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AIR POLLUTION ASPECTS
OF
VANADIUM 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) Ethylene
Aldehydes (includes acrolein Hydrochloric Acid
and formaldehyde) Hydrogen Sulfide
Ammonia Iron and Its Compounds
Arsenic and Its Compounds Manganese and Its Compounds
Asbestos Mercury and Its Compounds
Barium and. Its Compounds Nickel and Its Compounds
Beryllium and Its Compounds Odorous Compounds
Biological Aerosols Organic Carcinogens
(microorganisms) Pesticides
Boron and Its Compounds Phosphorus and Its Compounds
Cadmium and Its Compounds Radioactive Substances
Chlorine Gas Selenium and Its Compounds
Chromium and Its Compounds Vanadium and Its Compounds
(includes chromic acid) 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, Ph0D.
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
Vanadium is toxic to humans and animals, especially in
its pentavalent form. Human exposure through inhalation of
relatively low concentrations (less than 1,000 p.g/m3 ) has
resulted in inhibition of cholesterol synthesis, and chronic
exposure to environmental air containing vanadium has been
statistically related to mortality rates from heart diseases
and certain cancers. Exposure to high concentrations (greater
than 1,000 fig/in3 ) results in physiologically observable
effects of varying severity on the gastrointestinal and
respiratory tracts. In general, very little research has been
done on the toxicity of environmental concentrations of
vanadium.
No information has been found on the effects of vanadium
air pollution on commercial or domestic animals or plants.
Only one reference was found on the effects on materials:
vanadium in fuels was found to be corrosive to heating plants.
The major sources of vanadium air pollution are the
vanadium refining industries, alloy industries, and power
plants and utilities using vanadium-rich residual oils.
The concentration of vanadium in the atmosphere is moni-
tored by the National Air Sampling Network. The average
levels noted ranged from below detection (0.003 p.g/m3 ) to
0.30 (1964), 0.39 (1966), and 0.90 (1967)
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No information has been found on economic losses re-
sulting from vanadium air pollution, and little information
exists on the costs of abatement. One report on abatement
indicated that an economic gain resulted from extracting
vanadium from steam generators using vanadium-rich fuel. No
other information was found on abatement procedures specifi-
cally intended to control vanadium emissions; normal parti-
culate control methods are suitable.
The methods of quantitative analysis of vanadium in the
atmosphere that are available—including colorimetric, atomic
absorption spectroscopy, emission spectrography, and polaro-
graphy—provide sensitivities in the 0.001 |j.g/m3 range.
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CONTENTS
FOREWORD
ABSTRACT
1. INTRODUCTION . .
2. EFFECTS ,
2.1 Effects on Humans ....... 8
2.1..1 Exposure to Low Concentrations 8
2.1.2 Exposure to High Concentrations .... 13
2.1.3 Lethal Dose 15
2.1.4 Other Factors Determining Toxicity ... 16
2.2 Effects on Animals 17
2.2.1 Commercial and Domestic Animals .... 17
2.2.2 Experimental Animals 17
2.2.2.1 Vanadiu-n Pentoxide 17
2.2.2.2 Vanadium Trioxide 18
2.2.2.3 Vanadium Chloride 19
2.2.2.4 Vanadium Metal, Vanadium
Carbide, and Ferrovanadium. . 19
2.2.2.5 Sodium Metavanadate 20
2.2.2.6 Other Factors Determining
Toxicity 20
2.2.2.7 Absorption, Distribution, and
Excretion 22
2.2.2.8 Comparative Toxicity 23
2.3 Effects on Plants 25
2.4 Effects on Materials * 25
2.5 Environmental Air Standards 25
3. SOURCES 27
3.1 Natural Occurrence 27
3.1.1 Mineral Ores 27
3.1.2 Coal 28
3.1.3 Oil 29
3.1.4 Distribution of Deposits 30
3.2 Production Sources 30
3.2.1 Recovery of Vanadium-Oxide from Vanadium
Bearing Ores 30
3.2.2 Production of Vanadium Metal 32
3.2.3 Vanadium-Bearing Alloys 34
3.2.4 Vanadium Chemicals 34
3.2.5 Other Sources 34
3.2.6 Distribution 38
3.3 Product Sources 38
3.4 Environmental Air Concentrations 41
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4. ABATEMENT 45
5. ECONOMICS 47
6. METHODS OF ANALYSIS 48
6.1 Sampling Methods 48
6.2 Quantitative Methods 49
6.2.1 Colorimetric Methods 49
6.2.2 Atomic Absorption Spectroscopy .... 50
6.2.. 3 Polarography 50
6.2.4 Emission Spectrography 51
6.2.5 Other Methods 51
7. SUMMARY AND CONCLUSIONS 52
REFERENCES
APPENDIX
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LIST OF FIGURES
1. The Complex of Bio-Processes Inhibited by Vanadium ... 4
2. Production of Vanadium Pentoxide in the United States . 33
3. Productive and Potential Vanadium Sources by Type ... 64
4. Productive and Potential Vanadium Sources by
Deposits and Districts 64
5. Principal Areas of Vanadium and Uranium Mining and
the Seven Major Production Units of Vanadium
Concentrates 65
6. Water-Acid Leaching and Ion Exchange Process 66
7. Vanadium-Uranium Recovery by Solvent Extraction .... 67
8. Recovery of Vanadium from Phosphate Rock 68
9. Sodium Carbonate and Acid Leach Method of Vanadium-
Uranium Recovery 69
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LIST OF TABLES
1. Urinary Excretion of Vanadium and Ascorbic Acid Levels
in Workers Exposed to Vanadium Pentoxide Fumes .... 16
2. Lethal Doses of Vanadium, Molybdenum, Chromium, and
Tungsten Metals and Salts, Administered Intravenously
to Cats „ 21
3. Valence of Vanadium and Relative Median Lethal
Doses of Its Compounds 21
4. Classification of Vanadium and Other Metals by
Toxicity 24
5. Lethal Doses of Nine Metals Orally Administered to
Rattus Norvegicus (0.3 kg) 24
6. Concentrations of Vanadium in Domestic Coals 28
7. Comparative Concentrations of Vanadium Pentoxide and
Sulfur Dioxide in Three Typical Residual Oils .... 29
8. Concentrations of Vanadium Pentoxide and Sulfur
Dioxide in Petroleum from Various Regions 30
9. Distribution by State of 119 Industrial Units
Producing Major Vanadium Chemicals 35
10. Vanadium Consumed in the United States in 1966, by
Uses 39
11. Distribution of Minimum, Maximum, and Average Values
of Vanadium Concentration in the Environmental Air
of Some Communities in the United States 43
12. Rank Ordering of the 15 Communities with Highest
Vanadium Concentrations Based on Average, Maximum, and
Minimum Values, 1967 44
13. Concentrations of Fly-Ash and Vanadium at Inlets and
Outlets of Fly-Ash Collectors Used in Two Coal-Fired
Power Plants 46
14. Vanadium and Recoverable Vanadium in Ore and
Concentrate Produced in the United States, 1930-1965 . 70
15. Vanadium Consumed in the United States 71
16. Producers of Vanadium Chemicals 72
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List of Tables (Continued)
17. Concentration of Vanadium in the Air 76
18. Concentrations of Vanadium in the Air of 118
Communities of the United States, 1967 81
19. Concentrations of Vanadium in the Air of 79
Communities of the United States, 1966 86
20. Some Producers of Vanadium Products 89
21. Properties, Toxicity, and Uses of Vanadium and Some
Vanadium Compounds 90
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1. INTRODUCTION
Vanadium is moderately toxic to humans and animals.
Exposure to vanadium or its compounds at low concentrations
through inhalation has produced observable adverse effects on
the human organism. Chronic exposure to environmental air
concentrations has been statistically associated with the
incidence of cardiovascular disease and certain types of
cancer.
Vanadium is emitted into the atmosphere from such
sources as the industries producing the metal, its chemical
compounds, alloys, and other products, as well as power
plants and utilities consuming residual and crude oils and
coals containing vanadium. The present concentrations of
vanadium in the atmosphere of the United States are on the
order of a few micrograms per cubic meter; however, the fast-
increasing production and use of vanadium and its compounds,
added to the growing consumption of vanadium-bearing oils
and coals, will significantly augment the potential for air
pollution by vanadium.
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2. EFFECTS
Vanadium appears to be a trace metal essential for the
human body — and for mammals in general — but the final proof
of its essentiality is still lacking. In spectrographic
analysis of organs and muscle tissues of Americans, vanadium
has been detected only in lung and intestine: most positive
samples showed 0.01 |_ig or less of vanadium per gram of tissue.
Vanadium appears to be stored mostly in fat and serum.
Studies of the fate of vanadium in man point to the existence
of a vanadium homeostasis, but the exact mechanism is presently
7fi
not known .
Increasing knowledge of the role of essential and non-
essential trace metals in metabolic processes at cellular and
molecular levels has stimulated research on the biochemical
effects of vanadium. Vanadium has been found to inhibit the
synthesis of cholesterol, 8' 14' 21' 23 ' 24' 39'43 ' 61' 65' 84' 92' 10°
19 97 ft 1 ft 9
phospholipids, and other lipids. z'z 'OJ-'OZ Vanadium's
inhibitory role has been also studied with respect to amino
l'44 j_n generai anci theotic acid-^0 an(j uric
*7 C^1^.
particular, as well as the enzymatic activities of tyrosinase, '
xanthine reductase,6^ cystine, 10' 59,60 and nitriate reductase.
Studies have also been made of the adverse bioeffects of
vanadium on tissue oxidation. inhibition of sulfydril
8? 39
activity; blood lecithin content; excretion of corticoste-
13 40 45
roids; ' acetylcholine metabolism; liver acetylation process;
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inhibition of the activities of coenzymes A, Q, and i;6,49,50
69
inhibition of adenosene triphosphatases; and precipitation
of serum proteins.
The most-studied effect is the inhibition of cholesterol
synthesis. Vanadium has been found to interfere with the
formation and utilization of mevalonic acid, one of the inter-
mediate substances in the process of cholesterol synthesis
from acetyl groups. Furthermore, vanadium has been shown to
inhibit the metabolic activities of coenzymes A and Q, which
are involved in the early stages of cholesterol synthesis.
These coenzymes form various acetyl-coenzymes, which, in turn,
produce the necessary condensation of acetyl groups to form
mevalonic acid. There is also evidence that vanadium contri-
butes to depletion of cholesterol stored in the tissues and
reduces dietary cholesterol retention.
The interrelationship of the various metabolic processes
mentioned above is shown in Figure 1. The chain of cause-and-
effect relationships that link inhibition of cholinesterase
and other activities to a number of diseases is discussed in
the following paragraphs.
The role of cholinesterase consists of splitting acetyl-
choline into choline and acetic acid. Choline is an essential
nutrient that protects the tissues (mainly the liver) from
excess fat accumulation by converting fats into phospholipids.
Choline deficiency is also associated with fatty infiltration
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Folic Acid
Choline Cholinesterases
(Enzymes)
From Diet
Choline
Dehydrogenase
\ Inhibition
by
Vanadium
Coenzyme I -^
Acetyl Coenzyme A
Cortisone
Adrenosterone
FIGURE 1
The Complex of Bioprocesses Inhibited by Vanadium
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of the myocardium which can ultimately cause an infarct.
Sclerosis (Monckeberg type) has also been observed, with more
or less calcified lipid deposits in the aorta and coronary
vessels. Deficiency of choline causes a decrease in serum
albumin and an increase of phospholipids and the alpha-and
beta-globulins. Finally, choline is known to have a favorable
effect on growth, reproduction, and preganancy in both lower
and higher organisms.
Experimentally determined indications of choline deficiency
include growth retardation, anemia, high infant mortality,
kidney atrophy, fatty degeneration and cirrhosis of the liver,
necrosis of the kidney tubules, creatinuria, progressive
muscular dystrophy, and even death.
Since the role of vanadium as an inhibitor of cholinesterase
activity is well established, it is possible that the above
physiological effects are at least partially correlated with
the presence of vanadium. As will be shown in the following
sections, a positive correlation to some of these effects has
been established.
The importance of vanadium's indirect inhibitory effects
on the adrenocortical hormones may be assessed on the basis of
the following considerations. Cholesterol, as the name indi-
cates, is a member of the sterol group that belongs to the
larger group known as steroids, which are widely distributed
in nature and include many important hormones. Cholesterol,
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a cell constituent of most warm-blooded animals, is relatively
concentrated in the adrenal cortex, where it is a precursor
of the all-important adrenocortical hormones (see Figure 1).
The latter affect a great number of metabolic processes,
including salt, water, mineral, and carbohydrate metabolism.
It has been established that cholesterol can give rise to
all the corticosteroids (hormones, glucogenic steroids, and
androgens). Inhibition of the majority of these metabolic
processes is known to result in a great number of physiological
alterations.
The next most-studied aspect of vanadium is its role as
an inhibitor of cystine, cysteine, and methionine—the three
basic sulfur-containing amino acids. Cysteine forms and is
formed by cystine, and its decarboxylation results in the
formation of part of coenzyme A. Cystine is the sulfur-
containing constituent of skin, hair, and nails. Methionine
has a sulfur-bound methyl group which through enzymatic
activity is used in the production of adrenaline, choline,
and creatine.
Vanadium has been shown to interfere with tissue respira-
tion at the stage of dehydrogenation which is catalyzed by
coenzyme I. Inhibition of this coenzyme's activity by vana-
dium results in reduced incorporation of iron in the related
porphyrins which, in turn, inhibits hemoglobin synthesis.
The nonutilized portion of iron has been observed to accumulate
in the reticuloendothelial tissues after experimental exposure
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to vanadium. The metal's action is supported by its potential
inhibition of the activity of monoamineoxidase, which catalyzes
the oxidation of serotonin to 5-hydroxyindolacetic acid. The
urine content of this acid has been found to fall as a result
of experimental exposure to vanadium. Thus, inhibition of
monoamineoxidase may result in the accumulation of serotonin
in the central nervous system.
On the other hand, it has been found that the activity
of monoamineoxidase was considerably inhanced by 1.0 millimole of
vanadium(IIl) and vanadium(IV), but not vanadium(V). In this
respect, it has been suggested that vanadium is a co-factor
in tissue monoamineoxidase.
The conflicting evidence regarding the role of vanadium
in monoamineoxidase activity may be explained by the fact that
many trace metals can either inhibit or enhance a given
metabolic activity, depending on their level of concentration
and other relevant variables or parameters. Among 18 metals
tested, vanadium was found to be the major catalyst in the
oxidation of 5-hydroxytryptamine (serotonin), adrenaline, and
48
other important catecholamines. In insulin hypercalcemia,
the adrenaline level can rise to 10 times the normal and, in
patients with catecholamine-producing tumors, noradrenaline
levels 100 times greater than normal have been observed.
Adrenal hormones can cause high blood pressure and marked
reduction in the renal blood circulation, renal plasma circu-
lation, and glomerular filtration rate. They can also increase
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8
oxygen consumption and indirectly, production of corico-
steroids.
The exact etiological mechanism linking the above effects
to observed physiological changes in tissues and organs is
not known. Most of the observed adverse effects of vanadium
have occurred after human or animal exposure to relatively
high concentrations in relation to normal environmental con-
centrations of vanadium. Such effects are clinically observable
and, in most cases, can be specifically attributed to vanadium.
However, chronic exposure to the relatively low concentrations
observed in urban atmospheres usually does not produce any
103
clinically observable physiological changes. The effects
of vanadium, if any, on metabolic processes are not felt by
the person exposed, and the biochemical changes produced are
usually links in a chain of adverse effects that can result
from a multitude of pollutants as well as diseases. It is
for these reasons that such changes as a 10 percent decrease
in normal cholesterol and/or cystine levels become important
in considering the possible health effects of environmental
concentrations of vanadium.
2.1 Effects on Humans
2.1.1 Exposure to Low Concentrations
Very few studies have been made on the effects of human
exposure to low concentrations of vanadium in the environmental
air. In one of these studies, lower-than-normal plasma
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cholesterol levels were usually found among vanadium
processing workers in Colorado who had been exposed to vana-
dium levels of from 100 to 300 M.g/m3.44'96
In an experiment with two volunteers, exposure to vana-
dium pentoxide (V2O5) at a concentration of 1,000 |Jg/m3
resulted in coughing which persisted for 8 weeks. Another
five volunteers were exposed to an average concentration of
200 W.g/m3 (± 60 standard deviation) for about 8 hours. All
of them developed loose coughing the following day- Urinanal-
ysis showed a maximum concentration of 130 ug/liter three
days after the exposure, while maximum fecal concentration
was 3,000
In another instance, when 24 workers were exposed to
vanadium pentoxide at concentrations of from 18 to 925 M.g/m3,
it was found that serum cholesterol levels were approximately
43
10 percent below normal.
35
In a statistical study by Hickey et al., concentrations
of vanadium and nine other metals in the environmental air of
25 communities in the United States were correlated to
mortality indices (1962 to 1963) of eight categories of
prevailing diseases. Various techniques of correlation
analysis were used, including canonical analysis. In the
matrix of computed correlation co-efficients the following
values were obtained with respect to vanadium's association
with some of the diseases and pollutants:
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10
Vanadium—"diseases of the = 0.50 (fourth highest
heart" value after those
found for cadmium,
zinc, and tin)
Vanadium—nephritis =0.47 (third highest
after tin and
nickel)
Vanadium—"arteriosclerotic heart"= 0.47 (fourth highest
after cadmium,
zinc, and tin)
Vanadium—nickel = 0.94 (highest coefficient
of intercorrelation
among any two of the
ten metals)
Thus, vanadium (together with cadmium, zinc, and tin) was
found to correlate significantly with the above diseases and
highly with nickel. In subsequent canonical analysis, it was
found that the strongest relationship existed between vanadium
and "diseases of heart." Moreover, tests of statistical
significance of various combinations showed that the addition
of vanadium to cadmium produced a more than 10 percent
35
reduction (the highest) in the error of variance. The very
high intercorrelation between vanadium and nickel was not
explained in this study. As shown in the section devoted to
sources, the two metals together are major contaminants of
crude and residual oils, as well as constituents of the fly
ash from their industrial emission; sources.
89
In another statistical study by Stocks, mortality
from lung cancer was found to correlate significantly with the
concentration of particulates in many areas in Great Britain.
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Concentrations of 13 trace elements were correlated with lung
cancer mortality rates in 23 localities. The findings of the
study were as follows:
(1) Vanadium, together with arsenic and zinc, showed
weak associations with lung cancer.
(2) Vanadium showed a strong association—second only
to berryllium and arsenic—with bronchitis in males.
(3) Vanadium and beryllium were found to be associated
with pneumonia.
(4) Vanadium, beryllium, and molybdenum showed correla-
tions with other cancers, but only in males.
Thus vanadium ambient air concentrations showed statis-
tical correlations with bronchitis, pneumonia, lung cancer,
and other cancers. The estimated correlation coefficients
were the following:
Bronchitis, males = 0.620
Pneumonia, males = 0.805 (highest among 11 metals)
Pneumonia, females = 0.711 (second highest after beryllium)
Lung cancer, males = 0.770 (second highest after beryllium)
Other cancer,
except of
stomach, males = 0.556 (highest)
Both the above-mentioned studies represent efforts to
test statistically for significant correlations between
environmental concentrations of a number of trace elements
and mortality rates related to various diseases in urban centers.
35
The study by Hickey used more sophisticated techniques
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12
of statistical analysis. His study employed canonical rank
correlation to test for the combination of variables that
would maximize the correlation between pollutants and diseases;
it also tested for and found significant intercorrelations,
thus reducing the validity of conclusions based on the esti-
mated numerical values of the correlation coefficients. On
89
the other hand, the study by Stocks considered diseases
which are more well-defined than the majority of those con-
sidered in the study by Hickey.35 Further, it considered
such important parameters as population density, sex, and age.
However, the two studies cannot be compared, since the
correlations were run for different diseases (except for lung
cancer) and the sets of pollutants considered were not exactly
the same0 Nevertheless, it is interesting to note the differ-
ences in findings with respect to the relationship between
lung cancer mortality and vanadium concentrations. The
correlation coefficients estimated by the two studies are
00320 (Hickey)35 and 00770 (Stocks).89
o c
Hickey found that when vanadium was considered together
with cadmium the multiple correlation coefficient was 00767~
He points out that in addition to cadmium, vanadium in the
ambient air may contribute to diseases of the heart.
' Both studies were handicapped by the lack of long-term
data (time series), the omissions of important pollutants
(e.g., organic compounds) that are known to be causally
related to some of the considered diseases and that cannot be
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13
assumed to be constant; the unsatisfactory definition of diseases;
and the known and unknown intercorrelations (positive and/or
negative) among the pollutants as well as the diseases consid-
ered.35'89
Statistical correlation studies are useful mostly in
cases of relatively high average levels of atmospheric pollu-
tion in cities and towns where the meterorological conditions
35 89
include fairly prolonged temperature inversions. '
2.1.2 Exposure to High Concentrations
Practically all of the studies on high concentrations of
vanadium center on occupational exposures, mostly to vanadium
pentoxide (V-Oc).
In one study, exposure to inhalation of ^2^)^ dust by 18
workers engaged in pelletizing pure V2Og resulted in acute
103
illness of all those involved.
In other research, a normal young male was injected
intramuscularly with a sodium salt of vanadium (Na2V4On).
The first dose was 5,600 [ag of vanadium, followed by doses of
11,200 lag on the third and fourth days. The following effects
were subsequently observed: (1) increased levels of urea and
purine nitrogen, but relatively small increases in total
nitrogen; (2) an increased level of neutral sulfate in the
urine, but relatively small increases in total neutral
sulfate; and (3) a significant increase in fecal phosphorus
91
(27 percent,) but very small increase in total phosphorus.
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14
Occupational vanadium poisoning was first studied in 1911
among workers exposed to vanadium dust and fumes from Peruvian
ores. The effects described included paroxysmal cough leading
to hemoptysis. In more severe cases, tuberculosis developed,
which sometimes led to death. Among other symptoms were
irritation of throat, eyes, and nose; anorexia, tremors,
hysteria, and melancholia; and anemia, accompanied by reduc-
tions in hemoglobin and in the number of erythrocytes. At
tissue levels, the poisoned workers showed destruction of the
alveolar epithelium in the lungs and hemorrhagic nephritis.
Similar symptoms have since been reported by other investiga-
tors in various countries but at lower levels of intensity since
industrial precautions are increasing in number. The effects
described by various studies during the 1940's and 1950's
included bronchitis, pneumonia, conjuctivitis, rhinitis,
pharyngitis, laryngitis, and bronchopneumonia. The systemic
09 101
poisoning effect suggested by earlier investigations '
has not been confirmed by later and more detailed studies.
During the 1940's and 1950's similar effects were
described in cases of exposure to vanadium pentoxide and
vanadium trioxide contained in by-products of residual or
crude oil combustion.36'51'78"80'94 In practically all the
cases showing marked effects on the respiratory system,
exposures ranged from 1,000 to about 50,000 |ag of vanadium
per cubic meter. The average particle size was found to be
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15
less than 5 u* and sometimes less than 1 a, mostly in vanadium
Q Q
pentoxide in slag from residual oil combustion. Actually,
the intensity and incidence rate of effects have been found
to relate directly to the level of concentration and the
particle size: the higher the concentration, the greater the
intensity and the incidence rate of the observed effects.
Since concentrations in the above-stated range of values
are highly unlikely to occur in urban atmospheres, the type
of acute physiological effects described are limited to
occupational exposures.
In a recent study, the effects of vanadium on a bio-
chemical level were investigated in 13 workers who had been
engaged in the production of vanadium pentoxide for a period
of from 1 to 3 years and exposed to 480 to 2,650 |ag of
vanadium per cubic meter. Clinical findings, shown in Table
1, may suggest that the stated exposure resulted in a
derangement of the ascorbic acid metabolism.
2.1.3 Lethal Dose (LD)
The lethal dose of vanadium (through inhalation) for man
has been estimated by Stokinger to range from 60,000 to
120,000 |-ig. The LD for intravenous administration of V2O5
(as tetravanadate) to a man of average weight (70 kg) has
been estimated as 30,000 M.g.67 However, doses of 10,000 |ag
(intravenous) or 20,000 |J.g (intramuscular or subcutaneous)
were found to be tolerated in some instances.
*p. = micron.
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16
The emetic dose for the hexavanadate was estimated as
100,000 to 125,000 ng V2°5' while a dose of 60,000 p.g by any
route was well-tolerated.67
It is apparent that the range of values between lethal
and nonlethal doses of vanadium, as with other nonessential
metals, is very narrow.
TABLE 1
URINARY EXCRETION OF VANADIUM AND ASCORBIC ACID
LEVELS IN WORKERS EXPOSED TO VANADIUM PENTOXIDE FUMES97
Urinary Excretion Max Avg Min
Vanadium ( M.g/1 iter )
Exposed workers
Controls
Increase factor
259.3
11.0
23.5
92.7
6.9
13.4
21.0
3.5
6.0
Ascorbic Acid (Ug/3 hr)
Exposed workers 4,000 1,900 500
Controls 9,700 2,500 700
Percent of decrease 58.8 24.0 28.6
2.1.4 Other Factors Determining Toxicity
Route of Intake. Oral administration of the salt sodium
tetravanadate to normal men in 12 daily doses (7,000 |jg
vanadium) resulted in nearly total excretion, 12 percent
through the urine and about 88 percent in the feces. However,
when the salt was administered intravenously in six daily
doses, (approximately 20,000 |_ig vanadium) about 90 percent
91
was excreted, of which only 9 percent was recovered in the feces.
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17
Synergism. In one case of vanadium intoxication, zinc
oxide was found to act synergistically to produce after-
effects.56
Susceptibility to metabolic disturbances because of a
genetic defect (Wilson's disease) has been shown to increase
as a result of occupational exposure to vanadium.58
It has been reported that organic vanadium dust at
extremely low concentrations (1 |J.g/gm of tissue) may induce
disturbances of basic metabolic processes, including reduction
of cystine content, which are neither clinically detectable
90
nor felt by the subject.
2.2 Effects on Animals
2.2.1 Commercial and Domestic Animals
No information has been found on the effects of vanadium
air pollution on commercial or domestic animals.
2.2.2 Experimental Animals
2.2.2.1 Vanadium Pentoxide (V2O5)
Ten rabbits and rats were exposed in gas chambers to
inhalation of V2C>5 aerosol at a concentration of 8,000 to
18,000 [-ig/m3 for 2 hours daily over a period of 9 to 12
months. The acute and chronic poisoning which developed was
characterized by biochemical, functional, and morphological
abnormalities similar to those described below for vanadium
trioxide (VO). However, the median lethal concentration
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18
of V2O5 was found to be one-third to one-fifth that of
In the third month, the test rabbits began to show a
considerable decrease in the urine content of 5-hydroxyindo-
lacetic acid, which at the end of the experimental period
amounted to about one-third of the normal level.73
2.2.2.2 Vanadium Trioxide (V2O3)
Vanadium trioxide is also capable of causing acute or
chronic poisoning in experimental animals, depending on the
dose or concentration in the air. In another series of
experiments, 10 rabbits and rats were exposed in gas chambers
to inhalation of vanadium aerosol in concentrations ranging
from 40,000 to 70,000 |ag/m3 for 2 hours daily over a period
of 9 to 12 months. The observed effects included (1) hypo-
chromic anemia, (2) decrease in the hemoglobin level of from
75 percent to 67 percent of the normal, and (3) a 33 percent
decrease in the number of leuckocytes in the peripheral blood.
By the end of the second or third month of exposure,
chronic poisoning with V^Oo dust caused a decrease in albumin
and increase in globulin to the extent that the ratio of the
former to the latter was reduced by half. By the end of the
llth month, additional effects included (1) an increase in the
serum content of aminoacids (cysteine, arginine, histidine),
(2) a 10 percent increase in the nucleic acid in the blood,
(3) a 29.8 percent decrease in the serum content of sulfhydryl
groups, (4) a 50 percent decrease in the blood content of
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19
vitamin C, (5) a considerable increase in the blood content
of chloride, and (6) a drastic inhibition of tissue respira-
tion in the liver and brain. Finally, the organs of the
respiratory system at the end of the experimental period
showed such conditions as (1) suppurative bronchitis, (2)
septic broncho pneumonia, (3) pulmonary emphysema, (4) forma-
tion of cellular-dust foci with signs of necrobiosis in the
phagocytes, and (5) moderate interstitial pulmonary sclerosis.73
2.2.2.3 Vanadium Chloride
Rabbits and rats exposed to inhalation of VC13 showed
chronic poisoning effects similar to those described for V^Oo,
2 3
but the effects on tissues were more marked: they were
characterized by (1) protein and fatty dystrophies of the
cells of liver, kidney, and myocardium; (2) partial necrosis
of the tissues of some organs; and (3) reduction in ribonucleic
acid (RNA) and deoxyribonucleic acid (DNA) content of the
cells of liver, kidney, myocardium, stomach, intestine, and
lung. Thus VC13 proved to be more toxic than V2C>3 under the
same experimental conditions.
2.2.2.4 Vanadium Metal (V), Vanadium Carbide (VC) , and
Ferrovanadium (FeV)
The aerosols of vanadium, vanadium carbide, and
ferrovanadium are not considered highly toxic. However,
they produce certain local and general physiological reactions,
such as (1) catarrhal bronchitis; (2) pathological tissue
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20
proliferation; (3) a moderate degree of interstitial pneumono-
sclerosis; (4) marked catarrhal gastritis—a local effect
occurring after oral administration; and (5) pathohistological
alterations in the parenchyma, such as local nephritis, fatty
dystrophy of the hepatic cells, sclerosis of hepatic and renal
interstitial tissues, and perivascular edema in the myocardium
(a typical general toxic effect).
Exposure to iron-vanadium alloy dust was found to cause
slight and statistically insignificant changes in the blood
such as a decrease in the sulfhydryl groups and nucleic acids,
but marked and significant proteinuria. The vanadium of the
iron-vanadium alloy was found to be considerably more toxic
than free vanadium because of its higher solubility in bio-
material. Exposure to vanadium-carbon and vanadium dust was
found to produce slight, unstable, and statistically insigni-
7*3
ficant biochemical changes in the blood.
2.2.2.5 Sodium Metavanadate (NaVO3)
The relative toxicities of vanadium, molybdenum,
chromium, and tungsten and their sodium salts have been
66
determined in a series of experiments. Table 2 lists the
lethal doses of these substances as administered to cats,
based on fatalities occurring within 60 minutes.
2.2.2.6 Other Factors Determining Toxicity
Valence of Vanadium Atoms. Pentavalent compounds, such
as ¥205, NH4VO3, NaVO3, and Ca(VC>3)2, were found to be three
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21
TABLE 2
LETHAL DOSES OF VANADIUM, MOLYBDENUM, CHROMIUM, AND
TUNGSTEN METALS AND SALTS, ADMINISTERED INTRAVENOUSLY TO CATS
66
Metal
Vanadium
Tungsten
Chromium
Molybdenum
Lethal Dose
UgAg
body weight)
1,880
22,600
56,400
205,000
Compound
Sodium metavanadate
Sodium tungstate
Sodium chromate
Sodium molybdenate
Lethal Dose
( |ag/kg
body weight)
7,180
143,600
179,500
972,000
to five times more toxic than trivalent compounds under com-
parable experimental conditions, as measured by median lethal
concentrations.
73
This is shown in Table 3.
TABLE 3
VALENCE OF VANADIUM AND RELATIVE MEDIAN
LETHAL DOSES OF ITS COMPOUNDS73
V Compound
Valence of
V Atoms
Relative Value
of Median LD
Salts
NH4V03
vci3
VI2
Oxides
V2°5
V2°3
5
3
2
5
3
la
2.3
6.8
lb
5.6
110,000 ng of vanadium per kg body weight.
>23,000 (-ig of vanadium per kg body weight.
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22
Diet. Dietary V2O5 has been found to be toxic at 103
ppm of vanadium to rats fed a suboptimal (casein) diet, but
toxic only at 1,000 ppm of vanadium to rats fed an optimal
diet (consisting of Purina chow).
Tolerance. It has been shown that some animals develop
a certain amount of tolerance to vanadium. Experimental
animals may tolerate amounts of vanadium, administered in
gradually increasing doses, which would have been lethal if
administered in only one or two doses.26
Age. Variations in weight, growth, and ability to survive
have been found to relate to age in an experiment with rats
fed 100 ppm of vanadium for a lifetime (2 to 5 years).91
Antagonism and Synergism. At high concentrations,
vanadium has been shown to mobilize iron out of the liver and
spleen. However, in low concentrations, vanadium has been
found to mobilize iron into the liver and to enhance calcium
deposition in bone.
2.2.2.7 Absorption, Distribution, and Excretion
After rats had inhaled V^O^ dust (500 M-g/m3 of vanadium)
6 hours daily for 6 months, the amounts of vanadium absorped
at the end of this period per gram of tissue were 30 [Jg in
the lung, 0.8 (Jg in the kidney, 0.6 |_ig in the spleen, and
0.14 |ag in the liver. Forty days after the end of the
experimental period, the liver was found to retain the highest
percent (about 99 percent) of the absorbed amount, followed
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23
by the kidney (60 percent), the spleen (50 percent), and the
lung (10 percent). The mean value of urinary excretion of
vanadium for pigs was 140 |J.g of vanadium per liter of urine—
28 times higher than for the control animals.91 Vanadium was
excreted mostly through the kidneys when its sodium salt
(NaVO3*H2O) was administered intraperitoneally or intravenously
to experimental animals. When subtoxic single doses; were
given, renal excretion was found to be rapid, amounting to 60
percent in the first 24 hours. The above percentage was
22
independent of the number of doses administered. This fact
led to the conjecture that changes in urinary excretion of
vanadium reflected changes in its retention. About 10 percent
was excreted through the intestines and an approximately equal
percentage was retained in the skeleton, while traces were
found in all tissues. Rentention of vanadium pentoxide in the
91
tissues of rats was twice that of its sodium salt.
2.2.2.8 Comparative Toxicity
The elements can be classified according to their toxicity,
as measured by the lethal dose (LDgg) for small mammals, as
4T -,-, 13a
follows:
Highly toxic 1,001-10,000 |~ig/kg body wt
Moderately toxic 10,001-100,000
Slightly toxic 100,001-1,000,000
Relatively harmless >1,000,000
These classes can then be subdivided according to the
mode of intake. The comparative toxicity of vanadium and 12
other metals is shown in Table 4 and Table 21 in the Appendix.
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24
TABLE 4
CLASSIFICATION OP VANADIUM AND OTHER METALS BY TOXICITY13a
Highly Toxic Moderately Toxic Slightly J^oxic
Metal Oral Intravenous Oral Intravenous Oral Intravenous
Arsenic (As+3) x
Boron x x
Cadmium x x
Cobalt x
Chromium (Cr+6) x x(Cr+3)
Iron x
Fluorine x
Mercury x x
Manganese x
Nickel x
Selenium (Se+4) x
Vanadium (V+5) x x
Zinc x
The relative LD^Q values for nine of the above metals are
given in Table 5.
TABLE 5
LETHAL DOSES OF NINE METALS ORALLY ADMINISTERED
TO RATTUS NORVEGICUS (0.3 kg )15 , 20, 25 , 55 , 57, 83, 86
(Weight of Dry Diet=10 g Metal per Day)
Lethal Dose
Element _ ( uq/day )
Vanadium (V+5) 1,500
Selenium (Se+4) 1,000-2,000
Arsenic (As+3) 1,300-5,000
Mercury (Hg+2) 8,000
Cadmium (Cd+2) 16,000
Fluorine (P~) 30,000
Iron (Fe+2 or Fe+3) >60,000
Zinc (Zn+2) 150,000
Boron (Borate) 130,000-270,000
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25
2.3 gffects on Plants
No information was found on adverse effects of vanadium
on vegetation.
2.4 Effects on Materials
In boilers fired on residual oils, the accumulation of
ash on the external surfaces of superheater tubes causes a
loss of thermal efficiency and associated corrosion which at
high metal temperatures may result in premature failure of
the steam-raising equipment. Vanadium and sodium are considered
the most harmful of the ash-forming elements, and their in-
organic complexes (naphthanates) form a major part of the
superheater deposits. Furthermore, the corrosive action of
sodium-vanadium complexes at high temperatures is increased
by the oxides of sulfur produced during the combustion
99
process.
2.5 Environmental Air Standards
The 1967 American Conference of Governmental Industrial
Hygienists adopted the following values for those occupa-
tionally exposed:
Vanadium pentoxide (V2O5), dust 500 ng/m3
Vanadium pentoxide (V2C>5), fume 100 iag/m3
In the U.S.S.R., the following maximum allowable concen-
trations (MAC) have been adopted for occupational exposure
to industrial aerosols of vanadium compounds:
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26
Vanadium pentoxide—condensation aerosol 100 ug/m
Vanadium pentoxide—comminution aerosol 500 M-g/m
Vanadates and vanadium chlorides 500 [-ig/m3 *
Ferrovanadium and vanadium-aluminum alloys 1,000 |-ig/m
Vanadium carbide 4,000
*In terms of vanadium pentoxide.
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27
3. SOURCES
3.1 Natural Occurrence
3.1.1 Mineral Ores
More than 65 vanadium-bearing minerals have been identi-
fied. The most important of these are (1) patronite (V2Sg+S),
found only in Peru, and also containing iron, nickel, molybdenum,
phospborus, and carbon; (2) bravoite ((FeNi)S2), also found
in Peru; (3) sulvanite (3Cu2S-V2S5), found in Utah and Southern
Australia; (4) davidite, a titanium-iron ore found in Southern
Australia; and (5) roscoelite (CaO-3V2S5'9H2O), found in
Colarado and Utah. The last is a vanadium-bearing mica existing
as a mineral in a number of rich gold-bearing veins. It occurs
in important quantities as a secondary mineral in the sand-
stones of Colorado and Utah. Vanadium is also found in these
two States in such uranium-bearing sandstones as carnotite
(K2O-2U03-V2O5*3H2O), uravanite (2U03-3V205-15H2O), tyuyamunite
(CaO-2U03-2V205-4H20), and hewettite (2K20-2A12O3(Mg,Fe)O-3V2).
Recent reduction in domestic uranium output and continuing
increases in vanadium consumption have made it necessary to
seek other sources of vanadium, such as fetfrophosphorus,
obtained from Idaho and Montana phosphate rock deposits and
titaniferous magnetite ores bearing vanadium.
The concentration of vanadium in ores varies widely, from
5 to 25 percent. In roscoelite, V2O5 accounts for 20 percent
of the total ore. In most of the vanadium-bearing titanium
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28
ores, V2C>5 accounts for less than 1 percent (0.1 to 0.3 percent)
and is removed as an impurity. The phosphate rocks of Idaho
and Montana contain from 0.11 to 0.45 percent V205.
3.1.2 Coal
As early as 1892, V2C>5 was found to constitute 0.24 per-
cent of a lignite deposit in Argentina (38.22 percent of the
ash obtained). Similar concentrations were also found in Peru
and in certain Australian coals. The vanadium is usually
bound to the organic matter in the coal. Measurements of
vanadium concentrations in domestic coals are shown in Table 6.
TABLE 6
CONCENTRATIONS OF VANADIUM IN DOMESTIC COALS1
Vanadium in Ash Vanadium in Coal
Coal Source (j£) (ppm)
Northern Great Plains 0.001-0.058 16
Eastern Interior Region 35
Appalachian Region 21
Texas, Colorado, North Dakota,
South Dakota 0.01-0.1
West Virginia 0.018-0.039
Pensylvania (anthracite) 0.01-0.02
Buck Mountain Bed 0.11 176
Diamond Bed 0.09 92
It has been also found that in West Virginia coals the
concentration of vanadium is reasonably constant in the main
body of the coal but frequently high in thin sections of the
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29
coal between shale partings.
3.1.3 Oil
Vanadium compounds are major organometallic constituents
of crude oils. Concentrations vary from 0.01 percent in mid-
continental crude oil to 0.06 percent V9Or in Venezuelan crude
sLf ~S
., 16,73
oil.
Ash from combustion of residual oil (grade 6) varies from
0.002 to 0.3 percent (by weight), and its V2O5 content varies
from 2.7 percent in Texas crude to 63.2 percent (of total ash).
Comparative analysis of three typical residual oils is shown
in Table 7.
TABLE 7
COMPARATIVE CONCENTRATIONS OF VANADIUM PENTOXIDE AND
SULFUR DIOXIDE IN THREE TYPICAL RESIDUAL
Percent of Total Ash
California Texas Venezuela
Content
Vanadium Pentoxide
Sulfur Dioxide
Low Hiah Low Hiah Hiah
7.6 29.9 2.7 21.00 63
35.6 20.9 45.5 33.00 13
.2
.9
Average concentrations of vanadium pentoxide and sulfur
dioxide in petroleum from various areas—determined after
73
laboratory combustion—are shown in Table 8.
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30
TABLE 8
CONCENTRATIONS OF VANADIUM PENTOXIDE AND SULFUR DIOXIDE
IN PETROLEUM FROM VARIOUS REGIONS73
Percent of Total Ash
Place of Origin ¥205 SO2
California 5.1 15.0
Texas 1.4 1.4
Kansas 0.4 36.4
Iran I 14.0 2.6
Iran II 38.5 7.0
Sahara I 0.04
Sahara II 0.30
3.1.4 Distribution of Deposits
The geographical distribution of ores and deposits by
type and size is given in Figures 3 and 4 of the Appendix,
respectively. During the second half of the past decade,
practically all of the domestic vanadium output came from the
deposits in southeastern Utah and northeastern Arizona.
This area is shown in Figure 5 of the Appendix.
3.2 Production Sources
3.2.1 Recovery of Vanadium Oxide from Vanadium-Bearing Ores
Vanadium extraction methods include ion excange and sol-
vent extraction, which separate both uranium and vanadium from
combined extraction circuits in domestic mills. Daring the
1950's several new methods developed for the recovery of
uranium from carnotite and roscoelite were also used for
separate recovery of vanadium. Recovery of vanadium by solvent
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31
extraction was started in 1956 (by the Climax Uranium Co. in
Colorado), resulting in a vanadium recovery rate of 30
percent.
At some plants making chromium compounds, vanadium has
been recovered from chromite ore by an acid precipitation
method.
Vanadium has also been recovered by the Anaconda Company
from phosphate rock by a leach roasting process.
Experimental methods have been patented and developed for
recovering vanadium from titaniferous magnetites, ferrophos-
phorus ores, and crude oils.
In addition, methods have been developed in other
countries for recovering vanadium from (1) the complex ore
wulfenite, which also contains molybdenum, gold, silver, and
lead; (2) bauxites (Great Britain); (3) lead-zinc ores
(Northern Rhodesia); and (4) steel plant slag (Germany).
Flow sheets showing the processes and materials involved
in domestically used extraction methods are given in Figures
6 to 9 of the Appendix. No emission data could be found, but
given the estimated recovery rates (30 to 75 percent of the
vanadium) and the metal's low vaporization temperature, one
may form an idea of the corresponding rates of losses in the
air.
Slag from processing vanadium-bearing ores contains
considerable amounts of vanadium oxides. Crushing of this
slag produces aerosols containing lower oxides of vanadium as
-------
32
well as silica, calcium, iron, chromium, manganese, etc.
Furthermore, when calcines are produced from these slags, dust
forms which contains soluble vanadates at concentrations as
high as 5,000 Ug/m3 in the working environment. Vanadium
pentoxide, derived from calcium vanadate, is melted before it
72
is used in alloying.
3.2.2 Production of Vanadium Metal
The output from processing vanadium-bearing ores is an
oxide concentrate commercially known as vanadium pentoxide
(V2°s)' containing at least 80 percent V2C>5; most of the
remaining part is sodium monoxide and/or calcium oxide. Thus,
commercial vanadium pentoxide is actually a sodium and/or
calcium hexavanadate. From this compound, high purity ^2°5
is obtained that is suitable for reduction to vanadium metal.
While recovery of vanadium from ferrophosphorus has been
increasing during the 1960's, the greater part of domestic
production continues to come from Western vanadium and
uranium-vanadium ores. Production and consumption data are
given in Tables 14 and 15 of the Appendix.
The long-term trend in vanadium consumption can be best
seen in Figure 2 showing the domestic production of vanadium
pentoxide. During the 20-year period from 1946 to 1966,
production jumped from about 2 thousand to approximately 12
thousand short tons. Domestic mine production of vanadium
during the last 35 years displays a continued growth.
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33
Short tons
(Thousands)
12
10
4
Trend curve
1940 1950 1960 1970 1980
FIGURE 2
Production of Vanadium Pentoxide in the United States
-------
34
As sources less rich in vanadium are increasingly used,
the limitations imposed by the scarcity of the original sources
are removed. This plus the fact that improved recovery methods
are continuously being developed may maintain the upward trend
in vanadium production.
As mentioned earlier, vanadium pentoxide is melted before
its use in alloying. During the smelting process, vapor of
the pentoxide is produced that condenses into a highly dispersed
aerosol. Prior to alloying, the molten pentoxide is reduced in
electric furnaces to vanadium metal. The reduction process is
slow and proceeds from pentoxide to tetroxide, trioxide, oxide,
and finally the metal itself. The volatility of the pentoxide
is high, especially at temperatures above 3,000°F, as used in
alloying processes. Melting of ferrovanadium has been shown
to result in concentrations of the pentoxide in the air of the
working environment as high as 68,000 ug/m3, and concentrations
of lower oxides up to 450 p.g/m3 .
3.2.3 Vanadium-Bearing Alloys
No information on vanadium emissions in the industries
producing vanadium-bearing alloys has been found. Since the
major alloys are ferrovanadium, vanadium-aluminum and vanadium-
carbide, such a study should concentrate on the iron-, steel-,
and aluminum-alloy industries.
3.2.4 Vanadium Chemicals
The chemical industry is producing a great number of
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35
vanadium chemicals, the major ones of which are listed in
Table 16 of the Appendix. The geographical distribution is
given in Table 9 below and Table 20 in the Appendix.
TABLE 9
DISTRIBUTION BY STATE OF 119 INDUSTRIAL UNITS
PRODUCING MAJOR VANADIUM CHEMICALS28
State
New Jersey
New York
Pennsylvania
California
Ohio
Illinois
Texas
Other (six states)
Total
Number
of units
24
21
10
10
8
7
7
21
119
% of total
number
20
18
8
8
7
6
6
17
100
No study has been made of the chemical industry as a
source of vanadium emissions. Nevertheless, the fact that
New York and New Jersey rank first and second (see Table 9)
with respect to vanadium concentration in the environmental
air may be partially explained by the high concentration of
industrial units producing vanadium chemicals.
3.2.5 Other Sources
While steam and power plants using residual oil and oil
refineries are not production sources of vanadium, they are
nevertheless sources of vanadium emissions. Actually, most
-------
36
of the emission data that has been found relate to these
sources.
Vanadium emissions in the environmental air arise from
the combustion of vanadium-bearing oils in plants refining
crude oil and in plants using residual oils to generate heat
and power. In such cases, vanadium is a major component of
the particulate emissions, and its concentration in the air
is often used as an evidence of the presence of fly ash from
oil-fired units. Ranges reported for percentage of combus-
tibles in the fly ash are 50 to 75 and 30 to 40, but in 31
tests in one plant, the observed range of values was 61.1 to
95.2 percent. In a plant using residual oil, vanadium (as
VpOc-) was found to constitute 2.5 percent of the total solids
in particulate emissions—collected in an electrostatic
precipitator—at 230°F from burning PS400 oil. When Grade
4 API oil was used and particulates were collected in a glass
filter sock at 300°F, the concentration of vanadium was 4.7
81
percent.
In a study of the economics of crude oil desulfurization,
it was found that residual oil contained, in the usual process,
500 ppm of metals, the major ones being vanadium and nickel.
How much vanadium is lost to the air during the refining and
desulfurization processes is not known. Yet an idea can be
formed by considering the amounts of crude oil refined per
year and the fact that residual oil content varies from 23 to
500 ppm of vanadium, depending on the origin of the crude oil
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37
used and the type of desulfurization process.
With respect to the total emission of vanadium from
industrial and power plants, it must be noted that until World
War II nearly all of these plants were using coal. Since
World War II and especially during the last 15 years, coal has
been replaced by residual oil, mainly for economy. Neverthe-
less, during the 1960's increasing recovery of gasoline and
light fuel oils from the crude oil resulted in lower quality
and higher cost of residual oils lower quality meaning higher
concentration in the oil of organometallic compounds in general
and of vanadium in particular. The Venezuelan crude, which
amounts to a large portion of the oil consumed on the East
Coast, is noted for its high vanadium content. In 1966, 33
percent of the total imported crude oil and 52 percent of the
total imported residual oil, came from Venezuela; together
they amounted to 342,000 barrels.
Stack emissions of particulates from fuel oil combustion
(at 32°F, 1 atm) vary with the size of the combustion source.
For large sources the extreme range is from 0.005 to 0.205 g/
scf* of stack gas or 0.15 to 6.3 lb/1,000 Ib oil. The usual
range is 0.025 to 0.060 g/scf or 0.82 to 1.8 lb/1,000 Ib oil,
and the average value recommended in emission surveys is
0.033 g/scf of stack gas or 1 lb/1,000 Ib oil. For small
sources (less than 2,500 Ib/hr of oil) the extreme range is
from 0.000 to 0.330 g/scf or 0.00 to 10.0 lb/1,000 Ib oil.
*scf: standard cubic feet.
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38
The usual range is from 0.033 to 0.13 g/scf or 1.00 to 4.0
lb/1,000 Ib oil, and the value recommended for emission
on
surveys is 0.049 g/scf or 1.5 lb/1,000 Ib oil.
After calcining, the total mineral spinel of some
Bessemer, Thomas, and open-hearth slags formed in pig iron
processing was found to contain up to 67 percent vanadium
(as V2O3). During sintering, the mineral spinel oxidizes to
hematite and releases pentavalent vanadium.
3.2-6 Distribution
The Rifle Mine of Union Carbide Corporation started
production in February 1965 and is still the only mine pro-
ducing vanadium as its principal product. The other major
mills that recover vanadium from uranium-vanadium and
vanadium-uranium ores were (1965) operated by the following
54
companies:J^
(1) American Metal Climax, Inc., Grand Junction, Colo.
(2) Mines Development, Inc., Edgement, S. Dak.
(3) Union Carbide Corp., Rifle, Colo.
(4) Vanadium Corporation of America, Shiprock, N. Mex.
In 1965, the following companies recovered vanadium from
ferrophosphorus, a by-product in the production of elemental
phosphorus from Idaho phosphate rock:
(1) Kerr-McGee Corp., Soda Springs, Idaho
(2) Vitro Chemical Co., Salt Lake City, Utah
3.3 Product Sources
The major single use of vanadium is in alloying, partic-
ularly in the production of ferrovanadium, which consumes more
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39
than two-thirds of the vanadium produced. The next major uses
are in the production of chemicals and as a catalyst in indus-
trial processes. The distribution among the various major uses
of the total quantity consumed is shown in Table 10.
_ TABLE 10
VANADIUM CONSUMED IN THE UNITED STATES IN 1966, BY USES
54
Use
Vanadium Percent
Content of Total
(percent) Short Tons Consumption
Steel
High-speed
Hot-work tool
Other tool
Stainless
Other alloya
Carbon
Total steel
Gray and malleable
castings
Nonferrous alloys
Chemicals
Other0
Grand Total
0.1-4
501
99
173
38
2,950
818
4,579
0.1-0.15 40
2.5-85 594
183
85
5,481
9.1
1.8
3.1
0.7
53.9
14.9
83.5
0.7
10.9
3.3
1.6
100.0
alncludes some vanadium used in nonspecified high-speed
tool steels.
^Principally titanium-base alloys.
cPrincipally high-temperature alloys, welding rods, and
cutting and wear-resistant materials.
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40
Various vanadium compounds have been used as driers in
paints and varnishes and in making luster for pottery, porce-
lain, and glass.
Vanadium compounds are basically used as catalysts in
many important industrial processes, as follows:
Production of sulfuric acid
Oxidation of benzene to maleic acid
Oxidation of naphthalene to phthalic anhydride
Oxidation of anthracene to anthraquinone
Oxidation of chlorinated hydrocarbons to maleic and
fumaric acid
Oxidation of acrolein to acrylic acid
Oxidation of toluene or xylene
Oxidation of alkenyl and alkyl derivatives of
pyridine in presence of ammonia
Oxidation of amino acids
Oxidation of cyclohexanal to adipic acid
Oxidation of naphthalene to 1,4-naphthoquinone
Ammonia synthesis
Hydrogenation of carbon monoxide
Dehydration of organic acid to ketones
Dehydrocyclization of paraffins to aromatics such as
hexane to benzene
Dehydrogenation of butanes to butenes
Dehydrogenation of butenes to butadiene
Oxidizing agent in the formation of aniline dyes
Catalyst in petroleum cracking
The amount of vanadium used as a catalyst is still minor
compared with that presently consumed in metallurgy. However,
the number of metallurgical processes using vanadium is
increasing rapidly. For example, in 1956 the new plant of
the Vanadium Corporation of America at Cambridge, Ohio, began
to produce vanadium oxytrichloride for use as a catalyst in
producing ethylene-propylene synthetic rubbers.
Vanadium is also used for photography and ceramics, and
in atomic reactors.
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41
An important development is the use of vanadium pentoxide,
V^Og, as a substitute for platinum (Which is much more expen-
sive) in the manufacture of sulfuric acid by the contact
process. Probably half the world production of sulfuric acid
by this process is now made with vanadium pentoxide as the
catalyst, and it appears probably that it will eventually
replace platinum for this purpose.
No data have been found on vanadium emissions from
industrial units consuming vanadium or vanadium products.
3.4 Environmental Air Concentrations
Measurements of vanadium concentration in the environ-
mental air from 99 sampling stations in the United States
for the period 1954 to 1964 are given in Table 17 of the
2-4
Appendix. In 1964, the average ambient air concentrations
ranged from below detection (<0.003 i_ig/m3 ) to 0.30 |jg/m3 , and
the maximum value recorded was 0.88 (_ig/m3 .
In 1967, the average vanadium concentrations (quarterly
composites) in ambient air ranged from below detection
(<0.003 |ag/m3 ) to 0.90 |j.g/m3 in 149 communities (Table 18).68
Thirty-one of these communities showed concentrations below
the detection concentration. The maximum value recorded in
1967 was 1.4 |ag/m3 . In 1966, the average concentration in
129 communities ranged from below detection to 0.39 |jg/m3
Table 19). The maximum concentration in 1966 was 0.61
l_ig/m3 . The percent distribution of observed concentration
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42
values is shown for 1966 and 1967 in Table 11. Ranking of
the 15 communities with the highest concentration values is
shown in Table 12.
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43
TABLE 11
DISTRIBUTION OF MINIMUM, MAXIMUM, AND AVERAGE VALUES OF
VANADIUM CONCENTRATION IN THE ENVIRONMENTAL AIR OF
SOME COMMUNITIES IN THE UNITED STATES
(Quarterly Composite Values)68
Percent of Concent-ration Values in Each Interval5
1966b 1967C
Concentration Interval
(M-g) Min Max Avq Min Max Avq
X > 1.0000 — — — — 2.0 —
1.0000 > X>0.1000 4.7 15.5 10.9 6.0 15.4 12.8
0.1000 > X>0.0100 24.8 30.2 32.5 26.2 36.9 31.5
0.0100 > X>0.0010 31.7 15.5 17.8 45.7 24.9 34.9
0.0010 > X>0.0001 — _ — 1.3 — —
X < 0.0001 38.8 38.8 38.8 20.8 20.8 20.8
aNurriber of concentration values in each interval as
percent of the total for each category of values (Max, Min,
Avg).
In this year, 129 communities were sampled.
/—i
In this year, 149 communities were sampled.
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44
TABLE 12
RANK ORDERING OF THE 15 COMMUNITIES WITH HIGHEST VANADIUM
CONCENTRATIONS BASED ON AVERAGE, MAXIMUM, AND MINIMUM VALUES, 1967
(Quarterly Composite Values)68
Community
Concentrations
Avq
Max
Min
Avq
Rank
Max
Mm
New York, N.Y.
Paterson, N.J.
New Haven, Conn.
Jersey City, N.J.
Bayonne, N.J.
Perth Amboy, N.J.
Newark, N.J.
Providence, R.I.
Philadelphia, Pa.
Concord, N.H.
Baltimore, Md.
Wilmington, Del.
Washington, D.C.
Hartford, Conn.
Bayamon, P.R.
Scranton, Pa.
Marlton, N.J.
Warminster, Pa.
East Providence, R.I
905
565
490
487
445
390
345
271
264
258
200
190
165
160
132
1.40
1.20
0.74
1.10
0.99
0.86
0.62
0.35
0.43
0.51
0.35
0.24
0.23
0.21
0.31
0.32
0.24
0.24
.34
.14
.10
.18
.22
.092
.16
.076
.076
.072
.13
.13
.10
.11
1
2
2
4
5
6
7
8
9
10
11
12
13
14
15
1
2
6
3
4
5
7
10
9
8
11
14
13
12
14
15
1
2
10
3
2
11
4
12
13
14
6
7
9
8
-062
15
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45
4. ABATEMENT
No information has been found on abatement of air pollu-
tion by vanadium emitted from its production or product sources.
When additives such as magnesium oxide are used in oil-
fired burners, a chain of reaction's occurs resulting in the
reduction in the amount of fine particulates and amounts of
vanadium escaping to the atmosphere. The portion of total
particulates in the less than 10 [a range may be reduced from
60 to 40 percent in the case of high-vanadium content oils.
This is significant, since particulate-size distribution is
an important parameter of abatement efficiency. Centrifugal
collectors are preferred over electrostatic precipitators
because they reduce the difficulties associated with the acid
character of the ash, especially where bag filters and scrub-
bers are used. However, for any given particle-size distribu-
tion, the efficiency of various centrifuges may vary as much
as from 50 to 65 percent and from 70 to 85 percent, around the
particle size range of 5 |a, and 10 |j, respectively -
The use of efficient fly-ash control equipment in modern
coal-fired power plants may considerably reduce the emission
of particulates containing vanadium. The control equipment
most used are cyclones and electrostatic precipitators. When
additives are used, which result in the formation of larger
ash particles, cyclones are more efficient and economical to
use than electrostatic precipitators. The collection efficiency
-------
achieved in two coal-fired power plants using such equipment
is shown in Table 13.
TABLE 13
CONCENTRATIONS OF FLY-ASH AND VANADIUM AT INLETS AND OUTLETS
OF FLY-ASH COLLECTORS USED IN TWO COAL-FIRED POWER PLANTS32
Test Load
No. %
1 100
2 75
lc 100
2 100
3C 100
Fly -Ash Vanadium
Efficiency Ash ( |jg/m3 ) fly-ash
% % Inlet Outlet Inlet
94.0
92.3
82.6
45.4
81.3
UNIT Aa
15.1 8,500,000 460,000 6,180
15.8 8,000,000 180,000 5,150
UNIT Bb
8.8 16,900,000 1,810,000 11,910
8.1 4,600,000 1,150,000 2,290
8.1 14,000,000 1,760,000 7,100
in the
Outlet
230
390
1,580
1,350
1,420
aCorner-fired dry bottom unit rated at 940,000 Ib of steam per
hour at 1,050°F and using a cyclone-type separator followed by an
electrostatic precipitator (in Ohio).
Horizontally opposed fired, wet bottom unit rated at 150,000 Ib
per hour at 835°F and using a cyclone-type separator only (in Illinois)
c
With fly-ash reinfection.
In this study,32 vanadium and 16 other trace metals were
analyzed semiquantitatively by emission spectroscopy, and the
achieved accuracy was estimated as ± 50 percent of the measured
concentration values.
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47
5. ECONOMICS
Little information has been found on the economic costs
of vanadium air pollution or on the costs of its abatement.
One report77 discussed measures taken to reduce the
stack emissions from an oil-fired steam generator. Finely-
ground magnesium oxide is employed as an additive in the fuel
oil. The use of this additive, together with operating the
plant at low excess air, resulted in a significant reduction
in stack emissions plus recovery of boiler pit ash rich in
vanadium pentoxide. The residual oil used contained 250 to
1,000 ppm of vanadium pentoxide, and the boiler ash was found
to contain 32 to 43 percent V-Ocj. In 1965, the unit yielded
120 tons of ash at an average value of $260 per ton. In a
second boiler, an improved additive system yielded concen-
trations of vanadium pentoxide valued at $450 per ton.
In addition to the recovered vanadium, this emission
control system produced increased boiler efficiency and
reliability, reduced maintenance costs, and improved community
relations.
Data on the production and consumption of vanadium are
presented in Section 3 and in the Appendix (Tables 14 and 15).
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48
6. METHODS OF ANALYSIS
6.1 Sampling Methods
At low concentrations of vanadium in air, high volume
samplers are used, which operate during the 24-hour sampling
period 50 cubic feet of air per minute, or 2,200 cubic meters
of air. Preweighed glass-fiber filters (about 10 inches in
diameter) are used. The filters should be equilibrated at a
standard temperature (75° F), or less with relative humidity
of 50 percent or less, and then weighed to determine the
concentration of particulate matter. Afterwards, an aliquot
of the sample is ashed (at 100° C) and then extracted with
nitric and hydrochloric acids. For nonurban samples, extracts
are made that are up to five times more concentrated than
88
those for urban samples.
Kuz'micheva described the following sampling method
for the colorimetric determination of aerosols of vanadium
and its compounds in metallurgical plants. Air samples were
passed through filters of polyvinyl chloride fabric and then
placed in porcelain dishes, treated with 2 ml of a 50 percent
HNO-o solution, and evaporated to dryness. Ashing was done in
a muffle furnace at 500° C, and the residue was treated with
2 ml of a 10 percent NaOH solution which dissolved the
vanadium, leaving iron in the residue.
Membrane ultrafliters (having a pore width of 0.6 to 0.9
37
|~i) were used in a study by Jerman, who used a polarographic
method to determine vanadium concentrations in the air of
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49
alloy and chemical plants.
6.2 Quantitative Methods
6.2.1 Colorimetric Methods
A very simple, inexpensive, and specific method for the
determination of vanadium in air is the ring oven technique.
The relative error is said to be within the range from 5 to
10 percent, which at the microgram level compares well with
other more sophisticated methods. The limit of identification
is 0.01 ng, and its range 0.01 to 3.0 iag. The wavelength
used is 3184&, and the concentration giving 1 percent absorp-
tion is 1.5 MXJ of vanadium per ml.
Two other colorimetric techniques have been recently
described. The first is based on the oxidation of vanadium
and its compounds to vanadium pentoxide and its further
reaction with hydrogen peroxide in acid medium. This method
has a sensitivity of 17.8 \ig of vanadium pentoxide or 10 ug
of vanadium. The second method is based on the development
of a greenish-yellow color when pentavalent vanadium reacts
with sodium tungstate in neutral medium. The method is not
specific and there is interference from alkalies and mineral
acids. Kuz'micheva41 used a method based on the formation
of yellow phosphotungstovanadic acid when vanadium or vanadium
compounds react with phosphoric and sodium tungstate. The
determination was made on a 5-ml aliquot placed in colorimetric
test tubes. The sensitivity was 5 Mg of vanadium pentoxide
in 5 ml. No interference was observed by aluminum, calcium,
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50
silicon dioxide, or iron. Colored chromium compounds were
found to interfere when present in amounts greater than 40 |ag.
In general, colorimetric methods are being replaced by
more sophisticated and sensitive methods.
6.2.2 Atomic Absorption Spectroscopy
Vanadium in the range of 500 to 1,000 p.g per liter can
be determined by atomic absorption spectroscopy in an oxyacety-
lene or nitrous oxide-acetylene flame. For use with oxyacety-
lene flames, vanadium is extracted as vanadium cupferrate into
a mixture of ketone and acid, and the resultant product is
aspirated by the flame. For use with the nitrous oxide-
acetylene flame, an aqueous solution of vanadium is aspirated
74
directly-
6.2.3 Polaroqraphy
Only one paper described a polarographic method for the
determination of vanadium in air. The method described was
designed to be used for determining vanadium in the air of
the working environment in the alloy industry, where vanadium
is used as input, and in chemical manufacture, where vanadium
is used as a catalyst. Dusts in such environments contain
iron, aluminum, and magnesium, but these elements are not
expected to interfere with the test. Following mineralization
of the sample in 45 percent nitric acid, the polarographic
levels of vanadium were recorded from a conductive solution
of borax, ammonia, and chelaton III. The method is said to
•n -7
be sensitive to 1.5 |~tg/ml of vanadium pentoxide.
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51
6.2.4 Emission Spectrography
This method is used by the National Air Sampling
Network for the determination of vanadium concentration in
aliquots obtained from 24-hour samples after ashing and
Extraction. In 1966, improvements in sensitivity made this
method accurate enough for the determination of vanadium in
many nonurban air samples. The minimum detectable concentra-
tion of vanadium by this method is 0.003 ug/m3 for urban
samples and 0.0005 |_ig/m3 for nonurban samples.
6.2.5 Other Methods
Other analytical methods, used mostly for the deter-
53,102
mination of vanadium in biomaterial, are paper chromatography,
*? 1 4.7 "3ft
neutron radioactivation, ' electrophoresis, low-energy
18 85
X-ray mass absorption, and autoradiography.
Determinations of vanadium content have been made in
erythrocytes,95 bones,85 organ tissues, urine, ' 5 and
biomaterial in general. ' ' '
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52
7. SUMMARY AND CONCLUSIONS
Vanadium is toxic to humans and animals—especially its
pentavalent compounds. Exposure of humans through inhalation
of relatively low concentrations (less than 1,000 ug/m3) has
been found to result in inhibition of the synthesis of
cholesterol and other lipids, cysteine, and other amino acids,
and hemoglobin. Low concentrations also act as strong catalysts
on serotinin and adrenaline.
Chronic exposure to environmental air concentrations of
vanadium has been statistically associated with the incidence
of cardiovascular diseases and certain cancers.
Human exposure to high concentrations of vanadium (greater
than 1,000 |J.g/m3 ) results in a variety of clinically observable
adverse effects whose severity increases with increasing
concentrations. These effects include irritation of the
gastrointestinal and respiratory tracts, anorexia, coughing
(from slight to paroxysmal), hemoptysis, destruction of
epithelium in the lungs and kidneys, pneumonia, bronchitis and
bronchopneumonia, tuberculosis, and effects on the nervous
system ranging from melancholia to hysteria.
No information has been found on adverse effects of
atmospheric vanadium concentrations on vegetation or on
commercial or domestic animals.
What is known about the effects of vanadium on materials
related mostly to the corrosive action of vanadium, acting
(together with sulfur dioxide) on oil- and coal-fired boilers,
-------
53
especially those using vanadium-rich residual oils and coals.
The major sources of vanadium emissions are the
metallurgical processes producing vanadium metal and concen-
trates; the alloy industry; the chemical industry; power
plants and utilities using vanadium-rich residual oils and;
to a lesser extent, the coal and oil refining industries.
Vanadium production is concentrated in the states of Colorado,
Utah, Idaho, and New Mexico, while the highest concentration
of industries producing vanadium chemicals is found in New
Jersey and New York. Domestic vanadium consumption has more
than doubled since 1960, and the domestic mine production of
ores and concentrates increased from 1,482 short tons of
vanadium in 1945 to 5,226 short tons in 1965.
In communities in the United States in which vanadium
concentrations were measured, the average values (quarterly
composites) ranged from below detection (0.003 ug/m3) to
0.30(1964), 0.39(1966), and 0.90 (1967) ug/m3.
Little information is available on the economic losses
due to vanadium air pollution or on the costs of abatement.
One report indicated that measures taken to reduce the loss
of vanadium to the atmosphere from an oil-fired steam generator
resulted in recovery of commercially valuable vanadium
pentoxide, thereby producing a profit from air pollution
abatement. No other information was noted in the literature
on control procedures specifically intended to reduce air
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54
pollution by vanadium. However, customary methods used to
control particulate emissions in general are considered
suitable to the industrial processes using vanadium or
vanadium-containing fuels.
Methods of quantitative analysis of vanadium in the
environmental air include colorimetry, atomic absorption
spectroscopy, emission spectrography, and recently polar-
ography. The trend is toward more use of spectrographic
and spectrophotometric methods, some of which are more
sensitive than the other methods and easily automated.
Sensitivites on the order of 0.001 [ag/m3 are reported.
Based on the material presented in this report, further
study is suggested in the following areas:
(1) Determination of the relationships of low concentra-
tions of vanadium in various oxidation states with enzyme
inhibition, cardiovascular disease, and cancer.
(2) Determination of the concentration and valence of
vanadium near oil and coal burning industries (especially
those burning vanadium-rich oil), and the vanadium metallurgi-
cal and chemical industries.
(3) Evaluation of the abatement and economics of vanadium
air pollution control.
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55
REFERENCES
1. Abernethy. R. F., et al. , Rare Elements in Coal, U.S. Bur.
Mines Inform. Circ. 8163 (1963).
2. Air Pollution Measurements of the National Air Pollution
Network, U.S. Dept. of Health, Education, and Welfare,
Public Health Service, Cincinnati, Ohio (1958). Analysis
of Suspended Particulates, 1953-1957.
3. Air Quality Data, 1962, National Air Sampling Network, U.S.
Dept. of Health, Education, and Welfare, Public Health
Service, Cincinnati, Ohio.
4. Air Quality Data, 1964-65, National Air Sampling Network,
U.S. Dept. of Health, Education, and Welfare, Public Health
Service, Cincinnati, Ohio (1966).
5. Air Quality Data, 1966, National Air Sampling Network, U.S.
Dept. of Health, Education, and Welfare, Public Health
Service, Cincinnati, Ohio (1968).
6. Aiyar, A. S., et al., Effect of Vanadium Administration on
Coenzyme Q Metabolism in Rats, Proc. Soc. Exp. Biol. Med.
107:914 (1961).
7. Anbar, M., et al., Effect of Pyridoxal 5-Phosphate in the
Presence of Vanadyl Ions on the De-Iodination of Thyroxine,
Nature 196:1213 (1962).
8. Azarnoff, D. L., et al., A Specific Site of Vanadium Inhibi-
tion of Cholesterol Biosynthesis, Biochim. Biophys. Acta 51;
397 (1961).
9. Berg, L. R. , Effect of Diet Composition on Vanadium Toxicity
for the Chick, Poultry Sci. 45:1346 (1968).
10. Bergel, F., et al., A Model System for Cystein Desulphydrase
Action: Pyridoxal Phosphate—Vanadium, Nature 181(4624) ;1654
(1958).
11. Bernheim, F., et al., Action of Vanadium on Tissue Oxidation,
Science 88:481 (1938).
12. Bernheim, F., et al., Action of Vanadium on Oxidation of
Phospholipids by Certain Tissues, J. Biol. Chem. 127:353 (1939)
13. Blankenhorn, D. H., Management of Hypercholesterolaemia, GP
29.:135-42 (1964).
13a. Bowan, H. J. M., Trace Elements in Biochemistry (London:
Academic Press, 1966).
-------
56
14. Braun, H. A., et al. , Vanadium Inhibition of Cholesterol
Synthesis (Review), Nutr. Rev. 17(8):231 (1959).
15. Browning, E., Toxicity of Industrial Metals (London:
Butt erwo rth, 1961).
16. Burdock, J. L., Fly Ash Collection from Oil-Fired Boilers,
Paper presented at the 10th meeting of the New England Air
Pollution Control Association, Hartford, Connecticut (1966).
17. Bush, P. M., Vanadium—A Materials Survey, U.S. Bur. Mines
Inform. Circ. 8060 (1961).
18. Carter, R. W., et al., Low Energy X-Ray Mass Absorption Co-
efficients from 1.49 to 15.77 keV for Scandium, Titanium,
Vanadium, Iron, Cobalt, Nickel, and Zinc, Health Phys. 13;
593 (1967).
19. Chemical Week, Part Two: 1969 Buyer's Guide Issue—Chemicals,
p. 451, July 26, 1969.
20. Comar, C. L., et al., Mineral Metabolism (New York: Academic
Press, 1962).
21. Comar, D., et al., Concentration of Vanadium in the Rat and
Its Influence on Cholesterol Synthesis. Studies by the
Technic of Neutron Radioactivation and the Method of Isotopic
Equilibrium, Text in French, Bull. Soc. Chim. Biol. 49:
1357 (1967).
21a. Cortelyou, C. G., et_ al_. , A New Look at Disulfurization
Chem. Eng. Proqr. 64(1):53 (1968).
22. Costello, R. L., et al., Effect of Metavanadate Ion on the
Growth in Vitro of Mycobacterium Tuberculosis, J. Bacteriol.
T7_(6) :794 (1959).
23. Curran, G. L., Effect of Certain Transition Elements on
Hepatic Synthesis of Cholesterol in the Rat, J. Biol. Chem.
210 (2): 765 (1954).
24. Curran, G. L., et al., Reduction of Excess Cholesterol in
the Rabbit Aorta by Inhibition of Endogenous Cholesterol
Synthesis, J. EXP. Med. 103(1);49 (1956).
25. Cuthbertson, W. F. J., Proc. Nutr. Soc. 16:70 (1957).
26. Daniel, E. P-, Experimental Vanadium Poisoning in White
Rat, Public Health Repts. (U.S.) 53:765 (1938).
27. Dimond, E. G., et al., Vanadium: excretion, toxicity, lipid
effect in man, Amer. J. Clin. Nutr. 12:49-53 (1963).
-------
57
28. Directory of Chemical Producers (Menlo Park, Calif.:
Stanford Research Institute, 1968).
29. Button, W. P., Vanadiumism, J. Am. Med. Assoc. 46;1648
(1911).
30. Eriksen, N., et al.. The Precipitation of Serum Protein by
Acidified Sodium Orthovanadate in Neoplastic and Other
Diseases, Cancer Res-. 14(2):145 (1954).
31. Garcia-Blanco, J., et al., Differentiation of Various
Natural Amino Acids by Their Capacity of Reduction of
Vanadic Acid in Vanadic Salt, Text in Spanish, Rev. Espan.
Fisiol. 11(2);149 (1955).
32. Gerstle, R. W., et al., Air Pollutant Emissions from Coal-
Fired Power Plants: Report No. 2, J. Air Pollution Control
Assoc. 15(2);59 (1965).
33. Grippando, G., et al., Studies on Vanadium and Experimental
Caries. 1. Review and Comments on Data from the Literature,
Text in Italian, Ann. Stomat. (Roma) L5_:87 (1966).
34. Handbook of Chemistry and Physics, 41st ed. (Cleveland:
Chemical Rubber Publishing Co., 1960).
35. Hickey, J. R. , et al., Relationship Between Air Pollution
and Certain Chronic Disease Death Rates—Multivariate Sta-
tistical Studies, Arch Environ. Health 15(6):728 (1967).
36. Hickling, S., Vanadium Poisoning, N. Zealand M. J. (Welling-
ton), 51(322):607 (1958).
37. Jerman, L. von, et al._, Polarographische Bestimmung von
Vanadin in der Luft von Arbeitsraumen, Zeit. Hyg. (Berlin)
14_(1):12 (1968).
38. Kaser, .M. M. , et al. , The Separation and Identification of
Vanilmandelic Acid and Related Compounds by Electrophoresis
on Cellulose Acetate, J. Chromatoq. 29:378 (1967).
39. Kharauzov, N. A., Data on the Effect of Pharmacological
Agents on Cholesterol Metabolism and the Content of Lecithin
in the Blood (on Pharmacotherapy of Arteriosclerosis),
Text in Russian, Vestn. Akad. Med. Nauk USSR 16(11):40 (1961)
40. Kleinrok, Z., et al., The Influence of Vanadyl Sulfate on
Hypercholesterinemia Following a Single Injection of Choles-
terin, Text in Russian, Biul. Eksp. Biol. Med. 61:82 (1966).
-------
58
41. Kuz'micheva, M. N., The Determination of Vanadium in Air,
Text in Russian, Gigiena i Sanit. 3.1;229 (1966).
42. Kuz'micheva, M. N. , Determination of Vanadium in Biologic
Materials, Text in Russian, Gigiena i Sanit. 31;70 (1966).
43. Lewis, C. E., The Biological Actions of Vanadium. I. Effects
upon Serum Cholesterol Levels in Man, A.M.A. Arch. Ind.
Health 19 (5)-.419 (1959).
44. Lewis, G. E., The Biological Actions of Vanadium. III. The
Effect of Vanadium on the Excretion of 5-Hydroxyindolacetic
Acid and Amino Acids and the Electrocardiogram of the Dog,
A.M.A. Arch. Ind. Health 20:455 (1959).
45. Lisunkin, I., Acetycholine Metabolism in the Rat Brain
Following the Combined Action of Vanadyl Sulphate and Some
Phenylacetic Acid Derivatives, Text in Russian, Biul. Eksp.
Biol. Med. 57;80 (1964).
46. Lisunkin, I., Combined Effects of Vanadium and Some Phenyl-
acetic Acid Derivatives on the Acetylating Capacity of the
Liver in Rats, Text in Russian, Farmakol; Toksikol 28;450
(1965).
47. Livingston, H. D., et al., Estimation of Vanadium in Biolo-
gical Material by Neutron Activation Analysis, Anal. Chem.
.3_7:1285 (1965).
48. Martin, G. M., et al., Vanadium Catalysis of the Oxidation
of Catecholamines Dihydroxyphenylalanine and 5-Hydroxyindoles,
Nature 186;884 (1960).
49. Mascitelli-Coriandoli, E., et al., Effects of Vanadium upon
Liver Coenzyme A in Rats, Nature 183(4674);1527 (1959).
50. Mascitelli-Coriandoli, E., et al., Intracellular Thioctic
Acid and Coenzyme A Following Vanadium Treatment, Nature
1J34_( Suppl. 21):1641 (1959).
51. McTurk, L. C., et al., Health Hazards of Vanadium-Containing
Residual Oil Ash, Ind. Med. Surg. 25(1);29 (1956).
52. The Merck Index (Rahway, N.J.i Merck, 1968).
53. Miketukova, V., Detection of Metals on Paper Chromatograms
with Rhodamine B, J. Chromatoq. 24_:302 (1966).
54. Minerals Yearbook, Bureau of Mines, U.S. Govt. Printing
Office, Washington, D. C. (1950-1967).
-------
59
55. Mitchell, Comparative Nutrition of Man and Domestic
Animals (New York: Academic Press, 1962).
56. Molfino, P., Occupational Poisoning; Experimental Study,
Text in Italian, Rass. Med. Appl. Lavoro Ind. 9:362 (1938).
57. Monier, Williams, G. W. , Trace Elements in Food (New York:
Wiley, 1949).
58. Mountain, J. T., Detecting Hypersusceptibility to Toxic
Substances, Arch. Environ. Heajlth 6:537 (1963).
59. Mountain, J. T., et al., Studies in Vanadium Toxicology;
Reduction in the Cystine Content of Rat Hair, A.M.A. Arch.
Ind. Hycr. Occupational Med. 8(4):406 (1953).
60. Mountain, J. T. et al., Studies in Vanadium Toxicology.
III. Fingernail Cystine as an Early Indicator of Metabolic
Changes in Vanadium Workers, A.M.A. Arch. Ind. Health 12(5):
494 (1955).
61. Mountain, J. T., et al., Effect of Ingested Vanadium on
Cholesterol and Phospholipid Metabolism in the Rabbit,
Proc. Soc. Exptl. Biol. 92(3) :582 (1956).
62. Nicholas, D. J., et al., Effects of Cultural Conditions
on Nitrate Reductase in Photobacterium Sepia, J. Gen.
Microbiol. 35;401 (1964).
63. Pham-huu-Chanh, Comparative Action of Sodium Chromate,
Molybdate, Tungstate and Metavanadate on the Enzymatic
Action of Tyrosinase, Text in French, Agressoloqie _5_:3179
(1964).
64. Pham-huu-Chanh, Comparative Action of Sodium Chromate,
Molybdate, Tungstate and Metavanadate on Xanthine Dehydrase,
Text in French, Med. Exptl. 11:38 (1964).
65. Pham-huu Chanh, Comparative Action of Sodium Chromate,
Molybdate, Tungstate, and Metavanadate on Pseudocholines-
terase, Text in French, Agressologie 7:161 (1966).
66. Pham-huu-Chanh, et al., Comparative Toxicity of Sodium
Chromate, Molybdate, Tungstate and Metavanadate. 3. Tests
on Cats, Agressologie 8:51 (1967).
67. Proescher, F., et al., A Contribution to the Action of
Vanadium with Particular Reference to Syphilis, Am. J._
Syphilis 1:347 (1917).
-------
60
68. 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.
69. Rifkin, R. J., In Vitro Inhibition of Na+-K and Mg2+ ATPases
by Mono, Di and Trivalent Cations, Proc. Soc. Exptl. Biol.
Med. 120:802 (1965)..
70. Rockhold, L. W. , et al. , Vanadium Concentration of Urine;
Rapid Colorimetric Method for Its Estimation, Clin. Chem.
2.(3):188 (1956).
71. Roshchin, I. V., Hygienic Nature of Industrial Aerosol of
Vanadium, Text in Russian, Gigiena i Sanit. 11:49 (1952).
72. Roshchin, I. V., Hygienic Evaluation of Dust from Vanadium
Containing Slag, Gigiena i Sanit. 2j3:23 (1963).
73. Roshchin, I. V., Toxicology of Vanadium Compounds Used in
Modern Industry, Gigiena i Sanit. 32(4-6) (1967).
74. Sachdev, S. L., et al., Determination of Vanadium by Atomic
Absorption Spectrophotometry, Anal. Chim. Acta 37:12 (1967),
75. Sartosova, Z,, Determination of Vanadium in Urine, Text in
Czech, Pracovni Lekar 11:518 (1959).
76. Schroeder, H. A., et al., Abnormal Trace Metals in Man—
Vanadium, J. Chronic Diseases 16:1047 (1963).
77- Severs, B. C., The ABC's of Fireside Corrosion, Proc. Am.
Power Conf. 27:864 (1965).
78. Sjoberg, S. G., Vanadium Bronchitis after Cleaning of Oil
Burning Steam Boilers, Text in Swedish, Nord. Hyg. Tidskr.
3-4:45 (1954).
79. Sjoberg, S. G., Vanadium Dust, Chronic Bronchitis and
Possible Risk of Emphysema: A Follow-up Investigation of
Workers at a Vanadium Factory, Text in Swedish, Acta Med.
Scand. 154(5):381 (1956).
80. Sjoberg, S. G., et al., Skin-, Eye-, and Respiratory Tract-
Symptoms Associated with Cleaning of Oil-Fired Boilers; An
Investigation with Special Reference to Vanadium in Blood
and Urine, Text in Swedish, Nord. Hyg. Tidskr. 37(9-10);
229 (1956).
-------
61
81. Smith, W. S. , Atmospheric Emissions from Fuel Oil Combus-
tion, U.S. Public Health Serv. Publ. 999-AP-2 (1962).
82. Snyder, F., et al., Vanadium Inhibition of Phospolipid
Synthesis and Sulphydryl Activity in the Rat Liver, Nature
JL82.(4633):462 (1958).
83. Sollmann, T., A Manual of Pharmacology (Philadelphia:
Saunders, 1957).
84. Somerville, J., et al., Effect of Vanadium on Serum Choles-
terol, Am. Heart J. 64;54 (1962).
85. Soremark, R. et al., Autoradiographic Localization of
V-48-Labeled Vanadium Pentoxide (V2Os) in Developing Teeth
and Bones in Rats, Acta Odontol. Scand. 20;225 (1962).
86. Spector, W. S. , Handbook of Toxicology (Philadelphia:
Saunders, 1956).
87. Stephan, J., et al., Spectrographic Demonstration of
Vanadium in Some Human and Animal Organs and Alteration of
Its Presence, Text in German, Med. Exptl. 4;397 (1961).
88. Stern, A. C. (Ed.), Air Pollution, vol. II (New York:
Academic Press, 1968).
89. Stocks, P., On the Relation Between Atmospheric Pollution
in Urban and Rural Localities and Mortality from Cancer,
Bronchitis and Pneumonia, with Particular Reference to 3,
4 Benzopyrene, Beryllium, Molybdenum, Vanadium and Arsenic,
Brit. J. Cancer 14:397 (1960).
90. Stokinger, H. E., Organic Beryllium and Vanadium Dusts,
A.M.A. Arch. Ind. Health 12:675 (1955).
91. Stokinger, H. E., "Vanadium", in Industrial Hygiene and
Toxicology, F. A. Patty Ed. (New York: Interscience Pub-
lishers, 1963).
92. Tank, G., et al., Vanadium Inhibition of Cholesterol Syn-
thesis in Man, Nutr. Rev. 18:39 (1960).
93. Tempestini, O., et al., The Combined Action of Vanadium
and Fluorine in Experimental Caries in the White Rat,
Panminerva Med. 2:344 (1960).
94. Thomas, D. L. G., et al., Vanadium Poisoning in Industry,
Med. J. Australia 1(15);607 (1956).
-------
62
95. Valberg, L. S., et al., Detection of Vanadium in Normal
Human Erythrocytes, Life Sci. 3:1263 (1964).
96. Vintinner, F. J., et al., Study of the Health of Workers
Employed in Mining and Processing of Vanadium Ore, A.M.A.
Arch. Ind. Health 12J6):635 (1955).
97. Watanabe, H., et al., Some Clinical Findings on Vanadium
Workers, Japan. J. Ind. Health (Kawasaki) J3(7):23 (1966).
98. Williams, N., Vanadium Poisoning from Cleaning Oil-Fired
Boilers, Brit. J. Ind. Med. 9(1);50 (1952).
99. Wolski, A. A., et al., Proc. Am. Petrol. Inst. 40:423 (1960).
100. Wright, L. D., et al., The Site of Vanadyl Inhibition of
Cholesterol Biosynthesis in Liver Homogenates, Biochem.
Biophys. Res. Commun. 3:264 (1960).
101. Wyers, H., Some Toxic Effects of Vanadium Pentoxide, Brit.
J. Ind. Med. 3:177 (1946).
102. Yamakawa, K., et al., Organometallic Compounds. II. Gas
Chromatography of Metal Acetylacetonates, Chem. Pharm.
Bull. (Tokyo) ]J^:1405 (1963).
103. Zenz, C., et al., Acute Vanadium Pentoxide Intoxication,
Arch. Environ. Health 5:542 (1962).
104. Zenz, C., et al., Human Responses to Controlled Vanadium
Pentoxide Exposure, Arch. Environ. Health, 14:709 (1967).
-------
APPENDIX
-------
64
& Titaniferous magnetite
-o Nontitaniferous magnetite
X Titaniferous magnetite sands
o Sedimentary iron
^ Vanadiferous phosphates
Q V-bearing hydrothermal veins
n Uranium sandstones and limestones
A Vanadate ores
FIGURE 3
Productive and Potential Vanadium Sources by Type
17
14
12
o Less than 1 million pounds vanadium
or unknown, but probably small
® 1 10 million pounds vanadium
© 10 - 100 million pounds vanadium
• More than 100 million pounds vanadium
o Large deposits with very low vanadium
content or deposits of unknown size
with high vanadium content
1 Colorado Plateau
2 Black Hills, S.Dak. and Wyo.
3 Mammoth, Ariz.
4 San Bernardino Co., Calif.
5 Goodsprings, Nev.
6 Cutter, N.Mex.
7 Magdalena, N.Mex.
8 Phosphate deposits, Idaho
9 Vanadiferous shales, Idaho and Wyo.
10 Lake Sanford, N.Y.
11 Iron Mountain, Wyo.
12 Iron Mine Hill, R.I.
13 Duluth gabbro deposits, Minn.
14 Los Angeles Co., Calif.
15 Colorado, Caribou and Iron Mountain
16 Western North Carolina
17 Curry County, Oreg.
18 New Jersey deposits
19 Camp Floyd district, Utah
20 Alabama flake graphite
21 Colorado Front Range
FIGURE 4
Productive and Potential Vanadium Sources by Deposits and Districts17
-------
65
'(\~^-''.^'L— w T ° M' ' N 7^~-
[ -'V>'T1-4
^ —1 J A I
I" IT A /H
r— ~^-:,
^ J*v
^J7q i " r
0 R A
f
--' -- -^ --------- J o i_«__5Naturi"t^'_._i
/ • ' • 1^1
"
/
Monticello, |1 . »Placerville
,llle-,_
^"^--i ! i' !" j|
y !--<—!,—-L_X
/^ Durango x. i
A R" I Z
. ^Shiprock
L—-t-L-^
0 Nl A ! NEW M|E X I C',0
100 Miles i |
_J I '
A Vanadium deposits with a little uranium
• Uranium deposits yielding co-product vanadium
° Uranium deposits with little or no vanadium
6 Production units of vanadium concentrates
FIGURE 5
Principal Areas of Vanadium and Uranium Mining and the Seven
Major Production Units of Vanadium Concentrates
17
-------
66
Ore
Dry Grind
-10 to-14 mesh
-> Salt roast
I
'"I
Water leach
Tails Liquor
L
Acid leach
I I
Tails Uranium-vanadium-bearing liquor
Sludge
— i
T
i --- Vanadium-bearing liquor
Neutralization
and filtration
Waste Uranium-vanadium sludge
liquor
i
Sludge digestion
& vanadium precipitation
Ferric
vanadate
Impure uranium liquor
Alumina precipitation
I
Waste
sludge
r
i
Uranium precipitation
> l i
' li
Waste
liquor
Uranium drying
and packaging
Conditioning
& acid leach
i
i
t
CCD thickeners
I i
Tails |
i +
I Liquor
I Eluant
Ion exchange
columns
I I
I I
I I
I
rj
i
i
i
i
i
Uranium eluate
Concentrate to Atomic Energy Commission
FIGURE 6
:hing and Ion Exchange Process
-------
67
Solutions from
uranium ion exchange
I
Solutions from
uranium solvent extraction
Metallic Fe
h Vanadium & iron
reduction
I
Stripped organic solvent
storage tank
Vanadium extraction
Mixer-settler extraction units
Solvent cleanup
, step, mixer-settler.
extraction units
Na2CO3
Waste liquor
u
Barren liquor to waste
Vanadium-loaded
organic solvent
Stripped organic
solvent Vanadium stripping
NH,
NaCIO,
Mixer-settler extraction units
-10%H2 SO 4
storage tank
Vanadium-bearing
acid liquor
Vanadium precipitation .4-
Heat
Slurry
Vanadium filtration & fusion
Vanadium packaging
To sales
Waste
liquor
FIGURE 7
Vanadium-Uranium Recovery by Solvent Extraction
17
-------
68
Milk of lime
Soda ash
Milk of
lime
Phosphato-vanadic acid
Stream
Primary purification (1st step)
Primary purification (2nd step)
r
Primary purification (3rd step)
Pulp
Filtration and washing
4
Sulfuric acid
(if needed)
Residue low
in vanadium
Phosphoric
acid plant ,,
Filtrate
Wash water
Milk of lime
i - ,.
'
Sulfuric acid
(if needed)
Secondary purification
Pulp
Filtration or settlement
4 4
Residue or sludge Filtrate
high in vanadium I
Vj 05 precipitation
FIGURE 8
Recovery of Vanadium from Phosphate Rock
17
-------
69
Ore
Dry grind
I
-10 to -14 mesh
1
Salt roast ( 835°C)
A
Uraniu
vanadium
w nui buuium
1
Tails
I
Acid leach
I |
1 1
Liquor Tails
Carbonate
neutralization
m and ^ v
liquor Sludge
uaroonaie leacn
1
Liquor
1
Carnotite
precipitation
Filtrate
•\ '
Vanadium
recovery
C l-c
|
Salt, sawdust
and
carbonate added
i
Fusion
^ '
Uranium
concentrate
FIGURE 9
Sodium Carbonate and Acid Leach Method
of Vanadium-Uranium Recovery!?
-------
70
APPENDIX
TABLE 14
VANADIUM AND RECOVERABLE VANADIUM IN ORE AND CONCENTRATE
PRODUCED IN THE UNITED STATES, 1930-196554
(Short Tons of Contained Vanadium)
Year
Ore and Concentrate3
Recoverable Vanadium"
1930
1931
1932
1933
1934
1935
1936
1937
1938
1939
1940
1941
1942
1943
1944
1945
1946
1947
1948
1949
1950
1951
1952
1953
1954
1955
1956
1957
1958
1959
1960
1961
1962
1963
1964
1965
c
c
270.
2
6d
25d
70
543
807
992
1,081
1,257
2,220
2,793
1,764
1,482
636
1,059
894
1,580
2,298
3,040
3,588
4,643
4,930
4,983
5,635
7,294
7,266
7,392
8,800
5,343
5,221
3,862
4,362
5,226
c
c
c
c
c
c
c
c
c
c
c
c
c
c
c
c
510
821
670
1,188
1,598
2,126
2,571
3,057
3,026
3,286
3,868
3,691
3,030
3,719
4,971
5,817
4,750
3,897
5,049
6,160
aMeasured by receipts, at mills.
^Recoverable vanadium represents the vanadium that can
be recovered from ores produced but not necessarily processed
and is based upon the general recovery rate for mills produ-
cing vanadium pentoxide during a specific year.
GData not available.
dCarnotite ores only.
-------
71
APPENDIX
TABLE 15
VANADIUM CONSUMED IN THE UNITED STATES54
Year
1965
1964
1963
1962
1961
1960
1959
1958
1957
1956
*
1955
Short Tons
4,708
3,550
2,906
2,314
2,015
2,016
1,891
1,259
1,790
1,988
1,700
*First year data became
available.
-------
72
APPENDIX
TABLE 16
1 Q
PRODUCERS OF VANADIUM CHEMICALS^
Vanadium Acetylacetonate
Aceto Chemical Co. Inc., Flushing, N.Y.
Atomergic Chemetals Co. Div- Gallard-Schlesinger
Chemical Mfg. Corp, Carle Place, Long Island, N.Y.
Dynamit Nobel Sales Corp., Hackensack, N.J.
MacKenzie Chemical Works, Inc., Central Islip, N.Y.
Shepherd Chemical Co., Cincinnati, Ohio
Stauffer Chemical Co., Speciality Chemical Div.,
New York, N.Y.
Akron, Ohio
Chicago, 111.
Houston, Tex.
Los Angeles, Calif.
Wilmington, Del.
Troy Chemical Corp., Newark, N.J.
Var-Lac-Oid Chemical Co., Elizabeth, N.J.
Vanadium Carbide
Atlantic Equipment Engineers, Bergenfield, N.J.
Atomergic Chemetals, Carle Place, Long Island, N.Y.
Bram Metallurgical Chemical Co., Philadelphia, Pa.
Cerac, Inc., Butler, Wis.
Electronic Space Products, Inc., Los Angeles, Calif.
Var-Lac-Oid Chemical Co., Elizabeth, N.J.
Vanadium Dichloride
Atlantic Equipment Engineers, Bergenfield, N.J.
Atomergic Chemetals, Carle Place, Long Island, N.Y.
Foote Mineral Co., Exton, Pa.
Rocky Mountain Research, Inc., Denver, Colo.
Var-Lac-Oid Chemical Co., Elizabeth, N.J.
Vanadium (Metal)
Atlantic Equipment Engineers, Bergenfield, N.J.
Atomergic Chemetals, Carle Place, Long Island, N.Y.
Belmont Smelting and Refining Works, Inc., Brooklyn, N.Y.
Bram Metallurgical Chemical Co., Philadelphia, Pa.
Cerac, Inc., Butler, Wis.
Electronic Space Products, Inc., Los Angeles, Calif.
Foote Mineral Co., Exton, Pa.
Reading Alloys, Inc., Robesonia, Pa.
Union Carbide, Mining & Metals, Div. Birmingham, Ala.
Chicago, 111.
Cleveland, Ohio
Detroit, Mich.
Houston, Tex.
Los Angeles, Calif.
Phillipsburg, N.J.
Pittsburgh, Pa.
Portland, Oreg.
(continued)
-------
73
APPENDIX
TABLE 16 (Continued)
PRODUCERS OF VANADIUM CHEMICALS
Vanadium (Metal)(cont.)
United Mineral & Chemical Corp., New York, N.Y.
Var-Lac-Oid Chemical Co., Elizabeth, N.J.
Vanadium Oxytrichloride
Alfa Inorganics, Inc., Beverly. Mass.
Atomergic Chemetals, Ca'rle Place, Long Island, N.Y.
Foote Mineral Co., Exton, Pa.
Stauffer Chemical Co.,
Specialty Chemical Div., Akron, Ohio
Chicago, 111.
Houston, Tex.
Los Angeles, Calif.
Wilmington, Del.
Union Carbide, Mining & Metals Div., Birmingham, Ala.
Chicago, 111.
Cleveland, Ohio
Detroit, Mich.
Houston, Tex.
Los Angeles, Calif.
Phillipsburg, N.J.
Pittsburgh, Pa.
Portland, Oreg.
Var-Lac-Oid Chemical Co., Elizabeth, N.J.
Vanadium Pentoxide (Vanadic Acid Anhyd.ride)
Atlantic Equipment Engineers, Bergenfield, N.J.
Cerac, Inc., Butler, Wis.
Electronic Space Products, Inc., Los Angeles, Calif.
Foote Mineral Co., Exton, Pa.
Union Carbide, Mining & Metals Div., Birmingham, Ala.
Chicago, 111.
Cleveland, Ohio
Detroit, Mich.
Houston, Tex.
Los Angeles, Calif.
Phillipsburg, N.J.
Pittsburgh, Pa.
Portland, Oreg.
United Mineral & Chemical Corp., New York, N.Y.
Var-Lac-Oil Chemical Co., Elizabeth, N.J.
Vanadium Sulfate (Vanadyl Sulfate)
Atlantic Equipment Engineers, Bergenfield, N.J.
Atomergic Chemetals, Carle Place, Long Island, N.Y.
City Chemical Corp., New York, N.Y.
(continued)
-------
74
APPENDIX
TABLE 16 (Continued)
PRODUCERS OF VANADIUM CHEMICALS
Vanadium Sulfate (Vanadyl Sulfate)(Cont.)
Stauffer Chemical Co.,
Specialty Chemical Div., Akron, Ohio
Chicago, 111.
Houston, Tex.
Los Angeles, Calif.
Wilmington, Del.
Var-Lac-Oid Chemical Co., Elizabeth, N.J.
Vanadium Tetrachloride
Atomergic Chemetals, Carle Place, Long Island, N.Y.
Dynamit Nobel Sales Corp., Hackensack, N.J.
Foote Mineral Co., Exton, Pa.
D.F. Goldsmith Chemical & Metal Corp., Evanston, 111.
Stauffer Chemical Co.,
Specialty Chemical Div., Akron, Ohio
Chicago, 111.
Houston, Tex.
Los Angeles, Calif.
Wilmington, Del.
Union Carbide, Mining & Metals Div-,
Birmingham, Ala.
Chicago, 111.
Cleveland, Ohio
Detroit, Mich.
Houston, Tex.
Los Angeles, Calif.
Phillipsburg, N.J.
Pittsburgh, Pa.
Portland, Oreg.
Var-Lac-Oid-Chemical Co., Elizabeth, N.J.
Vanadium Tetroxide
Atomergic Chemetals, Carle Place, Long Island, N.Y.
City Chemical Corp., New York, N.Y.
Rocky Mountain Research, Inc., Denver, Colo.
Var-Lac-Oid Chemical Co., Elizabeth, N.J.
Vanadyl Acetate
Atomergic Chemetals, Carle Place, Long Island, N.Y.
City Chemical Corp., New York, N.Y.
Var-Lac-Oid Chemical Co., Elizabeth, N.J.
Vanadyl Acetonate
Troy Chemical Corp., Newark, N.J.
Vanadyl Oxalate
Atomergic Chemetals, Carle Place, Long Island, N.Y.
City Chemical Corp., New York, N.Y.
Rocky Mountain Research, Inc., Denver, Colo.
Var-Lac-Oid Chemical Co., Elizabeth, N.J.
(continued)
-------
75
APPENDIX
TABLE 16 (Continued)
PRODUCERS OF VANADIUM CHEMICALS
Vanadyl Sulfate
Atomergic Chemetals, Carle Place, Long Island, N.Y.
Chemical Commerce, Newark, N.J.
Var-Lac-Oid Chemical Co., Elizabeth, N.J.
-------
APPENDIX
TABLE 17
2-4
CONCENTRATION OF VANADIUM IN THE AIR
(Values of Individual Samples in |-ig/m3)
Location
Alabama
Birmingham
Alaska
Anchorage
Arizona
Phoenix
Tucson
California
Los Angeles
Berkeley
Pasadena
San Bernadiono
San Francisco
San Jose
San Leandro
Colorado
Denver
Connecticut
Waterbury
District of Columbia
Washington
Deleware
Wilmington
Florida
Tampa
Georgia
Atlanta
1954-59a
Max
.63
1.1
.30
.70
.20
.14
.30
.07
3.0
2.0
.94
3.8
Avq
.06
.10
.04
.07
.03
.03
.05
.03
.88
.33
.06
.22
1960
Max
.03
.01
.13
2.5
Avq
.01
.00
.02
.56
1961
Max
.10
Avq
.02
1962
Max
.01
.13
.08
.02
.35
Avq
.00
.03
.01
.00
.12
1963
Max
*
.05
.03
.08
.04
.28
.08
.04
Avq
.01
.01
.01
.00
.10
.03
.00
1964
Max
.01
.01
.00
.26
Avq
.00
.00
.00
.09
(continued)
-------
APPENDIX
TABLE 17 (Continued)
CONCENTRATION OF VANADIUM IN THE AIR
(Values of Individual Samples in |ag/m3)
Location
Illinois
Chicago
Cicero
East St. Louis
Indiana
East Chicago
Indianapolis
Gary
Hammond
Iowa
Des Moines
Kentucky
Louisville
Louisiana
New Orleans
Maryland
Baltimore
Massachusetts
Boston
Everett
Michigan
Detroit
Minnesota
Minneapolis
Missouri
St. Louis
Kansas City
Nebraska
Omaha
1954-59a
Max
.90
.07
1.4
.25
.08
4.3
3.0
3.0
2.10
.30
.20
.40
Avq
.09
.02
.18
.04
.01
1.3
.96
.86
.28
.05
.04
.06
1960
Max
.21
.01
Avq
.07
.00
1961
Max
•t_
.54b
ft
.05°
.01
Avq
.14b
ft
.02
.00
1962
Max
.06
.01
.04
.05
1.0
.02
.04
Avq
.02
.00
.02
.13
.01
.01
1963
Max
.17
.02
•
.08
.04
.03
.04
Avq
.05
.01
.02
.01
.01
.01
1964
Max
.08
.21
.01
.01
.65
.45
.02
.03
.02
Avq
.03
.04
.00
.00
.16
.21
.01
.01
.00
(continued)
-------
APPENDIX
TABLE 17 (Continued)
CONCENTRATION OF VANADIUM IN THE AIR
(Values of Individual Samples in |ag/m3 )
Location
Nevada
Las Vegas
New Jersey
Camden
Elizabeth
Jersey City
Newark
Paulsboro
Perth Amboy
Trenton
tsfew Mexico
Albuquerque
New York
Buffalo
New York
Rochester
North Carolina
Charlotte
Wins ton-Sal em
Ohio
Akron
Canton
Cincinnati
Cleveland
Columbus
Youngs town
Oklahoma
Oklahoma City
1954-59a
Max
1.20
1.80
6.00
2.34
1.20
1.20
9.98
1.54
.16
Avq
.30
.57
.30
.42
.29
.33
2.57
.02
.07
1960
Max
.03
.04
.01
.03
.02
Avq
.01
.01
.00
.01
.00
1961
Max
.01
.98b
3.60
.02
.01
.02
.01
Avq
.50b
.67
.01
.00
.01
.00
1962
Max
.60
.04
2.20
.03
.02
.01
.05
.01
Avq
.19
.01
.62
.01
.00
.01
.00
.00
1963
Max
f
1.00
.01
.01
.01
Avq
.41
.00
.00
.00
1964
Max
.72
.88
.03
.01
.01
Avq
.19
.30
.01
.00
.00
(continued)
00
-------
APPENDIX
TABLE 17 (Continued)
CONCENTRATIONS OP VANADIUM IN THE AIR
(Values of Individual Samples in M-g/m3 )
Location
Oregon
Eugene
Medf ord
Portland
Pennsylvania
Allentown
Altoona
Bristol
Chester
Johnstown
Philadelphia
Pittsburgh
Scranton
Williamsport
Tennessee
Memphis
Chattanooga
Texas
Bellaire
El Paso
Houston
Lake worth
Utah
Salt Lake City
Washington
Seattle
Tacoma
1954-59a
Max
.80
.03
.55
1.6
4.65
.07
.10
.40
.10
.07
.39
.40
1.30
Avq
.16
.01
.17
.25
.61
.02
.04
.02
.04
.01
.12
.06
.47
1960
Max
.99
Avq
.44
1961
Max
.06
.10
b
.32°
.73
•u
.75^
.01
Avq
.01
.02
T-,
.10°
.21
b
.12
.00
1962
Max
.61
.05
.00
.08
.09
Avg
.21
.01
.00
.03
.02
1963
Max
.04
§
.01
.45
.01
.05
Avq
.01
.00
.17
.00
.02
1964
Max
.06
.41
.01
.01
.01
.01
.08
Avq
.02
.16
.00
.00
.00
.00
.02
(continued)
-------
APPENDIX
TABLE 17 (Continued)
CONCENTRATIONS OF VANADIUM IN AIR
(Values of Individual Samples in |~ig/m3 )
Location
West Virginia
Charleston
Wisconsin
Milwaukee
Racine
Wyoming
Cheyenne
1954-59a
Max
.60
.48
Avq
.08
.20
1960
Max
.03
Avq
.02
1961
Max
.09
Avq
.03
1962
Max
Avq
1963
Max
•
Avq
1964
Max
.05
.01
.02
Avq
.01
.00
.00
The data in this column may include only one year or the average of all measurements
made during these years.
Values shown in Reference 3. Different values for same city and year, as stated in
Reference 4 are shown below.
Max
Chicago
Indianapolis
Allentown
Scranton
Newark
Avq
.35
.03
.21
.22
.62
.10
.01
.06
.07
.30
-------
81
APPENDIX
TABLE 18
CONCENTRATIONS OP VANADIUM IN THE AIR
OF 118 COMMUNITIES3- OF THE UNITED STATES,
(Quarterly Composite Values)
1967
68
Location
Alabama
Montgomery
Alaska
Anchorage
Fairbanks
Arizona
Phoenix
California
Glendale
Humboldt County
Long Beach
Los Angeles
Oakland
San Diego
San Francisco
Colorado
Denver
Connecticut
Hartford
New Haven
Delaware
Kent County
Newark
Wilmington
District of Columbia
Washington
Georgia
Atlanta
Hawaii
Honolulu
Illinois
Chicago
East St. Louis
Rockf ord
Springfield
Concentration
Min
.0033
.0027
.0032
.0031
.0036
.0009
.014
.0077
.018
.013
.023
.0034
.11
.74
.014
.027
.13
.10
.0037
.018
.0077
.0034
.0038
.0028
Max
.0033
.011
.0071
.0042
.022
.0012
.057
.034
.041
.034
.039
.0034
.21
.10
.035
.070
.24
.23
.0092
.026
.10
.007
.016
.0039
Ucr/m3 )
Avq
.0033
.0058
.0052
.0037
.0095
.0010
.026
.0189
.030
.021
.031
.0034
.16
.49
.029
.046
.19
.165
.0056
.021
.0589
.0058
.0084
.0033
Number of
Samples*3
1
4
3
2
4
2
4
4
4
4
2
1
2
4
4
4
4
4
3
3
4
3
3
4
-------
82
APPENDIX
TABLE 18 (Continued)
CONCENTRATIONS OF VANADIUM IN THE AIR
OF 118 COMMUNITIES3 OF THE UNITED STATES,
(Quarterly Composite Values)
1967
Location
Indiana
East Chicago
Hammond
Indianapolis
Monroe State Forest
Parke County
South Bend
Terre Haute
Iowa
Cedar Rapids
Des Moines
Dubuque
Kentucky
Covington
Lexington
Louisville
Louisiana
New Orleans
Maine
Acadia National Park
Maryland
Baltimore
Calvert County
Michigan
Detroit
Flint
Grand Rapids
Minnesota
Minneapolis
St. Paul
Mississippi
Jackson County
Missouri
Kansas City
St. Louis
Shannon County
Nebraska
Omaha
Nevada
Reno
Concentration (uq/m3)
Min
.026
.017
.0097
.001
.0012
.0031
.003
.0042
.0035
.0062
.0025
.0029
.0025
.017
.0090
.13
.0033
.0068
.0026
.0025
.0027
.0036
.0031
.0027
.0042
.0026
.0041
.018
Max
.10
.054
.020
.0017
.0012
.11
.0042
.011
.0035
.0062
.0031
.0033
.032
.056
.040
.35
.11
.016
.0030
.0025
.018
.077
.0044
.022
.025
.0026
.0041
.069
Avq
.0497
.0345
.0157
.0013
.0012
.0305
.0036
.0076
.0035
.0062
.0028
.0031
.0126
.034
.0295
.20
.0443
.0114
.0028
.0025
.0080
.0322
.0037
.0192
.0116
.0026
.0041
.0365
Number of
Samples13
4
4
4
3
2
4
2
2
1
1
2
2
3
4
4
4
4
4
2
1
3
3
4
3
3
1
1
4
(continued)
-------
APPENDIX
83
TABLE 18 (Continued)
CONCENTRATIONS OF VANADIUM IN THE AIR
OF 118 COMMUNITIES3 OF THE UNITED STATES, 1967
(Quarterly Composite Values)
Location
New Hampshire
Concord
Coos County
New Jersey
Bayonne
Marlton
Glassboro
Jersey City
Newark
Paterson
Perth Amboy
New Mexico
Rio Arriba County
New York
Cape Vincent
New York
North Carolina
Charlotte
Cape Hatteras
Ohio
Akron
Cincinnati
Cleveland
Columbus
Dayton
Toledo
Youngstown
Oregon
Curry County
Eugene
Medf ord
Portland
Pennsylvania
All en town
Altoona
Bethlehem
Clarion County
Erie
Lancaster
Philadelphia
Concentration ([Jq/m3 )
Min
.072
.0045
.22
.036
.017
.18
.16
.14
.092
.0014
.011
.34
.0057
.0045
.0058
.0037
.0070
.0056
.0037
.0051
.0041
.0011
.0043
.0031
.023
.027
.0039
.014
.0021
.0035
.017
.076
Max
.51
.012
.99
.24
.070
1.1
.62
1.2
.86
.0014
.014
1.4
.034
.0063
.013
.021
.0074
.0056
.014
.011
.0079
.0011
.013
.0033
.053
.12
.012
.13
.0024
.0037
.091
.43
Avq
.2585
.0074
.445
.1125
.052
.4875
.345
.565
.3905
.0014
.012
.905
.0182
.0050
.0063
.0101
.0072
.0056
.0093
.055
.0061
.0011
.0078
.0032
.0377
.0795
.0068
.063
.0025
.0036
.0415
.264
Number of
Samples*3
4
4
4
4
4
4
4
4
4
1
3
4
4
4
3
3
2
1
4
3
3
1
3
2
4
4
3
4
4
2
4
4
-------
APPENDIX
84
TABLE 18 (Continued)
CONCENTRATIONS OF VANADIUM IN THE AIR
OF 118 COMMUNITIESa OF THE UNITED STATES, 1967
(Quarterly Composite Values)
Location
Pennsylvania (cont. )
Pittsburgh
Reading
Scran ton
Warminster
West Chester
York
Puerto Rico
Bayamon
Guayamilla
Ponce
San Juan
Rhode Island
East Providence
Providence
Washington County
South Carolina
Columbia
Richland County
South Dakota
Black Hills Forest
Tennessee
Chattanooga
Knoxville
Nashville
Texas
Houston
Utah
Salt Lake City
Vermont
Orange County
Virginia
Hampton
Lynchburg
Norfolk
Shenandoah National Park
Portsmouth
Richmond
Roanoke
Concentration (uq/m3 )
Min
.0078
.019
.015
.030
.015
.041
.044
.013
.0062
.020
.062
.076
.035
.0034
.0046
.011
.0083
.0078
.0027
.0043
.0034
.0094
.011
.0037
.034
.0013
.012
.022
.0056
Max
.034
.21
.32
.24
.11
.21
.31
.10
.021
.10
.18
.35
.064
.017
.0061
.011
.010
.0078
.0038
.0043
.010
.10
.051
.019
.068
.0052
.068
.081
.022
Avq
.0164
.0315
.104
.0985
.0575
.1135
.132
.0382
.0127
.056
.1065
.2715
.0485
.0084
.0052
.011
.0091
.0078
.0032
.0043
.0059
.0646
.0282
.0097
.051
.0025
.034
.047
.0113
Number of
Samples13
4
4
4
4
4
4
4
4
4
4
4
4
4
3
3
1
2
1
2
1
3
4
4
3
4
4
4
4
4
-------
85
APPENDIX
TABLE 18 (Continued)
CONCENTRATIONS OF VANADIUM IN THE AIR
OF 118 COMMUNITIES3 OF THE UNITED STATES, 1967
(Quarterly Composite Values)
Location
Washington
Seattle
West Virginia
Charleston
Wisconsin
Door County
Kenosha
Milwaukee
Concentration ( uq/m3 )
Min
.013
.0056
.0010
.0048
.0027
Max
.030
.023
.0020
.0061
.0075
L Avg
.0225
.0156
.0015
.0054
.0048
Number of
Samples*3
4
4
2
2
4
aln 31 communities no value was observed above the
detection limit.
Number, out of four measurements, with observed values
above the detection limit (four decimal places).
-------
86
APPENDIX
TABLE 19
CONCENTRATIONS OF VANADIUM IN THE AIR
OF 79 COMMUNITIES3 OF THE UNITED STATES, 1966
(Quarterly Composite Values)
68
Location
Alabama
Mobile
Alaska
Anchorage
Arizona
Phoenix
California
Burbank
Los Angeles
Oakland
Pasadena
San Diego
San Francisco
Connecticut
Hartford
New Haven
Delaware
Kent County
Newark
Wilmington
District of Columbia
Washington
Georgia
Atlanta
Hawaii
Honolulu
Illinois
Chicago
Indiana
East Chicago
Hammond
Indianapolis
Monroe State Forest
New Albany
Parke County
South Bend
Kentucky
Covington
Louisville
Louisiana
New Orleans
Concentration_(jaq/m3J
Min
.012
.011
.007
.011
.007
.007
.010
.007
.029
.034
.110
.012
.034
.032
.048
.017
.013
.008
.014
.006
.008
.002
.006
.003
.008
.006
.007
.006
Max
.017
.014
.007
.039
.062
.022
.052
.030
.038
.320
.440
.057
.078
.170
.230
.038
0.59
.091
.092
.027
.016
.002
.006
.003
.160
.006
.007
.016
Avq
.013
.0124
.007
.0206
.022
.0147
.031
.0167
.0338
.1638
.3275
.0332
.0532
.1155
.1182
.0275
.0222
.0475
.0425
.0175
.0123
.002
.006
.003
.0502
.006
.007
.095
Number of
Samples13
4
3
1
3
4
4
2
4
2
4
4
4
4
4
4
2
4
4
4
4
3
1
1
1
4
1
1
4
• ' ' ' (continued)
-------
87
APPENDIX
TABLE 19 (Continued)
CONCENTRATIONS OF VANADIUM IN THE AIR
OF 79 COMMUNITIES21 OF THE UNITED STATES, 1966
(Quarterly Composite Values)
Location
Maine
Acadia National Park
Maryland
Baltimore
Calvert County
Michigan
Detroit
Minessota
Minneapolis
St. Paul
Mississippi
Jackson County
Missouri
Kansas City
St. Louis
New Hampshire
Concord
Coos County
New Jersey
Marlton
Camden
Glassboro
Jersey City
Newark
Perth Amboy
Trenton
New York
Cape Vincent
New York
North Carolina
Charlotte
Cape Hatteras
Ohio
Cincinnati
Dayton
Toledo
Youngs town
Oregon
Portland
Concentration ( M.q/m3 )
Min
.010
.110
.004
.006
.005
.006
.003
.013
.007
.029
.006
.027
.090
.020
.160
.150
.150
.074
.004
.250
.008
.004
.004
.003
.003
.003
.020
Max
.014
.350
.048
.007
.015
.014
.005
.013
.019
.100
.020
.110
.280
.052
.330
.340
.260
.150
.011
.610
.037
.007
.004
.004
.003
.008
.042
Avq
.042
.255
.025
.066
.010
.010
.0036
.013
.012
.093
.010
.0525
.1675
.0377
.2625
.2575
.1525
.110
.0067
.3875
.0195
.0057
.004
.0033
.003
.0023
.0305
Number of
Samples*3
4
4
4
3
2
2
3
1
3
4
4
4
4
4
4
4
4
4
4
4
4
4
1
3
1
3
4
(continued)
-------
88
APPENDIX
TABLE 19 (Continued)
CONCENTRATIONS OF VANADIUM IN THE AIR
OF 79 COMMUNITIES3 OF THE UNITED STATES, 1966
(Quarterly Composite Values)
Location
Pennsylvania
Clarion County
Lancaster
Philadelphia
Reading
Warminster
Puerto Rico
Bayamon
Guayanilla
Ponce
San Juan
Rhode Island
Providence
Washington County
South Carolina
Columbia
Greenville
Richland County
Tennessee
Chattanooga
Utah
Salt Lake City
Vermont
Burlington
Orange County
Virginia
Danville
Norfolk
Shenandoah National Park
Washington
Seattle
West Virginia
Charleston
Wisconsin
Milwaukee
__ Concentration
Min
.002
.023
.088
.035
.024
.030
.011
.014
.032
.055
.008
.004
.003
.002
.008
.003
.094
.005
.006
.016
.002
.011
.013
.003
Max
.002
.063
.200
.160
.280
.094
.017
.024
.130
.290
.061
.006
.036
.005
.008
.005
.120
.038
.015
.050
.004
.055
.016
.004
( Uq/m3 )
Avq
.002
.0442
.1332
.0925
.0945
.0625
.013
.018
.0692
.3412
.0317
.005
.015
.0033
.008
.004
.1022
.024
.0116
.0325
.003
.0285
.0142
.0035
Number of
Samples*3
3
4
4
4
4
4
3
4
4
4
4
2
3
3
2
2
4
4
3
4
2
4
4
3
aln 50 communities no value was observed above the
detection limit.
•'-'Number, out of four measurements, with observed values
above the detection limit (four decimal places).
-------
89
APPENDIX
TABLE 20
SOME PRODUCERS OF VANADIUM PRODUCTS28
Vanadium Oxides, Salts, Alloys, and Other Derivatives
Aceto Chemical Co., Inc.
City Chemical Corp.
Fairmount Chemical Co., Inc.
Foots Mineral Co.,
Vancoram Operations
Kerr-McGee Corp.
MacKenzie Chemical Works, Inc.
Ozark-Mahoning Co.
Semi-Elements, Inc.
The Shepherd Chemical Co.
Stauffer Chemical Co.
Industrial Chemical Div.
Specialty Chemical Div.
Susquehanna-Western, Inc.
Union Carbide Corp.
Mining and Metals Div.
U. S. Borax Research Corp.
Vitro Corp. of America
Flushing, N.Y.
Jersey City, N.J.
Newark, N.J.
Cambridge, Ohio
Shiprock, N. Mex.
Soda Springs, Idaho
Central Islip, N.Y.
Tulsa, Okla.
Saxonbur, Pa.
Cincinnati, Ohio
Houston, Tex.
Weston, Mich.
Edgemont, S. Bak,
Hot Springs, Ark
Maybell, Colo.
Niagara Falls, N.Y.
Rifle, Colo.
Riverton, Wyo.
Uravan, Colo.
Wilson Springs, Ark.
Anaheim, Calif.
Salt Lake City, Utah
-------
APPENDIX
TABLE 21
PROPERTIES, TOXICITY, AND USES OF VANADIUM AND SOME VANADIUM COMPOUNDS
52
Compound
Properties
Toxicity
Uses
Vanadium
Light gray or
white lustrous
powder or
fused hard
lumps
mp 1,717°C
bp 3,000°C
Insoluble in
water
The pentoxide dust has been
reported to be a respira-
tory irritant and to cause
skin pallor, greenish-black
tongue, chest pain, cough,
dyspnea, palpitation, lung
changes. When ingested,
causes gastrointestinal
disturbances. May also
cause a papular skin rash
In manufacture of rust
resistant vanadium steel
Vanadium
carbonyl
v(co)6
Blue-green
powder. Sen-
sitive to air.
Should be
stored under
nitrogen.
Decomposes at
60-70°C
May liberate CO.
Vanadium
See also
Vanadium
pentafluoride
VFC
Liquid, turns
yellow on expo-
sure to moist
air. mp 19.0°C
bp 47.9°C
(continued)
-------
APPENDIX
TABLE 21 (Continued)
PROPERTIES, TOXICITY, AND USES OF VANADIUM AND SOME VANADIUM COMPOUNDS
Compound
Properties
Toxicity
Uses
Vanadium
pentoxide
v2o5
Yellow to
rust-brown
orthorhoinbic
crystals
mp 690°C
As a catalyst in the oxida-
tion of S02 to 303, alcohol
to acetaldehyde, etc.; for
the manufacture of yellow
glass; as a depolarizer; as
developer in photography; in
form of ammonium vanadate as
mordant in dyeing and print-
ing fabrics and in manufac-
ture of aniline black
Vanadium
tetrafluoride
•n4
Brownish pow-
der. Very hy-
groscopic .
Deliquesces.
Decomposes
above 325°C
Vanadium
trifluoride
?3
Greenish-
yellow powder
mp above 800°C
Sublimes at
bright red heat
Vanadium
trioxide
Black powder
mp 1,940°C
Insoluble in
water
As a catalyst, e.g., when
making ethanol from ethylene
(continued)
-------
APPENDIX
TABLE 21 (Continued)
PROPERTIES, TOXICITY, AND USES OF VANADIUM AND SOME VANADIUM COMPOUNDS
Compound
Properties
Toxicity
Uses
Vanadium
trisulfate
v2(so4)3
Lemon-yellow
powder
See Vanadium
Vanadium
trisulfide
Greenish-
black powder
Decomposes
when heated
Vanadyl
arsenate
VOAsO4-5H2O
Yellow,
tabular
crystals
Vanadyl
dichloride
VOCIU
Green, very
deliquescent
tabular
crystals
No specific data.
Probably an irritant,
See Vanadium
As mordant in printing
fabrics
Vanadyl
sulfate
VOSO4-2H2O
Blue, crys-
talline
powder
Soluble in
water
See Vanadium
As mordant in dyeing and
printing textiles, manufac-
ture of colored glass; for
blue and green glazes on
pottery
(continued)
-------
APPENDIX
TABLE 21 (Continued)
PROPERTIES, TOXICITY, AND USES OF VANADIUM AND SOME VANADIUM COMPOUNDS
Compound
Properties
Toxicity
Uses
Vanadyl
trichloride
VOClo
Yellow liquid
emitting red
fumes
bp 126-127°C
Readily liberates highly
irritating HC1. See Vanadium
The metals:
VO+2
VOC12
voci3
NHVO.
Na2V4Og
Na
, c
= vanadyl
= vanadium oxydichloride (or vanadite)
= vanadium oxytrichloride (hypovanadate)
= ammonium metavanadate
= sodium vanadite
= sodium orthovanadate
= sodium pyrovanadate
= sodium tetravanadate
= sodium hexavanadate
Also a number of complex Vanadium-arsenic and Vanadium-antimony compounds
------- |