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AIR POLLUTION ASPECTS
OF
CADMIUM AND ITS COMPOUNDS
Prepared for the
National Air Pollution Control Administration
Consumer Protection & Environmental Health Service
Department of Health, Education, and Welfare
(Contract No. PH-22-68-25)
Compiled by Y. C. Athanassiadis
Litton Systems, Inc.
Environmental Systems Division
7300 Pearl Street
Bethesda, Maryland 20014
September 1969

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FOREWORD
As the concern for air quality grows, so does the con-
cern over the less ubiquitous but potentially harmful contami-
nants that are in our atmosphere.
Thirty such pollutants have
been identified, and available information has been summarized
in a series of reports describing their sources, distribution,
effects, and control technology for their abatement.
A total of 27 reports have been prepared covering the
30 pollutants.
These reports were developed under contract
for the National Air Pollution Control Administration
(NAPCA) by
Litton Systems, Inc.
The complete listing is as follows:
Aeroallergens (pollens)
Aldehydes (includes acrolein
and formaldehyde)
Anunonia
Arsenic and Its Compounds
Asbestos
- Barium and Its Compounds
~Beryllium and Its Compounds
Biological Aerosols
(microorganisms)
-Boron and Its Compounds
- Cadmium and Its Compounds
- Chlorine Gas
-Chromium and Its Compounds
(includes chromic acid)
Ethylene
Hydrochloric Acid
Hydrogen Sulfide
Iron and Its Compounds
-Manganese an~ Its Compounds
/ Mercury and Its Compounds
~Nickel and Its Compounds
_Odorous Compounds
Organic Carcinogens
- Pesticides
Phosphorus and Its Compounds
- Radioactive Substances
- Selenium and Its Compounds
-Vanadium and Its Compounds
-Zinc and Its Compounds
These reports represent current state-of-the-art
literature reviews supplemented by discussions with selected
knowledgeable individuals both within and outside the Federal
Government.
They do not however presume to be a synthesis of
available information but rather a summary without an attempt
to interpret or reconcile conflicting data.
The reports are

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necessarily limited in their discussion of health effects for
some pollutants to descriptions of occupational health expo-
sures and animal laboratory studies since only a few epidemio-
logic studies were available.
Initially these reports were generally intended as
internal documents within NAPCA to provide a basis for sound
decision-making on program guidance for future research
activities and to allow ranking of future activities relating
to the development of criteria and control technology docu-
ments.
However, it is apparent that these reports may also
be of significant value to many others in air pollution control,
such as State or local air pollution control officials,
as a
library of information on which to base informed decisions on
pollutants to be controlled in their geographic areas.
Addi-
tionally, these reports may stimulate scientific investigators
to pursue research in needed areas.
They also provide for the
interested citizen readily available information about a given
pollutant.
Therefore, they are being given wide distribution
with the assumption that they will be used with full knowledge
of their value and limitations.
This series of reports was compiled and prepared by the
Litton personnel listed below:
Ralph J. Sullivan
Quade R. Stahl, Ph.D.
Norman L. Durocher
Yanis C. Athanassiadis
Sydney Miner
Harold Finkelstein, Ph.D.
Douglas A. Olsen, PhoD.
James L. Haynes

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The NAPCA project officer for the contract was Ronald C.
Campbell, assisted by Dr. Emanuel Landau and Gerald Chapman.
Appreciation is expressed to the many individuals both
outside and within NAPCA who provided information and reviewed
draft copies of these reports.
Appreciation is also expressed
to the NAPCA Office of Technical Information and Publications
for their support in providing a significant portion of the
technical literature.

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ABSTRACT
Cadmium and cadmium compounds are toxic to humans and
animals; however,
the exact nature of the biological action of
cadmium is not fully understood.
It is known to be toxic to
practically all systems and functions of human and animal
organisms, and it is absorbed without regard to the level of
existing concentrations in the body, indicating the lack of a
homeostatic mechanism for the control of cadmium levels.
When inhaled, cadmium or cadmium compounds can produce
pulmonary emphysema and bronchitis, kidney damage resulting in
proteinuria, and gastric and intestinal disorders.
Atmospheric
concentrations of cadmium have been related statistically to
diseases of the heart.
Similar effects have been observed in
experimental animals.
Effects on the liver and brain have also
been observed.
Animal experiments also indicate that cadmium
may be carcinogenic.
No evidence has been found of the deleterious effects of
cadmium air pollution on plants or materials.
The major emission sources of cadmium are the metal
industries engaged in extraction, refining, machining, electro-
plating, and welding of cadmium materials.
Since cadmium is
produced as a by-product rather than as a primary product, the
refining of associated metals--such as zinc, lead, and copper--
provides the emission sources important to air pollution.
Cadmium is also used in the m~nufacture of pesticides and

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fertilizers, and both the production and consumption of these
products are potential air pollution sources.
The average ambient air concentration of cadmium was
0.002 ~g/m3 in 1964, and the maximum concentration was 0.350
~g/m3.
General air pollution control procedures used in the
metal industries are applicable to the abatement of cadmium
contamination; however, little information has been found on
specific applications of these procedures.
No information has been found on the economic costs of
cadmium air pollution or on the costs of its abatement.
Methods are available for the analysis of cadmium in the
ambient air.

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FOREWORD
ABs'r RACT
1.
CONTENrs
2.
INTRODUCTION.
. . . . . . .
. . . . . .
. . .
. . .
EE'FECTS
2.1
2.2
2.3
2.4
2.5
3.
SOURCES
. . . . .
. . .
. . . . . .
3.1
3.2
3.3
3.4
4.
. . . .
. . . .
Effects on Hu~ans . . . . . . . . . . . . . . .
2.1.1 Respiratory System. . . . . . . .
2.1.2 Cardiovascular Syste..rn . . . . . . . . .
2.1.3 Other Physiological Effects. . . . . .
2.1.4 Carcinogenesis. . . . . . . . . . . . .
Effects on &,imals .. . . . . . . . . . . . .
2.2.1 Commercial and D~mestic Animals. . . .
2.2.2 Experimental Animals. . . . . . . . . .
2.2.2.1 Respiratory System. . . . . .
2.2.2.2 Other Physiological Effects. .
2.2.2.3 Carcinogenesis. . . . . . . .
Effects on Plants. . . . . . . . . . . . . . .
Effects on Materials. . . . . . . . . . . . .
Environmental Air Standards. . . . . . . . . .
. . . . . . .
. . .
. . . .
. . . . .
. . .
Natural Occurrence
Productio~ Sources
Product Sources.
E~vironmental Air
. . . . .
. . . . .
. . . .
. . .
. . . . . .
. . . . .
. . . . .
. . . .
. . . . . .
Concentrations
. . . . . . .
ABATEMENT
. . . . .
APPENDIX B
. . .
. . . . . . . . . . . . .
5.
ECONOMICS
. . . .
6.
. . . . .
. . .
. . . . .
. . . .
ME'rHODS OF ANALYSIS
. . . . .
. . .
. . . . .
6.1
6.2
7.
. . .
Sampling Methods. . . . . . . . . . . . . . .
Quantitative Methods. . . . . . . . . . . . .
SUMlvL\RY AND CONCLUSIONS
. . . . .
R~FERENCES
. . . . . . . . .
. . .
. . . . . . .
. . . . . .
. . . . . . .
APPENDIX A .
. . .
. . .
. . . . . . . . . . . .
. . . .
. . . . . . . . . . . .
. . . . . . . . . . .
1
2
2
2
3
4
7
9
9
10
11
12
16
16
16
17
18
18
19
25
28
30
31
32
32
32
34
37
53
58

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LIST OF FIGURES
1.
Mean Concentrations of Cadmium '3.i1d Cadnium/Zinc Values
in Kidneys of 221 subject from the United States,
A;::cord in9 to Age. . . . . . . . . . . . . . . . . . . .
8
2.
U.S. Production of Cadmium
. . .
. . 22
. . .
. . .
. . . .

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10.
11.
12.
13.
14.
15.
16.
LIST OF TABLES
1.
Life Span of Rats
. . . .
. . .
. . . . .
. . . .
2.
Cadmium Concentrations in Zinc Refinery Dusts. .
3.
Cadmium Content in Exhaust Gas of Copper Smelting

War k s . . . . . . . . . . . . . . . . . . . . . .
4.
Production and Consumption of Cadmium and
Cadmium Compounds. . . . . . . . . . . .
. . . .
5.
Major U.S. Producers of Primary Cadmium as a
Metallurgical By-Product of Zinc . . . . . .
6.
Percentage of Cadmium Recovered per Ton

Recoverable Zinc. . . . . . . . . . . .
. . . .
7.
Major Uses of Cadmium.
. . . . .
. . .
. . . . .
8.
Cadmium Alloys and Solders and Their Cadmium

Content. . . . . . . . . . . . . . . . . . . . .
9.
Cadmium Content of Paints
. . . .
. . . . . . . .
Effects of Cadmium and Cadmium Compounds on

Humans. . . . . . . . . . . . . . . . . .
. . .
Presence of Cadmium in Human Tissues
. . . . . .
Properties, Toxicity, and Uses of Some Cadmium

Compounds. . . . . . . . . . . . . . . . . . . .
Effects of Cadmium and Cadmium Compounds on

.Ar1 irna 1 s . . . . . . . . . . . . . . . . . . . . .
Cadmium-Containing Pesticides.
. . . . . .
. . .
List of Companies Producing Cadmium Chemicals

( 1968 ) .....................
Concentration of Cadmium in the Air.
. . . . . .
11
20
20
23
24
25
25
26
26
59
60
61
66
69
71
78

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1
1.
INTRODUCTION
Cadmium is a relatively rare element discovered in
1817 by Strohmeyer, who gave it the name "cadmium" to indicate
its close association with zinc ores.
The industrial production of cadmium started in 1829 in
Upper Silesia and in 1907 in the United States.
Cadmium
production in the United States has been accelerating since
the beginning of the 20th century.
The cadmium industry's
steady growth is a result of an increasing number of industrial
uses--such as electroplating--and products--such as storage
batteries, semiconductors, atomic fission controls, fertilizers,
and pigments.
Industrial exposure to cadmium has been observed to cause
both chronic and acute poisoning.
Inhalation of cadmium fumes
or vapors causes damage mainly to kidneys, where the cadmium
tends to concentrate.
Moreover, most other body organs and
systems can be affected adversely by cadmium inhalation.
The most likely source of cadmium pollution is the
production and the handling of its compounds.
The inhalation
of fumes and vapors arising from retorts or condensers while
cadmium and cadmium oxide are being manufactured, and the
inhalation of dust in bagging have caused industrial cadmium
poisoning.
Recent studies indicating that cadmium may cause heart
disease and cancer have caused concern about the health
significance of low concentrations of cadmium in ambient air.

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2
2.
EFFECTS
2.1
Effects on Humans
Although human exposure to concentrations of cadmium in
the atmosphere has occurred for over 140 years, no systematic
study of the adverse effects of such exposure has yet been
made.
Nevertheless, studies conducted during the last 10-year
period have indicated that there is no system or function of
the human organism that has not been subjected to and damaged
(experimentally or otherwise) by an' effective concentration of
environmental cadmium.
Table 10 in APpendix B summarizes the specific effects
noted from intake of cadmium or cadmium compounds by humans.
Table 11 in Appendix B indicates the cadmium content of

91
various human tissues, as reported by Schroeder, et ale
The properties and toxicity of certain cadmium compounds are
presented in Table 12 (Appendix B).
Appendix A provides
additional information on the physical and chemical properties
of cadmium and some of its compounds.
2.1.1
Respiratory System
Pulmonary emphysema--the most typical symptom of chronic
cadmium poisoning due to inhalation of cadmium fumes, cadmium
oxide dust, or cadmium salts--is characterized by shortness of
breath and may be followed by bronchitis.
In pulmonary emphy-
serna the alveoli of the lungs are dilated and their walls
. d 12
overdlstende .

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3
The effects of inhaled cadmium on the respiratory system
are characterized by three overlapping phases:
edematous,
f'b . 27
proliferative, and 1 rogenlc.
The first phase, representing
the initial inflammation of some 50 square meters of irritated
pulmonary membrane, is similar in nature to that produced by
other deep-lung irritants.
Interstitial edema develops as a
result of extravasation of fluid from inflamed pulmonary
capillaries and often results in a separation of pulmonary
epithelium sheets from their underlying stromata.
Progressive
distention of interstitial tissues is followed by accumulation
of fluid in the alveoli, and often, precipitation of fibrin.
The second phase is characterized by metaplasia of the
alveolar epithelium and proliferation of histiocytes and
polypoidal lesions, resulting in destruction of alveoli and
proliferative interstitial pneumonitis.
The third, or fibro-
genic, phase has been observed in experimental animals surviving
acute cadmium exposures and also among exposed humans who
survived.
The associated pulmonary fibrosis is localized
around the bronchi and the vascular tubes.
Clinical examinations of five workers poisoned by
cadmium fumes while cutting cadmium-plated bolts with an
oxyacetylene torch showed severe pulmonary edema and alveolar
10
metaplasia of the lung.
2.1.2
Cardiovascular System
Perry and Schroeder,71 and later Schroeder alone,87,88
implicated cadmium as a cause of hypertension.
Their studies

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4
showed a correlation between the cadmium content of the kidneys
and hypertension in both humans and rats.
Stimulated by these
results, Carroll17 compared the death rates in 28 U.S. cities
and the cadmium concentration in the urban air.
He found a
significant correlation (r=0.76) between the cadmium concen-
tration and diseases of the heart (with the exception of rheu-
matic heart disease).
His study included hypertension,
arteriosclerosis, and other nonspecific heart diseases,
such
as congestive heart failure and myocardial degeneration.
In another study that related diseases of the heart to
concentrations of cadmium,
zinc, lead, vanadium, tin,
chromium,
and manganese in the urban air, cadmium concentration was
found to have the highest correlation to heart diseases,
d' 49
followed by vana lum.
In a study of 13 Japanese workers engaged in smelting
silver-cadmium alloys, exposure for even less than a year to
the resulting cadmium fumes (75 to 240 ~g/m3, averaging 130
3 d d ,100
~g/m ) pro uce anemla.
2.1.3
other Physiological Effects
Kidney damage is the most common and the best documented
of the effects of cadmium on the excretory system of human and
animal bodies.
Prolonged occupational exposure to cadmium dusts and
fumes produces proteinuria, i.e., excretion of urinary proteins
with molecular weights of 20,000 to 30,000.
Documentation

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5
relating cadmium exposure to proteinuria is relatively exten-
sive and detailed.
Friberg35 observed proteinuria in Swedish workers who
had been engaged in the alkaline battery industry.
These
workers had experienced comparatively short exposures (5 to 7

years) to low concentrations (200 to 15,000 ~g/m3) of cadmium
dust.
In one case, the proteinuria was detected when the
patient complained of lassitude 3 years after he had ceased
handling the cadmium.
A clinical study of 70 workers exposed to cadmium oxide
dust was reported by potts:7
These workers were exposed to
cadmium concentrations ranging from 100 ~g/m3 to 236,000 ~g/m3
over a 10~year period.
Proteinuria and anosmia were found in
31 (44 percent) and 45 (64 percent), respectively.
Potts
reported two cases of glycosuria, six of bronchitis, six of
peptic ulcers, and eight deaths.
Five of the eight deaths were
caused by cancer (three from cancer of the prostate).
He
makes no claim that these findings are causally associated with
cadmium exposure.
Japanese workers who had been exposed to dusts of
stabilizers (including cadmium stearate) in a vinyl chloride
film factory were found to have a high incidence of protein-
. 97
urla.
Another study of proteinuria due to cadmium oxide fumes
involved 79 persons, 55 of whom were workers exposed to the
fumes.
Piscator73 found that normal protein excretion in the

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6
urine averaged 50,000 ~g per day, while in the individuals
exposed to cadmium oxide fumes, protein excretion ranged from
70,000 to 2,600,000 ~g per day.
Furthermore,
this excretion
rate was found to be a function of the length of exposure.
The electrophoretic findings of this study were typical of
tubular proteinuria.
Quantitative determinations of proteinuria have shown
that the appearance of proteinuria is not a specific indica-
tion of cadmium exposure, as other diseases give rise to
. 74
similar reactlons.
Piscator75 also compared normal urlnary proteins with
excreted proteins from patients with occupational proteinuria
caused by chronic cadmium poisoning:
most of the excreted
proteins were identified as normal urinary proteins.
The study
concluded that the presence of large amounts of low molecular
weight (20,000 to 30,000) serum proteins in the urine of
patients with chronic cadmium poisoning is probably due to
tubular damage and the resulting reduction in efficiency of
protein absorption in the glomerular filtrate.
Another study reported that the autopsy of a worker
poisoned by cadmium fumes while cutting cadmium-plated bolts
10
with an oxyacetylene torch showed renal damage.
Nephrolithiasis was observed in about 25 percent of the
. 33,37
workers in the Swedish alkaline battery lndustry.
Kidney damage is now considered to be a classical
syndrome of chronic cadmium poisoning, and it has been shown

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7
to result from exposure to the soluble salts of cadmium sulfide
and cadmium stannate. 55
Tne variation, with respect to age, of cadmium mean con-
ceotrations and of the cajmium-to-zinc ratio found in kidneys
by Schroeder et al.91 is shown in Figure 1.
Maximum concen-
trations of cad:lliu:n and cad:llium to zinc were fO'clnd in the 40-
to-50-year age group.
concentrations declined thereafter.
Other observed and doclli~ented physiological effects of
cad'llium include gastric and intestinal diso::-ders and jamage,
loss of weight, and hepatic damage.
h' 85 f d '
Sakabe and Us 10 o~n gastr1c disturbances caused by
inhalation of cajmium stearate dust.
They suspected that the
inhaled dust (1 to 10 ~*) was deposited in the upper respira-
tory tract where the particles would be removed by ciliar
motion 3nd expectoration, then swallo'wed and hydrolyzed by
the acidic gastric juice.
potts77 reported that six men exposed to cadmium oxide
dust had peptic ulcers, of whom four have had partial
gastrectomies.
2.1.4
Carcinoqenesis
There is incomplete evidence that cadmium is carcinogenic
to humans, however,
its carcinogenicity in animals has been
demonstrated.
In 1965, potts77 reported that from a total of 70 ca&llium
*~=micron(s).

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ppm ash
7,000
6,000
5,000
4,000
3,000
2,000
1,000
. /'
/
\ /
\ /
'--'
.
1-9
.0- -- -
......,,"'" ~"""'....
,fY
x
x
"'-
,
,
.,
,. Zn
'--.
"-
"-
,
o "
'0
"" Cd
"
"
"
Age
1 0-19 20-29 30-39 40-49 50-59 60-69 70-79
FIGURE 1
8
Cd/Zn
0.7
0.6
0.5
0.4
0.3
0.2
o
0.1
80-
Mean Concentrations of Cadmium and Cadmium/Zinc Values in Kidneys
of 221 Subjects from the United States, According to Age91
.
--- - .............
./' .
x./'.
./

/.
/
/
/
/
/
,
" 0
/
0/
/
/
/
/
~-

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9
workers five deaths were due to cancer.
In the discussion that
followed the presentation of this paper, Kazantzis suggested
that these results indicate a possible role of cadmium as a
carcinogen.
He further pointed out that some cadmium compounds
have been shown to be carcinogenic to animals (see Section
2.2.2.3).
14
In another study ten different tissues obtained from
the Autopsy Service of the Los Angeles County Hospital were
analyzed for 13 trace metals.
Cadmium concentrations in
cancerous tissues obtained from lung and liver were found to
be nearly twice as high as those obtained from control tissues
(4,000 and 5,100 v~ 2,400 and 3,200 ~g/lOO g dry tissue).
2.2
Effects on Animals
Commercial and Domestic Animals
2.2.1
A few studies have been conducted on the effects of
cadmium that has been injected into farm animals or included in
their diets.
Although these studies are not directly related
to effects of cadmium in the environmental air, they serve to
assess the relative toxicity of cadmium to various species of
animals.
. 65 h
In a study by Mlller et ale tree cows were each glven
capsules of 3 grams of cadmium daily for 2 weeks.
Milk pro-
duction declined rapidly for several days after cadmium adminis-
tration was begun, and then increased to an intermediate level. Wher
cadmium administration ceased, milk production increased by 50

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10
percent and weight loss occurred.
Fecal excretion of cadmium
averaged 82 percent of the intake.
The cadmium content of
milk was less than 0.1 ppm, which was the low detectability
limit.
Less than 0.022 percent of the cadmium administered
appeared in the milk.
Lofts et al.60 reported that an intramuscular injection
(0.2 ml of a 0.04 molar solution) of cadmium chloride given
to wood pigeons and feral pigeons did not result in necrosis
of the seminiferous tubes.
However, they found that an intra-
testicular injection (0.1 ml of a 0.04 molar sOlution) of
cadmium chloride into pigeons of both species caused localized
necrotic damage and a general disruption of germ-cell coordi.
nation in the seminiferous epithelium.
A study5 was made of cadmium toxicity in swine by
feeding a ration containing a wormer (0.044 percent cadmium
anthranilate) to shoats in dry lot.
Some deaths occurred;
autopsies revealed anemia, enlarged spleen, numerous linear
ulcerations of stomach, enlarged mulberry-shaped heart, marked
fatty degeneration of liver and kidneys, and icterus.
Wi th-
drawal of the medicated feed eliminated the symptoms.
2.2.2
Experimental Animals
A most important category of health effects is one
characterized by complete absence of definite symptoms.
Effects on longevity and survivability of living organisms
belong to this category and can be causally associated with a

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11
pollutant only by extensive experiments employing refined and
well-designed statistical methods of analysis.
Schroeder et al.90 showed that the life span of rats and
mice fed cadmium was shorter than that of control groups.
In
this study 127 rats fed cadmium were compared with 104 control
rats.
The findings of the study are summarized in Table 1.
TABLE 1
90
LIFE SPAN OF RATS
Percent Dead
Aqe (days)
Control Cadmium-fed
50 percent
75 percent
100 percent
945-978
1,016-1,036
1,185-1, 400
805-822
902-996
1,213-1,278
Number of dead at 3 months of age
o
20
Data on some effects of specific doses of cadmium
compounds on animals are listed in Table 13 in Appendix B.
2.2.2.1 Respiratory System
Schroeder et al.90 found no significant difference in
the number of deaths caused by pneumonia in rats fed 5 ppm
cadmium acetate solution and a control group.
These investi-
gators observed at autopsy that 26 rats (Qr 31 percent) from
a total of 84 died of pneumonia while being fed cadmium.
In comparison, 25 (or 36 percent) of 70 rats in a control
group died of pneumonia.

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12
101
In another study, rats intermittently exposed to
cadmium chloride aerosol developed larger lungs, which con-
tained an air volume three times greater (1.5 ml) than the
normal; a lung-to-body weight ratio markedly greater (86.5 x

10-4) than the normal (4.2 x 10-4), and a decreased amount of
air per gram of body tissue.
The last symptom indicates loss
of distensibility, or increased rigidity.
Both macroscopic
and microscopic examinations showed pulmonary inflammation,
fibrosis, emphysema, loss of tissue elasticity, decrease of
functioning units (decrease in the number of alveoli), and
filling of alveoli with proliferated cells and debris.
2.2.2.2
Other PhVsioloqical Effects
A dose of 650 ~g/kg of cadmium injected as cadmium


sulfate in rabbits was found by Dalhamn and Friberg23 to
result in a 40 percent to 50 percent reduction in hemoglobin
within 10 weeksu as well as a 30 percent to 50 percent reduc-
tion in erythrocytes.
As a consequenceu the rabbits developed
pronounced anemia.

In a subsequent study. Carlson and Friberg16 showed that
rabbits injected daily for 1 to 6 weeks with solutions of
radioactive cadmium-llS (6S0 to 1,000 ~g/kg body weight)
developed anemia.
The erythrocytes contained more than 90
percent cadmium in whole blood, and the cadmium in the blood,
after repeated exposures, was at least partly bound to the
hemoglobin molecule.
The study concluded that it is possible

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13
that cadmium is transported to the bone ffi'irrOW, where it
inhibits the synthesis of hemoglobin and thus produces anemia
in animals and men.
. 22.. d
In another study, Dalhamn and Fr~berg ~nJecte cats
and rabbits with very small doses of cadmium (300 to 500 ~g
of cadmium per kilogram of body weight) in the form of cadmium
sulfate solution.
A reduction in blood pressure of 15 to 45
rom Hg was observed almost immediately.
The bloJd pressure
returned to normal in 1 to 3 minutes.
57
An investigation by Kennedy of the effect of injected
cadmium chloride (10, 15, and 20 ~ mOle/kg body weight) on
the serum calcium levels of rabbits showed hypocalcemia pro-
portional to the cadmium dose.
The experiments showed that
the serum calcium level dropped from 147 ~g/ml to 100 to 120
~g/ml due to increased renal excretion.
Dalhamn and Friberg23 found that a dose of cadmium
(650 ~g/kg) injected subcutaneously in rabbits resulted in
proteinuria in 16 of the 18 exposed animals in about 1 to 2
months after injections were begun.
24
Later they reported in a supplementary study (on 18
rabbits injected with 650 ~g cadmium per kilogram of body
weight in the form of a water solution of cadmium sulfate)
that microscopic examination of the sacrificed animals showed
pronounced damage to the renal tabuli.
Prolonged administration of small doses of soluble
cadmium salts to rats was shown to produce renal lesions,

-------
14
tabular atrophy, and interstitial fibrosis.
The lesions were
fo~nd to be very similar to those found in the case of renal

90
failure in man.
In a study by Schroeder et al.90 from a total of 46
rats fed cadmium, 35 animals suffered arteriosclerosis,
13 showed glomerular changes, and three had pyelonephritis.
90
Schroeder et al. also reported that upon microscopic
examination, 16 of 20 rats fed cadmium acetate suffered
hepatic sclerosis.
An investigation of rats fed cadmium stearate for 90
d~ys (0.03 percent cadmium diet) revealed histological changes
in the stomach and the intestines.
It was also shown that all
h . 104
test animals exhibited growt suppresslon.
A dose of 650 ~g metallic cadmium injected in rabbits
was found to result in loss of weight, splenic fibrosis, and
nephrosis in nearly all the exposed animals.23
An increasing number of investigations have been focus-
lng on the effects of exposure to cadmium concentrations on
the reproductive system in general, and the function of the
orchis in particular.
In one study, rats fed cadmium stearate (0.03 percent
cadmium diet) for 90 days showed histological damage in the

orchis.104 Other studies have focused on the destructive
. 1 . 68
effect of cadmium ions on testlcu ar tlssue, the sterili-
1 84 h .
zation of the male by cadmium sa ts, c anges ln the blood
vessels of the rat testis and epididymis produced by cadmium

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15
ch 1 . d 20 53 f f . .
. orl e, , the e ect of chryptorchldlsm and cadmium on
the rat testis,25 the path of cadmium91 in the spermatogenic

pathway,42 and the functioning of the testis and intratestic-
ular ovarian grafts in male rats following injection with
d. 62
ca mlum.
Most of the above-mentioned studies were conducted
during the 1960's.
Also during this period, two British studies
showed an association between cadmium and teratogenesis in
animals.42,84
51
Holmberg and Ferm have reported that cadmium sulfate is
teratogenic to the hamster embryo.
Following injection of 2
~g/g of cadmium sulfate into the lingual vein of pregnant
hamsters, 59 of 115 embryos were malformed.
Selenium was
found to significantly decrease the teratogenic action.
Comparatively very few studies have been made of the
effects on the nervous system of exposure to cadmium in the
atmosphere.

In a study by Schroeder et al.,90 of 84 rats fed cadmium
acetate (5 ppm), the deaths of 10 amimals were caused by
disorders of the nervous system.
The major symptoms were
vestibular disturbances, paralysis, convulsions, and "rolling
fits."
In the control group, only one of 70 animals died of
neurological disease.
A Russian study of chronaxie and conditioned reflexes of
animals exposed to inhalation of cadmium oxide aerosol showed
that a single inhalation of 13 to 18 ~g/liter as well as repeated
exposure to concentrations ranging from 1.8 to 2 ~g/liter

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16
produced disturbances of conditioned reflex activity-
In bath
acute and prolonged exposures, similar results appeared after
prolonged latent periods and were accompanied by lower reflex
h' 101
responses and, in some cases, ypnotlc phases.
2.2.2.3
Carcinoqenesis
Rats injected with cadmium chloride solution developed
sarcomas at the injection site (mesodermal tissues), while
comparable dose levels of zinc failed to produce tumors in
any of the tissue sites tested.4l
Sarcomas were also induced in rats by injections of
suspensions of cadmium metal powder,47,48 cadmium oxide, 56
cadmium sulfide (insoluble),54,56 and even cadmium sulfate
(soluble).44
Rat ferritin, an iron preparation knoT~. to be
contaminated with cadmium, produced tumors when injected into
rats.43
2.3
Effects on Plants
Cadmium reaches the soil as an impurity in phosphate
f '1' 9
ertl lzers.
When vegetables normally deprived of cadmium
were grown ln soil heavily fertilized with 20 percent
superphosphate, they absorbed the cadmium, and the roots be-
came progressively damaged.89 While contamination of soil
by atmospheric zinc has been studied, no similar study has
been made for cadmium.
2.4
Effects on Materials
No evidence was found in the literature regarding effects

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17
o~ materials resulting from cadmium air pollution.
2.5
Enviro~mental Air Standards
The American Conference of Governmental Industrial
H . . 99
yglenlsts has recommended the following cadmium threshold
limit values for industrial workers:
Cadmium oxide fumes
100 flg/m3
200 fl'~/m3
Cadmium metal dusts and soluble salts
The American Industrial Hygiene Association15 recommends
a maximum atmospheric concentration of 100 flg/m3, for cadmium
oxide fume.
In addition, they suggest that doses of 2,900,000
flg-min/m3 of oadmium oxide can be lethal; 1,100 flg/m3 for 8
hours can produce nonfatal intoxication and 500 to 2,500 flg/m3
over a 3-day period can produce cadmium pneumonitis.
~le U.S.S.R. has adopted the threshold limit value of
100 flg/m3 per 8 hours for cadmium oxide for industrial workers.
British Commonwealth countries have accepted the
following values for emission standards of cadmium in effluent
air or gases:
Great Britain 39,000 flg/m3
New South Wales 23,000 flg/m3
Queensland 23,000 flg/m3
Great Britain also limits the emissions of cadmium to
63,95
30 pounds per week (168 hours).

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18
3.
SOURCES
3.1
Natural Occurrence
Pure cadmium metal does not occur in nature.
It is a
relatively rare metal that occurs mainly in the form of
minerals in zinc, lead-zinc, copper-zinc, and lead-capper-zinc
ores.
In fact, cadmium is found in nearly all ores containing
zinc,
and its concentration is almost always in direct rela-
tion to that of zinc.
The cadmium-to-zinc weight ratio varies
from 0.0002 to 0.002.102
The following concentrations are
, d' h 1, 19,92
clte ln t e lterature:
Material
Cajmium Concentration
Earth 1 S crust
0.000055%
Geological reserves (percent of zinc reserves)
0.5%
Ores
Zinc blende
Pribramite
Polymetallic zinc
Zinc concentrates
ores
from sulfide ore
0.1-5.0'10
5.0%
0.01-0.5%
0.3-1.4%
Minerals (primary)
Greenockite (CdS)
Octavite (CdC03) rare
Sphalerite (CdS coating, crystal)
Xanthochroite (CdS coating, amorphous)
$77.6%
$61 . 5%

51.47%
The concentration of cadmium in soils has been estimated91
as follows:
Soil, field, unfertilized
0.55-2.45 ppm (wet weight)
SoiL tilled, unfertilized*
"'0.8
Soil, fertilized
3.38
*Virgin Islands, Agricultural Station.

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19
Cadmium concentrations have bee~ determined for the
. 91 61
followlng: '
Sea water (ppb)
0.075-0.32
Soft waters (~g/liter)
Natural water
600-14,600a
Water in private dwellings
0.0-77,OOOb
l,lOO-140,OOOc
M.micipal wdter
3.2
Production Sources
As there are no cadmium ores as such, cadmium is pro-
duced as a by-product in the refining of other metals, primarily
zinc.
Cadmium occurs in most of the polymetallic ores, and in
the selective flotatio:1 of the ores, cadmium accompanies the
primary metals and passes into the corresponding concentrates.
Therefore cadmium dust, fumes, and mists are commonly present
in the refinery processes involving zinc, copper, and lead, as
well as in the specific processes for extracting cadmium.
These production so~rces, therefore,
are sources of e~ission
of cadmium into the atmosphere.
The quantities emitted are a
92
function of the quantities of zinc, lead, and copper produced.
Little information has been found on the specific
emissions of ca~~ium in the metal refinery pr02ess.
However,
it is possible to estimate the a~Junt of cadmium discharged into
the atmosphere from data on production a~d emission of other
aConnecticut River in Vermont.
bStagnant, Brattleboro, Vt.
cFrom tap, plastic pipe; originating in
Hampshire.
lake in NeT'"

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2C)
metals.
Table 2 contains information on the relative amount
of cadmium a1!d cad.llium compounds contained in dusts from an
electrostatic precipitator controlling the roasting process
for zinc concentrates.
TABLE 2
CADMIUM CONCEN'rRATIONS IN ZINC REFINERY DUSTS19
Compound
Concen tra ti on
BY CHEMICAL ANALYSIS
Cadmium
0.42%
BY RATIO ANALYSIS
Cadmium sulfate
O. 54%
Cadlliun oxide
0.04%
Cadmium oxide-iron oxide
0.16%
Cadmium sulfide
0.03%
The cadmium content of gases projuced in the electro-
lytic refining of copper are presented in Table 3.
TABLE 3
CADMIUM CONTENT IN EXHAUST GAS OF COPPER SMELTING WORKS19
Activity
Ca&llium Content of Gas
(q/ton)*
Reverberatory smelting
1,500
Blast furnace smelting
2,000
3,200
Bessemer process
Total
6,700
*Grams of carunium in exhaust gas per metric ton of copper
produced.

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21
In 1948 in Pennsylvania, the Donora episode initiated
the first detailed measurement of cadmium emission rates in
the ambient air from one of the major sources of cadmium, a
zinc metallurgical plant.
The plant studied discharged a
total of 320 pou~ds of cadmium into the atmosphere per day
from the sinter plant and the spelter furnaces.

A study83 of the Hudson Bay Mining and Smelting Company,
Ltd., revealed that prior to an improvement in their methods
of recovering cadmium, the amount of cadmium in the dust
burden of the smelter stack flow ranged fro~ 0.3 to 0.4 tons/
day.
In the United States, the major cadmium plants use as
raw material copper-cadmium residues from electrolytic zinc
production, lead dusts from lead smelting furnaces, zinc
sulfide concentrates, and dust from the elctrostatic precipi-
tators of the multiple-hearth roaster furnaces.
The rapid growth of domestic cadmium production since
its beginning (1907) is shown in Figure 2.
Data on the
production of cadmium, cadmium oxide, and cadmium sulfide
for the period 1946 to 1966 are given in Table 4.
Table 5
lists the major producers of primary cadmium (as a by-product
in the production of zinc).

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Tons (000)
12
10
8
6
4
2
1900
1910
Hand.fitted trend curve
1920
1930
1960
1940
1950
FIGURE 2
U.s. Production of Cadmium
(IO-year averages)66

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TABLE 4
66
PRODUCTION AND CONSUMPTION OF CADMIUM AND CADMIUM COMPOUNDS
(Thousands of Pounds)
    DOMESTIC PRODUCTIQN AND CONSUMPTION   
  PRODUCTION      
 -          
 World          
 ProdJction      Shipments Imports   
 of      By For  Apparent 
Year Metal M,=ta1 Oxide Sulfide Producers Consumption Exports Consumption 
1966 26,600 10,460 W* 2,267 11,792 3,358 379 14,780 
1965 26,100 9,671 W* 1,575 8,128 2,121 73 10,431 
1964 28,250 10,458 W* 1,531 9,689 1,104 1,439 9,364 
1963 26,000 9,990 W* 1, 542 10,124 991 1,313 11, 482 
1962 25,800 11,137 1,481 1,329 12,057 1,117 717 12,146 
1961 25,700 10,466 1,075 1,115 10,222 1,079 702 10,184 
1960 21,700 10,180 W* 1,034 12,151 942 2,448 10,166 
1959 19,800 8,602 W* 1,243 11,273 1,638 900 11,471 
1958 19,800 9,673 W* 983 7,921 1,002 580 8,177 
1957 20,800 10,549 W* 1,041 10,091 1,586 693 10,999 
1956 20,000 10,614 W* 1,258 10,936 3,116 1,234 12,711 
1955 17,920 9,754 W* 1,095 11,453 927 1,394 10,689 
1954 15,900 9,552 838 1,045 8,207 402 999 7,424 
1953 15,710 9,767 956 1,229 8,282 1,555 66 9,627 
1952 13,702 8,567 531 898 8,048 1,479 301 9,008 
1951 13,514 8,311 529 955 8,052 90 606 7,171 
1950 13,239 9,190 505 1,571 9,620 630 353 9,546 
1949 11,506 8,227 493 999 8,455 157 566 7,486 
1948 10,728 7,776 292 1,097 7,953 10 956 7,818 
1947 10,876 8,508 393 1,303 8,489 20 303 7,727 
1946 8,924 6,471 318 1,226 6,812 17 140 6,984 
 *W = withdrawn (company confidential).    tV
    w

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24
TABLE 5
~~JOR U.S. PRODUCERS OF PRIMARY CADMIUM
AS A METALLURGICAL BY-PRODUCT OF ZINC13
Co:npany
L'Jcation
A'1lax
Asarco
Asarco
American Zinc
Anaconda
Bunker Hill
Eagle-.Picher
National Zinc
New Jersey Zinc
New Jersey Zinc
St. Joseph Lead
Blackwell, Okla. (zinc smelter)
Denver, Colo. (Globe cadmium plant)
Corpus Christi, Tex. (zinc smelter)
East St. Louis, Ill. (zinc smelter)
Great Falls, Mont. (zinc smelter)
Kellog, Idaho (zinc plant)
Henryetta, Okla. (zinc smelter)
Bertsville, Okla. (zinc smelter)
Depue, Ill. (zinc smelter)
Palmerton, Pa. (zinc smelter)
Herculaneum, Mo. (lead smelter)
Asarco and Anaconda produce approximately 60 percent of
the total output of cadmium in the United States.
Amax,
American Zinc, and New Jersey Zinc account for an additional
20 percent, while the remaining companies produce the balance.
The domestic production of cadmium has been decreasing
in proportion to the world's total production.
In 1946, th e
United States produced 73 percent of the world's production
of cadmium.
This figure had decreased to 53 percent by 1956,
and to a low of 39 percent in 1966.66
This decrease in the
relative domestic supply relates directly to the increased
imports of cadmium source materials from Mexico, Peru, and
Canada.
It also has influenced an increase in efficiency of
ca~'1lium recovery from the ore-extraction industries, as
revealed in Table 6.

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25
TABLE 6
19
PERCENTAGE OF CADMIUM RECOVERED PER TON RECOVERABLE ZINC
Year Percent Year Percent
1941 5.2 1948 7.2
1942 5.4 1949 8.2
1943 5.8 1950 9.0
1944 6.7 1951 7.3
1945 6.8 1952 6.5
1946 6.2 1953 8.2
1947 7.2 1954 9.6
3.3
Product Sources
The three major uses of cadmium are in the electroplating
process,
in alloys and solders, and in pigments and chemicals.
The distribution of cadmium uses is tabulated in Table 7 for
the years 1940 and 1955-56.
TABLE 7
19
MZ\JOR USES OF CADMIUM
Use
Percent of Consumption
1940 1955-56
Electroplating
Alloys and solder
Pigments and chemicals
Miscellaneous
59.8
23.9
10.0
6.3
58.1
10.9
27.3
3.7
Electroplating has consumed the largest portion of the
cadmium metal, and almost all of the oxide, sulfate, and
chloride produced.

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26
Tne percentage of cadmium in certain cadmium alloys and
solders is listed in Table 8.
TABLE 8
CADMIUM ALLOYS AND SOLDERS AND THEIR CADMIUM CONTENT96
Material
Percent of Cadmium
Alloys
Cad:11ium-nickel
Cadmium-silver-copper
93.65
97.65
Solders
Silver-cadmium
Zinc-tin-cadmium
Lead-tin-cadmium
93.00
16.00
5.00
22.50
26.00
22.00
40.00
10-26.00
8.00
Other-cadmium
The cadmium content of common paints is indicated in
Table 9.
TABLE 9
CADMIUM CONTENT OF PAINTS78
Material
Percent of Ca~~ium
Cadmium red
Li thopone 30'!o
Lithopone 60%
Stachtolith
Cadmium red +
Cadmium red +
Stachtoli th +
lithopone 60%
lithopone 30%
lithopone 60%
69.92
0.05
0.05
0.05
56.09
7.01
0.06

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27
Cadmium is a constituent of fertilizers:
common superphos-
phate fertilizers con.tain 50 to 170 ppm of cadmium.
Cadmium is
also used in pesticides.
Table 14 (Appendix B) lists some of
the important pesticides and their cadmium content.
Both fer-
tilizers and pesticides are impc>rtant to air pollution since
they are intentionally introduced into the natural environment,
usually in concentrations that can be hazardous to human,
animal,
and plant life.
A comparatively new and increasing use of cadmium is in
cadmium-nickel batteries for civil and military aircraft,
guided missiles, and spacecraft, as well as for portable
electrical appliances and power tools.
Cadmium metal and cadmium nitrate are used to control the
rate of nuclear fission and as reactor poison: cadmium soap
(stearate) is used as a stabilizer of polyvinyl chloride: and

diethyl cadmium is used in the production of tetraethyl lead.97
One of the newest uses of cadmium is in semico~ductors.
A listing of companies engaged in the production of
cadmium chemicals appears in Table 15 in Appendix B.
No data indicating the emission rate of cadmium into the
atmosphere from industrial users of cadmium products were found.
The following is a list of activities which are probable
sources of emission:

Manufacture of cad~ium-faced bearings45
production of alkaline batteries32-34-67,72
Casting of copper-cadmium alloysll
Electroplating34
1.
2.
3.
4.

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28
5.
6.
7.
Use of cadmium pigments (paints}79,81
Smelting of scrap metal (containing cadmium)
Welding of cadmium-plated metal parts
The United States Public Health Service39 reported, in
1964, the following occupations to be potentially hazardous
as a result of cadmium exposure:
Alloy making
Aluminum-solder making
Cadmium compound cOllecting-bag
Cadmium compound collecting-bag
Cadmium plating
Cadmium smelting
Cad~ium vapor-lamp making
Cadmium working
Ceramic making
Dental-amalgam making
Electric-instrument making
Electroplating
Engraving
Glassmaking
Incandescent-lamp making
Lithography
Lithopone working
Metallizing
Paint making
Paint spraying
Photoelectric-cell making
Pigment making
Small-arms ammunition making
Smoke-bomb making
Soldering
Solder making
Storage-battery making
Textile printing
Welding, cadmium alloy
Welding, cadmium-plated objects
Zinc refining
cleaning
handling
3.4
Environmental Air Concentrations
Measurements of cadmium concentration in the air have
been m~de by the National Air Sampling Network of the U.S.
1 h . 2,3 .
Public Hea t- SerVlce. Air Quallty Data figures reveal

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29
that the average atmospheric cO~2entration of cadmi~~ for 35
stations in the United States was 0.002 ~g/m3 in 1964, and


the maximum value recorded for this period was 0.350 ~g/m3.
Tabulated data for these stations are contained in Table 16
in Appendix B.

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30
4.
ABAT EI'1EN'r
No information was found in the literature on methods of
abatement peculiar to air pollution by cadmium or its cOlnpounds.
General control procedures for the prevention of air pollution
by dusts, fumes, and mists applicable to the ~etal refinery,
alloying, and machining industries are considered suitable to
these processes in the cadmium industry.
Robertson83 reported that in 1957 stack dust burden was
reduced in a Canadian copper mining and smelting company when
bag filters and cyclones were added to increase the recovery
of cadmium as a by-product.
A flue revision which vented the
dryer gas through cyclones, separated the roaster and rever-
berating gas streams, and routed each stream through two
existing electrostatic precipitators was supplementary to a
baghouse installation (12 parallel units each consisting of a
cooling train, a dust arrestor, and a fan).
The flue system
routed the furnace gases from the electrostatic precipitators
to the filtration equipment (glass cloth) and discharged the
filtered gas to the smelter stack.
AS a result of the added
processes, more than 35 tons/day of dust containing 1.46
percent cadmium were collected.

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31
5.
ECONOMICS
No information has been found on the economic costs of
cadmilli~ air pollution or on the costs of its abatement.
Data on the production and consumption of cadmium are
presented in Section 3.

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32
6.
METHODS OF ANALYSIS
6.1
Samplinq Methods
Dusts and fumes of cadmium compounds may be collected by
any method suitable for collection of other dusts and fumes;
the impinger, electrostatic precipitator, and filter are
commonly used.
The National Air Sampling Network uses a high
98
volume filtration sampler.
6.2
Quantitative Methods
Emission spectroscopy has been used by the National Air
Pollution Control Administration for cadmium analysis of
. 1,98
samples from the National Air Sampllng Network. The
samples are ashed and extracted to eliminate interfering
elements.
The minimum detectable cadmium concentration by
emission spectroscopy is 0.011 ~g/m3 for urban samples and
0.004 ~g/m3 for nonurban samples.
The different sensitivities
result from the different extraction procedures required for
4
urban samples.
Thompson et al.98 have reported that the National Air
Pollution Control Administration uses atomic absorption to
supplement analyses obtained by emission spectroscopy.
The
method has a minimum detectable limit of 0.0002 ~g/m3 based
3. 1
on a 2,000 m alr samp e.
Emission spectroscopy has also been used to determine


cadmium and other trace materials in mamm~lian tissues.14
A
resolution of 9,350 ~g/lOO 9 dry tissue was reported.

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33
. 28,59
Polarograph1c methods have also been used to
determine cadmium concentrations in air.
Ashing of the sample
is followed by neutralization and precipitation of cadmium
sulfate.
The sample is recorded using a polarographic
radiometer.
This procedure has also been used to determine
the presence of cadmium in urine, providing a measure of
concentrations between 10,000 to 70,000 ~g/liter.

86,93
A colorimetric method was used to determine the
concentration of cadmium in the air in a cadmium sterate
plant.
Dithizone was the coloring agent.
The method has a
sensitivity of 50 ~g for cadmium if less than 10,000 ~g of
interfering metals are present.

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34
7
SU~~RY AND CONCLUSIONS
Cad'TIium and cadmium compounds are toxic substances by
all means of administration, producing acute or chronic
symptoms varying in intensity from irritations to extensive
disturbances resulting in death.
However,
despite increasing
use of this metal and increasing attention to its toxic nature,
the exact manner in which it affects human or animal organisms
is not yet known.
Cadmium is toxic to practically all systems
and functions of the body, and is absorbed without regard to
the levels of cadmium already present, thereby indicating the
lack of a natural homeostatic mechanism for the control of
organic concentrations of cadmium.
Inhalation of cadmium fumes, oxides, and salts often
produces emphysema, which may be followed by bronchitis.
Prolonged exposures to airborne cadmium frequently cause
kidney damage resulting in proteinuria.
Cadmium also affects
the heart and liver.
Statistical studies of people living in
28 U.S. cities have shown a positive correlation between
heart diseases and the concentration of cadmium in the urban
air.
Cadmium may also be a carcinogen.
While there is little
evidence to support this conclusion from studies of industrial
workers, animal experiments have sho
-------
35
in-cestinal organs, and the nervous and reproductive systems.
No data were found on the effects of cadmium air pollution on
plants or materials.
The metals industry is the major source of emissions of
cadmium into the atmosphere.
Cadmium dusts and fumes are
produced in the extraction, refining, and pro2essing of
metallic cadmium.
Since cadmium is generally projuced as a
by-product in the refining of other metals, sU2h a3 zinc,
lead, and copper, plants refining these materials are sources
of cadmium emissions as well as of the basic metal.
Also,
because cadmium is present in small quantities in the ores of
these metals, cadmium emissions may occur inadvertently in
the refining of the basic metal.
Common sources of cadmium air pollution occur during the
use of cadmium.
Electroplating, alloying, and use of cadmium
in pigments can produce local contaminations of the atmosphere.
Also, since cadmium is added to pesticides and fertilizers,
the use of these materials can cause local air pollution.
In 1964, the average concentration of cadmium in the


ambient air was 0.002 IJ.g/m3, atld the maximum concentration
was 0.350 IJ.g/m3.
Air pollution control procedures are employed at some
metal refinery plants in order to recover the valuable cadmium
that would o"therwise escape into the atmosphere.
Electrostatic
precipitators, baghouses, and cyclones are effectively used

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36
for abatement.
However,
little information has been found on
the specific application of these procedures for the purpose
of controlling cad~ium air pollution.
The procedures for
recovering cadmium from exhaust in a copper extraction plant
collected significant quantities of valuable cadmium, at the
same
time reducing local air pollution levels.
No information has been found on the economic costs of
cadmium air pollution or on the costs o~ its abatement.
Methods are available for the analysis of cadmium in the
ambient alr.
Based on the material presented in this report, further
studies are suggested in the following areas:
(1)
Research into the effects of cadmium on human,
animal, and plant health.
Research into the carcinogenic effects of cadmium.
( 2 )
( 3 )
Quantitative analysis of the emissions of cadmium
into the atmosphere from industrial sources.

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37
REFERENCES
6.
8.
9.
1.
Air Pollution Measurements of the National Air Sampling
Network - Analyses of Suspended Particulates, 1957-1961,
U. S. Dept. of Health, Education, and Welfare, Public
Health Service Publication No. 978, U.S. Government
Printing Office, Washington, D. C. (1962).
2.
Air Quality Data, National Air Sampling Network, 1962,
U.S. Department of Health, Education, and Welfare, Public
Health Service, Division of Air Pollution, Cincinnati,
Ohio.
3.
Air Quality Data, National Air Sampling Network, 1964-
1965, U.S. Department of Health, Education, and Welfare,
Public Health Service, Division of Air Pollution,
Cincinnati, Ohio (1966).
4.
Air Quality Data from the National Air Sampling Networks
and Contributing State and Local Networks, 1966 ed., U.S.
Dept. of Health, Education, and Welfare, National Air
Pollution Control Administration Publication No. APTD
68-9, U.S. Government Printing Office, Washington, D.C.
(1968).
5.
Alber, C. L., Cadmium Toxicity in Swine, Vet. Med. 58:893
(1963).
Alsberg, C. L., et al., J. Pharmacol. 13: Proc. 504 (1919).
7.
Axelsson, B., et al., Renal Damage After Prolonged Exposure
to cadmium, Arch. Environ. Health 12:360 (1966).
Barrett, H. M., et al., Studies on the Toxicity of Inhaled
Cadmium. II. The Acute Lethal Dose of Cadmium Oxide for
Man, J. Ind. Hyq. & Toxicol. 29:286 (1947).
Barrows, H., The Agricultural Significance of Inorganic
Pollutants, Paper prepared for presentation Aug. 21, 1967,
at a symposium, Damage to Plants from Soil and Water
Pollution, sponsored by the American Phytopathological
Society, Washington, D. C.

-------
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
3;3
Beton, D. C., et al., Acute Cadmium Fume Poisoning - Five
Cases With One Death From Renal Necrosis, Brit. J. Ind.
Med. ld(14):292 (1966).
Bonnell, J. A., Emphysema and Proteinuria in Men Casting
Cadmium Alloys, Brit. J. Ind. Med. 12:181 (1955).
Bonnell, J. A., Cadmium Poisoning, Ann. Occupational Hyq.
8:45 (1965).
Brooks, D. B., Supply and Competition in Minor Metals
(Washington, D. C.: Resources for the Future, Inc., p.147 (1965)
Butt, E. M., Trace Metals in Health and Disease, Air
Pollution Medical Research Conference, San Francisco,
Calif. (1960).
Cadmium, Hygienic Guide Series, Am. Ind. Hyq. Assoc. J.
ll: 23 5 (1962 ) .
Carlson, L. A., and L. Friberg, The Distribution of Cadmium
in Blood After Repeated Exposure, Scan. J. Clin. & Lab.
Invest. 2:1 (1957).
Carroll, R. E., The Relationship of
Cardiovascular Disease Death Rates,
198: 177 (1966).
Cadmium in the Air to
J. Am. Med. Assoc.
Chemical Origins and Markets, Chemical Information Services,
Stanford Research Institute, Menlo Park, Calif. (1967).
Chizhikov, D. M., Cadmium, Translated from Russian (Oxford,
Eng.: Pergamon Press, 1966).
Clegg, E. J., et al., Changes in Blood Vessels of the Rat
Testis and Epididymis Produced by Cadmium Chloride,
J. Pathol. Bacteriol. 94:317 (1967}.
Crawford, T., et al., Prevalence and Pathological
of Ischaemic Heart Disease in a Hard-Water and in
Water Area Lancet 1:229-2)2 (1967).
, -
Changes
a Soft-

-------
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
39
Dalhamn, T., and L. Friberg, The Effect of Cadmium on
Blood Pressure and Respiration and the Use of Dimercaprol
(BAL) as Antidote, Acta Pharmacol. Toxicol. 10:199 (1954).
Dalhamn, T., and L. Friberg, Dimercaprol (2,3-Dimercap-
topropanol) in Chronic Cadmium Poisoning, Acta Pharmacol.
Toxicol. 11:68 (1955).
Dalhamn, T., and L. Friberg, Morphological Investigations
on Kidney Damage in Chronic Cadmium Poisoning: An Experi-
mental Investigation on Rabbits, Acta Pathol. Microbiol.
Scand. 40:475 (1957).
Davis, J. T., et al., The Effect of Cryptorchidism, Cadmium
and Anti-Spermatogenic Drugs on Fatty Acid Composition of
Rat Testis, J. Reprod. Fertility 14:407 (1967).
Dubois, L., et al., Polarographic Determination of Heavy
Metals in Air Samples, Anal. Chim. Acta 37:20 (1967).
Dunphy, B., Acute Occupational Cadmium poisoning - A
Critical Review of the Literature, J. Occupational Med.
2(1):22 (1967).
Ferret, D. J., et al., A Comparative Study of Three Recently
Developed Polarographs, Analyst 81:506 (1956).
Fitzhugh, O. G., et al., J. Pharmacol. Exptl. Therap.
1£:15 (1941).
Franklin, K. S., More About Cadmium Poisoning, Refriq.
Servo Contractinq 34(10):28 (1966).
Frear, D. E. H., Pesticide Handbook-Entoma. 1968 (State
College, Pa.: College Science Publishers, 1968).
Friberg, L., Proteinuria and Kidney
Exposed to Cadmium and Nickel Dust:
J. Ind. Hyq. 30:32 (1948).
Injury Among Workmen
Preliminary Report,
Friberg, L., Health Hazards in the Manufacture of Alkaline
Accumulators with Special Reference to Chronic Cadmium
Polishing, Acta Med. Scandp Suppl. 240,138:1-124 (1950).

-------
34.
35.
36.
37.
38.
39.
40.
41.
42.
43.
44.
45.
40
Friberg, L., Injuries Following Continued Administration
of Cadmium: Preliminary Report of a Clinical and Experi-
mental Study, Arch. Ind. Hyq. Occupational Med. ~:458
(1950) .
Friberg, L., Proteinuria in Chronic Cadmium poisoning
After Comparatively Short Exposure to Cadmium Dust,
A.M.A. Arch. Ind. Health 16:30 (1957).
Friberg, L., Chronic Cadmium poisoning, A.M.A. Arch. Ind.
Health 20:401 (1959).
Friberg, L., et al., Synpunkter pa den kroniska kadmium-
iorgiftningens prognos, Svenska Lakartidn. 49:2630 (1952).

Friberg, L., et al., Localization of Cdl15 in Different
Organs: An Autoradiographic Study, Acta Pathol. Microbiol.
Scand. 41:96 (1957).
Gafafer, W. M. (Ed.), Occupational Diseases - A Guide to
their Recognition, U. S. Public Health Service Publ. 1097
(1964).
Garri ty,
J. Am. Water Works Assoc. 40:1194 (1948).
L. V.,
Gunn, S. A., et al., Specific Response of Mesenchymal
Tissue to Carcinogenesis by Cadmium, Arch. Pathol. 83(6):
493 (1967).
Gunn, S. A., et al., Failure of 109Cadmium to Traverse
Spermatogenic Pathway, J. Reprod. Fertility 16:125 (1968).
Haddow, A., et al., Carcinogenicity of
and Metal-Carbohydrate Complexes, Rep.
Campaiqn 39:74 (1961).
Iron Preparations
Brit. EmP. Cancer
Haddow, A., et al., Cadmium Neoplasia: Sarcomata at the
Site of Injection of Cadmium Sulphate in Rats and Mice,
Brit. J. Cancer 18:667 (1964).
Hardy, H., et al., The Possibility of Chronic Cadmium
Poisoning, J. Ind. Hyq. Toxicol. 29:321 (1947).

-------
47.
48.
49.
50.
51.
52.
53.
54.
55.
56.
57.
41
46. Harrison, H. E., et al., The Effects and Treatment of
Inhalation of Cadmium Chloride Aerosols in the Dog,
J. Ind. Hyq. Toxicol. 29:302 (1947).
Heath, J. C., et al., Cadmium as a Carcinogen, Nature
193:592 (1962).
Hessling, Uber ein neues Anreichungsverfahren fur die
quantitative spektralanalytische Bestimmung von Kadmium
in organischem Material, Zentr. Arbeitsmed. Arbeits-
schutz ~:145 (1952).
Hickey, R. J., E. P. Schoff, and R. C. Clelland, Relation-
ship Between Air Pollution and Certain Chronic Disease
Death Rates, Arch. Environ. Health 15(6):728 (1967).
Holden, H., Cadmium Fume, Ann. Occupational Hyq. ~:5l
(196 5) .
Holmberg, R. E., and V. H. Ferm, Interrelationships of
Selenium, Cadmium and Arsenic in Mammalian Teratogenesis"
Arch. Environ. Health 18:873 (1969).
Johnstone, R. T., Occupational Medicine and Industrial
Hyqiene (St. Louis, Mo.: Mosby, pp. 265-275, 1948).
Kar, A. B., et al., In Vitro Action of Cadmium Chloride
on Isolated Seminiferous Tubules of the Rat Testis,
Acta BioI. Med. Ger. 16:665 (1966).
Kazantzis, G., et,. al., Indiuction of Sarcoma in the Rat by
Cadmium Sulphide Pigment, Nature 198:1213 (1963).
Kazantzis, G., et, al., Reroal Tubular Malfunction and Pulmonar1
Emphysema in Cadmium Pigment Workers, Quart. J. Med. 32:
16 5 (196 3) .
Kazantzis, G., et al., The Induction of Sarcoma in the Rat
by Cadmium Sulphide and by Cadmium oxide, Brit. J. Cancer
20:190 (1966)"
Kennedy, A., Hypocalcaemia in Experimental Cadmium Poison-
ing, Brit. J. Ind. Med. 23(4):313 (1966).

-------
58.
59.
60.
61.
62.
63.
64.
65.
66.
67.
68.
69.
70.
42
Kleinfeld, M., Acute Pulmonary Edema of Chemical Origin,
Arch. Environ. Health 10:942 (1965).
Levine, L., Polarographic Determination of Toxic Metal
Fumes in Air, J. Ind. Hyq. Toxicol. 27:171 (1945).
Lofts, B., et al., The Effects of Cadmium on the Avian
Testis, 'J. Reprod. Fertility 13: 155 (1967).
Lounamma, J., Trace Elements in Plants Growing Wild on
Different Rocks in Finland. A Semiquantitative Spectro-
graphic Survey, Ann. Botan. Soc. Vanamo 29:4 (1956).
Maekawa, K., et al., Behavior of the Testis and Intra-
testicular Ovarian Grafts in Male Rats Following Injection
with Cadmium, Acta Anat. Nippon 42:343 (1967).
Mahler, E. A. J., Standards of Emission Under the Alkali
Act, Paper III/12, Reprinted from the Proceedings (Part 1)
of the International Clean Air Congress (October 1966).
The Merck Index, 8th ed. (Rahway, N. J.: Merck, 1968).
Miller, W. J., et al., Relation of Dietary Cadmium to Cow
Performance and Cadmium in Milk, J. Dairy Sci. 50:979
(1967) .
Minerals Yearbook, Bureau of Mines, U. S. Govt. Printing
Office, Washington, D. C. (1946-66).
Nicaud, P., et al., Les Troubles de l'intoxication chronique
par 1e cadmium, Arch. Maladies Prof. 5-6:192 (1942).
Parizek, J., The Destructive Effect of Cadmium Ion on
Testicular Tissue and Its Prevention by Zinc, J. Endocrinol.
15: 56 (1957).
Pariz~k, J., Sterilization of the Male by Cadmium Salts,
J. Reprod. Fertility ~:294 (1960).
Patterson, J. C., Studies on the Toxicity of Inhaled Cadmium.
III. The Pathology of Cadmium Smoke Poisoning in Man and
in Experimental Animals, J. Ind. Hyq. Toxicol. 29:293 (1947).

-------
71.
72.
73.
74.
75.
76.
77.
78.
79.
80.
43
Perry, H. M., and H. A. Schroeder, Concentration of Trace
Metals in Urine of Treated and Untreated Hypertensive
Patients Compared with Normal Subjects, J. Lab. Clin.
Med. 45:936 (1955).
Pinto, S., Health Hazards in the Manufacture of Alkaline
Accumulators With Special Reference to Chronic Cadmium
Poisoning, by Lars Friberg: Book Review, Arch. Ind. Hyq.
Toxicol. ~:l20 (1950).
Piscator, M., Proteinuria in Chronic Cadmium Poisoning:
I. An Electrophoretic and Chemical Study of Urinary and
Serum Proteins From Workers with Chronic Cadmium Poison-
ing, Arch. Environ. Health 4:607 (1962).
Piscator, M., Proteinuria in Chronic Cadmium Poisoning:
2. The Applicability of Quantitative and Qualitative
Methods of Protein Determination for the Demonstration of
Cadmium Proteinuria, Arch. Environ. Health ~:325 (1962).
Piscator, M., Proteinuria in Chronic Cadmium Poisoning:
IV. Gel Filtration and Ion Exchange Chromatography of
Urinary Proteins From Cadmium Workers, Arch. Environ.
Health 12:345 (1966).
Potts, A. M., et al., Distribution and Fate of Cadmium in
the Animal Body, Arch. Ind. Hyq. Occupational Med. ~:175
(1950) .
Potts, C. L., Cadmium Proteinuria--The
Workers Exposed to Cadmium Oxide Dust,
~. ~:55 (1965).
Health of Battery
Ann. Occupational
pribil, R., and V. Vesely, Determination of Cadmium in the
Presence of Zinc and Lead via an EGTA Titration, Chemist-
Analyst 55:4 (Jan. 1966).
princi, F., A Study of Industrial Exposures to Cadmium,
J. Ind. Hyq. Toxicol. 29:315 (1947).
princi, F., et al., Prolonged Inhalation of Cadmium, Arch.
Ind. Hyq. Occupational Med. ~:65l (1950).

-------
81.
82.
83.
84.
85.
86.
87.
88.
89.
90.
91.
44
Prodon, L., Cadmium Poisoning: I. The History of Cadmium
Poisoning and the Uses of Cadmium, J. Ind. Hyq. Toxicol.
14: 132 (1932).
Raw Data Tabulations of the Measurements for Metals in
Quarterly Composites of 1966 and 1967, NASN Hi-Vol
Samples of Urban and Nonurban Sites, Air Quality and
Emission Data Division, National Air Pollution Control
Administration, Cincinnati, Ohio.
Robertson, D. J., Filtration of Copper Smelter Gases at
Hudson Bay Mining and Smelting Company, Limited, Can.
Mininq and Met. Bull. (Montreal) 18:674 (May 1960).
Roe, F. J. C., et al., Cadmium Neoplasia: Testicular
Atrophy and Leydig Cell Hyperplasia and Neoplasia in
Rats and Mice Following the Subcutaneous Injection of
Cadmium Salts, Brit. J. Cancer 18:674 (1964).
Sakabe, H., et al., Acute Cadmium Soap Poisoning in Industry,
Bull. Natl. Inst. Ind. Health ~:56 (1960).
Saltzman, B. E., Colorimetric Micro-Determination of Cadmium
with Dithizone, Anal. Chern. 25:493 (1953).
Schroeder, H. A., Cadmium as a Factor in Hypertension,
J. Chronic Diseases 18:647 (1965).
Schroeder, H. A., Cadmium, Chromium and Cardiovascular
Disease, The George E. Brown Memorial Lecture (October 22,
1966).. !n Press.
Schroeder, H. A., et al., Cadmium--Uptake by Vegetables
From Superphosphate in Soil, Science 140:819 (1963).
Schroeder, H. A., et al., Chromium, Cadmium and Lead in
Rats: Effects on Life Span, Tumors and Tissue Levels,
J. Nutr. 86:51 (1965).
Schroeder, H. A., et al., Essential Trace Metals in Man:
Zinc Relation to Environmental Cadmium, J. Chronic Diseases
~ (4) : 179 (196 7) .

-------
92.
93.
94.
95.
96.
97.
98.
99.
100.
101.
45
Schroeder, H. J., "Cadmium," in Mineral Facts and Problems,
Bureau of Mines Bulletin 630, U. S. Govt. Printing Office,
Washington, D. C. (1965).
Setterlind, A. N., et al., Microanalysis of Cadmium by the
Diphenylthiocarbazone (Dithizone) Method, Department of
Public Health, State of Illinois (1943).
Smith, J. C., et al., Determination of Cadmium in Urine
and Observations on Urinary Cadmium and Protein Excretion
in Men Exposed to Cadmium Oxide Dust, Biochem. J. 61:698
(1955) . -
Stern, A. C. (Ed.), Air Pollution, vol. 3, 2nd ed.
York: Academic Press, p. 633, 1968).
(New
Stokinger, H. E., "The Metals," in Industrial Hyqiene and
Toxicoloqy, F. A. Patty, Ed. (New York: Interscience, 1963).
Suzuki, S., et al., Proteinuria Due to Inhalation of Cadmium
Stearate Dust, Ind. Health ~:73 (1965).
Thompson, R. J., G. B. Morgan, and L. J. Purdue, Analyses
of Selected Elements in Atmospheric Particulate Matter by
Atomic Absorption, Preprint, presented at the Instrument
Society of America Symposium, New Orleans, La. (May 5-7,
196 9) .
Threshold Limit Values for 1967, Adopted at the 29th Annual
Meeting of the American Conference of Governmental Indus-
trial Hygienists, Chicago, Ill., May 1-2, 1967.
Tsuchiya, K., Proteinuria of Workers Exposed to Cadmium
Fume--The Relationship to Concentration in the Working
Environment, Arch. Environ. Health 14(6):875 (1967).
Vasilion, P., et al., Pressure-Volume Relations of Rat
Lung Exposed to Repetitive Irritation, U. S. Dept. of
Health, Education, and Welfare, National Center for Air
Pollution Control, Health Effects Research Program,
Cincinnati, Ohio (1966).

-------
102.
103.
104.
45
Vinogradov, A. P., The Geochemistrv of Rare and Dis-
persed Chemical Elements in Soils, 2nd ed. Translated
from Russian. (New York: Consultant's Bureau, 1959).
Wolf, K., et al., Aichtwirkung einer ebenen spiralformigen
Luftstromung, VDI Verf.-Techn. (1941).
Yoshikawa, H., et al., Experimental Studies on Cadmium
Stearate Poisoning, I. Dissociation Curve and Toxicity,
Bull. Natl. Inst. Ind. Health ~:61 (1960).

-------
47
OTHER REFERENCES
Ahlmark, A., et al., Further Investigation into Kidney Function
and Proteinuria in Chronic Cadmium Poisoning, Proc. Thirteenth
Intern. Congr. on Occupational Health (July 25-29, 1960).
Air Pollution Measurements of the National Air Sampling Network,
Analyses of Suspended Particulates, 1957-1961, U. S. Department
of Health, Education, and Welfare, Public Health Service,
Division of Air Pollution, Cincinnati, Ohio (1962).
Air Pollution Measurements of the National Air Sampling Net-
work, Analyses of Suspended Particulates, 1963, U. S. Depart-
ment of Health, Education, and Welfare: Public Health Service,
Division of Air Pollution, Cincinnati, Ohio (1965).
Axelsson, B., Kidney Damage in Workers From Long Exposure to
Cadmium (To be published).
Baader, E., Chronic Cadmium Poisoning, Ind. Med. 21:427 (1952).
Barrett, H. M., et al., Studies on the Toxicity of
Cadmium. I. The Acute Toxicity of Cadmium Oxide by
J. Ind. Hyq. Toxicol. 29:279 (1947).
Inhaled
Inhalation,
Blejer, H. P., Death Due to Cadmium Oxide Fumes, Ind. Med.
Surq. 35:363 (1966).
Blejer, H. P., et al., Acute Cadmium Fume Poisoning in Welders-
A Fatal and a Nonfatal Case in California, Calif. Med. 4:290
(1966).
Blejer, H. P., et al., Report of an Occupational Health Study
of Exposures to Cadmium Oxide Fumes, Study No. S-1800, State
of California Department of Public Health, Bureau of Occupational
Health, 1966 (unpublished).
Bonnell, J. A., et al., A Follow-Up Study of Men Exposed to Cad-
mium Oxide Fumes, Brit. J. Ind. Med. 16:135 (1959).
Bonnell, J. A., et al., Renal Lesions in Experimental Cadmium
Poisoning, Brit. J. Ind. Med. 17:69 (1960).

-------
48
Brant, J. W. A., Human Cardiovascular Diseases and Atmospheric
Air Pollution in Los Angeles, California, Intern. J. Air Water
Pollution 2:219 (1965).
Brant, J. W. A., et al., Human Respiratory Diseases and Atmo-
spheric Air Pollution in Los Angeles, California, Intern J.
Air Water Pollution ~:259 (1964).
Browning, E., Toxicity of Industrial Metals (London: Butter-
worth, p. 83 (1961).
Clarkson, T. W., et al., Urinary Excretion of Amino Acids by
Men Absorbing Heavy Metals, Biochem. J. 62:361 (1956).
Colony, J., et al., A Comparative Study of the Dithizone and
Polarographic Determination of Lead, Am. J. Clin. Pathol.
39: 652 (1963).
Cotter, H. L., et al., Cadmium Poisoning, Arch. Ind. Hyq.
Occupational Med. ~:495 (1951).
Decker, C. F., et al., A Study of the Distribution and Retention
of Cadmium-lIS in the Albino Rat, Arch. Biochem. 66:140 (1957).
Decker, L. E., et al., Chronic
Administered in Drinking Water
18:228 (1958).
Toxicity Studies. I. Cadmium
to Rats, A.M.A. Arch. Ind. Health
Deichmann, W. B., et al., Symptomatoloqy and Therapy of Toxi-
coloqical Emerqencies (New York: Academic Press, p. 101, 1964l
Dingle, J. H., et al., Water Composition and Cardiovascular
Health, Illinois Med. J. 125:25 (1964).
Documentation of Threshold Limit Values, American Conference
of Governmental Industrial Hygienists, Committee on Threshold
Limit Values, Cincinnati, Ohio (1962).
Drinker, P., et al., Industrial Dust, 2nd ed. (New York: McGraw-
Hill, 1954).
Elkins, H. B., The Chemistry of Industrial Toxicoloqy, 2nd ed.
(New York: Wiley, p. 309, 1958).

-------
49
Falk, H. L., et al., An Assessment of Factors Concerned With
the Carcinogenic Properties of Air Pollutants, in Symposium,
Analyses of Carcinogenic Air Pollutants, U. S. Dept. of Health,
Education, and Welfare, National Cancer Institute Monograph
No.9, (1962).
Fedderson, P. C., et al., Cadmium-Recovery Practice in Lead
Smelting, Metal Trans. pp. 110-117 (Feb. 1949).
Friberg, L., Further Investigations on Chronic
Poisoning: A Study on Rabbits With Radioactive
A.M.A. Arch. Ind. Hyq. 2:30 (1952).
Cadmium
Cadmium,
Friberg, L., Iron and Liver Administration in Chronic Cadmium
Poisoning and Studies of the Distribution and Excretion of
Cadmium, Acta Pharmacol. Toxicol. 11:168 (1955).
Friberg, L., Deposition and Distribution of Cadmium in Man in
Chronic Poisoning, A.M.A. Arch. Ind. Health 16:27 (1957).
Gilman, J. P. W., Metal Carcinogenesis: II. A
Carcinogenic Activity of Cobalt, Copper, Iron
Compounds, Cancer Res. 22:158 (1962).
Study on the
and Nickel
Goldsmith, J. R., Uses of Medical and Epidemiological
in the Control and Prevention of Air Pollution, Proc.
Med. 57:1034 (1965).
Research
Rov. Soc.
Gunn, S. A., et al., Zinc Protection Against Cadmium Injury to
Rat Testis, Arch. Pathol. 71:274 (1961).
Heath, J. C., et al., The Production of Malignant Tumours by
Cadmium in the Rat, Brit. J. Cancer 18:124 (1964).
Holden, H., Cadmium Poisoning, Public Health Rept. (U.S) 57:601
(1947) .
Ipsen, J., Relationships of Acute Respiratory Disease to Measure-
ments of Atmospheric Pollution and Local Meteorological Con-
ditions, Report of the Henry Phipps Institute, University of
Pennsylvania, Philadelphia (1965).
Kazantzis, Respiratory Function in Men Casting Cadmium
Brit. J. Ind. Med. 13:30 (1956).
Alloys,

-------
50
Knockaert, O. E., et al., A Polarographic Method for the Simul-
taneous Determination of Lead and Cadmium in Urine, Am. Ind.
Hyq. Assoc. J. Nov-Dec.:595 (1967).
Kotin, P., et al., Polluted
Factors in the Pathogenesis
45:236 (1964).
Urban Air and Related Environmental
of Pulmonary Cancer, Dis. Chest
Lane, R., et al., Fatal Emphysema in Two Men Making a Copper
Cadmium Alloy, Brit. J. Ind. Med. 11:118 (1954).
Lee, R. E., Jr., et al., Particle Size Distribution of Metal
Components in Urban Air, Presented at the American Chemical
Society Meeting, Miami Beach, Fla. (April 1967).
Mackenzie, R. D., et al., Chronic Toxicity Studies. II.
Hexavalent and Trivalent Chromium Administered in Drinking
Water to Rats, A.M.A. Arch. Ind. Health 18:232 (1958).
Melinikova, E. A., The Toxicity of Highly Dispersed Cadmium
Oxide Aerosol, U.S.S.R. Literature on Air Pollution and Re-
lated Occupational Diseases ~ (1960).
Monkrnan, J. L., Determination of Heavy Metals in Urine by
Polarography, Anal. Biochem. 6: 255 (1963).
Murthy, G. K., et al., Cadmium and Liver Content of Market Milk,
J. Dairy Sci. 51:610 (1968).
Neumann,A. J., Toxic Hazards in Industry as Illustrated by
Cadmium, Can. J. Public Health 52:443 (1961).
Occupational Diseases, U. S. Public Health Servo Publ. 1097,
U. S. Govt. Printing Office, pp. 102-103 (1964).
Patty, F. A. (Ed.), Industrial Hyqiene and Toxicoloqy, 2nd ed.
(New York: Interscience, pp. 1016-1017. 1963).
prodan, L., Experimental Cadmium Poisoning, J. Ind. Hyq. Toxicol.
14:174 (1932).
Saltzman, B. E., Micro-Determination of Chromium With Diphenyl-
carbazide by permanganate Oxidation, Anal. Chern. 34:1016 (1952).

-------
51
Sandell, E. B., Colorimetric Determination of Traces of
Metals (New York: Interscience, 1959).
Schroeder, H. A., Cadmium Hypertension in Rats, Am. J. Physiol.
207:62 (1964).
Schroeder, H. A., et al., Effect of Chromium, Cadmium and
Other Trace Metals on the Growth and Survival of Mice, J. Nutr.
80: 39 (1963).
Schroeder, H. A., et al., Hypertension in Rats by Injection
of Cadmium, Arch. Environ. Health 13:788 (1966).
Schroeder, H. J., Cadmium in the Fourth Quarter of 1965,
Mineral Industry Surveys, Bureau of Mines, U. S. Department
of the Interior, Washington, D. C. (Feb. 1966).
Schwartze, E. W., et al., Studies on the Pharmacology of
Cadmium and Zinc With Particular Reference to Emesis, J.
Pharmacol. Expt1. Therap. 21:1 (1923).
Smith, J. C., et al., Chemical and Histological Post-Mortem
Studies on a Workman Exposed for Many Years to Cadmium Oxide
Fume, Brit. J. Ind. Med. 14:246 (1957).
Smith, J. C., et al., Observations on Urinary Cadmium and
Protein Excretion in Men Exposed to Cadmium Oxide Dust and
Fume, Brit. J. Ind. Med. 14:240 (1957).
Smith, J. C., et al., Observations on the Urinary Protein of
Men Exposed to Cadmium Dust and Fume, Brit. J. Ind. Med. 18:70
(1961) .
Spolyar, L. W., et al., Cadmium Poisoning in Industry: Report
of Five Cases Including One Death, J. Ind. Hyq. Toxicol.
26: 232 (1944).
Stephens, G. A., Cadmium Pois~ning, J. Ind. Hyq. £:129 (1920).
Swensson, A., Changes in Blood, Bone Marrow and Spleen in
Chronic Cadmium poisoning, Proc., Twelfth Intern. Conqr. on
Occupational Health (1957).

-------
52
Tipton, I. H., et al., Spectrographic Determination of Trace
Elements in Human Tissue, U. S. Ato~ic Energy Commission, Oak
Ridge National Laboratory, Report CF-53-8-4 (March 11, 1963).
Townshend, R.
Fuction Tests
25:68 (1968).
H., A Case of Acute Cadmium Pneumonitis--Lung
During a Four-Year Follow Up, Brit. J. Ind. Med.
Wakim, K. G., Physiologic Basis for Anuria and Proteinuria,
J. Urol. 79:560 (1958).

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APPENDIX A

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APPENDIX A
54
PROPERTIES OF CADMIUM AND ITS COMPOUNDS27,36
A better understanding of ca~~ium's health effects
requires knowledge of its properties.
The physicochemical
properties of cadmium and its compounds that may relate to
their effects as air polluta~ts are given below.
1.
Cadmium Metal
A.
Physical Properties
Density (in g/cm3)
at p=l atm
at absolute zero
below melting point
at 320°C
at 800°C
Vapor Density (in g/liter)
at 320°C
400°C
500°C
600°C
700°C
766°C
Relative to air:
4.0
Melting Point
Boiling Point
8.63-8.69
8.65
8.38
8.02
7.50
0.0003
0.0033
0.032
0.175
0.66
1.36
320.920C
766.0 °c
Vapor Pressure: variation with respect to
temperature is given by the following two formulas:
log P (mm) = - 6,073 - 0.9 log T + 11.72 (127-321°)
 T    
log P (mm) - - 5,982 - 1.8 log T + 14.063 (321-877°)
 T    
 Vapor Pressure at 200°C: 0.0003 mm mercury
    at 800°C: 1,080.0 mm mercury
Cadmium is nonatomic in the vapor phase.
(continued)

-------
55
APPENDIX A (Continued)
B.
Chemical Properties
Group in Mendeleev's
Atomic weight
Atomic number
Valency: divalent
periodic ta"Jle
II
112.41
48
Oxidation:
in moist air,
cadmium vapor reacts with
water vapor to form cadmium oxide.
Cadmium powder burns in
the air with a red flame.
Solubility:
cadmium dissolves in mercury, forming
an amalgam.
The solubility in mercury is 3.3 percent at OoC~
5.9 percent at 250C~ and 24 percent at 100oC.
Cadmium comes
between iron and thorium in the electromotive series, thus
aluminum, zinc, and iron displace cadmium from solutions of
its salts~ but cadmium displaces copper and other nobler
metals from their solutions.
2.
Cadmium Oxide (CdO)
Cad~ium oxide can be prepared by the oxidation of
cadmium metal by the air in the presence of cadmium vapor or
the oxidation of its sulfide.
Melting point:* at atmospheric pressure it sublimes
without melting at 1,770oK.
Vapor pressure:
950oC=-3.15
1250oC=-1.43
(experimental)
variation with temperature at
3.385 (log P atm.)
1.404 (log P atm.)
(calculated)
Noticeable evaporation of cadmium oxide is observed
at 9000C to 1,000oC.
Solubility in water:
nearly insoluble
(continued)

-------
56
APPENDIX A (Continued)
3.
Cadmium Sulfide (CdS)
Vapor pressure variation with temperature is given
by the formula:

log P (rom) = 9.823 - 11,256
T
Some actual values are given below:
Temp.arature, °c
540
10-4
605
10-3
680
10-2
765
10-1
875
1,000
1,160
Pressure, rom Hg
1
10
100
Solubility in water:
1.5 x 10-10 mole/liter
Crystal dimensions
Greenockite
Hexagonal
Sphalerite
Cubic
of minerals:
°
a = 4.10 A
°
a = 5.82 A
°
c = 6.69 A
On heating to 700°-800°C, the hexagonal forms
reduce to the cubic form, and cadmium sulfide becomes brown
and then carmine red.
4.
Cadmium Sulfate (CdS04)
Density
Melting Point
Solubility in water:
4.96
1,000oC
OOC-74.50C
77.0oC-100oC
76.48-87.62g CdS04/100 g water (3CdS04'8H20)
73.02-60.77g CdS04/l00 g water (CdS04'H20)
Cadmium Chloride (CdC12)
5.
Density
anhydrous
at mp
4.05
3.345
Crystal (hexagonal) lattice dimensions
° °
a = 3.85 A c = 17.46 A
Melting point*
Melting Point*
564°-568°C
964°-970°C
(continued)

-------
57
APPENDIX A (Continued)
Vapor Pressure:
variation with temperature
at 6180C
721
864
930
3 mm Hg
28
316
610
Solubility in water:
numerous hydrates can be obtained.
A saturated aqueous solution of cadmium chloride
contains the following amounts of cadmium chloride per 100
grams of water:
CdC12'
°c
g
o
90
30
128.6
100
147
*Data for melting and boiling points are slightly
different from those stated in Table 12.

-------
APPENDIX B

-------
APPENDIX B
TABLE 10
EFFECTS OF CADMIUM AND CADMIUM COMPOUNDS ON HUMANS
Substance Concentration Exposure
Cadmium metal 530 ppm Single dose
Cadmium metal 67 ppm Single dose
Cadmium metal
13-15 ppm
Cadmium oxide
11,000 ~g/m3
120 minutes
Cadmium oxide 8,630 ~g/m3 
Cadmium oxide 2,500,000-2,900,000 ~g/m3
Cadmium oxide 600-2,800 ~g/m3
Cadmium oxide  >326,000 ~g 
Cadmium sulfide 500,000 ~g/kg wet wt
Cadmium sulfide 165,000-97,600 ~g/m3
2,589 minutes
1 minute
13-38 years
2-3 days
Effects
Cadmium gelatin produced
sickness in children
Cadmium in punch pro-
duced sickness in
children
Cadmium in popsicles
produced sickness in
children
Retention of cadmium by
kidneys, liver, pancreas,
brain, bone marrow, lung,
testes, myocardium,
thyroid, adrenal cortex,
and skin; very little
elimination in 16 days
Lethal
Lethal
Lethal
Lethal
Lethal
Anemia, giddiness, breath-
lessness, nausea, and
fatigue
R~ference
40
40
40
58
10
29
77
80
80
85
lJ1
1..0

-------
APPENDIX B
TABLE 11
91
PRESENCE OF CADMIUM IN HUMAN TISSUES
      Cases  Amount of 
      Number Percent Cadmium 
     Number With With Concentration 
Tissue     Investiqated Cadmium Cadmium ( I-lq/g) 
Muscle         
Diaphragm   91 7 8  
Other striated muscle  137 2 1  
Uterus     32 16 50  
Bladder    112 30 27 <50 
Gastrointestinal tract      
Esophagus   67 6 9  
Stomach    130 41 31  
Duodenum    68 56 82 50 
Jejunum    103 58 56 50 
Ileum     84 25 30  
Cecum     31 16 51  
Omentum    73 42 58  
Sigmoid flexure of the colon 108 23 21  
Rectum     42 12 30  
Upper respiratory tract      
Larynx     48 2 4 <50 
Trachea    60 12 20  
Genital Tract       
Ovary     16 31   
Testes     71 15 21  
Prostate    50 40 80  
Other         
Skin     21 0 0  
Thyroid gland   21 67  50 
Adrenal gland   15 73  50 
Fat     28 100  39 0'\
Bone     91 1 1 < 5 0

-------
APPENDIX B
COillPo'und
Cadmium acetate
Cd(CH3COO}2
TABLE 12
PROPERTIES, TOXICITY, AND USES OF SOME CADMIUM COMPOUNDS64
ProDerties
mp anhydrous
2550C
Cadmium bromide mp 5660
CdBr2  bp 9630
Cadmium carbonate Decomposes
CdC03   < 500
Cad::nium chloride mp 5680
CdC12  bp 9600
)
'1'0 x i c ii-v
Ingestion (metal and
soluble compounds):
increased saliva-
tion, choking,
vomiting, abdominal
pain, diarrhea,
tenesmus.
Inhalation (dust
and fumes): throat
dryness, cough,
headache, vomiting,
chest pain, irrita-
bility, pneumonitis
Same as above
Same as above
Same as above
TJf>PS
For producing iridescent effect on
porcelains and pottery; as a rea-
gent for determination of S, Se,
and Te in cadmium electroplating
In photography, process engraving,
and lithography
In photography; in dyeing and calico
printing; in the vacuum tube indus-
try; in manufacture of cadmium
yellow; special mirrors; as ice-
nucleating agent, lubricant; In
analysis of sulfides to absorb the
H2S
(continued)
0\
I-'

-------
APPENDIX B
TABLE 12 (Continued)
PROPERTIES, TOXICITY, AND USES OF SOME CADMIUM COMPOUNDS
Co:npound  Properties   Toxicity     Uses     
Cadmium cyanide Decomposes Very poisonous In copper bright electroplating
Cd{CN)2   >2000               
Cadmium fluoride mp 10490 Poisonous In manufacture of phosphors, glass;
CdF2  bp 17480    in nuclear reactor cO:ltrols  
Cadmium hydroxide Decomposes Same as Cadmium In storage battery electrodes 
Cd{OH)2   3000 acetate            
Cadmium iodide mp 3880 Same as Cadmium In electrodeposition of Cd; as
CdI2  bp 7870 acetate nematocide; in manufacture of phos-
       phors; as lubricant; in phot020n-
       ductors; in photography, pr02ess
       engraving, lithography    
Cadmium nitrate mp 59.50    In making other Cd salts; ln  
Cd{N03)2 bp 1320    photographic emulsions    
(continued)
0'\
!\J

-------
APPENDIX B
TABLE 12 (Continued)
PROPERTIES, TOXICITY, AND USES OF SOME CADMIUM COMPOUNDS
Compound
Cadmium oxide
CdO
Cadmium potassium
cyanide
K2Cd(CN)4
Cadmium salicylate
Cd(C7H503)2
Properties
mp >14260
bp,
Decomposes
900-10000
mp 4500
mp 2420
Toxicitv
Poisonous. Acute
poisoning occurs in
animals at the fol-
lowing concentra-
tions of cadmium
oxide (in ~g/m3 of
air inhaled): for
rats - 500,000 for
rabbits - 2,500,000
for dogs - 4,000,000
for monkeys -
1,500,000. For
humans, inhalation
of air containing
2,500,000 ~g/m3 for
ODe minute or air
containing 5,000,000
~g/m3 for ~ minute
is fatal. Also see
Cadmium acetate
Poisoning may occur
by ingestion,
absorption through
in jured sk in
Uses
In phosphorus, semiconductors,
manufacture of silver alloys, glass;
in storage battery electrodes; as
nematocide; as catalyst for organic
reactions; in cadmium electroplating;
in ceramic glazes.
Vet. use: as an ascaricide in swine
Med. use:
antiseptic
has been used as an
(continued)
0'\
LV

-------
APPENDIX B
                                   TABLE 12 (Continued)




                 PROPERTIES,  TOXICITY,  AND USES OF SOME CADMIUM COMPOUNDS
Compound
Cadmium selenide
CdSe
Cadmium succinate
C4H4Cd04
Cadmium sulfate
CdSO4
Cadmium sulfide
CdS
Cadmium telluride
CdTe
Cadmium tungstate
CdWO4
Properties
mp 1350°

mp 1000°
mp 1750100
atm
bp sublimes
in N2
mp 1041°

Toxicity
Low toxicity because
of insolubility

LD in dogs 27,000
i-igAg



Uses
In photoconductors , semiconductors,
photoelectric cells, and rectifiers;
in phosphors
As plant fungicide
In electrodeposition of Cd, Cu, and
Ni; in phosphors; in manufacture of
standard cadmium elements
As a pigment that is fast to light,
and not affected by H2S; as color
for soaps : for coloring glass yel-
low, coloring textiles, paper, rub-
ber; in printing inks, ceramic
glazes, fireworks. Med. use: for
seborrheic dermatitis
In semiconductor research, in
phosphors
In X-ray screens; in scintillation
counters; in phosphors; as catalyst
for organic reactions
                                                                                   (continued)

-------
APPENDIX B
Compound
Dimethylcadmium
Cd(CH3)2
Potassium
tetraiodocadmate
K2 EdI~ 2H20
TABLE 12 (Continued)
PROPERTIES, TOXICITY, AND USES OF SOME CADMIUM COMPOUNDS
Properties

mp 4_50 Decom-
poses with ex-
plosive vio-
lence when
heated above
1500- Catches
fire when drop-
ped on filter
paper and pro-
duces dense
clouds of first
white, then
brown cadmium
oxide smoke
Toxicitv
Uses
In organic synthesis; as
polymerization catalyst
See Cadmium acetate
Cadmium borate
Cad~llium bromate
Cad::nium bromide anhydrous
Cadmium chromate
Cadmium hexafluoroarsenate
Cadmium molybdate
Cd(B02)2.xH20
Cd(Br03)2-H20
CdBr2
CdCr04
Cd(ASF6)2
CdMo04
In testing for alkaloids, amlnes,
imines, heterocyclic nitroge~s,
peroxides In ether
Note:
More detailed information was not available on the following compounds:
Cadmium perchlorate
Cadmium phosphate
Cadmium phosphide
Cadmium zirconate
Potassium cadmium iodide
Potassium tetracyanocadmiate
Cd(C104)2-6H20
Cd3(P04)2
CdP
CdZr03
K2CdI4-2H20
K2Cd(CN)4
0'\
U1

-------
APPENDIX B
TABLE 13
EFFECTS OF CADMIUM AND CADMIUM COMPOUNDS ON ANIMALS
                Refer-
!substance Subiect Concentration  EXDosure   Rffp~t~  e:.12e
~admium metal Rats 135 ppm  Single dose Lethal      3
Cadmium metal R-lts 5-75 ppm Single dose Lethal      3
Cadmium metal Rats 0.1-10 ppm 1 year  Cadmium content of 3
         liver and kidney In- 
         creased in propor- 
         tion to quantity of 
         cadmium intake  
Cadmium metal Cats 20 ppm  Single dose Produced vomiting 6
Cadmium oxide Rats 500,000 ~g-min/m3 1 minute Acute pulmonary  70
         edema within 24  
         hOClrs;  pneum::mi tis 
         in 3-10 days; perma- 
         nent lung damage and 
         fibrosis     
Cadmium. oxide  Rats 150,000-1,300,000 10-15 minutes Acute pulmonary  8
   ~g/min/m3    edema within 24  
         hours;  pneumonitis 
  I     in 3-10 days; perna - 
         nent lung da:nage and 
         fibrosis     
Cadmium oxide Rats 800,000-1,000,000 1 minute Lethal; acute pu1- 70
    . / 3       ede::na wi tl:1in 
   ~g-mln m    monary  
         24 hOurs; pneumoniti, 
         in 3-10 days; pecma- 
         nent lung d:lma.3e and I 
         fibrosis     
()I
0'1
(continued)

-------
APPENDIX B
TABLE 13 (Continued)
EFFECTS OF CADMIUM AND CADMIUM COMPOUNDS ON ANIMALS
                    Refer- 
Substance Subiect Concentration   ,-". .~  R-F-FAr+-'"  ence 
Cadmium oxide Mice 660,000-1,130,000  15 minutes       8 
   I-lg-min/m 3                
~admium oxide Rabbits 630-3,690 I-lg/m 3  13-30 minutes       8 
~admium oxide Guinea 640,000-6,450,000  13-30 minutes       8 
  pigs I-lg/m3                 
!cadmium oxide Dogs 3,100,000-10,000,000  10-20 minutes Lethal     80 
  I-lg/m3                 
k:admium oxide Dogs 7,000I-lg/m 3    1,102 hours Reteiltion of cadmium 8 
              dust In tissues  
tadmium oxide Monkeys 4,500-28,200 I-lg/m3  10-30 minutes Lethal     8 
Icadmi LLLl chloride Mice 4,480 I-lg/kg body wt.  1-7 days Lethal     104 
k:admium chloride Mice 85-170 I-lg/1iter      Overall retention 76 
              10.5-23%    
tad~TIi urn chloride Rats 78,000-164,000 I-lg-min/m 3 6 months Tolerated   70 
~admium chloride Rats 250,000   . / 3  15 minutes Lethal; pulmonary 70 
I-lg-mln m  
              edema within 24  
              hours; pneumoni-  
              tis 3-10 days;  
              permanent lung  
              damage and fibro-  
              sis       
                    ---- 
                   (contin'..led) 
                     0'\
                     -.j

-------
APPENDIX B
Substance
~admium chloride
-'admium chloride
2admium chloride
2admium chloride
Cadmium stearate
2admium stearate
-'admium stearate
TABLE 13 (Continued)
EFFECTS OF CADMIUM AND CADMIUM COMPOUNDS ON ANIMALS
Subi ect
Rats
Rabbits
Dogs
Dogs
Mice
Mice
Rats
Concentration
170-340 ~g ions
250 ~g/kg body wt
320 ~g/liter
9,600,000 ~g-min/m3

9,310-18,570 ~g/m3/day

6,000-7,570 ~g/m3/day
0.1-1% of food
Exposure
Single dose
12-29 weeks
30 minutes
1 minute
1-7 days
1-7 days
90 days
Effects
Pleomorphic sarco-
mata 10-16 months
after injection;
carcinogenicity
observed only in
tissue of mesen-
chymal mesodermal
origin
Pulmonary edema
Lethal
Lethal
Lethal; LD 9,310 ~g
Growth suppression,
histological
changes In stomach,
intestine, testi-
cles, other organs
Anemia, giddiness,
breathlessness,
nausea, and fatigue
Refer-
ence
41
7
46
40
104
104
85
()\
co

-------
APPENDIX B
TABLE 14
CADMIUM-CONTAINING PESTICIDES31
     Chemical Ingredients    SUDPlier   
Use* Trade Name  Name %   Name   Location 
FID Stauffer Mer-Caid Anilinocadmium 6.25 Stauffer Chern. Co. N e'll York  
     dilactate         
FID Twin Light Granular Cadmium chloTid9,  Seacoast Labs, Inc. E. Brunswick, 
 Lawn Fungicide Thiram        N.J.  
F/s Ortho Lawn Disease Cadmium carbonate, 3.00 Chevron Chern. Co., Richmond,  
 Control    captan, 5-chloron  0 r tho Div.  Calif.  
     nitrobenzene         
F/s Or tho  La"NJ:1 and Cadmium carbo:1ate, 5.00 Chevron Ch 8..'11. Co., Richmon::l,  
 Turf Fun3icide Folpet, Thiram  Ortho Div.  Calif.  
                I
F/s Caddy    Cadmium chloride 20.10 Cleary, W.A., Corp. N. Brunswick, I
             N.J.  
F/s Vicad    Cadmium chloride  Vine land  Chern. Co. Vineland, N.J. 
F/s Cad-Trete  Cadmium chlorate, 8.30 Cleary, W.A., Corp. N. Brunswick, 
     hydrate, Thiram      N.J.  
F/s Cadminate  Cad;lliurn,   29.00 Mallinckrodt  St. Louis,  
     Cadmium succinate 60.00 Chemical Works  Mo.   
           I
F/s A3'way Fire Blight Cadmium s 1.11fate 14.00 A'3Way    ~
 Canker Paint         
()I
\..0
(continued)

-------
APPENDIX B
TABLE 14 (Continued)
CADMIUM-CONTAINING PESTICIDES31
      Chemical Ingredients     SUDDlier
Use* Trade Name  Name   %  Name  Location
F/s Ultra-Clor (General Cadmium,    1.10 Chevron Chern. Co. Richmond,
 Turf Fungicide) Cadmium succinate, 3.30      Calif.
     Mercuric dimethyl-       
     thiocarbamate, potas-       
     sium chromate,        
     mercury and chromium       
F/s Fura Turf  Phenylamine cadmium 12.80 Guard Ch em. Co., Ossining,
     dilactate    Inc.    N.Y.
F-I Ortho Lawn  Cadmium carbonate, 5.30 Chevron Chern. Co. Richmond
Is Fungicide  Cap tan,  Gamma (BHC)       Calif.
*F = Fungicides
D = Dusts; S = Sprays; and I = Insecticides.
--.J
o

-------
71
APPENDIX B
TABLE 15
LIST OF COMPANIES PRJDUCING CADMIUM CHEMICALS (1968)18
1.
CADMIUM ACE'rATE
J. T. Baker Chern. Co.
The Harshaw Chern. Co.
Mallinckrodt Chem. Works
Industrial Chern. Div.
The Shepherd Chern. Co.
Pnillipsburg, N.J.
Cleveland, Ohio
St. Louis, Mo.
Cincinnati, Ohio
2.
CADMIUM BENZOATE
Carlisle Chern. Works, Inc.
Reading, Ohio
CADMIUM BISULFATE AND
CADMIUM BROMATE
3.
4.
City Chern. Corp.
Jersey City, N.J.
5.
CADMIUM BROMIDE
The Dow Chernical Co.
Research Inorganic Chern. Co.
Midland, Mich.
Sun Valley, Calif.
6.
CADMIUM CARBONATE
Allied Chern. Corp.
Industrial Chern. Div.
Chernetron Corp.
McGean Chern. Co., Div.
The Shepherd Chern. Co.
Marcus Hook, Pa.
Cleveland, Ohio
Cincinnati, Ohio
7.
CADMIUM CHLORIDE
Allied Chern. Corp.
Industrial Chern. Div.
J. T. Baker Chern. Co.
Chernetron Corp.
McGean Chern. Co., Div.
W. A. Cleary Corp.
The Harshaw Chern. Co.
Mallinckrodt Chern. Works
Industrial Chern. Div.
Marcus Hook, Pa.
Phillipsburg, N.J.
Cleveland, Ohio
New Brunswick, N.J.
Cleveland, Ohio
St. Louis, Mo.
(continued)

-------
APPENDIX B
TABLE 15 (Continued)
72
10.
11.
12.
13.
14.
15.
16.
8.
CADMIUM CHROMATE
City Chern. Corp.
9.
CADMIUM CYANIDE
Aceto Chern. Co., Inc.
CADMIUM DICHRJMATE
City Chern. Corp.
CADMIUM ETHYLENEDIAMINE
Allied Chern. Corp.
Industrial Chern. Div.
Jersey City, N.J.
Flushing, N.Y.
Jersey City, N.J.
Marcus Hook, Pa.
CADMIUM 2-ErHYLHEX~OATE (CADMIUM OCTOATE)
Carlisle Chern. Works, Inc.
Advance Div.
The Shepherd Chern. Co.
Tenneco Chern. Inc.
Nuodex Div.
CADMIUM FERROCYANIDE
City Chern. Corp.
CADMIUM FLUOBORATE
Allied Chern. Corp.
Industrial Chern. Div-
Harstan Chern. Corp.
The Harshaw Chern. Co.
CADMIUM FLUORIDE
Allied Chern. Corp.
Industrial Chern. Div.
The Harshaw Chern. Co.
Crystal-Solid State Div.
Semi-Elements, Inc.
Sylvania Electric Products, Inc.
CADMIUM FORMATE
City Chern. Corp.
New Brunswick, N.J.
.Cincinnati, Ohio
Elizabeth, N.J.
Lang Beach, Calif.
Jersey City: N.J.
Marcus Hook, Pa.
Brooklyn, N.Y.
Cleveland, Ohio
Marcus Hook, Pa.
Cleveland, Ohio
Elyria, Ohio
Saxonburg, Pa.
Towanda, Pa.
Jersey City, N.J.
( continued)

-------
17.
18.
19.
20.
21.
22.
23.
APPENDIX B
TABLE 15 (Continued)
CADMIUM HYDROXIDE (CADMIUM HYDRATE)
Chernetron Corp.
McGean Chern. Co., Div.
The Shepherd Chern. Co.
CADMIUM IODIDE
Allied Chern. Corp.
Industrial Chern. Div.
J. T. Baker Chern. Co.
Mallinckrodt Chern. Works
Industrial Chern. Div.
R.S.A. Corp.
CADMIUM LACTATE
City Chern. Corp.
CADMIUM LAURATE
Tenneco Chern.
Nuodex Div.
Inc.
73
_.o.-_~-~-......_- -"- -_.
CADMIUM MOLYBDATE
City Chern. Corp.
Sylvania Electric Products, Inc.
CADMIUM NAPHTHENATE
Carlisle Chern. Works, Inc.
Advance Div.
The Harshaw Chern. Co.
The Shepherd Chern. Co.
Frederick A. Stresen-Reuter,
Tenneco Chern. Inc.
Nuodex Div.
Inc.
Cleveland, Ohio
Cincinnati, Ohio
Marcus Hook, Pa.
Phillipsburg, Pa.
St. Louis, Mo.
Ardsley, N.Y.
Jersey City, N.J.
Elizabeth, N.J.
Long Beach, Calif.
Jersey City, N.J.
Towanda, Pa.
New Brunswick, N.J.
Gloucester City, N.J.
Cincinnati, Ohio
Bensenville, Ill.
Elizabeth, N.J.
Long Beach, Calif.
Cincinnati, Ohio
CADMIUM NEO-DECANOATE
The Shepherd Chern. Co.
(continued)

-------
APPENDIX B
TABLE 15 (Continued)
74
25.
26.
27.
28.
29.
30.
31.
24.
CADMIUM NITRATE
-"""""------""""""'~---P.,--- -
Buffalo, N.Y.
Phillipsburg, N.J.
Cleveland, Ohio
Gloucester City, N.J.
St. Louis, Mo.
Cincinnati, Ohio
Cleveland, Ohio
Jersey City, N.J.
Marcus Hook, Pa.
Denver, Colo.
Phillipsburg, N.J.
Cleveland, Ohio
Elyria, Ohio
Jersey City, N.J.
Jersey City, N.J.
Jersey City, N.J.
Cincinnati, Ohio
Jersey City, N.J.
Allied Che~. Corp.
Industrial Chern. Div.
J. T. Baker Chern. Co.
Chemetron Corp.
McGean Chern. Co., Div.
The Harshaw Chern. Co.
Mallinckrodt Chern. Works
Industrial Chern. Div.
The Shepherd Chern. Co.
CADMIUM OXALATE
Chernetron Corp.
McGean Chern. Co., Div.
City Chern. Corp.
CADMIUM OXIDE
Allied Chemical Corp.
Industrial Chern. Div.
American Smelting & Refining C~
J. T. Baker Chern. Co.
Chernetron Corp.
McGean Chern. Co., Div-
The Harshaw Chern. Co.
CADMIUM POTASSIUM CHLORIDE
City Chern. Corp.
CADMIUM POTASSIUM CYANIDE
City Chern. Corp.
CADMIUM POTASSIUM IODIDE
City Chern. Corp.
CADMIUM PROPIONATE
The Shepherd Chern. Co.
CADMIUM SALICYLATE
City Chern. Corp.
(continued)

-------
APPENDIX B
TABLE 15 (Continued)
75
32.
33.
34.
35.
36.
37.
CAIl"1IUM SEBACATE
Mallinckrodt Chern. Works
Industrial Chern. Div.
CADMIUM SELENATE
City Chern. Corp.
CADMIUM SELENIDE (CADMIUM ORANGE)
Allied Chern. Corp.
Industrial Chem. Div.
The Glidden Co.
Hercules Powder Co.
Imperial Color & Chern. Dept.
The Harshaw Chern. Co.
Crystal-Solid State Div.
H. Kohnstamm and Co., Inc.
General Color Co., Div.
Research Inorganic Chern. Co.
Semi-Elements, Inc.
CADMIUM m-SILICATE
City Chern. Corp.
CADMIUM SILICOFLUORIDE
City Chern. Corp.
CADMIUM STEARATE
Argus Cnem. Corp.
Nopco Chern. Co.
Industrial Div.
S. B. Penick & Co.
M. W. Parsons-Plymouth
Synthetic Products Co.
witco Chern. Co., Inc.
Organic Chern. Div.
Div.
St. Louis, Mo.
Jersey City, N.J.
Marcus Hook, Pa.
Baltimore, Md.
Glen Falls, N.Y.
Cleveland, Ohio
Elyria, Ohio
Newark, N.J.
Sunn Valley, Calif.
Saxonburg, Pa.
Jersey City, N.J.
Jersey City, N.J.
Brooklyn, N.Y.
Cedartwon, Ga.
Richmond, Calif.
Newark, N.J.
Cleveland, Ohio
Chicago, Ill.
Los Angeles, Calif.
Perth Amboy, N.J.
(continued)

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APPEl'1DIX B
TABLE 15 (Co~tinued)
76
._---~--_.
38.
CADMIUM SULFATE
Allied Chern. Corp.
Injustrial Chem. Div-
J. T. Baker Chern. Co.
Chemetro~'1 Corp.
M~Gean Chern. Co., Div.
The Harshaw Chern. Co.
Mallinckrodt Chern. Works
Industrial Chern. Div.
Tne Shepherd Chern. Co.
39.
CADMIUM SULFIDE (CADMIUM YELLOW)
Allied Chern. Corp.
Industraal Chern. Div-
&~erican Smelting and Refining
The Ea'3'le-Picher Co.
The Glidden Co.
Hercules Powder Co.
Imperial Color & Chem. Dept.
The Harshaw Chern. Co.
Crystal-Solid State Div.
H. Kohnsta~TI and Co., Inc.
General Color Co., Div.
Research Inorganic Chern. Co.
Semi-Elements, Inc.
Smith Chem. & Color Co., Inc.
Sylvania Electric Products Inc.
Chern. and Metallurgical Div-
40.
CADMIUM SULFOSELENIDES (CADMIUM REDS)
B. F. Drakenfeld and Co., Inc.
The Glidden Co.
Hercules Powder Co.
Imperial Color & Chern. Dept.
H. Kohnstamrn and Co., Inc.
General Color Co., Div.
Smith Chern. & Color Co., Inc.
41.
CADMIUM TARTR~TE
City Chern. Corp.
Marcus Hook, Pa.
Phillipsburg, N.J.
Cleveland, Ohio
Cleveland, Ohio
St. LO'uis, Mo.
Cincinnati, Ohio
Marcus Hook, Pa.
Co. Denver, Colo.
Miami, Okla.
Baltimore, Md.
Glen Falls, N.Y.
Cleveland, Ohio
Elyria, Ohio
Newark, N.J.
Sun Valley, Calif.
Saxonburg, Pa.
Brooklyn, N.Y.
Towanda, Pa.
Washington, Pa.
Baltimore, Md.
Glen Falls, N.Y.
Newark, N.J.
Broo1
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42.
43.
44.
45.
46.
APPENDIX B
TABLE 15 (Continued)
CADMIUM TELLURIDE
City Chern. Corp.
The Eagle-Picher Co.
The Harshaw Chern. Co.
Crystal-Solid State
Div.
77
-------4____- ..- "-
--- - -- -. ----- - -
Semi-Elements, Inc.
CADMIUM THIOCYANATE
Ci ty Chern. Corp.
CADMIUM TUNGSTATE
North Metal and Chern. Co.
Semi-Elements, Inc.
Sylvania Electric Prod~ct& Inc.
CADMIUM ZIRCONATE
National Lead Co.
Titanium Alloy Manufacturing
Div.
Research Inorganic Chern. Co.
CADMIUM SUCCINATE (Pesticide)
Mallinckrodt Chern. Works
Jersey City, N.J.
Mia'Tli, Okla.
Cleveland, Ohio
Elyria, Ohio
Saxonburg, Pa.
Jersey City, N.J.
York, Pa.
Saxonburg, Pa.
Towan::1a, Pa.
Niagara Falls, N.Y.
Sun Valley, Calif.
St. Louis, Mo.

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APPENDIX B
TABLE 16

CONCENTR~TION OF CADMIUM IN THE AIR2,3
(~g/m3)
    1954-59 1960  1961  1962  1963  1964
    Max Avq Max Avq Max Ava Max Avq Max Ava Max Ava
Alabama              
Birmingham  .018          .029 
Huntsville           .008  
Arizona              
Phoenix    .068 .016   .000    .020 
Tucson     .140 .026        
California             
Los Angeles .020  .029 .009     .022   
Pasadena         .003    
Sa':1 Fra:1cisco       .051  .008   
Sa:1.ta Barbara        .000    
Colorado              
Denver   .087      .310  .065  .030 
Pueblo            .006  
Connecticut             
Norwich           .000  
Waterbury    .045 .015        
District of Columbia            
Washington        .048  .028  .009 
Florida              
St. Petersburg        .000    
Georgia              
Atlanta  .044        .020   
Idaho              
Boise     .000    .000    .000 
               -----'
(continue::J.)
-.j
CD

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APPENDIX B
TABLE 16 (Continued)
CONCENTRATION OF CADMIUM IN 'rHE AIR
(~g/m3)
   1954-59 1 60  1961  1962  1963  1964
   Max Avq Max Avq Max Ava Max Avq Max Avq Max Avq
Illinois             
Chicago  .017  .400 .033 .150    .054  .049 
Cicero        .047     
East St. Louis         .180   
Joliet           .000  
North Chicago          .000  
Springfield        .000    
Indiana             
East Chicago           .042 
Gary     .110 .018        
Indianapolis .040  .100 .029 .029       
Muncie           .000  
Iowa              
Cedar Rapids          .000  
Des Moines .009  .017    .000    .000 
Louisiana             
Lake Charles        .000    
New Orleans .019      .010  .000   
Maryland             
Baltimore .034  .044        .110 
Cumberland          .000  
Massachusetts            
Boston            .000 
Michigan             
Detroit  .051      .042  .017  .000 
Grand Rapids          .000  
Minnesota             
Minneapolis .027           
St. Paul         .ODO    ~
             c:::mtinued)
-.....J
'-0

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APPENDIX B
TABLE 16 (Continued)
CONCENTRAT ION OF CADMIUM IN THE AI R
(lJ.g/m3)
  1954-59  1960  1961  1962   1963  1964
  Max Avq Max Avq Max Avq Max Avq  Max Avq Max Avq
Missouri             
St. Louis .150      .420   .051  .290 
Monta1'1a             
HeLena            .049 
Nebraska             
Omaha     .110 .011       
Nevada              
Las Vegas     .000  .000   .000  .000 
Reno            .ODO  
New Mexico             
Albuquerque   .018 .003         
New Jersey         I    
Bayonne          .028  
Camden        .011 I    
Newark     .310 .056      .350 
Paterson           .002  
New York             
Buffalo       .011      
Glen Cove        .005     
Massena      .000       
Mount Vernon      .000       
New R'Jchelle     . .003       
New York     .210 .032 .180   .064  .040 
Rochester      .000       
Troy         .000     
North Carolina             
Asheville    .000         
Charlotte            .000 
Durham           .000  
             - 
(continued)
CD
o

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APPENDIX B
TABLE 16 (Co~tinued)
CONCENTR~TION OF CADMIUM IN THE AIR
(~g/m3)
   1954-59  1960  1961  1962  1963  1964
   Max Avq Max Avg Max Avq Max Avq Max Avq Max Avq
Ohio             
Akron    .130 .020        
Canton      .095 .023      
Cincinnati     .093 .021   .036  .110 
Cleveland        .037  .064  .038 
Columbus      .110 .026      
Dayton    .019         
Youngstown   .140 .024        
Oklaho:'11a             
Tulsa       .000      
Oklahoma City     .045 .015      
Oregon             
Eugene      .000       
Medford      .013 .001      
Portland  .028           
Pe~nsylvania            
Allento'tffi      .330 .068      
Altoona           .003  
Bethlehem     .140 .039      
Lancaster        .000    
Philadelphia .016    .290 .045   .046  .110 
Pittsburgh   .067    .095  .055  .028 
Scranton      .089 .024      
Roode Island            
East Providence          .000  
Tennesse             
Chattanooga     .039 .006   I  .014 
Nashville .016          
(continued)
CD
f-'

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APPENDIX B
TABLE 16 (Continued)
CONCENTRATION OF CADMIUM IN THE AIR
(~g/m3)
   1954-59  1960  1961  1962  19'03 1964 
   Max Avq Max Ava Max Avq Max Ava Max  Avq Max Ava
Texas            I   
           I   
El Paso         .310    .300 
HOUstO"1  .026            
Odessa            .000  
Tyler            .000  
Utah               
Sal t Lake City .028            
Washington              
Seattle  .011      .032  .000    
Spokane       .000       
Tacoma  .170      .000     .000 
West Virginia             
Charleston  .071 .015   .160 .043     I .000 
Huntington    .021        
Wisconsin              
Milwaukee  .043           .000 
Wyoming   i         
Cheyenne          .000 
CD
tV

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