Inorganic lead (EHC 165, 1995)

INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY

ENVIRONMENTAL HEALTH CRITERIA 165

INORGANIC LEAD

This report contains the collective views of an international group of
experts and does not necessarily represent the decisions or the stated
policy of the United Nations Environment Programme, the International
Labour Organisation, or the World Health Organization.

First draft prepared at the National Institute of Health Sciences,
Tokyo, Japan, and the Institute of Terrestrial Ecology, Monk's Wood,
United Kingdom

Published under the joint sponsorship of the United Nations
Environment Programme, the International Labour Organisation, and the
World Health Organization

World Health Organization
Geneva, 1995

The International Programme on Chemical Safety (IPCS) is a joint
venture of the United Nations Environment Programme, the International
Labour Organisation, and the World Health Organization. The main
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that could produce internationally comparable results, and the
development of manpower in the field of toxicology. Other activities
carried out by the IPCS include the development of know-how for coping
with chemical accidents, coordination of laboratory testing and
epidemiological studies, and promotion of research on the mechanisms
of the biological action of chemicals.

WHO Library Cataloguing in Publication Data

Inorganic lead.

(Environmental health criteria ; 165)

1.Lead - adverse effects 2.Environmental exposure
3.Guidelines I.Series

ISBN 92 4 157165 9 (NLM Classification: QV 292)
ISSN 0250-863X

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CONTENTS

ENVIROMENTAL HEALTH CRITERIA FOR INORGANIC LEAD

PREAMBLE

PREFACE

1. SUMMARY

1.1. Identity, physical and chemical properties, and analytical
methods
1.2. Sources of human exposure
1.3. Environmental transport, distribution and transformation
1.4. Environmental levels and human exposure
1.5. Kinetics and metabolism in laboratory animals and humans
1.6. Effects on laboratory animals and in vitro systems
1.7. Effects on humans
1.8. Evaluation of human health risks

2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL
METHODS

2.1. Physical and chemical properties of lead and its compounds
2.2. Analytical procedures
2.2.1. Sampling procedures
2.2.1.1 Sampling of environmental media
2.2.1.2 Sampling of biological materials
2.2.2. Analytical methods for lead
2.2.2.1 Analysis of lead in environmental
samples
2.2.2.2 Analysis of lead in biological materials
2.2.2.3 Analytical procedures for biomarkers of
lead exposure and effect
2.3. Conversion factors

3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE

3.1. Natural occurrence
3.1.1. Rocks and soils
3.1.2. Sediments
3.1.3. Water
3.1.4. Air
3.1.5. Plants
3.1.6. Environmental contamination from natural sources
3.2. Anthropogenic sources
3.2.1. Lead mining
3.2.2. Smelting and refining
3.2.3. Environmental pollution from production of lead
3.3. Consumption and uses of lead and its compounds
3.4. Sources of environmental exposure

4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION AND TRANSFORMATION

4.1. Transport and distribution between media
4.1.1. Atmospheric deposition
4.1.2. Transport to water and soil
4.1.3. Transport to biota
4.1.3.1 Aquatic organisms
4.1.3.2 Terrestrial organisms
4.2. Environmental transformation
4.2.1. Abiotic transformation
4.2.2. Biotransformation

5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE

5.1. Inhalation route of exposure
5.1.1. Ambient air
5.1.1.1 Emissions from motor vehicles
5.1.1.2 Stationary sources
5.1.2. Indoor air
5.1.3. Air in the working environment
5.1.4. Smoking of tobacco
5.2. Exposure by ingestion
5.2.1. Water
5.2.2. Food and alcoholic beverages
5.2.2.1 Food
5.2.2.2 Total intake from food
5.2.2.3 Alcoholic beverages
5.2.3. Dust and surface soils
5.2.3.1 Dust
5.2.3.2 Soil
5.2.3.3 Migration of lead from food containers
5.3. Miscellaneous exposure
5.3.1. Cosmetics and medicines
5.4. General population exposure
5.5. Blood lead concentrations of various populations
5.5.1. Adult populations
5.5.2. Children
5.5.3. Remote populations
5.6. Occupational exposure

6. KINETICS AND METABOLISM IN LABORATORY ANIMALS AND HUMANS

6.1. Absorption
6.1.1. Absorption after inhalation
6.1.1.1 Animal studies
6.1.1.2 Human studies
6.1.2. Absorption of lead from the gastrointestinal tract
6.1.2.1 Animal studies
6.1.2.2 Human studies
6.1.2.3 Nutritional status and lead absorption
via gastrointestinal tract

6.1.3. Dermal absorption
6.1.3.1 Human dermal absorption
6.1.4. The relationship of external lead exposure to blood
lead concentration
6.1.4.1 Ambient air
6.1.4.2 Food
6.1.4.3 Drinking-water
6.1.4.4 Soil and dust
6.1.4.5 Total lead intake
6.2. Distribution
6.2.1. Animal studies
6.2.2. Human studies
6.2.3. Transplacental transfer
6.3. Elimination and excretion
6.4. Biological indices of lead exposure and body burden
6.4.1. Blood lead
6.4.2. Tooth lead
6.4.3. Bone lead
6.4.4. Lead in urine
6.4.5. Lead in hair

7. EFFECTS ON LABORATORY ANIMALS AND IN VITRO TEST SYSTEMS

7.1. Biochemical effects
7.1.1. Haem synthesis and haematopoiesis
7.2. Nervous system effects
7.2.1. Higher order behavioural toxicity
7.2.2. Mechanisms of lead-induced behavioural toxicity
7.2.2.1 Conclusions
7.2.3. Sensory organ toxicity
7.3. Renal system
7.4. Cardiovascular system
7.5. Reproductive system
7.6. Effects on bone
7.7. Immunological effects
7.8. Mutagenicity
7.9. Carcinogenicity

8. EFFECTS ON HUMANS

8.1. Biochemical effects of lead
8.1.1. Haem synthesis
8.1.1.1 Protoporphyrin levels
8.1.1.2 Coproporphyrin levels
8.1.1.3 delta-Aminolaevulinic acid levels in
urine and blood
8.1.1.4 Aminolaevulinic acid dehydratase levels
8.1.1.5 delta-Aminolaevulinic acid synthase
8.1.1.6 Other effects of decreased haem
synthesis

8.1.2. Vitamin D
8.1.3. Dihydrobiopterin reductase
8.1.4. Nicotinamide adenine dinucleotide synthetase
8.1.5. Nutritionally affected groups
8.2. Haematopoietic system
8.2.1. Anaemia
8.2.2. Pyrimidine-5'-nucleotidase activity
8.2.3. Erythropoietin production
8.3. Nervous system
8.3.1. Historical perspective
8.3.2. Neurotoxic effects in adults
8.3.2.1 Central nervous system
8.3.2.2 Peripheral nervous system
8.3.2.3 Autonomic nervous system
8.3.3. Neurotoxic effects in children
8.3.3.1 Historical perspective
8.3.4. Population-based cross-sectional studies on
children
8.3.4.1 Tooth lead studies
8.3.4.2 Blood lead studies
8.3.4.3 Follow-up studies
8.3.4.4 Conclusions and limitations of
cross-sectional studies
8.3.5. Prospective epidemiological studies on children
8.3.5.1 Common elements
8.3.5.2 Study descriptions
8.3.5.3 Summary of differences between studies
8.3.5.4 Results of studies
8.3.5.5 Questions prospective studies have not
answered
8.3.5.6 Attempting a consensus
8.3.6. Task group overview and interpretation of
prospective studies on children
8.3.6.1 Rationale
8.3.6.2 The prospective studies
8.3.6.3 A quantitative assessment of the
cross-sectional studies
8.3.6.4 Task group overview of cross-sectional
studies
8.3.6.5 An interpretation of the overview of
prospective and cross-sectional studies
8.3.7. Hearing impairment in children
8.4. Renal system
8.4.1. Clinical studies
8.4.2. Epidemiological studies
8.4.2.1 Occupational cohorts
8.4.2.2 General population
8.4.2.3 Cohort mortality studies
8.5. Cardiovascular system
8.5.1. Blood pressure

8.5.1.1 Studies on occupationally exposed
cohorts
8.5.1.2 Studies in the general population
8.5.2. Other cardiovascular effects
8.5.2.1 Occupational studies
8.5.2.2 Studies in the general population
8.5.3. Summary
8.6. Gastrointestinal effects
8.6.1. Occupational exposure
8.6.2. Exposure of children
8.7. Liver
8.7.1. Occupational exposure
8.7.2. Exposure of children
8.8. Reproduction
8.8.1. Female populations
8.8.2. Male populations
8.8.3. Hormonal responses
8.8.4. Postnatal growth and stature
8.9. Effects on chromosomes
8.10. Carcinogenicity
8.10.1. Occupational exposure and renal cancer
8.10.2. Conclusion
8.11. Effects on thyroid function
8.11.1. Occupational groups
8.11.2. Effects in children
8.12. Immune system
8.12.1. Occupational exposure
8.12.2. Children
8.13. Effects on bone
8.14. Biomarkers for lead effects

9. EVALUATION OF HUMAN HEALTH RISKS

9.1. Exposure assessment
9.1.1. General population exposure
9.1.2. Occupational exposures
9.2. Critical issues related to exposure evaluation
9.2.1. Sampling and analytical concerns
9.2.2. Data presentation
9.3. Relationship between exposure and dose
9.4. Surrogate measures of dose
9.4.1. Blood
9.4.2. Urine
9.4.3. Bone
9.4.4. Tooth
9.4.5. Hair
9.5. Biochemical effects of lead
9.5.1. Haem synthesis
9.5.1.1 Urinary coproporphyrin
9.5.1.2 Urinary aminolaevulinic acid in children

9.5.1.3 Urinary aminolaevulinic acid in adults
9.5.1.4 delta-Aminolaevulinic acid dehydratase
9.5.2. Vitamin D metabolism
9.5.3. Dihydrobiopterin reductase
9.5.4. Haemopoietic system
9.5.4.1 Anaemia in adults
9.5.4.2 Anaemia in children
9.5.4.3 Erythrocyte pyrimidine-5'-nucleotidase
9.6. Nervous system
9.6.1. Adults
9.6.1.1 Central nervous system
9.6.1.2 Peripheral nervous system
9.6.1.3 Autonomic nervous system
9.6.2. Children
9.6.2.1 Type of effect
9.6.2.2 Magnitude
9.6.2.3 Reversibility/persistence
9.6.2.4 Age-specific sensitivity
9.6.2.5 Interactions/subgroups
9.6.3. Animal studies
9.7. Renal system
9.8. Liver
9.9. Reproduction
9.9.1. Female
9.9.2. Male
9.10. Blood pressure
9.11. Carcinogenicity
9.12. Immune system

10. RECOMMENDATIONS FOR PROTECTION OF HUMAN HEALTH

10.1. Public health measures
10.2. Public health programmes
10.3. Screening, monitoring and assessment procedures

11. FURTHER RESEARCH

12. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES

REFERENCES

RESUME

RESUMEN

NOTE TO READERS OF THE CRITERIA MONOGRAPHS

Every effort has been made to present information in the criteria
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Criteria monographs, readers are requested to communicate any errors
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A detailed data profile and a legal file can be obtained from the
International Register of Potentially Toxic Chemicals, Case postale
356, 1219 Châtelaine, Geneva, Switzerland (Telephone No. 9799111).

* * *

This publication was made possible by grant number 5 U01
ES02617-15 from the National Institute of Environmental Health
Sciences, National Institutes of Health, USA, and by financial support
from the European Commission.

Environmental Health Criteria

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The first Environmental Health Criteria (EHC) monograph, on
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The original impetus for the Programme came from World Health
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JMPR

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WHO TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR INORGANIC LEAD

Members

Professor S. Araki, Department of Public Health, Faculty of Medicine,
University of Tokyo, Japan

Dr P. Baghurst, Division of Human Nutrition, Commonwealth Scientific
Industrial Research Organization, Adelaide, Australia

Dr D. Bellinger, Neuroepidemiology Unit, Gardner House, Children's
Hospital, Boston, Massachusetts, USA

Dr I. Calder, Occupational and Environmental Health, South Australian
Health Commission, Adelaide, South Australia, Australia

Dr D.A. Cory-Slechta, Department of Environmental Medicine,
University of Rochester School of Medicine and Dentistry,
Rochester, New York, USA

Dr K. Dietrich, Department of Environmental Health, Division of
Biostatistics and Epidemiology, University of Cincinnati College
of Medicine, Cincinnati, Ohio, USA

Dr R.A. Goyer, Chapel Hill, North Carolina, USA (Chairman)

Dr M.R. Moore, University of Glasgow, Department of Medicine and
Therapeutics, Western Infirmary, Glasgow, Scotland

Dr C. Nam Ong, Department of Community, Occupational and Family
Medicine, National University of Singapore, National University
Hospital, Singapore

Dr S.J. Pocock, Department of Epidemiology and Population Sciences,
Medical Statistics Unit, University of London, London, England

Dr M.B. Rabinowitz, Marine Biological Laboratory, Woods Hole,
Massachusetts, USA

Dr M. Smith, Thomas Coram Research Unit, London, England

Dr G. Winneke, Medical Institute for Environmental Health,
Heinrich-Heine University, Düsseldorf, Germany (Vice-Chairman)

Observers

Dr C. Boreiko, Environmental Health, International Lead Zinc Research
Organization (ILZRO) Inc., Research Triangle Park, North
Carolina, USA

Dr N.H. Clark, Lead Industry Environment and Health Forum, Melbourne,
Victoria, Australia

Dr J.M. Davis, Environmental Criteria and Assessment Office, US
Environmental Protection Agency, Research Triangle Park, North
Carolina, USA

Professor G. Duggin, Toxicology Unit, Royal Prince Alfred Hospital,
Camperdown, Australia

Dr G.R. Neville, Queensland Health Department, Brisbane, Australia

Secretariat

Dr G.C. Becking, International Programme on Chemical Safety,
Interregional Research Unit, World Health Organization, Research
Triangle Park, North Carolina, USA (Secretary)

Dr K.R. Mahaffey, National Institute of Environmental Health
Sciences, Research Triangle Park, North Carolina, USA^a

Dr A.E. Robinson, Toronto, Ontario, Canada (Rapporteur)

^a Present address: US Environmental Protection Agency, Environmental
Criteria and Assessment Office, Cincinnati, Ohio, USA

ENVIRONMENTAL HEALTH CRITERIA FOR INORGANIC LEAD

A WHO Task Group on Environmental Health Criteria for Inorganic
Lead met in Brisbane, Australia, from 1 to 6 February 1993. The
meeting was sponsored by a consortium of Australian Commonwealth and
State Governments through a national Steering Committee chaired by
Dr Keith Bentley, Director, Health and Environmental Policy,
Department of Human Services and Health, Canberra. The meeting was
hosted and organized by the Queensland Department of Health,
Dr G.R. Neville being responsible for the arrangements. Dr G. Murphy,
Director of Public Health, Queensland, welcomed the participants on
behalf of the Organizers, and Dr T. Adams, Chief Commonwealth Medical
Advisor and Dr G. Johns, Parliamentary Secretary to Federal Minister
for Health, Housing and Community Services, welcomed the participants
on behalf of the Commonwealth Government. Dr Johns stressed the
importance attached to this IPCS meeting by the Commonwealth and State
Governments of Australia. Dr G.C. Becking, IPCS, welcomed the
participants on behalf of Dr M. Mercier, Director of the IPCS and the
three cooperating organizations (UNEP/ILO/WHO). The Task Group
reviewed and revised the draft criteria monograph, and made an
evaluation of the risks to human health from exposure to inorganic
lead.

The Task Group draft was prepared by Dr A.E. Robinson, Toronto,
Canada, using texts made available by Dr K.R. Mahaffey^a (National
Institute of Environmental Health Sciences, Research Triangle Park,
North Carolina, USA) and Dr E. Silbergeld (University of Maryland
School of Medicine, Baltimore, Maryland, USA), and the comments
received from the IPCS contact points for environmental health
criteria monographs. The draft was revised extensively by the Task
Group taking into account the comments from the IPCS contact points.

Dr G.C. Becking (IPCS Central Unit, Interregional Research Unit)
and Dr P.G. Jenkins (IPCS Central Unit, Geneva) were responsible for
the overall scientific content and technical editing, respectively, of
this monograph.

The efforts of all who helped in the preparation and finalization
of this publication are gratefully acknowledged.

^a Present address: US Environmental Protection Agency, Environmental
Criteria and Assessment Office, Cincinnati, Ohio, USA

ABBREVIATIONS

AAS atomic absorption spectrometry
AES atomic emission spectroscopy
ALA delta-aminolaevulinic acid
ALAD delta-aminolaevulinic acid dehydratase
ASV anodic stripping voltametry
EDTA ethylenediaminetetraacetic acid
FEP free erythrocyte porphyrin
GFAAS graphite furnace atomic absorption spectrometry
ICP inductively coupled plasma
IDMS isotope dilution mass spectrometry
MPb mobilization yield of lead
MSW municipal solid waste
PbB blood lead
PbT tooth lead
TML tetramethyllead
XRFS X-ray fluorescence spectroscopy
ZPP zinc protoporphyrin

PREFACE

Although many countries have initiated programmes to lower the
level of lead in the environment, human exposure to lead remains of
concern to public health officials worldwide. For over 20 years the
World Health Organization (WHO) and the International Programme on
Chemical Safety (IPCS) have been concerned about the health and
environmental effects of the levels of inorganic lead in the
environment. The evaluation of human health risks arising from
food-borne lead has been carried out by WHO on four occasions since
1972. In addition, health-based guidance values for lead in water, air
and the workplace have been developed by various Task Groups convened
by WHO. Environmental Health Criteria 3: Lead, published in 1977,
examined the effects of lead on human health and Environmental Health
Criteria 85: Lead - Environmental Aspects was published in 1989.

Since the publication of Environmental Health Criteria 3: Lead, a
large body of knowledge has accumulated concerning the effects of lead
on humans at low levels of exposure. Studies have emphasized the
effects of inorganic lead on infants and children, a high-risk
population. This monograph on inorganic lead reflects this research
emphasis; a major part of the monograph deals with the neurotoxic
effects of lead with emphasis on neurobehavioural development in
children. Less detail is presented on the health effects of the higher
levels of inorganic lead found in some workplaces, although such
exposures are still considered to pose a risk to humans in many
regions of the world.

This monograph deals only with the human health effects of
inorganic lead. No attempt has been made to evaluate the human health
effects of organo-lead compounds, although it was recognized that such
compounds when added to petrol (gasoline) are a major source of
inorganic lead in the environment. In view of the toxicity of many
organo-lead derivatives and the possible methylation of inorganic lead
in the environment, the IPCS plans to evaluate the risk to humans from
exposure to organo-lead compounds in a separate monograph.

As with all IPCS criteria monographs, no attempt has been made to
prepare an exhaustive bibliography of the extremely large amount of
lead-related literature published since 1977. Rather, an effort has
been made to review critically the studies on humans and experimental
animals that are essential for the evaluation of risks to human health
from exposure to all sources of inorganic lead.

1. SUMMARY

This monograph focuses on the risks to human health associated
with exposure to lead and inorganic lead compounds. Emphasis has been
given to data which have become available since the publication of
Environmental Health Criteria 3: Lead (IPCS, 1977). The environmental
effects of lead are discussed in Environmental Health Criteria 85:
Lead - Environmental Aspects (IPCS, 1989).

1.1 Identity, physical and chemical properties, and analytical
methods

Lead is a soft, silvery grey metal, melting at 327.5°C. It is
highly resistant to corrosion, but is soluble in nitric and hot
sulfuric acids. The usual valence state in inorganic lead compounds is
+2. Solubilities in water vary, lead sulfide and lead oxides being
poorly soluble and the nitrate, chlorate and chloride salts are
reasonably soluble in cold water. Lead also forms salts with such
organic acids as lactic and acetic acids, and stable organic compounds
such as tetraethyllead and tetramethyllead.

The most commonly used methods for the analysis of low
concentrations of lead in biological and environmental materials are
flame, graphite furnace and inductively coupled plasma atomic
absorption spectroscopy and anode stripping voltametry. Depending on
sample pretreatment, extraction techniques and analytical
instrumentation, detection limits of 0.12 µmoles lead/litre blood
(2.49 µg/dl) can be achieved. However, reliable results are obtained
only when specific procedures are followed to minimize the risk of
contamination during sample collection, storage, processing and
analysis.

1.2 Sources of human exposure

The level of lead in the earth's crust is about 20 mg/kg. Lead in
the environment may derive from either natural or anthropogenic
sources. Natural sources of atmospheric lead include geological
weathering and volcanic emissions and have been estimated at
19 000 tonnes/year, compared to an estimate of 126 000 tonnes/year
emitted to the air from the mining, smelting and consumption of over 3
million tonnes of lead per year.

Atmospheric lead concentrations of 50 pg/m³ have been found in
remote areas. Background levels of lead in soil range between 10 and
70 mg/kg and a mean level near roadways of 138 mg/kg has been
reported. Present levels of lead in water rarely exceed a few
micrograms/litre; the natural concentration of lead in surface water
has been estimated to be 0.02 µg/litre.

Lead and its compounds may enter the environment at any point
during mining, smelting, processing, use, recycling or disposal. Major
uses are in batteries, cables, pigments, petrol (gasoline) additives,
solder and steel products. Lead and lead compounds are also used in
solder applied to water distribution pipes and to seams of cans used
to store foods, in some traditional remedies, in bottle closures for
alcoholic beverages and in ceramic glazes and crystal tableware. In
countries where leaded petrol is still used, the major air emission is
from mobile and stationary sources of petrol combustion (urban
centres). Areas in the vicinity of lead mines and smelters are subject
to high levels of air emissions.

Airborne lead can be deposited on soil and water, thus reaching
humans through the food chain and in drinking-water. Atmospheric lead
is also a major source of lead in household dust.

1.3 Environmental transport, distribution and transformation

The transport and distribution of lead from fixed, mobile and
natural sources are primarily via air. Most lead emissions are
deposited near the source, although some particulate matter (< 2 µm
in diameter) is transported over long distances and results in the
contamination of remote sites such as arctic glaciers. Airborne lead
can contribute to human exposures by the contamination of food, water
and dust, as well as through direct inhalation. The removal of
airborne lead is influenced by atmospheric conditions and particulate
size. Large amounts of lead may be discharged to soil and water.
However, such material tends to remain localized because of the poor
solubility of lead compounds in water.

Lead deposited in water, whether from air or through run-off from
soils, partitions rapidly between sediment and aqueous phase,
depending upon pH, salt content, and the presence of organic chelating
agents. Above pH 5.4, hard water may contain about 30 µg lead/litre
and soft water about 500 µg lead/litre. Very little lead deposited on
soil is transported to surface or ground water except through erosion
or geochemical weathering; it is normally quite tightly bound
(chelated) to organic matter.

Airborne lead can be transferred to biota directly or through
uptake from soil. Animals can be exposed to lead directly through
grazing and soil ingestion or by inhalation. There is little
biomagnification of inorganic lead through the food chain.

1.4 Environmental levels and human exposure

In the general non-smoking adult population, the major exposure
pathway is from food and water. Airborne lead may contribute
significantly to exposure, depending upon such factors as use of

tobacco, occupation, proximity to motorways, lead smelters, etc., and
leisure activities (e.g., arts and crafts, firearm target practice).
Food, air, water and dust/soil are the major potential exposure
pathways for infants and young children. For infants up to 4 or 5
months of age, air, milk, formulae and water are the significant
sources of lead exposure.

Levels of lead found in air, food, water and soil/dust vary
widely throughout the world and depend upon the degree of industrial
development, urbanization and lifestyle factors. Ambient air levels
over 10 µg/m³ have been reported in urban areas near a smelter,
whereas lead levels below 0.2 µg/m³ have been found in cities where
leaded petrol is no longer used. Lead intake from air can, therefore,
vary from less than 4 µg/day to more than 200 µg/day.

Levels of lead in drinking-water sampled at the source are
usually below 5 µg/litre. However, water taken from taps (faucets) in
homes where lead is present in the plumbing can contain levels in
excess of 100 µg/litre, particularly after the water has been standing
in the pipes for some hours.

The level of dietary exposure to lead depends upon many lifestyle
factors, including foodstuffs consumed, processing technology, use of
lead solder, lead levels in water, and use of lead-glazed ceramics.

For infants and children, lead in dust and soil often constitutes
a major exposure pathway. Lead levels in dust depend upon such factors
as the age and condition of housing, the use of lead-based paints,
lead in petrol and urban density. The intake of lead will be
influenced by the age and behavioural characteristics of the child and
bioavailability of lead in the source material.

Inhalation is the dominant pathway for lead exposure of workers
in industries producing, refining, using or disposing of lead and lead
compounds. During an 8-h shift, workers can absorb as much as 400 µg
lead, in addition to the 20-30 µg/day absorbed from food, water and
ambient air; significant intake may occur from ingestion of large
inhaled particulate material.

1.5 Kinetics and metabolism in laboratory animals and humans

Lead is absorbed in humans and animals following inhalation or
ingestion; percutaneous absorption is minimal in humans. Depending
upon chemical speciation, particle size, and solubility in body
fluids, up to 50% of the inhaled lead compound may be absorbed. Some
inhaled particulate matter (larger than 7 µm) is swallowed following
mucociliary clearance from the respiratory tract. In experimental
animals and humans, absorption of lead from the gastrointestinal tract
is influenced by the physico-chemical nature of the ingested material,
nutritional status, and type of diet consumed. In adult humans
approximately 10% of the dietary lead is absorbed; the proportion is

higher under fasting conditions. However, in infants and young
children as much as 50% of dietary lead is absorbed, although
absorption rates for lead from dusts/soils and paint chips can be
lower depending upon the bioavailability. Diets that are deficient in
calcium, phosphate, selenium or zinc may result in increased lead
absorption. Iron and vitamin D also affect absorption of lead.

Blood lead (PbB) levels are used as a measure of body burden and
absorbed (internal) doses of lead. The relationship between blood lead
and the concentration of lead in exposure sources is curvilinear.

Once it has been absorbed, lead is not distributed homogeneously
throughout the body. There is rapid uptake into blood and soft tissue,
followed by a slower redistribution to bone. Bone accumulates lead
over much of the human life span and may serve as an endogenous source
of lead. The half-life for lead in blood and other soft tissues is
about 28-36 days, but it is much longer in the various bone
compartments. The percentage retention of lead in body stores is
higher in children than adults. Transfer of lead to the human fetus
occurs readily throughout gestation.

Blood lead is the most commonly used measure of lead exposure.
However, techniques are now available for measuring lead in teeth and
bone, although the kinetics are not fully understood.

1.6 Effects on laboratory animals and in vitro systems

In all species of experimental animals studied, including
non-human primates, lead has been shown to cause adverse effects in
several organs and organ systems, including the haematopoietic,
nervous, renal, cardiovascular, reproductive and immune systems. Lead
also affects bone and has been shown to be carcinogenic in rats and
mice.

Despite kinetic differences between experimental animal species
and humans, these studies provide strong biological support and
plausibility for the findings in humans. Impaired learning/memory
abilities have been reported in rats with PbB levels of
0.72-0.96 µmoles/litre (15-20 µg/dl) and in non-human primates at PbB
levels not exceeding 0.72 µmoles/litre (15 µg/dl). In addition, visual
and auditory impairments have been reported in experimental animal
studies.

Renal toxicity in rats appears to occur at a PbB level in excess
of 2.88 µmol/litre (60 µg/dl), a value similar to that reported to
initiate renal effects in humans. Cardiovascular effects have been
seen in rats after chronic low-level exposures resulting in PbB levels
of 0.24-1.92 µmol/litre (5-40 µg/dl). Tumours have been shown to occur
at dose levels below the maximum tolerated dose of 200 mg lead (as
lead acetate) per litre of drinking-water. This is the maximum dose
level not associated with other morphological or functional changes.

1.7 Effects on humans

In humans, lead can result in a wide range of biological effects
depending upon the level and duration of exposure. Effects at the
subcellular level, as well as effects on the overall functioning of
the body, have been noted and range from inhibition of enzymes to the
production of marked morphological changes and death. Such changes
occur over a broad range of doses, the developing human generally
being more sensitive than the adult.

Lead has been shown to have effects on many biochemical
processes; in particular, effects on haem synthesis have been studied
extensively in both adults and children. Increased levels of serum
erythrocyte protoporphyrin and increased urinary excretion of
coproporphyrin and delta-aminolaevulinic acid are observed when PbB
concentrations are elevated. Inhibition of the enzymes
delta-aminolaevulinic acid dehydratase and dihydrobiopterin reductase
are observed at lower levels.

The effects of lead on the haemopoietic system result in
decreased haemoglobin synthesis, and anaemia has been observed in
children at PbB concentrations above 1.92 µmol/litre (40 µg/dl).

For neurological, metabolic and behavioural reasons, children are
more vulnerable to the effects of lead than adults. Both prospective
and cross-sectional epidemiological studies have been conducted to
assess the extent to which environmental lead exposure affects
CNS-based psychological functions. Lead has been shown to be
associated with impaired neurobehavioural functioning in children.

Impairment of psychological and neurobehavioural functions has
been found after long-term lead exposure of workers.
Electrophysiological parameters have been shown to be useful
indicators of subclinical lead effects in the CNS.

Peripheral neuropathy has long been known to be caused by
long-term high-level lead exposure at the workplace. Slowing of nerve
conduction velocity has been found at lower levels. These effects have
often been found to be reversible after cessation of exposure,
depending on the age and duration of exposure.

The effect of lead on the heart is indirect and occurs via the
autonomic nervous system; it has no direct effect on the myocardium.
The collective evidence from population studies in adults indicates
very weak associations between PbB concentration and systolic or
diastolic blood pressure. Given the difficulties of allowing for
relevant confounding factors, a causal relationship cannot be
established from these studies. There is no evidence to suggest that
any association of PbB concentration with blood pressure is of major
health importance.

Lead is known to cause proximal renal tubular damage,
characterized by generalized aminoaciduria, hypophosphataemia with
relative hyperphosphaturia and glycosuria accompanied by nuclear
inclusion bodies, mitochondrial changes and cytomegaly of the proximal
tubular epithelial cells. Tubular effects are noted after relatively
short-term exposures and are generally reversible, whereas sclerotic
changes and interstitial fibrosis, resulting in decreased kidney
function and possible renal failure, require chronic exposure to high
lead levels. Increased risk from nephropathy was noted in workers with
a PbB level of over 3.0 µmol/litre (about 60 µg/dl). Renal effects
have recently been seen among the general population when more
sensitive indicators of function were measured.

The reproductive effects of lead in the male are limited to sperm
morphology and count. In the female, some adverse pregnancy outcomes
have been attributed to lead.

Lead does not appear to have deleterious effects on skin, muscle
or the immune system. Except in the case of the rat, lead does not
appear to be related to the development of tumours.

1.8 Evaluation of human health risks

Lead adversely affects several organs and organ systems, with
subcellular changes and neurodevelopmental effects appearing to be the
most sensitive. An association between PbB level and hypertension
(blood pressure) has been reported. Lead produces a cascade of effects
on the haem body pool and affects haem synthesis. However, some of
these effects are not considered adverse. Calcium homoeostasis is
affected, thus interfering with other cellular processes.

a) The most substantial evidence from cross-sectional and
prospective studies of populations with PbB levels generally
below 1.2 µmol/litre (25 µg/dl) relates to decrements in
intelligence quotient (IQ). It is important to note that such
observational studies cannot provide definitive evidence of a
causal relationship with lead exposure. However, the size of the
apparent IQ effect, as assessed at 4 years and above, is a
deficit between 0 and 5 points (on a scale with a standard
deviation of 15) for each 0.48 µmol/litre (10 µg/dl) increment in
PbB level, with a likely apparent effect size of between 1 and 3
points. At PbB levels above 1.2 µmol/litre (25 µg/dl), the
relationship between PbB and IQ may differ. Estimates of effect
size are group averages and only apply to the individual child in
a probabilistic manner.

Existing epidemiological studies do not provide definitive
evidence of a threshold. Below the PbB range of 0.48-0.72 µmol/
litre (10-15 µg/dl), the effects of confounding variables and
limits in the precision in analytical and psychometric
measurements increase the uncertainty attached to any estimate
of effect. However, there is some evidence of an association
below this range.

b) Animal studies provide support for a causal relationship between
lead and nervous system effects, reporting deficits in cognitive
functions at PbB levels as low as 0.53-0.72 µmol/litre
(11-15 µg/dl) which can persist well beyond the termination of
lead exposure.

c) Reduction in human peripheral nerve conduction velocity may occur
with PbB levels as low as 1.44 µmol/litre (30 µg/dl). In
addition, sensory motor function may be impaired with PbB levels
as low as about 1.92 µmol/litre (40 µg/dl), and autonomic nervous
system function (electrocardiographic R-R interval variability)
may be affected at an average PbB level of approximately
1.68 µmol/litre (35 µg/dl). The risk of lead nephropathy is
increased in workers with PbB levels above 2.88 µmol/litre
(60 µg/dl). However, recent studies using more sensitive
indicators of renal function suggest renal effects at lower
levels of lead exposure.

d) Lead exposure is associated with a small increase in blood
pressure. The likely order of magnitude is that for any two-fold
increase in PbB level (e.g., from 0.8 to 1.6 µmol/litre, i.e.
16.6 to 33.3 µg/dl), there is a mean 1 mmHg increase in systolic
blood pressure. The association with diastolic pressure is of a
similar but smaller magnitude. However, there is doubt regarding
whether these statistical associations are really due to an
effect of lead exposure or are an artifact due to confounding
factors.

e) Some but not all epidemiological studies show a dose dependent
association of pre-term delivery and some indices of fetal growth
and maturation at PbB levels of 0.72 µmol/litre (15 µg/dl) or
more.

f) The evidence for carcinogenicity of lead and several inorganic
lead compounds in humans is inadequate.

g) Effects of lead on a number of enzyme systems and biochemical
parameters have been demonstrated. The PbB levels, above which
effects are demonstrable with current techniques for the
parameters that may have clinical significance, are all greater
than 0.96 µmol/litre (20 µg/dl). Some effects on enzymes are
demonstrable at lower PbB levels, but the clinical significance
is uncertain.

2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL METHODS

2.1 Physical and chemical properties of lead and its compounds

Lead (atomic number, 82; relative atomic mass, 207.19; specific
gravity, 11.34) is a bluish or silvery grey soft metal. The melting
point is 327.5°C and the boiling point at atmospheric pressure 1740°C.
It has four naturally occurring isotopes (208, 206, 207, and 204 in
order of abundance), but the isotopic ratios for various mineral
sources may differ. This property has been exploited in
non-radioactive-tracer environmental and metabolic studies. The
physical and chemical properties of elemental lead and some lead
compounds are summarized in Table 1.

Although lead has four electrons in its valence shell, only two
ionize readily. The usual oxidation state of lead in inorganic
compounds is therefore +2 rather than +4. The inorganic salts of lead,
such as lead sulfide and the oxides of lead, are generally poorly
soluble in water. However, the nitrate, chlorate and, to a much lesser
degree, the chloride are water soluble. Some of the salts formed with
organic acids, e.g., lead oxalate, are also insoluble, but the acetate
is relatively soluble, as shown in Table 1.

Under appropriate conditions of synthesis, stable compounds are
formed in which lead is directly bound to a carbon atom. Industrially
synthesized lead-carbon compounds include tetraethyllead and
tetramethyllead, which are of importance as fuel additives and, hence,
are sources of environmental lead.

2.2 Analytical procedures

In recent years substantial advances have been made in developing
methods for the quantification of metals at low concentrations. In
order to provide improved quality assurance of such measurements,
various reference materials in different matrices have been produced
(Muramatsu & Parr, 1985). To ensure adequate quality control, the
analyst should choose a reference material that matches as closely as
possible the experimental samples to be analysed. Choices are based
upon matrix type and concentration of the element of interest. A
summary of data on 60 biological and 40 environmental (non-biological)
reference materials has been compiled by Muramatsu & Parr (1985).

With the increased interest in measuring lead in the low µg/kg
and µg/m³ range in both environmental and biological samples, there
is need for particular attention to analytical sensitivity and
reliability. As lower concentrations are measured, problems of
laboratory contamination become more significant and quality control
and quality assurance programmes are important. Because of these
concerns, all analytical results for lead should report the laboratory

Table 1. Physical and chemical data on lead and selected lead compounds^a

Name Synonym Relative atomic/ Melting point Boiling point Solubility in cold Soluble in
and formula molecular mass (°C) (°C) water (g/litre)

Lead Pb 207.19 327.502 1740 insoluble HNO₃; hot concentrated
H₂SO₄; hot water;
glycerine; alcohol (slightly)

Lead salts

acetate Pb(C₂H₃O₂)₂ 325.28 280 - 443

carbonate cerrusite PbCO₃ 267.20 315 (decomposes) 0.0011 acid; alkali; decomposes in
hot water

chlorate Pb(ClO₃)₂ 374.09 230 (decomposes) very soluble alcohol

chloride cotunite PbCl₂ 278.10 501 950 919 NH₄ salts; slightly in dilute
HCl and in NH₃; hot water
(33.4 g/litre)

nitrate Pb(NO₃)₂ 331.20 470 (decomposes) 376.5 alcohol; alkali, NH3; hot
water (1270 g/litre)

orthophosphate Pb₃(PO₄)₂ 811.51 1014 0.00014 alkali; HNO₃

oxalate PbC₂O₄ 295.21 300 (decomposes) 0.0016 HNO₃

dioxide plattnerite PbO₂ 239.19 290 (decomposes) insoluble dilute HCl; acetic acid
(slightly)

monoxide litharge PbO 223.19 888 0.017 dilute HNO₃; acetic acid

Table 1 (cont'd)

Name Synonym Relative atomic/ Melting point Boiling point Solubility in cold Soluble in
and formula molecular mass (°C) (°C) water (g/litre)

sulfate anglesite PbSO₄ 303.25 1170 0.0425 NH₄ salts; concentrated
H₂SO₄ (slightly)

sulfide galena PbS 239.25 1114 0.00086 acid

^a Data from Weast (1985)

performance for reference standards and for parallel blank
measurements of sample contamination for the entire analytical
process. Without these, the validity of the data should be questioned.

2.2.1 Sampling procedures

Particular attention should be paid to the cleanliness of
equipment and glassware and the purity of the chemicals to prevent
secondary contamination by lead.

For the collection of samples, standard trace element methods are
generally required (Behne, 1980) with adequate quality control
procedures (Friberg, 1988; Jorhem & Slorach, 1988, Vahter & Friberg,
1988). Quality control samples for blood, faeces, air filters and dust
have been described (Lind et al., 1988).

2.2.1.1 Sampling of environmental media

In air sampling, both high-volume samplers and low-volume
techniques have been used. It should be noted that the collection
characteristics of high-volume samplers are strongly affected by
particle size and the orientation of the sampler. For particles larger
than 5 µm in diameter the high-volume sampler system is unlikely to
collect representative samples (US EPA, 1986a). As in all sampling for
suspended particulate matter, the accuracy of volume meters should be
checked periodically. The size of the pores in filters for collecting
lead-containing particles should be small, possibly less than 0.2 µm
for glass-fibre filters (Lee & Goranson, 1972).

Depending on the purpose of sampling, care should be taken to
select the appropriate site for sampling devices and to achieve the
best possible sampling conditions by:

* estimating the amount of particulate required for analysis before
deciding on the sample volume and the sampling procedure;

* placing the sampling devices in the appropriate position (e.g.,
in the breathing zone, level with inlet tubes of house
ventilators, at window level in the case of a traffic-laden town
street, at a reasonable distance from the highway in uninhabited
zones, etc);

* taking the samples at appropriate rates and volumes (e.g., daily
breathing volumes, daily ventilating capacities of installations)
and for a sufficient time to make possible the estimation of the
average concentration (e.g., during a work-shift, or a 24-h or
longer period for general population exposure);

* taking into account the use of areas under study (cattle grazing,
recreational zones, children's playgrounds, etc).

In addition, whenever possible a procedure should be used that
makes it possible to evaluate particle-size distribution and the
physicochemical properties of the lead compounds involved, including
the shape of the particles and the state of their aggregation.

Lead may be found in water bound to particulate matter as soluble
complexes or soluble compounds. Techniques for sampling water must
take this into account. It is necessary to sample water without
fractionation (filtration) when total lead levels are required.
Because of the potential for metals from low ionic strength waters to
be adsorbed onto the surfaces of some containers, samples should be
acidified (US EPA, 1986a). Selection, cleaning, and conditioning of
storage and sample containers deserve special attention (Moody, 1982).

The preparation of soil and dust samples for lead analyses
usually involves drying (at 100°C), homogenization by grinding, and
sieving (Thornton & Webb 1975; Bolter et al., 1975). Brown & Black
(1983) have discussed the issues related to quality assurance and
quality control in the collection and analysis of soil samples. Most
reports of lead in soil provide the total elemental abundance either
by acid extraction or X-ray fluorescence. However, the leachable or
bioavailable fraction is of special interest.

For the study of the dietary intake of lead from food, two
general methods have been utilized. The advantages and disadvantages
of the "duplicate portions" technique and the equivalent composite
technique ("market basket") have been reviewed by Pekkarinen (1970).
Although the duplicate portions (duplicate diets) technique can define
variability in consumption, it is expensive, and the sampling and
analytical procedures involved are complicated and limit the number of
individuals included in any study. With the equivalent composite
technique, the economy and ease of collection must be considered in
the light of the variability of results obtained due to uncertainties
in knowledge of actual preparation techniques, including possible lead
levels in water used for processing in individual homes.

The quantity of lead likely to be leached from ceramic surfaces
by different foods and beverages may be assessed using dilute acetic
acid solutions (1 to 4%) at temperatures in the range 20 to 100°C for
times ranging from 30 min to more than 24 h (Laurs, 1976; Merwin,
1976).

Colorimetric methods are suitable for screening inorganic
materials such as pottery or paint for lead. Positive reactions
require confirmation by established quantitative methods. Spot tests
using dithizone, rhodizonate and iodide (Feigl et al., 1972) are
available.

2.2.1.2 Sampling of biological materials

The main problem in the sampling of body fluids and tissues for
lead analysis is potential secondary contamination with lead. The low
general population blood lead (PbB) levels in many regions of the
world are complicating screening efforts, requiring levels of
analytical precision and sensitivity that can be achieved only through
intensive QA/QC programmes. Issues related to such sampling have been
examined in detail by US EPA (1986a).

Special precautions are needed to ensure that all venous
blood-collecting and blood-storage materials are as free from lead as
possible (IPCS, 1977). All glass equipment involved in blood
collection and storage should be made of lead-free silicate glass,
rinsed first in mineral acid, then with copious amounts of
glass-distilled or deionized water. Polypropylene syringes have been
recommended (NAS-NRC, l972). Needles should be of stainless steel with
polypropylene hubs. Blood is often drawn directly from the needle into
vacuum tubes. It is wise to confirm periodically the absence of
significant amounts of lead in the anticoagulant used in the blood
container as well as monitoring the contamination level (blank) for
the entire analytical process.

New analytical techniques make it possible to determine lead
concentrations in microlitre quantities of blood. The trend towards
the procurement of micro-samples of blood by skin prick increases the
chance of secondary contamination of the blood. Systematic
investigation on the significance of this problem has been reported
(Mitchell et al., 1974; Mahaffey et al., 1979; DeSilva & Donnan,
1980). Mitchell et al. (l974) describe a procedure whereby sample
contamination can be reduced by spraying collodion over the cleansed
skin before lancing. The correlation between the concentration of lead
in micro-samples and in macro-samples obtained by venepuncture was
fairly good (r=0.92) over a wide range of PbB concentrations
(0.48-4.41 µmol/litre or 10-92 µg/dl whole blood). Mahaffey et al.,
(1979b) found that capillary blood levels in a comparison test were
systematically higher than corresponding venous blood levels; similar
elevations have been reported by DeSilva & Donnan (1980). Since about
1980 the requirement for reliable and accurate micro procedures has
resulted in the development of good protocols. Sinclair & Dohnt (1984)
described a procedure which resulted in the ability to collect
capillary samples with PbB levels only 3.3% higher than the presumably
correct venous value. This procedure has been used in the Port Pirie
Cohort Study (Baghurst et al., 1985, 1992) and for routine
surveillance in the Port Pirie Lead Decontamination Program (Calder et
al., 1990). Also, Lyngbye et al. (1990b) have shown that capillary
sampling without lead contamination is possible. Routine validation by
cross-comparison with venous blood samples should be undertaken on a
regular basis.

The same general precautions to avoid contamination must be taken
in the collection of urine samples as in the collection of blood
samples. Additionally, special care must be taken to prevent
precipitation during storage.

2.2.2 Analytical methods for lead

A number of analytical methods exist for determination of lead in
environmental and biological samples. These methods differ enormously
in their costs (e.g., sophisticated equipment, an adequate
infrastructure to maintain laboratory conditions and chemical
supplies) and personnel requirements (e.g., availability of skilled
personnel in adequate numbers for the work to be undertaken). Both
accuracy and precision of any of the methods can be affected greatly
by contamination of samples within the laboratory. It is important to
utilize the principles of a "clean" laboratory described by Patterson
& Settle (1976) and Everson & Patterson (1980).

It is not the purpose of this section to provide an exhaustive
description of the analytical methods that could be available to
detect and quantify lead levels in environmental and biological
samples. However, an attempt will be made to identify well-established
methods in current use and to provide information on their application
to assist in the interpretation of experimental and epidemiological
studies.

2.2.2.1 Analysis of lead in environmental samples

The most common methods used for the analysis of lead in samples
from air, water, dust, sediment, soil and foodstuffs are flame atomic
absorption spectrometry (AAS), graphite furnace atomic absorption
spectrometry (GFAAS), anodic stripping voltametry (ASV), inductively
coupled plasma-atomic emission spectroscopy (ICP-AES), and X-ray
fluorescence spectroscopy (XRFS). The reference method for the
determination of the absolute amounts of lead is by isotope dilution
mass spectrometry (IDMS) (Settle & Patterson, 1980; Grandjean & Olsen,
1984; US EPA, 1986a), but due to equipment costs and required
expertise, it is not widely used. Spectrophotometric methods, using
diphenylthiocarbazone as the colorimetric reagent, were widely used in
the past; they are less sensitive and are labour-intensive but are
still appropriate. The advantages and disadvantages were described by
Skogerboe et al. (1977).

Gould et al. (1988) utilized a citric acid solution on filter
paper to leach lead from glazed ceramic and/or enamelled metal-ware.
When treated with a lead-sensitive chromogen, there is a reaction
indicating the presence of lead on the paper. The minimal amount of
lead required to produce an observable reaction was 0.25 µg/cm²; the
maximum amount tested was 5 µg/cm². A colorimetric test based on the
use of sodium sulfide in solution is used to estimate lead in paint

films. It is possible to determine lead concentrations greater than
1 mg/cm² of dried paint 90% of the time when the method is used by a
trained chemical laboratory technician.

Table 2 summarizes the utility of several representative methods
for specific environmental media.

2.2.2.2 Analysis of lead in biological materials

Biological samples present special problems for the analyst
because of the low lead concentrations and matrix effects. Most
analytical techniques developed to detect and quantify lead can be
adapted to the analysis of such biological materials as blood, urine,
serum, cerebrospinal fluid, solid tissues, hair, teeth and bone.
However, certain techniques are more often used for specific matrices.

Currently, the most commonly used methods are AAS, GFAAS, ASV,
and ICP-AES. Spectrophotometric methods were commonly used in the past
and can be useful. Other specialized methods for lead analysis are
XRFS, neutron activation analysis (NAA), inductively coupled
plasma-mass spectrometry (ICP-MS), and IDMS. Table 3 summarizes the
utility of several analytical procedures applied to various biological
matrices. Included in this table are examples of the application of
XRFS (Christoffersson et al., 1986; Wielopolski et al., 1986; Nilsson
et al., 1991) for the determination in situ of the body burden of
lead.

2.2.2.3 Analytical procedures for biomarkers of lead exposure and
effect

Using standard clinical laboratory techniques, analytical
procedures have been developed: delta-aminolaevulinic acid (ALA);
delta-aminolaevulinic acid dehydratase (ALAD); urinary coproporphyrin
(CPU) and erythrocyte protoporphyrin (EP). All of these assays are
well established and reliable (Grandjean & Olsen 1984; US EPA, 1986a).
These biochemical parameters are influenced by physiological factors
other than lead. They lack the specificity and sensitivity of PbB
measurements as an index of either current lead exposures or body
stores of lead.

2.3 Conversion factors

1 µg/dl = 0.048 µmol/litre
1 µmol/litre = 20.7 µg/dl

Using the above conversion factor, blood lead concentrations are
given as µmol/litre with the equivalent µg/dl in brackets. Calculated
figures have not been rounded and added precision is not to be
inferred from the number of significant figures.

Table 2. Analytical methods for determining lead in environmental samples^a

Sample type Preparation method Analytical method Sample detection Percentage Reference
limit recovery

Air collect particulate matter on membrane ASV with mercury-graphite 0.16 µg/m³ 90-110 NIOSH (1977b)
(particulate filter; wet ash with HNO₃/HClO₄/H₂SO₄; electrode (NIOSH method
lead) dissolve in acetate buffer P&CAM 191)

Air collect particulate matter on cellulose ICP-AES (NIOSH method 0.34 µg/m³ 95-105 NIOSH (1981)
(particulate acetate filter; wet ash with HNO₃/HClO₄ P&CAM 351)
lead)

Air collect particulate matter on filter; AAS 0.1 µg/m³ 93 Scott et al.
(particulate dry ash; extract with HNO₃/HCl; dilute AES 0.15 µg/m³ 102 (1976)
lead) with HNO₃

Air sample on cellulose acetate filter; AAS 8 ng/litre 100-101 Nerin et al.
(particulate dissolve in HNO₃ with heat; add HCl/H₂O₂ (1989)
lead) and react in hydride generator with sodium
borohydride to generate lead hydride

Air collect sample on filter; spike filter with IDMS 0.1 ng/m³ NR Volkening et
(particulate ²⁰⁶Pb; dissolve filter in NaOH; acidify; al. (1988)
lead) separate lead by electrodeposition; dissolve
in acid

Water digest sample with acid; heat; dilute with AAS 1.0 ng/g NR Chau et al.
(total lead) water (1979)

Soil dry sample and sieve for XRF; digest sieved XRF NR 65-98 Krueger &
sample with HNO₃ and heat for AAS AAS NR 63-68 Duguay (1989)

Soil dry sample, dry ash; digest with acid AAS 2 µg/g 79-103 Beyer &
and dilute with water Cromartie (1987)

Table 2 (cont'd)

Sample type Preparation method Analytical method Sample detection Percentage Reference
limit recovery

Soil, waste, digest sample with acid; dilute with water AAS (EPA method 7420) 0.1 mg/litre NR US EPA (1986b)
and ground and filter GFAAS (EPA method 7421) 1 µg/litre NR
water

Soil, dust digest sample with hot acid; dry; redissolve AAS 12 ng/g > 80 Que Hee et al.
and paint in HNO₃ (1985b)

Sediment, fish, digest sample with acid; heat; dilute with AAS 50 ng/g NR Chau et al.
vegetation water (sediment) (1980)
(total lead) 10 ng/g (fish NR
and vegetation)

Milk add 50 µl (C₂H₅)4NOH in ethanol to 25 µl GFAAS NR NR Michaelson &
milk; heat and dilute with water to 125 µl Sauerhoff (1974)

Evaporated dry ash sample; dissolve in HNO₃ ASV 0.005 µg/g 99 Capar & Rigsby
milk (1989)

Agricultural dry ash sample with H₂SO₄ and HNO₃; DPASV 0.4 ng/g 85-106 Satzger et al.
crops dilute with water (1982)

Grains, milk, bomb digest sample with acid; heat or GFAAS 20 µg/g (bomb) 85-107 Ellen & Van
mussels, fish digest with acid and dry ash; dissolve 5 µg/g (dry ash) 75-107 Loon (1990)
in acid; dilute with water DPASV NR 82-120

Table 2 (cont'd)

Sample type Preparation method Analytical method Sample detection Percentage Reference
limit recovery

Citrus leaves chop or pulverize sample; digest with hot ICP-AES 10-50 µg/litre 75-82 Que Hee &
and paint acid; dry; redissolve in acid (citrus Boyle (1988)
leaves)
89-96
(paint)

^a AAS = atomic absorption; AES = atomic emissions spectroscopy; ASV = anode stripping voltametry; (C₂H₅)₄NOH = tetraethylammonium
hydroxide; DPASV = differential pulse anodic stripping voltametry; EPA = US Environmental Protection Agency; GFAAS = graphite furnace
atomic absorption spectrometry; HCl = hydrochloric acid; HClO₄ = perchloric acid; HNO₃ = nitric acid; H₂O₂ = hydrogen peroxide;
H₂SO₄ = sulfuric acid; ICP-AES = inductively coupled plasma/atomic emission spectroscopy; IDMS = isotope dilution mass spectrometry;
NaOH = sodium hydroxide; NIOSH = National Institute for Occupational Safety and Health; NR = not reported; XRF = X-ray fluorescence

Table 3. Analytical methods for determining lead in biological materials^a

Sample Preparation method Analytical method Sample detection Percentage Reference
type limit recovery

Blood wet ash sample with acid mixtures; ASV with mercury-graphite 0.192 µmol/litre 95-105 NIOSH (1977c)
dissolve residue in dilute HClO₄ electrode (NIOSH method (4 µg/dl)
P&CAM 195)

Blood wet ash sample with HNO₃; dissolve GFAAS (NIOSH method 0.48 µmol/litre NR NIOSH (1977e)
residue in dilute HNO₃ P&CAM 214) (10 µg/dl)

Blood dilute sample with Triton X-100^(R); add GFAAS 0.011 µmol/litre 93-105 Aguilera de
nitric acid and diammonium phosphate (0.24 µg/dl) Benzo et al.
(1989)

Blood dilute sample with ammonia solution ICP-MS 0.072 µmol/litre 96-111 Delves &
containing Triton X-100^(R); analyse (1.5 µg/dl) Campbell
(1988)

Blood dilute sample in 0.2% Triton X-100^(R) GFAAS approx. 0.072 97-150 Que Hee et
and water; analyse µmol/litre (approx. al. (1985a)
1.5 µg/dl)

Blood and wet ash sample with HNO₃, complex Spectrophotometry 0.144 µmol/litre 97 NIOSH (1977a)
urine with dephenylthiocarbazone and (NIOSH method (3.0 µg/dl) (blood);
extract with chloroform P&CAM 102) 0.0576 µmol/litre 97
(12 µg/litre) (urine)

Serum, filter sample if needed; dilute with ICP-AES 0.048-0.240 µmol/litre 85 (serum) Que Hee &
blood and acid or water (1.0-5.0 µg/dl) Boyle (1988)
urine

Urine wet ash sample with acid mixture and ASV with mercury-graphite 0.0192 µmol/litre 90-110 NIOSH (1977d)
dissolve in dilute HClO₄ electrode (NIOSH method (4 µg/litre)
P&CAM 200)

Table 3 (cont'd)

Sample Preparation method Analytical method Sample detection Percentage Reference
type limit recovery

Liver, bomb digest sample with acid and heat, GFAAS 20 µg/g (bomb); 85-107 Ellen & Van
kidney, or digest with acid and dry ash; dissolve (bomb); Loon (1990)
muscle in acid; dilute with water 5 µg/g (dry ashing) 75-107 (dry
ashing)

Bone direct partially polarized photons at XRF 20 µg/g NR Christoffersson
second phalanx of left forefinger et al. (1986)
(non-invasive technique)

Bone direct partially polarized photons at XRF 20 µg/g NR Wielopolski
anteromedial skin surface of mid-tibia et al. (1986)
(non-invasive technique)

Teeth clean and section tooth; digest with ASV NR 83-114 Rabinowitz
HNO₃; evaporate; redissolve in buffer et al. (1989)
solution

Teeth dry ash sample; crush; dry ash again; AAS NR 90-110 Steenhout &
dissolve in HNO₃ Pourtois
(1981)

^a AAS = atomic absorption spectrometry; ASV = anode stripping voltametry; GFAAS = graphite furnace atomic absorption spectrometry;
HClO₄ = perchloric acid; HNO₃ = nitric acid; ICP-AES = inductively coupled plasma-atomic emission spectroscopy;
ICP-MS = inductively coupled plasma-mass spectrometry; NIOSH = National Institute for Occupational Safety and Health;
NR = not reported; XRF = X-ray fluorescence

3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE

3.1 Natural occurrence

Because lead is relatively abundant in the earth's crust it is
found naturally throughout the world. The major natural sources of
lead are volcanic emissions, geochemical weathering, and emissions
from sea spray. A small amount of radioisotopic lead (²⁰⁷Pb) is
derived from the decay of radon gas released from geological sources.
It has been estimated that the worldwide natural emission rates of
lead are of the order of 19 000 tonnes/year (Nriagu & Pacyna, 1988),
with volcanic sources accounting for 6400 tonnes/year (Nriagu, 1979).

Owing to centuries of human exploitation of lead resources, it is
difficult to determine the natural content of lead in most ecosystems.
Data on environmental levels, uses, and sources of lead have been
summarized in a recent review (OECD, 1993).

3.1.1 Rocks and soils

The average concentration of lead in the earth's crust is between
10 and 20 mg/kg (IPCS, 1989). The major geological sources of lead are
in igneous and metamorphic rocks.

The soil is the most important repository in terrestrial
ecosystems for contaminants of anthropogenic origin (Nriagu & Pacyna,
1988; Nriagu, 1989). The lead content of soils (which are for
discussion purposes distinguished here from surface dusts) is greatly
influenced by anthropogenic activities and by long- and short-range
airborne transport of lead from various sources. Both dry and wet
deposition are important routes of input.

Lead in soil may be relatively insoluble (as a sulfate, carbonate
or oxide), soluble, adsorbed onto clays, adsorbed and coprecipitated
with sesquioxides, adsorbed onto colloidal organic matter, or
complexed with organic moieties in soil (US EPA, 1986a; IPCS, 1989).
Soil pH, content of humic and fulvic acids, and amount of organic
matter influence the content and mobility of lead in soils. Since
acidic conditions favour the solubilization and leaching of lead from
the solid phase, acidic soils tend to have lower lead concentrations
when analysed as dry soil. Humic and fulvic acids can also mobilize
lead, and certain complex organic molecules can act as chelators of
lead (IPCS, 1989).

Background levels of lead in soil are in the range of 10-70 mg/kg
(GEMS, 1985). Similar results have been found in studies of mobile
source contamination near highways; soil taken at distances of
50-100 m from highways (outside the range of immediate impact from
traffic emissions) usually shows levels of lead below 40 mg/kg. In the
1985, GEMS survey of selected countries, lead concentrations in
topsoil from Malta were found to have a mean of 54 mg/kg in areas at

least 5 m from roadways; less than one metre from roadways the mean
concentration was 138 mg/kg. A 1977 report from Sweden found a mean of
16 mg/kg in non-contaminated areas (GEMS, 1985).

3.1.2 Sediments

Sediments from freshwater and marine environments have been
studied for lead content. This compartment provides a unique record of
the history of changes in global lead fluxes (Patterson, 1983). Levels
of lead in sediments dated before the onset of the industrial
revolution in Western Europe show very low levels, less than 10% of
current levels (Flegal et al., 1987). The average background level of
lead in marine sediments off southern California was reported by
Flegal et al. (1987) to be 1.3 mg/kg.

3.1.3 Water

Flegal et al. (1987) estimate that the natural concentration of
lead in surface water is about 0.02 µg/litre. In general, lead is not
found in ground or surface waters at concentrations above 10 µg/litre
(IPCS, 1989).

Data from oceans indicate very low levels of lead in sea-water
samples not affected directly by significant sources of lead. Water
samples taken from an area of the Pacific, where annual windborne-
input fluxes of lead are estimated to be 3 mg/cm², have lead
concentrations of 3.5 ng/litre (0-100 m depth) and 0.9 ng/litre at
depths greater than 2500 m. In contrast, water samples taken from the
north Atlantic, where annual windborne-input fluxes of lead are
170 mg/cm², contain 34 ng lead/litre at the surface and 5 ng/litre
in depths below 2500 m (Patterson, 1983). Settle & Patterson (1980)
have estimated that prehistoric oceans contained 0.5 ng/litre lead.
Flegal et al. (1987) have estimated that over 95% of the lead in
off-shore surface waters is the result of windborne inputs. However,
in coastal waters near Monterey (California, USA), higher
concentrations of lead were found in sea water, sediments and
organisms; these elevations were related to specific sources by
systematic isotope analyses (Flegal et al., 1987).

3.1.4 Air

Anthropogenic inputs of lead from a range of sources have
resulted in global dispersion of both inorganic and organic species of
lead into the air, of which 80-90% is derived from alkyllead fuel
additives (WHO, 1987). Nriagu & Pacyna (1988) estimated that a total
of 330 000 tonnes of lead is discharged directly into the atmosphere
each year. Estimations of pre-industrial levels of lead in air from
natural origins (volcanic emissions, crustal weathering, radon decay
and sea-spray releases) are in the range of 0.01-0.1 µg/m³ (US NRC,
1980). The lowest level reported since 1975 is 0.076 ng/m³ measured
at the South Pole (US EPA, 1986a).

3.1.5 Plants

Lead occurs naturally in plants and results from both deposition
and uptake. There is a positive linear relationship between lead
concentrations in plants and soil (Davies & Thornton, 1989). As with
other environmental compartments, measurement of "background" levels
of lead in plants is complicated by the general contamination of the
globe from centuries of lead use, which has included direct
application of lead-containing chemicals in agriculture (see below)
and contamination of fertilizers with lead. Lead has been measured in
superphosphate fertilizer at concentrations as high as 92 mg/kg (Lisk,
1972). Sewage sludge, used as a source of nutrients in agriculture,
may contain even higher levels of lead. The concentration of lead in
sewage sludge is typically < 1000 mg/kg. Levels as high as 26 g/kg
have been measured in the USA (Chaney et al., 1984). Soil receiving
heavy sludge applications over long periods of time (years) contained
425 mg lead/kg; the concentration in untreated soil was 47 mg/kg
(Beckett, 1979).

3.1.6 Environmental contamination from natural sources

The contribution of natural sources of lead to human exposure is
small. As a result of various breakdown processes, rocks yield lead
which is transferred to the biosphere and the atmosphere, and,
ultimately, back to the earth's crust in the form of sedimentary
rocks. Soluble lead has for thousands of years entered the oceans with
river discharges, and the rate has been estimated by Patterson (1965)
to be around 17 000 tonnes/year. Sources contributing to airborne lead
are silicate dusts, volcanic halogen aerosols, forest fires, sea salts
aerosols, meteoric and meteorite residues, and lead derived from the
decay of radon. While the lead content of most coals is relatively
low, coal fly ash is enriched in lead (Hutton et al., 1988) and is a
source of environmental contamination.

3.2 Anthropogenic sources

World lead consumption has steadily increased over the period
1965-1990 and was about 5.6 × 10⁶ tonnes in 1990 (OECD, 1993).

Further review of the data summarized by OECD (1993) indicates a
change in consumption patterns worldwide. Although the consumption of
lead within the 24 countries of the OECD increased only slightly over
the decade from 1980 to 1990, consumption within less developed
economies (Africa and Asia) increased from 315 000 tonnes in 1970 to
844 000 tonnes in 1990.

3.2.1 Lead mining

Lead occurs in a variety of minerals, the most important of which
are galena (PbS), cerrusite (PbCO₃) and anglesite (PbSO₄). Galena
is by far the most important source of primary lead. It occurs mostly

in deposits associated with other minerals, particularly those
containing zinc. Mixed lead and zinc ores account for about 70% of
total primary lead supplies. Ores containing mainly lead account for
about 20% and the remaining 10% is obtained as a by-product from other
deposits, such as mixed copper-zinc deposits. The proportions of
various metals may differ in the ores of different countries. Silver
is the most important of the other metals frequently present in lead
deposits, but copper may also be present in concentrations high enough
to be commercially important. Other minor constituents of lead ores
are gold, bismuth, antimony, arsenic, cadmium, tin, gallium, thallium,
indium, germanium and tellurium.

The major countries producing lead from mining activity during
1987-1991 were the USA, Canada, Australia, Peru, the former USSR and
Mexico, as shown in Table 4. Other countries producing lead from lead
ores include China, the former Yugoslavia, Morocco, Spain, Sweden and
Tunisia. In general, the level of world production of lead from mining
activities has remained relatively constant at about 3.3 × 10⁶
tonnes between 1988 and 1991 (ILZSG, 1992); this represents roughly
60% of the world demand for lead.

Table 4. Major countries producing lead from ore and ore
concentrates^a

Country 1987 1988 1989 1990 1991

Canada 423 200 366 600 276 100 241 300 278 100

USA 318 300 395 700 419 300 495 200 483 300

Ex-USSR 510 000 520 000 500 000 490 000 --

Australia 489 200 462 000 495 000 570 000 579 000

Mexico 177 200 178 100 163 000 174 100 158 800

Peru 204 000 149 000 192 200 187 800 199 100

^a From: World Bureau of Metal Statistics (1992)

3.2.2 Smelting and refining

Smelting and refining are classified as either primary or
secondary, the former producing refined lead products from ores or
concentrates (primary lead) and the latter producing lead by
recovering it from lead-bearing scrap and waste materials (secondary
lead). Secondary lead is derived from processing what is termed new

scrap arising during manufacturing processes and recycled old scrap
arising from waste materials containing lead. Most scrap is from old
sources, of which the most important are lead plates from batteries,
solder, common babbitt, soft lead, lead solders, cable coverings, type
metals, dross and other lead-containing products. There has been an
increasing contribution of secondary lead sources to the total
worldwide production of lead, as shown in Table 5 (World Bureau of
Metal Statistics, 1992). Secondary sources of lead supplied between 35
and 40% of world production during the period from 1970 to 1990.

3.2.3 Environmental pollution from production of lead

Mining operations and the smelting and refining of both primary
and secondary lead are known to cause contamination of the nearby
environment. The nature and extent of contamination depends on many
factors, including the level of production, the effectiveness of
emission controls, climate, topography and other local factors.
Concentrations are usually highest within 3 km of the point source (US
EPA, 1989). A report from China found that lead levels in ambient air,
plants and soil increased proportionally with proximity to a large
primary smelter; at 50 m from the source, the air lead level was
60 µg/m³, the lead level in plants was 29.1 mg/kg, and soil lead
level was 170 mg/kg (Wang, 1984). However, some earlier studies have
shown air pollution and soil contamination as far as 10 km from
smelters (Djuric et al., 1971; Kerin, 1973; Landrigan et al., 1975).

Table 5. Relative contribution of primary and secondary sources
relative to world lead production (1987-1990)^a

1987 1988 1989 1990

Primary 422 100 3 414 200 3 286 500 3 324 500
Secondary 2 045 600 2 103 900 2 272 900 2 254 800

^a From: World Bureau of Metal Statistics (1992)

The impacts of lead mining and smelting can persist for long
periods of time. A study conducted in Wales, United Kingdom, in an
area where lead mining began 2000 years ago and ended in the middle of
the 20th century, found high concentrations of lead in soils (Davies
et al., 1985). In Port Pirie, Australia, a community with one of the
world's largest and oldest primary lead smelters, lead levels in soils
were found to be grossly elevated, and the incidence of elevated blood
lead levels in pregnant women and young children was also increased
above that found in other communities in Australia (Wilson et al.,
1986).

3.3 Consumption and uses of lead and its compounds

Lead has a combination of physical and chemical properties that
have made it extremely useful industrially, i.e. high density, high
opacity to gamma and X-ray energies, low sound conductance, a low
melting point, exceptional malleability, high corrosion resistance,
and stability. In 1990, 5.627 × 10⁶ tonnes of lead were consumed
worldwide (ILZSG, 1992). The twenty-four industrialized countries of
the OECD consumed approximately 65% of this amount, with eastern
Europe and the former USSR using 21%. Asia now utilizes about 9% of
the world's lead production.

The use patterns of refined lead vary from country to country.
The situation in 1990 in Mexico is shown in Table 6, while end-use
categories within OECD countries are summarized in Fig. 1, which
indicates the changes between 1970 and 1990 (OECD, 1993).

Table 6. Principal uses of refined lead in Mexico^a

Type of product 1988 1990
(%) (%)

Oxides 69.7 56.7
Batteries 9.2 17.9
Tetraethyllead 7.9 11.9^b
Cables 4.0 1.5
Others 9.2 11.9

^a ILZSG (1992)
^b This does not reflect the introduction of lead-free petrol
in 1990.

From Fig. 1, it is evident that the largest use of lead within
OECD countries is for battery production, whereas there has been a
large drop in the demand for lead-containing gasoline additives.
However, this pattern is not valid worldwide, e.g., concentrations in
petrol range from zero in such countries as Japan and Thailand to
1.12 g/litre in the Virgin Islands (Octel, 1991).

In the past the use of lead in the chemical industry for the
preparation of paints, pigments and coloured inks was widespread. Many
countries have now restricted this use, and concentrations of lead
greater than 0.06% (USA) and 0.5% (New Zealand) are not permitted in
indoor paints (Albert & Badillo, 1991; OECD, 1993). In 1982, data from
the United Kingdom (UK, 1982) indicated levels of lead between 2500
and 3000 mg/kg in decorative glass paints and up to 448 g/kg in
white-lead primer. Red-leadcontaining paints, still used widely to
paint structural steel works, can contain up to 661 g lead/kg.

Other disperse uses of lead include lead solders (now banned in
USA for use in drinking-water systems), ammunition (Novotny et al.,
1987), foil on wine bottles (Wai et al., 1979) and cosmetics and
folk-medicines (surma in Asia, Kohl in India, and Al Kohl in Saudi
Arabia and Kuwait) (Fernando et al., 1981).

3.4 Sources of environmental exposure

As noted above, lead is a ubiquitous pollutant in the global
ecosystem, as well as occurring naturally. Its uses have resulted in
increases in soil, water and air lead levels to one to two orders of
magnitude above those estimated to have prevailed prior to rapid
industrialization in the 18th and 19th centuries (Patterson, 1983).
Whereas in specific areas point sources may contribute significant
amounts of lead to the environment, on a global scale, the combustion
of alkyllead in petrol is the predominant source of increased lead in
all compartments of the environment. This has been hypothesized based
upon mass balance studies (Nriagu, 1979) and confirmed by the changes
in environmental lead levels which have followed the significant
reductions in worldwide use of alkyllead as a gasoline additive since
the mid-1980s. For example, lead concentrations in Greenland snow
decreased by a factor of 7.5 over a 20-year period from the late 1960s
(Boutron et al., 1991).

Nriagu & Pacyna (1988) have estimated the global emissions of
lead to the atmosphere resulting from anthropogenic uses (Table 7).
Current estimates (OECD, 1993) of emissions from mobile sources would
be about 30% of the 1983 amounts. Similarly estimates of emissions of
lead to soil in 1983 were made by Nriagu & Pacyna (1988) (Table 8).
Since lead is never degraded, all lead which is shifted from
geological sources by human technology eventually enters the
environment through disposal, although this can be slowed by recycling
and recovery.

Municipal solid waste (MSW), solid waste, hazardous waste, sewage
sludge, and industrial waste-water discharges all may contain lead at
concentrations as high as 50 g/kg. Although few measurements of
environmental lead concentrations in the vicinity of disposal sites
have been conducted, analyses of fly and bottom ash from municipal
incinerators show high concentrations (up to 50 g/kg) of lead (Wadge &
Hutton, 1987), and land disposal sites which have received incinerator
ash for a number of years show high levels of lead in soil (Hutton et
al., 1988).

Dusting and flaking of lead paint from surfaces can be a source
of lead contamination in surface dust and soil near houses or
buildings as well as contributing to the concentrations of lead in
household dust. This process is a function of the type of paint and
the age and state of repair of the structure. When lead paint is
present on structures, both interior and exterior dusts have higher

concentrations than otherwise would be expected (Thornton et al.,
1985). Abatement of lead paint may be a major local source of
environmental contamination, as shown by studies near school buildings
in London (Rundle & Duggan, 1986). Removal of lead-based paints from
bridges and water towers using improper techniques can also result in
significant environmental contamination. Direct application of
lead-contaminated sludge as fertilizers, and residues of lead arsenate
from use in agriculture can lead to the contamination of soil, surface
water and ground water. In local aquatic environments, pollution can
result from leaching of lead from lead shot, shotgun cartridges and
fishing weights (IPCS, 1989). Coal contains small amounts of lead,
which can be concentrated in fly ash from coal combustion (Wadge &
Hutton, 1987) or in stack emissions (Table 8).

Table 7. Estimated worldwide anthropogenic emissions of lead to
the atmosphere (1983)^a

Source category Emission rate (tonnes/year)

Coal combustion
- electric utilities 780-4650
- industry and domestic 990-9900

Oil combustion
- electric utilities 230-1740
- industry and domestic 720-2150

Pyrometallurgical non-ferrous metal production
- mining 1700-3400
- lead production 11 700-31 200
- copper-nickel production 11 000-22 100
- zinc-cadmium production 5520-11 500

Secondary non-ferrous metal production 90-1440

Steel and iron manufacturing 1070-14 200

Refuse incineration
- municipal 1400-2800
- sewage sludge 240-300

Phosphate fertilizers 60-270

Cement production 20-14 200

Wood combustion 1200-3000

Mobile sources^b 248 030

Miscellaneous 3900-5100

Total 289 000-376 000

(median 332 000)

^a Adapted from: Nriagu & Pacyna (1988), as in OECD (1993).
^b Current estimates (OECD, 1993) for mobile source emissions
would be about 30% of the 1983 amounts.

Table 8. Worldwide emissions of lead into soils (1983)

Source category Emission rate (tonnes/year)

Agricultural and food wastes 1500-27 000
Animal wastes, manure 3200-20 000
Logging and other wood wastes 6600-8200
Urban refuse 18 000-62 000
Municipal sewage sludge 2800-9700
Miscellaneous organic wastes, including excreta 20-1600
Solid wastes, metal manufacturing 4100-11 000
Coal fly ash, bottom fly ash 45 000-242 000
Fertilizer 420-2300
Peat (agricultural and fuel use) 450-2000
Wastage of commercial products 195 000-390 000
Atmospheric fall-out 202 000-263 000

Total yearly input to soils 479 090-1 038 800

Mine tailings 130 000-390 000

Smelter slags and wastes 194 000-390 000

Total yearly discharge on land 803 090-1 818 800

^a From: Nriagu & Pacyna (1988), adapted from OECD (1993);
many of these emissions remain localized due to the nature of
the particulate matter

4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION AND TRANSFORMATI