, and cadmium. Osteomalacia is the chief feature,
very like the industrial illness. (Editorial: Lancet 1971).
Prior to the onset of signs and symptoms, according to Barthelmy and
Moline, the teeth of the workers also exposed to cadmium had a
characteristic appearance which may serve as a warning that the
workers are absorbing dangerous amounts of cadmium. The enamel of the
teeth took on a yellow color which also discolored the tartar but not
the gingiva. Princi in the United States (1950) reported cadmium in
discolored teeth of workers exposed to cadmium in smelting after ten
years.
Hardy and Skinner (1947) in the United States reported an experience
of illness following a cadmium exposure during the lining of large
steel parts with cadmium. Air studies for an six-year period were
recorded showing workmen’s exposure varying from 0.6 mg/10m3 to
6.8 mg/10m3. The work period was lengthened during the war years.
Urinary values in the five cases reported varied from a trace of
cadmium per liter to 0.05mg/L. The five men reported that they had
external pain, throat irritation, and coughing. Four men had
gastrointestinal complaints of varying severity form anorexia to
nausea, vomiting, and epigastric pain which, in one worker, led to a
diagnosis of peptic ulcer. The man was a crane operator who took naps
and ate in his cab, spending more time there as he felt less well,
probably with resultant greater ingestion and inhalation of cadmium.
Two of the five men had hemoglobin values considered in the range of
iron deficiency.
Evidence of chronic cadmium toxicity in workers has accumulated from
reports of illness among workers exposed in storage battery and alloy
manufacturer in Sweden and England. Friberg described loss of weight,
pulmonary disease and the appearance of a low molecular weight protein
in the urine as evidence of chronic cadmium effect. This
author’s first report appeared in 1948 (Friberg, 1948) and these
observations have been amply confirmed (Lane and Campbell, 1954;
Bonnell, 1955; King, 1955; Kazantzis, 1956; Piscator, 1966). Finding
certain globulins in the serum proteins of workers with long-term
cadmium exposure led to the suggestion that an abnormal
antigen-antibody has been provoked (Piscator, 1966; Vigliani et al.,
1966). Kidney stones due to chronic cadmium poisoning are an
established complication. Chronic pulmonary insufficiency
characterized by a clinical picture of emphysema is a significant risk
in continued uncontrolled cadmium exposure. There are a few reports of
lung function abnormalities.
Bonnell describes a cadmium worker under his care with evidence of
severe airway obstruction . Kazantzis described abnormal ventilatory
and gas-distribution studies as evidence of cadmium-produced
emphysema. According to Buxton (1956), men suffering the emphysema of
chronic cadmium poison do not show the increase in total lung volume
characteristic of the emphysema of chronic bronchitis. Several reports
include anosmia, excess fatigue, and lowered hemoglobin as caused by
cadmium. An important feature of chronic cadmium poisoning, emphasized
by Bonnell et al. (1959) is the delay in onset of clinical illness in
some cases, demonstrating the fact that cadmium disease progresses
even though the worker’s exposure ceases. One Russian report
(Patty, 1963, p. 1015) describes direct action of cadmium on cortical
cells. This is based on study of motor chronaxia in cadmium-exposed
workers. Interpretation of this observation is difficult as the
conclusion is based on functional changes in the cortex easily
influenced by many factors. Kipling and Waterman (1967) raise the
question that lifelong exposures may be associated with a significant
increase in prostatic cancer. Pathologic changes considered due to
cadmium are found in lungs, kidney, and gastrointestinal tract. Lane
and Campbell (1954) consider cadmium emphysema unique, showing at
post-mortem a narrow zone of normal lung under the pleura and no
bullae at the periphery. Spencer (1962) does not agree but does note
the absence of severe fibrosis in the presence of advanced emphysema.
Hirst et al. (1973) assayed emphysematous lungs with age matched
controls, and only cadmium was elevated of metals tested for which
included sodium, potassium, calcium and zinc, as well as cadmium.
These authors suggest cigarettes as the source of cadmium.
Of unusual interest, due to cadmium effect on the renal tubules, is
the finding first described by Friberg (1948) of a low molecular
weight protein in the urine of workers free of symptoms or detectable
signs of illness. Its molecular weight is 20,000 to 30,000, lower than
any known serum protein. This cadmium proteinuria is not usually
demonstrable with routine methods used to detect albuminuria.
Twenty-five percent trichloroacetic acid will give reliable positive
reactions if such a protein is present, as will Heller’s ring
test. Piscator (1966) states that the amount of cadmium in urine is a
reflection of the extent of renal tubular damage. Excess excretion of
amino acid is considered due to the same cause rather than metabolic
abnormalities. Clarkson and Kench (1956) found aminoacidurina
(threonine and serine) in workers exposed to cadmium oxide dust.
Swedish workers similarly exposed were shown by Ahlmark et al. (1960)
to have low insulin clearance values and inability to concentrate
urine. These abnormalities were shown to increase with length of time
and level of cadmium exposure. Several authors (Schroeder and Nason,
1969; Peter, Yeager, and Witherup, 1973) have studied hair for metal
content hoping to discover useful correlations with exposure and body
content. Variables such as age, sex, and handling of the sample proved
cadmium values in hair of no use as a monitoring device.
The earlier incomplete reports of worker illness associated with
exposure to cadmium included in this section gave warning of the now
well recognized toxic effects of the metal.
In summary, it is established that intense exposures to cadmium oxide
can cause fatal pulmonary edema. Repeated exposures may damage the
kidneys, respiratory tract, and gastrointestinal tract, including the
liver (Kanzantzis et al., 1963). Old and new reports suggest cadmium
can cause changes in the skeleton and changes in the teeth. Piscator
is of the opinion that changes in calcium metabolism are secondary to
cadmium induced renal damage (M. Piscator, 1969: Personal
communication). Such job-related illness becomes more important as
cadmium pollution in air in industrialized countries exposes general
populations to unknown quantities of this toxic metal. This is
especially so because of cadmium-produced malignancy (Kipling and
Waterman, 1967).
Animal Studies
The literature describing animal experimentation with cadmium has
increased considerably in recent years. The Chemical Warfare Service
studied various aspects of the problem of cadmium poisoning and its
treatment during the Second World War (Tobias et al., 1946; Gilman et
al., 1946). Since Friberg’s studies (1948), there has been new
interest in the biological behavior of cadmium. Many animal studies
are reported, and only a summary of some will be attempted here.
Animal work has corroborated the gastrointestinal effects seen in man
after ingestion of cadmium. The emetic effect in cats has been often
used by pharmacologists. Prodan’s animal studies (1932) showed
that changes in the liver vary from generalized inflammation of the
cells to pronounced fatty infiltration. Pathologic changes are also
seen in the kidneys, especially in the convoluted tubes. Cadmium is
stored in the liver, bones, and kidneys. This is of interest in
considering that some of the gastrointestinal symptoms of subacute
illness may be due to the toxic effect of cadmium on liver function.
Prodan reported the kidney in his experimental animals retained much
of the administered cadmium and excreted it very slowly. Schwartze and
Alsberg (1923) also found that the kidney retained more cadmium than
did any other organ. The effect of cadmium on iron metabolism has been
reported in feeding experiments with rats (Wilson et al., 1941).
Cadmium chloride given to rats resulted in severe anemia. According to
Granick and Michailis (1942), cadmium is capable of precipitating
iron-containing protein, and it may be that , by so doing, it produces
a low hemoglobin as reported in animal and human experience.
The dental effects reported by Barthelmy and Moline (1946) and Prince
(1950) have no exact counterpart in animal experimentation. Several
investigators have studied the effect of cadmium on rats’ teeth
because, in common with fluorine, it has the property of bleaching.
Cadmium increases the susceptibility of the rats’ teeth to
dental caries rather than increasing resistance to decay as fluorine
does (Ginn and Bolker, 1944). However, we have found no reports of
effects in animals similar to the yellow pigmentation described in
cadmium workers.
Use of radioactive cadmium showed that 90 percent of cadmium
accumulated in the red blood cells. Lung changes and the unusual
proteinuria of cadmium workers occur in exposed rabbits (Friberg,
1952). A number of investigators find abnormal serum proteins in
cadmium-poisoned animals ( Axelsson and Piscator, 1966). British
workers using rats found cadmium highest in the kidney cortex, it was
also present in liver, pancreas, thyroid and spleen. (Buxton, 1956;
Kazantzis, 1956). Cadmium in high doses has been shown to produce
testicular atrophy in several mammalian species including Rhesus
monkey. Other experimental animal findings reported are damage to the
placenta, teratogenic effect, and hemorrhage in sensory nerves (Roe,
et al., 1964; Holmber and Ferm, 1969). In 1969 Kendry and Roe reviewed
accumulated evidence of cadmium toxicity on a wide variety of
biological systems.
Control of Toxic Effects
Cadmium should not be used where it may contaminate food or drink.
With the data at hand, the safe limit value for cadmium oxide fume now
in use (1972) is 0.1 mg/m3 ; for cadmium metal dust and soluble salts
0.2 mg/m3 is the allowable airborne concentration. Because of cadmium
retention in the body, these presently used levels may not protect
from harmful effects arising from long-term exposure. Elkins published
air data associated with illness (1959), confirming the relationship
between exposure and toxic effect as well as the value of engineering
controls. Urinary cadmium levels reflect absorption but do not
correlate with disease of intensity of exposure.
Periodic weighing of workers exposed to a cadmium risk provides the
chance to record vague gastrointestinal complaints, anosmia, and
chronic rhinitis as evidence of early cadmium poisoning. Regular
inspection of teeth, routine hemoglobin and urine analysis for
cadmium-induced proteinuria are valuable and reliable means for early
recognition of toxic cadmium effect.
Treatment
Following discovery of the favorable effect of British Anti-Lewisite
(BAL) in arsenic and mercury poisoning, the Chemical Warfare Service
(1946) made extensive studies (Gilman et al., 1946) of this material
in the treatment of acute cadmium intoxication. This report and that
of Dalhamm and Friberg (1955) showed the cadmium-BAL complex to be
nephrotoxic. Moeschlin suggests that BAL be used for acute pneumonia
due to cadmium (1965). Because of the fact that urinary cadmium
correlates poorly with toxic effect, and because of Friberg’s
report that intravenous ethylenediaminetetraacetic acid (EDTA) caused
renal damage if used for a prolonged period in animals (1956), EDTA
also is not recommended for therapy of chronic cadmium poisoning.
However, Friberg found no kidney damage on a single dose of
intravenous EDTA and increase in cadmium excretion up to 500 times. On
balance, the use of BAL or EDTA are not to be recommended for cadmium
intoxication of the basis of current knowledge. As in all chemical
pneumonias, that are symptomatic and present chest x-ray changes,
complete bed rest combined with oxygen therapy and the use of steroids
will reverse the abnormalities of cadmium pneumonia if used promptly
in adequate doses.
Schroeder et al., (1968) studying increase in body cadmium as a cause
of hypertension in rats, proposed the use of a zinc chelate as a means
of removing cadmium from the body. This has proven successful in
cadmium poisoning in animals and a zinc chelate is proposed for use in
humans. Moeschlin (1965) suggests that , in addition to removing the
worker from cadmium exposure, the use of intravenous calcium gluconate
(20ml of a 10 to 20 percent solution) and vitamin D (600,00 units
under the skin at weekly intervals for six doses). Moeschlin advises
such treatment at the earliest stage of chronic cadmium intoxication
- for example, when the “yellow ring” is seen on the
teeth.
NIOSH -Criteria Documents on Chemicals and Recommendations for
Occupational Health Standards
CADMIUM COMPOUNDS
THR = The oral toxicity of Cd and its compounds is HIGH. However, when
these materials are ingested, the irr and emetic action is so violent
that little of the Cd is absorbed and fatal poisoning does not as a
rule ensue. Cases of human Cd poisoning have been reported from
ingestion of food or beverages prepared or stored in Cd-plated
containers. The inhal of fumes or dusts of Cd primarily affects the
respiratory tract; the kidneys may also be affected. Even brief
exposure to high conc may result in pulmonary edema and death. Usually
the edema is not massive, with little pleural effusion. In fatal
cases, fatty degeneration of the liver and acute inflammatory changes
in the kidneys have been noted. Ingestion of Cd results in a
gastrointestinal type of poisoning resembling food poisoning in its
symptoms. Inhal of dust or fumes [54] may cause dryness of the throat,
cough, headache, a sense of constriction in the chest, shortness of
breath (dyspnea) and vomiting. More severe exposure results in marked
lung changes, with persistent cough, pain in the chest, severe dyspnea
and prostration which may terminate fatally. X-ray changes are usually
similar to those seen in broncho-pneumonia. The urine is frequently
dark. These symptoms are usually delayed for some hours after
exposure, and fatal conc may be breathed without sufficient discomfort
to warn the workman to leave the exposure. May Cd compounds are exper
(+) carc and neo [3,6,14] of the connective tissue, lungs and liver.
[50,51,2,17,52] There is some evidence of teratogenicity. [53]
Ingestion of Cd results in sudden nausea, salivation, vomiting and
diarrhea and abdominal pain and discomfort. Symptoms begin almost
immediately after ingestion. A yellow discoloration of the teeth has
been reported in workers exposed to Cd. cadmium oxide fumes can cause
metal fume fever resembling that caused by zinc oxide fumes.
CADMIUM BOROTUNGSTATE
Yellow triclinic crystals. Cd5(BW12O40)2 18H6O, mw: 6602.06, mp: 75°
THR = See cadmium compounds and boron compounds.
CADMIUM FLUORIDE
Cubic white crystals. CdF2, mw: 150.41, mp: 1100°, bp: 1758°, d: 6.64,
vap. press: 1 mm @ 1112°.
Acute tox data: Oral LD50 (guinea pig) = 150 mg/kg. [3]
THR = HIGH via oral route. Violent reaction with K. [19] See fluorides
and cadmium compounds.
CADMIUM FLUOBORATE
Acute tox data: Oral LDLO (rat) = 250 mg/kg; inhal LCLO (mouse) = 670
mg/m3 for 10 min. [3]
CADMIUM OXIDE
(1) amorphous, brown crystals; (2) cubic, brown crystals. CdO, mw:
128.41, mp (1): <1426°, mp(2): decomp @ 950°, bp: 1559°, d (1): 6.95,
d(2): 8.15, vap. press: 1 mm @ 1000°.
Acute tox data: Oral LD50 (rat) = 72 mg/kg. [3]
THR = HIGH via oral and inhal routes. See also cadmium. an exper (+)
carc. [3,6] Reacts violently with Mg. [19]
CADMIUM OXIDE FUME
Acute tox data: Inhal TCLO (man) = 8.63 mg/m3 for 5 hrs --- pulmonary
damage, inhal LC50 (rat) = 500 mg/m3; inhal LC50 (dog) = 4000 mg/m3
for 10 min. [3]
THR = HIGH irr via inhal route.
CADMIUM SOLDER
THR = A (S) carc. [14] See cadmium compounds.
hanson
news:9e9abe33.01110...@posting.google.com...
>
> I admire and respect your opinions. I even agree with you to a great
> extent. However, We have developed substitutes for Cadmium in
> braze alloys based on the following which references dangers of
> Cadmium.
> Tom
Thanks, Tom.
I fully agree with you that it's is not healthy to be exposed to and inhale
CdO fumes, and I would use your Zero-Cad brazing rods anytime over Cad
containing ones, provided that they perform as well all over. I do suspect
though that Cad containing brazing rods are for rare specialty applications
only, which I myself never ran across. Furthermore, my post was directed
to, as the post title says; "electrochemical deposition of Cd from
solution" and not what you refer to. Never the less, I highly appreciate
your information, and I hope that your plug will result in some sales for
your product. Post the name of your product, and where can it be bought.
Now, let me make some comments on your literature collection:
Thank you for your fine compilation, with which I am familiar. There is ten
times more info of this kind on the subject available in every local Enviro
agency.
Now, please note in your fine compilation about Cad dangers, that the word
"may" does appear 34 times. In other words "may", = perhaps, maybe/maybe
not, POTENTIALLY, but NOT with certainty references are made which besmear
the good name of cadmium and only advertises its POTENTIAL maybe-perhaps
undesirable possibilities.
Then also note in your fine compilation about Cad dangers, that the
assertive word "will" does occur only 6 times, 5 of which do not refer to
its toxicity, and the 6th "will" does say: "complete bed rest combined with
oxygen therapy and the use of steroids will reverse the abnormalities of
cadmium pneumonia if used promptly in adequate doses.
I don't mind the publication of such studies, anecdotal records and
conjectures at all. What galls me is the ungodly hysteria which is whipped
up over such POTENTIALS which never even reach the level of a general
public health concern. What galls me are the accompanying new tax burdens
which such frenzies create, and the cashing-in-on, the exploitation and
corruption of such nonexistent, only POTENTIAL dangers. They only REAL
thing all this does is, it feeds useless bureaucrats and allows enviro
turds to get grants to stir up more green shit.
These are the reason why I have stated: "Cadmium's EXTREMELY OVER
EXAGGERATED toxicity is nothing but classical enviro shit hype..etc."
In parting let me restate for the sake of collective sanity and reason:
Remember,
environmentalism is nothing ------
----- but sanitation driven to pathological extremes, .
Tom Walz
It is not our alloy. It is a standard AWS alloy.
I would agree with you and offer the further thought that Cadmium is
cheap and easy to detect.
I have met some of the people that have done this research and a
couple of them were good scientists. As good scientists they were
very careful in their phrasing. This would mean that they would use
"will" only if there is a proven, 100% cause / effect relationship.
Of course, your comments are accurate in all too many cases.
Tom