ipp A
Id I r\ Environmental Protection Health Effects Research Labors
Ag*.- Cincinnati,
REVIEWS OF THE ENVIRONMENTAL
EFFECTS OF POLLUTANTS:
LEAD
w
Health Effects Research Laboratory
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RESEARCH REPORTING SERIES
Research reports of the Office of Research and Development, U.S. Environmental
Protection Agency, have been grouped into nine series. These nine broad categories
were established to facilitate further development and application of environmental
technology. Elimination of traditional grouping was consciously planned to foster
technology transfer and a maximum interface in related fields. The nine series are:
1. Environmental Health Effects Research
2. Environmental Protection Technology
3. Ecological Research
4. Environmental Monitoring
5. Socioeconomic Environmental Studies
6. Scientific and Technical Assessment Reports (STAR)
7. Interagency Energy-Environment Research and Development
8. "Special" Reports
9. Miscellaneous Reports
This report has been assigned to the ENVIRONMENTAL HEALTH EFFECTS
RESEARCH series. This series describes projects and studies relating to the tolerances
of man for uhhealthful substances or conditions. This work is generally assessed from a
medical viewpoint, including physiological or psychological studies. In addition to
toxicology and other medical specialities, study areas include biomedical instrumenta-
tion and health research techniques utilizing animals — but always with intended
application to human health measures.
This document is available to the public through the National Technical Information
Service, Springfield, Virginia 22161.
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EPA-600/1-78-029
July 1978
REVIEWS OF THE ENVIRONMENTAL EFFECTS OF POLLUTANTS:
VII. LEAD
by
Mary Anne Bell, Robert A. Ewing, Garson A. Lutz,
Verna L. Holoman, Bernard Paris, and Horatio H. Krause
Battelle
Columbus Laboratories
Columbus, Ohio 43201
Assessment Chapter Author
Paul B. Hammond
Department of Environmental Health
University of Cincinnati
Cincinnati, Ohio 45219
Contract # 68-01-1837
Contract # 68-03-2608
Project Officer
Jerry F. Stara
Office of Program Operations
Health Effects Research Laboratory
Cincinnati, Ohio 45268
Date Published: October 1979
HEALTH EFFtOS RESEARCH LABORATORY
OFFICE OF RESEARCH AND DEVELOPMENT
U.S. ENVIRONMENTAL PROTECTION AGENCY
CINCINNATI, OHIO 45268
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DISCLAIMER
This report has been reviewed by the Health Effects Research Laboratory,
U.S. Environmental Protection Agency, and approved for publication. Approval
does not signify that the contents necessarily reflect the views and policies
of the U.S. Environmental Protection Agency, nor does mention of trade names
or commercial products constitute endorsement or recommendation for use.
ii
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FOREWORD
A vast amount of published material is accumulating as numerous research
investigations are conducted to develop a data base on the adverse effects
of environmental pollution. As this information is amassed, it becomes
continually more critical to focus on pertinent, well-designed studies.
Research data must be summarized and interpreted in order to adequately
evaluate the potential hazards of these substances to ecosystems and ulti-
mately to public health. The Reviews of the Environmental Effects of
Pollutants (REEPs) series represents an extensive compilation of relevant
research and forms an up-to-date compendium of the environmental effect data
on selected pollutants.
Reviews of the Environmental Effects of Pollutants: VII. Lead, includes
information on chemical and physical properties; pertinent analytical techni-
ques; transport processes to the environment and subsequent distribution and
deposition; impact on microorganisms, plants, and wildlife; toxicologic data
in experimental animals including metabolism, toxicity, mutagenicity,
teratogenicity, and carcinogenicity; and an assessment of health effects in
man. Hie large volume of factual information presented in this document is
summarized and interpreted in the initial chapter, "General Sunmary/Environ-
mental Assessment" which presents an overall evaluation of the potential
hazard resulting from present concentrations of lead in the environment.
This overview chapter represents a major contribution by Dr. Paul Hammond
of the University of Cincinnati, Dept. of Environmental Health. As a
recognized authority in the field, Dr. Hammond's professional interpretation
and synthesis of the literature gives great insight into past work and
projected research trends.
The REEPs are intended to serve various technical and administrative
personnel within the Agency in the decision-making processes, i.e. in the
development of criteria documents and environmental standards, and for
other regulatory actions. The breadth of these documents makes them a use-
ful resource for public health personnel, environmental specialists, and
control officers. Upon request these documents will be made available to
any interested individuals or firms, both in and out of the government.
Depending on the supply, the document can be obtained directly by writing to:
U.S. EPA
Environmental Criteria and Assessment Office
26 W. St. Clair Street
Cincinnati, Ohio 45268
F=±
F. Stara
Director
Environmental Criteria and
Assessment Office
iii
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PREFACE
Metallic lead was one of the earliest metals used by man. Since lead
is now the most widely used heavy metal, and since lead poisoning has plagued
mankind since antiquity, an enormous body of literature has developed on the
biological aspects of lead. Thus, the principal problem in preparing this
monograph was not in identifying and acquiring sufficient information to
adequately encompass the topic, but assembling and coordinating what became
a seemingly endless supply of pertinent and germane references. The wealth
of candidate material for inclusion in this document which was deemed too
significant to omit has resulted in a sizeable report.
In spite of the fact that lead has been studied so intensively for so
long, comprehensive reviews of the literature frequently disclose areas
warranting further investigation, and this review is no exception. For example,
it would appear that the area of subclinical effects in children is one de-
serving further examination. The neurotoxic effects of lead include permanent
damage to the central nervous system which may result in mental retardation,
hyperactivity syndrome, psychological impairment, and deficiency in fine
motor, adaptive, and language functions. The subclinical effects of lead
upon adults including the aged also have not been resolved.
Interest in lead has not abated, and important new literature continues
to appear. Also, as new and pending regulations governing the utilization
and handling of lead begin to show measurable results, its environmental
effects will begin to be altered from those described in this report, possibly
shifting towards more subtle health effects. Their evaluation will pose chal-
lenging problems in designing and executing the requisite research studies.
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ABSTRACT
Lead, one of the oldest metals known to man, has by far the largest
usage in the U.S. of any of the heavy metals, approaching 1.5 million
metric tons per year. The largest use, for gasoline antiknock additives,
results in the annual dispersion to the atmosphere of between 150,000 and
200,000 tons. Lead concentrations in the environment have increased signi-
ficantly since the industrial revolution. Lead contamination reaching the
environment is more or less immobilized in insoluble forms, e.g., as oxides,
carbonates, or phosphates. Lead is not biomagnified to any significant
extent in man's food chain. The transfer of lead to foods is minimized
by its low solubility in environmental media, and by the ability of soil
to bind lead ions. Although lead poisoning of animals does occur occasion-
ally, the contribution of animal products to human lead burdens is
negligible.
In earlier years acute lead poisoning was a common occupational problem
in the metals and pigments industries, and in the manufacture of antiknock
additives. Advances in industrial hygiene have virtually eliminated this
problem; the few remaining problems are now being seriously addressed by
new legislation.
The most serious toxicological problem at present appears to be lead
poisoning in children, primarily as a result of pica and lead-based paints
used on old homes. Legislation prompted by community action, mass screen-
ing, and improved therapy provide assurance that plumbism attributable to
paint sources will continue to decline and possibly be eventually eradicated.
In recent years, adverse effects of lead have manifested themselves,
especially in children, as minor neurological dysfunctions and impairments
of motor and mental abilities. The overall impact of these effects has
not been resolved.
Diet is the principal source of lead under normal circumstances; lead
from air is a minor contributor. While lead is detectable in all foods,
concentrations in food in cans with soldered side seams may exceed twice
those in the raw food before canning.
This study reviews the environmental impact of lead. It includes a
discussion of the physical and chemical properties, analytical methods,
the biological aspects in microorganisms, plants, animals, and humans,
environmental distribution and transformation and environmental inter-
actions and their consequences.
This report was submitted in fulfillment of Contract Nos. 68-01-1837
and 68-03-2608 by Battelle Memorial Institute under the sponsorship of the
U.S. Environmental Protection Agency. This report covers the period May 27,
1975 to February 28, 1978, and work was completed as of March 15, 1978.
vii
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CONTENTS
Foreword [[[
Preface [[[
Abstract [[[ iv
Figures [[[ xl
Tables [[[ xiv
Acknowledgement [[[ xix
1.0 General Summary /Environmental Assessment ...................... 1.1
1. 1 Introduction .......................................... 1> 1
1.2 Physical and Chemical Properties and Analysis ......... 1.2
1 . 3 Effects on Microorganisms ............................. 1.3
1.4 Effects on Plants ..................................... 1.3
1.5 Effects on Animals .................................... 1.5
1 . 6 Effects on Humans ..................................... 1.8
1.7 Environmental Distribution and Transformation ......... 1. 15
1.8 Environmental Interactions and their Consequences ..... 1.17
2.0 Physical and Chemical Properties and Analysis ................. 2.1
2.1 Summary ............................................... 2.1
2 . 2 Physical and Chemical Properties ...................... 2.2
2.2.1 Inorganic Compounds of Lead .................. 2.5
2.2.2 Organic Compounds of Lead .................... 2.7
2.2.3 Isotopes of Lead ............................. 2.10
2.3 Analysis for Lead ........................ , ....... ,,.., 2,10
2.3.1 Sample Storage and Preservation. ...,.,, ...... 2.11
2.3.2 Preparation of Samples for Analysis ---- . ..... 2.12
2.3.2.1 Biological Samples ......... . ........ 2.12
2.3.2.2 Aqueous Samples, ........ . ........... 2.15
2.3.2.3 Air Samples ......................... 2.15
2.3.2.4 Rock and Soil Samples ............... 2.15
2.3.2.5 Miscellaneous Samples ............... 2.16
2.3.3 Methods of Analysis .......................... 2.16
2.3.3.1 Atomic Absorption Spectroscopy ...... 2.22
2.3.3.2 Absorption Spectrophotome try. ....... 2.25
2.3.3.3 Electrochemical Techniques .......... 2.25
2.3.3.4 X-Ray Fluorescence .................. 2.26
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CONTENTS
(continued)
2.3.4 Comparison of Analytical Methods 2.29
2.3.4.1 Standards and Standardization 2.31
2.3.4.2 Intel-laboratory Comparisons 2.32
2.4 References 2.37
3.0 Effects on Microorganisms 3.1
3.1 Summary 3.1
3.2 Transformations and Metabolism 3.1
3.2.1 Biotransformations 3.1
3.2.2 Uptake and Absorption 3.3
3.3 Effects 3.3
3.4 References 3.11
4.0 Effects on Plants 4.1
4.1 Summary 4.1
4.2 Nonvascular Plants 4.2
4.2.1 Algae 4.2
4.2.1.1 Metabolism: Uptake, Absorption,
and Residues 4.2
4.2.1.2 Effects 4.3
4.2.2 Lichens, Fungi, and Bryophytes 4.4
4.2.2.1 Metabolism: Uptake, Absorption,
and Residues 4.4
4.2.2.2 Effects 4.8
4.3 Vascular Plants 4.8
4.3.1 Noncrop Plants 4.8
4.3.1.1 Metabolism: Uptake, Absorption,
and Residues 4.8
4.3.1.2 Effects 4.19
4.3.2 Crop Plants 4.22
4.3.2.1 Metabolism: Uptake, Absorption,
and Residues 4.22
4.3.2.2 Effects 4.32
4.3.3 Translocation in Vascular Plants 4.36
4.4 References 4.38
5.0 Effects on Animals 5.1
5.1 Summary 5.1
5.2 Invertebrates 5.1
5.2.1 Aquatic 5.2
5.2.1.1 Metabolism: Uptake, Absorption,
and Residues 5.2
5.2.1.2 Effects 5.4
5.2.2 Terrestrial 5.8
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CONTENTS
(continued)
5.2.2.1 Metabolism: Uptake, Absorption,
and Residues 5.8
5.2.2.2 Effects 5.9
5.3 Fish 5.9
5.3.1 Metabolism: Uptake, Absorption and
Residues 5.9
5.3.2 Effects 5.12
5.4 Birds 5.17
5.4.1 Metabolism: Uptake, Absorption, and
Residues 5.17
5.4.2 Effects 5.24
5.5 Mammals 5.27
5.5.1 Wild 5.27
5.5.1.1 Metabolism: Uptake, Absorption,
and Residues 5.27
5.5.1.2 Effects 5.30
5.5.2 Domestic 5.30
5.5.2.1 Metabolism: Uptake, Absorption,
and Residues 5.30
5.5.2.2 Effects 5.34
5.6 References 5.37
6.0 Effects on Humans 6.1
6.1 Summary 6.1
6.2 Metabolism 6.7
6.2.1 Uptake and Absorption 6.7
6.2.1.1 Inhalation 6.7
6.2.1.2 Ingestion , 6.9
6.2.1.3 Percutaneous Absorption 6.11
6.2.1.4 Placental Transfer 6.12
6.2.2 Transport and Distribution 6.14
6.2.3 Elimination 6.25
6.2.4 Mathematical Models of Lead Metabolism.... 6.28
6.3 Toxic Effects 6.28
6.3.1 Enzymatic and Cellular Responses to Lead.. 6.29
6.3.2 Organ System Toxicities 6.34
6.3.2.1 Renal Toxicity 6.34
6.3-2.2 Hematopoietic Toxicity 6.40
6.3.2.3 Nervous System Toxicity 6.54
6.3.2.4 Immune System Toxicity 6.67
6.3.2.5 Cardiovascular System Toxicity... 6.68
6.3.2.6 Endocrine System Toxicity 6.69
6.3.3 Factors Influencing or Modifying Toxicity. 6.70
6.3.4 Reproductive Effects: Fertility Reduction,
Mutagenicity, Teratogenicity 6.77
xi
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CONTENTS
(continued)
6.4
6.5
6.3.5
Carcinogenicity and Miscellaneous Bio~
Lead Toxicity in Children. , , . . , ,
6.4.1
6.4.2
6.4.3
6.4.4
6.4.5
Unique Features of Lead Poisoning in
Children , ,
6.4.1.1 Sources , ,
6.4.1.2 Absorption Patterns,
6.4.1.3 Manifestations: Learning Dis~
abilities and Hyperkinesis
Scope of Childhood Lead Poisoning Problem. . .
Sequellae of Excessive Childhood Lead
Treatment Modalities ,
Epidemiology
6.5.1
6.5.2
6.5.3
6.5.2.1 Mobile Emissions Sources
6.5.2.2 Stationary Emissions Sources
6.5.2.3 Miscellaneous Sources
Occupational Exposures ,.....,....,,....
6.5.3.1 Recent Field Investigations
6.5.3.2 Dose-Response Relationships -
6.81
6.84
6.84
6.84
6.85
6.91
6.95
6.97
6.97
6.100
6.102
6.102
6.116
6.116
6.118
6.124
6.128
6.129
Air and Blood 6.137
6.5.3.3 Effects of Chronic Exposure on
Mortality 6.139
6.6 Organic Lead 6.141
6.6.1 Uptake and Absorption 6.142
6.6.2 Tissue Distribution 6.144
6.6.3 Elimination 6.144
6.6.4 Toxic Effects 6.145
6.6.4.1 Acute Toxicities of Various
Organolead Compounds 6.145
6.6.4.2 Neuropathology and Neurologic
Effects 6.149
6.6.4.3 Metabolic Effects 6.151
6.6.4.4 Enzyme Effects 6.151
6.6.5 Epidemiologic Studies 6.151
6.7 References 6.156
7.0 Environmental Distribution and Transformation 7.1
7.1 Summary 7.1
7.2 Production and Uses of Lead 7.3
7.3 Distribution of Lead in the Environment 7.9
xii
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CONTENTS
(continued)
7.3.1 Distribution in Air ,.,,.. t,,,.,.,,. 7.9
7.3.2 Distribution in Water ...,,,,...,.,... 7.15
7.3.3 Distribtuion in Soil and Rock. 7.27
7.4 Environmental Fate of Lead 7.31
7.4.1 Mobility and Persistence in Air 7.31
7.4.2 Mobility and Persistence in Water 7.40
7.4.3 Mobility and Persistence in Soil..., , 7.43
7.4.4 Waste Waters 7.44
7.4.5 Sediments 7.45
7.5 References , 7,47
8.0 Environmental Interactions and Their Consequences 8.1
8.1 Summary 8.1
8.2 Environmental Cycling of Lead 8.1
8.3 Food Chains 8.9
8.3.1 Lead in Foods 8.9
8.3.1.1 Food and Forage Plants 8.10
8.3.1.2 Processed Fruit and Vegetable
Products , 8.14
8.3.1.3 Milk and Infant Formulas 8.14
xiii
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LIST OF FIGURES
Number Page
14
3.1 Effect of lead on incorporation of C-leucine into
t-RNA from E. coli 3.5
3.2 Effect of lead on growth of Rhodopseudomonas spheroides.. 3.6
3.3 Metal-ion antagonism in Rhodopseudomonas spheroides 3.7
3.4 Synergistic antagonism of Fe by Mn and Pb in
Rhodeopseudomonas spheroides 3.8
3.5 Pathway of tetrapyrrole synthesis in Rhodopseudomonas
spheroides 3.9
5.1 Tissue lead concentration of country and city pigeons.... 5.19
5.2 The dry weight concentrations of lead in Microtus,
Clethrionomys and Apodemus trapped at Group 1 (Al road
verges) and Group 3 (arable and woodland) sites 5.30
6.1 Levels of blood lead in volunteers exposed to 10.9
micrograms per cu meter lead sesquioxide 6.8
6.2 Semi-log plot of increase in lead body burden 6.10
6.3 Change in concentration of lead with age in kidney 6.17
6.4 Change in concentration of lead with age in pancreas 6.17
6.5 Change in concentration of lead with age in liver 6.18
6.6 Change in concentration of lead with age in aorta 6.18
6.7 Change in concentration of lead with age in lung 6.19
6.8 Change in concentration of lead with age in bone 6.21
6.9 Scheme showing role of intranuclear inclusion body
in metabolism of lead 6.35
6.10 Lead content of subcellular fractions from kidneys of
control and lead-fed rats 6.36
6.11 Correlation of lead content of kidney and different
doses of lead fed to rats for 10 weeks 6.39
6.12 Pathway of heme synthesis 6.44
6.13 Scheme of heme synthesis showing sites of lead effect.... 6.45
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LIST OF FIGURES
(continued)
Number
6-1^ Brain weights of CS7BI/65 mice at 30, 40, 60, and 90
days of age raised on diets containing 0 to 0.8
percent lead carbonate for 60 days after birth 6.56
6.15 Brain weights of CS7BI/6J mice at 30 and 60 days of age
raised on diets containing 0 or 0.08 percent lead
carbonate for 60 days after birth 6.56
6.16 The effect of increasing ceruloplasmin levels on
Erythrocyte lead in male Sprague-Dawley rats fed a
semipurified diet and 0.5 percent lead for 56 days 6.74
6.17 Percent of Black and Puerto Rican two-year old children
with lead level over 60 jig/100 ml., New York City,
1971 6.99
6.18 Mean blood lead concentrations for epidemiological
and experimental respiratory exposures 6.105
6.19 Blood lead levels and corresponding mean air-lead
levels 6.108
6.20 Blood lead versus total air lead 6.113
6.21 Lead and ALA levels in urine of organic lead workers 6.153
6.22 Comparison of reported urinary ALA-lead relationships
for exposures to inorganic lead with organic lead 6.154
7.1 Percent distribution of estimated emissions of lead
to air, 1975 7.12
7.2 Ranges, means, and medians of the concentration of
lead in the atmosphere of cities grouped according
to population 7.13
7.3 Lead profiles in the maj or oceans 7. 21
7.4 Lead content of cold tap water from three groups
of Glasgow houses 7.24
7.5 Lead pollution in Glasgow 7.25
7.6 Geometric means for lead fallout measurements in 77
cities by area and month 7.36
7.7 Gravitational fallout flux of lead and washout lead
concentration as a function of downwind distance
from edge of highway at T = 1000 sec 7.37
xvi
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LIST OF FIGURES
(continued)
Number Page
7.8 Long range transport of lead and lead deposited at
soil/air interface as a function of downwind distance
from edge of highway at T = 1000 sec 7.37
7.9 Concentration of lead in soil accumulation zone and bulk
soil residual lead content as a function of downwind
distance from edge of highway at T = 1000 sec 7.38
7.10 Comparison of predicted atmospheric lead concentration
and measured values on Interstate 25 as a function
of downwind distance from edge of highway at
Z = 1.2 meters 7.38
7.11 Concentrations of total suspended particulate and
lead in New York City air 7.39
7.12 Solubility and species distribution for Pb (II) in
soft water 7.41
7.13 Solubility and species distribution for Pb (II) in
hard water 7.42
8.1 Ecologic flow chart for lead showing possible cycling
pathways and compartments 8.2
8.2 Ecodiagram of lead in the environment and its effect
on man. 8.3
8.3 A network representation of a lead ecosystem model 8.28
8.4 Calculated annual budget for lead in salt marsh plots
under three treatments 8.32
8.5 Lead levels in dredge material disposal sites of Craney
Island and Lynnhaven Inlet compared with that of the
natural unpolluted marsh at Mobjack Bay, Virginia 8.33
8.6 Lead transfer in a dredge-spoil pond ecosystem 8.34
8.7 Lead concentrations in dredge-spoil pond ecosystem 8.35
8.8 Mean concentration of lead in water, biota, and sedi-
ments of the Illinois River 8.37
xvii
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LIST OF TABLES
Number Page
2.1 Physical Constants for Lead 2.3
2.2 Oxidation-Reduction Potentials for Lead 2.4
2.3 Solubilities of Inorganic Compounds of Lead 2.6
2.4 Properties of Tetraethyllead and Tetramethyllead 2.9
2.5 Typical Concentration and Separation Procedures Used
in Determining Lead in a Variety of Environmental
Samples 2.13
2.6 Analytical Methods for Determining Lead at Low Levels.... 2.17
2.7 Available NBS Primary Samples for Lead in Various
Environmental Samples 2.31
3.1 Microbial Me thy la t ion of Lead Compounds 3.2
3.2 Effect of Pb and Mn on Tetrapyrrole Synthesis in
Rhodopseudomonas spheroides 3.10
4.1 Lead Content of Bryophytes and Their Substrates 4.6
4.2 Natural Lead Levels in the Ash of Native, Noncrop
U.S. Plants 4.10
4.3 Lead in Grasses as a Function of Distance from Traffic
or Industries 4.15
4.4 Lead in Roadside Grass Samples 4.16
4.5 Concentrations of Lead in Leaves of Post Oak (Quercus
stellata) and Needles of Shortleaf Pine (Pinus
echinata) in Vicinity of Lead Smelter Operations 4.17
4.6 Concentration of Lead in Leaves of White Oak (Quercus
alba) and Leaves of Blueberry (Vaccinium pallidum) in
Vicinity of Lead Processing Operations 4.18
4.7 Lead Burdens of Trees Growing in the City of New
Haven, Connecticut 4. 20
4.8 Natural Lead Levels in the Ash of Crop Plants 4.23
4.9 Lead in Crops, Greenhouse Studies 4.28
4.10 Lead in Crops, Highway Studies 4.29
xix
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LIST OF TABLES
(continued)
Number Page
4.11 Concentration of Lead in Five Crops Grown at Three
Field Sites in 1968 4.30
4.12 Lead Content of Plants Grown in Greenhouse in 1963 4.31
4.13 Lead Content of Fruits and Vegetables Correlated with
Distance from Traffic and Traffic Load 4.33
5.1 Lead Accumulation in a Simulated Natural Environmental
System 5.5
5.2 Concentrations of Lead Lethal to or Tolerated by Six
Protozoan Species 5.6
5.3 Concentrations of Lead in Tissues of Sardine and Anchovy
from the Adriatic Sea 5.11
5.4 Concentrations of Lead Reported Toxic or Lethal
to Fish 5.13
5.5 Concentrations of Lead Compounds Reported Lethal
to Fish 5.14
5.6 Lead Concentrations in Livers of Lead Poisoned
Waterfowl 5.20
5.7 The Concentration of Lead in the Liver of Birds 5.21
5.8 Lead Concentrations in Tissue Samples from Ohio Ring-
Necked Pheasants 5.23
5.9 Mean Concentration of Lead in Tissue of Small Mammals
from Roadside and Control Sites 5. 28
5.10 Lead Concentrations in Tissue Samples from Various
Ohio Mammals 5.31
5.11 Lead Concentrations in Tissues from Urban and Rural Rats. 5.32
5.12 "Background" Bovine Lead Concentrations in Tissues and
Rumen Contents 5.35
5.13 Lead Content in Tissues and Rumen Contents from Cattle
with Clinical Lead Toxicosis 5.35
6.1 Tissue Lead Concentration in Children and Adolescents.... 6.13
6.2 Variation in Soft Tissue Lead Concentration with Geo-
graphical Location 6.16
6.3 Variation in Bone Lead Concentration with Age 6.20
6.4 Tissues Ranked on the Basis of Overall Mean Concen-
tration of Lead 6.23
xx
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LIST OF TABLES
Number (Continued) Page
6.5 Concentration of Lead for Tissues Increasing with Age.... 6.24
6.6 Lead Ingestion and Excretion of a Normal Human Subject... 6.26
6.7 Enzymatic Activities Enhanced by Lead 6.31
6.8 Enzymatic Activities Inhibited by Lead 6.32
6.9 Erythrocyte Delta-Aminolevulinic Acid Dehydratase
(ALAD) Activities in Different Blood Lead Groups 6.48
6.10 Erythrocyte Delta-Aminolevulinic Acid Dehydratase
(ALAD) Activities in Different Blood Lead Groups 6.49
6.11 Hemoglobin Value in Different Blood-Lead Groups,
Separately for Hen and Women 6.50
6.12 Concurrent Measurements of Erythrocyte ALAD Activities
and Urinary ALAU Concentrations in Different Blood-
Lead Groups 6.51
6.13 Effect of Lead on the Force of Contraction on Nerve
and Muscle Stimulation. 6.59
6.14 Summary of Functional Changes in Workers Exposed to
Inorganic Lead 6.64
6.15 Factors Influencing Lead Toxicity 6.71
6.16 Effect of Lead on Copper Metabolism in Male Rats 6.75
6.17 Cytogenetic Findings in Cultured Lymphocytes from
Shipyard Workers with an Occupational History of
Lead Exposure 6.79
6.18 Lead in Dirt in Detroit 6.86
6.19 Lead in Dirt in Rural Area: Fainted Frame Farmhouses.... 6.88
6.20 Lead and Lead-210 in Urine 6.89
6.21 Lead and Lead-210 in Excreta 6.90
6.22 Relative Contributions of Dietary and Ambient Air
Lead to Total Lead Absorption 6.92
6.23 Cases of Childhood Lead Poisoning Plus Fatalities in
New York City from 1954 to 1964 6.96
6.24 Data of Survey Areas for Chicago Blood-Lead Screening
Program: 1967-1968 6.98
6.25 Blood Lead Levels of Selected Human Populations 6.104
6.26 Mean Subject Air Lead Exposure 6.Ill
6.27 The Impact of Air Lead on Blood-Lead Levels: A Com-
parison of Actual Data to Predictions Using Mathe-
matical Model 6.115
xxi
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LIST OF TABLES
(continued)
Number
Page
6.28 Lead Accumulation by People Living Close to a Secondary
Smelter Compared to an Urban Control Group, and Some
Potential Sources of Lead Uptake 6.125
6.29 Blood-Lead Levels in School-Age Children as a Function
of Their Address 6.126
6.30 Intelligence and Behavior in School-Age Children as a
Function of Their Address During Their First Two
Years of Life 6.127
6.31 Description of Lead Plants Investigated, 1975-1976 6.130
6.32 Blood Lead Levels in Lead Plant Workers 6.131
6.33 Percentage of Workers with Symptoms of Lead Poisoning
by Blood Lead and Erythrocyte Protoporphyrin Level
at Three Lead Plants g m ^33
6.34 Frequency of Symptoms Among 22 Cases of Lead
Poisoning, Utah, 1976 6.135
6.35 Occurrence of Symptoms in Lead Smelting Plant Employees,
Minnesota, 1976 6.136
6.36 Effect of Concentration on Absorption of Tetraethyllead
in Rats 6.143
6. 37 Cutaneous Absorption of Lead Compounds 6.143
6.38 Toxicities of Some Lead Compounds 6.146
6.39 Comparative Mortality of Rats Following Inhalation of
Tetramethyllead or Tetraethy-llead, and Lead Content
of Their Tissues. 6.147
6.40 Comparative Mortality of Dogs Following Inhalation of
Tetraethyllead, and Lead Content of Their Tissues 6.148
6.41 Cumulative Diagnoses of TEL Workers Vs Non-TEL Workers... 6.155
7.1 Production and Consumption of Lead 7.4
7.2 Lead Consumption in the United States, by Product 7.6
7.3 Estimated Amounts of Lead in the Atmosphere from
Natural Sources 7.10
7.4 Concentration of Lead in Atmosphere 7.14
7.5 Lead in the Atmosphere 7.16
7.6 Regional Summary of Lead in Surface Waters of the U.S.... 7.18
xxii
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LIST OF TABLES
(continued)
Number Page
7.7 Distribution of Lead in Dissolved and Suspended Solids
of Two Tennessee Streams 7.18
7.8 Lead Content of the Waters of the Springfield, Missouri
Area 7. 20
7.9 Lead Content of Various Waters 7.22
7.10 Lead in Glasgow Water 7. 26
7.11 Lead Content in Roadside Soil and Grass as a Function
of Distance from Traffic and Soil Depth 7.29
7.12 Total Lead in Soils of the Missouri Lead Belt 7.30
7.13 Lead in Dirt in Detroit 7.32
8.1 Environmental Pathways for Lead Compounds 8.4
8.2 Lead Content of Cereals and Vegetables 8.11
8.3 Lead Content of Fruits 8.13
8.4 Lead Content of Processed Fruits and Vegetable
Products 8.15
8.5 Lead Uptake in Canned Vegetables, Fruits, and Juices 8.16
8.6 Lead Content of Milk and Infant Formulas 8.17
8.7 Lead Content of Meat, Fish, and Poultry Products 8.22
8.8 Lead Content of Beverages 8.23
8.9 Lead Content of Bread and Baked Products 8.24
8.10 Lead Content of Sugar, Spices, Condiments, and
Miscellaneous Foods 8.25
8.11 Comparison of Actual with Predicted Lead Concentrations
in Model Ecosystem 8.30
8.12 Lead Concentration in Mud in Lake Hamilton 8.38
xxiii
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Other Battelle-Columbus staff members contributed specialized expertise
in the preparation of this document, including particularly Dr. John H.
Litchfield, Dr. A. Philip Leber, and Dr. Robert D. Burkett.
The authors wish especially to acknowledge the valuable contributions
of Dr. Paul B. Hammond, of the Environmental Health Department of the University
of Cincinnati for his perceptive general summary/environmental assessment
chapter.*
We also wish to express our appreciation for the cooperation and support
received from EPA staff of the Health Effects Research Laboratory during the
preparation of this document. Unflagging support and encouragement was pro-
vided throughout the program by the project officer, Dr. Jerry F. Stara. He
was ably assisted by Donna J. Sivulka and later by Bonita M. Smith and Karen
L. Blackburn.** The support of Dr. John R. Garner, Director of HERL was much
appreciated.
* The following persons assisted in the preparation of this chapter:
Dr. David E. Koeppe, Department of Agronomy, University of Illinois; Dr.
A. L. Aronson, Dept. of Physiology and Biochemistry, New York State
Veterinary College, Cornell University; Dr. Gary TerHaar, Director,
Toxicology and Industrial Hygiene Department, Ethyl Corporation; Dr. T. G.
Tornabene, Department of Microbiology, College of Veterinary Medicine and
Biomedical Science, Colorado State University and Dr. R. K. Skogerboe,
Department of Chemistry, Colorado State University.
** Dr. Allan Susten and Rosa Raskin co-ordinated early processing of document
preparation.
xxv
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1.0 GENERAL SUMMARY/ENVIRONMENTAL ASSESSMENT
(Dr. Paul B. Hammond)
1.1 INTRODUCTION
This document is only one of several recent ones which have summarized
portions of the vast literature dealing with the impact of lead on human
health and the environment. Each has had a somewhat different purpose and
focus. Thus, Lead in the Environment (NSF/RA-770214) is basically a summary
of work conducted under the sponsorship of the National Science Foundation
RANN program. It focuses mainly on the characteristics and transport of lead
through the environment and on monitoring methodology. Air Quality Criteria
for Lead (EPA 600/8-77-017, December, 1977) on the other hand, is basically a
resource document intended for use in promulgating an air lead standard. As
such, it omits a review of the literature dealing with effects of lead on
bacteria, plants, domestic animals and wildlife. Similarly, the World Health
Organization's recent publication, Environmental Health Criteria 3-Lead, is
also concerned with critical evaluation of the literature dealing with the
impact of lead on human health only. The present document most closely re-
sembles "Airborne Lead in Perspective (NAS-NRC, 1972) as to breadth of coverage.
Indeed, it may be considered a direct descendant of that earlier document not
only as to the ground covered, but also as to the sponsorship by the Environ-
mental Protection Agency.
This introductory chapter provides a general summary of the more detailed
coverage provided in the subsequent chapters. In addition to this, it will
attempt an assessment of the current problems begging resolution. This assess-
ment expresses the views of specific contributors in behalf of a single agency.
No claim to omniscience is implied. If this document, and particularly this
chapter, triggers some controversy and debate in the scientific community,
the effort and expenditures involved will have been justified. The worst
that can happen is that no one will read it. This seems rather unlikely.
We find today that lead is an issue which sparks debate and even class action
suits by public interest groups, the economic and social impacts of which are
likely to be considerable.
In the interest of organization, the topics considered in the separate
chapters will be reviewed and commented upon in the order in which they
appear in the document.
1.1
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1.2 PHYSICAL AND CHEMICAL PROPERTIES AND ANALYSIS
There would probably be no great concern regarding lead today were it not
for the fact that it has certain useful properties which have prompted its
mining, smelting, and conversion to items of commerce.
Lead's high density, softness and relatively low melting point enable
easy forming and casting. It has good resistance to oxidation and is fairly
resistant to both alkaline and acid solutions. It and its alloys are readily
cast, spun, stamped, rolled, extruded, and drawn. It can be readily bonded
to other metals by various means. For all these reasons, it is used exten-
sively in the metallic form.
The inorganic compounds of lead are moderately to highly insoluble.
As a consequence, lead does not transfer readily from one phase in the environ-
ment to another, e.g., from rocks to water or from water to plants.
The organolead compounds in which lead is bound directly to one or more
carbon atoms have unique properties. They are volatile, lipid-soluble and
stable to most environmental conditions, susceptibility to photoxidation
excepted. Tetraethyllead and tetramethyllead are the most common compounds
of this class. Although they may occur in nature, the major known source
is synthesis by man for use as a gasoline additive.
The analysis for lead presents numerous problems ranging from losses
during sample storage and digestion to imprecisions during analysis resulting
from matrix effects, non-specificity of method and incomplete atomization as
in flameless atomic absorption methods. For most purposes, it appears that
accuracy and precision are more serious problems than sensitivity. This is
particularly evident in the case of analysis for lead in blood and urine.
Interlaboratory comparison programs have revealed that highly discrepant
results are common. The colorimetric dithizone method which was first devel-
oped more than forty years ago, is still considered reliable for most purposes
when used by experienced analysts. Atomic absorption spectroscopy and anodic
stripping voltammetry have largely displaced the colorimetric dithizone
method. When used by experienced analysts, these methods are more specific
and sensitive than are dithizone methods.
It seems clear that the current need is not so much for new methods
as it is for more effective use of current methods. Concerns about the
environmental impact of lead ultimately come down to a matter of relating
effects to amounts or concentrations of lead in environmental and biological
media. Assessments of risk are clearly dependent on reliable analytical
data. Investigators should participate in interlaboratory comparison pro-
grams and should report in their scientific publications the accuracy and
precision of their analytical methodology. There also is need for sensitive
methodology which would identify the chemical form in which lead is found in
various environmental media. This is necessary for studies involving the
1.2
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tracing of lead to sources of pollution, and for assessing the modes or
mechanisms of lead impact in various systems. In order for such analytical
methods to be useful, various separation and concentration methods must also
be developed as appropriate for the particular problem at hand.
1.3 EFFECTS ON MICROORGANISMS
So far as bacteria and viruses are concerned, there is only very
limited literature as to effects of lead and the possible significance thereof.
As a matter of fact, there are no reports regarding lead interactions with
viruses. Various species of bacteria are capable of converting trimethyllead
to tetramethyllead. It is also possible that bacteria can convert inorganic
lead to tetramethyllead, although this remains to be demonstrated.
-4
At relatively high.concentrations (10 M lead acetate) lead inhibits
the incorporation of C-leucine into E. coli t-RNA and thereby suggests
that lead might inhibit protein synthesis. However, it should be noted
that concentrations of lead approaching solubility limits have no detect-
able effect on growth rate and cell viability in two species of bacteria
which have been studied. It appears from the limited studies reported to
date that bacteria are relatively resistant to lead.
No high priority research needs are evident at this time in regard
to interactions of lead with microorganisms. This may be because the
research reported to date has focused too narrowly on individual species
of microorganisms rather than on total integrated microbial communities
It is possible that small effects on one or a few species in the world of
microcrobes have cooperative effects which we have simply failed to perceive.
1.4 EFFECTS ON PLANTS
Consideration of the impact of lead on plant life falls into two general
areas of concern. On the one hand, there is a concern for possible detri-
mental effects of lead on plants, either for economic reasons, as with
food crops, or for esthetic reasons, i.e., concern for the varied plant
life which is part of man's natural environment. There also exists the
possibility that plants can serve as a biomagnification mechanism for the
concentration and transfer of lead from soil and water to animal life, including
man himself. Research studies to date strongly suggest that there is little cause
for concern on either score. This is not to say that plants are totally
resistant to detrimental lead effects. Nor is it to say that plants cannot
under special circumstances serve as a medium for the transfer of toxic
amounts of lead to animals and man. As a matter of fact, plant and animal
foods constitute the major source of lead for the general population.
The National Academy of Sciences review, Airborne Lead in Perspective
(1972), considered a relatively large volume of research on lead uptake,
translocation, and effect in plants; it also pointed to research gaps
(such as the uptake of aerial particulate deposited Pb and the need for
root uptake studies of lead from naturally occurring soils). Over the
1.3
-------
ensuing years some of the questions asked by the 1972 report have been
answered, but in other instances problems of lead-environmental interactions
have proven to be even more complicated and elusive than had previously
been thought. The most substantial conclusion to arise from these studies
is that it is impossible to extrapolate effects of lead on plants grown under
one set of environmental conditions to other situations without the very
careful consideration of soil and plant factors affecting lead availability.
In most instances the source of lead with potential effects on plants
has been from aerosols. Since most such particles are relatively large,
their deposition is highly localized; i.e., within several hundred meters
of roadways in the case of lead emitted from auto exhausts. Lead from
aerosol sources is deposited on leaf surfaces and also comes in contact
with roots as a result of soil contamination. Both the vertical and hori-
zontal movement of this lead in soils has been assumed to be negligible
due to the very high affinity of lead for various soil components. This has
in general been the case, except where man has disturbed the soil through
tillage, possibly leaving the Pb-soil complex exposed to potential wind or
water-effected erosion. This movement is of course predominately horizontal.
In contrast to most plants, algae live predominantly in an aquatic en-
vironment where horizontal and vertical transfer of lead occurs with relative
ease at low concentrations. Algae clearly show a capacity to concentrate
lead by adsorption and absorption from their aquatic environment. The im-
plications of this biomagnification for higher forms of life are not known. So
far as effects of lead on algae are concerned, the inhibitory effects on
growth and metabolic processes which have been noted all occur at lead
levels in excess of 1 ppm. Such levels of water contamination seldom occur
in nature, even with the added burden of pollution from lead mine tailings
or municipal and industrial wastes.
Ascending to the world of lichen and fungi, one finds that the capacity
for biomagnification disappears. This is because these plants reside in
soils, which have a strong affinity of their own for lead. So far as toxic
effects are concerned, the evidence is too sparse to arrive at any firm con-
clusions, but there is no evidence to encourage the belief that these forms
of life are in any way threatened by the concentrations of lead they might
encounter even when residing in close proximity to point or line sources of
lead pollution.
The uptake of lead by vascular plants has received considerably more
attention than has been the case with lower forms of plant life. Aquatic
forms concentrate lead to a considerable extent, as do algae, probably mainly
by adsorption. Terrestrial vascular plants, however, show no concentrative
capacity, except for roots. As with lower forms of terrestrial plant life
this is no doubt due to the strong lead-binding capacity of soil.
l.U
-------
There is no question as to the potential toxicity for livestock of plants
contaminated with lead, but in all documented instances the contamination
has resulted from aerial deposition of lead from the fallout of lead smelters.
Transfer of lead to forage via the root system has never been demonstrated
to be a problem under either natural or soil-amended conditions. Even the
growth of plants in sewage sludge does not seem to result in any significant
elevation of plant lead content.
There have been a number of studies indicating that food crop yields
are reduced by lead, but only in soils containing concentrations far in
excess of what is ever likely to be encountered under field conditions.
As the world food supply dwindles, certain circumstances may arise in
which relatively moderate lead contamination of soil might reduce plant
yields. The most likely circumstance may be phosphorus deficiency. Most
evidence now available indicates that probably most lead absorbed by plant
roots is rapidly precipitated as a Pb-phosphate complex without translocation.
Reports indicate that lead in varied situations binds to many cellular com-
ponents, especially phosphate-containing membranes, nucleotides, nucleic
acids, and organelles; and that it also binds in vitro to insoluble ferric
hydroxide, is codeposited with Ca^+ in Pb-protein complexes and forms mer-
captides with the ~SH group of several amino acids. The significance of
the predominant Pb-phosphate complexation is seen in studies with corn and
several tree species where phosphate deficient plants exhibited a greater
toxic response to lead. These observations could have future agricultural
applicability since increases in land usage for agriculture will likely
come with cropping of marginal lands, many of which are low in phosphorus.
While suggestions have been made that a "healthy plant" can withstand most
stress factors better than one which is already stressed, it seems that of
all stresses which could have an impact on lead uptake and translocation
in the plant, phosphorus deficiency may possibly be the most important.
There is still a need to determine how much lead in plant food is due
to contamination on in the field and how much is due to various stages of
processing and storage. No systematic study has ever been reported in
which the flow of lead into and out of the raw plant food products has been
delineated.
1.5 EFFECTS ON ANIMALS
There have been numerous studies reported concerning the occurrence
and effects of lead in a broad range of animal species, both aquatic and
terrestrial.
1.5
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Many survey studies have been made on the concentrations of lead occurring
in fresh and marine waters and in the aquatic species residing therein. As
expected, experimental studies have shown that aquatic species accumulate
lead when the concentrations of lead in their environment increase. There
is no convincing evidence for biomagnification of lead in the aquatic food
chain however.
Concentrations of lead shown to be toxic are considerably higher than
that found to generally occur in natural waters. There is no evidence incri-
minating lead as producing adverse biologic effects in aquatic life in natural
waters in the United States. Fish kills have been reported, however, as
occuring in rivers near old lead mining areas in England. It was reasoned
that the concentration of lead in the rivers would rise sharply whenever
heavy rains effected leaching of lead from the surrounding areas.
It has been reported that methylation of lead can occur in an aquatic
environment. A confirmation of this finding and a definition of the factors
favoring the formation of this form of lead in an aquatic environment would
be of considerable interest.
In insects, the concentration of lead reflects the concentration in
the environment, as in aquatic animals. There is some evidence for biomagni-
fication whereby lead is concentrated in its progression from plant foods
to herbivores and on up to insect carnivores. Data concerning biological
effects in insects are relatively sparse. Changes in gene frequency in
Drosophila have been found to be significantly correlated with distance from
a lead smelter in Missouri. Similar studies in other insect species have
not been reported.
The impact of environmental lead on wildlife is difficult to assess
with one notable exception. It is clear that waterfowl have died in large
numbers resulting from the ingestion of spent lead shot. The problem has been
recognized for years and extensive efforts have been made to find a substitute
for lead shot. Soft iron approaches lead in suitability and for the past
two years this shot has been required for hunting in certain flyways. Lead
shot probably will be banned from even more flyways in future hunting seasons.
Certainly this should have a favorable effect in reducing the incidence of
lead poisoning in waterfowl. Hopefully, other problems will not be created
instead. For example, will more birds be wounded instead of killed because
of the less favorable ballistic qualities of soft iron? A few years ago,
hardening of the soft iron was considered to be a real problem - with a
resultant hazard to hunters in the forms of split gun barrels, especially
if the shotgun were equipped with a full choke.
A number of survey studies have been made which show that increased
body burdens of lead occur in terrestrial wildlife inhabiting areas contam-
inated with lead, e.g., roadsides, old apple orchards, and in the vicinity
of industrial lead operations. There is no evidence that these increased
1.6
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body burdens of lead are causing deaths. The difficulties in determining
population shifts, decreased life span, depressed growth or reproductive
difficulties in most wild animal species are obvious. Even if such effects
could be determined as occurring within localized areas of contamination,
the significance relative to the population at large would be questionable.
An extensive body of information exists on clinical lead poisoning in
domestic animals. The sources of poisoning, clinical signs in several
species and gross and microscopic lesions have been described in many
publications. Lead poisoning has been and still is a commonly diagnosed
toxicologic problem in veterinary medicine. For example, 80 to 100
episodes are reported annually from the Texas Veterinary Diagnostic Laboratory.
Lead poisoning accounted for 1.2% of all canine hospital admissions at the
Angell Memorial Animal Hospital between 1969 through 1971. Thus, the
ingestion of lead by animals in amounts sufficient to produce overt clinical
poisoning is important.
The sources of lead in domesticated animals vary greatly depending on
the environment and species peculiarities. Cattle are indiscriminate eaters
and most any lead-containing material may be ingested (for example, paint,
storage batteries, used motor oil and filters and certain types of grease
and putty). Forage contaminated from industrial lead operations or mines
has been incriminated as a source to cattle and also to horses and sheep.
Dogs, like cattle, are indiscriminate eaters and will consume a variety of
lead-containing materials (for example, plaster, paint, linoleum, and a variety
of lead objects). The sources of lead described above have been documented
repeatedly as being responsible for clinical cases of poisoning in animals.
There are other potential sources of lead to animals that have not
until recently received serious consideration. These include the ingestion
of soil by grazing animals and the addition of feed-grade mineral supplements
to feed products. It is conceivable that the ingestion of lead-containing
soil, in addition to the forage in certain areas, could result in the con-
sumption of lethal quantities of lead.
Horses are suspected of consuming considerably more soil while grazing
than cattle but studies designed to quantitate the amount ingested have not
been made. Ingestion of soil might account for the enormous differences
reported in toxic doses of lead to horses as compared to cattle, based upon
forage content of lead. Studies designed to quantitate the amount of soil
ingested by grazing horses should be most helpful in resolving this question.
Little definitive information is available on the effect of lead in
domestic animals at levels that are elevated, but insufficient to produce
poisoning. Limited data concerning cattle indicate that even when fodder
contained 100 ppm Pb, there was no effect on feed consumption, weight gain,
electrocardiogram patterns or respiratory rate. Examination of the cerebral
cortex, liver and kidney cortex by electron microscopy did not reveal any
1.7
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ultrastructural change!. In another study (dally Pb dotea of 5 to 6 mg/kg,
corresponding to a concentration In excess of 200 ppm In forage) steers
have been shown to grow normally for as long as 33 months. On the other
hand, 15 mg/kg/day fed to steers for 283 days resulted In the development
of anemia following the 42nd day of feeding, but no observable signs of
lead Intoxication were reported other than a slower rate of growth.
1.6 EFFECTS ON HUMANS
Evaluation of the hazards of lead exposure In man has been ongoing for
many years. Largely as a consequence of this research, the Incidence of
Illness and death attributable to lead has been drastically reduced, parti-
cularly during the past twenty years. Yet, for all that, research continues
at an ever-accelerating pace. Some new subtle effects of lead are being
reported. Just as lead In the environment has proven to be ubiquitous, so
have the biological effects In mammalian systems. Needless to say, most
current Information has been obtained utilizing animal models and In many
cases the doses of lead used to elicit responses have been extremely high.
In some Instances the human health Implications of animal studies have been
defined with a reasonable degree of certainty. In many other cases,wall-
designed studies In human populations have not been done.
Evaluation of toxlclty requires specification not only of an effect,
but also of the dose at which It occurs. In the broad sense of the word,
dose Includes all knowledge concerning transfer from the external environment
to the receptor site where the toxic effect Is elicited. Needless to say,
the receptor site Is usually either unknown or Is not accessible for study
In man. In the case of lead, the usual Indirect measure of dose Is the con-
centration of lead In the blood (PbB), conventionally expressed as yg Pb/dl.
There Is some knowledge as to how PbB relates to external doses via Inhal-
ation and IngestIon. Much also Is known about the relationship of PbB to
degree of effect (dose-effect relationship) or to the Incidence of occurrence
of an effect (dose-response relationship). Thus, PbB forms a vital link
between external dose and effect.
The major routes of absorption are the gastrointestinal tract and
the respiratory system. Efforts to determine the absorption of lead by
the human body at specified air lead concentrations have been only marginally
successful for various technical reasons. It has been necessary to resort
to PbB as an indirect measure of "dose" of air lead. For people who are
breathing fairly constant air lead concentrations, averaged over months,
the concentration of lead in the blood varies in accordance with the air
lead concentration. Analysis of data as to air lead vs. PbB from several
studies of adults Indicate that over the range of general ambient air lead
concentrations, 1 Mg Pb/m3 of air contributes 1-2 pg Pb per deciliter of
blood. This relationship seems also to apply to children. At higher air lead
concentrations, such as are encountered in industry, the incremental rise in
PbB is lower per unit air lead concentration.
1.8
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Direct determination of absorption of lead from the digestive tract
Is not beset with as many technical difficulties as is the case with inhaled
lead. Although the number of studies of lead absorption performed in people
Is extremely limited, the conclusions drawn are fairly consistent. Approxi-
mately 8 percent of total, normal dietary lead is absorbed in adults and 40-
50 percent is absorbed in the case of infants and preschool-age children.
Dietary Intake of lead in the general adult population is about 150-250
Mg/d. Limited information suggests that every 100 ug *b ingested in the diet
daily contributes about 6 ug to PbB. Thus, diet is the principal source
of lead under normal circumstances.
The relative contribution of various types of foods and beverages to
PbB is poorly understood. It is not enough to know the concentrations of
Pb in foods and the amounts consumed since bloavallablllty and absorption
may vary considerably. Thus, for example, the lead in foods high in calcium
is less well-absorbed than la the case when dietary calcium is low, and lead
in beverages consumed on an empty stomach is absorbed to a substantially
greater degree than lead in foods. Metallic lead particles such as are
found In the side seam region of lead soldered cans Is very poorly absorbed
compared to lead acetate Incorporated into the diet of experimental animals.
The availability for absorption of lead in paint chips is of special concern
because young children are known to chew and swallow paint chips. Animal
studies suggest that lead in this form Is substantially absorbed, though
probably not as well as lead in foods.
The absorption of inorganic lead salts from the skin Is negligible,
even at high concentrations. Lead soaps used in industrial lubricants,
however, are absorbed to a significant extent, probably because these soaps
are llpld-soluble.
The fetus absorbs lead freely from its maternal environment. This is
evident from numerous animal studies and some human autopsy studies. The
maternal-fetal system tends to equilibrate as indicated by the fact that
PbB's in the newborn correspond closely to the PbB's of their mothers.
Once absorbed, lead displays certain important features regarding
distribution. Within the blood, lead is concentrated mainly in the erythro-
cytes. Among the soft tissue structures, the liver, kidney, and aorta have
relatively high concentrations, whereas the concentration in brain, muscle
and heart is relatively low. All of these differences are relatively minor,
however, in contrast to the well-known propensity which lead has to accumulate
in bone. Approximately 90 percent of the lead in the body of adults resides
in the skeleton. The figure is lower for infants and young children.
Because of its slow rate of excretion, lead tends to accumulate in the
body to middle life and beyond. Accumulation la more pronounced in some
tissues and body fluids than in others. Thus, the concentration in the
1.9
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blood seems to reach a plateau early in life whereas in some tissues e.g.,
bone and large arteries, lead continues to increase to old age.
Excretion of lead is mainly by way of the urine and bile with losses
from exfoliating dermal structures and sweat making only minor contributions
to total excretion.
Mathematical models have been developed to describe the kinetics of
lead distribution and excretion. So far as excretion is concerned, the most
satisfactory model is a power function model. This says, in effect, that
the rate of excretion of a single dose of lead becomes progressively slower
with passing time. The model has not been rigorously tested.
The biological effects of lead in man are numerous. They occur at
different levels of lead exposure, the body being more sensitive to some
effects than to others. The critical organ is defined as the one exhibiting
adverse effects at the lowest level of exposure and the critical dose (gen-
erally expressed as PbB) is the one causing the critical effect. Other
biological effects, occurring at lower levels of lead exposure are termed
subcritical effects. There is still some controversy as to which effect
of lead is the critical one or, put another way, there is controversy as
to the maximum level of lead exposure which produces no adverse effects.
It is perhaps useful to work downward from the worst effects which
everyone will agree are adverse to those of uncertain health significance.
In that regard, it is also useful to distinguish between clinical effects
and subclinical effects. For the purposes of this review, clinical effects
are those which a subject can perceive and which a physician would normally
seek to correct. Subclinical effects are those which under normal circum-
stances do not result in a perceptible decrement in body function but which
could possibly reduce an individual's capacity to cope with a coexistent
body stress.
The principal organs and systems affected by lead are the kidneys, the
hematopoietic system and the central and peripheral nervous systems. In all
four cases a spectrum is seen, incuding both subclinical and clinical
effects. In addition, at least one effect occurs in the hematopoietic system
which is considered to be of dubious health significance and which therefore
may be classified as "subcritical".
Prolonged elevated lead exposure results in two general types of kidney
disease. The first affects the renal tubules and the second, commonly
referred to as chronic lead nephropathy, is characterized by slow develop-
ment of contracted kidneys with arteriosclerotic changes, interstitial
fibrosis and glomerular atrophy. In contrast to renal tubular disease caused
by lead, chronic lead nephropathy is relatively irreversible and has been
shown to lead to renal failure and death in workers with heavy lead exposure •
1.10
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The disease occurs too among heavy drinkers of lead-contaminated illicitly-
distilled whiskey. There also is some evidence that heavy, prolonged lead
exposure in childhood can cause death in middle life from chronic lead
nephropathy. This particular form of the disease has been identified only
in Queensland, Australia, from childhood exposure during a period of time
limited to the turn of the century.
It seems from available clinical and epidemiological evidence that
this disease occurs only when PbB's exceed 80 micrograms/dl for prolonged
periods, although one report suggests that exposures of only a few years with
PbB's below 80 may be sufficient to cause chronic lead nephropathy, at
least in adults.
The renal tubular disease caused by lead is seen in heavily exposed
adults and children. The intensity of lead exposure necessary to cause
renal tubular disease is probably at least as high as is required to cause
chronic lead nephropathy, although the duration of exposure required is perhaps
shorter. Limited data indicate that the condition is readily reversed by
treatment with chelating agents e.g., ethylenediamine tetraacetate (EDTA).
The health consequences also probably are less severe than for chronic lead
nephropathy. The disease state should nevertheless be classified as
"clinical". It consists of elevated renal excretion of amino acids, phos-
phate, and glucose, conditions which a physician would probably seek to
correct although they are not effects which normally would lead a subject
to seek medical attention in the first place, at least not in the absence
of other co-existent lead effects.
The effects of lead on the hematopoietic system are varied in nature.
They include shortened survival of circulating red cells and decreased
rate of hemoglobin synthesis in the bone marrow. Both of these general
effects contribute to the anemia which is characteristic of lead poisoning.
Anemia is clearly a clinical effect, one which a physician would normally
seek to correct. The minimal level of lead exposure which is necessary
to cause anemia is difficult to specify, if only because the clinical defini-
tion of anemia is imprecise. It is perhaps more to the point to consider
the minimal level of lead exposure at which a downward drift in blood hemo-
globin first appears, even within the accepted normal range. This minimal
level appears to be PbB = 40 in children and PbB = 50 in adults.
Numerous specific biochemical defects are known to occur which may
contribute to reduced circulating hemoglobin. Some are more lead-sensitive
than others. Thus, inhibition of erythrocytic ATP'ase, which may contribute
to a reduced lifespan of erythrocytes and inhibition of globin synthesis are
effects which probably occur only at levels of lead exposure somewhat higher
than for some other effects which concern the synthesis of heme.
Two enzymes in the pathway leading to heme synthesis are clearly
inhibited by lead at PbB's below 40. The first of these is heme synthetase,
a mitochondrial enzyme which catalyzes the final step in heme synthesis, the
1.11
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insertion of iron into protoporphyrin IX. Inhibition of this enzyme is
reflected in the appearance of elevated protoporphyrin IX in circulating
red cells, an effect which occurs at PbB's as low as 25 in adult males and
as low as 20 in adult females and children. At even lower levels of lead
exposure (PbB =15), the enzyme aninolevulinic acid dehydratase (ALAD)
which converts the heme precursor aminolevulinic acid (ALA) to the intermed-
iate porphobilinogen (PEG) is somewhat inhibited, both in blood and in some
other tissues. The consequence of inhibition of this enzyme is thought to
be elevation of the precursor ALA in blood plasma and urine. This effect
does occur, but only as PbB rises above 40. Thus, the significance of ALAD
inhibition at very low levels of lead exposure is uncertain and is considered
by most to be a subcritical effect.
The basic issue, for which there is no clear answer, is as to whether
elevation of erythrocytic protoporphyrin between PbB = 20 and PbB = 40 is
to be considered a critical or subcritical effect. The effect certainly
is compensated since hemoglobin levels are sustained at a normal level in
this range of lead exposure. The real issue is as to whether or not a person's
capacity to cope with a co-existent stress on hematopoiesis is in any way
compromised. Not much is known about this problem. There is a need for
more research to determine the health consequences of this compensated state,
and also to determine the implications of the effects of lead on the synthesis
of other hemoproteins essential to normal body function. It has been shown
that mixed function oxidase induction is reduced in lead exposure, suggest-
ing an inhibition of synthesis of the hemoprotein cytochrome P-450. This
effect, however, does not seem to occur at levels of lead exposure below
those affecting the concentration of hemoglobin in the blood. Effects on
other hemoproteins are virtually unknown.
There has been much controversy in recent years regarding the effects
of lead on the central nervous system. The concern has its origins in the
well-documented fact that very high lead exposure causes severe, often fatal
damage to the brain in both adults and children. It is also known that attacks
of lead encephalopathy in children and even severe lead poisoning in the absence
of encephalopathy can give rise to long-term effects on brain function includ-
ing mental retardation, altered sensory perception and slowed learning. Such
cases have resulted from high exposures (PbB _> 80).
In recent years, there have been studies reported of possible neuro-
logical and behavioral effects of lead in children whose PbB's were in the
range of 40-80. All of these studies have been retrospective in nature.
The majority of them focused on comparison of children with high and low
PbB's. In some cases, one or more PbB determinations were available at a
point in time prior to the neurobehavioral test. Although most of these
studies are flawed in one way or another, a number of them provide reasonably
good evidence that PbB's in excess of 50 may result in impairment measured
by sensitive psychometric tests. There also is fragmentary evidence to
1.12
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suggest that even moderately elevated lead exposure in utero may increase
the occurrence of mental retardation. As with the studies performed on
children with postnatal lead exposure, it is not possible to specify
either the critical period or level of exposure required to induce dele-
terious effects. Finally, it should be pointed out that neurobehavioral
effects may well be a result of the combined effects of lead and other
stressors, both physical and social. All studies reporting lead effects
have been conducted in socio-economically deprived populations.
The most satisfactory approach to problems of this type is the pros-
pective study, wherein a continuing profile of dose and effect are available.
Unfortunately, no such studies have been reported or, seemingly, are even
underway.
Numerous laboratory animal studies of neurobehavioral effects of pre-
natal and perinatal lead exposure have been reported. Although numerous
methodological problems have confounded the interpretation of these studies,
it does appear that moderate lead exposure does result in locomotor and operant
behavioral effects. Future studies are needed in which confounding variables,
e.g., nutritional status and litter size are more closely controlled.
Furthermore, multiple measurements of internal dose are needed in addition
to PbB, e.g., protoporphyrin and ALA excretion in order to provide better
interlaboratory comparison of data.
It should also be mentioned in passing that one laboratory has reported
subtle neurobehavioral effects in lead-exposed industrial workers (PbB >80).
This study was beset with many methodological problems and equipment failures.
A similar type of study conducted by another group of investigators was
negative. Thus, for the present at least, the occurrence of subtle neuro-
behavioral effects of moderate lead exposure in adults is uncertain.
The peripheral nervous system also is adversely affected by lead.
There are numerous reports of peripheral neuropathy in patients with
clinical lead poisoning but not necessarily in conjunction with clinical
neurological symptoms. Major effects reported are reduced nerve conduction
velocity and electromyographic deficits. These effects have been reported
to occur in both adults and children. Reduction of nerve conduction velocity
without clinical evidence of neuropathy has also been reported. It is not
certain at this time just where the lead exposure threshold for this effect
lies, but it is probably at a PbB of about 50 in both adults and children.
The effect must be considered adverse, particularly since certain factors
may be additive to the lead-induced effect. Thus, alcoholism and diabetes
also cause slowed nerve conduction, and there is some evidence of suggesting
that presence of the sickle cell trait may constitute a special risk for
this effect.
There are numerous other organs and systems in the body which are adver-
sely affected by lead, but the information at hand is insufficient to make
possible any judgements as to dose-effect and dose-response relationships.
1.13
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Until more is learned about these effects, estimates of acceptable maximal
lead exposure must rely on knowledge regarding effects on the hematopoietic
system, the kidney and the nervous system. It seems clear that the kidney
can be ruled out as the critical organ. Best estimates of threshold exposure
even for subclinical effects on the peripheral nervous system indicate a
PbB of about 50. On the other hand, the threshold for clinical effects
£E iti£ central nervous system may be about 50. This threshold is therefore
clearly the one of greater concern. It must be reiterated that estimated
thresholds have validity only for the populations which have actually been
studied. Since thresholds tend to fall progressively as sample size increases.
The true threshold for effects on the central nervous system of all children
critically exposed must be lower than applies to the sample. At present,
it is impossible to state how much lower the population threshold is.
The dose-response relationships for lead effects on the hematopoietic
system are much more clearly delineated than for any other lead effects,but
again, any estimated thresholds are based on limited population samples.
The only way to protect everyone from effects of poisons is to monitor
everyone - an obvious impossibility.
The hematopoietic system is, so far as can be discerned, the most
lead-sensitive system among the four under discussion, but which effect
should be considered the critical one? If the rise in erythrocytic proto-
porphyrin is to be considered the critical one, as has been proposed by
some, total lead exposure should be reduced to a point such that no woman or
child's PbB rises above 20 and no man's PbB rises above 25. Judgment con-
cerning the importance of achieving such a goal should be tempered by two
considerations. In the first place, the effect is a subclinical one.
Moreover, unlike the case with renal and, perhaps, neurobehavior effects,
this one is reversible with reduction of exposure.
Some of the miscellaneous effects of lead for which no estimates of
threshold are possible at present have been recognized for many years by
numerous investigators. Others have been reported only by one or two
investigators and therefore must be evaluated with appropriate reservations.
Beyond that, there also are some effects which have been reported to occur
in experimental animals and for which no human data are available.
It has long been known that lead causes colic. This effect occurs in
men who show other clinical signs of poisoning concurrently, e.g., anemia.
It seems unlikely therefore that this effect is particularly lead-sensitive.
The cardiovascular system undoubtedly also is affected by grossly elevated
lead exposure. The incidence of cerebrovascular deaths was reported to be
elevated among lead workers exposed during the first quarter of this century
but not among men exposed more recently. Hypertension has also been reported
to occur as a result of heavy lead exposure, although a more recent study
indicates that it does not occur under more recent industrial lead exposure
conditions. Toxic actions on the heart have also been reported, but, again,
1.1U
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only in cases of clinical poisoning.
During the latter part of the 19th century and on into the first quarter
of this century there were numerous reports of a high incidence of miscarriages
and stillbirths among women working in the lead trades. PbB's were not
available at that time, but it is likely that women today only rarely, if
ever, experience the high exposures which probably existed at that time.
There are single reports of ovulatory dysfunctions in women and of sperm
abnormalities in men working in the lead trades. These effects were observed
at relatively modest levels of elevated lead exposure. Further studies are
needed.
There are scattered reports of other effects in man, such as chromosal
absortnalities in lymphocytes and impaired thyroid function. The health
significance of these findings is obscure at present. Lead also has been
reported to be teratogenic, but only on the basis of laboratory animal
data.
Finally, the question of carcinogenicity has received some attention.
Lead definitely is carcinogenic in the rat and mouse. In these species it
causes renal adenomas and adenocarcinomas, but only at extremely high dose
relative to any likely level of human exposure. The renal tumors have been
reported by a number of independent investigators. There also is a single
report of lead-induced gliomas in rats. Among three epidemiological reports
of causes of death in people with elevated lead exposure, only one suggests
a possible association with cancer. The authors of this last-named report
conclude that even this association, of marginal statistical significance,
is to be discounted so far as a causal relationship is concerned.
1.7 ENVIRONMENTAL DISTRIBUTION AND TRANSFORMATION
Lead is widespread as a natural constituent of rocks and soils. Even
in areas most remote from human influences, the earth's crust contains
approximately 16 ppm Pb. Human activity has caused some increase in the
concentration of lead in the environment, particularly in and near large
centers of human population. So far as soil is concerned, the areas of
contamination are mainly the result of aerial transport from point sources
such as smelters and from heavily-traveled highways. The zone of soil
contamination extends only a few miles from smelters and only outward a few
hundred meters from heavily-traveled roadways. Haulage of lead ores in
trucks from mines to primary smelters is a minor additional source of road-
side contamination occurring in a few very limited areas.
In spite of the highly restricted zone of detectable soil contamination,
it would be incorrect to conclude that some long-range soil contamination
does not occur. Analysis of lead in glacial ice, museum specimens of wildlife
and plants, and successive rings of long-lived trees indicates that a sub-
stantial general dispersion of man-generated lead has occurred since the
1.15
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Industrial Revolution. This is no doubt attributable to aerial transport
from areas of technological activity. Transport models have as yet not been
very well developed to describe this process of dispersion.
The specific sources of man-generated lead pollution are numerous.
The major uses of lead are in the manufacture of storage batteries, antiknock
additives for automotive fuels, pigments, ammunition and solder. Nearly
one half of this lead originates from recycled metallic lead. U.S. production
has remained fairly stable in recent years. There is a suggestion of a
downward trend however, particularly in the categories of paint pigments and
antiknock fuel additives. These downward trends are likely to continue
because of restrictions on ambient air pollution and the use of lead in
household paints .
Although only sixteen percent of lead production goes into the manufacture
of fuel additives, it is estimated that combustion of lead-containing fuels
accounts for almost ninety percent of aerial emissions and secondary con-
tamination of soil, plants, and water by fallout. Among the several mis-
cellaneous sources of aerial emission, primary and secondary lead smelters
are of special concern. The fallout zone from these stationary sources is
quite small in comparison to the total zone of contamination along all U.S.
roadways. The gradient from source to baseline, however, is quite steep,
with exceedingly high aerial and soil lead concentrations sometimes
occurring in the immediate vicinity of the stacks. Although the degree of
soil contamination in the smoke zone of some lead smelters may be greater
than along highways, the total impact of highway fallout as a threat to the
public health probably is the more important of the. two* Nevertheless,
concentrations of lead as high as in the immediate vicinity of smelters
sometimes are reported for soils along major freeways.
Runoff from contaminated soils into water is extremely limited owing
to the precipitation of lead salts and the binding of lead ions to stream
sediment. There is a vertical gradient, however, of lead in oceans.
Concentrations near the surface are much greater than in deep waters.
Regional differences in surface concentrations are considerable. It is not
clear as to how much of the gradient is attributable to fallout over the
oceans as compared to runoff from streams. The median concentrations of
lead in U.S. streams generally is reported to be less than 10
Wastewaters entering treatment plants often have extremely high con-
centrations of lead Ov 100-900 pg/fc) in contrast to streams and oceans.
This probably mainly because wastewaters carry lead-bearing street dust
heavily contaminated with near-fallout of gasoline motor exhuast. This
dust often contains as much as 0.3 percent lead.
Although the lead content of city water supplies measured at the
reservoirs seldom exceeds 50 ug/£,. , water drawn from household taps often
exceeds this level. This is mainly due to the use of lead water pipes and,
worse, lead-lined water storage tanks. Low concentrations of dissolved solids
1.16
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(soft water) and an acidic pH exacerbate the problem. Under extremely
unfavorable conditions the lead concentration may exceed 1000 yg/1., as in
Glasgow, Scotland.
Perhaps the greatest single source of lead hazard to children is the
presence of lead-base paint on the exterior and interior of private dwellings.
Such surfaces are particularly hazardous when they are cracked or peeling.
Most cases of clinical lead poisoning in infants and young children have
been attributed to swallowing paint chips. The soil immediately surrounding
houses coated with lead-base paints also may be heavily contaminated as a
result of weathering. Although lead-base household paints have not been
used extensively since the 1940's, the hazard persists in old, run-down
neighborhoods. In such neighborhoods the number of pre-school children with
unduly elevated lead exposure is alarmingly high. As it happens, traffic
density and consequent soil and dust contamination also is generally high.
A major unresolved issue today is as to the relative contributions to lead
exposure of lead-bearing paint on the one hand and of lead-bearing dust and
soil on the other. The child who engages in the licking, chewing and swal-
lowing of foreign objects probably does not exhibit any preference for
paint vs. soil and dust, although even that cannot be affirmed with any
strong conviction. In any event, there is a great need today for research
concerning the sources of lead in young children. It is not simply a question
of establishing the relative importance of the suspect sources. It is also
a question of determining the concentrations of lead in the several media
which are minimally hazardous. Ultimately, decisions must be made as to
which level of lead in each of the several media calls for remedial action.
1.8 ENVIRONMENTAL INTERACTIONS AND THEIR CONSEQUENCES
This final chapter brings together some elements of most previous
chapters. It describes the movement of lead through the ecosystem with due
attention to possible biomagnification phenomena. As a broad generalization,
it seems fair to state that multi-stage biomagnification is not apparent in
the case of lead in the environment. Several properties of lead account
for this. To begin with, lead in most natural forms is relatively insoluble
and does not therefore tend to move readily across biological membranes.
For that matter, its insolubility tends to minimize its presence in water,
the natural solvent which conveys nutrients into living systems. A further
characteristic of lead tending to limit its transfer up the phylogenetic
scale is its affinity for calcareous structures such as bones and shells.
These elements in animal systems generally are rejected by predators, thereby
diluting rather than concentrating lead in the food chain. This is not to
deny that lead remains to this day a significant hazard to some forms of
life. Rather, it is to say that current problems are one-stage or, at best,
two-stage problems in which some inanimate form of lead interacts either
directly with the target species or by way of one transfer medium. Thus,
in the case of man and domesticated animals, lead is either inhaled or
swallowed directly from contaminated air or water or it is swallowed with
externally-contaminated food. Multiple stage transfer is not in evidence.
1.17
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Transfer of lead from plants to herbivore to carnivore in the insect world
seems to be an exception. Here there is evidence for biomagnifIcation.
The major source of lead for the average person is probably food and
beverages. This conclusion is based on two considerations. The first is in
regard to the relative insignificance of the other major transfer medium-air.
Few people inhale an average air lead concencration in excess of 2 yg Pb/m .
At best, this contribution to circulating blood lead concentration is
4 yg Pb/dl. Assuming a normal PbB of 15 yg/dl, this leaves 11 yg Pb/dl to
be accounted for. In the absence of any other widespread sources of lead
intake for the average mean, foods and beverages are generally held respon-
sible for the predominant remaining fraction of intake. It is therefore
important to consider the extent to which lead in foods and beverages is
reducible. Put another way, "To what extent are foods and beverages
contaminated by lead introduced either in production or in processing?".
The answers to this question are at present totally unsatisfactory. There
are absolutely no studies available in which the raw product has been exa-
mined as to its inital natural lead content, its initial man-generated lead
content and its addition and/or subtraction of lead in the course of pro-
cessing and presentation to the consumer. Certain isolated segments of the
overall problem have received attention. Thus, it is widely recognized that
the soldered seams of cans are potential sources of food contamination.
Certain foods have been found to double their lead content as a result of
the transfer of lead from solder to filler, especially during storage for
substantial periods of time. The significance of this transfer is still
unknown, however. More information is needed as to (1) the total dietary
contribution of such items and (2) the availability for absorption of the
solder contribution. It is recognized that contamination from solder is in
the form of microscopic pellets of metallic lead which are not nearly as
readily absorbed from the gastrointestinal tract as is lead present in foods
in the form of simple lead salts bound to natural ligands. There is a need
to establish more clearly the bioavailability of solder-derived lead.
It has been found recently that canned pet foods have very high con-
centrations of lead. These products are sometimes purchased by the poor
for human consumption. The source of this lead has not been determined.
1.18
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2.0 PHYSICAL AND CHEMICAL PROPERTIES AND ANALYSIS
2.1 SUMMARY
Lead is a soft, malleable, ductile, dense, bluish-gray metal with a
melting point of 372 C, and a boiling point of 1740 C. In the presence of
moisture, lead is readily coated with an oxide film, which with carbon dioxide
forms a basic white carbonate. Nitric acid converts lead to soluble lead ni-
trate. Lead is moderately resistant to both sulfuric and hydrochloric acids.
In the presence of oxygen, most organic acids react with lead to form the cor-
responding organolead salts. Lead may be hardened by alloying with small
amounts of metals such as antimony, arsenic and copper.
Most inorganic lead compounds are moderately to highly insoluble. This
low solubility in the aqueous phase of natural systems affects the behavior
of lead in the environment. As a consequence lead does not transfer readily
from soil to plants or into bodies of water (see Sections 4.1;7.3.2, and
8.3.2). Similarly, lead tends to accumulate wherever it is delivered and con-
sequently can become a hazard.
Of the organolead compounds, tetraethyllead and tetramethyllead (anti-
knock additives in gasolines) give rise to most of the lead that is released
into the atmosphere as a result of their combustion in the automobile engine.
The many other organic derivatives of lead are of minor importance compared
to the lead tetraalykyls.
For the determination of lead concentrations in biological and environmen-
tal samples, each sample type presents a different analytical problem. As a
result, much effort has been expended in developing suitable techniques for the
measurement of lead. Great care must be exercised in all steps involved in
lead analysis if reliable results are to be obtained. Sampling methods and
materials should be selected which will not introduce elements that will inter-
fere with the lead analysis. Lead-free storage containers should be used and
appropriate preservatives should be added to the sample for storage purposes.
As the first step in the analysis, sample preparation should be adapted
to the type of material being analyzed. The Association of Official Analytical
Chemists has adopted the wet ash extraction procedure (digestion) as the pre-
ferred method. However, dry and bomb ashing methods have proven suitable for
some samples. Nondestructive methods and methods of separation and preconcen-
trations based on density gradients and magnetic separation have been used where
preservation of the identity of the lead compounds has been important.
2.1
-------
For the actual lead determination, the colorimetric method based on
dithizone was the standard method for lead analysis in all types of samples
for many years. However, because of the need for rapid and reliable methods
for blood lead analysis in screening people for lead exposure, the atomic
absorption method (flameless technique) has generally become the method of
choice.
Optical emission spectrometric analysis for lead can cover wide concen-
tration ranges and is suitable for direct analysis of numerous types of sam-
ples, including soils, dried tissues, and solutions containing microgram
quantities of lead. With a plasma source, this method can be used for rapidly
measuring nanogram (10 ) levels of lead. Electrochemical methods such as
polarography can be used to determine lead accurately at the nanogram level.
Other methods for lead determination are spark source mass spectometry, X-ray
fluorescence, and activation analysis.
A considerable number on inter- and intralaboratory comparisons have
been carried out on a variety of environmental samples to detect sources of
error in the analytical procedures for lead. The results of these programs
show that extreme care is required throughout the entire procedure to achieve
high correlations among laboratories. The discrepancies among results from
different laboratories have often been attributed to sample handling problems
and to laboratory bias.
Interpretation of analytical results is complicated by the fact that at
the trace level concentrations being analyzed, analytical methods are not yet
available to determine the chemical form(s) in which lead is present. Satis-
factory analytical techniques have not been developed for determining individ-
ually the organic and inorganic lead that may be present in tissue. Thus,
except at macroconcentrations, results as reported are for total lead.
2.2 PHYSICAL AND CHEMICAL PROPERTIES
Lead is a soft metal with a bluish-gray color when freshly cut. Its
bright luster soon disappears upon exposure to air because of the formation
of lead oxide. The important physical constants of lead are presented in
Table 2.1. It is atomic number 82 in the periodic classification of the ele-
ments, and has several naturally occurring isotopes which result in an average
atomic weight of 207.19. Because lead has four electrons in its outer shell,
it falls in Group IV of the periodic table, and consequently, might be ex-
pected to show a normal valence of +4 in its compounds. However, the 2 "s"
electrons are difficult to ionize so the usual valence of lead in ionic com-
pounds is +2 rather than +4. In acid solutions lead is a fair reducing agent;
in alkaline solutions it is a rather strong reductant. The more important
oxidation-reduction potentials for lead and its compounds are presented in
Table 2.2 (Latimer, 1952).
Lead has good resistance to neutral solutions where the oxide and car-
bonate are the corrosion products, and is fairly resistant to alkaline solu-
tions. Lead is resistant to sulfuric, sulfurous, phosphoric and chromic acids,
2.2
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Table 2.1 PHYSICAL CONSTANTS FOR LEAD*
Melting point, C 347.43
Boiling point, C 1740
Specific gravity, at 20 C 11.3437
at 327.43 C 10.686
at 650.0 C 10.302
at 850.0 C 10.078
Vapor pressure, at 987 C, mm Hg 1-0
at 1167 C 10.0
at 1417 C 100.0
at 1508 C 200.0
at 1611 C 400.0
Surface tension, at 350 C, dyn/cm2 442
at 400 C 438
at 500 C 431
Viscosity, at 441 C, cp 2.116
at 551 C 1.700
at 703 C 1.349
at 844 C 1.185
Specific heat, at 0 C, cal/g 0.0297
at 20 C 0.0306
at 100 C 0.0320
at 327 C 0.0390
at 500 C 0.037
Latent heat of fusion, cal/g 5.86
Latent heat of vaporization, cal/g 203
Thermal conductivity, at 20 C, cal/(cm2) (C/cm) (sec) 0.083
at 100 C 27.021
at 327.43 C 94.6
at 600 C 107.2
at 800 C 116.4
Magnetic susceptibility, 10-6 egs units 0.12
Brine11 hardness (cast) 4.2
Element bond length, Pb-Pb- at 25 C, A 3.5003
Electrical resistivity, micro-ohms/cc at 20 C 20^648
Refractive index, sodium light 2.01
Velocity of sound, cm/sec x 105 1.227
Tensile strength, Ib/sq in at 20 C 1920
Linear coefficient of expansion, per C x 10~5 2.93
aAdapted from McKay. In: Encyclopedia of Chemical Technology, Vol. 12,
A. Standen (ed.), Used by permission of Interscience Publishers,
New York, (c) John Wiley and Sons, Inc., 1967.
2.3
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Table 2.2 OXIDATION-REDUCTION POTENTIALS FOR LEAD3
Reaction
+2
Pb -»• Pb + 2e
Pb+2 ->• Pb+A + 2e
Pb + SO ~2 ->• PbSO. + 2e
4 4
Pb + 20H~ •* PbO + H20 + 2e
Pb+2 -1- 2H00 -»• Pb00 + 4H+ + 2e
7 7
+ -2
PbSO. + 2H00 •»• Pb00 + 4H + SO. + 2e
422 4
PbO + 20H~ •*• Pb02 + H20 + 2e
Pb + 2C1~ + PbCl2 + 2e
Pb + 2Br~ •*• PbBr2 + 2e
Pb + 2I~ -*• Pbl2 + 2e
Pb + S'2 -*• PbS + 2e
AE°, volts
+ 0.126
- 1.7
+ 0.356
+ 0.58
- 1.455
- 1.685
- 0.248
+ 0.268
+ 0.280
+ 0.365
+ 0.980
aAdapted from Latimer, The Oxidation State of the Elements and
Their Potentials in Aqueous Solutions, 2nd Edition, (c) 1952,
pp 151-155. Reprinted by permission of Prentice-Hall, Inc.,
Englewood Cliffs, New Jersey.
2.U
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but it is moderately attacked by hydrochloric and hydrofluoric acids. It is
strongly corroded by nitric, acetic and formic acids and moderately affected
by organic chlorides and aqueous solutions of metal chlorides. In the presence
of oxygen most organic acids react with lead to form the corresponding organo-
lead salts (Hamner, 1974).
The equilibrium model for the chemistry of aqueous lead developed by
Stumm and Morgan (1970) indicates that at low pH and low pe (reducing con-
ditions) elemental lead can be readily dissolved. This has health implica-
tions, where soft water with little or no buffering capacity is at a low pH
and lead piping is used for potable water. Excessive lead concentrations in
such water have been observed in Great Britain and in certain locations in the
U. S. (see Section 7.3.2).
Lead's high density (11.3 grams per cubic centimeter), its softness, and
relatively low melting point enable easy forming and casting. These physical
characterists account for the numerous uses of lead (see Section 7.2).
Lead forms low-melting alloys with tin, arsenic, antimony, bismuth, cadmium,
and calcium, singularly and collectively. These alloys are fabricable by com-
mercial processes (Hack, 1967). Alloys are also made from secondary lead
which is recovered from scrap. Lead does not readily alloy with zinc, iron,
nickel, and other high-melting metals. Alloys of lead can be extruded, drawn,
rolled, cast, stamped, spun, and applied as a coating to other metals by hot
dipping, electroplating, or spraying (Lead Industries Association, 1952).
Thick layers of lead can be bonded to steel and other metals.
Refined primary lead is at least 99.85 percent pure; however, the
impurities making up the balance put it into four different grades which in turn
govern its use. "Corroding grade" lead (99.94 percent) is used in the manu-
facture of lead oxide for storage batteries and for pigments. The grades
designated as "chemical" lead and "acid-copper" lead are more generally used
for sheets and pipes in chemical installations because the small amount of copper
and silver present increase the strength and corrosion resistance. The fourth
grade "desilverized" lead, is used in general applications and in the manufac-
ture of alloys.
2.2.1 Inorganic Compounds of Lead
The divalent lead compounds resemble those of the alkaline earth elements.
The sulfate, nitrate, and carbonate compounds of lead are isomorphic with the
corresponding barium and strontium compounds. Many lead compounds have two or
more crystalline forms. The common inorganic compounds of lead (nitrate,
chlorate, and acetate) are water-soluble; the chloride is sparingly soluble; and
the sulfate, carbonate, chromate, phosphate, and sulfide are insoluble.
Values for the solubilities of common inorganic compounds of lead are
presented in Table 2.3 (Lange, 1961; Weast, 1974). Lead sulfide has a very low
solubility (approximately 0.8 mg/1) and its formation can serve as a convenient
method for the removal of lead from aqueous systems. Its solubility is higher
than might be_expected on consideration of the low solubility product
(Ksp =» 7 x 10~ ). This is due mainly to the hydrolysis of the sulfide ion.
(Kolthoff, et al., 1964).
2.5
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Table 2.3 SOLUBILITIES OF INORGANIC COMPOUNDS OF LEAD
a,b
Compound
Name
Acetate
Bromide
Carbonate
Chlorate
Chloride
Chr ornate
Fluoride
Hydroxide
Iodide
Nitrate
Oxalate
Oxide , mono-
Oxide, tetra-
Phosphate
Sulfate
Sulfide
Formula
Pb(OOCCH3)2- 3H20
PbBr2
PbCOg
Pb(C103)2'H20
PbCl2
PbCr04
PbF2
Pb(OH)2
PbI2
Pb(N03)2
Pb(OOC)2
PbO
Pb 0
-J *T
PbS04
PbS
Water Solubility,
g/100 ml
44.3
0.844
1.1 x 10~4
151.3
0.99
5.8 x 10~6
0.064
0.0155
0.063
56.5
1.6 x 10~4
1.7 x 10~3
5.3 x 10"5
1.4 x 10"5
4.25 x 10~3
8.6 x 10"5
Temperature,
C
20
20
20
18
20
20
20
20
20
20
18
20
20
20
25
20
Reprinted with permission from Handbook of Chemistry, 10th edition,
N.S. Lange (ed.) (c) McGraw-Hill Book Company, 1967.
Reprinted with permission from Handbook of Chemistry and Physics,
55th Edition, R.D. Weast (ed.). (c) CRC Press, Inc., 1974.
2.6
-------
Santillan-Medrano and Jurinak (1975) found that the solubility of lead
in noncalcareous soils appeared to be regulated by PbCOH)^, Pb3(P04)«, Pb^O
(P0,)_, Pb,(P04), OH, and was dependent on the pH. In calcareous soils
PbC03 was also significant. Reductions in lead uptake by plants of up to
one-half in the presence of excess phosphate have been observed (see Sections
4.3.1.1 and 4.3.2.1).
Lead monoxide (PbO), one of the most important industrial lead com-
pounds, exists in two forms. At ordinary temperatures, the monoxide exists
as reddish-yellow, tetragonal crystals commonly referred to as litharge. At
480 C this transforms into yellow orthorhombic crystals known as massicot.
Neither form of the oxide is appreciably soluble in water. Litharge dis-
solves only to the extent of 0.0017 gram/100 ml of water at 20 C, and mas-
sicot, 0.0023 gram/100 ml. The melting point of PbO is 888 C; it has appreci-
able volatility below this. PbO reacts readily with all common acids to form
the corresponding salts and dissolves in alkali, though with more dif-
ficulty. Hence, PbO serves as a starting point for the preparation of many
lead compounds (Thompson, 1967). The major uses of the inorganic and organic
compounds of lead are discussed in Section 7.2 (see also Table 8.1).
Red lead, Pb,0,, contains both divalent and tetravalent lead atoms in a
complex crystalline structure. It is prepared by the oxidation of PbO in air
at 500 C.
Lead dioxide, PbO^, is dark brown solid in which the lead atoms are
tetravalent. It is a vigorous oxidizing agent when heated (290 C). PbO_
can be produced in the laboratory by the anodic oxidation of solutions or lead
compounds. Commercially, it is produced by the treatment of an alkaline
slurry of red lead with chlorine (Klug and Brasted, 1958).
2.2.2 Organic Compounds of Lead
Organolead compounds are those in which the lead atom is bound directly
to one or more carbon atoms. Since Lowig's first synthesis of an organolead
compound in 1953, organolead chemistry has developed into one of the largest
areas of organometallic chemistry. It has been estimated that about 1200
organolead compounds were known in 1965 (Shapiro and Frey, 1968). Only a few
of these achieved commercial status.
The tetraorganolead compounds in which a tetravalent lead atom is bonded
to four organic groups through a carbon atom represent the most stable class of
organolead compounds. The four organic groups may be alkyl, aryl, cycloalkyl,
arylalkyL, thienyl, furyl and substituted derivatives thereof. The most
important of these compounds are the fuel additives, tetrathyllead (TEL) and
tetramethyllead (TML).
In general, the alkyl derivatives of lead are highly toxic compounds, and
are readily absorbed through the skin (see Section 6.2.1.2.3 and 6.3.2.3).
TEL and TML are clear, colorless liquids, volatile, nonpolar, nonionic, and
2.7
-------
soluble in many organic solvents such as hydrocarbons, chloroform, ether,
and absolute ethanol. They have very low water solubilities, and are rela-
tively unreactive in air, water or alkali (Shapiro and Frey, 1968). They
are, however, light-sensitive and undergo photochemical decomposition when
they reach the atmosphere; because they are readily broken down by light and
heat, their presence in the atmosphere is transient (National Academy of
Sciences, 1972).
At 50 millimeters of mercury, TEL boils at 108.4 C, and TML at 33.2 C.
TML decomposes on heating at 265 C, and TEL at 100 C (Shapiro and Frey, 1968).
Some of the other physical properties, as summarized by Gerarde (1964), are
presented in Table 2.4.
These compounds decompose readily during the combustion process, thus
freeing the radicals to prevent the extremely rapid burning of gasoline. The
so-called "regular" gasoline contains 3 to 4 milliliters of the tetralead
compounds per gallon. This concentration represents from 2 to 3 grams of lead
per gallon. To scavenge the lead from the engine, standard antiknock fluids
also contain ethylene dibromide and/or ethylene dichloride. The chief lead
emission products are (in particles of equivalent diameter between 2 and 10
micrometers) lead bromochloride (PbCl-Br) and (in particles smaller than 1
micrometer) the alpha and beta forms of ammonium chloride and lead bromo-
chloride (NH4Cl-2PbCl-Br, 2NH4Cl-PbCl-Br), minor quantities of lead sulfate
(PbS04) and the mixed oxide and halide (PbO-PbCl-Br-H20 National Academy
of Science, 1972). These combustion products, present as solids, are
the largest source of atmospheric lead pollution.
In addition to the tetralead derivatives, other types of organolead com-
pounds are of environmental significance, for example, hexamethyldilead, which
consists of six organic groups surrounding a pair of lead atoms:
(CH3)3Pb-Pb(CH3)3.
Lead can also be bonded to organic groups through an oxygen atom giving
rise to a variety of alkoxides, such as trimethyllead methoxide, (CH3)3PbOCH3.
Peroxide structures are also known, for example, tert-butyl trimethyllead
peroxide, (CH3)3 PbOOC(CH3)3 (Shapiro and Frey, 1968).
A large number of organolead compounds also are known in which the lead
is bonded to sulfur, for example, (CHg)JPbSCEL. A few compounds have been
prepared in which the sulfur is replaced by selenium or tellurium. Organolead
compounds in which the lead is bonded to nitrogen are types in which the nitro-
gen is part of a heterocyclic ring:
(Shapiro and Frey, 1968).
Very recently evidence has been presented (Wong, et al., 1975) for the
biotransformation of inorganic and organic lead into a tetraalkyl lead by micro-
organisms in lake sediments (see Section 3.2.1).
2.8
-------
Table 2.4 PROPERTIES OF TETRAETHYLLEAD "AND TETRAMETHYLL1AD
a
Physical Properties
Tetraethyllead
Tetramethyllead
Physical form
Chemical formula
Odor
10 Saturated liquid density
Co at 20 C
Vapor pressure at 20 C
Boiling point
Freezing point
Flash point (open cup)
Viscosity at 20 C
Refractive index
Solubility in water at 22 C
Solubility in gasoline
Watery white oily liquid
(CH ) Pb
Faint, fruity
1.65 g/ml
0.27 mm Hg
199 C
130.2 C
85 C
0.87 cps
1.520
0.18 ppm
Soluble in all proportions
Watery white oily liquid
(CH ) Pb
Faint, fruity (probably odorless
in chem. pure state)
1.99 g/ml
22.5 mm Hg
110 C
30.3 C
About 38 C
0.53 cps
1.512
18.0 ppm
Soluble in all proportions
Source: Gerarde. Reprinted with permission from Annual Reviews Pharmacology, (c) Annual Reviews,
Inc., 1964.
-------
2.2.3 Isotopes of Lead
There are four stable isotopes of lead, with the following abundances
(Lederer, et al., 1967):
Isotope Percent
Pb-204 1.4
Pb-206 25.1
Pb-207 21.3
Pb-208 52.7
Pb-204 has no radioactive progenitor. The Pb-206, Pb-207, and Pb-208 are
produced by the radioactive decay of uranium-238, uranium-235, and
thorium-232, with half-lives of 4.5,0.7, and 14 billion years, respectively
(Lederer, et al., 1967). There are four radioactive Isotopes of lead occurring
as members of these decay aeries. Pb-211, Pb-212, and Pb-214 have short half-
lives 36.1 min., 10.64 hr., and 26.8 rain., respectively. Pb-210 (Radlum-D),
the longest lived, however, has a half-life of about 20 years, sufficiently
long to be useful in environmental studies.
The stable isotope composition of naturally-occurring lead ores varies,
depending on their geological evolution, and this can be used to determine the
geological age of lead deposits. The isotopic composition may also be used
to determine the sources of lead contamination (see Section 7.2). However, be-
cause lead is so durable and so much of it is recycled, the pool of recycled
scrap and products derived from it (e.g., TEL) tends to average toward a
fairly uniform composition. While this complicates the tracing of the
orgin(s) of environmental lead by isotopic ratio measurements, the technique
has still proven useful.
2.3 ANALYSIS FOR LEAD
The variety of environmental samples is so great as to pose a different
analytical problem for each type of sample. Testing and surveillance of
potentially exposed persons require methods indicative of lead poisoning which
are reliable and rapid; biological samples pose their own distinctive problems.
Accurate determination of metals at the nanogram level exerts demands
upon investigators in their attempts to prescribe emission limits of harmful
materials and, more importantly, to understand the effect of these emissions
upon people. The complexity of environmental and biological samples to be
analyzed for trace levels of lead requires the utmost care in sampling,
storage, preparation, and analysis in order to obtain meaningful results. In
any analysis step lead can be lost or contamination occur to produce
erroneous results. Probably the greatest error occurs during the decomposition
of the sample for purposes of converting the lead to a form suitable for the
analysis. The decomposition may require hours of digestion or ashing. This
phase should be done in clean rooms, using clean reagents and vessels.
The following information represents steps being utilized in the search
for better and simpler methods and techniques for assessing lead contents
2.10
-------
in a wide range of materials. Not only are systematic approaches being taken
in the preparation of difficult samples where needed, but also direct sample
analyses are being made as more sensitive methods of analysis are developed.
Awareness of reliability problems associated with all phases of the
analytical processes Including sampling, storage, and preservation, chemical
treatment, and analysis has become evident.
2.3.1 Sample Storage and Preservation
Sampling techniques and conditions should be used which will collect
samples representative of the problem under study. For ambient air sampling,
Sawacki (1975) points out the difficulties experienced with filtering tech-
niques used to collect partlculate lead near highways. Variations in sampling
techniques, involving different filter materials or the use of scrubbers,
produced variation in the lead contents obtained due to variations in
the efficiences of the collection media used. Similar variations can occur in
sampling biological tissues unless steps are taken to homogenize the sample.
Attendant to sampling, the preservation of the integrity of the sample
during the interim between collection and analysis is an absolute requirement.
This is especially so for samples in forms which are susceptible to change,
e.g., water or some biological samples. The primary consideration in these
instances is to store the samples in previously cleaned and inert containers
to prevent loss by absorption and diffusion or contamination by desorption from
the container wall (U. S. Environmental Protection Agency, 1974). These con-
siderations should apply as well to the digested concentrates in preparation
for analysis.
The use of unclean containers for storage of either raw or chemically-
treated samples can produce unpredictable results. It has been shown (Issaq
and Ziellnski, 1974) that considerable loss of lead, as aqueous Pb(NO.)2,
occurred in less than 1 hour when stored without a stabilizing agent In mater-
ials such as Pyrex, Kimax, or polyethylene. Hydrogen peroxide was preferred
for this. The stability of lead chelates was investigated (Klnrade and Van
Loon, 1974), and It was found that the combined use of two agents, ammonium
pyrrolldine dithlocarbamate (APDC) and diethylammonium diethyldithiocarbamate
(DDDC) provide Indefinitely long stability compared to the rapid deterioration
when only one (APDC) was used. A similar multichelatlon treatment of water
samples (Sachdev and West, 1970) produced stable lead solutions that were made
slightly acidic.
Whole blood and urine samples (National Academy of Sciences, 1972)
are best collected and used in polypropylene, Teflon, or other lead-free
materials. A study of the effect of the aging of blood on the recoverability
of lead (Mitchell, et al., 1972) was performed using blood stored at three
different temperatures. Sample storage at 9 C was recommended on the basis
of stability. Additional information Indicates that after the addition of suf-
ficient quantities of heparin, blood can be stored at room temperature for
weeks (Braztel and Reed, 1974). In the frozen state, blood was not observed
to deteriorate (Lerner, 1975)
2.11
-------
Preservation of delta-aminolevulinic acid, an indirect indicator of
the presence of lead in urine specimens, was accomplished by acidifying, re-
frigerating, and storing in the dark (Vincent and Ullman, 1970). A good review
of the precautions to be taken in the sample treatment of biological fluids
is available (Anand, et al., 1975).
2.3.2 Preparation of Samples for Analysis
The criteria for trace metal analytical methods are specificity, sensi-
tivity, and precision. The achievement of these goals on samples containing
the substances sought in the nanogram range often requires the use of separa-
tion and preconcentration techniques to avoid spurious results.
Although beset with the everpresent possibility of analyte loss or gain,
most environmental samples are subjected to some form of chemical treatment.
The purpose of chemical treatments is to provide an analyte concentration that
is within the best range for good precision of the method and to reduce
possible interferences from the matrix components. A thorough description of
the destruction of organic matter in biological samples was given by Gorsuch
(1970). Reference is also made to another review by Tolg (1972) which de-
tails a large number of chemical treatments for a variety of sample types.
Table 2.5 lists some typical concentration/separation procedures used
for isolating the lead content of a number of different sample types. The
amount of literature directed toward both treatment and analysis of many
types of samples for lead is extensive. Investigators have determined bene-
ficial measures for reducing decomposition times and background blanks.
Some of these changes are presented below under the various sample types.
2.3.2.1 Biological Samples
The wet ash digestion procedure reported for plants and animal products
(Hoover, et al., 1969) was adopted as the AOAC (Association of Official Analyti-
cal Chemists) preferred method (Horwitz, 1975) after testing its ruggedness
in an interlaboratory comparison. Precautions are taken to insure the com-
plete co-precipitation of lead with strontium sulfate. This procedure may be
applicable to other biological samples requiring preconcentration procedures.
Both wet (digestion) and dry ashing procedures have been used for des-
troying the organic matrix of biological samples (Yeager, et al., 1971). These
workers obtained similar results using either approach, but preferred dry
ashing (as did Sutton, 1975) in silica dishes for reduced treating times.
However, as Tolg (1972) points out, dry-ashing in a muffle furnace at
400-800 C in the presence of air can lead to more or less loss of many
elements, including Hg, B, Pb, Zn, Cd, Ga, In, Tl, As, Sb, Fe, Cr, and Cu.
The addition of fluxes such as sulfur, phosphates, or sulfuric acid, reduces
the losses in many cases, but magnifies the risk of raising the blank value.
Interaction between the flux and the vessel - such as formation of insoluble
silicates from silica and porcelain - and the formation of difficulty-soluble
oxides, causes losses, which, together with the other disadvantages, render
2.12
-------
Table 2.5 TYPICAL CONCENTRATION AND SEPARATION PROCEDURES USED IK
DETERMINING LEAD IN A VARIETY OF ENVIRONMENTAL SAMPLES
Sample
Plant and animal
products
Biological
Bone
Tissue
Blood
L'rine
J'KCPS
Hsir
Water
Aabient air
Filter (pafi.-)
rilvcr (j>jp*r)
Til-...- (?-..cr;
Filter (fclass)
Filter
(cellulose)
Soils
Ccr.i:;i:t
Organic lead
Liquid i-xls
Acbient air
Palr.ts (solids)
P£incs (licxids)
Matrix
Separation
We- ash
Dry ash
Dry ash
Dry ash
Dry ai*h
3ry ash
Dry Ash
Chelation
lor. exchange
Dry ash
V.Vc ash
LTAd
Leach
Wet ash
Leach
Fusion
Bcrcb dis-
solution
Leach
Coaplexatlon
Ai'sorpcion
Leach
-
Reagents
or
Conditions
HCx04, HX03. HjSO^
SOO C/Silica dishes
SOO C/Sillcn dishes
SOO C/Silica dishes
500 C/Silica dishes
500 C/Silica dishes
SOO C/Silica dishes
DUCa/APDCb
Resin-Dowex 1
500 C
IIXOj. HC106
Ionized 0/100 C
HCl, HXO-
HXO--HC10.
J 1
HCl-HiXOj or
Sa2C03-KS03
HF-HNO.
J
Acetic acid
IC1
Charcoal
KSOj
-
Second
Separation
Salt con-
version
Chelation
Chelation
Chelation
Chelation
-
-
-
Evaporation
Evap.-diss.
-
Evap.-diss.
Evap. to low
vol.
Chelation
-
Ion excahnge
Electro-
chemical
-
-
Leach/
digestion
-
-
Reagents
or
Conditions Extraction
(NH4)2C03
APDCb Solvent
APUCb Solvent
APDCb Solvent
APDC Solvent
-
-
Solvent
Heat
HF-HN03
-
HF-HS03
Heat
Dithizone
-
Chelex 100
Cathodic-
anlon
.
Solvent
HCl, HN03. Chelation
HCIO^
-
Solvent
Pb Specie
Reagent Desired
Total
MIBKC Total
MIBKC Total
M1BKC Total
MIBKC Total
Total
-
KIBK? Soluble
Soluble
Inorganic
- Inorganic
Inorganic
Inorganic
Inorganic
Adsorbed
Total
Total
Acld-
extractable
MIBKf Organic Pb
Dithizone Organic Pb
Organic Pb
MIBKC Organic Pb
Overall
Treatment
Tice, hr
4
12
12
12
12
12
-
2
2
<4
>4
<4
12
1
24
2
3
2
2
24
2
1
References
Hoover et al.,(196*)
Yeager et al., (1971)
Yeager et al., (1971)
Ycnger et ai., (1971)
Yeager et al., (1971)
Yeager et nl., (1571)
Clarke and Wilson (1974)
U.S. EPA (1974)
Korkisch and Sorio (1575) ,
Mark et al. (1969)
Kometani (1972)
Konetar.i (197IJ
Konetani (1972)
Thompson et al., i!969)
Annual B-Tl; of ASTM
Standards C-97J)
Anderson (IV 7 4}
Froudiger and Kunr.cr (1972)
Arden and Gale (1974)
Krinitz (1974)
Campbell and Palner (1972)
ASTM (1972)
Eider (1971); Holak (1975)
Eider (1971)
bAaaonJ.uj pyrroliuine dlehiocarbanate.
Ijtfethylisobutylketone.
T.OW temperature
ashing.
-------
these procedures unsuitable for extreme trace analysis. Alternatively, Tolg
describes a method of low temperature ashing between 100 and 200 C in a
stream of oxygen with excitation by a high-frequency electromagnetic field.
Abu-Samra, et al., (1975) point out that wet-ashing methods seem to have
gained greatest acceptance among workers Interested in trace metals analysis.
Abu-Samra and his co-workers developed a procedure for rapid, safe, and
efficient ashing of biological samples using microwave heating. Complete di-
gestion was accomplished in minutes. Human tissues were solublllzed in a
comparatively short time (2 hours) when treated with alcholic tetramethyl
ammonium hydroxide (Gross and Parkinson, 1974).
Another technique intended to reduce the decomposition time of biological
materials is the bomb method (Paus, 1972). Initial work indicated this to be
comparable to wet ashing for the recovery of lead in seaweed and fish. This
procedure also dissolves all the fata and proteins which are more difficult
to decompose when using other concentration techniques. The presence of oils
in the concentrates may Interfere with the subsequent chelation of lead and
with the flame characteristics when the sample Is nebulized for atomic absor-
tlon spectroscopy (AAS).
A relatively rapid ion exchange technique recovers lead efficiently from
dilute solutions of blood and urine, and also from their acid leachate solu-
tions for analysis by atomic absorption (Lyons and Quinn, 1971).
Tracer studies were conducted to identify sources of error In the recovery
of lead in blood samples vla.several preparation techniques (Kopito, et al.,
1974). Thi' lead isotope ( Pb) was added as the nitrate or acetate. The four
concentration techniques tested were two procedures of protein precipitation
with trichloracetlc acid (TCA) and subsequent chelation and extraction; acid
digestions using TCA; and acid digestion coupled with coprecipltation with
bismuth. The final concentrates of these procedures were analyzed using
atomic absorption spectroscopy.
The experiments with the use of TCA singly showed that long incubation
periods (1 hour) are required for quantitative recoveries. Incubation periods
of short duration (10 minutes) yielded recoveries of only 85 percent, neces-
sitating sucesslve precipitation treatments. The procedure using TCA-mixed
perchloric acid reagent resulted in only 75 percent recovery of the Isotope.
For the wet ashing procedure, using a mixture of nitric and perchloric acids
at a termpereture of 150 C, total recovery of the tracer was found. In un-
covered beakers, lead contamination due to atmospheric fallout was observed.
Also, complete destruction of the organic matter is necessary for efficient
recovery of lead using the coprecipltation approach. This was made evident
In studio Involving tracer injection Into mice followed by analysis of their
blood.
2.lit
-------
2.3.2.2 Aqueoua Sample*—
In waters containing high amounts of humus lead may bo present as a
metallo-organlc. The humus may reduce the efficiency of extraction of lead
In some Instances (Paus, 1971). This work compared direct water analyses
with those obtained from the various extractive techniques (such as chelation
and Ion exchange) after destroying the humuH content. The combined extrac-
tive and analytical techniques can provide specific lead specie estimation
as to ionic, metallic or organic.
Ion exchange, resin-loaded papers have been used to separate tht lead
in waters for analysis by X-ray fluorescence (Lochmuller, et al. , 1974).
Low detection limits were demonstrated but quantitative estimates could not
be made.
2.3.2.3 Air Samples-
Samples collected on polystyrene membrane filters were dry ashed at
400 C and the resulting residues were dissolved in a mixture of acids in a
Teflon bomb (Ranweller and Movers, 1974). In the multielement analysis
of these solutions It was noticed that the lead blank for this membrane
was higher than that found for cellulose filters.
A unique technique for separating and concentrating air particulates
Into two particle size ranges utilized a dlchotomous sampler containing a
virtual impactor (Dcubay and Stevens, 1973). The sizes that were separated
included particles of leas than and greater than 2 micrometers. An analysis
of these fractions using X-ray fluorescense (XRF) revealed that lead is
highly concentrated in the smaller sizes characteristic of emissions from
auto exhausts.
Analysis of dustfall deposits on Impervious Teflon discs is subject
to less blank problems (Huntzicker, et al., 1975). Leachates of the discs
were evaporated to dryness, redlssolved and analyzed by atomic absorption.
Dry ashing of glass filter catches produced lower extractions of lead due
to the formation of insoluble silicate compounds (Kometani, et al., 1972).
However, various ashing procedures for filter papers performed well.
2.3.2.4 Rock and Soil Samples—
In order to further identify lead species deposited In soils from auto
exhaust systems, gradient density and magnetic separation methods were used
to separate lead compounds for X-ray diffraction studies (Olson and Skogerboe,
1975). The lead compounds are concentrated in the high density fraction
with the larger amount being present in the nonmagnetic aliquot.
Comparative leachlnga of soil were carried out using a mixture of sul-
furic and hydrochloric acids and ammonium acetate. There was a considerable
reduction in the lead extraction efficiency for the latter agent (Kahn,
et al., 1972).
2.15
-------
2.3.2.5 Miscellaneous Samples—
An automated procedure for determing lead in a large number of unleaded
gasolines was reported using a two-reagent extraction scheme (Heistand and
Shaner, 1974). Alcoholic iodine and dilute nitric acid solutions were used
for the lead separations. The results were mainly within the allowable
tolerance in comparison to the direct assay method (Annual Book of ASTM
Standards, 1973).
Lead in oils has been determined using comparatively short (minutes)
extraction of the lead additive and its subsequent estimation by titration
(Banerjee and Dutta, 1973). The reagents used were thioglycollic and
nitric acid.
Low-temperature (about 150 C) radio frequency ashing of coals was
performed in an oxygen atmosphere to yield unaltered ash to concentrate
lead and other metals for analysis by spectrographic methods (O1Gorman and
Walker, 1972).
2.3.3 Methods of Analysis—
The forgoing information is only a partial summary of the research
efforts which are being applied in the search for more rapid methods of
pretreatment of environmental samples without sacrificing efficient re-
coveries of lead. The necessity of reliance upon sample treatment will
become evident in the following comparisons of analytical methods avail-
able for determining lead at trace levels.
A comparatively large number of analytical methods are being used for
trace lead analysis. Table 2.6 lists these methods along with the pertinent
features and requirements to be met in the determination of lead for a
variety of samples. Included for each method are the general pretreatments
necessary for accomodation as to sample form and concentration. The other
factors which describe the suitability of a method—detection limit, sensi-
tivity, precision and accuracy—are reported from data found in the litera-
ture. Some workers use the terms sensitivity and detection limit inter-
changeably, so it is sometimes difficult to separate these parameters.
Wherever possible, the sensitivity values listed represent those for which
analyses can be made above the detection limit with reliability. The pre-
cision information is based on results obtained on replicate samples, and
the accuracy assessment is based upon comparisons from the analyses of the
same sample using at least two methods of analysis. These analytical limits
can and will vary among analysts depending upon equipment, operation and
diligence.
2.16
-------
Table 2.6 ANALYTICAL METHODS FOR DETERMINING LEAD AT T£W LEVELS
ro
*
H
Analytical
Method
Colorimetrlc
(dithizone)8
Atomic absorption . .
spectres copy (flame) *
Atomic absorption
spectroscopy
(flameless)c»k
Instrumental photon
activation analysis1*
X-ray fluorescence
apectrometrye •*
Spark source mass
8pectrometry*»k
Electrochemical
(anodic stripping
voltammetry ) 8»*
Atomic fluorescence
spectrometryh»k
Optical emission
spectrometry (arc
source) *»k
Optical emission
spectrometry
(plasma source)^
Required
Sample Fora
Liquid
Liquid
Liquid or solid
Liquid or solid
Liquid or solid
Solid
Liquid
Liquid or solid
Liquid or solid
Liquid
Important
Applications
Water and all other
samples which can be
chemically treated.
All samples after
chemical treatment.
All samples with varying
degrees of pretreatment.
All samples.
All samples.
All sample types with
treatment .
Hater direct; other
samples are converted.
All samples with varying
degrees of pretreatment.
All samples; some require
treatment.
All samples which can be
liquified.
State of
Measured
Lead
Lead dlthizone
complex
Free atoms
Free atoms
As is
As is
Ions
Amalgams
Excited atom
state
Vib rationally
excited atoms
Vib rationally
excited atoms
Detection
Limit for
Lead
<1 ppm
30 ppb
<1 ppb
12 ng/m3
1.5 ppb
(by volume)
1 ppn
(10 ng/cm2)
<0.1 ppm
0.5 ppb/
5 ml
1 ppb
(30 pi)
<1 ppm
2-8 ppb
(100 ul)
-------
Table 2.6 ANALYTICAL METHODS SUITABLE FOR DETERMINING LEAD AT LOW LEVELS
(cont'd)
Analytical
Method
Sample Preparation
Methodology
Interferences
ro
•
M
OO
Colorimetric
(dithizone)*
Atomic absorption
apectroscopy (flame)^>»'t
Atomic absorption
spectroscopy
(flamele8s)c»fc
Instrumental photon
activation analysis'1
X-ray fluorescence
apectrome try6»*•
Liquid is chelated with dithizone
and the complex is extracted with
an organic solvent. Double ex-
traction at high pH may be needed
to eliminate interference from
other metals.
Water samples may require con-
centration; biological samples,
soils, and other solids are
dissolved, chelated, and
extracted.
Water and biological fluids
require little treatment.
Solids may have to be digested
and extracted.
Most samples can be irradiated
directly. Radiochemlcal
separations may be needed in
some cases.
Filter catches can be analyzed
directly; soils and biological
samples should be dried, ground
to at least 44um, and pressed
into pellets. Water samples
require preconcentration by ion
exchange or anodic stripping*
Abaorbance of complex is
determined spectrophoto-
metrically at 510 nm.
Solution is nebulized and
lead is atomized with a
high temperature flame to
produce free atoms which
absorbs light of wave-
length 283.3 nm.
Lead la atomized by thermal
sources to provide absorb-
ing free atoms.
Samples are irradiated with
optimum electron energies,
and the resulting gamma
rays are measured with a
high resolution Ge(Li) de-
tector. Interference-
free 204 Pb line is used.
Samples are irradiated
with primary source of
X-rays to produce char-
acteristic secondary X-
raya for measurement by
energy or wavelength
dispersion.
Bi, Sn, and Fe in
moderate amounts.
Chemical and matrix
effects must be over-
come. Background may
vary.
Chemical and matrix
effects overcome by
proper standardization,
must be aware of furnace
emissions, nonrepro-
ducibillty, and back-
ground problems.
Overlapping of gamma
ray peaks may require
selection of less
sensitive wavelength.
Interelement effects,
scattering from primary
X-rays, overlapping
peaks.
-------
Table 2.6 ANALYTICAL METHODS SUITABLE FOR DETERMINING LEAD AT LOW LEVELS
(cont'd)
Analytical
Method
Sample Preparation
Methodology
Interferences
Spark source mass
spectrometry^ »^
Electrochemical
(anodic stri
voltamnetry)
(anodic stripping
ro
•
H
vo
Atomic fluorescence
spectrometry*1 »k
Optical emission
spectrometry (arc
source)*-''1
Optical emission
spectrometry
(plasma source)J
Biological fluids are lyophilized,
water samples are evaporated to
dryness, filter catches and .soils
can be used without chemical
treatment. All nonconductive
samples require addition of graphite
to form conductive electrodes.
Water samples as is, solids and
biological samples chemically
treated to provide a liquid.
Biological fluids and water can
be analyzed directly; other
samples may require treatment
for proper form.
Biological samples are dried or
ashed and then arced. Water
samples can be analyzed directly
or via dried residue. Soils and
air collections are arced
directly.
Soils must be chemically converted
to liquids; water and biological
fluids can be aspirated directly
or after slight dilution.
Radio frequency spark is
used to produce Ions with
the proper isotopic dis-
tribution for either photo-
graphic plate or electrical
detection readout.
Electrolytic reduction of
lead onto a Hg electrode
iollowed by its det_r-
tnination using a reverse
oxidation potential
according to its standard
electrode potential.
Lead is atomized by a heat
source and excited by a
light source to flucresce
and emit characteristic
radiation for measurement
upon deactlvation.
Samples are arced In a pure
graphite cup to produce
spectral lines of the
analyte. Readout of opti-
mum lead line (213.3 nm)
can b« done by film or
direct reader.
Sample solution is nebulized
into a hot, inductively
excited plasma of Argon gas
to convert almost all of the
analyte atoms to an excited
state to provide the
characteristic line spectra.
Organic matrix and
complex Ion formations,
high background from
major elements present.
Possible peak potential
overlaps, presence of
organolead prevents
total lead determination.
Chemical matrix effects
and fluorescent quench-
ing of desired radiation.
Spectral, chemical, and
lonization effects can
be overcome by simulation
of standards makeup with
matrix of samples.
No chemical effects, Pe
may interfere with lead
analysis; background
and instability should
be controlled.
-------
Table 2.6 ANALYTICAL METHODS SUITABLE FOR DETERMINING LEAD AT LOW LEVELS
(cont'd)
Analytical
Method
Color ime trie
(dithizone)3
Sensitivity Precision
— 20%
Accuracy
10%
Comments
Method is specific in
absence of interfering
metals.
ro
*
iv>
o
Atomic absorption
spectroscopy (flame) »
Atomic absorption
spectroscopy
(flameless)c»k
Instrumental photon
activation analysis'*
X-ray fluorescence
spectrometry6 »
Spark source mass
spect rometry*»^
Electrochemical
(anodic stripp,
voltammetry)B»
2.5 Mg/1 for
1% absorbance
3 x 10~10g per IX
absorbance (equivalent
to air concentration
of 0.1 ug/m3
W/25 ug/1
5-10%/10 wg/1
5-10%
±3x
0.1 wg/1
2-6% 0.1 ug/1
5% Method is specific.
Standards preparation
must simulate sample
matrix.
5-20% Method is specific. Small
(ul) volumes can be used.
Short overall analysis
time.
10% Specific, but equipment
cost and time of analysis
may be a disadvantage.
Method is rapid, precise,
and has multielement
capability. Standardiza-
tion can be a problem.
Good multielement coverage
at low levels, isotopic
dilution can provide
accurate determination of
trace metals.
Possibility of multi-
50 yg/1 element (6) determinations.,
equipment simple but
requires skill for
operation, specific.
>±3x (without
standards)
±10-25% (with
standards)
-------
Table 2.6 ANALYTICAL METHODS SUITABLE FOR DETERMINING LEAD AT LOW LEVELS
(cont'd)
Analytical
Method
Sensitivity
Precision
Accuracy
Comments
ro
•
ro
H
Atomic fluorescence
spectrometryh»fc
Optical emission
spectrometry (arc
source) i»"c
Optical emission
spectrometry
(plasma source)J
3 x 10~11g
per IX abs.
5Z/0.1
Pg/ml
1 ppm (25 mg
sample)
10 ppb
13% 20-2000
ppm level
5% 1 ppm level
— Multielement capability;
equipment commercially
unavailable; light source
problems include Instability,
nonreproducibility and
operation. Aqueous standards
can be used.
±20% Fast, multielement analysis
over a broad concentration
range.
5t Multielement analysis capa-
bility, a wide range of Fb
content can be determined
without the need for dilu-
tion, simple standards can
be used.
^Lerner (1975).
"Edmunds et al.,(1973); Kinrade and Van Loon (1974); Amore (1974).
^Edmunds et al.,(1973); Anderson and Mesman (1973); Gross and Parkinson (1974).
dAras et al.,(1973).
fGiauque et al.,(1973),
Fitchett et al.,(1974).
°Ediger and Coleman (1973); Searle et al.,(1973).
!?Browner (1974); Amos et al.,U971); Hlnefordner and Elser (1971).
TSeeley et al.,(1972); Bedroslan et al.,(1968).
^Greenfield et al.,(1975).
KColeman (1974).
-------
The following sections describe the analytical methods which have
been used in the overall analyses of lead in a variety of samples. Most
recorded work deals with chemically-treated samples using one of the many
techniques described earlier. Recent modifications and improvements in
analysis methods and techniques have tended to require little or no chemical
treatment of the sample, but in some of these cases reliability and general
acceptance of the technique have been less than desirable.
2.3.3.1 Atomic Absorption Spectroscopy (AAS)—
This method is based upon the formation and the subsequent absorption
properties of the atomic vapor of an analyte. The absorbance of a specific
wavelength of light is measured which is characteristic of the element to be
determined. For lead either 283.3 or 217nm can be used; the former is more
commonly used. Several atomizing techniques can be used for converting the
element sought into free atoms. These techniques provide varying degrees of
conversion efficiencies and are generally dependent upon the atomizing temp-
eratures attainable. These differences will be discussed below.
According to the literature, no method other than AAS has been as widely
accepted and compared as a standard for trace lead analysis in the last five
years. The advantages of low cost and ease of operation along with fulfilling
conventional analytical criteria has contributed to the acceptance of this
method. Improvements in atomization techniques during the last decade have ex-
tended the ability of atomic absorption spectroscopy to cope with the problem
of choosing a compromise between reductions in required sample pretreatment and
dependable results. The lowered detection limits and correspondingly more
rapid sample preparation and analysis are seen to reflect these improvements.
The atomizing capabilities presently available for AAS are the conventional
flame, semiflameless and flameless. Maximization of sensitivities for each
of these techniques can be achieved by adjusting the various operational
parameters (Hwang, et al., 1972).
The conventional flame technique of AAS requires liquid samples for ne-
bulization into air-acetylene or nitrous oxide-acetylene flame where atomization
of the analyte occurs. The concentration is determined by measuring the absorp-
tion effects on a spectral source comprised of the same element. Analyses are
carried out with an analyte concentration around 0.5-1 ppm or above. Therefore,
chemical treatment is generally a prerequisite for achieving both the proper
sample form and concentration range.
When analyzing plant samples by AAS, De Vries, et al., (1975) encountered
difficulties of a kind likely to be encountered with other biological samples.
Solutions of dry-ashed samples gave spurious results due to salt effects,
which appeared to be additive. In addition, recoveries of lead from dry-
ashed samples were generally low when compared with wet-ashed samples, due to
partial volatilization of metal salts, to fixation in an acid-insoluble
residue, or both. Wet-ashing eliminated this problem but it was found neces-
2.22
-------
sary to extract the sample into an organic solvent before analysis to attain
the desired sensitivity and to remove interferences. Samples were decomposed
with a nitric acid-perchloric acid mixture, diluted, buffered with citric
acid and extracted with APDC-MIBK for analysis. Small amounts of iron in
the standards and unknowns increased the stability of the solution and re-
producibility of the analysis.
A technique has been described by Hessel (1968) for determining lead
in blood erythrocytes using the flame source. Comparatively large volumes
of blood are chelated and extracted for comparison with synthetic standards.
The lead content in blood and urine samples is quite low. For blood analyses,
5 to 20 milliliters are often needed for adapting to the range of flame AAS.
This involves continual withdrawal of large volumes of blood which is
unattractive in clinical studies.
The disadvantages attendant to the use of flame techniques have re-
sulted in the development of the more sensitive and rapid semiflameless and
flameless approaches. The semiflameless techniques initially investigated
for this purpose use tantalum boats (Kahn and Sebestyen, 1970) and nickel
crucibles (Delves, 1970). With these modifications sensitivities are in-
creased by at least a factor of 10 over the flame method. Both approaches
utilize procedures of drying small quantities of samples in appropriate
containers placed near the flame of a conventional AAS unit. After drying,
the containers with their residues are inserted into the flame where temper-
atures are sufficiently high to vaporize and atomize the lead.
For analysis using the tantalum boat technique, volumes of less than
0.5 milliliter of blood or urine can be inserted directly, dried and measured
for lead within several minutes. Previously analyzed samples (secondary
standards) can be used for calibration. Reproducibility and comparison
of these results with those of other methods are variable. This may be due
to differences in tantalum boat positioning and to its deterioration.
The Delves technique requires addition of hydrogen peroxide to partially
oxidize the blood sample (10 microliters), and overall, takes about 5 minutes
for analysis. Standardization is accomplished by the standard additions pro-
cedure. Nonlinearity occurs at high lead levels thereby precluding the use
of standard additions at these levels. However, reproducibility and comparison
with other methods on similar samples are good. Evaluation of the Delves
technique has been made by numerous investigators. Many hospitals have
adopted the method after comparing results with those of several other methods
(Hicks, et al., 1973; Marcus, et al., 1975).
Lead may be analyzed from small amounts of capillary blood specimens.
Insufficient cleansing of the fingers prior to capillary sampling is a more
likely source of possible contamination of capillary blood samples than of
venous blood samples. Further simplification fo the Delves method is possible
by the collection of capillary blood onto filter paper; after drying, small
2.23
-------
ill new arn iHinrlitnl out l(u liiMfiilun Into the cup. Dispensing volume errors
ure eliminated using thl* approach (Cernlk, I9'/'I; Cooke, et al,, 1974), This
technique has also I IP en used for the direct determinat Ion of lead In urine and
WON I (Muni to provide excellent rewulti (Anderson and Mesman, 197)), Simultaneous
background correction whould be made fin this and many other types of MampleH
analyged hy atomic absorption.
The I Umnless technique provides high atomlsatlon temperature by resls-
tance heating of a graphite furnace or carbon i od assembly, Sensitivities are
Increased by up to 1 ordera ol magnitude OV«M the flame technique, However,
the prprim I mi of analyst* is much worse Chan lor flame methodw, typically 9 to 25
percent depending on the type ol atomitcer and type of aample (Coleman, 1974),
The graphite atomlier allows the direct Introduction of nolUI aamplaa, but auch
ttamplea are often lacking In reproduc l.bil 1 ty, The general procedure for anal-
yKtiiti email 10- to 30-mJcrolHpr volumew ol blood placed in the atomlxatlon cell
In to dry at a low temperature (100 C), ash at a higher temperature (300 C), and
then atomiie at 2300 c (Fernandas, 1973), Background correctlone are Decennary.
Alao, Dynthetlc aqueoue atandardn can he uaed, Comparison with reiulta obtained
by the conventional extraction-flame technique are often favorable,
Slight changes in pretreatment procedure^ nwnentlally eliminated Che need
for background correct lonw In the analyse ot lead In blood using a graphite
boat (Oarnys and Matouaek, I'J73). Alter adding nitric acid, the results which
were obtained showed excellent agreement with those determined by different pro-
cedures ol chemical treatment and atomlxatlon, Sources of errors encountered In
blood lead analysis using the graphite boat Is the subject of a publication by
Hally and K11 run-Smith (19/S),
Pur Cher Information on other Individual techniques ol nonflame analysis of
blood lead content Is available, This Includes the determination of lead in
human erythrocytes ualng the graphite furnace (Evensun and Pendergast, 1974) and
whole blood and plasma lead analyses using the carbon rod atomlier (Kubaslk, et
at., 1972| Matousek and 8tevens, 1971),
Applications of flame I ess acorn liters are being made for Che analyals by AA8
of participate samples collected from ambient air, Although lead is generally
present In urban air at or near 2 micrograms per cubic meter (often directly
determinate by flame technique*), Che direct analysis of parclculates on filter
media seems attractive, Sampling of small air volume! (100 Co 500 ce) through
hluh density graphite cups which are Inserted directly into a graphite furnace
provides rapid wpui cheeks of atmospheric lead pollution, The sensitivity re-
ported was 1n the 10* gram range (Woodriff and Lech, 1972), Standardisation
was made with aqueous solutions,
Monitoring ol lead concentrations in ah was performed by passing ambient
atr over Inductively heated graphite rods for atomliatlon and subsequent abaor-
bance measurement (Robinson. 1973), Analytical nenilclvltiea of 0,16 microgram
per cubic meter were achieved,
2.2it
-------
Flame loan and eemIf tameless atomic absorption can be u««*d to determine
load It) water wit hour preconeentratlun, Small volumes (mlcrol! ler*) of water
can ba analysed, Krrorw In precision appear to be caused liy inaccurate volume
dispensing, deterioration of the tantalum boat or graphite furnace and by the
possible Instability of stored samples, The following article* relate thane
problem* to the analysis of lead In water samples at iuw (ppb) concent.rat, IDIIM
(Edlger, et a)., 19741 Pernande* and Manning, I'J7I; Edmunds, et al., 1971). A
modification of the Delved cup technique was uwed successfully (Maine*, et al . ,
1973) for lead analyses of potable wateri. Mlcrollters or water were tntrinlui'tul
Along with gelatin Into the cups to yield remit to which were In excellent agi no
me tit with (he solvent extract Ion- f lame procedure.
Some form of preliminary chemical treatment of most biological material*
other than blood la apparently neee**arv for analysis hy flameless AAti, The
fact that the detection limits are lower than In flame appl lc*4t Ion* in an argu-
ment for their use even when such treatments are required.
Addition of graphite to pulverlied rock iamplea enhanced the atomliatlun
of lead £ur direct measurementn using an inductively heated graphite furnace.
However, only moderately prectme dau were obtained when compared to X-rav lluu-
rencenccs values (Langmyhr, et al., 1974).
/,3,3.'
-------
Various procedures are described below for the analyses of low lead con-
centrations in liquids or acid digests of solids. Pulsed voltammetric stripping
(PVS) was used to determine lead in the low ppb range in water, urine, blood
plasma and digested whole blood (Copeland, et al., 1973). Very good agreement
was found between results of this method and those obtained using nonflame AAS.
Analytical conditions were optimized (Hg film in place of a drop) to attain
higher sensitivities. Using linear scan anodic stripping voltammetry (ASV),
investigators determined the lead content of chemically-treated blood and urine
samples. The results agreed well with those obtained by flame AAS (Searle, et
al., 1973).
Other electrochemical techniques which may be used in the direct analysis
of lead in water in the ppb range are pulsed ASV (Crosmun and Dean, 1975); cath-
odic SV (Kinard and Propst, 1974); and alternating current ASV (Rojahn, 1972).
The electrochemical methods are specific for lead and usually provide a
means of multielemental analysis.
2.3.3.4 X-ray Fluorescense (XRF)—
XKF can be used for determining micro and trace quantities of lead in a wide
variety of samples. Ambient air filter samples can be measured directly with
the quality of the results being dependent upon suitable standardization, par-
ticle size and interelemental matrix interferences (lee, et al., 1972). The
latter may be reduced with proper standardization or the use of mathematical re-
lationships for corrective purposes. Unless present in sufficiently high quan-
tities, lead in water is best analyzed after concentration on ion exchange mem-
branes (Campbell, et al., 1966). Some biological materials (freeze-dried) can
be analyzed directly for semiquantitative data in the absence of simulated
standards (Giauque, et al., 1973).
Energy dispersive readout of XRF was used to measure microgram quantities
of lead in biological, rock, and air samples (Giaugue, et al., 1973). The biolog-
ical specimens were freeze-dried and pressed into thin wafers before irradation
with primary X-rays from a Mo target. Rocks were finely ground and redispersed
onto suitable membranes prior to measurement. Ambient air particulates were
analyzed directly on filters.
Gamma-ray excitation is used in a portable lead detector for screening
painted walls for potential lead ingestion sources (Laurer, et al., 1971).
Proton-induced X-ray emission analysis (PIXEA) using an energy-dispersive
readout was investigated for lead determinations in a variety of environmental
samples (Walter, et al., 1974; and Lochmuller, et al., 1974). The use of proton
excitation reduces the white radiation background and increases X-ray excitation
to provide greater sensitivities. The former investigators determined lead in
soil extracts, in leaf sections, dried body fluids, air catches, thin tissue
sections and proteins by direct measurement. Difficulties were experienced in
achieving quantitative results and suitable sensitivities.
2.26
-------
The combination of a primary source for sample irradiation and wavelength
dispersion was used to quantitatively determine lead in gasoline (von Lehmden,
et al., 1974).
2.3.3.5 Activation Analysis—
Environmental samples analyzed for lead by this method are better treated
by radiation sources other than neutrons. The low nuclear cross section of
lead and intereferences associated with neutron activation reduce the sensiti-
vity for lead considerably beyond that required for meaningful analysis in
many cases. Other forms of irradiation induce more sensitive lead reactions
so that lead can be determined in trace quantities in all forms of samples. In
conjunction with instrumental attachments, greater sensitivities can be obtained.
Photon irradiation (2 hours) performed directly on atmospheric (Aras, et al.,
1973) and soil (Chattopadhyay and Jervis, 1974) samples allowed the determination
of lead at accuracies competitive with other methods of analyses. Irradiation of
air particulates for one hour with He ions permitted the measurement of the pro-
duct Po , representing converted lead at low levels (Parsa and Markowitz, 1974).
Good precision was observed at microgram per cubic meter levels.
2.3.3.6 Spectrographic Methods—
The methods described in this section include mass and optical spectroscopy.
Various sources for excitation or ionization are available for Spectrographic
measurements, but only a few will be covered.
Emission spectroscopy has been a standard qualitative and semi-quantitative
laboratory tool for years. Samples are deposited on graphite or metal electrodes
and excited to produce spectra characteristic of the element. Comparison of the
spectra of known and unknown compounds provides qualitative identification of the
elements in the sample; if standards are used for the known samples, semiquanti-
tative and quantitative analysis is possible. Seeley, et al., (1972) compared
emission spectrography and AAS for the determination of lead transported to soils
from automobile exhausts. Soils were analyzed for lead by direct arcing in graph-
ite cups. Comparisons with digested samples analyzed by AAS agreed within 10
percent.
The combination of an inductively-coupled, plasma excitation source with
optical emission spectroscopy (ICP-OES) has been used to achieve extremely high
atomization temperatures for detection of lead at low nanogram levels. A small
volume of liquid sample is introduced into an argon plasma where excitation of
the free atoms occurs for their measurement. Attributes of ICP-OES are compared
with those of other methods (Fassel and Kniseley, 1974) along with its use for
the analysis of lead in a variety of samples (Greenfield, et al., 1975).
Spark source mass spectrometry (SSMS) is a highly sensitive analytical
technique. The sample is vaporized by a radio-frequency spark and the resul-
tant ions are spectrometrically measured according to their mass. Precision
2.2J
-------
can be improved through the use of an isotopic dilution technique. Spark source
mass spectrometry has been used for the analysis of biological specimens for
heavy metals including lead (Fitchett, et al., 1974). The samples were dried
and combined with conductive graphite to aid in sparking. Although detection
limits for lead were in the ppb range, the organic content interference required
proper graphite dilution ratios.
2.3.3.7 Atomic Fluorescence Spectroscopy (AFS)—
Compared to its related counterpart (AAS), AFS has not enjoyed the extent of
application to trace metal analysis. Both techniques show similar sensitivities
for lead determinations. Since AFS equipment is not generally commercially avail-
able, modification of existing AAS equipment is required for its use. The reader
is referred to publications outlining the potential of AFS (Browner, 1974; Wine-
fordner and Elser, 1971). Lead has been determined in blood and urine using the
flameless carbon rod atomizer (Amos, et al., 1971). Although lead levels deter-
mined were comparable to nonflame AAS values, considerable experimental difficul-
ties were experienced. This method appears to be in the developmental stages,
with its potential not yet fully developed.
2.3.3.8 Biological Methods For Determining Body Lead Exposure—
Considerable efforts are being made to develop analytical procedures suitable
for diagnostic use on persons suspected or known to have elevated lead exposure.
The effect of excessive lead on metabolism is reflected in its inhibition of
enzymes required in heme synthesis. The protoporphyrin IX content of blood which
reflects inhibition of heme synthesis in bone marrow can be determined with rela-
tive ease on microcapillary samples (Sassa, et al., 1973). Two milliliters of
whole blood provide a sufficient sample to determine the separated porphyrin
content fluorimetrically. This method and minor modifications developed by
others are somewhat non-specific. Porphyrins other than protoporphyrin IX regis-
ter fluorescence under the conditions of porphyrin extractions used. This is not
a major problem since other porphyrins are elevated only in the case of the rela-
tively rare porphyrin disease, e.g. erthrocytic protoporphyria. Nevertheless, in
recognition of this non-specificity, the results are expressed as micrograms of
"free" erthrocyte porphyrin (FEP) rather than as units of protoporphyrin. Log
FEP has been found to rise linearly with blood lead concentration in adults
(Haeger-Aronson, 1971) and children (Piomelli, 1973; Sassa, et al., 1973).
Lamola and Yamane (1974) found that the fluorescent porphyrin in the
erythrocytes of patients with lead intoxication or with iron deficiency anemia
is zinc protoporphyrin which is bound to globin moieties, probably at heme
binding sites. Measurement of the fluorescence at 594 nanometers of blood di-
rectly (without any extraction steps) can serve as a simple screening test for
lead intoxication. Experimental procedures developed by Lamola, et al., (1975)
have confirmed the simplicity and rapidity of the method. Small capillary
quantities of blood are diluted prior to measurement of their fluorescence.
This metabolite is stable in properly stored blood.
2.28
-------
The measurement of coproporphyrin in the urine has long been used as an
index of excessive lead exposure in industry. Coproporphyrin is first extracted
from the urine into either ethylacetate-acetic acid (Sano and Rimington, 1963)
or into diethyl ether (Askevold, 1951). Absorbance is then measured at 401 nm.
The methods are apparently specific since uroporphyrin, the only likely source
of interference, is not extracted under the conditions described above (Riming-
ton and Sveinsson, 1950).
The rate of urinary excretion of delta-aminolevulinic acid (ALA) also has
been used as an index of excessive lead exposure. The basic procedure commonly
used today was originally reported by Mauzerall and Granick (1956). The method and
subsequent modifications thereof depend on the formation of a colored complex of
pyrrole derivative of ALA with p-dimethylaminobenzaldehyde (DMAS). The method
is non-specific. DMAS forms colored complexes with many pyrroles formed by Knorr
condensation of aminoketones other than ALA, notably aminoacetone (AA), which
occurs in biological fluids. Modifications of the method of Mauzerall and
Granick separate AA from ALA prior to coupling with DMAB (Urata and Granick,
1963; Marver, et al., 1966). Like all enzymatic methods, ALAD activity is de-
pendent on such variables as pH and temperature of the enzyme-substrate prepar-
ation. Numerous specific assay procedures have been used, all of which vary in
such specific details (see, for example, Nikkanen, et al., 1972; Bonsignore,
et al., 1965; Tomokuni and Ogata, 1972).
2.3.4 Comparison of Analytical Methods
The applicability of an analytical method for determining lead in environ-
mental samples depends on the intended use of the results. As this relates to
health effects brought on by excessive lead exposures, it is imperative that the
methods provide the results rapidly and with accuracy as well as precision so
that treatment can be given to alleviate the condition. Conversely, for studies
involving lead in relation to source, emission routes, fate, chemical form,
elemental associations and mass balance, a fast analytical response is not re-
quired. To some extent these studies may also include the measurement of other
trace metals present along with lead. Therefore, the need of the investigator
for simultaneous multielement analyses will also dictate the method of choice.
The colorimetric dithizone method is still considered by many laboratories
as their adopted or backup method for determining lead in samples which have
been chemically treated. By taking the necessary precautions to eliminate inter-
ferences and insure complete recovery of lead as a complex during sample pre-
paration, this method is competitive with the more recently emphasized techniques.
In general, the method is reliable and where time is not a consideration, it can
be used with confidence.
Atomic absorption spectroscopy compares very favorably with both the estab-
lished and the new methods of analysis. It possesses the features which are de-
2.29
-------
sirable for an analytical method: specificity, low limit of detection, accuracy,
fast turn around time and comparative- ease of operation. Although capable of
analyzing up to 60 elements, sequential, rather than simultaneous, multlelemental
analyses are possible with the same sample solution. The flame atomizer requires,
in most cases, some form of sample treatment to obtain the proper sample concen-
tration and form. The flameless atomizer modifications have, to some extent,
eliminated the need for extensive pretreatment for some samples. Projected use
and continued exploration of this atomizing technique will undoubtedly result in
the direct, or with slight modification, insertion of other environmental samples
of interest. Present operational and stability problems of the latter atomizing
technique are also expected to be corrected with this Increased emphasis. The
widespread use of AAS for determining lead and other metals at trace levels is an
indication of its acceptance for reliability of analysis. Atomic fluorescence,
like atomic absorption, is capable of multielement analysis, but this capability
has not been commercially developed.
Optical emission spectometry (OES) techniques provide analyses which encom-
pass wide elemental and concentration ranges in the proper sample form and are
particularly suited to multielement analyses. The arc source OES Is suitable for
the direct analysis of soils and dried tissues and also for solutions which con-
tain lead in the microgratn range. The inductively coupled plasma source of OES
has great potential as a future method for rapidly determining lead and other
metals at the nanogram level in solution samples. The forte of these OES tech-
niques is in obtaining rapid survey characterization of samples requiring ele-
mental associations and base-line studies.
The electrochemical methods require comparatively simple equipment with
excellent sensitivity for lead in the analysis of liquid samples. Multielemental
analysis Is possible although the number of elements determinable is limited.
The Increased sensitivities gained from the various modifications of polarography
and anodic stripping make them well suited for determining lead at the nanogram
level. The precision and accuracy derived from these techniques compared favor-
ably with AAS.
Spark source mass spectrometry (SSMS) can be used for the direct analysis
of a variety of sample types. Semlquantltative information can be generated at
the sub-ppm level for most of the elements, including lead, without standardi-
zation. The high cost of equipment, the level of operator expertise required
and other attendant difficulties limit the use of SSMS for single element analysis.
Its use for multielement determinations can be very advantageous.
X-ray fluorescence can be used for the direct analysis of soils and atmos-
pheric filter catches and concentrates or residues of aqueous solutions. Standard-
ization is a problem in heterogeneous samples although the contents of lead among
samples can be determined with a reasonable level of accuracy relative to each
other. This method can also be used to determine lead in liquid fuels with a
greater degree of accuracy than that obtained with other samples because of the
ease of standard preparation. The simultaneous, multielement capability is
2.30
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available when using energy or wavelength dispersive readout techniques.
Proton or photon activation analysis offer the advantage of being able to
analyze for lead with little or no sample preparation. As with SSMS, equipment
availability and time of analysis preclude its wide use except in rare situations,
2.3.4.1 Standards and Standardization—
An accurate assessment of trace levels of lead in environmental samples
necessitates the use of methods of analysis which permit comparison. The low
concentrations of lead which are encountered preclude the use of absolute gravi-
metric methods. Standards can be classified as primary (certified), secondary
(previously analyzed), and synthetic (laboratory prepared).
Table 2.7 lists the National Bureau of Standards (NBS) standards of sig-
nificance to lead environmental studies which are presently available. The range
of lead concentrations offered in the liquid fuels allows working curves to be
obtained for accurate determinations of lead. The single-value lead standards
available for the other sample types can provide a good check on chemical treat-
ment recoveries and the evaluation of analytical procedures.
Table 2.7 AVAILABLE NBS PRIMARY SAMPLES FOR LEAD
IN VARIOUS ENVIRONMENTAL SAMPLES*
Sample SRM No. Pb Content
Orchard leaves 1571 45. ppm
Bovine liver 1577 0.34 ppm
Paint 1579 11.87%
Coal 1632 30. ppm
Coal fly ash 1633 70. ppm
Fuel oil 1634 (Fending Certification)
Liquid fuels 1636 12, 20, 28, 773 ug/g
1637 12, 20, 28 ug/g
1638 773 ug/g
8Adapted from Catalog of NBS Standard Reference Materials, NBS Special
Publication No. 260, 1975-76.
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Other standards are available, e.g., U. S. Environmental Protection Agency
water samples, and U. S. Geological Survey rock samples.
Secondary standards can be used when available and when appropriate. Pre-
viously analyzed blood samples have been used successfully with the flameless
techniques of AAS for calibration purposes. Preservation may be a problem with
their use over extended periods of time. Secondary standards possessing an ade-
quate concentration range of the analyte can be used as standards in the direct
analysis of fuels and air particulate catches by many techniques. Careful
storage of these standards will insure their stability for long periods.
Chemical treatment of the samples provides an added advantage in that
appropriate similar aqueous standards can be prepared to more closely resemble
the chemical makeup of the concentrate. Simulation of the sample matrix with the
standard compensates for interferences in many instances.
For AAS applications, standards with simulated matrices can be used sep-
arately, for comparison, or may be incorporated into the sample by employing
the method of additions technique. The latter technique is used to compensate
for interference effects. It does not accomplish this in every case, however.
Some indication of the variation in the results obtained with standards used
in the Delves cup procedure of determining lead in blood is provided by a study,
in which Olsen and Jatlow (1972) compared and related the addition of synthetic
standards in several matrices and cup treatments. They found that the direct
use of aqueous standards was successful if the nickel cups were first treated
with albumin. This modification eliminated the need for using the method of
additions which required more analyses per sample.
Synthetic aqueous standards can be used directly for optical emission
spectroscopy with an inductively-coupled plasma as the atomizing source. Because
of the high temperatures attained using this source, most interelement or matrix
problems associated with other atomizing techniques are considerably reduced.
Both the direct method and the method of additions can be used for the application
of solution standards in polarographic analyses with comparable success. Syn-
thetic standards in solid forms can be prepared for use in both mass and X-ray
spectrometry.
2.3.4.2 Interlaboratory Comparisons—
The constant desire and need for upgrading the results of determinations
of metals at trace levels has produced rapidly improving modifications of exist-
ing preparation techniques and analytical methods. These improvements not only
provide increased method sensitivities, but an awareness of the pitfalls of
sample contamination during its preparation for analysis. One of the important
activities in establishing the validity as well as the problem areas of an ana-
lytical method is interlaboratory comparison. Such cooperative studies provide
useful information on sample preparation techniques as well as providing direct
2.32
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comparisons of the methods in relation to their applicability and the validity of
results obtained. The results of most round robin comparisons have pointed out
the difficulties of and the need for better approaches to trace metal analysis.
The analysis of lead at trace concentrations, particularly in biological speci-
mens, is no exception. Fortunately, more awareness of the problems associated
with microanalytical techniques is being shown today. The results of past inter-
laboratory comparisons for a variety of samples containing lead at low concentra-
tions are reported in the following paragraphs.
2.3.3.2.1 Biological samples—A number of interlaboratory programs have been
conducted on the analysis of blood and urine for lead. Round robin analyses of
blood samples have been shown to produce varied results (Keppler, et al. , 1970).
In one interlaboratory effort to compare blood analyses involving over 60 lab-
oratories nearly one-half reported unacceptable data. Each laboratory used its
preferred laboratory method and seven different methods were represented in this
study. Not unexpectedly, it was reported that the laboratories were better able
to determine the relative differences between samples than accurately measure
the actual quantities present. No one method was totally acceptable. The poor
results were evidently caused by a number of reasons; the stipulation of which
can only be speculative.
In another comparison seven laboratories were asked to analyze one blood
sample of known lead content (Donovan, et al., 1971). The lead was double ex-
tracted. In most cases, the dithizone method of analysis was used. The dispen-
sing laboratory analyzed the pooled stock eleven times during a 3-month period
to assure its stability. The results of the laboratories ranged from 10 to 150
micrograms per 100 grams of blood; the mean value obtained by the referee lab-
oratory was 155 micrograms. Only 3 laboratories were within 3 sigma of the
mean value obtained by the referee laboratory. There was no correlation between
previous laboratory experience in blood lead analysis with the reliability of
results. In the same study, 20 laboratories took part in the analysis of one
urine sample for lead; only three reported results which fell within 3 sigma
of the mean value reported by the referee laboratory.
Twenty-two laboratories analyzed one aqueous, spiked solution of lead and
three different stabilized blood samples of unknown lead content (Berlin, et al.,
1973). The majority of the participants, after the extractive procedures, used
either AAS or the standard dithizone color method. On the spiked sample, 70
percent of the laboratories were within 10 percent of the added amount of lead.
The results of the blood samples, however, showed a large range in each case
with the greatest disparity being evident for the samples containing the lowest
amounts of lead. It was suggested that contamination could occur in any phase
of the procedure and was the cause of the spread obtained. As a result of that
study, it was deduced that these procedures were too imprecise to measure small
lead uptakes.
2.33
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Three experienced laboratories engaged in an analytical comparison of lead
in blood samples in 1973, and again in 1974 (Browne, et al., 1974). Two labor-
atories used MS and one, anodic stripping. At the 95 percent confidence
level, the mean difference between any two laboratories showing the greatest
variation was plus or minus 29 micrograms per 100 grams in 1973 and plus or minus
44 micrograms per 100 grams in 1974. In both years, one out of three laboratories
(not the same one) reported unacceptable data.
An extensive European, 66-laboratory program for the analysis of lead in
blood and urine was undertaken (Lauwerys, et al., 1975). The program was de-
signed to evaluate experience, analytical method and the precision of analysis.
Extreme care was taken in sampling, homogenizing and stabilizing the pooled
samples. The methods used for the lead analyses were primarily AAS (flame and
nonflame) and colorimetric dithizone. Samples consisted of 3 blood, 2 urine and
2 aqueous, spiked samples and were run in triplicate. The overall range of re-
ported lead contents varied as much as 2 orders of magnitude, with inter- and
intralaboratory coefficients of variation of 50 and 10 percent, respectively.
Experience and method of analysis did not appear to be a factor in the variation
of results. The discrepancies were attributed to the systematic errors peculiar
to each lab which may have arisen in their pretreatment, standardization, or
analysis techniques.
Twenty-six laboratories reported on the analysis of six samples of urine
containing various amounts of ALA, using three different techniques (Berlin,
et al., 1974). A considerable range of ALA levels was reported on the urine
samples taken from an unexposed subject; however, a better correlation was ob-
served for samples containing higher amounts of ALA. The conclusion was that
these procedures were not sufficiently precise to be relied upon in the deter-
mination of small differences in ALA.
The ALAD content in blood was analyzed in the cooperative effort of nine
laboratories (Berlin, et al., 1973). Using variations of the classical method
of Bonsignore (1965), reasonable agreements were obtained in the ratios of
enzymatic activities found in two blood samples. Standards were not prepared
for concentration estimates.
The difficulties and discrepancies in the analysis of lead in blood, as
indicated by numerous interlaboratory comparison studies, are such as to suggest
that (1) much more effort is needed to resolve these analytical problems; and
(2) doubts are introduced into the validity of past analytical data upon which
rests the understanding of the relationship between blood and lead.
While the above perhaps is not as disruptive as the discovery of the im-
portance of alkyl mercury compounds in understanding tod interpreting the environ-
mental effects of mercury, it still points up a need for further research on the
preparation and analysis of blood for trace levels of lead.
2.3.3.2.2 Foods—The lead content of four general food types was determined
in a collaborative study involving eight laboratories. The study included
2.3U
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specific procedures of chemical treatment and the proposed AOAC atomic absorption
analytical method (Hoover, et al., 1969; Hoover, 1972). The coefficient of vari-
ation was no greater than 10 percent and much less in most cases. General indi-
cations are that this overall procedure is reliable and can be used for the deter-
mination of lead in foodstuffs. Lead is generally present in foods at levels
below 1 ppm (see Section 8.3.1).
Eleven laboratories engaged in a round robin analysis of lead in evaporated
milk (Fiorini, et al., 1973). The stipulated overall analytical procedure in-
cluded dry ashing, chelation and extraction and analysis by either AAS or anodic
stripping. Lead was found to be present in evaporated milk at the fractional
ppm level. The coefficients of variation of the results at levels of 0.06 and
0.22 ppm were 43 and 4 percent for AAS and 28 and 6 percent for anodic stripping,
respectively. The AAS method was chosen as the official first action by the AOAC
because of the better agreement among the laboratories using this method.
Lead in fish was the subject of an effort of 19 laboratores (Gajan and
Larry, 1972). The fish, generally containing lead at the less than 1 ppm level,
were dry ashed at 500 C and dissolved in HC1. Lead was determined by AAS or
polarography. Preliminary acquaintance with the procedural steps was achieved
by attaining 90 percent lead recoveries on spiked fish samples. The results of
this study indicate that the recoveries as measured by the two analytical methods
were unusually efficient. The coefficient of variation for the polarographic and
AAS results were reported to be about 8 and 13 percent, respectively. The polar-
ographic method was chosen as the official first action by the AOAC because of
the lower blanks obtained; however, either method can be used to check the other.
Sixteen laboratories took part in a cooperative effort to determine lead in
apples at the less than 1 ppm level (Markus, 1974). The recoveries were quanti-
tative within experimental error and the coefficient of variation for the between-
laboratory comparisons was less than 5 percent after certain procedural changes
were made to lower the high blanks obtained in an initial study.
2.3.3.2.3 Environmental samples—The analysis of lead in seawater was performed
by seven laboratores (Patterson, 1974). Although the methods used for these
analyses (atomic absorption spectroscopy and anodic stripping voltammetry) were
subject to accuracy difficulties, efforts are being made to improve the use of
these methods in regard to reducing blanks and increasing the amount of lead
available for analysis. The deep water lead content as indicated by isotope
dilution mass spectrometry measurement may have been in the low nanogram per
kilogram of water range. This value disputes earlier investigators who reported
this level to be in the microgram range. The previously high lead results for
seawater were attributed to inadequate care in sampling and storage.
In another interlaboratory comparison of the analysis of ambient air for
lead (U. S. Department of Health, Education and Welfare, 1965) using the standard
dithizone method, a 30 percent difference in results from various laboratories
2.35
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for comparatively high concentrations of lead.
2.3.3.2.3 Fuels and emission products—Attempts were made to select the optimum
analytical method for the multielement analyses of fuels and associated by pro-
ducts (von Lehmden, et al., 1974). Nine laboratories were asked to analyze as
many as 28 elements in coal, fly ash, fuel oil and gasoline. Lead was one of the
elements to be analyzed. The methods used for these analyses included NAA, AAS,
SSMS, OES, ASV and XRF. The wide range of lead content (at the ppm level) re-
ported by the various laboratories indicated that the use of different sample
treatments and analytical methods can produce errors in the results. Reference
materials are needed for determining recovery efficiencies. It was also deter-
mned that variations for some elements in certain samples was due largely to
sample heterogenity. The results of thes<: types of studies clearly emphasize the
need for reference materials of an environmental nature. Without such materials,
it will continue to be difficult to pinpoint sources of error for the various
analysis methods and techniques.
2.36
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-------
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-------
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2.U5
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2.46
-------
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2.1*7
-------
3.0 EFFECTS ON MICROORGANISMS
3.1 SUMMARY
Evidence was presented that indicates that bacteria in anaerobic lake
sediments or incubated aquarium water can convert organic lead compounds into
volatile lead. The chemical mechanism in the formation of tetramethyllead
from trimethyllead acetate or lead acetate was not determined.
Inorganic lead was absorbed from culture media by bacteria and was found
to be associated with their cell membranes. The lipids associated with bac-
terial cell membranes appeared to play a role in the nucleation of lead that
resulted in lead inclusion bodies.
Inorganic lead (as lead salts or free ions) can inhibit bacterial growth,
cell viability, and enzyme activities, and some phases of lipid biosynthesis.
3.2 TRANSFORMATIONS AND METABOLISM
Only the bacteria will be discussed in this chapter. No references on
lead and viruses were found in the sources searched. For discussions of other
organisms sometimes considered as microorganisms, see the following sections:
algae and fungi (Section 4.2); zooplankton (Section 5.2); phytoplankton (Section
4.2) and protozoa (Section 5.2).
3.2.1 Biotransformations
Wong, et al., (1975) and Schmidt and Huber (1976) present evidence that
microorganisms (bacteria) convert organic lead compounds into volatile lead
(Table 3.1). Biologically active lake sediments and seeded aquarium waters
yielded tetramethyllead from trimethyllead acetate (Wong, et al., 1975) and
lead acetate (Schmidt and Huber, 1976), respectively. Pure cultures of
Pseudomonas, Alcaligenes, Acinetobacter, Flavobacterium, or Aeromonas, in
lake water or nutrient medium with or without sediment (Wong, et al., 1975)
and light also produced tetramethyllead from trimethyllead acetate. None of
the above biological seeds, however, had definite effects on the production
of jtetramethyllead from inorganic lead (Table 3.1). The mechanisms by which
Pb is converted to tetramethyllead through microbiological activities still
have to be investigated. Doubt has been cast on the significance of microbio-
logical conversion of specific organic lead compounds to tetramethyllead be-
cause of the failure of bacteria to convert inorganic lead compounds (Table
3.1).
Jarvie, et al., (1975) suggest that a possible chemical mechanism for the
formation of tetramethyllead from trimethyllead acetate in active, anaerobic
sediment systems is the intermediate formation of trimethyllead sulfide
3.1
-------
TABLE 3.1 MICROBIAL METHYLATION OF LEAD COMPOUNDS
2+ Incubation
Pb Salt Pb Cone., Microbial Time, Volatile Me4Pb
Added yg/ml System0 Weeks Produced, yg
Pb(N03)2
PbCl2
Pb(OH)2
Pb(CN)2
Pb02
PbBr2
C16H32°2-Pb
Me3PbOAcb
Pb(OAc)2
5
5
5
5
5
5
5
10
1
Lake sediment
Lake sediment
Lake sediment
Lake sediment
Lake sediment
Lake sediment
Lake sediment
Lake sediment
Incubated
aquarium
water
2
2
2
2
2
2
2
1;2;3;4 124;642d
550;256
1;2 106;103e
Reference
Wong et al,
(1975)
Wong et al,
(1975)
Wong et al,
(1975)
Wong et al,
(1975)
Wong et al,
(1975)
Wong et al,
(1975)
Wong et al,
(1975)
Wong et al,
(1975)
Schmidt and
Huber
(1976)
a Adapted from Wong et al, (1975) and
Trimethyllead acetate.
Apparently pure
Flavobacterium,
cultures Pseudomonas
Schmidt and Huber (1976).
, Acaligenes, Acinetobacter,
or Aeromonas were also tested with each Pb salt
with same
results reported with the exception of incubated aquarium water.
Reported as tetramethyl lead (Me^Pb) produced at 1 to 4 weeks, respectively.
Maximum amounts of volatile Pb produced; calculated as equivalent to
Me.Pb at 1 and 2 weeks respectively.
3.2
-------
followed by decomposition to give tetramethyllead. In anaerobic conditions,
this mechanism seems to be dominant in the formation of tetraethyllead from
triethyllead chloride. The authors envisage that trialkyllead salts com-
pete with inorganic sulfides to obtain the necessary sulfur. However, Schmidt
and Huber (1976) point out the probability that lead sulfide is precipitated
out of solution and that not enough lead may be in solution to allow appreci-
able alkylation to tetramethyllead.
3.2.2 Uptake and Absorption
Micrococcus luteus and Azotobacter sp. are highly capable of absorbing
substantial quantities of inorganic lead (Tornabene and Edwards, 1972).
M._ luteus and Azotobacter sp. were found to concentrate 490 and 310 milli-
grams of lead per gram of whole cells (dry-weight basis), respectively, from
culture media containing 2.5 mg PbBr^/ml. The cellular lead was largely as-
sociated with the cell wall plus membranes with very little associated with
the cytoplasmic fractions. The residual lead in the cellular membranes of
Micrococcus and Azotobacter accounted for 89.8 and 61.5 percent of the total
cellular lead, respectively. When Tornabene and Edwards (1973) exposed M.
luteus to lead chloride and lead bromide for 20 consecutive days, the greatest
portion of the cellularly-assimilated lead remained associated with the cell
membranes.
Tornabene and Peterson (1975) found that individual lipids in the cellular
membranes of bacteria, especially M^ luteus, do not provide specific stable
binding sites for lead. However, natural membrane lipid mixtures seem to have
a role in the nucleation of lead (i.e., the formation of lead inclusion bodies)
and consequently providing a possible vehicle for the transport of lead. Micro-
scopic examinations of control and lead-treated M. luteus cells supported the
in vitro studies by revealing electron dense inclusion bodies in membrane frag-
ments in only the lead-treated cells (Peterson, et al., 1975).
No further references to lead uptake by bacteria were found in the sources
searched.
3.3 EFFECTS
McConn, et al., (1967) have shown that the Bacillus subtilis neutral pro-
tease (bound to a zinc atom) is inhibited by an excess of Hg , Cd , Pb^ , and
Ni . The^zinc^in the native enzyme is readily exchanged with Hg , Cd ,
Pb , and Zn to form active compounds as demonstrated by their ability to
hydrolyze the synthetic substrate hippuryl L-leucinamide.
In experiments to qualitatively test the possible inhibitory effects of
heavy metals on a glutaminase isolated from Escherichia coli, Hartman (1968)
incubated metal ions with the enzyme for 5 minutes at 25 degrees prior to add-
ing glut amine. Glutaminase was inhibited 57 percent by one^(l) millimole
Pb (as lead acetate) and 100 percent by 0.1 millimole Hg (as mercuric ni-
trate). Cd (as cadmium acetate) was without effect at one (1) millimole.
-4 14
Lead (10 M lead acetate) inhibits the incorporation of C-leucine
into E. coli t-RNA (Ulmer and Vallee, 1969). The authors indicate that this
3.3
-------
inhibition is due to the interaction of lead with the enzyme aminoacyl syn-
thetase and the hydrolysis of leucyl t-RNA (see Figure 3.1). These experi-
ments suggest that lead might affect protein synthesis both by attacking the
synthesizing enzymes and bringing about the hydrolysis of t-RNA and, pre-
sumably, similar RNA species.
Inorganic lead inhibits the growth of the bacterium Rhodopseudomonas
spheroides, and appears to alter tetrapyrrole synthesis in this species
through a complex metal-ion antagonism involving coproporphyrinogen oxidase
(coprogenase) (see Figures 3.2 to 3.5 and Table 3.2). Through these studies
were derived the basis for the increased urinary coproporphyrin observed in
plumbism (Ulmer and Vallee, 1969).
Devigne (1968b) observed stimulated growth_j?f Sarcina flava in medium
containing relatively high concentrations of Pb . This was accompanied by
an increase in peptone degradation and in a number of biosynthetic reactions
with PbS appearing as the final metabolite. Using a telluric Micrococcus,
similar experimental results were obtained by Devigne (1968a). Growth of wild
and recombination-deficient strains of Bacillus subtilis was equally inhibited
by 0.5 M lead acetate and lead chloride in a rec-assay (method for screening
chemical mutagens) of fifty-six metal compounds. No evidence of mutagenic
activity was found for the lead compounds (Nishioka, 1975).
Sadler and Trudinger (1973), in a study of the inhibition of microorganisms
by heavy metals, concluded that for E. coli the order of decreasing toxicity
is: mercury, cadmium, lead, ferrous iron, copper, zinc.
According to Tornabene and Edwards (1972), lead bromide, lead iodide,
and lead bromochloride in concentrations approaching solubility limits had no
detectable effects on the overall growth rate and cell viability of Azotobacter
sp. and M. luteus. Tornabene and Edwards (1973), however, observed that in
the course of exposing Micrococcus luteus cells to lead (as lead bromide
and lead chloride) for 20 consecutive days, osmotically sensitive cells resulted.
These cells exhibited a loss of carotenoids but without any effect on the
Vitamin K content of the cells. Peterson, et al., (1975) later demonstrated
that M. luteus cells exhibited a sequence of changes in the quantity of total
cellular lipids with essentially no changes from normal cellular yields. The
lipid composition of cells cultivated five to six times was reduced by as much
as fifty percent. Those cells cultivated more than six times had progressively
greater quantities of lipid approaching that found in control cells. Those
cells with reestablished lipid contents showed no further effects from more
prolonged lead exposures. Chromatographic studies of each phase of cultivation
revealed relatively complete lipid compositions. This indicates that where
there were lipid reductions, lead had some inhibitory effect on a biochemical
parameter in the biosynthesis of lipids (Peterson, et al., 1975).
3.U
-------
12
10
CONTROL
/' PREINCUBATION WITH Pb. IO*4M
/
» * ^.•"*
X- \
ASSAY + Pb, IO'4M
8
MINUTES
12
Figure 3.1 Effect of lead on incorporation of -^C-leucine
t-RNA from 15^ coli. Addition of lead to the assay
mixture decreases the r_ate of •'•^C-leucine incorpor-
ation, most likely due to inhibition of the aminoacyl
synthetase. Preincubation of t-RNA with lead at
37 C decreases the extent of amino acid incorporation,
most likely due to hydrolysis of the nucleic acid.
Source: Ulmer and Vallee. Reprinted with permission
from Proceedings 2nd Annual Conference on Trace
Substances in Environmental Health (c) University
of Missouri, 1969.
3.5
-------
o>
o.
o
o» -
E 2
e>
"Medium S" (Lofcelles)
*Mn, 3ppm
Control
Control
Control
Pb
10
Fe. /.M
IOO
Figure 3.2 Effect of lead on growth of Rhodopseudoaonas sphereides.
At an iron concentration of 1 yM, lead markedly inhibits
sesianaerobic, light-grown cultures. This inhibition is
largely overcome by higher iron concentrations.
Source: Ulmer and Vallee. Reprinted with permission
from Proceedings 2nd Annual Conference on Trace Substances
in Environmental Health, (c) University of Missouri, 1969.
3.6
-------
0.3
Mn, ppm
30
Figure 3.3 Metal-ton antagonism in Rhodopseudomonas spheroides.
At low Fe concentrations (1 uM/liter) Mn, 0.03 ppm,
induces marked coproporphyrin excretion. In the
presence of 10 or 100 vM/liter Fe, increased copro-
porphyrin appears only at much greater Mn concentra-
tions. Source: Dlmer and Vallee. Reprinted with
permission from Proceedings 2nd Annual Conference
on Trace Substances in Environmental Health, (c)
University of Missouri, 1969.
3.7
-------
10
o
o» 8
E
01
o:
Q.
o:
o
a.
Q_
O
o
Fe,IO/xM ^ f~
Pb,lO'4M */ //\
1 ' i Fe>IOfiM
Fe.lOO/xM / »
+ Pb, IO'4M I
I
.03
0.3
Mn, ppm
Fe,IOO/iM
30
Figure 3.4 Synergistic antagonism of Fe by Mn and Pb in
Rhodopseudomonas spheroides. In the presence
of Pb, lesser concentrations of Mn induce
coproporphyrin excretion. Source: Ulmer and
Vallee. Reprinted with permission from Proceedings
Annual Conference on Trace Substances in Environ-
mental Health, (c) University of Missouri, 1969.
3.8
-------
GUCINE *
SUCCIXVL-CoA
> «-*HIHOLEVIlLISIC *.-|
»c
PROTOPORPHYRINOGEN < "Coprogentse", COPROPORPIIYR1NOCEN Ml <-
•H«C02
PROTOPORPHYRIN
»H
It
COPROPORPMYRIN 111 * II
FarrocheUtme
SS
HEME
I
PHRPIIOBI LIXOGEN
IIROPORPHVRI.SOCEN
• Nil,
UROPORPIIYRIN
•11
-* Mg I'ROTOPORPIIYRI.V
BACTERIOCIILCROPMYLL
Figure 3.5 Pathway of tetrapyrrole synthesis in Rhodopseudoinonas
spheroides. In the presence of Mh and Pb, copropor-
phyrin III is markedly increased while both principal
end-products, heme and bacteriochlorophyll, are
decreased (arrows). Source: Ulmer and Vallee.
Reprinted with permission from Proceedings 2nd Annual
Conference on Trace Substances in Environmental Health.
(c) University of Missouri, 1969.
3.9
-------
Table 3.2 EFFECT OF Pb AND Mn ON TETRAPYRROLE SYNTHESIS IN RHODOPSEUDOMONAS SPHEROIDES*
H
O
Metals Addedb
Fe Mn Pb
1x10"^ 2xlO~5M IxlO'T*
1
1 - +
1 + -
1 + +
10
10 - +
10 + -
10 + +
A
Coproporphyrin ,
yg/mgc
1.2
1.7
32.4
36.8
1.3
1.5
0.6
7.3
B
Bacteriochlorophyll ,
yg/mgc
5.8
3.4
1.4
1.4
7.6
10.8
3.3
2.2
C
Heme,
myM/mgc
0.8
1.0
0.5
0.5
1.0
0.9
1.0
0.7
D
Protoporphyrin ,
yg/mgc
0.8
1.1
<1.0
<1.0
1.6
1.4
0.3
0.1
a
Source: Ulmer and Vallee. Reprinted with permission from Proceedings 2nd Annual Conference on
Trace Substances in Environmental Health. (C) University of Missouri, 1969.
Lascelles Medium S with metals as indicated.
Tetrapyrrole concentration per mg cell protein.
-------
3.4 REFERENCES
Devigne, J.-P. 1968a. Precipitation du Sulfure de Plomb par un Micrococcus
Tellurique, Comp. Rend. Hebd. Seanc. Acad. Sci., Ser. D, Sci. Natil,
267(10:935-951.
Devigne, J.-P. 1968b. Une Bacterie Saturnophile, Sarcina flava BARY, 1887
Arch. Inst. Pasteru Trunis, 45:341-357.
Hartman, S. C. 1968. Glutaminase of Escherichia coli. I. Purification and
General Catalytic Properties, J. Biol. Chem., 243(5):853-863.
Jarvie, A. W. P., R. N. Markall and H. R. Potter. 1975. Chemical Alkylation
of Lead, Nature, 255(5505):217-218.
McConn, J. D., D. Tsuru and K. T. Yasunobu. 1967. Bacillus Subtilis Neutral
Protease. II. Exchange Properties of Zinc and Preparation of Some Metal
Derivatives. Arch. Biochem. Biophys., 120(3):479-486.
Nishioka, H. 1975. Mutagenic Activities of Metal Compounds in Bacteria.
Mut. Res., 31(3):185-189.
Peterson, S. L., L. G. Bennett and T. G. Tornabene. 1975. Effects of Lead
on the Lead Composition of Micrococcus luters Cells. Appl. Microbiol.,
29(5):669-679.
Sadler, W. R. and P. A. Trudinger. 1967. The Inhibition of Microorganisms
by Heavy Metals. Miner. Depos., 2(3):158-168.
Schmidt, U. and F. Huber. 1976. Methylation of Organolead and Lead (II)
Compounds to (CEL), Pb by Microorganisms. Nature, 259, 157-158.
Tornabene, T. G. and H. W. Edwards. 1972. Microbial Uptake of Lead.
Science, 176(4041):1334-1335.
Tornabene, T. G. and H. W. Edwards. 1973. Effects of Lead on Bacterial
Membranes, in: Trace Substances in Environmental Health — VII, Proc.
7th Ann. Conf. on Trace Substances in Environ. Health, University of
Missouri, Columbia, Mo., June 12-14, 1973. D. D. Hemphill (ed.), pp
263-266.
Tornabene, T. G. and S. L. Peterson. 1975. Interaction of Lead and Bacterial
Lipids. Appl. Microbiol., 29(5):680-684.
Ulmer, D. D. and B. L. Vallee. 1969. Effects of Lead on Biochemical Systems,
in: Trace Substances in Environmental Health - II, Proc. 2nd Ann. Conf.
on Trace Substances in Environ. Health, University of Missouri, Columbia,
Mo., July 16-18, 1968, pp 7-27.
Wong, P. T. S., Y. K. Chau and P. Luxon. 1975. Methylation of Lead in the
Environment, Nature, 254(5489):263-264.
3.11
-------
4.0 EFFECTS ON PLANTS
4.1 SUMMARY
The presence of lead in plants has received considerable attention
because of the potential hazard to animal and human health. Several sources
including soil, water, and air give rise to lead in plants.
Ubiquitous concentrations of lead are found in most soils but their
content varies according to the levels of lead in the parent material and to
various physical factors such as the weathering rate. Higher lead levels
in soil may be found near lead mines or industries using lead, where heavy-
metal-containing sewage sludge has been spread, and adjacent to well-used
roadways. Most of the lead compounds are deposited within a few meters of
the road, with contamination being restricted to the topsoil.
Depending on the type of plant, there are generally two pathways avail-
able for lead to enter: uptake by the roots and uptake by the foliage.
Lead is absorbed by plants from the soil, but generally not to any great
extent. There are many factors that determine lead availability and associ-
ation with plants, these include soil concentrations, pH, cation exchange
capacity, presence of other nutrients, natural chelating agents, and the
individuality of the plant species involved.
Lead in aerosol form can be absorbed by plant foliage and lead can
accumulate in particulate form on the foliage from aerial fallout. Critical
evidence on foliar absorption of lead is difficult to obtain because of an
inability to experimentally differentiate between lead deposited on, and
lead absorbed by, the foliar tissue. Deposition of lead on leaves is known
to be controlled by characteristics of the aerosol (size, chemical composi-
tion, cloud density), the leaf surface (roughness, pubescence, moisture),
and the environment in which the plant lives (relative humidity, wind speed).
The extent of lead accumulation in plants from particulate aerosols is now
thought to be minimal.
Lead concentrations within plant tissues are influenced by the factors
listed above as well as by lead pollution intensity, proximity to roadways
and lead industries, wind direction, distribution within plant organs,
cellular localization, and the amount of lead removed by washing with water.
Lead inhibits growth, reduces photosynthesis, and interferes with cell
division and regenerative processes in algae. Studies show considerable
similarity of lead effect on ^n vitro enzymes when care is taken to define
the medium parameters. No algal species have been reported to have any
built-up tolerance to lead. In contrast, lichens, some fungi, and bryophytes
U.I
-------
seem to have a pronounced, genetically-determined tolerance to lead. Some
lead chelates and organolead compounds, however, are fungicidal. Lichens
and bryophytes are capable of concentrating lead at levels that are much
higher than environmental levels without any effects. In fact, mosses and
Spanish moss (a vascular plant) are being used as bioindicators in regional
and local atmospheric lead surveys.
Some of the effects of lead on vascular plants include: (1) inhibition
of photosynthesis, transportation and water absorption; (2) reduction of
chlorophyll and ATP synthesis; (3) inhibition of enzymes unique to the
photosynthetic and respiratory processes; (4) reduction of mitosis and
subsequent growth; and (5) acceleration of abscission or defoliation and
pigmentation. Only one of the vascular plants, Agrostis tenuis (Rhode
Island bent) seems to have the chemical ability to precipitate lead from
cytoplasmic solution and thus render it inactive. The effects of lead on
vascular plants appear at this stage to be minimal. Probably the most
important adverse effects of lead from vascular plants are economic and may
result from ingestion of topical plant lead by grazing animals.
Many metabolic processes can potentially be affected by lead since
they are controlled or associated with enzymes having secondary or tertiary
structures which are potentially capable Of binding lead.
Environmentally, it would seem that a plant with sufficient nutrients,
moisture, temperature and light would be unlikely to be affected by lead
concentrations of less than 100 ppm in the plant tissue on a dry weight
basis.
4.2 NONVASCULAR PLANTS
4.2.1 Algae
4.2.1.1 Metabolism: Uptake, Absorption, and Residues—
Very little is known of the background lead concentrations in algae.
Most algal species probably have the capacity for concentration or uptake of
lead to levels above that in the water medium. For example, the concentra-
tion factor (ratio of an element in an organism to the concentration avail-
able in the medium.under equilibrium conditions) for lead by marine phyto-
plankton is 4 x 10 (National Academy of Sciences, 1971).
Day (1963) indicates that aquatic algae such as Spirogyra have the
capacity to remove suprisingly large quantities of elements from their en-
vironment. Spirogyra, growing in mine water containing a total of 16 ppm
heavy metals, contained 2,900 ppm zinc, 6,600 ppm lead, and 920 ppm copper
(on a dry weight basis). Gale, et al., (1973) found 8,035 ppm lead associ-
ated with Cladophora taken 0.31 kilometer below a tailings dam in Missouri's
New Lead Belt. There was a definite inverse linear relationship between
lead concentration on or in the algae and distance from the source of con-
tamination. Laboratory studies confirm that Cladophora happens to be one of
the forms which has been found to attract and bind relatively large amounts
U.2
-------
of lead. The researchers indicate that the data are suggestive of rapid
ion-exchange processes which bind the lead to the organic material of the
algal cells.
4.2.1.2 Effects—
The usual procedure in assessment of toxic and other effects of heavy
metals on algae is to observe the effect of the material on the test organ-
ism over a range of concentrations. For lead care must be taken to ensure
solubility, since lead is easily precipitated from solution by sulfates,
phosphates, chlorides, carbonates, etc. Even in demineralized water there
are enough ions present to limit solubility of the lead ion.
Although there is a large amount of literature on the toxicity of lead
to animals, and the literature is growing on toxicity to vascular plants,
few studies have been conducted on the effects of lead on algae.
Most of the studies on effects have involved exposure to various con-
centrations of lead with observations of resultant effects. Rice, et al.,
(1973) reported that lead at 0.1 parts per million had no effect on the
marine phytoplankton Phaeodactylum tricornutum, Chaetoceros galvestonensis,
and Cyclotella nana, but did inhibit growth in the freshwater green alga
Chlorella. Studies by Hannan and Patouillet (1972) are supportive: lead at
0.1 ppm and 1.0 ppm had no significant effect upon growth of Phaeodactylum,
but lead at 0.1 ppm did inhibit temporarily growth by Chlorella. Banks
(1972) exposed Chlorella pyrenoidosa to concentrations of 1.0 ppm and 10.0
ppm lead as lead acetate. Banks reported that 1.0 ppm of lead in modified
Bristol's solution did not affect cell number or content of chlorophylls ji
and b_ during 15 days of culturing; however, 1.0 ppm lead in demineralized
•water decreased cell number by approximately 10 percent. At 10 ppm lead
the number of cells was reduced to 52 percent of the control after 5 days.
Although autospore formation was not impaired at this concentration, chloro-
phyll content was reduced after 15 days of culturing such that chlorophyll
a., chlorophyll b_ and total chlorophyll were 46, 76, and 53 percent of the
control, respectively. The presence of^demineralized water does support
the concept that the association of Pb with other ions in the growth
medium and in the cells tends to complex lead and render it inactive meta-
bolically.
Other investigations have reported that lead in solution inhibits algal
growth. Monahan (1973) found that lead, as lead chloride, at concentrations
which ranged from 50 through 500 ppm reduced cell density in cultures of the
green alga Hormotila blennista under both light and dark environments.
Whitton (1970) investigated a variety of natural algal populations to deter-
mine if any had built up a tolerance to heavy metal - zinc, copper, lead -
pollution. No tolerance to elevated lead concentrations was found. The
fixation of labelled CO- was used by Malanchuk and Gruendling (1973) to
measure the toxicity of Pb(N03)2 at 10, 20, and 30 ppm Pb to Anabaena sp.,
Chlamydomonas reinhardti, Cosmarium botrytis, Navicula pelliculosa, and
Ochromonas malhamensis, all freshwater organisms. The concentration of lead
which caused a 50 percent reduction of CO- fixation as compared to the
U.3
-------
control defined the ED_n (median effective dose). The ED _'s reported by
Malanchuk and Gruendling (1973) were 15 to 18 ppm Pb for Anabaena, Chlamydo-
monas, and Navicula; 5 ppm for Cosmarium; an ED_n for Ochromonas was not
obtained. Lead nitrate at 4.1 ppm Pb produced no deleterious effects on
the photosynthetic rate in giant kelp, Macrocystis pyrifera, during a 4-day
exposure (North and Clendenning, 1958,cited in McKee and Wolf, 1963).
Light-induced oxygen evolution in Chlamydomonas reinhardti was inhibited
by lead ions. This photosynthetic phase was found to be ten times as sensi-
tive to cadmium and lead ions as it is to copper and mercury ions. In
contrast, the chlorophycean Dunaliella bioculata exhibited decreasing sensi-
tivity in the order: mercury, lead, cadmium (Overnell, 1975).
Hessler (1974 and 1975) has studied the effects of lethal and sub-
lethal concentrations of lead chloride on the marine unicellular green
flagellate alga, Platymonas subcordiformis. Lead concentrations between
2.5 and 10 ppm were sub lethal to P^. subcordi f ormis and delayed cell division
and daughter cell separation. Lead at 60 ppm was lethal to the test organ-
ism. Hessler (1974) noted several abnormalities due to lead treatment of
this alga: (1) loss and alteration of flagella, and (2) impairment of
motility. In subsequent research, Hessler (1975) reported that the incid-
ence of mutant types above spontaneous frequency in £. subcordif ormis was
not raised upon exposure of the alga to sublethal and lethal concentrations
of lead.
Lead interferes with cap formation and regeneration in the unicellular
marine alga, Acetabularia mediterranea. Bonotto and Kirchmann (1973)
found that (1) cap formation, which is necessary for reproduction in
Acetabularia, in nucleate as well as in anucleate cells is rapidly (4 days)
inhibited by 1 to 10 ppm concentration of Pb (N0.)«, and (2) cap growth,
regeneration of nucleate basal fragments, and growth of regenerating stalks
are less sensitive to lead treatment than cap initiation which is the morpho-
genic process most sensitive to lead exposure.
Momentary bubbling of biologically-generated tetramethyllead (TML)
into a culture of Scenedesmus quadricauda decreased primary productivity and
cell growth by 85 and 32 percent, respectively, as compared to controls.
Cells exposed to TML also tended to clump. Similar results were obtained
with Ankistrodesmus falcatus (Wong, et al., 1975). Of the organometallic
compounds used in algistatic tests, the triphenyllead and tributyllead
adjuncts appeared to confer the greatest toxicity to Enteromorpha sp.
Hexaphenyldilead also appeared to be an active algistat (Skinner, 1974).
4.2.2 Lichens, Fungi, and Bryophytes
4.2.2.1 Metabolism: Uptake, Absorption, and Residues—
Lichens have a marked capacity for inorganic cation uptake. In fact,
some species, e.g., Cladonia spp. and Stereocaulon spp., appear as consistent
components of mine communities. Puckett, et al., (1973) studied metal-ion
uptake by lichens and found that iron, copper, and lead accumulations
accounted for 76 to 87 percent of the total metal uptake. 4,144 to 4,310 ppm
U.U
-------
Pb was absorbed by Umbilicaria muhlenbergii from lead nitrate solutions
containing 16,575 ppm Pb Cladonia mitis and IJ. muhlenbergii. collected near
a smelter, were found to contain 414 to 497, and 559 to 642 ppm Pb ,
respectively, as determined by total wet oxidation. Holl and Hampp (1975)
cite the use of the lichen Parmelia physodes as a bioindicator for the in-
tensity of lead emission. At a distance of 1,000 meters from the highway
the thalli contained 35 ppm (unwashed) and 19 ppm (washed) lead.
Experimental studies of lead uptake in Cladonia rangiformis revealed
that all the lead, whether taken up naturally or artificially, is bound in
an exchangeable form to insoluble anionic sites within the cell wall. The
association of lead was shown to take place in the presence of living cells
and is therefore, considered to be a purely physical process. Samples of
£. rangiformis collected in a relatively lead-free area versus a disused
lead mining complex reflected the composition of the underlying soil. In
the lead mining complex, lichens growing in soil containing 27,500 ppm
lead had a lead concentration of 1,100 ppm. Those growing in the relatively
lead-free area with a soil lead content of 20 ppm had a lead concentration
of 25 ppm (Brown and Slingsby, 1972).
Only one reference to the uptake of lead by fungi has been found.
Washed mycelia of Aspergillus clavatus cultured at 24 C in 1 percent glucose,
0.5 percent peptone, 0.5 percent yeast extract, and 1 gram per liter lead
oxide concentrated 1,080 ppm lead after 35 days of exposure. The lead con-
tent of the culture medium was 32 ppm giving a resultant concentration ratio
(mycelium:medium) of 34 (Siegel, et al., 1973).
Numerous species of mosses have been recorded as members of communities
on metal-contaminated soils. Liverworts are much rarer on contaminated soils.
Bryophytes (mosses and liverworts) growing in such areas or in relatively
contamination-free areas have been found to have a greater lead content than
the substrates on which they grow (see Table 4.1). Enrichment of upper
soil horizons has been attributed to the action of these plants which con-
centrate elements and then, by decomposition, release them into the surface
soil (Antonovics, et al., 1971; Shacklette, 1965a,b).
Mosses accumulate nutrients, including heavy metals, through their
aerial regions. This association may arise from aerial particles or as
ions from dilute solutions. These properties have allowed the use of cer-
tain mosses in monitoring short-term metal accumulation from aerosol and
precipitation sources (Ratcliffe, 1975). Ruhling and Tyler (1970) showed
that the woodland moss Hylocomium splendens absorbed heavy metal ions from
dilute solutions in the order Cu > Pb > Ni > Cb > Zn > Mn. These observa-
tions were made over a wide range of concentrations and seem to be independent
of other heavy metals or essential nutrients. Rhytiediadelphus squarrosus
incorporated lead into the nuclei of cells of plants exposed to le,a^ acetate
solutions. Studies cited by Skaar, et al., (1973) revealed that Pb was
incorporated into both nuclear and mitochondrial fractions. Extracellular
Pb binding has also been observed by Brown and Bates (1972) in Grimmia
doniana by a passive physical process. Ratcliffe (1975) has presented
evidence that a number of suspended moss samples including Dicranella
-------
Table 4.1 LEAD CONTENT OF BRYOPHTYES AND THEIR
SUBSTRATES*
Bryophyte Species
Anomodon rostratus
A. rostratus
Atrichum angustatum
Batramla pomiformis
Bazzania trilobata
Brachythecium rutabulum
B. salebrosum
Bryum capillare
Cirriphyllum boscli
Climacium americanum
Conocephalum conicum
C . conicum
Dicranella heteromalla
Dicranum scoparium
D. scoparium
Entondon seductrix
Grimmia apocarpa
G. laevigata
Hedwigia ciliata
H. ciliata
H. ciliata
H. ciliata
H. cilita
Hypnum curvifolium
Leucobryum glaucum
Har chant ia polymorpha
Ash, Percent
9.5
13.5
9.7
26.5
14.0
11.8
20.5
10.3
11.7
11.3
13.0
32.0
7.0
13.8
12. D
13.5
11.3
41.0
7.3
16.3
5.7
8.8
10.3
8.7
1.67
59.5
Lead Content
Percent
0.03
0.3
0.1
0.015
0.03
0.05
0.07
0.03
0.05
0.03
0.05
0.01
0.07
0.07
2.0
0.07
0.2
0.03
0.2
0.15
0.15
0.1
0.3
0.07
2.0
0.0025
Ash Lead Content of .
Substrate, Percent
0.0025 (soil)
0.006 (limestone)
0.003 (soil)
0.002 (lithosol)
0.002 (soil)
0.003 (soil)
0.015 (soil)
0.005 (felsite
porphyry)
0.001 (lithosol)
0.001 (lithosol)
<0.001 (limestone)
0.0075 (chert)
<0.0025 (soil)
<0.001 (soil)
0.01 (lithosol)
0.015 (quartzose
sandstone)
0.01 (arkosic sand-
st^ne)
0.0015 (granite)
0.01 (arkosic sand-
st jne)
0.0025 (quartzose
sandstone)
0.0015 (granite)
0.015 (quartzose
sandstone)
0.006 (dolomite •
limestone)
0.001 (lithosol)
0.01 (lithosol)
0.0015 (soil)
U.6
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TABLE 4.1 LEAD CONTENT OF BRYOPHYTES AND THEIR
SUBSTRATES3
(Continued)
Bryophyte Species
Mnium affine
M. cuspidatum
Polytrichum commune
P._ juaiperinum
?. juniperinum
P. juniperinum
P. ohioense
Thelia asprella
T.. lescurii
TJiuidium recognitum
Neisia micros toma
W. viridula
Ash, Percent
46.8
8.3
8.0
3.5
8.2
s.:»
8.7
13.3
12. /
10.2
15.2
17.3
Lead Content
Percent
0.002
0.07
0.1
0.02
0.07
0.07
0.1
0.03
0.03
0.05
0.3
0.05
Ash Lead Content of ,
Substrate, Percent
0.0015 (soil)
0.0015 (soil)
0.0015 (rock asphalt)
0.001 (soil)'
0.003 (soil)
0.0025 (soil)
0.0015 (granite)
0.015 (bark of Juniperus
virginiana)
0.003 (lithosol)
0.001 (lithosol)
0.006 (dolomite lime-
stone)
<0.001 (doloiite lime-
stone)
, .
aAdapted from Shacklette (1965b).
K
Dry weight basis.
U.T
-------
heteromalla, Ceratodon purpureus, Sphagnum papillosum, and S^. subsecundum
can be used to monitor atmospheric lead fallout from a battery factory.
As with other mosses, Hypnum cupressiforme var. filiforme rapidly comes
to equilibrium with aerial lead and other heavy metal concentrations. This
species loses lead very slowly (Roberts and Goodman, 1973). Briggs (1972)
found that lead values in Marchantia polymorpha, even at great distances
from roads, were due to contamination. The lead contents corresponded to
the respective traffic intensity and did not significantly correlate with
the soil lead content.
4.2.2.2 Effects—
Lead was determined by Brown and Slingsby (1972) to be almost exclu-
sively ionically-bound within the cell walls of lichens. These authors
believe that under natural conditions, although excessive quantities of this
potentially toxic element have been recorded from the thalli of lichens, lead
is unlikely to have any direct effects on metabolism of the lichen. No
other reference to toxicity of lead to lichens has been found in the sources
searched.
Free lead ions at 269 ppm slightly reduced the accumulation of but did
not suppress spore formation in the fungus Aspergillus niger. Because of
their poor solubility in water, inorganic lead salts in a culture medium are
not toxic to _A. niger. Chelates such as lead thiopicolinanilide or lead
diethyldithiocarbamate have strong fungicidal properties (Zlochevskaya and
Rabotnova, 1966; Zlochevskaya and Rukhadze, 1968). Twenty-three organolead
compounds were screened for fungicidal activity against sixteen fungal
species isolated from paint films. Three of the compounds (tributyllead
2-ethyl hexanoate, tributyllead acetate, and triphenyllead acetate) exhibited
fungicidal activity at 0.01 percent lead in unweathered and leached vinyl
copolymer emulsion paint systems. Tributyllead .acetate (0.05 percent lead)
was fungicidal in a vinyl copolymer paint even after 250 hours of artificial
weathering (Skinner, 1974).
Although fungi have been shown to be consistent, if not abundant,
components of mine soils, there is surprisingly little evidence of tolerant
races among the fungi. A tolerant species of penicillium which withstands
external lead concentrations of 100 times those of nontolerant species has
been found to be associated with a nonnuclear plasmid.
4.3 VASCULAR PLANTS
4.3.1 Noncrop Plants
4.3.1.1 Metabolism: Uptake, Absorption, and Residues—
The amount of lead reported in plant material varies widely and is
dependent on lead levels in the plant's environment. Natural or background
lead concentrations in the ash of several native plant species sampled from
U.8
-------
a variety of geochemical environments have been summarized by Connor and
Shacklette (1975) and are included in Table 4.2.
Lead taken up by aquatic vegetation is believed to be bound primarily
to the surface. Available evidence suggests that lead is bound to anionic
sites on the surface of aquatic plants by the process of cation exchange.
Gale, et al., (1975) found that extensive washing of aquatic vegetation
from the New Lead Belt of Missouri in distilled, tap, or stream water
failed to remove the bound lead. Scirpus americanus has a capacity for con-
centrating lead from its environment such that it is thought to be capable
of serving as a depolluting agent. Eleocharis smallii and Bidens cernua are
possibly capable of doing the same. Scirpus, Eleocharis, and Bidens were
exposed to solutions containing 0.5 to 1.5 ppm lead for 72 hours. In the
1.5-ppm lead environment, the stems and rhizomes of J3. americanus accumulated
54 and 885 ppm, respectively. In the same environment JJ. smallii accumulated
342 ppm in stems and 3,320 ppm in rhizomes. jJ. cernua accumulated 140 and
625 ppm in stems and rhizomes, respectively; the flowers and leaves had 28.3
ppm (Carbonneau and Tremblay, 1972). Analyses of shoots of Spartina alter-
niflora (cordgrass) growing in several salt marshes in Massachusetts revealed
that they contained 5.4 to 23.2 ppm Pb on a dry weight basis. Increased
contamination, either from the proximity to human activity or through the
experimental additions of fertilizer, resulted in greater lead concentra-
tions in the plants (Banus, et al., 1974). Drifmeyer and Odum (1975) studied
the effect of the disposal of heavy-metal-containing dredge-spoil as a source
of heavy metals to salt-marsh biotav The authors found that lead levels in
Phragmites communis (common reed), Spartina alterniflora (salt-marsh cord-
grass) , and j^. patens (saltmeadow hay) were significantly higher in plants
growing on the dredge-spoil sites than in the control areas. Lead accumula-
tion values were as follows for the three plant species: JP. communis, 4.4
plus or minus 5.3 ppm (dredge-spoil) and 0.5 plus or minus 0.6 ppm (natural
marsh); j>. alterniflora, 5.1 plus or minus 1.2 ppm (dredge spoil) and 1.9
plus or minus 0.7 ppm (natural marsh) ; and j>. patens, 9.1 plus or minus 2.9
ppm (dredge-spoil) and 0.8 plus or minus 1.4 ppm (natural marsh).
Spanish moss (Tillandsia usnebides) has been used as an indicator of
atmospheric lead pollution since it is an epiphyte which derives all its
nutrients from the air by means of leaf and stem absorption. Martinez,
et al., (1971) analyzed eight Spanish moss samples from sites near and at
some distance (0.16 to 0.48 kilometer) from heavily-traveled roadways. They
found lead concentrations were greatest in samples taken near highways, with
a maximum of 0.085 percent (850 ppm) in dry samples, whereas those more
distant from highways contained as little as 0.0051 percent (51 ppm).
Shacklette and Connor (1973) confirmed the above findings and noted that the
typical lead concentration is the ash of 123 Spanish moss samples (70 to
50,000 ppm) exceeded the upper limit of the expected 67 percent range (8,800
to 45,000 ppm) in comparison to the lead content of the ash of soil-rooted
plants (1,600 to 400,000 ppm) from the conterminous United States. Greater-
than-average amounts of lead were found in samples from industrial and high-
way locations. The extremely high lead concentrations reflect the fact that
most samples were taken at sites near highways.
U.9
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Table 4.2 NATURAL LEAD LEVELS IN THE ASH OF NATIVE, NON-
CROP U.S. PLANTS3
Sample and Collection Locality
Black cherry, steins; Georgia
Black cherry, leaves; Georgia
Blackgum, stems; Georgia
Blackgum, leaves: Georgia
Buckbush; Missouri
Glaciated prairie
Un glaciated prairie
Cedar glade
Oak-hickory forest
Oak-hickory-pine forest
Cedar; Missouri
Cedar glade
Glaciated prairie
Unglaciated prairie
Cedar glade
Oak-hickory forest
Oak-hickory-pine forest
Hickory, pignut; Kentucky
Hickory, shagbark; Kentucky
Hickory, shagbard; Missouri
Oak-hickory forest
Oak-hickory-pine forest
Maple, red, stems; Georgia
Maple, red, leaves; Georgia
Observed Range,
ppm
30 -
<10 -
<10 -
<10 -
<10 -
70 -
<10 -
10 -
50 -
7C -
100 -
70 -
150 -
30 -
50 -
7f -
50 -
50 -
20 -
100 -
120 -
70 -
80 -
30 -
100 -
<10 -
30 -
<10 -
30 -
1,000
2,000
700
500
1,000
3,000
2,000
1,000
500
1,000
2,000
1,000
1,500
1,500
200
150
100
1,500
200
700
940
500
510
200
300
700
2,000
700
700
Mean, Geometric
ppm Deviation
210
270
33
58
250
480
57
96
200
210
300
260
420
100
86
91
70
120
64
210
260
170
220
100
190
120
230
41
100
2.71
4.64
4.65
2.40
2.88
2.34
2.01
2.56
1.76
1.91
1.85
1.88
1.84
2.06
1.54
1.42
1.26
3.25
2.16
1.61
1.51
1.57
1.65
1.66
1.65
2.59
3.13
2.92
2.21
U.10
-------
Table 4.2 NATURAL LEAD LEVELS IN THE ASH OF NATIVE, NON-
CROP D.S. PLANTS*
(Continued)
Sample and Collection Locality
Oak, black; Kentucky
Oak, post; cedar glade; Missouri
Oak, red; Kentucky
Oak, white; Kentucky
Oak, white; Missouri
Oak-hickory forest
Oak-hickory-pine forest
Oak, willow; floodplain
forest; Missouri
Persimmon, stems; Georgia
ersimmon , leaves ; Georgia
Pine, shortleaf; oak-hickory-
pine forest; Missouri
Sassafras, steins; Georgia
Sassafras, leaves; Georgia
Sumac, winged, stems; Georgia
Sumac, winged, leaves; Georgia
Sumac, smooth; Missouri
Floodplain forest
Glaciated prairie
Unglaclated prairie
Cedar glade
Oak-hickory forest
Oak-hickory-pine forest
Sweet gum, stems; Georgia
Sweetgum, leaves; Georgia
Sweet gum; floodplain forest;
Missouri
Observed Range,
ppm
70
63
30
70
90
10
50
30
50
30
<10
<10
<10
<1C
100
30
<10
30
30
<1C
<10
<10
30
<20
<20
<20
<20
<20
<20
<10
<10
<10
20
20
- 500
- 240
- 700
- 200
- 260
- 700
- 440
- 500
- 1,000
- 500
700
- 1,500
700
- 500
- 1,500
- 700
- 1,000
- 200
- 500
- 1,500
- 700
- 500
- 700
- 200
- 100
- 150
- 150
- 150
- 300
- 700
- 700
- 200
- 300
- 300
Mean,
ppm
150
140
80
120
150
150
180
100
140
120
110
150
24
68
250
210
140
83
95
110
110
67
120
26
32
28
42
30
61
120
110
45
91
65
Geometric
Deviation
1.63
1.46
1.87
1.34
1.52
1.92
1.49
,•
1.85
1.72
1.85
2.90
3.85
4.13
2.59
1.70
2.37
4.91
1.66
2.28
3.91
3.09
2.29
2.25
2.28
1.82
2.11
2.17
2.36
2.23
2.86
3.31
2.47
2.07
2.09
aAdapted from Connor and Shacklette (1975).
U.ii
-------
Sewage sludge from an urban-Industrialized area of Atlanta, Georgia,
containing high levels (up to 2,750 ppra) of lead were sodded to fescue
(Festuca arundinacea). 1754 ppm increased the lead content of the plant
tissue from 3 to 120 times. Additions of microelements to the sewage sludge
doubled the amount of lead in fescue tissue above that contained with sewage
sludge treatments alone (Boswell, 1975).
Wild oats (Avena fatua L.) have been proved to be a sensitive indicator
of atmospheric inputs of lead (Rains, 1975). Dried plant material sampled
for two seasons accumulated lead from the atmosphere with little or no in-
puts from lead-contaminated soils. The contaminated, above-ground plant
tissue was also shown to retain lead deposited thereon from the atmosphere
during the growing season, with only small amounts contributed from the
soil. The wild oats were very sensitive to changes in input levels of
atmospheric lead. A nearby smelter was closed during the winter after the
first growing season. In the following year, the lead content was only a
fraction of the content in the previous growing season. Similar results
were obtained by Rains (1971). Leaching with water and the winter rains
were ineffective in removing lead from the tissue.
Jones, et al., (1973a) found that the uptake of lead by intact peren-
nial ryegrass (Lolium perenne var. 523) plants in solution cultures con-
taining lead nitrate was very rapid and complete. Lead bound in roots was
not released by exchange with calcium or barium ions. The total uptake, or
lead burden, increased with increasing rates of lead addition and ranged
from 280 to 9,970 micrograms of lead per three plants harvested. The con-
centration of lead in shoots at the first harvest ranged from 0.2 to 58.4 ppm
and that in the corresponding roots from 5.5 to 5,310 ppm. Jones, et al.,
f!973b) studied the lead status of sixteen soils in which perennial rye-
grass was grown, with and without added sulfur, in a controlled environment
cabinet with carbon-filtered air. The lead concentration in the tops of
healthy plants (those with adequate sulfur) was lower than in the roots.
The mean lead content at the fourth harvest was 5.0 and 12.9 ppm, respec-
tively, in the tops and roots. Marked Increases in lead concentration in
the tops of sulfur-deficient plants coincided with decreases in dry-matter
yield.
Ter Haar, et al., (1969) utilized specially-constructed chambers In a
greenhouse for experiments to determine uptake and retention of lead by
perennial ryegrass and radishes. Ryegrass plants were grown in normal
(0.96 microgram Pb per cubic meter) or filtered air (0.03 ndcrogram Pb per
cubic meter) while distilled water or water containing 40 micrograms Pb
as PbCl« per liter was applied either to the leaves or soil surface. The
lead content of grass grown in filtered air was 2.5 ppm while that grown in
unfiltered air was 5.2 ppm. The mean lead concentration in grass grown
with distilled water was 4 ppm; with lead-containing water, 3.9 ppm; under
foliar application of water, 4 ppm; and under soil application, 3.7 ppm.
These data compare favorably with the respective values of 4.9 ppm and 3.5
ppm reported by Jones and Hatch (1945) and Marten and Hammond (1966).
Dedolph, et al., (1970), in experiments designed to determine the contribu-
tion of lead in soil, water, and air to that in perennial ryegrass and
U.12
-------
radishes, found that ryegrass derived 2 to 3 ppm Pb from soil sources. Leaf-
lead levels in excess of that from soil were derived from, and quantitatively
related to atmospheric concentrations in the growth chambers (an average of
0.09 and 1.45 micrograms Pb per cubic meter, respectively, in filtered and
unfiltered air). Lead added to water at 40 micrograms per liter as PbCl. did
not affect the concentration In the grass.
Marten and Hammond (1966) grew bromegrass plants which had been propa-
gated from the same clone in lead-contaminated soils. Three crops were
harvested; after the second harvest chelates were added to the soils. The
most significant fact derived from the experiment was that even the greatest
grass lead concentration (34.5 ppm) was far below that which would be toxic
to animals consuming the grass. The addition of the chelates resulted in a
distinct rise in lead concentration only in grass growing in the most con-
taminated soils.
The removal of metals by 30-day-old barley seedlings (Hordeurn vulgare
L., cv. Tralll) from two topographically associated soils having pH's of 5.9
and 7.9 (free carbonates) was studied following the application of 0.35,
6.9, 13.8 and 27.6 metric tons (0, 3.8, 7.6, 15.2, and 30.4 tons) per hectare
of sewage sludge (Dowdy and Larson, 1975a). The total uptake of zinc, lead,
nickel, and chromium was greater from the sludge-amended acid soil than from
the calcareous soil. Lead uptake increased by 50 percent with the addition
of 27,3 metric tons (30 tons) per hectare.
Rolfe (1973) studied lead uptake by seedlings of eight tree species.
Experiments were done with additive lead chloride additions from 0 to 600
parts per million, and additive phosphate additions from 0 to 336 kilograms
per hectare. The uptake of lead was reduced to approximately 1/2 when the
higher level of phosphate was added to the soil.
An area of immense concern is that of lead uptake by vegetation near
well-traveled roadways or lead-producing or lead-utilizing Industries (mines,
mills, and smelters). Dedolph, et al., (1970) obtained average lead con-
centrations of 15, 8.4, and 7.9 ppm dry weight, respectively, in leaves of
ryegrass grown in field plots 12.2, 36.6, and 155 meters (40, 120, and 510
feet) from the road. Hemphill (1974) and Hemphlll, et al., (1974) found
that forage plants and soils along ore-truck routes in Missouri's Lead Belt
contained elevated levels of lead and other toxic metals, which decreased
with increasing distance from the highway. Lead concentrations in or on
unwashed vegetation along the ore-truck routes averaged 280 ppm dry weights
on the road right-of-way, and 34 ppm at 91.4 meters (100 yards), 11.6 ppm
at 182 meters (200 yards), and 6.5 ppm at 365 meters (400 yards) from the
highway. Blueberries had a maximum of 537 ppm along the truck routes and
172 ppm at 91,4 meters from the routes.
Evidence for the accumulation of toxic levels of lead in forage plants
was the deaths of several horses beginning in 1970 (see Section 5.5.2).
Lagerwerff and Specht (1970) found that lead concentrations in grass samples
(tall fescue, blue grass, and orchard grass) decreased with distance from
traffic. The concentration also decreased with depth in soil profiles.
According to a study conducted by Graham and Kalman (1974), lead levels in
U.13
-------
grass at all points up to 91 meters from the roadway in a suburban setting
surpassed the amounts that are potentially hazardous to horses and cattle.
In fact, the levels were nearly 200 times that of natural levels of 5 ppm
as reported by Motto, et al., (1970). A limited number of observations
by Graham and Kalman (1974) also indicated an inverse relationship between
concentration of lead and distance from roads as has been verified by
Schuck and Locke (1970) and Page, et al., (1971). Tables 4.3 and 4.4
further summarize somewhat different findings of lead in grasses as
related to distance from traffic or industry.
On- and off-road samples of plants from Missouri were analyzed for
the presence of lead. All vegetation clearly showed a roadside effect.
Grass samples from Kansas City averaged 29 and 9.7 ppm of lead, respec-
tively, in on- and off-road samples; those from Pacific averaged 17 ppm
and 4.5 ppm. Red cedar trees (Juniperus virginiana), sampled at widely
scattered sites in southern Missouri, averaged 16 ppm in on-road samples
and 7 ppm in off-road samples. One cedar tree sampled in Centerville, a
major lead-mining district, had 1,200 ppm lead. Cedars and grass growing
within 15.2 meters (50 feet) of pavement had lead contents two to three
times the amounts found in companion species taken 91.4 meters (300 feet)
from the pavement (Connor, et al., 1971a). An intensive study of cedars
in Centerville, Missouri, showed a geometric mean concentration of 5,800
ppm lead in the ash of fifteen samples. Such high concentrations were
considered to be a roadside effect and to reflect vehicular transport
of lead-bearing ores from mine to smelter, rather than an unusual
occurrence of lead minerals in the bedrock (Conner, et al., 1971b).
Keith (1969) analyzed elm, maple, and oak trees and soils from the
Upper Mississippi Valley mining district, and from an area outside but
continguous to the district for lead and zinc content. Stems contained
about twice as much lead (78 to 135 ppm from the mineralized area; 102 to
150 ppm, nonmineralized area) as did the leaves (26 to 62 ppm, mineralized
area; 29 to 61 ppm, nonmineralized area) from the same stems. Lead
appeared to be slightly more concentrated in trees from the nonmineralized
area whereas zinc was more highly concentrated in trees from the mineral-
ized area. This can possibly be explained as a function of regional
geology. Outside the mining district, more acidic conditions prevailed.
These conditions allowed for the solubility and mobility of lead compounds.
Buchauer (1973) found that a statistically significant correlation existed
among lead contents for six tree species growing near two zinc smelters.
Red oak seedlings were planted at various distances from one of the
smelters. The surviving seedlings were harvested and analyzed after two
growing seasons. At distances of 1 to 40 kilometers from the smelter,
leaves had 100 to 11 ppm; stems, 35 to less than 10 ppm; and taproots,
less than 100 ppm of lead, respectively.
Henphill and Pierce (1975) studied the accumulation of lead in or on
vegetation in an area in Missouri's New Lead Belt which encompassed four
mines and mills and one smelter, and an area outside the New Lead Belt with
a smelter at the center. The data summarized in Tables 4.5 and 4.6 show
that vegetation in the near vicinity of smelters and, to a lesser extent,
4.14
-------
Table 4.3 LEAD IN GRASSES AS A FUNCTION OF DISTANCE FROM TRAFFIC OR INDUSTRIES
Distance from Road,
m
0 - 7.5
7.5 - 15
15 - 150
Ov«»r 150
0
7.5
^K
23
37.5
67.5
Region of a smelter
7.6 - 30
0 - 336.7
0 - 336.7
Lead Content,
ppm, dry weight
80a
66
45
20
664b
454
198
139
68
500C
20 - 60
8 - 341 (fescue)
5.8 - 344 (purple top)
References
Cannon and Bowles (1962)
Motto et al., (1970)
Rains (1971)
Chow (1970)
Hemphill et al., (1974)
8 - 32 (U.S. 1, Beltsville,
Maryland)
8-32 (Washington-Baltimore
Parkway, Bladensburg,
Maryland)
S - 32 (1-29, Platte City,
Missouri)
8-32 (Seymour Road, Cincinnati,
Ohio)
26.3 - 68.2 Lagerwerff and Specht (1970)
18.5 - 51.3
7.5 - 21.3
7.6 - 31.3
.Ash; average content.
Highest values from unwashed grass samples.
Highest value from a survey of four seasons.
U.15
-------
Table 4.4 LEAD IN ROADSIDE GRASS SAMPLES
Distance from
Highway, ft
0
25
75
125
175
225
Av.
12,800
Vehicles
per 24 hi
_
63
76
_
—
_
-
14,700
Vehicles
pei24hr
_
—
_
_
—
35
-
17,700
Vehicles
per24hr
_
_
_
31
_
_
-
19,700
Vehicles
per 24 hi
Lead Content
133
84
65
41
41
34
66.3
41,000
Vehicles
pei 24 hi
, Not Washed,
14)
66
103
—
60
56
85.2
45,600
Vehicles
pei 24 hi
ppm
118
192
—
66
46
41
92.6
48,600
Vehicles
pet 24 hi
_
154
66
45
66
48
75.8
48,600
Vehicles
pei 24 hi
664
454
198
139
-
68
304.6
54,700
Vehicles
pei 24 hi
219
139
83
78
61
59
106.5
Aveiage
255.0
164.6
98.5
66.7
54.8
46.3
112.0
Lead Content, Washed, ppm
0
25
75
125
175
225
Av.
40
37
64
58
47
50
49.3
40
23
34
43
35
31
34.3
91
64
46
26
_
_
56.8
133
58
59
58
18
36
60.3
136
85
80
55
46
58
76.7
71
80
—
46
31
32
510
128
62
50
36
45
31
58.7
492
262
77
59
-
44
186.8
98
83
60
45
62
43
65.2
136.6
83.8
58.8
47.3
40.6
40.6
69.8
Source: Motto, et al,, Reprinted with permission from Environmental Science and
Technology, (c) American Chemical Society, 1970.
-------
Table 4.5 CONCENTRATION OF LEAD IN LEAVES OF POST OAK
(Quercus stellata) AND NEEDLES OF SHORTLEAF
PINE (Pinus echinata) IN VICINITY OF LEAD
SMELTER OPERATIONS3
Micrograms per
Distance from
Smelter (mi.)
0-0.5
0.5 - 1.0
1.0 - 1.5
1.5 - 2.0
More than 2.0
Post Oak
Range of
Values
230-8125
71-3800
50-1580
45- 640
18-1360
Mean
3776.70
771.40
250.00
192.80
168.97
Gram - Dry Weight
Short leaf
Range of
Values
420-11750
101- 1475
52- 1050
62- 412
22- 661
Pine
Mean
3546.36
497.37
273.56
142.85
123.29
"Adapted from Hemphill and Pierce (1975).
U.IT
-------
Table 4.6 CONCENTRATION OF LEAD IN LEAVES OF WHITE OAK
(Quercus alba) AND LEAVES OF BLUEBERRY
(Vaccinium pallidum) IN VICINITY OF LEAD
PROCESSING "OPERATIONS
Micrograms
per gram -
White Oak
Range of
Distance Miles Values
Mean
n
Dr-- Weii!
:hc
Blueberry
Range of
Values
Mean
n
Fletcher Mine and Mill
0
1
2
3
4
5
- 1
- 2
- 3
- 4
- 5
- 6
39
16
20
10
12
12
.0
.5
.0
.8
.5
.5
- 70.0
- 26.5
- 57.7
-124.0
- 36.5
39.0
35.9
22.6
20.7
29.5
22.6
1
6
6
10
15
11
In Vicinity
1
2
3
4
5
6
- 2
- 3
- 4
- 5
- 6
- 7
75
122
39
28
23
26
.8
.0
.8
.2
.5
.0
-1221.0
- 557.0
- 155.0
- 276.0
- 228.0
- 121.0
574.3
299.0
80.2
93.0
75.6
54.5
3
7
4
10
12
9
39.0
16.5
16.5
11.5
5.8
5.9
-132.0
- 40.0
- 27.5
- 42.5
- 73.9
- 24.0
85.
25.
20.
20.
27.
17.
5
8
6
6
1
7
2
5
5
12
17
11
of Smelter
141.0
93.0
21.0
34.2
24.0
29.0
-874.0
-338.0
-146.0
-181.0
-155.0
-101.0
495.
203.
76.
68.
64.
41.
3
9
1
6
3
6
3
10
5
11
10
11
Adapted from Hemphill and Pierce (1975).
U.18
-------
in the vicinity of mines and mills, accumulated levels of lead that are
manyfold that of background levels.
Six species of trees (sugar maple, pin oak, yew, Norway maple,
Eastern hemlock, and Norway spruce) growing in the City of New Haven, Con-
necticut, were found to have a mean lead tissue concentration in the pre-
ceding growing season that exceeded most lead concentrations determined for
trees in areas with geologic lead deposits or adjacent to primary highways
(Smith, 1972; Smith, 1973). Washing and analysis with an electron micro-
probe failed to provide conclusive evidence with regard to the specific
location of the lead on or in the tissue sampled. The highest lead con-
centrations were associated with the leaves of pin oak and Norway maple.
The maximum lead concentration observed was 760 ppm dry weight in a washed
hemlock twig (see Table 4.7). In contrast, Smith (1973) found that twigs
and leaves of sugar maple growing in remote sections of northern New
Hampshire and Vermont contained 0 to 20 ppm lead on a dry weight basis. The
analysis of bark from white pine (Pinus strobus) and elm (Ulmus americanus)
trees growing adjacent to densely travelled streets with an electron probe
microanalyzer revealed that lead, chlorine, and bromine were associated with
particles, about 7 micrometers in diameter, held on the rough surface or
embedded in the surface cells of the bark (Heichel and Hankin, 1972). Here-
tofore, there has been no information on the form or composition of lead
residues on or in plants. These findings show that lead on or embedded in
plant surfaces, especially rough ones, may be associated with at least two
other elements, chlorine and bromine, and suggests their origin from automo-
bile exhausts. Using an aerosol generator and wind tunnel fumigation system,
Wedding, et al., (1975) found that the gross deposition of lead aerosols on
rough, pubescent leaves of sunflowers (Helianthus annuus L.) was ten times
greater than on the smooth, waxy leaves of the tulip poplar (Liriodendron
tulipifera). The findings of Page, et al., (1971) with consumer crops confirm
the above data on lead aerosol deposition on plant leaves (see Section 4.3.2.1)
4.3.1.2 Effects—
There is surprisingly little information in the open literature on the
effects of lead and its compounds on vascular, noncrop plants. However, it
is reasonable to expect similar effects (reduction of photosynthesis,
mitosis, and water absorption) on many species of this group of plants as
have been shown for vascular, crop plants (see Section 4.3.2.2).
Low lead concentrations (as lead acetate) reduced root growth and leaf
and flower production of hyacinth bulbs (Holl and Hampp, 1975; National
Academy of Sciences, 1972). Bougainvillaea sp. (five plants) exposed to
approximately 7 ppm tetraethyllead vapor at 25 C for a 3-day period exhibited
14 percent defoliation or abscission. Fourteen days were required for total
recovery from the 3-day, organolead exposure (Siegel, et al., 1973).
Root growth of sheep fescue (Festuca ovina) was retarded, markedly
reduced, and stopped by 10, 30, and 100 ppm of Pb(NO,)2, respectively.
Three parts per million lead in the form of a pure lead nitrate solution was
highly toxic to all plants of _F. ovina, while in a Knopp's culture medium
U.19
-------
Table 4.7 LEAD BURDENS OF TREES GROWING IN THE
CITY OF NEW HAVEN, CONNECTICUT3
Species
Pin oak
(Quercus palustris)
Sugar maple
(Acer saccharum)
Norway maple
(Acer platanoides)
Eastern hemlock
(Tsuga canadensis)
Yew
(Taxus spp.)
Norway spruce
(Picea abies)
Tissue
Organ
Leaves
Twigs
Leaves
Twigs
Leaves
Twigs
Leaves
Twigs
Leaves
Twigs
Leaves
Twigs
Analyzed
Number of
Trees
12
12
7
7
32
32
8
8
10
10
4
4
Lead (micrograms
per gram, dry weight)
Unwashed
70-200
25-110
25-315
21-315
20-515
25-290
40-203
97-510
50-318
50-318
100-390
100-390
Washed
55-220
25-125
35-120
38-195
45-485
10-300
25-180
155-760
70-371
70-371
100-240
100-240
a Source: Smith. Reprinted with permission from Environmental
Science and Technology, (c) American Chemical Society, 1973.
U.20
-------
many plants showed little reduction in root growth at 25 ppm. Certain
nutrients in the medium obviously had an antagonistic effect on the toxicity
of lead (Wilkins, 1957). Tests have shown that plants (Agrostis tenuis,
Deschampsia flexuosa, Festuca ovina) grown near a lead mine exhibited a low
sensitivity to lead. In addition, calcium was found to ameliorate lead
toxicity in IT. ovina and j\. tenuis. Lead-resistant A^. tenuis populations
exhibit an adaptation to very low calcium and phosphate concentrations.
High lead contents of soil lower phosphate concentrations which are essen-
tial for plants. The need of plants for calcium diminishes in the absence
of large concentrations of heavy metals. Generally, plants show a greater
susceptibility to heavy metals when their calcium content is small. Lead
tolerance in JF. ovina is genetic involving a single gene (Antonovics, et al.,
1971; Bradshaw, 1952; Holl and Hampp, 1975; Lagerwerff, et al., 1973; NAS,
1972; Wilkins, 1957).
Perennial ryegrass (Lolium perenne var. S23) roots showed a pronounced
blackening at the tips similar to that described by other investigators for
onions, beans, and maize after exposure to lead nitrate in solution (Jones,
et al., 1973a). Relatively low concentrations of lead inhibited photo-
synthesis and transpiration of detached sunflower leaves (Hilianthus annuus)
primarily by interfering with stomatal function. The degree of stomatal
opening was determined experimentally to decrease log-linearly with increas-
ing concentrations of lead from 10 to 1,000 micromoles. Net photosynthesis
was reduced by 50 percent when leaf tissue lead concentrations were 0.93
micromole per gram (193 ppm). Transpiration was similarly reduced (Bazzaz,
et al., 1974a).
Whole plant studies of the effect of lead, cadmium, nickel, and thallium
on net photosynthesis and transpiration were conducted by Carlson, et al.,
(1975) to obtain some measure of the damage of heavy metals to physiological
processes taking place in the leaves of intact plants. Corn and sunflower
plants were grown in hydroponic culture and treated with various levels of
lead chloride and other metal salts. Lead did not cause a statistically
significant reduction in net photosynthesis at the treatment levels used.
Even at lead concentrations up to 500 ppm, net photosynthetic and trans-
piration rates of lead-treated plants were not significantly different than
those of control plants. These data suggest that lead is not translocated
in appreciable quantities from hydroponic media through the root system and
into leaf tissue of intact plants during short-term experiments.
Lead chloride concentrations of 41 to 410 ppm in watering solutions
reduced the height, stem and root dry weights, and root/shoot ratio of
loblolly pine (Pinus taeda) and red maple (Acer rubrum) seedlings in two
forest soils. Increasing amounts of lead resulted in progressively smaller
pine needles accompanied by the appearance of a milky-green hue, and,
finally, in overall necrosis at the higher levels. The root systems also
became reduced and blackened. Lead treatments caused an increase in red
pigmentation (anthocyanin content) and an accelerated casting of red maple
leaves (Davis and Barnes, 1973).
Little (1973). in a study of heavy metal contamination of tree leaves
(Ulmus glabra, elm; Crataegus monogyna, hawthorn; Salix alba, willow;
U.21
-------
oak), concluded that considerable proportions of the total
lead burden are removed by washing. Since much of the metal appears to be
bound to membranes and cell wallH and only small amounts are released on
boiling, it neems likely that comparatively small amounts of the metal are
metabolically active within the leaves. This might offer an explanation
for the absence of toxicIty symptoms in species exposed to aerial fallout
versus them- species where all the metal in the leaves Is of soil origin.
4. 1.2 Crop Plants
4.J.2.1 Metabollsmi Uptake, Absorption, and Residues—
Data available on the uptake by plants of lead from natural sources are
relatively sparse. Table 4.8 summarizes natural lead levels In some of the
crop plantH in the conterminous United States. For at least 30 years, lead
added to the soil, often as an arsenate insecticide, and to air and water
i rom automobile exhausts and industries has resulted In uptake by plant
roots but only a slight Increase in lead content of the stem and leaves
(Lagerwerff, 1972).
Once the lead Is Inside the plant, it seems to be retained by cell
membranes, mitochondria, and chloroplasts, Sabnls, et al., (1969) found a
nonenzymlc, discrete deposition of lead, osmium, and tungsten at specific
sites on the thylakoid membranes of Chloroplasts in the tissue of pea
tendrils (Piaum j[«.tlvujn var. Alaska). The authors found that as long as
lead was in the incubation medium, the,deposits.were obtained irrespective
of the presence or absence of ATP, Mg , or Ca in various combinations
or alone. Even when plants were grown in the dark for 24 hours to eliminate
the effects of photophosphorylation and any traces of endogenous ATP or when
lead was added to the fixtures used to prepare the tissues for electron
microscopy, the deposits were still visible. Malone, et al., (1974) ex-
posed corn plants to lead In a hydroponic solution either as a citrate or
an EDTA chelate or aa PbCl,, or Pb(NO,,)2. Light and electron microscopic
studies showed that the roots generally accumulated a surface lead precipi-
tate and slowly accumulated lead crystals in cell walls. Lead taken up by
the roots was concentrated in dletyosome vesicles which fused with one an-
other to encase the lead deposit. Movement of the lead deposits toward the
outside cell wall resulted in the lead being finally localized In the cell
wall out Hide Die plasmalemma. Similar deposits were observed In stems and
leaves, suggesting that lead was transported and deposited in a similar
manner.
Oatb (Avena satlva) and lettuce (Lactua satlye var. Black-seeded
Simpson) grown in soils with a stable Isotope tracer showed about the same
lead concentration associated with the diffuse roots as in the soil, while
in leaves the concentration of lead derived from soil uptake was only 0.5
to 10 percent as much (Rablnowltz, 1972). The author examined lettuce
grown in the Salinas Valley. Southern California, and found 3 to 25 ppm
lead; he viewed the excess aa being due to airborne lead absorbed by the
leaves. Expressed on a fresh-weight basis the lettuce contained 0.15 to
1.5 ppm lead, about the average for food which is about 0.3 ppm. John (1972)
U.22
-------
Table 4.8 NATURAL LEAD LEVELS IN THE ASH OP CROP
PLANTS8
Sample and Collection Locality
Asparagus; Wisconsin
Bean, lima; Georgia
Bean, snap; Georgia
Beet, red; Wisconsin
Blackeyed peas; Georgia
Cabbage; Georgia
Carrot; Wisconsin
Corn; Georgia
Corn; Missouri
Floodplaln forest
Glaciated prairie
Corn; Wisconsin
Onion | Wisconsin
Potato; Wisconsin
Tomato; Georgia
Observed Range, Mean,
ppm ppm
23 - 300 87
<10 - 50 <10
<10 - 50 <10
<10 - 70 <10
<10 - 30 <10
<10 - 25 <10
<10 - 70 <10
•10 - 20 <10
<10 - 25 -10
<10 - 70 7.1
<20 - 50 <20
<20 - 30 -20
<10 - 150 <10
<10 - 25 <10
<10 - 50 <10
<10 - 300 <10
mv - I • 1 1 |M • « ....„„,.... , .
aAdaptad from Connor and Shacklette (1975).
It.23
-------
found that the lead content of lettuce and oats was related to soil lead
and other soil properties including pH, extract able aluminum, and total
nickel. When 500 ppm lead (as lead nitrate) was added to the soil, the
lead content of lettuce averaged 54 ppm while that of oat shoots and oat
roots averaged 20 and 57 ppm, respectively.
Miller, et al., (1975) found that uptake of lead into shoots of 6-week-
old corn plants decreased with an increase in soil pH, cation exchange ca-
pacity, and available phosphorus. Maximum accumulation of lead occurred at
the 2,000-ppm lead chloride treatment level. According to MacLean, et al.,
(1969), the lead content of oats and alfalfa grown in four soils pretreated
with PbCl (0 to 1,000 ppm) varied inversely with the organic matter content
and pH of the soils. The amount of lead taken up was reduced upon addition
of phosphate or lime to acid soils. The mean lead content for oat grain,
oat straw, and alfalfa tops, respectively, was 0.7 to 4.3 ppm, 1.3 to 9.8
ppm, and 1.5 to 8.5 ppm.
Corn plants, grown in sand and water with Hoagland's nutrient solution,
accumulated large quantities of lead when lead nitrate was applied to the
sand. When evaluating the quantity of lead accumulated, the age of the
plant at the time of lead treatment was found to be very Important along
with the phosphate condition of the plant. The highest amounts of lead
accumulated by old leaves receiving lead and in the absence of phosphate
were 2,029 plus or minus 437 ppm and 936 plus or minus 78 ppm, respectively.
Young leaves accumulated 11,640 plus or minus 100 ppm and 19,200 plus or
minus 242 ppm in the same order (Miller and Koeppe, 1971), Baumhardt and
Welch (1972) found that the lead content (ppm) of corn stover grown in a
field which received lead acetate treatments of 0 and 3,200 kilograms per
hectare was: 2.4 and 37.8 for whole young plants, 3,6 to 27*6 for leaves
at tasselling, and 4.2 and 20.4 for whole plants at grain harvest. The lead
content of grain averaged 0.4 ppm lead and was not affected by added
lead.
Bazzaz, et al., (1974b) found that lead accumulation trends in corn and
soybeans were similar at lower treatment levels but were slightly different
at higher levels. The uptake by corn Increased sharply as the amount of
lead chloride in the growth medium increased. Maximum accumulation of about
450 ppm occurred at a medium concentration of 1,000 ppm. The maximum accumu-
lation for soybeans was 151 ppm grown in a medium with the same lead con*
centration. Lagerwerff, et al., (1973) grew corn and alfalfa plants In
potted Chester silt loam at two soil pH levels (5.2 and 7.2) and with HC1-
extractable soil lead (as PbCl^) levels of 12, 64, 113, and 212 ppm. Most
treatments were carried out in a greenhouse where the plants were exposed
to aerial lead from nearby traffic as veil as leaded-paint particulates from
the greenhouse windows. No clear relationship was established between up*
take and soil lead content in the leaves and stalk of the upper section of
corn. In the lower section lead content in the leaves and stalk Increased
from 53 to 110 ppm, and from 4.6 to 12,5 ppm, respectively, as the soil con-
tent Increased from 12 to 212 ppm lead at pH 5.2. As the extractable lead
content of the soil Increased from 12 to 212 ppm, the differences between
rinsed and unrinsed samples of the first clipping of alfalfa tops increased
-------
from 1.6 to 9.5 ppm, and from 3.2 to 4.9 ppm lead on a dry-weight basis at
soil pH 5.2 and 7.2, respectively. A similar trend was shown with the sec-
ond clipping. Page, et al., (1971) found that alfalfa plants lost 50 per-
cent of their lead by rinsing once with water.
Corn plants grown on soil treated with municipal sludge for 35 years
did not show an appreciable accumulation of lead in the grain as compared to
control crops (Kirkham, 1975). In general, the roots, stems, leaves, and
husks had much higher lead concentrations than those of control plants. The
lead concentration in roots was 540 ppm compared to less than 5 ppm in grain.
The concentration of lead and other metals in the grain of sludge-treated
plants was not greater than that in grain from control plants. These data
show that very little lead was translocated to the above-ground portions even
in sludge-amended soils. In contrast, Anderson and Nilsson (1972) noted a
50 percent increase in extract able soil lead and the lead content of vege-
tation (5.2 ppm, background level; 7.7 ppm, sludge added; when sewage sludge
(containing 293 ppm lead) was used as a plant nutrient source on cultivated
soils.
The uptake of metals by seven vegetable crops (carrots, lettuce, peas,
potatoes, radishes, sweet corn, and tomatoes) after 0, 102, 205, and 450
tons per hectare of sewage sludge was applied to coarse, sandy soil was
studied by Dowdy and Larson, (1975b). Lead uptake was insignificant and did
not exceed 1.0 ppm in the root and tuber tissue, although 230 kilograms lead
per hectare was added. The low values (less than 1 ppm) contrast with values
of 20 to 25 ppm lead in radish roots (Lagerwerff, 1971) grown on soil con-
taining 70 to 370 kilograms lead per hectare. The edible fruiting tissue had
little or no increase in the iron, manganese, copper, lead, and boron con-
tents with applications of sludge. The data indicate, in this case, that
lead-containing sewage sludge added to soil does not significantly affect
tissue-lead content.
In those instances where lead toxicitles to animals and humans have
occurred, the sources of lead in the foods and feeds were not due to plant
absorption from soils but were caused by contamination during processing,
storage, or deposition from lead in air onto plant surfaces (Page, 1974;
see Sections 5.5 and 8.3.1). Menzies (1974) points out that lead is gener-
ally Inactivated in sludge by being tied up with phosphorus. This accounts
in part, for the insignificant amounts of lead that are usually absorbed by
plants growing on sludge-amended soil. Furthermore, lead or other trace
element levels in higher plants grown on sludge-amended soils are dependent
on the amount of sludge applied, composition of the sludge, soil pH, and
plant species.
John and VanLaerhoven (1972a) grew oat seedlings and lettuce in silty
clay loam soil that received lead (as PbCU), lime, and nitrogen treatments.
Lettuce leaf lead content (140.6 ppm) was highest at the 1,000-ppm treat-
ment level. When soil was limed, only small increases were found. In oat
tops lead Increased from 3.2 to 57.4 ppm as a result of adding 1,000 ppm
lead to unlimed soil whereas the corresponding Increase for limed soil was
only from 5.6 to 16.8 ppm. Oat root lead content was not significantly
-------
affected. When lead and nitrogen were added simultaneously, the lead con-
tent of both plant species varied depending on the source of lead and rate
of nitrogen applied. Application of low levels of nitrogen reduced uptake
of lead by lettuce and oat roots only.
Cox and Rains (1972) tested liming at 0, 2, and 4 metric tons per nee-
tare (0, 3.6, and 7.1 tons/acre) as a means for reducing lead uptake by five
plant species (Glycine max, Triticum aestivum, Trifolium subterraneum, Zea
mays and Avena sativa) from two lead-contaminated soils. 2 and 4 metric
tons lime per hectare reduced lead concentrations in the tops of 10-week-
old plants of all species. Uptake was decreased by lime simply because of
lower availability of soil lead. At maturity, Glycine max growing in soil
limed at the rate of 0 to 1.8 metric tons (0 to 2 tons) per acre, accumula-
the following amounts of lead: 37.2 to 36.8 ppm (seed pods) and 62.3 to 25.3
ppm (seeds) in the 0- to 10-cm soil horizons, and 30.4 to 23.7 ppm (seed
pods) and 60.4 to 27.6 ppm (seeds) in the 10- to 30-cm soil horizons.
Lagerwerff (1971) grew radish plants in an open field 200 meters from
traffic and in a growth chamber located in a windowless room to determine
uptake of cadmium, lead, and zinc by radish from soil and air. A tenfold
increase in the lead content of soil was reflected in an increase in the lead
content of radish by a factor of less than two. The tops and roots of radish
grown inside on a low lead content soil of pH 5.9 already had 13.3 and 19.4
ppm lead on a dry-weight basis, respectively. The highest lead content in
radish roots grown outside at pH 5.9 was about 119 ppm; at pH 7.2, the content
was about 89 ppm. Radish tops grown outside accumulated approximately 148
ppm at pH 5.9 and about 85 ppm at pH 7.2
Ter Haar, et al., (1969) grew radishes in specially-constructed growth
chambers with normal (0.96 microgram Pb per cubic meter) or filtered air (0.3
microgram Pb per cubic meter) while either distilled or lead-containing water
(40 micrograms Pb per liter as PbCl_) was applied to the leaves or soil sur-
face. The concentration of lead in radish leaves grown in filtered air was
2.3 ppm; in unfiltered air, 2.7 ppm; with distilled water, 2.7 ppm; with
lead-containing water, 2.2 ppm; under foliar application of water, 2.2 ppm;
and under soil application of water, 2.7 ppm. The lead content of the hypo-
cotyls grown in filtered air was 2 ppm; in unfiltered air, 1.8 ppm; in dis-
tilled water, 2 ppm; in lead-containing water, 1.8 ppm; under foliar appli-
cation of water, 1.5 ppm; and under soil application, 2.3 ppm.
Dedolph, et al., (1970) obtained essentially the same results as did
Ter Haar, et al., (1969) using filtered air with a lead content of 0.09 micro-
gram per cubic meter and unfiltered air containing 1.45 micrograms per cubic
meter. Radishes were grown in field plots 12.2, 36.6, and 155 meters (40,
120, and 510 feet) from the road under the following conditions in the order
given: 82, 45, and 27 ppm, soil lead content and an atmospheric lead concen-
tration of 2.32, 1.71, and 1.07 micrograms Pb per cubic meter in the air.
Lead content (ppm) of radish leaves was 16.4, 10.8, and 2.8 and that of rad-
ish roots was 0.7, 0.8, and 0.8, respectively, under the conditions cited
above. Ter Haar (1970 and 1973) grew several food crops in greenhouses
supplied with filtered and ambient air and in plots planted perpendicular
U.26
-------
to a busy highway. Inedible portions of the plants, bean leaves, corn and
soybean husks, and oat, wheat, and rice chaff showed a two- or threefold
increase in lead concentration when grown near the road or in the greenhouse
with unfiltered air. Tables 4.9 and 4.10 summarize the results obtained.
John and VanLaerhoven (1972b) studied lead uptake by seven food crops
(leaf lettuce, spinach, broccoli, cauliflower, oats, radishes and carrots)
in a growth chamber experiment which involved three rates of PbCl? soil ap-
plications. Lettuce and spinach leaves and the tuberous portions of radish
and carrot plants accumulated markedly higher lead concentrations than did
the edible portions of the three other plant species. In all plants parts,
lead concentrations increased as more lead was added to the soil. Differences
among lead concentrations in tissues of these plants were most evident with
the high lead treatment, 1,000 milligrams lead per kilogram. Concentrations
in root portions ranged from 396.6 to 867.7 milligrams lead per kilogram and
increased with the following sequence of plant species: oats, cauliflower,
carrots, broccoli, and lettuce. Among the above-ground plant parts, lettuce
and spinach leaves, with 54.2 and 39.3 milligrams lead per kilogram, respec-
tively, contained approximately twice the lead levels found in any other
aerial portion. The least lead concentration was found in oat grain.
Motto, et al., (1970) grew five crops (carrots, corn, lettuce, potatoes,
and tomatoes) at three distances from highways in New Jersey having various
traffice densities. The same crops were grown in the greenhouse with soil
from the surface 15.2 centimeters (6 inches) of field plots and in acid-washed
sand to which soluble lead was added. Analysis of plants grown in the field
revealed that the highest lead levels were associated with leaves; lower
levels were in the roots. These same plants grown in the greenhouse exhibited
lower levels in the leaves relative to the roots. The overall results, as
summarized in Tables 4.11 and 4.12, showed that the lead content of plants
and soils increased with increasing traffic volume and decreased with increas-
ing distance from highways. Most of the lead accumulation was within 30.5
meters (100 feet) of highways. The edible portion of carrots, corn, potatoes,
and tomatoes contained the lowest amounts of lead and showed the least effect
of increased lead supply. Edible portions of lettuce contained a larger
amount of lead.
Page, et al., (1971) ascertained the lead content of 27 varieties of con-
sumer crops and plants growing near some major southern California highways.
The data, too voluminous to repeat here, cover the effects of distance from
the highway, and the effect of washing on the lead content of both edible
and inedible portions of the plants. Exposed tissues of plants grown very
close to major highways contained more lead than similar tissues of plants
grown some distance from highways. Beyond 150 meters lead in or on vegeta-
tion was no longer related to distance from the highway and appeared to be gov-
erned by regional effects as opposed to local effects. Exposed tissues of
plants with flexible, rough, hairy surfaces, and close to highways accumulated
more lead per unit time than did those with smooth surfaces. Duration of ex-
posure was found to be important. Tomatoes, for example, picked at various
stages of maturity, showed increased lead as the season progressed. Lead in
parts of plants not in direct contact with the atmosphere such as root, pod,
U.27
-------
TABLE 4.9. LEAD IN CROPS, GREENHOUSE STUDIES*
(micrograms per gram dry weight)
Air
Soil
Leaf lettuce
Cabbage head
Cabbage-unharvested leaves
Tomatoes
Beans
Bean leaves
Sweet corn
Kernel
Cob
Husk
Carrots
Potatoes
Wheat
Unfllteied
Air
1.45Mg/m3
17.1
6.6C
1.0
4.5
0.59
1.4
20.9*
0.22
0.43C
6.9*
1.7
0.30
0.18
Filtered
Air
0.09jig/m3
17.1
3.2
1.1
5.8
0.72
1.2
7.9
0.27
0.69
1.8
11
0.33
0.16
LSD6
_
—
1.3
0.35
1.6
0.26
0.52
8.8
0.22
0.24
1.5
1.9
0.12
0.06
^Source: Ter Haar. Reprinted with permission
from Environmental Science and Technology.
(c) American Chemical Society, 1970.
3Least significant difference.
"Different from other values in row at 95 percent
level of confidence.
U.28
-------
TABLE 4.10 LEAD IN CROPS, HIGHWAY STUDIES3
(micrograms per gram dry weight)
Feet from Road
Air
Soil
Leaf lettuce
Cabbage head
Cabbage-unharvestcd leaves
Tomatoes
Beans
Potatoes
Sweet corn
Kernel
Cob
Husk
Soybeans
Beans
Husk
Oats
Kernel
Chaff
Carrots
Wheat
Kernel
Chaff
30
2.3c«ig/m3
65C
6.5
0.56
6.4C
1.3
1.96
0.48
0.39
0.74
12.6C
0.28°
15.9°
0.47
31. 4C
1.6
0.62
17.8C
120
l.T^Mg/m3
40"
5.0
0.86
8.9"
1.2
1.2
0.64
0.21
0.55
6.6
0.12
8.0"
—
15.5
-
0.42
9.8d
520
1 1.1 Mg/m3
25
4.8
0.83
4.0
1.6
0.90
0.40
0.83e
0.68
5.7
0.10
5.3
0.53
12.8
1.5
0.48
6.2
LSD6
—
3.1
0.44
1.3
1.3
0.47
0.27
0.31
0.21
3.6
0.10
0.22
0.37
15.5
0.61
0.17
1.6
a
Source: Ter Haar. Reprinted with permission from
Environmental Science and Technology. (Q) American
Chemical Society, 1970.
Least significant difference.
^Different from others at 95 percent level of confidence.
U.29
-------
Table 4.11 CONCENTRATION OF LEAD IN FIVE CROPS GROWN
AT THREE FIELD SITES IN 1968a
Traffic Volume
1 2,500 Cars per
Distance from
highway, ft
Air lead. Mg/m3
Soil lead, ppm
at 0-6 in.
Lead content.
ppm, of:
Carrot
Tops
Roots
Corn
Tassel
Leaves
Stalk
Husk
Outer
Inner
Roots
Kernel
Cob
Lettuce
Leaves
Roots
Potato
Leaves
Stems
Roots
Tuber
Tomato
Leaves
Stem
Root
Fruit
30
1.4
54
18
3.8
31
19
3.6
11
5.0
6.0
3.8
8.0
12
16
36
12
22
0.5
36
9.0
11
18
100
1.1
38
11
5.3
7.4
17
3.7
5.0
5.2
3.9
3.6
3.2
13
15
31
8.4
23
1.5
25
9.8
15
3.0
24 hr
250
1.0
33
14
3.9
7.8
14
0.9
6.8
14
5.4
3.1
16
-
—
21
7.8
18
1.0
17
6.9
14
14
47, 100 Cars per 24 hr
30
4.5
134
37
6.2
179
86
5.6
\
J "
19
0.0
0.4
24
24
87
15
33
16
76
27
27
4.6
100
17
138
26
9.5
144
47
3.6
5ft
•U
14
0.2
0.0
21
27
47
11
49
3.0
82
25
35
17
250
2.4
300
21
9.4
69
36
0.2
2f
.0
19
0.2
0.4
14
39
29
14
58
3.0
40
31
50
2.8
49,000 Cars per
30
5.2
229
53
9.1
-
88
6.2
—
—
54
-
—
56
61
-
—
—
—
88
29
37
3.6
100
3.3
130
22
10
-
51
3.4
-
—
19
-
-
35
32
-
—
—
-
52
13
12
1.2
24 hr
250
15
89
17
5.0
-
40
3.6
-
-
-
-
-
-
-
-
-
-
-
44
7.7
9.6
3.2
aSource: Motto, et al. Reprinted with permission
from Environmental Science and Technology.
(c) American Chemical Society, 1970.
U.30
-------
Table 4.12 LEAD CONTENT OF PLANTS GROWN IN GREENHOUSE IN 1963"
Soil
Sand
tppm 0-13 cm)
Carrot
Tops
Roots
Corn
Tassel
Leaves
Stalk
Husk
Outer
Inner
Roots
Kernel
Cob
Lettuce
Leaves
Roots
Potato
Leaves
Stems
Roots
Tuber
Tomato
Leaves
Stem
Root
Fruit
164
18
16
24
74
5.2
17
...
...
14
1.3
1.2
8.7
94
41
39
• • •
6.2
25
13
51
3.6
95
14
6
• • .
18
3.9
4.1
» •
* * *
4.7
1.6
1.1
7.6
11
31
16
• * •
3.7
18
4.7
13
3.4
76
• • •
9
* • •
• • •
. • •
4.9
* * «
• • *
10
2.1
1.7
6.9
12
33
13
* • •
3.7
19
4.2
13
3.5
0
Pb | ppw
8.7
3.1
7.8
11
0.6
• • •
2.9
3.9
3.7
1.0
2.4
5.7
7.6
11
7.6
30
1.0
8.1
3.6
17
3.6
Treatment fonm PM
1
16
7.9
8.1
19
11
• • •
7.9
7.3
12
1.7
2.7
12
108
7.8
29
200
0.6
8.1
24
418
2.5
"2
19
18
7.4
39
28
• • •
15
13
22
2.8
4.3
16
182
12
55
451
2.6
15
89
690
2.3
4
27
21
9.2
88
44
• . .
23
16
35
3.3
10
37
332
12
123
764
1.2
16
87
739
2.1
a
Source: Motto, et al. Reprinted with permission from Environmental Science and
Technology, (c) American Chemical Society, 1970.
-------
and husk crops was not substantially influenced by proximity to highly tra-
veled roads. Corn kernels, lima beans, and carrots, and sugar beet roots all
contained comparatively small amounts of lead which were not significantly
related to distance from the highway.
One hundred thirty-two samples of a variety of fruits and vegetables
grown near heavily traveled highways primarily in California were analyzed
for lead. The concentrations of the lead residues are summarized in Table
4.13 (Klelnman, 1968).
4.3.2.2 Effects-
Roll and Hampp (1975) in reviewing the literature on lead and plants
cited the few cases in which lead was found to increase plant growth or yield.
Lead increased the yield of barley, corn, wheat, buckwheat, and other crop
plants as well as sugar yield from sugar beets while the tuber mass and starch
content of potatoes decreased. Baumhardt and Welch (1972) found that corn
grain yields were neither decreased nor enhanced by additions of lead acetate
to soil. Yields with added lead were 96 to 103 percent as great as yields
from controls. The data showed that lead additions as high as 3,200 kilo-
grams per hectare had no effect on grain yield of corn. Lagerwerff, et al.,
(1973) found that total corn yield was not significantly affected by liming
the soil or amending the soil with graded amounts of lead chloride. With
alfalfa, yield was only affected by soil lead concentration when the soil was
limed.
Garber (1974) subjected various agricultural and garden plots to varying
quantities of lead-containing fly dusts typical of foundry operations and
observed the effects on growth and yield. Lead had a strong, Inhibiting
effect on the growth and pod yield of bush beans. Bean plants at the highest
lead concentration (10,000 ppm) had leaves which were only half as well
developed as those of control plants, and which showed reddish-brown mottling
along the leaf veins as well as a strong chlorosis in newly-formed leaves.
The number of nodules on the roots exposed to 2,000 ppm lead was small,
while at 10,000 ppm lead, no nodules were formed. Tomatoes, bean sprouts,
and lettuce showed a yield reduction when treated with 120 grams of lead-
containing dust per square meter. Potatoes, in contrast, Increased yield
at the higher treatment level. Considerable yield reductions were also
found for peas, lettuce, and carrots in loamy sand soils. John and
VanLaerhoven (1972a) found that lead application (1,000 ppm Pb singly as
PbCl-, PbCO, or Pb(N03)_ or In combination) reduced lettuce yield signifi-
cantly whereas yields or oat top growth and roots were not affected. The
interaction between lime and lead treatments had a significant effect upon
yields of lettuce and oat shoots, but had no effect on yield of roots.
Liming reduced lead uptake by above-ground plant portions to a much greater
degree than by oat roots.
Great variations in lead sensitivity of various cultured grasses have
been demonstrated. Zea mays (maize) and Secale cereale (rye) were not sen-
sitive to lead acetate concentrations of 10 to 100 milligrams of lead
per liter. Barley, oats, and especially wheat showed damage symptoms even
4.32
-------
Table 4.13 LEAD CONTENT OP FRUITS AND VEGETABLES CORRELATED
WITH DISTANCE FROM TRAFFIC AND TRAFFIC LOAD*
Distance from
Crop Plant Highway"3
Grapefruit
Oranges
Lemons
Cantaloupe or
honeydew
Strawberries
Collarda
Lettuce
Endive
Spinach
Broccoli
Cabbage
Turnip greens
Rape
Tomatoes
Pole beans
Potatoes
Carrots
Radishes
Celery
Cauliflower
1
3
2
1
3
3
2
3
2
2
1
3
3
3
2
1
1
2
3
3
Traffic Loadc
M
H
H,L
L
H.L
M
M
M,L
L
H.M.L
M,L
H
H
H,M,L
L
M
M,L
L
M
H
Growth Period,
weeks
13
13
12-16
7-8
22
12
12-14
12
28
8-12
8-27
18
13
12
12
10
12
8
26-28
8-12
Highest
Average
Value for lead
Content , ppm
0.08
0.12
0.18
0.16
0.15
0.90
0.26
0.05
0.27
0.30
0.03
0.31
0.25
0.05
0.12
0.02
0.09
0.06
0.16
0.03
"Modified from Kleinman (1968).
bl • 9 to 22.9 meters (0 to 25 yards); 2 - 22.9 to 229 meters (25 to 250 yards);
3 - above 229 meters (250 yards).
°H - Heavy; M - Medium; L - Light.
U.33
-------
at low lead concentrations. There was visible damage to Hordeum vulgare
(barley) 4 days after exposure to 0.1 M Pb(NO ) , ending in death (Holl and
Hampp, 1975).
Baumhardt and Welch (1972) found that corn grown in a field to which
lead acetate concentrations of 0 to 3,2000 kilograms of lead per hectare had
been added showed no effect in terms of emergence and plant height. Neither
were any morphological, color, maturity nor other growth differences visu-
ally observed during a 2-year study. Miller, et al., (1975) found that lead
and cadmium together inhibited corn root elongation, but not individually.
Soil properties were not found to be directly related to the effects of lead
and/or cadmium although the greatest reduction of growth was seen in low
cation exchange capacity (CEC) and low pH soils. According to Miller and
Koeppe (1971), as little as 24 ppm lead as PbCl« in sand culture caused a
stunting of growth of corn plans under phosphate-deficient conditions.
Phaseolus vulgaris (bean) plants were visibly damaged as soon as 30
minutes after exposure to a concentration of 33,000 ppm lead nitrate. There
was a loss of turgor pressure and death after 24 hours. A lead concentra-
tion of 3.3 ppm enhanced growth activity whereas the limiting concentration
which caused no damage or growth stimulation was 330 ppm. Leaves not fully
differentiated at the beginning of lead exposures were chlorotic. Phaseolus
was damaged by 30 ppm lead as the sulfate alone, or in combination with
other nutrient salts in solution culture. No increase in toxicity from 0 to
30 ppm was detected. Lead nitrate and acetate in concentrations exceeding
100 ppm reduced the germination of cress and mustard seeds and retarded sub-
sequent growth, to concentrations of 1,000 to 2,000 ppm completely inhibited
seed germination (Holl and Hampp, 1975; Zimdahl and Arvik, 1973). These
authors also indicated that high lead concentrations inhibit root growth con-
siderably. Remarkably thick roots with abnormally long root hairs were ob-
served on cereals after lead treatment. In contrast, an abnormal thinning
of roots accompanied by a reduction of root hair numbers has also been
reported. A 93 percent inhibition of root ontogeny of germinating lettuce
seeds was observed at a lead concentration of 330 ppm.
An inhibition of mitosis accompanied by reduced growth was observed in
Allium cepa (onion) and Zea mays (maize) when the nutrition solutes contained
rising quantities of lead. Differentiating young plant tissues have been
found to be much more sensitive to lead than mature tissues (Holl and Hampp,
1975). Radu (1971) found that the lead ion at a concentration of at least 6
ppm is a mitotic poison. Experiments conducted with Allium cep (onion) and
Vicia faba (vetch) in vivo using lead nitrate resulted in altered mitotic
figures. Stathmokinetic effects were elicited. Higher lead concentrations
induced chromosomal modifications. According to Levan (1945), mitosis in
onion root tips induced by lead nitrate has been found to be indistinguishable
from that induced by colchicine in terms of spindle disturbances and chromatid
formation. Ahlberg, et al., (1972) subjected an exposed clone of onion bulbs
to varying concentrations of alkyl lead compounds. Disturbances of the miotic
spindle fiber mechanism occurred at even very low concentrations (10 and
10~ M). The ethyl compounds exerted a stronger effect on the spindle fiber
mechanism than the methyl compounds. Applying the highest dosage, a strong
-------
inhibition of mitosis was noted with triethyllead and trimethyllead after 6 and
24 hours of treatment, respectively. Small, but significant increases of chro-
mosome bridges and fragments as we,Ll as micronuclei were observed with triethyl-
lead concentration of at least 10~ M. The trimethyllead compounds did not
produce a corresponding effect. Barker (1972) grew explanted tissues of cauli-
flower, lettuce, potato and carrot on media containing varying concentrations
of lead acetate. Lettuce was responsive to lead at 0.5 ppm and the growth of
carrot explants was significantly slowed at 0.005 ppm and drastically hampered
at 5 ppm. Toxicity to the growth of cauliflower and potato was noted between
0.5 and 5 ppm. None of the tissues showed discoloration or other gross morpho-
logical abnormalities.
Hampp and Lendzian (1974) found that the syntheses of both types of
chlorophyll in 16-day-old oat seedlings was reduced in proportion to increas-
ing amounts of lead ions. Concentrations as low as 50 micromoles (14 ppm)
PbCl_ had a statistically significant effect. 0 to 500 micromoles inhibited
chlorophyll _b syntheses to a greater extent than that of chlorophyll a. At
higher concentrations the ratio of chlorophyll _a to chlorophyll t> tended
toward unity.
A pronounced inhibition of transpiration and water uptake in spinach
leaves was demonstrated in the presence of less than 100 micromoles Pb(II).
A rise in lead concentration [exceeding 100 micromoles Pb(II)] however, was
not accompanied by a proportional increase of inhibition. There was a pro-
nounced inhibition of gas turnover when 25 micromoles of lead were applied.
There was a greater inhibition of C0? uptake in.the light period than of C0?
release in the dark period. The intensity of C0~ fixation by isolated
spinach chloroplasts was reduced by all lead concentrations tested (2 to 200
micromoles lead nitrate). ATP syntheses in illuminated chloroplasts was also
reduced (Holl and Hampp, 1975). Corn (Zea May_s) and soybean (Gly_cin_e max )
plants grown in media receiving lead treatments of showed decreased net photo-
syntheses and transpiration at increased treatment levels. Treatment in-
cluded application of solutions containing 0, 250, 500, 1,000, 2,000 and
4,000 ppm lead in one liter of solution providing 0, 15.6, 31.3, 62.5, 125
and 250 milligrams of lead per plant. Sixteen individual trays of seedlings
of corn and soybeans were used. At 250 milligrams of lead per plant photo-
syntheses was only 10 percent of maximum in soybeans, but 47 percent in corn
although the tissue lead content was much higher than that of soybeans.
Transpiration exhibited similar trends to photosynthesis (Bazzaz, et al.,
1974b).
Lead significantly affects the photosynthesis process in plants. In
fact, photosynthesis is more sensitive to lead than the respiration appa-
ratus. Miles, et al., (1972) report that lead salts (chloride) inhibited
electron transport in Photosystem II of the chloroplasts in spinach (Spin-
acia oleracea) and tomato (Lycopersicum esculentum) leaves as contrasted to
that in Photosystem I. Holl and Hampp (1975) report a case in which Photo-
system I in spinach chloroplasts was inhibited in the presence of lead ions.
The inhibition was less pronounced than that for Photosystem II. Bazzaz and
Govindjee (1974) found that lead chloride inhibits or stimulates Photosystem
II activity depending on the pH of the reaction media. At pH 7.8, an inhi-
bition of 16 to 39 percent with 0.75 to 9 millimoles PbCl2 was observed;
4.35
-------
however, a stimulatory effect of 20 percent was observed with 9 millimoles
PbCl- at pH 6.5. Light intensity was 2 x 10 ergs cm" sec . One ml
samples containing 5 to 8 micrograms ehloroplast were suspended in buffer and
50 micromoles 3 - (3, 4-dichlorophenyl) 1, 1-dimethylurea.
In spinach root and leaf homogenates, several enzymes unique to the
photosynthetic process exhibited changes in activities in the presence of
5 to 200 micromoles of lead nitrate (Roll and Hampp, 1975). Five micro-
moles of lead nitrate inhibited ribulose diphosphate carboxylase, and lactate
dehydrogenase showed a similar but less pronounced decrease in activity.
Pyruvate kinase activity was enhanced by all lead nitrate concentrations
tested, reaching an optimum at 20 micromoles. The NAD- and NADP-dependent
triose phosphate dehydrogenase systems were mostly activated at the respec-
tive lead concentrations of 100 to 500 micromoles and 100 to 1,100 micro-
moles. In plant tissues, lead ions have been found to lower the concentra-
tions of metabolites such as acetyl coenzyme A, malic acid and other soluble
organic acids, and kardenolides.
Koeppe and Miller (1970) and Miller and Koeppe (1971) have found that
lead affects mitochondrial respiration. In corn mitochondria, lead chloride
(10 to 62 micromoles per liter) stimulated the oxidation of exogenous,
reduced NADH by 174 to 640 percent whereas 12.5 micromoles per liter of lead
chloride inhibited succinate oxidation by more than 80 percent. When inor-
ganic phosphate was included in the reaction media, the subsequent addition
of lead was not effective due to the low solubility of lead phosphate. When
the addition of lead was followed by the addition of phosphate, succinate
oxidation inhibition was released but there was no reduction in the stimula-
tion of oxidation of NADH. It was therefore concluded that high concentra-
tions of lead in plants will not be effective due to the precipitation of
lead if sufficient phosphate is present.
4.3.3 Translocation in Vascular Plants
Contaminant movement within vegetation depends on soil-plant-water
relations. Luxmoore, et al., (1975) coupled an atmosphere-soil-plant-water
relations model with a plant growth and uptake model to describe the two
pathways for contaminant movement in vegetation: water movement from roots
to leaves and sugar translocation from leaves to roots. Most of the lead
studies, though limited in number, indicate that lead is either unavailable
to the plant or is "fixed" in the roots and only small amounts are trans-
located to the above-ground parts of the plant even when the plants are
grown on soil containing substantial amounts of lead. This is due not only
to the solubility of lead in the soil but to some internal factors which
govern the mobility of lead within the plant. This phenomenon varies among
plant species (Hemphill, 1972; MacLean, et al., 1969; Marten and Hammond,
1966; Mitchell and Reith, 1966; Rabinowitz, 1972; Rolfe, 1973; Rule, et al.,
1975). Significant increases in lead content of top growth due to soil
application of lead have been reported by Jones and Hatch (1945) and Warren
and Delavault (1962).
Banus, et al., (1974) have found that lead is rapidly transported from
salt marsh sediments to the leaves and shoots of marsh grasses, especially
-------
those of cordgrass (Spartina alterniflora). It was previously thought that
grass roots were very effective barriers of the movement to lead to other
parts of the plant. Jones and Clement (1972) and Jones, et al., (1973a)
studied the uptake of lead by roots and its transport to shoots using peren-
nial ryegrass (Lolium perenne var. S23) in solution culture rather than
complex soils. The proportion of lead reaching the shoots at first harvest
(7 days after lead additions) was 3.5 to 22.7 percent of the total uptake,
the lower value being for plants with the greatest burden. Transport to the
shoots continued throughout experimental periods of 21 and 28 days, but did
not exceed 28.9 percent of the total uptake. At the highest level of added
lead, there was some indication that the rate of transport increased with
time. The experiments showed that the roots of actively-growing ryegrass
plants readily take up lead but pass only a small proportion to the shoots.
In contrast, Jones, et al., (1973b) found that when perennial ryegrass is
growing in soil, the roots restrict the movement of lead into the tops of
high-yielding plants, but when growth is limited by a sulfur deficiency the
concentration in the tops increases markedly. During the winter period
when the growth rate is low, considerably increases have been observed in
the lead content of grass shoots (Jones and Clement, 1972; Jones, et al.,
1973a). Mitchell and Reith (1966) reported lead increases from 0.8 to 1.5
ppm in August/September to 5.1, 11.9, and 21.8 ppm in late November in rye-
grass, cocksfoot, and mixed pasture grasses, respectively. The above in-
creases were confined to the months of restricted growth. The lead was
transported to the stem prior to winter dormancy possibly by the way of the
phloem. This same phenomenon was found in leaves of deciduous trees and in
wild oats (Rains, 1971; Zimdahl and Arvik, 1973).
Rabinowitz (1972) verified foliar absorption and subsequent transloca-
tion of lead halide aerosols by oats (Avena sativa) and lettuce (Lactua
sativa var. Black-Seeded Simpson) grown near the San Diego Freeway which
reportedly carried 360,000 cars per day. Four to ten parts per million of
atmospheric lead was absorbed by the leaves and translocated downward in the
plants to the central taproots. John and VanLaerhoven (1972a) believe that
since higher levels of lead were found in oat roots than in tops, translo-
cation of lead is of a restricted nature. Based on their findings, the
authors postulated that liming may restrict the translocation of lead from
roots to above-ground portions. According to a calculated transport index,
there was an enhancement of lead movement into the above-ground portion of
the oat plants when lead was added to the soil.
Generally, the translocation of lead in plants cannot be considered an
isolated phenomenon, rather it is related to such factors as involvement of
chelates, ion concentration in the medium, pH, and chemical equilibrium pre-
valent in the soil medium in question. The uptake can probably be controlled
through modification of the soil with the appropriate minerals which affect
these chemical equilibria. For example, Miller and Koeppe (1971) found that
corn plants grown in a soil deficient in phosphate allowed a very substantial
uptake and translocation of lead. Because of the buffering capabilities of
soils and plant roots, as well as absorption and precipitation phenomena,
most lead in soils is not going to be translocated to above-ground regions of
plants. However, uptake can be appreciable following alterations in the
environmental state of the plant as well as the physiological condition of
the plant.
4.37
-------
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4.46
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5.0 EFFECTS ON ANIMALS
5.1 SUMMARY
Much evidence exists for elevated amounts of lead residues in wild ani-
mals as a result of environmental pollution from a variety of lead sources.
In aquatic systems, both freshwater and marine, a variety of benthic and
pelagic organisms including worms, mollusks, and fishes, accumulate lead;
in some cases these levels exceed the "norm" or baseline level for the par-
ticular organism. However, excluding grossly polluted streams associated
with some mining operations, that lead is deleterious to aquatic populations
and communities in nature has not been demonstrated. Numerous laboratory
investigations of short-term and chronic effects of lead on fishes have been
made. The behavior of lead in aquatic systems, and thus the availability of
lead to the biota, have not been resolved. It is generally believed that
lead is precipitated from the water column to bottom sediments, remaining
there with little effect on or translocation to the aquatic flora and fauna.
However, there is recent evidence that methylation of inorganic lead can
occur in an aquatic environment. This may eventually be shown to be signifi-
cant.
Biotranslocation and magnification of lead in certain components of ter-
restrial ecosystems have been demonstrated. In areas of high lead emission
from automobile exhaust, predaceous insects were found to have higher lead
levels than those insects which fed upon plants. This indicates a biomagni-
fication of lead from herbivore to carnivore trophic levels.
Lead poisoning remains a serious health problem in waterfowl, especially
for mallard ducks. Lead shot from spent shotgun shells is the source of
poisoning. Evidence obtained from starling and pigeon populations suggests
that lead residue levels in nongame birds are higher in urban areas.
Poisoning of domestic animals - cattle, horses, and pets - is most fre-
quently attributable to ingestion of lead contained in lead-based paints,
linoleum, storage batteries, putty, and used motor oil. Airborne lead from
mining, smelting, and lead-using industries has poisoned cattle and horses
in localized areas by contaminating hay and pasturage. Airborne lead from
vehicular exhaust emission is suspected in one instance of causing lead
poisoning in zoo animals. Small, wild mammals which inhabit areas adjacent
to major highways have elevated body burdens of lead.
5.2 INVERTEBRATES
Because of the importance of invertebrates as components of food chains
providing food sources for a large number of organisms occupying higher
trophic levels, the uptake, accumulation, and toxicity of lead have been
studied in a variety of invertebrate species.
5.1
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5.2.1 Aquatic
5.2.1.1 Metabolism: Uptake, Absorption, and Residues—
Drifmeyer and Odum (1975) investigated the uptake of lead, zinc, and
manganese by salt-marsh biota living in two diked, dredge-spoil disposal
areas in Virginia which had received heavy metal-containing dredge-spoil.
Eighty-two specimens of the grass shrimp (Palaemonetes pugio) showed a
significant (0.01 confidence level) difference in whole-body lead contents
between grass shrimp collected from ponds inside diked, spoil-disposal
areas where lead levels averaged 11.0 plus or minus 1.8 ppm, and grass
shrimp from natural marsh areas where the concentration of lead averaged
0.2 plus or minus 0.3 ppm.
Warnick and Bell (1969) studied the acute toxicity of lead in three
species of aquatic insects. Individuals that were killed in these static
tests absorbed 0.05, 0.12, and 0.08 mg of lead, respectively, for Acroneura
(stonefly), Ephemerella (Mayfly), and Hydropsyche (Caddisfly).
Gale, et al., (1973) found that lead levels in consumer organisms in
Missouri's New Lead Belt decreased as the distance from tailings ponds in-
creased. At distances of 0.3 to 6.7 kilometers (0.2 to 4.2 miles) down-
stream from a tailings pond which holds combined mine and mill effluents,
lead levels in crayfish and snails were 69 to 28 ppm, and 116 to 39 ppm
dry weight, respectively. These levels approach background values at 8 to
9.7 km (5 to 6 miles) downstream.
Shells of the freshwater clam Corbicula manillensis are considered
good monitors of total lead increase over baseline concentrations in water
at pH 7 or above (Clarke and Clarke, 1974). Empty Corbicula shells were
collected from the Harpeth River in Nashville, Tennessee. One group was
analyzed for their lead content while others were placed in 70 liters of
lead-spiked [16 ppm Pb(NO )_], deionized water or 70 liters of deionized
water buffered at pH 8.38 for 3 months. Those shells analyzed without
further experimentation had an average lead content of 1.9 ppm. Those
exposed to lead-spiked, deionized water and to lead-free, deionized water
had average lead concentrations of 69.5 and 4.1 ppm, respectively. Clam
species from the Illinois River which had an average concentration of 28
ppm of lead in bottom sediments were found to contain the following amounts
of lead (averages in parentheses): Fusconaia flava, 1.8 to 5.1 (3.7) ppm;
Amblema plicata, 1.1 to 7.5 (2.7) ppm; and Quadrula quadrula, 0.9 to 3.8
(2.2) ppm (Mathis and Cummings, 1973). These same authors reported 6 to
39 ppm lead (17 ppm, average concentration) for the tubificids Limnodrilus
hoffmeisteri and Tubifex tubifex.
The uptake of heavy metals from seawater or estuaries by the animal
living therein may occur on the body surface, across the general body
surface, or on specialized areas such as the gills or the shell. Bryan (1971)
indicated that lead, zinc, and cadmium are stored in the hepatopancreas
(digestive gland) of the clam Scrobicularia plana and in the renal organs
of the scallop, Chlamys opercularis. Anderlini (1974) analyzed the gills,
5.2
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mantle, digestive gland, and foot of 74 specimens of the red abalone from
five sites on the California coast for eight heavy metals. Lead concentra-
tions were below detection (less than 0.1 ppm, dry weight) in the gills,
mantle and foot. Highest concentrations of lead were in the digestive gland
(9 to 40.8 ppm). Schwimer (1973) determined levels of lead and fourteen
other metal ions in the herbivorous gastropod Olivella biplicata, the preda-
tory gastropod Polinices lewisii, and the predatory sea star Pisaster
brevispinus collected at three different sites in California including a
sewage outfall. Lead levels were found to be greatest for Olivella (4.6 to
11.8 ppm) and in the soft parts of Polinices (2.6 to 7.4 ppm). Pisaster
tended to concentrate lead in the rays with a high lead value of 26.6 to
35.2 ppm. Polinices shells accumulated the greatest amounts: anterior
shell, 10 to 22.4 ppm; shell spire, 21.7 to 39.1 ppm; and anterior shell,
18.1 to 34.5 ppm; shell spire, 21.7 to 39.1 ppm; and anterior shell, 18.1
to 34.5 ppm. Olivella shells accumulated 15.9 to 25.5 ppm. In the Mytilus
edulis the largest amount of lead is accumulated in the kidney. (Schulp-
Baldes, 1974).
Graham (1972) analyzed 6 species of mollusks from 11 locations in
California for lead, silver, cadmium, chromium, copper, manganese, and zinc.
The species examined included 2 herbivorous gastropods (Acmaea digitalis and
Tegula funebralis), one predatory snail (Thais emarginata), 2 bivalves living
on hard substra (Mytilus Californianus and Medulis), and 2 burrowing clams
(protothaca staminla, and Tapes semidecussata). These species live in the
intertidal zone, and near cities where they are exposed to atmospheric
lead fallout from automobile exhaust. M. Californianus was also found in
the vicinity of a sewer outfall. The lead content of the shells of these
mollusks averaged less than 9 ppm lead on a dry-weight basis. Body-lead
levels were as follows: Acmaea digitalis 931 ppm; M. Californianus 23.4 ppm;
Tegula funebralis 9.8 ppm; M. edulis 7.9 ppm; Protothaca staminea 5.2 ppm;
and Tapes semidecussata, less than 2.2 ppm.
In Mobile, Alabama, where the mean water-lead levels ranged from 0.5 to
3.0 micrograms per liter (ppb) Kopfler and Mayer (1973) found in oysters an
average of 0.67 to 0.88 milligram lead per kilogram (ppm) wet weight. This con-
centration is about two times that of the average value for Atlantic Coast
oysters. Pringle, et al., (1968) studied the uptake and concentration rates
of approximately ten trace metals including lead in the Northern quahaug or
hard-shell clam (Mercenaria mereenaria), the soft shell clam (Mya arenaria),
the American (Eastern) and Pacific oysters (Crassostrea Virginia and C. gigas)
in their natural environment. Anatomical uptake of lead as well as depletion
studies were conducted using the Eastern oyster. There were species differences
in the uptake and concentration of lead. Temperature, salinity, dissolved
oxygen, pumping rates, and the physiological conditions of the animal are all
closely related to uptake and the concentration level. Clams (Mya and Mercenaria)
and oyster (Crassostrea) collected along the Atlantic and Pacific coasts con-
tained the following lead concentrations in parts per million (ppm) of wet
weight: Eastern oyster, 0.10 to 2.30; Pacific oyster, 0.10 to 4.50; soft-shell
clam, 0.10 to 10.20; and hard-shell clam or Northern quahaug, 0.10 to 7.50.
Along the Atlantic coast the Eastern oyster, soft-shell clam, and Northern
quahaug had average lead concentrations of 0.47, 0.70, and 0.52 ppm, respective-
ly. The Pacific oyster had an average lead concentration of less than 0.20
5.3
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ppm at various times of the year. Trace metal depletion studies carried out
for 21 days showed that the Eastern oyster loses lead at the rate of 0.48 to
0.91 milligram per kilogram per day. There appeared to be a direct relation-
ship between the uptake rate and its depletion for any molluscan species. The
results of studies on the uptake and concentration of lead in the Eastern oyster,
Northern quahaug, and soft-shell clam subjected to a simulated natural environ-
ment are summarized in Table 5.1. Under the same experimental conditions with
the oyster and soft-shell clams, doubling the level of lead will result in
twice the rate of uptake and tissue concentration reached in the same time
period. The four environmental lead levels (0.025, 0.05, 0.1, and 0.2 ppm)
gave identical results as to the concentration order in the anatomical storage
studies. Anatomical areas in the order of their increasing lead concentration
(ppm) were: muscle, 9 to 115; mantle edge, 15 to 192; mantle, 14 to 212;
remaining body parts, 18 to 237; gill, 23 to 274, gonad, 26 to 235; and
digestive gland, 28 to 368. The high lead concentrations in the liver (diges-
tive gland) and gill indicate that these organs serve as areas for lead stor-
age in the oyster. This correlates with the presence of large number of
chelating organic ligands in these tissues.
Valiela, et al., (1974) found that the growth of Mercenaria mercenaria
and Crassostrea virginica, bivalves found in tidal creeks in salt marshes along
the East Coast, was not affected by the addition of sewage sludge containing
0 to 81.3 mg Pb/m and urea fertilizers to salt-marsh plots. Growth of
Modilolus demissus, a mussel inhabiting the marsh surface was enhanced in
all fertilized treatments. However, no increases in lead content were ob-
tained in any of the three species.
5.2.1.2 Effects-
Several studies have been conducted on the toxicity of lead to freshwater
and marine protozoans. Apostol (1973) found that lead acetate at 500 milli-
grams per liter killed Paramecium caudatum; concentrations at 100 milligrams
per liter only inhibited growth of this species. Carter and Cameron (1973)
reported that lead nitrate was much more toxic to the ciliated protozoan
Tetrahymena pyriformis in soft water than in hard water: 96-hr LT_0 was 42
ppm for soft water, and greater than 250 ppm for hard water. Growth of cul-
tured Cristigera, a bacterivorous marine ciliate, was reduced 8.5 percent at
a lead nitrate level of 0.15 ppm (Gray and Ventilla, 1973). Table 5.2 from
Ruthven and Cairns (1973) illustrates the response of several free-swimming
protozoans to lead as lead nitrate.
Karbe (1973) exposed the colonial hydroid Eirene viridula to varying
concentrations of lead nitrate in natural seawater to assess the response
of the polyps to pollutants. One to ten parts per million lead induced
morphological changes and tissue reorganization of hydranths. The thresh-
old lead concentration giving acute effects was 1 to 3 ppm. Siegel, et
al., (1973) on exposure of planaria and Oniscus (Isopoda) to tetraethyl-
lead recorded 50 percent survival times of 576 and greater than 1,000
minutes, respectively. Brown and Ahsanullah (1971) studied the toxicity
of six metal salts including lead nitrate to Artemia salina (brine shrimp)
and Ophryotrocha labronica (polychaete), and the effect of three selected
5.U
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Table 5.1 LEAD ACCUMULATION IN A SIMULATED NATURAL
ENVIROmtENTAL SYSTEM AT 20 Ca
Shellfish Species
Soft- shell clam
Soft-shell clam
Soft- shell clam
Northern quahaug
Eastern oyster
Eastern oyster
Eastern oyster
Eastern oyster
Environmental
Lead Level,
0.1
0.2
0.2
0.2
0.025
0.05
0.1
0.2
Total
Accumulation,
mg/kg
112
235
260
35
17
35
75
200
Accumulation
Time,
days
70
40
84
56
49
49
49
49
Accumulation
Rate,
mg/kg/day
1.60
5.80
3.10
0.63
0.35
0.71
1.50
4.00
aModified from Pringle et al.,(1968)
-------
Table 5.2 CONCENTRATIONS OF LEAD NITRATE LETHAL TO
OR TOLERATED BY SIX FREE-SWIMMING PROTOZOAN
SPECIES3
Concentration, ppm
Species
Chilomonas
Peranema
Tetrahymena
Paramecium multimicronucleatum
Euglena gracilis
Blepharisma
Lethalb
320
>100
56
100
Tolerated0
5.6
1000
24
24
1000
42
aSource: Ruthven and Cairns. Reprinted with permission
from Journal of Protozoology (c) Journal of Protozoology (1973).
b
Lethal concentration - lowest concentration at which all
organisms die in 10 minutes.
cTolerated concentration - highest concentration at which
some organisms were living after 3 hours.
5.6
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metal salts on their growth rates. Lead was among the metals with low
toxicity. Lead at 10 ppm was least toxic of the six metals to Artemia and
Ophryotrocha, with LC5_ being more than 600 and 576 hours, respectively,
for Ophyrotrocha and Artemia adults. Exposure to a lead concentration of
10 ppm did not significantly suppress the growth of Ophryotrocha whereas
exposure to 5 and 10 ppm lead significantly suppressed the growth rate of
Artemia.
The toxicities of lead (as lead chloride) and other metals in Lake
Superior water to Daphnia magna were evaluated on the basis of a 48-hr LC _,
a 3-week LC , and a 3-week 16 and 50 percent reproductive impairment (de-
crease in the number of young born). The acute 48-hr LC,-0 was 450 micrograms
per liter when the daphnids had been fed. The lead concentrations giving a
3-week LC5Q, and 50 and 16 percent reproductive impairments were 300, 100,
and 30 ppo, respectively. Reproductive impairment was found to be a more
sensitive measure of toxicity than survival. Lead was found to stimulate
glutamic oxalacetic transaminase activity and to cause a decrease in weight,
but there was little change in the protein content (Biesinger and Christensen,
1972). McKee and Wolf (1963) in their review of toxicity data point out
that 0.01 to 1 ppm lead chloride in various kinds of water was deleterious
to Daphnia magna after 10 days' exposure. In Lake Erie water 128 ppm lead
chloride was found to be lethal to Cyclops vernalis. Wilder (1952) reported
that lobsters died within 20 days when kept in lead-lined tanks but survived
60 days or longer in steel-lined tanks.
Whitley (1968) exposed two turbificid worms, L. hoffmeisteri and T.
Uibifex to 1 milligram of lead (as lead nitrate) per liter of modified Knop's
solution. The 72-hr TLm (median tolerance limit) was 27.5 ppm at pH 8.5
and 49 ppm at pH 6.5. Warnick and Bell (1969) conducted static bioassays
to determine the toxicity of some heavy metals to aquatic insects. With a
high test concentration of 64 ppm, 96-hour TLm values were not found. Fifty
percent survival times (LC-_) were as follows: Acroneuria, greater than 14
days at 64 ppm, Ephemerella, 7 days at 16 ppm, and Hydropsyche, 7 days at
32 ppm.
Pringle, et al., (1968) exposed American (Eastern and Pacific) oysters
to four environmental lead concentrations (0.025, 0.05, 0.1, and 0.2 ppm).
At lead concentrations of 0.025 and 0.05 ppm, the oysters appeared to be
in good gross physiological condition. However, at 0.1 and 0.2 ppm,
considerable toxicity was noted and the following anatomical changes occurred:
(1) atrophy and diffusion of gonadal tissue; (2) less identifiable and
lighter-colored hepatopancreas, (3) considerable edema, and (4) disappearing
or less distinct mantle edge.
Calabrese, et al., (1973) studied the effect of eleven inorganic metal-
lic salts on the survival of American or Eastern oyster embryos. The 48-
hour LC_ and LC5_ for lead nitrate were 0.5 and 2.45 ppm, respectively. Lead
concentrations greater than 6 ppm were necessary for 100 percent mortality.
Calabrese and Nelson (1974) found that lead nitrate was lethal to hard-shell
clam embryos at 1.2 ppm. LCn, LC_0, and LC5Q ranges for hard-shell clam
embryos were 0.40, 0.78, and 0.72 ppm, respectively, in synthetic seawater.
5.7
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Cleland (1953) found that approximately 200 ppm lead as lead nitrate in
seawater produced abnormalities in the eggs of sea urchins. A concentration
of only 124 ppm lead was required to suppress membrane elevation. At this
concentration subsequent cleavage was mostly normal and polyspermic.
5.2.2 Terrestrial
5.2.2.1 Metabolism: Uptake, Absorption, and Residues—
Price, et al., (1974) sampled insect communities at sites for the level
of lead emissions from motor vehicle exhausts. They found no significant dif-
ferences in the lead content of insects among sample sites within the same
traffic density and vegetation category, or among samples taken at different
times of the year. However, in areas of high lead emission insects had aver-
age lead levels (ppm, oven dry weight) of 10.3, 15.5, and 25 for species that
suck plant juices, chew plant parts, and prey on other insects, respectively.
This does indicate a biomagnification of lead from herbivore to carnivore
trophic levels. In low-lead emission areas insects in the same feeding cate-
gories had average lead contents of 4.7, 3.4, and 3.3 ppm. Giles, et al.,
(1973) determined the lead content of Japanese beetles (Papillia japonica),
damselflies (Agrion maculaturn), and the European mantid (Mantis religiosa)
collected along Baltimore, Maryland's major north-south freeway (1-83), which
in 1970 had an average daily traffic count of 13,000 vehicles, and in a con-
trol area 480 meters west of the freeway. Japanese beetles had 7.1 and 9.0
ppm lead, respectively, in control and freeway areas. Their host plants (wild
carrot and evening primrose) contained 3.0 and 4.3 ppm, respectively, in the
control area and 9.4 and 15.7 ppm in the freeway area. Since these insects
are strong fliers, there is a possibility of intermingling of individuals
from the control and freeway areas. This species spends only a few months of
its life cycle above ground thereby limiting the time lead can be accumulated
from feeding on contaminated plant parts. The damselfly is a weak flier so
the imagoes were probably indicative of environmental conditions of the
collection sites. In the control area lead levels in damselfly imagoes ranged
from 6.83 to 6.97 ppm; in the freeway area, 7.08 to 9.09 ppm. European
mantid nymphs and imagoes in the control area had respective lead levels of
2.04 ppm, and 1.27 and 1.94 ppm. In the freeway area 7.35 ppm (nymphs), and
3.52 and 14.80 ppm (imagoes) lead were present. It did appear that measur-
able amounts of atmospheric lead were being concentrated by these insect
predators.
Nehring (1976) studied the acute toxicity of some heavy metals to a
mayfly (Ephemerella grandis) and a stonefly (Pteronarcys californica).
Flow through methods were used, with a dilution water whose alkalinity and
hardness varied from 30 to 70 ppm (as Ca C0g) between tests, but not more
than 10 ppm within a test. The 14-day LC values were greater than 19.2
ppm lead for the stonefly, and 3.5 ppm lead for the mayfly.
Gish and Christensen (1973) found that lead, cadmium, nickel, and
zinc in soils and earthworms decreased with increasing distances—3, 6, 12,
24, and 48 meters (10, 20, 40, 80, and 160 feet) from the Baltimore-
Washington Parkway and U.S. Highway No. 1. Highest lead concentrations in
soils and in earthworms along either highway were found in plots closest
to the roadway. Lead concentrations in soils and earthworms along the
5.8
-------
Parkway with a traffic density of 47,800 and 44,500 cars per day were 228
and 93 ppm, and 121 and 107 ppm, respectively. Along U.S. No. 1 with a
traffic density of 25,100 and 25,600 cars per day, soils had 63.7 and 83.5
ppm lead and earthworms had 64 and 76.7 ppm lead. The maximum lead level
accumulated by earthworms was 331 ppm which might be lethal to animals that
feed on earthworms. The mean lead concentrations for the two highways com-
bined at distances of 3 to 48 meters (10 to 160 feet) from the roadway were
468 to 53.4 ppm (soils) and 270 to 52.7 ppm (earthworms). Lead levels in
earthworms averaged 0.95 times those in the soils. The ratios of lead in
earthworms to those in soil tended to increase as distance increased. Lead
levels at 3 meters (10 feet) from the roadway, though higher at other distan-
ces, were half those in the soil. At other distances, the levels were ap-
proximately equal. Differential accumulation by earthworms (AJLabophera,
Lumbricus, and Octolasium) of cadmium, lead, and zinc in six soil series in
east Tennessee was determined by Van Hook (1974). Mean lead concentrations
in soils and earthworms were 27 and 4.7 ppm, respectively. The mean earth-
worm concentration factor for lead was 0.2, ranging from 0.1 in Emory soil
to 0.3 in Captina soil. Lead was not biologically accumulated by earthworm
species studied. Based on the results obtained, Van Hook believes that
earthworms could serve as useful biological indicators of increased lead,
cadmium, and zinc contamination of soils because of the fairly consistent
relationship between element concentrations in earthworms and soils. These
invertebrates are key components in natural food chains and are a food source
for many small mammals and birds.
5.2.2.2 Effects-
Lower (1975) used the vinegar fly, Drosophila melanogaster, to monitor
the environmental enrichment of lead, cadmium, cpper and zinc at geographical-
ly separated lead smelting facilities in Missouri. Changes in gene frequency
in five of ten isozyme loci in Drosophila were significantly correlated with
distance from a smelter which has been operated since 1968 at Bixby, Missouri.
Enrichment also occurred at other locations. At lead concentrations of 12 to
1,200 ppm, the frequencies of alleles decreased at the four loci which had
been definitely correlated, with lead and cadmium. The changes in frequencies
occurred over a distance of 11 kilometers with the greatest change in the first
5 kilometers. Seasonal changes in gene frequencies did not mask those changes
associated with distance from the Bixby smelter or metal concentrations. The
author postulates that intensive selection pressure is the cause of the
changes. This study further confirms that lead interferes with mitotic and
other essential functions (see Sections 4.3.2.2 and 6.3.1.). Further in-
vestigations utilizing D^ melanogaster might clarify the mode of action
of lead and other heavy metals within animal cells.
5.3 FISH
5.3.1 Metabolism; Uptake, Absorption, and Residues
Naturally occurring levels of lead in fishes are subject to variations
due to age and species, fluctuations and differences in water chemistry,
and geographical location. A survey of 419 fishes from 49 New York State
waters reported concentrations of lead (analyzed colorimetrically) ranging
5.9
-------
generally from 0.3 to 1.5 ppm; a few specimens contained as high as 3 ppm
(Pakkala, et al., 1972). In this study no correlation was drawn between
the lead concentrations found in fish and the proximity to large cities,
industrial effluents, rural areas or known lead deposits. A study of trace
metals in Cayuga Lake lake trout (Salvelinus namaycush), aged 1 to 12 years,
showed lead levels (decapitated and eviscerated fish) between 4.4 ppb and
22 ppb (Tong, et al., 1974). While highest concentrations for lead occur-
red in fishes 1 and 2 years old, no significant (P = 0.05) correlation be-
tween age and concentration was drawn.
Holcome, et al. , (1976) studied the long term effects of lead on three
generations of brook trout. They found that the greatest accumulation of
lead occurred in the kidney, liver, and gill tissue. Kidney and liver lead
residues from second generation fish reached an equilibrium at various ex-
posure concentrations, then tended to remain at that level or decrease with
continuing exposure. The maximum mean residue levels for liver and kidney
samples, respectively, were 68 and 215 ppm lead in tissue for first genera-
tion fish and 50 and 179 ppm lead in tissue for second generation fish
exposed to 119 ppb lead. Lead residues in gill tissue did not reach an
equilibrium based on ppm lead but tended to increase with continuing
exposure. Muscle tissue did not accumulate lead to any substantial ex-
tent. The mean average lead residue values for all muscle tissue for
test fish and controls were 2.1 and 1.1 ppm lead, respectively.
Lead has been found to accumulate at higher concentrations in certain
fish tissues. In a study of fishes from a lake located near a lead mine
in Sweden, concentrations of lead were 12 ppm in liver, 5.7 ppm in gills,
and 1.4 ppm in muscle (Wetterberg, 1966). Stevens and Brown (1974) found
less than 0.2 ppm of lead, dry weight, in muscle, liver, epigonal and gonad
tissue of 98 percent of blue sharks studied; some individuals contained
concentrations of lead as high as 1.8 ppm in epigonal plus gonad tissue.
In a study of flounders, Hardisty, et al., (1974) found the highest lead
concentrations to be in brain tissue (3.85 to 43.6 ppm). These authors also
found that lead levels in muscle tissue rarely exceed 20 percent of the values
for liver, heart, or kidney, which range from 20 to 30 ppm for flounders. The
largest flounders (length and age class) exhibited the highest concentrations
of lead; no consistent seasonal variation was apparent. Chow, et al., (1974),
found that 3 percent of all lead in tuna resides at a concentration of 0.003
ppm in fresh muscle; 52 percent resides in epidermis at 2 ppm. Muscle com-
prises 75 percent of the total body weight; epidermis amounts to one quarter
of 1 percent, yielding a total body burden of lead in albacore tuna of
0.008 ppm. (Interestingly, Chow, et al., (1974) state that contamination by
industrial lead raises the concentrations of lead in tuna processed for
human consumption about 1,000 times that found in living tuna. Concentrations
in the mucosal slime could only raise muscle concentrations by a factor of
20 by contamination.) Table 5.3 presents lead values found in tissues of
sardines and anchovies (Gilmartin and Revelante, 1975). Increased lead
concentrations in skin tissue during the winter sampling were possibly due
to resuspension of sediments by the wind.
Chow, et al., (1974) claim that values reported for lead in materials
such as sea water and fish tissue may be erroneously high. They state
5.10
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Table 5.3 CONCENTRATIONS OF LEAD IN TISSUES OF SARDINE
AND ANCHOVY FROM THE ADRIATIC SEA3
Lead Concentration, ppm. Wet Weight
Sardine :
June 9, 1972
July 10, 1972
August 17, 1972
September 29, 1972
October 31, 1972
December 5, 1972
Mean
Anchovy :
June 9, 1972
July 10, 1972
August 17, 1972
October 3, 1972
October 31, 1972
December 6, 1972
Mean
Skin
4.5
4.9
4.3
5.3
3.3
6.8
4.9
2.7
5.2
5.7
1.6
7.0
6.5
4.8
Gills
3.0
4.5
2.6
1.9
2.4
3.1
2.9
4.3
3.7
3.9
2.6
3.1
3.9
3.6
Muscle
0.4
0.1
ND
ND
ND
ND
0.1
ND
ND
ND
ND
1.2
0.3
0.3
Digestb
ND
•ND
ND
2.2
0.7
0.3
0.5
ND
0.4
0.3
1.3
0.7
0.4
0.5
b
Liver
ND
ND
ND
ND
ND
ND
ND
ND
ND
1.1
1.5
3.4
11.0°
1.2
Total
Fish
1.23
0.94
0.82
0.84
1.38
1.40
1.1
0.99
0.99
0.51
0.73
1.16
1.37
1.0
a
Adapted from Gilmartin and Revelante (1975)
ND = not detected.
Suspect value - excluded from mean.
5.11
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"not one oceanographic laboratory of superior status could, as of September,
1973, collect and analyze lead in coastal surface seawater by atomic absorption
or anodic stripping voltammetry techniques and report reliable results."
Based upon their findings of lead concentrations in tuna they state further
"These new findings strongly suggest, as in the case of seawater, that recent
studies of the hazards of lead pollution may be misleading if they are based
on analyses of plant and animal tissues determined by routine analytical
methods carried out without the use of clean-laboratory techniques and without
the necessary sensitivity and accuracy." The method these workers employed
was stable isotope dilution using thermal ionization source high-resolution
mass spectrometers and special clean-laboratory techniques. They found that
tuna muscle, uncontaminated by handling, contained approximately 0.0003 ppm
lead (wet weight). However, commercial canned tuna muscle contained amounts
of lead in the order of 0.1 to 0.9 ppm.
Much evidence exists for elevated amounts of lead in fishes because
of environmental pollution. Fingerling brook trout previously exposed to
increased invironmental lead concentrations due to snowmobile exhaust
(4.1 ppb of lead before freezing and 135 ppb after ice-melt) were found to
contain nine to sixteen times more lead than control fishes (Adams, 1974;
Adams, 1975). Lead levels in muscle tissue of the wooly sculpin (Clinocottus
analis) were found to increase from a rural tidepool area of California to an
area receiving atmospheric lead pollution (Alley, et al., 1974). For this
species, "control" levels were 0.6 ppm; fishes from polluted areas contained
2.7 ppm and 4.9 ppm. Fagenkopf and Neuman (1974) obtained similar results
in a study of lead concentrations in fish tissue from a hatchery (1.41 ppb)
and from the West Gallatin River in Montana (2.56 to 2.96 ppb). Mean concen-
trations of lead found in bone, liver, and gill tissue from the two sites
were 0.95 and 3.85 ppm, 0.61 and 1.56 ppm and 0.62 and 2.43, respectively. Van
Coillie and Rousseau (1974) found that the lead content in scales from fishes
in waters of undetectable lead concentration was 2.89 times lower than in
scales from fishes in water of 3.0 to 13.0 ppb lead. Mathis and Cummings
(1973) reported on the lead in sediments, water, and biota of the Illinois
River. A concentration gradient ranging from the highest level in worms,
intermediate levels in clams, and lowest levels in fish fillets was found
for lead. There was no statistical significant difference (P = 0.05)
between the lead concentration of the muscle tissue of omnivorous and
carnivorous fish.
Although there is evidence for methylation of lead by bottom s diment
microorganisms, its implication for fish contamination is not presently
known (Wong, et al., 1975).
5.3.2 Effects
Elevated lead concentrations have been proven to be toxic or deleterious
to fishes. Table 5.4 presents a compilation of lead concentrations which
were found lethal or toxic to fish under the conditions specified. Table
5.5 presents a similar compilation for lead compounds.
5.12
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Table 5.4 CONCENTRATIONS OF LEAD REPORTED TOXIC
OR LETHAL TO FISHa
Concentration
of Lead,
ppm
0.1
0.1
0.1-0.2
0.2
0.21
0.25
0.33
0.34
1.0
1.0
1.4
1.4
2.8
4.0
5.5
6.3
10.0
17.0
27.0
40.0
63.0
Type of
Water
—
—
Very soft
Soft
—
Fresh
—
1000-3000 mg/1
of dissolved
solids^
—
V S°ft
Tap
Fresh
Soft
Stream water
Tap
—
—
Tap
—
—
Time of
Exposure
—
r—
i • '
48-hr TLm
Long term
8.5 days
18-24 hr
48-hr TLm
—
10-12 hr
—
24 & 28 hr TLm
—
—
16-183 days
80-hr
80-hr
Species of Fish
Fish
Sticklebacks
Sticklebacks
Fish
Guppy
Fish
Minnows, brown trout
and sticklebacks
Sticklebacks and
coho salmon
Carp
Sticklebacks
Rainbow trout
Bluegill sunfish
Fish
Rainbow trout
Trout
Bluegill sunfish
Goldfish
Goldfish
Catfish
Goldfish
Goldfish
Adapted from McKee and Wolf (1963).
5.13
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Table 5.5 CONCENTRATIONS OF LEAD COMPOUNDS REPORTED
LETHAL TO FISH3
Lead Compound
Lead acetate
Lead ar senate
Lead chloride
Lead nitrate
Concentration ,
ppm
5.
10.
10.
25.
0.33
0.58
0.16
0.53
3.
5.
10.
10.
10.
16.
16.
100.
165.
240.
830.
3320.
8300.
16600.
44000.
53000.
Type of
Water
—
—
Stream
—
Fresh
Time of
Exposure
4-16 hr
12 days;
renewed every
2 days
24-hr
Lake Erie
Tap
Tap
—
—
Natural
Tap
Hard
—
—
Hard
Distil-
led
Highly
turbid
—
—
—
—
—
w —
r*ri
12-hr
2-hr; 1.4
mg/1 dissolved
oxygen
2.5-hr
24 and 48-
hr TLm
4 Days
—
20-hr
80-hr
—
96-hr TLm
3-hr
2.2-hr
1.5-hr
1.4-hr
44 min
40 min
Type of Fish
Minnows
Goldfish
Trout
Trout
Fish
White fish fry
Stickleback
Minnows , stickle-
backs, and brown
trout
Topminnows
Goldfish
Trout
Bluegill sunfish
Goldfish
Goldfish
Minnows
Goldfish
Fish
Mosquitofish
Minnows
Minnows
Minnows
Minnows
Minnows
Minnows
aAdapted from McKee and Wolf (1963).
5.1U
-------
It is commonly theorized (McKee and Wolfe, 1963; Pakkala, et al.,
1972) that in waters containing lead salts, a film of coagulated mucus forms,
first over the gills, then over the whole body of the fish (possibly the
result of a reaction of lead with an inorganic constituent or mucus), Death
is then by suffocation. A report by Aronson (1971) states that recovery
does occur when this mucosal film is shed and that analysis of the film
accounts for virtually all the lead in solution.
Certain species of fishes are more susceptible to lead than others.
The action of lead on goldfish is the same as for trout, sticklebacks,
and minnows, yet goldfish are more resistant. Goldfish appear to tolerate
1 ppm lead in soft tap water (Jones, 1938). In soft tap water 0.1 to 0.2
ppm lead proved fatal to sticklebacks (McKee and Wolf, 1963). Variations
in tolerance may be related to the nature of the gill secretions; goldfish
produce copious amounts (Aronson, 1971b).
More subtle effects have been shown to occur at chronic exposures to
lead. An early study by Dawson (1953) of 16- to 183-day exposures of cat-
fish (Ameriurus nebulosus, genus name since changed to Noturus) to 5 ppm
lead acetate renewed every 48 hours yielded early evidence of blood cell
injury and elicited a mild regenerative response. After several weeks
exposure, Dawson reported the occurrence of injured erythrocytes, progres-
sive anemia, and marked regenerative response in peripheral blood. During
lead poisoning the erythropoletic activity of the spleen was greatly reduced
and the organ itself became smaller and paler. In fishes killed by lead
poisoning, Dawson reported an extreme dilation of the gall bladder. The
prolonged exposures of this study gave evidence of lead absorption. Similar
physiological effects have been noted in guppies at long-term exposures.
Lead has been found to interfere with enzyme activities (see also
Section 6.3.1). Jacklm, et al., (1970) found lead to inhibit alkaline
phosphatase activity in ±n vitro studies on killifish (Fundulus heter-
oclitus), but increased activity of the same enzyme in in vivo studies,
both at 96-hour TLm concentrations (i.e., 188.0 ppm).
Experiments on various life stages of fishes indicate that susceptibility
to lead is greatest during embryo and fingerling stages. Highest mortality
rates in life stages of brook trout (Salvelinus fontinalis) occur among
alevins upon exposure to lead nitrate (Christensen, 1975). Alkaline
phosphatase and acetylcholine esterase activity were increased at 525 ppb
of lead in tissue or water. A decrease in weight in response to 134 ppb
and 525 ppb of lead was also noted.
Mclntyre (1972) reports severe embryo deformation in the eggs of
brook trout at 500 ppb of lead. Similar deformation as well as increased
incidence of blacktail syndrome occurs in fathead minnows at 240 ppb.
Lead concentrations of 25 ppm administered daily as a single dose
under diurnal fluctuations of temperature and disolved oxygen conditions
reduced growth of fingerling brook trout (Dorfman and Whitworth, 1969).
5.15
-------
Of the factors possibly influencing the toxicity of lead to fishes
such as dissolved oxygen concentration, pH of solution, volume and number
of exchanges of experimental solution, and duration of exposure, water
temperature and, particularly, water hardness appear to be important
controlling factors. A 10-degree C rise in temperature has been shown to
reduce survival time by 50 percent (Aronson, 1971). An increase in water
hardness from 14 to 53 milligrams per liter (expressed as calcium carbonate)
decreased lead concentration from 8 to 1.6 ppm by precipitation. Fifty ppm
of calcium destroyed the toxic effect of 1 ppm of lead (McKee and Wolf, 1963).
Calcium has been shown to antagonize toxic lead effects by increasing sur-
vival times of fishes exposed to 1 ppm of lead nitrate with an increase of
calcium nitrate or chloride concentration. In this case, lead toxicity is
not reduced by precipitation, but by prevention of the coagulation of mucus
(Jones, 1938).
In an extensive study of chronic lead exposure to rainbow trout,
Davies and Everhart (1973) determined toxic levels for lead nitrate in hard
and soft waters. Since lead may form complexes or precipitate in hard
water, the concentration of the metal was expressed on a total and dissolved
lead basis. On a total lead concentration basis, the 96-hr TL,.- (50 percent
tolerance limit) was 471 ppm and the MATC (maximum acceptable toxicant con-
centration) was 0.12 to 0.36 ppm. The MATC was determined by the occurrence
of abnormal black tails. On a dissolved lead basis, the 96 hr TL-- was 1.38
ppm and the MATC 0.018 to 0.32 ppm. Lead was considered to be completely
dissolved in soft water. The 18-day TL-- in soft water was 140 ppb and the
MATC was between 6 to 11.9 ppb. The authors developed an application factor
approach that may be utilized to compare the toxicity of lead in different
water qualities where the soluble or free lead in water is determined.
This same study by Davies and Everhardt (1973) investigated the occur-
rence of physical abnormalities in the F.. generation of brook-stock rainbow
trout that were used in the soft water bloassay. Again, no growth or
hematological differences were apparent after 6 months' exposure to lead
concentrations ranging from 3.1 to 95.6 ppb. Black tails, spinal curvatures
and/or eroded caudal fins occurred at concentrations of 11.9 ppb and greater.
No effects were noted at lower concentrations. From this entire study, the
maximum acceptable lead level for rainbow trout is very near 11.9 ppb.
From this survey it can be concluded that the effects of lead on
fishes may be so severe as to cause direct mortality or be so subtle as
to be manifested only after an exposure of considerable duration. Body
surfaces, internal organs or metabolic activities may be affected. De-
trimental effects include not only mortality but also abnormal behavior
rendering the fish more vulnerable to predation. Interference with
metabolic activity, while not only eliciting abnormal behavior, may subject
the fish to attack by disease or parasites. Reproductive success may also
be limited due to the high susceptibility of embryos and fingerlings to
lead effects.
Lead concentrations in water are subject to complex chemical interactions.
Toxicities may be enhanced or reduced by fluctuation in temperature, dissolved
oxygen or concentrations of minerals. There is need for further investiga-
tion to determine maximum acceptable levels under various water chemistry
conditions. ,
5.16
-------
5.4 BIRDS
Concentration of lead in tissues of birds and physiological effects of
lead on birds have mainly been studied in waterfowl, particularly with re-
spect to the ingestion of lead shot (Anderson, 1975; Bellrose, 1959; Coburn,
et al., 1951; Karstad, 1971; Longcore, et al., 1974a; Longcore, et al.,
1974b). The mallard (Anas platyrhynchos) is the duck most frequently assoc-
iated with lead poisoning dieoffs. Use of shotguns in marshes and lakes by
hunters concentrates lead shot on the bottom of heavily hunted areas. The
spent shot is eaten by waterfowl as if it were seeds or grit. As the shot
are held in the duck's gizzard, the lead is absorbed into the body, causing
an estimated 2 to 3 percent of the American waterfowl population to die
annually from lead poisoning (Stickel, 1969). Mortalities due to lead
ingestion by Canadian and United States waterfowl (mostly mallards, mottled
ducks, redheads, and black ducks) have been estimated to be 1.6 to 2.4
million annually out of fall flight population of 100 million ducks. This
great loss has prompted the preparation of an environmental impact statement
on the use of steel shot for hunting waterfowl (U.S. Department of the
Interior, 1976).
Although waterfowl (includes ducks, geese, and swans) has been the
major bird group studied for lead poisoning, other bird groups have also
been analyzed for lead concentration in various tissues and/or examined for
the presence of lead shot. Studies of lead in nonwaterfowl game species
include species-specific studies of the sora rail (Porzana Carolina)
(Artmann and Martin, 1975) and ring-necked pheasant (Phasianus colchicus)
(Lynch, 1973: Anderson and Stewart, 1969), and a general survey of 28 bird
species, including grouse, ptarmigan, rails, doves, and ring-necked pheasants
(Bagley and Locke, 1967). USDI (1976) lists cases of lead poisoning in
godwits, California gulls, and several species of the order Gruiformes (rails,
gallinules, and coots).
Investigations of lead in nongame bird species are not nearly as numer-
ous as studies involving game birds. Bagley and Locke (1967) reported on
lead concentrations in six nongame bird species. Snyder, et al., (1973)
reported on lead levels in eggs of Cooper's hawks (Accipiter cooperii).
Two reports on starlings (Sturnus vulgaris) discussed lead levels at
monitoring sites throughout the United States (Martin and Nickerson,
1973; Martin, 1972). Lincer and McDuffie (1974) reported on lead levels
in American kestrel (Falco sparverius) eggs. Lead poisoning in a prairie
falcon (Falco mexicanus) was described by Benson, et al., (1974). Finally,
two studies analyzing lead levels in herons (Hoffman and Curnow, 1973)
and common terns (Sterna hirundo) (Connors, et al., 1975) found that lead
concentrations in most specimens were below the detection limits of the
analytical procedure used.
5.4.1 Metabolism: Uptake. Absorption, and Residues
Extensive studies of naturally-occurring lead levels in single species
include analysis of starlings (Martin, 1972; Martin and Nickerson, 1973),
pigeons (Tansy and Roth, 1970), and ring-necked pheasants (Anderson and
Stewart, 1969). Whole body, wet-weight lead residues of starlings sampled
5.17
-------
throughout the United States varied from 0.4 ppm at Yakima, Washington, to
a high of 13.3 ppm at Chicago, Illinois, with a mean level of 3.18 ppm for
all sample sites (Martin, 1972). Lead residue levels were highest in birds
from urban areas, reflecting the greater exposure of starlings to automotive
and industrial contamination. The mean lead content per unit weight of hard
(feathers, nails, beak, femur) and soft tissues (liver, kidney) of randomly
procured Philadelphia City pigeons was significantly higher than the cor-
responding values for country pigeons (see Figure 5.1). Interestingly, blood-
lead levels of the city birds were as low as, if not lower than, their country
counterparts (Tansy and Roth, 1970).
Lead concentrations in the liver are considered to be the most useful of
all tissue types in diagnosing lead poisoning (Longcore, et al., 1974a) and
high levels are indicative of severe, recent exposure. Therefore, most studies
have included liver analysis in their sampling plan. One of the best sum-
maries of lead concentrations in livers of lead-poisoned waterfowl (Table 5.6)
indicates that lead levels of 6 to 20 ppm in the liver of waterfowl are diag-
nostic of active lead intoxication (Longcore, et al., 1974a). On the other
hand, background levels of lead in eleven species of waterfowl with no known
history of lead exposure averaged 0.5 to 1.5 ppm (Bagley and Locke, 1967; see
Table 5.7).
One of the most complete studies of naturally-occurring lead levels in
liver tissues of a variety of birds was done by Bagley and Locke (1967) on
28 species of wild birds. They found that the average background lead con-
centrations in the livers of these birds varied from 0.5 to 3.7 between
species (see Table 5.7). Lead levels in livers of ringnecked pheasants from
Illinois varied from 0.09 to 0.84 ppm (Anderson and Stewart, 1969). Lynch
(1973 found a geometric median concentration of 1.59 ppm (see Table 5.8) in
the livers of ring-necked pheasants.
Lead residues in bones are normally higher than those in liver, but seem
to be less diagnostic of lead poisoning (Stickel, 1969). Lead accumulates
in bone from both acute, high-level exposure or chronic, low-level exposure.
Therefore, high bone lead levels are not suitable for diagnosing lead
poisoning, but do indicate chronic exposure to lead.
Lead is stored in the bones of waterfowl and may be present in varying
amounts depending on several factors, including diet, and duration and
levels of exposure. High levels of lead (67 to 73.6 ppm) were found to
occur in wing bones of mallards, for example, as a result of ingestion of
a single lead shot. Food in the form of commercially prepared duck ration
reduced the amount of lead (2.3 ppm) absorbed and deposited in the bones
(USDI, 1976). Longcore, et al. (1974a) found a geometric mean lead con-
centration in the tibia of lead-dosed mallards that died to be 137 ppm.
Lead levels in femurs of eleven Ohio ring-necked pheasants had a
median of 8.0 ppm and a range of 1.8 to 17.1 ppm, wet weight (Lynch, 1973;
see Table 5.8). The average background lead concentration in tibias of 12
species of wild birds varied from 2.0 ppm in eleven Canada geese (Branta
canadensis) to 13 ppm in 18 snow geese (Chen hyperborea) (Bagley and Locke,
1967).
5.18
-------
1000
1-3 Fledgling
4-9 Adult
10-16 Adult
EZBONE
• FEATHERS
KIDNEY
100
123456789 10 II 12 0 W 15 16
Country City
PIGEONS
Figure 5.1 Tissue lead concentration of country and
city pigeons. Source: Tansy and Roth.
Reprinted with permission from Journal of
Air Pollution Control Association.
(c) Air Pollution Control Association, 1970.
5.19
-------
Table 5.6 LEAD CONCENTRATIONS IN LIVERS OF
LEAD POISONED WATERFOWL3
Species
Canada geese
Canada geese
(2 separate
die-of f s)
Canada geese
Canada geese
Canada geese
Canada geese
Mallards
Mallards
Mallards
(2 separate
groups)
Mallards
Whistling swan
Mallard
Mute swan
Mallard
Mallard
Black duck
Source
"die-off"
"die-off"
expt'l.
expt ' 1 .
"die-off"
"die-off"
expt'l.
expt'l.
expt'l.
expt ' 1 .
"die-off"
"die-off"
expt ' 1 .
(died: corn diet)
(died: comm. mix
pellet diet)
(survived: comm.
mix pellet diet)
"die-off"
Amount Lead
Average
18
12
22
20
19
26
21
33
44
12
40
51
28
12
—
29
23
1
25
(ppm, wet wt.)"5
Range
9-27
1-20
12-53
5-32
8-42
12-44
10-45
20-64
23-80
8-14
11-16
16-76
18-37
12
1-70
5-45c
8-66
19-26
1-3
25
References
Adler (1944)
Bagley et al . ,
(1967)
Cook & Trainer
(1966)
Karstad (1971)
Locke et al.
(1967)
Locke & Bagley
(1967a)
Bates et al.
(1968)
Coburn et al . >
(1951)
Barrett & Karstad
(1971)
Locke et al. >
(1966)
Chupp & Dalke
(1964)
Erne & Borg
(1969)
Andrews et al. ,
(unpublished data,
Patuxent Wildlife
Research Center)
Locke & Bagley
(1967b)
Q
Adapted from Longcore et al. (1974a).
cValues rounded to nearest whole number.
This range of values for more than half of the livers examined,
5.20
-------
Table 5.7 THE CONCENTRATION OF LEAD IN THE
LIVER OF BIRDSa
American coot
(Fulica americana)
American scoter
(Oedemia njgra americana)
Bald Eagle
(Haliaeetus leucocephalus)
Black duck
(Anas rubripes)
Brant
(Branta bernicla)
Brown pelican
(Pelecanus occidentalis)
Canada goose
(Branta canadensis)
Canvasback
(Aythya valisineria)
Cowbird
(Molothrus ater)
Domestic goose
(Anser cygnoides)
Dusky grouse
(Dendragapus obscurus)
Great blue heron
(Ardea herodias)
Green wing teal
(Anas carolinensis)
Hooded merganser
(Lophodvtes cucullatus)
Average,
ppmk
2.0
0.5
0.6
0.5
1.3
0.8
0.5
0.5
3.7
0.6
1.1
0.7
1.5
0.9
Range,
ppmb
2.0
0.3-0.9
0.6
0.4-0.6
0.9-1.9
0.4-1.3
0.3-0.8
0.5
2.0-5.0
0.3-0.8
1.1
0.7
1.5-1.6
0.6-1.2
No. of
Samples
1
10
1
2
11
16
11
4
4
4
1
1
2
3
Source
3
2
2
2
2
2
1
2
2.
1
1
2
3
2
5.21
-------
Table 5.7 THE CONCENTRATION OF LEAD IN THE
LIVER OF BIRDS3
(Continued)
King rail
(Rallus elegans)
Mallard
(Anas platyrhynchos)
Mourning dove
(Zenaidura macroura)
Osprey
(Pandion haliaetus)
Pintail
(Anas acuta)
Ring-necked pheasant
(Phasianus colchicus)
Rock ptarmigan
(Lagopus mutus)
Sandhill crane
(Grus canadensis)
Shove ler
(Spatula clypeata)
Snow goose
(Chen hyper borea)
Surf scoter
(Melanitta perspecillata)
Whistling swan
(Olor columbianus)
White-winged scoter
(Melanitta fusca)
Wood duck
(Aix sponsa)
Average,
ppmb
2.0
0.9
3.3
1.5
0.9
0.5
2.1
0.7
1.1
1.2
0.9
0.8
0.8
1.5
Range,
pprni'
2.0
0.3-2.0
0.4-7.0
1.5
0.9
0.2-1.0
2.0-3.0
0.7
1.0-1.2
0.8-1.8
0.4-2.0
0.8
0.3-1.8
0.7-2.0
No. of
Samples
1
16
27
1
1
21
7
1
3
18
23
1
18
5
Source0
2
1
2
2
3
1
3
2
3
2
2
2
2
2
^agley and Locke. Reprinted with permission from Bulletin of
Environmental Contamination and Toxicology, (c) Springer-Verlag New York,Inc.,
X7D/ .
cWet weight basis.
(1) = Pen raised; (2) = captured or shot; (3) = found dead.
5.22
-------
Table 5.8 LEAD CONCENTRATIONS IN TISSUE SAMPLES
FROM OHIO RING-NECKED PHEASANTS3
Tissue
Brain
Breast
muscle
Feather
Femur
Kidney
Leg muscle
Liver
Ovary
No.
Analyzed
1
33
18
11
2
14
11
1
No.
Positive15
0
8
9
11
0
2
9
0
Pb Concentration, ppm, Wet Weight
XiS.D.c
n.d.d
1.61±0.66
6.7015.22
8.8314.53
n.d.
0.99+0.79
1.7510.43
n.d.
Median
n.d.
n.d.
0.66
7.98
n.d.
n.d.
1.59
n.d.
Range
n.d.
n.d. -2. 59
n.d. -19. 66
1.76-17.12
n.d.
n.d. -1.60
n.d. -2. 41
n.d.
aSource: Lynch, from M.S. Thesis, The Ohio State University 0-973),
Reprinted with permission of the author,
^Number of tissue samples with detectable lead concentrations.
cMean+one standard deviation of tissue samples with detectable lead
concentrations.
dn.d.-no lead detected. Below detection limit of 0.03 ppm lead.
5.23
-------
Lead concentrations in brain tissues appear to have some value in
diagnosing lethal lead toxicosis (Longcore, et al., 1974a). Lead levels
in mallard brain tissue of more than 3 ppm indicate acute exposure to lead.
Lead levels in brains of lead-dosed ducks that died of lead poisoning
averaged 4.6 ppm and ranged from 2.1 to 10.6 ppm.
Lead concentrations in kidneys are also quite useful in diagnosing
lead poisoning. High levels in the kidney are indicative of recent, high
exposure to lead. Lead levels of 20 ppm in kidney tissue of mallards
indicate acute exposure to lead. The average lead level in kidneys of lead-
dosed mallards that died was 175.7 ppm (Longcore, et al., 1974a).
Lead concentrations of 10 ppm in clotted blood from mallard hearts
are indicative of acute exposure to lead. In mallards dosed with lead shot,
lead levels in blood from hearts averaged 10.2 ppm for ducks that died
(Longcore, et al., 1974b). High concentrations of lead in red blood cells
of lead-poisoned mallards also have been reported by Clemens, et al., (1975).
Many other bird tissues such as breast muscle, feathers, leg muscle,
ovary, gall bladder, spleen, and lung have been analyzed for lead concen-
trations, but only lead levels in liver, brain, kidney, and blood appear
to have value in indicating lead poisoning (Longcore, et al., 1974a; Lynch,
1973; see Table 5.8).
Presumably raptors feeding on ducks containing lead shot could accidently
ingest lead shot. USDI (1976) indicates that there are only two published
reports of secondary lead poisoning in birds (an Andean condor, Vultur
gryphus and a prairie falcon, Falco mexicanus, both of which were in capti-
vity). The prairie falcon was fed a diet of mallard duck heads, some of
which contained at least one shot and/or lead residues of 2 to 55.8 ppm
(muscle tissue) and 4.7 to 32.6 ppm (brain) (Benson, et al., 1974). The
Andean condor had been fed hunter-killed cottontail rabbits, squirrels
and groundhogs (Locke, et al., 1969).
5.4.2 Effects
The typical signs and lesions of lead poisoning in waterfowl are well
described. Lead-poisoned waterfowl that are fairly well advanced in lead
intoxication usually exhibit the following signs of poisoning:
1) varying degree of emaciation (loss of up to 40 percent
of original body weight, and prominent keel portion of
the sternum)
2) reduced activity with reluctance to fly
3) lowered food intake
4) palsy (wing droop)
5) bile staining of vent area
6) tendency to seek isolation and cover
7) loss of ability of walk or stand (USDI, 1976).
-------
The internal lesions associated with lead-poisoning in waterfowl in-
clude :
1) lack of fat.
2) atrophy of striated muscle, liver and kidneys
3) excess fluid in the pericardial sac
4) distended gall bladder
5) atrophied gizzard with grinding pads hardened and
bile-stained
6) proventriculus impacted with food and grit
7) anemia and paleness of the whole body (USDI, 1976).
Lead poisoning typically causes a variety of lesions in ducks, such
as emaciation, proventricular impaction, green-stained and eroded gizzard
lining, atrophied liver, distended gall bladder, hydropericardium, and
acid-fast intranuclear inclusions in kidney tubules. These abnormal
changes were monitored in mallard drakes exposed to particulate lead in
four concentrations (0, 17.8, 89.0, and 178 grams per square meter) in
simulated marsh areas over a 14-week period. None of the above lesions
was noted at necropsy in the control (no particulate lead) or low (17.8
grams per square meter) treatment groups. In the 178 grams per square meter
treatment group, all lesions were noted and in the 89.0 grams per square
meter treatment group, all but two lesions (distended gall bladder and hydro-
pericardium) were noted at necropsy (Irwin and Karstad, 1972).
Waterfowl poisoned by lead shot frequently have lesions in heart
muscle and muscle of arteries and arterioles. Myocardial infarctions and
lesions associated with fibrinoid necrosis of the media of arterioles and
small arteries were found in 75 percent of 67 lead-poisoned waterfowl. Also,
infarcts were noted in striated muscles and smooth muscles of the gastro-
intestinal tract (Karstad, 1971).
The first sign of lead poisoning in ducks in usually a marked anorexia
and lethargy, probably due to the beginning of the muscle paralysis which
follows next. Green staining of feathers from bile occurs late in the lead-
poisoning process, often prior to death (Coburn, et al., 1951).
The erythrocyte count normally drops in early stages of lead poison-
ing in ducks, returns to normal during the intermediate stages of poisoning,
and has a rapid decline preceding death. Cells also change to such shapes
as dumbbell-, bottle-, sickle-, and tear-shaped forms. The percentage of
red cells altered may be as high as 36 percent in acutely poisoned ducks
(Coburn, et al,, 1951). The levels of delta-aminolevulinic acid dehydratase
(ALAD), an enzyme in the biosynthetic pathway for hemoglobin, in the blood
of adult mallards on a nutritionally adequate diet and dosed with one number
4 lead pellet decreased to less than 20 percent of ALAD levels in undosed
birds (U.S. Department of the Interior, 1976).
Anemia and emaciation are normally found in lead-poisoned ducks, with
a total absence of any fatty tissues. Tissues noticeably reduced in size
in lead-poisoned ducks include the liver and gizzard muscle (Coburn, et al.,
1951).
5.25
-------
As with the deposition of lead in tissues of birds and other animals
including humans, diet influences the toxic effects of lead (see Section
6.3.2.1). The U.S. Department of the Interior report (1976) reviews re-
search in which toxic effects of lead (including mortalities) were reduced
in mallard ducks when they were fed commercial duck ration as opposed to
no food or grain diets. The texture of the diet may have some influence
on lead toxicity. Longcore, et al., (1974b) showed that the presence or
absence of grit, and the type of grit affected toxicity of ingested lead
shot. In ducks fed crushed oyster shell grit (contains calcium), a rapid
rate of shot erosion was somewhat offset by the concomitant increased chance
of voidance of the lead shot. The net result was less, but more rapid,
mortality among ducks with grit than in ducks without grit. Anderson and
Stewart (1969) found that trace metals, such as lead, are less likely to
induce toxic conditions in ring-necked pheasants where calcium is abundant
in the soil.
Toxicological symptoms of young Japanese quail fed lead (as lead ace-
tate) at the level of 500 and 1,000 ppm included inhibition of normal
growth and anemia.
The performance of juvenile bobwhite quail (Colinus virginianus)
receiving up to 1,500 ppm of dietary lead as lead acetate was not signifi-
cantly influenced during a 6-week experimental.period. Feeding 3,000 ppm
lead acetate was associated with a significant depression of body weight
and an increase in mortality (Damron and Wilson, 1975). Feeding growing
quail up to 2,000 ppm lead from either lead acetate or powdered lead or
five lead shot per week caused no significant effects upon either body
weight or mortality. No significant trends were noted in body weight, feed
intake, or organ weight of adult quail that received up to 1,500 ppm lead
from lead acetate. Dosing adult bobwhite quail cocks with ten or more lead
shot per week caused a significant increase in mortality, and more than 90
percent of those dosed with 30 shot per week died by the end of 4 weeks
(Damron and Wilson, 1975).
A few studies have been addressed to the effect of lead on sexual
development and reproductive performance in birds. Wetmore (1919) reported
that lead may be important in producing sterility in birds that in other
respects appeared to have recovered from lead poisoning. Cheatum and
Benson (1945) reported that drakes recovering from lead poisoning did not
exhibit a significant loss of fertility. Feeding 1500 ppm lead as lead
acetate to bobwhite quail did not result in any detectable effect on semen
quality (Damron and Wilson, 1975). On the other hand, feeding 500 to 1000
ppm lead as lead acetate to young Japanese quail interferred with normal
sexual development in the males (Morgan, et al., 1975). Females may be
more sensitive to the effects of lead than males; it has been reported that
female Japanese quail exhibited reproductive problems at dietary intakes as
low as 1 ppm (Edens, et al., 1976.
Toxicity experiments on chick embryos (Callus domesticus) revealed that
lead chloride is highly toxic, giving survival rates of 74 to 23 percent
when used at 0.001 to 5 ppm. Survivors treated with lead displayed a high
frequency of anomalies (Birge, et al., 1975).
5.26
-------
The end result of the changes caused by lead poisoning is that a bird
has little or no intake of nutrients and cannot retain or process nutrients
it does have. Protein metabolism and thus, the immune mechanisms, are
probably interfered with. In consequence, lead-poisoned birds are subject
to both predation and disease (Stickel, 1969). Sublethal doses of lead
acetate cause increased mortality in chicks administered bacterial endo-
toxins (U.S. Department of the Interior, 1976).
5.5 MAMMALS
5.5.1 Wild
5.5.1.1 Metabolism: Uptake, Absorption, and Residues—
Investigations have been conducted to evaluate lead contamination in
tissues of roadside small mammals, especially mice, and to assess the patho-
logical effects, if any, of lead on these organisms. Small mammals which
inhabit roadside areas are exposed to increased levels of environmental lead.
In general, it has been found that lead levels in roadside mammal popula-
tions are higher than those levels found in populations distant from road-
ways. Table 5.9 summarizes data from several investigations.
Jefferies and French (1972) found that there is a differential between
the concentrations of lead in small mammals of woodland and field areas and
those living on roadside verges (see Figure 5.2) and also between those
living on the verges of major and minor roads. Although there was a 9.2
times difference in the concentrations in the vegetation of major road
verges and field areas (307 to 33.4 ppm, dry weight, respectively), pre-
sumably due to surface coating on the former, there was only a 1.7 times
(or lower) difference in the concentrations in mammals. ' Mammals living
on verges had a mean of 4.2 ppm, dry weight (1.3 ppm, wet weight) in two
species.
Despite greater present-day levels of lead aerosols in the environment,
Raymond and Forbes (1975) did not find significant differences in the lead
burden of hair from natural wild mice as compared to that obtained from
musuem specimens.
Braham (1973) reported that lead in California sea lions (Zalophus
californianus) was highest in hard tissue and lowest in soft tissue. Lead
in bone and teeth ranged from 14.0 to 62.8 ppm and from 11.3 to 15.1 ppm,
respectively, whereas, lead in fat and muscle ranged from undetectable to
0.6 ppm and from 0.3 to 3.2 ppm, respectively.
Mierau and Favara (1975) found no evidence of lead poisoning in the
wild mice populations which they investigated. Further, the exposure level
required to produce recognizable lead poisoning in captive deer mice was
about five times higher than that measured in the wild roadside mice popu-
lations.
A survey of lead in tissue of Ohio upland game animals has been com-
pleted by Lynch (1973). Table 5.10 is from Lynch1s study and indicates
lead levels in deer, rabbit, and squirrels. Of the muscle tissue analyzed
only two samples, one from rabbit and one from squirrel, exceeded 7 ppm.
5.27
-------
Table 5 ,9 MEAN CONCENTRATION OF LEAD IN TISSUE OF SMALL MAMMALS FROM
ROADSIDE ANP CONTROL SITES
(ppra, dry weight)
Organism
Tissue
Control Site Roadside Site
References
\J\
•
ro
oo
Deer mouse
Peromyscua maniculatus
White-footed mouse
(Peromyscua leucopus)
Meadow vole
(Microtus
pennsylvanicus)
Short-tailed shrew
(Blarina brevicauda) ^
Shrew
(Sorex sp.)
Deer mouse
(Peromyscus maniculatus)
Townsend chipmunk
(Eutamias townsendii)
Meadow vole
CMicrotua sp.)
Brain
Lung
Liver
Stomach
Kidney
Muscle
Bone
Whole body
Whole body
Whole body
Whole body
Hair
(unwashed)
0.14
1.06
3.28
4.84
2.7
2.6
4.9
2.6 - 5.4
6.0
<0.57 - 0.84
<0.58
0.92 - 3.29
1.64
1.87 - 8.46
0.49
14.0 - 52.i
4.4
8.6
14.0
235.6
Mierau & Favara (1975)
and
Welch & Dick (1975)
Schlesinger & Potter (1974)
Quarles et al.,(1974)
Ovaries et al.,(1974)
Quarles et al.,(1974).
Schlesinger & Potter (1974)
Raymond & Forbes (1975)
-------
—10
*
E
2" 9
Z
O 8
O
u
o
<
iu
O
O
O
i-
306-7
42-5
33-4 Vegetation
Microtui
CUthrionomyi
Apodvmus
Group I
Group 2
SITES
Group 3
Figure 5.2
The dry weight concentrations of lead in Microtus,
Clethrionomys and Apodemus trapped at Group 1 (Al
road verges) , Group 2 (minor road verges) and
Group 3 (arable and woodland) sites. The broken
line joins the means for the three species (two
at Group 3 sites). The mean level of lead (d/w
ppm) on the vegetation at these sites is also
given. Source: Jefferies and French. Reprinted with
permission from Environmental Pollution, (c) Applied
Science Publishers, Ltd., 1972.
5.29
-------
TABLE 5.10 LEAD CONCENTRATIONS IN TISSUE SAMPLES FROM VARIOUS OHIO MAMMALS*
Tissue
Brain
Hair
Kidney
Leg muscle
Liver
Metacarpal
Brain
Embryo
Femur
Kidney
Leg Muscle
Liver
Testes
Brain
Femur
Kidney
Leg Muscle
Liver
Testes
No.
Analyzed
14
8
35
26
24
38
6
1
24
40
22
16
1
3
21
18
24
13
2
No,
Pb Concentration, ppm, Wet Weight
Positive5 X+S.D.^
6
6
33
7
11
38
4
1
24
32
10
9
1
2
21
15
7
4
2
White-Tailed Deer
1.45+1.01
5.92+5.11
1.06+1.60
0.95+0.69
0.74+0.32
4.82+1.73
Cottontail Rabbits
9.64+3.52
0.625+0.00
7.77+2.48
1.35+0.88
1.92+0.00
5.92+4.01
0.36+0.00
Squirrels
2.04+1.74
7.68+3.07
0.47+0.01
3.28+4.33
2.04+1.17
1.42+0.14
Median
n.d.
2.18
0.32
n.d.
n.d.
4.57
7.22
0.625
7.91
0.86
n.d.
2.63
0.362
0.536
7.56
0.235
n.d.
n.d.
1.47
Range
n.d. -2. 91
n.d. -14. 4
n.d. -6. 27
n.d. -2. 37
n.d. -1.34
2.49-11.04
n.d.d!2.22
0.625
2.49-11.92
n.d. -3. 92
n.d. -8. 63
n.d. -16. 76
0.362
n.d.d3.56
2.65-14.16
n.d. -2. 92
n.d. -13. 49
n.d. -3. 24
1.31-1.59
aSource: Lynch (1973). Reprinted with permission
of the author.
^Number of tissue samples with detectable lead concentrations.
cMean + one standard deviation of tissue samples with detectable lead
concentrations.
dn.d.-no lead detected. Below detection limit of 0.03 ppm lead.
5.30
-------
Mouw, et al., (1975) found that wild rats captured in an urban area
had markedly elevated tissue lead, particularly in the major lead-storage
tissues (bone and kidney) which was twentyfold higher, as compared to rural
rats. The fecal levels were fourfold higher in urban rats (see Table 5.11).
5.5.1.2 Effects—
Bazell (1971) reported that a large portion of animals housed at the
Staten Island Zoo suffer from lead poisoning. Bazell suggested that major
source of lead to these animals appeared to be atmospheric pollution, al-
though lead paint might also be a factor. The animals affected include
leopards, a variety of other cats, snakes, and primates. Those animals
kept in outdoor cages had the highest lead burdens. The effects of lead
upon those animals at the Staten Island Zoo (incidence of lead poisoning of
captive animals at the Bronx Zoo has also occurred) included death, hair
loss, paralyzation, and loss of muscular coordination. Although Bazell
attributed air pollution as a major source of lead for zoo animals, it seems
unlikely in view of the fact that lead poisoning in domestic cats, as
opposed to dogs, is exceedingly rare.
Studies of lead poisoning in wild animals at the National Zoological
Park, Washington, D.C., indicated a cause-effect relationship between
leaded paint and lead intoxication of caged animals (Zook, et al., 1972).
Postmortem diagnosis of primates, parrots, and fruit bats indicated that
these animals were subjected to lead poisoning.
Changes in several biologic indices (depression of delta-aminolevulinic
acid dehydratase in the kidney and red blood cells, presence of renal intra-
nuclear inclusion bodies, and increased kidney weight) confirmed lead-
poisoning in urban rats versus rural rats (Mouw, et al., 1975). There were
no ovarian cysts or testicular degeneration in the wild rats as has been
seen in lead-poisoned laboratory rats (see Section 6.3.2).
Evidence to substantiate the effect of lead contamination on the popu-
lation dynamics of wild mammals is at present lacking, due no doubt to the
extreme difficulty in assessing cause-effect mortality factors which oper-
ate upon wild annimals under natural conditions.
5.5.2 Domestic
5.5.2.1 Metabolism: Uptake, Absorption, and Residues—
Lead poisoning generally is considered to be the most common cause of
accidental poisoning of domestic animals. The condition is diagnosed most
frequently in cattle and dogs (Aronson, 1972). Common histories of exposure
in dogs include chewing on objects painted with lead-based paints, eating
linoleum, or ingesting lead materials such as shotgun slugs or curtain
weights. Case histories indicate that lead poisoning in cattle is usually
the result of a single ingestlon of a material containing a large quantity
of lead (Osweiler, et al., 1973). The major source of lead to domestic
stock continues to be lead paints (Buck, 1970 and 1975). Other sources of
lead include used motor oil, discarded lead storage batteries and oil fil-
5.31
-------
Table 5.11 LEAD CONCENTRATIONS IN TISSUES FROM URBAN AND RURAL
RATSa'b
Lead Concentration, ppm
Sample
Source
Blood
Liver
Kidney
Lung
Brain
Bone
Feces
No. of
Samp les
39
21
25
23
22
24
19
Urban
Mean + SE
0.55 + 0.04
3.34 + 0.45
22.7 + 2.8
1.24 + 0.20
1.11 + 0.17
200.00 + 19
178.00 + 30
No. of
Samples
28
19
20
19
19
18
19
Rural
Mean + SE
0.17 + 0.02
0.44 + 0.09
1.14 + 0.28
0.24 + 0.03
0.21 + 0.06
10.3 + 1.9
46.6 + 6.0
Significant
Differences,
P Value
.001
.001
.001
.001
.001
.001
.001
3
Source: Mouw, et al. Reprinted with permission from Archives
b Environmental Health, (c) American Medical Association, 1975.
Data are from 41 urban rats (26 males and 15 females, body weight = 382
Too a.8?, an? 28 rural rats (2° males and ei8ht females, body weight -
c322 + 14 gin) .
A large fraction of the lung (10/19) and brain (12/19) samples from
rural rats were entered as the minimum detectable concentration (0.2
yg/gm) for these tissues. This manipulation has reduced the apparent
SE for these two values and (probably) elevated the mean, but is un-
likely to have affected the statistical conclusion.
5.32
-------
ters, machinery grease, putty, linoleum, and lead caulking. Poisoning in
cattle can also arise from long-term ingestion of crops and/or pasture for-
age contaminated by lead settling out from fumes and dust emitted from lead-
and copper-smelting operations (Aronson, 1972; Dorn, et al., 1974; Dorn,
et al., 1975; Orheim, et al., 1974). The latter is the principal transfer
mechanism involved in lead poisoning of horses (Aronson, 1971; Knight and
Burau, 1973).
Most field investigations of lead contamination of domestic animals
have taken the form of comparison of tissue burdens among test animals,
those in the vicinity of a lead source, and control animals. Orheim, et
al., (1974) found no difference in lead concentration of blood and milk
between dairy cattle within the "fallout" zone of a lead smelter versus
control cattle. However, lead levels in the hair of the test versus control
animals were significantly different. Dorn, et al., (1974) also
reported significant lead accumulation in washed bovine hair. Investiga-
tions carried out on a test farm exposed to production sources of lead re-
vealed increased concentrations of lead in the milk of test cows as compared
to control cows (Dorn, et al., 1975). The highest concentration measured
in milk was 0.35 ppm. This figure is close to the maximum of 0.3 ppm re-
ported by Aronson and Hammond (1964) in milk from cows exposed to a high
intake of lead.
When Allcroft (1950) fed calves large quantities of lead (0.1 to 0.5
gram per kilogram body weight), there was a marked and rapid rise in the
blood lead level and if the animal survived, the lead content of the blood
did not revert to normal for many months. When given as the metal or the
finely ground ore galena, lead was absorbed to a much smaller extent than
when given as the acetate, phosphate, basic carbonate, oxide and wet or
dry paint. After the ingestion of the various lead compounds mentioned
above, the highest concentrations, by far, were found in the kidney cortex
(297 ppm) and liver tissue (126 ppm). Allcroft (1950) considers the kidney
cortex content to be of specific diagnostic value.
According to Buck (1975), determination of blood lead concentrations
offers the best antemortem evidence for the presence or absence of lead
poisoning in cattle. Blood-lead concentrations greater than 0.35 ppm in
cattle should be judged as evidence of unusual exposure. Tables 5.12 and
5.13 give background and contaminated lead concentrations in various bovine
tissues.
Laboratory experiments which used sheep as the test animal have been
conducted. Carson, et al., (1973) maintained sheep on daily regimens of
food spiked with 4.5 and 2.3 ppm of lead for 27 weeks. Results showed
mean blood-lead levels of 0.30 and 0.17 ppm, respectively, in the two test
groups. No clinical signs of lead poisoning in the sheep were observed.
Five groups of foals were fed rations that differed in calcium and
phosphorus content for 26 weeks. During the last 15 weeks of the experi-
ments, some of the foals in each ration group were fed 30 ppm lead carbo-
nate daily. The addition of lead at the 30 ppm level significantly in-
creased (P less than 0.05) lead concentrations in whole blood liver, kidney,
vertebra, and ribs, but not in metacarpal diaphysis or epiphysis, brain,
5.33
-------
lung, or muscle. The calcium and phosphorus content of the rations fed
did not have a significant influence on whole blood-lead values. In fact,
the lead values were highest in the group of foals fed the largest amounts
of calcium. The amount of calcium and, to a less extent, phosphorus in
the ration had a significant influence on the amount of liver-tissue lead
(Willoughby, et al., 1972b). In some cases, the concentration of lead in
the livers of foals fed the least amount of calcium and phosphorus were
twice as high as values from foals fed greater amounts of these minerals.
5.5.2.2 Effects—
Since lead accumulates in the body, chronic exposure to small amounts
of lead may lead to toxicosis in domestic livestock. For cattle, the
daily intake of approximately 6 to 7 milligrams of lead per kilogram body
weight can result in toxicosis (Hammond and Aronson, 1964). Acute, lethal,
single exposures are in the magnitude of 400 to 600 milligrams of lead per
kilogram of body weight for calves and 600 to 800 milligrams of lead per
kilogram of body weight for adult cattle, (Buck, 1975). These values are
influenced by the form of lead ingested and other environmental factors.
Allcroft and Blaxter (1950) showed that, in the case of young calves, 0.2
to 0.4 gram of lead (as lead acetate, carbonate or oxide) per kilogram of
body weight was sufficient to cause death in a few days. Horses are more
susceptible and approximately 2 milligrams of lead per kilogram body
weight can lead to lead poisoning (Aronson, 1971). Lead poisoning in
domestic animals appears to affect all major organs and organ systems, in
particular the central nervous system and the blood vascular system.
Christian and Tryphonas (1971) made gross and microscopic examinations
of nine cattle, ranging in age from 3 months to 6 years, affected with
naturally occurring lead poisoning of 1 to 32 days' duration. Gross brain
lesions consisting of cerebrocortical softening, yellowish discoloration,
and cavitation were seen only in cattle with prolonged clinical illness
(affected more than 9 days). Tips of most cerebral gyri were affected;
lesions were most severe in the occiptal lobes. In cattle with acute
poisoning, microscopic lesions varied from diffuse capillary activation to
scattered focal areas of status spongiosus and necrosis of the cerebral
cortex. In cattle with subacute and chronic poisoning, the microscopic
lesions were located at the gyral tips and ranged somewhat from different
degrees of status spongiosus, astrocytic swelling, and nerve cell degenera-
tion to severe cavitation and vascular proliferation.
The majority of lead poisoning incidents reported for horses have been
attributed to consumption of vegetation contaminated by lead from local
mines and smelters. Knight and Burau (1973) researched two incidents of
lead poisoning on two horse ranches located within the "fallout" area of a
lead smelter. Contaminated vegetation consumed by the horses proved to be
the lead source. Symptoms of chronic lead poisoning in the horses was
evidenced by anorexia, loss of body weight, muscular weakness, anemia,
laryngeal hemiplegia, elevated urine lead concentration following chelation
therapy, and inhalation pneumonia preceding death.
Schmitt, et al., (1971) found that excessive amounts (up to 264 ppm)
of lead in ingested forage were found to be the primary cause of a debilitating
5.3U
-------
Table 5.12 "BACKGROUND" BOVINE LEAD CONCENTRATIONS
IN TISSUES AND RUMEN CONTENTS3
Specimen
Analyzed
Blood
Liver
Kidney
Rumen contents
No. of
Samples
92
197
181
52
Mean Lead
Content,
ppm, Wet Weight
0.103 (±0.044)C
1.12 (±1.36)
1.21 (±1.69)
1.07 (±1.44)
Source: Buck. Reprinted with permission from Journal American
Veterinary Medical Association, (c) American Veterinary Medical
Association, 1975.
Data from records of the Iowa State University Veterinary
Diagnostic Laboratory, 1967-1970.
CStandard Deviation.
Table 5.13 LEAD CONTENT IN TISSUES AND RUMEN CONTENTS
FROM CATTLE WITH CLINICAL LEAD TOXICOSIS3
Specimen
Analyzed
Liver
Kidney
Blood
Rumen contents
No. of
Cases
100
105
50
52
Lead Content,
Mean
26.40
50.30
0.81
400.80
ppm, Wet Weight^
Range
1.0 - 83.0
3.0 - 200
0.19 - 3.80
0.0 - 11,875
aSource: Buck.Reprinted with permission from Journal American
Veterinary Medical Association, (c) American Veterinary Medical
Association, 1975.
bData from records of the Iowa State University Veterinary Diagnostic
Laboratory, 1967-1971*
5.35
-------
disorder in six horses. This represents a daily intake of lead of 5.5 mg/kg
based on estimates of forage consumption by horses (Aronson, 1972). Necro-
psy findings included depletion of adipose tissues with generalized emaciation,
edematous synovial membranes, erosive and rough joint surfaces, and exostoses
of the articulating bones, especially metacarpals. The more significant
histopathological findings were diffuse edema and necrosis of individual nerve
cells, hepatic cell degeneration, and a slight to moderate degree of
nephrosis. Many epithelial cells of the collecting renal tubules and
some of the nuclei of hepatic cells showed intranuclear inclusion bodies,
suggesting the presence of lead.
Groups of young, growing horses were fed toxic amounts of lead only,
zinc only and the same amounts of lead and zinc together. Those fed lead
only developed pharyngeal and laryngeal paralysis ("roaring") whereas
those fed zinc only and lead and zinc together developed the same clini-
cal syndrome which included swelling at the epiphyseal region of the
long bones, stiffness and lameness. Animals fed lead only did not become
anemic, and weight loss did not occur until after there was an interference
in swallowing. Zinc appeared to have prevented the development of clini-
cal signs of lead poisoning in the young, growing horses (Willoughby,
et al., 1972a).
Zook, et al., (1969) found that lead poisoning is a common disease
of young dogs, especially in the summer and fall. The signs of poisoning
were characterized by gastrointestinal dysfunction (colic, vomiting, and
diarrhea) and nervous disorders (convulsions, hysteria, nervousness,
behavior changes). Their blood consisted of numerous stippled and im-
mature (especially nucleated) erythrocytes in the absence of severe anemia.
Clarke (1973) pointed out that there are practically no references to lead
poisoning in the cat. The cat is resistant to the absorption of lead in
large quantities; however, it succumbs to repeated administration of small
doses. In cases where cats were poisoned, they showed both gastric
(anorexia, vomiting) and nervous (epileptiform convulsions, dashing about
as if mad) symptoms. They were very thirsty, somewhat constipated and
partially paralyzed, with hyperaesthesia of the skin. Some degenerative
changes were noted in the liver and kidneys. The intestines were contracted
and there was a blue color in the tongue and throat.
5.36
-------
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6.0 EFFECTS ON HUMANS
6.1 SUMMARY
The metabolism of lead is concerned with uptake and absorption, distribu-
tion, transport, elimination, and biological half-life of both inorganic and
organic compounds of lead.
Lead may be taken into the body by inhalation, ingestion or percutaneous
absorption, and placental transfer. It may enter the respiratory system in the
form of particles, gases or vapors. Various estimates place pulmonary reten-
tion rates of inhaled lead in the range of 37-50 percent. Because lead alkyls
in the air are broken down by light and heat, their presence in the air is
transient and it is believed that they contribute little to the inhalation
burden. Of greater importance are the inorganic lead compounds emitted by
automobiles using leaded gasolines. Under normal conditions, not more than
5 to 10 percent of ingested lead in food is absorbed from the gut. The frac-
tion absorbed from liquids taken between meals may be considerably greater.
The amount of lead absorbed from the gut in animals appears to be less than
in man. Lead is absorbed mainly from the small intestine, to a lesser extent
from the colon, and not at all from the stomach. Skin absorption of lead com-
pounds is of importance only in the case of lead alkyls and lead salts of
naphthenic and fatty acids.
Following absorption nearly all the inorganic lead in the blood is assoc-
iated with the erythrocytes. The bonding sites on the maternal erythrocytes
are not saturated. It is then distributed to various tissues and is highest
in bone and hair; intermediate in aorta, liver, and kidney; and lowest in
heart and brain. In the steady state, more than 90 percent resides as a re-
latively nondiffusible fraction in the skeleton. The concentration of lead in
the bone rises steadily to about the fourth decade, reaches a plateau, and
then decreases in many cases in the seventh and eighth decade. Fluctuations
in the amount of lead intake, either through inhalation or ingestion cause
movements into and out of various compartments of the body lead pool (e.g.,
hard tissue, soft tissue, pluma, erythrocytes, etc.). Equilibration of the
various compartments occurs after a relatively small lead intake is achieved.
Only then do lead levels in tissues and fluids accurately reflect body pool.
Exposure to lead through placental transfer of inorganic lead probably
has greater potential for injury to the embryo, fetus, and neonate than has
exposure during adulthood. Flacental transfer of inorganic lead has been
widely reported.
Extensive studies of tissue lead distribution have been reported. A
detailed investigation of blood-lead levels of male residents in 19 cities
in the continental United States showed wide variations from one city to
another as did individual values in each city. Concentrations of lead in the
aorta have been found to be positively correlated with aorta calcium concen-
trations. Levels of lead in shed deciduous teeth are elevated in cases of
6.1
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known lead poisoning and in children who reside in areas where lead poisoning
is endemic. Lead is normally found in higher concentrations (on a weight per
weight basis) in hair than in any other tissue. The high lead content has
been found in the hair of city dwellers or those living near a lead smelter
as compared to those living in a rural area. Traffic policemen within cities
have a higher average lead content in their hair than members of the general
population.
The organic lead compounds have no special affinity for bone, but high
concentrations may appear in the brain and liver. The metabolism of tetra-
alkyl lead proceeds via the highly toxic trialkyl lead which in turn is con-
verted to inorganic lead.
The principal routes of elimination of lead from the body are via feces
and the urine. Fecal excretion of both inorganic and organic lead is greater
than urine excretion. For inorganic lead the ratio in man is about 2:1. The
excretion of lead through the kidney is hampered by the high degree of inter-
action of lead with ligands present in erythrocytes and/or plasma proteins.
About 90 percent of the lead in the feces represents lead which has passed
unabsorbed through the gut.
Indirect estimates of lead have been made by balance studies in human
subjects. Data derived from urine and blood samples of individuals exposed
to known concentrations of atmospheric lead oxide have been used to develop
mathematical models describing lead uptake and excretion kinetics. Estimates
of half-times for lead in bone have varied from 64 days in the spine of rats
to 7500 days in the skeleton of a dog. Research continues on the development
of a suitable metabolic model which incorporates lead uptake and excretion
kinetics for humans exposed to atmospheric lead.
Most of what is known about lead toxicity applies to (1) adults exposed
in the industrial setting and (2) children who have ingested large amounts of
lead. Symptoms these two groups may exhibit include abnormalities in the
blood (red blood cell stippling, anemia, decreased ALAD activity) and in
kidney function (glycosuria, hyperphosphaturia and hyperamino aciduria. In
addition children are more susceptible to lead encephalopathy with a poten-
tially fatal outcome.
In the last 5 years, increasing emphasis has been placed on the more
subtle aspects of lead toxicity which seems to be appropriate considering
the nature of contemporary lead exposure. For most individuals, ingested
lead is more likely to be derived from water, soil, food, and ambient air
than from occupational exposures or industrial emissions.
Lead, like cadmium and mercury, forms mercaptides with the -SH group of
cysteine and less stable complexes with other amino acid side chains. This
apparently results in an inhibitory action on a number of enzymes. An exam-
ple is the strong inhibition of lipoamide dehydrogenase, an enzyme crucial ,
to cellular oxidation, by lead (as Pb ) concentrations as low as 6.5 x 1.0
M. This inhibition probably occurs through binding to the dithiol configura-
tion at the active catalytic center. Activities of several other enzymes
(e.g., ATPases, aldolase, glucose-6-phosphate dehydrogenase (G-6-PD), adenyl
cyclase, microsomal enzymes, acetylcholinesterase) are affected by lead.
6.2
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Within the cell, lead has greatest affinity for mitochondrial membranes
and nuclei. Altered nucleic acid content (RNA and DNA) of leukocytes have been
observed in adult cases of plumbism. Lead binds with an acidic protein
fraction to form discrete intranuclear inclusion bodies within the kidney
tubule cells of chronically poisoned rats, rabbits, and humans.
The affinity of mitochondria for lead results in morphological and
functional alterations which have been verified in various animal species.
Mitochondrial accumulation of lead in the kidneys inhibits ADP-stimulated
respiration. Impairment of energy metabolism by lead may be responsible
for the reduced transport function of the kidney.
Inorganic lead toxicity may give rise to clinical syndromes such as ab-
dominal colic, anemia, acute or chronic encephalopathy, peripheral neuropathy,
and chronic nephropathy. Manifestations of organolead poisoning are domina-
ted by the involvement of the central nervous system and differ from inorganic
lead toxicity. Absorption of the gasoline antiknock additives, TEL or TML,
results in similar symptomatology. The principal manifestations of exposure
to TEL are insomnia, asthenia, ataxia, tremors, neuromuscular pain, hallucina-
tions, mania, delusions, and psychosis.
Lead has varying effects on different organ systems. In the kidney, lead
interferes with tubular sodium absorption perhaps through marked inhibition
of Na /K ATPase in lead-poisoned animals. It also inhibits tubular reabsor-
ption of glucose, and amino acids and phosphate.
The effects of lead on hematopoiesis include two aspects: (1) the in-
fluence on circulating erythrocytes resulting in, for example, altered osmotic
and mechanical fragility and (2) the impairment of the production of hemo-
globin resulting from the effects of lead upon bone marrow.
Heme synthesis is severely affected by lead. This is reflected in the
high levels of excreted porphyrin precursors in the urine. One of the most
lead-sensitive enzymes involved in heme synthesis is delta-aminolevulinic
acid dehydratase (ALAD). A decrease in ALAD activity in mature erythrocytes
is a very early sign of lead exposure. ALAD activity decreases exponentially
when blood-lead levels increase. The effective threshold is not certain but
probably is below PbB = 20 micrograms/100 ml.
Many children living in slum housing have been observed to have elevated
blood-lead levels and decreased red cell ALAD levels. Reversal of the ALAD
deficit in lead-poisoned erythrocytes has been accomplished with glutathione
reductase (GSH) in vitro and, to some extent, in vivo. Chelation therapy,
especially EDTA, also reverses ALAD inhibition.
The immunologic impairment of lead is reflected in its decreasing of the
normal Vitamin C content of the adrenal gland. Chronic lead exposure at
high doses reduces the effectiveness of the immune system in experimental
animals.
No evidence has been forthcoming to implicate any cardiovascular disease
in humans following chronic lead exposure. Lead has been found to exert a
6.3
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depressing effect upon the endocrine function of such glands as the thyroid,
pituitary, adrenal cortex, and juxtaglomerular apparatus.
Pediatric lead poisoning follows persistent lead ingestion usually over
a period of several months. For early recognition of the disease, a high
index of suspicion and judicious use of four laboratory tests - blood exami-
nation for anemia and erythrocytic stippling; roentgenograms of the long
bones for "lead lines"; plain x rays of the abdomen, looking for radiopaque
flecks within the intestine; and a urinalysis especially checking for copro-
porphyrinuria - are indicated.
A positive correlation has been reported between mental retardation
and high levels of lead in drinking water. One study showed that as levels
of lead increased, general cognitive, verbal and perceptual abilities de-
creased in a group of preschool children.
Lead ingestion in children has been linked to minimal brain dysfunction
or "hyperkinesis". One study reports an association between hyperactivity
and raised lead levels. A large body-lead burden may exact consequences
that have been hitherto unrealized. Sensitive techniques now available in
the behavioral and neurosciences are being used to detect altered motor
activity, motor performance and other previously undetectable abnormalities
in these animal models.
Chelation therapy is the method of choice for treating plumbism in the
United States. The three chelating agents used are edathamil calcium diso-
dium (CaEDTA), 2, 3-dimercaptopropanol (BAL), and d-penicillamine (PCA).
CaEDTA administered intramuscularly evokes a great increase in lead excre-
tion in children and adults with high lead exposure. In adults with mild
plumbism, parenteral CaEDTA is the most effective of the chelating agents.
A study of chromosomal abnormalities in lead workers showed that those
having blood-lead levels of 62 to 88 micrograms per 100 ml had gap-break
type aberrations of chromatids and increases in tetraploid mitoses and the
mitotic index.
Severe lead intoxication has long been associated with sterility, ab-
ortion, stillbirths, and neonatal deaths in man and other animals. Litter
size, embryonic growth, and fetal development have been reduced in labora-
tory animals by inorganic lead. Damage to reproductive organs and inter-
ference with estrus cycles by inorganic lead have also been noted. Men'
occupationally exposed to lead have been reported to exhibit substantial
increases in spermatogenic abnormalities (asthenospermia, hypospermia, and
teratospermia).
Teratogenic effects of inorganic lead in animals are manifested by co-
genital skeletal malformations. Human fetuses in utero may be a group at
particular risk because inorganic and organic lead cross the placenta. One
human case has been noted where the mother, exposed to illegal whiskey con-
taining lead, gave birth to an infant with neurological defects, intrauterine
growth retardation, and postnatal failure to thrive.
6.U
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Renal, adrenal, thryoid, prostate, and pulmonary adenomas, renal adeno-
carcinomas and testicular carcinomas have been found in rats and mice given
lead phosphate, lead acetate, and basic lead acetate via dietary and/or
parenteral routes. Lymphomas have been found to result from the subcutane-
ous injection of TEL. By contrast, epidemiological evidence to date does
not indicate that lead has a similar carcinogenic effect in humans.
As in the toxicity of other materials, factors such as dietary calcium,
phosphorus, copper, protein, and Vitamin D, season of the year, drugs, and
exposure to other metals can alter severity of intoxication.
Epidemiological surveys in normal adults indicate mean blood-lead
levels are approximately 20 micrograms per 100 grams of whole blood (range
5 to 30 micrograms per 100 grams whole blood). Persons in daily occupational
contact with motor vehicles in confined spaces show blood-lead levels in the
40- to 50-microgram range.
Epidemiologic studies of blood-lead levels in general and occupational
groups show a logarithmic regression on estimated atmospheric exposure.
Experimental results at the same and higher levels show a dose-reponse re-
lationship which fits the same regression. The data imply that long-term
increases in atmospheric lead will result in progressively smaller incremen-
tal increases in blood lead per unit increase in air lead concentration.
Orchardists and their children in the Wenatchee area of Washington State,
who had been exposed to lead arsenate were examined for toxicological effects
of lead. In the orchardists, both blood- and urine-lead concentrations
ranged from slightly higher to the same values as controls. Studies on the
children indicated that their urinary lead and arsenic concentrations were
nearly twice as high as those of a control group. There was no indication
of adverse effects of lead arsenate exposure on the health of the Wenatchee
orchardists or their children.
Average blood-lead levels in adults living near heavily-traveled free-
ways in Los Angeles County were substantially higher than those found in
adults living near the ocean, or at least 1.6 kilometers (1 mile) from the
freeway. However, the high blood-lead levels were similar to other Los
Angeles populations and lower than those reported for some other urban popu-
lations.
Poor personal hygiene and play habits of children living in areas where
the lead content of house dust, outdoor dust, and soil is considerably ele-
vated from, for example, a secondary smelter, can result in excessive lead
absorption. However, the increases recorded do not appear to cause clear-
cut symptoms of lead poisoning. It is uncertain whether or not subtle
neurological changes occur from such exposure.
The Seven-City Study showed a positive, but not a significant correla-
tion between average blood-lead levels and average annual airborne lead
exposures ranging in concentration from 0.17 to 3.39 micrograms per cubic
meter. Although extensive, the study was inconclusive on this point because
air samples did not accurately reflect air lead exposure of the subjects.
6.5
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The life expectancy of lead workers in an environment in which occu-
pational exposures to lead were controlled in conformity to currently re-
commended environmental and biologic standards was approximately the
same as that of all U.S. males.
Slowed nerve conduction has been observed in storage battery factory
workers whose blood-lead levels had never exceeded 70 micrograms per 100
milliliters of blood. There were no signs of functional neuromuscular dis-
turbances , however.
Fragmentation of bullets during firing, explosive vaporization of
primer, and aerosolization of lead suboxide particles during bullet molding
appear to have been the major sources of mild lead poisoning among instruc-
tors at an indoor pistol range.
Epidemiologic features of excessive lead absorption in children include
prevalence of pica in preschool children, seasonal variation, age distri-
bution of cases, association with dilapidated and deteriorating houses and
race. Today in the United States, plumbism in children is believed to be due
almost entirely to the repetitive eating of leaded house paint. The in-
terior woodwork, painted plaster, and wallpaper of houses built prior to
1940 may contain layers of flaking lead-pigment paints which have never been
removed. Several such flakes may contain far more than the average per-
missible (300 micrograms) daily intake of lead.
At least 600,000 U.S. children reportedly have high levels of blood
lead. In 1971 a survey in 27 cities showed that 21 percent of inner-city
children had symptoms of excessive lead exposure. As many as 2.9 million
American children might run the risk of lead poisoning.
The maximum daily permissible intake (DPI) of lead from all sources
without excessive body lead-burden in children has been considered to be 300
micrograms. The DPI should preclude increases in the total body burden of
lead in children between 1 and 3 years of age as well as in older children.
This DPI was based on the assumption that lead absorption in children is
similar to absorption in adults, a presumption which has recently been shown
to be incorrect.
In children, blood-lead levels less than 40 micrograms of lead per 100
grams of whole blood are assumed to indicate negligible risks with normal
daily dietary intake accounting for most of the ingestion. The biological
significance of 50 to 80 micrograms of lead per 100 grams of blood is un-
clear. Levels greater than 80 micrograms of lead per 100 grams of blood
signify an unacceptable risk to health. Early studies in New York City in-
dicated that lead poisoning in children results in death in about 15 to 20
percent of the cases, and neurological and mental disturbances from encepha-
lopathy in 25 percent of the cases. The apparent increased incidence of
lead poisoning (comparison of 1964 with 1954) is believed due to the vigor-
ous case-finding programs that resulted in the discovery of cases in the
asymptomatic state prior to the onset of encephalopathy. Encouraging was
the sharp decrease in the number of deaths (8 percent in 1964).
6.6
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The screening in New York City in 1971 of 100,000 children, age 1
to 6 years, showed that 2 percent of these children had blood levels of
60 micrograms or greater. Significant elevated blood-lead levels were
found three times more often among black children than among Puerto Rican
children. Seasonal variations of blood-lead levels showed a summer peak.
The New York City results are typical of lead studies in inner-cities
having old and dilapidated housing that accentuate the lead paint problem.
The principal cause of elevated lead in dirt around frame houses in
selected urban areas has been attributed to lead paint on these houses.
Using a naturally occurring tracer lead isotope, dust, and air-suspended
particulate were found not to be the sources of elevated lead body burdens
of children residing in these areas.
Deleterious health effects, for example, mental disorders and school
performance, as evidenced by psychologic referrals and problems of at-
tention and concentration, were observed in children who were treated for
severe lead poisoning and in children without diagnosed lead poisoning who
had elevated blood-lead (over 50 micrograms) levels.
6.2 METABOLISM
6.2.1 Uptake and Absorption
6.2.1.1 Inhala t ion—
Besides the free lead ion, the inorganic lead products include such in-
dustrially used compounds as the acetate, arsenate, carbonate, chloride,
chromate, oxides, suboxides and the sulfate. Industrial lead poisoning usu-
ally results from inhalation of aerosol lead emitted in the form of dust,
fume, mist, or vapor. When inhaled, the small lead particles (less than 1
to 2 micrometers in diameter) tend to be retained by the respiratory tract
to be absorbed or coughed up and swallowed later.
Kehoe (1961a,b; 1964) studied the deposition of lead sesquioxide in the
human respiratory tract, using particles with mass median equivalent diameters
(MMED) of 0.25 and 2.9 micrometers. The deposition of the smaller particles
was 36 percent and was 46 percent for the larger particles. Mehani (1966)
found deposition values ranging from 39 to 47 percent, but unfortunately
failed to determine particle size. Hursh and Mercer (1970) assessed the
percentage of lead deposited after inhalation of natural aerosols on which
lead-212 was adsorbed. They found a range of 27 to 62 percent, which was de-
pendent on particle size.
Rabinowitz, et al., (1974) calculated the quantity of lead absorbed from
a typical urban atmosphere (lead concentration equals 1 to 2 micrograms per
cubic meter) to be 15 plus or minus 3 micrograms per day.
Bingham (1970), using a technique of harvesting alveolar macrophages
from excised mammalian lungs, found that rats inhaling minute quantities of
lead sesquioxide (10 and 150 micrograms per cubic meter) for periods of 3
to 12 months showed a temporary decrease in the number of cells compared
6.7
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with rats inhaling filtered air (0.1 microgram per cubic meter). The func-
tional significance of this effect and the applicability to humans is un-
known.
Macrophages probably do play a role in respiratory uptake of lead in
humans. The rapid absorption from this route noted by Chamberlain, et al.,
(1975) is possibly a result of phagocytosis. This route of entry causes
lead to enter directly into the blood stream.
By phagocytosis and other routes, inhaled lead eventually reaches the
bloodstream. Coulston (1973) and Knelson, et al., (1973) describe a study
in which twenty human volunteers were exposed to 10.9 micrograms per cubic
meter of lead sesquioxide 23 hours per day for 4 months (see Figure 6.1).
In the exposed group the blood lead concentration increased to nearly twice
their pre-exposure levels while the level remained relatively unchanged in
the controls. During the final six weeks of the experiment, there was no
apparent increase in the blood lead of the exposed men, the level remaining
at about 35 micrograms per 100 milliliters of blood. After about 6 weeks
of exposure the ALAD activity had decreased to about one-half the pre-expos-
ure value in the men (see Section 6.3.2.2).
0 5 10 IS 20
WEEKS OF EXPOSURE
Figure 6.1 Levels of blood lead in volunteers exposed to
10.9 micrograms per cubic meter lead sesquioxide.
Source: Coulston. Reprinted with permission from
Environmental Quality and Safety, Vol.2.,
F. Coulston and F. Korte (eds.),
(c) Academic Press, Inc., 1973.
Data from the investigation by Knelson, et al., (1973) on the biological
effects of long-term human exposure to airborne lead was used to prepare a
mathematical model of the kinetics of respiratory lead uptake. Adult male
subjects were subjected to two 18-week exposures at mean lead concentrations
of 10.9 plus or minus 3.1 micrograms per cubic meter and 3.2 plus or minus
0.6 micrograms per cubic meter. Baseline blood-lead concentrations before
6.8
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exposure began were 19.6 plus or minus 4.8 micrograms per deciliter. These
investigators found that increases in total blood lead observed at the two
levels of exposure were closely related to the logarithm of the body burden
(see Figure 6.2). A mathematical model was developed which enables one to
compute the relationship between total lead and potential increase in body
burden. From this relationship, distribution between two theoretical com-
partments with rapid and slow turnover can be inferred. About 90 percent of
the total body burden is believed to go into a slow compartment. Substantial
increases in blood lead are forecasted even for respiratory doses well below
those commonly encountered in ambient air. Towards the end of the actual
exposures approximately 10 percent of the potential increase in body burden
might show as increased total blood-lead content.
Experimental studies of prolonged exposure to artificially generated
lead aerosols have been reported by Griffin, et al., (1975). The lead
aerosol employed resembled that of ambient air in size but differed chemi-
cally. Subjects were exposed for 23 hours a day to lead levels of 3.2 and
10.9 micrograms per cubic meter. The experiments were continued for over 4
months to allow time for equilibration of blood lead to the new exposure levels,
The exposures resulted in respective increases of 2.0 and 1.4 microgram per
100 ml of blood per 1 microgram per cubic meter in air.
6.2.1.2 Ingestion—
The absorption of lead in the intestine has also been shown to be in-
creased by high fat, low protein and high protein diets, and to be decreased
by high mineral diets (Barltrop and Khoo, 1975). Similarly, an extensive
review by Karhausen (1973) suggested that other important factors determining
absorption include: (1) the chemical form of the lead ingested, (2) dietary
calcium level; (3) vitamin D intake; (4) dietary composition; (5) load of
lead; and, (6) gastric acidity. Generally, the uptake of lead from the gut is
less complete than it is from the lungs. Kehoe (1961a), in a detailed
investigation of lead metabolism, found that net absorption of lead from
the gastro-intestinal tract is approximately 10 percent in normal adult
subjects.
In humans, lead is absorbed mainly from the small intestine, to a lesser
extent from the colon, and not at all from the stomach. The coefficient of
intestinal absorption is about 0.08 in adults and has been reported to be as
high as 0.53 in some children (Alexander, et al., 1973).
Rabinowitz, et al., (1975) used stable isotope and balance studies to
investigate the human uptake of dietary and atmospheric lead. Four healthy
adult males were maintained in a hospital metabolic unit for periods up to
six months with controlled diets and environments. The subjects ate constant
diets which were low in lead content but supplemented with stable isotopes of
lead, which served as a nonradioactive tracer distinct from other (atmospheric
and internal) sources of lead.
The alimentary absorption rates of both the lead nitrate tracer and food
6.9
-------
LEAD UPTAKE FROM
RESPIRATORY EXPOSURE
37X RETENTION e*' *' u6""1
«
15 M3 VENTILATION
004 MG/OAT
4.9 L. BLOOD VOL.
j •
3.9 UG'M>
OOI7 MCXDAT
INC HAS! IN tODT IUIOCN (MC)
Figure 6.2 Semi-log plot of increase in total blood-
lead content and potential increase in body
burden. Adapted from Knelson et al.,(1973).
6.10
-------
lead varied among the individuals from 6 to 14 percent. Absorption rates
as high as 50 percent were seen when lead nitrate or sulfide were admini-
stered while fasting. The presence of food in the gut inhibited lead ab-
sorption by up to eightfold. Perhaps substances within food compete with
lead for absorption sites or perhaps unabsorbable portions of food bind the
lead. The data obtained in this study show that gastrointestinal absorption
of lead salts is not a simple function of lead intake, but varies among sub-
jects and depends on chemical form.
Reduction of dietary calcium increases the absorption of lead and cad-
mium (Fleischman, et al., 1968; Six and Goyer, 1970). The great demand for
calcium in children, and pregnant and lactating women will cause high calcium
absorption rates which may decrease the absorption of lead. Six and Goyer
(1972) showed that lowering dietary iron increases lead absorption. Low pro-
tein increased lead uptake (Milev, et al., 1970, cited in Waldron and Stofen,
1974; see Section 6.3.3 and Table 6.15).
The availability of lead in a paint film is of special concern in regard
to the hazard of lead base paint in children. Gage and Litchfield (1969) have
shown that the absorption of lead naphthenate is reduced by half as a result
of its incorporation into a dried paint film. Similarly, Kneip, et al.,
(1974) have shown in monkeys that lead octoate in ground paint is only about
one-third as readily absorbed as lead octoate independent of the paint matrix.
The absorption of various salts of lead has recently been studied in some
detail (Barltrop and Meek, 1975). Various lead salts showed similar degrees
absorption, but metallic lead (180-250 mm diameter) was absorbed only about 14
percent as well as lead acetate. This is of some importance in the evaluation
of the contribution made to dietary lead by the small particles of lead solder
found in the side seam region of metal cans (Barltrop and Meek 1975).
Experimental studies suggest that absorption of lead is age-dependent.
Kostial, et al., (1971a,b) observed that neonate rats have a higher absor-
ption of lead when compared to adult rats. This may be related to the high-
er absorption of calcium in young rats. In animals, the amount of lead ab-
sorbed from the gut appears to be less than in man and the form in which it
is administered does not appear to affect its absorption (Forbes and Reina,
1972).
203
Gruden and Stantic (1975) studied the in vitro transfer of Pb through
the wall of the duodenum, jejunum and ileum in 6- and 26-week-old female,
albino rats. Lead transport through, and lead uptake in the wall were prac-
tically the same in all segments. No influence of age on these parameters of
lead metabolism was observed. In contrast, these investigators cite research
in which very young rats (5 to 7 days old) were found to absorb over 50 per-
cent of applied lead, a figure fifty times larger than observed with 16-week
old rats.
6.2.1.3 Percutaneous Absorption—
Penetration of lead through intact skin has not been studied extensively.
There are some data suggesting that inorganic lead salts are not absorbed
6.11
-------
significantly by this route (Lang and Kunze, 1948). A case report, however,
by Hamilton and Hardy (1974) notes percutaneous absorption of inorganic lead
resulting from the application of a theatrical grease paint which contained
40 percent lead oxide. Lead soaps used in industrial lubricants, however,
are absorbed to a significant extent (Hine, et al., 1969).
6.2.1.4 Placental Transfer—
The inorganic forms of lead have a greater potential for injury to the
embryo, fetus, and neonate than to the mature adult. Placental transfer of
inorganic lead has been reported (Scanlon, 1971; Harris and Holley, 1972;
Blanchard, 1966; Palmisano, et al., 1969). Cord blood was found to have
lead in concentrations approximating those found in maternal blood (Scanlon,
1971; Harris and Holley, 1972 and Rajegowda, et al., 1972). Scanlon (1971)
has found lead concentrations as high as 39 micrograms per 100 milliliters
in the umbilical cord of infants in an urvan environment.
Barltrop (1969, cited in Waldron and Stofen, 1974), in a study of nor-
mal humans, found that placental transfer of lead began as early as the
twelfth week of gestation and that the lead content in fetal tissues increas-
ed throughout pregnancy. Fetal bone was found to have the highest tissue-
lead level (80 micrograms per gram). Lower lead levels were found in the
placenta, heart, kidney, liver, and blood. The total amount of lead transfer-
red per day during pregnancy appeared to be less than 303 micrograms.
Chaube, et al., (1972) detected lead in two-thirds of first trimester
human embryonic and fetal specimens. The fifty embryos and fetuses ranged
in age from 31 to 261 days gestation. In fetal tissues, lead was found in
77 percent of the liver samples, 15 percent of the brain samples, and 30
percent of the kidney samples analyzed. In the embryos the concentration of
lead ranged from 0.38 to 2.0 micrograms per gram of wet tissue. Only two
fetuses had detectable lead in the brain. In the liver, the concentration
ranged from 0.84 to 4.04 micrograms per gram of wet tissue, and in the kid-
ney from 0.9 to 2.3 micrograms per gram of wet tissue.
The blood of neonates contains lead in concentrations similar to that
in cord blood (Kubasik and Volosin, 1972). This is supported by Schroeder
and Tipton (1968) who found lead in significant concentrations in neonates
of several nationalities (including stillbirths), indicating considerable
placental transfer (see Table 6.1).
Haas, et al., (1973), cited by the Task Group on Metal Accumulation
(TGOMA, 1973) reporting on 294 sets of maternal and fetal blood samples, found
maternal lead levels to average 16.9 micrograms per 100 milliliters, with
fetal lead levels averaging 15 micrograms per 100 milliliters. The cor-
relation coefficient between maternal and newborn blood levels was 0.57, which
is substantial.
Finklea, et al., (1972, cited in TGOMA, 1973) found that lead is bound
to and crosses the placenta. Fetal blood levels were lower than maternal
levels, with erythrocytes showing a greater differential than whole blood.
6.12
-------
Table 6.1 TISSUE LEAD CONCENTRATION IN CHILDREN AND ADOLESCENTS
ON
•
H
U>
Place of
Origin
n Aorta
Liver
Kidney
Pancreas
Mean Lead
America
Stillborn
0-19
Africa
India
Japan
22
23
5
9
3
65
24
-
82
27
53
74
100
100
64
38
62
39
90
98
—
31
18
44
26
Lung Testis
Concentration,
18
18 9
23
68 76
34 72
Heart
Brain
Spleen
Bone
ppm ash
25
5
0
33
15
10
0
13
10
13
37
10
-
50
23
«.
2
-
10
27
Source: Schroeder and Tipton. Reprinted with permission from Archives Environmental Health.
(c) American Medical Association, 1968.
-------
6.2.2 Transport and Distribution
Following absorption nearly all the lead in the blood is associated with
the erythrocytes. It is then distributed to various tissues with concentrations
being highest in bone and hair; intermediate in liver, kidney, and aorta, and
lowest in heart and brain. Schroeder and Tipton (1968) have observed that in
or near a steady state of lead retention in the human body, more than 90 per-
cent resides as a relatively nondiffusible fraction in the skeleton. The
body tends to reject lead at a rate commensurate with the rate of ingestion.
Therefore, both the blood and urine lead levels vary as a function of the
amount of ingested lead. Since only about 10 percent of the ingested lead is
absorbed into the body, lead concentrations in the feces reflect short-term
fluctuations in lead ingestion, while the urine and blood levels are more indi-
cative of lead ingestion over long periods of time.
Within the blood, lead is associated with the erythrocytes or the plasma
proteins, and a small quantity is in a free, ionized state. Approximately
95 percent of the lead in the circulating blood is attached to the red cell.
This percentage, however, is dose-dependent and subject to interpersonal varia-
tions , according to a review by Waldron and Stofen (1974). The rate of lead
uptake by the erythrocytes from the plasma is temperature-dependent as well,
according to Clarkson and Kench (1958).
Since lipid-free stroma does not bind lead effectively, the lipids and
lipid proteins in the cell membrane seem to act as strong lead binding sites
(Vincent, 1958, Teisinger, et al., 1958; see Section 6.3.1). The fact that
lead is bound to plasma proteins is not surprising since other heavy metals
like mercury and cadmium also show a strong affinity for ligands such as
phosphates, cysteinyl and histidyl side chains of proteins, purines, pteridines,
and porphyrins (Vallee and Ulmer, 1972). Suggestions for the manner in which
lead is bound to the erythrocyte reviewed by Waldron and Stofen (1974) include
a peptized lead phosphate sol, a colloidal lead phosphate, a diglyceryl phos-
phate, mixed salts with calcium and chloride, and a protein-phenolic complex.
The affinity of lead toward sulfhydryl (SH) groups suggests a series of reac-
tions on the membrane which lead to a S-Pb-S complex (Fassow and Tillman, 1955).
Barltrop and Smith (1971) have reexamined the lead-binding properties of
human erythrocytes with respect to the cell fraction in which binding occurs.
Their results suggest that lead is bound to the cell contents rather than to
stromal material. This was confirmed by the absence of significant binding of
lead when washed stroma replaced hemolyzed erythrocytes. These were some
indications that the lead was bound to both hemoglobin and some low molecular
weight material.
Lead disappears from the blood at a rate which indicates first-order re-
action kinetics and may be the sum of three exponential functions (Castellino
and Aloj, 1964). Stover (1959) concluded that lead rapidly transferred to the
extravascular spaces from the plasma as the latter level declined. To maintain
dynamic equilibrium between red-cell and plasma lead, on the one hand, and extra-
cellular and intracellular lead on the other, it is suggested that the ionic
fraction of the plasma lead is transferred slowly to other body compartments.
6.1U
-------
A similar rationale applies to the lead concentration in urine, with blood
showing a somewhat lesser fluctuation than urine (Kehoe, 1961a-d).
Extensive studies of soft-tissue lead distribution have been reported by
Schroeder and Tipton (1968), and their colleagues (Schroeder and Balassa, 1961;
Tipton and Cook, 1963; Tipton and Shafer, 1964; Tipton, et al., 1965) and their
data confirmed by Barry and Mossman (1970). Tables 6.1 and 6.2 show the varia-
tions in lead tissue concentrations with geographical origin. In general, the
aorta has the highest concentration followed by the liver and kidney. The
brain and the heart show consistently low values.
Schroeder and Balassa (1961) and Schroeder and Tipton (1968) found that
concentrations of lead in the soft tissues, for example, kidney, pancreas,
liver, lung, and aorta increase with age up to age 40-50, the rise being par-
ticularly sharp in the aorta (see Figures 6.3 through 6.7).
Age-linked accumulations of lead in tissues of Americans were also found
for larynx, trachea, and prostate (Schroeder and Balassa, 1961). In aortas
collected at autopsy from 18 male residents of Baltimore the highest aortic
levels of lead were found in those persons 38 years or older (Poklis, 1975).
The lead content of the trachea at autopsy from 17 Baltimore residents sampled
in 1972 ranged from 0.6 to 8.8 micrograms per gram of fresh tissue (Poklis and
Freimuth, 1975). Contrary to the observation of Schroeder and Tipton (1968),
no significant correlation of tracheal lead and age was demonstrated by these
data. The mean tracheal lead concentration of the samples collected in 1972
was compared with the mean lead concentration of Baltimore residents reported
in 1957. From the increase in tracheal lead, it may be concluded that from
1957 to 1972 there was an increase in the lead "body burden" of Baltimore
residents. While the increase may not have been sufficient to affect public
health of Baltimore residents, it does reflect an increase in lead exposure
in the Baltimore environment.
Bone contains approximately 90 percent of the total body burden of lead
which is deposited in the form of the insoluble tertiary lead phosphate.
Data by Schroeder and Balassa (1961) and Schroeder and Tipton (1968) indicate
that the concentration of lead in the bones rises steadily to about the 4th
decade, reaches a plateau, and then decreases in the 7th or 8th decade (see
Table 6.3 and Figure 6.8).
Barry and Mossman (1970) and Barry (1973) concluded that there is no de-
crease in bone lead with old age and suggested that the drop reported by some
of the earlier investigators was due to the small number of samples. This
confirms earlier work by Morris (1940) who found positive correlation coef-
ficients between age and lead concentration in femur, ribs, and vertebrae
with values of 0.48, 0.36, and 0.28, respectively. He concluded that more
lead was stored in the long bones than in either ribs or the vertebrae, al-
though there is not a general consensus as to which contains the greatest
concentration of lead. Holtzman (1963) demonstrated that the concentration
of lead-210 was higher in trabecular than in cortical bone. The lead in
the skull bones seemed to be most representative of the mean for the total
6.15
-------
Table 6.2 VARIATION IN HUMAN SOFT TISSUE LEAD CONCENTRATION WITH GEOGRAPHICAL LOCATION3
ON
Place of origin
N
Aorta
Liver
Kidney
Pancreas Lung
Mean Lead
Nine American
cities
San Francisco
Switzerland
Africa
Middle East
Far East
150
27
9
54
37
74
140
220
32
71
140
91
130
160
59
64
70
97
98
54
45
36
62
63
49
65
42
24
34
39
Testis
Concentration ,
47
38
32
28
42
43
12
20
23
29
32
35
Heart
ppm ash
5
10
14
5
24
19
Brain
5
5
5
5
14
10
Spleen
27
44
20
21
40
33
Bone
43
-
-
-
26
30
a
Source: Schroeder and Tipton. Reprinted with permission from Archives Environmental Health.
(c) American Medical Association, 1968.
-------
150-
100
8
50
i i i i i i i n
Leod In kidney
45 15
Days
2030405060 70 a09O
Age in yeors
Figure 6.3 Change in concentration of lead with age in
kidney. Numbers in brackets in this and
Figs 6.3-6.7 indicate number of cases in that
decade when <9.
Source: Shroeder and Balassa. Reprinted with
permission from Journal Chronic Diseases.
(c) Pergamon Press, 1961.
150-
100
I
so
i i i
Leod in pancreas
I
I
I
I
I
I
I
10 20 30 40 50 60 70 80 90
Age in years
Figure 6.4 Change in concentration of lead with age in
pancreas.
Source: Shroeder and Balassa, Reprinted with
permission from Journal Chronic Diseases.
(c) Pergamon Press, 1961,
6.17
-------
200-
120
I I I I
Lead in liver
I I I I
(7)
(2)
•
I I
10 20 30 40 50 6O 70 80 90
Age in years
Figure 6.5 Change in concentration of lead with age
in liver.
Source: Shroeder and Balassa. Reprinted
with permission from Journal Chronic Diseases.
(c) Pergaraon Press, Inc. 1961.
300-
200
o
i
100
Leod in oorto
• (6)
10 20 30 40 50 60 70 80 90 100
Age in years
Figure 6.6 Change in concentration of lead with age
in aorta.
Sour.ce: Shroeder and Balassa. Reprinted with
permission from Journal Cfirohic Diseases.
(c) Pergamon Press, Inc., 1961
6.18
-------
I I I I I I I
Lead hi lung
(7)
O 45 10 2O 30 4O 50 60 70 80 90
Days
Age in years
Figure 6.7 Change in concentration of lead with age in
lung.
Source: Schroeder and Ralassa.
Reprinted with permission from Journal of
Chronic Diseases, (c) Pergamon Press, Inc., 1961.
6.19
-------
Table 6.3 VARIATION IN BONE LEAD
CONCENTRATION WITH AGE3
Mean Lead
Concentration,
Age, years n yg/g ash
0-1
1-9
10-19
20-29
30-39
40-49
50-59
60-69
70-79
80+
4
2
9
11
27
9
9
5
2
1
<1-0
2-5
11-3
16-8
43-1
37-2
31-2
34-2
10-0
22-0
a
Source: Schroeder and Tipton. Reprinted with
permission from Archives Environmental Health.
(c) American Medical Association, 1975.
6.20
-------
50
40-
:30
20
10
I I I I
Lead in bone
(1)
0 45 10 20 30 40 50 60 70 80 90
Days
Age in years
Figure 6.8 Change in concentration of lead with age in
bone.
Source: Schroeder and Balassa. Reprinted
with permission from Journal Chronic Diseases.
(c) Pergamon Press, Inc., 1961.
6.21
-------
skeleton. Rib concentrations deviated most from the mean and concentrations in
the tibia were very low.
Gross, et al., (1975) assayed 29 tissues per individual from autopsies of
46 white males ranging in age from 20 to 84 years (see Table 6.4). Of the 46
individuals reported, 43 had normal blood-lead concentrations of 40 micrograms
per 100 milliliters or less; two individuals had slightly elevated blood-
lead concentrations (43 micrograms and 41 micrograms per 100 milliliters);
and one had 106.5 micrograms per 100 milliliters. On a wet-weight basis (see
Table 6.4 ), calcified tissues (bones and aorta) contained the highest con-
centration of lead; the glandular tissues (liver, kidney, and pancreas) were
intermediate; and the remaining tissues (which were mostly of a nonglandular
nature) had the lowest concentrations of lead. Table 6.5 shows the distri-
bution of lead in the bones and aorta. The low lead values for the bones of
the individual in the 5th decade may reflect a chance selection of individuals
with low lifetime lead exposures. A rapid increase of lead in the aorta was
found after the 5th decade.
Gross and Pfitzer (1975) found that concentrations of more than 2 micro-
grams per gram of lead in the aorta were associated with severe atherosclero-
sis involving calcium deposits. As reflected in the skeletal lead, the over-
all body content of lead increased with age, but many soft tissues did not
change and several decreased in lead concentrations with age. The lead con-
tent of the liver, kidneys, pancreas, jejunum, stomach, and adrenals decreased
significantly with a trend for lead in the blood, skin, cecum, and bladder to
decrease as well.
In an assay of the tissues of 129 human postmortem subjects, Barry (1975)
found that the tissues of men contained about 30 percent more lead than the
tissues of women. Lead increased with age in bones in both sexes but not in
most of the soft tissues. Children had lower lead concentrations than adults
irrespective of sex. Over 90 percent of the adult burden of lead was in the
bone, of which over 70 percent was in dense bone. Occupationally-exposed men
aged 55 years or more had mean bone burdens of lead of 595 milligrams compared
with 205 milligrams in unexposed men of similar age. Their soft tissue burdens
were 16 and 8.5 milligrams, respectively. The cortex and basal ganglia of the
brain of males with no known occupational exposure to lead had mean lead levels
of 0.10 and 0.09ppm, respectively. The respective concentrations in females
were 0.12 and 0.11 ppm. Men aged 29 to 82 years occupationally exposed to
lad had mean lead levels of 0.65 and 0.29 ppm, respectively, in the cerebral
cortex and basal ganglia. The data for exposed subjects compared favorably
with that of Gross, et al., (1975). Hair concentrations did not seem to pro-
vide a useful index of lead absorption.
Sumino, et al., (1975) determined the amounts of fifteen heavy metals in
fifteen male and fifteen female Japanese cadavers (average weight 55 kilo-
grams, average age 39 years). The highest level of lead was found in the
adrenal glands (1.2 plus or minus 0.79 ppm). The average lead content of
the female tissue was higher than in male tissue, except in the liver. Sig-
nificant differences were found in small intestine (P equals 0.01), lung,
brain, adrenal glands, and spleen (P equals 0.05). No difference with ages
6.22
-------
Table 6.4 TISSUES RANKED ON THE BASIS OF OVERALL
MEAN CONCENTRATIONS OF LEADa»b
ppm, wet-weight basis
Tissue
Tibia
Skull
Rib
Vertebrae
Aorta
Liver
Nodes
Kid. cor.
Kid. med.
Pancreas
Spleen
Lung
Adrenal
Blood
Prostate
N
45
44
45
44
45
45
41
45
44
45
43
42
41
43
41
14.
13.
7.
4.
1.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
X/SD
09/11
81/9.
14/4.
42/2.
65/1.
98/0.
86/0.
79/0.
48/0.
46/0.
33/0.
36/0.
25/0.
21/0.
20/0.
.22
09
19
52
82
53
93
42
22
23
15
12
12
09
22
r
0.53C
0.50C
0.38d
0.21
0.52C
-0.34d
0.15
-0.53C
-0.38d
-0.45C
-0.02
0.13
-0.38d
-0.29
-0.08
Tissue
Thyroid
Testes
Je j unum
Brain, grey
Brain, white
Fascia
Stomach
Bladder
Skin
Heart
Cecum
Muscle
Urine
Adipose
N
40
43
45
39
41
43
45
43
43
43
45
44
8
43
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
X/SD
17/0.
15/0.
12/0.
11/0.
11/0.
11/0.
10/0.
09/0.
08/0.
08/0.
07/0.
07/0.
11
09
05
05
04
05
05
04
03
04
03
03
06/0.11
04/0.
01
r
0.30
-0.26
-0.30d
-0.18
-0.09
-0.05
-0.32
-0.02
-0.11
-0.12
-0.07
-0.23
0.24
0.11
Source: Gross, et al. Reprinted with permission from Toxicology and
Applied Pharmacology, (c) Academic Press, Inc., 1975.
Shown are number of tissues (N) , their means +SD and correlation of
tissue concentrations vs age.
p <0.05.
6.23
-------
Table 6.5 CONCENTRATIONS OF LEAD FOR TISSUES
INCREASING WITH AGEa'
ppm, wet-weight basis
Decade, years
Tissue
Tibia
Skull
ON
ro Rib
Vertebrae
Aorta
20-29
6.6110.92
(6)
7.2711.76
(6)
4.0611.92
(6)
3.4811.50
(6)
0.4010.18
(6)
30-39
9.3714.64
(4)
9.07+4.31
(4)
5.48+3.82
(4)
2.9811.84
(4)
0.8610.71
(4)
40-49
10.7715.09
(8)
12.85+5.12
(8)
8.0414.13
(8)
4.9811.52
(8)
0.75+0.16
(8)
50-59
9.6814.43
(9)
10.13+4.21
(9)
4.8311.55
(9)
2.8811.20
(9)
1.1410.46
(9)
60-69
18.5718.34
(11)
19.6018.17
(11)
9.7714.36
(ID
6.66+3.24
(ID
2.8312.55
(ID
70-79
28.36121.37
(6)
21.76118.06
(5)
9.42+4.65
(6)
4.1712.26
(6)
3.3212.18
(6)
Source: Gross, et al. Reprinted with permission from Toxicology and Applied Pharmacology.
(c) Academic Press, Inc. 1975.
Shown are the decade means +SD. The number of tissues in each decade are shown in parentheses.
-------
was found. The median lead concentration in the cerebrum and cerebellum
was 0.19 and 0.22 ppm, respectively.
Lead is normally found in higher concentrations (on a weight per weight
basis) in hair than in any tissue. Kopito, et al., (1967), in a study of 93
presumably healthy children under 17 years of age from the greater Boston
area, found a mean lead concentration of 31 micrograms per gram of hair.
Several studies have shown that lead concentrations in hair and teeth
vary among groups of individuals, depending on the amount of lead in their
immediate environments. These are discussed in Section 6.5.2.
6.2.3 Elimination
The principal routes of elimination of lead from the body are through
the feces and urine. Secondary routes include sweat, milk, falling hair,
and discarded and desquamated skin. Kehoe has suggested that the contribu-
tion of food, beverages and water digested and of the total urine and feces
excreted can be used to determine the net balance of lead intake versus out-
put over a period of many months (Kehoe, 1961- a-d; see Table 6.6)
Kehoe's work indicates that in conditions approximating a steady-state
in which oral input roughly parallels urinary and fecal output, the urinary
excretion is about 10 percent of the oral output and the fecal output is
close to 90 percent. Most of the lead in the feces represents lead which
has passed unabsorbed through the gut. The contribution to total excretion
of inhaled lead was not determined, a factor which would have likely elevated
the estimated proportion of the total lead intake excreted via the urine.
Several investigations have indicated that lead excreted (rather than
that passing unabsorbed through the intestine) in the feces derives pre-
dominantly from the bile. For example, Blaxter and Cowie (1946) found that
7.5 percent of a dose of lead acetate administered to sheep was excreted in
6 days. Eighty-one percent of that was in the bile.
After intraveneous administration of lead-212, the fecal route probably
contributes as much as the urinary route to total excretion. In a study on
two human subjects, Booker, et al., (1969), found no lead-212 in the feces
during the first 24 hours after injection but found 4.4 and 5.6 percent in
the urine. During the second 24 hours, however, they found 1.4 percent in
the urine and 1.5 percent in the feces.
The excretion of lead through the kidney is hampered by the high degree
of interaction of lead and other heavy metals with ligands present in erythro-
cytes and/or plasma proteins. Vostal and Heller (1968) investigated lead
excretion in man and dogs and found that the renal tubule reabsorbed a con-
stant amount of lead. The effect was pH-dependent, increased at low pH and
decreased or was entirely absent at high pH.
Rabinowitz, et al., (1973), studied lead excretion as oart of a 8gUdY of
the kinetics of lead metabolism using stable lead isotope ( Pb and Pb)
6.25
-------
Table 6.6 LEAD INGESTION AND EXCRETION OF
A NORMAL HUMAN SUBJECT3
8-Week
Periods
1st
2nd
3rd
4th
5th
6th
7th
Subtotal
8th
9th
Subtotal
Total
Lead
Ingested, mg
13.59
13.31
13.16
11.51
9.30
9.24
12.75
82.86
22.21
18.17
40.38
123.24
Lead
Total
11.95
15.13
13.82
11.59
8.93
9.05
13.74
84.21
17.61
15.05
32.66
116.87
Excreted ,
In Feces
10.45
13.63
12.45
10.41
7.88
8.16
12.86
75.84
15.85
13.76
29.61
105.45
mg
In Urine
1.50
1.50
1.37
1.18
1.05
0.89
0.88
8.37
1.76
1.29
3.05
11.42
Net Change
in Body
Lead, mg
+1.64
-1.82
-0.66
-0.08
+0.37
+0.19
-0.99
-1.35
+4.60
+3.12
+7.72
+6.37
a Source: Kehoe (1961a-d). Reprinted from Journal Royal Institute
Public Health Hygiene.
6.26
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tracers. A normal, healthy man ate a constant, low-lead diet (156 micro-
grams lead per day for 160 days while living in a metabolic unit. It was
found that 8.3 plus or minus 0.4 percent of the ingested Pb was absorbed
into the blood, where it had a mean life of 27 days. Fifty-four percent of
this lead was lost from blood through the urine, which had an isotopic compo-
sition identical with whole blood; the remainder was transferred to the soft
tissues and skeleton. The net absorption of lead was 25 micrograms per day
with a mean urinary excretion of 28 micrograms per day. Loss of lead from
hair, nails, and sweat was approximately 4 micrograms per day. Therefore
the total lead output exceeded dietary intake by 17 micrograms per day,
which presumably came from the atmosphere. This value agreed generally with
that derived from the analysis of isotopic blood data.
The estimates of half-time for lead in bone have varied from 64 days in
the spine of rats (Torvik, et al., 1974) to 7,500 days in the skeleton of a
dog (Fisher, 1969). The half-time varies with different bones, presumably
due to the relative proportions of cortical and trabecular bone. The
International Commission on Radiological Protection (ICRP) has used 10 years
as the biological half-l|£g for lead in bones of humans (ICRP, 1959). Fol-
lowing a single dose of Pb in dogs, disappearance of the label from blood
was followed for 280 days. The biological half-life of lead in the body was
estimated to be 1940 days (Hursh, 1973).
Prerovska and Teisinger (1970), in a study of the excretion of lead and
its biological activity several years after termination of exposure, con-
cluded that there are at least two compartments for lead in bone. Hammond,
et al., (1967) also suggested an additional compartment consisting of lead
firmly bound to soft tissue. This conclusion is consistent with the obser-
vation by Goyer and Mahaffey (1972) and Moore and Goyer (1974) who found that
lead binds firmly with nuclear protein in rats. Studies in animals by
Bolanowska, et al., (1968) and Bolanowska and Piotrowski (1968, 1969) have
furnished mathematical models for the elimination of lead based upon an ex-
ponential model for a four-component system:
(1) A rapid exchange compartment (blood and internal organs);
(2) The skin and muscles;
(3) The exchangeable part of lead in bones; and
(4) A very slowly exchangeable part of lead in bone.
Body retention for bone-seekers is best described by a power function of the
form:
At"n
where,
R = fraction of original dose at time t;
A = a constant equal to the fraction of the assimilated dose at t = 1;
and
n = a constant equal to the slope of a linear log - log plot of R
against t, is a coefficient characterizing the loss from the body.
6.27
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6.2.4 Mathematical Models of Lead Metabolism
Some researchers have examined the total uptake of lead by humans.
This involves multiple routes of entry, each with characteristic absorption
patterns.
Rustagi (1964, 1965) and Sterling (1964) propose the use of the log-
normal distribution for the random phenomena of the intake and output of
trace metals, including lead, in the human system. Some results of the
queuing theory in probability are indicated through the use of this mathe-
matical model for the expected amount stored in the body.
Lutz, et al., (1970) developed a mathematical model to represent the
environmental transport of lead from several sources, with the subsequent
uptake of lead by man. In particular, the submodels for airborne transport
of lead and lead in the body were developed. The model developed for the
airborne transport of lead was used to calculate the airborne concentrations
of lead in the atmosphere due to emissions of lead from several sources.
The predicted output is for an average steady-state airborne lead concentra-
tion, as the model was not developed to predict time-varying airborne lead
concentrations.
The submodel, which represents the flow of lead into, within, and out
of an individual was developed to predict the distribution and quantity of
lead in several body organs. Since measurement of the blood-lead level of
an individual is a clinical method of investigating the effect of lead on an
individual, the blood-lead levels due to several modes of intake of lead,
including inhalation of various concentrations of airborne lead and ingestion
of normal amounts and above normal amounts, were calculated. The approach
of developing a mathematical model to quantitatively predict blood-lead
levels due to intake by ingestion or inhalation was found to be valid within
the accuracy of this preliminary modeling effort.
In order to approximate total lead uptake more accurately it is
desirable to first consider each route separately. It should be noted, how-
ever, that humans are never limited to a single path of lead entry and
studies which do so are abstractions for the purpose of controlled experimen-
tation.
6.3 TOXIC EFFECTS
The present-day environmental problem of lead may be viewed at three
levels. First, there is the problem of sporadic episodes of acute lead in-
toxication. These are largely accidental or the result of ignorance of the
danger of lead. Second is the problem of clinical and subclinical intoxica-
tion of large numbers of children in urban ghetto areas who are living in
pre-World War II housing. This is largely a socioeconomic problem but it is
left to members of the medical community to promulgate information regarding
the dimensions of the problem. The third aspect of the environmental prob-
lem concerns the question of the possible harmful effects of body stores of
lead.
6.28
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An answer to this question depends on increased knowledge of the bio-
logic effects of lead, particularly regarding the effect of trace quantities
on cellular function (Goyer, 1971a).
Many organs and systems have been shown to be adversely affected by
lead. These effects will be discussed in succeeding sections of this
chapter. Much of what is known concerning effects has been adduced only in
isolated cellular or subcellular systems. The implications for the health
of man are uncertain in such cases but should be further investigated when
the level of lead in the study is within an order of magnitude of likely
human exposure levels.
6.3.1 Enzymatic and Cellular Responses to Lead
The basic mechanism of chemical toxicities is ultimately associated
with the chemical and physical properties of the toxic agent. Metal toxicity
is the inherent capacity of the metal to adversely affect any biological
activity. This is the result of a metal interacting with an enzyme, an
enzyme substrate, or a protein, thereby leading to changes in metabolic or
physiologic processes.
Toxicity may also result from interference with essential metal metabo-
lism, and from interactions with macromolecules causing conformational
changes and disturbances in cell membrane permeability. Lead exhibits high
affinity for most biological anions. For example, the solubility product
for.lead phosphate is 10 , making binding between the two ionic species
(Pb and PO,) most likely both inside and outside living cells (Venugopal
and Luckey, 1975).
Although the enzymes affected by lead mainly are involved in heme
synthesis, activities of other enzymes are also influenced by lead. These
activities may be manifested in two general ways: (1) increased enzyme
activity in the blood plasma due to tissue damage, or (2) decreased enzyme
activity due to an inhibitory action on certain enzymes in tissues or in the
blood (de Bruin, 1971).
Ulmer and Vallee (1969) and Vallee and Ulmer (1972) have reported the
effects of lead on diverse biological systems ranging in complexity from
isolated biochemical systems to whole animals. Vallee and Ulmer (1972)
indicate that lead, like mercury and cadmium, forms mercaptides with the -SH
group of cysteine and less stable complexes with other amino acid side chains.
This apparently is inhibitory to a number of enzymes.
I [
The stability constants of ^complexes of Pb with serine and^threojjiine
are_^equivalent to those with Zn and greater than those with Cu , Ni ,
Co , and Mn . proteins with large numbers of free -SH groupgs, e.g.,
thionein bind Pb firmly both in vitro and in vivo.
Lead inhibits most^enzymes^bearing a single functional^SH group less
readily than either Hg or Cd . The concentrations of Pb _3 generally
required to inhibit -SH and other enzymes in vitro, i.e., 10 to 10 M,
6.29
-------
is far in excess of those levels observed in tissues and fluids from indi-
viduals with clinically evident Pb intoxication. However, much lower con-
centrations of Pb inhibit a small, select group of enzymes, i.e.,
lipoamide dehydrogenase, certain ATPases, and deltaaminolevulinic acid (ALAD)
dehydrase (Valle^and Ulmer, 1972). In fact, Ulmer and Vallee (1969) found
that lead (as Pb ) in concentrations as low as 6.5 x 10~ M strongly
inhibits lipoamide dehydrogenase, an enzyme crucial to cellular oxidation.
This probably occurs through binding to the dithiol configuration at the
active catalytic center. Protection is afforded by coenzymes and substrates
and the inhibition is reversed by EDTA.
Increased activity of the transaminases (serum glutamic oxaloacetic
transaminase and serum glutamic pyruvic transaminase) have been described by
some investigators while such effects have not been observed by others.
Animal studies of enzyme enhancement and depression were reviewed by Vallee
and Ulmer (1972) and are summarized in Tables 6.7 and 6.8.
There is some indication that lead absorption by man may increase the
activity of aldolase and catalase while depressing the activity of alkaline
phosphatase, cholinesterase, and carbonic anhydrase. These effects were
reviewed by de Bruin (1971). Workers with moderate elevations of blood lead
have been found to have red blood cells with reduced adenosine hyphosphatase
activity (Hasan, et al., 1967a,b). The clinical implications of this enzyme
alteration are unknown, although it is quite possibly a factor in the
shortened erythrocyte life span which occurs upon exposure to high levels of
lead.
In a study of the detoxication mechanism in the rat, Wagstaff (1972)
observed that ingestion of lead acetate was followed by increased activity
of microsomal enzymes. No rats died due to lead acetate consumption T>ut
body weight gains were depressed. Male rats fed lead acetate had elevated
cytochrome P-450.
The effect of lead acetate on phenobarbital, a microsomal enzyme stimu-
lant, was additive or even synergistic in liver weight increases, hexobarbital
sleep time, and in vitro enzyme activities. Concurrent ingestion of pheno-
barbital with lead decreased toxicity. The physical appearance of lead-fed
rats was improved, impairment of body weight gain was practically eliminated,
and storage of lead in liver tissue was decreased 39 percent by phenobarbital.
Contrary to these findings, rates of P-450 mediated drug metabolism in
adults and children appear to be prolonged in some cases of high exposure
(Alvares, et al., 1975; Alvares, et al., 1976). Furthermore, even in rats,
contradictory observations have been made indicating depression of P-450
dependent drug metabolism (Scoppa, et al., 1973).
Nathanson and Bloom (1975) found that very low concentrations of lead
nitrate inhibit adenyl cyclase in mammalian (rat) brain tissue. In cere-
bellar homogenates, enzyme activity was inhibited by concentrations of lead
nitrate or lead chloride as low as 0.1 micromolar; 50 percent inhibition
occurred at about 3 micromolar; and almost complete inhibition occurred at
6.30
-------
Table 6. 7 ENZYMATIC ACTIVITIES ENHANCED BY LEADC
Enzyme
Source
Alkaline phosphatase
Cytochrome oxidase
Glucose-6-P dehydrogenase
Glutamic dehydrogenase
Glutamic oxaloacetic transamlnase
Glutamic pyruvate transaminase
Lactic dehydrogenase
Sorbital dehydrogenase
Steroid 3 3-ol-dehydrogenase
Guinea pig urine
Canine intestine
Guinea pig kidney
Guinea pig serum and urine
Sheep red cells; guinea pig serum
Sheep plasma and red cells
Guinea pig serum and kidney
Guinea pig serum
Rabbit adrenal
Source: Vallee and Ulmer. Reprinted with permission from Annual Reviews
Biochemistry, (c) Annual Reviews, Inc., 1972.
6.31
-------
Table 6.8 ENZYMATIC ACTIVITIES INHIBITED BY LEAD'
a
Enzyme
Source
Acetyl cholinesterase
Acid phosphatase
Alkaline phosphatase
6-ALA dehydrase
Aminopeptidase
ATPases
Carbonic anhydrase
Cytochrome oxidase
Diaphorase
Fructose-1,6-diphosphatase
Glucose-6-P dehydrogenase
Glutamic dehydrogenase
Succinic dehydrogenase
Rat red cells
Equine serum
Sheep brain
Rabbit liver and kidney
Rabbit and human serum
Rabbit muscle, intestine
Rabbit blood vessels
Rat lung
Mammamlian red cells
Cat and guinea pig liver
Rabbit muscle, blood vessels
Human red cells
Guinea pig kidney
Human blood
Canine intestine
Rabbit muscle
C_. utilis
Rat red cells
Human red cells
Guinea pig kidney
Canine intestine
a Source: Vallee and Ulmer. Reprinted with permission from Annual
Reviews Biochemistry, (c) Annual Reviews, Inc. 1972.
6.32
-------
100 micromolar. Lead ions also inhibited noradrenaline-stimulated activity,
independent of the concentration of adenosine triphosphate (ATP) and tissue
protein present in the reaction mixture. In cases of experimental lead
intoxication in which rats displayed symptoms of hyperactivity, brain lead
levels varied from 3.0 to 6.0 micromoles, a concentration in which adenyl
cyclase activity was inhibited by 50 to 70 percent. These animal studies
of Nathanson and Bloom (1975) support the suggestion that inhibition of
adenyl cyclase may mediate some of the toxic manifestations of lead in the
nervous system and other organ systems in man.
Phillips, et al., (1971) investigated the effects of lead ingestion on
the body burden of DDT, liver Vitamin A and microsomal enzyme activity in the
rat. Lead ingestion at 100 to 200 ppm (as lead acetate) for 36 and 90 days
had no effect on the disappearance of DDT residues (and metabolites) from
adipose tissue of rats. Lead alone and lead fed to DDT pretreated animals
had no effect on body weight gain, liver weights, liver Vitamin A, liver
protein, in vitro liver carboxylesterase activity and phenobarbital sleeping
times.
Suketa, et al., (1975) found that the amount of delta-aminolevulinic
acid (ALA) increased four times in lead-intoxicated rats compared with con-
trols. The formation of ALA in the liver homogenate of lead-intoxicated rats
was increased by the addition of ethylenediamine-tetraacetic acid (EDTA),
suggesting that the increase of ALA in the liver of lead-intoxicated rats may
be due to the activation of ALA synthetase by lead rather than due to the
inhibition of ALA dehydratase by lead. While the full physiological conse-
quences of the lead inhibition of enzymes are not generally understood,
research has focused on enzymes of the hematological system (see Section
6.3.2.2).
Within cells, lead has the greatest affinity for mitochondrial membranes
and nuclei (Goyer and Moore, 1974). Lead forms complexes with the phosphate
groups of nucleotides and nucleic acids and catalyzes a nonenzymatic hydro-
lysis of nucleosidetriphosphates (particularly ATP). Lead also hydrolyzes
FNA/Ln other systems, and brief exposure of phenylalanyl and lysyl tBNA to
Pb inhibits their binding to ribosomes as reviewed by Vallee and Ulmer
(1972).
Nuclear lead binds with an acidic protein fraction and accumulates to
form a discrete inclusion body which has a characteristic ultrastructure
(Goyer and Moore, 1974). A common occurrence in humans and animals who
suffer from lead intoxication is the presence of discrete, densely-staining
intranuclear inclusion bodies within hepatic parenchyma! cells and renal
tubular cells. When the renal tubular cell is presented with large concen-
trations of lead, intracytoplasmic concretions are formed. The relation-
ship of these concretions to the. lysosomal system has not been demonstrated
but dense staining bodies do form in secondary lysosomes derived from de-
generating lead-intoxicated mitochondria (Goyer and Moore, 1974).
Two forms of lead-containing, intranuclear inclusion bodies isolated
from kidney tubule cells of chronically lead-poisoned rats seem also to be
6.33
-------
present in rabbits and man. Goyer (1971a) proposed that these inclusion
bodies act as a protective mechanism by converting toxic lead into a non-
diffusible form, thus diminishing its effects on mitochondria and other
physiological receptors (see Figure 6.9). Inclusion bodies appear in acid-
fast-stained smears of the urinary sediment of children, which may provide
a technique for assessing kidney toxicity following lead exposure (Landing
and Nakai, 1959). The subcellular distribution of lead in the kidney fol-
lowing the feeding of lead to rats for 4 months is shown in Figure 6.10.
These data show that the largest increase in lead content is in the nucleus
where most is bound to an inclusion body (see Section 6.3.2.1).
The high affinity of mitochondria for lead results in morphological and
functional alterations. Alteration of mitochondrial structure or cellular
oxidation processes, or both, has been verified in canine intestine, rabbit
liver, human placenta, rat liver, rat kidney, and corn mitochondria (see
Section 6.3.1). In many instances, inhibition is reversed by EDTA accord-
ing.to Vallee and Ulmer (1972). These authors also report that lead ions
(Pb ) bind to insoluble ferric hydroxide and to ferritin in vitro, which
suggests that iron storage is altered in this condition.
Mitochondrial swelling has been demonstrated in renal tubular cells of
lead-poisoned humans and animals (Goyer, 1971a). Experimentally lead-poisoned
animals possess mitochondria with impaired respiratory and phosphorylative
abilities. The effects of lead on mitochondria appear to result from: (1)
inhibition of certain enzymes such as succinic dehydrogenase; (2) activation
of energy-dependent ion movement and the resulting increased respiration
supporting these movements; (3) energy-dependent movement of lead itself; and
(4) effects of lead on substrate uptake and retention (Scott, et al., 1971).
Walton (1973) suggests that the effects of lead on the mitochondria are two-
fold; (1) prevention of ATP synthesis and interference with the maintenance
of ionic concentration gradients across the membrane; and (2) hydrolysis of
ATP, formation of complexes with the thiol groups of mitochondrial enzymes
such as those involved in cytochrome synthesis, and reaction with ions such
as phosphates.
In a study on the cytotoxicity of lead, Beck, et al., (1973) report
that lead oxide and airborne dust have a toxic effect on line L cells as
manifested by division inhibition and disturbance of cell permeability and
intermediary metabolism. The reproduction of connective tissue cells in the
human fetus is also impaired. Bullate vacuolation is caused both by lead
oxide and airborne dust and is comparable in alveolar macrophages, line L
cells, and connective tissue cells in the human fetus.
6.3.2 Organ System Toxicities
6.3.2.1 Renal Toxicity—
A large body of evidence implicates lead as a causative agent in kidney
disease. Goyer and Rhyne's (1973) review of the pathological effects of lead
indicates that in humans suffering from acute lead toxicity (encephalopathy,
lead-induced anemia), the kidney exhibits nonspecific degenerative changes
in the tubular lining. The proximal tubular cells are the most seriously
6.34
-------
ICAPILLARY
PROXIMAL RENAL TUBULAR LINING CELL
LUMEN
INORGANIC «d
UBAND-BOUND
Figure 6.9 Scheme showing role of intranuclear inclusion
body in the metabolism of lead. Source: Goyer.
Reprinted with permission from Laboratory
Investigations, (c) International Academy of
Pathology, 1971.
6.35
-------
60 r
50
LJ
O
CE
a.
0>
X
o
30
Ul
_» 20
o«
10 -
55.5
1°
O CONTROL
£3 LEAD-FED
200
*4.e
0.61
±0.28
0.045 0.138
*0.01I ±0.019
MITOCHONDRIA NUCLEI INCLUSION
BODIES
Figure 6.10 Lead content of subcellular
fractions from kidneys of
control and lead-fed rats.
Source: Goyer. Reprinted
with permission from Laboratory
Investigations, (c) International
Academy of Pathology, 1971.
6.36
-------
affected, manifesting inclusion bodies within their nuclei. In many
instances, hyperaminoacidemia is seen when blood levels are greater than 80
micrograms lead per 100 milliliters (Chisolm, 1962). This toxicity seems to
be completely reversible in many instances.
Renal tubular dysfunction in lead toxicity is thought to arise from the
effects of lead on mitochondrial function. This has great significance in
terms of toxicity becuase of the high affinity of mitochondria for lead
(see Section 6.3.1).
Mitochondrial accumulation of lead in kidneys is potentially damaging
for normal renal function, as ADP-stimulated respiration in mitochondria is
completely inhibited on incubation with lead. Mitochondria from the proximal
convoluted tubules of lead-loaded rats generally show a reduced rate of
respiration and partial uncoupling of oxidative phosphorylation, perhaps as
a consequence of altered outer membrane structure. This impairment of
energy metabolism may be responsible for the reduced transport function of
the kidney and therefore the occurrence of aminoaciduria and glycosuria in
lead toxicity. The respiratory abnormalities in renal mitochondria may
result from their reduced cytochrome content. (Rhyne and Goyer, 1971).
Renal cells, though functionally impaired, are still viable, even at
cellular lead concentrations which are lethal to mitochondria in in vitro
studies. This suggests some protective mechanism operating within the renal
cell to limit mitochondrial uptake of lead, which may be the role of renal
intranuclear inclusion bodies. As concentrations of lead in renal tubular
lining cells increase, much of the additional metal is found in the nuclear
fraction, with over 50 percent of this in the form of inclusion bodies.
Renal lead is thus maintained in a nondiffusible, nontoxic form until the
cell in which the inclusion body exists is itself excreted in the urine. In
this way the kidney can excrete large amounts of lead without excessive
damage to the tubular lining cells (see Section 6.3.1).
At blood-lead concentrations of 150 micrograms per 100 milliters or
more, the Fanconi triad (hyperaminoaciduria, glycosuria, and hypophosphatemia
accompanied by hyperphosphaturia) is seen in approximately one-third of the
patients wich acute lead encephalopathy (Leaf, 1966). This indicates some
degree of tubular damage. The aminoaciduria is related to the severity of
clinical toxicity, and disappears following chelation therapy and cessation
of lead intake.
The association between chronic lead exposure and nephropathy has been
controversial. Hamilton and Hardy (1974) reviewed studies made 40 or more
years ago which indicated a positive association. One report suggested that
industrial lead workers had three times the incidence of kidney damage as
compared to the controls. In Queensland, Australia, a high incidence of
deaths from chronic nephritis was reported in persons who had experienced,
when children, acute plumbism from the ingestion of leaded paint. Subse-
quently, many of these same people in Queensland developed renal gout
(Emmerson, 1968). Women were overrepresented among these lead gout patients
compared to patients with idiopathic gout. Also, lead gout patients have
6.37
-------
normal triglyceride and cholesterol levels but those with idiopathic gout
develop hypertriglyceridemia (Emmerson and Knowleds, 1971).
Studies in the U. S. have not confirmed these results. Tepper (1963)
found no evidence for chronic renal disease in persons who had confirmed
lead intoxication as children 10 to 30 years previously. He suggested that
the Queensland children were exposed to lead over a more protracted period
of time than the American children. In contrast to the Australian people,
the American subjects exhibited no excess in lead body burden as demon-
strated by the administration of EDTA.
Goyer and Rhyne (1973) cited reports which suggested that prolonged
industrial lead exposure induced chronic nephropathy and renal failure in
countries where occupational exposure to lead was not closely controlled.
Studies with Japanese lead workers indicated that 10 workers excreted lead
in the urine, ranging in concentration from 168 to 603 micrograms lead per
liter, whereas controls (office workers) excreted 12 to 98 micrograms per
liter (Goyer, et al., 1972). In the lead group significant elevations were
also seen for alpha-amino nitrogen excretion, urinary delta-aminolevulinic
acid and urinary coproporphyrins, but only one of the 10 workers exhibited
hyperaminoaciduria. Similarly, Cramer, et al., (1974) found no excess
aminoaciduria in lead workers whose exposure varied from 4 to 20 years.
Kidney biopsies in five of the seven workers demonstrated mitochondrial
changes and ultrastructural changes in the proximal tubules of all five men,
and lead inclusions were found in the nuclei of two. Renal function tests
were normal in all except one worker who had a reduced glomerular filtration
rate.
The existence of lead nephropathy resulting from occupational exposure
to lead appears to be well substantiated in American lead workers. Among
eight subjects suspected of excessive occupational exposure to lead, detailed
examination of renal function identified abnormalities in four (Wedeen, et al.,
1975). The glomerular filtration rate was less than 87 milliliters per
minute per 1.73 square meters in one subject with asymptomatic renal failure
and in three subjects with preclinical renal dysfunction. A survey of death
certificates from 7,032 battery and smelting workers (Cooper and Gaffey,
1975) revealed a "consistent excess of deaths from 'other hypertensive1 and
'chronic nephritis or other renal sclerosis'". These and other findings
suggest that occupational lead nephropathy may indeed represent a signifi-
cant health hazard in the United States lead industry and is by no means
unusual among lead workers.
Many of the signs that appear in humans suspected of suffering from
lead toxicity also occur in experimental animals which are fed lead. These
include hyperaminoacidemia, intranuclear inclusion bodies, proximal tubular
damage, and hyperuricemia (Goyer and Rhyne, 1973). These authors concluded
that "chronic" effects of lead on the kidney are dependent on a particular
renal content of lead over a prolonged period of time, and that lead is
certainly capable of inducing a chronic nephropathy. Figure 6.11 depicts a
scheme which relates lead concentrations of drinking water to kidney lead
content and various pathological conditions which appear in rats after 10
6.38
-------
o
Ul
tti
o
t-
IU
o
4
Ul
1000
100
10
1.0
0.08 0.20 0.40 1.20 4.00 10.0
mg of LEAD per ml of DRINKING WATER
Figure 6.11
Correlation of lead content of
kidney and different doses of lead
fed to rats for 10 weeks with various
parameters of lead toxicity. Source: Goyer
and Ryne. Reprinted with permission from
International Review Experimental Pathology,
(c) Academic Press, Inc. 1973.
6.39
-------
weeks of exposure to lead, Schroeder (1973) also noticed that 250 micro-
grams of lead (as lead acetate) per 100 milliliters given to rats in drink-
ing water since weaning caused substantial increases in glycosuria and pro-
teinuria. The former study perhaps relates more closely to the lead ex-
posure of industrial workers who often are found to have intranuclear
inclusion bodies, whereas the latter is a closer approximation to other
groups not exposed to the high lead environment.
Choie and Richter (1972) found that a single dose of lead (0.05 milli-
gram per gram of body weight) as lead acetate induced characteristic intra-
nuclear inclusions in the epithelium of proximal tubules in rat kidneys
within 1 to 6 days. The development of the intranuclear inclusions is thus
an acute manifestation of lead poisoning, not a delayed one, as has been
thought hitherto.
Goyer (1971b) reported that rats tolerate long-term feeding of a diet
containing one percent lead as lead acetate, with the kidneys undergoing
a series of pathological changes. These changes commence with proximal
tubular dysfunction and progress to cellular hyperplasia, medullary cysts
and interstitial fibrosis. Renal adenocarcinoma develops in a large per-
centage of the rats (see Section 6.3.5). There is no evidence, however,
that lead poisoning or chronic, subclinical lead intoxication in man is
related to cancer in the kidney or any other organ of man.
The endocrine function of the kidney following lead intake has been
partially evaluated. Sandstead, et al., (1970) noted that nine men with
confirmed subclinical lead intoxication failed to respond to a low sodium
diet in the normal manner. The subjects' plasma renin activity and aldo-
sterone secretion rate did not reach the normal range. Lead induces a
marked inhibition of Na /K ATPase from renal homogenates of lead-poisoned
animals which interferes with tubular Na absorption. This indicates that
lead acts as an antagonist to sodium conservation by the kidney.
6.3.2.2 Hematopoietic Toxicity—
De Bruin (1971) identified three different aspects of the effects of
lead on hematopoiesis:
(1) The influence of lead on circulating erythrocytes;
(2) The impairment of the production of hemoglobin resulting from
the effects of lead upon the bone marrow; and
(3) The stimulation of erythropoiesis in the bone marrow.
In relation to these effects the following biochemical events can be ob-
served:
(1) In urine:
Porphyrinurla: increased excretory output of coproporphyrin 3.
Elevated excretion of delta-aminolevulinic acid (5-aminolevulinic
acid [ALAD]). Slight rise of urinary level of porphobilinogen.
6.UO
-------
(2) In blood:
a. In serum: Increased content of ALA.
b. In mature erythrocytes in peripheral blood: Elevated con-
centration of protoporphyrin 9 and the coproporphyrins.
Increase in concentration of iron unattached to hemoglobin
Decrease in hemoglobin level
Reduction in numbers of erythrocytes
Decrease in aminolevulinic acid dehydratase (ALAD)
Occurrence of punctate basophilia
Occurrence of siderocytes
Occurrence of reticulocytosis
Increase in their osmotic resistance
Enhancement of their outflow of potassium
Shortening of their survival
(3) In the bone marrow cells:
Occurrence of morphological changes, i.e., basophilia, siderocytes,
increased numbers of erythroblasts and, sometimes, of megaloblasts
and macroblasts
Degenerative alterations of mitochondria in association with
presence of ferritin molecules
(4) In tissue cells:
Accumulation of porphyrins in liver, kidney, and in cells of bone
marrow in some species of experimentally poisoned animals.
Albahary (1972) further described several effects of chronic inorganic
lead poisoning on the bone marrow and peripheral blood. For example, the
mitochondria and the ribosomes of the erythroblasts and the reticulocytes
are known to be damaged, leading to the formation of basophilic stippled
cells when stained by basic dyes and to abnormalities of heme synthesis.
These phenomena, to which the effect of lead in some other tissues (liver,
kidney) may be added, cause secondary porphyria, imperfect utilization of
iron, and perhaps a minimal globinopathy similar to that in thalassenda
minor. Lead inhibits medullary erythropoiesis and increases the fragility
of red cell membranes which shortens their life span.
Anemia is often seen as a manifestation of acute or chronic lead
poisoning and may be the only clinical sign of chronic exposure to low
levels of lead (Goyer and Ehyne, 1973). It appears to be the combined
result of impaired heme synthesis and the hemolytic action of lead. The
integrity of red cell membranes and globin play a role in the anemia of lead
poisoning. Stippling of red blood cells is often seen in lead-induced
anemia along with microcytic and hypochromic cells. Stippled cells are
more prevalent among immature red cells in the marrow than in peripheral
blood (Waldron, 1966). The appearance of granules in red blood cells was
6.U1
-------
used as an indication of lead intoxication in the past, but this is a very
nonspecific test.
Altered osmotic and mechanical fragility of erythrocytes may be due to
lead impairment of glycolytic enzyme activity (Goyer and Rhyne, 1973),
although experimental support is lacking. Damage of the red blood cell by
the liberation of free acids, subsequent to the (1) formation of a lead-
inorganic phosphate complex with red cells or plasma; (2) formation of lead
diglycerol sulfate; and (3) coagulation and flocculation of a peptide lead
phosphate sol on the cell membrane have all been proposed (Vallee and Uliner,
1972).
On incubation in vitro, lead causes human and rabbit erythrocytes to
leak K whereas controls take up K . A corresponding decrease in the activ-
ity of erythrocytic membrane Na /K -dependent adenosine triphosphatase
(ATPase) along with an increase in cellular adenosine triphosphate (ATP)
may underlie the K loss. A second dose of lead to recovered cells does
not increase K permeability; this will occur, however, if chelation
"therapy" is used (Hasan, et al., 1967b; Passow, et al., 1961). Red blood
cells taken from men occupationally exposed to lead exhibited the behavior
described above (Hasan, et al., 1967a). The membrane ATPase levels return
to normal when exposure to lead ceases or EDTA therapy has been started.
The effect on the membrane is an early response to lead and appears
long beforeclinical symptoms are obvious. There is also an effect on the
uptake of P by red blood cells which is reduced in men having severe
exposure to lead.
According to de Kretser and Waldron (1963), Aub, et al., (1926) ob-
served that leaded red cells were less resistant to mechanical trauma than
normal cells, an observation which has also been reported by some other
workers. Other research, however, has shown the mechanical fragility to be
normal in lead poisoning. De Kretser and Waldron (1963) found that there
was no increase in the mechanical fragility of cells leaded in vitro until
the concentration of lead was greater than 10 micrograms per milliliter, and
that at a concentration of 45 micrograms Pb per milliliter, saturation
was reached. It should be noted that these concentrations are greatly in
excess of the usual in vivo solutions.
Red cell survival is shortened in lead poisoning. Using tritiated
diisopropyl fluorophosphate as a tracer for red blood cells, Hernberg, et
al., (1967) showed that the red cell half-life was shortened in humans
occupationally exposed to lead. The half-life decreased to less than 105
days at blood lead concentrations of 80 micrograms per 100 grams of whole
blood. In acute lead poisoning, hemolysis is the predominant factor.
decreasing the life span of red cells.
In normal red cell precursors, the synthesis of heme and globin is
finely balanced but in diseases such as sideroblastic anemia and iron-
deficiency anemia, a defect in heme synthesis leads to a disturbance of
globin synthesis. Defective globin synthesis occurs in lead poisoning
6.42
-------
according to White and Harvey (1972) who indicate that the abnormal synthesis
of alpha and beta globin chains plays a role in the pathogenesis of lead
poisoning anemia. When heme-deficient reticulocytes are incubated with
lead in vitro, polysomal disaggregation occurs. This supports an alternative
explanation that the disordered globin synthesis in lead poisoning is due
in part to heme deficiency.
A detailed examination of the steps in the synthesis of heme (see
Figures 6.12 and 6.13) indicates that lead can to some extent affect steps
of heme synthesis, although the degree of inhibition and the concentration
of the required elements vary considerably. Lead interference in heme
synthesis is reflected in the high levels of excreted porphyrin precursors
in the urine (Milic, et al., 1973).
The most lead-sensitive enzymes are: (1) ALA dehydratase (ALAD) which
converts delta-aminolevulinic acid to porphobilinogen; and (2) ferro-
chelatase which aids the incorporation of iron into protoporphrinogen
thereby forming hemes. Inhibition both at these sites, and in the conver-
sion of coproporphyrinogen to protoporphyrinogen is indicated in experi-
mental lead toxicity in animals and in lead poisoning in man by the accumu-
lation and excretion of porphyrins and their precursors.
A decreased activity of ALAD in mature erythrocytes is considered to be
a very early biological sign of exposure to lead. ALAD appears, in vivo and
in vitro, to be extremely sensitive to the effect of inorganic lead. ALAD
activity becomes inhibited even during the very first days of new lead ex-
posure, and its activity is closely and inversely correlated with the con-
centration of lead in blood even within the "normal blood-lead range", i.e.,
0.7 to 1.9 micromoles per liter (15 to 40 micrograms per 100 milliliters).
Recent studies have shown that erythrocyte ALAD is inhibited to some degree
at far lower blood-lead (PbB) concentrations. Although Hernberg, et al., (1970)
suggested there is no threshold for this effect, more recent research (Tola,
et al., 1973; Granick, et al., 1973) suggests there is a threshold for ALAD
inhibition of 10-20 micrograms per 100 milliliters in adults and about 15
micrograms per 100 milliliters in children.
Hernberg (1973) believes that it is possible that the inhibition
measured in vitro merely represents a reduction of "reserve enzyme capacity"
that is not essential. However, the ALAD test provides, at the very least,
a sensitive method for registering biological effects of low lead doses.
Lauwerys, et al., (1973) compared the effect of inorganic lead and
cadmium on blood ALAD in 77 workers occupationally exposed to cadmium, and
in 73 control workers. The substantial negative correlation found between
log ALAD and PbB (r = -0.660) or PbU (urine lead) (r = -0.501) confirmed
the existence of an inverse relationship between ALAD activity in red blood
cells and PbB even within the "normal" PbB range of 10 to 40 micrograms per
100 milliliters. The potential effect of cadmium on ALAD in the general
population should be considered negligible compared to the effect of lead,
since ALAD activity and CdB were not correlated. Previous studies by the
senior investigator indicate that among three heavy metals - mercury, lead,
6.43
-------
a\
m
•P-
H2N-CH2-COOH +
Glycine
Piotoporphyrinogen IX'
MI ^~t* "*&&
P M C
Protoporphyrin III -No. IX'
^ 1 Heme Synthetase
4 fe+-;-
Heme Proteins
Hgb
Myoglobin
Cytochrome-
Catalase
Etc.
0
HOOC- CH2-CH2- C-COOH
« -Ketoglutarate
DPN+
CoASH
0
unnr-rn -TH -f*-^-pnA —
Succinyl CoA
M P
P M
Coproporphyrin 1
Auto-oxid.
Coproporphyrmogen 1
'i> *
Coproporphyrinogen III
I Auto-cxid.
M P
M|-T~l— .M
pL-i pip
P M
Coproporphyrin III
Purmes. Formate
fo] y
Succinate
Pyridoxal-P | ' V™i 1 -CO?
i-ALA
SvnthEtase a-Amino-jM-etoadipic Acid
A P *
TT
*LLJJp
P A
Uroporphyrin 1
1 Auto-oxid.
Urodecarboxylase uroporpfy""ogen 1 ^XA.
^^^5"'/>
Phyriaporphyrinogen III ^v
Urodecatylai; Uroporphyfinogen '" ^^
1 Auto-oxid.
A P
P A
Uroporphyrin III
_ HOOC-CH2-CH2-C-CHO
A -Ketoglutaraldehyde
{Alternate
-NH3
1 9
HOOC-CH2-CH2- C-CH2-NH2
i Aminolevulinic Acid
»-ALA a^
Dehydrase Cyclization
..COOH
HOOC CH2
^J"'
i * H
NH2
Porphobilinogen
Sf JOeaminase
^^ Polypyrryl Methane
5«
A— CH2COOH
P-- CH2CH2COOH
M-- CH3
V-- CH-CH2
* Known sites of Pb inhibition
Figure 6.12 Pathway of heme synthesis. Source: Goldsmith. Reprinted with
permission from Journal Air Pollution Control Association.
(c) Air Pollution Control Association, 1969.
-------
Mitochondrion
Ferrltln, ferruginous
HEME I
_. f FerrochelaUse
n 4 Fe«*
PROTO
1
micelles
> Glyclne •¥ Succlnyl-CoA
LA LA
synthetase —
Pb
PROTO'GEN + Fe1* "-CYTOC
' t
COPRO'CEN m
1
-•-ALA
^*
PEG
' 1
ALA
- dehydraUse
Pb
Figure 6.13
Scheme of heme synthesis showing sites of lead
effect. PEG, porphobilinogen; UROPOR III,
uroporphyrinogen III; COPRO III, coproporphyrin-
ogen III; PROTO, protoporphyrin; CoA, coenzyme A,
ALA, aminolevulinic acid; CYTO C, cytochrome £.
Source: Gayer and Ryne. Reprinted with permission
from International Review Experimental Pathology.
(c) Academic Press, Inc., 1973.
6.U5
-------
cadmium - only lead significantly influences the ALAD activity of red blood
cells. Lauwerys, et al., (1973) suggest that further investigations of
various parameters (e.g., age, pregnancy, drugs) which may influence ALAD
are justified as well as those on any biological significance of the
inhibition of this enzyme.
Lauwerys, et al., (1974) investigated the relationship between urinary
delta-aminolevulinic acid excretion and the inhibition of red cell delta-
aminolevulinate dehydratase by lead. They used venous blood collected in
heparinized tubes from 83 male workers occupationally exposed to lead and
from 84 control workers. ALAD activity decreased exponentially as a function
of PbB concentration. The coefficient of correlation between log ALAD and
PbB (in the range 0 to 75 micrograms per 100 milliliters PbB) was -0.76,
confirming previous reports. The results indicate the threshold for ALA
excretion is at a PbB Level of 45 micrograms per 100 milliliters. This
confirms earlier studies in industrial populations (Selander and Cramer,
1970) and in children (National Academy of Sciences, 1972) indicating a PbB
threshold for elevated ALAD of approximately 40 micrograms per 100 milliliters.
The average ALAD concentration at a PbB concentration of 45 micrograms
per 100 milliliters was 37 percent higher than that found at a PbB concen-
tration between 10 and 20 micrograms per 100 milliliters. When PbB ex-
ceeded 45 micrograms per 100 milliliters, ALAD increased rapidly. At a
PbB of 55 micrograms per 100 milliliters, its concentration was already
twice that found at a PbB level of 10 micrograms per 100 milliliters
(Lauwerys, et al., 1974).
Different characteristics of erythrocyte ALAD between workers with
a history of occupational lead exposure and normals were observed by
Tomokuni (1975). In the blood of lead workers, when the hemolysates were
heated at 60 C for 5 minutes, the activity of the erythrocyte ALAD increased
up to about 3.6-fold times initial level and the optimum in pH-activity
curve changed from pH 6.0 to 6.6. On the contrary, in normal blood, the
optimum in the pH activity curve was but little changed by the same heating
process, even though the erythrocyte ALAD activity was increased up to about
1.3-fold of the initial level.
Secchi and Alessio (1974) and Haeger-Aronsen, et al., (1971) showed
that there is an inverse relation between blood-lead levels and erythrocyte
ALAD in individuals with diverse occupational exposures to lead. Weissberg,
et al., (1971) demonstrated that many children living in slum housing had
elevated blood-lead levels and decreased red cell ALAD levels. Lead
workers examined at different intervals following the cessation of lead
exposure exhibited a rapid return to normal urinary ALA levels (within
4 months), but ALAD levels were only 25 percent normal at 4 months, and
80 percent at 16 months (Haeger-Aronsen, et al., 1974).
The effect of blood-lead concentration (PbB), age, sex and time of
exposure upon erythrocyte aminolevulinic acid dehydratase (ALAD) activity
6.h6
-------
was investigated by Tola (1973) in 1,370 workers (1,199 men, 171 women)
under different conditions of exposure to lead. A close negative correla-
tion was observed between blood lead (PbB) and ALAD in 1,147 workers.
Furthermore, the ALAD activities in groups arranged according to PbB values
(see Tables 6.9 and 6.10) show the close relationship between PbB and ALAD.
PbB had a statistically significant effect on the ALAD levels in
workers. The exposure groups were significantly different from one another
in ALAD activity (p less than 0.001) when PbB intervals of 10 micrograms per
100 milliliters were utilized. At PbB-intervals of 10 micrograms per 100 milli-
liters, the differences between the groups were statistically significant
only up to the 60 to 69 micrograms per 100 milliliters PbB group, reaching a
level of maximum depression from 70-100 micrograms per 100 milliliters. No
difference was observed between the ALAD activities at the same blood-lead
levels in men and women. Duration of exposure exerted an effect independent
of PbB, such that the ALAD activity was lower after less than one year's
exposure than in exposures of longer duration. ALAD activity was found to
be higher in the age group of 24 years or less than at more advanced ages,
controlling for blood-lead levels. Measurements were made of the blood
hemoglobin in 1,269 workers, and of ALAD in 285 workers (see Tables 6.11
and 6.12). The hemoglobin level did not differentiate between PbB groups,
and was not correlated with PbB and ALAD.
Blood-lead levels and erythrocyte ALAD activity in people living
around a secondary lead smelter were investigated in 1970 by Nordman, et
al., (1973). There was a statistically significant negative correlation
between PbB and the distance of habitation from the emission source and a
positive correlation between the PbB's and the monthly dustfall lead within
the area. Higher levels of PbB closer to the emitting source were accom-
panied by a decrease in ALAD activity. ALAD proved to be a useful test in
the demonstration of even a low-grade increase in lead absorption.
Secchi, et al., (1974) studied the delta-aminolevulinic acid de-
hydratase (ALAD) activity of erythrocytes and of liver tissue in subjects
not occupationally exposed to lead. A considerable heterogeneity in the
levels of ALAD activity of erythrocytes was confirmed in this group of
subjects, an expression of the individual variability in lead absorption
from lead in food and the atmosphere. In the group of 22 subjects studied
(both sexes, between 24 and 69 years of age), there was a correlation
between the values of erythrocyte ALAD activity and the values of ALAD
activity of liver tissue. This correlation of erythrocyte and liver ALAD
activity had been reported earlier for suckling rats by Millar, et al.,
(1970). The above research demonstrates again that ALAD inhibition is a
useful index of lead exposure.
Baboon studies showed that while blood-lead concentrations increased
very slowly during a chronic oral regimen of lead salts, ALAD decreased to
a minimum value immediately (Goldstein, et al., 1975). The continued in-
take of lead had no further depressant effect on ALAD activity following
the first day of treatment.
6.U7
-------
Table 6.9 ERYTHROCYTE 6-AMINOLEVULINIC ACID DEHYDRATASE (ALA-D) ACTIVITIES IN
DIFFERENT BLOOD-LEAD (Pb-B) GROUPS3
(grouping at Pb-B intervals of 10 yg/100 ml)
o\
•
CD
Pb-B
fig/100 ml
< 9
10—19
20—29
30—39
40—49
50—59
60—69
70—79
80—89
90—99
100<
n
5
182
327
161
108
67
43
45
32
15
9
*
721
941
716
507
353
226
146
121
77
58
49
Men
x— SD
370
663
490
332
210
139
73
67
38
30
25
fimol
ALA-D
PBG/h/1
RBC
Women
x+SD
1405
1325
10-16
775
595
366
295
216
154
110
94
pb
me O
< 0.001
< 0.001
< 0.001
< 0.001
< 0.001
__ V,
ns o
< 0.001
nsb
nsu
n
11
71
34
8
9-
4
6
8
1
1
••
X
1033
952
646
260
258
265
146
91
125
25
••
X— SD
818
697
446
161
206
194
95
48
* *
••
x + SD
1304
1300
934
421
324
363
227
173
, ,
••
pb
nsb
< 0.001
< 0.001
nsb
nsb
<0.05
nsb
n
16
253
361
169
117
71
49
53
33
16
9
X
923
944
709
491
345
228
146
110
78
55
49
Total
x— SD
600
673
486
314
207
142
75
64
39
28
25
x-fSD
1419
1324
1034
770
575
366
286
209
155
105
94
pb
n« **
< 0.001
< 0.001
< 0.001
< 0.001
< 0.001
nsD
< 0.001
nsD
n«D
a
^-Source: Tola (1973) Reprinted from Work, Environment, Health.
p-value of difference between the mean ALA-D activities of the successive Pb-B groups.
ns » not significant (p > 0.05).
-------
Table 6-10 ERYTHROCYTE 6-AMINOLEVULINIC ACID DEHYDRATASE (ALA-D) ACTIVITIES IN
DIFFERENT BLOOD-LEAD (Pb-B) GROUPS3
(grouping at Pb-B Intervals of 20 vg/100 ml)
VO
Ph-R
jug/100 ml
<19
20—39
40—59
60—70
80<
ALA-D
fimol PBG/h/1 RBC
Men
n
187
488
175
R8
5G
*
035
C30
208
133
66
x— SD
652
417
173
70
33
x+SD
1341
070
516
253
132
pb
< 0.001
< 0.001
< 0.001
< 0.001
n
82
42
13
14
2
X
062
543
2GO
112
56
Women
x— SO
721
320
204
61
x+SD
1302
022
332
203
pb
< 0.001
< 0.001
< 0.001
< 0.00 1
n
269
530
188
102
SB
*
943
631
205
i:)0
66
Total
X— SD X+SD
668 1330
407 977
173 504
08 245
33 131
Pb
< 0.001
< 0.001
< 0.001
< 0.001
^Source: Tola (1973). Reprinted from Work, Environment Health.
p-value of difference between the mean ALA-D activities of the successive Pb-B groups.
-------
Table 6.11 HEMOGLOBIN VALUES IN DIFFERENT
BLOOD-LEAD (Pb-B) GROUPS,
SEPARATELY FOR MEN AND WOMEN3
Hemoglobin
/ig/100 ml
< 9
10—19
20—29
30—39
40—19
50—59
60— 09
70—79
80—89
90<
n
5
238
373
178
11G
70
44
41
29
17
Men
x SD
14.5
14.8
14.9
15.0
15.0
15.0
14.9
14.7
14.4
14.8
.7
.0
.0
.0
.0
.0
.0
.0
.0
.4
Women
n
11
72
36
9
9
4
C
7
1
1
X
12.4
13.5
13.8
13.6
13.1
14.1
13.0
12.0
10.2
12.0
SD
1.6
0.9
1.0
1.0
0.9
0.8
0.8
0.7
m .
••
Source: Tola (1973). Reprinted from
Work, Environment, Health.
6.50
-------
Table 6.12 CONCURRENT MEASUREMENTS OF ERYTHROCYTE
6-AMINOLEVULINIC ACID DEHYDRATASE (ALA-D)
ACTIVITIES AND URINARY 6-AMINOLEVULINIC
ACID (ALA-U) CONCENTRATIONS IN DIFFERENT
BLOOD-LEAD GROUPSa
(285 workers)
Pb-B
ftgflQQ ml
< 9
10—19
20—29
30—39
40—49
50—59
60—09
70—79
80—89
90<
n
12
31
20
43
51
38
47
27
16
X
978
741
479
315
204
158
109
83
46
AT-A-D
/rniol PBG/h/1
x— SD
• *
645
481
332
179
128
82
62
44
24
RBC
x+SD
1483
1143
690
551
324
305
191
155
89
X
» •
6
7
6
6
10
11
18
28
32
ALA-U
mg/1
x — SD
• •
4
6
4
3
6
5
8
13
11
x-SD
8
10
y
13
18
23
38
58
95
Source: Tola (1973). Reprinted from Work, Environment, Health.
6.51
-------
Hammond (1973) investigated the effect of EDTA (ethylenediamine-
tetraacetate) on the activity of delta-aminolevulinic acid dehydratase
(ALAD) and the excretion of lead in the urine of lead-intoxicated rats.
Inhibition of ALAD was greater in blood than in liver, and EDTA treatment
of rats given lead gave rapid reactivation of ALAD in the liver but had
little effect on lead-induced ALAD inhibition in the blood. EDTA-induced
lead excretion in the urine was inversely proportional to the liver ALAD
activity.
Garber and Wei (1973) found that ALAD activities of three mice strains
used in their investigation were significantly different, and suggested
that this was due to genetic control of the rate of enzyme synthesis rather
than different enzyme characteristics. The results indicate that inhibition
of delta-aminolevulinic acid dehydratase activity is not related to acute
or subacute lead toxicity as measured by lethality, body weight loss, liver
and kidney weight changes or decrease in hematocrits.
The reversal of the ALAD deficit in lead-poisoned erythrocytes has been
demonstrated in vitro with reduced glutathione (GSH). In vivp_ administra-
tion of GSH to workers with lead-intoxication improved the decreased erythro-
cyte ALAD activity to some extent, which would be expected since the
endogenous GSH concentration in erythrocytes is known to decrease moderately
in workers intoxicated with lead (Roels, et al., 1975). These investigators
compared the in vivo effect of inorganic lead and cadmium on glutathione
reductase system (GSH) and delta-aminolevulinate dehydratase (ALAD) in
human erythrocytes in 84 men employed in a Belgian cadmium- and lead-pro-
ducing plant. A control group of 26 persons was also examined.
The logarithm of the PbB was found to be significantly negatively
correlated with log ALAD activity (r = -0.760) and with GSH (r = -0.423).
Log CdB was associated with neither ALAD nor GSH activity. An in vivo
investigation of the GSH regeneration rate of intact erythrocytes demon-
strated that the overall activity of the glutathione oxidation-reduction
pathway is not impaired in lead- and cadmium-exposed workers with signifi-
cantly increased PbB and CdB. This suggests that the moderate decrease in
endogenous erythrocyte GSH in lead-exposed workers might result from lead-
induced impairment of the erythrocytic mechanism for glutathione synthesis
(Roels, et al., 1975).
Persons with depressed levels of ALAD who exhibit no overt signs of lead
toxicity may be developing subclinical symptoms of toxicity. Since ALAD in
circulating erythrocytes has no known synthesizing or other functions, it is
questionable if lead inhibition of this enzyme is toxicologically important.
However, ALAD deficits which occur in brain and liver following lead ex-
posure may be very important as the synthesis of heme-containing respiratory
enzymes depend on ALAD (Millar, et al., 1970; Secchi, et al., 1974).
Chisolm, et al., (1975) studied a group of 18 children, 14 of whome
had blood-levels above 50 micrograms per 100 milliliters but none of whom
had symptoms of lead toxicity. Linear relationships were found among
urinary lead and EDTA-chelatable lead (indicators of lead dose), and the
6.52
-------
indicators of heme synthesis depression (urinary delta-aminolevulinic acid
and erythrocyte protoporphyrin). Blood-lead levels did not correlate well
with either indicator of lead's effect on heme synthesis. The authors
suggest that the use of the chelatable lead-test (urinary lead following
calcium-EDTA treatment) is the best measure of soft tissue lead concentra-
tions, superior to measures of PbB.
Many believe the determination of free erythrocyte porphyrin (FEP) or
zinc protoporphyrin (ZPP) to function as screening tests for excessive lead
exposure. The correlation between FEP or ZPP and PbB is moderately good.
Correlation coefficients between FEP and PbB of 0.65, 0.9 and 0.77 have been
obtained in children (Chisolm, et al., 1975; Piomelli, 1973; Lamola, et al.,
1975) and a correlation coefficient of 0.87 was obtained by Lamola, et al.,
(1975) in adults. Correlation is improved when the lead exposure conditions
are stable owing to the fact that the appearance of protoporphyrin in the
blood reflects an event which occurred earlier in the bone marrow, before
the erythroid cells reached the blood. (Sassa, et al., 1973).
In addition to serving as useful screening tests for lead exposure,
elevation of protoporphyrin reflects an undesirable effect of lead on hemato-
poiesis. It is reasonable to consider the accumulation of an essential
metabolite, e.g., protoporphyrin, as a critical effect. That is, accumula-
tion of protoporphyrin is probably an indicator of disturbed funtion due to
lead absorption.
Marginal elevation of FEP may represent a compensatory increase in heme
synthesis. Blood, hemoglobin decrements only occur at lead exposure levels
somewhat greater than the threshold levels for a rise in FEP. Thus, the
data of Pueschel, et al., (1972) and of Betts, et al., (1973) show that a
lead-related fall in blood hemoglobin in children is seen only as PbB rises
above 40. Tola, et al., (1973) noted a slight drop in blood hemoglobin
related to lead exposure in industry with PbB's of approximately 50 micro-
grams per 100 millileters.
A threshold for increased erythrocytic protoporphyrin has not been ad-
equately defined. Piomelli (1973) estimated a PbB threshold of 40 micro-
grams lead per 100 milliliters in children. On the other hand, Roels, et al.,
(1975) estimated a threshold of 20-30 in women and children and 25-35 micro-
grams per 100 milliliters in men. In the lead air quality criteria document
(U.S. Environmental Protection Agency, 1977) average thresholds (lowest-observed
effect levels) proposed on the basis of a number of studies were 15 to 20 micro-
grams per 100 milliliters in children and 20 to 25 for adult males.
Also in the EPA document it is argued that while certain of the initial.
hematological effects (such as ALAD inhibition) constitute relatively mild,
non debilitating symptoms at low blood lead levels, they nevertheless signal
the onset of steadily intensifying adverse effects as blood lead levels increase.
Thus, elevation of free erthyrocyte protoporphyrin is suggested as a significant
early measure of lead exposure.
If these estimates are correct and if elevation of erythrocytic proto'-
porphyrin is to be viewed as a critical effect, the exposure level (PbB) at
which it occurs would represent the lowest critical effect yet found.
6.53
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6.3.2.3 Nervous System Toxicity—
6.3.2.3.1 Pathology—The pathological lesions noted in lead-induced CNS
anomalies include cerebral edema, encephalopathy, increased cerebro-spinal
fluid pressure, proliferation and swelling of endothelial cells, dilation
of capillaries and arterioles, glial cell proliferation, focal necrosis, and
neuronal degeneration (Goyer and Rhyne, 1973). These conditions, however,
do not differentiate between symptomatology and/or pathology due to alkyl
lead from that of inorganic lead. This section will focus primarily on in-
organic lead neurotoxicity, leaving organic lead toxicity to be discussed
separately in Section 6.6.
Lead encephalopathy is the most serious acute manifestation of lead in-
toxication. It rarely occurs in adults and only following the rapid absorp-
tion of large amounts of inorganic lead. Children are much more susceptible
to lead-induced neuropathy than are adults (see Section 6.3.2.3.5). Acute lead
encephalopathy usually has a sudden onset, typically with intractable seizures,
followed by coma and cardiorespiratory arrest. In fatal cases, death usually
occurs within 48 hours of the initial seizure unless life support is provided.
The prodroma may include paralysis or weakness, sluggishness, poor memory, and
hyperirritability. The onset and course of symptoms are unpredictable and
may abate if the patient is removed from the source of lead (National Academy
of Sciences, 1972). A source of lead which has been implicated in causing adult
encephalopathy in the U.S. is "moonshine" whiskey. Whitfield, et al., (1972)
studied such patients and found that many exhibited symptoms ranging from con-
fusion to repeated seizures, coma and death. Most had anemia; lateralizing,
neurologic signs were observed in 35 percent of the patients. Pentschew (1965)
autopsied patients who had died from lead encephalopathy and found no cerebral
edema in 3 out of 20 cases. This author points out that swelling of capillary
endothelial cells and astrocytic proliferation are the most common features in
lead encephalopahty. Cerebral edema may result from the convulsive episodes
which accompany the intoxication.
Neuropathological changes were produced in suckling mice by adding 0.5
to 1.0 percent of lead carbonate to the diet of the maternal animals im-
mediately after they had given birth (Rosenblum and Johnson, 1968). Intoxica-
ted neonates displayed faulty growth and development, and revealed hematologic
evidence of lead intoxication. Neuropathologic findings included abnormally
large numbers of fibrous, intercapillary strands in several cerebral loci,
and astrocytosis in the hippocampus. The latter was recognied most easily in
sections stained with phosphotungstic acid hematoxylin. In addition, metallic
impregnations for astrocytes and microglia revealed consistent differences be-
tween experimental and control material suggesting a general alteration in the
properties of glia and/or cerebral tissue of intoxicated mice. In addition
to the study by Rosenblum and Johnson (1968), important papers on experimen-
tally induced, and histopathological evaluation of, lead encephalopathy in dif-
ferent species include: (1) Pentschew and Garro (1966); (2) Lampert (1966);
(3) Thomas, et al., (1971); (4) Thomas and Thomas (1974); (5) Clasen, et al.,
(1974); (6) Krigman, et al., (1974); (7) Bouldin and Krigman (1975); (8)
Thomas, et al., (1973); (9) Wells, et al., (1976); (10) Hopkins and Dayan
(1974).
-------
The histological findings in suckling mice differ from those of suckling
rats (Pentschew and Garro, 1966). Studies using maternal transfer of lead
to developing neonates to study the effect of lead on brain have been critically
reviewed by Michaelson (1973).
Patel, et al., (1974) describe the effect of inorganic lead on metabolic
compartmentation in the 19-day-old rat brain. Lead was ingested by suckling
rats through the milk of mothers fed a diet containing 4.5 percent lead
acetate. Assessment of metabolic compartmentation of brain amino acids was
made by comparing the metabolism of [2- C]-glucose and [ H]-acetate which
were injected simultaneously into the suckling rats. Changes in the rate
of conversion of both precursors into amino acids associated with the
tricarboxylic acid cycle were observed.
In the brain of young rats ingesting lead, the specific radioactivity
of glutamate, aspartate, gamma-aminobutyrate and glutamine were all signi-
ficantly lowered relative to that of glucose. Glutamine labelling was the
most affected. In comparison with controls, the total amount of H in^either
water or acid-soluble constituents of the brain was the same, but the H con-
tent of the amino acids was significantly reduced in the lead-treated rats.
In both groups, glutamine had the highest specific radioactivity but the time
courses of the labelling of glutamine were different. In spite of the dif-
ferences in the metabolism of [ H]-acetate, metabolic compartmentation of
glutamate, assessed by a glutamine: glutamate-specific radioactivity ratio
higher than 1, was evident even in the brain of the lead-treated animals,
although the values of the ratio at 5 and 10 minutes were less than in con-
trols. There was no evidence of a diminished supply of substrates to the
brain in lead intoxication. The overall changes in this study were consis-
tent with a retardation in the biochemical maturation of the brain in terms
of development of glucose metabolism and metabolic compartmentation (Patel,
et al., 1974). Michaelson (1973) indicates that the regimen employed leads
to low body weights of animals suckling from mothers fed lead acetate. This
depressed body weight has been cited by all investigators using the Pentschew
and Garro (1966) model for getting lead into a suckling developing neonate.
Few investigators have controlled for the contribution of undernutrition in
these lead studies. A retardation in the age-dependent increase in the con-
version of glucose carbon into amino acids was observed in studies in the
brain of undernourished infant rats (Balazs and Patel, 1973).
In a study undertaken to determine the growth retardation in mouse pups
exposed to lead and to determine the effects in brain development, Maker, et
al., (1975) observed a dose-related retardation as high as 50 percent of con-
trols in body growth, brain development, and sexual and behavioral maturation
(see Figure 6.14). Although dams fed 0.4 percent or more of lead (as lead
acetate or carbonate) ate less than control mice, this investigation con-
cluded that undernutrition is apparently not the major cause of retardation
since varying the litter size did not greatly modify the detrimental effect
of the diet. However, it is known that varying litter size has little ef-
fect on growth rate of pups until you exceed 10 pups per dam so comparing 3
pups vs 6 pups as described by Maker, et al.,(1975) does not contribute to
the resolution of the question. Small brain size and retardation of bone
growth were characteristic in the lead-fed mice (see Figure 6.15).
6.55
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f
i
50 OATS
iOWrtS
900AW
e ous .*
o ta» .4 o oa .4 .» .»
\PbCO»INOlET
o .1
Figure 6.14 Brain weights of C57/BI/6J mice at 30, 40, 60, and 90
days of age raised on diets containing 0, 0.08, 0.15,
0.4, 0.5, or 0.8 percent lead (carbonate) for 60 days
after birth. The standard deviation of mean brain
weights are indicated.
•a
Source: Maker, et al. Reprinted with permission from
Environmental Research, (c) Academic Press, Inc., 1975.
CS7BI/6J
4SC
400
«0
-
-
1
.
" 1 1
so a
»T£
6
oc
J
IAV
s
X.
!• .
p.
CO
XPbCO, IN DIET
Figure 6.15 Brain weights of C57/BI/6J mice at 30 and 60 days of age
raised on diets containing 0 or 0.08 percent lead as
PbCOs for 60 days after birth are compared to those of a
litter (PF) pair fed. At 30 days, 2 of the pair-fed pups
were allowed an ad libitum diet containing 0.8 percent
lead carbonate. The brain weights of these pups after 30
days on this diet (i.e., at age 60 days) are shown (PB/30)
Source: Maker, et al. Reprinted with permission from
Environmental Research, (c) Academic Press, Inc., 1975.
6.56
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Goiter and Michaelson (1975) found that the daily oral administration
of lead acetate solution (1.09 milligrams of lead) to suckling rats does
not influence growth relative to coetaneous controls and that lead-exposed
animals show periods of increased motor activity. Endogenous levels of
brain dopamine were unchanged whereas norepinephrine was increased, this sug-
gests a possible relationship between lead exposure during earliest de-
velopmental periods, increased motor activity and brain norepinephrine, rather
than brain dopamine.
Hopkins and Dayan (1974) investigated the pathology of experimental lead
encephalopahty in two adult and one infant baboon. Lead carbonate was given
by repeated intratracheal injections under light anesthesia. The main patho-
logical findings were widespread edema and focal cortical necroses. The
mechanisms by which lead produces these changes were not identified. Hopkins
and Dayan (1974) unfortunately do not adequately describe experimental proto-
cols, exposure levels, timing of exposure, blood lead levels, brain lead
levels and how this relates to the 3 deaths out of the 15 animals who origi-
nally entered the study in 1970.
Clasen, et al., (1974a)administered lead subacetate (0.5 gram) and 1000
units of Vitamin D to 4 newly weaned rhesus monkeys three times a week. Be-
tween 6 and 18 weeks the animals suddenly developed ataxia, nystagmus, gen-
eralized weakness and convulsions. The authors claim that this experimental
model resembled acute encephalopathy seen in humans more closely than encephalo-
pahty experimentally produced in the rat; Clasen, et al., did not provide
information as to the basis for the difference of opinion on this point be-
tween their work and that of Pentschew and Garro (1969), however.
Lead poisoning was diagnosed in four primates by finding toxic amounts
of lead in tissues (Sauer, et al., 1970). Abnormalities in the brain and
spinal cord were characterized by vascular lesions and demyelination. These
finding suggest a new animal model for the study of demyelination and
strengthen the supposition that lead may be a factor in some idiopathic
demyelinating diseases. A preliminary report which suggests this possibility
concerns the accidental poisoning of four primates who had suffered from
accidental lead intoxication for various lengths of time before death
in the Washington, B.C. Zoo. A detailed study of a larger number of similar
cases is reportedly being prepared for publication. Dr. B. C. Zook of the
Washington Zoo and George Washington Medical College has recently published
a number of significant papers on experimental lead poisoning in primates.r
an accidental poisoning of four primates in which accidental lead intoxica-
tion existed for various lengths of time before death occurred in the
Washington, D.C. Zoo. The authors do state that "A detailed study of a larger
number of similar cases is being prepared for publication." Between the time
of this paper (1970) and the preparation of this document (1977) Dr. B. C. Zook
of the Washington Zoo and George Washington Medical College has published a
number of significant papers on experimental lead poisoning in primates.
6.57
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6.3.2.3.2 Neuromuscular and synaptic transmission effects—Both or-
ganic and inorganic lead have been found to interfere with the transmission
of nerve impulses and, therefore, neuromuscular function. Investigations
dealing primarily with inorganic lead compounds will be discussed here;
studies relating to alkyl lead compounds will be discussed separately in the
organic lead section (6.6.4).
Silbergeld, et al., (1974a and 1974b) presented evidence for a junctional
effect of lead on neuromuscular function. To separate the effects of lead on
nerves from the effects on muscle, these investigators carried out in vitro
studies of isolated phrenic-nerve diaphragm preparations from male Sprague-
Dawley rats. The diaphragms with both phrenic nerves attached were removed
from the rats and separated into two hemidiaphragms, each with a nerve
trunk attached. The nerve-muscle preparation was modified so that prepara-
tions could be stimulated separately either through the nerve or muscle.
One hemidiaphragm with its phrenic nerve was exposed to lead, as lead chlor-
ide, in a range of concentrations from 1 x 10 M to 1 x 10 M. Its pair
was run simultaneously as a control. Krebs-Ringer-bicarbonate solution was
used in all experiments. The most significant finding was that lead and
calcium might interact at the presynaptic (junctional) level and thereby
alter the metabolism of acetylcholine. Studies were also conducted on nerve-
muscle preparations from mice chronically exposed to lead acetate added to
their drinking water (Silbergeld, et al., 1974b). The studies from exposed
animals are questionable since exposed animals were only 60 percent of their
normal weight and similar studies using weight-matched mice were not conduc-
ted. The experiments demonstrated that lead, in concentrations greater than
1 x 10 M significantly decreased the force of contraction of the rat hemi-
diaphragm muscle on phrenic nerve stimulation (see Table 6.13). The latency
between nerve stimulation and contraction was also increased. Over the same
range of concentrations, the force of contraction was not affected when the
muscle was stimulated directly (Silbergeld, et al., 1974a and 1974b).
Silbergeld, et al., (1974b) found that the effects of lead on force of
contraction and latency were dose- and time-related. Responses to exogenous
acetylcholine or acetyl-beta-methylcholine were not affected by lead. These
results suggest that lead does not significantly interact with motor end-
plate receptors to change the response to the neurotransmitter acetylcholine.
Therefore, the in vitro effects of lead, at least, are confined to prejunc-
tional sites of the peripheral motor nerves. The electrical properties of
the nerve and/or transmitter function may be involved in the induction of
these effects. Such effects may be responsible for the production of ataxia,
muscle weakness and paraplegia in both animals and humans chronically exposed
to lead.
The authors stated that phrenic nerve hemidiaphragm preparations taken
from mice chronically exposed to lead were found to be functionally dif-
ferent from preparations taken from unexposed mice of the same age. Muscles
from exposed animals generated a significantly smaller force of contraction
on stimulation of either the nerve or the muscle. Since the experiment did
not control for undernutrition, it is conceivable that this mode of response
is characteristic of undernourished animals independent of lead exposure.
6.58
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Table 6. 13 EFFECT OF LEAD ON THE FORCE OF
CONTRACTION ON NERVE AND MUSCLE
STIMULATION AFTER TREATMENT
FOR 2 HOURS3
Concentration of
Lead (x 10 M)
0
1
5
8
10
n
15
4
3
6
1
Percentage of Initial
on Stimulation
Nerve
97.5 + 2.5b
97.5 + 2.5
77.8 + 9.7
60.8 + 5.4
47.7
Force of Contraction
through :
Muscle
98.0 + 2.0
98.0 + 2.0
97.5 + 2.5
97.5 + 2.5
96.5
aSource: Silbergeld, et al. Reprinted with permission from
Nature, (c) Macmillan; Ltd. (1974).
+ s.e.m.
6.59
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Whereas the Silbergeld studies used physiologic measures (i.e., force
of contraction and latency), Manalis and Cooper (1973) employed electro-
physiologic measures to monitor intracellular responses from individual end-
plates such as frequency of miniature end-plate potentials. Manalis and Cooper
(1973) demonstrated that lead influences both pre- and postsynatpic events in
neuromuscular transmission with the presynaptic ones being most sensitive.
Experiments were performed in vitro on isolated sciatic nerve satorius muscle
preparations of the frog (Rana pipiens). Superficial neuromuscular junctions
were located optically with a compound microscope (magnification x 400). Stan-
dard microelectrode and phtotgraphic techniques were used to monitor intra-
cellular responses from individual end plates. Responses were recorded first
while the preparation was bathed in a control Ringer's solution, then in the
presence of lead, added as PbCl , and finally after the lead had been washed
out. Acetylcholine was applied directly to the end-plate receptors by ionto-
phoresis from a micropipette in order to test for post-synaptic effects of
lead.
These investigators observed that lead increases the frequency of minia-
ture end-plate potentials. As is the case with other ions which inhibit
the phasic release of the neurotransmitter, it is not known with which ligands
of the presynaptic membrane lead combines. If this were known some insight
might be gained concerning the involvement of these ligands in excitation-
secretion coupling. The salient features in this report were: (1) lead
effects on evoked transmitter release were greater than on spontaneous re-
lease and (2) in agreement with other workers, the effect of lead is pri-
marily presynaptic and not on the postsynaptic or neuromuscular function.
Furthermore, the threshold end plate potential was reduced by 0.01 M lead
within less than one minute whereas no significant increases in the fre-
quency of the miniature end plate (mep) potentials were detected when this
amount of lead was added to normal Ringer's Solution.
It is interesting to note that Manalis and Cooper (1973) reported that
0.01 M (2.1 ppb) produced measurable effects and this concentration is quite
comparable to that of Silbergeld, et al., (1974a,b) who showed that lead con-
centration greater than 1 x 10~ M (0.01 mM, 2.1 ppb) significantly decreased
the force of contraction. Thus, there appears to be some agreement as to the
moles concentration of lead needed to elicit this neuromuscular physiological
effect.
Kostial and Vouk (1957) studied the perfused superior cervical ganglion
of the cat to study the effect of lead (5-40 micromoles) on synaptic trans-
mission and on the release of acetylcholine from preganglionic nerve endings.
They found that lead in concentrations as low as 12.1 micromolar (1.21 x
10 M) blocked ganglionic transmission and reduced the output of acetylcho-
line. The release of acetylcholine or the uptake of choline and subsequent
synthesis of choline is known to have a requirement for calcium ions (Katz
and Miledi, 1967). Kostial and Vouk is one of the earliest papers in this
line of research to show that calcium ions (10 mM) relieve the block pro-
duced by lead ions and restored acetylcholine output.
6.60
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Relative to the introduction of Pb and Ca Kober and Cooper (1976)
studied the interaction of lead and^alcium and presented data which infers
that lead competitively inhibits Ca -mediated transmitter release from pre-
synaptic terminals. This^was suggested by experiments in which the effects
of lead on the up^ke^f Ca by presynaptic terminals resulted in a three-
fold increase in Ca uptake. Calcium uptake of stimulated lead-blocked
ganglia was reduced by 91 percent (to 9 percent) of control, indicating
that lead strongly blocks the uptake of calcium normally associated with the
arrival of action potential at the presynaptic nerve terminals.
From this and the work of others a model for the mechanism by which
lead interfers with normal neutronal activity is emerging. This is that lead
blocks transmission by competitive antagonism of spike-evoked entry of
Ca into presynaptic terminals and a subsequent reduction of transmitter
release.
6.3.2.3.3 Peripheral neuropathy—Goyer and Rhyne (1973) and Haley (1971)
have reviewed the literature and found peripheral neuropathy to be one of
the more common manifestations of chronic lead toxicity in adults. Lead-
induced peripheral neuropathy or "lead palsy" is manifested by motor weak-
ness of the extensor muscles of the hands or feet, resulting in "hand drop"
or foot drop. Lead neuropathy may be bilateral, although it is usually
unilateral. Other muscles which are affected are the extraocular muscles of
the eye. In an early clinical study of neuropathy in lead-poisoned adults,
nearly two-thirds of 55 patients were found to have some degree of muscle
weakness and almost one-half had wrist drop (Thomas, 1904).
Although peripheral neuropathy is considered to be one of the more
common symptoms of chronic lead toxicity in adults (Goyer and Rhyne, 1973)
children may also develop peripheral neuropathy with chronic lead poisoning.
Whereas wrist drop is the most common manifestation of lead neuropathy in
adults, foot drop and generalized weakness are more common in children (Seto
and Freeman, 1964). Altered peripheral nerve conduction velocity has been
reported in adults with 1 to 17 years of industrial exposure and whose Bl-Pb
never exceeded 70 micrograms/100, as discussed in detail below by Seppalainen,
et al., (1975). Similar altered peripheral nerve conduction velocity in
chronic lead-intoxicated children has been reported by Feldman, et al., (1973).
In this instance conduction velocity was measured in children known to have
had one or more of the following: (1) Blood-Pb greater than 40 micrograms/
100 ml, (2) U-Pb greater than 600 mg/24 hr following acetic acid provocation,
(3) radiographic evidence of lead lines or radiopaque flecks in the gastroin-
testinal tract. It has been recently postulated that children with sickle
cell disease have an increased risk of developing neuropathy with exposure to
lead. Clinical documentation to support this belief has been provided by
Erenburg, et al., (1974), Anku and Harris, (1974) and Athreya and Oski, (1975).
Whether skeletal muscle is directly affected by lead remains unresolved.
Early investigators suggested that lead produced a primary myopathy but lead
content of skeletal muscle in lead intoxication is usually not very high.
Also, electromyography of affected patients does not show a myopathic pattern
(Preiskel, 1958). Experimentally it has been shown that lead ions reduce the
6.61
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output of acetylchollne and that calcium reverses this effect of lead.
Whether lead afreets gangllonlc transmission In man Is not known. Haley
(1971) mentions reports which suggest that the neuromuscular lesions result
from the degenerative, neural action of lead, or from the selective damage
of blood vessels supplying the nerves. These suggestions stem from Russian,
Indian, Italian, and German reports and deserve careful evaluation.
Knowledge of the lesions In lead-Induced peripheral neuropathy has ev-
olved from study of experimental models beginning In the 1880'H with the
obm-rvation that guinea pigs with chronic lead Intoxication develop a peri-
pheral neuropathy characterized by aegmental degeneration of myelln sheaths.
Recent extension of these experiments by Fullerton (1966) has confirmed the
1requent occurrence of segmental demyellnatlon and of axonal degeneration.
Lampert and Schochet (1968) and Schlaepfer (1968, 1969) have shown that In
rats segmental demyellnation and remyellnatlon are related to Schwann cell
degeneration and proliferation. Schlaepfar (1969) has also demonstrated
Wallerlan degeneration of posterior nerve roots of sciatic and tlblal nerves,
which suggests a cellular basis for lead-Induced paretheala and sensory nerve
loss. Similar loss of nerve structural Integrity has been reported In the 8th
nerve of guinea pig (Goidzik-Zolnieckiewlcz, and Moszyriskl, 1969) and the vesti-
bular system of the adult squirrel monkey (Wllplzeskl, 1974). Ganglion cells
show no consistent pathological alterations, but surrounding capsular cells con-
tain Increased numbers of organelles and dense bodies (Schlaepfer, 1969). A
detailed clinical description In adult lead industry worker has been provided by
Seppalalnen and Hernberg (1972) and Seppalainen, et al., (1975).
Subclinical neuropathy was studied In 39 male lead workers, of which
31 had a diagnosis of poisoning but all were without clinical signs of
neurological impairment (Seppalainen and Hernberg, 1972). Standard electro-
myograms revealed abnormalities (fibrillations and/or diminished number of
motor units) In 24 men. The mean maximum conduction velocities (MCV) of
the ulnar and median nerve were significantly lower in the group of lead
workers as compared with an age-matched control group. The conduction ve-
locity of the slower fibers (CVS) of the ulnar nerve proved to be a very
sensitive Indicator of lead damage. A combination of this variable and the
distal latency of the median nerve discriminated lead workers from controls
better than any other combinations. The findings were consistent with slight
neuropathy, and show that lead also affects certain portions of the fibers
In the proximal part of the nerve.
The lack of correlation between the severity of subclinical nerve damage
and the Intensity of lead effects suggests that nerve damage is produced
independently of other manifestations of poisoning. There is a dearth of
information on the value of present acceptable limits of lead exposure from
the point of view of the nervous system.
Catton, et al., (1970) obtained evidence in a group of lead battery
workers of subclinical peripheral nerve fiber damage without clinical
evidence of a neurological lesion. Of the 19 men examined, 13 had blood
levels about 80 micrograms/100 milliliters and 7 had hemoglobin levels
below 12 grams/100 milliliters, showing that considerable exposure to lead
was occurring.
6.62
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Some relationship was found between the peripheral nerve damage, length
of expoaure to lead, and the preaance of anemia, but there was little relation-
ship with blood-lead level*. In thia reapect, the neuropathy behaved like
anemia of lead poisoning, which other workers have found to correlate poorly
with the blood-lead level (Williami, 1966),
Several of the symptoms of amyotrophic lateral sclerosis (muscle faaci-
culations, proximal girdle atrophy) are seen in lead industry workers sus-
pected of having motor neuron disease. In spite of suggestive clinical evi-
dence (Campbell and Williams, 1969) a cauae and effect relationship between
lead and motor neuron disease has not been established (Currier and Haerer
(1968),
Petkau, et al., (1974) found that lead levels in neural and muscular
tissues were significantly elevated in patients with thia disease, regard-
less of whether or not they had previous occupational exposure to lead.
The findings of normal lead concentrations in the lead-containing com-
partments of humans with multiple sclerosis would Indicate no association
between multiple sclerosis and lead poisoning (acute or chronic). The ef-
fects of lead might be Induced by mobilization therapy (Wasterman, et al.,
1974), The complexities of this issue are discussed by Hammond in the
National Academy of Sciences document (1972). Also, there has been
another recent paper by Conradi, et al., (1976) on the topic of abnormal
tissue distribution of lead in myotrophic lateral sclerosis. In this study.
the lead content of cerebrospinal fluid was found to be significantly ele-
vated 2.84 + 1.19 (range 1.56 to 5.30) when compared to 28 control subjects
having non-degenerative neurological disorders (1.41 + 0.49 micrograma/100
grams (range 0.89 to 2.61),
6.3.2.3.4 Behavior affects—A recent NIOSH report (Repko, et al,, 1975)
examined 80 behavior parameters and five measures of body burden of lead in
industrial workers (Table 6.14). The experimental group consisted of 316
individuals employed in lead storage battery companies, and the control
group was derived from workers of similar age, sex, race, education, but
with no occupational exposure to lead.
The following are the salient points in their findings:
(1) Blood ALAD activity was a better indicator of
functional capacity than were blood lead levels,
urinary Pb, ALA, or coproporphyrina. Decreasing
levels of blood ALAD correlated with decreased
auditory acuity and eye-hand coordination, increased
muscular tremor, and decreased endurance/strength
ratios In men with 70 micrograms Pb per 100 milli-
meters of blood or above.
(2) Of the intellectual functions tested, none indicated
a decreased capacity in their experimental group.
The authors, however, suggested in retrospect that
6.63
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Table 6.14 SUMMARY OF FUNCTIONAL CHANGES IN WORKERS EXPOSED TO INORGANIC LEAD*
ON
0\
Test Area
Signal Detection
Pattern
Discrinination
Mental Arithaetic
Visual Acuity
Auditory Acuity
Trenor
Miscular Strength,
Endurance 4 Recovery
Eye-Hand Coordination
iBMdiate Recall
Subjective Feelings
Functional Predictors of Criterion Performance
Category Primary Secondary
Matchkeeping
Sensory-Perceptual
Intellectual
Sensory
Sensory
Neuromuscular
NeuroBuscular
Neuronuscular
Intellectual
Psychological
Age Education
Age Education
Education Age
Age ALA
it.A.n _._..
ALA-D PbU
Age Enployment
Significant Change in
Correlations Dlrectrdh
of Change
PbU. PbB, ALA-D Decrease
ALA-D Decrease
PbU^PbB, ALA-D Increase
PbU, ALA-D Decrease
Functional Capacity t.
Indicated PbB Level
Nhere Change Occurs
80-89ug%
70-79ug%
70-79|ig%
70-79pg%
70-79|ig*
Adapted from Repko et al.,(1975).
"^bB—Blood lead.
'T'bU—Urine lead.
-------
these particular tests were not appropriate for
industrial workers (one test being too easy, the
other too difficult).
(3) In psychological tests, significant increases in
hostility, depression, and general dysphoria were
detected in lead workers as compared to controls.
No biochemical parameter correlated with these
particular observations.
Behavior dysfunction usually occurred in workers with blood-lead levels
of 70 micrograms per 100 milliliters or above. Blood ALAD levels are inver-
sely related to blood lead concentrations, and are more sensitive indicators
of functionality. Therefore, it was recommended that a combination of blood
ALAD activity below 21 units, and a blood level above 70 micrograms per 100
milliliters be used as an indicator for further evaluation of a worker's medi-
cal status. Another alternative is to remove the worker from the lead en-
vironment. Whether these criteria are appropriate for other individuals in
high-lead environments deserves further consideration.
Several criticisms of Repko, et al., (1975) deserve mention. First is
the possibility that biased responses on questionnaire items were evoked
due to the prior information the subjects were given concerning the purpose
of the study. For example, each volunteer was given complete and comprehen-
sive explanation of the study including the expected results of the research.
Information obtained from such preconditioned subjects is apt to be biased
in the direction of these expected results.
Second, it should also be noted that audiometric tests were conducted
without the use of a sound chamber and with ambient background sound levels
of 65 - 80 dbA. Although audiologists would not consider this good practice
for testing auditory acuity, neither lead-exposed nor non exposed workers
should have been affected preferentially by a test administered to both
groups under adverse conditions.
In addition, one could dispute some of Repko, et al's,, (1975) interpre-
tation of the psychological tests. For example, the authors concluded that
lead workers had significant increases in hostility, depression and general
dysphoria over controls. Interestingly, however, individual subjective
states for anxiety, depression and hostility indicate no significant relation-
ship existed between Multiple Affect Adjective Check List (MAACL) and the
clinical measures for either the experimental or control group. There was
also a great deal of variability in the data of all MAACL measures. The
relationship between blood lead and the psychological measures employed was
by no means uniform. The dysphoria measure showed a saw tooth effect when
plotted. Peak dysphoria effects occurred at 70 and 100 micrograms/100 milli-
liters while troughs were seen at 60 and 90 micrograms/100 milliliters lead
in blood. Clearly, there is no apparent explanation for the phenomenon from
a physiologic standpoint. Repko's findings are best regarded as speculative
until further research under better methodological conditions is carried out.
6.65
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McCallum (1972) discusses the possible health effects of lead in the
environment on adults. He recommends the use of a battery of psychological
tests in men exposed to a known lead hazard, but without clinical poisoning.
These tests would be geared to detect early symptoms of lead poisoning and
would be related to blood lead levels, urine coproporphyrin, and ALA excre-
tion.
Bryce-Smith and Waldron (1974b) have presented a review on the neural
and behavioral toxicity of lead in children and adults. The authors ob-
tained information from: (1) prisoners who have elevated blood-lead and
urinary-ALA values; (2) hyperkinetic children with abnormal lead metabolism
and who often respond to EDTA therapy; (3) lead workers who underwent per-
sonality and behavioral changes; and (4) experimental animal models. They
concluded that lead probably is a significant causative factor in the anti-
social bahavior of children and adults. Unfortunately, the work of Bryce-
Smith is not original research, but rather a highly selected collection of
papers and personal communications. The document states that the authors
obtained information from: (1) Prisoners who have elevated blood lead and
urinary-ALA values - what is not brought out in this document is that Bl-Pb
and U-ALA were determined in two different prison populations, the former in
Switzerland (Lob and Desbaumes, 1971) and the latter in America, (Barnes,
et al., 1972). Where Bl-Pb was done U-ALA was not; where U-ALA was done
Bl-Pb was not. What the document also doesn't bring out is that Lob and
Desbaumes subsequently (1976) retracted the 1971 report and concluded that
the blood lead levels obtained in 1971 by polarography were too high. The
mean actual value determined by AAS for prisoners does not differ signifi-
cantly from the value for the non-occupationally exposed population. Lob
and Desbaumes go on to state, "Unfortunately the blood lead concentrations
published in our 1971 paper were taken by other authors (Bryce-Smith, 1972,
Bryce-Smith and Waldron, 1974b as supporting the hypothesis relating lead
and blood to anti-social and criminal behavior."
In connection with the second point, that hyperkinetic children with
abnormal lead metabolism often respond to chelation therapy, Bryce-Smith
and Waldron, 1974a) are referring to the work of David (1976) which in
fact does not substantiate claims made by Bryce-Smith and Waldron (1974a)
(based on earlier personal communication with David) that chelation therapy
has been found to cure hyperactive behavior in children.
Conclusion: Within the past 5 years a considerable volume of literature
has developed on neonatal lead exposure, brain development, neurochemistry,
and behavior. Controversy exists as to the meaningfulness of this re-
search. There are serious flaws in experimental design, and many secondary
effects (i.e., nutritional status) confused the results and make objective
evaluation of these data difficult. More recent preliminary studies
(abstracts) report opposite findings or no change in catecholamines. Pro-
tocols for exposure are so varied that definite conclusions for lead effects
on brain neurotransmitters must await more meaningful experimentation.
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6.3.2.4 Immune System Toxicity—
There is little evidence on the impairment of immunologic mechanisms
from lead, as reviewed by de Bruin (1971). Lead-treated animals, subsequently
subjected to active immunization, develop lesser quantities of gamma-globulin
than normal (control) animals. The activity of lysozyme seems to be reduced
progressively in the spleen and blood serum of dogs poisoned by the prolonged
administration of inorganic lead salts. In a group of employees in a lead-
processing plant, the mean activity of lysozyme was found to be subnormal,
and the lowest values were found in the most severely affected persons. The
immunologic impairment of lead is reflected by a decreased Vitamin C content
in the adrenal gland.
Studies by Drs. Rafael Trejo and Nicholas Di Luzio suggest that the
accumulation of lead in the lysosome appears to be sufficient to disrupt
its activity, to the point at which it can no longer detoxify endotoxin
(Anon., 1971). Later work by these same investigators demonstrated that en-
hancement by lead of endotoxin lethality is not due to impaired phagocytosis
but rather to some effect on endotoxin detoxification. (Trejo, et al., 1972).
Roller and Kovacic (1974) found that chronic exposure of mice to lead
(as lead acetate) in drinking water (1375, 137.5, or 13.75 ppm) produced a
significant decrease in antibody synthesis, particularly IgG, indicating that
the memory cell is involved. There was a reduction in the number of spleen
cells producing 19S or IgM antibody at each dose of lead. The largest dose
resulted in a fivefold decrease in antibody-forming cells as compared to
the controls, but even those mice receiving the lowest dose had a significant
decrease in the number of 7S or IgG plaque-forming cells. Rabbits given
2,500 ppm lead as lead acetate in drinking water for 70 days and then ino-
culated with pseudorabies virus as the antigen had significantly lower
neutralizing antibody titers (marked immuno-suppression) than did the controls
(Roller, 1973). These results indicate that reduced antibody synthesis may
be responsible for the increased mortality from bacterial and viral diseases
in animals that are chronically exposed to lead.
Lead decreases normal responsiveness to bacterial endotoxins in rats
as evidenced by increased mortality rates following Salmonella enteritidis
endotoxin administration (Cook, et al., 1974). When lead and E. coli endo-
toxin were administered to baboons in doses which were individually sub-
toxic, morphologic changes appeared in their livers suggesting a synergistic,
toxic action of the two agents (Hoffman, et al., 1973). Cook, et al., (1975)
reviewed the effects of lead on endotoxin-induced pathology. When rats are
dosed with 5 milligrams of lead acetate per rat (a dose which equals one-
tenth the LD,.Q for 300-gram rats) , the dose of bacterial endotoxin that
would kill 100 percent of the population is 2,000 to 10,000 times less than
for rats receiving no lead. Young rats are more sensitive to such inter-
actions than are adult animals. Schroeder (1973) also noticed that male
rats and mice fed 25 micrograms of lead (as lead acetate) per liter in
drinking water had a higher susceptibility to bacterial infections.
Mice exposed to daily doses of 100 and 250 micrograms of lead nitrate
in 0.5 milliliter of saline for 30 days showed greater susceptibility to
challenge with Salmonella tvphimurium than controls which had received no
6.67
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lead (Hemphill, et al. , 1971). There was a tenfold difference in the LD^
of the j>_. typhimurium organisms between the control and the lead-treated
mice. The susceptibility of the lead-treated mice to a strain of S. typhimu-
rium with limited pathogenicity was markedly increased.
• A single, normally well-tolerated, intravenous injection of lead acetate
(5 milligrams) increased the sensitivity of rats to the endotoxins of
various gram-negative bacteria about 100,000 times above normal (Selye,
et al., 1966). Under the conditions of the experiments used, the mortality
and organ changes normally produced by the intravenous injection of 100
micrograms of E. coli endotoxin were essentially the same as those obtained
by use of one nanogram in lead-sensitized rats. The sensitizing effect of
lead acetate for E. coli endotoxin was greatest when the two agents were
given simultaneously.
Viral-induced diseases in mice were aggravated by administering lead
acetate in the drinking water (Gainer, 1974). Mortality from viral inocula-
tions was higher in lead-treated mice than in controls. In addition, lead-
pretreated mice exhibited splenomegaly following viral inoculations
(Rauscher virus) and higher mortalities. Large titers of virus were re-
covered from the spleens of the lead-treated animals. The suggested mechani-
sm for this action is that lead antagonizes interferon synthesis, thus
lowering natural defenses to viral infections. Goyer and Rhyne (1973) point out
that proof of such a relationship may be difficult to establish in affected
humans.
Many people die per year in the U.S. from Gram-negative bacteremia
and endotoxemia, but no epidemiological studies have been reported on the
relative risks of such infections to people with increased lead exposure.
6.3.2.5 Cardiovascular System Toxicity—
Concern in the past that lead contributed to hypertension and other
cardiovascular diseases in humans was most prevalent when industrial hygienic
measures surrounding lead workers were unregulated. The review by Goyer and
Rhyne (1973) mentions reports of myocardial abnormalities in acutely intoxi-
cated children. In a followup study (based on regular control over 20 years)
of 364 lead workers in a battery factory, Cramer and Dahlberg, (1966) found
that regular health examinations and good working conditions resulted in an
incidence of hypertension not greater than that found in the general popu-
lation.
There is epidemiological evidence that heavy industrial lead exposure
at one time caused increased incidence of death from cerebrovascular disease
(cerebral hemorrhage, thrombosis and arteriosclerosis) (Dingwall-Fordyce
and Lane, 1963). The increased incidence of death from this class of
diseases was associated with a degree of lead exposure which probably no
longer exists. A more recent epidemiological study of causes of death
among lead workers does not indicate any excess deaths due to cerebrovascular
diseases (Cooper and Gaffey, 1975). The workers studied were not as heavily
exposed as earlier workers, but the vast majority had PbB's greater than 40
micrograms per 100 milliliters. Thus, it seems highly unlikely that lead is
responsible for deaths at the exposure levels which are experienced by the
general population.
6.68
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An association between the accumulation of lead in aortas and severe
atheromatous lesions has been observed in humans (see Section 6.2.2), but
no causal relationship has been established. Studies of lead-induced athero-
sclerosis in experimental animals have also been inconclusive. Increased
serum lipoprotein and cholesterol, and cholesterol deposits in the aorta have
been reported with heavy lead exposure in rats and rabbits (Sroczynski, et
al. , 1967). Others, however, have failed to produce athersclerotic lesions
using similar doses of lead in rabbits (Prerovska, 1973).
6.3.2.6 Endocrine system Toxicity—
The clinical effects of lead on the hematopoietic, neuromuscular, and renal
systems coupled with the adverse biochemical phenomena which have been ob-
served suggested to Sanstead (1973) that lead may also impair the function
of the endocrine system. Standard tests of endocrine function on the thyroid,
pituitary, adrenal cortex, and juxtaglomerular apparatus of patients who had
acquired their lead by drinking moonshine indicated impairment of function in
many cases. Six of eighteen patients demonstrated a decreased excretion of
pituitary gonadotrophic hormones. Nine of sixteen had low (less than 10 per-
cent) 24-hour thyroid uptakes of iodine. Three of them were hyporesponsive
to thyroid-stimulating hormone. The adrenal response to exogenous ACTH was
decreased in five of ten while eight of twenty excreted low amounts of 17
OHCS following oral metapyrone. Plasma cortisol levels were low in seven of
eight given metapyrone. Two of four metapyrone nonresponders were also poorly
responsive to insulin hypoglycemia. In contrast, growth hormone responses to
hypoglycemia were normal in eight. The renin-aldosterone response (see
Section 6.3.2.1) to acute sodium deprivation was impaired in nine of eleven
patients. Sodium deprivation for 10 to 28 days did not result in an approp-
riate increase in renin or aldosterone in four subjects.
The effect of lead ingestion (1 percent lead acetate) on in vitro steroid
synthesis of the rat adrenal gland was investigated by Wright, et al., (1975).
Blood-lead concentrations rose to 85 micrograms per 100 milliliters of whole
blood in 1 week and stayed at or above this level for the 8-week experimental
period.
Lead ingestion resulted in an increase in adrenal weight during the first
4 weeks of lead exposure, followed by a return to near control values. The
net-percent conversion of C-progesterone by adrenal tissue to 11-deoxycor-
ticosterone, aldosterone, and deoxycortisol first rose, then returned to
near or below control values, in a variable pattern, by the 8th week. The
data suggest an initial stimulation of the adrenal gland function during
the early stages of lead intoxication followed by either an adaptation by
or an exhaustion of the adrenal. In contrast, de Bruin (1971) reports on
research in which steroids were found to decrease during the initial period
of the lead poisoning of animals, but increased considerably during ad-
vanced stages of intoxication.
Absorption of lead appears to exert a depressing effect upon the thyroid
gland (de Bruin, 1971). Sheep poisoned by prolonged lead absorption in
increased quantities have been found to have an abnormally low level of
6.69
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protein-bound iodine, an indication of reduced thyroid activity. According
to de Bruin no protein-bound iodine observations have been made in
connection with the occupational exposure of humans to lead.
6.3.3 Factors Influencing or Modifying Toxicity
Goyer and Mahaffey (1972) and Mahaffey (1974) listed age, season of the
year (body temperature, dehydration, ultraviolet light), dietary calcium
and phosphorus, iron deficiency, dietary protein, dietary Vitamin D, ascorbic
acid, alcohol, other metals, coexistent diseases, and the intracellular
complexing of lead (see Section 6.3.1) as factors that influence the sus-
ceptibility of humans and other animals to the toxic effects of lead. Some
of these parameters are outlined in Table 6.15. Some factors cannot be
controlled (age, season, some diseases), while others such as diet and
living in high-risk lead environments can be.
Six and Goyer (1970) investigated the influence of lowered dietary cal-
cium on a variety of biological parameters in rats fed a dose of lead (200
ppm lead acetate) which does not produce subclinical lead toxicity when
accompanied by a lab chow diet. Lowering dietary calcium at the above lead
dosage greatly increased the body burden of lead as was shown by increased
absorption and urinary excretion of lead and increased lead levels in blood,
soft tissue, and bone. Pathologic changes reflecting overt lead toxicity
were greater in rats fed the low-calcium diet, including increased excretion
of delta-ALA, increased frequency and size of intranuclear inclusion bodies
and renal tubular cells, increased kidney size, and aminoaciduria.
Quarterman, et al., (1972) found that the susceptibility of rats to
lead was increased severalfold by lowered calcium intake. A lowered phosph-
orus intake had a similar effect on lead retention in rats and the effects
of calcium and phosphorus deficiency were additive. Transfer of lead from
the mother to the newborn and to weanling pups was greater in the calcium-
deficient rats. Although it has been reported that lead retention in rats
cannot be decreased by increasing dietary calcium intake above normal
requirements, addition of calcium and phosphorus to the milk ration of
newborn rats has decreased their lead absorption (Quarterman, et al., 1972).
On the other hand, milk itself enhances lead absorption in rats. (Kello and
Kostial, 1973). The mechanisms underlying these interactions are presently
unclear. There are, however, some similarities in calcium and lead metabo-
lism. For example: Vitamin D also affects lead metabolism by increasing
its blood and bone concentrations (Sobel, et al., 1940); lead and calcium
distribution in the body are influenced in a similar manner by phosphorus
(Potter, et al., 1971); and calcium and phosphorus occur with lead in
intranuclear inclusion bodies (Carroll, et al., 1970). Furthermore, there
is some similarity between the energy-dependent lead uptake by heart mito-
chondria and energy-dependent calcium accumulation (Scott, et al., 1971).
Although toxic manifestations of a certain lead dosage may be observed
only with a calcium- or phosphorus-deficient diet, there is no evidence
that the lead actually induces a deficiency state with regard to these ele-
ments. However, lead does cause some disturbance in the metabolism of
these elements, with reductions in serum calcium (Six and Goyer, 1970).
6.70
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TABLE 6.15. FACTORS INFLUENCING LEAD TOXICITY3
Factor
Correlation with
Lead Toxicity
Species
Age
Season
Dietary copper deficiency
Dietary calcium and
phosphorus deficiency
Protein deficiency
Vitamin D excess
Vitamin C excess
Vitamin E deficiency
Nicotinic acid
treatment
Drinking of alcohol
Iron deficiency
Cadmium exposure
Diseases
Hemoglobin S or C
Thalassemia
Glucose-6-phosphate
dehydrogenase deficiency
Chronic renal disease
Negative
Increased toxicity
in summer vs.
winter
Positive
Positive
Positive
Positive
Negative
Positive
Negative
Positive
Positive
Positive
All positive
Human, rats
Humans; increased tem-
perature increased
toxicity in rabbits
and mice.
Rats
Rats, humans?
Rats
Rats
Guinea pigs
Rats
Rabbit, rats?, humans?
Humans
Humans, rats
Rats
Humans
Humans, rats
Compiled from Goyer and Mahaffey (1972); Goyer and Rhyne (1973)-,
Klauder et al.,(1973); Levander et al.,(1975); Mclntire and Angle
(1972)? and Quarterman et al., (1973).
6.71
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Low-calcium and low-phosphorus diets greatly increased skeletal uptake
of lead by adult female rats given 200 ppm lead acetate in the drinking water
(Quarterman, et al., 1973). The subsequent release of this incorporated lead
was strongly inhibited by low calcium diets. However, the uptake and release
of lead was not related to the calcium:phosphorus ratio of the diet or to the
degree of skeletal resorption or to the plasma calcium concentrations. The
calcium and phosphorus content of the weanling carcasses was unaffected by
the maternal diet.
Experimental studies suggest that absorption of lead varies as a func-
tion of age. Forbes and Reina, (1972) and Kostial, et al., (1971a,b) ob-
served that nursing rats have a much higher absorption of lead when compared
to adult rats. This may be related to the higher absorption of calcium in
young rats.
Six and Goyer (1972) studied the synergistic toxic effect of low dietary
iron and lead ingestion in rats which had been fed a subtoxic dose of lead
(200 ppm lead acetate) in drinking water along with a purified diet containing
adequate iron (25 ppm), calcium, and phosphorus, or a diet deficient only in
iron (5 ppm). During the 10-week study period, there was a marked exacerba-
tion of lead toxicity symptoms in the iron-deficient rats. The effects were
similar to those reported for calcium-deficient rats except that, in this
case, lead distribution between bone and soft tissues was not affected. Iron
deficiency did result in an increased retention of lead in liver, kidney,
and bone, and an increased urinary excretion of lead. Biochemical parameters
of lead toxicity including urinary excretion of delta-ALA were greater in
iron-deficient rats fed lead than in rats receiving adequate diets and lead.
There is no obvious explanation for the strong effect of iron deficiency
on lead absorption and retention (Six and Goyer, 1972). There seems to be a
common absorption pathway for iron, zinc, cobalt, and manganese (Forth and
Rummel, 1971). In iron-deficient rats, absorption of these other elements
is generally increased by two to three times, while the absorption of lead
is much greater.
Calcium and iron intakes are most likely to be inadequate in children
and pregnant women who are also found to be most susceptible to hematopoietic
effects of lead and possibly to other effects as well. There is a need for
further research to establish to what degree lead absorption and the mani-
festation of lead toxicity are affected in children consuming diets which
are only marginally adequate in calcium, phosphorus, and iron.
One preliminary indication is that of Angle and Stelmak, (1975). They
found that iron supplementation in children increases blood lead and that
such supplementation does not alleviate the anemia differentially for high
vs low blood lead children.
Mooty, et al., (1975) investigated the relationship of diet to lead
poisoning in 46 children, aged 24 to 47 months (25 controls and 21 subjects)
chosen according to low and high blood lead levels. The major finding in
this study is that there was no significant difference in their protein,
6.72
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caloric or iron intake, leaving unanswered what factor(s) must account for
the occurrence of lead poisoning in the subjects (see Section 8.3.1.6).
On the other hand, lead absorption has been shown to be increased by high
fat, low protein, and high protein diets, and decreased by high mineral diets
(Barltrop and Khoo, 1975).
Thawley (1975) investigated the toxic interactions among lead, zinc,
and cadmium with varying levels of dietary calcium and Vitamin D in rats.
Male Sprague-Dawley rats (95 to 100 grams live weight) received dietary
lead (0.5 percent), zinc (0.63 percent) and cadmium (90 ppm) individually
and in combination with each other (the inorganic compounds supplying these
metals were not given). These diets were eaten for 42 days with two levels
of calcium (0.1 and 0.9 percent) and three levels of Vitamin D (0, 2,000,
and 50,000 international units per kilogram of feed).
The most significant findings of this study were:
(1) A marked increase in the toxic effects, as well as blood,
liver and kidney concentrations of lead, zinc, and
cadmium in animals fed a calcium-
deficient ration;
(2) A general increased toxicity of lead, zinc and cadmium
as dietary Vitamin D levels increased from deficient
to excess;
(3) An alleviation of the toxic symptoms (viz., increased
ALA excretion and reticulocytosis) and a reduction of
lead in blood liver, kidney, and bone by the concurrent
administration of lead with zinc or lead with cadmium.
Reports that the incidence of swayback, a copper-deficiency syndrome
in sheep, may be associated in some areas with elevated lead contents in
pastures led to a study of the effects of lead on copper metabolism in rats.
Klauder, et al., (1973) found that lead toxicity in rats was increased by
a dietary deficiency of copper. They also had evidence for a protective role
of copper in reducing lead toxicity, and conversely for a depressive effect
which lead had on copper metabolism (see Figure 6.16 and Table 6.16). Inges-
tion of lead caused anemia in the low-copper rats (which was not evident in
the rats receiving a normal amount of copper), reduced serum ceruloplasmin
and copper in rats receiving the normal copper (with no depression of hemo-
globin), and depressed zinc in rats getting low copper. Retention of lead in
kidney and liver was inversely proportional to dietary copper levels. The
very pronounced inverse relationship which was evident in all parameters
(see Table 6.16) indicated a protective effect of copper at the higher
levels. As shown in Figure 6.18t the amount of lead present in the erythro-
cytes of the rats, each of which was exposed to the 0.5 percent dietary lead,
was inversely related to the amount of copper and ceruloplasm in the serum.
This implies a mutual antagonism between these elements.
6.73
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90 100 BO 200 2»
ERYTHROCYTE LEAD (pg/IOOmO
Figure 6.16
The effect of increasing ceruloplasmin levels on
erythrocyte lead in male Sprague-Dawley rats fed
a semipurified diet and 0.5% Pb for 56 days. The
groups received 0.5, 1.5, and 2.5 yg Cu/g diet.
Source: Klauder. Reprinted with permission from
Proceedings 6th Annual Conference on Trace Substances
in Environmental Health, (c) University of Missouri,
1973.
6.7U
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Table 6.16 EFFECT OF LEAD ON COPPER METABOLISM IN
MALE RATSa'b
Hematocrit (%)
Hemoglobin
(g %)
Serum Cu
(yg %)
Serum Zn
(yg %)
Ceruloplasmin
(mg %)
Low
Cuc
48.5
12.2
6.0
138
6.7
Normal
Cud
51.4
13.2
57.2
124
29.1
Low Cu
+Pbe
36.2
8.1
7.5
98
2.8
Normal Cu
+ Pbe
51.2
12.3
12.4
121
10.7
Source: Klauder, et al. Reprinted with permission from Proceedings
6th Annual Conference on Trace Substances in Environmental Health.
(c) University of Missouri, 1973.
Parameters affected by lead acetate given in the copper-deficient
semi-purified diet to male Sprague-Dawley (SD) rats for 56 days.
LOW copper diet contained 0.5 ppm Cu.
Normal copper diet contained 2.5 ppm Cu.
e+Pb diet contained 0.5% Pb.
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In contrast, Rubino, et al., (1958) showed that lead-exposed workers
have increased erythrocyte-copper concentrations which is contradictory to
what would be expected from the above results. He, therefore, believes that
it is far from certain that a biologically significant copper-lead
interaction exists, especially since the lead dosage used by Klauder, et al.,
(1973) was excessively high. Other reports of possible effects of lead
on copper metabolism imply that some other copper-antagonist is responsible
for the results obtained (Bremner, 1974).
Another possible interaction of copper and lead is a reduction in trans-
placental movement of lead when maternal copper levels are high (Baumslag,
1975). Willoughby, et al., (1972) found that young horses who were fed
diets containing toxic amounts of lead and/or zinc had marked differences in
clinical symptoms with the combined metals producing symptoms of zinc (but
not of lead) toxicity. Tissue distribution of lead was altered by zinc in-
take; there was a large decrease in bone lead and increase in hepatic and
renal lead concentrations. The finding of increased tissue lead content and
decreased susceptibility to lead toxicity is as yet unexplained. The in-
creased zinc intake almost certainly would have increased both renal and
hepatic metallothionein content and may possibly have increased lead binding
in this form with consequent detoxication, although Webb's (1972) data does
not support this. Alternatively, the effect on lead metabolism may arise
from effects of zinc on bone mineralization. It would be of interest to
establish whether more physiological and nontoxic amounts of zinc can also
offer protection against lead toxicity.
Alcohol ingestion has been implicated clinically as exacerbating lead
toxicity. This apparent synergism might result from lowered nutrient in-
take by the alcoholic consumer, a metabolic interrelationship, or the pre-
sence of both lead and ethanol in illicitly distilled beverages (Anon, 1974).
Mahaffey, et al., (1974) found that chronic consumption of ethanol by rats
with controlled nutrient and energy intake during a 10-week study did not
markedly affect the toxicity of orally ingested lead acetate (200 ppm).
However, lead ingestion increased renal lead concentration from 0.7 ppm wet
tissue to 6.4 ppm in the absence of ethanol and 16.6 ppm in the presence of
ethanol. Ethanol increased the number of renal inclusion bodies in the
kidneys of lead-eating rats. Bone and liver lead were not influenced by
ethanol, and liver morphology was influenced by ethanol, but not by lead.
It thus appears that any clinical synergism between lead toxicity and alco-
hol ingestion results from a lower nutrient intake or increased exposure to
lead. Both lead and ethanol inhibit the enzyme aminolevulinic acid dehy-
drase, indicating some common biochemical effects. This has been reported
in man and in rats (Moore, et al., 1971). Negative aeroionization reduces
the toxic effects of lead (Straus, et al., 1973). Ninety rabbits were used
to study the effect of lead (as lead acetate) administered intravenously,
subcutaneously, or orally over 10 to 20 days, while simultaneously submitting
the animals to moderate negative aeroionization. The experimental animals
had lower mortality rate and a lower concentration of lead, and less altera-
tion of the enzymes glutamino-pyuvic-transaminase in the serum, and cholines-
terase in the blood.
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Ghelberg, et al., (1973) investigated the effect of an anabolic therapy
using methandrostenolone on white rats which had been given 950 milligrams
of lead acetate per kilogram body weight in aqueous solution administered
intraperitoneally over 7 months. A reduction of the concentration of lead
was observed in the kidney, brain and femur, and improvements were noted
in the serum fraction, and in the enzyme activity of the liver and the
small intestine.
Mclntire and Angle (1972) observed that black children who are deficient
in the enzyme glucose-6-phosphate dehydrogenase have a higher lead concentra-
tion than those in whom the enzyme is normal. Since the serum lead concen-
tration is actually lower than in normal children, this can be attributed to
an increased binding of lead to the red cell.
6.3.4 Reproductive Effects; Fertility Reduction, Mutagenicity,
Teratogenicity
The effects of lead on human reproductive functions per se have received
little study in recent years. Consequently, much of what appears in the
literature concerning human reproductive effects comes from very old studies
of workers exposed to levels of lead orders of magnitude higher than today's
lead workers, or alternatively from rather unscientific foreign reports of
similar age. Lancranjam's (1975) study is the only recent investigation
focusing exclusively on human fertility effects (specifically spermatogenic
abnormalities) under reasonably well defined levels of lead exposure. Some
cell culture studies of mutational activity of lead are also available.
Many laboratory animal studies are included in this section, therefore,
because they serve as indicators of potential human effects and because the
requisite human experimentation needed to clarify these effects is either
unethical or absent. Nuclear polyploidy and abnormalities in mitosis have
been noted in bone marrow cells by a number of investigators. Chromosomes
from leukocyte cultures from mice fed a diet containing 1 percent lead
acetate showed an increased number of gap-break type aberrations (Muro and
Goyer, 1969). The observed chromosomal abnormalities largely involved only
single chromatids. Failure to have a paired defect (break or gap) in both
chromatids of a chromosome suggested that damage occurred after the deoxyri-
bonucleic acid (DNA) synthetic phase of the cell cycle. There is a possible
relationship between increased deoxyribonuclease activity and chromosome
damage as a marked increase in DNA has been demonstrated in urine from lead-
poisoned rats (Muro and Goyer, 1969). These findings are of interest with
respect to the known effect of lead on reduction of fertility and possible
oncogenesis and teratogenesis. Gap-break type aberrations of chromatids have
been reported among lead workers having blood lead levels ranging from 62 -
88 micrograms/100 milliliters (Goyer and Rhyne, 1973). A variety of nonspecific
changes in chromosome morphology (adhesions and spiralizing defects), and
increases in tetraploid mitoses and the mitotic index were also noted.
6.77
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The mutational activity of inorganic lead in lead workers was further
examined by studying the chromosomes of cultured blood lymphocytes (Forni
and Secchi, 1973). Significant increased rates of chromatid aberrations,
and unstable chromosomal changes were seen in current workers as compared
to controls or workers who had been removed from lead exposure for 18 or
more months. None of the groups exhibited changes in stable chromosomes.
O'Riordan and Evans (1974) studied the extent of chromosomal damage,
and correlation between the level of damage and the lead levels in blood
and urine within a population of men occupationally exposed to oxides of
lead. The population consisted of seventy male workers employed by a ship-
breaking yard. Thirty-five men, aged 21 to 63 years (Group 1), were engaged
as burners to cut the hulls and all metal structures of ships, and their
lengths of exposure ranged from 3 months to 43 years with an average weekly
exposure time of 50 hours. The remaining thirty-five men (controls) were of
comparable age. Their findings (see Table 6.17) did not reveal any consistent
and significant differences in the incidence of chromosome-type and chromatid-
type aberrations between Groups 1 and 2 or among classes A, B, C, and D.
Moreover, the results within any class were similar to those obtained from
previous surveys of adult males from a variety of groups that were not con-
sidered to be unduly exposed to known or suspected mutagens.
Chromosomes from the peripheral blood lymphocytes of 14 workers from a
zinc industry who showed signs of differing degrees of lead poisoning were
studied by Deknudt, et al., (1973). According to the type and duration of
exposure, the workers examined were classified into three groups: Group I:
People exposed to a high level of zinc and low levels of lead and cadmium;
Group II: People exposed to high levels of the three minerals; and Group III:
People exposed to high levels of lead and cadmium in the absence of zinc. The
aberrations observed were dicentrics, rings, chromatid exchanges as well as
gaps and fragments. Exposure to zinc and cadmium did not seem to increase
the number of cells with, severe chromosomal anomalies, thus lead intoxication
was considered to be responsible for these chromosomal aberrations.
Excess chromosomal breaks have been found in children suffering from
lead poisoning, both acute and chronic (Shaw, 1970).
The older literature concerning industrial lead poisoning makes frequent
reference to stillbirths, miscarriages and sterility among women working in
the lead trades as well as among the wives of workers (Cantarow and Trumper,
1974; Oliver, 1914).
Lancranjan, et al., (1975) investigated the reproductive ability of men
occupationally exposed to lead. They found that workmen having lead absorp-
tion ranging from slight to high (as judged by blood and urine analyses for
lead, ALA and coproporhyrins) exhibited a substantial increase in spermato-
genic abnormalities (asthenospermia, hypospermia and teratospermia). Al-
though Leydig androgen function was not affected, germinal insufficiency
appeared to result from a direct, toxic effect of lead on the gonads and did
not occur through the hypothalamopituitary system. Studies with laboratory
animals indicate that the ingestion of lead by either parent results in the
reduction of both size and number of offspring.
6.78
-------
Table 6.17 CYTOGENETIC FINDINGS IN CULTURED LYMPHOCYTES FROM SHIPYARD WORKERS
WITH AN OCCUPATIONAL HISTORY OF LEAD EXPOSURE (GROUP 1), AND FROM
SHIPYARD CONTROLS (GROUP 2) AND OTHER ADULT MALES8
Blood
Lead
Level
(ug per
Category 100 B!
A. Morail <40
B. Accept- 40-80
able
C. bees- 80-120
slve
D. Danger- >120
ous
Total Group 1 —
(Exposed)
Total Group 2 ~
(Control) c
Other Biles
Cells with Chroaatid Aberrations
Ho. of
Men
Studied
12
(Group 2)
16
(Group 1)
17
(Group 2)
33
(total)
15
(Group 1)
2
(Group 2)
17
(total)
4
(Group 1)
35
31
285
Total
Cells
Scored
1,200
1,600
1,700
3.300
1,500
200
1,700
400
3.500
3.100
3.107
Percent
Norwl
Cells
91.5
93.33
94.50
94.47
93.87
94.29
94.09
94.50
93.90
93.43
4
9o. DO
Total
Ho.
51
71
70
141
72
10
82
25
168
131
68
Chroaatid
and
IsochroBitid Chroaatid
Percent
4.25
4.43
4.12
4.27
4.80
5.00
4.90
6.25
5.16
4.46
2.18
Gaps
53
68
73
141
68
10
78
25
161
136
65
Breaks
0
7
1
8
5
1
6
0
12
2
4
Chroaatid
Interchanges
0
9
2
4
0
0
0
0
2
2
0
Total
Mo.
5
7
6
13
13
1
14
3
23
12
36
Cells
Percent
0.42
0.44
0.35
0.39
0.87
0.50
0.82
0.75
0.69
0.42
1.16
with ChroBosoae Aberrations
Dicen tries
2
1
0
1
0
0
0
0
1
2
2
Acentric
Pragaents
5
6
5
11
7
1
8
3
16
11
9
Mo.
Structurally
Abnormal
Chroaosoaes
0
5
2
7
3
0
3
0
8
2
16
aSource: O'Riordan and Evans. Reprinted with permission from
Nature, (c) Macmillan, Ltd. (1974).
^Number of structurally abnormal monocentric chromosomes observed which
were not associated with an acentric fragment.
cData obtained from previous MRC surveys of othe adult male groups with
no history of undue exposure to known or suspected mutagens (lymphocyte
culture time <
^Includes nonmodal cells.
-------
Goyer and Rhyne (1973) cited a study in which the paternal ingestion of
lead in rats resulted in the retardation of embryonic growth of offspring
and reduced numbers of weaned pups per litter. While this may have been
indicative of defective spermatozoa, no morphological or functional differen-
ces were noted between sperm from control and lead-fed parents. Maternal
effects of lead were exhibited by reduced litter size, retardation of fetal
development, and impaired postnatal survival. The ovaries of lead-burdened
females (rats and rhesus monkeys) showed a reduced number of developing fol-
licles.
When both male and female rats and mice were exposed to 25 ppm of lead
(as lead acetate) in drinking water, the offspring had increased numbers of
breeding failures, runts, young deaths and dead litters (Schroeder, 1973).
Unspecified inorganic lead salts administered to pregnant mice and rats in
low doses (25 ppm) in drinking water produced runting, reproductive failure
and shortened life spans (Schroeder and Mitchener, 1971).
Hilderbrand, et al., (1973) investigated the effect of lead acetate on
reproduction and metabolism in rats. Eighty sexually mature males and eighty
sexually mature females were maintained in a controlled environment with a
constant temperature of 25.5 C. The males and females were divided into
three groups with each group containing 20 rats. Group 1 served as controls;
Group 2 was treated orally with 5 micrograms of lead acetate for 30 days;
and Group 3 was treated with 100 micrograms of lead acetate for 30 days.
These dosages were presumably administered daily although the authors do not
specifically say so. Results of this investigation revealed the following:
(1) In males, when the lead concentration in the blood increased
from 14 to 26 micrograms per 100 milliliters, impotence and
prostatic hyperplasia resulted.
(2) When the lead level increased to 50 micrograms per 100 milli-
liters, testicular damage occurred and spermatogenesis was
inhibited.
(3) In the female, when lead concentration in blood increased from
14 to 30 micrograms per 100 milliliters, irregularity of estrus
occurred.
(4) When lead levels reached 30 micrograms per 100 milliliters,
persistent vaginal estrus occurred after normal estrus,
and the development of ovarian follicular cysts with a
reduction in the number of corpora lutea was noted.
(5) No toxicity or mortality occurred in the treated animals.
Stowe and Goyer (1974) also observed that the reproduc-
tive performance of male rats is reduced as a result of
lead exposure. The parentally transmitted effect includes
reduction of litter size, weights of offsprings and reduced
survival rates of the offsprings.
Teratogenic effects of lead have been demonstrated in experimental animals.
Specific congenital-skeletal malformations were induced in golden hamster
6.80
-------
embryos by treating pregnant hamsters with lead acetate, lead chloride, and
lead nitrate (Ferm and Carpenter, 1967). The malformations were primarily
localized within the developing sacral and tail vertebrae and were charac-
terized by varying degrees of tail malformations ranging from stunting to
complete absence of the tail. Minor degrees of this malformation were
compatible with life, and the fertility of several affected newborns which
had been reared to adulthood did not appear to be affected.
Ferm (1969) injected female hamsters intravenously with cadmium sulfate
(2 milligrams per kilogram) and lead acetate (25 and 50 milligrams per kilo-
gram) on the 8th day of gestation. The combination of the metals revealed
that the frequency and severity of clefts in the lip and palate usually caused
by cadmium were reduced in the presence of lead, while the posterior tail
malformations caused by lead appeared to be potentiated in the presence of
cadmium. Ferm supports the possibility of cadmium and lead interacting ad-
ditively on certain enzyme systems in the case of tail bud malformation and
of lead blocking the effect of cadmium on the differentiating visceral arch
system preventing the facial abnormalities. Ferm and Ferm (1971) showed
that when female golden hamsters are given lead nitrate intravenously at a
dose level of 25 or 50 milligrams per kilogram on the 8th and 9th days of
gestation, the embryonic resorption and malformation rates rose with in-
creasing doses of lead. Likewise, rats exhibited similar effects following
the intravenous administration of lead nitrate to the dams (McClain and
Siekierka, 1975). Interestingly, no such effects could be produced by oral
feeding of lead. Fournier and Rosenberg (1973) found no significant terato-
genicity in lead acetate-treated rats and rabbits over the controls.
McClain and Becker (1972) found tetraethyllead, tetramethyllead, and
tetramethyllead chloride to be essentially nonteratogenic in Sprague-Dawley
rats. Embryo or fetal toxicity was observed to accompany the administration
of the organolead compounds and was characterized by growth retardation and
delayed ossification of bone. Marked fetal effects were observed only in
maternal animals that exhibited severe organolead toxicity and were, there-
fore, severely debilitated.
6.3.5 Carcinogenicity and Miscellaneous Biochemical Effects
Grandjean (1973) reviewed studies which suggest that lead and cancer are
related. Some cancers were related geographically to elevated lead levels
in soil and drinking water. Others showed that cancer patients had elevated
levels of lead in the lungs and liver regardless of the site of cancer.
A followup of 425 workers exposed to lead in a storage battery factory
was conducted by Dingwall-Fordyce and Lane (1963). They reported "no
evidence to suggest that malignant disease was associated with lead absorp-
tion".
Similarly, a recent epidemiological study of causes of death among U.S.
lead workers indicated that although deaths from neoplasms were higher than
would be expected (based on the mortality rates among males in the general
population of the U.S.), the incidence was not elevated to the point of
statistical significance (Cooper and Gaffey, 1975).
6.81
-------
In contrast to man, rodents are susceptible to lead-induced cancers.
Sunderman (1971) reviewed reports of renal, adrenal, thyroid, prostate,
and pulmonary adenomas, renal adenocarcinomas, and testicular carcinomas
in rats and mice which had received lead phosphate, lead acetate, and
basic lead acetate via dietary and/or parenteral routes. Lymphomas result-
ing from the subcutaneous injection of tetraethyllead were also reported.
Cerebral gliomas (usually poorly differentiated, malignant tumors) were
induced in rats with dietary lead subacetate and 2-acetylaminofluorene (AAF)
(Oyasu, et al., 1970). Twenty-five gliomas and 3 extracerebral intracranial
tumors were found in 988 Wistar and caesarean-delivered (Sprague-Dawley)
rats of which 663 were in experimental, and 325 in control groups. The
tumors usually developed after 52 weeks of age. The highest incidence (8.6
percent) of gliomas was in animals ingesting lead subacetate and the differ-
ence compared with the incidence among controls, (0.3 percent) was statistical-
ly significant (P less than 0.05). In animals given 2-AAF (with or without
olive oil, carbon tetrachloride, or ethionine) the incidence (2.5 percent)
of gliomas was lower and their development was usually delayed until after
60 weeks of age but the incidence (5.5 percent) among rats that survived 60
weeks or more was statistically significant (P less than 0.05) when compared
with that of 325 control rats in which only one glioma was found.
A similar interaction of lead and benzo-[a]-pyrene vis-a-vis tumorigenesis
has been reported in hamsters (Kobayashd and Okamoto, 1974).
An increased incidence of lung cancer has been reported in lead, copper,
and zinc smelter workers and in the residents of communities surrounding
smelters (Anon, 1975a). However, the report adds that the arsenic emitted
from these plants may be the actual cause of the cancer. Lead chromate has
been linked to cancer in Europe (Anon, 1975b). The chromate ion has long
been suspected as being carcinogenic (Furst and Haro, 1969), and is pro-
bably the active moiety in lead chromate. NIOSH is currently working on
new criteria documents for lead and zinc chromates. Some paint manufacturers
have also issued alerts concerning these pigments.
Martell (1975) postulates that tiny amounts of radioactive lead are ab-
sorbed by tobacco plants as they grow. The lead, he believes, is inhaled
in the lungs with cigarette smoke, where it lodges and gives off alpha
rays that destroy lung cells, or the radioactive lead particles spread
throughout the body and cause some bone, stomach, and liver cancers.
Summarily, the entire issue of the carcinogenic potential of lead in
humans must be considered unresolved.
Urbanska-Bonenberg and Smigla (1973) carried out clinical investigations
and several routine biochemical examinations on 230 persons professionally
exposed to inorganic lead and on several control groups. They concluded that
the liver is somewhat resistant to lead and that under conditions of occupa-
tional exposure to lead, abnormalities of liver function may be due to other
potentially pathogenic factors, for example, viral hepatitis and alcohol
abuse. Abnormalities of liver function were also confirmed in rats subjected
to subacute poisoning with lead acetate.
6.82
-------
Numerous miscellaneous effects have been reported in the literature (e.g.,
elevated cholesterol levels in heavily lead-exposed humans and animals, modi-
fications of proteins in blood serum albumin fraction, alpha, beta and gamma
globulins in lead-poisoned humans and animals, shifts in metallic components
of tissues and body fluids associated with changes in lead intake, etc.)
These effects are reviewed by de Bruin (1971). The physiological significance
of many of these effects, however, are totally obscure at the present time.
The affinity of lead sulfhydryl (-SH) groups (see Section 6.3.1) allows
for reaction involving free thiol groups (e.g., glutathione) in the body.
Such reactions spare certain enzymes to a greater or lesser extent. A re-
duction of the glutathione content of the erythrocytes in the presence of
sufficient concentrations of lead has been observed both in vitro and in vivo
(Bonsignore, 1967; Vergnano, 1967).
Related to the reaction of lead with thiol groups is the appearance of
Heinz bodies which are formed by the oxidation of thiol groups bound to glo-
bin in hemoglobin. It is quite likely that there is a link between reduction
in erythrocyte glutathione in lead exposure and the appearance of Heinz
bodies since these result from the oxidative degradation of hemoglobin (Beutler,
1969).
It has been suggested that lead interferes with enzymatic degradation of
tryptophan, of which 5-hydroxyindoleacetic acid (HIAA) is a final metabolite
in a minor pathway. This metabolite was found in increased quantities in
the urine of 227 children who lived in the vicinity of lead-processing in-
dustries. A well-defined relationship has been observed between the propor-
tion of cases with increased urinary concentrations of HIAA and the concentra-
tion of lead in the air of the area (Ghelberg, 1966)The HIAA determinations
were not quantitative and were not correlated with other indices of lead ex-
posure. Others have noted a rise in urinary excretion of HIAA in moderate
lead exposure (Urbanowicz, et al., 1969; Dugandzec, et al., 1973). Schicle,
et al., (1974) on the other hand, were unable to find any significant ele-
vation of HIAA excretion in a group of lead workers with levels of exposure
greater than in the earlier studies.
6.83
-------
6.4 LEAD TOXLCITY IN CHILDREN
6.4.1 Unique Features of Lead Poisoning in Children
Considerable research effort has gone into the study of the features of
lead poisoning unique to children. Although there are many such special
features, they can be broken down into three categories: (1) Children have
different modes of exposure than adults (e.g., eating non-nutritive lead-
containing substances such as paint, dust, and soil). (2) The lead which
is ingested seems to be absorbed at a higher rate than in adults. Also,
children's developing nervous systems make them especially vulnerable to
lead toxicity. (3) Manifestations of lead overexposure in childhood may
include disorders of higher mental functioning (e.g., learning disabilities
and hyperkinesis) which are effects unique to this group.
The exposure of children to lead has very unique characteristics.
The vast majority of lead poisoning cases in children are due to eating
leaded house paint (National Academy of Sciences, 1972). An important feature
of this problem in preschool children is "pica" which is the repetitive in-
gestion of non-food materials. It has been suggested that the sweet taste of
leaded chips reinforces this action. An essential element in lead poisoning
risk for children is the age of the home. Older housing (30 years old or
more) which is in disrepair gives easy access to paint peelings which may con-
tain up to 40 percent lead by weight. Many articles have been written des-
cribing the problems associated with the childhood ingestion of leaded-paints
(Hartman, et al., 1960; Griggs, et al., 1964; de la Burde and Shapiro, 1975;
Jacob zine r, 1966).
There are other sources of lead with a special relevance to children.
These include street dust, surface or garden soil in areas of high traffic
density, household dust, pencil, toy and furniture paint, improperly glazed
earthenware, ashes from burning lead-battery casings, newsprint with leaded
inks, toothpaste, and toothpaste tubes (Lin-Fu, 1973a,b; Eaton, et al., 1975;
National Academy of Sciences, 1972). It should be noted, however, that the
most significant source is still leaded paints (World Health Organization,
1977).
6.4.1.1 Sources—
To determine the relative contribution of different sources of lead,
Lockeretz (1975) measured the lead content of teeth of children in five
different environments in metropolitan areas. In each case, the mother
lived in the area during pregnancy, and the child lived continuously in the
same area until the tooth that was used in this study was shed. The five
parameters studied were—lead paint, no lead paint, suburb, industrial, and
public housing. Comparisons of populations based on lead levels in individual
teeth showed the difference between areas with and without a lead paint
problem, respectively, but showed no effects attributable to traffic density
or industrial sources. Tooth-lead content was examined in children whose
exposure to environmental lead differed with respect to four sources: lead
paint; automobile exhausts; atmospheric industrial lead emissions; and mills.
The only clear difference was that, in the area with a lead paint problem,
children in both regular housing and in the projects had an average level
-------
almost twice as high as the other areas. In areas that have no lead paint
problem no difference was observed between those that had high and low
traffic densities.
Ter Haar and Aronow (1974) investigated the childhood lead problem in
terms of (1) the major sources of lead in dirt around houses where children
play, and (2) the extent to which children take in dust and air-suspended
particles. Dirt was sampled at nine sites around each of 18 frame houses
in widely scattered urban areas of Detroit. Dirt was also sampled around
7 farm houses in an area remote from traffic, located about 30 miles north
of the nearest city, and about 50 miles north of Detroit. The data from
the survey of the urban areas (see Tables 6.18 and 6.19) showed that the
principal cause of elevated lead in the dirt in the yards is leaded paint
on these houses. For the second part of the study, these investigators
determined the amount of air-suspended particulate or dustfall a child
might eat. They used a naturally occurring tracer, lead-210, which is
present in dust but nearly absent from paint. The results (see Tables
6.20 and 6.21) showed that children with pica (and other evidence of high
lead intake) and normal children excreted identical amounts of lead-210.
Consequently, dust and air-suspended particulate were not the sources of
lead in these urban children.
In an in vitro laboratory study of the lead in printed matter, Bogden,
et al., (1975) found that dangerous quantities of lead, up to 200 micro-
grams, could be extracted from small pieces of printed paper at pH values in
the range of human gastric fluid, i.e., 1 to 2. Lead was not extracted
at pH values in the range of human saliva. Children who merely chew printed
matter are not in danger of absorbing lead, but pica-prone children who
swallow printed material may absorb toxic amounts of lead.
6.4.1.2 Absorption Patterns—
The absorption of ingested lead in children is believed to be more
extensive than in adults (Section 6.2.1). Absorption coefficients for
adults are in the range of 8 to 10 percent, while some children absorb up
to 53 percent of ingested lead (Alexander, et al., 1973). It is clear that
the relationship between environmental lead sources and blood lead will be
different for adults and children.
The maximum daily permissible intake (DPI) of lead from all sources
without excessive body-lead burden in children was at one time considered to
be 300 micro grains (King, 1971). Barltrop suggested more recently that this
figure should be 133 micrograms per day (Golz, 1973). King defines intake
as the amount of lead ingested in the diet and nonfood substances, and the
amount retained in respiratory exchange. Sources of data on which the DPI
was based were:
(1) Levels of lead in the blood of exposed and nonexposed children
and of those with frank lead poisoning;
(2) The results of experimental lead ingestion by adults;
(3) Measurements of fecal output of lead in exposed and nonexposed
children;
6.85
-------
Table 6.18 LEAD IN DIRT IN DETROIT3
OO
.ON
Lead in Dirt, yg/g dry dirt
Within 2 Ft of Houseb
House Type House
Painted frame 1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
Front
1919
4121
439
237
920
126
n.d.
3420
179
17590
262
295
556
1256
n.d.
1077
768
4068
Back
3001
674
2193
2539
2184
233
n.d.
n.d.
372
4951
1585
292
246
655
162
1660
1094
3535
Sides
1170
7284
1116
1117
1211
186
1457
1380
611
5552
5694
140
446
1206
1083
1894
220
1452
748
6003
2548
925
1447
916
n.d.
5120
1060
7000
3402
104
254
4243
373
1460
1483
1278
10 Ft
from House
Front
985
536
278
216
191
58
n.d.
621
139
305
197
170
229
208
280
708
952
1530
Back
351
289
608
131
223
157
n.d.
831
122
207
219
149
285
149
252
1220
614
1410
Near
Sidewalk
449
1301
326
1482
309
343
627
355
820
422
506
152
266
1958
299
425
227
1017
Curb
660
432
610
680
320
321
404
1957
555
918
338
220
328
331
701
419
708
400
Gutter
596
1079
508
n.d.
738
1270
645
1827
1047
1387
1168
n.d.
1046
550
n.d.
935
1277
415
Average
2349
1586 2257
1846
447
425
627
572
966
-------
Table 6.18 LEAD IN DIRT IN DETROIT3
(Continued)
00
Lead in Dirt, pg/g dry dirt
Within 2 Ft
House Type House
Brick 19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
Average
Front
380
606
78
1030
352
687
104
183
382
377
146
146
491
140
480
150
366
227
351
Back
222
168
169
701
344
197
107
1915
835
283
463
203
172
72
2350
131
442
243
501
of House^
Sides
106
217
96
838
883
91
194
474
597
1160
173
102
187
1090
800
173
213
276
426
146
128
1540
725
486
222
95
1210
4610C
1500
231
269
113
40
632
251
281
2290
595
10 Ft
from House
Front
77
125
103
148
203
219
88
312
168
228
103
108
39
201
316
153
111
111
156
Back
72
94
48
188
480
97
75
329
816
163
80
84
50
119
417
77
244
175
200
Near
Sidewalk
246
438
1130
485
416
263
87
248
249
403
154
169
86
117
301
261
317
465
324
Curb
301
711
431
881
966
303
147
324
148
2420
469
330
403
408
395
428
750
1210
612
Gutter
564
1670
2085
1360
3170
656
1070
578
487
1410
765
600
423
3140
867
304
2380
298
1213
^Adapted from Ter Haar and Aronow (1974).
Many of samples for painted frame house contained readily visible paint chips, especially house 10;
n.d. denotes not determined.
CHouse next door was a painted frame house. This value not included in average.
-------
Table 6.19 LEAD IN DIRT IN RURAL AREA:
PAINTED FRAME FARMHOUSESa
House
1
2
3
4
5
6
7
Average
Lead
2 Ft
From House*5
2162
450
6338
1896
5184
840
831
2529
in Dirt, yg/g
10 Ft
From House^
417
429
2093
199
556
428
141
609
dry dirt
20 Ft
From House^
67
144
166
74
640
107
268
209
Background
9
27
26
74
12
63
94
44
a.Source: Ter Haar and Aronow (1974). Reprinted from Environmental
Health Perspectives.
Each value is the average for'four samples, one collected on each
side of the house.
6.88
-------
Table 6.20 LEAD AND LEAD-210 IN URINEa
Collection
1
2
3
4
5
6
7
8
9
10
11
12
13
14
Stable Pb,
yg/i
147
153
121
Treatment with
(oral) began
3820
1960
2030
6140
1400
2880
1170
3210
2530
1125
1780
21°Pb,
pCi/1
0.23
0.28
0.74
D-Penicillamine
0.27
0.18
0.42
b
0.27
0.51
0.48
b
b
b
0.40
Treatment began with calcium
disodium ethylenediaminetetra-
acetic acid and 2,3-dimercap-
to-1-propanol (muscularly)
15 4180 0.55
aSburce: Ter Haar and Aronow (1974) Reprinted
from Environmental Health Perspectives
Sample was partly used in the hospital, leaving
too small an amount for 210Pb determination.
6.89
-------
Table 6.21 LEAD AND LEAD-210 IN EXCRETA2
Normal Children
Stable Pb,
yg/g dry
3
2
3
7
7
3
3
5
4
4
Average
210pb,
pCi/g dry
0.019
0.021
0.027
0.120
0.087
0.041
0.026
0.028
0.044
0.024
0.044
Hospitalized
Stable Pb,
Ug/g dry
19
20
18
49
4
7
40
1640
Average
Children
210Pb,
pCi/g dry
0.046
0.018
0.024
0.047
0.050
0.039
0.063
0.037
0.040
Source: Ter Haar and Aronow (1974). Reprinted from
Environmental Health Perspectives.
6.90
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(4) The initial effects of lead intake;
(5) Rates of increase in levels of lead in the blood of exposed
children; and
(6) Sequelae of lead poisoning.
This daily permissible intake was developed at a time when it was not
known that the absorption of lead from the gastrointestinal tract of chil-
dren is considerably greater than that of adults. The rationale for it is
therefore outdated. Various authors have more recently published data on
fecal lead excretion of normal children and of children with abnormal lead
exposure. On the basis of these data and assuming 40 to 50 percent
absorption, it can now be specified that "normal" oral lead intake for
children 1-5 years of age is approximately 10 micrograms/kg/day. An
excellent review of these data is provided by Mahaffey, (1977).
Though definitive data are lacking, some estimate can be derived of
the relative contributions of ambient air lead and dietary lead to total
absorption. Table 6.22 presents estimates based on the studies of Alexander
(1974) in children and of Rabinowitz (1974) in adults. The most notable
aspect of Table 6.22 is that for normal, non-pica children, exposures to
lead in ambient air accounts for a much smaller proportion of their total
lead uptake than it does for adults (U.S. Environmental Protection Agency,
1976). For example, EPA calculated that an increment of 3 microgram/m in
ambient air lead concentration would result in an increase of 11 percent in
average daily lead absorption in children. The same increment would result
in an increase of 46 percent in average daily absorption in adults. For
controlling body lead in an adult, diet and ambient air are approximately
equal in importance; while for a child, diet is by far the more significant
factor.
6.4.1.3 Manifestations: Learning Disabilities and Hyperkinesis—
Some manifestations of lead poisoning in children are quite similar to
those in adults, and can be found in Section 6.3.2. Certain behavioral
outcomes such as mental retardation and hyperkinesis are of particular
interest in children.
The relation of blood-lead levels to cognitive and perceptual perfor-
mance function was determined for 80 black preschool children (Perino and
Emhart, 1974). Their lead levels were below the criteria set for lead
poisoning (not greater than 60 micrograms per 100 milliliters of blood),
but regression analysis revealed that the effect of blood lead on perfor-
mance was statistically significant. As the lead level increased, general
cognitive, verbal and perceptual abilities decreased. Lead levels were not
related significantly to parental intelligence, birth order, birth weight,
and number of siblings.
This study provided a clear separation of the "study group" with
elevated blood leads from low exposure "controls". Most previous studies of
this type suffer from considerable overlap in the blood lead levels of the
two groups. There was also a significant correlation between lead level and
the amount of parental education. While results of this study are
6.91
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Table 6.22 RELATIVE CONTRIBUTIONS OF DIETARY AND AMBIENT AIR LEAD
TO TOTAL LEAD ABSORPTION3
yg/Day-Person
Airborne Lead, ug/m A Absorption „
Physiological
Parameter
Intake
Diet
Air
Total
Absorption
Diet
Air
Total
Excretion
Urine
Hair, sweat
Total
Retention
2
Child"
159
16
175
82
7
89
51
_£
(63)
(26)
5 With A + 3 ug Pb/m'
Adultc Child Adult Child Adult
360 159 360
40 40 100 +24 +60
400 199 460 +24 +60
33 82 33
17 17 40 +10 +23
50 99 73 +10 +23
38
12
50
0
aSource: U. S. Environmental Protection Agency (1976).
bAlexander (1974).
CRabinowitz (1974).
6.92
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suggestive of a role of lead in intelligence performance, it may very well
be that more highly educated parents are the underlying "cause" of both low
blood lead (through regulating their children's behavior) and of superior
mental functioning (through tutoring and more effective parenting).
Beattie, et al., (1975) conducted studies of the relationship between
mental retardation and blood lead in Glasgow, Scotland, an area where
extremely high levels of lead have been recorded in drinking water. One
hundred fifty four children were examined, half of whom were classified as
mentally retarded, and half were normal. The mean blood-lead level in the
children tested was 25.4 micrograms per 100 milliters of whole blood
compared with 17,8 for the controls and this correlated with the higher
water-lead levels measured in the children's homes. None of the children
from the control group came from homes with lead levels greater than 800
micrograms per liter, whereas eleven from the mentally retarded groups were
exposed to as much as 2,000 micrograms per liter.
Another portion of the study looked at the effects of high lead con-
centrations (800 micrograms per liter or above) in Glasgow drinking water
during pregnancy and in the first year following birth. They found that
a strong correlation exists between high lead content and the development
of mental retardation in the children from the age of 2 to 5. The combina-
tion of soft water and lead in plumbing contributed to the elevated levels
in drinking water, both of which are preventable sources of lead (see
Section 7.3.2).
There are a number of methodological issues which Beattie, et al., (1975)
neglected, including matching of controls, confounding effects of social
class, and comparison of biological parameters in the two groups. Until
methodologically adequate studies are conducted, there appears insufficient
justification for a claim that lead in drinking water causes mental retarda-
tion.
Landrigan, et al., (1975c) compared children between the ages of 3 and
15 years with blood lead levels of 40-60 micrograms per 100 milliliters to
children with blood lead levels below 40 micrograms per 100 milliliters.
Higher blood lead was weakly associated with lower I.Q. and slower motor
skills, but was not associated at all with hyperactivity. Ethnicity and
socioeconomic status were controlled in this study, but unfortunately age
and sex were not. This tends to weaken the conclusions.
Another study found no relationship between blood lead and Intelligence,
reading ability, or hyperactivity (Landsdown, et al., 1974). Methodological
weaknesses make both of the above studies somewhat suspect (World Health
Organization, 1977).
Pueschel (1974) examined the neurological and psychomotor functions in
58 children with an increased lead burden 1-1/2 to 3 years after an in-depth
study of various neurological and psychomotor functions was made. Of these
children 23 to 27 percent had minor neurological dysfunction and various
forms of motor impairment during each evaluation. While the initial
psychological assessment showed low average mental abilities in the majority
of children, a significant increase in certain areas of intellectual
6.93
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functioning was observed during a follow-up examination. Unfortunately, the
control group was not administered any of the psychological tests, conse-
quently no data is offered with which to compare the results of the 58 sub-
jects. Although an improvement in certain areas of intellectual function
is reported, there was no change with respect to neurologic evaluation of
fine motor function or on the visual motor integration test.
de la Burde and Choate (1972) studied children exposed to a high-risk
lead environment with a positive coproporphyrin test but no diagnostic signs
of toxicity. They were found to have low IQ's, disturbed fine and gross
motor performance, and suspect behavioral profiles. Unfortunately blood-
lead levels or radiographic studies were not done on the children who
served as controls.
Human studies relating lead to hyperactivity are linked to animal
studies such as those of Silbergeld and Goldberg (1973, 1974) discussed in
Section 6.3.2.4.
Lead ingestion in children has been linked to minimal brain dysfunction
or "hyperkinesis" (David, et al., 1972; David, 1974b). Hyperactive children
were compared with nonhyperactive controls on two measures reflecting the
presence of body lead (blood lead levels and urinary-lead levels) following
a dose of the chelating agent, penicillamine. In this study the hyper-
active children chosen were without known psychosis or neurological disease.
The etiology of their hyperactivity was unknown. Higher lead values were
seen for both measures in hyperactive children as compared to the controls.
A total of 52 percent of the hyperactive group had blood-lead levels of 25
micrograms per 100 milliliters or above while only 25 percent of the con-
trols were in this range. Similarly, 62 percent of the hyperactive group
excreted 81 micrograms of lead per liter or above while only 13 percent of
controls were in this range. Although the differences in blood levels were
small for the two groups (26.2 for hyperactives and 22.1 for controls),
the urine lead values were 144 and 77, respectively. This supports the
authors' contention that probably many of the children had eaten paint
and dirt when they were younger and that much of the lead being stored in
the bones was subsequently released by the penicillamine treatment. It was
concluded by David (1974b) that there is an association between hyper-
activity and raised lead levels and that a large body-lead burden may
exact consequences that have been hitherto unrealized. Although this demon-
strates a (statistical) association, no inferences of causality are justified.
It may be that lead causes hyperactivity, hyperactivity causes lead ingestion,
or some third factor (e.g., low social class) is the true predictor of both
lead ingestion and hyperkinesis. Further research is necessary to determine
which of these relationships is accurate.
In order to fully appreciate the significance of the effects of lead on
the physical and mental functioning of children, the magnitude of the prob-
lem must be recognized. Knowledge of the mechanisms and toxicity of lead in
children must ultimately be applied to populations in terms of preventive
and rehabilitative care. To address these issues, the descriptive epidemio-
logy of lead poisoning in children and population based intervention pro-
grams will be discussed.
6.94
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6.4.2 Scope of Problem of Childhoad Lead Poisoning
According to McFeatters (1976), the U. S. Department of Housing and
Urban Development estimates at least 600,000 U.S. children have high levels
of lead in their blood. In 1971, a U.S. Public Health Service survey in 27
cities showed 21 percent of inner-city children had symptoms of lead poison-
ing. The National Committee for the Prevention of Childhood Lead Poisoning
believes as many as 2.9 million American children run the risk of lead
poisoning.
Accurate blood-lead determinations should provide the basis of any
mass screening for childhood lead intoxication (American Academy of Pedi-
atrics, 1969). Pending improvements in the analysis of lead in blood, the
urinary ALA test and the analyses of lead in hair offer the best substi-
tutes for the purpose of mass screening. Early detection efforts should be
directed at children 12 to 18 months of age. Each abnormal test calls for
thorough clinical evaluation of the patient and, at the very least, a con-
firmatory blood-lead determination.
In the absence of mass screening programs for lead poisoning itself,
early recognition relies on identifying the child with pica. Suspicion of
lead poisoning and indications for blood-lead analysis and other laboratory
tests include: (1) pica in the child by history or observation either in the
clinic or house; (2) symptoms of plumbism; (3) nutritional anemia, especially
after 12 months of age; (4) aberrant behavior; (5) developmental delay,
especially in speech development. Parental attributes which increase the
risk of lead poisoning in the child include: (1) a working mother who does
not monitor her toddler's activities during her absence; (2) the arrival of
a newborn infant and possible lack of attention to the toddler; (3) a
depressed, psychotic, or alcoholic mother; and (4) a history of pica in the
mother or previous children of the mother.
Childhood plumbism in the United States is largely a disease of the
big cities and especially of the inner-city areas where old deteriorated
housing prevails. The interior woodwork, painted plaster, and wallpaper
of houses built prior to 1940 may contain layers of flaking lead-pigment
paints which have never been removed. Several such flakes may contain far
more than the average daily intake of lead. Thus, children with a history
of pica are likely candidates for lead poisoning. In New York City, lead
poisoning in children used to result in deaths in about 15 to 20 percent of
cases, and to neurologic and mental disturbances from encephalopathy in
over 25 percent of cases. As shown in Table 6.23, of the more than 61,000
poisonings reported to the New York City Poison Control Center between 1954
and 1964, 3 percent or approximately 1,700 cases were due to lead (Jacobziner,
1966; Lutz, et al., 1970), and 128 of these were fatal. The apparent
increased incidence of lead poisoning (comparison of 1964 with 1954) is
believed due to the vigorous case-finding program, resulting in the dis-
covery of cases in the asymptomatic state prior to onset of encephalopathy.
The sharp decrease in the number of deaths In recent years in encouraging.
Jacobziner (1966) found that 54 percent of all deaths from lead poison-
ing occurred in 2-year-old children. Lead encephalopathy is encountered much
6.95
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Table 6.23 CASES OF CHILDHOOD LEAD POISONING
PLUS FATALITIES IN NEW YORK CITY
FROM 1954 to 1964a
Year
1954
1955
1956
1957
1958
1959
1960
1961
1962
1963
1964
Total
Cases
80
115
99
85
116
171
146
181
198
338
509
2,038
Deaths
12
18
9
9
21
12
18
6
9
7
7
128
Case Fatality
15.0
15.7
9.1
10.6
18.1
7.0
12.3
3.3
4.5
2.1
1.4
6.3
^Adapted from Jacobziner (1966) and Lutz et al., (1970)
Deaths per 100 cases.
6.96
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more frequently during the summer months but asymptomatic lead poisoning
is a year-round disease. Forty-five percent of the total cases reported
between 1954 and 1964 occurred between June and September, but the exact
reason for this is not known.
6.4.3 Massive Intervention Programs
In Baltimore the child lead-poisoning problem was first recognized in
1931, and since 1935, the Health Department's Bureau of Laboratories had
provided free blood-lead determinations to physicians and hospitals (Lutz,
et al., 1970). In 1949 a public health nurse was appointed to investigate
reported instances of abnormal lead ingestion by children and to correct
the condition. In 1951, the city adopted legislation to prohibit the use
of heavily-leaded paints for interiors of dwellings. No deaths from child-
hood lead poisoning occurred in 1965 and childhood lead poisoning cases
dropped to 32, the lowest since 1952. The Baltimore experience shows that
fatalities from lead can be reduced or prevented. Also, it demonstrates
that in an effective campaign, the number of deaths should decline as the
number of cases rise, if there is speed and efficiency of treatment.
The Chicago Board of Health in October, 1966, began a mass screening
program using a blood-lead test to detect lead poisoning in children
living in substandard conditions (Sachs, et al., 1970). Atomic absorption
spectroscopy made it possible to screen 5,000 specimens in 1 month and to
test a total of 68,744 children in 1967 and 1968 (see Table 6.24). Of the
68,744 children, 5.7 percent (3,935) had lead values of 50 micrograms per
100 grams of whole blood. Children with elevated lead values were referred
to a special clinic established by the Chicago Board of Health for the
diagnosis and treatment of lead poisoning. Twenty-nine percent of these
referrals were treated with chelating agents and the remainder were screened
periodically until their lead level returned to normal. There were no
deaths from lead poisoning among the 68,744 tested in 1967 and 1968. The
incidence of high-blood levels among children living in the same areas
declined from 8.5 percent in 1967 to 3.8 percent in 1968. Blood-lead values
were lowest in November through January and highest in June.
Guinee (1973) reports on a large screening program in New York City to
detect elevated blood-lead levels in young children. In 1971, 100,000
children, age 1 to 6 years, were tested. Two percent of these children had
blood levels of 60 micrograms or greater. Significantly elevated blood-
lead levels were found three times more often among black children than
among Puerto Rican children (see Figure 6.17). Seasonal variation of blood-
lead levels again showed a summer peak which persisted when age and race
were standardized. As would be expected, elevated blood-lead levels were
usually attributable to the ingestion of chips of old lead paint found on
the interior surfaces of deteriorating dwellings.
6.4.4 Sequellae of Excessive Childhood Lead Exposure
Albert, et al., (1974) assessed the nature and magnitude of the
deleterious health effects of overexposure to lead in children. The study
6.97
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Table 6.24 DATA OF SURVEY AREAS FOR CHICAGO BLOOD-LEAD SCREENING PROGRAM - 1967-1968a
NO
00
Urban
AIM
1
2
3
4
5
6
7
8
9
Total*
A
Number of
Children
Under 5 Years
(1960 Census)
10,000
15.100
22.00C
22,300
13.700
24.500
20.500
15,300
4, -500
147,900b
1967
B
Number
T«stedb
2,500
1,700
2,000
5,200
4,100
6.600
3,400
2,200
300
28,000
Percent
of A
25
11
9
23
30
27
17
14
7
19
Number With
High Lead6
157
73
262
509
316
393
432
218
19
2,379 •
Percent
of B
6.3
4.3
13.1
9.8
7.7
6.0
12.7
9.9
6.3
8.5
C
Number
Tested*
3,100
1.800
3.000
5.500
4,900
7,700
7.000
6.100
1.700
40,800
196S
Percent
of A
31
12
14
25
36
3^
34
40
38
28
Number With
High Lead6
53
56
166
270
142
277
356
227
9
1.556 •
Percent
of C
1.7
3.1
5.5
4.9
2.9
3.6
5.1
3.7
0.5
3.8
D
Number
Tested1*
5,600
3.500
5.000
10,700
9,000
14,300
10,400
8,300
2,000
68,800
Totals for 1967-1968
Percent
of A
56
23
23
48
66
58
51
54
44
47
Number With
High Lead0
210
129
428
779
458
670
788
445
28
3,935 -
Percent
of D
3.8
3.7
8.6
7.3
5.1
4.7
7.6
5.4
1.4
5.7
aAdapted from Lutr et al., (1970).
Figures given to the nearest hundred.
°Hlgh lead equals 50 mlcrograns lead per 100 mlllillters whole blood or higher.
-------
10
9
8
7
6
* 5
fc>
S.
Puerto Rican (5422)
Jan.
Feb.
Mar.
Apr.
May
Jun.
July
Aug.
Sep.
Oct
Nov.
Dec.
Figure 6.17 Percent of Black and Puerto Rican two-year old children
with lead level of _> 60 vg/100 ml on first blood sample,
by month, New York City, 1971. Adapted from Guinee
(1973).
6.99
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stemmed from concerns about the health of children in city slums who ingest
leaded paint, but remain asymptomatic. The health implication of rising
levels of lead in the environment from automotive emissions was also
addressed. The study sample was derived mainly from a registry of children
on whom blood-lead determinations had been made by the New York City Depart-
ment of Health, supplemented by siblings of the registry cases and children
from a lead belt area who had extractions of deciduous teeth in dental
clinics. Information was obtained through parental interview, medical
records, and psychometric evaluation. The data show that deleterious health
effects occur both in children who were treated for severe lead poisoning
and in children without diagnosed lead poisoning who had elevated blood-lead
(equal or greater than 60 micrograms per 100 grams) levels. In the absence
of diagnosed lead poisoning or elevated blood-lead levels, excess lead ex-
posure, (measured in terms of high levels of lead in teeth) was not associ-
ated with deleterious health effects.
A screening and follow-up study on children with an increased lead
burden was carried out by Pueschel, et al., (1972). In a house-to-house
survey of an impoverished section of Boston, preschool children were studied
for lead poisoning with the use of a simple and inexpensive screening pro-
cedure based upon the analysis of lead in hair by atomic absorption. Ninety-
eight of 705 children screened in this fashion were found to have an in-
creased lead burden. Chelation therapy was administered and environmental
elimination of exposure to lead-containing substances was initiated. Fiftys
eight children with an increased lead burden underwent comprehensive study
and 1-1/2 years later reexamination took place: minor neurological dys-
function and various forms of motor impairment were observed in 22 percent
to 27 percent of the children during each evaluation (Pueschel, 1974).
Initial psychological assessment revealed low average mental abilities in the
majority of children; 1-1/2 years later a significant increase in certain
areas of intellectual functioning was noted.
6.4.5 Treatment Modalities
Chelation therapy has been cited by several investigators as the method
of choice for returning blood-lead levels back to normal in cases (children
or adult) of chronic or acute plumbism. The three chelating agents used to
treat plumbism in the United States are edathamil calcium disodium (CaEDTA),
2,3-dimercaptopropanol (BAL) and d-penicillamine (PCA) (Chisolm, 1974). PCA
is available in oral dosage form only (250-mg capsules) and is classified by
the FDA as an investigational drug when used for lead poisoning. Equimolar
amounts of these agents infused in rats under identical experimental con-
ditions showed PCA to be appreciably inferior to CaEDTA and BAL in terms
of the quantity of lead mobilized and excreted. Furthermore, a transitory
Increase in the lead content of some soft tissues was noted during mobiliza-
tion with PCA, but not with CaEDTA or BAL. For all three drugs, the vast
bulk of lead mobilized was derived from osseous tissue, presumably marrow,
and the portion of lead loosely bound to bone. In children with acute
symptomatic plumbism and in asymptomatic children with greater than 100 micro-
grams Pb per 100 milliliters of whole blood, combined BAL-CaEDTA at a maximum
safe dosage is more effective than CaEDTA alone in terms of the amount and
6.100
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rapidity of diuresis of lead, reversal of metabolic abnormalities and, in
critically ill patients, survival.
In adults with mild plumbism, parenteral CaEDTA is most effective, but
oral PCA is superior to oral CaEDTA. Studies of children likewise show
that CaEDTA administered intramuscularly evokes a considerably greater
diuresis of lead than does oral PCA. The available data indicate that CaEDTA
(or BAL-CaEDTA) should be used initially as the primary drugs. As a second-
ary drug, oral PCA is both adequate and much more convenient for long-term
therapy when recurrent excessive intake can be controlled (Chisolm, 1974).
6.101
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6.5 EPIDEMIOLOGY
A wide variety of epidemiologic studies have attempted to describe and
quantify the health effects associated with lead exposure. The identifica-
tion of especially susceptible segments of the population has also been a
constant objective of these studies. Epidemiologic studies have been con-
ducted in three general types of settings based on the characteristic levels
of exposure: (1) studies of general populations in which lead exposure occurs
at ambient conditions with no unusual sources of exposure (e.g., point sources
or occupational). Inter-city comparisons are most representative of this type.
(2) Intermediate level studies which examine populations selected on the
basis of some unusual condition of exposure. Typically such persons are
chronically exposed to ambient lead concentrations higher than those of the
general population, yet substantially below industrial exposure levels.
Persons residing in close proximity to freeways, working in dense vehicular
traffic or living near smelters or other stationary sources of lead emissions
are examples of "intermediate" exposure groups. (3) Studies of occupational
groups exposed to air lead concentrations many times higher than general
populations or "intermediate" groups; these groups represent the high extremes
of the dose-response spectrum.
Attempts to establish a dose-response relationship between environmental
lead concentrations and adverse health effects and/or the relative contribu-
tion of each of the various sources of exposure to body burden have met with
only limited success. The underlying difficulty in such an analysis stems
from the multiplicity of sources of lead exposure and the difficulty in
accurately quantifying individual exposure.
6.5.1 General Populations
The risk to general populations from lead in air has become a matter of
considerably concern (and the subject of many studies) in recent years. As
Hammond (1977) has pointed out, studies of the fate of inhaled lead in man
using conventional deposition and clearance measurements have not provided
much useful information on the contribution of lead in ambient or industrial
air to the internal dose at specified air lead concentrations. A more in-
direct but nonetheless useful approach to the problem proceeds from the
assumption that the concentration of lead in the blood is proportional to the
combined level of total uptake via many modes of exposure. It follows, then,
that each environmental source (mainly air, food, and water) would contribute
to the blood lead concentration in direct proportion to the total daily lead
uptake. Although such a relationship has never been rigorously demonstrated,
the studies discussed in this section, taken together, place the contribution
of air lead to blood lead in the range of about 0.6-2.0 microgram/100 ml in
blood per microgram lead/m in air.
The earliest large-scale study of general populations was the "Three
Cities Study" conducted in Los Angeles, Philadelphia, and Cincinnati, in the
early 1960's (U.S. Department of Health, Education and Welfare, 1965). In
addition to the general population, several groups whose exposure level is
more representative of the "intermediate" exposure category (i.e., policemen,
6.102
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traffic controllers, garage employees, etc.) were also included as separate
study groups.
The principal finding was that although significant differences in mean
blood lead concentrations could not be found between the cities, persons who
lived or worked in close vicinity of dense vehicular traffic such as traffic
policemen, garage mechanics, and parking lot attendants had higher blood
lead levels than others not similarly exposed. These data are shown in Table
6.25.
Goldsmith and Hexter (1967) calculated a logarithmic dose-response regres-
sion of blood lead concentrations from air levels. The data were mean blood
lead levels and average estimated ambient air exposure from the cities included
in the "Three Cities Study" (U.S. Dept. of Health, Education, and Welfare,
1965). Under the assumption that the major source of variation in ambient air
lead was vehicular traffic, Goldsmith and Hexter calculated particle sizes and
consequent retention rates on the basis of 50-80 percent (by weight) particles
< 1.0 micrometer equivalent diameter. This is believed to be the characteristic
particle size associated with automotive emissions. In general, ambient levels
were measured by fixed samplers. Although it is recognized that they may not
be truly representative of individual exposures, the authors felt they repre-
sented reasonable estimates of population averages. Goldsmith and Hexter con-
cluded that a plotting of lead concentration in blood against lead concentra-
tion suggested a dose-response relationship. Data from four experimental sub-
jects exposed to known, high concentrations of lead sesquioxide (Kehoe, 1966)
are also plotted along the regression line to reinforce the validity of the
relationship. The regression line itself was calculated only on the basis of
the epidemiologic data, however. Figure 6.18 shows the regression line des-
cribed by the equation:
log blood lead = 1.265 + 0.2433 log atmospheric concentration.
The contribution of air lead to blood lead, as inferred from the Goldsmith
and Hexter (1967) regression, is about 1.3 microgram of lead per 100 ml of
blood per 1 microgram of lead per m in air.
The authors concluded that "the close correspondence between the experi-
mental and epidemiologic data (obtained from Kehoe, 1966 and "Three Cities
Study", respectively) make it seem likely that this relationship will be
valid for a population having a dietary, beverage and cigarette smoking in-
take similar to that of American males".
Goldsmith and Baxter's proposed dose-response regression has been
criticized on several grounds: (1) Ambient exposures were only estimates
and were not necessarily measured at the same times and places at which the
populations were exposed. Thus, air and blood levels even within the same
exposure group (data points) are not related in any consistent, specific
fashion. (2) The validity of calculating a regression line based on lead
absorption from atmospheric lead has been challenged on the basis of the
variable contribution of lead from other, more important sources of intake
such as food and cigarettes, (National Academy of Sciences, 1972). (3) The
6.103
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Table 6.25 BLOOD LEAD LEVELS OF SELECTED HUMAN
POPULATIONS*1
Type of Population
Mean Blood Lead,
yg/100 ml
Population without known occupational Male Females
exposures:
Remote California mountain 12 9
Composite rural U.S. 16 10
Suburban Philadelphia 13 13
Composite Urban U.S. 21 16
Los Angeles aircraft workers 19 17
Pasadena city employees 19 12
Downtown Philadelphia 24 18
Population with known occupational
exposures:
Cincinnati policeman
Cincinnati trafficman
Cincinnati automobile test-lane
inspectors
Cincinnati garage workers
Boston Sumner tunnel employees
25
30
31
31
30
lSource: U. S. Department of Health, Education, and Welfare (1965)
-------
oc
0.1
600
Estimated Average Respiratory Exposure, yg Pb/nf
Figure 6.18
Mean blood lead concentration for epidemiologic
and experimental respiratory exposures with re-
gression from epidemiologic data only. Redrawn
from Goldsmith and Hexter.
Source: National Academy of Sciences, (1972).
6.105
-------
authors do not describe the methods of deriving their regression line nor
do they present data on statistical tests of "goodness of fit" of the cal-
culated regression line. (4) The methods used for deriving estimated "ave-
rage" exposure levels for occupational groups (e.g., policemen, garage
workers, and tunnel workers) are described only as a weighted average of
presumed occupational and ambient exposure which were themselves estimated.
(5) There are certain difficulties in interpreting findings, especially at
the low end of the dose - response regression line. Lines representing con-
fidence limits are hyperbolic and diverge markedly when applied to extrapo-
lations at either end of the regression line; there is little validity to
extrapolations beyond the range encompassed by actual observations. For a
discussion on the matter of confidence limits calculated around a regression
line see Goldwater (1972). The NAS report also comments on this phenomenon
concluding the regression line cannot be applied with confidence to exposure
conditions affecting the general population; this also applies to the general
population of most large urban centers, inasmuch as average ambient air con-
centrations even in these centers do not generally exceed 2 micrograms per
cubic meter.
In earlier studies such as the Three Cities Study, multiple uncontrolled
variables associated with the various population groups have confused appra-
isal of actual integrated exposure and construction of the correct dose-
response relationship. Because blood lead levels are determined by many
factors in addition to respiratory absorption of lead in ambient air, the
effects of these variables must either be controlled through statistical pro-
cedures or made as homogeneous as possible in the initial selection of the
study subjects. Unless personal monitoring devices are used, one cannot
establish the total integrated exposure over months or years for police
officers, garage mechanics, "drivers", "commuters", aircraft workers or
other similar groups. Occupational factors as well as variations in diurnal
mobility patterns between individuals may markedly influence exposure level,
yet these factors are not reflected in air sampling at fixed locations.
Tepper and Levin (1972) reported the findings of a survey of air and
population lead levels in selected American communities, commonly referred
to as the "Seven Cities Study". Among the cities surveyed were Cincinnati,
Philadelphia, and Los Angeles, which had been extensively surveyed in 1961-
1962 as part of the earlier "Three Cities Study". Also included were New
York City, Metropolitan Washington (D.C.), Greater Chicago, Houston, and
Los Alamos, New Mexico. These cities were selected on the basis of popu-
lation density, level of industrialization and geographical location in
order to represent a broad spectrum of these variables. The principal ob-
jective of the study was to evaluate the relationship between atmospheric
lead levels and the concentrations of lead in blood of persons exposed to
the atmospheres in question.
The Seven Cities Study focused particular attention on the definition
of populations having a specific, consistent relationship to known air
levels of lead. Unlike the Three Cities Study, populations sampled in the
present study were women volunteers living within a prescribed distance
(within a 1-mile radius) from the reference air sampling station. Moreover,
6.106
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the blood lead and air measurements were made concurrently. By confining
the observations to members of one sex, requiring that the subject reside
not more than 1 mile from the sampling apparatus, and eliminating as com-
pletely as possible extraneous, occupational lead exposures, the authors
hoped to select a group which would accurately reflect absorption of ambient
community atmospheric lead via the respiratory system.
In addition to the groups of women described above, husbands of 100
Los Alamos participants were also included as a separate study group.
Estimates of alimentary lead intake were obtained from measurement of
the urine and feces of a subsample of 20 volunteers in each region. Each
participant collected all excrement for a 10-day period. The principal
findings were:
(1) Concerning changes in atmospheric levels of lead during the interval 1961-62
to 1968-69, the reported data demonstrate higher lead levels at most of
the study sites during the more recent of the two periods. A careful
examination of experimental methodology tends to exclude the possi-
bility that this change is an artifact reflecting changes in tech-
nique.
(2) Since the F-ratio (testing the difference in blood lead levels among
locations) was significant, individual comparisons were conducted
between urban and suburban populations in the same metropolitan areas
to examine whether or not blood lead levels reflect degree of urban-
ization for smokers and nonsmokers. In both smoking categories the
Philadelphia urban groups were higher than the suburban; the Chicago
urban groups were higher than the suburban and in New York the urban
groups were also higher than the suburban. The probability of obtain-
ing 6 relationships in this direction (urban > suburban) out of 6
comparisons is approximately equal to 1/2 = 1/64 = 0.015, if one assumes
either direction to be equally likely. Consequently, it appears that
urban blood lead levels are higher than those from nearby suburban areas.
(3) Figure 6.19 presents mean blood lead levels and corresponding mean
air lead levels at the sites where both were measured. The associa-
tion between these mean values was measured by means of the Pearson
Product Moment Correlation Coefficient and Kendall's Rank Correla-
tion Coefficient. The values obtained were 0.412 and 0.354, respec-
tively, for all data. Corresponding values for nonsmokers only were
0.400 and 0.345. The values were not significant at the 5 percent
level. It was therefore concluded that there is no association
between average blood and air lead concentrations.
(4) The observations that urban levels of blood lead are significantly
higher than suburban levels, but that air concentrations of lead are
not clearly reflected in blood lead levels generally, suggest that
other variables are more important than ambient air lead levels in
determining concentrations of lead in the blood. The precise nature
of the variables, which evidently differ in the several regions studied,
6.107
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00
o
o
0.03
- 0.02
o
o
0.01
• Los Alamos f/i
• Okeana (162)
Houston (191) •
^ — Port Woshingto
• "t£- Ardmore (15 O)
Lombard (2O8)* ~"~ Washington A
_ • Rittenhouse (L
Bridgeport f/47)*
• Greenwich Vil
• Pasadena (19;.
BLOOD LEAD LEVELS
AS A FUNCTION OF
AIR LEAD LEVELS
fj* number of people
- - 1
LO 2S) 3J3
Lead in air, yg/m^
Figure 6.19 Blood lead levels and corresponding mean air
lead levels.
Source: Adapted from Tepper and Levin, 1972.
6.108
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remains undefined. Presumably alimentary lead intake plays a signi-
ficant role; however this was not clearly evident in the short-term
metabolic study. Climatic factors may also be relevant.
(5) The analysis of fecal lead levels conducted to appraise alimentary
lead intake, did not demonstrate high or low levels compensating for
respiratory exposures so as to obscure effects of the latter.
(6) The relationship between age and blood lead level was examined by
means of regression analysis and was found to be of no general signi-
ficance.
(7) The influence of smoking upon blood lead levels was determined to be
clearly significant. The blood lead level of smokers exceeded that
of non-smokers and previous smokers. The relationship held true for
males as well as females in the husband-wife pairs in Los Alamos.
(8) The examination of blood lead levels in husband-wife pairs in Los
Alamos revealed a significant difference between males and females.
The basis for this difference was not established. Probably, it can-
not be attributed to occupational factors, for the work of each in-
dividual was characterized and conducted under comprehensive and
detailed industrial hygiene supervision. Generally, men smoke more
than do women; however, the blood lead in males remained higher than
in female smokers and non-smokers.
Since men have generally higher hematocrit levels than women and since
lead is transported in association with red blood cells, the possi-
bility exists that higher blood lead concentrations in men reflect a
higher level of circulating red cells.
Although both men and women of the studied Los Alamos couples consumed
diets presumably similar in composition, the men consumed a generally
greater quantity of food. It is therefore likely that the alimentary
exposure of men to lead may be greater than that of women.
In summary, the Seven Cities Study failed to find a significant corre-
lation between air lead and blood lead levels over an air lead range of 0.17-
3.39 micrograms/m?. Such a finding should not be unexpected, however, due
to the narrow range of ambient conditions examined, the relatively small
contribution to total intake (only about 20-30 percent) contributed by air
at such low exposure levels, and the fact that the air data were obtained
from fixed outdoor sampling stations which cannot estimate individual expo-
sure levels precisely enough.
Azar, et al., (1975) examined the effects of air lead exposure indices
of lead absorption such as blood lead, urine lead,D-ALA, (delta aminolev-
ulinic acid) and ALAD (aminolevulinic acid dehydratase) activity. Personal
air samplers were used to monitor the air lead exposure of 30 male subjects
in each of 5 locations in the United States, 24 hours a day for periods
6.109
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ranging from 2-4 weeks. During this period, blood samples were obtained for
blood lead and ALAD activity analyses and urine samples were analyzed for
lead, D-ALA excretion, osmolarity and creatinine. Smoking data was obtained
by means of a questionnaire. Two types of personal samplers were used to
quantify level of airborne lead exposure. One type of unit was equipped with
a cyclone device, which could separate respirable from non-respirable parti-
cles. These were used in the two taxicab studies. The second type was a
Case11a unit which was more portable, but since it did not have the cyclone
device, only total air lead exposure was measurable.
The five sites were selected to represent a wide range of air lead ex-
posures. Taxicab drivers were studied in Philadelphia and Los Angeles.
Participants at Starke, Florida, Barksdale, Wisconsin and Los Angeles were
thought to be representative of non-occupationally exposed groups.
The average exposure, urine and blood responses were computed for each
subject in the study. Statistical analyses were based on these within
subject averages. Site specific averages were computed based on individual
averages at each site. These were subjected to an analysis of variance to
determine whether there were significant differences between average urine
and blood responses at the five sites. The relationship between air lead
and the blood and urine responses were evaluated using regression techniques.
Homogeneity of the slopes were checked by multiple regression techniques and
the data were analysed in both natural physical units and logarithmic units
(base 10 logarithms of the natural units). The logarithmic relationship
gave the best fit to the data.
Table 6.26 shows air-lead exposure levels which were calculated by
combining the work exposure ("on duty") with the home exposure ("off duty")
on a time-weighted basis. When a cyclone device was used, the data are
referred to as "Respirable" and when not used, as "Total". Exposures
ranged from a low of 0.22 micrograms/m at Starke to a high of 9.12 micro-
grams /m obtained from a Los Angeles cab driver. Respirable air lead ex-
posures were significantly less than total exposures, indicating that a
significant quantity of the lead was contained in particles >10 microns in
diameter which do not penetrate the lung. (These large particles could be
swallowed, however.)
3
Despite air lead levels approaching 10 micrograms/m , only one individ-
ual in 150 had abnormal blood or urine levels. The source of exposure in
this case was not lead from ambient air but rather from moonshine whiskey.
(This subject was not included in subsequent analyses.) Statistical anal-
ysis of the site specific data showed that there was no significant correla-
tion between air and blood lead at any of the five sites, indicating either
(1) that there is in fact no correlation between air lead and blood lead,
or (2) thirty subjects is too few to demonstrate significance, or (3) the
range of data is too narrow to show significance, or (4) variables other
than air lead (e.g., lead ingested from food and drink) are overwhelming
any effect which air lead might have on blood lead. An analysis of the data
for 149 of the subjects using a multiple regression technique indicated that
variables other than air lead were affecting blood lead.
6.110
-------
TABLE 6.26 MEAN SUBJECT AIR LEAD EXPOSURE
a\
Lead Concentration, ug/m
On Duty
Site
Philadelphia, Pa
Cab drivers
Starke, Fla.
Barksdale, Wise.
Los Angeles, Calif.
Cab drivers
Los Angeles, Calif.
Office workers
Total
5.10 ±
2.01 +
2.84 +
9.42 +
3.05 +
1.11
2.52
5.19
.98
.76
Respirable
4.
1.
N.
7.
N.
34+ .86
39 + 2.39
D.b
48 + .92
D.
± 1 S.D.
Off Duty
Total
1.48 +
0.37 +
0.36 +
4.22 +
3.07 +
.23
.31
0.14
1.28
.81
Combined Exposure
Total
2.62 +
0.81 +
1.01 +
6.10 +
3.06 +
.42
.82
1.43
1.02
.75
Respirable
2
0
N
5
N
.37 +
.64 +
.D.
.37 +
.D.
.34
0.78
1.02
aSource: Azar et al. Reprinted from Lead: Environmental Quality and
Safety Supplement, Vol 2, T.B. Griffin, and J. H. Knelson (Eds.)
(c) George Thiem Verlag, Stuttgart (1975).
bN.D. = Not determined.
-------
Figure 6.20 shows that the data tended to clump into 5 subgroups by
location. The average relationship between air lead exposure and blood
lead concentration was obtained by drawing a line with a slope of 0.153
through the average blood lead concentration for 149 subjects. The result-
ing line was defined by the equation: log blood Pb = 1.2257 + 0.153 log
air Pb. The slope of this regression was significantly (p < 0.01) differ-
ent from zero (95 percent Confidence Limits, C. L. = + 0.079). Approxi-
mately 56 percent of the variance in blood Pb is not explained by air Pb
(R = 0.436). Figure 6.20 also shows the regression lines obtained when
the data from all sites are combined and adjusted to a common slope of
0.153. This is justified since the slopes are homogeneous. There was a
significant correlation between log air lead level and log blood lead
level after pooling data from all sites. The contribution of air lead to
blood lead was found to be approximately 1.0 microgram of lead per 100 ml
of blood per 1 microgram per m of air over the range of air lead concentra-
tions studied. This estimate is somewhat less than that estimated from
Goldsmith and Hexter's (1967) equation (i.e., 1.0 vs. 1.3 microgram/100 ml
for each 1 microgram lead in air, respectively).
The slope of this regression line (0.153) is less than that found by
Goldsmith and Hexter (1967) and considerably less than that based on the
theoretical calculations of the Environmental Protection Agency shown in
Figure 6.22 as "EPA line".
Hammond (1977, personal communication) has applied the mathematical
model described by Azar, et al., (1973) to empirical data published by
Rabinowitz (1974); Griffin, et al., (1975); Fugas, et al., (1973); Prpic-
Majik, et al., (1973); and Williams, et al., (1969) in order to compare
actual data to predictions derived from the model.
The regression equation developed by Azar, et al., (1973; 1975) is as
follows:
3
log PbB = 1.226 + 0.153 • log microgram Pb/m
where
PbB . = blood lead level
Pb/m = air lead level.
This equation says, in effect,-that for this particular population
the average PbB at 1 microgram Pb/m was:
log PbB = 1.226 = 16.8 microgram/100 ml
3
since the term (0.153 • log microgram Pb/m ) reduces to zero when air Pb = 1
microgram/m .
For any other population under study, the constant for PbB at air lead =
1 microgram Pb/m will be unique to that population and will depend upon all
sources of lead intake. In order to solve for the constant describing log
6.112
-------
f
8
7
6
5
0»
O
o
1
"S 8
J 7
00 6
5
4
10°
^1
Log Blood Pb*l.226 + 0.153 Log Air Pb
0
e ~—
f • • • •
o —..—
Legend
Within Site Slope
Phila. Cab
L.A. Cab
L.A. Office
Barksdaie.Wis.
Starke.Fla.
E.P.A. Line
icr'
5678910° 2
Total Air Lead,/ig/m*
4 5678 9K)1
Figure 6.20 Blood lead versus total air lead
Source: Azar, et al, Reprinted from Lead: Environmental
Quality and Safety Supplement, Vol. 2.
T. B. Griffin and J. H, Khelson (Eds.)
(c) George Thiem Verlag, Stuttgart, 1975.
6.113
-------
3
PbB at 1 microgram Pb/m , baseline PbB at a known small air lead concentra-
tion can be used. Taking an example, Coulston, et al., (1972) determined
PbB in a group of men known to breathe air lead at 0.2 microgram/m through-
out the day. Solving for the term bina = b+c,
a = log observed PbB
b = unknown constant
c = 0.153 • observed air lead, microgram Pb/m .
Using the Azar model, it is necessary to calculate a new constant for
any particular group, log PbB at 1 microgram Pb/m . In Table 6.27 the base-
line data_for PbB at low, known air lead is given. Data for log Pb at 1 micro-
gram Pb/m are then calculated. This is the constant b described above.
3
Using the calculated constant for log PbB at 1 microgram Pb/m , the pre-
dicted PbB at the high air lead concentration is compared to the actual PbB
measured. Finally, the contribution of air lead to PbB as actually observed
is given.
Predictions are also provided for PbB's at several air lead concentra-
tions breathed for 40 hours per week against a background PbB of 23.5 with
an assumed nonoccupational air lead of 1 microgram/m .
It is evident from these data that the Azar model for regression of PbB
on air lead predicts fairly accurately the group mean PbB's which have actu-
ally been observed among workers and human volunteers whose air lead expo-
sures were fairly accurately known. It is also evident that as air lead
increases, its impact on PbB, as designated in the last column of the table,
becomes progressively smaller. Thus, excursions of air lead exposure over
the suggested maximum of 100 microgram/m would likely have only modest
impact on the internal dose as reflected in PbB's. The physiological basis
for such a phenomenon is not known.
Certain seeming discrepancies occur in,Table 6.27. For example, an
average air lead exposure of 27 microgram/m (Prpic-Majic, 1973; Fugas, 1973)
yields a predicted PbB of 46.8 while an average air lead exposure of 72.2
microgram/m is predicted (last horizontal column) to yield a somewhat lesser
PbB of 45.2. This discrepancy is due to the fact that in the former case
PbB at 1 microgram/tn is 28.3 (antilog 1.4513) while in the latter case it is
only 23.5. This only serves to highlight the fact that the impact of air lead
on blood lead is very much dependent upon the background of non-air sources of
lead.
It may be argued that the Azar model is invalid for industrial situa-
tions in which the particle size range and chemical composition of the lead
aerosols may be quite different from those encountered in the general ambient
air situation prevailing in the Azar study. Nevertheless, predicted values
based on the Azar regression equation are quite consistent with the limited
experimental data available concerning industrial exposure.
While all of the studies presented in this section have some objectionable
features the estimates of the contribution of air lead to blood lead which
-------
Table 6.27 THE IMPACT OF AIR LEAD ON BLOOD-LEAD LEVELS; A COMPARISON OF ACTUAL DATA
TO PREDICTIONS USING MATHEMATICAL MODEL3»b
o\
•
H
H
Baseline
PbB at
11.2
21.8
20.1
22.1
22.1
23.5
23.5
23.5
23. 5C
23. 5d
23. 5e
23. 5f
•*/.'
0.2
0.2
0.2
0.2
0.2
1.0
1.0
1.0
1.0
1.0
1.0
1.0
log PbB at
1 ug Pb/m3
1.1561
1.4454
1.4101
1.4513
1.4513
1.3711
1.3711
1.3711
1.3711
1.3711
1.3711
1.3711
"High" Air Exposure
Hg Pb/m3
1.6
3.2
10.9
35
27
51
37
33
24.6
36.5
48.4
72.2
log (ig Pb/m3
0.2041
0.5051
1.0374
1.5441
1.4314
1.7076
1.5682
1.5185
1.3909
1.5623
1.6848
1.8585
PbB
Predicted
15.4
33.3
37.1
48.7
46.8
42.9
40.8
40.1
38.4
40.7
42.5
45.2
Actual
12.9
27.6
36.4
44.3
42.9
50.1
39.7
39.5
—..
-_
__
--
M-g PbB/
Hg/m3
1.2
1.9
1.5
0.64
0.78
0.53
0.45
0.42
_..
--
_.
—
Reference
Rabinowitz, 1974
Griffin, et al.
Ditto
1975
Fugas, et al., 1973
and Prpic-Majic,
et al., 1973
Ditto
Williams, et al.
Ditto
"
, 1969
Source: Hammond, P. B. (1977, personal communication).
bAzar, et al., 1973.
Prediction assuming inhalation of 100 Hg/m3 air lead 40h/wk. + 1 M-g/m3 for remainder of week (128 h)
(avg. » 24.6 3
Prediction assuming 150 Hg/m 40h/wk. + 1 ug/m3 128/wk. (avg. =36.5 Hg/«3) .
Prediction assuming 200 Hg/m3 40h/wk. + 1 ng/m3 128/wk. (avg. - 48.4 Hg/m3).
Prediction assuming 300 M«/m3 40h/wk. + 1 ^g/m3 128/wk. (avg. - 72.2 |ig/m3).
-------
they have provided are remarkably consistent. These estimates suggest that
each microgram/m of lead in air contributes approximately 0.6 to 2.0 micro-
gram lead per 100 ml of blood. These data are also in agreement with esti-
mates derived from occupational groups presented in Section 6.5.3.
6.5.2 Intermediate Levels of Exposure
Studies of persons regularly exposed to unusually high ambient lead
concentrations (over 10 microgram/m for all or part of the day) both from
mobile and stationary sources have been much more successful than general
population studies in demonstrating relationships between levels of lead in
air and those in blood. Actually, it is only under these circumstances that
respiratory intake of lead accounts for an appreciable percentage of total
absorption. It should be mentioned that few of the persons in the inter-
mediate category are exposed to sustained levels of over 10 microgram/m for
more than a few hours a day.
Chronic exposure to intermediate levels of lead from mobile sources may
occur either as a result of residing in close proximity to high traffic
density (i.e., freeways) or from occupations which involve exposure to above
average amounts of automotive exhaust either indoors or outdoors. Police-
men, taxi drivers, garage attendants and mechanics are the most common ex-
amples. Populations residing near stationary sources of lead emissions such
as primary and secondary smelters and battery plants have also been studied.
The effects of exposure to higher than average amounts of lead among the
Wenatchee orchardists and their families have also been reported.
6.5.2.1 Mobile Emissions Sources—
Thomas, et al., (1967) attempted to determine-whether persons living near
freeways in Los Angeles County have increased levels of lead in blood. Fifty
adults who had resided for at least 3 years within 76.2 meters (250 feet) of
a freeway were compared with 50 who had resided for a like period near the
ocean or at least 1.6 kilometers (1 mile) from a freeway. Average blood-lead
levels were substantially higher in the population sample living near the
freeway. However, blood-lead levels of these individuals were similar to
other Los Angeles populations and lower than those reported for some other
urban populations. The observed difference between the two population samples
is consistent with the existence of coastal-inland atmospheric lead and blood-
lead gradients within the Los Angeles Basin.
The effect of distance of residence from highways upon blood-lead levels
among black females has been investigated (Daines, et al., 1972). Average
annual air-lead levels on the front porches of homes located 3.7, 38.1, and
121.9 meters away from a highway were 4.60, 2.41, and 2.24 micrograms per
cubic meter, respectively. There was no significant difference between the
outside air-lead concentrations at 38 and 122 meters, but both were different
from the air-lead concentration at 3.7 meters from the highway. This rapid
nonlinear decrease in airborne lead with distance from the source has been
observed for mobile as well as stationary lead sources. Concentrations of
lead in dustfall also decrease rapidly with increasing distance from the
6.116
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source. Average annual air-lead levels in the front room of houses at the
three sampling points also reflected this nonlinear decrease, being 2.3,
1.50, and 1.57 micrograms per cubic meter as the distances increased.
Average blood-lead levels in the study subjects were 23.1, 17.4, and
17.6 micrograms of lead per 100 grams at 3.7, 38.1, and 121.9 meters,
respectively. The average blood-lead levels at the two more distant sam*-
pling sites differed significantly from the average at 3.7 meters, but did
not differ significantly from each other.
Among the homes closest to the highway (3.7 meters), air-lead and
blood-lead levels were significantly lower for subjects whose homes were
air-conditioned than for similar subjects in homes without air-conditioning.
Significant differences in air-lead, but not in blood-lead levels were ob-
served for subjects in homes at 33.4 and 457 meters from a turnpike. The
average outdoor air-lead levels at 33.4 meters and 457 meters were 1.95 and
1.73 micrograms per cubic meter; blood leads at these sites averaged 15.7
and 16.1 micrograms per 100 grams, respectively. In this experiment the
air-lead levels, though statistically different, would not necessarily be
reflected in higher blood-lead levels, because daily respiratory lead ab-
sorptions nearer the turnpike would only amount to about 1 microgram of
lead per day more than at the distant site (U.S. Environmental Protection
Agency, 1972).
Groups exposed to above-average amounts of automotive exhaust outdoors,
such as policemen, may or may not have lead levels above those of comparable
nonexposed groups according to a U.S. Environmental Protection Agency (1976)
report. Differences, when present, are small (10 to 20 percent), but ranges
are sometimes above normal limits. However, groups similarly exposed indoors
(U.S. Dept. of Health, Education and Welfare, 1965; Tola, et al., 1972;
Gothe, et al., 1973) such as parking garage employees, consistently have 20
to 40 percent higher levels than ordinary groups and a greater number of in-
dividuals with above-normal levels (blood lead of 40 microgram/100 ml or
higher). Groups exposed in automotive repair facilities (U.S. Dept. of
Health, Education and Welfare, 1965; Tola, et al., 1972) consistently have
higher levels (20 to 100 percent higher) because exposure to solder, bat-
teries, etc., is added to exposure to automotive exhaust. The range of
levels is increased, and many are above 40 microgram Pb/100 g blood, as shown
by the Three Cities Study.
Lawther, et al., (1972) studied airborne inorganic lead and its uptake
by inhalation using three different types of data: (1) measurements of air-
borne concentrations of inorganic lead compounds taken in a busy London
street and at a control site away from traffic, (2) measurements of the
blood-lead concentrations in London taxi drivers using day workers as the
test group and night workers as the controls; and (3) visual appearance of
particles collected from the general atmosphere of London, from a busy
London street and from the exhaust gases of petroleum and diesel engines.
Blood-lead and carboxyhemoglobin levels were studied among London taxi
drivers on both the day and the night shift. Significant differences were
6.117
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found in blood carboxyhemoglobin, but not in blood-lead levels, when com-
paring smoking and non-smoking day-shift drivers to similar night-shift
drivers. Lawther, et al., (1972) concluded that the day drivers had a
greater exposure to motor car exhaust than the night-shift drivers because
they had significantly higher blood carboxyhemoglobin levels and therefore
"it would seem that little of the lead found in their blood is attributable
to the lead they inhale while driving in London streets". Unfortunately,
both differences in smoking intensity between smoking groups, as well as
actual differences in air and dietary lead exposure could explain these
results and neither was measured. Furthermore, information was not obtained
regarding the exposure of the drivers when they were off duty (U.S. Environ-
mental Protection Agency, 1972). Thus, the relative contribution of auto-
motive exhaust versus other sources of lead remains unresolved.
Iwata, et al., (1971) described the effects of lead in auto exhaust
on traffic controllers. The study measured lead in areas representative of
the controller's work environment, along with medical examinations for signs
of lead toxicity. Lead concentrations in air ranged from 3.3 micrograms per
cubic meter to 9.6 micrograms per cubic meter. Medical examinations were
carried out on 17 traffic controllers (Group I) and 14 indoor policemen
(Group II). Subjective symptoms included headache and nettle rash, sore
throat, nausea, constipation, lumbago, and dizziness. More complaints were
found in Group I. No difference was found between the two groups in terms
of whole blood specific gravity, amount of blood pigment, and punctate,
basophilic erythrocyte level. A coproporphyrin test of the urine of one sub-
ject in Group I was positive. The average level of lead in urine ranged from
14.1 to 25.9 micrograms per liter in Group I and 10.4 to 26.2 micrograms per
liter in Group II. The average level of lead in blood ranged from 12.3 to
24.5 micrograms/100 ml in Group I and 10.1 to 17.3 micrograms/100 ml in
Group II, indicating slightly higher levels in Group I, however, these
differences were not large enough to be statistically significant.
Landrigan, et al., (1975b) discovered three cases of mild lead poisoning
among instructors at an indoor pistol range. These cases were characterized
by blood-lead levels greater than 100 microgram/100 ml of blood, free erythro-
cyte protoporphyrin levels greater than 450 micrograms/100 ml of red blood
cells, abdominal pain, and, in one instance, by slowing of motor and sensory
nerve conduction velocity. Fragmentation of bullets during firing, explosive
vaporization of primer, and aerosolization of lead suboxide particles during
bullet molding appear to have been the major sources of airborne lead.
6.5.2.2 Stationary Emissions Sources—
Stationary sources of lead emissions can be divided into three cate-
gories :
(1) Primary smelters where ore is processed. Because lead ore
generally will contain other metals (such as zinc, cadmium,
bismuth, and arsenic), effects observed in exposure studies
may not always be caused by lead alone.
6.118
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(2) Secondary lead smelters and lead processing plants.
(3) Miscellaneous sources. These may include industrial processes
where the main objective is not to obtain or process lead. An
example is the recovery of copper from cables coated with poly-
vinyl chloride plastic, during which lead from the plastic may
be released.
A recent Environmental Protection Agency report has summarized the
studies which have examined the effects of lead exposure on persons resid-
ing near stationary lead emitting sources (U.S. Environmental Protection
Agency, 1976). Extensive investigations of the effects of lead exposure
on people living near primary smelters have been performed in El Paso,
Texas; Helena Valley, Montana; Kellogg, Idaho,; and the Meza Valley in
Yugoslavia. Highlights of each of these studies will be discussed briefly.
The smelter at El Paso, Texas, has been operating since the late 1800's
and produces not only lead but also copper and zinc (Landrigan, et al.,
1975a; Texas Morbidity and Mortality Weekly Report, 1973). In addition to
these metals, cadmium and arsenic are known to be emitted. The estimated
lead emissions were 292 metric tons in 1969; 511 tons in 1970; and 312
tons in 1971. These figures, however, are only for stack emissions; it
is not known how much lead may have been emitted from fugitive emissions
via ventilation, windows, etc.
The areas studied included the so-called Smeltertown Section, a resi-
dential area less than 183 meters (200 yards) west of the smelter as well
as some nearby communities farther downwind known to be impacted by the
smelter emissions. The concentrations of lead in air are presented in detail
by The U.S. Environmental Protection Agency (1976) and in the published reports
referred to above. Daily lead^concentrations in Smeltertown in 1972 ranged
from 0.49 to 75.0 micrograms/m . For 86 sampling days in 1972, the average
level was 6.6 micrograms/m . Air lead levels fell off rapidly with distance,
reaching background values at 4 to 5 km from the smelter. High concentra-
tions of lead were found in the soil, being greatest in the area nearest
the smelter (geometric mean 1791 ppm lead). High concentrations of lead in
house dust were also found, ranging from 400 to 58,800 ppm.
Determinations of lead in blood showed that 70 percent of children 1
to 4 years old living nearest the smelter had concentrations > 40 micrograms/
100 ml; whereas high blood levels were not so common in older children and
adults. Children with blood-lead levels of 40 micrograms/100 ml or above
lived in homes where the geometric mean lead content of house dust was 6450
ppm compared to 2070 ppm for children with blood-lead levels under 40 micro-
grams/100 ml. Landrigan, et al., (1975a) concluded that the main factor
causing elevated blood levels in these children was ingestion or inhalation
of dust containing lead. Data on dietary intake of lead have not been ob-
tained, but because the climate in El Paso and the nearness to the smelter
prevents any farming in the area, it is probable that the lead intake via
food for this study population does not differ markedly from other areas in
El Paso (U.S. Environmental Protection Agency, 1976).
6.119
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A smelting complex in East Helena, Montana, also has been investigated as
a source of airborne lead pollution. Zinc, cadmium, and arsenic are known
to be emitted in addition to lead. The precise quantity of lead emissions
is not known (U.S. Environmental Protection Agency, 1976).
Air concentrations of lead were measured in 1969, and in East Helena
the average concentration at several stations varied from 0.4 to 4 micro-
grams/m ; the maximum 24-hour value was found to be 15 micrograms/m . In
the further distant city of Helena, the average concentration was 0.1 micro-
gram/m . Lead in soil was found to be 4000, 600, and 100 ppm at distances
of 1.6, 3.2, and 6.4 km (1, 2, and 4 miles), respectively, from the smelting
complex; whereas, in uncontaminated soil near the Helena Valley it was 16
ppm., Deposited lead (dustfall) was found to vary from 3 to 108 mR/m2/month
in East Helena; whereas, in Helena it varied from 1 to 7 mg/m2/month.
Studies on humans were limited to children; lead in hair and blood
were found to be higher in East Helena than in Helena. Averages were 15.6
and 11.6 micrograms/100 ml in blood and about 40 and 13 ppm in hair (Hammer,
et al., 1972). Both blood lead and hair lead findings are suggestive of
greater lead exposures near the smelter. The blood values indicate that
lead absorption, although elevated near the source, was within normal limits.
No adverse health effects on these children have been noted.
The U.S. Environmental Protection Agency (1976) reported preliminary
data on air lead in the vicinity of a lead-zinc smelter at Kellogg, Idaho,
which showed that during 6 months in 1921 the average concentration of lead
in air was between 6 and 8 micrograms/m . Children from this area had a
mean blood level of 20.9 micrograms/100 ml and a mean hair-lead level of
about 100 ppm. Based on air lead determinations, the exposure seems to be
about twice as high as in East Helena, which is supported by the finding
that lead in hair was twice as high. This exposure resulted in about 5
micrograms/100 ml higher lead values in blood. Subsequent studies in Kellogg
indicated that 22 percent of children 1 to 9 years of age living within 1
mile of the smelter had blood lead levels of 80 micrograms/100 ml or higher
and that all but one child in this area had a blood-lead level of at least
40 micrograms/100 ml (Anon., 1974).
Another survey in the area showed elevated blood lead levels in a high
percentage of children living as far as 4.02 km (2.5 miles) from the smelter.
A possible explanation for the difference in the surveys is that the earlier
study involved primarily fourth-grade boys, whereas the second included
mainly younger children. Moreover, two different laboratories whose quanti-
fication techniques have never been compared were used for the analyses
(U.S. Environmental Protection Agency, 1976).
At the 300-year-old "Mezica" lead-zinc mine in Yugoslavia, a smelting
plant was constructed in 1896. This caused considerable lead contamination
of the topographically closed, long valley of the Meza river. Consequently,
for many generations inhabitants have had lifelong exposure to relatively
6.120
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high ambient lead. From 1968 a broad ecological and epidemiological study
was conducted on a population composed mostly of women and children (Graovac-
Leposavic, et al., 1973). The aims of this study were:
(1) To determine whether the population is unduly exposed to lead;
(2) To establish the level of the exposure in relation to the geo-
graphic location to the source of contamination;
(3) To discover the integrated lead exposure (lead body burden)
from birth; and
(4) To find out by medical, biochemical and toxicologic methods any
possible effects attributable to lead exposure.
For detailed study 286 persons were selected, together with 52 controls.
Medical, biochemical, toxicological, hematological and genetic investigations
were performed.
Many tests for evaluation of body burden were applied. The authors
felt that determination of ALA represented the most suitable test. To estab-
lish integrated exposure, lead mobilization by CaEDTA injection was performed
in 209 persons. It was established that lead body burden in exposed persons
was up to 10 times higher than in unexposed controls.
Of 15 randomly selected persons, 13 showed some chromosome aberrations
in the lymphocytes of the blood, which seems to be characteristic for lead
effects. Applying the methods on the exposed population in the valley, it
was not possible to reveal any express clinical signs of lead toxicity. The
most significant changes were established in the enzyme system of porphyrin
biosynthesis, chromosome aberrations and lead body burden.
It is clear from the preceding discussion that emissions from primary
smelters may cause elevated blood levels and other signs of increased lead
burdens in populations living near the emission sources. In El Paso and
Kellogg, fairly high concentrations in blood of children in these areas were
associated with increases in ALA excretion. Emissions from the El Paso
smelter seem to have been of the same magnitude as those from the Meza
smelter, but much higher air-lead concentrations have been found in Meza,
probably as a result of different meteorological factors. Elevated lead
levels in blood and urine and increases in ALA-U are, of course, results of
lead exposure. Other reported symptoms, such as bone pains in Meza Valley,
are probably not caused by lead. As pointed out earlier, primary lead
smelters emit other metals, and nonspecific effects may well be caused by
these or other contaminants (U.S. Environmental Protection Agency, 1976).
Efforts should be made to separate effects of such contaminants from lead
effects.
A recent EPA report (U.S. Environmental Protection Agency, 1976)
investigated mortality patterns in counties containing primary smelters in
comparison with contiguous, non-smelter counties to determine whether
smelter emissions produced any noticeable health effects in terms of disease-
specific mortality.
6.121
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Several findings were consistent among all, or most of the sites ex-
amined. A majority of smelter counties showed an excess of deaths from 5
categories of deaths:
(1) All causes combined
(2) Cancer of the liver and biliary passages
(3) Cancer of the trachea, lung and bronchus
(4) Cancer of the kidney
(5) Cancer of the bladder.
Excesses from other (non-cancer) causes of death were frequently found in
one or two of the smelter counties. These excesses were predominantly
from respiratory diseases such as bronchitis, emphysema, asthma and pneu-
monia. Excess deaths from arteriosclerosis and small vessel disease were
also seen in some smelter counties, however this pattern was not consistent.
These findings are interesting in view of the fact that traditionally,
lead has not been thought to be a carcinogen in man, although it has been
shown to induce cancer in rodents.
Two major faults emerge in this study, however. The first is the possi-
bility that the effect is real (i.e., there is a genuine excess of cancer)
but these effects might be attributable to factors other than lead. For
instance, a variety of other carcinogens are known to be present in smelter
emissions. Secondly, the study was unable to adjust for certain demographic
factors which are independently associated with cancer risk (population,
population density, income, race, education, and socioeconomic status). There-
fore one has no assurance that smelter and non-smelter counties are comparable
with respect to these factors. Findings from this study should be viewed
with skepticism, however, this type of approach offers some possibilities if
an adequate study design could be developed.
A good example of exposure from secondary smelters has recently been
given by Nordman, et al., (1973). A random sample of 621 individuals 16
years old or older in an area near a secondary smelter in Finland was selected.
Three hundred and thirty four individuals responded, of whom 41 were rejected
for various reasons. Lead and ALAD in blood were determined in the remaining
293 individuals. The results were related to distance from the source and
to dustfall levels of lead, which had been determined at 80 stations during
a 1-month period. Significant negative correlations were found between
distance from source and lead or ALAD in blood. This was especially pro-
nounced in a group of women who spend most of their time at home. On a group
basis, lead in blood was also found to be correlated to dustfall. However,
blood-lead levels were generally below 30 micrograms/100 ml, and only in a
group of males living in a zone where the dustfall was about 100 mg/m /month
was the average 30 micrograms/100 ml. This dustfall is of the same magnitude
as reported from East Helena.
Exposure from both a primary and secondary smelter in the inner city
area of Omaha, Nebraska, has been reported (Mclntire and Angle., 1972; Angle
and Mclntire, 1974). In the report, the authors did not take into account
6.122
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traffic density, but in a more recent study they concluded that elevated
blood levels of lead could be related to proximity to a battery plant,
traffic density, and substandard housing. (U.S. Environmental Protec-
tion Agency, 1976).
Martin (1974) reported an epidemiological survey of lead works of
various types to determine possible adverse health effects on mothers and
children living in the area. At a point approximately 100 meters from the
factory chimney, average atmospheric lead concentrations of 3.0 micrograms/
m were found. Occasional 24-hour concentrations ranged up to a maximum
of 28 micrograms/m . An extensive series of measurements of lead deposits
was made in the vicinity and monthly figures of up to 392 micrograms/m were
found; environmental dusts contained concentrations of up to 5 percent, and
soil concentrations ranged from 0.15 to 4.9 percent.
Initial results indicated that of 39 children under the age of 5 years
living within 400 meters of the factory, 41 percent had blood levels of
above 40 micro grams/100 ml whereas of 80 children living in the 400- to
500-meter range of the factory only 13.7 percent had blood-lead values above
this level. Similarly, of 252 children attending local schools, 17 percent
(44 children) were found with blood levels above 40 micrograms; 6 of these
were over 60 micrograms. Of the 26 mothers living within the 400-meter
range, 3 had blood-lead levels over 40 micrograms/100 ml, whereas of 53
living in the 400- to 500-meter range none exceeded this level. Three of
the 4 children under school age with the highest blood leads, (75, 74, and
65 micrograms/100 ml), were living close to the works and 2 of these had
fathers working there. In the third, the child's only known exposure to
abnormal quantities of lead was the result of his proximity to the works.
In the fourth, who lived in the 400- to 500-meter range, there was evidence
of pica. Where raised blood levels were found, investigations were carried
out in the home to exclude as far as possible sources of raised lead intake
other than'.those derived from the factory. Apart from the occasional case
of pica, no abnormal source was established. Thus, the principal cause of
the raised levels was presumably emissions to the atmosphere from the factory,
windborne dusts, or dusts from vehicles entering and leaving the works, or
lead taken home on the person or clothing of a parent working in the factory,
as described in Section 6.5.3.1.
Roberts, et al., (1974) report on the dispersal of lead and associated
health effects of lead contamination near two secondary smelters located in
different parts of Toronto. Each smokestack is about 100 meters south of a
residential area and 100 to 200 meters north of an elevated expressway
carrying 50,000 to 150,000 cars per day. Lead emissions from the two
smelters were estimated at 15,000 to 30,000 kilograms per year. The high
rate of lead fallout around the secondary lead smelters was attributed to
episodal large-particulate emissions from low-level fugitive sources rather
than from stack fumes. The lead content of dustfall, and consequently that
of soil, vegetation, and outdoor dust, decreased exponentially with distance
from the two smelters.
6.123
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Blood samples were collected from 286 people close to the first smelter,
1425 people close to the second smelter and 1231 people in a similar socio-
economic urban control group. To determine the major source of increased
lead absorption, blood and hair samples were obtained from 16 families
living within 15 meters of the first smelter and 8 urban control families liv-
ing in houses of similar age and upkeep. Lead content of potential sources
of lead exposure in the smelter area and in the urban control group are shown
in Table 6.28.
Between 13 and 30 percent of the children living in the contaminated
areas had absorbed excessive amounts of lead (more than 40 micrograms/100 ml
of blood and more than 100 micrograms/gram of hair) as compared with less
than 1 percent in a control group. A relationship between blood and hair
was established which indicated that the absorption was fairly constant for
most children examined. It seemed that the ingestion of contaminated dirt
and dusts rather than "paint pica" was the major route of lead intake.
Metabolic changes were found in most of the 21 children selected from those
with excessive lead absorption; 10 to 15 percent of this group showed subtle
neurological dysfunctions and minor psychomotor abnormalities.
The total population of children under the age of 17 living in a working
class area exposed to undue amounts of lead from lead smelter was examined in
an investigation of the relationship between blood-lead levels, general
intelligence, reading ability, and rate of behavioral disorder (Lansdown, et
al., 1974). As shown in Tables 6.29 and 6.30, these investigators found that
distance from the factory producing the lead pollution was related to blood-
lead level and any measure of mental functioning. Lower levels of intelli-
gence and higher rates of disturbance were attributed to social factors,
rather than excessive lead exposure.
Both Roberts, et al., (1974) and Landrigan, et al., (1975a) showed that
children living in close proximity of ore smelters have elevated blood lead
concentrations. Also, both studies found that lead in soil, in dustfall and
in the blood of children were strongly correlated with distance from the
smelter stack.
In addition, Roberts, et al., (1974) linked their findings of behavioral
abnormalities (hyperkinesis) among children hospitalized for excessive lead
absorption with similar findings of David (1974a,b). Roberts, et al., how-
ever, do not define the clinical diagnostic criteria used to classify the
children as hyperactive in their study. Thus, while there seems to be
reason to suspect that there may be a relationship between elevated blood
lead and hyperkinesis, inadequacy of study design and/or ill-defined criteria
for diagnosing hyperactivity have been serious shortcomings of past studies.
For this reason, many experts relegate these findings to unconfirmed reports
requiring scientific documentation in future studies.
6.5.2.3 Miscellaneous Sources—
There have been very few epidemiologic studies of groups exposed to
lead in which a large number of factors were documented and the results in
6.12U
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Table 6.28 LEAD ACCUMULATION BY PEOPLE LIVING CLOSE TO A
SECONDARY SMELTER COMPARED TO AN URBAN CONTROL
GROUP, AND SOME POTENTIAL SOURCES OF LEAD UPTAKE3
Matrix Units
Blood (ug/100 ml)
Hair (ug/g)
Tap water (yg/
liter)
Paint (percent
by weight)
2
Dustfall (mg/m
per 30 days)
Suspended parti-
cles (ug/m3)
Outdoor dust
(ug/g, D.W.d)
House dust
(ug/g, D.W.)
Garden soil
(ug/g, D.W.)
Vegetables, washed
Lettuce leaf
(ug/g, F.W.e)
Radish tuber
(ug/g, F.W.)
Tomato fruit
(ug/g, F.W.)
A.M.b
31
52
6.8
1.23
553
3.84
5828
2055
2626
8.6
4.6
0.33
Smelter
G.M.C
27
41
5.9
0.72
158
3.01
2416
1550
1715
2.9
1.7
0.32
Area
Range
12-61
14-166
2-14
0.13-4.64
35-2334
1-10
578-39,500
470-8400
355-8750
0.7-40
0.6-28
0.25-0.40
Urban
A.M.
19
17
1.40
1.30
25
0.93
1002
845
110
0.9
0.3
0.24
Control Area
G.M.
17
13
1.3
0.89
23
0.82
924
713
99
1.0
0.3
0.23
Range
8-40
3-39
1-2.4
0.11-2.62
17-36
0.30-2.54
500-1561
351-2010
57-240
0.8-1.1
0.2-0.4
0.10-0.30
•a
Source: Roberts, et al. Reprinted with permission from Science.
(c) American Association for the Advancement of Science, 1974.
Arithmetic mean.
c
'Geometric mean.
Dry weight.
Fresh weight.
6.125
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Table 6.29 BLOOD-LEAD LEVELS IN SCHOOL-AGE CHILDREN
AS A FUNCTION OF THEIR ADDRESS*»&
Distance from
Factory, m
0-100
100-200
200-300
300-400
400-500
Blood-Lead, ug/100 ml
Number
3
27
58
88
30
Mean
40
37
32
32
10
S.D.
15
12
8
5
10
Range
28-57
22-65
18-60
23-45
15-63
aSource: Landsdown, et al. Reprinted, with
permission, from Lancet, (c) The Lancet, Ltd. (1974)
^Correlation between address and lead level:
r = 0.176 (P<0.05).
6.126
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Table 6.30 INTELLIGENCE AND BEHAVIOUR IN SCHOOL-AGE
CHILDREN AS A FUNCTION OF THEIR ADDRESS
DURING THEIR FIRST TWO YEARS OF LIFEa>b»c
Distance from
Factory, m
0-200
200-300
300-400
400-500
500+
Number
17
33
27
6
138
Mean I.Q.
107
101
106
110
96
Percent
Disturbed
0
15.6
22.2
0
30.1
Percent
Hyperactive
6.6
37.5
26.9
16.6
40.0
aSource: Landsdown, et al. Reprinted, with permission, from
Lancet, Ltd. (1974).
Comparison between children within 500 meters of the dump
and those at 500 meters or more:
I.Q.i t = 4.057 (P<0.01)
Disturbance: x^ = 9.4 (P<0.01)
Hyperactivity: x2 = 3.3 (P>0.05).
CA11 but 14.5 percent of the sample spent their first 2 years
at the same address.
6.12T
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different exposure groups compared. One of the earliest of such studies
concerned the orchardists in the Wenatchee area of Washington state who
were exposed to lead arsenate,reported by Neal, et al., (1941) and followed
up in a later study by Nelson, et al., (1973).
The lead concentrations observed were not as high as those sometimes
seen in other industrial exposures, but that makes them particularly impor-
tant because urinary lead levels ranged from slightly higher than that com-
monly found in urban conmunities up to levels typically seen among workers
having moderate lead exposures in industry.
Among the factors studied in assessing the health of the orchardists
were weight, blood pressure, diseases of the cardiovascular system, skin
disorders, eye irritation, chronic nervous diseases, blood dyscrasias, kid-
ney disease, pulmonary tuberculosis, visual acuity, syphilis, neoplastic
disease, and fertility. Insofar as comparative data for other populations
were available, no evidence was found that incidence of any of these con-
ditions was altered by the exposure. Special attention was given to the
medical examination of children because in the Wenatchee area, orchards
surrounded the communities or the houses in which they lived. Consequently,
there were unusual opportunities for children to be exposed to lead arsen-
ate insecticide sprays and spray residues on branches, leaves, and grass, in
addition to residues ingested on apples. In only one respect did these
children differ from children in other districts: their urinary lead and
arsenic concentrations were nearly twice as high as those of a group of 18
children measured at the same time in Washington, D.C. (who had a mean
urine lead content of 0.026 milligram per liter; standard deviation,
0.0128). In reviewing this study, National Academy of Sciences (1972) con-
cluded that there was no indication of adverse effects of lead arsenate
exposure on the health of the Wenatchee children.
A follow-up study of this population was undertaken in 1968 (Nelson,
et al., 1973). Over 97 percent of the original participants were success-
fully traced. There was an attrition of 452 by death among the 1231 origi-
nal subjects. The overall mortality rate proved to be less than average for
the area. There was also no correlation with exposure to lead and mortality.
6.5.3 Occupational Exposures
Occupational lead exposures represent the high end of the dose-response
spectrum; it is among workers who mine, smelt, refine, and manufacture lead-
containing or lead-painted products that the highest and most prolonged lead
exposures are seen. Consequently, the study of occupational groups provides
valuable maximal human health effects both in terms of high concentration
and chronicity of exposure.
The clinical pattern of occupational lead intoxication has changed
during the 20th century in that the incidence and severity of poisoning has
decreased substantially in recent years. Whereas acute and occasionally
fatal lead poisoning was seen early in the 20th century, today's cases are
frequently diagnosed at an earlier, asymptomatic stage on the basis of
6.128
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abnormalties of biochemical, neurological, or renal function. Neverthe-
less, excessive lead absorption and its attendant health effects remain a
serious and prevalent occupational hazard in the lead industries today.
The findings of several recent surveys reported in this section indicate
that present standards and work practices of the lead industry do not
adequately protect lead workers from adverse health effects.
6.5.3.1 Recent Field Investigations—
Epidemiologic-studies conducted between 1975 and 1976 in five different
lead facilities across the United States have shown unacceptably high blood
lead levels and symptoms of lead poisoning in every plant studied (Center
for Disease Control, 1977). The sites investigated included four secondary
smelters and one lead chemicals plant (Eagle-Picher Industries, Joplin,
Missouri), which produces such lead compounds as lead oxides, lead peroxide,
lead sulfate, and lead silicate.
Information concerning the plants included in the investigation is
given in Table 6.31. Hematologic, neurologic and renal damage due to lead
were consistently reported. Inappropriate medical management (misuse of
chelating drugs) and poisoning of worker's children from home contamination
with lead dust were also observed in one or more of the plants.
Investigations at the Memphis, Tennessee, secondary lead smelter were
prompted by reports of excessive blood-lead levels and clinical lead
poisoning at this plant. Ninety-two percent of current employees and one
former employee were examined, revealing blood-lead levels up to 184 micro-
grams /100 ml. Sixty-seven percent of the workers had blood lead concentra-
tions above the currently proposed occupational standard of 60 micrograms/
100 ml. Table 6.32 summarizes the distribution of blood-lead levels at
the Memphis facility as well as from the other four sites. The highest
levels were seen in production area workers, many of whom exhibited the
following classical signs of lead poisoning:
Abdominal pain (17 percent)
Gastrointestinal dysfunction (22 percent)
Joint pain (28 percent)
Neuromuscular symptoms (27 percent)
Anorexia (23 percent)
Lead neuropathy (8.5 percent) weakness of wrist extensor muscles
Anemia (13 percent) defined by hemoglobin <_ 60 microgram/100 ml.
Three workers were anemic; neurological symptoms including wrist weak-
ness, ankle drop and tremors were noted in a few workers. Symptoms compati-
ble with lead poisoning were noted in 38 percent of the 53 workers examined.
The most notable finding at this plant was the high incidence of renal
function abnormality. Thirty-two percent of the workers had elevated blood
urea nitrogen (BUN _> 20 mg/100 ml). Further studies revealed significant
impairment of renal tubular and glomerular function in 7 workers which may
represent early stages of lead nephropathy.
6.129
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Table 6.31 DESCRIPTIONS OF LEAD PLANTS INVESTIGATED, 1975-1976*
os
•
H
Date of Study
November 1975
March 1976
May 1976
January 1976
March 1976
Location
Memphis, Tenn.
Joplin, Missouri
Eagan, Minnesota
Salt Lake City, Utah
Atlanta, Georgia
Type of Plant
Secondary smelter
Lead chemicals plant
Secondary smelter
Secondary smelter
Secondary smelter
Date Plant Began
Lead Processing
1948
—
1948
1975
—
Pounds of Lead
Processed per
Month
2.3 million
—
1.5 million
30,000-250,000
—
Source: Center for Disease Control, 1977.
-------
Table 6.32 BLOOD LEAD LEVELS IN LEAD PLANT WORKERS*
o\
•
H
Number of Workers In Each Group, Percent
Blood Lead Level
yg/100 ml
< 40
40 - 59
60 - 79
_> 80
Total tested
Memphis ,
Tenn.
14(18%)
12(15%)
26(33%)
26(33%)
78
Joplin ,
Mo.
1(2%)
7(17%)
21(50%)
13(31%)
42
Atlanta ,
Ga.
6(15%)
6(15%)
17(44%)
10(26%)
39
Salt Lake
City, Utah
1(3%)
5(17%)
2(7%)
21(72%)
29
Eagan,
Minn.
3(8%)
6(16%)
17(45%)
12(32%)
38
Total
25(11%)
36(16%)
83(37%)
82(36%)
226
Source: Center for Disease Control (1977).
-------
Investigations at the secondary lead smelter at Salt Lake City, Utah,
revealed unequivocal lead poisoning in 52 percent of those examined; two
hospitalized workers had blood lead levels over 250 micrograms/100 ml. In
addition, 36 percent of the workers were anemic. These cases of acute
lead poisoning were related to a change in process involving the conversion
of two small rotary furnaces previously used to process antimony to lead
processing. Inadequate ventilation was felt to be responsible for the
elevated air lead levels in the plant.
The median blood lead level of 38 workers at the secondary lead
smelter at Eagan, Minnesota, was 72.5 microgram/100 ml. Seventy-six per-
cent had levels _> 60 microgram/100 ml. Weakness of wrist and/or ankle
extensor muscles was seen in 10.5 percent of the workers; 26 percent had
tremor of the outstretched hands.
At the Atlanta, Georgia, secondary lead smelter, 70 percent of the
plants' 39 employees had blood lead levels >_ 60 microgram/100 ml. The per-
centage of workers with blood lead levels >^ 80 microgram/100 ml varied
between 43 percent in January, 1975 (when a lead exposure problem was first
identified) to 26 percent in February 1976. Workers at this plant who were
treated with intravenous chelation were permitted to remain on the job
during therapy, a practice condemned by the medical profession.
An important finding of the overall study was that blood lead and
erythrocyte protoporphyrin (EP) were well correlated with symptoms of lead
toxicity. Persons reporting symptoms during the year previous to testing
had significantly higher blood lead levels than those without symptoms.
Erythrocyte protoporphyrin (EP) levels were also well correlated (r = 0.76)
with zinc protoprophyrin levels. Furthermore, the higher the blood lead or
EP level, the greater the proportion of symptomatic workers. This correla-
tion was better in circumstances where the duration of exposure was rela-
tively short as in the Memphis facility (average duration of employment was
5 months) than in plants where the average duration of exposure was longer.
In Eagan, Minnesota, and Joplin, Missouri, the average duration of exposure
was 4 and 20 years, respectively. These data are shown in Table 6.33.
Forty-nine percent of workers with blood lead levels from 60-79 micro-
grams/100 ml reported symptoms consistent with lead poisoning during the
year preceding examination. Twenty-three percent of workers with blood
lead levels from 60-79 micrograms/100 ml were experiencing symptoms at the
time of the examination. Since many of the symptoms reported were non-
specific, (i.e., headaches, joint pain, constipation) a similar question-
naire was administered to a control group composed on local workers having
no known occupational lead exposure. The prevalence of reported symptoms
consistent with lead toxicity was much lower among unexposed workers than
among lead workers.
Anemia, defined by hemoglobin levels < 14 g/100 ml, was noted in 14
percent of workers at the Memphis plant and 31 percent at the Salt Lake
City facility. The clinical significance of anemia depends upon the degree
of hemoglobin depression, however, classical symptoms of anemia (i.e.,
6.132
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Table 6.33 PERCENTAGE OF WORKERS WITH SYMPTOMS OF LEAD POISONING
BY BLOOD LEAD AND ERYTHROCYTE PROTOPORPHYRIN LEVEL AT
THREE LEAD PLANTSa»b
Ratio, Percent of Symptomatic Workers
by Blood Lead Level (yg/100 ml)
Location
Tennessee
Missouri
Minnesota
Tennessee
Missouri
Minnesota
<40
40-59
60-79
1/13 (8) 2/12 (17) 7/26 (27)
[0/1 (8)]° 4/7 (57) 7/21 (33)
[0/2 (0)] 2/6 (33) 9/14 (64)
Erythrocyte Protoporphyrin Levelj
<100
2/26 (8)
[1/1 (100)]
[0/2 (0)]
100-199
2/13 (15)
4/10 (40)
1/5 (20)
200-299
11/16 (69)
10/15 (62)
[0/4 (0)]
>80
18/26 (69)
7/13 (54)
5/12 (42)
yg/100 ml
>300
13/21 (62)
9/15 (60)
15/23 (65)
Source: Adapted from Center for Disease Control (1977).
Two or more of symptoms of lead poisoning during past year.
f%
[ ] = 5 members or less.
6.133
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tiredness, fatigue, etc.) are not generally seen until hemoglobin decreases
below 8 g/100 ml. Decrement in work performance has been documented at
hemoglobin levels of 11-13 g/100 ml according to the authors (Center for
Disease Control, 1977). A dose-response effect between hemoglobin level
and work performance was noted throughout the range of hemoglobin levels
from 3-17 g/100 ml and no threshold effect was observed. Resistance to
infection is also depressed in anemic persons although no precise informa-
tion regarding the magnitude or threshold level for this effect is available.
Manifestations of lead toxicity also varied with duration of exposure.
After brief exposure, (2-3 months) gastrointestinal sysmptoms predominated
whereas constitutional symptoms and joint pains were relatively more common
after prolonged exposure (over 1 year). Also, conditions of acute exposure
lead to relatively more gastrointestinal symptoms than chronically exposed
workers. Highest rates of gastrointestinal symptoms were noted in lead poi-
soning cases in Salt Lake City (3-4 months duration) while workers chronic-
ally exposed in the Eagan, Minnesota, plant exhibited more nonspecific,
constitutional symptoms such as tiredness, weakness, irritability, and joint
pain (Tables 6.34 and 6.35).
The relationship between duration of exposure to lead and manifestations
is summarized below.
(1) Anemia - With one exception, anemia was observed only after
two or more months of exposure.
(2) Neuropathy - Several workers showed wrist extensor or ankle
weakness after 2-7 months of exposure. The lowest blood lead
level associated with neuropathy was 78 micrograms/100 ml;
most neuropathy cases had blood lead levels above 80 micro-
grams/100 ml.
(3) Nephropathy - No definite relationships were noted between
duration of exposure and development of overt lead nephropathy.
Some abnormalities of renal function were correlated with dur-
ation of lead exposure. At the Missouri plant, 32 percent of
workers tested had elevated blood urea nitrogen (BUN). These
workers had worked at the plant for 45-31 years. Eight per-
cent of the Tennessee workers had elevated BUN levels and 8
percent of the Minnesota workers had elevated serum creatinine
levels. With the exception of 3 workers who were all exposed
to lead less than 2 months, no worker with less than 3-1/2
years of exposure had abnormal renal functions tests.
A survey of 228 children living in the area surrounding the Memphis,
Tennessee smelter showed no excessive lead absorption, however young children
of smelter workers were found to have elevated blood lead levels and 8 were
hospitalized and treated for lead poisoning. Examination of 31 children (ages
1-9) at the Eagan, Minnesota plant revealed blood lead levels >_ 30 mLcrograms/
100 ml in 16 percent of the children, indicating increased lead absorption.
6.13U
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Table 6.34 FREQUENCY OF SYMPTOMS AMONG 22 CASES OF LEAD
POISONING, UTAH, 1976a
Symptom
Abdominal cramps
Nausea
Diarrhea
Headache
Dizziness
Anorexia
Vomiting
Paresthesias
Constipation
Fatiguability
Myalgias
Weight loss
Irritability
Chest pain
Muscle weakness
Tremor
Joint pains
Number
19
18
12
12
12
12
9
9
8
8
7
6
5
5
4
4
4
Percent
86
82
55
55
55
55
41
41
36
36
32
27
23
23
18
18
18
aSource: Adapted from Center for Disease Control
(1977).
6.135
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Table 6.35 OCCURRENCE OF SYMPTOMS IN LEAD SMELTING
PLANT EMPLOYEES, MINNESOTA, 1976a
Symptoms
Tiredness
Loose bowel movements
Irritability
Joint pains
Muscle weakness
Loss of appetite
Headache
Leg cramps
Constipation
Nausea*5
Trouble sleeping
Vomit ing ^
Abdominal pain
Weight lossc
Shakes
Number with
Sympton
17
11
9
9
9
7
6
6
6
5
4
4
3
2
2
Percent With
Symptom
52
33
27
27
27
21
18
18
18
16
12
13
9
6
6
Source: Adapted from Center for Disease Control (1977).
Excluding 1 employee with symptom due to ulcers.
°Excluding 2 employees with symptom due to diet. Of the
2 with weight loss not related to diet, 1 lost 20 pounds
in 15 months and 1 lost 22 pounds in 7 months.
6.136
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Based on findings presented in the previous discussion, it is obvious
that the currently accepted upper limit of a safe blood lead level (80
micrograms/100 ml) does not provide adequate protection against lead tox-
icity. If lead toxicity is to be prevented, the biologic monitoring system
must remove the worker from exposure prior to the onset of illness. Clearly
the present 80 micrograms/100 ml level does not provide adequate protection
since anemia and other overt symptoms of lead intoxication were observed at
blood lead levels below 80 micrograms/100 ml.
In the five facilities investigated, no workers showing evidence of lead
related anemia, wrist weakness or lead related renal disease were associated
with a blood lead level < 60//g/100 ml. In fact, very few workers with blood
lead levels <. 60 micrograms/100 ml had any symptoms consistent with lead in-
toxication. The authors concluded that the data in the report clearly support
the setting of a biologic threshold limit value of 60 micrograms/100 ml for
occupationally exposed populations and furthermore that this value should be
revised downward in the event that deleterious health effects at blood lead
levels <• 60 micrograms/100 ml can be demonstrated in the future (Center for
Disease Control, 1977).
6.5.3.2 Dose-Response Relationships: Air and Blood—
Preliminary findings of a study by National Institute for Occupational
Safety and Health (NIOSH) at the General Motors Corp. Delco-Remy battery
plant in Muncie, Indiana, provide new information on the relationship between
air and blood-lead levels (Wall Street Journal, 1977). NIOSH analyzed the
data on lead levels in the blood of about 500 plant workers as well as the
lead level in the air. Investigators found that the plant kept lead levels
in the blood of over 90 percent of its workers at 60 micrograms/100 ml or_
lower by maintaining air exposures at a maximum of about 100 micrograms/m
in most work areas.
The studies of Williams, et al., (1969) and Williams (1972) cited
in The OSHA Proposed Occupational Exposure Standard (U.S. Department of
Labor, 1975) may be used to estimate the potential contribution of lead
in air to blood lead levels. The air exposure data used by Williams, et al.,
(1969) was based on measurements obtained from workers in various departments
of a storage battery factory who wore personal samplers for a full work shift
for 2 weeks. Considerable variations were found both among departments
and among individual personal samples. The study presents a correlation
between the mean blood lead level, together with the upper and lower ranges,
with air lead levels. In order to provide a maximum blood lead value of
60 micrograms/100 ml, the mean blood lead level in a population of workers
must be maintained at about 40 micrograms/100 ml since a mean of about 40
micrograms/100 ml will result in a range in workers of approximately 20
micrograms at the lower limits to 60 micrograms at the upper limits. The
Williams data suggest that air lead levels of 200 micrograms/m correspond
to a range of 48-92 micrograms/100 ml of lead in blood with a mean level
of 70 micrograms/100 ml (84 micrograms/100 ml = 80 micrograms/100 g).
Similarly, air lead levels of 150 micrograms/m correspond to a range of
38-82 micrograms/100 ml with a mean blood lead level of 60 micrograms/100
ml. It is apparent, therefore, that airborne lead levels of 200 or 150
6.13T
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micrograms/m would result in unacceptable blood lead levels, i.e.,
greater than 60 micrograms/100 ml, for a significant number of employees
(U.S. Department of Labor, 1975).
o
Based on data from 103 employees, air lead levels of 200 micrograms/m
produced a mean blood level of 70 micrograms/100 ml; some workers had over
80 micrograms lead/100 ml in blood (Williams, 1975). Interestingly, the data
on air lead and corresponding blood lead levels reported by Short Associates
(1976) tends to confirm the relationship.described above.
Data correlating somewhat lower blood lead levels, such as 60 micrograms/
100 g, to air lead levels are not definitive. Thus, the regression equation
relied upon in Williams' study is based upon data which do not contain a
critically important value—the blood lead level corresponding to an air lead
level of 52 micrograms/m .
If it is assumed that the Williams regression equation is correct, an
air lead level of 50 micrograms/m would correspond to a mean blood lead
level of 40 micrograms/100 g, with an upper limit of approximately 60 micro-
grams/100 g. However, as noted above, critical data are missing which leaves
doubt as to the correctness of this projection. The regression equation is
unduly weighted by data at either extreme, and extrapolation of this equation
to predict the air lead—blood—lead relationship beyond the limits of measured
data is somewhat speculative. In any event, the study by Williams, even with
its limitations, provides the best available data with respect to the air
lead—blood lead relationship in industrial exposure situations. Clearly,
the Williams study shows that to achieve a mean blood lead level of 40 micro-
grams/100 g would require an 8 hour air lead concentration of less than 150
micrograms/m based on a time-weighted average (U.S. Department of Labor, 1975).
Based on Williams, et al., (1969) calculations, it appears that an increase
of 1 microgram/m in the weekly time weighted average concentration of lead in
air would correspond to an increase of approximately 1 microgram/100 ml in
blood lead.
Prpic-Majic, et al., 1973, and Fugas, et al., 1973, report data for a
study of 52 workers in unspecified lead trades. The time weighted average
concentration of respirable lead particles was 35 micrograms/m ; the mean
blood lead level of the group was 44.3 micrograms/100_ml. A control group
living in an area having air lead at 0.2 micrograms/m and a mean blood lead
level of 22.4 micrograms/100 ml was used to establish baseline levels of
blood lead due to non-air sources of 22.1 micrograms/100 ml (0.3 micrograms/
100 ml in the control group was due to air). Since the air lead level in
the occupational environment was 35 micrograms/m , it was concluded that
1 microgram of lead per m in air contributes 0.6 micrograms/100 ml of blood
(22.1 micrograms/m -t 35 micrograms/m ).
The studies of Prpic and Majic, et al., (1973), Fugas, et al., (1973)
and Williams (1975) suggest that the incremental increase in blood lead
per unit increase in lead in air is somewhat less at air lead levels charac-
teristic of industry than those in the usual outdoor ambient range (i.e.,
6.138
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3 3
0.2-10.0 micrograms/m ) where an increase of 1 microgram/m in air is said
to lead to an increase of 1 microgram/100 ml or slightly greater in blood
(U.S. Environmental Protection Agency, 1972; Environmental Health Resource
Center, 1973). This finding was also confirmed by Hammond (1977) as dis-
cussed in Section 6.5.1 and Table 6.27.
6.5.3.3 Effects of Chronic Exposures on Mortality—
Dingwall-Fordyce and Lane (1963) carried out a retrospective mortality
study in a cohort of British workers who retired from work between 1926 and
1960. All members of the study group had at least 25 years of service;
workers were classified according to three grades of exposure: "heavy",
"medium" or "none" based on average urinary lead concentration records. The
heavy exposure group (average urinary lead 100-250 micrograms/liter over the
past 20 years of employment) had higher than normal death rates from cerebro-
vascular diseases. Included in this category are cerebral hemorrhage,
thrombosis and arteriosclerosis. Interestingly, the trend of excess deaths
in the heavy exposure group was most pronounced among men who retired prior
to 1951. Such a finding is most likely related to technological changes
which improved exposure conditions. Deaths from malignant neoplasms were
not above the rate expected (based on the general population rates) in any
of the exposure categories.
Malcolm (1971) also published the results of a mortality study which
examined men exposed to lead at "moderate" levels. The average blood lead
level of the group was 65 micrograms/100 ml. He found no evidence of signifi-
cant ex-cess mortality from heart disease, pulmonary disease, cerebrovascular
accidents, cancer, renal disease and other miscellaneous causes among the
group.
Cooper and Gaffey (1975) undertook a study of men who worked in lead
production facilities and battery plants to determine whether or not their
mortality patterns differed significantly from those of men not occupationally
exposed to lead. This investigation took the form of a retrospective study in
six lead-production facilities and ten battery plants. The former included
one primary smelter, two refineries, and three recycling plants. A group
of 7032 men who had been employed in these plants between 1946 and 1970 was
followed to determine whether they were still alive at the end of 1970.
Their observed mortality by cause was compared with that of all United States
males.
Lead absorption in many of the men was greatly in excess of currently
accepted standards based upon urinary and blood-lead concentrations avail-
able for a portion of the group. Seventy-eight percent of 47 smelter workers
had blood lead levels 21 80 micrograms/100 ml or more over the period from
1946-1961. After 1965, data based on 489 workers showed 35 percent had
blood lead _> 80 micrograms/100 ml. Levels from the battery workers were
somewhat lower than those of the smelter workers. Over all levels of exposure,
duration and job classifications, 81.5-95.7 percent of the workers had blood
lead levels >_ 40 micrograms/100 ml.
6.139
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There were 1356 deaths reported; death certificates were obtained for
1267. The standardized mortality ratio (SMR) for all causes was 107 for
smelter workers and 99 for battery plant workers indicating a fairly close
approximation of the U.S. male population whose SMR = 100 by definition.
Deaths from neoplasms were in slight excess in smelters, but not signifi-
cantly increased in battery plants. There were no excess deaths from kidney
tumors. The SMR for cardiovascular-renal disease was 96 for smelter workers
and 101 for battery plant workers, i.e., roughly the same as for the general
population but not as good as might be expected in an employed population
(which commonly has an all-causes SMR of 60-90 percent of that of the gen-
eral population). There was definitely no excess in deaths from either
stroke or hypertensive heart disease. However, deaths classified as "other
hypertensive disease" and "unspecified nephritis or renal sclerosis" were
higher than expected. The actual numbers of deaths in these last-named
categories combined (41 where 19.5 expected) represented about 3 percent of
all certified deaths. In these observations, the possible interactive
effects between lead and other renal toxic agents such as cadmium cannot
be ruled out, however. The life expectancy of lead workers was calculated
to be approximately the same as that of all U.S. males.
6.1UO
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6.6 ORGANIC LEAD
In general, the alkyl derivatives of lead are highly toxic compounds,
and are readily absorbed through the skin. TEL and TML are clear, colorless
liquids, volatile, nonpolar, nonionic, and soluble in many organic solvents
such as hydrocarbons, chloroform, ether, and absolute ethanol. They have
very low water solubilities, and are relatively unreactive in air, water or
alkali (Shapiro and Frey, 1968). The high solubility of alkyl lead compounds
in body fluids is the basis for toxicity through percutaneous absorption
whereas the volatility of these compounds (particularly when added to gaso-
line) underlies the hazard potential among workers engaged in the production
of these compounds. Those chronically exposed to evaporating gasoline may
also be at risk, although few studies have been conducted. Because alkyl
lead compounds are light-sensitive and undergo photochemical decomposition
when they reach the atmosphere; their presence in the atmosphere is transient
(National Academy of Sciences, 1972). The full complement of organic lead
compounds was identified in Section 2.2.2. Suffice it to say that the most
significant organolead compounds from a toxicological viewpoint are the lead
alky Is, tetraethyl and tetramethyl. Additionally, a number of lead com-
pounds of organic acids, such as lead naphthenate,lead octoate, etc., used
in the paints and plastics industry are significant although these are, by
industry convention, classified as inorganic compounds. Their behavior in
biological systems also appears more similar to inorganic lead than to that
of the lead alkyIs.
Lead soaps of organic acids are commonly used as driers by the paint,
varnish, printing ink and linoleum industries. Soaps of mixed acids of
linseed oil and rosin acids are known as linoleate driers and resinate
driers, respectively. Lead stearates, tallates, naphthenates, and octoates
(chiefly 2-ethylhexoate) are also produced and marketed in the United States
as paint driers. The hazards encountered in the handling and use of driers
and metallic soaps are associated with the toxicity of the metal present,
the solvents contained, and their activity as oxidation catalysts. Although
little data are available regarding the specific toxicities of these com-
pounds, in general, the LD5Q values appear to be several orders of magnitude
higher than those of TEL and TML. While many of the symptoms of acute
poisoning by inorganic and organic lead are similar, they can be distinguished
diagnostically. Organolead poisoning results in elevated levels of lead in
the urine but less consistently in the blood. Likewise, red blood cell
stippling, anemia, and alterations in urinary porphyrins are not consistently
seen with organic lead exposure, particularly in acute episodes.
In general, the alkyl (tri- and tetraalkyl) derivatives of lead are
highly toxic compounds which are absorbed by inhalation, ingestion or percutan-
eous absorption. These compounds are probably distributed in a nonionic form
and, being lipid-soluble, are concentrated in the brain, body fat and liver.
Because of this selective distribution, manifestations of lead poisoning
are dominated by involvement of the central nervous system and differ from
those of inorganic lead poisoning (Gerarde, 1964; Schepers, 1964).
6.1U1
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6.6.1 Uptake and Absorption
Kehoe (1925, 1927) showed that tetraethyllead WfRor is readily absorbed
through the pulmonary epithelium. Using radium-D ( Pb) as a marker,
Mortensen (1942) studied the uptake of tetraethyllead in the lungs of rats.
The amount absorbed was proportional to the concentration of vapor in the
inhaled air, although the proportion decreased at high concentrations (see
Table 6.36). Because lead alkyIs are broken down by light and heat, their
presence in the air is transient and it is believed that they contribute
little to the inhalation burden.
Ingestion is a much less probable route for uptake and absorption of
organic lead compounds than inhalation and skin absorption. In general,
lead soaps are hydrolyzed and possibly converted to metal chlorides and free
acids when ingested. Any toxicity would be associated with the metal present
(Kirk-Othmer, 1965). The lead content varies somewhat according to the type
of metallic soap and also according to the viscosity of the product, rang-
ing from about 18 percent lead in the resinate paste products to approximately
37 percent lead in solid naphthenates. Lead content of the tallates, lino-
leates, and 2-ethylhexoates are intermediate, averaging from 16-26 percent
lead (Payne, 1954). Hazards from inhalation and skin contact may also arise
when solvents are combined with the lead soaps, particularly in the liquid
driers. In such situations, the solvents probably represent a greater toxico-
logical hazard than the lead in the paint driers. One estimate places the
total number of persons directly exposed to lead in the manufacture of paint
driers in the United States at less than 250; thus, it is a relatively in-
significant source of lead exposure compared to the primary and secondary
lead and storage battery industries which employ about 25,000 persons who are
potentially exposed to much higher levels (Short Associates, 1976). Further,
the usage of many types of paint driers, especially the linoleates, resinates,
stearates, and tallates has markedly declined in the past decade, further
reducing any possible hazard.
Pettinati, et al., (1959) and Rassetti, et al., (1961) point out that
percutaneous absorption is of importance only in the case of lead alkyIs and
lead salts of naphthenic and fatty acids. Eldridge (1924) reported that tetra-
ethyllead was absorbed rapidly through the skin in both dogs and guinea pigs.
In a study of the rate of percutaneous absorption of tetraethyllead and
inorganic lead compounds, Lang and Kunze (1948) found the amount of lead in
the kidney from application of tetraethyllead was significantly elevated
relative to the controls who received various forms of inorganic lead (Table
6.37).
Tetraalkyl lead compounds are volatile, highly lipid-soluble, and would
be expected to pass through biological membranes including the placenta.
McClain and Becker (1972) reported that trimethyllead crossed the placental
barrier to only a limited extent at low maternal doses. At higher doses,
transport was much greater, probably because binding sites in maternal erythro-
cytes were saturated at the higher dose.
6.1U2
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Table 6.36 EFFECT OF CONCENTRATION ON ABSORPTION
OF TETRAETHYLLEAD IN RATSa
Vapor
Concentration,
mg/liter
Mean TEL Absorbed,
mg/kg
Ratio of Amount
Absorbed to
Concentra t ion
0.07
0.15
0.51
1.03
2.50
7.00
0.24
0.53
1.52
3.19
6.34
16.90
3.4
3.5
3.0
3.1
2.5
2.4
a.
Source: Mortensen. Reprinted, with permission,from Journal
Industrial Hygiene and Toxicology, (c) Williams and Wilkins
Co. (1942).
Table 6.37 CUTANEOUS ABSORPTION OF LEAD COMPOUNDS'
Compound
Arsenate
Oleate
Acetate
Tetraethyl
Quantity
Applied ,
mg/g
102
148
77
106
Lead
Concentration
in Kidneys,
Wet Wt.
0.85
1.30
1.80
64.20
Control
0.55
0.59
0.82
0.82
aSource: Lang and Kunze. Reprinted, with permission, from
Journal Industrial Hygiene and Toxicology, (c) Williams
and Wilkins Co.
6.1U3
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6.6.2 Tissue Distribution
The distribution of the organic lead salts differs markedly from the
inorganic salts of lead. Bolanowska (1968) investigated the distribution
and excretion of triethyllead in rats following intravenous administration
of tetraethyllead. Twenty-four hours after administration of tetraethyllead,
50 percent of the total lead in the internal organs was in the form of tri-
ethyllead; the highest levels were found in the liver, blood, kidney, and
brain. Cremer (1959) found that tetraethyllead was rapidly converted to
triethyllead in the liver. Triethyllead then remained stable in vivo for
several days before it was excreted in the feces and urine at a rate equiva-
lent to not more than 1 percent of the daily dose. Inorganic lead consti-
tuded the remainder of the in vivo lead beginning 24 hours after injection.
The triethyllead ion is identified as responsible for the toxic effects
of tetraethyllead. There is evidence that tetramethyl- and tetrapropyllead
compounds are metabolized to the trialkyl form much more slowly than tet-
raethyllead is converted to triethyllead. This may account for their being
comparatively less toxic, although once formed, trimethyllead compounds are
as toxic as the triethyllead compounds (Cremer and Callaway, 1961). Unlike
those of inorganic lead, the organic lead compounds have no special affinity
for bone but a high affinity for lipoid tissues, especially those consti-
tuting the nervous system. Therefore, the central nervous system is the
site of greatest concentration.
Schepers (1964) observed that the concentration in the brain is much
lower than in the liver and lungs, even though the affects of organic lead
compounds are mainly in the central nervous system in experimental animals.
After inhalation of toxic amounts of tetraethyllead the concentration of
lead in the skeleton and in blood is negligible, whereas after inhalation of
toxic amounts of tetramethyllead, the concentration of lead in blood may
exceed that in any other tissue including the skeleton. Following inhala-
tion by rats, tetraethyllead can be recovered unchanged from the liver
(Stevens, et al., 1956), although it is rapidly metabolized in the liver to
inorganic lead so that chronic exposure may result in distribution and in a
toxic syndrome characteristic of inorganic lead (Cremer, 1959).
6.6.3 Elimination
There are few data on the excretion of alkyl lead compounds such as
tetraethyllead and tetramethyllead. Sanders (1964) states that in both in-
organic and organic lead intoxication the urine will probably be found to
have an abnormally high concentration of lead. In tetraethyllead intoxica-
tion, it is likely to be considerably higher than it is in inorganic lead
poisoning since lead absorbed in this manner is more rapidly excreted.
In considering the kinetics of organic lead excretion, it should be
noted that TEL and TML have a far shorter residence time in the blood and
other tissues than does inorganic lead. Kehoe and Thamann (1931) found that
in rabbits, following skin absorption, the absorbed tetraethyllead decomposed
in the tissues after a period of 3 to 14 days. Both its distribution and
6.M
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excretion followed quantitatively that of water-soluble lead compounds. In
a study of the excretion of triethyllead in rats, Bolanowska (1968) found
that 24 hours after the administration of TEL, 50 percent of the total lead
in the soft organs was in the form of triethyllead. Triethyllead concentra-
tion in vivo then remained steady for several days, and was excreted in the
feces and urine at a rate equivalent to not more than 1 percent of the
daily dose of TEL. Inorganic lead constituted the remainder of the in vivo
lead 24 hours after TEL injection, and no diethyllead was found, even shortly
after administration of TEL. Diethyllead was fairly stable jLn vivo, but less
so than triethyllead. Bolanowska notes the presence of triethyllead in
humans who died up to 20 days after acute poisoning with TEL.
6.6.4 Toxic Effects
6.6.4.1 Acute Toxicity of Various Organolead Compounds—
The absorption of lipid-soluble alkyl lead compounds, either through
the skin or the lungs may result in central nervous system manifestations
including insomnia, asthenia, tremors, headache, neuromuscular pain,
hallucinations, mania, delusions, and convulsions. The results of the ad-
ministration of single, lethal doses of TEL or TML progress from hyper-
irritability and tremors to convulsions and death. Chronic exposure to
alkyl lead also leads to neurotoxicity with similar symptomatology as that
following acute exposure.
The toxicities of TEL and TML are shown in Table 6.38, in comparison
with those for several inorganic lead compounds. The comparative mortality
of rats and dogs following inhalation of TML or TEL is shown in Tables 6.39
and 6.40.
The trialkyl ionic metabolites of TEL and TML are thought to be the
toxic lead species. The in vivo conversion of tetralkyllead to trialkyllead
is well established and is known to occur in the liver of humans. TEL is
converted rapidly to the more toxic trialkyl derivative, while the conver-
sion of TML to its trialkyl derivative is much slower. Therefore, the
toxicity of the tetraalkyl compounds apparently depends on the rate of con-
version to the more toxic trialkyl derivative (Gerarde, 1964).
The intraperitoneal injection of t rime thy Head induces in rats signs
of central nervous system toxicity (tremors and convulsions) at low doses.
The LD5Q by this route is 25.5 milligrams per kilogram. The intraperitoneal
LD5Q for triethyllead in rats is 11.2 milligrams per kilogram, and the
intravenous LD5Q in rats for tetraethyllead is 15.4 milligrams per kilogram
(Gerarde, 1964;. TetramethyHead is less toxic than trimethyllead, and a
dose of 34 milligrams per kilogram given intravenously to rats causes no
signs of poisoning. Large, oral doses of tetramethyllead (250 to 500 milli-
grams per kilogram) fed to rats produced signs of intoxication identical
to those elicited by trimethyllead. An immediate toxic reaction was
observed in rabbits dosed intraperitoneally with 7.5 and 15 milligrams per
kilogram of trimethyllead. The intravenous dosing of 20 and 40 milligrams
of tetramethyllead did not produce toxic manifestations in the rabbit
(Gerarde, 1964).
-------
Table 6.38 TOXICITIES OF SOME LEAD COMPOUNDS'
Dosage
Compound
Lead metal (powder)
Lead acetate
Lead carbonate
Lead dioxide
Lead nitrate
Tetraethyllead
Tetramethyllead
Animal
Rat
Rat
Rabbit
Dog
Guinea pig
Guinea pig
Rat
Rat
Rabbit
Rabbit
Rat
Route
IP
IP
IV
IV
Oral
IP
IP
IP
SC
IV
Oral
Toxic
Dose
LD
LD5Q
LD
LD
MLD
LD5Q
LD
MLD
MLD
MLD
LD5Q
Compound,
mg/kg
_
150
50
300
1000
220
270
10
32
22
108
Metal,
mg/kg
1000
95
32
191
860
173
169
6.4
20.4
14
83
Adapted from Venugopal and Luckey (1975) and Schepers (1964).
6.1U6
-------
Table 6.39 COMPARATIVE MORTALITY OF RATS FOLLOWING INHALATION OF TETRAMETHYLLEAD
OR TETRAETHYLLEAD, AND LEAD CONTENT OF THEIR TISSUES3
ON
•
H
Compound
Tetramethyllead
Tetcaethyllead
Control
Concentration
of
Compound
in Air
Breathed,
•g/m3
63.0
49.0
22.0
12.0
46.0
22.0
12.0
0
Duration
of Exposure
hours.
10 X 7
18 X 7
35 X 7
150 X 7
5X7
14 X 7
150 X 7
150 X 7
Mortality
(Died/Exposed)
M F Total
5/5 4/5 9/10
5/5 4/5 9/10
5/5 3/5 8/10
4/5 0/5 4/10
3/5 5/5 8/10
4/5 5/5 9/10
0/5 0/5 0/10
0/10 0/10 0/20
Average Interval
between Last
Period of
Exposure and
Death, days
2
0.25
2
lc
050C
40C
3
0.25
1
39d
12
No.
Pooled
for Chemical
Analysis
5
8
8
4
3
3
8
9
4
5
20
Average
Concentration
of Pb in
Major
Viscera?
mg/100 g
10.12
10.06
7.54
5.47
2.25
0.67
1.99
2.99
0.78
0.43
0/12
Average
Concentra tion
of Pb in
Urine ,
rag/liter
_
8.38
4.53
1.94
_
-
5.22
0.39
'Source: Gerarde. Reprinted with permission from Annual Reviews Pharmacology, (c) Annual Reviews, Inc.,
Viscera included: lung, liver, kidney, spleen, heart, and brain.
Q
Of the ten rats that inhaled 12 mg per cubic meter, four died after 116 periods. These fatalities were
complicated by intercurrent infections. Three of the remainder were killed one-half day after the 150th
period, and the remaining three were killed 40 days later.
Killed for further examination.
-------
Table 6.40 COMPARATIVE MORTALITY OF DOGS FOLLOWING INHALATION OF
TETRAETHYLLEAD, AND LEAD CONTENT OF THEIR TISSUES*1
ON
•
H
CD
Concentration
Compound
Tetrane thy Head
Tetraethyllead
Control
Inititlal
Body
Weight,
kg
10.8
9.0
5.4
11.0
11.6
11.0
10.6
13.2
5.9
10.2
6.8
of
Compound
in Air
Breathed,
mg/m
44.0
23.0
12.0
12.0
4.0
4.0
42.0
22.0
12.0
12.0
0
Duration
Exposure Before
Fatal Outcome,
hours
8 X 7C
9X7
15 X 7
14 X 7
107 X 7
84 X 7
7 X 7C
30 X 7
29 X 7
24 X 7
>130 X 7
Average Interval
Between Last
Period of
of Exposure
and Death, days
1
0
1
2
0
0
0.25
0
3
0
-
Average
Concentration
of Pb in
Major
Viscera,
tng/100 g
1.03
0.85
0.69
0.74
0.79
-
1.22
2.96
1.02
0.67
0.05
Average
Concentration
of Pb in
Urine,
mg/ liter
4.02
4.52
0.64
0.59
10.20
2.29
2.42
0.16
Average
Concentration
of Pb in
Blood,
mg/100 g
00.13
0.05
0.04
0.06
0.12
0.14
0.06
0.02
Source: Gerarde. Reprinted with permission from Annual Reviews Pharmacology, (c) Annual Reviews, Inc., 1964.
Viscera included: lung, liver, kidney, spleen, heart, and brain.
Each line represents the period of survival of a single dog subjected to exposure to an alkyllead
compound. (Two control dogs were killed at the end of the period of time indicated).
-------
6.6.4.2 Neuropathology—
The pathological lesions noted in lead induced CNS anomalies include
cerebral edema, encephalopathy, increased cerebrospinal fluid pressure,
proliferation and swelling of endothelial cells, dilation of capillaries
and arterioles, glial cell proliferation, focal necrosis and neuronal
degeneration. (Goyer and Khyne, 1973).
Many of these symptoms are also common to inorganic lead poisoning as
well.
One investigator has attempted to distinguish between CNS toxicity
caused by organic and inorganic lead compounds. This is the monograph pre-
pared by Pentschew (1958) based principally on earlier work of Tolgskaya
and Reznikov (1955). These authors discussed the physiologic differences
between encephalopathy caused by organic lead compounds versus that attribut-
able to inorganic lead. It is notable that TEL encephalopathy is character-
ized by insufficient vascular tension. The fact that inorganic lead
attached to the ethyl radical is incapable of exerting its pressure-increas-
ing action on vessels is probably connected with the simultaneous onset of
disturbances of the central blood pressure regulation in the direction of
hypotension. For this reason the epileptic attacks, so characteristic as
a sign of inorganic lead encephalopathy, are absent in TEL poisoning. Some
relationship probably exists also between blood pressure and vascular ten-
sion and the increase in brain volume in the form of edema and swelling of
the brain. This is generally absent in TEL encephalopathy.
Other indications that the lesions themselves may not be similar in
organic and inorganic poisoning are the reports that following recovery
from TEL encephalopathy, a large part of the damage is reversible since many
experience complete remission of neurologic and psychic symptoms associated
with TEL poisoning. This is not the case with inorganic lead encephalopathy,
especially in children, where permanent neurological sequellae are to be
expected.
Niklowitz (1974) investigated the ultrastructural effects on nerve cell
components of selected brain areas (frontal cortex, cerebellum, hippocampus)
after exposure of rabbits to tetraethyllead (TEL).
A single dose of 100 milligrams per kilogram of TEL led, after a lat-
ency period of 12 to 18 hours, to neurological disorders such as convulsions,
and produced significant lesions of components of pyramidal cells and atro-
glial cells. These developed before the onset of major neurological signs of
toxicity.
Two types of degenerative cell changes were identified: cellular
pyknosis and cellular hydrops, each specific to certain cell layers of
selected brain areas. The subcellular manifestations of nerve cells under-
going hydropic degeneration exhibit a distinct pattern. The following
sequence of appearance of structural alterations was determined: (1) folding
6.149
-------
of the nuclear membrane; (2) swelling and severe lesions of mitochondria;
(3) hypertrophy of Golgi complexes; and (4) patchy chromatolysis of the
ergastoplasm. Progressive hypertrophy of Golgi saccules and vacuolization
of ergastoplasm areas lead to a vacuolar hydropic degeneration of affected
nerve cells.
In each brain area an accumulation of lead of approximately 150 nano-
moles per gram dry weight took place after exposure of rabbits to TEL.
Simultaneously, a statistically significant decrease occurred in the content
of copper, iron, and zinc.
Cytomorphological measures were not made at the same time intervals as
measures on trace metals. Niklowitz and Yeager's metal analysis (1973) in
these rabbits showed that they received TEL 100 mg/kg intraperitoneally and
were decapitated after showing clinical signs of convulsions. The histo-
pathology study was a time course event preceding convulsions and the metal
analysis study was at height of toxic response. It would not be surprising
that many other measures of brain chemistry at the time of convulsion follow-
ing a lethal dose of TEL show changes relative to non-treated animals.
Rats injected with leaded gasoline (1,000 ppm of tetrae thy Head per 100
grams of body weight) showed excessive tension and excitement by the 6th or
7th day. One to 3 days after both leaded gas and nonleaded white gas injec-
tions, the delta, theta, and alpha brain waves decreased significantly. The
electrocorticogram from 6 to 7 days after leaded gasoline injection showed
marked alpha and theta waves suggestive of the direct action of triethyllead
on the brain stem reticular formation (Saito, 1973). 1 mg TEL per 100 e
body weight (10 mg/kg i.p.) is the minimum lethal dose (MLD) for the rat.
While it is reasonable to study the toxicity of high doses of intoxicants
(TEL) in attempts to understand mechanism of action, the neuronal effects or
electrical activity elicited at near lethal doses may be totally absent at
reasonable environmental doses. The author's suggestion that TEL has a direct
effect on brain stem reticular system without discussing dose effect relation-
ships has limited meaning.
Triethyllead inhibits catecholamine effect on smooth muscle contrac-
tion. Consequently, there has been some speculation that the toxicity of
triethyllead and particularly its action on the central nervous system can
be explained by a combination of effects which might result from an upset
of cholinergic and adrenergic central pathways due to the formation of
endogenous psychotogenic complexes. This speculation is based on uncon-
firmed claims that adrenochrome, which is an -intermediate in the conversion
of catecholamines to trihydroxyindole products, is an hallucinogenic agent.
Galzigna, et al., (1973) found that triethyllead dramatically increases
the duration of the succinylcholine-induced myoneural block of cholinergic
transmission. This is explained by the competition between triethyllead
and succinylcholine for serum cholinesterase. Triethyllead is able to
antagonize the effect of norepinephrine in vivo but alone is without any
effect on normal contractile activity.
6.150
-------
6.6.4.3 Metabolic Effects—
Few studies have focused specifically on the metabolic effects of
alkyliead compounds.
Trimethyl- and triethyllead decrease oxygen consumption when added to
rat brain and cortex slices in vitro. Tetramethyl- and tetraethyllead did
not have this effect except at much higher concentrations (amount unknown).
A decrease in in vitro oxygen consumption was also found in brain slices
taken from rats previously exposed to triethyl- and tetraethyllead (Gerarde,
1964). Glucose metabolism in brain slices is also inhibited by the diethyl-,
triethyl-, tripropyl- and trimethyllead compounds.
TEL has effects on neurotransmitter metabolism in the brain of experi-
mental animals (Cremer and Callaway, 1961). The mechanism of this action
was studied by assessing the effects of triethyllead in vitro on the cholin-
esterase activity of rat diaphragm and in vivo on serum cholinesterase in the
dog. The highest inhibition of acetylcholinesterase activity of the rat
diaphragm obtained with two concentrations (0.4 and 0.8 milliliter) of the
substrate acetylthiocholine was about 25 percent of normal activity. The
inhibition was noncompetitive. As with other aspecific cholinesterase
inhibitors, triethyllead was able to induce a maximal inhibition of 25 to
30 percent on the true cholinesterase activity of the rat diaphragm prepa-
ration. Maximum inhibition of serum cholinesterase was observed 15 minutes
after the administration of 6 milligrams per kilogram triethyllead to dogs
and full recovery occurred 45 minutes after administration (Galzigna, et al.,
1973).
6.6.4.4 Enzyme Effects—
In view of the high sensitivity of ALAD to lead, the levels of enzyme
activity in the blood of men occupationally exposed to lead alkyIs, partic-
ularly tetraethyllead, were measured (Miller, et al., 1972). The enzyme
activity in an exposed group of men was significantly less (P less than
0.001) than in a control group, the respective mean values being 220 and
677 units of enzyme activity.
Tetraethyllead is metabolized in the body via triethyllead and die-
thyllead ions. Diethyllead ion was found to inhibit ALA dehydratase activity
at concentrations greater than 5 x W~ M, although the degree of inhibition
was less than that obtained with Pb . These results suggest that exposure
to tetraethyllead can cause a decrease in erythrocyte ALA dehydratase activity
(Miller, et al., 1972). The effect of known inhibitors on ALA dehydratase
activity, such as alcohol consumption and cigarette smoking were not taken
into account in the group of workers investigated.
6.6.5 Epidemiologic Studies
Gerarde (1964) states that because of the large dilution factor (3 to
4 milliliters per gallon of gasoline) of TEL, the normal use of "leaded"
6.151
-------
gasoline does not present a lead intoxication hazard. However, human ex-
posure to TEL during the cleaning of leaded-gasoline tanks has led to
fatalities (Shapiro and Frey, 1968). Robinson (1974) has presented evi-
dence of absorption of alkyl lead antiknock compounds among occupationally
exposed workers. Delta-aminolevulinic acid and lead were measured in the
urine of 123 men of various ages and lengths of service, all working as
operators or maintenance men in an area of production of alkyl lead anti-
knock compounds (tetraethyllead and tetramethyllead). Results are shown
in Figure 6.21. The levels of ALA and lead in urine were found to have a
relatively low positive correlation of 0.52. Figure 6.22 suggests that a
given elevation of urinary lead excretion probably is associated with a
lower level of urinary ALA excretion when the exposure is to organic lead.
It is not clear whether this difference might be related primarily to
differences in circumstances of exposure or to differences in metabolism
(biotransformation) due to exposure to a different form of lead. For
example, there have been no experimental studies reported to indicate
what effect, if any, tetraethyllead or tetramethyllead might have on por-
phyrin metabolism and, hence, on urinary ALA excretion. In summary, the
investigation by Robinson (1974) shows that absorption of organic lead as
indicated by increased urinary levels, is associated with an increase in
urinary ALA levels. However, the mechanism through which this effect is
produced was not identified.
Proper protection of workers has virtually eliminated the problem of
TEL or TML poisoning over the last 30 years. Robinson (1976) made a detailed
comparison of extensive medical information (results of periodic medical
examinations, of medical records of absence from work due to nonoccupational
illness, and of cumulative medical diagnoses) for workers with 20 years or
more tetraethyllead (TEL) service to a matched (for age, sex, race, and
length of service) group of workers with no occupational lead (TEL or other)
exposure. The comparison showed no significant health differences between
the two populations. Table 6.41 shows the results of the cumulative diagno-
ses. The conclusion was that, under the conditions that have existed at
the Baton Rouge, Louisiana, plant, workers having long occupational exposure
to levels of lead (chiefly TEL) sharply in excess of that of the general
public, but within a range termed "safe" by current industrial medical
standards, have not suffered detectable impairment of health.
In cities alkyl lead levels were reported "not to reach 10 percent of
inorganic levels" (National Academy of Science, 1972). In fact, much of
the lead burned in gasoline (see Section 7.4.1) is not exhausted in forms
which can remain suspended in the atmosphere. To date, no information
exists on the effects of chronic, low-level exposure to airborne alkyl lead.
6.152
-------
24
ON
•
U)
14)
OS
NormalRange
lor Ifctnwy
Lead
• •• « • • •• ••• •
•
• ••• •• • *oi
> • •
•
Normal Range
for Urinary
ALA
I t 1
0.05
0.10
0.15
Urinary Lead, mg/filar
Ot30
OJ5
Figure 6. 21 Lead and ALA levels in urine of organic lead (TEL, TML) workers.
Source: Robinson. Reprinted with permission from Archives of
Environmental Health, (c) American Medical Association, 1974.
-------
ON
•
H
2.5
2.0
1
8
vs
1.0
0.5
Hneflw-Aronwn.
dcKrelser & Waldron*
/ (Estimated)
0.05
0.10
0.15 0.20
Urinary Load, mg/lller
025
0.30
0.35
Figure 6. 22 Comparison of reported urinary AIA-lead relationships for exposures to
inorganic lead with results of present study involving organic lead (TEL,
TML). Source: Robinson. Reprinted with permission from Archives of.
Environmental Health, (C) American tyedical Association, 1974.
-------
Table 6.41 CUMULATIVE DIAGNOSES OF TEL WORKERS VS
NON-TEL WORKERS,a»b
TEL
Diagnosis
Hypertension
Myocardial infarction
Angina pectoris (without MI)
Arrhythmia (only)
Abnormal EKG (only)
Cerebrovascular disease
Other peripheral artery disease
Phlebitis, thrombophlebitis
Anemia
Polycythemia
Other blood disease
Pyelonephritis
Other renal disease (except stones)
Renal stones
Liver disease
Gallbladder disease
Gastric or duodenal ulcer
Colitis
Chronic lung disease
Peripheral neuritis
Alcoholism
Neuropsychiatric
Thyroid disease
Diabetes mellitus
Gout
Rheumatoid arthritis
Lumbago
Cancer of skin
Other cancer
Glaucoma
Cataracts
Obesity, 20-29 percent
Obesity _> 30 percent
No diagnosis
Obesity only diagnosis
Total Diagnoses
Diagnoses per person
No. Men
18
3
2
2
1
1
1
5
1
-
-
3
-
7
2
4
16
-
5
1
2
1
-
3
4
-
22
7
-
1
-
42
40
22
37
194
—
Percent
12.9
2.2
1.4
1.4
0.7
0.7
0.7
3.6
0.7
-
-
2.2
-
5.0
1.4
2.9
11.5
—
3.6
0.7
1.4
0.7
-
2.2
2.9
-
15.8
5.0
-
0.7
-
30.2
28.8
15.8
26.6
—
1.4
NonTEL
No. Men
27
5
3
1
7
—
2
4
-
1
-
2
3
12
4
3
18
—
2
-
-
3
2
7
3
1
26
4
-
3
-
29
39
29
22
211
—
Percent
19.4
3.6
2.2
0.7
5.0
-
1.4
2.9
-
0.7
-
1.4
2.2
8.6
2.9
2.2
12.9
-
1.4
-
-
2.2
1.4
5.0
2.2
0.7
18.7
2.9
-
2.2
-
20.9
28.1
20.9
15.8
-
1.5
aSource: Robinson. Reprinted with permission, (c) Journal of
Occupational Medicine, 1976.
"139 persons each group, 20 (or more) years.
6.155
-------
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7.0 ENVIRONMENTAL DISTRIBUTION AND TRANSFORMATION
7.1 SUMMARY
Lead occurs only to the extent of about 16 ppm of the earth's crust;
however, its ores (which are the source of primary lead) are concentrated
in reasonably large deposits. U.S. production of lead from domestic ores
in 1975 was 560,000 metric tons (621,000 short tons). World production
during 1973 was 6.9 million metric tons (7.6 million short tons). U.S.
consumption of primary and secondary lead during 1975 was 1.17 million
metric tons (1.3 million short tons). Nearly one-half of the total used
(597,000 metric tons) was secondary lead. Secondary lead is obtained from
storage batteries and alloys.
The major uses of lead are in the manufacture of antiknock additives
for automotive fuels, storage batteries and accessories, pigments, ammuni-
tion, and solder. Minor uses include cable coverings and pipes, alloys
with antimony, copper and tin, sheet lead, and bearing metals.
Extremely high soil and dust fall levels of lead have been found around
secondary smelters. However, the monthly geometric means of the air lead
concentrations close to the smelters averaged 1 to 5.3 micrograms per cubic
meter of air, and were only about double those for urban sites (0.8 to 2.4
micrograms per cubic meter).
It is estimated that before the industrial revolution, the lead content
of marine waters was about 0.02 to 0.04 parts per billion (ppb). At the
present time oceanic surface waters contain about ten times that much lead.
The lead content of inland lakes and rivers of the U. S. has been found to
be of the order of 10 to 50 ppb. Lead-mining areas show the highest concen-
trations in surface waters with some localities exceeding the 50 ppb limit
imposed by the U.S. Public Health Service. Lead-based industries can con-
tribute large amounts of lead to nearby streams depending on the processing
of the plant effluents. Up to 800 ppb has been detected in unfiltered water
from lead smelter tailings- ponds. In drinking water the main source of con-
tamination is the use of lead pipes in older plumbing. Occasionally this
may result in levels above the permissible limit, particularly if the water
is soft and the pH is below 7.0.
Secondary smelters, automobile exhausts, and houses where lead paint has
been used on the exterior, are considered major sources of soil contamination
with lead. Lead levels of 16,000 to 40,000 micrograms per gram of soil have
been found around a secondary smelter. These values declined to background
levels within 300 to 400 meters of the stack. Although the high concentra-
tions of lead in the soil near houses may be due to weathering of lead-based
7.1
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paints, there also is strong evidence that automobile exhausts contribute
to soil lead near the roadway. Greatly elevated levels of lead have been
found in soils and vegetation along rights-of-way of lead ore truck routes
Contamination generally was limited to a distance of 100 meters or less
from the road. The concentrations of lead in street dust from 77 mid-
western cities in the U.S. assayed 1,500 to 2,400 milligrams per kilogram
(ppm) of dust. Since levels in industrial areas averaged approximately
1,600 milligrams per kilogram of dust, vehicular sources appear to be major
contributors.
Large amounts of lead can be found in the soil near roadways as the
automobile exhaust provides enough lead to raise the concentration to 400
to 500 ppm. An even greater concentration of lead in soils can be found
in the vicinity of houses where lead paint has been used on the exterior.
Concentrations of several thousand ppm may exist in the soil immediately
adjacent to the house.
The persistence of lead which has been dispersed in the atmosphere
depends on the physical form of the lead and on meteorological factors.
In general, about half the particulate lead from automotive sources is
removed from the air by gravitational effects and is deposited near the road-
way. About 30 percent of the lead consumed stays in the oil, oil filter,
and muffler. The remaining lead consists of aerosols that remain in the
atmosphere until brought down by precipitation. The average residence time
of lead in the atmosphere has been found to be about 10 days.
Apparently a significant portion of the lead introduced into surface
waters by precipitation and runoff is not soluble and consequently is
removed from the water by sedimentation. Probably more important is the
absorption of lead in soil particles. Precipitation and contamination by
fallout from industrial and vehicular sources also increase the lead content
of soils. However, little of this lead enters healthy plant life because
it is not present in a readily available form. Contamination of surface
soil by inorganic forms of lead may be subject to rapid leaching by water,
and under some circumstances lead can be removed fairly rapidly in this
fashion. Lead contamination of water by the leaching of landfills could
become a problem if the soil chemistry of lead is favorable.
Wastewaters entering treatment plants have been found to contain from
about 100 to 1,000 micrograms per liter of lead depending on the industrial-
ization and the automobile traffic density of the area. Waste-waters dis-
charged into coastal waters can bring the lead concentration in harbors up
to several hundred micrograms per liter. The effluent from sewage treatment
plants usually contains substantially less lead than the incoming wastewater.
The primary effluent may contain only half as much lead, and the secondary
effluent from one-fifth to one-fourth as much. The lead then is removed with
the sludge, where it may constitute a problem if the sludge is spread on
agricultural land. However, in actual field operations and in laboratory
tests in which some metal toxicity has been observed in terms of reduced
growth of plants, lead has not been found to be the cause of the toxicity.
7.2
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Lead introduced into lakes and streams concentrates in the sediments.
It is rapidly removed from water when it passes through soil and bottom
sediments. This is due to the high capacity of organic matter to bind the
lead more firmly.
The amount of lead in sediments has increased by about a factor of ten
in the last 80 to 100 years in populated areas. Concentrations of several
hundred ppm by weight of lead have been found in the upper layers of sedi-
ments. In areas in which lead has been mined, the lead concentration in
sediments can be several thousand ppm by weight.
In a position paper on the health implications of airborne lead, the
U.S. Environmental Protection Agency has pointed out that man-made sources
of lead contribute most of the lead entering the environment, and that the
combustion of leaded gasoline is the single most significant contributor.
Accordingly, reduction of airborne lead constitutes an accessible means for
reducing potential human exposure to environmental lead.
As can be inferred from data on the projected projection and consumption
of lead for lead alkyIs, environmental lead from the combustion of gasoline
will continue to decline. In 1977, 190,000 metric tons of lead will be used
in the production of lead alkyIs, 145,000 tons of which will be used domestic-
ally, with the remaining 45,000 tons being exported. However, by 1985 pro-
jections are for 90,000 tons divided equally between domestic consumption and
exports. These estimates assume that, (1) lead additions will not be signi-
ficantly below the 0.5 g/gal mandated by EPA regulations, and (2) exports of
lead alkyIs will continue at present levels.
A large number of organometallic compounds of manganese have been in-
vestigated as antiknock agents. Of these, probably methylcyclopentadienyl-
manganese tricarbonyl is the most satisfactory. However, it is not marketed
as a primary antiknock but is included in several antiknock blends.
7.2 PRODUCTION AND USES OF LEAD
Lead, one of the oldest known metals, occurs only to the extent of about
16 ppm of the earth's crust (8 and 20 ppm, respectively, in alkaline and
acidic rocks) or 15 grams per ton (de Treville, 1964). Its ores which occur
chiefly as sulfide in galena (86.8 percent Pb), carbonate in cerussite (77.5
percent Pb), and sulfate in anglesite (68.3 percent Pb) are concentrated in
reasonably large deposits. Lead is produced commercially by roasting galena
in an oxidizing atmosphere.
Lead is introduced into the environment as a result of the many uses
to which it is put by man. Consequently, the amount of lead produced and its
distribution among the various applications are important to environmental
considerations. Data on the production of lead in the United States for the
7-year period, 1969-75, are presented in Table 7.1 (Ryan and Hague, 1974;
1976).
7.3
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TABLE 7.1 PRODUCTION AND CONSLVIPTION Of LEAD
(Short tons unless otherwise specified)
United States:
Production:
Domestic ores, recoverable lead content
Value thousands
Primary lead (refined) :
From domestic ores and base
bullion ,,., ,
From foreign ores and base bullion
Antimonial lead (primary lead
Secondary lead (lead content)
Exports of lead materials excluding scrap
Imports, general:
Lead in ore and matte
Lead in base bullion
Lead in pigs, bars, and old-
Stocks December 31 (lead content) :
At primary smelters and refineries
A fc *. «*.«M..««M — 1 *._
*»t consuinet plants ~—~~ — — ——«—•.•— •..«..
Consumption of metal, primary and
SGCOnQoLy ™ " ' ''^•"•^^•"•^"^^^•"•^ •^••"••"•"•^•i ™ "•• ~m* M «
Price: Common lead, average, cents per
pound —————•--- .---
1970
571,767
$178,609
528,086
138,644
UA^S
, OJJ
597,390
7,747
112,406
296
251,480
192,985
1 ^ S07
J. Jj f j\Jf,
1,360,552
15.69
1971
578,550
$159,679
573,022
76,933
1 A 11 fi
J.O | J.J.O
596,797
0,925
65,998
41
198,970
121,660
125 577
^ttj , j 1 1
1,431,514
13.89
1972
618,915
$186,046
u
577,398
103,001
81 AS
, J>O*/
616,597
8,376
101,514
895
245,625
145,573
118 544
AAW y J*»*T
1,485,254
15.03
1973
603,024
$196,465
567,256
107,260
n223
y fnf*J
654,286
66,576
102,483
4
180,788
89,847
124,121
1,541,209
16.29
1974
663,870
$298,742
673,024
92,946
90 67
»OD /
698,698
61,982
94,299
831
119,197
121,051
166 589
^ w j mt\jy
1,599,427
22.53
1975
621,464
$262,230
530,215
105,907
? 71 S
£ , H.J
658,456
21,256
87,560
462
105,876
156,330
133 315
4L*J-J y •J A^
1,297,098
21.53
World:
Production:
M-f -*•* __ ________ - ___
ru.iic — -- - ------ — — —
Price: London, common lead, average,
cents per pound ---------------
3,741,546? 3,742,950 3,802,086 3,852,190 3,832,499 3,787,804
3,628,422b 3,590,730 3,744,660 3,800,753 3,858,205 3,713,691
1.3.76
11.52
13. *8
70.47
26.83
18.73
f Adapted from Ryan and Hague (1974;1976).
Revised.
Quotation for 1969-71 at New York and for 1972 and 1973 on a nationwide, delivered basis.
-------
The consumption of lead in the United States by product usage for the
years 1972-75 is shown in Table 7.2 (Byan and Hague, 1974, 1976). Its use
in storage batteries utilizes by far the largest amount (634,000 metric tons
or 699,000 short tons in 1975), but approximately one-half of this was sal-
vaged from old batteries and the lead recycled. Gasoline antiknock additives,
tetraethyllead and tetramethyllead (Section 2.2.1), comprised the second
largest use in 1975 (189,200 metric tons or 208,600 short tons). The annual
increase in lead consumption in the U.S. during the 10-year period 1962-1971
averaged 2.9 percent, resulting largely from an increased demand for batteries
and gasoline additives (U.S. Environmental Protection Agency, 1973).
The trend to unleaded gasoline reduced the lead used for antiknock
compounds by approximately 38,000 metric tons (16.7 percent) in 1975 from
1974 consumption, which was itself down about 8.7 percent from 1973. This
trend can be expected to accelerate as new cars operating on unleaded gaso-
line replace older cars on the road. Also, a trend toward smaller and more
economical cars contributed to a declining rate of growth of gasoline con-
sumption.
Until recently, uses of lead in pigments and for a variety of metal
products applications have accounted for the remainder of the lead that is
consumed.
Lead is employed for containers in tank linings for many corrosive
liquids. The metal and its alloys are used in solders, type metal, bearings,
pipe, cable covering, plumbing, and ammunition. Lead is very effective as a
sound absorber, serves as a radiation shield around X-ray equipment and
nuclear reactors, and is used to absorb vibration.
There are various uses for specific lead compounds. The major use for
lead oxide, PbO, is in the preparation of storage battery plates. The par-
tially oxidized material (black oxide of lead) is preferred. The most exten-
sive use for the fully oxidized PbO is in the manufacture of glasses, glazes,
and vitreous enamel.
Another important oxide of lead is red lead or minium, pb_0,. Much of
this material is used in the manufacture of storage batteries, But a signifi-
cant amount forms the pigment for red lead paint which is used in large
quantities as a corrosion-resistant coating on iron and steel. Cutting and
welding of steel which has been protected in this fashion result in the vola-
tilization and decomposition of the lead oxide and consequently constitute a
health hazard in the absence of precautionary measures.
Lead dioxide, PbO-, is used as the positive plate of the lead storage
battery. PbO_ is used as an oxidizing agent in the manufacture of dyes,
chemicals, matches, pyrotechnics, and synthetic rubbers (Klug and Brasted,
1958).
In past years, paint pigments consumed a great deal of the lead output.
Several of the most stable inorganic colors were based on lead compounds,
and many of the older homes and items of furniture were painted with these
7.5
-------
TABLE 7.2 LEAD CONSUMPTION IN THE UNITED STATES, BY PRODUCT
(Short tons)
Product
Metal products:
Ammunition
Bearing metals
Brass and bronze
Calking lead
Casting metals
Collapsible tubes
jjOUL.""""™™ ™"rL™^~™-~'~~~*~~— .— •—
Pipes, traps, bends
Sheet lead
tnldor- T_^__, ...
Storage batteries:
Battery grids,
posts, etc
Battery oxides
Terne metal
Type metal
Tot il
Pigment i :
UK4fj> 1aa«1_ __— — —
Red l-'.ad and
Pigment colors
nt-tio-r - -- ... -
Chemicals :
Gasoline antiknock
additives
Miscellaneous
chemicals
Total
Miscellaneous uses:
Annealing
Galvanizing
Lead plating
Weights and ballast
Total
Other, unclassified uses
£
Grand total
1972
84,699
15,915
19,805
45,930
22,483
7,139
4,020
4,592
17,780
23,667
71,289
347,225
379,367
504
19,944
1,064,359
2,814
69,799
16,264
377
89,214
278,340
849
279,189
4,239
1,397
638
21,302
27,666
24,826
1,485,254
1973
81,479
15,657
22,735
43,005
20,057
7,220
2,860
4,985
21,291
23,394
71,770
365,557
403,890
2,658
21,922
1,108,480
1,749
89,577
16,963
477
108,766
274,410
944
275,354
3,974
1,294
744
20,848
26,860
21,749
1,541,209
1974
87,090
14,609
22,240
43,426
19,739
7,507
2,488
4,404
16,455
21,294
66,280
391,479
460,402
2,300
20,516
1,180,229
1,996
96,163
17,336
718
116,213
250,502
708
251,210
4,097
1,664
498
21,418
27,677
24,098
1,599,427
1975
75,081
12,184
13,404
22,099
14,296
7,711
2,216
3,205
14,233
24,859
57,344
326,714
372,700
1,511
16.211
963,768
2,498
65,457
10,618
499
79,072
208,605
181
708,786
2,629
1,228
376
20,018
24,251
21,221
1,297,098
fAdapted from Ryan and Hague (1974;1976).
Includes lead content of leaded zinc ox de and other pigments.
°Includes lead which went directly from scrap to fabricated products.
7.6
-------
lead colors. Lead chromates have provided yellow, orange, and red pigments.
The normal chromate, PbCrO , is the brilliant pigment chrome yellow. By
formulating with alkalis to make basic lead chromates, the oranges can be
obtained. The chrome reds can be obtained by making the basic lead chromate
from white lead instead of from the usual lead acetate solution. The many
gradations of color between yellow and red are obtained by formulating mix-
tures of the different lead chromates. Chrome green, the most important green
pigment, is actually a mixture of yellow lead chromate and Prussian blue.
The oldest white paint pigment, basic lead carbonate, 2PbCO -Pb(OH)_,
commonly known as white lead, has been used extensively in the past for Both
interior and exterior white paints for dwellings. However, a series of
Federal laws, beginning with the Lead Based Paint Poisoning Prevention Act
(LBPPPA) , have effectively eliminated lead based paints from this market.
The LBPPPA was first enacted in 1971 (P.L. 91-695) to deal with the problems
of childhood lead poisoning caused by the ingestion of lead-based paints.
The original act prohibited, after January 13, 1971, the use of lead-based
paint in residential structures constructed or rehabilitated by the Federal
government, or with Federal assistance in any form. The term "lead-based
paint" was defined as any paint containing more than 1 percent lead in the
dried paint film.
The LBPPPA was amended in 1973 (P.L. 93-151), which among other things
redefined "lead-based paint" to mean any paint with over 0.5 percent lead in
the dried film. The LBPPPA was again amended in 1976 by enactment of the
National Consumer Health Information and Health Promotion Act (P.L. 94-317).
Under this Act the Consumer Product Safety Commission issued on August 10,
1976, (41 FR 33636) proposed regulations governing lead-based paint and
certain other consumer products, banning as hazardous products:
(1) Lead-containing paint and similar surface-coating materials
containing more than a safe level of lead.
(2) Toys and other articles intended for use by children bearing
lead-containing paint or other similar surface-coating material
containing more than a safe level of lead.
(3) Articles of furniture bearing lead-containing paint or other
similar surface-coating materials containing more than a safe
level of lead.
On February 16, 1977, (42 FR 9404), The Consumer Product Safety Com-
mission announced its decision that available scientific information is
insufficient to establish that a level of lead in paint above 0.06 percent
but not over 0.5 percent is safe. The result of this decision is to classify
any paint manufactured after June 22, 1977 containing more than 0.06 percent
lead as lead-based paint, under the Lead-Based Paint Poisoning Prevention
Act (LBPPPA).
Final regulations were issued September 1, 1977, (42 FR 44192) confirm-
ing the proposed regulations. Certain exceptions were made for a few special-
ized coatings not used by consumers and with little likelihood of access to
7.7
-------
children. These included a number of agricultural and industrial equipment
coatings, traffic paints, graphic art coatings, and touch-up coatings for
appliances, etc.
Pursuant to these various pieces of legislation to control exposure to
lead-based paints in dwellings, the Department of Housing and Urban Develop-
ment (HUD) issued July 13, 1976, (41 FR 28876) regulations revising 24 CFR
Part 35 governing numerous controls on HUD-associated housing constructured
prior to 1950. These regulations, among other things:
(1) Require HUD to notify purchasers and tenants of HUD-associated
housing constructed prior to 1950 of the hazards of lead-based
paint poisoning.
(2) Prohibit the use of lead-based paint in HUD-associated housing.
(3) Provide for the elimination, to the extent practicable, of lead-
based paint hazards in HUD-associated housing (and similarly in ^
Federally-owned housing prior to sale for residential habitation).
In the area of insecticides, lead arsenate was employed as the acid salt,
PbHAsO,. In the World War II era hundreds of millions of pounds of this
compound were produced for the control of the gypsy moth. The production and
usage of lead arsenate have been declining, as the advent of the organic
pesticides has resulted in replacement of lead arsenate by other compounds.
Total lead consumption in 1975 for all miscellaneous lead chemicals (see Table
7.2) was only 164 metric tons (181 short tons). However, the lead content of
soils in orchards and similar agricultural areas is probably the result of
the accumulation of lead over the many years of usage of lead arsenate.
Organolead compounds such as hexamethyldilead are used in the manufacture
of organolead intermediates. A large number of alkyl- or aryl-substituted
lead acetate derivatives such as tributyllead acetate, triethyllead acetate
and triphenyllead acetate are used as fungicidal agents in paints (Shapiro
and Frey, 1968; Section 4.2.2.2).
Either directly or indirectly, virtually 100 percent of the tetraethyllead
(TEL) produced in the United States is used to make antiknock additives for
gasolines. The usage pattern for tetramethyllead (TML) is identical with
that for TEL except it is preferentially used in aviation and premium gaso-
lines because of its superior performance in gasolines having a high aromatic
hydrocarbon content.
Thioalkyl lead compounds are used as anti-mildewing agents in the cotton
industry. They also have various medical applications as antiinflammatory
"All surface conditions identified as immediate hazards are to be thor-
oughly cleaned (washed, sanded, wire-brushed, scraped or otherwise cleaned)
as to remove all cracked, scaling, peeling, chipping, and loose paint on
applicable surfaces. Surfaces shall then be repainted with two coats- of
a suitable non-leaded paint."
7.8
-------
and antiandrogenic agents. Nitrogen-containing, heterocyclic, organolead
compounds are known for their excellent biocidal activity (Shapiro and Frey,
1968).
Further uses of various lead compounds are shown in Table 8.1 .
7.3 DISTRIBUTION OF LEAD IN THE ENVIRONMENT
As a result of the widespread use of lead and its compounds, it is
ubiquitous in the environment. It will be found in all three forms—gaseous,
liquid, and solid. Since man acquires his body burden from all three sources,
one domain cannot be considered singly, to the exclusion of the others.
Pinkerton, et al., (1974), in following up this approach, suggest that ambient
air, soil, dustfall, water, and if possible, food and house dust should be
included in multimedia indices of environmental trace-metal exposure in
humans.
7.3.1 Distribution in Mr
Natural sources of atmospheric lead are airborne dust and gases diffusing
from the earth's crust. These gases include radon-222, one of the daughter
products of the radioactive decay of uranium-238, which is present in varying
abundance in the rocks of the earth. Being a gas it can escape from the
earth's crust into the atmosphere. Radon-222 decays.radioactively to form a
chain of solid radioactive daughter products, the end product of which is
stable lead-206. The longest-lived daughter product is lead-210 which has a
half-life of approximately 20 years. Diffusion of radon-222 into the atmos-
phere results in the presence of lead-210 in amounts ranging from 7 x 10
disintegration per minute per kilogram of air at ground level to 10 times
that amount at an altitude of 47,000 feet (Burton and Stewart, 1960). This
increase with altitude can be attributed both to nuclear test explosions and
diffusion effects in the atmosphere, troposphere, and stratosphere.
For the continental United States, the baseline concentration for total
atmospheric lead has been suggested to be 0.0080 microgram per cubic meter
(Chow, et al., 1972). This value is the annual average lead aerosol concen-
tration measured at White Mountain, California, at a virtually uninhabited
site at an elevation of 3,800 meters, far above the thermal inversion.
Patterson (1965) estimated that the contribution of lead in the atmos-
phere from natural sources ranees from 5 x 10 microgram per cubic meter for
silicate dusts down to 2 x 10~ microgram per cubic meter for meteoric
sources (see Table 7.3).
By far the largest amount of lead that reaches the atmosphere results
from the combustion of the tetraethyl- and tetrame thy Heads that are used as
antiknock agents in gasolines. Averaged over 50,000 miles of driving, about
70 percent of the lead burned is exhausted as particulate matter. The com-
bustion of leaded gasoline accounts for by far the largest portion of all
lead now reaching the environment (U.S. Environmental Protection Agency, 1977)
7.9
-------
Table 7.3 ESTIMATED AMOUNTS OF LEAD IN THE
ATMOSPHERE FROM NATURAL SOURCES*1,
Lead Concentration>
Source Vg/m3
—,
Silicate dust 5 x 10_5
Volcanic halogen aerosols 3 x 10_,
Volcanic silicate smoke 6 x 10_,
Forest fire smoke 6 x 10_,
Aerosolic sea salts 1 x 10_g
Meteoritic and meteoric smoke 2 x 10
aSource: Patterson, Reprinted with permission from
Archives Environmental Health, (c) American Medical
Association, 1965
7.10
-------
Chow and Johnstons (1965) verified that the lead in aerosols of the Los
Angeles Basin, California, had the same isotopic composition as the lead in
the antiknock gasoline sold in that area. In 1968, when all gasoline was
leaded, about 98 percent of the atmospheric lead could be attributed to that
source (National Academy of Sciences, 1972). The combustion of leaded gaso-
line continues to be by far the largest contributor to atmospheric lead. As
of 1975, this was estimated to amount to 142,000 metric tons (U.S. Environ-
mental Protection Agency, 1977). Additionally, some 10 percent of the lead
in the gasoline accumulates in the crackcase oil; combustion of waste lubri-
cating oil adds another 10,400 metric tons or so to that emitted from the
exhaust pipe. The total of automobile antiknock-related air emissions is
almost 95 percent of all emissions (Figure 7.1).
Systematic measurements of lead in the atmosphere of a city began in
1941 in Cincinnati, Ohio, but the work was interrupted by World War II and
not resumed until the 1950fs, at which time a number of U.S. cities were
included. The 1941 data from Cincinnati gave an average lead concentration
of 5.1 micrograms per cubic meter. Cholak (1964) reported that investiga-
tions in Cincinnati from 1941 to 1962 showed a continual and gradual downward
trend in both mean and median concentrations of lead in air. The mean con-
centration of 5.1 micrograms per cubic meter in 1941 decreased to 1.43 micro-
grams per cubic meter in 1962 while the median level fell to 1.27 micrograms
in 1962. After 1954, no concentration above 8 micrograms of lead per cubic
meter of air was found. The higher average values and ranges found from 1941
to 1951 may have been partly due to the manner of sampling during this period,
and therefore were somewhat biased.
Analysis of samples from 24 cities in the United States during 1954 to
1955 yielded a mean concentration ranging from 1.47 to 1.99 micrograms of
lead per cubic meter, while median values ranged from 1.2 to 1.42 micrograms.
Cities with a population above 2 million had significantly higher mean and
median values; Los Angeles had the highest mean level of concentration (5.5)
as shown in Figure 7.2.
Other data indicate that lead concentration levels in the atmosphere
subsequently increased, at least up to 1970, a not unreasonable phenomenon
considering the increases in consumption of gasoline additives during this
period. Chow (1973), in summarizing the findings of the Tri-City Project,
conducted in 1961-1962 in Los Angeles, Philadelphia, and Cincinnati, and of
the Seven-Cities Project, conducted in 1968-1969 in these same three cities,
plus New York, Chicago, Houston, and Washington, D.C., points out that in
Los Angeles the average lead concentration in the Basin increased 56 percent
over this period, an annual increase of 7 percent compounded. In Philadelphia
and Cincinnati, the increases were more moderate, 19 percent and 17 percent,
respectively. Of the 19 sampling sites, lead concentrations increased in 17,
and decreased in 2 (National Academy of Sciences, 1972).
An extensive study to determine the variation in the annual, seasonal,
monthly, and diurnal average distributions of lead and total particulate
matter in the atmosphere of Cincinnati, Los Angeles, and Philadelphia was
carried out by continuous sampling from June 1961 through May 1962 (U.S.
Department of Health, Education, and Welfare, 1965a,b). A summary of the
results in Table 7.4 shows that the general urban concentrations ranged from
7.11
-------
Gasoline Consumption
87.9% 1142,0001)
Other 2.3% (3780 T)
Lead Alkyl (1000 T)
Secondary Lead Smelting (755 T)
Fossil Fuel Combust on (500T)
Type Metal (435 T)
Cement Mfg (300T)
Metallic Lead Products (290T)
Lead Pigments (HOT)
Misc (IOOT)
Waste-oil Combustion
£5% (10,430 T)
Iron a Steel 1.4% (23IOT)
Waste Incineration
1.0% (I630T)
Primary Nonferrous Metals
1.0% (1625 T)
Figure 7.1. Percent distribution of estimated emissions of lead
to air, 1975, in metric tons. Data from U.S.
Environmental Protection Agency (1977).
T.12
-------
<
cc
o
o
cc
u
fnni
O
100 SAMPLES
MEAN CONC.
- = MEDIAN CONC.
1229 SAMPLES
(A
O
5
L
loop i
1000 M 2000M
7.2
600M town a>ggM >20OOM
POPULATION CLASS
Bar graph showing ranges, means, and medians of the concentration
of lead in the atmosphere of cities grouped according to popula-
tion. Source: Cholak. Reprinted with permission from Archives
Environmental Health, (c) American Medical Association, 1964.
7.13
-------
Table 7.4 CONCENTRATION OF LEAD IN THE ATMOSPHERE*
Annual average values
Downtown
Outlying area
All stations
Seasonal distributions
(all stations) :
Summer
Fall
Winter
Spring
Diurnal distributions
(annual — all stations
stated as a fraction
of annual mean) :
2300-0300
0300-0700
0700-1100
1100-1500
1500-1900
1900-2300
Atmospheric
Cincinnati
2
1
1.4
1.3
1.7
1.3
1.3
1.3
1.1
1.4
0.8
0.9
1.0
3
Lead Concentration, yg/m
Los Angeles
3
2
2.5
1.9
2.8
3.1
2.1
1.0
1.1
1.2
0.7
0.8
1.1
Philadelphia
3
1
1.6
1.4
1.9
1.9
1.4
0.9
0.8
1.4
0.8
1.1
1.1
Adapted from U-, S. Department of Health, Education and Welfare (1965a).
-------
about 1 to 3 micrograms per cubic meter depending on the area sampled.
The average concentration of lead for all samples collected during the year
was 1.4 micrograms per cubic meter in Cincinnati, 2.5 in Los Angeles, and
1.6 in Philadelphia. The highest average concentration for all samples
collected during a single month at any single sampling site was 3.1 micro-
grams per cubic meter in Cincinnati, 6.4 in Los Angeles, and 4.4 in Phila-
delphia. The highest individual concentrations were 6.4 micrograms per
cubic meter in Cincinnati, 11.4 in Los Angeles, and 7.6 in Philadelphia.
A uniform sampling procedure was used in each of the cities, and the samples
were analyzed by the same technique.
Measurements made in Helena, Montana, during the summer and fall of 1969
showed an average daily lead concentration of 0.1 microgram per cubic meter
with maximum daily levels up to 0.7 microgram per cubic meter (U.S. Environ-
mental Protection Agency, 1972). However, in East Helena where an industrial
smelter complex is located, the lead concentration averaged 0.4 to 4 micro-
grams per cubic meter depending on location. The maximum daily concentration
observed there was 15 micrograms per cubic meter. Within a 1-mile radius of
the smelter, the fallout of lead on the ground ranged from 30 to 140 milli-
grams per square meter; an area of 0.05 to 0.18 square meter would contain
the body-burden limit for lead.
Enrichment factors which involve the ratio of metal concentrations in
the atmosphere to that in the earth's crust, and which are normalized by
relating to the aluminum content were determined for the Boston area by
Gordon, et al., (1973). For lead an enrichment factor of 5,800 was calcu-
lated, a value significantly larger than that for any of the other 22
elements included in the study. A similar calculation made for air over
the North Atlantic Ocean indicated an enrichment factor of 2,200 for lead
(Duce, et al., 1975).
Chow (1973) compiled data from various parts of the world which indi-
cate that lead concentrations may range from a low of 2 x 10 to 71.3
micrograms per cubic meter (Table 7.5).
7.3.2 Distribution in Water
The lead content of various surface waters of the U.S. have been
reported by Kroner and Kopp (1965). Samples were taken from the Great
Lakes and from five large rivers: Colorado, Columbia, Ohio, Mississippi,
and Missouri. The concentration ranges found for lead were, respectively.
in micrograms per liter (ppb): Ohio River, 10 to 30; Mississippi River, 10
to 50; Columbia River, 4 to 50; Great Lakes, 3 to 20. Unusual values were
shown for the Mississippi River (80, 100, 200), the Great Lakes (90) and
for the following (range values were not given): Colorado River (60, 600),
Missouri River (20, 90). The frequency of detection, in percent, was:
Ohio River, 11; Colorado River, 6; Missouri River, 3; Mississippi River, 11;
Columbia River, 29; Great Lakes, 20.
In more extensive sampling of U.S. surface waters in 1970, three cate-
gories were sampled: (1) sources of public water supplies of large cities;
7.15
-------
Table 7.5 LEAD IN THE ATMOSPHERE'
Cone.,
yg/m3
Period
Significance
0.0002
0.0005
0.0006
0.001
0.004
0.008
0.07
0.32
0.42
0.7
1.5
2.0
2.0
2.1
3.5
3.2
5.4
3.6
7.6
8.1
10.1
25.0
71.3
200.0
Annual average
Annual average
Annual average
Annual average
Annual average
24 h average
30-day average
90-day average
Annual average
Annual average
Daytime
Daytime
Annual average
Monthly average
Weekly average
8 h per day
8 h per day
Novaya Zemlya, USSR, 1966
Thule, Greenland, 1965
Calculated 'natural1 atmosphere
Mid-Pacific Ocean, 1967
South Pole, 1971
White Mountain, California, 1971
Laguna Mountain, California, 1971
Tashkent, USSR, 1966
La Jolla, California, 1971
USSR limit for general population
California limit for general population
US limit for general population
WHO limit
San Diego, California, 1971
High Street, Warwick, England, 1965-66
Fleet Street, London, 1962
Fleet Street, London, 1971
Los Angeles, California, 1968-69
Los Angeles, California, highest 1968-69
San Diego, California, highest 1968
USSR limit for industrial exposure
Average Los Angeles freeways, 1961-62
Recorded during peak traffic in Los Angeles
US unofficial limit for industrial exposure, 1966
Source: Chow. Reprinted with permission from Chemistry in Britain.
(c) The Chemical Society, 1973.
7.16
-------
(2) water courses downstream from major municipal and industrial complexes;
and (3) U.S. Geological Survey hydrologic bench-mark stations (Durum and
Hem, 1972). Analyses of 727 samples taken in various parts of the country
gave lead values ranging from 1 to 890 ppb with median values from 1 to 6
ppb. As shown in Table 7.6, lead was present in almost two-thirds of the
samples. The data have a regional pattern showing that lead occurred most
frequently in the northeast and southeast portions of the country.
Regional studies in California covering 383 samples from miscellaneous
water sources (Bradford, 1971) showed median values for lead of about the
same magnitude as those presented in Table 7.6. The water sources sampled
included surface waters, wells, agricultural drainage, domestic wastes,
metal and chemical processing plant effluents, rivers, bays, and oil well
brines. In general, the mean values for lead were only slightly higher
than the medians, indicating that extremes did not have much influence on
the averages. An exception to this was the category of domestic wastewaters
which had a mean of 34 ppb as compared to a median of 10. One extreme value
of 2,000 ppb was encountered in a processing plant effluent.
Another regional study involving Champaign County, Illinois, consisted
of monitoring two streams, one draining an agricultural area and the other
draining the cities of Champaign and Urbana (Rolfe and Edgington, 1973).
Suspended solids were removed with a 5-nd.crometer filter, and were analyzed
separately from the liquid fraction. The concentration of dissolved lead
generally ranged from 0 to 15 ppb while that in the suspended solids was
significantly higher and varied a great deal. In the urban drainage, lead
in the suspended solids ranged from 2 to 29 times as much as that in the
liquid fraction. For the rural area, lead content ranged from equal amounts
to 5 times as much. The larger amount from urban sources was attributed to
lead particulate being deposited on paved city streets and being washed off
by rains.
Other comparisons of the soluble lead and lead in particulate matter
have been made for Cayuga Lake, New York, and its tributaries. Soluble lead
was present in the lake at an average concentration of 0.12 ppb while it
averaged 0.91 ppb in the tributary streams (Mills and Oglesby, 1971; Kubota,
et al., 1974). Lead in the particulate matter that was filtered from the
streams was reported as averaging 2.06 ppb. Particulate lead was concluded
to be a better indicator of the impact of urbanization than soluble lead,
which did not show much difference between streams flowing through rural and
urban areas.
Similar data were collected for two streams in Tennesse, of which one
was chosen because it lies near mineral outcrops which would provide metal
content to the water (Perhac, 1972). A considerably higher lead content
was measured in these streams which averaged 15 ppb. The water samples were
divided into three fractions by ultracentrifugation: coarse particulate,
colloidal, and dissolved solids. The highest lead concentration was found
in the colloids from three of the four samples as shown in Table 7.7. The
lowest concentrations were in the dissolved solids with the coarse particu-
lates in between. However, because the amount of insoluble material in the
7.17
-------
Table 7.6 REGIONAL SUMMARY OF LEAD IN SURFACE
WATERS OF THE U.S.S
Region
New England
and Northwest
Southeast
Central
Southwest
Northwest
Lead
Maximum
890
44
84
34
23
Concentration
Minimum
1
1
1
1
1
, ppb
Median
6
4
1
1
1
Not
Detected
Percent
8
27
51
61
62
Detected
Percent
92
73
49
39
38
a Source: Durum and Hem. Reprinted, with permission, from Annals of New York
Academy of Science, (c) New York Acadeny of Science. (1972).
Table 7.7 DISTRIBUTION OF LEAD IN DISSOLVED AND SUSPENDED
SOLIDS OF TWO TENNESSEE STREAMS3
Sample No.
Lead Concentration, ppm
1234
Percentage of Total Lead
1234
Dissolved solid
Coarse particulate
Colloid
77
124
62
75
213
2820
84
653
2820
96
123
<850
95.0
5.0
Trace
90.9
7.6
1.5
87.9
9.3
2.8
89.5
10.1
0.4
Source: Durum and Hem. Reprinted, with permission, from Annals of New York
Academy of Science, (c) New York Academy of Science. (1972).
7.18
-------
streams was relatively small, most of the total lead was contained in the
dissolved solids portion. Sample 1 was taken upstream of the mineralization
of one stream and showed the lowest lead concentration. Samples 2 and 3
were taken in the same stream but below the mineralization. The marked
enrichment of lead in the colloidal fraction suggests that adsorption by
small particles may be a significant mechanism in the transport of lead in
water.
Although the air and soil in the East Helena, Montana, contain more
lead than the national average because of the presence of a smelter, the
water in the area did not show excess levels of lead. Concentrations from
1 to 40 ppb were found in the Helena area which are no greater than those
found in other parts of the country (U.S. Environmental Protection Agency,
1972).
Water in areas in which lead has been mined can be expected to have
greater than average amounts of lead. The Springfield region of Missouri
which has been mined for lead was surveyed by Proctor, et al., (1973) for
the lead content of surface waters and wells. In some localized areas the
lead content of the drinking water exceeded the acceptable PHS limit of 50
micrograms per liter. However, most water samples had a lead content below
this limit. As shown in Table 7.8, seasonal variations occurred, and sur-
face waters contained the most lead in fall and winter whereas well waters
showed greater lead content during the wet summer period.
The lead profiles in the major oceans of the world were determined by
Chow (1968) who used mass spectrometric techniques to analyze samples from
various depths as well as locations. The results, which are shown in Figure
7.3, indicate that there are no essential differences in lead concentrations
in deep waters below the 1,000-meter level. In the surface layers, however,
lead is present in greater amounts in the Pacific and Mediterranean waters
than in the central Atlantic which is away from land influences. Chow also
cited data by other investigators (see Table 7.9) which show that values
found in different places ranged from 0.02 microgram per kilogram in ocean
depths to 8 micrograms per kilogram in surface waters off Europe. According
to Goldberg (1971) about 250,000 metric tons of lead are annually washed out
over the oceans and about 100,000 metric tons over the continents in corres-
pondence to their relative areas.
In a survey of water pollution control in the primary nonferrous metals
industry made for EPA by Battelle-Columbus Laboratories (Hallowell, et al.,
1973), effluents from the tailings ponds were reported to contain anywhere
from no lead to 800 ppb. The combined process and cooling waters from lead
smelters and refineries which were released into streams contained from 70
to 157 ppb of lead. The streams into which the wastes were released original-
ly contained from 0 to 50 ppb, as measured at points considered unaffected
by plant effluents.
The contribution of lead pipes to the level of lead in drinking water
can be significant. In a recently completed study for EPA, a Tufts University
group found that Boston City water contains 25.5 percent more lead than the
federally permissible level of 50 ppb (Anon., 1975). The high lead content
7.19
-------
Table 7.8 LEAD CONTENT OF THE WATERS OF THE
SPRINGFIELD AREA, MISSOURI3
ro
o
Water
Concentration, ppb
Seasons
Mean
Max.
Min.
Standard Deviation
Surface
Shallow wells
(<500 ft)
Deep wells
(>500 ft)
1
2
3
1
2
3
1
2
3
6.47
2.8
0.17
3.03
5
2.94
1.51
2.67
2.45
70
5.7
1
11.25
15
32
6.25
8
12
0
0.5
0
0.75
1
0
0.01
0
0
12.63
1.5
0.36
2.94
3.55
8.15
1.69
2.41
3.97
Source: Proctor, et al. Reprinted with permission from Proceedings 7th
Annual Conference on Trace Substances in Environmental Health, (c) University
of Missouri, 1973.
31 = fall and winter, dry.
2 * spring, dry.
3 = later summer, very wet.
-------
1000-
,2000-
3000-
4000
02
LEAD IN SEA WATER -
0.3
Figure 7.3 Lead profiles in the major oceans.
Source: Chow. Reprinted with
permission from Journal of Water
Pollution Control Federation.
(c) Water Pollution Control Federation,
1968.
7.21
-------
TABLE 7.9 LEAD CONTENT OF VARIOUS MARINE WATERS3
Concentration
Source of Seawater ppb
Florida Key 3-5b
North Sea—Surface 2
Brittany-Surface 3-8
Gullmarfjord-Surface 5-8
Japan Coast-Surface 4
English Channel-Surface 5
Washington Coast-to 100 m 0.1
English Channel 0.6 -1.5
Atlantic-to 5,300 m 0.02-0.10
Pacific-to 4,000 m 0.02-0.35
Bermuda-to 3,000 m 0.03-0.07
aSource: Chow. Reprinted with permission from Journal of
Water Pollution Control Federation, (c) Water Pollution
Control Federation, 1968.
Limit of sensitivity of method.
7c22
-------
was attributed to the acidity of the city water which is sufficient to
corrode old lead pipes in the water supply system. Boston water supplies
come from watersheds lying to the north where the rock is igneous rather
than sedimentary, so that the water composition falls in the small select
group in the U.S. with very low dissolved solids. Thus, the City of Boston
has soft, low pH water and an old piping system in which lead water pipes
are still in use, a combination known to cause excessive dissolution of lead.
It is planned to adjust the pH to reduce the corrosion of the old lead pipes;
2,000 metric tons (2,200 tons) of sodium hydroxide will be required annually
to accomplish this (Anon., 1975).
Glasgow, Scotland, is one of the largest soft water areas in the United
Kingdom, and is an old city in which there are a number of houses which con-
tain not only lead pipes, but also lead water storage tanks (one nearly 200
years old). Not surprisingly, some amazing lead concentrations (up to 2,000
to 3,000 ppb) were observed in the domestic water supplies of some homes
(Goldberg, 1974). The results of the study by Goldberg underline the possible
danger to health of lead plumbing in a soft water area such as Glasgow.
Investigations were carried out on the clinical and metabolic effects of
lead acquired by drinking soft domestic water from lead plumbing systems in
23 households (71 inhabitants). Three groups were studied: Group 1, com-
prising families whose house had a lead-lined tank for storage of drinking
water plus lead piping; Group 2, where there was no lead tank but lead piping
in excess of 18 meters (60 feet), Group 3, where there was less than 18 meters
of lead piping carrying the drinking water supply. The results are shown in
Figures 7.4 and 7.5. The lead content of water from cold water taps was up
to eighteen times the upper acceptable limit and was proportional to the
amount of lead in the plumbing system. The blood lead of 71 inhabitants of
these houses showed a significant positive correlation with water lead con-
tent. Delta-aminolevulinic acid dehydratase activity, an extremely sensitive
indicator of lead exposure, showed a significant negative correlation with
water-lead content. Atmospheric lead was within acceptable limits in all but
one house and no significant correlation could be found with biochemical
measurements. A small number of clinical abnormalities were found but could
not be directly attributed to lead toxicity.
Addis and Moore (1974) also investigated the possible environmental
hazard from lead plumbing in a soft water area such as Glasgow. For their
studies, the houses were divided into two groups; those less than 20 years
old (Group A) and those more than 20 years old (Group B). This division was
chosen because before 1939 these houses were constructed with lead plumbing
and until 1967 lead link pipes were used to connect the domestic copper sys-
tem to the cast iron main. Table 7.10 contains the results of their investi-
gation. The mean lead level of the water in the Group B houses was about 350
ppb; in 82 percent of the houses in this group the lead concentration in the
water was greater than 100 ppb (the WHO acceptable limit). Associated with
this increase in water lead levels was a significant 1.5-fold elevation of
blood lead in the occupants of older houses. When the water lead (PbW) and
the blood lead (PbB) levels were compared for all subjects in the study, a
significant linear regression was found with regression coefficient
7.23
-------
IJOO -
1400 -
1300-
1200 -
1100 -
1000 -
900 -
WATER LEAD
W/llue 800 -
700 -
600-
500 -
400 -
300 -
200 -
100 -
(M
<•
(•
•k
I I
1 1 1
GROUP GROUP GROUP
1 2 3
Figure 7.4 Lead content of cold tap water from
three groups of Glasgow houses
Source: Goldberg (1974). Reprinted
from Environmental Health Perspectives.
-------
40-1-
30H
BLOOD
LEAD
(A)
10-
MEAN±2SEH
\ i
GROUPS
AU
Dehydrate
600-
500-
400-
_VAIBMK\
1
*
I 1
(B)
•200-
100-
GROUPS
Figure 7.5 Lead pollution in Glasgow. (A) Blood levels of inhabitants
of houses in the three groups. (B) Erythrocyte ALA dehydra-
tase levels of the inhabitants of the houses of the three
groups. Adapted from Goldberg (1974). Reprinted from
Environmental Health Perspectives.
7.25
-------
Table 7.10 LEAD IN GLASGOW WATER*
No . in group
Mean age of house
Time of residence
Age of resident
Sex ratio
(female :male)
Water lead (ppb)
Blood lead (pg/100 ml)
Group A
(<20 yr)
12
13.5 + 4.4
8.8 + 5.3
41.3 + 18.8
2 : 1
34.6 + 29.5
19.8+ 8.4
Group B
(>20 yr)
38
42.6 +
16.1 +
46.7 +
29 :
353.1 +
30.5 +
4.2
12.5
17.8
9
255.6
10.6
Significance
N~Sb
NS
P<0.001
P<0.01
S-aminolaevuliflic 27.8+13.2 22.3+10.4 NS
acid dehydratase
(units)
ALAD
Residence>5 yr 30.4 + 12.9(10) 18.9 + 5.1(30) P<0.005
(No. of subjects)
aSource: Addis and Moore. Reprinted with permission from Nature.
(c) Macmillan, Ltd. (1974).
bNot significant.
7.26
-------
r = 0.417 using the Equation PbB = 0.018 PbW + 22.9.
Of particular interest was the observation that for all residents in the
survey, there was a significant negative exponential regression relationship
between erythrocyte ALAD activities and water lead levels, using the equa-
tion ALAD = 25.7e u'uuut) ™w
7.3.3 Distribution in Soil and Rock
The earlier work on measurement of lead in soils and rocks has been
summarized by de Treville (1964) who reported data which were compiled
mainly at the Kettering Laboratory. These data indicate that an average
value for the earth's crust is 16 ppm with alkaline rocks contributing about
8 ppm and acidic rocks about 20 ppm. Alluvial soil gave values as low as
0.04 ppm, while agricultural soil in New Jersey contained as much as 95.7
ppm. In old residential sections of cities where lead paints were used for
many years, values as high as 360 ppm were found. In the vicinity of lead
ores the soil was reported to have up to 10,000 ppm of lead.
In more recent work, Connor, et al., (1971) examined the effect of road-
side location on the lead content of rocks, subsurface soils, and vegetation.
The analyses showed the general trend of "on-road" samples of vegetation con-
taining more lead than the "off-road" samples. However, none of the three
rock types (limestone, shale, and sandstone) sampled showed any accumulation
of lead in the "on-road" samples. In fact, shale showed the opposite effect
which was attributed to geological origins. Connor, et al., were unable to
demonstrate any effect of distance from the road for soil taken a few centi-
menters below the surface. Zimdahl (1971, 1972) reported that for certain
samples of Colorado roadside soils lead concentrations decreased from 1,040
ppm at the surface to 250 ppm at a depth of 13-15 cm (5 to 6 in.).
Comparison of the lead content of urban soils in a region which included
industrial, agricultural, and residential areas showed that there was about
2.7 times as much lead in industrial soil as in residential soil (Klein, 1972).
The agricultural soils contained slightly less lead than those in residential
areas.
A very high lead concentration was found near a heavily-traveled express-
way in Chicago. The soil contained as much as 7,600 ppm at distances up to
13.7 meters from the expressway, and 900 ppm up to 45.7 meters (Khan, et al.,
1973). The amount of lead varied with the seasons in a fashion similar to
the seasonal variations in average monthly traffic volumes on the express-
way. Lead levels were lowest during fall and winter, increased during spring,
and reached their highest values during the summer.
The accumulation of lead in soils over a period of about 40 years was
compared for areas of high and low motor vehicle traffic densities in the
Los Angeles area (Page and Ganje, 1970). The sampling sites were more than
1.6 kilometers from any major highway. No lead accumulations as a function
of time were observed where motor vehicle traffic was less than 80 vehicles
per 2.6 square kilometers (square mile). In areas where the traffic density
7.27
-------
exceeded 580 vehicles per 2.6 square kilometers, the surface concentration
of lead (2.5-cm depth) increased by a factor of 2 to 3, which amounted to an
accumulation of 15 to 36 ppm of lead. The highest value recorded for any
of the locations was 52 ppm.
Lagerwerff and Specht (1970) present data typical of the depth profiles
for lead found by various investigators. Table 7.11 summarizes the results,
and shows about a 65 to 75 percent reduction in lead content in the top 5
centimeters of soil for samples taken at points 8 to 32 meters from a high-
way. In every case the amount of lead decreased with depth of sample.
The presence of a lead smelter can cause very high lead levels in near-
by soils. In the Helena, Montana, study cited previously, the upper 2.54
centimeters of uncultivated soil were found to contain 4,000, 600, and 100
ppm of lead at distances from the smelter of 1.6, 3.2, and 6.4 kilometers
(1, 2, and 4 miles), respectively (U.S. Environmental Protection Agency,
1972).
Roberts, et al., (1974) found that a high rate of lead fallout around
two secondary lead smelters originated mainly from large-particulate
emissions from low level fugitive sources rather than from stack fumes.
The lead content of dustfall, and consequently, of soil, vegetation, and
outdoor dust, decreased exponentially with distance from the two smelters.
Lead emissions from the two smelters were estimated to be 15,000 to 30,000
kilograms per year. Regression analysis of the concentrations indicated
an exponential decrease with distance, from values of 40,000 and 16,000
ndLcrograms per gram of soil close to smelter A and smelter B, respectively,
to an urban background of 100 to 500 micrograms per gram of soil, which
accounted for 60 to 80 percent of the variability in data. Although the
monthly geometric means of the lead concentration in particles close to the
smelters (1 to 5.3 micrograms per cubic meter of air) were only double those
for urban sites (0.8 to 2.4 micrograms per cubic meter) the range of the
daily concentrations was much greater, producing a marked log normal distri-
bution.
Hemphill, et al., (1974) studied roadside lead contamination in soils
along highways used for transport of lead concentrate in the Missouri lead
belt. As shown in Table 7.12, lead values approaching 3,800 micrograms per
gram (ppm) of dry weight were found at zero distance from the road. Along
control routes high lead values of 384 micrograms per gram of dry weight
were observed. The total lead in soils decreased rapidly at 100 to 300
meters. The investigators suggested that the elevated levels of lead in the
soil near the control routes are probably due to contamination from motor
fuel and possibly other sources.
The use of lead paints on the exterior of houses has been found to
result in locally high concentrations of lead in soils. Soil samples taken
near old houses in Cincinnati built prior to 1900 had lead concentrations
which ranged from 32.5 to 7,620 ppm. In general there was a correlation
between soil lead, and the lead content of the exterior paint on the houses
(Bertinuson and Clark, 1973). This work also demonstrated that much more
7.28
-------
Table 7.11 LEAD CONTENT IN ROADSIDE SOIL AND GRASS AS A
FUNCTION OF DISTANCE FROM TRAFFIC AND SOIL
DEPTH1
a
ro
vo
Site
I
West of U.S. 1, near Plant
Industry Station,
Beltsville, Maryland
II
West of southbound lanes,
Washington-Baltimore Parkway,
Bladensburg, Maryland
III
West of Interstate 29,
Platte City, Missouri
IV
North of Seymour Road,
Cincinnati, Ohio
Distance
from
Road, m
8
16
32
8
16
32
8
16
32
8
16
32
Grass
68.2
47.5
26.3
51.3
30.0
18.5
21.3
12.5
7.5
31.3
26.0
7.6
Lead Content
Soil Profile
Layer,
0-5 cm
522
378
164
540
202
140
242
140
61
150
101
55
, yg/g dry weight
Soil Profile
Layer,
5-10 cm
460
260
108
300
105
60
112
104
55
29
14
10
Soil Profile
Layer ,
10-15 cm
416
104
69
98
60
38
95
66
60
11
8.2
6.1
a
Source: Lagerwerff and Specht. Reprinted with permission from Environmental Science and
Technology, (c) American Chemical Society.
-------
TABLE 7.12 TOTAL LEAD IN SOILS OF THE MISSOURI LEAD BELT3
Distance
From Road
Right-of-Way, m (yd)
0
91
183
274
91
183
274
0
(100)
(200)
(300)
0
(100)
(200)
(300)
Lead, yg/gm Dry Weight
Low
16.7
12.7
20.0
33.0
10.7
9.3
8.3
13.3
Mean
Ore Truck Routes
809.6
32.5
36.0
52.0
Control Routes
75.6
23.2
17.3
17.3
High
3,792.0
80.0
48.0
55.0
384.0
49.0
27.0
20.0
No. of
Samples
56
28
11
5
24
16
9
5
aSource: Hemphill, et al. Reprinted with permission from Archives Environmental
Health, (c) American Medical Association, 1974.
In 1 to 6-inch zone.
7.30
-------
lead could be accumulated in the soil around a house with lead paint than at
the roadside where heavy automobile traffic passed (10,200 vehicles per day).
The house contribution to soil lead was about 30 times greater than that
from the road. This source of lead can be accentuated if the old paint is
chipped and scraped from the wood and then allowed to disperse in the vi-
cinity. One such measurement showed that lead in the soil 15 to 30 meters
from the house was 165 to 185 ppm when the old paint was removed. A year
later the lead content had increased to 440 to 490 ppm (Bogden and Louria,
1975).
It has long been recognized that the eating of leaded paint is a main
cause of lead poisoning and elevated blood leads of children living in
dilapidated housing. In this connection, Ter Haar and Aronow (1974) deter-
mined the source of lead in dirt to which children are normally exposed.
Dirt samples were taken in old urban areas around 18 painted frame houses and
18 houses of brick construction (Table 7.13). The data suggested that (1)
weathered lead-based paint is a major contributor to soil lead, and (2)
vehicular sources probably make a significant contribution to soil lead near
the sidewalks.
High local concentrations of lead might be expected to occur in soils
where plants and trees have been sprayed with lead arsenate. In past years
this compound was used as an insecticide but has been presently supplanted
by organic compounds. However, the soil of an orchard which had been sprayed
with lead arsenate for many years was found to contain about 50 to 65 ppm
of lead. This is not an unusually high value; however, it is significantly
greater than the 15 to 20 ppm which is typical of uncontaminated areas
(Vandecaveye, et al., 1936).
7.4 ENVIRONMENTAL FATE OF LEAD
7.4.1 Mobility and Persistence in Air
The physical form of lead in the atmosphere is important to its sub-
sequent disposition. Large particles will fall out near the emission source
while the smallest particles will persist for relatively long times. Aerosol
lead may be emitted to the atmosphere in the form of dust, fume, mist or
vapor depending on the source and the method of generation. Dusts are the
larger particles (1 to 150 micrometers in diameter) that result from mechan-
ical processes such as grinding. Fumes range in size from 0.12 to 1 micro-
meter and result from chemical processes. Mists result from condensation of
vapors on submicroscopic dust particles, and vapors are evaporated liquids.
The particle size distribution of lead aerosols in several large cities
was found by Robinson and Ludwig (1967) to have a fairly wide range. Measure-
ments made at 59 sites in Los Angeles, San Francisco, Cincinnati, and Chicago
gave a mass median equivalent diameter (MMED) of 0.25 micrometer with 25 per-
cent of the particles smaller than 0.16 micrometer, and 25 percent larger
than 0.43 micrometer. Lee, et al., (1968) found a MMED of 0.18 micrometer
for lead aerosols in Cincinnati and 0.42 micrometer in a suburb. In this
7.31
-------
TABLE 7.13 LEAD IN DIRT IN DETROIT3
Lead Concentration, ppm
Painted Frame Houses Brick Houses
Location Mean Range Mean Range
Within 0.6 m of house
front
back
sides
2349
1586
2257
1846
(126-17590)
(162-4951)
(140-7284)
(104-7000)
351
501
426
595
(78-1030)
(72-2350)
(91-1160)
(40-2290)
3 m from house
front
back
Near sidewalk
curb
Gutter
447
425
627
572
966
(58-1530)
(149-1410)
(152-1958)
(320-1957)
(415-1827)
156
200
324
612
1213
(39-316)
(72-480)
(86-1130)
(147-2420)
(304-3170)
*J
Adopted from Ter Haar and Aronow (1974).
7.32
-------
case, 75 percent of the aerosols were less than 1 micrometer. Other work in
California (Mueller, 1970) indicated that 50 to 90 percent of the lead parti-
cles in the urban air are smaller than 1 micrometer. In a later study, Lee,
et al., (1972) reported atmospheric lead particle mass median equivalent
diameters ranging from 0.42-0.69 micrometers in six U.S. cities.
Very large lead particulates ranging in size from 300 to 3,000 micro-
meters in diameter were discovered to have "fallen out" of automobile exhaust(s)
within 4.9 to 6.1 meters (16 to 20 feet) of the car (Habibi, 1970). More
than 95 weight percent of this lead was present as coarse particles, and the
total quantity amounted to 10 percent of the lead originally contained in the
gasoline consumed.
The chemical form of lead in automobile exhausts changes rather rapidly
as the components react with moisture, carbon dioxide, and sulfur dioxide in
the atmosphere. PbBrCl is the principal, initial component although there
is evidence that exhaust particles are bromine-rich compared to stoichio-
metric PbBrCl (Boyer and Laitinen, 1975). Measurements made by Ter Haar and
Bayard (1971) showed that the amount of (PbO) PbBrCl in the exhaust is
almost as great as that of PbBrCl. These two compounds accounted for 31.4
and 32.0 percent of the lead, respectively. Other halogen compounds and
their percentages were: PbCl- (10.4), PbOHCl (7.7), PbBr (5.5), (PbO)
PbCl (5.2), PbOHBr (2.2), ana (PbO) PbBr (1.1). The nonhalogen compounds
founa were: PbOx (2.2), PbC03 (1.2)7 (PbOJ PbCO- (1.0), and PbSO, (0.1).
After 18 hours, measurements showed that about 75 percent of the bromide
and 30 to 40 percent of the chloride compounds had disappeared. The lead
oxides, carbonate, and oxycarbonate then constituted 65 percent of the sample.
On longer exposure to the atmosphere the carbonate content increased and
some of the lead was converted to sulfate. Particulate samples collected
in the vicinity of a rural road which would represent "aged exhaust" had a
lead distribution of PbCO (30.2), (PbO)_ PbCO (27.5), PbO (20.5), PbO-
PbSO, (5.0), and PbSO, (3.2). The remaining 15 percent of £he lead was
distributed among the chloride and bromide compounds. Consequently, by the
time lead aerosols are removed from the atmosphere, they are converted almost
completely to carbonates and sulfates.
The presence of alkyl lead vapors (from gasoline) in ambient air has
been reported by several investigators. Purdue, et al., (1973) in a study
on organic lead concentration in an underground parking garage, and in
general ambient air of six major U.S. cities, found that in the parking
garage, lead was 11.7 micrograms per cubic meter, of which 16.7 percent was
organic lead. However, in the six major cities the organic lead concentra-
tion was lower (about 10 percent) relative to the total lead. Since the
concentrations of organic lead found approached the detection limit of the
method, there is some uncertainty concerning the accuracy of the data.
Snyder, et al., (1967), in a study in Los Angeles found that about 2 percent
of the lead was organic. Differences in the concentration of organic lead
found relative to particulate lead might be attributed to differences in
proximity to the lead source. Uniformly low levels (under 10 percent of
the total lead), except for two brief periods were reported by Laveskog
(1971) who studied the presence of lead in the air at several locations in
7.33
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Stockholm. These low levels occurred near a gasoline station and were
attributed to evaporation of fuel spills. Colwill and Hickman (1973) con-
finned Laveskog's concept. Harrison, et al., (1975a) found that organic lead
levels ranged from 0.02 microgram per cubic meter in a tunnel to 0.59 micro-
gram per cubic meter six meters from a gasoline pump.
The mass balance for automobile-related lead was developed for the Los
Angeles basin by Huntzicker, et al., (1975). Lead calculated to be attrib-
utable to automobile exhaust was estimated to be 17.6 plus or minus 2.6
metric tons per day. In addition to the exhaust components, the evaporation
of antiknock compounds was considered since tetramethyllead has a vapor
pressure of 24 torr at 20 C and tetraethyllead, 0.15 torr (Schwarzbach, 1973).
However, the contribution estimated for evaporation of antiknock compounds
amounted to only 0.3 ton per day. The total amount of lead thus generated
was considered to be spread over the region. Deposition near the source
accounted for 9.5 plus or minus 2.2 tons per day; deposition far from the
source amounted to 2.0 plus or minus 1.0 tons per day, and lead removed by
wind was 5.6 plus or minus 3.0 tons per day. Essentially all of the auto-
related lead (17.1 plus or minus 3.9 metric tons per day) could be accounted
for in terms of these mechanisms.
The movement of particulate lead compounds was monitored along a
heavily traveled freeway in Cincinnati, at a nearby park, and in a resi-
dential area about 3.2 kilometers (2 miles) away (Cholak, et al., 1968).
The findings indicated an average concentration of 7.8 micrograms per cubic
meter at the freeway, 1.7 at the park site, and 1.1 at the residential site,
both leeward of the source of lead. The concentration of lead in the air
at the latter site was approximately the same as that of 6 years previously.
Concentrations of lead at the freeway site did not vary with the seasons
and most likely reflected the uniformity of vehicular traffic on the road-
way. At both of the other stations, concentrations were higher during the
summer and fall months than during the winter and spring months. The mass
median equivalent diameter of the lead particles was found to be approximately
0.30 micrometer with 70 percent of the lead particles being less than 1
micrometer. The size data indicated that most of the lead in dusts removed
from the air by filtration is mainly in the size range considered "respirable".
Not all of the small lead particles in the atmosphere can be attributed to
automobiles, however, because emissions from a coal-burning power plant have
been found to contain lead (3 percent) in the finer particles that are not
collected even by a high efficiency electrostatic precipitator (Klein, et al.,
1975).
Concentrations of dustfall at the three Cincinnati stations varied from
16.5 metric tons per square kilometer (47 tons per square mile) at the highway
to 8.4 metric tons per square kilometer (24 tons per square mile) at the
other two stations. Concentrations of lead in the dustfall at the freeway
averaged 0.51 percent while at the other two stations they were only 0.12
percent. Thus, the average monthly quantity of lead at the freeway was
approximately twice that at the other two sites, a main factor in the con-
tamination of soil and vegetation near the highway (Cholak, et al., 1968).
Data on concentration of lead in soils and grass roots and blades showed
7.34
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variations according to the distance from the roadway with most of the
contamination occurring within 30.4 meters (100 feet). The top 0.63 centi-
meter (0.25 inch) of soil contained the highest concentration of lead which
suggests surface contamination due to partial washout of lead from the
atmosphere, but principally from the settling of the larger lead particles
generated at the roadway.
In a study carried out in 1968 by EPA, 77 cities in the central U.S.
were monitored for lead and other metals in dustfall from the atmosphere
(Hunt, et al., 1971). Residential, commercial, and industrial areas were
distinguished. As shown in Figure 7.6, the fallout of lead was highest in
industrial areas, followed closely by commercial areas. Residential fallout
was about one-half of industrial fallout. The monthly variation was not
considered statistically significant.
A model for short range environmental transport and accumulation of
automotive lead near open highways was developed by Vaitkus, et al., (1973).
Atmospheric transport of lead from a highway (Interstate-25 in Colorado) and
its removal from the atmosphere by gravitational settling, washout, and
rainout were coupled with migration and retention in soil. Figures 7.7 to
7.9 show the values calculated from the model for the various ways of
removing atmospheric lead. The model was found to predict lead levels
reasonably well over the downwind distance to 60 meters, but was low beyond
that distance (see Figure 7.10).
Kleinman, et al., (1973) computed a dispersion factor for trace metals
in the atmosphere which was defined as the product of the morning mixing
height and the surface wind speed. Measurements of lead and several other
metals made at various locations in New York City during 1972 showed a
marked seasonal variation involving a spring minimum and a summer maximum.
Values for lead (see Figure 7.11) ranged from a minimum about 1 microgram
per cubic meter in spring to a maximum of 4 micrograms per cubic meter in
summer. The correlation between the dispersion factor and the lead concen-
tration was highly significant at the 95 percent level. By measuring the
concentration of lead-212 in vertical profiles at the Empire State Building,
New York City, Assaf and Biscaye (1972) estimated that the residence time of
air within the street layer was of the order of 5 minutes.
Rainfall removes lead from the atmosphere. The residence time of lead-
210 in rainwater was calculated by Burton and Stewart (1960) to be 22 days
for particles whose whole airborne life is spent in the troposphere. How-
ever, Francis, et al., (1970) found a residence time of only 9.6 days for
filtered rainwater samples and attributed Burton's higher value to a signi-
ficant dust component in the sample.
Snow is also effective in removing lead from the atmosphere. Hamilton
and Miller (1971) found an average lead concentration of 410 ppb, and a
maximum value of 1,090 ppb in snow collected in Columbus, Ohio. No rain
data are provided for a direct comparison to precipitation as rain. A study
of the lead concentration in snow in Ottawa, Ontario, was undertaken to
assess the effects of snow disposal practices. One hundred and forty-nine
7.35
-------
t.ai
2.00
i «n
DUSTFALL loge
i 1
1.40
1.20
IAA
•UU
1 III
: Eh
- g«
: B-
i i i
RES COMM IND
AREA
1 1 1 1
_
—
r— i
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tr g-
—
i i i i _
SEPT OCT HOV DEC
MONTH
9.00
8.00
7.00
i
5.00 J
1
4.00 Q
300
Figure 7.6 Geometric means and 95 percent confidence
intervals for lead fallout measurements
in 77 cities by area and month. Source;
Hunt et al. Reprinted with permission
from Proceedings 4th Annual Conference
on Trace Substances in Environmental Health.
(c) University of Missouri. 1971.
7.36
-------
0L*8.0pq-fri" •••e" . VLSD «9,0m
80
Figure 7.7
DOWNWIND DISTANCE D ,m«tarc
Gravitational fallout flux of lead and
washout lead concentration as a function
of downwind distance from edge of highway
at T = 1000 sec.
Source: Vaitkus, et al. Reprinted with
permission from Proceedings 7th Annual
Conference on Trace Substances in Envrion-
mental Health, (c) University of Missouri,
1973.
Oi»8.0ttQ-iif'-s«c , VLSD>9.0m
50
DOWNWIND DISTANCE D. (Mters
loo00
Figure 7.8 Long-range transport of lead and lead
deposited at soil/air interface as a
function of downwind distance from
edge of highway at T = 1000 sec.
aSource: Vaitkus, et al. Reprinted with
permission from Proceedings 7th Annual
Conference on Trace Substances in Environ-
mental Health, (c) University of Missouri,
1973.
-------
Ul
SO «XX
7.9 Concentration of lead in soil accumulation zone
and balk soil residual lead content as a function
of downwind distance from edge of highway at T = 1000
sec.
7.10 Comparison of predicated atmospheric
lead concentration and measured
values on Interstate 23 as a function
of downwind distance from edge of high-
way at z = 1.2 meters.
Source: Vaitkns, et al. Reprinted with permission from Proceedings of 7th Annual Conference on Trace
Substances in Environmental Health, (c) University of Missouri, 1973.
-------
IW
140
IW
in
no
too
•0
•0
70
10
N
4
I
I
I
0
TbMI lu»p»nd»d Amtiiutofl
l CinlifMonholion
MflM-B'Oni
* l*(l«ick Avl-B'Oni
Jon
Mir Apr Moy Jun« July At* »«pi Oci Nw 0*e
Figur* 7.11 Concantratloni of total suspended particulat*
and lt«d In N«w York City air. Source: Klsinman,
•t al. R«prlnt«d with Ptrmiiaion from Procaadlnga
7th Annual Confaranca on Traca Subatancea in
Environmental Health, (c) University of Miaaouri,
1973.
7,39
-------
samples from eleven snow dumps within the city gave widely ranging values of
20 to 50,000 ppb, with an average of 4,800 (La Barre, et al., 1973). It is
of particular significance that the runoff from these snow dumps contained
an average of only 110 ppb. Hence, much less lead would be introduced into
streams if the snow were dumped on nearby land rather than directly into the
water. This viewpoint is supported by the data of Hirao and Patterson (1974)
who measured lead concentrations in Thompson Canyon which is located in the
crest of the high Sierra in California. Lead is coprecipitated with snow in
that region as very little moisture falls as rain. It was found that 98
percent of the industrial lead entering the canyon as aerosols remains there.
The chelating humus fraction of the soil apparently extracts most of the
lead from snow meltwaters because very little lead was found in streams
leaving the canyon.
7.4.2 Mobility and Persistence in Water
In the absence of suspended solids the solubility of lead in water is
dependent on pH, salt content, and partial CO pressure. Equilibrium cal-
culations show that the total solubility of lead in hard water is about 30
ppb and 500 ppb in soft water (Davies and Everhart, 1973). In soft water
with a pH of 5.4 or less, PbSO, is present and limits the lead concentration
in solution. Above pH 5.4, PbCO- and Pb2(OH)_CO, are the limiting factors
in lead concentration. In hard water a pH greater than 6.0 is the level at
which the above carbonates are present and cause a corresponding limitation.
The most important factor in determining lead solubility in both of these
waters is the carbonate concentration which in turn depends on the partial
pressure of C09 and the pH. The equilibria involved in the solubility of
lead are presented in Figures 7.12 and 7.13 for soft and hard water,
respectively. The Cp, lines gives the concentration of the lead in solu-
tion.
Because most natural waters have a pH greater than 7, the upper limit
on the concentration of lead that occurs in lakes, rivers, or underground
water is determined by the solubilities of lead carbonate and lead hydro-
ide. This solubility limit can be low for the more alkaline and moderately
mineralized waters which are commonly used for water supplies in much of the
U.S. Fortunately, treatment of city water supplies usually keeps the pH high
enough to maintain lead at a low concentration. Hence, lead concentrations
will be below the 50 micrograms per'liter standard for drinking water of the
U.S. Public Health Service. However, where dissolved solids in water are
low and the pH is less than 7, lead can be present in amounts greater than
the above standard (Hem and Durum, 1973). When particulate matter is
present, the lead content of water can be much greater than the equlibrium
solubility due to adsorption of lead ions on particle surfaces. The actual
thermodynamic equilibrium solubility is unchanged, however.
Because at least twice as much lead is found in atmospheric precipita-
tion as in water supplies, Lazrus, et al., (1970) concluded that there is
some process by which lead is depleted after precipitation reaches the earth's
surface. Other investigators have reported lead in suspended matter to be
insoluble in surface waters, and to be removed by natural sedimentation or
-------
15 -
13
pH
Figure 7.12 Solubility and species distribution for Pb (II) in soft
water. Adapted from Davies and Everhart (1973).
-------
pH
Figure 7.13 Solubility and species distribution for Pb (II)
in hard water. Adapted from Davies and Everhart (1973)
-------
filtration (National Academy of Sciences, 1972). The lead present in pre-
cipitation appears to contribute more to the pollution of sediments than to
the pollution of water; therefore it is unlikely that precipitation will
have a significant effect on the concentration of this element in potable
waters (Harrison, et al., 1975b).
Some insight into the cycle of lead in water can be gained from the
ratios of the various lead isotopes. Lead in surface ocean waters and recent
precipitation is isotopically different from that found in marine sediments
deposited in the geologic past. The isotope composition of lead in surface
waters is typical of a mixture of lead ores from mines (Chow, 1968). Lead
from man-made sources is obviously being discharged into the rivers and
thence into the oceans.
It has been calculated that industrial lead is being added to the oceans
at about ten times the rate of introduction by natural weathering (Chow and
Patterson, 1959 and 1962). This additional lead in the oceans can be trans-
ported downward by physical processes of mixing and diffusion. However, one
of the most effective agents in removing it from the surface layer is the
biological process associated with sedimentation.
7.4.3 Mobility and Persistence in Soil
The nature of the lead compounds in soil that originate in automobile
exhausts and that are formed near roadways was determined by Olson and
Skogerboe (1975). Samples were collected from the top centimeter of surface
soil or from street dust in four different parts of the U.S. Lead sulfate
accounted for the major portion of the lead present in the samples. A small
amount of PbO*PbSO, and traces of lead oxides were found in some of the
specimens, while PbS was detected in a sample from the Missouri Lead Belt.
In view of the work by Ter Haar and Bayard (1971) which showed that only
about 3 percent of the aerosol lead in "old" exhaust particulates was PbSO,,
it appears that much of the conversion to lead sulfate occurs after the lead
compounds are deposited on the soil.
Lead can also be held by the humic acids in soil, either through forma-
tion of salts or by coordination. When humic acids from various soils were
treated with a lead solution, the carbonyl (C=0) functionality disappeared,
and the carboxylic acid (COOH) function was converted to the corresponding
salt (Hildebrand and Blum, 1974). As the pH of the soil humus was decreased
from 8 to 3, the amount of lead fixed was reduced from 112 to 24 millequiva-
lents per 100 grams of humus. These results show that soil condition has
an important effect on the amount of lead retained.
In general, lead deposited on the soil is retained near the surface,
and its concentration drops off rapidly with depth of the soil. However,
it has been observed that this retention does not always occur, and that
sodium chloride is capable of leaching the lead from surface layers
(Vandenbeele and Wood, 1972). Such a situation would occur where salt is
used to melt snow and ice on highways.
7.43
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There is some evidence that lead tends to be moved upward in the earth's
crust. Swaine and Mitchell (1960) found that in Scottish soils there was
approximately twice as much lead at the surface as there was at a depth of
125 centimeters. The soils analyzed were in uncultivated areas far from
any industrial or vehicle contamination. Wright, et al., (1955) also
reported similar results for Canadian soils from four areas. Swaine and
Mitchell (1960) speculated that the decay of plant material formed some
insoluble lead complex which concentrated near the surface.
If the lead is strictly of inorganic origin, it apparently can be
leached from the soil at a fairly rapid rate. Roberts and Goodman (1973)
examined surface soils in the vicinity of smelters at intervals after perman-
ent shutdowns of the smelters. Soil depletion of the lead was relatively
fast. At two badly contaminated sites (104 and 328 micrograms per gram of
soil) the surface 5 centimeters lost lead at a rate that would get it down
to background values within 2 to 5 years. A site with less lead (9.6 micro-
grams per gram of soil) and a dense grass cover lost lead at a much slower
rate, and would take some 30 years to reach background.
Other evidence for fairly rapid removal of lead by leaching was ob-
tained by Clark (1973) in an investigation of the leachate from landfills.
Trace metals in the leachate were determined, and the lead concentration
was found to be high as 500 ppb at a northern Illinois site. This value is
ten times the allowable amount for U.S. Public Health standards and five
times that permitted by the Illinois Pollution Control Board.
7.4.4 Wastewaters
It can be expected that the metal content of wastewaters will be greater
than that of natural waters. Measurements made in Pittsburg, Pennsylvania,
at the Allegheny County treatment plant for the first 6 months of 1973 showed
that the incoming water contained an average of 119 ppb of lead (Davis and
Jacknow, 1975). Of this amount about 75 ppb could be attributed to residential
and commercial sources; the remainder was industrial. Primary treatment at
the plant reduced the lead concentration to 55 ppb, and the secondary treat-
ment, to 22. Similar measurements made at Muncie, Indiana, for 1972-73 showed
a lead concentration of 920 ppb in the treatment plant influent. The amount
of lead in the plant effluent was reduced to 170 ppb in 1972, but only to 270
in 1973. In this case the residential contribution to the 920 ppb was found
to be only 120 ppb.
The waters of New York harbor are heavily contaminated by industrial
wastes from a variety of sources. They contain from 130 to 700 ppb of lead
depending on the location (Klein, et al., 1974). The highest values occurred
in the lower East River, and the lowest were in Jamaica Bay and the Long
Island waters.
A very extensive investigation of lead and other heavy metals in the
wastewater effluents of the Hyperion Treatment Plant, Los Angeles, California,
was conducted by Chen, et al., (1974). The lead concentration in the primary
effluent was found to be 110 ppb with a reduction to 42 in the secondary
7.44
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effluent. Most of the lead was in the dissolved state with less than 20
percent retained by 0.2 micrometer filters. The secondary treatment removed
less than 40 percent of the dissolved lead. The digested sludge from the
plant contained 530 ppm by weight of lead.
Morel, et al., (1975) in a study of a chemical equilibrium model of Los
Angeles County sewage concluded that lead should be present as the very in-
soluble sulfide, PbS. It also was concluded that at low dilution and moderate
oxidation conditions, lead carbonate will precipitate because of the high con-
centration of carbonate in the sewage. The significant effect of oxidation
is the dissolution of lead sulfide.
The effect of mixing wastewaters with seawater was also examined for the
discharge from the Hyperion plant in Los Angeles (Rohatgi and Chen, 1975).
Suspended solids in primary effluent containing 156 ppm by weight of lead
released 53 percent of their lead content when equilibrated with seawater at
a 5 to 1 dilution. The digested sludge particulates originally containing
875 ppm by weight of lead released 49 percent of the lead after 15 minutes
(50 to 1 dilution) but after equilibration this was reduced to 38 percent. Hence,
mixing with seawater is quite effective in reducing the amount of lead held
on the wastewater solids. This effect may be the result of surface desorption
caused by a high dilution ratio, the oxidation of sulfide, or complexing by
anions in the seawater.
Wastewaters from a lead mine are potential sources of lead pollution.
Proper management of wastes can keep the amount of lead discharged at a
relatively low level. Stream monitoring in the New Lead Belt of Missouri has
shown that lead concentrations in streams receiving mine effluents can be kept
below 50 ppb. Values obtained during 1969-70 ranged from 0 to 40 ppb of lead
(Jennett and Wixson, 1972). Heavy metals in mine wastes are precipitated
rapidly in settling and treatment lagoons by making the mine water more basic
(pH 7.5 to 8.2), thereby maintaining low levels of metals in the nearby
streams.
7.4.5 Sediments
Significant concentrations of lead have been found in sediments from
regions which have a high volume of automobile traffic or heavy industrial-
ization. Measurements made on sediment cores from selected lakes in Wisconsin
have shown that in populated areas the top 5 centimeters of sediments contained
from 28 to 124 ppm by weight of lead. By contrast, sediments from remote
lakes which never received any sewage effluent contained only from 3 to 10 ppm
of lead (Iskandar and Keeney, 1974). In addition, it was noted that even at
a depth of 50 centimeters in sediments from lakes in populated areas, there
was more lead than in the top layer of sediment in isolated lakes.
Similar examination of two sedimentary cores from Lake Washington in
Seattle, Washington, showed an increase in lead content from 30 to 400 ppm by
weight during the past 80 years. The increased lead concentration paralleled
the population increase of the area. The two major sources of lead during
the period were believed to be a lead smelter in Tacoma, Washington, from
1890 to 1913, and automobile exhausts from the 1920's to the present (Crecelius
and Piper, 1973).
7.1*5
-------
Sediment samples from four lakes in Indiana were found to have lead con-
centrations of 7, 163, 184, and 345 ppm by weight. In the absence of character-
ization of the lakes, it is likely that automotive and industrial sources of
lead can be associated with the high values. Data on sediments from a Gary,
Indiana, borrow pit subject to such influences showed values which generally
ranged from 200 to 493 ppm (Peyton and Mclntosh, 1974).
Bottom sediments from the Illinois River near Peoria, Illinois, were
analyzed by Mathis and Cummings (1973). The lead content proved to range
from 3 to 140 ppm by weight, giving a mean value of 28 ppm. The latter value
was 10,000 times greater than the mean for lead concentration in the river
water (0.002 ppm). By way of comparison, the sediments of three nonindustrial-
ized streams contained an average of 17 ppm of lead.
Core samples of sediment collected in the delta area of the Coeur d'Alene
River in Idaho were mostly fine silt typical of mine tailings. For over 80
years mining and smelting wastes had been discharged into the river. The top
layer of the sediments contained from 3,000 to 6,300 ppm by weight of lead.
There was no significant decrease in metal content in the sediments collected
at the river's mouth even at a depth of 52 centimeters. The lead content in
the sedimentary layers followed the decreasing order clay, organic matter,
silt, sand (Maxfield, et al., 1974).
The effect of a lead-zinc mineralized area on the heavy metal content of
sediments in downstream reservoirs was investigated by Pita and Hyne (1975).
Bottom sediments were collected from five reservoirs in Oklahoma, Kansas, and
Missouri. In two of the reservoirs the lead concentration in sediments was
less than 25 ppm, and in the other three average values of about 50 ppm were
found. Soil in this region contains about 22 ppm lead, so the sediment was
enriched with respect to the soil. Separation of sediment components accord-
ing to specific gravity showed that lead was concentrated in the 2.0 to 2.9
fraction. This indicates that lead was included with clay minerals either
as ions or as organometallic complexes.
Sediments collected in the coastal basins of Southern California receive
lead at rates from two to seven times greater than those that existed before
man-made sources of pollution contributed to lead levels. Values for the
Santa Monica, San Pedro, and Santa Barbara Basins were 0.9, 1.7, and 2.1
micro grains per square centimeter of sea bottom per year as compared to natural
rates of 0.24, 0.26, and 1.0, respectively (Chow, et al., 1973).
The possible solubilization of lead in bottom sediments by nitrilotri-
acetic acid has been explored by Gregor (1972). This compound was proposed
as a substitute for phosphates in detergents. As little as 2 ppm of
nitrilotriacetic acid was found to be capable of solubilizing some lead in
the sediments, and 20 ppm of the acid increased soluble lead from 0.03 to
0.61 ppm in one case. Hence, the presence of complexing agents in water can
cause lead concentrations to exceed the U.S. Public Health Service standard
of 0.05 ppm.
-------
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-------
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7.50
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7.51*
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8.0 ENVIRONMENTAL INTERACTIONS AND THEIR CONSEQUENCES
8.1 SUMMARY
Various processes interact to redistribute lead in the environment. Or-
ganisms can take up lead from these media and, in some cases, can concentrate
and accumulate lead. A variety of foods have a low, but measurable lead con-
tent. In some marine organisms elevated lead levels seem to be related to
increased lead levels in the water. However, biomagnification of lead was
not found in the different aquatic organisms.
In foods, the available data indicate that the edible portions of crop
plants, including leaves, roots, and fruits generally have a lower lead
content than the inedible portions. Also, the levels consumed in fresh fruit
and vegetables are well below levels considered significant from the human
health standpoint.
On the basis of a recent Market Basket Survey, the estimated daily aver-
age intake of lead by a U.S. adult is in the range of 57 to 233 micrograms.
The comparable daily intake in the United Kingdom has been estimated at 200
and 20 micrograms for food and beverages, respectively. Absorption of in-
gested lead has been estimated to normally lie in the 8 to 10 percent range for
adults and in the 40 to 50 percent range for infants and preschool-age children
(see Section 6.2.1.2).
Comprehensive work has been initiated on the movement of lead within the
various components of ecosystems. The transfer of lead through a simplifed
estuarine food web and a laboratory model ecosystem with a terrestrial/aquatic
interface has been described.
8.2 ENVIRONMENTAL CYCLING OF LEAD
In Section 7.3 the sources, distribution, and fate of lead in air, water
and soil were described. In addition to background levels from geochemical
sources, elevated levels of lead may result from industrial mining, refining,
and processing steps and from the disposal of various municipal wastes. Fi-
gures 8.1 and 8.2 illustrate the environmental cycling of lead. Table 8.1
describes the environmental pathways for various lead compounds. Although
the input of lead by the combustion of leaded fuels is considered to be the
major environmental source of lead, other sources such as food, industrial
wastes, paints, waste oils and storage batteries also contribute to the en-
vironmental burden. The fallout of lead-containing dust and its removal by
rain or snow result in lead being deposited on soil and in water. The lead
will then either be (1) retained in the soil and at least part of it become
8.1
-------
OTHER LEAD-
CONTAINING
PRODUCTS
Figure 8.1
Ecologic flow chart for lead showing
possible cycling pathways and compartments,
Adapted from National Academy of Sciences,
(1972).
8.2
-------
Lead Ores(Oalena*
Sources Manufacturing and Industrial Processes
Airborne Emission from.,— Industrial Wastes "—«• Lead Objects—i
Autos and Industry -*^ I Paint
I Piaster(Pica)
I 1 ft*?
Distribution Soil ash by rain ^ R|vers>LoheSjOceon5 Pottery
Edible Plant Life Drinking Water ^^Aquatic Life
Vinhalatii
Pharmacodynamics
rPoul try. Meat /
1 intake by Man".
Feces
Blood Cells (non-diffusible)
Plasma (Ugand bound.diffusible)
Health Effects CNS^" Reticuloeytes Kidney Miscellaneous Effects
Encephalopathy Peripheral Anemia Tubular dysfunction Endocrine
Neuropathy I Reproductive
I Cylogenetic
Urinary excretion
Bone (non-diffusible)
Figure 8.2 Ecodiagram of lead in the environment and its effect
on man. Source: Fishbein. Reprinted with permission
from The Science of the Total Environment, (c)
Elsevier Scientific Publishing Company, 1974.
8.3
-------
Table 8.1 ENVIRONMENTAL PATHWAYS FOR LEAD COMPOUNDS*
Chemical Compounds
Source
Tiansport Path
Effect
Uses
Lead acetate
Industrial processing
Lead alloys
Industrial processing
Power generation
Transportation
Lead antimonate
Lead arscnaie
Industrial processing
Industrial processing
Agriculture
Lead anenite
Industrial processing
Agriculture
Lead azide
Lead borate
Industrial processing
Industrial processing
Lead carbonate
Industrial processing
Air
Water
Land
Air
Water
Land
Fisheries
Physiological
Physiological
Air
Water
Land
Air
Water
Land
Food
Consumer
products
Air
Water
Land
Food
Consumer
products
Air
Water
Land
Air
Water
Land
Air
Water
Land
Physiological
Physiological
Physiological
Physiological
Physiological
Dyeing and printing cottons
Manufacture of lead salts
Astringent (veterinary)
Paint drier
Lead coating of metals
Slush coatings
Type metals foe printing
Batteries
Battery grids
Bearing metals
Solders
Fusible alloys
Communication cables
Pipe and sheet in chemical
installations
Corrosion protection coatings
Pigment
Staining glass
Crockery and procelain
Insecticides
Veterinary medicine
Primer in explosives
Paint drier and production of
conductive coatings
Class
Pottery
Porcelain
Chinaware
Paints
Ceramics
Glazes
Processing of; archment
-------
Table 8.1 ENVIRONMENTAL PATHWAYS FOR LEAD COMPOUNDS8
(cont'd)
Chemical Compounds
Lead chloride
Lead chromate
Lead cyanamld
Lead dioxide
Lead fluorosilicate
Lead fumaiaie
Lead Iodide
Lead linoleate
Lead molybdate
Lead monoxide.
litharge
Source
Industrial processing
Industrial processing
Industrial processing
Industrial processing
Mining
Industrial processing
Industrial processing
Industrial processing
Industrial processing
Industrial processing
Mining
Industrial processing
Transport Path
Alt
Water
Land
Direct contact
Alz
Water
Land
Direct contact
Air
Water
Land
Direct contact
Air
Water
Land
Direct contact
Air
Water
Land
Contact
Air
Water
Land
Direct contact
Air
Water
Land
Direct contact
Air
Water
Land
Direct contact
Air
Water
Land
Air
Water
Land
Consumer
service
Contact
Effect
Physiological
Physiological
Physiological
Physiological
Physiological
Physiological
Physiological
Physiological
Physiological
Physiological
Uses
Manufacturing of white lead dyes
Solder and flux
Pigment
Printing of fabrics
Decorating china and porcelain
Corrosion inhibitors
(Antltust paints)
Electrodes
Dyes
Rubber substitutes
Manufacture pigments
Analytical purposes
Electrolyte in electrolytic
refining of lead
Plastiiols
Phonograph records
Electrical insulation
Bronzing, priming
Photography
Driers in paints
Paint
Pigment
Ointments
Plasters
Glaze
Flux
Pigments
Analytical
Driers
8.5
-------
Table 8.1 ENVIRONMENTAL PATHWAYS FOR LEAD COMPOUNDS*
(cont'd)
Chemical Compounds
Sources
Transport Path
Effect
Uses
Lead naphthenaie
Industrial processing
Lead nitrate
Lead oleate
Industrial processing
Industrial processing
Lead orthophosphate Industrial processing
Lead phosphate
Industrial processing
Lead selenlde
Lead silicate
Lead stannate
Industrial processing
Mining
Industrial processing
Industrial processing
Air
Water
Land
Direct contact
Home environment
Work environment
Air
Water
Land
Contact
Air
Water
Land
Direct contact
Home environment
Work environment
Air
Water
Land
Home environment
Work environment
Neighborhood
environment
School environment
Consumer products
Food
Waste
Air
Water
Physiological
Driers In palm
Physiological
Physiological
Match industry
Pyrotechnics
Chemical intermediates
Driers in paint
Physiological
Stabilizer for plastics
Pigments
Antlcorrosive agents
Physiological
Stabilizer for plastics
Home environment
Work environment
Neighborhood
environment
School
environment
Consumer products
Food
Waste
Air
Water
Lead
Environment
Air
Water
Land
Environment
Air
Water
Land
Environmental
contact
Physiological
Physiological
Physiological
Semiconductor
Infrared detector
Glass ceramics
Ceramics
8.6
-------
Table 8.1 ENVIRONMENTAL PATHWAYS FOR LEAD COMPOUNDS8
(cont'd)
Chemical Compounds
Lead tubacetate
Lead tulfate
Lead mlfide
Lead telluride
Lead tetraoxlde.
tedlead
Lead tetraethyl
Lead tetrarnethyl
Trialkyl 01 alkyl
aiyl lead
Lead tbiocyanate
Lead thlosulfate
Sources
Industrial processing
Industrial processing
Mining
Mining
Industrial processing
Mining
Industrial processing
Industrial processing
Industrial processing
Power generation
Industrial processing
Power generation
Transportation
Agriculture
Industrial processing
Industrial processing
Industrial processing
Transport Path
Air
Water
Land
Food
Air
Water
Land
Contact
Air
Watet
Land
Contact
Air
Water
Land
Contact
Air
Water
Land
Air
Water
Land
Direct contact
Food
Air
Water
Land
Direct contact
Food
Air
Water
Land
Direct contacr
Food
Ait
Water
Land
Contact
Air
Water
Land
Contact
Effect
Physiological
Physiological
Physiological
Physiological
Physiological
Physiological
Physiological
Physiological
Physiological
Physiological
Uses
Sugar analysis
Pigments
Batteries
Lithography
Fabrics
Photoelectric cell
Infrared detector
Photosensitive resistor circuits
Photoelectric cell
Infrared detector
Photosensitive resistor circuits
High voltage lightning arrested
Dyes
Chemicals
Matches
Pyrotechnics
Curing agents (rubber substitute)
Antiknock
Fungicide
Antiknock
Fungicide
Filling of Gelger counters
Polymerization
Catalysts
Stabilizers for PVC1
Electroplating
Lubricating oils
Biocfdal agents
Primer in explosives
Matches
Dyes
Rubber accelerator
Lead mirrors
8.7
-------
Tobla 8.1 KNVJRONMENTAI, PATHWAYS FOR LEAD COMPOUNDS*
(cont'd)
Chemical Compound! lource
Tiampon Path
I(f*ci
UMI
L«ad il(*nd«
Uad lungiuw
van*d*u
Mining
InduiitUI proc«Mln|
Mining
IruluiiiUI
InduiirUI proMiiing
InduiuUI procMitng
All
W«ur
Und
Conitei
Air
Wiwr
Und
Air
Wtur
Land
Contact
Air
Water
Land
Thyitologloal Plgnwm
Ccramla
Pnyilologlcal Pigment
Plgmani
Phyiiologlcal Plgimnt
*Adapt«d from Lute et A!. (1970).
8.8
-------
available for plant and animal uptake, or (2) some will be leached Into ground-
watar. Baaldaa waatewater ditchargea, lead can be removed from land masse*
by runoff to surface watere. The lead In theae waters will appear In sedl-
mcnta and be ready to reenter the environmental cycle, except that ocean
aedlmenta conatltute, in part, an ultimate alnk for waterborne lead.
8.3 FOOD CHAINS
8.3.1 Lead in Pooda
Lead entera planta and anlmala which are conaumed aa human food from the
following aourcea:
1, Air—Duatfall and airborne particles that contain
lead may settle on aoll or' on leavea and sterna of
planta.
2. Soil—Lead la preaent In all soils. The content
Is Increaaed by lead from duatfall or rainfall.
3. Water—Lead la widely distributed in natural water*,
both fresh and marine. Rainfall alao contains
lead derived from atmospheric particles.
The lead content of food or forage plants la related to the amount that
la applied topically to axpoaed areas of edible leavea, atema, and fruit by
rainfall or duatfall, and to the amount that Is translocated from soil and
surface and/or ground watera through the roota to atema, leaves, and fruit
(Bathaa and Bethen, 1975; Ewing and Pearson, 1973; Kehoc at al., 1968; Haley,
1969; Lagerwerff, 1970; Leland et al., 1975; Ter Haar, 1970; aee Sections 4.1
and 4.3.3). Lead may accumulate differentially in different portlona of plants,
in varying quantities depending upon weather, proximity to highways, traffic
patterns, etc. (Brandt, 1970j Dedolphet al., 1970; Harley, 1970; Leland et al .,
1975; Motto et al., 1970; Schuck, 1970; Schuck and Locke, 1970). The lead con-
tent of portlona that are eaten by human or livestock are most Important from
the health standpoint (Haley, 1969; International Lead Zinc Research Organiza-
tion, 1972 a,b; Kolbya et al., 1974; Lagerwerff, 1970; Ter Haar, 1970).
For meats, milk, eggs and other products from domestic livestock, the
lead content is related to that of the feed, forage and water conaumed by
tha anlmala (Engal at al., 1971; Ewlng and Pearaon, 1973; Cues, 1970; Lynch
et al., 1974), In the caae of fish and shellfish, the lead content Is rela-
ted to that of the aquatic (freah, bracklah or marine) environment and to the
uptake of lead by organisms such aa plankton In the food chain (Dorn et al.,
1972; Leland et al., 1975; Loutlt et al., 1973).
In addition to the lead derived from air, soil, and water, foods may con-
tain lead derived from glazed vessels and metal containers sealed with lead
soldar (Clark, 1972; Harrie and Elsea, 1967; Klein and Namer, 1970; Mitchell
and Aldoua, 1974). L«ad poisoning has occurred from tha consumption of
8.9
-------
homemade apple cider made in lead-lined earthenware vessels and illegal alco-
hol or "moonshine" produced in old automobile radiators in the Southeastern
states (Palmisano et al., 1969; Walls, 1969). Lead has been eliminated from
food processing equipment, but old cooking utensils lined with lead alloys
evidently still exist, at least in the United Kingdom (Eg'an,' 1972).
8.3.1.1. Food and Forage Plants—
A substantial body of published data exists on the lead content of food
and forage crops, including cereals, vegetables and fruits. Tables 8.2 and
8.3 summarize typical values for the lead content of cereals and vegetables,
and of fruits, respectively.
The available data on portions of crop plants whose lead content is de-
rived from both air and soil indicate that soil uptake is the more important
source. Lead from the air generally deposits on the leaves and outer portions
of edible plants such as husks, as well as on the soil. It appears that up-
take of lead through the stomata of leaves may be considerably less than that
taken up from soil through the roots (Dedolph et al., 1970; Ter Haar, 1970).
However, crops grown close to highways (within 30.4 meters or 100 feet) having
a heavy traffic volume may have high levels of lead contamination on the
leaves and outer portions (Lacasse, 1970; Motto et al., 1970; Ter Haar, 1970).
The question of whether or not lead is translocated from the leaves or roots
to other portions of crops has not been resolved (Dedolph et al., 1970;
Lacasse, 1970; Lagerwerff, 1970; see Section 4.3.3). The available data
indicate that the edible portions of crop plants including leaves, roots and
fruits generally have a lower lead content than inedible portions. Data ob-
tained by the Food and Drug Administration from analyses of "market basket"
samples of food purchased in retail establishments indicate that levels of
lead consumed in fresh fruits and vegetables are well below levels considered
significant from the human health standpoint (Kolbye et al., 1974).
Leafy wastes from food crops that contain high levels of lead may be a
hazard to domestic livestock if used as a component of feed. For example,
note in Table 8.2 the considerably higher lead content of corn stalks, leaves,
and husks as compared to the kernels, and of unharvested cabbage leaves as
compared to the head. The type of lead poisoning in cattle and horses is
more fully discussed in Section 5.5.2.
Possible hazards from lead contamination of homegrown vegetables has only
recently been considered. A warning, for example, was recently issued by the
Idaho Department of Health and Welfare to residents within a 6.4-km (4-mile)
radius of a lead smelter that homegrown vegetables may have high levels of
lead (Anon, 1975). It is likely, however, that vegetable contamination in
smelter areas is primarily a problem of deposition of lead particularly on
the external portions of the plants rather than high concentrations of lead in
the plant tissues themselves. Thus, thorough washing should remove most of
the lead deposited on the surface. In any event, unless the garden provides a
substantial proportion of the total diet, the effects of lead contribution
8.10
-------
TABLE 8.2 LEAD CONTENT OF CEREALS AND VEGETABLES
Products
Wheat, heads
grain
Oats, heads
Corn, tassels
leaves
stalks
kernels
cobs
Barley, heads
Rye, heads
grass
Cabbage, heads
unhar vested leaves
Cauliflower, hearts
leaves
Broccoli, flowers
stalks
Brussel sprouts
Collar ds
Celery
Spinach
Watercress
Lettuce, leaves
roots
Lettuce, Romaine, outer leaves
inner leaves
Artichokes, outer leaves
inner leaves
Potatoes, leaves
stems
roots
tubers
Lead Content,
ppm Sample State Reference
1.0-2.0
0.16-0.18
0.3-2.0
19-1742
30-329
3.1-13
0-2.6
0.9-5.6
0.5-2.0
0.3-7.0
2.4-14.2
1.0-1.1
< 0.01-0. 51
4.5-5.8
0.9
2.0
0.19-0.30
0.04
< 0.01-0. 24
0.25-0.50
< 0.01-0. 02
0.01-0.02
0.10-0.25
0.01-0.33
8.7-159
3.2-6.6
1.0-9.0
20-150
0.10-0.18
< 0.01-0.01
0.04
<0.01
20-530
14-53
7.6-100
1.2-14
0.30-0.33
< 0.01-0. 14
Dry
Dry
Dry
Dry
Dry
Dry
Dry
Dry
Dry
Dry
Dry
Dry
Wet
Dry
Dry
Dry
Wet
Wet
Wet
Wet
Wet
Wet
Wet
Wet
Dry
Dry
Dry
Dry
Dry
Wet
Wet
Wet
Dry
Dry
Dry
Dry
Dry
Wet
Warren and De la vault (1962)
Ter Haar (1970)
Warren and De la vault (1962)
Motto et al.,(1970)
Motto et al.,(1970)
Motto et al. , (1970)
Motto et al.,(1970)
Motto et al.,(1970)
Warren and Delavault (1962)
Warren and Delavault (1962)
Dedolph et al.,(1970)
Ter Haar (1970)
Thomas et al.,(1972)
Ter Haar (1970)
Warren and Delavault (1962)
Warren and Delavault (1962)
ILZRO (1972a)
ILZRO (1972a)
Thomas et al.,(1972)
ILZRO (1972a)
ILZRO (1972a)
Thomas et al.,(1972)
ILZRO (1972a)
Thomas et al.,(1972)
Motto et al.,(1970)
Ter Haar (1970)
Warren and Delavault (1962)
Motto et al.,(1970)
ILZRO (1972a)
ILZRO (1972a)
ILZRO (1972a)
ILZRO (1972a)
Motto et al.,(1970)
Motto et al.,(1970)
Motto et al. ,(1970)
Motto et al. ,(1970)
Ter Haar (1970)
Thomas et al.,(1972)
8.11
-------
TABLE 8.2 LEAD CONTENT OF CEREALS AND VEGETABLES
(Continued)
Products
Potatoes, tubers, peel
tubers, inner portion
Onions
Beets, roots
tops
Carrots, .tops
leaves
stems
roots
inner portion
Leeks
Radish, leaves
roots
Peas, pods and peas
pods
peas
Beans
Beans, leaves
Cucumbers
Tomatoes, leaves
blades
petioles
stems
fruit
peels
pulp
Rhubarb, stems
leaves
Mushrooms
Lead Content
(ppm)
7.4-10.4
0.02
3.3-4.1
<0. 01-0. 38
1.6-6.0
1.0-6.0
2.0-10.0
25-218
4.0-7.0
83-152
16-23
0.05-0.06
3.3-24
1.7-2.1
2.0
<0.01
0.04-0.07
2.3-16.4
0.8-2.0
0-0.2
<0. 01-0. 02
<0.01-0.02
0.03
0.15-0.26
1.2-1.4
7.9-20.9
0.01-0.03
37-276
31-87
8-16
3.9-166
0.59-0.72
0.01-0.14
3.6-16
3.1-6.8
2.0-4.0
8.0-11.0
0.03-0.04
Sample State
Dry
Wet
Dry
Wet
Unspecified
Dry
Dry
Dry
Dry
Dry
Dry
Wet
Dry
Dry
Wet
Dry
Wet
Wet
Dry
Dry
Unspecified
Wet
Wet
Unspecified
Unspecified
Dry
Dry
Wet
Dry
Dry
Dry
Dry
Dry
Wet
Dry
Dry
Dry
Dry
Wet
Reference
Motto et al., (1970)
ILZRO (1977a)
Motto et al., (1970)
Thomas et al.,(1972)
de Treville (1964)
Warren and Delavault
Warren and Delavault
Motto et al.,(1970)
Warren and Delavault
Motto et al., (1970)
Motto et al.,(1970)
ILZRO (1972a)
Motto et al., (1970)
Ter Haar (1970)
Thomas et al., (1972)
Warren and Delavault
ILZRO (1972a)
Thomas et al., (1972)
Dedolph et al., (1970)
Dedolph et al., (1970)
de Treville (1964)
ILZRO (1972a)
ILZRO (1972a)
de Treville (1964)
de Treville (1964)
Ter Haar (1970)
Ter Haar (1970)
Thomas et al., (1972)
Motto et al.,(1970)
Motto et al.,(1970)
Motto et al.,(1970)
Motto et al.,(1970)
Ter Haar, 1970
Thomas et al.,(1972)
Motto et al.,(1970)
Motto et al.,(1970)
Warren and Delavault
Warren and Delavault
Thomas et al.,(1972)
(1962)
(1962)
(1962)
(1962)
(1962)
(1962)
8.12
-------
TABLE 8.3 LEAD CONTENT OF FRUITS
Products
Lead Content,
ppm
Sample State
References
Apples, whole fruit
skin
flesh
Pears, whole fruit
skin
flesh
Peaches
Cherries
Plums
0.12-0.3
<0.01-0.37
<0.01-0.24
<0.01-0.05
0.18
0.02-0.04
<0.01-0.23
<0.01-0.03
0.04-0.08
0.12
0.06-0.16
Unspecified
Wet
Wet
Wet
Unspecified
Wet
Wet
Wet
Unspecified
Unspecified
Wet
de Treville (1964)
Thomas et al., (1972)
Thomas et al., (1972)
Thomas et al., (1972)
de Treville (1964)
Thomas et al., (1972)
Thomas et al., (1972)
Thomas et al., (1972)
de Treville (1964)
de Treville (1964)
Thomas et al., (1973)
8.13
-------
from contaminated produce should be diluted in the total pool of food con-
sumed so that this source probably would contribute very little total lead
in a well balanced diet.
8.3.1.2. Processed Fruit and Vegetable Products—
Table 8.4 summarizes reports of analyses of lead contamination in canned,
frozen, and dehydrated fruit and vegetable products. The lead content of
frozen beans, peas and carrots was below the detectable limit of the analyti-
cal method used. Interestingly, these products together with frozen spinach
and frozen potatoes had a lower lead content than that of the corresponding
fresh products given in Table 8.2. The canned fruit products listed in Table
8.4 had significantly higher lead contents (99.9 percent confidence level)
than the corresponding fresh products listed in Table 8.3.
It is believed that these differences between fresh and canned products
result from the release of lead from solder used along the seam of the can.
Fruits and vegetables that are processed are washed thoroughly. This treat-
ment removes a portion of the lead on the surface of leaves, roots, or fruit
as indicated in data published by International Lead Zinc Research Organiza-
tion (1972a).
Analyses of the lead content of canned tomato paste by Mitchell and
Aldous (1974) revealed that higher lead levels (up to 500 micrograms per
liter) were obtained in samples taken near the soldered seam than in samples
taken in the center or opposite side of the can. Since the pH of tomato paste
is approximately 4.0, they concluded that lead was leached from the soldered
seam. This effect was particularly evident after the open cans were held at
room temperature for 24 hours. Products in cans having a high seam length to volume
ratio (>1.25 and 0.75 to 1.25) had a higher lead content than those in cans having
a lower ratio (<0.75). The high ratio cans included mainly baby food and other
small juice cans.
A survey conducted by the National Canners Association (1977) examined
lead content of various common vegetables, fruits, and juices prior to can-
ning and after storage in the caii for 1-1/2, 3, 6, and 12 months. The NCA
data (Table 8.5) offers strong support that: (1) food can absorb substantial
quantities of lead from cans, and (2) lead concentration in canned food in-
creases with the length of storage. Several foods such as grapefruit juice,
orange drink, corn, and tomatoes approximately doubled their initial lead
content after 1 year in storage.
8.3.1.3. Milk and Infant Formulas—
There is considerable concern about the lead content of milk and pro-
cessed milk products since these foods comprise a substantial proportion of
the diet of infants and children. Various data, past and present, exist with
respect to lead levels in milk, processed milk products, infant formulas and
human milk. These data are assembled by product in chronological order in
Table 8.6.
-------
TABLE 8.4 LEAD CONTENT OF PROCESSED FRUITS
AND VEGETABLE PRODUCTS
Products
Lead Content,
ppm Sample State
References
Beans, frozen
Beans, baked
Carrots, frozen
Corn, canned
Peas , frozen
Peas, canned
Spinach, canned
Spinach, frozen
Potatoes, frozen
Tomatoes, canned
Apples, canned
Apricots, canned
Apricots, dried
Black currants, canned
Damsons, canned
Grapefruits, canned
Oranges, canned
Peaches, canned
Pineapples, canned
Plums, canned
Prunes, canned
Raisins
Rhubarb, canned
Strawberries, frozen
Fruits and vegetables,
<0.01
0.19-0.67
<0.01
0.00-3.00
<0.01
0.00-1.46
0.13-0.95
0.07
0.01
0.32-0.63
0.12-1.14
0.52-1.48
0.24
0.17-3.90
0.37-0.74
0.19-0.54
0.10-0.22
0.26-0.50
0.14-0.54
0.17-0.98
0.15-0.73
0
0.10-2.57
0.02
dried 1.0-2.0
Wet
Wet
Wet
Wet
Wet
Wet
Wet
Wet
Wet
Wet
Wet
Wet
Unspecified
Wet
Wet
Wet
Wet
Wet
Wet
Wet
Wet
Unspecified
Wet
Wet
Unspecified
ILZRO (1972a)
Thomas et al.,(1973)
ILZRO (1972a)
National Canners
Association (1977)
ILZRO (1972a)
National Canners
Association (1977)
Thomas et al.,(1973)
ILZRO (1972a)
luZRO (1972a)
Tlomas et al.,(1973)
Thomas et al.,(1973)
Thomas et al.,(1973)
de Treville (1964)
Thomas et al.,(1973)
Thomas et al.,(1973)
Thomas et al.,(1973)
Thomas et al.,(1973)
Thomas et al.,(1973)
Thomas et al.,(1973)
Thomas et al.,(1973)
Thomas et al. ,(1973)
de Treville (1964)
Thomas et al.,(1973)
ILZRO (1972a)
de Treville (1964)
8.15
-------
Table 8.5 LEAD UPTAKE IN CANNED VEGETABLES,
FRUITS, AND JUICES*
Food Product
Lead Concentration,
ppmb
Percent Contributed
by Can
Corn
initial
6 months
1 year
Green beans
initial
6 months
1 year
Peas
initial
6 months
1 year
Tomatoes
initial
6 months
1 year
Applesauce
initial (mean)
6 months
1 year
Frtit cocktail
initial
6 months
1 year
Grapefruit juice
initial
6 months
1 year
Tomato juice
initial
6 months
1 year
Orange drink
initial
6 months
1 year
0.46
0.59
0.93
0.48C
0.35
0.39
0.33
0.40
0.37
0.31
0.55
--
0.27
0.32
0.38
0.22C
0.21
--
0.04
0.09
0.30
0.25
0.28
--
0.05
0.11
0.11
92
95
49
54
80
78
89
—
75
79
62
--
100
100
82
--
91
91
aSource: National Canners Association,(1977).
Values are means of approximately 12-50 samples.
cAnomalous mean, caused by distribution extremely skewed to
the right.
8.16
-------
Table 8.6 LEAD CONTENT OF MILK AND INFANT FORMULAS
Milk Product
Canned evaporated Bilk
sklBBed
regular
Infant Formula
Concentrate
Year of
Sampling
1971
1972-73
1968
1971
1972-73
1972-74
1973
1973-74
1972-73
Mean, ppa
1.04
0.06
0.81C
0.36
0.11
0.14
0.202
0.125
0.12
0.083
0.09
0.09
Range
0.30-2.30
0.04-0.07
0.30-0.40
0.04-0.22
0.03-0.91
0.01-0.820
0.02-0.37
0.01-0.46
0.04-0.12
0.06-0.13
Method d
AASd
AAS
AAS
HAAS
undetermined
AAS
HAAS
AAS
Reference
Lamm et al., 1973
Lamm and Rosen, 1974
Murthy and Rhea, 1971
Lamm et al., 1973
Laura and Rosen, 1974
Ministry of Agriculture, Fisheries
and Food, 1975
Mitchell and Aldous, 1974
U.S. DHEU (FDA), 1975
Schmidt, 1974
Lamm and Rosen, 1974
National Canners Association, 1973
(unpublished) cited la Kolbye et el
Kolhye et al. 1974
Ready to serve (diluted)
Modified Milk I
Modified Milk II
Lamb Meat Base
Soya Base
Homogenized Milk (cow)
ktuaan areast Kilk
1968
1968
1968
1968
1972-73
1972-74
1971
1972-73
1973
1972-74
1971
1972-73
0.170
0.210
0.256
0.272.
0.033b
0.05
0.04
0.005s
0.04
0.02
0.005
0.0426
0.042
0.049
0.02
0.005
0.019*
0.012
0. -0.08
0.02-0.07
0.009-0.1540
0.023-0.079
0. -0.065
0.006-0.202
AAS
AAS
AAS
AAS
HAAS
undetermined
AAS
HAAS
AAS
not stated
dlthixone
AAS
photon activation
AAS
HAAS
AAS
AAS
Murthy and Rhea, 1971
Murthy and Rhea, 1971
Murthy and Rhea, 1971
Murthy and Rhea, 1971
Lamm and Rosen, 1974
Ministry of Agriculture, Fisheries
and Food. (London) 1975
Lama et al. , 1973
Lamm and Rosen, 1974
Mltchel and Aldous, 1974
Ministry of Agriculture, Fisheries
and Food, 1975
Brandt and Bentz, 1971
Plnkerton et al. , 1973
Dutllhand Das, 1971
Lamm et al. , 1973
Lamm and Rosen, 1974
Murthy and Rhra. 1971
nurthy and Rhea, 1971
* Detection limit 0.005 ppo.
Seamed can* and bottle* averaged.
Average of four brands.
AAS • flame atomic absorption spectrophotoBetry, HAAS
* Median, rather than Bean.
nonflame AAS.
8.17
-------
Numerous articles in recent years have discussed the difficulty of
accurately quantifying lead in milk in the parts per billion range (Lamm
and Rosen, 1974; Brandt and Bentz, 1971; Kolbye et al., 1974 and Dutilh and
Das, 1971). Differences as large as tenfold between different investigators
and/or analytical techniques in analysis of the same product are not uncommon.
Cooperative studies involving several laboratories using standardized methods
of sample preparation and analytic techniques on identical samples have re-
vealed poor performance and extreme variability between laboratories. Accur-
acy worsens as the level of lead decreases, particularly as the lead level de-
creases below 1 ppm, which is typical.of milk products. In addition, the ubi-
quity of lead magnifies the possibility for sample contamination. On the other
hand, trace metal loss during destruction of the sample matrix also contributes
to error. These problems notwithstanding, several generalizations can be made
from the data shown in Table 8.6.
The lead content of human breast milk and fresh, homogenized cow's milk
(market milk) are quite low in comparison to those milk products which have
been canned, evaporated or mixed with additives (i.e., infant formulas.) This
is as expected, for the lead concentration of the plasma is low and remarkab-
ly constant over a wide range of red blood cell lead levels (Lamm and Rosen,
1974), and, since only a small fraction of total plasma can be ultrafiltered
through a molecular weight cut-off of approximately 2,000, one should antici-
pate a naturally low level of lead in milk.
Lynch, et al., (1974) also confirmed that very little lead is excreted
via the milk, even after administration of substantial amounts of lead. 11.0
milligrams of lead, as Pb(CO_)?, per kilogram of body weight was administered
to Holstein cows. This lead level did not produce serious physiological changes
despite a large body burden. The lead content of whole milk (5.9 ppb), was
lower than the mean lead content (49 ppb) of market milk as determined in a
national survey by Murthy, et al., (1967). However, the lead content of milk
did not decrease to background levels until 34 days after dosing the cattle.
Lead content of milk can also be influenced by the lead content of feed and
grass, particularly near highways, and the licking of metal objects or painted
surfaces by cows.
Pinkerton, et al., (1973) collected human milk from mothers in a breast-
feeding club in Cincinnati, Ohio, and bovine milk from individual cows on farms
producing milk for the Cincinnati area (Table 8.6). Chemical analyses re-
vealed that human breast milk contained about one-fourth the lead of bovine
milk. Median milk lead values were 0.010 and 0.042 ppm, respectively, for
humans and cows. Based on this study, a bottle-fed infant could theoretically
take in about thirty times the lead of an exclusively breast-fed infant.
Whereas analyses of human milk and homogenized cow's milk have shown low
levels of lead, past studies have indicated serious contamination problems in
canned evaporated milk. Lead content of other processed milk products (e.g.,
infant formulas) is generally intermediate between the levels of "natural"
milks and those of canned evaporated milk (Table 8.6). Data in 1968 on four
brands of evaporated milk indicated concentrations of 0.8 ppm; four brands of
infant formulas averaged about 0.4 ppm lead (Murthy and Rhea, 1971).
8.18
-------
As recently as 1974, levels of 0.5 ppm were frequently found in canned
milk when levels below 0.2 ppm would have been expected on the basis of
concentration of whole milk (Kolbye, et al., 1974). These and other avail-
able data suggest the need for further research, particularly with regard
to solder and flux operations in canning evaporated milk. Unlike other food
products, evaporated milk traditionally has been packed in a can having a
soft solder plug.
Murthy and Rhea (1971) reported that the ratio of tin to lead in the
filling solder affected lead uptake by evaporated milk. When the ratio was
60:40 and large amounts of solder were allowed access to the milk, lead up-
take of 0.34-1.60 ppm was observed whereas samples not exposed to solder had
0.05-0.37 ppm. No significant difference was seen in lead uptake by evapora-
ted milk between a 50:50 filling solder and a 10:90 for internal seams. With
solder pellets present inside, canned milk showed 0.10-0.54 ppm lead (Engst
and Waggon, 1965).
The evaporated milk industry was informed of the need to reduce these
levels and the industry has responded by instituting changes in canning
operations and improving quality control procedures. A general declining
trend from levels as high as 0.5 ppm to 0.1 ppm over the past 5-7 years is
evident from Table 8.6.
The data obtained by Lamm and Rosen (1974) showed a decrease in lead con-
tent of evaporated milk and infant formulas in a 1972-73 survey as compared to
that determined in a 1971-72 (Lamm, et al., 1973) survey. These results have
quite reasonably been questioned on the basis of a change from flame to non-
flame atomic absorption spectrometric analyses (Holliday, et al., 1974; Sarett,
1974). As shown in Table 8.6, Lamm and Rosen's (1974) data shows significantly
lower levels for all milk products (including market milk and human milk) than
Lamm, et al.'s (1973) study. Thus, much of the discrepancy between the two
studies is probably attributable to analytical techniques, rather than an actual
decrease of the magnitude suggested (ca 10X).
Mitchell and Aldous (1974) obtained higher lead levels in canned evapora-
ted milk (mean, 0.20 ppm; range, 0.01 to 0.28 ppm) using flame atomic absorp-
tion spectrometry than did Lamm and Rosen (1974) using a nonflame method (mean,
0.10 ppm; range, 0.04 to 0.22 ppm).
More recent Food and Drug Administration (FDA) analyses indicated that
the mean lead content of 80 canned, evaporated milk samples was 0.125 ppm,
with a range of 0.02 to 0.37 ppm (Kolbye, et al., 1974). The results of an
industrial survey of 3000 canned, evaporated milk samples using a FDA-approved
method showed a mean value of 0.12 ppm Pb, with the highest level in the range
of 0.01 to 0.46 (U.S. DHEW, 1974).
The food industry has been moving toward elimination of the plug-type
metal container. This should aid in minimizing the levels of lead in
evaporated milk and related products.
8.19
-------
In addition, the importance of evaporated milk in infants nutrition
has been in a long-term declining trend over the past 20 years. As reported
by Fomon (1974), whereas in 1958 the feeding of about 42 percent of infants
through 2 months of age was based on evaporated milk formulas, this had de-
creased to about 2 percent by 1972.
Evaporated milk has largely been replaced by formulas based on soybeans,
more nutritionally complete and more easily digested by infants than cow's
milk. Evidence in support of this comes from the results of two surveys con-
ducted by one of the major formula producers (Martinez, personal communication,
1977), which indicated the following proportions of infants using evaporated
milk formulas:
Evaporated Milk, percent
1976 1971
Hospital period 0.1 0.8
to 2 months 1.0 4.2
3-4 months 2.2 4.0
5-6 months 2.2 3.5
These infant formulas are available either concentrated, requiring dilution
before use, or ready-to-use. Both types are packed in regular side-seamed
cans, and do not use the plug-type evaporated milk style can.
The use of canned milk (condensed and evaporated) has in general also
been in a long-term declining trend in the United States, as indicated by
U.S. Department of Agriculture 1977 Statistics.
Year Millions of lb
1967 1,572
1968 1,497
1969 1,376
1970 1,214
1971 1,186
1972 1,102
1973 1,057
1974 1,000
1975 924
1976 862
1977 788
Commercial infant formulas are packed in the usual rigid seamed cans and
available information does not indicate a present hazard from lead contamina-
tion in these formulas.
Analyses of infant formulas packed in 8-ounce and 30-ounce seamed cans
and in 4-ounce glass nursettes did not reveal any significant differences
in the lead content of the product in either of these types of containers
(Lamm and Rosen, 1974). This finding has not been replicated in other
studies, however. Lamm and Rosen's (1974) survey as well as a National
Canner's Association survey showed averages of 0.08 and 0.09 ppm, respectively.
Similarly, FDA spot analyses showed an average of 0.09 ppm in four major brands
of infant formula concentrates. Diluted for use, the lead values would be re-
duced by 50 percent, making them comparable to market milk.
8.20
-------
8.3.1.4 Meat, Fish and Poultry Products—
Table 8.7 presents a summary of the lead content of meat, fish and poultry
products. The lead content of organ meats such as heart, kidney and liver of
swine and turkeys (not shown) is usually higher than that of muscle (Dalton
and Malanoski, 1969). However, the lead content of beef liver appears to be
quite low compared to that of beef muscle.
The lead content for cured and smoked meat products given in Table 8.7 was
reported by Kirkpatrick and Coffin (1973) on a fresh-weight basis. When these
are corrected to a dry-weight basis, the highest lead level of bacon, ham, and
picnic shoulders will be lower than that for pork muscle reported by Dalton and
Malanoski (1969). According to Hankin, et al., (1975b), seven market samples
of fresh beef and pork liver that were analyzed by the atomic absorption spectro-
metric method of Dalton and Malanoski (1969) contained 1.4 to 1.6 ppm Pb. Liver-
wurst sampled sporadically contained from 0 to 7.6 ppm Pb apparently depending
upon the lead content of the ingredients used.
8.3.1.5 Beverages, Bakery Products, Sugar and Condiments—
Tables 8.8 to 8.10 present summaries of the lead content of beverages,
bakery products, sugar, condiments and miscellaneous foods.
It does not appear that any of these products except fruit juices, both
adult and infant types, contain sufficient quantities of lead to be of concern
from the standpoint of a total dietary intake. These products have a pH in the
range of 2.7 to 3.9. Mitchell and Aldous (1974) reported that the mean lead
level of canned, infant products was 202 micrograms per liter as compared to 35
micrograms per liter in bottled products. They explain the higher levels in
cans on the basis of the acidity of these products combined with leaching of
lead from the seams in cans possessing a high seam to volume ratio.
8.3.1.6 Lead in the Human Diet—
No evidence exists at the present time of any effect of lead as a bene-
ficial trace element in human nutrition. Various estimates have been made of
the total human exposure to lead from food sources. In the United Kingdom,
Tolan and Elton (1973) analyzed food samples that were representative of the
average diet, and estimated that the adult daily intake of lead from food and
beverages was 200 and 20 micrograms, respectively. According to Meranger and
Smith (1972), lead was not present in sufficient levels in Canadian diets to
cause concern. A FDA estimate based on historical data of U.S. adult intake
of 337 micrograms of lead per day has been superseded by a 1972 Market Basket
Survey estimate range of 57.4 to 233 micrograms per day. The latter estimate
was based on actual analyses and varying assumptions concerning the actual
lead content of samples having trace levels (Kolbye, et al., 1974). These
authors point out the limitations in the various analytical methods for de-
tecting lead in foods at levels below 1 ppm.
Kolbye, et al., (1974) cite a dietary survey of 333 infants in the United
States, aged 1 to 12 months, in which the estimated dietary lead intake was
8.21
-------
Table 8.7 LEAD CONTENT OF MEAT, FISH, AND POULTRY PRODUCTS
Products
Lead Content,
ppm
References
Beef, roast chuck 0.71
bone of leg 3.60
hamburger 0.248b
liver 0.089b
Pork, fresh, muscle 0.54-1.33
Meat, canned, cured3 0.01-0.30
Wiener (smoked or 0.04-0.16
unsmoked
bologna 0.01-0.26
meat loaves 0.01-0.26
salami 0.01-0.30
pastrami and other 0.01-0.42
liverwurst 1.80-7.60
bacon 0.01-0.16
ham 0.01-0.16
picnic shoulders 0.01-0.12
corned beef products 0.01-0.28
Fish, fresh
cod, fresh, Icelandic 0.32
clams, hard, Atlantic 0.28
crab, body meat, Pacific 0.45
lobster, Atlantic 0.55
shrimp, Alaskan 0.50
Fish, canned
tuna, initial 0.34
canned,6 months 0.44
after packing
sardines, Dutch 0.72
Poultry
chicken, fryer 0.127°
turkey, fresh, muscle 2.93-3.35
Eggs, chicken 0.174b
Meat, fish, and poultry 0.015
(composite)
U.S. DHEW (1975)
Kehoe (1976)
U.S. DHEW (1975)
U.S. DHEW (1975)
Dalton and Malanoski (1969)
Kirkpatrick and Coffin (1973)
Kirkpatrick and Coffin (1973)
Kirkpatrick and Coffin (1973)
Kirkpatrick and Coffin (1973)
Kirkpatrick and Coffin (1973)
Kirkpatrick and Coffin (1973)
Hankin et al., (1975b)
Kirkpatrick and Coffin (1973)
Kirkpatrick and Coffin (1973)
Kirkpatrick and Coffin (1973)
Kirkpatrick and Coffin (1973)
Zook et al., (1976)
Zook et al., (1976)
Zook et al., (1976)
Zook et al., (1976)
Zook et al., (1976)
National Canners
Association (1977)
National Canners
Association (1977)
Reith et al., (1974)
U.S. DHEW (1975)
Dalton and Malanoski (1969)
U.S. DHEW (1975)
Kolbye et al., (1974)
aData on canned, cured meats are expressed on a wet-weight basis.
''Mean.
8.22
-------
TABLE 8.8 LEAD CONTENT OF BEVERAGES
Products
Lead Content,
ppm
References
Drinking water (U.S.)
Lemonade
Soda
Soft drinks (Holland)
Carbonated beverages
Tea
0.015
0.004
0.004
0.02
< 0.008
0.20-0.74
ALCOHOLIC BEVERAGES
Beer (Cincinnati)
Beer (Holland)
Wine (Holland)
Brandy (India)
Rum (India)
Dry Gin (India
Whiskey (India)
FRUIT JUICES
Lime juice
Lemon juice
Diluted fruit drinks, canned
Orange juice, canned frozen
concentrate
Tomato juice, canned
Orange juice, infant
Apple juice, infant
0.01-0.29
0.03
0.13
0.05-0.60
0.024-0.057
0
0.027
0.30
0.57
0.251
0.135
0.338
0.308-0.655
0.207-0.907
U.S. EPA (1975)
de Treville (1964)
de Treville (1964)
Keith et al.,(1974)
Meranger (1970)
Ministry of Agriculture,
Fisheries, and Food (1975);
Reith et al.,(1974)
de Treville (1964)
Reith et al.,(1974)
Reith et al.,(1974)
de Treville (1964)
de Treville (1964)
de Treville (1964)
de Treville (1964)
Meranger (1970)
Meranger (1970)
U.S. DHEW (1975)
U.S. DHEW (1975)
U.S. DHEW (1975)
U.S. DHEW (1975)
U.S. DHEW (1975)
Median value.
8.23
-------
TABLE 8.9 LEAD CONTENT OF BREAD
AND BAKED PRODUCTS3
Lead Content
Products ppmb
Bread, whole wheat 0.42
Bread, white 0.41
Rolls, hamburger 0.45
Doughnuts, cake 0.45
Biscuit mix 0.24
Flour, all purpose 0.51
Source: Zook, et al. Reprinted with permission
from Cereal Chemistry, (c) American Association
of Cereal Chemists, 1970.
Means lead content, dry weight basis.
8.2U
-------
TABLE 8.10 LEAD CONTENT OF SUGAR, SPICES, CONDIMENTS,
AND MISCELLANEOUS FOODS
Produc ts
Lead Content,
ppm
References
Sugar 0.004-0.13
Corn syrup 0.21-0.49
Pepper, black 0.22
red 0.4
Ginger 0.08
Turmeric 0.4
Mustard seed 0.4
Cloves 0.15
Cinnamon 0.03
Salt 0.2-0.45
Coffee 0.07
Cocoa beans 0.15
Baking powder 5.0-10.0
Refined soybean oil, canned 0.02-0.10
Oils, fats, and shortening 0.02
de Treville (1964); Haley (1969);
Kolbye et al., (1974); Ministry
of Agriculture, Fisheries, and
Food (1975)
de Treville (1964)
de Treville (1964); Haley (1969)
de Treville (1964); Haley (1969)
de Treville (1964); Haley (1969)
de Treville (1964); Haley (1969)
de Treville (1964); Haley (1969)
de Treville (1964); Haley (1969)
de Treville (1964); Haley (1969)
de Treville (1964); Haley (1969)
Reith et al.,(1974)
Reith et al.,(1974)
de Treville (1964); Haley (1969)
Bergner and Rudt (1968)
Kolbye et al., (1974)
8.25
-------
93 plus or minus 36 micrograms per day. In contrast, Lanzola, et al., (1973)
estimated that the daily dietary intake of lead by children in Italy from the
4th to 12th month of life increased from 172 to 289 micrograms. Definitive
information from balance studies is lacking on the absorption and retention of
lead from the gastrointestinal tract in infants and small children. However,
preliminary studies indicate that absorption rates in small children may be
5 to 10 times that of adults.
According to Mahaffey (1974), susceptibility to lead toxicity depends upon
age, season of the year (body temperature, dehydration, ultraviolet light),
calcium, phosphorus, vitamin D, dietary protein, ascorbic acid, nicotinic acid,
alcohol, and other heavy metals. In rat studies, the toxicity of a given con-
centration of lead increased significantly when dietary intakes of calcium or
iron were reduced to 20 percent of the recommended level. If these findings
can be generalized to children the effects of high lead intake in children
having dietary deficiencies of calcium and iron might be significantly increased
(see Section 6.3.2.1).
Forty-six children, aged 24 to 47 months, selected on the basis of blood
levels of lead were studied by Mooty, et al., (1975) to determine any relation-
ship between dietary intake and plumbism (lead poisoning). There were no sig-
nificant differences in protein, caloric, or iron intake of children having
low blood levels of lead (10 to 25 micrograms per 100 milliliters) as compared
with children having high levels (greater than 50 micrograms per 100 millilit-
ers). However, pica, defined as chronic ingestion of crayons, clay, starch,
soil, pencils, matches, paper, chipped paint and plaster was more prevalent in
the children showing plumbism.
8.3.2 Terrestrial Ecosystems
There are numerous reports showing that plants take up lead and generally
the concentrations in plants grown in high lead soils is greater than those
grown in low lead soils. The lead content differs in various parts of the
plants, roots often having the highest concentration. Translocation studies
(see Section 4.3.3) indicate that lead is either unavailable to the plant or
is "fixed" in the roots and only small amounts are translocated to the above-
ground parts of the plant.
Following uptake, lead in the plant is distributed throughout the plant
and is returned to the ground either upon removal or decay of portions of
the plant. Factors that determine lead availability and its uptake and dis-
tribution within plants are identified in Section 4.1. Thus, lead can be
leached from soil and the litter layers where it is available for uptake by
various plants, microbes and soil invertebrates. Biological breakdown of
plant materials makes lead available to soil-dwelling organisms associated with
many complicated food chains and the lead they consume may subsequently become
available to organisms of the next trophic level. As described in Section
4.2.2.1, lichens, fungi, mosses, and liverworts have a considerable capacity
for lead uptake. The lichen Parmelia physodes has been used as a bioindicator
for the intensity of lead near a smelter (Holl and Hampp, 1975). Enrichment
8.26
-------
of upper soil horizons has been attributed to mosses and liverworts which
concentrate elements including lead, and then by decomposition, release them
into the surface soil (Antonovics, et al., 1971; Shacklette»1965a,b). Spanish
moss (Tillandsia usneoides), a vascular plant, has also been used as an indi-
cator of lead pollution. Tissues of mosses have been found to contain de-
creasing lead contents with increasing distances from lead industries (Lee,
1972). However, at 800 meters from the contamination source, the amount of
lead in mosses was two to three times greater than in the same species col-
lected in uncontaminated areas.
Hemphill (1974) and Hemphill, et al., (1974) found that forage plants
and soils along ore-truck routes in Missouri's Lead Belt contained elevated
levels of lead and other toxic metals which decreased as distance from the
highway increased. Lead concentrations averaged 280 ppm dry weight on the
roads1 rights-of-way and 34 ppm at 91.4 meters (100 yards), 11.6 ppm at 182.8
meters (200 yards), and 6.5 ppm at 365.6 meters (400 yards) from the highway.
Blueberries had a maximum of 537 ppm along the truck routes and 172 ppm at
91.4 meters (100 yards) from the routes. The deaths of several horses in 1970
was attributed to the accumulation of toxic levels of lead in forage plants
along the highway. In areas of high lead emission, insects had average lead
levels (ppm, oven dry weight) of 10.3, 15.5, and 25, respectively, for species
that suck plant juices, chew plant parts, and prey on other insects (Price,
et al., 1974). These figures indicate a biomagnification of lead from herbi-
vore to carnivore trophic levels. In low lead emission areas insects in the
same feeding categories had average lead contents of 4.7, 3.4, and 3.3 ppm.
Giles, et al., (1973) found that measurable quantities of lead were being con-
centrated by Japanese beetles (Papillia japonica), damselflies (Agrion maculaturn)
and the European mantid (Mantis religiosa) which were collected in 1970 along
Interstate 83, Baltimore, Maryland's major north-south freeway. Gish and
Christensen (1973) found that lead, cadmium, nickel, and zinc in soils and
earthworms decreased with increasing distance from the Baltimore-Washington
Parkway and U.S. Highway No. 1. The mean lead concentrations for the two
highways combined were 468.3 to 53.4 ppm (soils) and 269.8 to 52.7 (earthworms)
at distances of 3-48 meters (10-160 feet) from the roadway, respectively. The
maximum lead level accumulated by earthworms was 331.4 ppm.
In a study of cadmium, zinc, and lead distribution in East Tennessee
Van Hook (1974) found mean lead concentrations in soils and earthworms were 27
and 4.7 ppm, respectively. The mean earthworm concentration factor for lead
was 0.2, ranging from 0.1 in Emory soil to 0.3 in Captina soil.
Rolfe, et al., (1972) conducted a study at the University of Illinois
aimed at understanding and modeling the movements and effects of heavy metals
(initially lead) in the environment. A model has been constructed which
stimulates the movements and projects the accumulation points of lead in a 76-
square mile watershed ecosystem in Champaign County, Illinois. The model in-
cludes components of both aquatic and terrestrial ecosystems and defines the
ecosystem by a network of nodes and branches. The nodes generally represent
the components of the ecosystem, and the branches indicate possible transport
mechanisms between nodes. The basic network of 17 nodes and 44 branches shown
in Figure 8.3 has been expanded to 36 nodes and 121 branches to accommodate
zonation of the system. Nodes such as primary producers, herbivores, and
8.27
-------
Figure 8.3 A network representation of a lead ecosystem
model. Adapted from Rolfe et al., (1972).
8.28
-------
carnivores are defined generally in this preliminary model, but future refine-
ment and data availability may permit more detailed examination of these com-
partments. The procedure to simulate the flow of lead through the network
consists of four steps: (1) generation of a distribution factor for each
branch; (2) seasonal adjustment of the distribution factors; (3) updating of
the nodal accumulation by adding the external inflows; and (4) distribution of
the lead in the nodes through exiting branches (including self-loops). A for-
mula is developed which yields nodal lead content changes between time periods.
A computer program which performs the distribution provides the user with nodal
accumulations and concentrations, including averages, standard deviations, mini-
ma, and maxima. Plots of nodal accumulations or concentrations may also be ob-
tained. Table 8.11 shows typical results of 100 cycle (2 years) simulation
using a zoned network of 36 nodes and 121 branches. Additional refinements in
the system should permit (1) the study and prediction of lead transport and ac-
cumulation in ecosystems, and (2) the development of alternatives of lead pol-
lution control.
The environmental fate and effects of cadmium and lead were studied in a
laboratory model ecosystem with a terrestrial/aquatic interface, using silica
sand, Bloomfield soil (sandy loam) and Drummer soil (silty clay loam) as sub-
strates (Lu, et al, 1975). Applications were made directly to the substrates
as lead and cadmium chloride and as sewage sludge as a source of heavy metals.
The mobilization and incorporation of cadmium and lead into food chain organisms
were inversely proportional to sorption capacity of the substrate and were
highest in silica sand and lowest in Drummer soil. Following the applica-
tion of sewage sludge there was clear-cut mobilization and transfer of cadmium,
copper, lead, and zinc into food chains, alga (Oedogonium cardiacurn), daphnia
(Daphnia magna), mosquito larva (Culex pipiens quinquefasciatus), snail (Physa),
and fish (Gambusia affinis). Cadmium exerted a particularly adverse affect on
the various organisms in the model ecosystem suggesting that its presence in
relatively high levels in sewage sludge could become a limiting factor in its
use on soils and for crop production.
8.3.3 Aquatic Ecosystems
Several completed and on-going studies have been reported on lead concen-
trations in aquatic ecosystems. Wolf and Rice (1972) have detailed the fol-
lowing major information needs for estimating mineral reservoirs in estuaries:
(1) Determining the relative amounts of different physio-chemical forms of
an element or radioiosotope in natural waters, their relative stabi-
ties, and the ease of introconversion between the various forms.
(2) Determining the relative biological availabilities of these dif-
ferent physiochemical forms to various types of biota.
(3) Determining trophic structure of the entire ecosystem.
The role of microorganisms—as sources of metallic
elements to consumers in detritus-based food chains,
as producers of organic-metal complexes, and as reminerali-
zers of metals previously incorporated into plant or animal
tissues—is particularly poorly understood.
8.29
-------
TABLE 8.11 COMPARISON OF ACTUAL WITH PREDICTED LEAD CONCENTRATIONS IN
MODEL ECOSYSTEM
• Node
Soil & soil sink
Plants & litter
Herbivores
Carnivores
I
Predicted
63
5
5
3
Actual0
50
35
12
12
Average
Concentration in Zone
II
Predicted
26
0.78
0.7
0.4
Actual0
23
18
5
9
• ppm
III
Predicted
17
0.03
0.04
0.02
Actual0
13
5
4
4
IV
Predicted
128
41
16
10
Actual0
115
38
-
-
a Source: Rplfe, et al. Reprinted, with permission from J, Environmental Systems, Cc) Baywood Publishing Co.
Actual concentrations are based on preliminary data.
-------
(4) Determining feeding rates and assimilation efficiencies for
carbon and metallic elements at each major trophic inter-
action.
(5) Determining biological retention of metallic elements in
the major organisms consumed by man.
(6) Determining the interactions of variable environmental
parameters on reservoir size and transfer rates at each
step in the overall system.
As a minimum, this information is necessary for any type of ecosystem to
determine the extent of mineral cycling. Although data exist on points one
and two for several ecosystems, few studies explain the remaining points and
no studies were found in which all points of information were determined for
the same ecosystem.
Banus, et al., (1975) measured the amounts of lead, zinc, and cadmium in
various components of a salt-marsh ecosystem that had been experimentally
treated with two levels (8.4 and 25.2 grams per square meter) of metals-
containing sludge fertilizers. Figure 8.4 summarizes the annual budget of
lead at three treatment levels including a control. It was found that lead
entering the salt marsh was largely retained by the surface sediments but 6
to 8 percent was taken up by marsh grasses. Lead in grass tops was exported
as detritus to deeper waters but this loss was only about 3 to 4 percent of
the entering lead. Nitrogen added in conjunction with the metals resulted in
an increased movement of the metals into coastal waters due to increased
production of grasses and increased metal contents of the grass tops.
Drifmeyer and Odum (1975) investigated disposal of heavy-metal-containing
dredge spoil and its possible uptake by salt-marsh biota. Fine-grained dredge
spoil had considerably higher levels of lead, zinc, and manganese than did
natural salt-marsh sediment. Large differences in the metals content of the
spoil were found; these were dependent on the sediment type. Lead levels in
the grass shrimp (Palaemonetes pugio), mumichog (Fundulus heteroclitus),
common reed (Phragmites communis), saltmarsh cordgrass (Spartina alterniflora),
and saltmeadow hay (Spartina patens) were significantly higher (at the 0.01
confidence level) than in these same species from the natural saltmarsh (see
Figure 8.5). Concentrations of lead and manganese tended to decrease markedly
with increasing trophic levels in both detritus-based and grazing food chains
of the dredge-spoil pond (see Figure 8.6). Combining information on lead levels
obtained by Drifmeyer and Odum (1975) with that on the feeding behavior of the
above species, Drifmeyer (1975) was able to: (1) verify that lead from polluted,
dredged material does enter the food web; and (2) determine the probable pathways
of lead transfer in the dredge-spoil pond ecosystem (see Figure 8.7).
It is evident from the research data that material dredged from polluted
waterways may constitute a source of lead uptake by salt-marsh plants and ani-
mals. Lead from polluted dredge spoil enters and is transferred without biologi-
cal magnification through a simple sediment-marsh grass-detritus-grass shrlmp-
mumichog food web.
8.31
-------
Uotf
Lotus to MO :
to grate:
to Mdinwntt:
Sources:
Control
tf
Soil morth
12-6
U
Atmotph.
Low
Fertilizer
High
Fertilizer
tf
Soil morth
2-8
tl
Soil marsh
5-4
<1 v\
li \>
157
Figure 8.4 Calculated annual budget for lead in salt marsh
plots under the three treatments. All values
are in mg Pb m~ . The boxes indicate pools
while the arrows show annual fluxes. Source:
Banus, et al. Reprinted with permission from
Estuarine Coastal Marsh Science, (c) Academic
Press Inc., (London) Ltd., 1975.
8.32
-------
1
DREDGE SPOIL NATURAL MARSH
POND
30-
28-
26-
24-
22-
20-
18-
.O
O.
E "
Q.
Q- -
ID-
S'
4-
. 26:0
•
z
IU
s
5
411
W>
5
fiC
O
x "-0 a
X 1 l O
"• O
08 ¥ •» .
^ ••• i/i *•
s 1 i Ills
6.2 i a | i " 5
•« « g Vt f
4.5 - 3 s s
? M s 1 *
U pUBMHM • •
1 ft O
Figure 8.5 Lead levels in dredged material disposal
sites of Craney Island and Lynnhaven in-
let compared with that of the natural,
unpolluted marsh at Mobjack Bay, Virginia.
Source; Drifmeyer. Reprinted with permission
from World Dredging and Marine Construction.
(c) Symcon Publishing Corporation, 1975.
8.33
-------
Detritus Food-Chain
Grazing Food-Chain
_sr Palaemonetes
pugio
(11.0)
detritus
(11.5)
Spartina
alterniflora
(5.1)
sediment
(26.0)
Fundulus
heteroclitus
(4.5)
Cyprinodon
^ variegatus
(3.3)
\
Gambusia
affinis
(8.4)
Algae
(29.0)
j uvenile
Figure 8.6.
Pb transfer Cppm dry-weight) in a dredge-spoil pond ecosystem.
Note the decrease in Pb levels with each successive trophic level
in both simple food-chains. Arrows indicate trophic interactions.
Source: Drifmeyef and Odum. Reprinted, with permission, from
Environmental Conservation, (c) Foundation for Environmental
Cons ervat ion. (19 75).
8.3U
-------
Fundulus heteroclitus
4.5
11.0
Pa Lqemqnetes
pugio
Cyprinodon
vorieqotui
3.3
Figure 8.7 Average lead concentrations in dredge-spoil
pond ecosystem, ppm dry wt. Arrows indicate
probable pathways of lead transfer. Source:
Drifmeyer. Reprinted with permission from
World Dredging and Marine Construction.
(c) Symcon Publishing Corporation, 1975.
8.35
-------
Mechanistically, Bella and McCauley (1971, cited in Drifmeyer and Odum,
1975) observed that heavy metals may be adsorbed on particulate matter in
estaurine water and these metal-laden particles may be pelletized by various
animals and deposited in the estaury. Schubel (1972) noted that some filter-
feeding and deposit-feeding organisms may be exposed to diets with relatively
high concentrations of adsorbed heavy metals.
Gale, et al., (1973 and 1975) have investigated the various experimental
factors and current industrial practices which may affect stream conditions in
Missouri's New Lead Belt. These investigators have concluded that the most
serious threat to aquatic life and environmental stability are (1) the release
of gangue with varying amounts of residual metal ores, and (2) the release of
toxic milling reagents into receiving streams. Aquatic vegetation and leaf
litter material have been shown to bind large quantities of lead. Lead is
bound to the anionic sites on the surface of aquatic plants or in leaf litter
by ion exchange. Ion exchange capacities of mixed live algal cultures averag-
ed approximately 65 milliequivalents of lead per 100 grams dry weight. Similar
cation exchange capacities for leaf litter collected in the region of the
smelter approximated 180 milliequivalents of lead per 100 grams dry weight.
Biomagnification of lead was not found in the different aquatic organisms.
Rather, the elevated total body concentrations of lead in fish, tadpoles, cray-
fish, and aquatic arthropods were associated with gastrointestinal contents
with some additional lead bound or chelated to the mucous membranes of gills
or to the mucous covering body surfaces. The investigators believe that under
present operational conditions, lead toxicity will not become a problem to
aquatic life forms in Missouri's New Lead Belt. However, further research is
suggested to determine the cause of increased algal growth below the industrial
outfalls, and particularly, the factors which permit the dominance of diatomac-
eous forms and the exclusion of normal consumer organisms in some of the pro-
blem streams.
Mathis and Cummings (1971) found that the lead content of sediments in
the Illinois River was approximately 10,000 times greater than the water (see
Figure 8.8). Mud samples taken from Lake Hamilton (Arkansas) and analyzed
for trace elements (Nix, 1970) are shown in Table 8.12. The downstream en-
richment (lower station numbers) of the bottom muds probably reflects the use
of the reservoir.
Sediment in lakes and rivers represent a sink for lead in the ecosystem.
However, it is still in the ecosystem and may be leached under appropriate con-
ditions. Mathis and Cummings (1971) found that the content of lead in clams,
worms and fish was much higher than that in the water. Worms contained lead
in concentrations of the same magnitude as that found in the bottom sediments.
The fish had considerably lower concentrations of lead; the carnivorous fish
had slightly lower concentrations of lead than the noncarnivorous fish.
Schroeder and Balassa (1961) reported a range of 0.17 to 2.5 ppm of lead
in seafood with an average of 0.5 ppm and only one sample exceeding 0.87 ppm.
Barley (1970) reported a concentration of 0.31 ppm in shellfish. Pringle,
et al., (1968) reported average wet-weight concentrations of 0.47, 0.70 and
0.52 ppm in Eastern oysters, soft-shell clams, and Northern quahogs, respec-
tively. The ability of the Eastern oyster to concentrate lead was shown by
8.36
-------
100
10
.1
.01
.001
n
Cwniv— Noncamiv-
orouf orou* dim
Fhhei
Woffns
Bottom
Sediment*
Figure 8.8 Mean concentration of lead in water, biota,
and sediments of the Illinois River. Adapted
from Mathis and Cummings (1971).
8.37
-------
Table 8.12 LEAD CONCENTRATION IN MUD IN LAKE HAMILTON3
Station
Number
1
2
3
4
5
6
7
8
Water Depth
meters
34
28
22
15
11
9
7
5
Lead
Concentration ,
Wg/g
20
60
50
35
20
10
—
5
3Adapted from Nix (1970).
8.38
-------
exposing oysters to flowing seawater containing lead concentrations of 0.025,
0.05, 0.1, 0.2 milligrams per liter. After 49 days, the total accumulations
of lead amounted to 17, 35, 75, and 200 ppm (wet weight). The highest con-
centrations of lead in the oyster occurred in the digestive gland and the
lowest concentration in the muscle tissue. Oysters exposed to the lower
concentrations appeared normal. However, oysters exposed to the higher ex-
perimental lead concentrations showed considerably atrophy and diffusion of
the gonadal tissue; edema; and a less distinct hepatopancreas and mantle edge.
The interference of lead with algal growth and development is described
in Section 4.2.1.2. The concentration of lead by noncrop vascular plants in
aquatic systems is described in Section 4.3.1.1. Translocation of lead in
terms of soil-plant-water relations is discussed in Section 4.3.3. Variations
in lead concentrations in certain fish tissues and evidence that elevated
amounts of lead in fishes result from pollution are presented in Section 5.3.1.
8.39
-------
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8.1*7
-------
TECHNICAL REPORT DATA
(Please read Instructions on the reverse before completing)
1. REPORT NO.
EPA-6QQ/1-78-Q2Q
4. TITLE AND SUBTITLE
Reviews of the Environmental Effects of Pollutants: VII
Lead
3. RECIPIENT'S ACCESSION NO.
6. REPORT DATE
Jlilv 197R
6. PERFORMING ORGANIZATION CODE
7. AUTHOR(S)
M. A. Bell, R. A. Ewing, G. A. Lutz, V. L. Holoman,
B. Paris, and H. H. Krause
8. PERFORMING ORGANIZATION REPORT NO.
I. PERFORMING ORGANIZATION NAME AND ADDRESS
Battelle-Columbus Laboratories
505 King Avenue
Columbus, Ohio 43201
10. PROGRAM ELEMENT NO.
LHA fill
LHA 616
, CONTRACT/
11. CONTRACT/GRANT NO.
68-03-2608
68-01-1837
12. SPONSORING AGENCY NAME AND ADDRESS
Health Effects Research Laboratory, Cin-OH
Office of Research and Development
U.S. Environmental Protection Agency
Cincinnati, Ohio 45268
13. TYPE OF REPORT AND PERIOD COVERED
Final. 5/75-3/78
14. SPONSORING AGENCY CODE
EPA/600/10
15. SUPPLEMENTARY NOTES
16. ABSTRACT
This document is a review of the scientific literature on the biological and environ-
mental effects of lead. Included in the review are a general summary and a compre-
hensive discussion of the following topics as related to lead and specific lead
compounds: physical and chemical properties; occurrence; synthesis and use; analytical
methodology; biological aspects in microorganisms, plants, wild and domestic animals,
and humans; distribution mobility, and persistence in the environment; and an assess-
ment of present and potential health and environmental hazards, including lead in
packaged foods. More than 950 references are cited. The document also contains an
evaluation of potential hazard resulting from lead contamination in the environment
and suggests current research needs.
17.
KEY WORDS AND DOCUMENT ANALYSIS
a.
DESCRIPTORS
b.lDENTIFIERS/OPEN ENDED TERMS C. COSATI Field/Group
*Pollutants
Toxicology, Carcinogenicity
Lead
Lead
06F
06T
8. DISTRIBUTION STATEMENT
Release to public
19. SECURITY CLASS (This Report)
Unclassified
21. NO. OF PAGES
476
20. SECURITY CLASS (Thispage)
Unclassified
22. PRICE
EPA Form 2220-1 (Rev. 4-77) PREVIOUS EDITION is OBSOLETE
S.kQ
U S GOVERNMENT PRINTING OFFICE 1979-640-079/235
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