VANADIUM PENTOXIDE ANDOTHER INORGANIC VANADIUM COMPOUNDS

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necessarily represent the decisions or the stated policy of the United Nations Environment Programme, the International Labour Organization, or the World Health Organization.

Concise International Chemical Assessment Document 29

VANADIUM PENTOXIDE AND

OTHER INORGANIC VANADIUM COMPOUNDS

Note that the layout and pagination of this pdf file are not identical to the printed CICAD

First draft prepared by

Dr M. Costigan and Mr R. Cary, Health and Safety Executive, Liverpool, United Kingdom, and

Dr S. Dobson, Centre for Ecology and Hydrology, Huntingdon, United Kingdom

Published under the joint sponsorship of the United Nations Environment Programme, the International Labour Organization, and the World Health Organization, and produced within the framework of the Inter-Organization Programme for the Sound Management of Chemicals.

World Health Organization

Geneva, 2001

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and the World Health Organization (WHO). The overall objectives of the IPCS are to establish the scientific basis for assessment of the risk to human health and the environment from exposure to chemicals, through international peer review processes, as a prerequisite for the promotion of chemical safety, and to provide technical assistance in strengthening national capacities for the sound management of chemicals.

The

Inter-Organization Programme for the Sound Management of Chemicals (IOMC) was

established in 1995 by UNEP, ILO, the Food and Agriculture Organization of the United Nations, WHO, the United Nations Industrial Development Organization, the United Nations Institute for Training and Research, and the Organisation for Economic Co-operation and Development (Participating Organizations), following recommendations made by the 1992 UN Conference on Environment and Development to strengthen cooperation and increase coordination in the field of chemical safety. The purpose of the IOMC is to promote coordination of the policies and activities pursued by the Participating Organizations, jointly or separately, to achieve the sound management of chemicals in relation to human health and the environment.

WHO Library Cataloguing-in-Publication Data

Vanadium pentoxide and other inorganic vanadium compounds.

(Concise international chemical assessment document ; 29) 1.Vanadium compounds - adverse effects 2.Risk assessment

3.Environmental exposure I.International Programme on Chemical Safety II.Series

ISBN 92 4 153029 4 (NLM Classification: QV 290)

ISSN 1020-6167

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The Federal Ministry for the Environment, Nature Conservation and Nuclear Safety, Germany, provided financial support for the printing of this publication.

Printed by Wissenschaftliche Verlagsgesellschaft mbH, D-70009 Stuttgart 10

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iii

FOREWORD . . . 1

1. EXECUTIVE SUMMARY . . . 4

2. IDENTITY AND PHYSICAL/CHEMICAL PROPERTIES . . . 6

3. ANALYTICAL METHODS . . . 6

3.1 Workplace air monitoring . . . 6

3.2 Biological monitoring . . . 6

3.3 Environmental monitoring . . . 7

4. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE . . . 8

5. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION . . . 9

5.1 Chemical speciation of vanadium . . . 9

5.2 Essentiality of vanadium . . . 9

5.3 Bioaccumulation . . . 9

5.4 Leaching and bioavailability in soils . . . 10

6. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE . . . 10

6.1 Environmental levels . . . 10

6.1.1 Air . . . 10

6.1.2 Surface waters and sediments . . . 11

6.1.3 Biota . . . 11

6.1.4 Soil . . . 12

6.2 Human exposure . . . 12

7. COMPARATIVE KINETICS AND METABOLISM IN LABORATORY ANIMALS AND HUMANS . . . 14

8. EFFECTS ON LABORATORY MAMMALS AND IN VITRO TEST SYSTEMS . . . 14

8.1 Single exposure . . . 15

8.1.1 Vanadium pentoxide . . . 15

8.1.2 Other pentavalent vanadium compounds . . . 15

8.1.3 Tetravalent vanadium compounds . . . 15

8.1.4 Trivalent vanadium compounds . . . 15

8.2 Irritation and sensitization . . . 15

8.3 Effects of inhaled vanadium compounds on the respiratory tract . . . 16

8.4 Other short-term exposure studies . . . 17

8.5 Medium-term exposure . . . 18

8.5.1 Vanadium pentoxide and other pentavalent vanadium compounds . . . 18

8.6 Long-term exposure and carcinogenicity . . . 19

8.6.1 Vanadium pentoxide and other pentavalent vanadium compounds . . . 19

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iv

8.7 Genotoxicity and related end-points . . . 19

8.7.1 Studies in prokaryotes . . . 19

8.7.1.1 Vanadium pentoxide . . . 19

8.7.1.2 Other pentavalent vanadium compounds . . . 19

8.7.1.3 Tetravalent vanadium compounds . . . 19

8.7.1.4 Trivalent vanadium compounds . . . 19

8.7.2 In vitro studies in eukaryotes . . . 19

8.7.2.4 Trivalent vanadium compounds . . . 21

8.7.3 Sister chromatid exchange . . . 21

8.7.4 Other in vitro studies . . . 21

8.7.5 In vivo studies in eukaryotes (somatic cells) . . . 22

8.7.6 In vivo studies in eukaryotes (germ cells) . . . 22

8.7.6.2 Other pentavalent and tetravalent vanadium compounds . . . 23

8.7.7 Supporting data . . . 23

8.8 Reproductive toxicity . . . 23

8.8.1 Effects on fertility . . . 23

8.8.1.1 Vanadium pentoxide and other pentavalent vanadium compounds . . . 23

8.8.2 Developmental toxicity . . . 24

8.9 Immunological and neurological effects . . . 25

9. EFFECTS ON HUMANS . . . 26

9.1 Studies on volunteers . . . 26

9.2 Clinical and epidemiological studies for occupational exposure . . . 27

9.3 Epidemiological studies for general population exposure . . . 29

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v

10. EFFECTS ON OTHER ORGANISMS IN THE LABORATORY AND FIELD . . . 30

10.1 Aquatic environment . . . 30

10.2 Terrestrial environment . . . 30

11. EFFECTS EVALUATION . . . 32

11.1 Evaluation of health effects . . . 32

11.1.1 Hazard identification and dose–response assessment . . . 32

11.1.2 Criteria for setting tolerable intakes or guidance values for vanadium pentoxide . . . 33

11.1.3 Sample risk characterization . . . 33

11.1.4 Uncertainties . . . 34

11.2 Evaluation of environmental effects . . . 34

12. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES . . . 35

REFERENCES . . . 36

APPENDIX 1 — SOURCE DOCUMENTS . . . 42

APPENDIX 2 — CICAD PEER REVIEW . . . 42

APPENDIX 3 — CICAD FINAL REVIEW BOARD . . . 43

INTERNATIONAL CHEMICAL SAFETY CARDS . . . 44

RÉSUMÉ D’ORIENTATION . . . 48

RESUMEN DE ORIENTACIÓN . . . 51

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1 FOREWORD

Concise International Chemical Assessment Documents (CICADs) are the latest in a family of publications from the International Programme on Chemical Safety (IPCS) — a cooperative programme of the World Health Organization (WHO), the International Labour Organization (ILO), and the United Nations Environment Programme (UNEP). CICADs join the Environmental Health Criteria documents (EHCs) as authoritative documents on the risk assessment of chemicals.

International Chemical Safety Cards on the relevant chemical(s) are attached at the end of the CICAD, to provide the reader with concise information on the protection of human health and on emergency action. They are produced in a separate peer-reviewed procedure at IPCS. They may be complemented by information from IPCS Poison Information Monographs (PIM), similarly produced separately from the CICAD process.

CICADs are concise documents that provide sum- maries of the relevant scientific information concerning the potential effects of chemicals upon human health and/or the environment. They are based on selected national or regional evaluation documents or on existing EHCs. Before acceptance for publication as CICADs by IPCS, these documents undergo extensive peer review by internationally selected experts to ensure their completeness, accuracy in the way in which the original data are represented, and the validity of the conclusions drawn.

The primary objective of CICADs is characterization of hazard and dose–response from exposure to a chemical. CICADs are not a summary of all available data on a particular chemical; rather, they include only that information considered critical for characterization of the risk posed by the chemical. The critical studies are, however, presented in sufficient detail to support the conclusions drawn. For additional information, the reader should consult the identified source documents upon which the CICAD has been based.

Risks to human health and the environment will vary considerably depending upon the type and extent of exposure. Responsible authorities are strongly encouraged to characterize risk on the basis of locally measured or predicted exposure scenarios. To assist the reader, examples of exposure estimation and risk characterization are provided in CICADs, whenever possible. These examples cannot be considered as representing all possible exposure situations, but are

provided as guidance only. The reader is referred to EHC 170¹ for advice on the derivation of health-based tolerable intakes and guidance values.

While every effort is made to ensure that CICADs represent the current status of knowledge, new information is being developed constantly. Unless otherwise stated, CICADs are based on a search of the scientific literature to the date shown in the executive summary. In the event that a reader becomes aware of new information that would change the conclusions drawn in a CICAD, the reader is requested to contact IPCS to inform it of the new information.

Procedures

The flow chart shows the procedures followed to produce a CICAD. These procedures are designed to take advantage of the expertise that exists around the world — expertise that is required to produce the high- quality evaluations of toxicological, exposure, and other data that are necessary for assessing risks to human health and/or the environment. The IPCS Risk Assess- ment Steering Group advises the Co-ordinator, IPCS, on the selection of chemicals for an IPCS risk assessment, whether a CICAD or an EHC is produced, and which institution bears the responsibility of the document production, as well as on the type and extent of the international peer review.

The first draft is based on an existing national, regional, or international review. Authors of the first draft are usually, but not necessarily, from the institution that developed the original review. A standard outline has been developed to encourage consistency in form.

The first draft undergoes primary review by IPCS and one or more experienced authors of criteria documents in order to ensure that it meets the specified criteria for CICADs.

The draft is then sent to an international peer review by scientists known for their particular expertise and by scientists selected from an international roster compiled by IPCS through recommendations from IPCS national Contact Points and from IPCS Participating Institutions. Adequate time is allowed for the selected experts to undertake a thorough review. Authors are required to take reviewers’ comments into account and revise their draft, if necessary. The resulting second draft

1 International Programme on Chemical Safety (1994) Assessing human health risks of chemicals: derivation of guidance values for health-based exposure limits.

Geneva, World Health Organization (Environmental Health Criteria 170).

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S E L E C T I O N O F H I G H Q U A L I T Y N A T I O N A L / R E G I O N A L A S S E S S M E N T D O C U M E N T ( S )

CICAD PREPARATION FLOW CHART

F I R S T D R A F T P R E P A R E D

R E V I E W B Y I P C S C O N T A C T P O I N T S / S P E C I A L I Z E D E X P E R T S

F I N A L R E V I E W B O A R D ²

F I N A L D R A F T³

E D I T I N G

A P P R O V A L B Y D I R E C T O R , I P C S

P U B L I C A T I O N S E L E C T I O N O F P R I O R I T Y C H E M I C A L

1 Taking into account the comments from reviewers.

2 The second draft of documents is submitted to the Final Review Board together with the reviewers’ comments.

3 Includes any revisions requested by the Final Review Board.

R E V I E W O F C O M M E N T S (P R O D U C E R / R E S P O N S I B L E O F F I C E R), P R E P A R A T I O N

O F S E C O N D D R A F T ¹ P R I M A R Y R E V I E W B Y I P C S (REVISIONS AS NECESSARY)

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3 is submitted to a Final Review Board together with the

reviewers’ comments.

A consultative group may be necessary to advise on specific issues in the risk assessment document.

The CICAD Final Review Board has several important functions:

– to ensure that each CICAD has been subjected to an appropriate and thorough peer review;

– to verify that the peer reviewers’ comments have been addressed appropriately;

– to provide guidance to those responsible for the preparation of CICADs on how to resolve any remaining issues if, in the opinion of the Board, the author has not adequately addressed all comments of the reviewers; and

– to approve CICADs as international assessments.

Board members serve in their personal capacity, not as representatives of any organization, government, or industry. They are selected because of their expertise in human and environmental toxicology or because of their experience in the regulation of chemicals. Boards are chosen according to the range of expertise required for a meeting and the need for balanced geographic

representation.

Board members, authors, reviewers, consultants, and advisers who participate in the preparation of a CICAD are required to declare any real or potential conflict of interest in relation to the subjects under discussion at any stage of the process. Representatives of nongovernmental organizations may be invited to observe the proceedings of the Final Review Board.

Observers may participate in Board discussions only at the invitation of the Chairperson, and they may not participate in the final decision-making process.

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1. EXECUTIVE SUMMARY

This CICAD on vanadium pentoxide and other inorganic vanadium compounds was based on a review of human health concerns (primarily occupational) prepared by the United Kingdom’s Health and Safety Executive (HSE, in press). This review focuses on exposures via routes relevant to occupational settings, but it also contains environmental information. Data identified as of November 1998 were covered. A further literature search was performed up to May 1999 to identify any additional information published since this review was completed. An Environmental Health Criteria monograph (IPCS, 1988) was used as a source document for environmental information. As no more recent source document was available for environmental fate and effects, the literature was searched for additional information. Information on the nature of the peer review and availability of the source documents is presented in Appendix 1. Information on the peer review of this CICAD is presented in Appendix 2. This CICAD was approved as an international assessment at a meeting of the Final Review Board, held in Helsinki, Finland, on 26–29 June 2000. Participants at the Final Review Board meeting are listed in Appendix 3. The International Chemical Safety Cards on vanadium trioxide (ICSC 0455) and vanadium pentoxide (ICSC 0596), produced by the International Programme on Chemical Safety (IPCS, 1999a,b), have also been reproduced in this document.

Vanadium (CAS No. 7440-62-2) is a soft silvery- grey metal that can exist in a number of different oxidation states: !1, 0, +2, +3, +4, and +5. The most common commercial form is vanadium pentoxide (V₂O₅; CAS No.

1314-62-1), and this exists in the pentavalent state as a yellow-red or green crystalline powder.

Vanadium is an abundant element with a very wide distribution and is mined in South Africa, Russia, and China. During the smelting of iron ore, a vanadium slag is formed that containvanadium pentoxide, which is used for the production of vanadium metal. Vanadium pentoxide is also produced by solvent extraction from uranium ores and by a salt roast process from boiler residues or residues from elemental phosphate plants. During the burning of fuel oils in boilers and furnaces, vanadium pentoxide is present in the solid residues, soot, boiler scale, and fly ash.

Atmospheric emissions from natural sources have been estimated at 8.4 tonnes per annum globally (range 1.5–49.2 tonnes). By far the most important source of environmental contamination with vanadium is combustion of oil and coal; about 90% of the approximately

64 000 tonnes of vanadium that are emitted to the atmosphere each year from both natural and anthropogenic sources comes from oil combustion.

The environmental chemistry of vanadium is complex. In minerals, the oxidation state of vanadium may be +3, +4, or +5. Dissolution in water rapidly oxidizes V³⁺

and V⁴⁺ to the pentavalent state, the most usual form of the metal in the environment. Vanadate, the pentavalent species in solution, may polymerize (mainly to dimeric and trimeric forms), particularly at higher concentrations of the salts. Within tissues of organisms, V³⁺ and V⁴⁺

predominate because of largely reducing conditions; in plasma, V⁵⁺ predominates.

Vanadium is probably essential to enzyme systems that fix nitrogen from the atmosphere (bacteria) and is concentrated by some organisms (tunicates, some polychaete annelids, some microalgae), but its function in these organisms is uncertain. Whether vanadium is essential to other organisms remains an open question.

There is no evidence of accumulation or biomagnification in food chains in marine organisms, the best studied group.

There is very limited leaching of vanadium through soil profiles.

Higher levels of vanadium have been reported in air close to industrial sources and oil fires. Representa- tive deposition rates are 0.1–10 kg/ha per annum for urban sites affected by strong local sources, 0.01–

0.1 kg/ha per annum for rural sites and urban ones with no strong local source, and <0.001–0.01 kg/ha per annum for remote sites.

Most surface fresh waters contain less than 3 µg vanadium/litre; higher levels of up to about 70 µg/litre have been reported in areas with high geochemical sources. Data on levels of vanadium in surface water close to industrial activity are few; most reports suggest levels approximately the same as the highest natural ones. Seawater concentrations in the open ocean range from 1 to 3 µg/litre, and sediment concentrations range from 20 to 200 µg/g; the highest levels are in coastal sediments.

A few organisms concentrate vanadium, with up to 10 000 µg/g in ascidians and 786 µg/g in polychaete annelids. Most other organisms contain generally less than 50 µg/g and usually much lower concentrations.

Estimates of total dietary intake of humans range from 11 to 30 µg/day. Levels in drinking-water range up to 100 µg/litre. Some groundwater sources supplying

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5 potable water show concentrations above 50 µg/litre.

Levels in bottled spring water may be higher.

In humans, there is limited toxicokinetic information suggesting that vanadium is absorbed following inhalation and is subsequently excreted via the urine with an initial rapid phase of elimination, followed by a slower phase, which presumably reflects the gradual release of vanadium from body tissues. Following oral administration, tetravalent vanadium is poorly absorbed from the gastrointestinal tract. There were no dermal studies available.

In inhalation and oral studies in laboratory animals, absorbed vanadium in either pentavalent or tetravalent states is distributed mainly to the bone, liver, kidney, and spleen, and it is also detected in the testes. The main route of vanadium excretion is via the urine. The pattern of vanadium distribution and excretion indicates that there is potential for accumulation and retention of absorbed vanadium, particularly in the bone. There is evidence that tetravalent vanadium has the ability to cross the placental barrier to the fetus.

The one acute inhalation study available reported an LC₆₇ of 1440 mg/m³ (800 mg vanadium/m³) following a 1-h exposure of rats to vanadium pentoxide dust. Oral studies in rats and mice resulted in LD₅₀ values in the range 10–160 mg/kg body weight for vanadium pentoxide and other pentavalent vanadium compounds, while tetravalent vanadium compounds have LD₅₀ values in the range 448–467 mg/kg body weight. No information is available concerning dermal toxicity.

Eye irritation has been reported in studies in vanadium workers. No skin irritation was reported in 100 human volunteers following skin patch testing with 10% vanadium pentoxide, although patch testing in workforces has produced two isolated reactions. No clear information is available from animal studies with regard to the potential of vanadium compounds to produce skin or eye irritation or skin sensitization.

In a group of human volunteers, a single 8-h exposure to 0.1 mg vanadium pentoxide dust/m³ caused delayed but prolonged bronchial effects involving exces- sive production of mucus. At 0.25 mg/m³, a similar pattern of response was seen, with the addition of cough for some days post-exposure. Exposure to 1.0 mg/m³ produced persistent and prolonged coughing after 5 h.

A no-effect level for bronchial effects was not identified in this study.

Repeated inhalation exposure to the dust and fume of vanadium pentoxide is associated with irritation of the eyes, nose, and throat. Wheeze and dyspnoea are commonly reported in workers exposed to vanadium

pentoxide dust and fume. Overall, there are insufficient data to reliably describe the exposure–response relation- ship for the respiratory effects of vanadium pentoxide dust and fume in humans.

Pentavalent and tetravalent forms of vanadium have produced aneugenic effects in vitro in the presence and absence of metabolic activation. There is evidence that these forms of vanadium as well as trivalent vanadium can also produce DNA/chromosome damage in vitro, both positive and negative results having emerged from the available studies. The weight of evidence from the available data suggests that vanadium compounds do not produce gene mutations in standard in vitro tests in bacterial or mammalian cells.

In vivo, both pentavalent and tetravalent vanadium compounds have produced clear evidence of aneuploidy in somatic cells following exposure by several different routes. The evidence for vanadium compounds also being able to express clastogenic effects is, as with in vitro studies, mixed, and the overall position on clasto- genicity in somatic cells is uncertain. A positive result was obtained in germ cells of mice receiving vanadium pentoxide by intraperitoneal injection. However, the underlying mechanism for this effect (aneugenicity;

clastogenicity) is uncertain. It is also unclear how these findings can be generalized to more realistic routes of exposure or to other vanadium compounds.

The nature of the genotoxicity database on vanadium pentoxide and other vanadium compounds is such that it is not possible to clearly identify the threshold level, for any route of exposure relevant to humans, below which there would be no concern for potential genotoxic activity.

No useful information is available on the carcino- genic potential of any form of vanadium via any route of exposure in animals¹ or in humans.

A fertility study in male mice, involving exposure to sodium metavanadate in drinking-water, suggests the possibility that oral exposure of male mice to sodium metavanadate at 60 and 80 mg/kg body weight directly caused a decrease in spermatid/spermatozoal count and in the number of pregnancies produced in subsequent matings. However, significant general toxicity (decreased body weight gain) was also evident at 80 mg/kg body weight.

1 The authors of this document are aware that a 2-year inhalation bioassay in rodents has recently been completed at the US National Toxicology Program.

However, results are not available at this time.

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There are a number of developmental studies on pentavalent and tetravalent vanadium compounds, and a consistent observation is that of skeletal anomalies.

Interpretation of these studies is difficult because of unconventional routes of exposure and evidence of maternal toxicity that may itself contribute to the effects seen in pups.

The toxicological end-points of concern for humans are genotoxicity and respiratory tract irritation.

Since it is not possible to identify a level of exposure that is without adverse effect, it is recommended that levels be reduced to the extent possible.

Acute LC₅₀ values for aquatic organisms range from 0.2 to about 120 mg/litre, with the majority lying between 1 and 12 mg/litre. More ecotoxicologically relevant end-points were development of oyster larvae (significantly reduced at 0.05 mg vanadium/litre) and reproduction of Daphnia (21-day no-observed-effect concentration at 1.13 mg/litre). There are few terrestrial studies. Most plant studies have been on hydroponic cultures where effects occurred at 5 mg/litre and higher;

these studies are difficult to interpret in relation to plants growing in soil.

Concentrations in environmental media are sub- stantially lower than reported toxic concentrations. Few data are available on concentrations at specific industrial sites, and it is not possible to conduct a risk assessment on this basis. However, reported concentrations appear to be similar to the highest natural concentrations, suggesting that risk would be low. Local measurements must be carried out to assess risk in any particular circumstance.

2. IDENTITY AND PHYSICAL/CHEMICAL PROPERTIES

Vanadium can exist in a number of different oxidation states: !1, 0, +2, +3, +4, and +5. The most common commercial form of vanadium is vanadium pentoxide (V₂O₅), in which vanadium is in the +5 oxidation state. Other forms of vanadium in the +5 oxidation state mentioned in this review derive from the vanadate ion (VO₃^–) and include ammonium metavanadate (NH₄VO₃), sodium metavanadate (NaVO₃), and sodium orthovanadate (Na₃VO₄). Compounds in the +4 oxidation state are derived from the vanadyl ion (VO²⁺)

— for example, vanadyl dichloride (VOCl₂) and vanadyl sulfate (VOSO₄). Compounds containing vanadium in the +3 oxidation state include vanadium oxide (V₂O₃). Table 1

provides some physicochemical properties of vanadium compounds that are referred to in this review.

Vanadium (CAS No. 7440-62-2) is a soft silvery- grey metal with a relative molecular mass of 50.9.

Vanadium pentoxide (CAS No. 1314-62-1) is the most commonly used vanadium compound and exists in the pentavalent state as a yellow-red or green crystalline powder of relative molecular mass 181.9. Other common synonyms include vanadic anhydride and divanadium pentoxide.

Vapour pressures (and hence Henry’s law con- stants) and octanol/water partition coefficients are not available for vanadium compounds.

3. ANALYTICAL METHODS

3.1 Workplace air monitoring

Airborne monitoring is largely based on measurement of vanadium, rather than vanadium pentoxide. The Health and Safety Executive has published MDHS 91 Metals and metalloids in workplace air by X-ray fluorescence spectrometry (HSE, 1998). This method can be used for measuring vanadium and vanadium

compounds in workplace air, but no method performance data are available for vanadium.

The US National Institute of Occupational Safety and Health (NIOSH, 1994) and the US Occupational Safety and Health Administration (OSHA, 1991) have published methods that are suitable for measuring vanadium and vanadium compounds in workplace air.

Both are generic methods for metals and metalloids in which samples are collected by drawing air through a membrane filter mounted in a cassette-type filter holder, dissolved in acid on a hotplate, and analysed by inductively coupled plasma – atomic emission spectrometry (ICP-AES). For both methods, the lower limit of the working range is approximately 0.005 mg/m³ for a 500-litre air sample, although these methods are not widely available.

3.2 Biological monitoring

The measurement of vanadium in end-of-shift urine samples is appropriate for biological monitoring of vanadium exposure and has been widely used to monitor occupational exposure to vanadium compounds in a number of industrial activities (Angerer & Schaller, 1994).

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Table 1: Physical/chemical properties of vanadium and selected inorganic vanadium compounds.

Solubility (g/litre) Compound

CAS number

Molecular/

atomic mass

Melting point (°C)

Boiling point (°C)

Cold water

(20–25 °C) Hot water Other solvents Vanadium, V 7440-62-2 50.942 1890 ± 10;

1917

3380 Insoluble Insoluble Not attacked by hot or cold hydrochloric acid or cold sulfuric acid, but soluble in hydrofluoric acid, nitric acid, and aquaregia Vanadium

pentoxide, V2O5

1314-62-1 181.9 690 1750 8 No data Soluble in acid/alkali;

insoluble in absolute alcohol

Sodium metavanadate, NaVO3

13718-26- 8

121.93 No data No data 211 388 (at 75

°C)

No data

Sodium orthovanadate, Na3VO4

13721-39- 6

183.91 850–856 No data Soluble No data Soluble in alcohol

Ammonium metavanadate, NH4VO3

7803-55-6 116.98 200

(decomposes)

No data 58 Decomposes Soluble in ammonium

carbonate

Vanadium oxytrichloride, VOCl3

7727-18-6 Soluble,

decomposes

No data Soluble in alcohol, ether, acetic acid

Vanadyl sulfate, VOSO4

27774-13- 6

Very soluble No data No data

Vanadyl oxydichloride, VOCl2

10213-09- 9

Decomposes No data Soluble in dilute nitric acid

Vanadium trioxide, V2O3

1314-34-7 Slightly

soluble

Soluble Soluble in nitric acid, hydrofluoric acid, alkali

Vanadium is eliminated in the urine with a half-life of 15–40 h (Sabbioni & Moroni, 1983). Pre-shift and post-shift urine vanadium levels measured at the beginning and the end of a working week will, therefore, give a measure of daily absorption and accumulated dose from exposures over the preceding days. A further study of workers exposed to vanadium pentoxide (Kawai et al., 1989) demonstrated the utility of measuring mid- shift urinary vanadium as an indicator of exposure.

Blood vanadium levels were also determined but offered no advantage over urine measurements. As non- invasive sampling is normally preferred for routine biological monitoring, the measurement of vanadium in urine is generally recommended.

In biological monitoring studies of occupational vanadium exposure, urinary levels of vanadium associated with airborne exposures have been measured (see Table 4 in section 6.2).

Urinary vanadium may be determined accurately by several analytical techniques (Hauser et al., 1998;

HSE, in press). Electrothermal atomic absorption

spectrophotometry (AAS), with pre-concentration by chelation and solvent extraction, is the most widely used analytical method for the determination of vanadium in urine, and validated methods have been described in the literature. This analytical method gives typical detection limits of 0.1 µg/litre for vanadium in urine, with analytical precisions of 11% relative standard deviation at 1 µg/litre and 4% at 10 µg/litre.

3.3 Environmental monitoring

Various methods have been described for analysis of vanadium in air, surface waters, and biota (e.g.,

Ahmed & Banerjee, 1995). Flameless AAS (NIOSH, 1977) gives a detection limit of 1 ng/ml in air, corresponding to an absolute sensitivity of 0.1 ng vanadium. ICP-AES has a working range of 5–2000 µg/m³ for a 500-litre air sample (NIOSH, 1994). Direct aspiration and graphite furnace AAS methods for determining vanadium compounds in water were reported in US EPA (1983). The detection limits for these two methods are 200 and 4 µg/litre, respectively (US EPA, 1986). Instrumental neutron activation analysis gave detection limits of 0.01 µg/g in

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the context of sea mammal tissues (Mackey et al., 1996).

The instrumental detection limit was 0.1 ng/ml using inductively coupled plasma – mass spectrometry (Saeki et al., 1999).

4. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE

Vanadium is a relatively abundant element with a very wide distribution; however, workable deposits are very rare. Vanadium occurs in the minerals vanadinite, chileite, patronite, and carnotite. It constitutes about 0.01% of the crust of the Earth (Budavari et al., 1996). It is derived mainly from titaniferous magnetites containing 1.5–2.5% vanadium pentoxide, which are mined in South Africa, Russia, and China (HSE, in press). During the smelting of iron ore, a vanadium slag is formed that contains 12–24% vanadium pentoxide, which is used for the production of vanadium metal. Worldwide production of vanadium was stable at just over 27 000 tonnes per annum between 1976 and 1990. Estimated production in 1990 was 30 700 tonnes, comprising approximately 15 400 tonnes from South Africa, 4100 tonnes from China, 8200 tonnes from the former USSR, 2100 tonnes from the USA, and under 900 tonnes from Japan (Hilliard, 1992). Vanadium pentoxide is also produced by solvent extraction from uranium ores and by a salt roast process from boiler residues or residues from elemental

phosphate plants. Ferrovanadium can be obtained from vanadium pentoxides or vanadium slags by the alumino- thermic process.

All crude oils contain metallic impurities, including vanadium, which is present as an organometallic

complex. The vanadium concentration in the oils varies greatly, depending on their origin. The concentration of vanadium in crude oil ranges from 3 to 260 µg/g and in residual fuel oil from 0.2 to 160 µg/g (NAS, 1974). During the burning of fuel oils in boilers and furnaces, the vanadium is left behind as vanadium pentoxide in the solid residues, soot, boiler scale, and fly ash. The vanadium content of these residues varies from less than 1%

up to almost 60%. Vanadium is also present in coal, typically at a concentration between 14 and 56 ppm (mg/kg).

Vanadium is used in the United Kingdom in certain ferrovanadium alloys, being added in relatively small proportions at the refining stage of steelmaking.

Titanium-boron-aluminium (TiBAl) rod, containing less than 1% vanadium, is used by the secondary aluminium industry as a grain refiner. The hard metals industry uses small amounts of vanadium carbide in the production of tungsten carbide tool bits. Pure vanadium, imported from

outside the United Kingdom, is used in very small quan- tities for research purposes.

Vanadium pentoxide is used as the catalyst for a variety of gas-phase oxidation processes, particularly the conversion of sulfur dioxide to sulfur trioxide during the manufacture of sulfuric acid. The most frequently used vanadium pentoxide catalyst contains 4–6%

vanadium as vanadium pentoxide on a silica base.

Vanadium pentoxide is also used in some pigments and inks used in the ceramics industry to impart a colour ranging from brown to green. Pigments and inks are made containing up to about 15% vanadium pentoxide, the higher-concentration ones being supplied in an oil base rather than as a dry powder.

Vanadium pentoxide can be used as a colouring agent and to provide ultraviolet filtering properties in some glasses. Normally, the vanadium content in the batch materials is less than 0.5%.

Atmospheric emissions of vanadium from natural sources have been estimated at 8.4 tonnes per annum globally (range 1.5–49.2 tonnes). Natural sources, in order of importance, are continental dusts, volcanoes, seasalt spray, forest fires, and biogenic processes (Nriagu, 1990).

By far the most important source of environmental contamination with vanadium is combustion of oil, with coal combustion as the second most important. Of the estimated total global emissions from both natural and anthropogenic sources of 64 000 tonnes per annum to the atmosphere, 58 500 tonnes come from oil combustion, with more than 33 500 tonnes of this accounted for by the developing economies in Asia and just under 14 500 tonnes by Eastern Europe and the former USSR. There are considerable regional variations in vanadium emissions. For example, emissions to the Great Lakes area fell between 1980 and 1995, whereas those to the Mediterranean basin have continued to rise, dominated by emissions from a few countries (Turkey 20%, Egypt 19%, and Lebanon 15% of the total) (Nriagu

& Pirrone, 1998).

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5. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION

5.1 Chemical speciation of vanadium The chemistry of vanadium is extremely complex, and the reader is referred elsewhere for detailed discussion of the origin, speciation, bioaccumulation, and complex-forming chemistry of the metal related to the environment and biological systems (Crans et al., 1998).

A simple summary of vanadium chemistry is presented here.

Under environmental conditions, vanadium may exist in oxidation states +3, +4, and +5. V³⁺ and V⁴⁺ act as cations, but V⁵⁺, the most common form in the aquatic environment, reacts both as a cation and anionically as an analogue of phosphate.

In minerals, the oxidation state of vanadium may be +3, +4, or +5, but all mineral dissolution rapidly oxidizes V³⁺ and V⁴⁺ to the pentavalent state. Dry weathering produces dusts that may be distributed over great distances; deposition of dust into water will also lead to exclusively pentavalent vanadium. Vanadium is a non- volatile metal, and atmospheric transport is via particulates. In fuel oils and coal, vanadium is present as very stable porphyrin and non-porphyrin complexes (Yen, 1975; Fish & Komlenic, 1984) but is emitted as oxides when these fossil fuels are burned. The native oxides are sparingly soluble in water but undergo hydrolysis to generate “vanadate” in solution. Vanadate is often used as a generalized term for vanadium species in solution. Speciation of vanadium in solution is complex and highly dependent on vanadium concentration.

Under most common environmental conditions of pH and redox potential, and at the low concentrations reported for vanadium in natural waters, the vanadate is largely monomeric. At higher concentrations, such as those used in toxicity testing, dimeric and trimeric forms may predominate, and this can have an effect on how the vanadium compounds interact with biological systems (Crans et al., 1998).

Within tissues in organisms, V³⁺ and V⁴⁺ predominate because of largely reducing conditions; in plasma, however, which is high in oxygen, V⁵⁺ is formed (Crans et al., 1998).

5.2 Essentiality of vanadium

Vanadium has been characterized as a constituent of several enzyme systems and complexes within living organisms. Nitrogen-fixing bacteria and cyanobacteria contain nitrogenases, which catalyse the reduction of

atmospheric nitrogen to ammonia. The best characterized nitrogenase is molybdenum-dependent, and its detailed structure has been published (Chan et al., 1993).

Although it has been known for a long time (Bortels, 1936) that vanadium could substitute for molybdenum as a trace element in nitrogen-fixing bacteria, only recently has it been studied in detail. The structure of the vanadium-dependent enzyme is not fully known but is assumed to be similar to the molybdenum–iron protein (Chan et al., 1993). The vanadium enzyme has been shown to function under conditions of low molybdenum, but it may also operate under all conditions; genetic variants lacking the molybdenum–iron enzyme and relying exclusively on the vanadium–iron enzyme are known.

Vanadium-dependent haloperoxidases have been found in marine macroalgae and also in a lichen and fungus. Amavadin, a complex molecule centred on vanadium, is found in fungi of the genus Amanita; its function is not known, but it may act as a mediator in electron transfer. In ascidians (Tunicata; Protochordata), commonly called sea squirts, it has been suggested that vanadium interacts with tunichromes, oligopeptides that are the building blocks of the tunic. In fan worms (Polychaeta; Annelida), a function for vanadium in oxygen absorption and storage has been suggested.

Recent reviews on the role of vanadium in biological systems include those by Rehder & Jantzen (1998), Wever & Hemrika (1998), Chasteen (1990), and Sigel &

Sigel (1995), where details of the chemistry of vanadium in biological systems can be found.

Whether vanadium is an essential trace element for mammals remains an open question. Deficiency states have been described for goats and chicks, consisting of reproductive anomalies and deleterious effects on bone growth (Nielsen & Uthus, 1990). However, there is disagreement on results, and, if vanadium is essential, requirement levels of the order of a few nanograms per day are likely (Mackey et al., 1996).

5.3 Bioaccumulation

Ascidians have been known to accumulate large residues of vanadium since a first report in 1911 (Henze, 1911). The metal accumulates in blood cells (vanado- cytes). The highest reported concentration is 350 mmol/

litre in the blood cells of Ascidia gemmata (Michibata et al., 1991), a concentration factor above that in seawater of 10⁷. Recent reviews of accumulation and the signifi- cance of vanadium in these organisms include those by Kustin & Robinson (1995), Michibata (1996), and Michibata & Kanamori (1998). Recently (Ishii et al., 1993), high vanadium accumulation was demonstrated for

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polychaetes of the genus Pseudopotamilla; polychaetes of other genera did not accumulate the metal.

Pseudopotamilla occelata showed concentrations in whole soft body ranging from 320 to 1350 mg/kg dry weight. Distribution, speciation, and possible physio- logical roles of the metal are discussed in Ishii (1998).

Apart from the specific accumulators mentioned above, organisms generally do not concentrate or accumulate vanadium from environmental media to a high degree, and there is no indication of biomagnification in food chains. Miramand & Fowler (1998) reviewed reported levels of vanadium in marine organisms and calculated concentration factors for components of a typical marine food chain based on average seawater concentrations of 2 ng/g. Concentration factors for primary producers ranged from 40 to 560, for primary consumers from 40 to 150, for secondary consumers from approximately 20 to 150, and for tertiary consumers from approximately 2 to 400. Although vanadium

concentrations are higher in sediment than in open seawater, only one study has attempted to quantify uptake from sediment using ⁴⁸V; the ragworm Nereis diversicolor accumulated vanadium from the sediment with a low transfer factor of about 0.02 (Miramand, 1979).

Using labelled food, assimilation coefficients have been calculated for several marine organisms. For the carnivorous invertebrates Marthasterias glacialis, Sepia officianalis, Carcinus maenus, and Lysmata seticaudata, assimilation coefficients of 88% (Miramand et al., 1982), 40% (Miramand & Fowler, 1998), 38%, and 25% (Miramand et al., 1981) were reported, respectively.

Biological half-lives in the same organisms were 57, 7, 10, and 12 days, respectively. A high proportion of the vanadium was present in the digestive gland (63–98.8%).

For a single fish species (Gobius minutus), assimilation was much lower, at 2–3%, with a half-life of 3 days (Miramand et al., 1992), and accumulation was also low in a bivalve feeding on suspended matter (Mytilus galloprovincialis), at 7%, with a half-life of 7 days (Miramand et al., 1980). Comparison of uptakes via food and directly from water showed that invertebrates accumulated much of the vanadium from food

(Miramand & Fowler, 1998). Recent studies on bioaccumulation of vanadium in pinnipeds and cetaceans in Swedish (Frank et al., 1992), northern Pacific (Saeki et al., 1999), and Alaskan/Atlantic (Mackey et al., 1996) waters have shown a correlation of residues with age,

comparable to other metal residues. Liver showed the highest accumulation of the metal of all tissues analysed.

However, bone, which might be expected to accumulate the element, was not analysed. Alaskan sea mammals showed the highest levels, ranging up to 1.2 µg/g wet weight. The authors suggest a unique dietary source, a unique geochemical source, or anthropogenic input to

the Alaskan marine environment as possible explanations (Mackey et al., 1996).

Marine biota are thought to contribute to the sedimentation of vanadium from seawater via shells, faecal pellets, and moult. Coastal sediments appear to be a sink for vanadium (Miramand & Fowler, 1998).

5.4 Leaching and bioavailability in soils A field study conducted over 30 months examined movement of vanadium added to the top 7.5 cm of coastal plain soil and its availability to bean plants. Less than 3% of applied metal moved down the soil profile.

Extractable concentrations decreased over the first 18 months of the study and remained constant thereafter.

Uptake of vanadium into the roots and upper parts of the bean plants did not change significantly between 18 months and the end of the experiment but was reduced during the initial period, suggesting reduced bioavailability over time as a result of binding to soil materials (Martin & Kaplan, 1998).

6. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE

6.1 Environmental levels

A very substantial literature exists on environmental levels of vanadium. The metal has been monitored in geographical areas with naturally high occurrence of the metal (mainly volcanic regions) where local water con- tributes to drinking supplies, and vanadium has been used to monitor general industrial contamination, since it is a common component of oil and coal. In addition, accumulation of the metal has been studied intensively for marine organisms, since vanadium is known to accumulate in a few species (section 5). In this section, representative levels are presented. The reader is referred to several recent reviews for more detailed coverage of the literature in each of the subsections following.

6.1.1 Air

Earlier measurements of vanadium in air were reviewed by Schroeder et al. (1987); most measurements were performed in the 1970s, with a few in the early 1980s. A review of later measurements and comparison with the earlier review were conducted by Mamane &

Pirrone (1998). The ranges they reported are presented in Table 2, together with reported concentrations down- wind of the Kuwait oil fires in 1991–1992. The ranges are very large, and there is no simple explanation for the

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Table 2: Ranges of concentrations of vanadium in air.

Area

Atmospheric concentration

(ng/m³) Reference Urban air

Rural air Remote areas^a

0.4–1460 2.7–97 0.001–14

Schroeder et al., 1987

Urban air Rural air Remote areas

0.5–1230 0.4–500

0.01–2

Mamane & Pirrone, 1998

Dhahran, Saudi Arabia, during Kuwait oil fires

2.4–1170 (in the PM10

fraction)

Sadiq & Mian, 1994

a Includes the Arctic and oceanic islands in the Atlantic and Pacific.

variation; possible causes are reviewed by Mamane &

Pirrone (1998), although they can draw no firm conclusions.

Vanadium in air from oil combustion tends to be in smaller particulate fractions. In arid areas with dust storms, high levels of vanadium have been reported;

here, particle size tends to be much larger (Mamane &

Pirrone, 1998).

Bulk precipitation concentration ranges have been reported at 4.1–13 µg/litre for the rural United Kingdom (Galloway et al., 1982) and 0.12–0.65 µg/litre (mean 0.45 µg/litre) in Switzerland (Atteia, 1994). Wet deposition in an area of New England remote from anthropogenic input showed concentrations of vanadium ranging from 0.2 to 1.16 µg/litre (average 0.67 µg/litre) and in Bermuda ranging from 0.049 to 0.111 µg/litre (average 0.096 µg/litre) (Church et al., 1984). Ice and snow levels in northern Norway and Alaska were 0.31 and 0.13 µg/litre, respectively (Galloway et al., 1982), and two ice core levels in Greenland were reported at 0.022 and 0.016 µg/litre. Levels in rain ranged from 1.1 to 46 µg/litre for rural and urban sites in North America and Europe (Galloway et al., 1982).

Based on these reported concentrations, Mamone

& Pirrone (1998) calculated representative total deposition rates of vanadium at 0.1–10 kg/ha per annum for urban sites affected by strong local sources, 0.01–

0.1 kg/ha per annum for rural sites and urban ones with no strong local source, and <0.001–0.01 kg/ha per annum for remote sites.

6.1.2 Surface waters and sediments Most surface fresh waters contain less than 3 µg vanadium/litre (Hamada, 1998). The vanadium content of water from the Colorado River basin (USA) ranged from 0.2 to 49.2 µg/litre, with the highest levels associated with uranium–vanadium mining (Linstedt & Kruger,

1969). A wider survey of Wyoming, Idaho, Utah, and Colorado in the USA showed vanadium concentrations of 2.0–9.0 µg/litre (Parker et al., 1978). Unfiltered water from the source area of the Yangtze River in China contained between 0.24 and 64.5 µg/litre, whereas concentrations in filtered water ranged from 0.02 to 0.46 µg/litre (Zhang & Zhou, 1992). The highest levels reported are in surface waters in the area of Mount Fuji in Japan. Two springs had 14.8 and 16.4 µg/litre, and five river samples showed between 17.7 and 48.8 µg/litre (Hamada, 1998).

Data on concentrations of vanadium in wastewater and local surface water are few, and studies are old;

reliability for present-day operations is questionable. A single concentration of 2 mg/litre for surface water from 1961, reported in IPCS (1988), seems much higher than other more recent reports, where levels of up to 60 µg/litre in industrial areas seem more likely.

Seawater concentrations have been reviewed by Miramand & Fowler (1998). Most reported concentrations in the open ocean have been in the range 1–3 µg/litre, with the highest reported value at 7.1 µg/litre. Sedi- ment concentrations range from 20 to 200 µg/g dry weight, with higher levels in coastal sediments.

6.1.3 Biota

Ranges of concentrations of vanadium in marine organisms are given in Table 3, based on a review of the literature in Miramand & Fowler (1998), where the original references can be found. The ranges include values from areas of likely local contamination from industrial sources. With the exception of ascidians (tunicates), some annelids, and molluscs, concentrations of vanadium in marine organisms are low. The range for planktonic species is heavily influenced by a single study showing accumulation up to 290 mg/kg dry weight; this was mainly into shells of planktonic forms of molluscs. Generally, planktonic organisms show

concentrations of vanadium around 1 mg/kg.

There are fewer data for freshwater organisms. The most comprehensive study of organisms was conducted in the Mount Fuji area of Japan, where concentrations in organisms from water with high (43.4 µg/litre) and lower (0.72 or 0.4 µg/litre) concentrations of vanadium were compared. Water plants from the high-vanadium area contained 21.8 ± 11.3 µg/g dry weight of the metal (range 5.6–43.7 µg/g), compared with 0.79 ± 0.52 µg/g (range 0.22–1.91 µg/g) in the low-vanadium area. A green microalga in the high-concentration area contained the highest reported concentration of the metal, at 118–168 µg/g dry weight. The vanadium concentration in rainbow trout (Oncorhynchus mykiss) farmed in water from these areas was measured: bone concentrations

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Table 3: Concentrations of vanadium in marine organisms.^a

Organism

Concentration of vanadium (mg/kg dry weight)

Phytoplankton 1.5–4.7

Zooplankton 0.07–290

Macroalgae 0.4–8.9

Ascidians 25–10 000

Annelids 0.7–786

Other invertebrates 0.004–45.7

Fish 0.08–3

Mammals <0.01–1.04 (fresh weight)

a From Miramand & Fowler (1998).

were 0.87, 4.77, and 17.2 µg/g and kidney concentrations were 0.43, 2.38, and 4.63 µg/g for water concentrations of 0.72, 43.4, and 82.7 µg/litre, respectively. In all cases, muscle concentrations were low and did not differ between areas (0.016–0.024 µg/g) (Hamada, 1998). A pooled sample of 279 larval razorback sucker (Xyrauchen texanus) from the Green River in Utah, USA, showed a vanadium concentration of 1.7 mg/kg dry weight. The Green River receives irrigation drainage and typically shows higher concentrations of a range of elements compared with the input streams (Hamilton et al., 2000).

A single study detected vanadium in 19 out of 120 canvasback ducks (Aythya valisineria) wintering in Louisiana, USA; the maximum concentration in duck liver was 0.94 µg/g dry weight (Custer & Hohman, 1994).

The mean vanadium concentration in four species of Japanese waterfowl ranged from 3.69 to 8.11 µg/g dry weight in kidney and from 0.39 to 3.69 µg/g in liver tissue (Mochizuki et al., 1999).

6.1.4 Soil

At distances of 600–2400 m from a metallurgical plant producing vanadium pentoxide, to a depth of 10 cm, the surface layer of the soil contained 18–136 mg vanadium/kg dry weight (Lener et al., 1998). The back- ground concentration for the area is not stated, although levels at 600 m from the plant are clearly elevated compared with those at greater distances. Concentrations in soil globally are very variable. Schacklette et al. (1971) found concentrations in soils in the USA ranging from

<7 to 500 mg/kg, with the median at around 60 mg/kg and the 90th percentile at 130 mg/kg. The average worldwide soil concentration is around 100 mg/kg (Hopkins et al., 1977).

6.2 Human exposure

The quantitative data available to the authors of this document are restricted mainly to the occupational environment (HSE, in press). Information on control measures has been derived from industry sources in the United Kingdom.

The main activity where workers can be exposed to vanadium in the United Kingdom is the cleaning of oil- fired boilers and furnaces where vanadium pentoxide is a major component of the boiler residues. It is estimated that 1000 workers in the United Kingdom are employed by specialist boiler maintenance contractors, although they probably spend less than 20% of their time cleaning oil-fired boilers. Measured vanadium exposures (total inhalable fraction) can approach 20 mg/m³ (during task), but can be lower than 0.1 mg/m³. The lowest results are obtained where wet cleaning methods are used. Respira- tory protective equipment is usually worn during boiler cleaning operations.

Handling of catalysts in chemical manufacturing plants is carried out by specialist contractors. Fewer than 50 workers in the United Kingdom are exposed to vanadium pentoxide during such activities. Exposure depends on the type of operations being carried out.

During the removal and replacement of the catalyst, exposures can be between 0.01 and 0.67 mg/m³. Sieving of the catalyst can lead to higher exposures, and results of between 0.01 and 1.9 mg/m³ (total inhalable vanadium) have been obtained. Air-fed respiratory protective equipment is normally worn during catalyst removal and replacement and sieving.

Fewer than 200 workers in the United Kingdom are exposed to vanadium during the manufacture of

ferrovanadium alloys and TiBAl rod. The limited exposure data available indicate exposures below the limit of detection of 0.01 mg/m³. No data have been found to quantify exposures during the manufacture of TiBAl rod.

There are fewer than 50 workers who are exposed to vanadium compounds in the United Kingdom during the manufacture of vanadium-containing pigments for the ceramics industry. Exposure is controlled by the use of local exhaust ventilation, and measured data indicate that levels are normally below 0.2 mg/m³ (total inhalable fraction).

Occupational exposure data are also available from Finland, including personal monitoring data from a range of work processes in a vanadium refining plant (Kivilu- oto, 1981). Generally, two samples were taken per person over a 2-month period. The mean respirable fraction

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Table 4: Biological monitoring studies of occupational vanadium exposure.

Industry

Sample

matrix No. of subjects

Measured air V (mg/m³) (TWA)

Urine V (µg/litre)

(range) Reference

V2O5 production Urine 58 Up to 5 28.3 (3–762) Kucera et al., 1992

Boiler cleaning Urine 4 2.3–18.6

(0.1–6.3)

2–10.5 White et al., 1987

Incinerator workers Urine 43 Not known <0.1–2 Wrbitsky et al., 1995

Boiler cleaners Urine 10 (!RPE)^a 10 (+RPE)

Not known 92 (20–270)

38

Todaro et al., 1991

Boiler cleaners Urine 30 0.04–88.7 (0.1–322) Smith et al., 1992

V alloy production Urine 5 Not known 3.6 (0.5–8.9) Arbouine, 1990

Pigment manufacture

Urine 8 Not known 2.3 (0.8–6.3) Arbouine, 1990

V2O5 staining Urine 2 (<0.04–0.13) <4–124 Kawai et al., 1989

Unexposed (general population)

Urine 213 012 0.22 (0.07–0.5)

<0.4

<0.1

Kucera et al., 1992 White et al., 1987 Smith, 1992

a RPE = respiratory protective equipment.

(particle size 5 µm or less) of the dust was 20%. The highest values (expressed as total inhalable vanadium) were obtained in the laboratory (range 0.25–4.7 mg/m³, mean shift length exposure 1.7 mg/m³) and the smelting room (0.055–0.47 mg/m³, mean 0.21 mg/m³), but were usually much lower for other processes (around 0.002–

0.18 mg/m³, mean 0.005–0.037 mg/m³).

Biological monitoring studies of occupational vanadium exposure also indicate the magnitude of airborne exposures (Table 4). A further recent example is detailed (Kucera et al., 1992, 1994, 1998; see also sections 7 and 9): a group of workers from the Czech Republic involved in the manufacture of vanadium pentoxide from slag rich in vanadium for periods of 0.5–33 years (mean duration of exposure 9.2 years) was exposed to airborne vanadium concentrations of 0.016–4.8 mg/m³. Urinary vanadium content was 3.02–769 ng/ml, compared with 0.066–53.4 ng/ml in controls. In blood, vanadium levels were 3.1–217 ng/ml, compared with 0.032–0.095 ng/ml in controls. The vanadium content in the hair of exposed and non-exposed persons was in the range of 0.103–203 mg/kg and 0.009–3.03 mg/kg, respectively, and the vanadium content in the fingernails was in the range of 0.260–614 mg/kg and 0.017–16.5 mg/kg, respectively.

Determinations of the vanadium content were carried out by both radiochemical and instrumental neutron activation analyses in all instances.

Estimates given in IPCS (1988) for total dietary intake of the general population in food range from 11 to 30 µg/day (adults). The mean vanadium concentration in drinking-water in Cleveland, USA, was 5 µg/litre, with a maximum of 100 µg/litre (Strain et al., 1982). Wells close

to a vanadium slag processing plant in the Czech Republic showed concentrations ranging from 0.01 to 0.44 µg/litre; the local municipal supply contained 0.01 µg/litre (Lener et al., 1998). Groundwater in the vicinity of Mount Fuji in Japan contains high vanadium levels from leaching of larval flows rich in the metal;

measured concentrations in deep wells were between 89 and 147 µg/litre, levels higher than those measured in spring water (Hamada, 1998). A sample of drinking-water from Kanagawa Prefecture in Japan contained a

vanadium concentration of 22.6 µg/litre, the highest value in a survey of Japanese cities and 21 cities in the USA (Tsukamoto et al., 1990). The water here was influenced by Mount Fuji groundwater. Groundwater in the region of Mount Etna in Sicily has been used as a source of drinking-water. The western basin showed the highest levels of vanadium; 33% of samples had concentrations between non-detectable and 20 µg/litre, 54%

between 20 and 50 µg/litre, and 13% higher than 50 µg/litre (Giammanco et al., 1996). Older studies summarized in IPCS (1988) report drinking-water concentrations up to 70 µg/litre, although the majority of samples contained less than 10 µg/litre, and in many the metal was undetectable. Levels in bottled waters from mineral springs may contain much higher levels of vanadium;

one study of bottled waters from Switzerland reported a range of 4–290 µg/litre (Schlettwein-Gzell & Mommsen- Straub, 1973).

The mean concentration of vanadium in cigarettes was 1.11 ± 0.35 µg/g, and the mean concentration in cigarette smoke was 0.33 ± 0.06 µg/g (Adachi et al., 1998).